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Sample records for fatal pulmonary edema

  1. Fatal re-expansion pulmonary edema in a young adult following tube thoracostomy for spontaneous pneumothorax

    PubMed Central

    Sharma, Sunil; Madan, Karan; Singh, Navneet

    2013-01-01

    Re-expansion pulmonary edema (RPE) is a rare but potentially fatal complication that can occur following rapid lung expansion while managing patients with pleural effusion or pneumothorax. In this case, fatal outcome occurred due to RPE in a previously healthy young adult male patient subsequent to tube thoracostomy for spontaneous pneumothorax. While managing patients with pneumothorax or large pleural effusions, precautions should be taken to avoid rapid re-expansion of the previously collapsed lung in order to reduce the probability of development of this complication. PMID:23744860

  2. Fatal re-expansion pulmonary edema in a young adult following tube thoracostomy for spontaneous pneumothorax.

    PubMed

    Sharma, Sunil; Madan, Karan; Singh, Navneet

    2013-06-05

    Re-expansion pulmonary edema (RPE) is a rare but potentially fatal complication that can occur following rapid lung expansion while managing patients with pleural effusion or pneumothorax. In this case, fatal outcome occurred due to RPE in a previously healthy young adult male patient subsequent to tube thoracostomy for spontaneous pneumothorax. While managing patients with pneumothorax or large pleural effusions, precautions should be taken to avoid rapid re-expansion of the previously collapsed lung in order to reduce the probability of development of this complication.

  3. Molecular Pathology of Pulmonary Edema in Forensic Autopsy Cases with Special Regard to Fatal Methamphetamine Intoxication.

    PubMed

    Du, Yu; Jin, Hong-Nian; Zhao, Rui; Zhao, Dong; Xue, Ye; Zhu, Bao-Li; Guan, Da-Wei; Xie, Xiao-Li; Wang, Qi

    2016-11-01

    Pulmonary edema is a common finding in fatal methamphetamine intoxication. However, the underlying mechanism remains poorly understood. This study investigated the molecular pathology of alveolar damage involving pulmonary edema in forensic autopsy cases. Seven candidate reference genes (RPL13A, YWHAZ, GUSB, SDHA, GAPDH, B2M, and ACTB) were evaluated in the lung by the geNorm module in qBase(plus) software. RPL13A, YWHAZ, and GUSB were identified as the most stable reference genes. Using these validated reference genes, intrapulmonary mRNA expressions of matrix metalloproteinases (MMPs), intercellular adhesion molecule-1 (ICAM-1), claudin-5 (CLDN-5), and aquaporins (AQPs) were examined. Relative mRNA quantification using TaqMan real-time PCR assay demonstrated higher expressions of all markers except for AQP-5 in fatal METH intoxication cases. These findings suggested alveolar damage and compensatory response in fatal METH intoxication cases. Systematic analysis of gene expressions using real-time qPCR is a useful tool in forensic death investigation.

  4. Pulmonary edema

    MedlinePlus

    ... Saunders; 2015:chap 23. Matthay MA, Martin TR, Murray JF. Pulmonary edema. In: Broaddus VC, Mason RJ, Ernst JD, et al, eds. Murray & Nadel's Textbook of Respiratory Medicine . 6th ed. Philadelphia, ...

  5. Fatal pulmonary edema due to nitric acid fume inhalation in three pulp-mill workers.

    PubMed

    Hajela, R; Janigan, D T; Landrigan, P L; Boudreau, S F; Sebastian, S

    1990-02-01

    Three young men died of rapidly progressive pulmonary edema of delayed onset after inhalation of fumes from an accidental nitric acid explosion. Electron microscopy revealed altered neutrophils and necrotic endothelial cells in alveolar capillaries. Immunohistochemistry showed small and large serum proteins, including immunoglobulin M, in the edema fluid and hyaline membranes. Increased permeability is a consequence of direct microvascular injury by inhaled nitrogen dioxide. However, our findings, implicating neutrophils and serum-derived mediators in the pathogenesis of the pulmonary edema, are consistent with recent proposals on their roles in the maintenance and/or progression of edema initiated by toxic inhalations.

  6. Molecular pathology of pulmonary edema in forensic autopsy cases with special regard to fatal hyperthermia and hypothermia.

    PubMed

    Wang, Qi; Ishikawa, Takaki; Michiue, Tomomi; Zhu, Bao-Li; Guan, Da-Wei; Maeda, Hitoshi

    2013-05-10

    Fatalities due to an extreme ambient temperature might present with poor or nonspecific pathologies; thus, the diagnosis of the cause of death in such cases is one of the most difficult tasks in forensic pathology. The present study investigated the molecular pathology of alveolar damage involving pulmonary edema with special regard to hyperthermia (heatstroke) and hypothermia (cold exposure) in forensic autopsy cases (total, n=122; within 48 h postmortem). Intrapulmonary mRNA and immunohistochemical expressions of matrix metalloproteinases (MMPs), intercellular adhesion molecule-1 (ICAM-1), claudin-5 (CLDN-5) and aquaporins (AQPs) were examined. Relative mRNA quantification using Taqman real-time PCR assay demonstrated higher expressions of all markers except for AQP-5 in fatal hyperthermia, and higher expression of MMP-9 in fatal hypothermia. Acute cardiac death, mechanical asphyxiation, fire fatality and intoxication did not present any characteristic findings. In immunostaining, only MMPs showed evident differences among the causes of death: MMP-9 was intensely positive in most cases of hyperthermia and hypothermia, but MMP-2 expression was evident only in hyperthermia. These findings suggest alveolar damage involving pulmonary edema, characteristic of fatal hyperthermia and hypothermia. Systematic analysis of gene expressions using real-time PCR might be a useful procedure in forensic death investigation.

  7. Fatal pulmonary edema in white-tailed deer (Odocoileus virginianus) associated with adenovirus infection.

    PubMed

    Sorden, S D; Woods, L W; Lehmkuhl, H D

    2000-07-01

    Sporadic sudden deaths in adult white-tailed deer occurred from November 1997 through August 1998 on an Iowa game farm. Three of the 4 deer necropsied had severe pulmonary edema, widespread mild lymphocytic vasculitis, and amphophilic intranuclear inclusion bodies in scattered endothelial cells in blood vessels in the lung and abdominal viscera. Immunohistochemistry with bovine adenovirus 5 antisera and transmission electron microscopy demonstrated adenoviral antigen and nucleocapsids, respectively, within endothelial cells. Adenovirus was isolated in cell culture from 1 of the affected deer. The isolate was neutralized by California black-tailed deer adenovirus antiserum. These findings indicate that adenovirus should be considered in the differential diagnosis of both black-tailed and white-tailed deer with pulmonary edema and/or hemorrhagic enteropathy.

  8. Reexpansion pulmonary edema.

    PubMed

    Tarver, R D; Broderick, L S; Conces, D J

    1996-01-01

    Reexpansion pulmonary edema is a rare complication attending the rapid reexpansion of a chronically collapsed lung, such as occurs after evacuation of a large amount of air or fluid from the pleural space. The condition usually appears unexpectedly and dramatically-immediately or within 1 h in 64% of patients and within 24 h in the remainder. The clinical manifestations are varied; they range from roentgenographic findings alone in asymptomatic patients to severe cardiorespiratory insufficiency. The radiographic evidence of reexpansion pulmonary edema is a unilateral alveolar filling pattern, seen within a few hours of reexpansion of the lung. The edema may progress for 24-48 h and persist for 4-5 days. Human data on the pathophysiology of reexpansion pulmonary edema derive from small series of patients, case reports, and reviews of the literature. On the other hand, a larger body of data exists on experimental reexpansion pulmonary edema in cats, monkeys, rabbits, sheep, and goats. This review examines the clinical and experimental evidence for reexpansion pulmonary edema. In addition, we detail the historical background, clinical setting, treatment, and outcome of reexpansion pulmonary edema.

  9. Lethal Factor, but Not Edema Factor, Is Required to Cause Fatal Anthrax in Cynomolgus Macaques after Pulmonary Spore Challenge

    PubMed Central

    Hutt, Julie A.; Lovchik, Julie A.; Drysdale, Melissa; Sherwood, Robert L.; Brasel, Trevor; Lipscomb, Mary F.; Lyons, C. Rick

    2015-01-01

    Inhalational anthrax is caused by inhalation of Bacillus anthracis spores. The ability of B. anthracis to cause anthrax is attributed to the plasmid-encoded A/B-type toxins, edema toxin (edema factor and protective antigen) and lethal toxin (lethal factor and protective antigen), and a poly-d-glutamic acid capsule. To better understand the contribution of these toxins to the disease pathophysiology in vivo, we used B. anthracis Ames strain and isogenic toxin deletion mutants derived from the Ames strain to examine the role of lethal toxin and edema toxin after pulmonary spore challenge of cynomolgus macaques. Lethal toxin, but not edema toxin, was required to induce sustained bacteremia and death after pulmonary challenge with spores delivered via bronchoscopy. After intravenous challenge with bacilli to model the systemic phase of infection, lethal toxin contributed to bacterial proliferation and subsequent host death to a greater extent than edema toxin. Deletion of protective antigen resulted in greater loss of virulence after intravenous challenge with bacilli than deletion of lethal toxin or edema toxin alone. These findings are consistent with the ability of anti–protective antigen antibodies to prevent anthrax and suggest that lethal factor is the dominant toxin that contributes to the escape of significant numbers of bacilli from the thoracic cavity to cause anthrax after inhalation challenge with spores. PMID:25285720

  10. Lethal factor, but not edema factor, is required to cause fatal anthrax in cynomolgus macaques after pulmonary spore challenge.

    PubMed

    Hutt, Julie A; Lovchik, Julie A; Drysdale, Melissa; Sherwood, Robert L; Brasel, Trevor; Lipscomb, Mary F; Lyons, C Rick

    2014-12-01

    Inhalational anthrax is caused by inhalation of Bacillus anthracis spores. The ability of B. anthracis to cause anthrax is attributed to the plasmid-encoded A/B-type toxins, edema toxin (edema factor and protective antigen) and lethal toxin (lethal factor and protective antigen), and a poly-d-glutamic acid capsule. To better understand the contribution of these toxins to the disease pathophysiology in vivo, we used B. anthracis Ames strain and isogenic toxin deletion mutants derived from the Ames strain to examine the role of lethal toxin and edema toxin after pulmonary spore challenge of cynomolgus macaques. Lethal toxin, but not edema toxin, was required to induce sustained bacteremia and death after pulmonary challenge with spores delivered via bronchoscopy. After intravenous challenge with bacilli to model the systemic phase of infection, lethal toxin contributed to bacterial proliferation and subsequent host death to a greater extent than edema toxin. Deletion of protective antigen resulted in greater loss of virulence after intravenous challenge with bacilli than deletion of lethal toxin or edema toxin alone. These findings are consistent with the ability of anti-protective antigen antibodies to prevent anthrax and suggest that lethal factor is the dominant toxin that contributes to the escape of significant numbers of bacilli from the thoracic cavity to cause anthrax after inhalation challenge with spores.

  11. Postobstructive pulmonary edema.

    PubMed

    Udeshi, Ashish; Cantie, Shawn Michael; Pierre, Edgar

    2010-09-01

    Postobstructive pulmonary edema (POPE; also known as negative pressure pulmonary edema) is a potentially life-threatening complication in which pulmonary edema occurs shortly after the relief of an upper airway obstruction. The incidence of POPE has been reported to be as high as 1 in 1000 general anesthetic cases and commonly presents as acute respiratory distress that requires immediate intervention. This review examines the 2 subclasses of POPE and describes the etiologic factors, pathophysiology, clinical manifestations, diagnostic criteria, and treatment strategies associated with each. The aim of this review was to equip clinicians with the knowledge base necessary to identify patients at increased risk for POPE and to expeditiously diagnose and treat this potentially catastrophic complication.

  12. Reperfusion pulmonary edema

    SciTech Connect

    Klausner, J.M.; Paterson, I.S.; Mannick, J.A.; Valeri, C.R.; Shepro, D.; Hechtman, H.B. )

    1989-02-17

    Reperfusion following lower-torso ischemia in humans leads to respiratory failure manifest by pulmonary hypertension, hypoxemia, and noncardiogenic pulmonary edema. The mechanism of injury has been studied in the sheep lung lymph preparation, where it has been demonstrated that the reperfusion resulting in pulmonary edema is due to an increase in microvascular permeability of the lung to protein. This respiratory failure caused by reperfusion appears to be an inflammatory reaction associated with intravascular release of the chemoattractants leukotriene B{sub 4} and thromboxane. Histological studies of the lung in experimental animals revealed significant accumulation of neutrophils but not platelets in alveolar capillaries. The authors conclude that thromboxane generated and released from the ischemic tissue is responsible for the transient pulmonary hypertension. Second, it is likely that the chemoattractants are responsible for leukosequestration, and third, neutrophils, oxygen-derived free radicals, and thromboxane moderate the altered lung permeability.

  13. An uncommon cause of acute pulmonary edema.

    PubMed

    Nepal, Santosh; Giri, Smith; Bhusal, Mohan; Siwakoti, Krishmita; Pathak, Ranjan

    2016-09-01

    Acute cardiogenic pulmonary edema secondary to catecholamine-induced cardiomyopathy is a very uncommon and fatal initial presentation of pheochromocytoma. However, with early clinical suspicion and aggressive management, the condition is reversible. This case report describes a patient who presented with hypertension, dyspnea, and cough with bloody streaks, and who recovered within 48 hours after appropriate treatment.

  14. Negative-Pressure Pulmonary Edema.

    PubMed

    Bhattacharya, Mallar; Kallet, Richard H; Ware, Lorraine B; Matthay, Michael A

    2016-10-01

    Negative-pressure pulmonary edema (NPPE) or postobstructive pulmonary edema is a well-described cause of acute respiratory failure that occurs after intense inspiratory effort against an obstructed airway, usually from upper airway infection, tumor, or laryngospasm. Patients with NPPE generate very negative airway pressures, which augment transvascular fluid filtration and precipitate interstitial and alveolar edema. Pulmonary edema fluid collected from most patients with NPPE has a low protein concentration, suggesting hydrostatic forces as the primary mechanism for the pathogenesis of NPPE. Supportive care should be directed at relieving the upper airway obstruction by endotracheal intubation or cricothyroidotomy, institution of lung-protective positive-pressure ventilation, and diuresis unless the patient is in shock. Resolution of the pulmonary edema is usually rapid, in part because alveolar fluid clearance mechanisms are intact. In this review, we discuss the clinical presentation, pathophysiology, and management of negative-pressure or postobstructive pulmonary edema.

  15. Clinical and radiologic features of pulmonary edema.

    PubMed

    Gluecker, T; Capasso, P; Schnyder, P; Gudinchet, F; Schaller, M D; Revelly, J P; Chiolero, R; Vock, P; Wicky, S

    1999-01-01

    Pulmonary edema may be classified as increased hydrostatic pressure edema, permeability edema with diffuse alveolar damage (DAD), permeability edema without DAD, or mixed edema. Pulmonary edema has variable manifestations. Postobstructive pulmonary edema typically manifests radiologically as septal lines, peribronchial cuffing, and, in more severe cases, central alveolar edema. Pulmonary edema with chronic pulmonary embolism manifests as sharply demarcated areas of increased ground-glass attenuation. Pulmonary edema with veno-occlusive disease manifests as large pulmonary arteries, diffuse interstitial edema with numerous Kerley lines, peribronchial cuffing, and a dilated right ventricle. Stage 1 near drowning pulmonary edema manifests as Kerley lines, peribronchial cuffing, and patchy, perihilar alveolar areas of airspace consolidation; stage 2 and 3 lesions are radiologically nonspecific. Pulmonary edema following administration of cytokines demonstrates bilateral, symmetric interstitial edema with thickened septal lines. High-altitude pulmonary edema usually manifests as central interstitial edema associated with peribronchial cuffing, ill-defined vessels, and patchy airspace consolidation. Neurogenic pulmonary edema manifests as bilateral, rather homogeneous airspace consolidations that predominate at the apices in about 50% of cases. Reperfusion pulmonary edema usually demonstrates heterogeneous airspace consolidations that predominate in the areas distal to the recanalized vessels. Postreduction pulmonary edema manifests as mild airspace consolidation involving the ipsilateral lung, whereas pulmonary edema due to air embolism initially demonstrates interstitial edema followed by bilateral, peripheral alveolar areas of increased opacity that predominate at the lung bases. Familiarity with the spectrum of radiologic findings in pulmonary edema from various causes will often help narrow the differential diagnosis.

  16. Reexpansion pulmonary edema in children

    PubMed Central

    Rodrigues, Antonio Lucas L.; Lopes, Carlos Eduardo; Romaneli, Mariana Tresoldi das N.; Fraga, Andrea de Melo A.; Pereira, Ricardo Mendes; Tresoldi, Antonia Teresinha

    2013-01-01

    OBJECTIVE To present a case of a patient with clinical and radiological features of reexpansion pulmonary edema, a rare and potentially fatal disease. CASE DESCRIPTION An 11-year-old boy presenting fever, clinical signs and radiological features of large pleural effusion initially treated as a parapneumonic process. Due to clinical deterioration he underwent tube thoracostomy, with evacuation of 3,000 mL of fluid; he shortly presented acute respiratory insufficiency and needed mechanical ventilation. He had an atypical evolution (extubated twice with no satisfactory response). Computerized tomography findings matched those of reexpansion edema. He recovered satisfactorily after intensive care, and pleural tuberculosis was diagnosed afterwards. COMMENTS Despite its rareness in the pediatric population (only five case reports gathered), the knowledge of this pathology and its prevention is very important, due to high mortality rates. It is recommended, among other measures, slow evacuation of the pleural effusion, not removing more than 1,500 mL of fluid at once. PMID:24142327

  17. Pulmonary Edema in Myasthenic Crisis

    PubMed Central

    Anand, Uttara Swati; Arulneyam, Jayanthi

    2013-01-01

    We report a previously asymptomatic 50-year-old lady who came with myasthenic crisis as initial presentation of myasthenia gravis. She developed pulmonary edema following intravenous immunoglobulin administration and had ischemic changes in ECG and left ventricular dysfunction on echocardiography. She improved with diuretics, dobutamine, and fluid restriction alone. This is the first report in English-language medical literature describing the association between myasthenic crisis and likely takotsubo cardiomyopathy-related pulmonary edema following intravenous immunoglobulin administration. PMID:24829832

  18. Sympathetic crashing acute pulmonary edema

    PubMed Central

    Agrawal, Naman; Kumar, Akshay; Aggarwal, Praveen; Jamshed, Nayer

    2016-01-01

    Sympathetic crashing acute pulmonary edema (SCAPE) is the extreme end of the spectrum of acute pulmonary edema. It is important to understand this disease as it is relatively common in the emergency department (ED) and has better outcomes when managed appropriately. The patients have an abrupt redistribution of fluid in the lungs, and when treated promptly and effectively, these patients will rapidly recover. Noninvasive ventilation and intravenous nitrates are the mainstay of treatment which should be started within minutes of the patient's arrival to the ED. Use of morphine and intravenous loop diuretics, although popular, has poor scientific evidence. PMID:28149030

  19. Sympathetic crashing acute pulmonary edema.

    PubMed

    Agrawal, Naman; Kumar, Akshay; Aggarwal, Praveen; Jamshed, Nayer

    2016-12-01

    Sympathetic crashing acute pulmonary edema (SCAPE) is the extreme end of the spectrum of acute pulmonary edema. It is important to understand this disease as it is relatively common in the emergency department (ED) and has better outcomes when managed appropriately. The patients have an abrupt redistribution of fluid in the lungs, and when treated promptly and effectively, these patients will rapidly recover. Noninvasive ventilation and intravenous nitrates are the mainstay of treatment which should be started within minutes of the patient's arrival to the ED. Use of morphine and intravenous loop diuretics, although popular, has poor scientific evidence.

  20. Late-onset pulmonary edema due to propofol.

    PubMed

    Inal, M T; Memis, D; Vatan, I; Cakir, U; Yildiz, B

    2008-08-01

    Pulmonary edema after the administration of propofol has rarely been reported. In this case report, we describe pulmonary edema due to the administration of propofol during a Cesarean section and while in the intensive care unit. The skin tests demonstrated strong positive weal and flare reactions to propofol. The patient was treated successfully with mechanical ventilatory support. This report emphasizes that this fatal complication may be seen with propofol and underlying mechanisms and therapeutic approach are discussed.

  1. Neurogenic Pulmonary Edema in Aneurysmal Subarachnoid Hemorrhage.

    PubMed

    Saracen, A; Kotwica, Z; Woźniak-Kosek, A; Kasprzak, P

    2016-01-01

    Neurogenic pulmonary edema (NPE) is observed in cerebral injuries and has an impact on treatment results, being a predictor of fatal prognosis. In this study we retrospectively reviewed medical records of 250 consecutive patients with aneurysmal subarachnoid hemorrhage (SAH) for the frequency and treatment results of NPE. The following factors were taken under consideration: clinical status, aneurysm location, presence of NPE, intracranial pressure (ICP), and mortality. All patients had plain- and angio-computer tomography performed. NPE developed most frequently in case of the aneurysm located in the anterior communicating artery. The patients with grades I-III of SAH, according to the World Federation of Neurosurgeons staging, were immediately operated on, while those with poor grades IV and V had only an ICP sensor's implantation procedure performed. A hundred and eighty five patients (74.4 %) were admitted with grades I to III and 32 patients (12.8 %) were with grade IV and V each. NPE was not observed in SAH patients with grade I to III, but it developed in nine patients with grade IV and 11 patients with grade V. Of the 20 patients with NPE, 19 died. Of the 44 poor grade patients (grades IV-V) without NPE, 20 died. All poor grade patients had elevated ICP in a range of 24-56 mmHg. The patients with NPE had a greater ICP than those without NPE. Gender and age had no influence on the occurrence of NPE. We conclude that the development of neurogenic pulmonary edema in SAH patients with poor grades is a fatal prognostic as it about doubles the death rate to almost hundred percent.

  2. Glyphosate Poisoning with Acute Pulmonary Edema

    PubMed Central

    Thakur, Darshana Sudip; Khot, Rajashree; Joshi, P. P.; Pandharipande, Madhuri; Nagpure, Keshav

    2014-01-01

    GlySH-surfactant herbicide (GlySH), one of the most commonly used herbicides worldwide, has been considered as minimally toxic to humans. However, clinical toxicologists occasionally encounter cases of severe systemic toxicity. The US Environmental Protection Agency (EPA) states that ‘GlySH’ is of relatively low oral and acute dermal toxicity. It does not have anticholinesterase effect and no organophosphate-like central nervous system (CNS) effects. The clinical features range from skin and throat irritation to hypotension and death. Severe GlySH-surfactant poisoning is manifested by gastroenteritis, respiratory disturbances, altered mental status, hypotension refractory to the treatment, renal failure, and shock.[1] GlySH intoxication has a case fatality rate 3.2–29.3%. Pulmonary toxicity and renal toxicity seem to be responsible for mortality. Metabolic acidosis, abnormal chest X-ray, arrhythmias, and elevated serum creatinine levels are useful prognostic factors for predicting GlySH mortality.[2] There is no antidote and the mainstay of treatment for systemic toxicity is decontamination and aggressive supportive therapy. We report a case of acute pulmonary edema, which is a rare but severe manifestation of oral GlySH poisoning, where patient survived with aggressive supportive therapy. PMID:25948977

  3. Independent ventilation and ECMO for severe unilateral pulmonary edema after SLT for primary pulmonary hypertension.

    PubMed

    Badesch, D B; Zamora, M R; Jones, S; Campbell, D W; Fullerton, D A

    1995-06-01

    Single lung transplantation (SLT) is now accepted therapy for selected cases of severe pulmonary hypertension. A recognized complication is the postoperative development of reperfusion edema in the graft, a potentially fatal cause of respiratory failure. Because reperfusion edema may be a reversible process, temporizing support measures can be life-saving. We report the case of a 48-year-old woman who developed severe reperfusion edema following right SLT for primary (unexplained) pulmonary hypertension. Extracorporeal membrane oxygenation (ECMO) was instituted. Independent lung ventilation was later begun and resulted in markedly improved oxygenation allowing withdrawal of ECMO. We conclude that reperfusion edema following SLT for pulmonary hypertension may be uniquely amenable to treatment with independent lung ventilation and ECMO if needed.

  4. Interstitial Pulmonary Edema Following Bromocarbamide Intoxication

    PubMed Central

    Sugihara, H.; Hagedorn, M.; Bōttcher, D.; Neuhof, H.; Mittermayer, Ch.

    1974-01-01

    Bromocarbamides are sleep-inducing drugs which can lead, in man, to intoxication and death due to respiratory failure. To prove whether hemodynamic factors or the changed endothelial permeability induce pulmonary edema, animal experiments were performed. The fine structural changes in pulmonary edema in rabbits were observed at 60, 90 and 120 minutes after oral administration. The major findings were a) large blebs between capillary endothelium and alveolar epithelium and b) interstitial edema of the vessel wall. The bleb contents were much less electron dense than the blood contents in the capillary. Colloidal carbon did not enter the bleb or the edematous interstitial tissue. Exogenous peroxidase uptake in pinocytotie vesicles increased in pathologic cases. The hemodynamic measurements in animal receiving artificial respiration which maintained the blood pO2 at a steady state showed similar blebs in the pulmonary vessels, indicating that anoxia is not the major cause of the vascular lesion. Moreover, pulmonary arterial pressure and pulmonary vascular resistance could be held in the normal range in artificially respirated animals under bromocarbamide intoxication. Thus, hemodynamic factors are not likely to play a pathogenetic role in bringing about pulmonary edema. The chief, early factor is the increased endothelial permeability due to increased cytoplasmic transport. From this a practical suggestion for treating patients with bromocarbamide intoxication is derived: the usual fluid replacement in shock patients should be handled with great care to avoid fluid overload of the lung. ImagesFig 1Fig 2Fig 3Fig 4Fig 5Fig 6 PMID:4835993

  5. [Negative pressure pulmonary edema: 3 case reports].

    PubMed

    Ortíz-Gómez, J R; Paja Martí, I; Sos-Ortigosa, F; Pérez-Cajaraville, J J; Arteche-Andrés, M A; Bengoechea, C; Lobo-Palanco, J; Ahmad-Al-Ghool, M

    2006-01-01

    Negative pressure pulmonary edema is a complication, described since 1977, caused by upper airway obstruction in both children and adults. Although its aetiopathogeny is multifactorial, especially outstanding is excessive negative intrathoracic pressure caused by the forced spontaneous inspiration of a patient against a closed glottis, that causes high arteriole and capillary fluid pressures that favor transudation into the alveolar space The resulting pulmonary edema can appear a few minutes after the obstruction of the airway or in a deferred way after several hours. The clinical manifestations are potentially serious, but normally respond well to treatment with supplemental oxygen, positive pressure mechanical ventilation and diuretics. Diagnostic suspicion is important for acting promptly. We report three clinical cases with acute negative pressure pulmonary edema.

  6. [Acute pulmonary edema as a nursing emergency].

    PubMed

    Navarro Aldana, M C

    2001-01-01

    The presence of Acute Pulmonary Edema represents a severe emergency condition that requires immediate and efficient treatment; otherwise, imminent death of the patient occurs. Therefore it is of utter importance to perform frequent reviews of the literature to keep up with the newest procedures to warrant the best quality nursing care of our patients. This article reviews the physiopathology, clinical manifestations, and medical treatment of the Acute Pulmonary Edema, emphasizing on the nursing aspects of the treatment and pointing out the need to treat the predisposing cardiac alteration as soon as possible.

  7. Pulmonary edema induced by intravenous ethchlorvynol.

    PubMed

    Conces, D J; Kreipke, D L; Tarver, R D

    1986-11-01

    The intravenous injection of ethchlorvynol is an uncommon cause of noncardiac pulmonary edema. Two cases of intravenous ethchlorvynol-induced pulmonary edema are presented. The patients fell asleep after injecting the liquid contents of Placydil capsules (ethchlorvynol) and awoke several hours later with severe dyspnea. Arterial blood gases demonstrated marked hypoxia. Chest radiographs revealed bilateral diffuse alveolar densities. The patients' symptoms and radiographic findings resolved after several days of supportive care. Changes in the lung caused by ethchlorvynol may be the result of direct effect of the drug on the lung.

  8. Diagnosis and management of cardiogenic pulmonary edema.

    PubMed

    Alwi, Idrus

    2010-07-01

    Acute cardiogenic pulmonary edema (ACPE) is a common cardiogenic emergency with a quite high in-hospital mortality rate. ACPE is defined as pulmonary edema with increased secondary hydrostatic capillary pressure due to elevated pulmonary venous pressure. Increased hydrostatic pressure may result from various causes including excessive administration of intravascular volume, obstruction of pulmonary venous outflow or secondary left ventricular failure due to left ventricular systolic or diastolic dysfunction. ACPE must be distinguished from pulmonary edema associated with injury of alveolar capillary membrane caused by various etiologies, i.e. direct pulmonary injury such as pneumonia and indirect pulmonary injury such as sepsis. Numerous clinical manifestations may differentiate ACPE and Non-ACPE. ACPE usually presents with a history of acute cardiac catastrophe. Physical examination reveals a low-flow state, S3 gallop, jugular venous distention and fine crepitant rales with auscultation. The diagnosis of pulmonary edema is made based on symptoms and clinical signs are found through history taking, physical examination, ECG, chest X-ray, echocardiography and laboratory tests including blood gas analysis and specific biomarkers. Medical treatment of ACPE has 3 main objectives, i.e.: (1) reduced venous return (preload reduction); (2) reduced resistance of systemic vascular (afterload reduction); and (3) inotropic support in some cases. Treatment that can be administered includes: vasodilator when there is normal or high BP, diuretics when there is volume overload or fluid retention, and inotropic drugs when there is hypotension or signs of organ hypoperfusion. Intubation and mechanical ventilation may be necessary to achieve adequate oxygenation.

  9. Acute nonhemodynamic pulmonary edema with nifedipine in primary pulmonary hypertension.

    PubMed

    Prigogine, T; Waterlot, Y; Gottignies, P; Verhoeven, A; Decroly, P

    1991-08-01

    A 34-year-old man with primary pulmonary hypertension developed acute nonhemodynamic pulmonary edema after a loading dose of nifedipine. Changes of the vascular permeability induced by the drug acting on the arteriolar wall of the capillary system could be an explanation.

  10. Negative pressure pulmonary edema in healthy cosmetic surgery patients.

    PubMed

    Dieu, Tam; Upjohn, Edward

    2003-01-01

    Anesthetic complications are uncommon in young and healthy patients undergoing cosmetic surgery. We report 2 cases of negative pressure pulmonary edema (NPPE) in young patients, 1 who underwent rhinoplasty and another who underwent augmentation mammaplasty and suction-assisted lipoplasty of the thighs and buttocks This rare and potentially fatal complication requires admission to an intensive-care unit and delayed discharge. Although cases of NPPE have been reported in the medical and anesthetic literature, NPPE in plastic surgery has never been reported previously.

  11. Acute Pulmonary Edema Associated With Propofol: An Unusual Complication

    PubMed Central

    Waheed, Mian Adnan; Oud, Lavi

    2014-01-01

    Propofol is frequently used in the emergency department to provide procedural sedation for patients undergoing various procedures and is considered to be safe when administered by trained personnel. Pulmonary edema after administration of propofol has rarely been reported. We report a case of a 23-year-old healthy male who developed acute cough, hemoptysis and hypoxia following administration of propofol for splinting of a foot fracture. Chest radiography showed bilateral patchy infiltrates. The patient was treated successfully with supportive care. This report emphasizes the importance of this potentially fatal propofol-associated complication and discusses possible underlying mechanisms and related literature. PMID:25493132

  12. The evolution of scuba divers pulmonary edema.

    PubMed

    Edmonds, Carl

    2016-01-01

    The evolution of scuba divers pulmonary edema is described. When discovered in 1981, it was believed to be a cold-induced response in a submerged, otherwise healthy, scuba diver. The clinical features are described and discussed, as are the demographics. An alleged prevalence of 1.1% was complicated by problematic statistics and an apparent increase in reported cases. Recurrences both while diving and swimming or snorkeling were common. More recent case reports and surveys are described, identifying predisposing factors and associations, including cardiac pathology. Stress cardiomyopathies, reversible myocardial disorder or Takotsubo cardiomyopathy, may complicate the presentation, especially in older females. Relevant cardiac investigations and autopsy findings are reviewed. Disease severity and potential lethality of scuba divers pulmonary edema became more apparent early this century, and these influence our current recommendations to survivors. First aid and treatment are also discussed.

  13. Influenza leaves a TRAIL to pulmonary edema.

    PubMed

    Brauer, Rena; Chen, Peter

    2016-04-01

    Influenza infection can cause acute respiratory distress syndrome (ARDS), leading to poor disease outcome with high mortality. One of the driving features in the pathogenesis of ARDS is the accumulation of fluid in the alveoli, which causes severe pulmonary edema and impaired oxygen uptake. In this issue of the JCI, Peteranderl and colleagues define a paracrine communication between macrophages and type II alveolar epithelial cells during influenza infection where IFNα induces macrophage secretion of TRAIL that causes endocytosis of Na,K-ATPase by the alveolar epithelium. This reduction of Na,K-ATPase expression decreases alveolar fluid clearance, which in turn leads to pulmonary edema. Inhibition of the TRAIL signaling pathway has been shown to improve lung injury after influenza infection, and future studies will be needed to determine if blocking this pathway is a viable option in the treatment of ARDS.

  14. Characterization of an epizootic of pulmonary edema in swine associated with fumonisin in corn screenings.

    PubMed

    Osweiler, G D; Ross, P F; Wilson, T M; Nelson, P E; Witte, S T; Carson, T L; Rice, L G; Nelson, H A

    1992-01-01

    In 1989, corn screenings were associated with acute interstitial pulmonary edema, hydrothorax, and death in swine. Attack rate was 5-50%, case fatality rate was 50-90%, and clinical course was 1-2 days. Screenings from farms with pigs affected with pulmonary edema contained 20-330 micrograms fumonisin B1 per gram. Screenings containing 92 micrograms fumonisin B1 per gram fed to weanling pigs caused pulmonary edema and death. Sterilized corn inoculated with Fusarium moniliforme and diluted 1:1 with clean corn contained fumonisin B1 (17 micrograms/g) and caused acute pulmonary edema when fed for 5 days. Survivors developed subacute hepatotoxicosis with individual hepatocellular necrosis, hepatomegalocytosis, and increased numbers of mitotic figures. Similar liver lesions occurred in pigs given fumonisin B1 intravenously at 0.8 mg/kg body weight for 14 days.

  15. Reexpansion pulmonary edema: review of pediatric cases.

    PubMed

    Kira, Shinichiro

    2014-03-01

    Reexpansion pulmonary edema (RPE) is an increased permeability pulmonary edema that usually occurs in the reexpanded lung after several days of lung collapse. This condition is recognized to occur more frequently in patients under the age of 40 years, but there has been no detailed analysis of reported pediatric cases of RPE to date. For this review, PubMed literature searches were performed using the following terms: 're(-)expansion pulmonary (o)edema' AND ('child' OR 'children' OR 'infant' OR 'boy' OR 'girl' OR 'adolescent'). The 22 pediatric cases of RPE identified were included in this review. RPE was reported in almost the entire pediatric age range, and as in adult cases, the severity ranged from subclinical to lethal. No specific treatment for RPE was identified, and treatment was administered according to the clinical features of each patient. Of the 22 reported cases, 10 occurred during the perioperative period, but were not related to any specific surgical procedures or anesthetic techniques, or to the duration of lung collapse. Pediatric anesthesiologists should be aware that pediatric RPE can occur after reexpansion of any collapsed lung and that some invasive therapies can be useful in severe cases. © 2013 John Wiley & Sons Ltd.

  16. High altitude pulmonary edema in mountain climbers.

    PubMed

    Korzeniewski, Krzysztof; Nitsch-Osuch, Aneta; Guzek, Aneta; Juszczak, Dariusz

    2015-04-01

    Every year thousands of ski, trekking or climbing fans travel to the mountains where they stay at the altitude of more than 2500-3000m above sea level or climb mountain peaks, often exceeding 7000-8000m. High mountain climbers are at a serious risk from the effects of adverse environmental conditions prevailing at higher elevations. They may experience health problems resulting from hypotension, hypoxia or exposure to low temperatures; the severity of those conditions is largely dependent on elevation, time of exposure as well as the rate of ascent and descent. A disease which poses a direct threat to the lives of mountain climbers is high altitude pulmonary edema (HAPE). It is a non-cardiogenic pulmonary edema which typically occurs in rapidly climbing unacclimatized lowlanders usually within 2-4 days of ascent above 2500-3000m. It is the most common cause of death resulting from the exposure to high altitude. The risk of HAPE rises with increased altitude and faster ascent. HAPE incidence ranges from an estimated 0.01% to 15.5%. Climbers with a previous history of HAPE, who ascent rapidly above 4500m have a 60% chance of illness recurrence. The aim of this article was to present the relevant details concerning epidemiology, pathophysiology, clinical symptoms, prevention, and treatment of high altitude pulmonary edema among climbers in the mountain environment. Copyright © 2014 Elsevier B.V. All rights reserved.

  17. Use of the Gamow Bag by EMT-basic park rangers for treatment of high-altitude pulmonary edema and high-altitude cerebral edema.

    PubMed

    Freeman, Kimberly; Shalit, Marc; Stroh, Geoffrey

    2004-01-01

    As part of an emergency medical system protocol, national park service rangers certified at the level of an emergency medical technician-basic (EMT-B) are taught to recognize and treat high-altitude pulmonary edema and high-altitude cerebral edema. In Sequoia and Kings Canyon National Parks, this is done with the assistance of physician on-line medical control as a backup. High-altitude pulmonary edema and high-altitude cerebral edema are both potentially fatal altitude illnesses that can be particularly problematic in the backcountry, where evacuation may be delayed. We report a case of high-altitude pulmonary edema and high-altitude cerebral edema occurring at moderate altitude that was successfully treated by park rangers with the Gamow Bag.

  18. [Pertussis infection and fatal pulmonary hypertension].

    PubMed

    Menif, K; Bouziri, A; Khaldi, A; Hamdi, A; Belhadj, S; Benjaballah, N

    2010-11-01

    Pertussis is ranked among the leading causes of childhood mortality. The most catastrophic clinical complication of pertussis in infants, intractable pulmonary hypertension with shock, is not very well known. We describe the clinical course of a fatal case of severe pertussis complicated by refractory pulmonary hypertension and shock in a 2-month-old infant. Copyright © 2010. Published by Elsevier SAS.

  19. Drug-induced pulmonary edema and acute respiratory distress syndrome.

    PubMed

    Lee-Chiong, Teofilo; Matthay, Richard A

    2004-03-01

    Noncardiogenic pulmonary edema, and, to a lesser extent, acute respiratory distress syndrome (ARDS), are common clinical manifestations of drug-induced lung diseases. Clinical features and radiographic appearances are generally indistinguishable from other causes of pulmonary edema and ARDS. Typical manifestations include dyspnea, chest discomfort, tachypnea, and hypoxemia. Chest radiographs commonly reveal interstitial and alveolar filling infiltrates. Unlike pulmonary edema that is due to congestive heart failure, cardiomegaly and pulmonary vascular redistribution are generally absent in cases that are drug-related. Rare cases of drug-induced myocarditis with heart failure and pulmonary edema have been described. Results from laboratory evaluation and respiratory function tests are nonspecific.

  20. Pulmonary tissue volume in dogs during pulmonary edema.

    PubMed

    Peterson, B T; Petrini, M F; Hyde, R W; Schreiner, B F

    1978-05-01

    Pulmonary tissue volume (Vt) and pulmonary capillary blood flow (Qc) were measured in anesthetized dogs by analyzing end-expiratory concentrations of dimethyl ether (DME), acetylene (C2H2), and sulfur hexafluoride during a 30-s rebreathing maneuver. Vt was compared to the postmortem lung weight of control dogs and dogs with hemodynamic and nonhemodynamic (alloxan) pulmonary edema. Qc was compared to the cardiac output measured by dye dilution. A 100-ml increase in alveolar volume (VA) in the range of 1-2 liters resulted in a 9 +/- 3 ml increase in Vt. Vt measured at a VA of 1.9 liters measures 114 +/- 18% of the postmortem lung weight in 20 control dogs and in 6 dogs with moderate edema (lung weight < 250% of predicted). Vt measured only 53 +/- 14% of the lung weight in 11 dogs with more severe edema. DME and C2H2 gave the smae mean values of Vt, but the reproducibility of a series of 3-7 measurements was greater with DME (coefficient of variation was 5% with DME and 8% C2H2). Qc measured 96 +/ 15% of the cardiac output during the rebreathing maneuver, but the maneuver caused a 4-40% fall in the cardiac output. These data show that Vt determined by rebreathing DME is between 86% and 135% of the lung weight in dogs with pulmonary edema until the lung weight is greater than 250% of the predicted value.

  1. [Pulmonary edemas due to acute heroin poisoning].

    PubMed

    Francois, G; Faizende, J; Reboul, J

    1975-01-01

    Their frequency is estimated with difficulty, although on autopsy pulmonary edema is found almost routinely. It is a major complication of overdoses (48 p. 100 of severe intoxications). Their formation can be suspected, when after the first phase of respiratory depressions, with coma, myosis, and a variable latent period, a second attack of respiratory insufficiency occurs with tachypnea, and cyanosis. The chest X-ray shows diffuse alveolar infiltration, sparing the apices. The heart being generally of normal size. Rapid disappearance of this infiltrate (24 to 48 hours) enables the elimination of two diagnoses: pneumonia due to inhalation of gastric fluid, an infectious pneumonia. Their pathogenesis remains very debatable: - in the majority of cases abrupt L.V.F. can be eliminated: -on the other hand it could be an allergic accident of the anaphylactic type, or local liberation of histamine, or a local toxic action on the pulmonary capillaries; - hypoxia, secondary to respiratory depression, could lead to pulmonary edema, by the same mechanism as at altitude; - finally, owing to the central neurological disorders a neurogenic theory can be put forward. Their treatment is essentially a combination of Nalorphine with oxygen therapy (by mask, or if necessary by assisted, controlled ventilation) with prevention of inhalation of gastric fluid (gastric emptying) or curative treatment of possible aspiration by antibiotics, and cortico-steroids. Diuretics can be useful, as well as cardiotonics.

  2. New Compton densitometer for measuring pulmonary edema

    SciTech Connect

    Loo, B.W.; Goulding, F.S.; Simon, D.S.

    1985-10-01

    Pulmonary edema is the pathological increase of extravascular lung water found most often in patients with congestive heart failure and other critically ill patients who suffer from intravenous fluid overload. A non-invasive lung density monitor that is accurate, easily portable, safe and inexpensive is needed for clinical evaluation of pulmonary edema. Other researchers who have employed Compton scattering techniques generally used systems of extended size and detectors with poor energy resolution. This has resulted in significant systematic biases from multiply-scattered photons and larger errors in counting statistics at a given radiation dose to the patient. We are proposing a patented approach in which only backscattered photons are measured with a high-resolution HPGe detector in a compact system geometry. By proper design and a unique data extraction scheme, effects of the variable chest wall on lung density measurements are minimized. Preliminary test results indicate that with a radioactive source of under 30 GBq, it should be possible to make an accurate lung density measurement in one minute, with a risk of radiation exposure to the patient a thousand times smaller than that from a typical chest x-ray. The ability to make safe, frequent lung density measurements could be very helpful for monitoring the course of P.E. at the hospital bedside or outpatient clinics, and for evaluating the efficacy of therapy in clinical research. 6 refs., 5 figs.

  3. Pheochromocytoma-induced acute pulmonary edema and reversible catecholamine cardiomyopathy mimicking acute myocardial infarction.

    PubMed

    Pineda Pompa, Luis Ramón; Barrera-Ramírez, Carlos Felipe; Martínez-Valdez, Jesús; Rodríguez, Pedro Domínguez; Guzmán, Carlos E

    2004-04-01

    Acute noncardiogenic pulmonary edema and catecholamine-induced cardiomyopathy as the first presentations of pheochromocytoma are uncommon events, but usually rapidly fatal. A 36-year-old man presented acute pulmonary edema in a setting of hypertensive emergency after arthroscopy, later developing catecholamine-induced cardiotoxicity mimicking an acute myocardial infarction, with elevation of cardiac damage markers, normal coronary arteries, and with full recovery from electrical abnormalities. Magnetic resonance imaging revealed a right adrenal mass. Elevated levels of catecholamines and metanephrines, and a positive 131I-metaiodobenzylguanidine scan confirmed a pheochromocytoma. Once the patient had been hemodynamically stabilized, he was successfully operated.

  4. [A rare form of acute pulmonary edema: case report].

    PubMed

    Ricardo, José; Anaya, Maria José; Barbosa, Mário; André, Nelson; Magno, Pedro; Morais, José; Proença, Gonçalo; Rabaçal, Carlos; Gil, Victor

    2011-10-01

    We report the case of a 21-year-old man who underwent appendectomy under general anesthesia and developed acute pulmonary edema immediately after extubation. We then review the literature, focusing on the pathophysiology and the most important aspects of diagnosis and treatment of post-extubation pulmonary edema.

  5. [Formation of hemodynamic pulmonary edema in irradiated bodies].

    PubMed

    Kurygin, G V; Kopylov, V N; Girs, E F; Chizhov, P A

    1978-09-01

    Experiments on albino rats demonstrated that high doses of ionising radiation producing pronounced leukopenia increased the animal resistance to pulmonary edema under the effect of adrenaline. This effect was especially manifest on the 4th day of irradiation. Relatively low doses (up to 100 r) as well as separate irradiation of the head, chest, or the abdomen induced pulmonary edema.

  6. Noncardiac Pulmonary Edema induced by Sitagliptin Treatment

    PubMed Central

    Belice, Tahir; Yuce, Suleyman; Kizilkaya, Bayram; Kurt, Aysel; Cure, Erkan

    2014-01-01

    A 74-year-old male patient with type 2 diabetes mellitus admitted to the emergency department with the complaints of progressive breathlessness, dry cough, and swollen lower extremities. Our patient had type 2 diabetes mellitus and hypertension for 3 years. His HbA1c was not within the target range so sitagliptin was added to on-going therapy. After 1 week of starting sitagliptin therapy, even though the patient had not heart failure he applied to the emergency department with a complaint of dyspnea. The cardiovascular safety and efficacy of many anti-hyperglycemic agents such as sitagliptin, saxagliptin are unclear. Our case has shown that dipeptidyl peptidase 4 inhibitors may cause pulmonary edema. Hence, it should be used with cautious, especially in patients with heart failure. PMID:25657966

  7. Serotonin syndrome presenting as pulmonary edema

    PubMed Central

    Shah, Nilima Deepak; Jain, Ajay B.

    2016-01-01

    Serotonin syndrome (SS) is a potentially life-threatening condition resulting from excessive central and peripheral serotonergic activity. Clinically, it is a triad of mental-status changes, neuromuscular abnormalities, and autonomic disturbances. It can be caused by intentional self-poisoning, overdose, or inadvertent drug interactions. We report the case of a 58-year-old male with type 2 diabetes mellitus and obsessive compulsive disorder who developed pulmonary edema as a possible complication of SS. SS was caused by a combination of three specific serotonin re-uptake inhibitors (fluoxetine, fluvoxamine, and sertraline), linezolid, and fentanyl. The hospital course was further complicated by difficult weaning from the ventilator. SS was identified and successfully treated with cyproheptadine and lorazepam. The case highlights the importance of effective consultation-liaison and prompt recognition of SS as the presentation may be complex in the presence of co-morbid medical illness. PMID:26997733

  8. Noncardiac Pulmonary Edema induced by Sitagliptin Treatment.

    PubMed

    Belice, Tahir; Yuce, Suleyman; Kizilkaya, Bayram; Kurt, Aysel; Cure, Erkan

    2014-01-01

    A 74-year-old male patient with type 2 diabetes mellitus admitted to the emergency department with the complaints of progressive breathlessness, dry cough, and swollen lower extremities. Our patient had type 2 diabetes mellitus and hypertension for 3 years. His HbA1c was not within the target range so sitagliptin was added to on-going therapy. After 1 week of starting sitagliptin therapy, even though the patient had not heart failure he applied to the emergency department with a complaint of dyspnea. The cardiovascular safety and efficacy of many anti-hyperglycemic agents such as sitagliptin, saxagliptin are unclear. Our case has shown that dipeptidyl peptidase 4 inhibitors may cause pulmonary edema. Hence, it should be used with cautious, especially in patients with heart failure.

  9. Pheochromocytoma presenting with pulmonary edema and hyperamylasemia.

    PubMed Central

    Munk, Z.; Tolis, G.; Jones, W.; Fallen, E.; McLean, P.

    1977-01-01

    A 28-year-old woman was admitted to hospital with acute pulmonary edema, mild abdominal discomfort and hyperamylasemia. From the 2nd hospital day hypertensive episodes occurred daily. The furosemide screening test for renovascular hypertension revealed elevated plasma renin activity (PRA) but an intravenous pyelogram revealed a right suprarenal mass and no evidence of renovascular compression. Elevated values of plasma and urinary catecholamines indicated a pheochromocytoma, and a single chromaffin tumour was resected. It is important to monitor left ventricular filling pressure during operative removal of a pheochromocytoma. Postoperatively the patient had normal blood pressure and PRA. Decreased urinary amylase clearance and abnormal pancreatic and salivary amylase isoenzymes were found. Images FIG. 1 FIG. 4 PMID:844016

  10. [Cardiogenic and non cardiogenic pulmonary edema: pathomechanisms and causes].

    PubMed

    Glaus, T; Schellenberg, S; Lang, J

    2010-07-01

    The development of pulmonary edema is divided in cardiogenic and non-cardiogenic. Cardiogenic edema pathogenically is caused by elevated hydrostatic pressure in the pulmonary capillaries due to left sided congestive heart failure. Non-cardiogenic pulmonary edema is categorized depending on the underlying pathogenesis in low-alveolar pressure, elevated permeability or neurogenic edema. Some important examples of causes are upper airway obstruction like in laryngeal paralysis or strangulation for low alveolar pressure, leptospirosis and ARDS for elevated permeability, and epilepsy, brain trauma and electrocution for neurogenic edema. The differentiation between cardiogenic versus non-cardiogenic genesis is not always straightforward, but most relevant, because treatment markedly differs between the two. Of further importance is the identification of the specific underlying cause in non-cardiogenic edema, not only for therapeutic but particularly for prognostic reasons. Depending on the cause the prognosis ranges from very poor to good chance of complete recovery.

  11. Diagnosing pulmonary edema: lung ultrasound versus chest radiography.

    PubMed

    Martindale, Jennifer L; Noble, Vicki E; Liteplo, Andrew

    2013-10-01

    Diagnosing the underlying cause of acute dyspnea can be challenging. Lung ultrasound may help to identify pulmonary edema as a possible cause. To evaluate the ability of residents to recognize pulmonary edema on lung ultrasound using chest radiographs as a comparison standard. This is a prospective, blinded, observational study of a convenience sample of resident physicians in the Departments of Emergency Medicine (EM), Internal Medicine (IM), and Radiology. Residents were given a tutorial on interpreting pulmonary edema on both chest radiograph and lung ultrasound. They were then shown both ultrasounds and chest radiographs from 20 patients who had presented to the emergency department with dyspnea, 10 with a primary diagnosis of pulmonary edema, and 10 with alternative diagnoses. Cohen's κ values were calculated to describe the strength of the correlation between resident and gold standard interpretations. Participants included 20 EM, 20 IM, and 20 Radiology residents. The overall agreement with gold standard interpretation of pulmonary edema on lung ultrasound (74%, κ = 0.51, 95% confidence interval 0.46-0.55) was superior to chest radiographs (58%, κ = 0.25, 95% confidence interval 0.20-0.30) (P < 0.0001). EM residents interpreted lung ultrasounds more accurately than IM residents. Radiology residents interpreted chest radiographs more accurately than did EM and IM residents. Residents were able to more accurately identify pulmonary edema with lung ultrasound than with chest radiograph. Physicians with minimal exposure to lung ultrasound may be able to correctly recognize pulmonary edema on lung ultrasound.

  12. Exercise-Induced Pulmonary Edema in a Triathlon

    PubMed Central

    Yamanashi, Hirotomo; Koyamatsu, Jun; Nobuyoshi, Masaharu; Murase, Kunihiko; Maeda, Takahiro

    2015-01-01

    Introduction. Family physicians have more opportunities to attend athletic competitions as medical staff at first-aid centers because of the increasing popularity of endurance sports. Case. A 38-year-old man who participated in a triathlon race experienced difficulty in breathing after swimming and was moved to a first-aid center. His initial oxygen saturation was 82% and a thoracic computed tomography scan showed bilateral ground glass opacity in the peripheral lungs. His diagnosis was noncardiogenic pulmonary edema associated with exercise or swimming: exercise-induced pulmonary edema (EIPE) or swimming-induced pulmonary edema (SIPE). Treatment with furosemide and corticosteroid relieved his symptoms of pulmonary edema. Discussion. Noncardiogenic pulmonary edema associated with endurance sports is not common, but knowledge about EIPE/SIPE or neurogenic pulmonary edema associated with hyponatremia, which is called Ayus-Arieff syndrome, is crucial. Knowledge and caution for possible risk factors, such as exposure to cold water or overhydration, are essential for both medical staff and endurance athletes. Conclusion. To determine the presence of pulmonary edema associated with strenuous exercise, oxygen saturation should be used as a screening tool at a first-aid center. To avoid risks for EIPE/SIPE, knowledge about these diseases is essential for medical staff and for athletes who perform extreme exercise. PMID:26229538

  13. Unilateral pulmonary edema during laparoscopic resection of adrenal tumor

    PubMed Central

    Prakash, Smita; Nayar, Pavan; Virmani, Pooja; Bansal, Shipra; Pawar, Mridula

    2015-01-01

    Despite technological, therapeutic and diagnostic advancements, surgical intervention in pheochromocytoma may result in a life-threatening situation. We report a patient who developed unilateral pulmonary edema during laparoscopic resection of adrenal tumor. PMID:26330724

  14. Reexpansion pulmonary edema after chest drainage for pneumothorax: A case report and literature overview

    PubMed Central

    Verhagen, M.; van Buijtenen, J.M.; Geeraedts, L.M.G.

    2014-01-01

    Background Reexpansion pulmonary edema (RPE) is a rare complication that may occur after treatment of lung collapse caused by pneumothorax, atelectasis or pleural effusion and can be fatal in 20% of cases. The pathogenesis of RPE is probably related to histological changes of the lung parenchyma and reperfusion-damage by free radicals leading to an increased vascular permeability. RPE is often self-limiting and treatment is supportive. Case report A 76-year-old patient was treated by intercostal drainage for a traumatic pneumothorax. Shortly afterwards he developed reexpansion pulmonary edema and was transferred to the intensive care unit for ventilatory support. Gradually, the edema and dyspnea diminished and the patient could be discharged in good clinical condition. Conclusion RPE is characterized by rapidly progressive respiratory failure and tachycardia after intercostal chest drainage. Early recognition of signs and symptoms of RPE is important to initiate early management and allow for a favorable outcome. PMID:26029567

  15. Diagnosis, Prevention and Management of Postoperative Pulmonary Edema

    PubMed Central

    Bajwa, SJ Singh; Kulshrestha, A

    2012-01-01

    Postoperative pulmonary edema is a well-known postoperative complication caused as a result of numerous etiological factors which can be easily detected by a careful surveillance during postoperative period. However, there are no preoperative and intraoperative criteria which can successfully establish the possibilities for development of postoperative pulmonary edema. The aims were to review the possible etiologic and diagnostic challenges in timely detection of postoperative pulmonary edema and to discuss the various management strategies for prevention of this postoperative complication so as to decrease morbidity and mortality. The various search engines for preparation of this manuscript were used which included Entrez (including Pubmed and Pubmed Central), NIH.gov, Medknow.com, Medscape.com, WebMD.com, Scopus, Science Direct, MedHelp.org, yahoo.com and google.com. Manual search was carried out and various text books and journals of anesthesia and critical care medicine were also searched. From the information gathered, it was observed that postoperative cardiogenic pulmonary edema in patients with serious cardiovascular diseases is most common followed by noncardiogenic pulmonary edema which can be due to fluid overload in the postoperative period or it can be negative pressure pulmonary edema (NPPE). NPPE is an important clinical entity in immediate post-extubation period and occurs due to acute upper airway obstruction and creation of acute negative intrathoracic pressure. NPPE carries a good prognosis if promptly diagnosed and appropriately treated with or without mechanical ventilation. PMID:23439791

  16. Lung ultrasound for monitoring cardiogenic pulmonary edema.

    PubMed

    Cortellaro, Francesca; Ceriani, Elisa; Spinelli, Monica; Campanella, Carlo; Bossi, Ilaria; Coen, Daniele; Casazza, Giovanni; Cogliati, Chiara

    2016-07-29

    Several studies address the accuracy of lung ultrasound (LUS) in the diagnosis of cardiogenic pulmonary edema (CPE) evaluating the interstitial syndrome, which is characterized by multiple and diffuse vertical artifacts (B-lines), and correlates with extravascular lung water. We studied the potential role of LUS in monitoring CPE response to therapy, by evaluating the clearance of interstitial syndrome within the first 24 h after Emergency Department (ED) admission. LUS was performed at arrival (T0), after 3 (T3) and 24 (T24) hours. Eleven regions were evaluated in the antero-lateral chest; the B-lines burden was estimated in each region (0 = no B-lines, 1 = multiple B-lines, 2 = confluent B-lines/white lung) and a mean score (B-Score, range 0-2) was calculated. Patients received conventional CPE treatment. Blood chemistry, vital signs, blood gas analysis, diuresis at T0, T3, T24 were also recorded. A complete echocardiography was obtained during hospitalization. Forty-one patients were enrolled. Respiratory and hemodynamic parameters improved in all patients between T0 and T3 and between T3 and T24. Mean B-score significantly decreased at T3 (from 1.59 ± 0.40 to 0.73 ± 0.44, P < 0.001) and between T3 and T 24 (from 0.73 ± 0.44 to 0.38 ± 0.33, P < 0.001). B-score was higher in the lower pulmonary regions at any time. At final evaluation (T24) 75 % of apical and only 38 % of basal regions were cleared. LUS allows one to assess the clearance of interstitial syndrome and its distribution in the early hours of treatment of CPE, thus representing a possible tool to guide therapy titration.

  17. Neurogenic pulmonary edema following Cryptococcal meningoencephalitis associated with HIV infection.

    PubMed

    Kondo, Reiichiro; Sugita, Yasuo; Arakawa, Kenji; Nakashima, Shinji; Umeno, Yumi; Todoroki, Keita; Yoshida, Tomoko; Takase, Yorihiko; Kage, Masayoshi; Oshima, Koichi; Yano, Hirohisa

    2015-08-01

    Neurogenic pulmonary edema (NPE) is a clinical syndrome characterized by the acute onset of pulmonary edema following a significant central nervous system insult. Only a few cases of NPE after Cryptococcal meningitis have been reported. We report a case of NPE following Cryptococcal meningoencephalitis. A 40-year-old man with no medical history was hospitalized for disturbance of consciousness. Blood glucose level was 124 mg/dL. Non-contrast head computed tomography showed no abnormalities. Lumbar puncture revealed a pressure of over 300 mm H2 O and cerebrospinal fluid (CSF) confirmed a white blood cell count of 65/mm(3) . The CSF glucose level was 0 mg/dL. The patient was empirically started on treatment for presumptive bacterial and viral meningitis. Four days after, the patient died in a sudden severe pulmonary edema. Autopsy was performed. We found at autopsy a brain edema with small hemorrhage of the right basal ganglia, severe pulmonary edema and mild cardiomegaly. Histologically, dilated Virchow-Robin spaces, crowded with Cryptococci were observed. In the right basal ganglia, Virchow-Robin spaces were destroyed with hemorrhage and Cryptococci spread to parenchyma of the brain. No inflammatory reaction of the lung was seen. Finally, acute pulmonary edema in this case was diagnosed as NPE following Cryptococcal meningoencephalitis. After autopsy, we found that he was positive for serum antibodies to human immunodeficiency virus. © 2015 Japanese Society of Neuropathology.

  18. Fatal pulmonary infection due to Mycobacterium fortuitum.

    PubMed Central

    Lessing, M P; Walker, M M

    1993-01-01

    Environmental (atypical, opportunist, other) mycobacteria were first isolated nearly a century ago. The classification of these "other than Mycobacterium tuberculosis" organisms was initially chaotic until Runyon proposed a scheme of four groups in 1959. Mycobacterium fortuitum is a member of group IV: Rapid growers. These ubiquitous terrestrial and aquatic forms contaminate water supplies, reagents, and clinical samples. They may colonise the respiratory systems of patients whose local defence mechanisms have been impaired or those with congenital and acquired immune defects. They can also cause disease in immunocompetent individuals. There have been fewer than 20 published cases of pulmonary infection caused by M fortuitum. A further case is reported of fatal pulmonary infection in an elderly patient with long standing chronic obstructive airways disease (COAD). He had left upper zone shadowing on chest radiography and lung abscesses at post mortem examination yielded only M fortuitum. PMID:8463423

  19. [Acute pulmonary edema secondary to acute upper airway obstruction].

    PubMed

    Sánchez-Ortega, J L; Carpintero-Moreno, F; Olivares-López, A; Borrás-Rubio, E; Alvarez-López, M J; García-Izquierdo, A

    1992-01-01

    We report a 72 years old woman with mild arterial hypertension and no other pathological history who presented an acute pulmonary edema due to acute obstruction of the upper airway secondary to vocal chord paralysis developing during the immediate postoperative phase of thyroidectomy. The acute pulmonary edema resolved after application of tracheal reintubation, mechanical ventilation controlled with end expiratory positive pressure, diuretics, morphine, and liquid restriction. We discuss the possible etiopathogenic possibilities of this infrequent clinical picture and we suggest that all patients who suffered and acute obstruction of the upper airways require a careful clinical surveillance in order to prevent the development of the pulmonary syndrome.

  20. Three plasma metabolite signatures for diagnosing high altitude pulmonary edema

    NASA Astrophysics Data System (ADS)

    Guo, Li; Tan, Guangguo; Liu, Ping; Li, Huijie; Tang, Lulu; Huang, Lan; Ren, Qian

    2015-10-01

    High-altitude pulmonary edema (HAPE) is a potentially fatal condition, occurring at altitudes greater than 3,000 m and affecting rapidly ascending, non-acclimatized healthy individuals. However, the lack of biomarkers for this disease still constitutes a bottleneck in the clinical diagnosis. Here, ultra-high performance liquid chromatography coupled with Q-TOF mass spectrometry was applied to study plasma metabolite profiling from 57 HAPE and 57 control subjects. 14 differential plasma metabolites responsible for the discrimination between the two groups from discovery set (35 HAPE subjects and 35 healthy controls) were identified. Furthermore, 3 of the 14 metabolites (C8-ceramide, sphingosine and glutamine) were selected as candidate diagnostic biomarkers for HAPE using metabolic pathway impact analysis. The feasibility of using the combination of these three biomarkers for HAPE was evaluated, where the area under the receiver operating characteristic curve (AUC) was 0.981 and 0.942 in the discovery set and the validation set (22 HAPE subjects and 22 healthy controls), respectively. Taken together, these results suggested that this composite plasma metabolite signature may be used in HAPE diagnosis, especially after further investigation and verification with larger samples.

  1. Three plasma metabolite signatures for diagnosing high altitude pulmonary edema

    PubMed Central

    Guo, Li; Tan, Guangguo; Liu, Ping; Li, Huijie; Tang, Lulu; Huang, Lan; Ren, Qian

    2015-01-01

    High-altitude pulmonary edema (HAPE) is a potentially fatal condition, occurring at altitudes greater than 3,000 m and affecting rapidly ascending, non-acclimatized healthy individuals. However, the lack of biomarkers for this disease still constitutes a bottleneck in the clinical diagnosis. Here, ultra-high performance liquid chromatography coupled with Q-TOF mass spectrometry was applied to study plasma metabolite profiling from 57 HAPE and 57 control subjects. 14 differential plasma metabolites responsible for the discrimination between the two groups from discovery set (35 HAPE subjects and 35 healthy controls) were identified. Furthermore, 3 of the 14 metabolites (C8-ceramide, sphingosine and glutamine) were selected as candidate diagnostic biomarkers for HAPE using metabolic pathway impact analysis. The feasibility of using the combination of these three biomarkers for HAPE was evaluated, where the area under the receiver operating characteristic curve (AUC) was 0.981 and 0.942 in the discovery set and the validation set (22 HAPE subjects and 22 healthy controls), respectively. Taken together, these results suggested that this composite plasma metabolite signature may be used in HAPE diagnosis, especially after further investigation and verification with larger samples. PMID:26459926

  2. The pathogenesis of pulmonary edema in acute pancreatitis.

    PubMed Central

    Warshaw, A L; Lesser, P B; Rie, M; Cullen, D J

    1975-01-01

    Acute pulmonary edema appeared 3 or more days after the onset of acute pancreatitis in 7 patients, an approximate incidence of 8%. The severity of pancreatitis in these patients was characterized by massive requirements for intravenous colloid and by marked hypocalcemia. In addition, at least 5 of the 7 patients had very high serum levels of triglycerides at the time of hospital admission. Hemodynamic studies during pulmonary edema showed normal central venous pressure, pulmonary artery pressure, pulmonary capillary wedge pressure, and pulmonary vascular resistance. Cardiac index was appropriately elevated. Respiratory treatment, consisting of endotracheal intubation and controlled ventilation with PEEP, was successful in allowing reversal of the pulmonary injury and recovery of respiratory function within 1-2 weeks in all cases. Two patients died later from pancreatic abscesses. The findings indicate that a distinct form of pulmonary injury may occur in acute pancreatitis, characterized by loss of integrity of the alveolar-capilllary membrane, leading to pulmonary edema. The mechanism of injury is not known but may be caused by circulating free fatty acids, phospholipase A, or vasoactive substances. The pulmonary membrane lesion appears to heal during the period of intensive respiratory support. Images Fig. 1. PMID:1101836

  3. Negative pressure pulmonary edema following choking on a cookie.

    PubMed

    Toukan, Yazeed; Gur, Michal; Bentur, Lea

    2016-07-01

    A 12-year-old boy developed severe acute respiratory distress during a school break requiring resuscitative measures. The episode started shortly after a short choking episode with a cookie. History, physical examination, laboratory results, chest X-ray, and clinical course supported the diagnosis of negative pressure pulmonary edema (NPPE). NPPE occurring outside a hospital setting, especially following a short episode of choking on a cookie, is rarely reported in children. Understanding the pathophysiological mechanisms contributing to pulmonary edema can help in distinguishing NPPE from other causes of fulminant respiratory distress, and especially from other causes of noncardiogenic pulmonary edema. Pediatr Pulmonol. 2016;51:E25-E27. © 2016 Wiley Periodicals, Inc.

  4. Poststreptococcal glomerulonephritis with pulmonary edema presenting as respiratory distress.

    PubMed

    Chiu, Chih-Yung; Huang, Yhu-Chering; Wong, Kin-Sun; Hsia, Shao-Hsuan; Lin, Chi-Jen; Lin, Tzou-Yien

    2004-11-01

    Acute poststreptococcal glomerulonephritis(PSGN) is characterized by an abrupt onset of edema,hypertension, and hematuria. Although the association of pulmonary edema with acute glomerulonephritis has been established, it is uncommon for children with PSGN to present with respiratory distress due to pulmonary edema. We encountered six such patients, aged 6-10 years, during a 10-month period. The demographic data, clinical manifestations, laboratory data, radiographic pictures, and clinical courses were collected. All patients presented to the primary pediatricians with dyspnea and alveolar infiltrates with bilateral pleural effusions on plain chest radiographs that were misinterpreted as pneumonia initially. The diagnosis of PSGN was de-layed until the awareness of the presence of pulmonary edema complicating PSGN. Subsequent urinalysis and blood pressure measurement all showed microscopic hematuria and hypertension. Elevated serum antistreptolysin 0 titers and depressed serum complement C3 levels confirmed the diagnosis of PSGN. Two patients progressed to respiratory failure because of a delayed diagnosis of PSGN. All patients recovered without sequelae following appropriate diuresis and antihypertensive therapy. We conclude that in preschool and school-age children who present with dyspneic respirations and a chest radiograph showing radiographic features of pulmonary edema, proper evaluation including blood pressure recording and urinalysis should be performed immediately. Prompt diagnosis and early therapy of PSGNmay avoid mortality and unnecessary therapeutic intervention.

  5. Anti-thymocyte globulin induced non-cardiogenic pulmonary edema during renal transplantation.

    PubMed

    Parikh, Beena K; Bhosale, Guruprasad P; Shah, Veena R

    2011-10-01

    Non-cardiogenic pulmonary edema (NCPE) is a clinical syndrome characterized by simultaneous presence of severe hypoxemia, bilateral alveolar infiltrates on chest radiograph, without evidence of left atrial hypertension/congestive heart failure/fluid overload. The diagnosis of drugrelated NCPE relies upon documented exclusion of other causes of NCPE like gastric aspiration, sepsis, trauma, negative pressure pulmonary edema. We describe a 28year-old, 50 kg male with ASA risk III posted for laparoscopic renal transplantation, who developed NCPE after 4 hours of administration of rabbit anti-human thymocyte immunoglobulin (ATG). He was successfully treated with mechanical ventilatory support and adjuvant therapy. This report emphasizes that this fatal complication may occur with use of ATG.

  6. Asymmetric pulmonary edema after scorpion sting: a case report.

    PubMed

    Razi, Ebrahim; Malekanrad, Elaheh

    2008-01-01

    A 12-year-old boy was referred with acute asymmetric pulmonary edema (APE) four-hour after scorpion sting to Emergency department. On admission, the main clinical manifestations were: dyspnea, tachypnea, and tachycardia. Chest x-ray revealed APE predominantly on the right hemithorax. The patient was treated with oxygen, intravenous frusemide and digoxin and discharged on the sixth hospital day in a good condition. This case report emphasizes the occurrence of asymmetric pulmonary edema after severe scorpion envenomation within few hours immediately after the sting.

  7. Neurogenic pulmonary edema: successful treatment with IV phentolamine.

    PubMed

    Davison, Danielle L; Chawla, Lakhmir S; Selassie, Leelie; Tevar, Rahul; Junker, Christopher; Seneff, Michael G

    2012-03-01

    Neurogenic pulmonary edema (NPE) is a clinical syndrome characterized by the acute onset of pulmonary edema following a significant CNS insult. The cause is believed to be a surge of catecholamines that results in cardiopulmonary dysfunction. Although there are myriad case reports describing CNS events that are associated with this syndrome, few studies have identified specific treatment modalities. We present a case of NPE caused by an intracranial hemorrhage from a ruptured arteriovenous malformation. We uniquely document a rise and fall of serum catecholamine levels correlating with disease activity and a dramatic clinical response to IV phentolamine.

  8. RESEARCH ON THERAPY OF PULMONARY EDEMA ASSOCIATED WITH OXIDIZERS

    DTIC Science & Technology

    pulmonary edema. Rutin in large doses caused a decrease in mortality and an increase in survival time of exposed rats. Intravenous infusion of isoproterenol...caused a decrease in mortality in rabbits exposed to N02. The effectiveness of hyperbaric oxygen, hydrocortisone, rutin and bethanechol against

  9. Pulmonary edema induced by calcium-channel blockade for tocolysis.

    PubMed

    Bal, Laurence; Thierry, Stéphane; Brocas, Elsa; Adam, Marie; Van de Louw, Andry; Tenaillon, Alain

    2004-09-01

    Nicardipine is used in the treatment of premature labor. There are no previous reports in the anesthesia literature of serious side effects associated with this drug. We report a case of pulmonary edema induced by nicardipine therapy for tocolysis in a pregnant 27-yr-old patient admitted to our hospital for preterm labor with intact membranes at 27 wk of gestation.

  10. Post-anesthetic pulmonary edema in two horses.

    PubMed

    Kaartinen, M Johanna; Pang, Daniel S J; Cuvelliez, Sophie G

    2010-03-01

    CASE 1: A two-year old, 462 kg Standard bred horse was anesthetized for arthroscopy and castration. During anesthesia, hyperemia of the mucosal membranes and urticaria were noticed. During 5 hours of anesthesia subcutaneous edema of the eyelids and neck region developed. In the recovery box, the orotracheal (OT) tube was left in situ and secured in place with tape. Following initial attempts to stand, the horse became highly agitated and signs consistent with pulmonary edema developed subsequently. Arterial hypoxemia (PaO(2): 3.7 kPa [28 mmHg]) and hypocapnia (PaCO(2): 3.1 kPa [23 mmHg]) were confirmed. Oxygen and furosemide were administered. The horse was assisted to standing with a sling. Therapy continued with bilateral intra-nasal oxygen insufflation. Ancillary medical therapy included flunixin meglumine, penicillin, gentamycin and dimethylsulfoxide. Following 7 hours of treatment the arterial oxygen tensions began to increase towards normal values. CASE 2: An 11-year old, 528 kg Paint horse was anesthetized for surgery of a submandibular mass. The 4-hour anesthetic period was unremarkable. The OT tube was left in situ for the recovery. During recovery, the horse was slightly agitated and stood after three attempts. Clinical signs consistent with pulmonary edema and arterial hypoxemia (PaO(2): 5 kPa [37.5 mmHg]) subsequently developed following extubation. Respiratory signs resolved with medical therapy, including unilateral nasal oxygen insufflation, furosemide, flunixin meglumine and dimethylsulfoxide. The diagnosis of pulmonary edema in these horses was made by clinical signs and arterial blood-gas analysis. While pulmonary radiographs were not taken to confirm the diagnosis, the clinical signs following anesthesia support the diagnosis in both cases. The etiology of pulmonary edema was most likely multifactorial.

  11. Predominant vasogenic edema in a patient with fatal cerebral air embolism.

    PubMed

    Tanaka, Ryota; Shimada, Yoshiaki; Shimura, Hideki; Oizumi, Hideki; Hattori, Nobutaka; Tanaka, Shigeki

    2012-08-01

    Cerebral air embolism (CAE) is a rare neurologic complication that can occur in patients undergoing various medical procedures or trauma. CAE can sometimes result in death caused by severe brain edema. In spite of these implications, the pathophysiologic mechanisms and radiologic features of fatal CAE remain to be elucidated. In this case report, a patient with carcinomatous pleuritis lost consciousness and developed quadriplegia and had generalized seizures during intrathoracic lavage. Serial computed tomography (CT) revealed the presence of air in intracranial blood vessels following severe brain edema; these are typically observed on the CT scans of patients with fatal CAE. Diffusion-weighted imaging (DWI) of the brain obtained at 24 hours after the onset of CAE revealed scattered cortical gyriform high signal intensity often observed in CAE cases, whereas the apparent diffusion coefficient and T2-weighted imaging revealed diffuse hyperintensity in the subcortical deep white matter, indicating vasogenic edema. Our case showed predominant vasogenic edema rather than cortical ischemic changes in the subcortical deep white matter area. These findings indicate that diffuse subcortical vasogenic edema could be the main cause of mortality in fatal CAE. Copyright © 2012 National Stroke Association. Published by Elsevier Inc. All rights reserved.

  12. Resolution of increased permeability pulmonary edema in rats.

    PubMed Central

    Havill, A. M.; Gee, M. H.

    1987-01-01

    The rate and sequence of interstitial and alveolar fluid removal from the lung after the occurrence of pulmonary edema were examined. Rats were given intraperitoneal injections of 20 mg/kg alpha-naphthylthiourea (ANTU), resulting in an increased permeability edema with alveolar flooding. Animals were killed at intervals between 2 and 48 hours after ANTU for the gravimetric determination of extravascular lung water (Qwl/dQl) and histologic study of the lung. Interstitial fluid volume was quantified by a morphometric technique. The assumptions were made that edema fluid equaled the experimental Qwl/dQl minus the normal Qwl/dQl, and that the edema fluid volume equaled the sum of interstitial and alveolar fluid volume. It was found that between 2 and 4 hours after the induction of pulmonary edema, fluid was removed from the alveolar space faster than it was removed from the interstitial space. Between 4 and 48 hours after ANTU, the fluid removal rate from both compartments was much slower, and interstitial fluid was removed at a faster rate than alveolar fluid. It is hypothesized that the later phase of fluid removal from the lung is dependent on the removal of protein. Images Figure 1 PMID:3109247

  13. [Acute heart failure: acute cardiogenic pulmonary edema and cardiogenic shock].

    PubMed

    Sánchez Marteles, Marta; Urrutia, Agustín

    2014-03-01

    Acute cardiogenic pulmonary edema and cardiogenic shock are two of the main forms of presentation of acute heart failure. Both entities are serious, with high mortality, and require early diagnosis and prompt and aggressive management. Acute pulmonary edema is due to the passage of fluid through the alveolarcapillary membrane and is usually the result of an acute cardiac episode. Correct evaluation and clinical identification of the process is essential in the management of acute pulmonary edema. The initial aim of treatment is to ensure hemodynamic stability and to correct hypoxemia. Other measures that can be used are vasodilators such as nitroglycerin, loop diuretics and, in specific instances, opioids. Cardiogenic shock is characterized by sustained hypoperfusion, pulmonary wedge pressure > 18 mmHg and a cardiac index < 2.2l/min/m(2). The process typically presents with hypotension (systolic blood pressure < 90 mmHg or a decrease in mean arterial pressure > 30 mmHg) and absent or reduced diuresis (< 0.5 ml/kg/h). The most common cause is left ventricular failure due to acute myocardial infarction. Treatment consists of general measures to reverse acidosis and hypoxemia, as well as the use of vasopressors and inotropic drugs. Early coronary revascularization has been demonstrated to improve survival in shock associated with ischaemic heart disease.

  14. Evaluation of meteorological and epidemiological characteristics of fatal pulmonary embolism

    NASA Astrophysics Data System (ADS)

    Törő, Klára; Pongrácz, Rita; Bartholy, Judit; Váradi-T, Aletta; Marcsa, Boglárka; Szilágyi, Brigitta; Lovas, Attila; Dunay, György; Sótonyi, Péter

    2016-03-01

    The objective of the present study was to identify risk factors among epidemiological factors and meteorological conditions in connection with fatal pulmonary embolism. Information was collected from forensic autopsy records in sudden unexpected death cases where pulmonary embolism was the exact cause of death between 2001 and 2010 in Budapest. Meteorological parameters were detected during the investigated period. Gender, age, manner of death, cause of death, place of death, post-mortem pathomorphological changes and daily meteorological conditions (i.e. daily mean temperature and atmospheric pressure) were examined. We detected that the number of registered pulmonary embolism (No 467, 211 male) follows power law in time regardless of the manner of death. We first described that the number of registered fatal pulmonary embolism up to the nth day can be expressed as Y( n) = α ṡ n β where Y denotes the number of fatal pulmonary embolisms up to the nth day and α > 0 and β > 1 are model parameters. We found that there is a definite link between the cold temperature and the increasing incidence of fatal pulmonary embolism. Cold temperature and the change of air pressure appear to be predisposing factors for fatal pulmonary embolism. Meteorological parameters should have provided additional information about the predisposing factors of thromboembolism.

  15. Evaluation of meteorological and epidemiological characteristics of fatal pulmonary embolism.

    PubMed

    Törő, Klára; Pongrácz, Rita; Bartholy, Judit; Váradi-T, Aletta; Marcsa, Boglárka; Szilágyi, Brigitta; Lovas, Attila; Dunay, György; Sótonyi, Péter

    2016-03-01

    The objective of the present study was to identify risk factors among epidemiological factors and meteorological conditions in connection with fatal pulmonary embolism. Information was collected from forensic autopsy records in sudden unexpected death cases where pulmonary embolism was the exact cause of death between 2001 and 2010 in Budapest. Meteorological parameters were detected during the investigated period. Gender, age, manner of death, cause of death, place of death, post-mortem pathomorphological changes and daily meteorological conditions (i.e. daily mean temperature and atmospheric pressure) were examined. We detected that the number of registered pulmonary embolism (No 467, 211 male) follows power law in time regardless of the manner of death. We first described that the number of registered fatal pulmonary embolism up to the nth day can be expressed as Y(n) = α ⋅ n (β) where Y denotes the number of fatal pulmonary embolisms up to the nth day and α > 0 and β > 1 are model parameters. We found that there is a definite link between the cold temperature and the increasing incidence of fatal pulmonary embolism. Cold temperature and the change of air pressure appear to be predisposing factors for fatal pulmonary embolism. Meteorological parameters should have provided additional information about the predisposing factors of thromboembolism.

  16. [The role of BDNF in brain ischemia pulmonary edema].

    PubMed

    Zhang, Yun-Hui; Wang, Ting-Hua

    2012-11-01

    Brain ischemia pulmonary edema(BIPE)is a critical type of the neurogenic pulmonary edema (NPE), with acute development and progression and high mortality. The study on mechanism of BIPE has important scientific significance and substantial practice values. NPE, as a complicated physiopathology condition, is not resulted from single factor but systemic events including the changes in nervous system, body fluid regulation and endocrine involved in central nervous system after the injury. The studies on this topic in this current issue suggested that brain-derived neurotrophic factor (BDNF) could involve in the pathogenesis procedure of NPE following brain ischemia, which indicated that the crucial role of BDNF in the NPE after BIPE. The findings of these studies pave a way for the treatment of BIPE by using BDNF administration in future clinic trail.

  17. Aripiprazole induced non-cardiogenic pulmonary edema: a case report.

    PubMed

    Cetin, Mustafa; Celik, Mustafa; Cakıcı, Musa; Polat, Mustafa; Suner, Arif

    2014-01-01

    Aripiprazole is a second-generation antipsychotic drug with partial dopamine agonistic activity. Although the adverse cardiovascular effects of both typical and atypical antipsychotics are well known, similar data on aripiprazole, which was recently introduced, are scarce. Herein we report a 35-year-old female that presented to our emergency department with non-cardiogenic pulmonary edema. Chest X-ray and thoracic CT showed pulmonary edema and bilateral pleural effusion. Anamnesis showed that she had been taking sertraline 200 mg d-1 for obsessive-compulsive disorder for a long time and that aripiprazole10 mg d-1 was added for augmentation 2 months prior to presentation. We think that the CYP 2D6 inhibitor sertraline might have played a role in increasing the plasma concentration and toxicity of aripiprazole in the presented patient.

  18. Pulmonary edema following transcatheter closure of atrial septal defect

    PubMed Central

    Chigurupati, Keerthi; Reshmi, Liza Jose; Gadhinglajkar, Shrinivas; Venkateshwaran, S.; Sreedhar, Rupa

    2015-01-01

    We describe an incident of development of acute pulmonary edema after the device closure of a secundum atrial septal defect in a 52-year-old lady, which was treated with inotropes, diuretics and artificial ventilation. Possibility of acute left ventricular dysfunction should be considered after the defect closure in the middle-aged patients as the left ventricular compliance may be reduced due to increased elastic stiffness and diastolic dysfunction. Baseline left atrial pressure may be > 10 mmHg in these patients. Associated risk factors for the left ventricular dysfunction are a large Qp:Qs ratio, systemic hypertension, severe pulmonary hypertension and paroxysmal atrial fibrillation. PMID:26139760

  19. [Late pneumomediastinum revealed by acute pulmonary edema in hemodialysis].

    PubMed

    El Amrani, Mohamed; El Kabbaj, Driss; Benyahia, Mohammed

    2014-04-01

    Central venous catheterization occupies an important place in the treatment of end stage renal disease pending the creation of an arteriovenous fistula. However, this procedure is not devoid of complications. We report a case of late pneumomediastinum revealed by an acute pulmonary edema in a young patient on hemodialysis, and we discuss its characteristics. Copyright © 2014 Association Société de néphrologie. Published by Elsevier SAS. All rights reserved.

  20. Postobstructive pulmonary edema after biopsy of a nasopharyngeal mass.

    PubMed

    Mehta, Keyur Kamlesh; Ahmad, Sabina Qureshi; Shah, Vikas; Lee, Haesoon

    2015-01-01

    We describe a case of 17 year-old male with a nasopharyngeal rhabdomyosarcoma who developed postobstructive pulmonary edema (POPE) after removing the endotracheal tube following biopsy. He developed muffled voice, rhinorrhea, dysphagia, odynophagia, and difficulty breathing through nose and weight loss of 20 pounds in the preceding 2 months. A nasopharyngoscopy revealed a fleshy nasopharyngeal mass compressing the soft and hard palate. Head and neck MRI revealed a large mass in the nasopharynx extending into the bilateral choana and oropharynx. Biopsy of the mass was taken under general anesthesia with endotracheal intubation. Immediately after extubation he developed oxygen desaturation, which did not improve with bag mask ventilation with 100% of oxygen, but improved after a dose of succinylcholine. He was re-intubated and pink, frothy fluid was suctioned from the endotracheal tube. Chest radiograph (CXR) was suggestive of an acute pulmonary edema. He improved with mechanical ventilation and intravenous furosemide. His pulmonary edema resolved over the next 24 h. POPE is a rare but serious complication associated with upper airway obstruction. The pathophysiology of POPE involves hemodynamic changes occurring in the lung and the heart during forceful inspiration against a closed airway due to an acute or chronic airway obstruction. This case illustrates the importance of considering the development of POPE with general anesthesia, laryngospasm and removal of endotracheal tube to make prompt diagnosis and to initiate appropriate management.

  1. Postobstructive pulmonary edema after biopsy of a nasopharyngeal mass

    PubMed Central

    Mehta, Keyur Kamlesh; Ahmad, Sabina Qureshi; Shah, Vikas; Lee, Haesoon

    2015-01-01

    We describe a case of 17 year-old male with a nasopharyngeal rhabdomyosarcoma who developed postobstructive pulmonary edema (POPE) after removing the endotracheal tube following biopsy. He developed muffled voice, rhinorrhea, dysphagia, odynophagia, and difficulty breathing through nose and weight loss of 20 pounds in the preceding 2 months. A nasopharyngoscopy revealed a fleshy nasopharyngeal mass compressing the soft and hard palate. Head and neck MRI revealed a large mass in the nasopharynx extending into the bilateral choana and oropharynx. Biopsy of the mass was taken under general anesthesia with endotracheal intubation. Immediately after extubation he developed oxygen desaturation, which did not improve with bag mask ventilation with 100% of oxygen, but improved after a dose of succinylcholine. He was re-intubated and pink, frothy fluid was suctioned from the endotracheal tube. Chest radiograph (CXR) was suggestive of an acute pulmonary edema. He improved with mechanical ventilation and intravenous furosemide. His pulmonary edema resolved over the next 24 h. POPE is a rare but serious complication associated with upper airway obstruction. The pathophysiology of POPE involves hemodynamic changes occurring in the lung and the heart during forceful inspiration against a closed airway due to an acute or chronic airway obstruction. This case illustrates the importance of considering the development of POPE with general anesthesia, laryngospasm and removal of endotracheal tube to make prompt diagnosis and to initiate appropriate management. PMID:26744691

  2. [Re-expansion pulmonary edema after iatrogenic pneumothorax. A propos of 1 case].

    PubMed

    Benezet, O; Gervais, C; Arich, C; Taulelle, M; Alsabadani, B; Fabre, S

    1983-01-01

    Re-expansion pulmonary edema (RPE) due to pneumothorax aspiration can lead to a fatal outcome, as in the case reported, the chronic nutritional deficiency and hypoproteinemia that it provokes probably playing a contributing role. Pathogenesis and factors affecting prognosis of RPE are discussed. These include the duration of the pulmonary collapse, though this is not an essential factor, the alterations in alveolar surfactant activity possibly related to the chronicity of the collapse, and the abruptness of aspiration which is, in contrast, a determining mechanical factor. Finally, the hypoproteinemia present in certain cases could facilitate fluid extravasation towards the alveolus. It is concluded that aspiration should be a gentle procedure in all cases, and should be conducted with extreme caution in the presence of hypoproteinemia.

  3. Our patients followed up with a diagnosis of neurogenic pulmonary edema

    PubMed Central

    Sarı, Mehmet Yusuf; Yıldızdaş, Rıza Dinçer; Yükselmiş, Ufuk; Horoz, Özden Ögür

    2015-01-01

    Neurogenic pulmonary edema is a clinical situation which developes as a result of central nervous system injury. It is rare in the childhood. Neurogenic pulmonary edema is a clinical diagnosis. Although the pathogenesis is not elucidated well, there is increase in pulmonary interstitial and alveolar fluid. The main principle in treatment of neurogenic pulmonary edema is supportive treatment and decreasing intracranial pressure as in acute respiratory distress syndrome. In this article, clinical properties of our two patients diagnosed with neurogenic pulmonary edema developed as a result of central nervous system injury are presented. PMID:26884694

  4. Ethyl pyruvate protects rats from phosgene-induced pulmonary edema by inhibiting cyclooxygenase2 and inducible nitric oxide synthase expression.

    PubMed

    Chen, Hong-li; Bai, Hua; Xi, Miao-miao; Liu, Riu; Qin, Xu-jun; Liang, Xin; Zhang, Wei; Zhang, Xiao-di; Li, Wen-li; Hai, Chun-xu

    2013-01-01

    Phosgene is a poorly water-soluble gas penetrating the lower respiratory tract which can induce acute lung injury characterized by a latent phase of fatal pulmonary edema. Pulmonary edema caused by phosgene is believed to be a consequence of oxidative stress and inflammatory responses. Ethyl pyruvate (EP) has been demonstrated to have anti-inflammatory and anti-oxidative properties in vivo and in vitro. The potential therapeutic role of EP in phosgene-induced pulmonary edema has not been addressed so far. In the present study, we aim to investigate the protective effects of EP on phosgene-induced pulmonary edema and the underlying mechanisms. Rats were administered with EP (40 mg kg(-1)) and RAW264.7 cells were also incubated with it (0, 2, 5 or 10 µm) immediately after phosgene (400 ppm, 1 min) or air exposure. Wet-to-dry lung weight ratio (W:D ratio), nitric oxide (NO) and prostaglandin E(2) (PGE(2)) production, cyclooxygenase2 (COX-2) and inducible nitric oxide synthase (iNOS) expression, and mitogen-activated protein kinases activities (MAPKs) were measured. Our results showed that EP treatment attenuated phosgene-induced pulmonary edema and decreased the level of NO and PGE(2) dose-dependently. Furthermore, EP significantly reduced COX-2 expression, iNOS expression and MAPK activation induced by phosgene. Moreover, specific inhibitors of MAPKs reduced COX-2 and iNOS expression induced by phosgene. These findings suggested that EP has a protective role against phosgene-induced pulmonary edema, which is mediated in part by inhibiting MAPK activation and subsequently down-regulating COX-2 and iNOS expression as well as decreasing the production of NO and PGE(2). Copyright © 2011 John Wiley & Sons, Ltd.

  5. Acute pulmonary edema after diazepam-ketamine in a dog.

    PubMed

    Boutureira, Joseph; Trim, Cynthia M; Cornell, Karen K

    2007-09-01

    An 8-year-old mixed-breed dog was anesthetized for colonoscopy. Moderate sedation was produced by premedication with glycopyrrolate, acepromazine, and hydromorphone, and anesthesia was induced by IV injection of diazepam and ketamine. Frothy, reddish-colored fluid flowed from the endotracheal tube immediately after endotracheal intubation but ceased after several minutes. Furosemide was injected IV. Anesthesia was maintained by sevoflurane in oxygen. Ventilation and arterial blood pressure were satisfactory, however, after oxygen was administered to maintain normal hemoglobin saturation. Radiography revealed changes consistent with a diagnosis of pulmonary edema. The following day, ventricular premature contractions developed and atrial dissociation, valvular regurgitation, and pulmonary hypertension were diagnosed on echocardiography. The proposed etiology is either profound transient hypotension and/or pulmonary hypertension induced by ketamine. The cardiac abnormalities that were present the following day suggest that myocardial dysfunction after induction of anesthesia was more severe than was apparent as assessed by routine physical examination and monitoring methods.

  6. [Non-cardiogenic pulmonary edema, acute respiratory distress syndrome].

    PubMed

    Skalická, Hana; Bělohlávek, Jan

    2015-01-01

    Non-cardiogenic pulmonary edema is a clinical syndrome manifested by rapidly progressive respiratory distress leading, without therapy, to severe respiratory insufficiency and subsequent multiorgan failure. The pathophysiological causes are: the change in the pressure gradients in the pulmonary capillaries, the impaired membrane permeability of the alveolocapillary in the lungs, and impaired lymphatic drainage. Unlike in cardiogenic pulmonary edema, cardiac disease is not a cause, and there is no increase in wedge pressure (< 18 mm Hg). The aetiological base is diverse and includes more clinical pathological factors. The diagnosis and evaluation are usually very difficult due to the rapidly deteriorating clinical condition of the patients. A decisive, quick and comprehensive approach, using all available invasive and non-invasive methods is necessary. The basic steps of treatment are: the use of different types of ventilatory support in order to achieve adequate oxygenation, dealing with possible hemodynamic instability, and, when needed, other specific procedures. It is always important to keep in mind that this is a very serious condition with a high mortality rate. And there is a need for fast and efficient access to the best specialized clinic.

  7. High-Altitude Pulmonary Edema in Mountain Community Residents.

    PubMed

    Ebert-Santos, Christine

    2017-09-01

    Ebert-Santos, Christine. High-altitude pulmonary edema in mountain community residents. High Alt Med Biol. 18:278-284, 2017.-High-altitude pulmonary edema (HAPE) affects lowlanders ascending quickly to elevations above 2440 m. Mountain resident children with no travel can sometimes develop HAPE as was observed over 30 years ago (Fasules et al., 1985). This is not well known and children instead are diagnosed as having pneumonia or asthma. In our clinic at 2800 m, we see children presenting with severe hypoxemia, clinical, and radiographic findings consistent with HAPE despite no recent travel. We call this mountain resident HAPE. We reviewed records of 48 patients with pulmonary symptoms. Analysis included vital signs, pulse oximetry, laboratories, physical findings, and clinical course. We identified 33 residents with HAPE and no travel, five with reentry HAPE, two visitors with classic HAPE, six residents with pneumonia, and two with asthma. Also, 48 X-rays on hypoxemic children seen between 2006 and 2017 were reviewed. Five showed definite HAPE with follow-up X-rays within 48 hours confirming rapid clearing on oxygen, 27 showed findings consistent with HAPE or viral pneumonia and no repeat study. Children living at elevation presenting with hypoxemia are commonly misdiagnosed. Rapid improvement with oxygen and little to no improvement with bronchodilators are more consistent with HAPE, and thus, antibiotics and other treatments can be avoided.

  8. Pulmonary Edema Assessed by Ultrasound: Impact in Cardiology and Intensive Care Practice.

    PubMed

    Blanco, Pablo A; Cianciulli, Tomás F

    2016-05-01

    Pulmonary edema is a frequent condition found in adult patients hospitalized in cardiology wards and intensive care units. Ultrasonography is a diagnostic modality with a high sensitivity for the detection of extravascular lung water, visualized as B lines, and usually caused by cardiogenic or noncardiogenic pulmonary edema. This paper highlights a simple method for the assessment of patients with pulmonary edema, which allows for a differential diagnosis of its possible mechanism and contributes to therapeutic intervention guiding and monitoring.

  9. Pulmonary edema following scorpion envenomation: mechanisms, clinical manifestations, diagnosis and treatment.

    PubMed

    Bahloul, Mabrouk; Chaari, Anis; Dammak, Hassen; Samet, Mohamed; Chtara, Kamilia; Chelly, Hedi; Ben Hamida, Chokri; Kallel, Hatem; Bouaziz, Mounir

    2013-01-10

    Scorpion envenomation is common in tropical and subtropical regions. Cardio-respiratory manifestations, mainly cardiogenic shock and pulmonary edema, are the leading causes of death after scorpion envenomation. The mechanism of pulmonary edema remains unclear and contradictory conclusions were published. However, most publications confirm that pulmonary edema has been attributed to acute left ventricular failure. Cardiac failure can result from massive release of catecholamines, myocardial damage induced by the venom or myocardial ischemia. Factors usually associated with the diagnosis of pulmonary edema were young age, tachypnea, agitation, sweating, or the presence of high plasma protein concentrations. Treatment of scorpion envenomation has two components: antivenom administration and supportive care. The latter mainly targets hemodynamic impairment and cardiogenic pulmonary edema. In Latin America, and India, the use of Prazosin is recommended for treatment of pulmonary edema because pulmonary edema is associated with arterial hypertension. However, in North Africa, scorpion leads to cardiac failure with systolic dysfunction with normal vascular resistance and dobutamine was recommended. Dobutamine infusion should be used as soon as we have enough evidence suggesting the presence of pulmonary edema, since it has been demonstrated that scorpion envenomation can result in pulmonary edema secondary to acute left ventricular failure. In severe cases, mechanical ventilation can be required.

  10. Is High Altitude Pulmonary Edema Relevant to Hawai‘i?

    PubMed Central

    2014-01-01

    High altitude clinical syndromes have been described in the medical literature but may be under recognized in the state of Hawai‘i. As tourism increases, high altitude injuries may follow given the easy access to high altitude attractions. Visitors and clinicians should be aware of the dangers associated with the rapid ascent to high altitudes in the perceived comfort of a vehicle. This paper will review the basic pathophysiology, prevention, and treatment of the most serious of the high altitude clinical syndromes, high altitude pulmonary edema. PMID:25478294

  11. Negative Pressure Pulmonary Edema Associated with Anterior Cervical Spine Surgery

    PubMed Central

    Yoneda, Masana; Tanaka, Yasuhito

    2014-01-01

    We report a very rare case of negative pressure pulmonary edema (NPPE) that occurred immediately after anterior cervical discectomy and fusion (ACDF). The patient was a 25-year-old man who sustained a facet fracture-dislocation of C5 during a traffic accident. After ACDF, he developed NPPE and needed mechanical ventilation. Fortunately, he recovered fully within 24 hours. NPPE is a rare postoperative complication that may occur after cervical spine surgery. The aims of this report are to present information regarding the diagnosis and emergent treatment of NPPE, and to review the previous literature regarding this serious complication. PMID:25558327

  12. Is high altitude pulmonary edema relevant to Hawai'i?

    PubMed

    Cornell, Seth Lewis

    2014-11-01

    High altitude clinical syndromes have been described in the medical literature but may be under recognized in the state of Hawai'i. As tourism increases, high altitude injuries may follow given the easy access to high altitude attractions. Visitors and clinicians should be aware of the dangers associated with the rapid ascent to high altitudes in the perceived comfort of a vehicle. This paper will review the basic pathophysiology, prevention, and treatment of the most serious of the high altitude clinical syndromes, high altitude pulmonary edema.

  13. Acute pulmonary edema secondary to hyperbaric oxygen therapy

    PubMed Central

    Obiagwu, Chukwudi; Paul, Vishesh; Chadha, Sameer; Hollander, Gerald; Shani, Jacob

    2015-01-01

    Hyperbaric oxygen therapy (HBOT) has been shown to be effective in the treatment of diabetic ulcers, air embolism, carbon monoxide poisoning and gas gangrene with minimal adverse effects. Very few cases of HBOT causing acute pulmonary edema (PE) has been described; with a study on dogs suggesting that a complication of this therapy could be PE. We describe the case of an 80-year-old man with a history of stable systolic heart failure and diabetes mellitus presenting with acute PE following treatment with HBOT for diabetic foot. PMID:25988073

  14. Acute pulmonary edema following inflation of arterial tourniquet.

    PubMed

    Santhosh, M C B; Pai, R B; Rao, R P

    2014-10-01

    Arterial tourniquets are used as one of the methods for reducing blood loss and for allowing blood free surgical field. A 20-year-old, 45 kg healthy female with a sphere shaped pendunculated hemangioma in the popliteal fossa of her left lower limb was applied with arterial tourniquet after exsanguination. The procedure was performed under general anesthesia. Soon after exsanguination and tourniquet inflation, the patient developed pulmonary edema which subsided after deflating the tourniquet. The clinical evolution, treatment and pathophysiology of this complication are described.

  15. Pulmonary Embolism Masquerading as High Altitude Pulmonary Edema at High Altitude

    PubMed Central

    Lohani, Benu; Murphy, Holly

    2016-01-01

    Abstract Pandey, Prativa, Benu Lohani, and Holly Murphy. Pulmonary embolism masquerading as high altitude pulmonary edema at high altitude. High Alt Med Biol. 17:353–358, 2016.—Pulmonary embolism (PE) at high altitude is a rare entity that can masquerade as or occur in conjunction with high altitude pulmonary edema (HAPE) and can complicate the diagnosis and management. When HAPE cases do not improve rapidly with descent, other diagnoses, including PE, ought to be considered. From 2013 to 2015, we identified eight cases of PE among 303 patients with initial diagnosis of HAPE. Upon further evaluation, five had deep vein thrombosis (DVT). One woman had a contraceptive ring and seven patients had no known thrombotic risks. PE can coexist with or mimic HAPE and should be considered in patients presenting with shortness of breath from high altitude regardless of thrombotic risk. PMID:27768392

  16. Pulmonary Embolism Masquerading as High Altitude Pulmonary Edema at High Altitude.

    PubMed

    Pandey, Prativa; Lohani, Benu; Murphy, Holly

    2016-12-01

    Pandey, Prativa, Benu Lohani, and Holly Murphy. Pulmonary embolism masquerading as high altitude pulmonary edema at high altitude. High Alt Med Biol. 17:353-358, 2016.-Pulmonary embolism (PE) at high altitude is a rare entity that can masquerade as or occur in conjunction with high altitude pulmonary edema (HAPE) and can complicate the diagnosis and management. When HAPE cases do not improve rapidly with descent, other diagnoses, including PE, ought to be considered. From 2013 to 2015, we identified eight cases of PE among 303 patients with initial diagnosis of HAPE. Upon further evaluation, five had deep vein thrombosis (DVT). One woman had a contraceptive ring and seven patients had no known thrombotic risks. PE can coexist with or mimic HAPE and should be considered in patients presenting with shortness of breath from high altitude regardless of thrombotic risk.

  17. Pulmonary Edema in Healthy Subjects in Extreme Conditions

    PubMed Central

    Garbella, Erika; Catapano, Giosuè; Pratali, Lorenza; Pingitore, Alessandro

    2011-01-01

    There are several pieces of evidence showing occurrence of pulmonary edema (PE) in healthy subjects in extreme conditions consisting of extreme psychophysical demand in normal environment and psychophysical performances in extreme environment. A combination of different mechanisms, such as mechanical, hemodynamic, biochemical, and hypoxemic ones, may underlie PE leading to an increase in lung vascular hydrostatic pressure and lung vascular permeability and/or a downregulation of the alveolar fluid reabsorption pathways. PE can be functionally detected by closing volume measurement and lung diffusing capacity test to different gases or directly visualized by multiple imaging techniques. Among them chest ultrasonography can detect and quantify the extravascular lung water, creating “comet-tail” ultrasound artefacts (ULCs) from water-thickened pulmonary interlobular septa. In this paper the physiopathological mechanisms of PE, the functional and imaging techniques applied to detect and quantify the phenomenon, and three models of extreme conditions, that is, ironman athletes, climbers and breath-hold divers, are described. PMID:21766015

  18. Pulmonary edema in healthy subjects in extreme conditions.

    PubMed

    Garbella, Erika; Catapano, Giosuè; Pratali, Lorenza; Pingitore, Alessandro

    2011-01-01

    There are several pieces of evidence showing occurrence of pulmonary edema (PE) in healthy subjects in extreme conditions consisting of extreme psychophysical demand in normal environment and psychophysical performances in extreme environment. A combination of different mechanisms, such as mechanical, hemodynamic, biochemical, and hypoxemic ones, may underlie PE leading to an increase in lung vascular hydrostatic pressure and lung vascular permeability and/or a downregulation of the alveolar fluid reabsorption pathways. PE can be functionally detected by closing volume measurement and lung diffusing capacity test to different gases or directly visualized by multiple imaging techniques. Among them chest ultrasonography can detect and quantify the extravascular lung water, creating "comet-tail" ultrasound artefacts (ULCs) from water-thickened pulmonary interlobular septa. In this paper the physiopathological mechanisms of PE, the functional and imaging techniques applied to detect and quantify the phenomenon, and three models of extreme conditions, that is, ironman athletes, climbers and breath-hold divers, are described.

  19. Fatal Cerebral Edema With Status Epilepticus in Children With Dravet Syndrome: Report of 5 Cases.

    PubMed

    Myers, Kenneth A; McMahon, Jacinta M; Mandelstam, Simone A; Mackay, Mark T; Kalnins, Renate M; Leventer, Richard J; Scheffer, Ingrid E

    2017-04-01

    Dravet syndrome (DS) is a well-recognized developmental and epileptic encephalopathy associated with SCN1A mutations and 15% mortality by 20 years. Although over half of cases succumb to sudden unexpected death in epilepsy, the cause of death in the remainder is poorly defined. We describe the clinical, radiologic, and pathologic characteristics of a cohort of children with DS and SCN1A mutations who developed fatal cerebral edema causing mass effect after fever-associated status epilepticus. Cases were identified from a review of children with DS enrolled in the Epilepsy Genetics Research Program at The University of Melbourne, Austin Health, who died after fever-associated status epilepticus. Five children were identified, all of whom presented with fever-associated convulsive status epilepticus, developed severe brain swelling, and died. All had de novo SCN1A mutations. Fever of 40°C or greater was measured in all cases. Signs of brainstem dysfunction, indicating cerebral herniation, were first noted 3 to 5 days after initial presentation in 4 patients, though were apparent as early as 24 hours in 1 case. When MRI was performed early in a patient's course, focal regions of cortical diffusion restriction were noted. Later MRI studies demonstrated diffuse cytotoxic edema, with severe cerebral herniation. Postmortem studies revealed diffuse brain edema and widespread neuronal damage. Laminar necrosis was seen in 1 case. Cerebral edema leading to fatal brain herniation is an important, previously unreported sequela of status epilepticus in children with DS. This potentially remediable complication may be a significant contributor to the early mortality of DS. Copyright © 2017 by the American Academy of Pediatrics.

  20. Takotsubo Cardiomyopathy in the Setting of Immersion Pulmonary Edema: Case Series

    PubMed Central

    Sorrentino, Dante; Azuma, Steven

    2015-01-01

    Immersion Pulmonary Edema is a unique medical condition being increasingly described in the medical literature as sudden-onset pulmonary edema in the setting of scuba diving and or swimming. Case reports have associated immersion pulmonary edema with cardiac dysfunction, but there are no known case reports describing submersion pulmonary edema resulting in Takotsubo cardiomyopathy. We report on three patients with unique presentations of immersion pulmonary edema with associated Takotsubo cardiomyopathy. All three cases occurred in O‘ahu, Hawai‘i and were seen by the same cardiologist within a span of seven years. Each patient was scuba diving with sudden dyspnea with pulmonary edema on chest X-ray. Cardiac catheterization revealed no significant epicardial stenosis. Wall motion abnormalities resolved. EKG's showed typical evolution of symmetric T wave inversion. Immersion pulmonary edema and Takotsubo cardiomyopathy may occur together and may be more common than initially thought. Dyspnea has been long known to be stressful as in “waterboarding.” Stressful events are known to trigger Takotsubo cardiomyopathy. Takotsubo cardiomyopathy should be considered as a possible complication of immersion pulmonary edema and EKG's, troponins, echocardiogram and in the appropriate situation cardiac catheterization should be considered.

  1. Acute pulmonary edema caused by takotsubo cardiomyopathy in a pregnant woman undergoing transvaginal cervical cerclage

    PubMed Central

    Lee, Jae-Young; Kwon, Hyun-Jung; Park, Sang-Wook; Lee, Yu-Mi

    2017-01-01

    Abstract Background: The physiological changes associated with pregnancy may predispose pregnant women to pulmonary edema. Other known causes of pulmonary edema during pregnancy include tocolytic drugs, preeclampsia, eclampsia, and peripartum cardiomyopathy. Methods: We describe a rare case of pulmonary edema caused by takotsubo cardiomyopathy in a pregnant woman at 14 weeks of gestation who was undergoing emergency transvaginal cervical cerclage. Results: Intraoperative chest radiography revealed severe pulmonary edema and echocardiography indicated moderate left ventricular dysfunction with akinesia of the mid to apical left ventricular wall segment, which is reflective of takotsubo cardiomyopathy. Conclusion: With early detection and appropriate management, the patient was stabilized in a relatively short period of time. Based on her clinical signs and symptoms, we suspect that the pulmonary edema was caused by takotsubo cardiomyopathy. PMID:28072695

  2. Electron Microscopy Observation of Human Pulmonary Ultrastructure in Two Patients with High-Altitude Pulmonary Edema.

    PubMed

    Droma, Yunden; Kato, Akane; Ichiyama, Takashi; Kobayashi, Nobumitsu; Honda, Takayuki; Uehara, Takeshi; Hanaoka, Masayuki

    2017-09-01

    We examined the pulmonary ultrastructure in tissue from two patients with high-altitude pulmonary edema (HAPE) by electron microscopy. In one case, we found that neutrophils were trapped in pulmonary capillary lumen of alveolar-capillary wall and part of the cytoplasm of a neutrophil protruded and adhered to the capillary endothelium. There were several degranulated vacuoles in the cytoplasm of the neutrophil. The pulmonary capillary wall was deformed, thickened, and swollen and there was evidence of degeneration. In another case, infiltration of neutrophils and macrophages, proliferation of type II pneumocytes, and numerous red blood cells were also observed in alveolar air space. These electron microscopic ultrastructural observations illustrate for the first time damage to the pulmonary alveolar-capillary barrier in lung tissue of humans with advanced HAPE.

  3. [Nursing assessment and management of patients with cardiogenic pulmonary edema].

    PubMed

    Wang, Yu-Jyuan; Liao, Chieh-Yin; Kao, Chi-Wen

    2012-02-01

    Cardiogenic pulmonary edema (CPE) is a clinical health problem that induces impaired gas exchange, dyspnea and hypoxia. This serious condition results in acute respiratory failure and high mortality rate. This article suggests an effective approach to CPE patient clinical symptom assessment and management. In accordance with evidence-based methods, we searched Cochrane, CINAHL and ScienceDirect and identified four Oxford Ia or Ib reports that employed a randomized controlled trial, systematic review and meta-analysis. Results suggest that prompt application of a non-invasive positive ventilator, especially continuous positive or bi-level positive airway pressure, can help patients reduce intubation risks, ICU stay days, and mortality rates. The authors hope to see more clinical trials on this topic to support evidence-based clinical nursing care.

  4. Pulmonary edema of environmental origin--newer concepts

    SciTech Connect

    Cordasco, E.M.; Demeter, S.R.; Kester, L.; Cordasco, M.A.; Lammert, G.; Beerel, F.

    1986-06-01

    Pulmonary edema of non-cardiac origin is usually an urgent clinical problem, which has recently increased in frequency throughout the world in the past few years. This is partly due to sociological factors and to pre-eminent advances in industrial technology. Recent severe massive toxic gas explosions have had national and worldwide implications. Therefore, urgent and appropriate therapy is of utmost importance in most of these patients. The use of high flow oxygen with Constant Positive Pressure Breathing are the main inhalational therapeutic approaches. Newer modalities of treatment include: (1) earlier Fiberoptic bronchoscopy in those individuals afflicted with aspiration problems and (2) certain specific chemical blocking agents for the management of phosgene intoxication and hydrogen sulfide toxicity. Preventive environmental measures are also important.

  5. A Rare Cause of Pulmonary Edema in the Postoperative Period.

    PubMed

    Chatterjee, Kshitij; Mittadodla, Penchala S; Colaco, Clinton; Jagana, Rajani

    2017-02-01

    With the increasing longevity of the population, the annual rates of hip arthroplasties performed have been steadily increasing over the past decade. Given the presence of medical comorbidities in the older patients, the peri-operative care of these individuals requires multi-specialty care, now more than ever. Hip arthroplasty is generally well tolerated, with early mortality after the procedure being <1%. Bone cement implantation syndrome (BCIS) is an entity that is occasionally encountered during or after the surgery. It is characterized by hypoxemia, hypotension, cardiac arrhythmias, and cardiac arrest leading to death, in severe cases. We report a case of a middle-aged female who developed refractory hypotension and pulmonary edema while undergoing hemiarthroplasty for a pathological femoral neck fracture and experienced cardiac arrest in the immediate postoperative period. Critical care physicians must familiarize themselves with promptly diagnosing and managing BCIS.

  6. A Rare Cause of Pulmonary Edema in the Postoperative Period

    PubMed Central

    Chatterjee, Kshitij; Mittadodla, Penchala S.; Colaco, Clinton; Jagana, Rajani

    2017-01-01

    With the increasing longevity of the population, the annual rates of hip arthroplasties performed have been steadily increasing over the past decade. Given the presence of medical comorbidities in the older patients, the peri-operative care of these individuals requires multi-specialty care, now more than ever. Hip arthroplasty is generally well tolerated, with early mortality after the procedure being <1%. Bone cement implantation syndrome (BCIS) is an entity that is occasionally encountered during or after the surgery. It is characterized by hypoxemia, hypotension, cardiac arrhythmias, and cardiac arrest leading to death, in severe cases. We report a case of a middle-aged female who developed refractory hypotension and pulmonary edema while undergoing hemiarthroplasty for a pathological femoral neck fracture and experienced cardiac arrest in the immediate postoperative period. Critical care physicians must familiarize themselves with promptly diagnosing and managing BCIS. PMID:28250610

  7. Ibuprofen prevents synthetic smoke-induced pulmonary edema

    SciTech Connect

    Shinozawa, Y.; Hales, C.; Jung, W.; Burke, J.

    1986-12-01

    Multiple potentially injurious agents are present in smoke but the importance of each of these agents in producing lung injury as well as the mechanisms by which the lung injury is produced are unknown. In order to study smoke inhalation injury, we developed a synthetic smoke composed of a carrier of hot carbon particles of known size to which a single known common toxic agent in smoke, in this case HCI, could be added. We then exposed rats to the smoke, assayed their blood for the metabolites of thromboxane and prostacyclin, and intervened shortly after smoke with the cyclooxygenase inhibitors indomethacin or ibuprofen to see if the resulting lung injury could be prevented. Smoke exposure produced mild pulmonary edema after 6 h with a wet-to-dry weight ratio of 5.6 +/- 0.2 SEM (n = 11) compared with the non-smoke-exposed control animals with a wet-to-dry weight ratio of 4.3 +/- 0.2 (n = 12), p less than 0.001. Thromboxane B, and 6-keto-prostaglandin F1 alpha rose to 1660 +/- 250 pg/ml (p less than 0.01) and to 600 +/- 100 pg/ml (p greater than 0.1), respectively, in the smoke-injured animals compared with 770 +/- 150 pg/ml and 400 +/- 100 pg/ml in the non-smoke-exposed control animals. Indomethacin (n = 11) blocked the increase in both thromboxane and prostacyclin metabolites but failed to prevent lung edema.

  8. [High altitude pulmonary edema. An experiment of nature to study the underlying mechanisms of hypoxic pulmonary hypertension and pulmonary edema in humans].

    PubMed

    Schwab, Marcos; Jayet, Pierre-Yves; Allemann, Yves; Sartori, Claudio; Scherrer, Urs

    2007-01-01

    High altitude constitutes an exciting natural laboratory for medical research. Over the past decade, it has become clear that the results of high-altitude research may have important implications not only for the understanding of diseases in the millions of people living permanently at high altitude, but also for the treatment of hypoxemia-related disease states in patients living at low altitude. High-altitude pulmonary edema (HAPE) is a life-threatening condition occurring in predisposed, but otherwise healthy subjects, and, therefore, allows to study underlying mechanisms of pulmonary edema in humans, in the absence of confounding factors. Over the past decade, evidence has accumulated that HAPE results from the conjunction of two major defects, augmented alveolar fluid flooding resulting from exaggerated hypoxic pulmonary hypertension, and impaired alveolar fluid clearance related to defective respiratory transepithelial sodium transport. Here, after a brief presentation of the clinical features of HAPE, we review this novel concept. We provide experimental evidence for the novel concept that impaired pulmonary endothelial and epithelial nitric oxide synthesis and/or bioavailability may represent the central underlying defect predisposing to exaggerated hypoxic pulmonary vasoconstriction and alveolar fluid flooding. We demonstrate that exaggerated pulmonary hypertension, while possibly a condition sine qua non, may not be sufficient to cause HAPE, and how defective alveolar fluid clearance may represent a second important pathogenic mechanism. Finally, we outline how this insight gained from studies in HAPE may be translated into the management of hypoxemia related disease states in general.

  9. Risk of fatal pulmonary embolism with oral contraceptives.

    PubMed

    Poulter, N R

    2000-06-17

    This commentary addresses the New Zealand study (case report) of a fatal pulmonary embolism (PE) associated with oral contraceptive (OC) use by L. Parkin and colleagues. The study significantly adds to the knowledge on the relationship between fatal PE and OC use, because most of the evidence up to now has related to nonfatal venous thromboembolic events (VTE). Several areas of the study, however, are criticized. These include the method used, definition, and the adjustment of data. However, these criticisms have been offered explanations in this commentary. It is noted that data from the study indicated that OCs containing desogestrel or gestodene are associated with higher risks of fatal PE than are those containing levonorgestrel. This is consistent with most previous studies comparing the effects of second-generation progestogens on VTE. Overall, data support previous pragmatic recommendations that second-generation pills, which contain levonorgestrel, are the combined OCs of choice.

  10. TEVAR for Flash Pulmonary Edema Secondary to Thoracic Aortic Aneurysm to Pulmonary Artery Fistula.

    PubMed

    Bornak, Arash; Baqai, Atif; Li, Xiaoyi; Rey, Jorge; Tashiro, Jun; Velazquez, Omaida C

    2016-01-01

    Enlarging aneurysms in the thoracic aorta frequently remain asymptomatic. Fistulization of thoracic aortic aneurysms (TAA) to adjacent structures or the presence of a patent ductus arteriosus and TAA may lead to irreversible cardiopulmonary sequelae. This article reports on a large aneurysm of the thoracic aorta with communication to the pulmonary artery causing pulmonary edema and cardiorespiratory failure. The communication was ultimately closed after thoracic endovascular aortic aneurysm repair allowing rapid symptom resolution. Early diagnosis and closure of such communication in the presence of TAA are critical for prevention of permanent cardiopulmonary damage. Copyright © 2016 Elsevier Inc. All rights reserved.

  11. Neurogenic pulmonary edema due to ventriculo-atrial shunt dysfunction: a case report.

    PubMed

    Cruz, Ana Sofia; Menezes, Sónia; Silva, Maria

    2016-01-01

    Pulmonary edema is caused by the accumulation of fluid within the air spaces and the interstitium of the lung. Neurogenic pulmonary edema is a clinical syndrome characterized by the acute onset of pulmonary edema following a significant central nervous system insult. It may be a less-recognized consequence of raised intracranial pressure due to obstructive hydrocephalus by blocked ventricular shunts. It usually appears within minutes to hours after the injury and has a high mortality rate if not recognized and treated appropriately. We report a patient with acute obstructive hydrocephalus due to ventriculo-atrial shunt dysfunction, proposed to urgent surgery for placement of external ventricular drainage, who presented with neurogenic pulmonary edema preoperatively. She was anesthetized and supportive treatment was instituted. At the end of the procedure the patient showed no clinical signs of respiratory distress, as prompt reduction in intracranial pressure facilitated the regression of the pulmonary edema. This report addresses the importance of recognition of neurogenic pulmonary edema as a possible perioperative complication resulting from an increase in intracranial pressure. If not recognized and treated appropriately, neurogenic pulmonary edema can lead to acute cardiopulmonary failure with global hypoperfusion and hypoxia. Therefore, awareness of and knowledge about the occurrence, clinical presentation and treatment are essential. Copyright © 2013 Sociedade Brasileira de Anestesiologia. Published by Elsevier Editora Ltda. All rights reserved.

  12. [Continuous spectrophotometry as a method to study pulmonary edema in isolated canine pulmonary lobe].

    PubMed

    Palomar Lever, A; Furuya Meguro, M E; Gómez González, A; Martínez Guerra, M L; Gertrudiz Salvador, N; Oppenheimer, L; Sandoval Zárate, J

    1996-01-01

    The aim of this paper is to introduce the spectrophotometric method to the study of pulmonary edema in isolated ex-vivo canine pulmonary lobe preparation. This spectrophotometric method is based on the on-line measure of light transmission in a column of blood, that is proportional to hematocrit. A second light is used to follow Evans blue dyed proteins. With this method we were able to measure the amount of edema in 10 isolated canine lobes. Both the filtration and reflection coefficient of the membrane as well as the characteristics of the filtrate could be calculated. The filtration coefficient was 0.6 +/- 0.4 ml/min (1.3 +/- 0.9 ml/min/100 g pulmonary, tissue) at maximum capillary pressure and the reflection coefficient was 0.53 +/- 0.07. With the spectrophotometric method we have the capability to study different aspects of lung edema formation. This method has the advantage of being exact and independent from pressure and volume induced vascular changes. It also allows the measurement of solute transport.

  13. Prevention of Unilateral Pulmonary Edema Complicating Robotic Mitral Valve Operations.

    PubMed

    Moss, Emmanuel; Halkos, Michael E; Binongo, Jose N; Murphy, Douglas A

    2017-01-01

    Unilateral pulmonary edema (UPE) has been reported after mitral operations performed through the right side of the chest. The clinical presentation is compatible with an ischemia-reperfusion injury. This report describes modifications to robotic mitral valve operations that were designed to reduce UPE. We reviewed 15 patients with UPE after robotic mitral valve operations from 2006 through 2012. Technique modifications to reduce right lung ischemia were used from 2013 through June 2015. Modifications included alterations in patient position, ventilation, and perfusion factors. The incidence of UPE before and after modifications was determined, as was perfusion factors and outcomes in a higher-risk patient subgroup with pulmonary hypertension and prolonged bypass procedures. The incidence of UPE was 1.4% (n = 15) in 1,059 consecutive robotic mitral valve procedures using the standard technique and 0.0% in 435 consecutive procedures using the modified technique (p < 0.02). All patients with UPE had pulmonary hypertension and bypass times of greater than 120 minutes. Patients in the higher-risk subgroup had significantly lower systemic temperature (31°C [range, 30°-32°C] versus 34°C [range, 33°-34°C]; p < 0.01) and higher mean perfusion pressure (67mm Hg [range 62-72 mm Hg] versus 54 mm Hg [range, 52-57 mm Hg]; p < 0.01) on bypass using the modified technique. The incidence of UPE in higher-risk patients was significantly reduced using the modified technique (0% versus 5.6%; p < 0.01) without any increase in overall morbidity or mortality. The incidence of UPE in patients undergoing robotic mitral valve operations has been significantly reduced using a modified technique, without increasing the perioperative complication rate. Further work is necessary to validate this protocol and understand the pathophysiology of postoperative UPE. Copyright © 2017 The Society of Thoracic Surgeons. Published by Elsevier Inc. All rights reserved.

  14. Edema

    MedlinePlus

    Edema means swelling caused by fluid in your body's tissues. It usually occurs in the feet, ankles ... it can involve your entire body. Causes of edema include Eating too much salt Sunburn Heart failure ...

  15. [Effectiveness of oxygen therapy for pulmonary edema in patients with hypertensive crisis before hospitalization].

    PubMed

    Dolgikh, V T; Epifanov, V G; Lukach, V N

    2003-01-01

    The oxygen therapy, involving the KI-3M respiratory apparatus administered in the positive pressure regimen on expiration (8-10 cm aq. c.), used, before hospitalization, within the complex therapy of patients with pulmonary edema triggered by hypertensive crisis arrests fast enough the pulmonary edema, cuts the working time of an ER crew and promotes the ER efficiency. The key clinical manifestations of pulmonary edema were found to begin to go down on minutes 5 to 10 after the administration of artificial lungs ventilation (ALV) by oxygen with the positive pressure being on expiration end; such signs were totally stopped in 20-25 minutes.

  16. Fatal Pulmonary Embolus After Uterine Artery Fibroid Embolisation

    SciTech Connect

    Hamoda, Haitham; Tait, P.; Edmonds, D. K.

    2009-09-15

    We report a 44-year-old woman who developed a fatal pulmonary embolus after uterine artery fibroid embolisation (UAE). Bilateral UAE was carried out through a single right-femoral artery puncture. The largest fibroid in the anterior fundal wall measured 4.5 cm, and the largest fibroid in the posterior fundal wall measured 6 cm. The appearances after UAE were satisfactory, and the procedure was apparently uneventful. No immediate complications were noted. The patient developed sudden-onset shortness of breath and went into cardiac arrest 19 h after the procedure. Postmortem autopsy confirmed that the cause of a death was a pulmonary embolism. To our knowledge this is the first reported case in the United Kingdom in which death occurred from a pulmonary embolus after UAE.

  17. Non-cardiogenic pulmonary edema, rhabdomyolysis and myocardial injury following heroin inhalation: a case report

    PubMed Central

    Bazoukis, G; Spiliopoulou, A; Mourouzis, K; Grigoropoulou, P; Yalouris, A

    2016-01-01

    Background: Heroin use by non-injecting routes of administration (snorting, swallowing, “chasing the dragon”) is considered to be safer but is not risk-free for fatal overdose or serious side effects. We report the case of an adolescent who was transferred unconscious to the emergency department after heroin inhalation. Description of the case: A 17-year-old male was transferred to the emergency department unconscious (Glasgow coma scale: 6/15) after heroin inhalation. He was treated with non-rebreather mask and intravenous infusion of naloxone with gradual improvement of consciousness and arterial blood gasses. The chest computed tomography showed signs of acute respiratory distress syndrome. Laboratory exams on the second day of hospitalization showed elevated creatine kinase (CK) and troponin-I levels while his electrocardiography (ECG) showed J-point elevation in V1, V2, and V3 precordial leads. On the second day of hospitalization the pulmonary infiltrates were not present in his chest X-ray while on the eighth day, troponin-I and CK levels were normalized without dynamic ECG changes and the patient was discharged uneventfully. Conclusion: Heroin inhalation may cause severe complications, such as non-cardiogenic pulmonary edema, rhabdomyolysis or myocardial injury. Hippokratia 2016, 20(1): 84-87 PMID:27895451

  18. High altitude pulmonary edema, down syndrome, and obstructive sleep apneas.

    PubMed

    Richalet, Jean-Paul; Chenivesse, Cécile; Larmignat, Philippe; Meille, Laurent

    2008-01-01

    A 24-year-old adult with a Down syndrome was admitted in December 2006 at the Moutiers hospital in the French Alps for an acute inaugural episode of high altitude pulmonary edema (HAPE) that occurred in the early morning of day 3 after his arrival to La Plagne (2000 m). This patient presented an interventricular septal defect operated on at the age of 7, a hypothyroidism controlled by 50 microg levothyrox, a state of obesity (BMI 37.8 kg/m(2)), and obstructive sleep apneas with a mean of 42 obstructive apneas or hypopneas per hour, treated with continuous positive airway pressure (CPAP). The patient refused to use his CPAP during his stay in La Plagne. At echocardiography, resting parameters were normal, with a left ventricular, ejection fraction of 60%, a normokinetic right ventricle, and an estimated systolic pulmonary artery pressure (sPAP) of 30 mmHg. At exercise, sPAP rose to 45 mmHg and the right ventricle was still normokinetic and not dilated. An exercise hypoxic tolerance test performed at 60 W and at the equivalent altitude of 3300 m revealed a severe drop in arterial oxygen saturation down to 60%, with an abnormal low ventilatory response to hypoxia, suggesting a defect in peripheral chemosensitivity to hypoxia. In conclusion, patients with Down syndrome, including adults with no cardiac dysfunction and regular physical activity, are at risk of HAPE even at moderate altitude when they suffer from obstructive sleep apneas associated with obesity and low chemoresponsiveness. This observation might be of importance since an increasing number of young adults with Down syndrome participate in recreational or sport activities, including skiing and mountaineering.

  19. [Cardiogenic pulmonary edema - truth and myths in the perspective of emergency medicine].

    PubMed

    Osterwalder, J J

    2012-09-19

    This critical analysis of the traditional pathophysiological approach to the diagnosis and treatment of cardiogenic pulmonary edema calls into question some long-established ideas and interventions that ought to be replaced by better evidence-based concepts.

  20. Emergent Unilateral Renal Artery Stenting for Treatment of Flash Pulmonary Edema: Fact or Fiction?

    PubMed Central

    Khan, Asaad Akbar; McFadden, Eugene Patrick

    2015-01-01

    Flash pulmonary edema is characteristically sudden in onset with rapid resolution once appropriate therapy has been instituted (Messerli et al., 2011). Acute increase of left ventricular (LV) end diastolic pressure is the usual cause of sudden decompensated cardiac failure in this patient population. Presence of bilateral renal artery stenosis or unilateral stenosis in combination with a single functional kidney in the susceptible cohort is usually blamed for this condition. We describe a patient who presented with flash pulmonary edema in the setting of normal coronary arteries. Our case is distinct as our patient developed flash pulmonary edema secondary to unilateral renal artery stenosis in the presence of bilateral functioning kidneys. Percutaneous stent implantation in the affected renal artery resulted in rapid resolution of pulmonary edema. PMID:25793128

  1. Refractory Pulmonary Edema Caused by Late Pulmonary Vein Thrombosis After Lung Transplantation: A Rare Adverse Event.

    PubMed

    Denton, Eve J; Rischin, Adam; McGiffin, David; Williams, Trevor J; Paraskeva, Miranda A; Westall, Glen P; Snell, Greg

    2016-09-01

    After lung transplantation, pulmonary vein thrombosis is a rare, potentially life-threatening adverse event arising at the pulmonary venous anastomosis that typically occurs early and presents as graft failure and hemodynamic compromise with an associated mortality of up to 40%. The incidence, presentation, outcomes, and treatment of late pulmonary vein thrombosis remain poorly defined. Management options include anticoagulant agents for asymptomatic clots, and thrombolytic agents or surgical thrombectomy for hemodynamically significant clots. We present a rare case highlighting a delayed presentation of pulmonary vein thrombosis occurring longer than 2 weeks after lung transplantation and manifesting clinically as graft failure secondary to refractory pulmonary edema. The patient was treated successfully with surgical thrombectomy and remains well. We recommend a high index of suspicion of pulmonary vein thrombosis when graft failure after lung transplantation occurs and is not responsive to conventional therapy, and consideration of investigation with transesophageal echocardiography or computed tomography with venous phase contrast in such patients even more than 2 weeks after lung transplantation.

  2. Management of acute cardiogenic pulmonary edema: a literature review.

    PubMed

    Johnson, Jeremy M

    2009-01-01

    Acute cardiogenic pulmonary edema (CPE) is a pathology frequently seen in patients presenting to emergency departments (EDs) and can usually be attributed to preexisting cardiovascular disease. Heart failure alone accounts for more than 1 million hospital admissions annually and has one of the highest ED morbidity and mortality to date (). Historically, CPE has been managed by the treating clinician in a manner that is based largely on anecdotal evidence. Furosemide (Lasix), morphine, and nitroglycerin have historically been the baseline standard for drug therapy in CPE management. A lack of drastic improvement in the patient's condition over the course of the ED visit may reflect a management style that results in higher morbidity and mortality for CPE patients. Several recent articles provide evidence-based outcomes that suggest changing standard therapy along with the adjunctive use of other medications. These articles also describe treatment modalities that result in a marked improvement in the management of patients with CPE along with decreases in adverse outcomes and hospital length of stay. The goal of this article is to present a summary of the evidence regarding the management of CPE and discuss the implications for current practice.

  3. Profiling of ARDS Pulmonary Edema Fluid Identifies a Metabolically Distinct Subset.

    PubMed

    Rogers, Angela J; Contrepois, Kevin; Wu, Manhong; Zheng, Ming; Peltz, Gary; Ware, Lorraine B; Matthay, Michael A

    2017-03-03

    There is considerable biologic and physiologic heterogeneity among patients who meet standard clinical criteria for acute respiratory distress syndrome (ARDS). In this study, we tested the hypothesis that there exists a sub-group of ARDS patients who exhibit a metabolically distinct profile. We examined undiluted pulmonary edema fluid obtained at the time of endotracheal intubation from 16 clinically phenotyped ARDS patients and 13 control patients with hydrostatic pulmonary edema. Non-targeted metabolic profiling was carried out on the undiluted edema fluid. Univariate and multivariate statistical analyses including principal components analysis (PCA) and partial least squares discriminant analysis (PLSDA) were conducted to find discriminant metabolites. 760 unique metabolites were identified in the pulmonary edema fluid of these 29 patients. We found that a subset of ARDS patients (6/16, 38%) presented a distinct metabolic profile with the overrepresentation of 235 metabolites compared to edema fluid from the other 10 ARDS patients, whose edema fluid metabolic profile was indistinguishable from those of the 13 control patients with hydrostatic edema. This "high metabolite" endotype was characterized by higher concentrations of metabolites belonging to all of the main metabolic classes including lipids, amino acids, and carbohydrates. This distinct group with high metabolite levels in the edema fluid was also associated with a higher mortality rate. Thus, metabolic profiling of the edema fluid of ARDS patients supports the hypothesis that there is considerable biologic heterogeneity among ARDS patients who meet standard clinical and physiologic criteria for ARDS.

  4. Post extubation negative pressure pulmonary edema due to posterior mediastinal cyst in an infant.

    PubMed

    Dubey, Prakash Kumar

    2014-01-01

    A 3-month-old male child underwent uneventful inguinal herniotomy under general anesthesia. After extubation, airway obstruction followed by pulmonary edema appeared for which the baby was reintubated and ventilated. The baby made a complete recovery and extubated after about 2 h. A post-operative computed tomography scan revealed a posterior mediastinal cystic mass abutting the tracheal bifurcation. Presumably, extrinsic compression by the mass on the tracheal bifurcation led to the development of negative pressure pulmonary edema.

  5. Noncardiogenic Pulmonary Edema after Amlodipine Overdose without Refractory Hypotension and Bradycardia

    PubMed Central

    Hedaiaty, M.; Eizadi-Mood, N.; Sabzghabaee, A. M.

    2015-01-01

    Amlodipine overdose can be life-threatening when manifesting as noncardiogenic pulmonary edema. Treatment remains challenging. We describe a case of noncardiogenic pulmonary edema without refractory hypotension and bradycardia after ingestion of 500 milligram amlodipine with suicidal intent. Mechanical ventilation, dexamethasone, atrovent HFA (ipratropium), pulmicort inhalation, and antibiotic therapy were used for the management. Length of hospital stay was 11 days. The patient was discharged with full recovery. PMID:26075111

  6. The dysfunction of ATPases due to impaired mitochondrial respiration in phosgene-induced pulmonary edema.

    PubMed

    Qin, Xu-Jun; Li, Ying-Na; Liang, Xin; Wang, Peng; Hai, Chun-Xu

    2008-02-29

    Phosgene is a toxic gas that is widely used in modern industry, and its inhalation can cause severe pulmonary edema. There is no effective clinical treatment because the mechanism of phosgene-induced pulmonary edema still remains unclear. Many studies have demonstrated that the Na(+)/K(+)-ATPase plays a critical role in clearing pulmonary edema and the inhibition of Na(+)/K(+)-ATPase protein expression has been found in many other pulmonary edema models. In the present study, after the mice were exposed to phosgene, there was serious pulmonary edema, indicating the dysfunction of the ATPases in mice. However, in vitro enzyme study showed that there were increases in the activities of the Na(+)/K(+)-ATPase and Ca(2+)-ATPase. Further investigation showed that the ATP content and mitochondrial respiratory control ratio (RCR) in the lungs decreased significantly. The oxidative stress product, malondialdehyde (MDA), increased while the antioxidants (GSH, SOD, and TAC) decreased significantly. These results indicate that mitochondrial respiration is the target of phosgene. The dysfunction of ATPases due to impaired mitochondrial respiration may be a new mechanism of phosgene-induced pulmonary edema.

  7. Prevalence of pulmonary edema among the deceased cases with acute Methadone poisoning: A report from Iran

    PubMed Central

    Eizadi-Mood, Nastaran; Naeini, Seyed Amir Hossein Madani; Hedaiaty, Mahrang; Sabzghabaee, Ali Mohammad; Moudi, Maryam

    2016-01-01

    Objective: Methadone poisoning is common in our society, mainly in drug addicts. One of its lethal complications is pulmonary edema. Therefore, we evaluated the prevalence of pulmonary edema in the deceased cases with methadone poisoning and its possible relationship with some medical variables. Methods: In this cross-sectional study which was done in 2014, we have investigated the deceased patients with methadone toxicity who underwent autopsy at Isfahan Forensic Medicine Department (Iran). All variables including age, gender, and autopsy findings were recorded and analyzed. Demographic characteristics and medical complications of the patients were compared between the patients with or without pulmonary edema in the autopsy findings. Findings: There were 64 cases who died with methadone poisoning during the 1-year study period. The average age of cases (±standard deviation) was 32.1 ± 10.29 years, among which 92.2% were male. Based on the autopsy findings, 64.1% were diagnosed with pulmonary edema. There was no statistically significant relationship between pulmonary edema and age, gender, history of addiction, and hepatic or cardiovascular complications. Conclusion: Pulmonary edema is a common finding in deceased methadone poisoning cases and must be considered and ruled out in patients with acute methadone toxicity. PMID:27843967

  8. Pulmonary edema after resection of a fourth ventricle tumor: possible evidence for a medulla-mediated mechanism.

    PubMed

    Keegan, M T; Lanier, W L

    1999-03-01

    A well-recognized fact is that some patients may have development of pulmonary edema in association with disorders of the central nervous system. The origin of this phenomenon, known as neurogenic pulmonary edema, is unclear but may result, in part, from select pulmonary venoconstriction modulated by autonomic outflow from the medulla oblongata. We describe a 21-year-old man who had development of pulmonary edema in association with surgical resection of a brain tumor that was close to the medulla. Other than the possibility of medullary dysfunction, which could have occurred after surgical manipulation, no other risk factor for pulmonary edema was identified. Of note, the patient's blood pressure remained normal throughout the perioperative period, and no fluid overload or primary cardiac dysfunction was evident. This case supports the theory that the medulla is an important anatomic site of origin for neurogenic pulmonary edema and that alterations in medullary function can induce pulmonary edema in humans, independent of systemic hypertension.

  9. Transthoracic lung ultrasound in normal dogs and dogs with cardiogenic pulmonary edema: a pilot study.

    PubMed

    Rademacher, Nathalie; Pariaut, Romain; Pate, Julie; Saelinger, Carley; Kearney, Michael T; Gaschen, Lorrie

    2014-01-01

    Pulmonary edema is the most common complication of left-sided heart failure in dogs and early detection is important for effective clinical management. In people, pulmonary edema is commonly diagnosed based on transthoracic ultrasonography and detection of B line artifacts (vertical, narrow-based, well-defined hyperechoic rays arising from the pleural surface). The purpose of this study was to determine whether B line artifacts could also be useful diagnostic predictors for cardiogenic pulmonary edema in dogs. Thirty-one normal dogs and nine dogs with cardiogenic pulmonary edema were prospectively recruited. For each dog, presence or absence of cardiogenic pulmonary edema was based on physical examination, heartworm testing, thoracic radiographs, and echocardiography. A single observer performed transthoracic ultrasonography in all dogs and recorded video clips and still images for each of four quadrants in each hemithorax. Distribution, sonographic characteristics, and number of B lines per thoracic quadrant were determined and compared between groups. B lines were detected in 31% of normal dogs (mean 0.9 ± 0.3 SD per dog) and 100% of dogs with cardiogenic pulmonary edema (mean 6.2 ± 3.8 SD per dog). Artifacts were more numerous and widely distributed in dogs with congestive heart failure (P < 0.0001). In severe cases, B lines increased in number and became confluent. The locations of B line artifacts appeared consistent with locations of edema on radiographs. Findings from the current study supported the use of thoracic ultrasonography and detection of B lines as techniques for diagnosing cardiogenic pulmonary edema in dogs.

  10. Noninvasive mechanical ventilation in chronic obstructive pulmonary disease and in acute cardiogenic pulmonary edema.

    PubMed

    Rialp Cervera, G; del Castillo Blanco, A; Pérez Aizcorreta, O; Parra Morais, L

    2014-03-01

    Noninvasive ventilation (NIV) with conventional therapy improves the outcome of patients with acute respiratory failure due to hypercapnic decompensation of chronic obstructive pulmonary disease (COPD) or acute cardiogenic pulmonary edema (ACPE). This review summarizes the main effects of NIV in these pathologies. In COPD, NIV improves gas exchange and symptoms, reducing the need for endotracheal intubation, hospital mortality and hospital stay compared with conventional oxygen therapy. NIV may also avoid reintubation and may decrease the length of invasive mechanical ventilation. In ACPE, NIV accelerates the remission of symptoms and the normalization of blood gas parameters, reduces the need for endotracheal intubation, and is associated with a trend towards lesser mortality, without increasing the incidence of myocardial infarction. The ventilation modality used in ACPE does not affect the patient prognosis.

  11. Perforin Expression by CD8 T Cells Is Sufficient To Cause Fatal Brain Edema during Experimental Cerebral Malaria.

    PubMed

    Huggins, Matthew A; Johnson, Holly L; Jin, Fang; N Songo, Aurelie; Hanson, Lisa M; LaFrance, Stephanie J; Butler, Noah S; Harty, John T; Johnson, Aaron J

    2017-05-01

    Human cerebral malaria (HCM) is a serious complication of Plasmodium falciparum infection. The most severe outcomes for patients include coma, permanent neurological deficits, and death. Recently, a large-scale magnetic resonance imaging (MRI) study in humans identified brain swelling as the most prominent predictor of fatal HCM. Therefore, in this study, we sought to define the mechanism controlling brain edema through the use of the murine experimental cerebral malaria (ECM) model. Specifically, we investigated the ability of CD8 T cells to initiate brain edema during ECM. We determined that areas of blood-brain barrier (BBB) permeability colocalized with a reduction of the cerebral endothelial cell tight-junction proteins claudin-5 and occludin. Furthermore, through small-animal MRI, we analyzed edema and vascular leakage. Using gadolinium-enhanced T1-weighted MRI, we determined that vascular permeability is not homogeneous but rather confined to specific regions of the brain. Our findings show that BBB permeability was localized within the brainstem, olfactory bulb, and lateral ventricle. Concurrently with the initiation of vascular permeability, T2-weighted MRI revealed edema and brain swelling. Importantly, ablation of the cytolytic effector molecule perforin fully protected against vascular permeability and edema. Furthermore, perforin production specifically by CD8 T cells was required to cause fatal edema during ECM. We propose that CD8 T cells initiate BBB breakdown through perforin-mediated disruption of tight junctions. In turn, leakage from the vasculature into the parenchyma causes brain swelling and edema. This results in a breakdown of homeostatic maintenance that likely contributes to ECM pathology. Copyright © 2017 American Society for Microbiology.

  12. The risk factors and prognostic implication of acute pulmonary edema in resuscitated cardiac arrest patients

    PubMed Central

    Kang, Dae-hyun; Kim, Joonghee; Rhee, Joong Eui; Kim, Taeyun; Kim, Kyuseok; Jo, You Hwan; Lee, Jin Hee; Lee, Jae Hyuk; Kim, Yu Jin; Hwang, Seung Sik

    2015-01-01

    Objective Pulmonary edema is frequently observed after a successful resuscitation in out-of-hospital cardiac arrest (OHCA) patients. Currently, its risk factors and prognostic implications are mostly unknown. Methods Adult OHCA patients with a presumed cardiac etiology who achieved sustained return of spontaneous circulation (ROSC) in emergency department were retrospectively analyzed. The patients were grouped according to the severity of consolidation on their initial chest X-ray (group I, no consolidation; group II, patchy consolidations; group III, consolidation involving an entire lobe; group IV, total white-out of any lung). The primary objective was to identify the risk factors of developing severe pulmonary edema (group III or IV). The secondary objective was to evaluate the association between long-term prognosis and the severity of pulmonary edema. Results One hundred and seven patients were included. Total duration of cardiopulmonary resuscitation (CPR) and initial pCO2 level were both independent predictors of developing severe pulmonary edema with their odds ratio (OR) being 1.02 (95% confidence interval [CI], 1.00 to 1.04; per 1 minute) and 1.04 (95% CI, 1.01 to 1.07; per 1 mmHg), respectively. The long term prognosis was significantly poor in patients with severe pulmonary edema with a OR for good outcome (6-month cerebral performance category 1 or 2) being 0.22 (95% CI, 0.06 to 0.79) in group III and 0.16 (95% CI, 0.04 to 0.63) in group IV compared to group I. Conclusion The duration of CPR and initial pCO2 level were both independent predictors for the development of severe pulmonary edema after resuscitation in emergency department. The severity of the pulmonary edema was significantly associated with long-term outcome. PMID:27752581

  13. Pulmonary edema in meningococcal septicemia associated with reduced epithelial chloride transport.

    PubMed

    Eisenhut, Michael; Wallace, Helen; Barton, Paul; Gaillard, Erol; Newland, Paul; Diver, Michael; Southern, Kevin W

    2006-03-01

    To test the hypothesis that meningococcal septicemia-related pulmonary edema is associated with a systemic abnormality of epithelial sodium and chloride transport and to investigate an association with hormones regulating Na transport. Prospective observational study. The 24-bed pediatric intensive care unit and pediatric wards of Royal Liverpool Children's Hospital. Consecutive children admitted to the pediatric intensive care unit and pediatric wards with a diagnosis of meningococcal septicemia and children (controls) with noninfectious critical illness receiving ventilatory support in the pediatric intensive care unit. We measured sweat and saliva electrolytes, renal electrolyte excretion, nasal potential difference, and aldosterone, thyroxine, and cortisol levels. Pulmonary edema was diagnosed by chest radiography and its severity quantified by calculation of ventilation index at admission and duration of mechanical ventilation. We recruited 17 patients with severe meningococcal septicemia (nine patients with pulmonary edema), 14 patients with mild meningococcal septicemia, and 20 controls. Sweat and saliva Na and Cl concentrations and renal Na excretion were significantly (p < .05) higher in patients with pulmonary edema compared with controls. Nasal potential difference and amiloride response in patients with pulmonary edema were not significantly different to controls, but response to a low Cl solution was reduced in the nasal airway of patients with pulmonary edema (p < .05). Sweat and saliva chloride concentrations correlated significantly and better with ventilation index and duration of ventilation than sodium concentrations. Aldosterone, thyroxine, and cortisol levels were not significantly different between groups. We have confirmed that meningococcal septicemia-related pulmonary edema is associated with reduced systemic sodium and chloride transport. Features of reduced Cl transport were most closely associated with markers of respiratory compromise

  14. Edema

    MedlinePlus

    ... and symptoms Pregnancy Edema can be a side effect of some medications, including: High blood pressure medications Nonsteroidal anti-inflammatory drugs Steroid drugs Estrogens Certain diabetes medications called ...

  15. [Pulmonary hypertension and lung edema at high altitude. Role of endothelial dysfunction and fetal programming].

    PubMed

    Schwab, Marcos; Allemann, Yves; Rexhaj, Emrush; Rimoldi, Stefano F; Sartori, Claudio; Scherrer, Urs

    2012-01-01

    High altitude constitutes an exciting natural laboratory for medical research. While initially, the aim of high-altitude research was to understand the adaptation of the organism to hypoxia and find treatments for altitude-related diseases, over the past decade or so, the scope of this research has broadened considerably. Two important observations led to the foundation for the broadening of the scientific scope of high-altitude research. First, high-altitude pulmonary edema (HAPE) represents a unique model which allows studying fundamental mechanisms of pulmonary hypertension and lung edema in humans. Secondly, the ambient hypoxia associated with high-altitude exposure facilitates the detection of pulmonary and systemic vascular dysfunction at an early stage. Here, we review studies that, by capitalizing on these observations, have led to the description of novel mechanisms underpinning lung edema and pulmonary hypertension and to the first direct demonstration of fetal programming of vascular dysfunction in humans.

  16. [The x-ray diagnosis of a predisposition to nephrogenic pulmonary edema in glomerulonephritis patients].

    PubMed

    Kamenetskiĭ, M S; Pervak, M B; Tkachenko, G D; Vernikov, B L

    1995-01-01

    To develop criteria for determining predisposition to pulmonary edema in patients with glomerulonephritis, clinical, laboratory and X-ray examinations were made in 697 patients with glomerulonephritis at different stages of its development. X-ray examination included chest tele X-ray and its densitometric analysis. Twenty two patients underwent computerized tomography with histographic analysis. In 106 patients, X-ray findings were compared with the volume of circulating blood, cardiac and stroke indices. Changes in the lungs and pleural cavities were found in 22.7%, pulmonary edema was revealed in 15.7% of the patients. The prognostically unfavourable criteria for the development of pulmonary edema were found to be Stage II pulmonary venous hypertension with hypervolemia and peripheral edemas. The densitometrically detected increase in the density of the lower lungs in patients with Stage II venous hypertension suggests early manifestations of interstitial edema of the lung and the narrowing of the histogram angle limited by its ascending and descending lines is indicative of the fact that interstitial edema progresses to alveolar one.

  17. Increased pulmonary vascular permeability as a cause of re-expansion edema in rabbits

    SciTech Connect

    Pavlin, D.J.; Nessly, M.L.; Cheney, F.W.

    1981-01-01

    In order to study the mechanism(s) underlying re-expansion edema, we measured the concentration of labeled albumin (RISA) in the extravascular, extracellular water (EVECW) of the lung as a measure of pulmonary vascular permeability. Re-expansion edema was first induced by rapid re-expansion of rabbit lungs that had been collapsed for 1 wk by pneumothorax. The RISA in EVECW was expressed as a fraction of its plasma concentration: (RISA)L/(RISA)PL. The volume of EVECW (ml/gm dry lung) was measured using a /sup 24/Na indicator. Results in re-expansion edema were compared with normal control lungs and with oleic acid edema as a model of permeability edema. In re-expanded lungs, EVECW (3.41 +/- SD 1.24 ml/g) and (RISA)L/(RISA)PL 0.84 +/- SD 0.15) were significantly increased when compared with normal control lungs (2.25 +/- 0.41 ml/g and 0.51 +/- 0.20, respectively). Results in oleic acid edema (5.66 +/- 2.23 ml/g and 0.84 +/- 0.23) were similar to re-expansion edema. This suggested that re-expansion edema is due to increased pulmonary vascular permeability caused by mechanical stresses applied to the lung during re-expansion.

  18. Platelet-rich plasma extract prevents pulmonary edema through angiopoietin-Tie2 signaling.

    PubMed

    Mammoto, Tadanori; Jiang, Amanda; Jiang, Elisabeth; Mammoto, Akiko

    2015-01-01

    Increased vascular permeability contributes to life-threatening pathological conditions, such as acute respiratory distress syndrome. Current treatments for sepsis-induced pulmonary edema rely on low-tidal volume mechanical ventilation, fluid management, and pharmacological use of a single angiogenic or chemical factor with antipermeability activity. However, it is becoming clear that a combination of multiple angiogenic/chemical factors rather than a single factor is required for maintaining stable and functional blood vessels. We have demonstrated that mouse platelet-rich plasma (PRP) extract contains abundant angiopoietin (Ang) 1 and multiple other factors (e.g., platelet-derived growth factor), which potentially stabilize vascular integrity. Here, we show that PRP extract increases tyrosine phosphorylation levels of Tunica internal endothelial cell kinase (Tie2) and attenuates disruption of cell-cell junctional integrity induced by inflammatory cytokine in cultured human microvascular endothelial cells. Systemic injection of PRP extract also increases Tie2 phosphorylation in mouse lung and prevents endotoxin-induced pulmonary edema and the consequent decreases in lung compliance and exercise intolerance resulting from endotoxin challenge. Soluble Tie2 receptor, which inhibits Ang-Tie2 signaling, suppresses the ability of PRP extract to inhibit pulmonary edema in mouse lung. These results suggest that PRP extract prevents endotoxin-induced pulmonary edema mainly through Ang-Tie2 signaling, and PRP extract could be a potential therapeutic strategy for sepsis-induced pulmonary edema and various lung diseases caused by abnormal vascular permeability.

  19. The Effects of Aquaporin-1 in Pulmonary Edema Induced by Fat Embolism Syndrome

    PubMed Central

    Zhang, Yiwei; Tian, Kun; Wang, Yan; Zhang, Rong; Shang, Jiawei; Jiang, Wei; Wang, Aizhong

    2016-01-01

    This study was designed to investigate the role of aquaporin1 (AQP1) in the pathologic process of pulmonary edema induced by fat embolism syndrome (FES) and the effects of a free fatty acid (FFA) mixture on AQP1 expression in pulmonary microvascular endothelial cells (PMVECs). In vivo, edema was more serious in FES mice compared with the control group. The expression of AQP1 and the wet-to-dry lung weight ratio (W/D) in the FES group were significantly increased compared with the control group. At the same time, inhibition of AQP1 decreased the pathological damage resulting from pulmonary edema. Then we performed a study in vitro to investigate whether AQP1 was induced by FFA release in FES. The mRNA and protein level of AQP1 were increased by FFAs in a dose- and time-dependent manner in PMVECs. In addition, the up-regulation of AQP1 was blocked by the inhibitor of p38 kinase, implicating the p38 MAPK pathway as involved in the FFA-induced AQP1 up-regulation in PMVECs. Our results demonstrate that AQP1 may play important roles in pulmonary edema induced by FES and can be regarded as a new therapy target for treatment of pulmonary edema induced by FES. PMID:27455237

  20. Swimming-induced immersion pulmonary edema while snorkeling can be rapidly life-threatening: case reports.

    PubMed

    Cochard, G; Henckes, A; Deslandes, S; Noël-Savina, E; Bedossa, M; Gladu, G; Ozier, Y

    2013-01-01

    It is well known that immersion pulmonary edema can be life-threatening for divers using a self-contained underwater breathing apparatus (scuba). Swimming-induced pulmonary edema in otherwise healthy individuals is not an object of dispute but its real severity is not well known and is probably underestimated. We report two cases of life-threatening acute respiratory distress while swimming and snorkeling, one of which is well documented for swimming-induced pulmonary edema. The interest of these case reports lies in the suddenness of these life-threatening events. Such accidents can mimic a loss of consciousness due to cardiac dysrhythmia and lead to drowning. In the case of swimming-induced pulmonary edema, the prognosis is far better than for a cardiac disorder, but it is also dependent on the efficiency of the supervision. Swimmers, divers, race organizers and supervising physicians should be given knowledge of this pathology and its potentially acute occurrence. Adequate organizational dispositions are mandatory to prevent swimming-induced pulmonary edema-related deaths.

  1. Beta-adrenergic agonist therapy accelerates the resolution of hydrostatic pulmonary edema in sheep and rats.

    PubMed

    Frank, J A; Wang, Y; Osorio, O; Matthay, M A

    2000-10-01

    To determine whether beta-adrenergic agonist therapy increases alveolar liquid clearance during the resolution phase of hydrostatic pulmonary edema, we studied alveolar and lung liquid clearance in two animal models of hydrostatic pulmonary edema. Hydrostatic pulmonary edema was induced in sheep by acutely elevating left atrial pressure to 25 cmH(2)O and instilling 6 ml/kg body wt isotonic 5% albumin (prepared from bovine albumin) in normal saline into the distal air spaces of each lung. After 1 h, sheep were treated with a nebulized beta-agonist (salmeterol) or nebulized saline (controls), and left atrial pressure was then returned to normal. beta-Agonist therapy resulted in a 60% increase in alveolar liquid clearance over 3 h (P < 0.001). Because the rate of alveolar fluid clearance in rats is closer to human rates, we studied beta-agonist therapy in rats, with hydrostatic pulmonary edema induced by volume overload (40% body wt infusion of Ringer lactate). beta-Agonist therapy resulted in a significant decrease in excess lung water (P < 0.01) and significant improvement in arterial blood gases by 2 h (P < 0.03). These preclinical experimental studies support the need for controlled clinical trials to determine whether beta-adrenergic agonist therapy would be of value in accelerating the resolution of hydrostatic pulmonary edema in patients.

  2. The Effects of Aquaporin-1 in Pulmonary Edema Induced by Fat Embolism Syndrome.

    PubMed

    Zhang, Yiwei; Tian, Kun; Wang, Yan; Zhang, Rong; Shang, Jiawei; Jiang, Wei; Wang, Aizhong

    2016-07-21

    This study was designed to investigate the role of aquaporin1 (AQP1) in the pathologic process of pulmonary edema induced by fat embolism syndrome (FES) and the effects of a free fatty acid (FFA) mixture on AQP1 expression in pulmonary microvascular endothelial cells (PMVECs). In vivo, edema was more serious in FES mice compared with the control group. The expression of AQP1 and the wet-to-dry lung weight ratio (W/D) in the FES group were significantly increased compared with the control group. At the same time, inhibition of AQP1 decreased the pathological damage resulting from pulmonary edema. Then we performed a study in vitro to investigate whether AQP1 was induced by FFA release in FES. The mRNA and protein level of AQP1 were increased by FFAs in a dose- and time-dependent manner in PMVECs. In addition, the up-regulation of AQP1 was blocked by the inhibitor of p38 kinase, implicating the p38 MAPK pathway as involved in the FFA-induced AQP1 up-regulation in PMVECs. Our results demonstrate that AQP1 may play important roles in pulmonary edema induced by FES and can be regarded as a new therapy target for treatment of pulmonary edema induced by FES.

  3. Acute pulmonary thromboembolism in a case of fatal child abuse.

    PubMed

    Rahimi, R; Zulkifli, Z F; Omar, E; Ismail, H; Md Noor, S

    2017-04-01

    Child abuse is a worldwide problem. The four major types of abuse include physical abuse, child neglect, psychological maltreatment and sexual violence. We describe a fatal case of child abuse which presented with numerous old and recent soft tissue injuries all over the body. The injuries on the legs have immobilized the victim for quite some time, giving rise to deep vein thrombosis, leading to death as a result of acute pulmonary thromboembolism. This case demonstrates presence of both elements of abuse and neglect in one victim. As this category of crime involves a helpless child, we would also like to reiterate that the community has an obligation to prevent such tragedies and educating the public to recognize the signs and symptoms of abuse would be of utmost important. Ultimately, the community must also be responsible for reporting such offences and the act of silence is akin to condoning a crime witnessed.

  4. Clinical Features of Patients with Diffuse Alveolar Hemorrhage due to Negative-Pressure Pulmonary Edema.

    PubMed

    Contou, Damien; Voiriot, Guillaume; Djibré, Michel; Labbé, Vincent; Fartoukh, Muriel; Parrot, Antoine

    2017-08-01

    Diffuse alveolar hemorrhage (DAH) with negative-pressure pulmonary edema (NPPE) is an uncommon yet life-threatening condition. We aimed at describing the circumstances, clinical, radiological, and bronchoscopic features, as well as the outcome of patients with NPPE-related DAH. We performed a retrospective, observational cohort study, using data prospectively collected over 35 years in an intensive care unit (ICU). Of the 149 patients admitted for DAH, we identified 18 NPPE episodes in 15 patients, one admitted four times for recurrent NPPE-related DAH. The patients were primarily young, male, and athletic. The NPPE setting was postoperative (n = 12/18, 67%) or following generalized tonic-clonic seizures (n = 6/18, 33%). Hemoptysis was almost constant (n = 17/18, 94%), yet rarely massive (>200 cc, n = 1/18, 6%), with anemia observed in 10 (56%) episodes. The DAH triad (hemoptysis, anemia, and pulmonary infiltrates) was observed in 50% of episodes (n = 9/18), and acute respiratory failure in 94% (n = 17/18). Chest computed tomography revealed diffuse bilateral ground glass opacities (n = 10/10, 100%), while bronchoscopy detected bilateral hemorrhage (n = 12/12, 100%) and macroscopically bloody bronchoalveolar lavage, with siderophage absence in most (n = 7/8, 88%), indicating acute DAH. While one episode proved fatal, the other 17 recovered rapidly, with a mean ICU stay lasting 4.6 (2-15) days. Typically, the evolution was rapidly favorable under supportive care. NPPE-related DAH is a rare life-threatening condition occurring primarily after tonic-clonic generalized seizure or generalized anesthesia. Clinical circumstances are a key to its diagnosis. Early diagnosis and recognition likely allow for successful management of this potentially serious complication, whereas ictal-DAH appears ominous in epileptic patients.

  5. [Hypervolemic redistribution mechanism in pulmonary edema in patients with isolated left ventricular failure].

    PubMed

    Shteĭngardt, Iu N; Inzel', T N

    1981-04-01

    The authors examined 90 patients with ischemic heart disease and isolated left-ventricular insufficiency by impedance plethysmography and determined the body total water content by means of tritium oxide in 32 of them. It was established that there is no essential increase in total body water and volumes of circulating blood and plasma at the peak of manifestations of isolated left-ventricular insufficiency. The redistribution of some of the blood from the periphery of systemic circulation to the center, mainly into the pulmonary circulation, possibly plays the principle role in the genesis of pulmonary circulation hypervolemia and pulmonary edema in approximately half of the cases. The same mechanism with its reverse direction occurs in successful treatment and correction of hypervolemia of pulmonary circulation and pulmonary edema.

  6. New Developments in the Pathogenesis of Smoke Inhalation-Induced Pulmonary Edema

    PubMed Central

    Witten, Mark L.; Quan, Stuart F.; Sobonya, Richard E.; Lemen, Richard J.

    1988-01-01

    Smoke inhalation causes most of the deaths in fire-related injuries, with pulmonary edema as a major determinant in the outcome of smoke-inhalation injury. The pathophysiology of pulmonary edema is thought to be related to the products of incomplete combustion. Damage to the integrity of the alveolar epithelium is one of the determinants of the development of smoke-induced pulmonary edema. In recent studies using lung clearance of aerosolized pentetic acid (DTPA [diethylenetriaminepentaacetic acid]) labeled with technetium Tc 99m to assess the permeability of the alveolar epithelium, several factors were identified that may increase a person's susceptibility to smoke-induced acute lung injury. These are increased initial alveolar permeability and alterations in the number and activity of alveolar macrophages. Clinical measurement of 99mTcDTPA clearance may provide a sensitive and convenient method for the early detection and serial assessment of smoke-induced alveolar epithelial permeability changes. Images PMID:3277334

  7. Cardiogenic Pulmonary Edema in a Dog Following Initiation of Therapy for Concurrent Hypoadrenocorticism and Hypothyroidism.

    PubMed

    Paik, Jooyae; Kang, Ji-Houn; Chang, Dongwoo; Yang, Mhan-Pyo

    A 5 yr old intact female cocker spaniel dog weighing 7.8 kg was referred with anorexia, vomiting, and depression. At referral, the dog was diagnosed initially with typical hypoadrenocorticism, and 2 d later, concurrent primary hypothyroidism was detected. Hormonal replacement therapies, including fludrocortisone, prednisolone, and levothyroxine, were initiated, but a few days later the dog became abruptly tachypneic, and thoracic radiographs indicated the development of pulmonary edema. Echocardiography showed that there were abnormalities indicating impaired left ventricular function, although the heart valves were normal. Following treatment with pimobendan and furosemide, the pulmonary edema resolved. The dog had no recurrence of the clinical signs after 10 mo of follow-up, despite being off all cardiac medications; consequently, the cardiac failure was transient or reversible in this dog. The case report describes the stepwise diagnosis and successful treatment of cardiogenic pulmonary edema after initiation of hormonal replacement therapy for concurrent hypoadrenocorticism and hypothyroidism in a dog.

  8. [Cardiogenic pulmonary edema following β2 agonist infusion for acute, severe asthma].

    PubMed

    Bahloul, M; Chaari, A; Dammak, H; Medhioub, F; Abid, L; Chtourou, K; Rekik, N; Chelly, H; Kallel, H; Bouaziz, M

    2015-09-01

    We report the case of a severe acute pulmonary edema secondary to the administration of salbutamol to a patient admitted for severe asthma. The diagnosis of acute pulmonary edema was suspected on the clinical examination, chest radiography, biological (plasmatic Pro-BNP rate) and echocardiographic findings. Rapid improvement under dobutamine and mechanical ventilation argue in favour of cardiogenic pulmonary edema. The young age of our patient, the absence of history of cardiovascular disease and the chronology of this complication onset regarded to salbutamol infusion could suggest β2 agonist involvement in this event. The improvement of cardiac function on echocardiography and the normal results obtained with myocardial perfusion scintigraphy performed 35 days later show the left ventricular reversible dysfunction.

  9. Acute Pulmonary Edema in an Eclamptic Pregnant Patient: A Rare Case of Takotsubo Syndrome.

    PubMed

    Karamchandani, Kunal; Bortz, Brandon; Vaida, Sonia

    2016-09-23

    BACKGROUND Acute pulmonary edema in a pregnant patient is associated with significant morbidity and mortality. Takotsubo syndrome, or stress-induced cardiomyopathy, is a rare cause of acute pulmonary edema in a pregnant patient, especially prior to delivery of the fetus. CASE REPORT We describe a case of a pregnant patient who presented with acute pulmonary edema and eclampsia and was found to have Takotsubo syndrome. To the best of our knowledge, eclampsia as a precipitating factor for Takotsubo syndrome has not been described in literature. CONCLUSIONS Clinicians taking care of pregnant patients should be aware of the potential link between eclampsia and Takotsubo cardiomyopathy. Prompt correction of the precipitating cause along with supportive management as described is the key to a successful outcome.

  10. Acute Pulmonary Edema in an Eclamptic Pregnant Patient: A Rare Case of Takotsubo Syndrome

    PubMed Central

    Karamchandani, Kunal; Bortz, Brandon; Vaida, Sonia

    2016-01-01

    Patient: Female, 35 Final Diagnosis: Takotsubo cardiomyopathy Symptoms: Seizures Medication: — Clinical Procedure: Cesarean section Specialty: Critical Care Medicine Objective: Rare co-existance of disease or pathology Background: Acute pulmonary edema in a pregnant patient is associated with significant morbidity and mortality. Takotsubo syndrome, or stress-induced cardiomyopathy, is a rare cause of acute pulmonary edema in a pregnant patient, especially prior to delivery of the fetus. Case Report: We describe a case of a pregnant patient who presented with acute pulmonary edema and eclampsia and was found to have Takotsubo syndrome. To the best of our knowledge, eclampsia as a precipitating factor for Takotsubo syndrome has not been described in literature. Conclusions: Clinicians taking care of pregnant patients should be aware of the potential link between eclampsia and Takotsubo cardiomyopathy. Prompt correction of the precipitating cause along with supportive management as described is the key to a successful outcome. PMID:27658947

  11. Cocaine-induced myocardial infarction associated with severe reversible systolic dysfunction and pulmonary edema.

    PubMed

    Arzola-Castañer, Daniel; Johnson, Charles

    2004-12-01

    Myocardial infarction (MI) associated to cocaine use was originally reported in 1982 and cases are being encountered more frequently in our milieu. The literature regarding this diagnosis has included mostly cases of cocaine associated chest pain and MI without serious sequelae. A lesser number of reports however focus on the clinical presentation of severe myocardial dysfunction and severe pulmonary edema, with the mechanism for pulmonary edema still being debated. Although previously described individually, these manifestations are thought to be an uncommon complication of cocaine ingestion. In this article the subject is reviewed and we report our experience with two patients that presented to our care with severe pulmonary edema and concomitant severe left ventricular systolic dysfunction that resolved spontaneously with supportive therapy. It is felt that this clinical picture after cocaine use may be more common than expected. In this article we discuss the possible mechanisms associated to this presentation as well as review the literature regarding this subject.

  12. Effect of magnesium sulfate and nifedipine on the risk of developing pulmonary edema in preterm births.

    PubMed

    Xiao, ChengWei; Gangal, Mihnea; Abenhaim, Haim A

    2014-09-01

    To evaluate the risk of developing pulmonary edema in women exposed to nifedipine, magnesium sulfate (MgSO4), or both in a preterm setting. We carried out a retrospective case-control study at a large tertiary care center from 2007 to 2012. Cases of pulmonary edema were age, and gestational age matched to controls at a ratio of 1 case to 4 controls. Logistic regression analysis was used to estimate the effect of nifedipine and/or MgSO4 on the development of pulmonary edema while controlling for predetermined confounding variables. Stepwise logistic regression analysis was used to evaluate additional risk factors of pulmonary edema. A total of 150 charts were reviewed (28 cases and 122 controls). Nifedipine did not increase the odds of developing pulmonary edema [adjusted odds ratio (OR)=1.22 (confidence interval (CI) 0.50, 3.01), P=0.67], whereas exposure to MgSO4, or both MgSO4 and nifedipine, significantly increased the risk of developing pulmonary edema [adjusted OR=3.91 (CI 1.44, 10.65), P=0.008 and adjusted OR=4.75 (CI 1.15, 19.71), P=0.032, respectively]. In the stratified analysis, this association persisted even in nonpreeclamptic women [nifedipine: adjusted OR=0.91 (CI 0.33, 2.52), P=0.852; MgSO4: adjusted OR=3.51 (CI 1.26, 9.76), P=0.016; both: adjusted OR=3.39 (0.76, 15.07), P=0.108]. Other independent risk factors for pulmonary edema were multi-fetal pregnancy, azithromycin, and erythromycin administration. MgSO4 treatment is strongly associated with the development of pulmonary edema when used either as a tocolytic agent or for seizure prophylaxis. In light of the availability of safer alternatives, MgSO4 should be used for tocolysis only in cases whereby the benefits clearly outweigh the risks.

  13. Pulmonary edema following closed-circuit oxygen diving and strenuous swimming.

    PubMed

    Shupak, Avi; Guralnik, Ludmila; Keynan, Yoav; Yanir, Yoav; Adir, Yochai

    2003-11-01

    Acute pulmonary edema may be induced by diving and strenuous swimming. We report the case of a diver using closed-circuit, scuba equipment who developed acute dyspnea, hemoptysis, and hypoxemia following a dive in 18 degreesC (64.4 degrees F) water and physical exertion during the swim back to shore. With the growing popularity of recreational scuba diving, emergency physicians are liable to be faced with increasing numbers of diving-related medical problems. Diving-induced pulmonary edema should be included in the differential diagnosis of acute hypoxemia, sometimes accompanied by acid-base abnormalities, when this is seen in a diver.

  14. A case of negative pressure pulmonary edema in an asthmatic patient after laparoscopic cholecystectomy.

    PubMed

    Rasheed, Asim; Palaria, Urmila; Rani, Dolly; Sharma, Shatrunjay

    2014-01-01

    Negative pressure pulmonary edema is often misdiagnosed or can go clinically unrecognized by anesthesiologists. It is characterized by a markedly low intrapleural pressure which leads to exudation of fluid and red blood cells in the interstitium. Recognition of patients with predisposing factors for upper airway obstruction is important in the diagnosis which is often confused with pulmonary aspiration of gastric contents. Signs and symptoms are subtle and edema is usually self-limited. Our patient was management conservatively with maintenance of a patent airway and administration of supplemental oxygen and had a successful outcome.

  15. Negative pressure pulmonary edema after nasal fracture reduction in an obese female patient: a case report

    PubMed Central

    Choi, Eunkyung; Yi, Junggu; Jeon, Younghoon

    2015-01-01

    Postoperative negative pressure pulmonary edema (NPPE) is a rare, but well-known life-threatening complication of acute upper airway obstruction (UAO) which develops after general anesthesia. The pronounced inspiratory efforts following UAO lead to excessive negative inspiratory pressure, which may cause acute pulmonary edema. Early recognition and prompt treatment of NPPE is necessary to prevent patient morbidity and mortality. In addition, the physician should carefully manage the patient who has risk factors of UAO to prevent this situation. We experienced a case of NPPE following laryngospasm after tracheal extubation in an obese patient who underwent open reduction of orbital wall and nasal bone surgery. PMID:26316826

  16. A case of negative pressure pulmonary edema in an asthmatic patient after laparoscopic cholecystectomy

    PubMed Central

    Rasheed, Asim; Palaria, Urmila; Rani, Dolly; Sharma, Shatrunjay

    2014-01-01

    Negative pressure pulmonary edema is often misdiagnosed or can go clinically unrecognized by anesthesiologists. It is characterized by a markedly low intrapleural pressure which leads to exudation of fluid and red blood cells in the interstitium. Recognition of patients with predisposing factors for upper airway obstruction is important in the diagnosis which is often confused with pulmonary aspiration of gastric contents. Signs and symptoms are subtle and edema is usually self-limited. Our patient was management conservatively with maintenance of a patent airway and administration of supplemental oxygen and had a successful outcome. PMID:25886111

  17. Percutaneous balloon atrioseptostomy for left heart discharge in extracorporeal life support patients with persistent pulmonary edema.

    PubMed

    Bignon, Mathieu; Roule, Vincent; Dahdouh, Ziad; Sabatier, Rémi; Lognoné, Thérèse; Malcor, Guillaume; Idali, Moussa; Ivascau, Calin; Massetti, Massimo; Grollier, Gilles

    2012-02-01

    In severe myocardial dysfunction, extracorporeal life support (ECLS) can preserve organ perfusion. Occasionally, the high resulting afterload can lead to refractory pulmonary edema. We report our experience with percutaneous balloon atrioseptostomy used in this circumstance to discharge the left heart and prevent worsening pulmonary congestion. Between October 2002 and December 2009, 5 patients, with a mean age of 39 years, who were under peripheral ECLS underwent percutaneous balloon atrioseptostomy for refractory worsening pulmonary edema as determined by clinical, radiological, and echocardiographic criteria. Myocardial dysfunction was related to drug poisoning in 2 cases and to myocarditis in the 3 others. Atrioseptostomy successfully improved pulmonary edema and echocardiographic indices of left ventricular function in all cases. Four patients were eventually discharged. The fifth patient died in hospital due to multiorgan failure. In our experience, percutaneous balloon atrioseptostomy appeared to be a rapid, effective, and minimally invasive technique for offloading the left heart of patients with a reversible cardiac dysfunction under ECLS and suffering from refractory pulmonary edema. ©2011, Wiley Periodicals, Inc.

  18. Hypothyroidism and non-cardiogenic pulmonary edema: are we missing something here?

    PubMed Central

    Nikolla, Dhimitri; Metta, V V S Ramesh

    2015-01-01

    Summary We report the case of a 42-year-old female with a history of hypothyroidism and asthma presenting with progressive dyspnea and orthopnea after 2 days of an upper respiratory tract infection (URTI). Based on the clinical and radiological findings, the patient was admitted as a case of cardiogenic pulmonary edema secondary to possible viral myocarditis. However, a normal brain natriuretic peptide (BNP) level with a normal ejection fraction (EF) on echocardiogram changed our working diagnosis from cardiogenic to non-cardiogenic pulmonary edema. Further questioning revealed a history of nocturnal snoring, frequent awakening, and daytime fatigue, suggesting a possible sleep apnea syndrome (SAS). In conclusion, we believe that SAS was the missing link between our patient's hypothyroidism and non-cardiogenic pulmonary edema. Learning points Always keep an open mind and look for a pathology that would explain the whole clinical scenario.The involvement of the respiratory system in hypothyroidism can range from SAS, pulmonary hypertension, hypoventilation, and severe respiratory failure.Hypothyroidism and SAS should be considered in the differential diagnosis of non-cardiogenic pulmonary edema.Patients should be instructed to take levothyroxine on an empty stomach 30–60 min before food to avoid erratic absorption of the hormone. PMID:25866647

  19. Epithelial sodium channel is involved in H2S-induced acute pulmonary edema.

    PubMed

    Jiang, Lei; Wang, Yixin; Su, Chenglei; Sun, Hao; Zhang, Huazhong; Zhu, Baoli; Zhang, Hengdong; Xiao, Hang; Wang, Jun; Zhang, Jinsong

    2015-01-01

    Acute pulmonary edema is one of the major outcomes of exposure to high levels of hydrogen sulfide (H2S). However, the mechanisms involved in H2S-induced acute pulmonary edema are still poorly understood. Therefore, the present study is designed to evaluate the role of epithelial sodium channel (ENaC) in H2S-induced acute pulmonary edema. The Sprague-Dawley rats were exposed to sublethal concentrations of inhaled H2S, then the pulmonary histological and lung epithelial cell injury were evaluated by hematoxylin-eosin staining and electron microscopy, respectively. In addition to morphological investigation, our results also revealed that H2S exposure significantly decreased the alveolar fluid clearance and increased the lung tissue wet-dry ratio. These changes were demonstrated to be associated with decreased ENaC expression. Furthermore, the extracellular-regulated protein kinases 1/2 pathway was demonstrated to be implicated in H2S-mediated ENaC expression, because PD98059, an ERK1/2 antagonist, significantly mitigated H2S-mediated ENaC down-regulation. Therefore, our results show that ENaC might represent a novel pharmacological target for the treatment of acute pulmonary edema induced by H2S and other hazardous gases.

  20. New concepts about the pathophysiology of pulmonary edema.

    PubMed

    Staub, N C

    1988-07-01

    Three new concepts concerning lung liquid and protein exchange are considered. The first is that the microvascular surface area is as important as the microvascular hydrostatic pressure in assessing filtration in the lung. One of the problems in differentiating hemodynamic from increased permeability edema is the inability to determine whether the microvascular surface area has changed. Several agents, as well as exercise, affect liquid filtration. A new, dynamic procedure that is more sensitive for the detection of increased permeability than static measurements of lung water content is described, along with its limitations. The second concept is that water and electrolytes are cleared from the alveoli by a separate mechanism from protein. Water clearance is fast and occurs mainly by an active process, which can be inhibited by amiloride or phloridzin and accelerated by beta-agonists. The mechanism appears to depend on metabolically regulated sodium transport across the alveolar epithelium. Protein clearance is very slow and is relatively independent of alveolar concentration. The protein clearance mechanism is unknown but may involve transcytosis. The third concept is that during edema formation there are two pathways for liquid clearance in addition to the lymphatic system: into the pleural space and along the bronchovascular connective tissue into the mediastinum. During recovery from edema, reabsorption into blood is important if the edema liquid has a low protein osmotic pressure. Clearance into the mediastinum may be the major pathway for liquid sequestered in the loose, binding connective tissue.

  1. Acute pulmonary edema caused by takotsubo cardiomyopathy in a pregnant woman undergoing transvaginal cervical cerclage: A case report.

    PubMed

    Lee, Jae-Young; Kwon, Hyun-Jung; Park, Sang-Wook; Lee, Yu-Mi

    2017-01-01

    The physiological changes associated with pregnancy may predispose pregnant women to pulmonary edema. Other known causes of pulmonary edema during pregnancy include tocolytic drugs, preeclampsia, eclampsia, and peripartum cardiomyopathy. We describe a rare case of pulmonary edema caused by takotsubo cardiomyopathy in a pregnant woman at 14 weeks of gestation who was undergoing emergency transvaginal cervical cerclage. Intraoperative chest radiography revealed severe pulmonary edema and echocardiography indicated moderate left ventricular dysfunction with akinesia of the mid to apical left ventricular wall segment, which is reflective of takotsubo cardiomyopathy. With early detection and appropriate management, the patient was stabilized in a relatively short period of time. Based on her clinical signs and symptoms, we suspect that the pulmonary edema was caused by takotsubo cardiomyopathy.

  2. Pulmonary edema and hemorrhage after acute spinal cord injury in rats.

    PubMed

    He, Bo; Nan, Guoxin

    2016-04-01

    Respiratory complications are a major cause of morbidity and mortality during the first days after acute spinal cord injury (ASCI). However, the pathophysiology of respiratory insufficiency resulting from spinal cord injury that involves lower levels is less well understood. The aim of the present study was to investigate pulmonary pathophysiology after ASCI. This is an experimental animal study of ASCI investigating pulmonary pathophysiology after ASCI. Eighty-four (N=84) rats were divided into two groups: a sham surgery (n=42) and an injury group (n=42). In the injury group, ASCI was induced at the level of the tenth thoracic vertebra by a modified Allen method. Rats were sacrificed 6 hours, 12 hours, 24 hours, 3 days, 1 week, 2 weeks, and 4 weeks after surgery. Pulmonary edema was assessed by calculating the ratio of the wet-to-dry lung weight (W:D). Pulmonary edema and hemorrhage were evaluated by observing gross and microscopic morphology. The study was funded by Natural Science Foundation of China (NSFC, 81272172). The funder of the present study had no capacity to influence the scholarly conduct of the research, interpretation of results, or dissemination of study outcomes. In the injury group, W:D was significantly increased 12 hours after surgery compared with the sham surgery group; W:D peaked 3 days after ASCI (p<.05). Gross morphologic observations showed hemorrhagic lesions on the lung tissue 12 hours after ASCI and pulmonary edema 24 hours after ASCI. Pulmonary edema peaked 3 days after ASCI and was obviously decreased 1 week after ASCI. Hemorrhage was apparent until 2 weeks after ASCI. Light microscopy showed congestion of pulmonary capillaries 6 hours after ASCI. The pulmonary alveoli were filled with erythrocytes and serous extravasate 12 hours after ASCI. Hemorrhage and edema were observed in the interstitium and lung alveoli 24 hours after ASCI. Early pathologic changes such as pulmonary congestion, hemorrhage, and edema after injury may be the

  3. Diagnosis and treatment of presumptive postobstructive pulmonary edema in a Florida panther (Puma concolor coryi).

    PubMed

    Fiorello, Christine V; Cunningham, Mark W; Cantwell, Shauna L; Levy, Julie K; Neer, Erin M; Conley, Kenneth; Rist, Paul M

    2007-06-01

    A free-ranging, adult male Florida panther (Puma concolor coryi) was immobilized and evaluated for hematuria following routine capture. Prior to anesthetic recovery, the panther was fitted with a telemetry collar. After an initially quiet recovery, the panther began thrashing in the transport cage, and was again immobilized. Pink foam was evident from the nostrils, and crackles were ausculted over the chest, indicating pulmonary edema. Postobstructive pulmonary edema was diagnosed based on history, clinical signs, radiographic evaluation, and blood gas analysis. The animal was treated intensively for several hours with diuretics, oxygen, and manual ventilation. The panther responded rapidly to therapy and was released back into the wild 48 hr after presentation. Postobstructive pulmonary edema, also called negative-pressure pulmonary edema, may be underrecognized in veterinary medicine. In this case, the telemetry collar, in conjunction with anesthetic recovery in a small transport crate, may have contributed to tracheal obstruction. Wildlife veterinarians and biologists should be aware of the risk of airway obstruction when placing tracking collars, and animals should be continuously monitored during anesthetic recovery to ensure the presence of a patent airway.

  4. Efficacy of pimobendan on survival and reoccurrence of pulmonary edema in canine congestive heart failure

    PubMed Central

    MIZUNO, Masashi; YAMANO, Shigeki; CHIMURA, Shuichi; HIRAKAWA, Atsushi; TAKUSAGAWA, Yoshimi; SAWADA, Tamotsu; MAETANI, Shigeki; TAKAHASHI, Arane; MIZUNO, Takeshi; HARADA, Kayoko; SHINODA, Asako; UCHIDA, Shuhei; TAKEUCHI, Junichiro; MIZUKOSHI, Takahiro; ENDO, Masaaki; UECHI, Masami

    2016-01-01

    The aim of this study was to evaluate the efficacy of pimobendan with conventional therapies on survival and reocurrence of pulmonary edema in dogs with congestive heart failure (CHF) caused by myxomatous mitral valve disease (MMVD). Records of 197 client-owned dogs from 14 veterinary hospitals were included in this study. Dogs were administered conventional treatments with or without pimobendan. Sixty-four dogs received a standard dose of pimobendan (0.20–0.48 mg/kg every 12 hr (q12hr)), 49 dogs received a low dose of pimobendan (0.05–0.19 mg/kg q12hr), and 84 dogs received conventional therapy alone. Dogs in the standard-dose and low-dose pimobendan groups had significantly longer median survival times than dogs in the conventional group (334, 277 and 136 days, respectively; P<0.001). The reoccurrence rate of pulmonary edema in the standard-dose group was significantly lower than in the low-dose and conventional groups (43%, 59% and 62%, respectively; P<0.05). Combination of pimobendan with a conventional treatment regimen significantly prolonged survival time after an initial episode of pulmonary edema in dogs with CHF caused by MMVD. There was no difference in survival between dogs administered standard and low doses of pimobendan, but pimobendan did prevent the reoccurrence of pulmonary edema in a dose-dependent manner. PMID:27644192

  5. Flash pulmonary edema in patients with renal artery stenosis--the Pickering Syndrome.

    PubMed

    Pelta, Anna; Andersen, Ulrik B; Just, Sven; Bækgaard, Niels

    2011-02-01

    We report the prevalence of flash pulmonary edema in patients consecutively referred for balloon angioplasty of uni- or bilateral renal artery stenosis (PTRA), and describe the characteristics of this special fraction of the patients. We further report two unusual cases. Review of medical records from 60 patients consecutively referred for uni- or bilateral PTRA from 2004-2005 in Copenhagen County. Eight out of 60 patients had one or more episodes of flash pulmonary edema before PTRA. Compared with the remaining patients, they had a higher prevalence of bilateral stenosis (50% vs 27%) and coronary artery disease (75% vs 28%). However, only one of eight had severe systolic dysfunction of the left ventricle. After PTRA, two recurrences of flash pulmonary edema were observed. One was caused by severe restenosis and did not recur after aorto-renal bypass surgery. The other one was caused by rapid atrial fibrillation and did not recur after pacemaker and medical treatment. Flash pulmonary edema can be observed in patients with unilateral as well as bilateral stenosis. The prognosis is usually excellent upon treatment of the stenoses. Recurrences are rare unless restenosis occurs, and therefore, regular control, e.g. by Doppler-ultrasound examination is recommended.

  6. Efficacy of pimobendan on survival and reoccurrence of pulmonary edema in canine congestive heart failure.

    PubMed

    Mizuno, Masashi; Yamano, Shigeki; Chimura, Shuichi; Hirakawa, Atsushi; Takusagawa, Yoshimi; Sawada, Tamotsu; Maetani, Shigeki; Takahashi, Arane; Mizuno, Takeshi; Harada, Kayoko; Shinoda, Asako; Uchida, Shuhei; Takeuchi, Junichiro; Mizukoshi, Takahiro; Endo, Masaaki; Uechi, Masami

    2017-01-20

    The aim of this study was to evaluate the efficacy of pimobendan with conventional therapies on survival and reocurrence of pulmonary edema in dogs with congestive heart failure (CHF) caused by myxomatous mitral valve disease (MMVD). Records of 197 client-owned dogs from 14 veterinary hospitals were included in this study. Dogs were administered conventional treatments with or without pimobendan. Sixty-four dogs received a standard dose of pimobendan (0.20-0.48 mg/kg every 12 hr (q12hr)), 49 dogs received a low dose of pimobendan (0.05-0.19 mg/kg q12hr), and 84 dogs received conventional therapy alone. Dogs in the standard-dose and low-dose pimobendan groups had significantly longer median survival times than dogs in the conventional group (334, 277 and 136 days, respectively; P<0.001). The reoccurrence rate of pulmonary edema in the standard-dose group was significantly lower than in the low-dose and conventional groups (43%, 59% and 62%, respectively; P<0.05). Combination of pimobendan with a conventional treatment regimen significantly prolonged survival time after an initial episode of pulmonary edema in dogs with CHF caused by MMVD. There was no difference in survival between dogs administered standard and low doses of pimobendan, but pimobendan did prevent the reoccurrence of pulmonary edema in a dose-dependent manner.

  7. RADIOGRAPHIC APPEARANCE OF PRESUMED NONCARDIOGENIC PULMONARY EDEMA AND CORRELATION WITH THE UNDERLYING CAUSE IN DOGS AND CATS.

    PubMed

    Bouyssou, Sarah; Specchi, Swan; Desquilbet, Loïc; Pey, Pascaline

    2016-12-22

    Noncardiogenic pulmonary edema is an important cause of respiratory disease in dogs and cats but few reports describe its radiographic appearance. The purpose of this retrospective case series study was to describe radiographic findings in a large cohort of dogs and cats with presumed noncardiogenic pulmonary edema and to test associations among radiographic findings versus cause of edema. Medical records were retrieved for dogs and cats with presumed noncardiogenic edema based on history, radiographic findings, and outcome. Radiographs were reviewed to assess lung pattern and distribution of the edema. Correlation with the cause of noncardiogenic pulmonary edema was evaluated with a Fisher's exact test. A total of 49 dogs and 11 cats were included. Causes for the noncardiogenic edema were airway obstruction (n = 23), direct pulmonary injury (n = 13), severe neurologic stimulation (n = 12), systemic disease (n = 6), near-drowning (n = 3), anaphylaxis (n = 2) and blood transfusion (n = 1). Mixed, symmetric, peripheral, multifocal, bilateral, and dorsal lung patterns were observed in 44 (73.3%), 46 (76.7%), 55 (91.7%), 46 (76.7%), 46 (76.7%), and 34 (57.6%) of 60 animals, respectively. When the distribution was unilateral, pulmonary infiltration involved mainly the right lung lobes (12 of 14, 85.7%). Increased pulmonary opacity was more often asymmetric, unilateral, and dorsal for postobstructive pulmonary edema compared to other types of noncardiogenic pulmonary edema, but no other significant correlations could be identified. In conclusion, noncardiogenic pulmonary edema may present with a quite variable radiographic appearance in dogs and cats.

  8. Update on pulmonary edema: the role and regulation of endothelial barrier function.

    PubMed

    Patterson, C E; Lum, H

    2001-01-01

    Discovery of the pathophysiologic mechanisms leading to pulmonary edema and identification of effective strategies for prevention remain significant clinical concerns. Endothelial barrier function is a key component for maintenance of the integrity of the vascular boundary in the lung, particularly since the gas exchange surface area of the alveolar-capillary membrane is large. This review is focused on new insights in the pulmonary endothelial response to injury and recovery, reversible activation by edemagenic agents, and the biochemical/structural basis for regulation of endothelial barrier function. This information is discussed in the context of fundamental concepts of lung fluid balance and pulmonary function.

  9. Non-cardiogenic pulmonary edema complicating electroconvulsive therapy: short review of the pathophysiology and diagnostic approach.

    PubMed

    Manne, Janaki R; Kasirye, Yusuf; Epperla, Narendranath; Garcia-Montilla, Romel J

    2012-08-01

    Acute pulmonary edema complicating electroconvulsive therapy is an extremely uncommon event that has rarely been described in the literature. Different theories, including one suggesting a cardiogenic component, have been proposed to explain its genesis. The present report describes a classic presentation of this condition with review of its potential mechanisms and diagnostic approach. After successful completion of a session of electroconvulsive therapy, a 42-year-old woman with major depressive disorder developed acute systemic high blood pressure, shortness of breath, and hemoptysis. A chest radiograph demonstrated diffuse bilateral pulmonary infiltrates. Initially cardiogenic pulmonary edema was presumed, but an extensive diagnostic work-up demonstrated normal systolic and diastolic left ventricular function, and with only supportive measures, a complete clinical and radiographic recovery was achieved within 48 hours. The present case does not support any cardiogenic mechanism in the genesis of this condition.

  10. ["Flash" pulmonary edema as a clinical manifestation of renovascular hypertension].

    PubMed

    Kalimonovska-Ostrić, Dimitra; Ivanović, Branislava; Ostrić, Vladimir; Knezivić, Vesna; Stojanov, Vesna; Simić, Dragan

    2003-01-01

    One of the clinical manifestations of renovascular hypertension (RVH) may be a recurrent pulmonary oedema both in the absence or in the presence of systolic left ventricular dysfunction. This type of pulmonary oedema characterized as "flash" pulmonary oedema is ascribed to elevated angiotensin II concentrations with consequent hypertension as well as to volume overload resulting from decreased pressor natriuresis when there are significant stenoses of both or one renal arteries. The investigation included 30 patients with RVH treated by percutaneous transluminal angioplasty of the stenosed renal artery (PTRA) and/or stent implantation (PTR-ST) and 30 patients with surgical resection of the abdominal aortic aneurysm (AAA). The first group was divided in two subgroups according to the etiology of renal artery stenosis (RAS). In the subgroup with fibromuscular dysplasia (FMD) the mean age was 37.5 years, in the subgroup with atherosclerotic renal artery stenosis (ARAS) 54.8 years and in the group with operated AAA 68.6 years. There were more females than males only in the FMD subgroup (10:3). Two patients of the first group experienced pulmonary oedema, both in the subgroup with atherosclerotic renal artery stenosis associated with atherosclerosis of other arteries. Normalization of the blood pressure following PTRA in both and an uncomplicated course after a surgical myocardial revascularization in one of them illustrates the importance of renal revascularization. Pulmonary oedema occurred preoperatively in four out of 30 patients with abdominal aortic aneurysm in whom significant renal artery stenoses coexisted. Two patients died despite surgery, one patient is clinically stable and the medicament treatment of heart failure is inevitable in the fourth with a left ventricular aneurysm following myocardial infarction. The occurrence or recurrence of pulmonary oedema in the absence of other explanation should suggest the possibility of bilateral or unilateral renal

  11. Polytetrafluoroethylene fume-induced pulmonary edema: a case report and review of the literature.

    PubMed

    Hamaya, Rikuta; Ono, Yuko; Chida, Yasuyuki; Inokuchi, Ryota; Kikuchi, Ken; Tameda, Tadanobu; Tase, Choichiro; Shinohara, Kazuaki

    2015-05-14

    Polytetrafluoroethylene is ubiquitous in materials commonly used in cooking and industrial applications. Overheated polytetrafluoroethylene can generate toxic fumes, inducing acute pulmonary edema in some cases. However, neither the etiology nor the radiological features of this condition have been determined. For clarification, we report an illustrative case, together with the first comprehensive literature review. A previously healthy 35-year-old Japanese man who developed severe dyspnea presented to our hospital. He had left a polytetrafluoroethylene-coated pan on a gas-burning stove for 10 hours while unconscious. Upon admission, he was in severe respiratory distress. A chest computed tomographic scan showed massive bilateral patchy consolidations with ground-glass opacities and peripheral area sparing. A diagnosis of polytetrafluoroethylene fume-induced pulmonary edema was made. He was treated with non-invasive positive pressure ventilation and a neutrophil elastase inhibitor, which dramatically alleviated his symptoms and improved his oxygenation. He was discharged without sequelae on hospital day 11. A literature review was performed to survey all reported cases of polytetrafluoroethylene fume-induced pulmonary edema. We searched the PubMed, Embase, Web of Science and OvidSP databases for reports posted between the inception of the databases and 30 September 2014, as well as several Japanese databases (Ichushi Web, J-STAGE, Medical Online, and CiNii). Two radiologists independently interpreted all chest computed tomographic images. Eighteen relevant cases (including the presently reported case) were found. Our search revealed that (1) systemic inflammatory response syndrome was frequently accompanied by pulmonary edema, and (2) common computed tomography findings were bilateral ground-glass opacities, patchy consolidation and peripheral area sparing. Pathophysiological and radiological features were consistent with the exudative phase of acute respiratory

  12. [Hyponatremic encephalopathy with non-cardiogenic pulmonary edema. Development following marathon run].

    PubMed

    Wellershoff, G

    2013-04-01

    This article presents the case of a 52-year-old woman who developed exercise-associated hyponatremia (EAH) complicated by non-cardiogenic pulmonary edema after a marathon run. The condition of EAH is a potentially life-threatening complication of endurance exercise. The main cause seems to be inadequate intake of free water during or following exercise with enduring antidiuresis due to nonosmotic stimulation of ADH secretion. Known risk factors are female gender, slow running pace and lack of weight loss. Emergency therapy is fluid restriction and bolus infusion of 3% NaCl solution to rapidly reduce brain edema.

  13. Concurrent early-onset peripartum cardiomyopathy in a preeclampsia patient with acute pulmonary edema.

    PubMed

    Belen, Erdal; Tipi, Fahri Fatih; Helvaci, Aysen; Bayyigit, Akif

    2015-01-01

    We herein report the case of a preeclampsia patient with comorbid peripartum cardiomyopathy (PPCMP). A 22-year-old woman in the 26th week of gestation was admitted with acute pulmonary edema. Hypertension and proteinuria were detected, and echocardiography showed an ejection fraction of 33%. It is remarkable that PPCMP particularly that associated with preeclampsia was observed in the early gestational period. In conclusion, while dyspnea and pretibial edema are often noted during normal pregnancies, the potential for PPCMP should be considered if these symptoms are excessive and/or comorbid paroxysmal nocturnal dyspnea and orthopnea are present, even in patients with preeclampsia.

  14. Nifedipine for Treatment of High Altitude Pulmonary Edema.

    DTIC Science & Technology

    1992-07-30

    cohsistent effect on spirometry. In addition, we undertook a survey of pulmonary hypertension (PHT) at high altitude, and surprisingly discovered excessive...Systems model #503), auscultation of all lung fields, and systemic blood pressure both supine and standing. Forced vital capacity, peak expiratory flow...the same chew and swallow manner. The protocol called for repeat dosing every thirty minutes, depending upon the blood pressure response of the

  15. Inhibition of chlorine-induced pulmonary inflammation and edema by mometasone and budesonide.

    PubMed

    Chen, Jing; Mo, Yiqun; Schlueter, Connie F; Hoyle, Gary W

    2013-10-15

    Chlorine gas is a widely used industrial compound that is highly toxic by inhalation and is considered a chemical threat agent. Inhalation of high levels of chlorine results in acute lung injury characterized by pneumonitis, pulmonary edema, and decrements in lung function. Because inflammatory processes can promote damage in the injured lung, anti-inflammatory therapy may be of potential benefit for treating chemical-induced acute lung injury. We previously developed a chlorine inhalation model in which mice develop epithelial injury, neutrophilic inflammation, pulmonary edema, and impaired pulmonary function. This model was used to evaluate nine corticosteroids for the ability to inhibit chlorine-induced neutrophilic inflammation. Two of the most potent corticosteroids in this assay, mometasone and budesonide, were investigated further. Mometasone or budesonide administered intraperitoneally 1h after chlorine inhalation caused a dose-dependent inhibition of neutrophil influx in lung tissue sections and in the number of neutrophils in lung lavage fluid. Budesonide, but not mometasone, reduced the levels of the neutrophil attractant CXCL1 in lavage fluid 6h after exposure. Mometasone or budesonide also significantly inhibited pulmonary edema assessed 1 day after chlorine exposure. Chlorine inhalation resulted in airway hyperreactivity to inhaled methacholine, but neither mometasone nor budesonide significantly affected this parameter. The results suggest that mometasone and budesonide may represent potential treatments for chemical-induced lung injury.

  16. Inhibition of chlorine-induced pulmonary inflammation and edema by mometasone and budesonide

    PubMed Central

    Chen, Jing; Mo, Yiqun; Schlueter, Connie F.; Hoyle, Gary W.

    2013-01-01

    Chlorine gas is a widely used industrial compound that is highly toxic by inhalation and is considered a chemical threat agent. Inhalation of high levels of chlorine results in acute lung injury characterized by pneumonitis, pulmonary edema, and decrements in lung function. Because inflammatory processes can promote damage in the injured lung, anti-inflammatory therapy may be of potential benefit for treating chemical-induced acute lung injury. We previously developed a chlorine inhalation model in which mice develop epithelial injury, neutrophilic inflammation, pulmonary edema, and impaired pulmonary function. This model was used to evaluate nine corticosteroids for the ability to inhibit chlorine-induced neutrophilic inflammation. Two of the most potent corticosteroids in this assay, mometasone and budesonide, were investigated further. Mometasone or budesonide administered intraperitoneally 1 h after chlorine inhalation caused a dose-dependent inhibition of neutrophil influx in lung tissue sections and in the number of neutrophils in lung lavage fluid. Budesonide, but not mometasone, reduced the levels of the neutrophil attractant CXCL1 in lavage fluid 6 h after exposure. Mometasone or budesonide also significantly inhibited pulmonary edema assessed 1 day after chlorine exposure. Chlorine inhalation resulted in airway hyperreactivity to inhaled methacholine, but neither mometasone nor budesonide significantly affected this parameter. The results suggest that mometasone and budesonide may represent potential treatments for chemical-induced lung injury. PMID:23800689

  17. Inhibition of chlorine-induced pulmonary inflammation and edema by mometasone and budesonide

    SciTech Connect

    Chen, Jing; Mo, Yiqun; Schlueter, Connie F.; Hoyle, Gary W.

    2013-10-15

    Chlorine gas is a widely used industrial compound that is highly toxic by inhalation and is considered a chemical threat agent. Inhalation of high levels of chlorine results in acute lung injury characterized by pneumonitis, pulmonary edema, and decrements in lung function. Because inflammatory processes can promote damage in the injured lung, anti-inflammatory therapy may be of potential benefit for treating chemical-induced acute lung injury. We previously developed a chlorine inhalation model in which mice develop epithelial injury, neutrophilic inflammation, pulmonary edema, and impaired pulmonary function. This model was used to evaluate nine corticosteroids for the ability to inhibit chlorine-induced neutrophilic inflammation. Two of the most potent corticosteroids in this assay, mometasone and budesonide, were investigated further. Mometasone or budesonide administered intraperitoneally 1 h after chlorine inhalation caused a dose-dependent inhibition of neutrophil influx in lung tissue sections and in the number of neutrophils in lung lavage fluid. Budesonide, but not mometasone, reduced the levels of the neutrophil attractant CXCL1 in lavage fluid 6 h after exposure. Mometasone or budesonide also significantly inhibited pulmonary edema assessed 1 day after chlorine exposure. Chlorine inhalation resulted in airway hyperreactivity to inhaled methacholine, but neither mometasone nor budesonide significantly affected this parameter. The results suggest that mometasone and budesonide may represent potential treatments for chemical-induced lung injury. - Highlights: • Chlorine causes lung injury when inhaled and is considered a chemical threat agent. • Corticosteroids may inhibit lung injury through their anti-inflammatory actions. • Corticosteroids inhibited chlorine-induced pneumonitis and pulmonary edema. • Mometasone and budesonide are potential rescue treatments for chlorine lung injury.

  18. Susceptibility to high-altitude pulmonary edema is associated with a more uniform distribution of regional specific ventilation.

    PubMed

    Patz, Michael D; Sá, Rui C; Darquenne, Chantal; Elliott, Ann R; Asadi, Amran K; Theilmann, Rebecca J; Dubowitz, David J; Swenson, Erik R; Prisk, G Kim; Hopkins, Susan R

    2017-04-01

    High-altitude pulmonary edema (HAPE) is a potentially fatal condition affecting high-altitude sojourners. The biggest predictor of HAPE development is a history of prior HAPE. Magnetic resonance imaging (MRI) shows that HAPE-susceptible (with a history of HAPE), but not HAPE-resistant (with a history of repeated ascents without illness) individuals develop greater heterogeneity of regional pulmonary perfusion breathing hypoxic gas (O2 = 12.5%), consistent with uneven hypoxic pulmonary vasoconstriction (HPV). Why HPV is uneven in HAPE-susceptible individuals is unknown but may arise from regionally heterogeneous ventilation resulting in an uneven stimulus to HPV. We tested the hypothesis that ventilation is more heterogeneous in HAPE-susceptible subjects (n = 6) compared with HAPE-resistant controls (n = 7). MRI specific ventilation imaging (SVI) was used to measure regional specific ventilation and the relative dispersion (SD/mean) of SVI used to quantify baseline heterogeneity. Ventilation heterogeneity from conductive and respiratory airways was measured in normoxia and hypoxia (O2 = 12.5%) using multiple-breath washout and heterogeneity quantified from the indexes Scond and Sacin, respectively. Contrary to our hypothesis, HAPE-susceptible subjects had significantly lower relative dispersion of specific ventilation than the HAPE-resistant controls [susceptible = 1.33 ± 0.67 (SD), resistant = 2.36 ± 0.98, P = 0.05], and Sacin tended to be more uniform (susceptible = 0.085 ± 0.009, resistant = 0.113 ± 0.030, P = 0.07). Scond was not significantly different between groups (susceptible = 0.019 ± 0.007, resistant = 0.020 ± 0.004, P = 0.67). Sacin and Scond did not change significantly in hypoxia (P = 0.56 and 0.19, respectively). In conclusion, ventilation heterogeneity does not change with short-term hypoxia irrespective of HAPE susceptibility, and lesser rather than greater ventilation heterogeneity is observed in HAPE-susceptible subjects. This suggests that

  19. Scorpion sting envenomation presenting with pulmonary edema in adults: a report of seven cases from Nepal.

    PubMed

    Bhadani, Umesh Kumar; Tripathi, Mukesh; Sharma, Sanjib; Pandey, Rajesh

    2006-01-01

    Scorpion sting is a common problem in villages of Eastern Nepal. The life-threatening complications of myocarditis and pulmonary edema is known in red scorpion in India but not reported in Nepal. This condition requires urgent attention and ICU care from few hours to days. Delay in recognition and the hypoxemia increase the morbidity and mortality. Illiteracy, ignorance, poverty, traditional faith healers trying treatment in remote areas, lack of transport in difficult terrains and the non availability of ventilation facility in nearby hospital, add to delay in appropriate treatment. Seven young adult patients admitted in a span of two years with history of scorpion sting presenting with pulmonary edema required ICU care. They were successfully managed with the positive pressure ventilation with PEEP, cardiac support with inotropes and fluid balance. Magnitude of problem, clinical presentation and management done is emphasized.

  20. A case of recurrent swimming-induced pulmonary edema in a triathlete: the need for awareness.

    PubMed

    Smith, R; Brooke, D; Kipps, C; Skaria, B; Subramaniam, V

    2016-08-03

    This report discusses a rare case of a 55-year-old female triathlete who developed recurrent episodes of swimming-induced pulmonary edema (SIPE). She had two hospital admissions with pulmonary edema after developing breathlessness while swimming, including a near-drowning experience in an open water swim. With increasing popularity of triathlon and open water sports, this case highlights the importance of a greater awareness of SIPE among health professionals, event organizers, and athletes. This report explores the previous reported cases in triathletes and those who have suffered recurrent episodes. It is paramount that an accurate diagnosis is made as these individuals may be at an increased risk of future life-threatening episodes.

  1. Radiographically Severe but Clinically Mild Reexpansion Pulmonary Edema following Decompression of a Spontaneous Pneumothorax

    PubMed Central

    Harner, William E.; Crawley, Eric A.

    2014-01-01

    The case is a 48-year-old female who presented with mild dyspnea on exertion and cough with unremarkable vital signs and was found to have a large right sided pneumothorax. She underwent small bore chest tube decompression with immediate reexpansion of the collapsed lung. However, she rapidly developed moderate hypoxemia and radiographic evidence of reexpansion pulmonary edema (REPE) on both the treated and contralateral sides. Within a week, she had a normal chest X-ray and was asymptomatic. This case describes a rare complication of spontaneous pneumothorax and highlights the lack of correlation between symptoms, sequelae, and radiographic severity of pneumothorax and reexpansion pulmonary edema. Proposed pathophysiologic mechanisms include increased production of reactive oxygen species with subsequent loss of surfactant and increased vascular permeability, and loss of vasoregulatory tone. PMID:25165607

  2. Delayed Pneumoperitoneum and Acute Pulmonary Edema Secondary to Acute Gastric Dilatation

    PubMed Central

    Ahn, Jae Yun; Kim, Jong Kun

    2015-01-01

    Pneumoperitoneum caused by acute gastric dilatation (AGD) is a very rare complication. We report a case of pneumoperitoneum and acute pulmonary edema caused by AGD in a patient with Parkinson’s disease. A 78-year-old woman presented with pneumonia and AGD. We inserted a nasogastric tube and administered empirical antibiotics. We performed an endoscopy, and perforation or necrosis of the stomach and pyloric stenosis were not observed. Thirty-six hours after admission, the patient suddenly developed dyspnea and shock, and eventually died. We suspected the cause of death was pneumoperitoneum and acute pulmonary edema caused by AGD during the conservative treatment period. Immunocompromised patients with chronic illness require close observation even if they do not show any symptoms suggestive of complications. Even if the initial endoscopic or abdominal radiologic findings do not show gastric necrosis or perforation, follow-up with endoscopy is essential to recognize complications of AGD early. PMID:26668807

  3. Negative Pressure Pulmonary Edema Following Septoplasty Surgery Triggering Acute Subendocardial Myocardial Infarction

    PubMed Central

    Kaya, Zeynettin; Tuncez, Abdullah; Gök, Umut; Gül, Enes Elvin; Altunbaş, Gökhan

    2014-01-01

    Negative pressure pulmonary edema (NPPE) is defined as fluid transudation into the pulmonary interstitium which occurs as a result of elevated negative intrathoracic pressure caused by the upper respiratory tract obstruction and strong inspiratory effort. NPPE is usually seen during emergence from general anesthesia in the early post-operative period especially after upper respiratory tract surgery. We present a case of a 37-year-old male patient who underwent septoplasty operation and developed NPPE which could not diagnosed and progressed to acute subendocardial myocardial infarction. PMID:25104982

  4. Acute pulmonary edema due to rosiglitazone use in a patient with diabetes mellitus.

    PubMed

    Cekmen, Nedim; Cesur, Mustafa; Cetinbas, Riza; Bedel, Pasa; Erdemli, Ozcan

    2006-01-01

    Rosiglitazone is a peroxisome proliferator active receptor. gamma agonist, which increases insulin sensitivity in adipose tissue, muscle, and liver. Rosiglitazone is a member of the thiazolidinedione group, and because of its significantly positive effect on glycemic control, it is especially preferred in type 2 diabetic patients with a high cardiovascular disease risk. This drug, because of its decreasing effect on insulin resistance, is used alone or combined with type 2 diabetic drugs. A 73-year-old female patient was admitted to the emergency department with dyspnea, pink frothing phlegm, cyanosis, and tiredness. She was lethargic, uncooperative, and had no orientation. In arterial blood gases, hypoxemia and hypercapnia were found. She was taken to the general intensive care unit, and oxygen was applied via mask. The patient had a history of 10 years of diabetes mellitus, hypertension, and atherosclerotic cardiac disease, and she was using rosiglitazone for the past 6 weeks. Her chest x-ray was taken, and acute pulmonary edema was diagnosed. In her last echocardiography, which was performed 1 year before, no signs indicating cardiac failure and pleural effusion could be found. Therefore, it was concluded that pulmonary edema occurred as a complication of rosiglitazone use. After stabilizing the patient's vital signs, blood glucose levels, and lactate levels, medical treatment of diabetes mellitus was rearranged, and she was discharged on the seventh day after her admittance. In a patient with diabetes mellitus who has been admitted to the intensive care unit because of acute pulmonary edema, for differential diagnosis, use of rosiglitazone should be kept in mind during the determination of treatment. Therefore, the authors aim to discuss the effect of rosiglitazone on creating acute pulmonary edema with a case report presentation.

  5. [Acute Postoperative Negative Pressure Pulmonary Edema Caused by the Compression of Brachiocephalic Artery].

    PubMed

    Tagawa, Miki; Iwai, Hidetaka; Fukatsu, Ken; Shimada, Mami; Hirabayashi, Yoshihiro

    2016-06-01

    We report a case of negative-pressure pulmonary edema occurring by tracheal obstruction caused by the brachiocephalic artery. The patient had deformed thorax with cerebral palsy, which deformed thorax placing the brachiocephalic artery high over the trachea, resulting in close and tight contact between the artery and trachea. Additional deformity of the thorax associated with myotonic attacks after general anesthesia might shorten the distance between the sternal notch and the vertebral body, resulting in the tracheal obstruction by the artery.

  6. Acute pulmonary edema and airway hemorrhage in a goat during sevoflurane anesthesia.

    PubMed

    Adami, C; Levionnois, O; Spadavecchia, C

    2011-02-01

    A goat was scheduled for experimental surgery under general anesthesia. The first attempt of performing endotracheal intubation failed and provoked laryngeal spasm. After repeated succesful intubation of inhalation anesthesia was delivered in high concentrations of sevoflurane. Suddenly hypertension and tachycardia were observed, followed by foamy airway secretion and then severe airway hemorrhage. The authors hypothesize that laryngeal spasm provoked respiratory distress and pulmonary edema. The delivered high concentrations of sevoflurane probably enhanced a hyperadrenergic response, predisposing to the development of airway hemorrhage.

  7. Basiliximab induced non-cardiogenic pulmonary edema in two pediatric renal transplant recipients.

    PubMed

    Dolan, Niamh; Waldron, Mary; O'Connell, Marie; Eustace, Nick; Carson, Kevin; Awan, Atif

    2009-11-01

    We report two cases of non-cardiogenic pulmonary edema as a complication of basiliximab induction therapy in young pediatric renal transplant patients identified following a retrospective review of all pediatric renal transplant cases performed in the National Paediatric Transplant Centre, Childrens University Hospital, Temple Street, Dublin, Ireland. Twenty-eight renal transplantations, of which five were living-related (LRD) and 23 were from deceased donors (DD), were performed in 28 children between 2003 and 2006. In six cases, transplantations were pre-emptive. Immunosuppression was induced pre-operatively using a combination of basiliximab, tacrolimus and methylprednisolone in all patients. Basiliximab induction was initiated 2 h prior to surgery in all cases and, in 26 patients, basiliximab was re-administered on post-operative day 4. Two patients, one LRD and one DD, aged 6 and 11 years, respectively, developed acute non-cardiogenic pulmonary edema within 36 h of surgery. Renal dysplasia was identified as the primary etiological factor for renal failure in both cases. Both children required assisted ventilation for between 4 and 6 days. While both grafts had primary function, the DD transplant patient subsequently developed acute tubular necrosis and was eventually lost within 3 weeks due to thrombotic microangiopathy and severe acute antibody-mediated rejection despite adequate immunosuppression. Non-cardiogenic pulmonary edema is a potentially devastating post-operative complication of basiliximab induction therapy in young pediatric patients following renal transplantation. Early recognition and appropriate supportive therapy is vital for patient and, where possible, graft survival.

  8. The Effects of Portulaca oleracea on Hypoxia-Induced Pulmonary Edema in Mice

    PubMed Central

    Yue, Tan; Xiaosa, Wen; Ruirui, Qi; Wencai, Shi; Hailiang, Xin

    2015-01-01

    Abstract Tan Yue, Wen Xiaosa, Qi Ruirui, Shi Wencai, Xin Hailiang, and Li Min. The effects of Portulaca oleracea on hypoxia-induced pulmonary edema in mice. High Alt Med Biol 16:43–51, 2015—Portulaca oleracea L. (PO) is known as “a vegetable for long life” due to its antioxidant, anti-inflammatory, and other pharmacological activities. However, the protective activity of the ethanol extract of PO (EEPO) against hypoxia-induced pulmonary edema has not been fully investigated. In this study, we exposed mice to a simulated altitude of 7000 meters for 0, 3, 6, 9, and 12 h to observe changes in the water content and transvascular leakage of the mouse lung. It was found that transvascular leakage increased to the maximum in the mouse lung after 6 h exposure to hypobaric hypoxia. Prophylactic administration of EEPO before hypoxic exposure markedly reduced the transvascular leakage and oxidative stress, and inhibited the upregulation of NF-kB in the mouse lung, as compared with the control group. In addition, EEPO significantly reduced the levels of proinflammatory cytokines and cell adhesion molecules in the lungs of mice, as compared with the hypoxia group. Our results show that EEPO can reduce initial transvascular leakage and pulmonary edema under hypobaric hypoxia conditions. PMID:25761168

  9. Acute pulmonary edema in a storehouse of moldy oranges: a severe case of the organic dust toxic syndrome.

    PubMed

    Yoshida, K; Ando, M; Araki, S

    1989-01-01

    A woman who was 41 y of age developed pulmonary edema after massive fungal inhalation at an orange storehouse. A provocation test by exposure in the work-place was positive. Neither immunological studies with fungi isolated nor other clinical and histological examinations showed any evidence of hypersensitivity pneumonitis. This is the first report of a subject with organic dust toxic syndrome who developed pulmonary edema associated with the handling of moldy oranges.

  10. Pattern of fluid accumulation in NO2-induced pulmonary edema in dogs. A morphometric study.

    PubMed Central

    Vassilyadi, M.; Michel, R. P.

    1988-01-01

    To ascertain whether the pattern of fluid accumulation could be altered by an agent introduced through the airways, the authors studied the physiology and morphology of 11 dogs exposed to 150-494 ppm.hr NO2 and compared them with 3 new and 5 previously reported control dogs. NO2 caused a partly reversible decrease in systemic arterial pressure and cardiac output, a fall in arterial PO2, and rapid shallow breathing, while pulmonary arterial and wedge pressures remained normal. Post mortem, lower (LL) and middle (ML) lobes were frozen, sections fixed for light microscopy by freeze-substitution, and wet weight/dry weight (W/D) ratios were measured. Alveolar edema was graded, and the distribution of interstitial edema around arteries and veins and within bronchovascular bundles was studied with morphometry: edema ratios (ER) were calculated as area of interstitium/area of vessel or airway. We found that NO2 produced an exposure-dependent increase in lung water (r = 0.73), and that both LL and ML had similar W/D ratios (7.77 and 8.39, respectively) and percent alveolar edema (30% and 34%). Morphometry of interstitial edema showed that the ER for vessels and airways of edematous LL were essentially similar to controls, while those of the ML were markedly increased. It is concluded that NO2 produces exposure-related lung edema and preferential alveolar flooding with probable secondary interstitial accumulation. The discrepancies in interstitial edema between middle and lower lobes may be due to differences in lung volume or in ventilation. Images Figure 6 Figure 9 PMID:3337206

  11. Case fatality rate with vena cava filters in hospitalized stable patients with cancer and pulmonary embolism.

    PubMed

    Stein, Paul D; Matta, Fadi; Sabra, Michel J

    2013-09-01

    In view of the high risk of pulmonary embolism in patients with cancer, we tested the hypothesis that stable patients with pulmonary embolism who have cancer might be a subset of patients who would show a lower case fatality rate with vena cava filters than without filters. Stable patients with pulmonary embolism and cancer at discharge from short-stay hospitals throughout the US from 1998-2009 were identified from the Nationwide Inpatient Sample. Patients with pulmonary embolism who had a diagnostic code for shock, ventilatory support, thrombolytic therapy, or pulmonary embolectomy were excluded because such patients have been shown to have lower case fatality rate with filters. In-hospital all-cause case fatality rate was lower with vena cava filters in stable patients with pulmonary embolism and solid malignant tumors providing they were aged >30 years, but there was variability according to type of tumor and age of patient. On average, case fatality rate among those >30 years with filters was 7070 of 69,350 (10.2%) (95% confidence interval, 10.0-10.4) versus 36,875 of 247,125 (14.9%) (95% confidence interval, 14.8-15.1) without filters (P <.0001) (relative risk 0.68). Among stable patients with hematological malignancies, case fatality rate, except in the elderly, was higher among those with vena cava filters than those without filters. Stable patients with pulmonary embolism and solid malignant tumors who are older than age 30 years appear to be a subset of patients with pulmonary embolism who would benefit from vena cava filters, but this needs to be tested prospectively. Copyright © 2013 Elsevier Inc. All rights reserved.

  12. Morphometric analysis of oleic acid-induced permeability pulmonary edema: correlation with gravimetric lung water.

    PubMed

    Darien, B J; Saban, M R; Hart, A P; MacWilliams, P S; Clayton, M K; Kruse-Elliott, K T

    1997-07-01

    The technique used most commonly to quantitate pulmonary edema in in vivo animal models is postmortem gravimetric analysis (wet:dry) ratio. To determine whether lung water can be quantitated morphometrically, as accurately as by the commonly used gravimetric analysis, perivascular edema (cuff) area to vessel area ratio was correlated to wet:dry ratio. Anesthetized pigs were given either oleic acid (20 mg/kg/h, intravenously) or physiologic saline. At 4 h, lungs were excised and cuff:vessel and wet:dry ratio analysis was performed. The intermediate lobe was clamped across its main stem bronchus to maintain peak inspiratory inflation, excised, frozen in liquid nitrogen, and stored at -70 degrees C until cryostat sectioning and quantification of perivascular interstitial edema (cuff) area. Gravimetric analysis (wet:dry ratio) was performed on the remaining lung. Mean cuff:vessel and wet:dry analyzes showed that lung water increased significantly (p < .01) in the oleic-acid treated group (4.9 +/- .22 and 6.78 +/- .47, respectively), compared with the saline group (.03 +/- .02 and 2.55 +/- .27, respectively). The correlation coefficient between mean cuff:vessel and wet:dry ratios was .86 (p = .0016). This study demonstrates that cuff:vessel ratio analysis can be used to identify the distribution of edema fluid versus vessel diameter, and seems to be as effective a technique as gravimetric analysis to quantitate lung water changes in acute lung injury models. Moreover cuff:vessel ratio analysis can differentiate modest changes in pulmonary edema by direct quantitation, an important end-point not provided by wet:dry analysis. Therefore, it may be a more sensitive technique when investigating therapeutic interventions in in vivo models of acute lung injury.

  13. Morphine blocks the Mesobuthus tamulus venom-induced augmentation of phenyldiguanide reflex and pulmonary edema in anesthetized rats

    PubMed Central

    Akella, Aparna; Tiwari, Anil K.; Rai, Om P.; Deshpande, Shripad B.

    2016-01-01

    Objective: Pulmonary edema, a manifestation of scorpion envenomation syndrome, is attributed to cardiogenic or noncardiogenic factors. Morphine is a drug used for cardiogenic pulmonary edema and its effect on Mesobuthus tamulus (MBT) venom-induced changes is not known. Therefore, we hypothesized that morphine blocks the MBT venom-induced augmentation of phenyldiguanide (PDG) reflex and pulmonary edema. Materials and Methods: Experiments were performed on anesthetized adult female rats. Trachea and jugular vein were cannulated, and the electrocardiographic potentials were recorded by connecting needle electrodes in limb lead II configuration. PDG (10 ΅g/kg, IV, bolus injection) responses were elicited by bolus injection initially, after saline/morphine (1 mg/kg) and after injecting MBT venom (100 μg/kg). The time-response area of the PDG-induced bradycardiac response after treatment was calculated as % of the initial PDG response area. At the end of experiments, lungs were excised for determination of pulmonary water content. Results: PDG produced bradycardiac response that lasted for >60 s. MBT venom augmented the PDG reflex response by 2.5 times. In morphine pretreated group, augmentation of bradycardiac response induced by MBT venom was absent. MBT venom increased the pulmonary water content, and the increase was absent in morphine pretreated animals. Conclusion: The results reveal that morphine prevents the MBT venom-induced augmentation of PDG reflex response and pulmonary edema. Thus, morphine can be useful in scorpion envenomation syndrome associated with pulmonary edema. PMID:26997727

  14. Morphine blocks the Mesobuthus tamulus venom-induced augmentation of phenyldiguanide reflex and pulmonary edema in anesthetized rats.

    PubMed

    Akella, Aparna; Tiwari, Anil K; Rai, Om P; Deshpande, Shripad B

    2016-01-01

    Pulmonary edema, a manifestation of scorpion envenomation syndrome, is attributed to cardiogenic or noncardiogenic factors. Morphine is a drug used for cardiogenic pulmonary edema and its effect on Mesobuthus tamulus (MBT) venom-induced changes is not known. Therefore, we hypothesized that morphine blocks the MBT venom-induced augmentation of phenyldiguanide (PDG) reflex and pulmonary edema. Experiments were performed on anesthetized adult female rats. Trachea and jugular vein were cannulated, and the electrocardiographic potentials were recorded by connecting needle electrodes in limb lead II configuration. PDG (10 ΅g/kg, IV, bolus injection) responses were elicited by bolus injection initially, after saline/morphine (1 mg/kg) and after injecting MBT venom (100 μg/kg). The time-response area of the PDG-induced bradycardiac response after treatment was calculated as % of the initial PDG response area. At the end of experiments, lungs were excised for determination of pulmonary water content. PDG produced bradycardiac response that lasted for >60 s. MBT venom augmented the PDG reflex response by 2.5 times. In morphine pretreated group, augmentation of bradycardiac response induced by MBT venom was absent. MBT venom increased the pulmonary water content, and the increase was absent in morphine pretreated animals. The results reveal that morphine prevents the MBT venom-induced augmentation of PDG reflex response and pulmonary edema. Thus, morphine can be useful in scorpion envenomation syndrome associated with pulmonary edema.

  15. Three-view bedside ultrasound for the differentiation of acute respiratory distress syndrome from cardiogenic pulmonary edema.

    PubMed

    Mantuani, Daniel; Nagdev, Arun; Stone, Michael

    2012-09-01

    Bedside ultrasound is being increasingly used by emergency physicians (EPs) for the differentiation of acute dyspnea in critically ill patients. Lung ultrasound is emerging as a highly sensitive tool in diagnosing alveolar interstitial edema with the presence of diffuse “B-lines” arising from the pleural line. However, when used independently, lung ultrasound is unable to differentiate between cardiogenic and noncardiogenic causes of pulmonary edema. This case report describes a rapid 3-view or “triple scan” sonographic examination to differentiate acute respiratory distress syndrome (ARDS) from cardiogenic pulmonary edema.

  16. Molecular pathology of pulmonary surfactants and cytokines in drowning compared with other asphyxiation and fatal hypothermia.

    PubMed

    Miyazato, Takako; Ishikawa, Takaki; Michiue, Tomomi; Maeda, Hitoshi

    2012-07-01

    Drowning involves complex fatal factors, including asphyxiation and electrolyte/osmotic disturbances, as well as hypothermia in cold water. The present study investigated the molecular pathology of pulmonary injury due to drowning, using lung specimens from forensic autopsy cases of drowning (n = 21), acute mechanical asphyxia due to neck compression and smothering (n = 24), and hypothermia (cold exposure, n = 11), as well as those of injury (n = 23), intoxication (n = 13), fire fatality (n = 18), and acute cardiac death (n = 9) for comparison. TaqMan real-time reverse transcription polymerase chain reaction was used to quantify messenger RNA (mRNA) expressions of pulmonary surfactant-associated proteins A and D (SP-A and SP-D), tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-10. SP-A and SP-D mRNA levels were lower for drowning, mechanical asphyxiation, fire fatality, and acute cardiac deaths than for hypothermia and injury. TNF-α, IL-1β, and IL-10 mRNA levels were higher for drowning or for drowning and injury than for other groups; there was no significant difference between fire fatality, involving airway injury due to inhalation of hot/irritant gases, and other control groups. These observations suggest characteristic molecular biological patterns of pulmonary injury involving suppression of pulmonary surfactants and activation of early-phase mediators of inflammation in drowning, with high mRNA expression levels of pulmonary surfactants in fatal hypothermia; however, there was no significant difference among these markers in immunohistochemical detection, except for SP-A. These mRNA expressions can be used as markers of pulmonary injury to assist in investigations of the pathophysiology of drowning and fatal hypothermia in combination with other biochemical and biological markers.

  17. Case Report: Bilateral reexpansion pulmonary edema following treatment of a unilateral hemothorax

    PubMed Central

    de Wolf, Steven P; Deunk, Jaap; Cornet, Alexander D; Elbers, Paul WG

    2014-01-01

    Bilateral re-expansion pulmonary edema (RPE) is an extremely rare entity. We report the unique case of bilateral RPE following a traumatic, unilateral hemopneumothorax in a young healthy male. Bilateral RPE occurred only one hour after drainage of a unilateral hemopneumothorax. The patient was treated with diuretics and supplemental oxygen. Diagnosis was confirmed by excluding other causes, using laboratory findings, chest radiography, pulmonary and cardiac ultrasound and high resolution computed tomography. His recovery was uneventful. The pathophysiology of bilateral RPE is not well known. Treatment is mainly supportive and consists of diuretics, mechanical ventilation, inotropes and steroids. In case of a pulmonary deterioration after the drainage of a traumatic pneumothorax, bilateral RPE should be considered after exclusion of more common causes of dyspnea. PMID:25713699

  18. Pulmonary edema and blood volume after aneurysmal subarachnoid hemorrhage: a prospective observational study

    PubMed Central

    2010-01-01

    Introduction Pulmonary edema (PED) is a severe complication after aneurysmal subarachnoid hemorrhage (SAH). PED is often treated with diuretics and a reduction in fluid intake, but this may cause intravascular volume depletion, which is associated with secondary ischemia after SAH. We prospectively studied intravascular volume in SAH patients with and without PED. Methods Circulating blood volume (CBV) was determined daily during the first 10 days after SAH by means of pulse dye densitometry. CBV of 60-80 ml/kg was considered normal. PED was diagnosed from clinical signs and characteristic bilateral pulmonary infiltrates on the chest radiograph. We compared CBV, cardiac index, and fluid balance between patients with and without PED with weighted linear regression, taking into account only measurements from the first day after SAH through to the day on which PED was diagnosed. Differences were adjusted for age, bodyweight, and clinical condition. Results In total, 102 patients were included, 17 of whom developed PED after a mean of 4 days after SAH. Patients developing PED had lower mean CBV (56.6 ml/kg) than did those without PED (66.8 ml/kg). The mean difference in CBV was -11.3 ml/kg (95% CI, -16.5 to -6.1); adjusted mean difference, -8.0 ml/kg (95% CI, -14.0 to -2.0). After adjusting, no differences were found in cardiac index or fluid balance between patients with and without PED. Conclusions SAH patients developing pulmonary edema have a lower blood volume than do those without PED and are hypovolemic. Measures taken to counteract pulmonary edema must be balanced against the risk of worsening hypovolemia. Trial registration NTR1255. PMID:20331893

  19. Role of tidal volume, FRC, and end-inspiratory volume in the development of pulmonary edema following mechanical ventilation.

    PubMed

    Dreyfuss, D; Saumon, G

    1993-11-01

    Mechanical ventilation with high peak inspiratory pressure and large tidal volume (VT) produces permeability pulmonary edema. Whether it is mean or peak inspiratory pressure (i.e., mean or end-inspiratory volume) that is the major determinant of ventilation-induced lung injury is unsettled. Rats were ventilated with increasing tidal volumes starting from different degrees of FRC that were set by increasing end-expiratory pressure during positive-pressure ventilation. Pulmonary edema was assessed by the measurement of extravascular lung water content. The importance of permeability alterations was evaluated by measurement of dry lung weight and determination of albumin distribution space. Pulmonary edema with permeability alterations occurred regardless of the value of positive end-expiratory pressure (PEEP), provided the increase in VT was large enough. Similarly, edema occurred even during normal VT ventilation provided the increase in PEEP was large enough. Furthermore, moderate increases in VT or PEEP that were innocuous when applied alone, produced edema when combined. The effect of PEEP was not the consequence of raised airway pressure but of the increase in FRC since similar observations were made in animals ventilated with negative inspiratory pressure. However, although permeability alterations were similar, edema was less marked in animals ventilated with PEEP than in those ventilated with zero end-expiratory pressure (ZEEP) with the same end-inspiratory pressure. This "beneficial" effect of PEEP was probably the consequence of hemodynamic alterations. Indeed, infusion of dopamine to correct the drop in systemic arterial pressure that occurred during PEEP ventilation resulted in a significant increase in pulmonary edema. In conclusion, rather than VT or FRC value, the end-inspiratory volume is probably the main determinant of ventilation-induced edema. Hemodynamic status plays an important role in modulating the amount of edema during lung overinflation

  20. Chest ultrasonography in emergency Cesarean delivery in multi-valvular heart disease with pulmonary edema during spinal anesthesia.

    PubMed

    Samanta, Sukhen; Samanta, Sujay; Ghatak, Tanmoy; Grover, V K

    2014-05-01

    Valvular heart disease in a parturient presenting for Cesarean section is challenging. A 25 year old primigravida parturient with severe mitral stenosis, mild mitral regurgitation, mild aortic regurgitation, and mild pulmonary arterial hypertension required Cesarean delivery after developing pulmonary edema. Low-dose spinal with hyperbaric bupivacine 0.5% 1.8 mL plus 25 μg of fentanyl was used for anesthesia. Chest ultrasonography (US) and transthoracic echocardiography (TTE) were used for monitoring purposes. Spinal-induced preload reduction improved the pulmonary edema, as evidenced by chest US. Chest US and TTE helped in fluid management.

  1. Fatal theophylline toxicity precipitated by in situ pulmonary artery thrombosis.

    PubMed Central

    Davies, R. J.; Hawkey, C. J.

    1989-01-01

    A 57 year old man developed theophylline toxicity in association with acute pulmonary artery thrombosis. The plasma half life of theophylline was prolonged suggesting impaired metabolism secondary to acute right heart failure. PMID:2780453

  2. A 45-Year-Old Man With Recurrent Dyspnea and Hemoptysis during Exercise: Exercise-Induced Pulmonary Hemorrhage/Edema

    PubMed Central

    Kim, Dae Sung; Lee, Minhyeok; Kwon, Oh Jung; Jeong, Inbeom; Son, Ji Woong; Na, Moon Jun

    2015-01-01

    A 45-year-old man presented with dyspnea and hemoptysis during exercise. A chest computed tomography (CT) revealed multifocal diffuse patchy ground glass opacity and interlobular septal thickening in both the lungs. Permeability pulmonary edema or pulmonary hemorrhage was suspected. Serologic studies for autoimmune disorders and vasculitis were negative. There was no laboratory evidence of coagulopathy, other hematopoietic disease or infectious disease. Considering correlation with exercise, we diagnosed exercise-induced pulmonary hemorrhage (EIPH) or exercise-induced pulmonary edema (EIPE). The patient was managed with antifibrinolytics, antibiotics, and antitussive agent. After a week, follow-up chest CT revealed completely resolved pulmonary hemorrhage. About 2 months after the first event, he visited again with dyspnea and hemoptysis during running. In the present study, we report a case of recurrent pulmonary hemorrhage after exercise. PMID:26508928

  3. Exercise-induced interstitial pulmonary edema at sea-level in young and old healthy humans

    PubMed Central

    Taylor, Bryan J.; Carlson, Alex R.; Miller, Andrew D.; Johnson, Bruce D.

    2014-01-01

    We asked whether aged adults are more susceptible to exercise-induced pulmonary edema relative to younger individuals. Lung diffusing capacity for carbon monoxide (DLCO), alveolar-capillary membrane conductance (Dm) and pulmonary-capillary blood volume (Vc) were measured before and after exhaustive discontinuous incremental exercise in 10 young (YNG; 27±3 yr) and 10 old (OLD; 69±5 yr) males. In YNG subjects, Dm increased (11±7%, P=0.031), Vc decreased (−10±9%, P=0.01) and DLCO was unchanged (30.5±4.1 vs. 29.7±2.9 ml/min/mmHg, P=0.44) pre- to post-exercise. In OLD subjects, DLCO and Dm increased (11±14%, P=0.042; 16±14%, P=0.025) but Vc was unchanged (58±23 vs. 56±23 ml, P=0.570) pre- to post-exercise. Group-mean Dm/Vc was greater after vs. before exercise in the YNG and OLD subjects. However, Dm/Vc was lower post-exercise in 2 of the 10 YNG (−7±4%) and 2 of the 10 OLD subjects (−10±5%). These data suggest that exercise decreases interstitial lung fluid in most YNG and OLD subjects, with a small number exhibiting evidence for exercise-induced pulmonary edema. PMID:24200644

  4. Reexpansion pulmonary edema after surgery for spontaneous pneumothorax in a patient with anorexia nervosa

    PubMed Central

    Ozawa, Yuichiro; Ichimura, Hideo; Sakai, Mitsuaki

    2016-01-01

    Introduction Several adverse effects on the pulmonary system in patients with anorexia nervosa (AN) have been reported. We present a case of AN who presented with a complicated reexpansion pulmonary edema (RPE) after video-assisted thoracic surgery (VATS) for spontaneous pneumothorax. Presentation of case A 23-year-old woman with severe anorexia nervosa (weight: 25 kg, body mass index: 8.96 kg/m2) underwent VATS for spontaneous pneumothorax. Five hours after the surgery, she immediately presented acute cardiorespiratory insufficiency. Chest radiography showed an infiltrating shadow in the entire right lung. She was diagnosed with reexpansion pulmonary edema that was treated with methylprednisolone pulse therapy and mechanical ventilation. She recovered and was extubated on postoperative day 4. The chest drain tube was removed on postoperative day 5. Discussion Bullectomy or ligation of bullae for spontaneous pneumothorax in a patient with AN has never been reported. In our case, bullae were identified in preoperative CT and we chose ligation of the bullae instead of the bullectomy using automatic suture device because of poor wound healing concerned. Conclusion We present a case of RPE after VATS for spontaneous pneumothorax in a patient with AN. Malnutrition owing to AN results in critical complications such as RPE. PMID:27158490

  5. Crystalloid or colloid fluid loading and pulmonary permeability, edema, and injury in septic and nonseptic critically ill patients with hypovolemia.

    PubMed

    van der Heijden, Melanie; Verheij, Joanne; van Nieuw Amerongen, Geerten P; Groeneveld, A B Johan

    2009-04-01

    To compare crystalloid and colloid fluids in their effect on pulmonary edema in hypovolemic septic and nonseptic patients with or at risk for acute lung injury/acute respiratory distress syndrome. We hypothesized that 1) crystalloid loading results in more edema formation than colloid loading and 2) the differences among the types of fluid decreases at high permeability. Prospective randomized clinical trial on the effect of fluids in 24 septic and 24 nonseptic mechanically ventilated patients with clinical hypovolemia. Patients were assigned to NaCl 0.9%, gelatin 4%, hydroxyethyl starch 6%, or albumin 5% loading for 90 minutes according to changes in filling pressures. Twenty-three septic and 10 nonseptic patients had acute lung injury/acute respiratory distress syndrome (p < 0.001). Septic patients had greater pulmonary capillary permeability, edema, and severity of lung injury than nonseptic patients (p < 0.01), as measured by the pulmonary leak index (PLI) for Gallium-labeled transferrin, extravascular lung water (EVLW), and lung injury score (LIS), respectively. Colloids increased plasma volume, cardiac index, and central venous pressure (CVP) more than crystalloids (p < 0.05), although more crystalloids were infused (p < 0.05). Colloid osmotic pressure (COP) increased in colloid and decreased in crystalloid groups (p < 0.001). Irrespective of fluid type or underlying disease, the pulmonary leak index increased by median 5% (p < 0.05). Regardless of fluid type or underlying disease, EVLW and LIS did not change during fluid loading and EVLW related to COP-CVP (rs = -.40, p < 0.01). Pulmonary edema and LIS are not affected by the type of fluid loading in the steep part of the cardiac function curve in both septic and nonseptic patients. Then, pulmonary capillary permeability may be a smaller determinant of pulmonary edema than COP and CVP. Safety factors may have prevented edema during a small filtration pressure-induced rise in pulmonary protein and thus fluid

  6. A multicenter prospective cohort study of volume management after subarachnoid hemorrhage: circulatory characteristics of pulmonary edema after subarachnoid hemorrhage.

    PubMed

    Obata, Yoshiki; Takeda, Junichi; Sato, Yohei; Ishikura, Hiroyasu; Matsui, Toru; Isotani, Eiji

    2016-08-01

    OBJECT Subarachnoid hemorrhage (SAH) is often accompanied by pulmonary complications, which may lead to poor outcomes and death. This study investigated the incidence and cause of pulmonary edema in patients with SAH by using hemodynamic monitoring with PiCCO-plus pulse contour analysis. METHODS A total of 204 patients with SAH were included in a multicenter prospective cohort study to investigate hemodynamic changes after surgical clipping or coil embolization of ruptured cerebral aneurysms by using a PiCCO-plus device. Changes in various hemodynamic parameters after SAH were analyzed statistically. RESULTS Fifty-two patients (25.5%) developed pulmonary edema. Patients with pulmonary edema (PE group) were significantly older than those without pulmonary edema (non-PE group) (p = 0.017). The mean extravascular lung water index was significantly higher in the PE group than in the non-PE group throughout the study period. The pulmonary vascular permeability index (PVPI) was significantly higher in the PE group than in the non-PE group on Day 6 (p = 0.029) and Day 10 (p = 0.011). The cardiac index of the PE group was significantly decreased biphasically on Days 2 and 10 compared with that of the non-PE group. In the early phase (Days 1-5 after SAH), the daily water balance of the PE group was slightly positive. In the delayed phase (Days 6-14 after SAH), the serum C-reactive protein level and the global end-diastolic volume index were significantly higher in the PE group than in the non-PE group, whereas the PVPI tended to be higher in the PE group. CONCLUSIONS Pulmonary edema that occurs in the early and delayed phases after SAH is caused by cardiac failure and inflammatory (i.e., noncardiogenic) conditions, respectively. Measurement of the extravascular lung water index, cardiac index, and PVPI by PiCCO-plus monitoring is useful for identifying pulmonary edema in patients with SAH.

  7. Therapeutic efficacy of milrinone in the management of enterovirus 71-induced pulmonary edema.

    PubMed

    Wang, Shih-Min; Lei, Huan-Yao; Huang, Mei-Chih; Wu, Jing-Min; Chen, Chun-Ta; Wang, Jieh-Neng; Wang, Jen-Ren; Liu, Ching-Chuan

    2005-03-01

    Hand, foot, and mouth disease and herpangina are the major clinical manifestations of enterovirus 71 (EV71) infections. Brain-stem encephalitis and pulmonary edema are severe complications that can lead to death. This study was designed to evaluate the potential therapeutic effect of milrinone, a phosphodiesterase (PDE) inhibitor, in the treatment of patients with EV71-induced pulmonary edema. We conducted a historically controlled trial of 24 children with severe EV71-induced pulmonary edema from April 1998-June 2003 in southern Taiwan. Patients were divided into groups treated before and after the introduction of milrinone therapy. Etiological diagnosis was established by viral cultures and confirmed by specific immunofluorescence and neutralization tests. All 24 patients were below 5 years of age. The mortality was lower in the milrinone-treated vs. nontreated group (36.4% vs. 92.3%, P=0.005). Sympathetic tachycardia was decreased in patients treated with milrinone compared to controls (144 +/- 17/min vs. 206 +/- 26/min, P=0.004). A marked decrease in IL-13 (77 +/- 9 pg/ml vs. 162 +/- 88 pg/ml, P=0.001) was observed in milrinone-treated patients compared to controls. There was a significant reduction in white blood cell (10,838 +/- 4,537/mm3 vs. 19,475 +/- 7,798/mm3, P=0.009) and platelet (257 +/- 45 x 10(3)/mm3 vs. 400 +/- 87 x 10(3)/mm3, P=0.001) counts in milrinone-treated patients compared to controls. These results were associated with improvement in sympathetic regulation and decrease in IL-13 production. Milrinone therapy may provide a useful therapeutic approach for this highly lethal disorder.

  8. A delayed, unusual non-cardiogenic pulmonary edema after intravascular administration of non-ionic, low osmolar radiocontrast media for coronary angiography.

    PubMed

    Kang, Min-Ho; Nah, Jong-Chun

    2013-07-01

    Non-cardiogenic pulmonary edema (NCPE) is a rare adverse reaction to iodinated radiocontrast media (RCM), in which all previous cases were immediate reactions. A 56-year-old male was given iopamidol, a non-ionic, low osmolar RCM, during coronary artery angiography. He developed pulmonary edema and fever a day after the procedure. Despite diuretic therapy, the patient's pulmonary edema worsened and his high fever persisted. The patient's pulmonary edema was eventually resolved with intravenous steroid treatment. We interpreted the patient's condition as NCPE manifesting as a delayed reaction to RCM. To our knowledge, our case is the first to show NCPE as a delayed hypersensitivity reaction.

  9. A Case of Salicylate Intoxication Complicated by Coagulopathy, Pulmonary Edema, and Pancreatitis.

    PubMed

    Ayalon, Itay; Alder, Matthew Noble; Langner, Travis Ryan; Hafberg, Einar Thor; Miethke, Alexander Gerhard; Kaplan, Jennifer Melissa

    The large availability of salicylic acid products makes them an often encountered source of poisoning in the emergency department. Even though in most cases the prognosis is good, with a low incidence of long-term morbidity and mortality, complications do occur, and some of those can be life threatening. We present an unusual case of salicylate intoxication in an adolescent in which several uncommon complications (severe coagulopathy, pulmonary edema, and pancreatitis) conjoined together. We review the literature and discuss the complications pathogenesis and differential diagnosis. We suggest that these potentially life-threatening complications be acknowledged, investigated, and rapidly treated.

  10. Delayed renal dysfunction and flash pulmonary edema post endovascular abdominal aneurysm repair.

    PubMed

    Carron, Pierre-Louis; Piliero, Nicolas; Heitz, Morgane; Kribs, Marc; Rodière, Mathieu; Jousse, Patrick; Gunther-Calvino, Silvia; Thony, Frédéric

    2016-04-01

    After endovascular aortic repair (EVAR), the deterioration in long-term renal function is probably multifactorial. Preoperative renal failure is an independent risk factor. Postoperative renal dysfunction can be associated with inadvertent renal artery occlusion, renal artery complications as stenosis, plaque dislodgement, or dissection. Ischemic nephropathy can accelerate hypertension and circulatory congestion. We report a case of coverage of the renal arteries symptomatic with flash pulmonary edema and renal failure 15 months after EVAR, suggesting a delayed endograft migration. The patient had complete resolution of symptoms and renal function after renal artery stenting with placement between endograft and aneurysm to the left renal artery.

  11. High Altitude Pulmonary Edema in an Experienced Mountaineer. Possible Genetic Predisposition

    PubMed Central

    Whitlow, Kenneth S.; Davis, Babette W.

    2014-01-01

    High altitude pulmonary edema (HAPE) is a form of high altitude illness characterized by cough, dyspnea upon exertion progressing to dyspnea at rest and eventual death, seen in patients who ascend over 2,500 meters, particularly if that ascent is rapid. This case describes a patient with no prior history of HAPE and extensive experience hiking above 2,500 meters who developed progressive dyspnea and cough while ascending to 3,200 meters. His risk factors included rapid ascent, high altitude, male sex, and a possible genetic predisposition for HAPE. PMID:25493133

  12. An Unusual Type of Localized Hypertrophic Cardiomyopathy With Wolf Parkinson White Syndrome Presenting With Pulmonary Edema

    PubMed Central

    Vatan, Mehmet Bulent; Gunduz, Huseyin; Gurel, Safiye; Kocayigit, Ibrahim; Vural, Ahmet; Demirtas, Saadet; Cakar, Mehmet Akif; Gunduz, Yasemin

    2012-01-01

    Hypertrophic cardiomyopathy (HCM) is an autosomal dominant heart disease that is the most common genetic cardiac disorder. The disease is characterized by excessive thickening of the left ventricular myocardium. The anterior portion of the interventricular ventricular septum is often involved. Asymmetric hypertrophy of apical site, left ventricular free wall, and right ventricle are less common in hypertrophic cardiomyopathy that occur in 1% cases. We report a case of a patient with an unusual type of hypertrophic cardiomyopathy and Wolf Parkinson White (WPW) presenting with pulmonary edema.

  13. Medial defects of the small pulmonary arteries in fatal pulmonary hypertension in infants with trisomy 13 and trisomy 18.

    PubMed

    Tahara, Masahiro; Shimozono, Saiko; Nitta, Tetsuya; Yamaki, Shigeo

    2014-02-01

    Congestive heart failure is a major cause of early death in patients with trisomy 13 or 18 and congenital heart disease (CHD). Pulmonary artery banding for these patients early in life is preferred to protect the lungs from high pulmonary flow rates and improve survival. We performed open lung biopsies in 11 patients with trisomy 13 or 18 accompanied by CHD and severe pulmonary artery hypertension (PAH) between 2009 and 2011. Two (18.2%) of these 11 patients had medial defects of the small pulmonary arteries. One patient with trisomy 13 and an atrial septal defect developed lung hemorrhage and lung edema at the age of 9 months and died at the age of 13 months. The lumens of the small pulmonary arteries of the other patient with trisomy 18 and a ventricular septal defect became occluded due to the intimal proliferation of fibrous tissues at the age of 2 months. This patient died at the age of 27 months. The deaths of both patients were associated with heart-related factors. Patients with medial defects are vulnerable to intimal proliferation in the small pulmonary arteries. More patients with trisomy 13 or 18 and CHD might have similar pulmonary vascular changes. The small pulmonary arteries of patients with trisomy 13 and 18 should be further analyzed.

  14. Swimming-Induced Pulmonary Edema: Pathophysiology and Risk Reduction With Sildenafil

    PubMed Central

    Moon, Richard E.; Martina, Stefanie D.; Peacher, Dionne F.; Potter, Jennifer F.; Wester, Tracy E.; Cherry, Anne D.; Natoli, Michael J.; Otteni, Claire E.; Kernagis, Dawn N.; White, William D.; Freiberger, John J.

    2016-01-01

    Background Swimming-induced pulmonary edema (SIPE) occurs during swimming or scuba diving, often in young individuals with no predisposing conditions, and its pathophysiology is poorly understood. This study tested the hypothesis that pulmonary artery and pulmonary artery wedge pressures are higher in SIPE-susceptible individuals during submerged exercise compared to the general population and are reduced by sildenafil. Methods and Results Ten study subjects with a history of SIPE (mean age 41.6 years) and 20 control subjects (mean age 36.2 years) were instrumented with radial artery and pulmonary artery catheters and performed moderate cycle ergometer exercise for 6–7 minutes while submersed in 20°C water. SIPE-susceptible subjects repeated the exercise 150 minutes after oral administration of 50 mg sildenafil. Work rate and mean arterial pressure during exercise were similar in controls and SIPE-susceptibles. Average VO2 and cardiac output (CO) in SIPE-susceptibles and controls were: VO2 2.42 L.min−1 vs. 1.95 L.min−1, P=0.2; CO 17.9 L.min−1 vs. 13.8 L.min−1, P=0.01). Accounting for differences in CO between groups, mean pulmonary artery pressure (MPAP) at CO=13.8 L.min−1 was 22.5 mmHg in controls vs. 34.0 mmHg in SIPE-susceptibles (P=0.004) and the corresponding pulmonary artery wedge pressure (PAWP) 11.0 mmHg vs. 18.8 mmHg (P=0.028). After sildenafil, there were no statistically significant differences in MPAP or PAWP between SIPE-susceptibles and controls. Conclusions These observations confirm that SIPE is a form of hemodynamic pulmonary edema. The reduction in pulmonary vascular pressures after sildenafil with no adverse effect on exercise hemodynamics suggests that it may be useful in SIPE prevention. Clinical Trial Registration Information ClinicalTrials.gov. Identifier: NCT00815646. PMID:26882910

  15. Fatal Pulmonary Tumor Embolic Microangiopathy in Young Lady without Known Primary Malignancy

    PubMed Central

    Al-Azem, M. Ali; Hanafy, Ahmed; Nakkar, Talal

    2014-01-01

    Pulmonary embolism (PE) is a common cause of morbidity and mortality in hospitalized patients. Malignancy, prolonged recumbence, and chemotherapy are renowned risk factors for development of clinically significant PE. Cancer exerts a multitude of pathophysiological processes, for example, hypercoagulability and abnormal vessels with sluggish circulation that can lead to PE. One of the peculiar characteristics of tumor cells is their ability to reach the circulation and behave as blood clot—not a metastasis-occluding the pulmonary circulation. We present a case of fatal pulmonary embolism diagnosed histologically to be due to tumor cell embolism. PMID:25478243

  16. Pulmonary Edema

    MedlinePlus

    ... these air sacs take in oxygen and release carbon dioxide. Normally, the exchange of gases takes place without ... arteries) to your lungs. There, the blood releases carbon dioxide and picks up oxygen. The oxygen-rich blood ...

  17. Unilateral pulmonary edema: a rare initial presentation of cardiogenic shock due to acute myocardial infarction.

    PubMed

    Shin, Jeong Hun; Kim, Seok Hwan; Park, Jinkyu; Lim, Young-Hyo; Park, Hwan-Cheol; Choi, Sung Il; Shin, Jinho; Kim, Kyung-Soo; Kim, Soon-Gil; Hong, Mun K; Lee, Jae Ung

    2012-02-01

    Cardiogenic unilateral pulmonary edema (UPE) is a rare clinical entity that is often misdiagnosed at first. Most cases of cardiogenic UPE occur in the right upper lobe and are caused by severe mitral regurgitation (MR). We present an unusual case of right-sided UPE in a patient with cardiogenic shock due to acute myocardial infarction (AMI) without severe MR. The patient was successfully treated by percutaneous coronary intervention and medical therapy for heart failure. Follow-up chest Radiography showed complete resolution of the UPE. This case reminds us that AMI can present as UPE even in patients without severe MR or any preexisting pulmonary disease affecting the vasculature or parenchyma of the lung.

  18. Pioglitazone-induced congestive heart failure and pulmonary edema in a patient with preserved ejection fraction

    PubMed Central

    Jearath, Vaneet; Vashisht, Rajan; Rustagi, Vipul; Raina, Sujeet; Sharma, Rajesh

    2016-01-01

    Pioglitazone-induced heart failure is known in patients with underlying heart disease, but is not well documented in patients with normal left ventricular function. Pioglitazone has been very popular as it is an insulin sensitizer and insulin resistance is prevalent among Indians. Fluid retention exacerbates pre-existing heart failure or precipitates heart failure in a patient with underlying left ventricular dysfunction. However, pathogenesis of heart failure in a patient with normal left ventricular function is not known. Probably it is due to dose-related effect on pulmonary endothelial permeability, rather than alterations in left ventricular mass or ejection fraction. We report a patient who developed congestive heart failure and pulmonary edema with normal left ventricular function within 1 year of starting pioglitazone therapy. We have to be careful in monitoring all possible side effects during followup when patients are on pioglitazone therapy. PMID:27127397

  19. Nicardipine-Induced Acute Pulmonary Edema: A Rare but Severe Complication of Tocolysis

    PubMed Central

    Serena, Claire; Begot, Emmanuelle; Cros, Jérôme; Hodler, Charles; Fedou, Anne Laure; Nathan-Denizot, Nathalie; Clavel, Marc

    2014-01-01

    We report four cases of acute pulmonary edema that occurred during treatment by intravenous tocolysis using nicardipine in pregnancy patients with no previous heart problems. Clinical severity justified hospitalization in intensive care unit (ICU) each time. Acute dyspnea has begun at an average of 63 hours after initiation of treatment. For all patients, the first diagnosis suspected was pulmonary embolism. The patients' condition improved rapidly with appropriate diuretic treatment and by modifying the tocolysis. The use of intravenous nicardipine is widely used for tocolysis in France even if its prescription does not have a marketing authorization. The pathophysiological mechanisms of this complication remain unclear. The main reported risk factors are spontaneous preterm labor, multiple pregnancy, concomitant obstetrical disease, association with beta-agonists, and fetal lung maturation corticotherapy. A better knowledge of this rare but serious adverse event should improve the management of patients. Nifedipine or atosiban, the efficiency of which tocolysis was also studied, could be an alternative. PMID:25215245

  20. Nicardipine-induced acute pulmonary edema: a rare but severe complication of tocolysis.

    PubMed

    Serena, Claire; Begot, Emmanuelle; Cros, Jérôme; Hodler, Charles; Fedou, Anne Laure; Nathan-Denizot, Nathalie; Clavel, Marc

    2014-01-01

    We report four cases of acute pulmonary edema that occurred during treatment by intravenous tocolysis using nicardipine in pregnancy patients with no previous heart problems. Clinical severity justified hospitalization in intensive care unit (ICU) each time. Acute dyspnea has begun at an average of 63 hours after initiation of treatment. For all patients, the first diagnosis suspected was pulmonary embolism. The patients' condition improved rapidly with appropriate diuretic treatment and by modifying the tocolysis. The use of intravenous nicardipine is widely used for tocolysis in France even if its prescription does not have a marketing authorization. The pathophysiological mechanisms of this complication remain unclear. The main reported risk factors are spontaneous preterm labor, multiple pregnancy, concomitant obstetrical disease, association with beta-agonists, and fetal lung maturation corticotherapy. A better knowledge of this rare but serious adverse event should improve the management of patients. Nifedipine or atosiban, the efficiency of which tocolysis was also studied, could be an alternative.

  1. Pioglitazone-induced congestive heart failure and pulmonary edema in a patient with preserved ejection fraction.

    PubMed

    Jearath, Vaneet; Vashisht, Rajan; Rustagi, Vipul; Raina, Sujeet; Sharma, Rajesh

    2016-01-01

    Pioglitazone-induced heart failure is known in patients with underlying heart disease, but is not well documented in patients with normal left ventricular function. Pioglitazone has been very popular as it is an insulin sensitizer and insulin resistance is prevalent among Indians. Fluid retention exacerbates pre-existing heart failure or precipitates heart failure in a patient with underlying left ventricular dysfunction. However, pathogenesis of heart failure in a patient with normal left ventricular function is not known. Probably it is due to dose-related effect on pulmonary endothelial permeability, rather than alterations in left ventricular mass or ejection fraction. We report a patient who developed congestive heart failure and pulmonary edema with normal left ventricular function within 1 year of starting pioglitazone therapy. We have to be careful in monitoring all possible side effects during followup when patients are on pioglitazone therapy.

  2. [Fatal pulmonary mycosis in a diabetic and cirrhotic patient].

    PubMed

    Ayadi-Kaddour, Aïda; Braham, Emna; Marghli, Adel; Ismail, Olfa; Helal, Imen; Mlika, Mona; Kilani, Tarak; El Mezni, Faouzi

    2015-04-01

    Pulmonary mucormycosis is a rare, devastating, opportunistic fungal infection, caused by the ubiquitous filamentous fungi of the Mucorales order of the class of Zygomycetes. This infection occurs principally in some particular conditions, specially in diabetic patients and immunocompromised host, and rarely in cirrhotic patients. The diagnosis of mucormycosis can only be confirmed by pathological and mycological examination of biopsy specimens. We report a case of pulmonary mucormycosis in a 68-year-old woman with underlying liver cirrhosis and diabetes mellitus. Endoscopic and radiologic findings supported the diagnosis of hydatid cyst of the lung. The patient underwent surgical resection and was started on amphotericin B, after pathological examination. Unfortunately, she succumbed to the infection within one month of surgery.

  3. Negative pressure pulmonary edema after craniotomy through the endonasal transsphenoidal approach

    PubMed Central

    Ou, Mengchan; Luo, Zhen; Liu, Juan; Yang, Yaoxin; Li, Yu

    2015-01-01

    We describe a case of negative pressure pulmonary edema that occurred in the post-anesthesia care unit in a patient who had undergone transsphenoidal resection of a pituitary adenoma. Negative pressure pulmonary edema is an uncommon complication of general anesthesia. In this case, the patient’s nasal cavity had been filled with surgical packs and she had not become accustomed to breathing through her mouth, in addition to her large tongue and small oropharyngeal cavity, residual effect of anesthetic may resulting in tongue falling which caused airway obstruction. The main causative factor is excessive negative intrathoracic pressure generated by the patient’s spontaneous forced inspiration in an effort to overcome the airway obstruction. It typically developed rapidly, and may be life threatening if not diagnosed promptly. After re-intubation for a short period of mechanical ventilation with positive end expiratory pressure (PEEP 10 cm H2O) and a bolus of intravenous furosemide, the patient recovered rapidly and discharged 8 days after surgery. PMID:26131257

  4. High Altitude Pulmonary Edema Without Appropriate Action Progresses to Right Ventricular Strain: A Case Study.

    PubMed

    Mills, Logan; Harper, Chris; Rozwadowski, Sophie; Imray, Chris

    2016-09-01

    Mills, Logan, Chris Harper, Sophie Rozwadowski, and Chris Imray. High altitude pulmonary edema without appropriate action progresses to right ventricular strain: A case study. High Alt Med Biol. 17:228-232, 2016.-A 24-year-old male developed high altitude pulmonary edema (HAPE) after three ascents to 4061 m over 3 days, sleeping each night at 2735 m. He complained of exertional dyspnea, dry cough, chest pain, fever, nausea, vertigo, and a severe frontal headache. Inappropriate continuation of ascent despite symptoms led to functional impairment and forced a return to the valley, but dyspnea persisted in addition to new orthopnea. Hospital admission showed hypoxemia, resting tachycardia, and systemic hypertension. ECG revealed right ventricular strain and a chest X-ray revealed right lower zone infiltrates. This case demonstrates that HAPE can develop in previously unaffected individuals given certain precipitating factors, and that in the presence of HAPE, prolonged exposure to altitude with exercise (or exertion) does not confer acclimatization with protective adaptations and that rest and descent are the appropriate actions. The case additionally demonstrates well-characterized right ventricular involvement.

  5. Respiratory Failure in a Child Due to Type 2 Postobstructive Pulmonary Edema.

    PubMed

    Austin, Andrea L; Kon, Alexander; Matteucci, Michael J

    2016-01-01

    Postobstructive pulmonary edema (POPE), sudden pulmonary edema after upper airway obstruction, is an important disease entity for pediatric emergency physicians to recognize and initiate prompt treatment. Type 1 POPE occurs after a sudden, severe upper airway obstruction, whereas type 2 POPE develops after acute relief of chronic airway obstructive. A 12-year-old boy, with a history of untreated sleep apnea, on postoperative day 2 from appendectomy, was brought to the emergency department in respiratory distress. The patient required urgent intubation, and copious pink frothy fluid was suctioned from the endotracheal tube. He was initially difficult to oxygenate, but with ventilator setting changes including a high positive end-expiratory pressure, the patient improved. He was discharged on hospital day 3 with nighttime BiPAP for home use. Type 2 POPE should be considered in a patient presenting with respiratory distress and a history of sleep apnea. Optimal ventilator management includes use of PEEP in the 10 to 15 cm H2O range. The roles of diuretics and steroids are controversial. Most patients will do well after a brief period of ventilatory support (24-48 hours). With the rise of ambulatory surgery, pediatric emergency physicians must be attuned to both the surgical and anesthetic complications that occur in the early postoperative period.

  6. Effect of partial liquid ventilation on pulmonary vascular permeability and edema after experimental acute lung injury.

    PubMed

    Lange, N R; Kozlowski, J K; Gust, R; Shapiro, S D; Schuster, D P

    2000-07-01

    We evaluated the effects of partial liquid ventilation (PLV) with two different dosages of the perfluorocarbon LiquiVent (perflubron) on pulmonary vascular permeability and edema formation after oleic acid (OA)-induced acute lung injury in dogs. We used imaging with positron emission tomography to measure fractional pulmonary blood flow, lung water concentration (LWC), and the pulmonary transcapillary escape rate (PTCER) of (68)Ga-labeled transferrin at 5 and 21 h after lung injury in five dogs undergoing conventional mechanical ventilation (CMV), five dogs undergoing low-dose PLV (perflubron at 10 ml/kg), and four dogs undergoing high dose PLV (perflubron at 30 ml/kg). A positive end-expiratory pressure of 7.5 cm H(2)O was used in all dogs. After OA (0.08 ml/kg)- induced lung injury, there were no significant differences or trends for PTCER or LWC at any time when the PLV groups were compared with the CMV group. However, lung tissue myeloperoxidase activity was significantly lower in the combined PLV group than in the CMV group (p = 0.016). We conclude that after OA-induced lung injury, the addition of PLV to CMV does not directly attenuate pulmonary vascular leak or lung water accumulation. Rather, the benefits of such treatment may be due to modifications of the inflammatory response.

  7. [Re-expansion pulmonary edema as a complication of a spontaneous pneumothorax drainage--a case review].

    PubMed

    Toporcer, T; Il'ková, J; Lakyová, L; Belák, J; Radonak, J

    2008-07-01

    Reexpansion pulmonary edema is an iatrogenic complication occurring after reinflation of the collapsed lung of a patient with pneumothorax or fluidothorax. The following risk factors have been associated with reexpansion pulmonary edema: younger age, longer duration of a lung collapse, its large extend and a quick lung reexpansion. We report a case of 26-years-old man. The patient was admited to the second surgical clinic FNLP, Kosice because of a spontaneous pneumothorax. A chest tube was inserted in local anesthesia in the right anterior axilar line and the fourth intercostal space. An active negative pressure of 20 cm H2O was applied. Dyspnea, decrease of blood pressure, tachycardia, tachypnoe and expectoration of pink sputum were recorded after negative pressure application. Oxygen saturation decreased to 90% despite the addition of oxygen. Glucocorticoids, diuretic stimulants, analgesic and bronchodilatators were administered. Chest X-rays and computer tomography showed a strong ipsilateral pulmonary edema and an incipient contralateral pulmonary edema. The patient was stabilized and after 16 hours continuous oxygen administration was not longer needed. Because of continuous pneumothorax, a video assisted thoracoscopic surgery was performed on the seventh day after the chest tube insertion. After 13 days of hospitalization the patient was discharged in good condition without any further complications to the ambulatory care. Reexpansion pulmonary edema is a rare complication of the chest tube insertion and thoracocentesis because of pneumothorax and fluidothorax. The mortality of reexpansion pulmonary edema reaches up to 20%. Chest tube insertion and thoracocentesis are therapeutic procedures to be performed solely on medical department which can provide artificial lung ventilation.

  8. Pulmonary aspergilloma with renal oxalosis: fatal effect at a distance.

    PubMed

    Vaideeswar, Pradeep; Sakhdeo, Uma M

    2009-05-01

    Some species of the fungus Aspergillus, especially Aspergillus niger, produce oxalic acid as a fermentation byproduct. The acid combines with calcium ions at physiological pH to form insoluble calcium oxalate crystals that are mainly deposited at local sites. This is often seen in the lungs, where the crystals tend to potentiate the destructive capacity of the fungus. In rare instances, there is hyperoxaluria and deposition of the crystals in the renal tubules. We report this rare occurrence in a 59-year-old man with pulmonary aspergilloma and acute renal failure. To the best of our knowledge, this is the fifth case to be reported.

  9. [Pulmonary pathology in fatal human influenza A (H1N1) infection].

    PubMed

    Duan, Xue-jing; Li, Yong; Gong, En-cong; Wang, Jue; Lü, Fu-dong; Zhang, He-qiu; Sun, Lin; Yue, Zhu-jun; Song, Chen-chao; Zhang, Shi-Jie; Li, Ning; Dai, Jie

    2011-12-01

    To study the pulmonary pathology in patients died of fatal human influenza A(H1N1) infection. Eight cases of fatal human influenza A (H1N1) infection, including 2 autopsy cases and 6 paramortem needle puncture biopsies, were enrolled into the study. Histologic examination, immunohistochemitry, flow cytometry and Western blotting were carried out. The major pathologic changes included necrotizing bronchiolitis with surrounding inflammation, diffuse alveolar damage and pulmonary hemorrhage. Influenza viral antigen expression was detected in the lung tissue by Western blotting. Immunohistochemical study demonstrated the presence of nuclear protein and hemagglutinin virus antigens in parts of trachea, bronchial epithelium and glands, alveolar epithelium, macrophages and endothelium. Flow cytometry showed that the apoptotic rate of type II pneumocytes (32.15%, 78.15%) was significantly higher than that of the controls (1.93%, 3.77%). Necrotizing bronchiolitis, diffuse alveolar damage and pulmonary hemorrhage followed by pulmonary fibrosis in late stage are the major pathologic changes in fatal human influenza A (H1N1) infection.

  10. Hypoxemia and low Crs in vagally denervated lambs result from reduced lung volume and not pulmonary edema.

    PubMed

    Lalani, Salim; Remmers, John E; MacKinnon, Yolanda; Ford, Gordon T; Hasan, Shabih U

    2002-08-01

    Vagal denervation performed in the intrathoracic region in newborn lambs leads to hypoxemia and decreased respiratory system compliance (Crs), which could result from atelectasis and/or pulmonary edema. The objective of the present study was to quantify the relative roles of alveolar derecruitment and pulmonary edema as underlying cause(s) of respiratory failure. Vagal denervation was performed in the intrathoracic region and below the recurrent laryngeal nerves in six newborn lambs within 24 h of birth, whereas six were sham operated. Pre- and postinflation Crs was measured to investigate the presence of alveolar derecruitment. Pulmonary edema was assessed with lung wet-dry-to-wet and lung tissue wet-to-dry ratios, total protein, and FITC-BSA recovery in lung tissue and bronchoalveolar lavage. Compared with that in the sham-operated animals, Crs was significantly lower in vagally denervated animals. However, postinflation, pulmonary system compliance obtained by quasi-static lung inflation and deflation to 30 cmH2O showed no significant difference between the sham-operated and denervated lambs. The lung wet-dry-to-wet and lung tissue wet-to-dry ratios, total protein, and FITC-BSA recovery in lung tissue and bronchoalveolar lavage were similar in denervated and sham-operated groups. We provide evidence that reduced lung volume and not pulmonary edema is associated with intrathoracic vagal denervation and is the likely underlying mechanism for hypoxemia and low Crs.

  11. Use of non-invasive ventilation in acute pulmonary edema and chronic obstructive pulmonary disease exacerbation in emergency medicine: predictors of failure.

    PubMed

    Passarini, Juliana Nalin de Souza; Zambon, Lair; Morcillo, André Moreno; Kosour, Carolina; Saad, Ivete Alonso Bredda

    2012-09-01

    This study analyzed acute respiratory failure caused by acute pulmonary edema, as well as chronic obstructive pulmonary disease exacerbation, that was treated with non-invasive mechanical ventilation to identify the factors that are associated with the success or failure non-invasive mechanical ventilation in urgent and emergency service. This study was a prospective, descriptive and analytical study. We included patients of both genders aged >18 years who used non-invasive mechanical ventilation due to acute respiratory failure that was secondary to acute pulmonary edema or chronic obstructive pulmonary disease exacerbation. Patients with acute respiratory failure that was secondary to pathologies other than acute pulmonary edema and chronic obstructive pulmonary disease or who presented with contraindications for the technique were excluded. Expiratory pressures between 5 and 8 cmH2O and inspiratory pressures between 10 and 12 cmH2O were used. Supplemental oxygen maintained peripheral oxygen saturation at >90%. The primary outcome was endotracheal intubation. A total of 152 patients were included. The median non-invasive mechanical ventilation time was 6 hours (range 1 - 32 hours) for chronic obstructive pulmonary disease patients (n=60) and 5 hours (range 2 - 32 hours) for acute pulmonary edema patients (n=92). Most (75.7%) patients progressed successfully. However, reduced APACHE II scores and lower peripheral oxygen saturation were observed. These results were statistically significant in patients who progressed to intubation (p<0.001). BiPAP (Bi-level Positive Airway Pressure portable ventilator), as continuous positive airway pressure use increased the probability of endotracheal intubation 2.3 times (p=0.032). Patients with acute pulmonary edema and elevated GCS scores also increased the probability of success. Respiratory frequency >25 rpm, higher APACHE II scores, BiPAP use and chronic obstructive pulmonary disease diagnosis were associated with

  12. VA/Q distribution during heavy exercise and recovery in humans: implications for pulmonary edema

    NASA Technical Reports Server (NTRS)

    Schaffartzik, W.; Poole, D. C.; Derion, T.; Tsukimoto, K.; Hogan, M. C.; Arcos, J. P.; Bebout, D. E.; Wagner, P. D.

    1992-01-01

    Ventilation-perfusion (VA/Q) inequality has been shown to increase with exercise. Potential mechanisms for this increase include nonuniform pulmonary vasoconstriction, ventilatory time constant inequality, reduced large airway gas mixing, and development of interstitial pulmonary edema. We hypothesized that persistence of VA/Q mismatch after ventilation and cardiac output subside during recovery would be consistent with edema; however, rapid resolution would suggest mechanisms related to changes in ventilation and blood flow per se. Thirteen healthy males performed near-maximal cycle ergometry at an inspiratory PO2 of 91 Torr (because hypoxia accentuates VA/Q mismatch on exercise). Cardiorespiratory variables and inert gas elimination patterns were measured at rest, during exercise, and between 2 and 30 min of recovery. Two profiles of VA/Q distribution behavior emerged during heavy exercise: in group 1 an increase in VA/Q mismatch (log SDQ of 0.35 +/- 0.02 at rest and 0.44 +/- 0.02 at exercise; P less than 0.05, n = 7) and in group 2 no change in VA/Q mismatch (n = 6). There were no differences in anthropometric data, work rate, O2 uptake, or ventilation during heavy exercise between groups. Group 1 demonstrated significantly greater VA/Q inequality, lower vital capacity, and higher forced expiratory flow at 25-75% of forced vital capacity for the first 20 min during recovery than group 2. Cardiac index was higher in group 1 both during heavy exercise and 4 and 6 min postexercise. However, both ventilation and cardiac output returned toward baseline values more rapidly than did VA/Q relationships. Arterial pH was lower in group 1 during exercise and recovery. We conclude that greater VA/Q inequality in group 1 and its persistence during recovery are consistent with the hypothesis that edema occurs and contributes to the increase in VA/Q inequality during exercise. This is supported by observation of greater blood flows and acidosis and, presumably therefore

  13. VA/Q distribution during heavy exercise and recovery in humans: implications for pulmonary edema

    NASA Technical Reports Server (NTRS)

    Schaffartzik, W.; Poole, D. C.; Derion, T.; Tsukimoto, K.; Hogan, M. C.; Arcos, J. P.; Bebout, D. E.; Wagner, P. D.

    1992-01-01

    Ventilation-perfusion (VA/Q) inequality has been shown to increase with exercise. Potential mechanisms for this increase include nonuniform pulmonary vasoconstriction, ventilatory time constant inequality, reduced large airway gas mixing, and development of interstitial pulmonary edema. We hypothesized that persistence of VA/Q mismatch after ventilation and cardiac output subside during recovery would be consistent with edema; however, rapid resolution would suggest mechanisms related to changes in ventilation and blood flow per se. Thirteen healthy males performed near-maximal cycle ergometry at an inspiratory PO2 of 91 Torr (because hypoxia accentuates VA/Q mismatch on exercise). Cardiorespiratory variables and inert gas elimination patterns were measured at rest, during exercise, and between 2 and 30 min of recovery. Two profiles of VA/Q distribution behavior emerged during heavy exercise: in group 1 an increase in VA/Q mismatch (log SDQ of 0.35 +/- 0.02 at rest and 0.44 +/- 0.02 at exercise; P less than 0.05, n = 7) and in group 2 no change in VA/Q mismatch (n = 6). There were no differences in anthropometric data, work rate, O2 uptake, or ventilation during heavy exercise between groups. Group 1 demonstrated significantly greater VA/Q inequality, lower vital capacity, and higher forced expiratory flow at 25-75% of forced vital capacity for the first 20 min during recovery than group 2. Cardiac index was higher in group 1 both during heavy exercise and 4 and 6 min postexercise. However, both ventilation and cardiac output returned toward baseline values more rapidly than did VA/Q relationships. Arterial pH was lower in group 1 during exercise and recovery. We conclude that greater VA/Q inequality in group 1 and its persistence during recovery are consistent with the hypothesis that edema occurs and contributes to the increase in VA/Q inequality during exercise. This is supported by observation of greater blood flows and acidosis and, presumably therefore

  14. VA/Q distribution during heavy exercise and recovery in humans: implications for pulmonary edema.

    PubMed

    Schaffartzik, W; Poole, D C; Derion, T; Tsukimoto, K; Hogan, M C; Arcos, J P; Bebout, D E; Wagner, P D

    1992-05-01

    Ventilation-perfusion (VA/Q) inequality has been shown to increase with exercise. Potential mechanisms for this increase include nonuniform pulmonary vasoconstriction, ventilatory time constant inequality, reduced large airway gas mixing, and development of interstitial pulmonary edema. We hypothesized that persistence of VA/Q mismatch after ventilation and cardiac output subside during recovery would be consistent with edema; however, rapid resolution would suggest mechanisms related to changes in ventilation and blood flow per se. Thirteen healthy males performed near-maximal cycle ergometry at an inspiratory PO2 of 91 Torr (because hypoxia accentuates VA/Q mismatch on exercise). Cardiorespiratory variables and inert gas elimination patterns were measured at rest, during exercise, and between 2 and 30 min of recovery. Two profiles of VA/Q distribution behavior emerged during heavy exercise: in group 1 an increase in VA/Q mismatch (log SDQ of 0.35 +/- 0.02 at rest and 0.44 +/- 0.02 at exercise; P less than 0.05, n = 7) and in group 2 no change in VA/Q mismatch (n = 6). There were no differences in anthropometric data, work rate, O2 uptake, or ventilation during heavy exercise between groups. Group 1 demonstrated significantly greater VA/Q inequality, lower vital capacity, and higher forced expiratory flow at 25-75% of forced vital capacity for the first 20 min during recovery than group 2. Cardiac index was higher in group 1 both during heavy exercise and 4 and 6 min postexercise. However, both ventilation and cardiac output returned toward baseline values more rapidly than did VA/Q relationships. Arterial pH was lower in group 1 during exercise and recovery. We conclude that greater VA/Q inequality in group 1 and its persistence during recovery are consistent with the hypothesis that edema occurs and contributes to the increase in VA/Q inequality during exercise. This is supported by observation of greater blood flows and acidosis and, presumably therefore

  15. Rapid Fatal Outcome from Pulmonary Arteries Compression in Transitional Cell Carcinoma

    PubMed Central

    Voutsadakis, Ioannis A.; Masouris, George; Tsapakidis, Konstantinos; Papandreou, Christos N.

    2009-01-01

    Transitional cell carcinoma of the urinary bladder is a malignancy that metastasizes frequently to lymph nodes including the mediastinal lymph nodes. This occurrence may produce symptoms due to compression of adjacent structures such as the superior vena cava syndrome or dysphagia from esophageal compression. We report the case of a 59-year-old man with metastatic transitional cell carcinoma for whom mediastinal lymphadenopathy led to pulmonary artery compression and a rapidly fatal outcome. This rare occurrence has to be distinguished from pulmonary embolism, a much more frequent event in cancer patients, in order that proper and prompt treatment be initiated. PMID:20111732

  16. A fatal case of pulmonary chromobacterium violaceum infection in an adult.

    PubMed

    Cheong, B M K

    2010-06-01

    Chromobacterium violaceum is a gram negative, facultative anaerobic coccobacillus. Human infections are rare and usually occur after exposure to contaminated soil or water. Infections can present with fulminant septicemia, multiple abscesses and rapidly spreading soft tissue infections. Here we present a fatal case of pulmonary Chromobacterium violaceum infection following aspiration of drain water. Treatment with fluroquinolones in combination with either co-trimoxazole or amikacin has been described in successfully treated cases.

  17. Pediatric Pulmonary Arterial Hypertension and Hyperthyroidism: A Potentially Fatal Combination

    PubMed Central

    Trapp, Christine M.; Elder, Robert W.; Gerken, Adrienne T.; Sopher, Aviva B.; Lerner, Shulamit; Rosenzweig, Erika B.

    2012-01-01

    Context: Patients with pulmonary arterial hypertension (PAH) who develop hyperthyroidism are at risk for acute cardiopulmonary decompensation and death. Cases and Setting: We present a series of eight idiopathic PAH/heritable PAH pediatric patients who developed hyperthyroidism between 1999 and 2011. Institutional Review Board approval was obtained; informed consent was waived due to the retrospective nature of the series. All eight patients were receiving iv epoprostenol; five of the eight patients presented with acute cardiopulmonary decompensation in the setting of hyperthyroidism. In the remaining three patients, hyperthyroidism was detected during routine screening of thyroid function tests. The one patient who underwent emergency thyroidectomy was the only survivor of those who presented in cardiopulmonary decline. Evidence Synthesis: Aggressive treatment of the hyperthyroid state, including emergency total thyroidectomy and escalation of targeted PAH therapy and β-blockade when warranted, may prove lifesaving in these patients. Prompt thyroidectomy or radioactive iodine ablation should be considered for clinically stable PAH patients with early and/or mild hyperthyroidism to avoid potentially life-threatening cardiopulmonary decompensation. Conclusions: Although the association between hyperthyroidism and PAH remains poorly understood, the potential impact of hyperthyroidism on the cardiopulmonary status of PAH patients must not be ignored. Hyperthyroidism must be identified early in this patient population to optimize intervention before acute decompensation. Thyroid function tests should be checked routinely in patients with PAH, particularly those on iv epoprostenol, and urgently in patients with acute decompensation or symptoms of hyperthyroidism. PMID:22622024

  18. Acute pulmonary edema following liposuction due to heart failure and atypical pneumonia.

    PubMed

    Wollina, Uwe; Graf, Andreas; Hanisch, Volkmar

    2015-05-01

    Microcannular liposuction in tumescent anesthesia is the most effective treatment for painful lipedema. Tumescent anesthesia is an established and safe procedure in local analgesia when performed according to guidelines. Major adverse effects are rare. In patients with advanced lipedema, however, the commonly presented comorbidities bear additional risks.We report on post-surgical acute pulmonary edema after tumescent liposuction according to guidelines in a 52-year-old female patient with lipedema of the legs. We discuss in detail possible scenarios that might be involved in such emergency. In the present case the most likely was a retarded community acquired atypical pneumonia with aggravation of pre-existent comorbidities.A combined treatment with intravenous b-lactam antibiosis, positive pressure ventilation, and continuous venovenous hemodialysis and filtration resulted in complete remission in a couple of days. In conclusion, tumescent liposuction of advanced lipedema patients should only be performed in well-trained centers with sufficient infrastructure.

  19. Experience of step-wise protocol using noninvasive positive pressure ventilation for treating cardiogenic pulmonary edema.

    PubMed

    Momii, Hidetoshi; Tashima, Yuki; Kadokami, Toshiaki; Narita, Sumito; Yoshida, Masayoshi; Ando, Shin-ichi

    2012-08-01

    Initiating and weaning procedure of noninvasive positive pressure ventilation (NIPPV) on acute cardiogenic pulmonary edema (ACPE) has been determined empirically, and the total time of its use has been sometimes prolonged unnecessarily. A simple protocol for its use may facilitate initiation and avoids prolongation of the NIPPV treatment. We designed a step-wise protocol for NIPPV use and retrospectively examined the clinical outcome of our protocol for initiation and weaning of NIPPV in 45 patients with ACPE. Almost all patients recovered from respiratory distress successfully. There was no intubation nor complication related to NIPPV. In most of the cases, maximal-end expiratory pressure was less than 7-cm H2O. The mean duration of NIPPV was 19.5±28.0 h and the median duration was 8.0 h (interquartile range=14.0 h). This simple step-wise NIPPV protocol for ACPE can facilitate quick and safe initiation and termination of the treatment.

  20. Diffuse alveolar hemorrhage from systemic lupus erythematosus misdiagnosed as high altitude pulmonary edema.

    PubMed

    Li, Suzhi; Wang, Yuliang; Huang, Xuewen; Cao, Jingxin; Yang, Dingzhou

    2015-03-01

    A 26-year-old woman presented with dyspnea and dry cough soon after arriving on the Qinghai-Tibet Plateau (3650 m). Chest radiograph showed diffuse patchy infiltrates. The initial diagnosis was high altitude pulmonary edema (HAPE). However, the patient had no sputum or moist rales, and supplemental oxygen and intravenous aminophylline produced no improvement. Chest HRCT revealed symmetric and diffuse ground glass opacities. Further examination found anemia, leukopenia, urine abnormalities, and increased erythrocyte sedimentation rate. Antibodies for ds-DNA and ANA were positive. Hemoptysis and arthralgia developed after a few days. Finally the patient was diagnosed with diffuse alveolar hemorrhage secondary to systemic lupus erythemetosus. When considering a diagnosis of HAPE, careful attention to physical signs, and a clinical course that is atypical for HAPE should prompt evaluation for other disease processes; HRCT can be useful in this setting.

  1. Neurogenic pulmonary edema combined with febrile seizures in early childhood-A report of two cases.

    PubMed

    Tasaka, Keiji; Matsubara, Kousaku; Hori, Masayuki; Nigami, Hiroyuki; Iwata, Aya; Isome, Kenichi; Kawasaki, Yu; Nagai, Sadayuki

    2016-01-01

    Neurogenic pulmonary edema (NPE) is a clinical entity that can occur following central nervous system disorders. However, NPE occurs quite rarely in early childhood, and there has only been one report about pediatric NPE associated with febrile seizures. Two cases are reported here. One case involved a 2-year-old girl who presented with febrile seizures, which rapidly progressed to severe NPE. Since the NPE occurred in the emergency department room, the patient was able to be resuscitated via immediate endotracheal intubation. The other case involved an 11-month-old boy who developed respiratory distress following a 50-min episode of febrile status epilepticus. Both patients required respiratory management in the intensive care unit. However their conditions were dramatically improved within several days and fully recovered without any sequelae.

  2. Severe preeclampsia, pulmonary edema, and peripartum cardiomyopathy in a primigravida patient.

    PubMed

    Cunningham, Curt; Rivera, Jesse; Spence, Dennis

    2011-06-01

    Peripartum cardiomyopathy (PPCM) is a rare form of heart failure of unknown etiology that is associated with late pregnancy and the early postpartum period. Although the complete pathogenesis of PPCM is not completely understood, the signs and symptoms are identical to those of left ventricular heart failure. The diagnosis of PPCM is made in a parturient only after other causes of heart failure are ruled out. Management of PPCM is similar to that of congestive heart failure with a few exceptions, such as avoiding the use of angiotensin-converting enzyme inhibitors during pregnancy. This report describes the presentation and anesthetic management of a parturient who was admitted with a diagnosis of severe preeclampsia in whom pulmonary edema and heart failure developed, necessitating emergency cesarean delivery under general anesthesia. The patient was subsequently given a diagnosis of PPCM.

  3. Endothelial selectins in acute mountain sickness and high-altitude pulmonary edema.

    PubMed

    Grissom, C K; Zimmerman, G A; Whatley, R E

    1997-12-01

    Mechanical or inflammatory injury to pulmonary endothelial cells may cause impaired pulmonary gas exchange in acute mountain sickness (AMS) and noncardiogenic pulmonary edema in high-altitude pulmonary edema (HAPE). This study was designed to determine whether markers of endothelial cell activation or injury, plasma E- and P-selectin, were increased after ascent to high altitude, in AMS or in HAPE. We collected clinical data and plasma specimens in control subjects at sea level and after ascent to 4,200 m, and in climbers with AMS or HAPE at 4,200 m. Data analysis was performed using standard nonparametric statistical methods, and results reported as mean+/-SD. National Park Service medical camp at 4,200 m on Mt. McKinley (Denali), Alaska. Blood samples and clinical data were collected from 17 healthy climbers at sea level and again after ascent to 4,200 m, and from a different group of 13 climbers with AMS and 8 climbers with HAPE at 4,200 m. Climbers with AMS were divided into normoxic (n=7) and hypoxemic (n=6) groups. Using an enzyme immunoassay technique, plasma E-selectin concentrations were found to be increased in the 17 control subjects after ascent to 4,200 m (17.2+/-8.2 ng/mL) as compared to sea level (12.9+/-8.2 ng/mL) (p=0.001). Plasma E-selectin concentrations were also increased in subjects with hypoxemic AMS (30.6+/-13.4 ng/mL) and HAPE (23.3+/-9.1 ng/mL) compared to control subjects at sea level (p=0.009). Increased plasma E-selectin concentration significantly correlated with hypoxemia (p=0.006). Plasma P-selectin concentrations were unchanged after ascent to 4,200 m and in subjects with AMS and HAPE. Because E-selectin is produced only by endothelial cells, increased plasma E-selectin after ascent to high altitude and in hypoxemic climbers with AMS and HAPE provides evidence that endothelial cell activation or injury is a component of hypoxic altitude illness.

  4. A pig model for blunt chest trauma: no pulmonary edema in the early phase.

    PubMed

    Couret, David; de Bourmont, Sophie; Prat, Nicolas; Cordier, Pierre-Yves; Soureau, Jean-Baptiste; Lambert, Dominique; Prunet, Bertrand; Michelet, Pierre

    2013-08-01

    Chest trauma remains a leading cause of trauma-death. Since lung contusion is one of the most important lesions implicated, the aim of this experimental study was to evaluate the cardiorespiratory consequences of an isolated lung contusion model. Twenty-eight anesthetized pigs were studied during four hours. We induced a right lung contusion with five bolt shots (70 joules each) using a 22-caliber charge in twenty of them. Eight others pigs constituted the control group. The trauma consequences were assessed by histology, measurements of arterial oxygenation, plasma cytokines, pressure-volume mechanics, hemodynamic monitoring using the PiCCO system and a pulmonary artery catheter. The extra-vascular lung water was measured using the gravimetric method. Histology confirmed an isolated right lung contusion without cardiac injury. Compared to baseline values, the trauma group was characterized by a decrease in cardiac index (3.3 ± 0.8 vs 3.9 ± 1.2 l/min/m(2); P < .05) and mean arterial pressure (80 ± 21 vs 95 ± 16 mmHg; P < .05) without preload or afterload modification. Oxygenation (PaO2/FiO2: 349 ± 87 vs 440 ± 75; P < .05) and static compliance (26.3 ± 7.4 vs 30.3 ± 7.8 ml/cmH2O; P < .05) were also impaired during two hours compared to baseline. No edema was noticed in either group whatever the lung considered. All measured cytokines were below the detection threshold. An isolated right lung contusion is associated with rapid but transient cardiorespiratory impairments. Despite the large extent of the lung contusion, no pulmonary edema appeared during the period studied. Copyright © 2013 Elsevier Inc. All rights reserved.

  5. Effectiveness of prehospital continuous positive airway pressure in the management of acute pulmonary edema.

    PubMed

    Hubble, Michael W; Richards, Michael E; Jarvis, Roger; Millikan, Tori; Young, Dwayne

    2006-01-01

    To compare the effectiveness of continuous positive airway pressure (CPAP) with standard pharmacologic treatment in the management of prehospital acute pulmonary edema. Using a nonrandomized control group design, all consecutive patients presenting to two participating emergency medical services (EMS) systems with a field impression of acute pulmonary edema between July 1, 2004, and June 30, 2005, were included in the study. The control EMS system patients received standard treatment with oxygen, nitrates, furosemide, morphine, and, if indicated, endotracheal intubation. The intervention EMS system patients received CPAP via face mask at 10 cm H2O in addition to standard therapy. Ninety-five patients received standard therapy, and 120 patients received CPAP and standard therapy. Intubation was required in 8.9% of CPAP-treated patients compared with 25.3% in the control group (p = 0.003), and mortality was lower in the CPAP group than in the control group (5.4% vs. 23.2%; p = 0.000). When compared with the control group, the CPAP group had more improvement in respiratory rate (-4.55 vs. -1.81; p = 0.001), pulse rate (-4.77 vs. 0.82; p = 0.013), and dyspnea score (-2.11 vs. -1.36; p = 0.008). Using logistic regression to control for potential confounders, patients receiving standard treatment were more likely to be intubated (odds ratio, 4.04; 95% confidence interval, 1.64 to 9.95) and more likely to die (odds ratio, 7.48; 95% confidence interval, 1.96 to 28.54) than those receiving standard therapy and CPAP. The prehospital use of CPAP is feasible, may avert the need for endotracheal intubation, and may reduce short-term mortality.

  6. Role of oxidative stress and NFkB in hypoxia-induced pulmonary edema.

    PubMed

    Sarada, Sagi; Himadri, Patir; Mishra, Chitaranjan; Geetali, Pradhan; Ram, Mastoori Sai; Ilavazhagan, Govindan

    2008-09-01

    Hypoxia is well known to increase the free radical generation in the body, leading to oxidative stress. In the present study, we have determined whether the increased oxidative stress further upregulates the nuclear transcription factor (NFkB) in the development of pulmonary edema. The rats were exposed to hypobaric hypoxia at 7620 m (280 mm Hg) for different durations, that is, 3 hrs, 6 hrs, 12 hrs, and 24 hrs at 25+/-1 degrees C. The results revealed that exposure of animals to hypobaric hypoxia led to a significant increase in vascular leakage, with time up to 6 hrs (256.38+/-61 rfu/g) as compared with control (143.63+/-60.1 rfu/g). There was a significant increase in reactive oxygen species, lipid peroxidation, and superoxide dismutase levels, with a concurrent decrease in lung glutathione peroxidase activity. There was 13-fold increase in the expression of NFkB level in nuclear fraction of lung homogenates of hypoxic animals over control rats. The DNA binding activity of NFkB was found to be increased significantly (P<0.001) in the lungs of rats exposed to hypoxia as compared with control. Further, we observed a significant increase in proinflammatory cytokines such as IL-1, IL-6, and TNF-alpha with concomitant upregulation of cell adhesion molecules such as ICAM-I, VCAM-I, and P-selectin in the lung of rats exposed to hypoxia as compared with control. Interestingly, pretreatment of animals with curcumin (NFkB blocker) attenuated hypoxia-induced vascular leakage in lungs with concomitant reduction of NFkB levels. The present study therefore reveals the possible involvement of NFkB in the development of pulmonary edema.

  7. Radiation induced endothelial cell retraction in vitro: correlation with acute pulmonary edema.

    PubMed

    Onoda, J M; Kantak, S S; Diglio, C A

    1999-01-01

    We determined the effects of low dose radiation (<200 cGy) on the cell-cell integrity of confluent monolayers of pulmonary microvascular endothelial cells (PMEC). We observed dose- and time-dependent reversible radiation induced injuries to PMEC monolayers characterized by retraction (loss of cell-cell contact) mediated by cytoskeletal F-actin reorganization. Radiation induced reorganization of F-actin microfilament stress fibers was observed > or =30 minutes post irradiation and correlated positively with loss of cell-cell integrity. Cells of irradiated monolayers recovered to form contact inhibited monolayers > or =24 hours post irradiation; concomitantly, the depolymerized microfilaments organized to their pre-irradiated state as microfilament stress fibers arrayed parallel to the boundaries of adjacent contact-inhibited cells. Previous studies by other investigators have measured slight but significant increases in mouse lung wet weight >1 day post thoracic or whole body radiation (> or =500 cGy). Little or no data is available concerning time intervals <1 day post irradiation, possibly because of the presumption that edema is mediated, at least in part, by endothelial cell death or irreversible loss of barrier permeability functions which may only arise 1 day post irradiation. However, our in vitro data suggest that loss of endothelial barrier function may occur rapidly and at low dose levels (< or =200 cGy). Therefore, we determined radiation effects on lung wet weight and observed significant increases in wet weight (standardized per dry weight or per mouse weight) in < or =5 hours post thoracic exposure to 50 200 cGy x-radiation. We suggest that a single fraction of radiation even at low dose levels used in radiotherapy, may induce pulmonary edema by a reversible loss of endothelial cell-cell integrity and permeability barrier function.

  8. Baroreflex failure increases the risk of pulmonary edema in conscious rats with normal left ventricular function.

    PubMed

    Sakamoto, Kazuo; Hosokawa, Kazuya; Saku, Keita; Sakamoto, Takafumi; Tobushi, Tomoyuki; Oga, Yasuhiro; Kishi, Takuya; Ide, Tomomi; Sunagawa, Kenji

    2016-01-15

    In heart failure with preserved ejection fraction (HFpEF), the complex pathogenesis hinders development of effective therapies. Since HFpEF and arteriosclerosis share common risk factors, it is conceivable that stiffened arterial wall in HFpEF impairs baroreflex function. Previous investigations have indicated that the baroreflex regulates intravascular stressed volume and arterial resistance in addition to cardiac contractility and heart rate. We hypothesized that baroreflex dysfunction impairs regulation of left atrial pressure (LAP) and increases the risk of pulmonary edema in freely moving rats. In 15-wk Sprague-Dawley male rats, we conducted sinoaortic denervation (SAD, n = 6) or sham surgery (Sham, n = 9), and telemetrically monitored ambulatory arterial pressure (AP) and LAP. We compared the mean and SD (lability) of AP and LAP between SAD and Sham under normal-salt diet (NS) or high-salt diet (HS). SAD did not increase mean AP but significantly increased AP lability under both NS (P = 0.001) and HS (P = 0.001). SAD did not change mean LAP but significantly increased LAP lability under both NS (SAD: 2.57 ± 0.43 vs. Sham: 1.73 ± 0.30 mmHg, P = 0.01) and HS (4.13 ± 1.18 vs. 2.45 ± 0.33 mmHg, P = 0.02). SAD markedly increased the frequency of high LAP, and SAD with HS prolonged the duration of LAP > 18 mmHg by nearly 20-fold compared with Sham (SAD + HS: 2,831 ± 2,366 vs. Sham + HS: 148 ± 248 s, P = 0.01). We conclude that baroreflex failure impairs volume tolerance and together with salt loading increases the risk of pulmonary edema even in the absence of left ventricular dysfunction. Baroreflex failure may contribute in part to the pathogenesis of HFpEF.

  9. Swimming-induced pulmonary edema in a tropical climate: a case report.

    PubMed

    Kwek, Wmj; Seah, M; Chow, W

    2017-01-01

    Swimming-induced pulmonary edema (SIPE) occurs during strenuous physical exertion in cold water and has been reported in scuba divers, free-diving competitors, combat swimmers, and triathletes. We describe a case of SIPE in a combat swimmer in warm tropical waters. A 21-year old diver trainee developed dyspnea, chest discomfort and hemoptysis after performing a 2-km sea swim in water temperatures of around 30°C. Over a two-hour period, his oxygen saturations deteriorated. Chest X-ray showed pulmonary edema. He was admitted to the general ward for observation and was given supportive treatment. His symptoms resolved over two days. Repeat CXR was normal. He was reviewed and certified fit to continue with diver training. Much of the earlier literature on SIPE describes the development of symptoms after exposure to temperate waters as one main risk factor. This case highlights the risk of development of SIPE in warm tropical waters. With a low reported incidence of SIPE in warm waters, this condition is likely to be underdiagnosed. There is therefore a need to increase local awareness of SIPE in the medical community. A deliberate effort to collate data on SIPE in our local community will help us to better understand the pathophysiology of SIPE in the context of a tropical climate. Development of SIPE in tropical waters suggests that other risk factors may be predominant. There should be a high index of suspicion when any strenuous in-water activity is conducted so that timely treatment may be instituted.

  10. Postobstructive pulmonary edema in a 40-year-old man after suffocation by a swimming pool cover.

    PubMed

    Tsung, Ann H; Slish, John H; Lisenbee, Nathaniel P; Allen, Brandon R

    2013-11-01

    Postobstructive pulmonary edema (POPE) is a form of sudden onset, noncardiogenic pulmonary edema that can occur after the relief of an upper airway obstruction. Since POPE is an uncommon diagnosis made in the emergency department (ED), this case is presented to increase emergency physicians' awareness of the etiology, pathophysiology, and management of this type of edema. This is a case of bilateral POPE in a 40-year-old man with no history of cardiac or pulmonary disease who experienced near suffocation due to the vacuum effect of a swimming pool cover. On presentation to the ED, the patient's symptoms included bilateral pleuritic pain over the anterior chest, shortness of breath, and inspiratory cough. He was tachycardic and tachypneic, with an oxygen saturation of 92% on room air. Pertinent physical examination findings included shallow breathing and right-sided rhonchi. The initial arterial blood gas on room air demonstrated a PaO2/FiO2 ratio of 304 mm Hg. Cardiac enzymes and the electrocardiogram result were normal. The patient's chest radiograph was interpreted as having marked bilateral pulmonary edema. The patient was admitted to the Medicine Intensive Care Unit and placed on noninvasive positive pressure ventilation (NIPPV). The patient was clinically asymptomatic and was discharged after 72 h. Emergency physicians should consider the diagnosis of POPE in a symptomatic patient if there is evidence of pulmonary edema immediately after a history of hanging, suffocation, strangulation, choking, naloxone administration, or other forms of upper airway obstruction. Rapid initiation of NIPPV with or without diuretics, steroids, or fluid restriction can lead to symptom resolution within 24 to 48 h. Published by Elsevier Inc.

  11. Postobstructive Pulmonary Edema following Tonsillectomy/Adenoidectomy in a 2-Year-Old with Poland-Moebius Syndrome

    PubMed Central

    Powell, Tanisha; Sharma, Nirupma; McKie, Kathleen T.

    2016-01-01

    A 2-year-old male with Poland-Moebius syndrome was transferred from a local hospital to the Pediatric ICU at Children's Hospital of Georgia for suspected postobstructive pulmonary edema (POPE) after tonsillectomy/adenoidectomy (T&A). The patient's respiratory status ultimately declined and he developed respiratory failure. Imaging suggested pulmonary edema as well as a left-sided pneumonia. Echocardiogram showed pulmonary hypertension and airway exam via direct fiberoptic bronchoscopy revealed tracheomalacia and bronchomalacia. He developed acute respiratory distress syndrome (ARDS) and remained intubated for ten days. This case highlights the association between congenital upper body abnormalities with cranial nerve dysfunction and the development of POPE with delayed resolution of symptoms. Patients with upper body abnormalities as above are at great risk of postoperative complications and should therefore be managed in a tertiary-care facility. PMID:26942029

  12. Neonatal high-permeability pulmonary edema based on serial cytokine profiles and KL-6 in serum: case report.

    PubMed

    Nakamura, Toshihiko; Nakamura, Mari; Takahashi, Naoto

    2017-03-22

    A newborn male with pulmonary edema was delivered at term by elective Caesarian section. Cytokine profiles of 17 cytokines and KL-6 in cord blood and serial serum values were investigated. The cord blood values of all 17 cytokines and KL-6 were within normal limits. Subsequently, IL-6, IL-8, IL-10, IL-13, IL-17, and IFNγ rapidly elevated during the first several hours after birth and dramatically decreased thereafter, whereas KL-6 rose to 611 U/ml on the 3(rd) day of life and then gradually decreased. These cytokines may induce pulmonary permeability, and KL-6 secreted in lining fluid could result in influx into the bloodstream. This is the first report that we have differentiated neonatal pulmonary edema from TTN by the measurement of serial cytokine profiles and KL-6 in serum.

  13. Elevated pulmonary artery pressure and brain natriuretic peptide in high altitude pulmonary edema susceptible non-mountaineers

    PubMed Central

    Gupta, Rajinder K.; Himashree, G.; Singh, Krishan; Soree, Poonam; Desiraju, Koundinya; Agrawal, Anurag; Ghosh, Dishari; Dass, Deepak; Reddy, Prassana K.; Panjwani, Usha; Singh, Shashi Bala

    2016-01-01

    Exaggerated pulmonary pressor response to hypoxia is a pathgonomic feature observed in high altitude pulmonary edema (HAPE) susceptible mountaineers. It was investigated whether measurement of basal pulmonary artery pressure (Ppa) and brain natriuretic peptide (BNP) could improve identification of HAPE susceptible subjects in a non-mountaineer population. We studied BNP levels, baseline hemodynamics and the response to hypoxia (FIo2 = 0.12 for 30 min duration at sea level) in 11 HAPE resistant (no past history of HAPE, Control) and 11 HAPE susceptible (past history of HAPE, HAPE-S) subjects. Baseline Ppa (19.31 ± 3.63 vs 15.68 ± 2.79 mm Hg, p < 0.05) and plasma BNP levels (52.39 ± 32.9 vs 15.05 ± 9.6 pg/ml, p < 0.05) were high and stroke volume was less (p < 0.05) in HAPE-S subjects compared to control. Acute hypoxia produced an exaggerated increase in heart rate (p < 0.05), mean arterial pressure (p < 0.05) and Ppa (28.2 ± 5.8 vs 19.33 ± 3.74 mm Hg, p < 0.05) and fall in peripheral oxygen saturation (p < 0.05) in HAPE-S compared to control. Receiver operating characteristic (ROC) curves showed that Ppa response to acute hypoxia was the best variable to identify HAPE susceptibility (AUC 0.92) but BNP levels provided comparable information (AUC 0.85). BNP levels are easy to determine and may represent an important marker for the determination of HAPE susceptibility. PMID:26892302

  14. Superior Vena Cava Stent Migration into the Pulmonary Artery Causing Fatal Pulmonary Infarction

    SciTech Connect

    Anand, Girija Lewanski, Conrad R.; Cowman, Steven A.; Jackson, James E.

    2011-02-15

    Migration of superior vena cava (SVC) stents is a well-recognised complication of their deployment, and numerous strategies exist for their retrieval. To our knowledge, only three cases of migration of an SVC stent to the pulmonary vasculature have previously been reported. None of these patients developed complications that resulted in death. We report a case of SVC stent migration to the pulmonary vasculature with delayed pulmonary artery thrombosis and death from pulmonary infarction. We conclude that early retrieval of migrated stents should be performed to decrease the risk of serious complications.

  15. [Pulmonary edema due to venous air embolism during craniotomy: a case report].

    PubMed

    Ishida, Kumiko; Hishinuma, Miwako; Miyazawa, Mikiko; Tanaka, Toshiyuki; Iwasawa, Ken; Kitoh, Takeshi

    2008-10-01

    We present a 35-year-old healthy male patient who developed pulmonary edema (PE) probably due to venous air embolism during craniotomy in the semi-sitting position for arteriovenous malformation (AVM). Anesthesia was maintained with oxygen, nitrous oxide, propofol and fentanyl. During craniotomy, end-tidal carbon dioxide pressure decreased suddenly from 26 to 9 mmHg. Concurrently, a decrease in oxygen saturation from 99% to 91% occurred. There were no serious changes in blood pressure and heart rate. A "mill-wheel murmur" was confirmed. PE due to venous air embolism was suspected. The operation was discontinued and the patient was transferred to the intensive care unit. In the post-operative period, the patient developed PE and made a full recovery within a week. Four months later, the patient was scheduled again for surgical excision of AVM in the semi-sitting position in the same way as the first time. Anesthesia was maintained with oxygen, air, propofol and fentanyl. Transoesophageal echocardiography and pulmonary artery catheter were used. Saline was filled at the surgical site to prevent aspiration of air bubbles and surgical procedure was performed carefully without large vein injury and uneventfully. During neurosurgical intervention in the sitting position, special attention should be paid to entry of air bubbles into the venous system which may lead to PE.

  16. [Efficacy and safety of non-invasive positive pressure ventilation therapy in acute pulmonary edema].

    PubMed

    Sarullo, Filippo Maria; D'Alfonso, Giovanni; Brusca, Ignazio; De Michele, Piero; Taormina, Andrea; Di Pasquale, Pietro; Castello, Antonio

    2004-03-01

    Non-invasive positive pressure ventilation (NIPPV) is an effective treatment for acute respiratory failure in patients with chronic obstructive pulmonary disease. We assessed the efficacy and safety of this therapy in acute cardiogenic pulmonary edema (ACPE). In addition to routine therapy consisting of oxygen, nitrates and diuretics, 60 patients (39 male, 21 female, mean age 72.5 +/- 15.8 years) were started on full mask NIPPV using a Sullivan VPAP II ventilator delivering pressure support 15 cm H2O, PEEP 5 cm H2O, FiO2 100%. Pressure support were titrated to achieve oxygen saturation (SaO2) > 95%. Physiological measurements were obtained in the first 2 h and at 3 h, 4 h, and 10 h. Outcome measures included arterial blood gas (ABG), Borg dyspnea score, vital signs, and need for endotracheal intubation (ETI). Initial mean values on FiO2 100% by non nonrebreather mask: pH 7.11 +/- 0.25, paCO2 67.7 +/- 17.5 mmHg, paO2 71.5 +/- 29.7 mmHg, SaO2 83 +/- 12%, lactate concentrations 4.7 +/- 2.3 mmol/L, Borg score 8.6 +/- 1.3, respiratory rate (RR) 41 +/- 7. At 60 minutes of NIPPV, improvement was statistically significant: pH 7.35 +/- 0.18 (difference 0.24; p < 0.0001), paCO2 43 +/- 13 mmHg (difference 24.7; p < 0.0001), paO2 102 +/- 10 mmHg (difference 30.5; p < 0.0001), SaO2 99 +/- 5% (difference 16; p < 0.0001), lactate concentrations 1.2 +/- 0.8 (difference 3.5; p < 0.0001) Borg score 3.6 +/- 0.9 (difference 5; p < 0.0001), RR 24.6 +/- 5 (difference 17.1; p < 0.0001). NIPPV duration ranged from 40 minutes to 24 hours (median 3 hours, 30 minutes). Fifty-six patients (93.4%) improved allowing cessation of NIPPV. ETI was required in four (6.6%) of 60 patients. There were non complications of NIPPV. In this study of acute cardiogenic pulmonary edema, NIPPV is an effective treatment and may help prevent ETI.

  17. Raised HIF1α during normoxia in high altitude pulmonary edema susceptible non-mountaineers.

    PubMed

    Soree, Poonam; Gupta, Rajinder K; Singh, Krishan; Desiraju, Koundinya; Agrawal, Anurag; Vats, Praveen; Bharadwaj, Abhishek; Baburaj, T P; Chaudhary, Pooja; Singh, Vijay K; Verma, Saroj; Bajaj, Amir Chand; Singh, Shashi Bala

    2016-05-23

    High altitude pulmonary edema (HAPE) susceptibility is associated with EGLN1 polymorphisms, we hypothesized that HAPE-susceptible (HAPE-S, had HAPE episode in past) subjects may exhibit abnormal HIF1α levels in normoxic conditions. We measured HIF1α levels in HAPE-S and HAPE resistant (HAPE-R, no HAPE episode) individuals with similar pulmonary functions. Hemodynamic responses were also measured before and after normobaric hypoxia (Fi02 = 0.12 for 30 min duration at sea level) in both groups. . HIF1α was higher in HAPE-S (320.3 ± 267.5 vs 58.75 ± 33.88 pg/ml, P < 0.05) than HAPE-R, at baseline, despite no significant difference in baseline oxygen saturations (97.7 ± 1.7% and 98.8 ± 0.7). As expected, HAPE-S showed an exaggerated increase in pulmonary artery pressure (27.9 ± 6 vs 19.3 ± 3.7 mm Hg, P < 0.05) and a fall in peripheral oxygen saturation (66.9 ± 11.7 vs 78.7 ± 3.8%, P < 0.05), when exposed to hypoxia. HIF1α levels at baseline could accurately classify members of the two groups (AUC = 0.87). In a subset of the groups where hemoglobin fractions were additionally measured to understand the cause of elevated hypoxic response at baseline, two of four HAPE-S subjects showed reduced HbA. In conclusion, HIF 1 α levels during normoxia may represent an important marker for determination of HAPE susceptibility.

  18. Raised HIF1α during normoxia in high altitude pulmonary edema susceptible non-mountaineers

    PubMed Central

    Soree, Poonam; Gupta, Rajinder K.; Singh, Krishan; Desiraju, Koundinya; Agrawal, Anurag; Vats, Praveen; Bharadwaj, Abhishek; Baburaj, T. P.; Chaudhary, Pooja; Singh, Vijay K.; Verma, Saroj; Bajaj, Amir Chand; Singh, Shashi Bala

    2016-01-01

    High altitude pulmonary edema (HAPE) susceptibility is associated with EGLN1 polymorphisms, we hypothesized that HAPE-susceptible (HAPE-S, had HAPE episode in past) subjects may exhibit abnormal HIF1α levels in normoxic conditions. We measured HIF1α levels in HAPE-S and HAPE resistant (HAPE-R, no HAPE episode) individuals with similar pulmonary functions. Hemodynamic responses were also measured before and after normobaric hypoxia (Fi02 = 0.12 for 30 min duration at sea level) in both groups. . HIF1α was higher in HAPE-S (320.3 ± 267.5 vs 58.75 ± 33.88 pg/ml, P < 0.05) than HAPE-R, at baseline, despite no significant difference in baseline oxygen saturations (97.7 ± 1.7% and 98.8 ± 0.7). As expected, HAPE-S showed an exaggerated increase in pulmonary artery pressure (27.9 ± 6 vs 19.3 ± 3.7 mm Hg, P < 0.05) and a fall in peripheral oxygen saturation (66.9 ± 11.7 vs 78.7 ± 3.8%, P < 0.05), when exposed to hypoxia. HIF1α levels at baseline could accurately classify members of the two groups (AUC = 0.87). In a subset of the groups where hemoglobin fractions were additionally measured to understand the cause of elevated hypoxic response at baseline, two of four HAPE-S subjects showed reduced HbA. In conclusion, HIF 1 α levels during normoxia may represent an important marker for determination of HAPE susceptibility. PMID:27210110

  19. Prevalence and severity of left atrial edema detected by electron beam tomography early after pulmonary vein ablation.

    PubMed

    Okada, Taro; Yamada, Takumi; Murakami, Yoshimasa; Yoshida, Naoki; Ninomiya, Yuuichi; Shimizu, Takeshi; Toyama, Junji; Yoshida, Yukihiko; Ito, Teruo; Tsuboi, Naoya; Kondo, Takahisa; Inden, Yasuya; Hirai, Makoto; Murohara, Toyoaki

    2007-04-03

    The aim of this study was to investigate the prevalence and severity of left atrial (LA) edema after pulmonary vein (PV) ablation and its effect on the cardiac function. Though extensive LA catheter ablation has been demonstrated to be more effective in curing paroxysmal atrial fibrillation (PAF) than segmental ostial pulmonary vein isolation (S-PVI), it might cause life-threatening complications, including congestive heart failure associated with LA edema. Fifty patients underwent S-PVI (Group S) and 27 underwent circumferential PV antrum ablation (Group C) for drug-refractory PAF. Enhanced electron beam tomography (EBT) was performed before, 1 or 2 days after, and 1 month after the PV ablation, and transthoracic ultrasound cardiography (UCG) was performed 1 month after the PV ablation in all patients. The EBT assessment revealed LA edema immediately after the PV ablation in 47 Group S patients and all Group C patients. The severity of the LA edema, number of radiofrequency applications, and amount of radiofrequency energy delivered during the PV ablation was significantly greater in Group C than in Group S. One month after the PV ablation, in all patients, the EBT assessment revealed that those edematous changes had disappeared, and the UCG assessment showed no reduction in the cardiac function. Left atrial edema was observed in a large portion of the patients immediately after the PV ablation, and the severity of the LA edema depended on the extent and amount of the radiofrequency energy delivered in the PV ablation. The LA edema soon disappeared naturally and did not reduce the cardiac function.

  20. A rare presentation of patent ductus arteriosus in an adult patient with normal pulmonary hypertension and limb edema

    PubMed Central

    Pishgoo, Bahram; Saburi, Amin; Khosravi, Arezoo

    2014-01-01

    BACKGROUND Patent ductus arteriosus (PDA) at childhood is one of the five major and frequent congenital abnormalities, but it can be rarely seen in adults. Pulmonary hypertension (PHTN) and other presentations such as heart failure and edema are the identified complications of longstanding PDA, but adult case with no permanent heart symptoms and PHTN was rare. We reported a rare case of with an obvious PDA and normal pulmonary pressure. CASE REPORT A 61-year-old woman presented with dyspnea (New York Heart Association class 2), chest pain, and lower limb edema. Echocardiogram showed; normal left ventricular chamber size and function, normal size of both atria. Furthermore, an obvious PDA (diameter = 6-7 mm) connecting the aortic arch to the pulmonary artery was reported in echocardiography. No lung congestion and evidence for PHTN was reported by computed tomographic angiography [Pulmonary capillary wedge pressure (PCWP) = 30 mmHg]. The patient was treated with antihypertensive drugs and after 1 and 3 months follow-up, edema and other symptoms were resolved. CONCLUSION Finally, we conclude that PDA in adulthood can present with nonspecific cardiovascular symptoms, and it seems that PHTN is not a fixed echocardiographic finding in these patients. PMID:25477985

  1. Retrospective study of adenovirus in autopsied pulmonary tissue of pediatric fatal pneumonia in South China.

    PubMed

    Ou, Zhi-Ying; Zeng, Qi-Yi; Wang, Feng-Hua; Xia, Hui-Min; Lu, Jun-Peng; Xia, Jian-Qing; Gong, Si-Tang; Deng, Li; Zhang, Jian-Tao; Zhou, Rong

    2008-09-21

    Adenovirus are the important pathogen of pediatric severe pneumonia. The aim of this study is to analyze the infection, subtype and distribution of adenovirus in autopsied pulmonary tissue of fatal pneumonia in infants and children, and the relationships between adenovirus infection and respiratory illness in South China. Nested PCR was performed on DNA extracted from autopsied lung tissue from patients who died of severe pneumonia, and the positive nested PCR products were cloned and sequenced. The adenovirus in autopsied pulmonary tissue was also analyzed by immunohistochemistry assay in a blind way. In the 175 autopsied pulmonary tissues, the positive percentage of adenovirus was 9.14% (16/175) and 2.29% (4/175) detected with nested PCR and immunohistochemistry, respectively. There are three cases of adenovirus serotype 3, twelve cases of adenovirus serotype 4 and one case of serotype 41 determined by sequencing of the cloned positive nested PCR products. Adenovirus is an important cause of severe pneumonia, and these data suggest that adenovirus serotype 4 might be an important pathogen responsible for the fatal pneumonia in Guangzhou, South China.

  2. A new view of pulmonary edema and acute respiratory distress syndrome.

    PubMed

    Ketai, L H; Godwin, J D

    1998-07-01

    The old division of lung edema into two categories--cardiogenic (hydrostatic) and noncardiogenic (increased permeability)--is no longer adequate. For instance, it fails to distinguish between the capillary leak caused by acute respiratory distress syndrome from that caused by interleukin-2 treatment. Further, it fails to account for the capillary leak ('stress-failure') that may accompany edema. A modern view of edema must recognize the natural barriers to the formation and spread of edema. These barriers are the capillary endothelium and the alveolar epithelium. Varying degrees of damage to them can account for the varying radiographic and clinical manifestations of lung edema. Thus, interleukin-2 administration causes increased endothelial permeability without causing alveolar epithelial damage. The result is lung edema that is largely confined to the interstitium, causing little hypoxia and clearing rapidly. However, acute respiratory distress syndrome, which is characterized by extensive alveolar damage, causes air-space consolidation, severe hypoxia, and slow resolution. Thus, a reasonable classification of lung edema requires at least four categories: 1) hydrostatic edema; 2) acute respiratory distress syndrome (permeability edema caused by diffuse alveolar damage); 3) permeability edema without alveolar damage; and (4) mixed hydrostatic and permeability edema. The authors emphasize the importance of the barriers provided by the capillary endothelium and the alveolar epithelium in determining the clinical and radiographic manifestations of edema. In general, when the alveolar epithelium is intact, the radiographic manifestations are those of interstitial (not air-space) edema; this radiographic pattern predicts a mild clinical course and prompt resolution.

  3. Sleep and Breathing in High Altitude Pulmonary Edema Susceptible Subjects at 4,559 Meters

    PubMed Central

    Nussbaumer-Ochsner, Yvonne; Schuepfer, Nicole; Ursprung, Justyna; Siebenmann, Christoph; Maggiorini, Marco; Bloch, Konrad E.

    2012-01-01

    Study objectives: Susceptible subjects ascending rapidly to high altitude develop pulmonary edema (HAPE). We evaluated whether HAPE leads to sleep and breathing disturbances that are alleviated by dexamethasone. Design: Double-blind, randomized, placebo-controlled trial with open-label extension. Setting: One night in sleep laboratory at 490 m, 2 nights in mountain hut at 4,559 m. Participants: 21 HAPE susceptibles. Intervention: Dexamethasone 2 × 8 mg/d, either 24 h prior to ascent and at 4,559 m (dex-early), or started on day 2 at 4,559 m only (dex-late). Measurements: Polysomnography, questionnaires on sleep and acute mountain sickness. Results: Polysomnographies at 490 m were normal. In dex-late (n = 12) at 4,559 m, night 1 and 3, median oxygen saturation was 71% and 80%, apnea/hypopnea index 91.3/h and 9.6/h. In dex-early (n = 9), corresponding values were 78% and 79%, and 85.3/h and 52.3/h (P < 0.05 vs. 490 m, all instances). In dex-late, ascending from 490 m to 4,559 m (night 1), sleep efficiency decreased from 91% to 65%, slow wave sleep from 20% to 8% (P < 0.05, both instances). In dex-early, corresponding sleep efficiencies were 96% and 95%, slow wave sleep 18% and 9% (P < 0.05). From night 1 to 3, sleep efficiency remained unchanged in both groups while slow wave sleep increased to 20% in dex-late (P < 0.01). Compared to dex-early, initial AMS scores in dex-late were higher but improved during stay at altitude. Conclusions: HAPE susceptibles ascending rapidly to high altitude experience pronounced nocturnal hypoxemia, and reduced sleep efficiency and deep sleep. Dexamethasone taken before ascent prevents severe hypoxemia and sleep disturbances, while dexamethasone taken 24 h after arrival at 4,559 m increases oxygenation and deep sleep. Citation: Nussbaumer-Ochsner Y; Schuepfer N; Ursprung J; Siebenmann C; Maggiorini M; Bloch KE. Sleep and breathing in high altitude pulmonary edema susceptible subjects at 4,559 meters. SLEEP 2012;35(10):1413-1421. PMID

  4. Managing High-Altitude Pulmonary Edema with Oxygen Alone: Results of a Randomized Controlled Trial.

    PubMed

    Yanamandra, Uday; Nair, Velu; Singh, Surinderpal; Gupta, Amul; Mulajkar, Deepak; Yanamandra, Sushma; Norgais, Konchok; Mukherjee, Ruchira; Singh, Vikrant; Bhattachar, Srinivasa A; Patyal, Sagarika; Grewal, Rajan; Chopra, Bhushan

    2016-12-01

    Yanamandra, Uday, Velu Nair, Surinderpal Singh, Amul Gupta, Deepak Mulajkar, Sushma Yanamandra, Konchok Norgais, Ruchira Mukherjee, Vikrant Singh, Srinivasa A. Bhattachar, Sagarika Patyal, and Rajan Grewal. High-altitude pulmonary edema management: Is anything other than oxygen required? Results of a randomized controlled trial. High Alt Med Biol. 17:294-299, 2016.-Treatment strategies for management of high-altitude pulmonary edema (HAPE) are mainly based on the observational studies with only two randomized controlled trials, thus the practice is very heterogeneous and individualized as per the choice of treating physician. To compare the response to different modalities of therapy in patients with HAPE in a randomized controlled manner. We conducted an open-label, randomized noninferiority trial to compare three modalities of therapy (Therapy 1: supplemental O2 with oral dexamethasone 8 mg q8 hours [n = 42], Therapy 2: supplemental O2 with sustained release oral nifedipine 20 mg q8 hours [n = 41], and Therapy 3: only supplemental O2 [n = 50]). Bed rest was mandated in all patients. The study was conducted in a cohort of previously healthy young lowlander males at an altitude of 3500 m. Baseline characteristics of the patients were comparable in the study arms. Complete response was defined as clinical and radiological resolution of features of HAPE, no oxygen dependency, a normal 6-minute walk test (6MWT) on 2 consecutive days, and normal two-dimensional echocardiography. Results were compared by analysis of variance using SPSS version 16.0. There was no statistical difference in duration of therapy to complete response between the three groups (Therapy 1: 8.1 ± 4.0 days, Therapy 2: 6.7 ± 3.9 days, Therapy 3: 6.8 ± 3.2 days; p = 0.15). There were no deaths in any of the groups. We conclude that oxygen and bed rest alone are adequate therapy for HAPE and that adjuvant pharmacotherapy with either dexamethasone or nifedipine

  5. Fatal Pulmonary Infection Due to Multidrug-Resistant Mycobacterium abscessus in a Patient with Cystic Fibrosis

    PubMed Central

    Sanguinetti, Maurizio; Ardito, Fausta; Fiscarelli, Ersilia; La Sorda, Marilena; D'Argenio, Patrizia; Ricciotti, Gabriella; Fadda, Giovanni

    2001-01-01

    We report a case of fatal pulmonary infection caused by Mycobacterium abscessus in a young patient with cystic fibrosis, who underwent bipulmonary transplantation after a 1-year history of severe lung disease. Fifteen days after surgery he developed septic fever with progressive deterioration in lung function. M. abscessus, initially isolated from a pleural fluid specimen, was then recovered from repeated blood samples, suggesting a disseminated nature of the mycobacterial disease. Drug susceptibility testing assay, performed on two sequential isolates of the microorganism, showed a pattern of multidrug resistance. Despite aggressive therapy with several antimycobacterial drugs, including clarithromycin, the infection persisted, and the patient died. PMID:11158161

  6. Combination of constant-flow and continuous positive-pressure ventilation in canine pulmonary edema.

    PubMed

    Sznajder, J I; Becker, C J; Crawford, G P; Wood, L D

    1989-08-01

    Constant-flow ventilation (CFV) maintains alveolar ventilation without tidal excursion in dogs with normal lungs, but this ventilatory mode requires high CFV and bronchoscopic guidance for effective subcarinal placement of two inflow catheters. We designed a circuit that combines CFV with continuous positive-pressure ventilation (CPPV; CFV-CPPV), which negates the need for bronchoscopic positioning of CFV cannula, and tested this system in seven dogs having oleic acid-induced pulmonary edema. Addition of positive end-expiratory pressure (PEEP, 10 cmH2O) reduced venous admixture from 44 +/- 17 to 10.4 +/- 5.4% and kept arterial CO2 tension (PaCO2) normal. With the innovative CFV-CPPV circuit at the same PEEP and respiratory rate (RR), we were able to reduce tidal volume (VT) from 437 +/- 28 to 184 +/- 18 ml (P less than 0.001) and elastic end-inspiratory pressures (PEI) from 25.6 +/- 4.6 to 17.7 +/- 2.8 cmH2O (P less than 0.001) without adverse effects on cardiac output or pulmonary exchange of O2 or CO2; indeed, PaCO2 remained at 35 +/- 4 Torr even though CFV was delivered above the carina and at lower (1.6 l.kg-1.min-1) flows than usually required to maintain eucapnia during CFV alone. At the same PEEP and RR, reduction of VT in the CPPV mode without CFV resulted in CO2 retention (PaCO2 59 +/- 8 Torr). We conclude that CFV-CPPV allows CFV to effectively mix alveolar and dead spaces by a small bulk flow bypassing the zone of increased resistance to gas mixing, thereby allowing reduction of the CFV rate, VT, and PEI for adequate gas exchange.

  7. Transcatheter closure of atrial septal defect protects from pulmonary edema: septal occluder device gradually reduces LR shunt.

    PubMed

    Murakami, Tsutomu; Nakazawa, Gaku; Horinouchi, Hitomi; Torii, Sho; Ijichi, Takeshi; Ohno, Yohei; Amino, Mari; Shinozaki, Norihiko; Ogata, Nobuhiko; Yoshimachi, Fuminobu; Yoshioka, Koichiro; Ikari, Yuji

    2017-01-01

    A 56-year-old woman was diagnosed as atrial septal defect (ASD) with pulmonary hypertension; pulmonary blood flow/systemic blood flow (Qp/Qs) of 2.3, pulmonary artery pressure (PAP) of 71/23(39) mmHg and diastolic dysfunction of left ventricle. PAP was improved after medical therapy; therefore, transcatheter ASD closure was performed. Seven days later, left-sided heart failure occurred, however, the improvement of Qp/Qs (1.7) and PAP of 51/21(32) was confirmed. Diuretic therapy was introduced which led to further decrease of PAP 40/12(25) and Qp/Qs (1.1). Because of gradual decrease of Qp/Qs, this patient appeared to be protected from acute pulmonary edema.

  8. Global end-diastolic volume is associated with the occurrence of delayed cerebral ischemia and pulmonary edema after subarachnoid hemorrhage.

    PubMed

    Watanabe, Akihiro; Tagami, Takashi; Yokobori, Shoji; Matsumoto, Gaku; Igarashi, Yutaka; Suzuki, Go; Onda, Hidetaka; Fuse, Akira; Yokota, Hiroyuki

    2012-11-01

    Predictive variables of delayed cerebral ischemia (DCI) and pulmonary edema following subarachnoid hemorrhage (SAH) remain unknown. We aimed to determine associations between transpulmonary thermodilution-derived variables and DCI and pulmonary edema occurrence after SAH. We reviewed 34 consecutive SAH patients monitored by the PiCCO system. Six patients developed DCI at 7 days after SAH on average; 28 did not (non-DCI). We compared the variable measures for 1 day before DCI occurred (DCI day -1) in the DCI group and 6 days after SAH (non-DCI day -1) in the non-DCI group for control. The mean value of the global end-diastolic volume index (GEDI) for DCI day -1 was lower than that for non-DCI day -1 (676 ± 65 vs. 872 ± 85 mL/m, P = 0.04). Central venous pressure (CVP) was not significantly different (7.8 ± 3.1 vs. 9.4 ± 1.9 cm H2O, P = 0.45). At day -1 for both DCI and non-DCI, 11 patients (32%) had pulmonary edema. Global end-diastolic volume index was significantly higher in patients with pulmonary edema than in those without this condition (947 ± 126 vs. 766 ± 81 mL/m, P = 0.02); CVP was not significantly different (8.7 ± 2.8 vs. 9.2 ± 2.1 cm H2O, P = 0.78). Although significant correlation was found between extravascular lung water (EVLW) measures and GEDI (r = 0.58, P = 0.001), EVLW and CVP were not correlated (r = 0.03, P = 0.88). Thus, GEDI might be associated with DCI occurrence and EVLW accumulation after SAH.

  9. [Significance of extravascular lung water index, pulmonary vascular permeability index, and in- trathoracic blood volume index in the differential diagnosis of burn-induced pulmonary edema].

    PubMed

    Lei, Li; Jiajun, Sheng; Guangyi, Wang; Kaiyang, Lyu; Jing, Qin; Gongcheng, Liu; Bing, Ma; Shichu, Xiao; Shihui, Zhu

    2015-06-01

    To appraise the significance of extravascular lung water index (EVLWI), pulmonary vascular permeability index (PVPI), and intrathoracic blood volume index (ITBVI) in the differential diagnosis of the type of burn-induced pulmonary edema. The clinical data of 38 patients, with severe burn hospitalized in our burn ICU from December 2011 to September 2014 suffering from the complication of pulmonary edema within one week post burn and treated with mechanical ventilation accompanied by pulse contour cardiac output monitoring, were retrospectively analyzed. The patients were divided into lung injury group ( L, n = 17) and hydrostatic group (H, n = 21) according to the diagnosis of pulmonary edema. EVLWI, PVPI, ITBVI, oxygenation index, and lung injury score ( LIS) were compared between two groups, and the correlations among the former four indexes and the correlations between each of the former three indexes and types of pulmonary edema were analyzed. Data were processed with t test, chi-square test, Mann-Whitney U test, Pearson correlation test, and accuracy test [receiver operating characteristic (ROC) curve]. There was no statistically significant difference in EVLWI between group L and group H, respectively (12.9 ± 3.1) and (12.1 ± 2.1) mL/kg, U = 159.5, P > 0.05. The PVPI and LIS of patients in group L were respectively 2.6 ± 0.5 and (2.1 ± 0.6) points, and they were significantly higher than those in group H [1.4 ± 0.3 and (1.0 ± 0.6) points, with U values respectively 4.5 and 36.5, P values below 0.01]. The ITBVI and oxygenation index of patients in group L were respectively (911 197) mL/m2 and (136 ± 69) mmHg (1 mmHg = 0.133 kPa), which were significantly lower than those in group H [(1,305 ± 168) mL/m2 and (212 ± 60) mmHg, with U values respectively 21.5 and 70.5, P values below 0.01]. In group L, there was obviously positive correlation between EVLWI and PVPI, or EVLWI and ITBVI (with r values respectively 0.553 and 0.807, P < 0.05 or P < 0.01), and

  10. ECG abnormalities predict neurogenic pulmonary edema in patients with subarachnoid hemorrhage.

    PubMed

    Chen, Wei-Lung; Huang, Chi-Hung; Chen, Jiann-Hwa; Tai, Henry Chih-Hung; Chang, Su-Hen; Wang, Yung-Cheng

    2016-01-01

    The study aims to assess if electrocardiographic (ECG) abnormalities could predict the development of neurogenic pulmonary edema (NPE) within 24 hours in cases of spontaneous subarachnoid hemorrhage (SAH). We studied prospectively a cohort of 269 adult patients with nontraumatic SAH in an emergency department of a university-affiliated medical center. A 12-lead ECG was taken for these patients. The patients were stratified into NPE and non-NPE based on serially clinical and radiologic findings. The ECG abnormalities were compared between these 2 groups of patients. Compared with the non-NPE (n = 229), the NPE (n = 40) had significantly higher World Federation of Neurological Surgeons class (P < .001), higher Hunt-Hess scale (P < .001), and higher prevalence of diabetes mellitus (P = .033). In addition, the percentage of ECG morphological abnormality was significantly higher in NPE, in which nonspecific ST- or T-wave changes (NSSTTCs) are significantly higher. Multiple logistic regression model identified World Federation of Neurological Surgeons class (95% confidence interval [CI], 2.6-13.3; P < .001), abnormal Q or QS wave (95% CI, 1.1-9.1; P = .038), and NSSTTCs (95% CI, 1.2-7.5; P = .016) as the significant variables associated with NPE. Electrocardiographic abnormalities, especially abnormal Q or QS wave and NSSTTCs, may predict the development of NPE within 24 hours in adult patients with spontaneous SAH. Copyright © 2015 Elsevier Inc. All rights reserved.

  11. Angiotensin II receptor 1 gene variants are associated with high-altitude pulmonary edema risk

    PubMed Central

    Zhu, Xikai; Li, Xun; Ouyang, Yongri; He, Xue; Zhang, Zhiying; Zhang, Yuan; Kang, Longli; Yuan, Dongya

    2016-01-01

    Previous studies demonstrated that Angiotensin II Receptor 1 (AGTR1) may play an important role in the development of high-altitude pulmonary edema. We envisaged a role for AGTR1 gene variants in the pathogenesis of HAPE and investigated their potential associations with HAPE in a Han Chinese population. We genotyped seven AGTR1 polymorphisms in 267 patients with diagnosed HAPE and 304 controls and evaluated their association with risk of HAPE. Statistically significant associations were found for the single nucleotide polymorphisms (SNPs) rs275651 (p = 0.017; odds ratio [OR] = 0.65) and rs275652 (p = 0.016; OR = 0.64). Another SNP rs10941679 showed a marginally significant association after adjusting for age and sex in the additive genetic model (adjusted OR = 1.44, 95% CI = 1.01-2.04, p = 0.040). Haplotype analysis confirmed that the haplotype “AG” was associated with a 35% reduction in the risk of developing HAPE, while the haplotype “AA” increased the risk of developing HAPE by 44%. These results provide the first evidence linking genetic variations in AGTR1 with HAPE risk in Han Chinese individuals. PMID:27732943

  12. Involvement of water channel Aquaporin 5 in H2S-induced pulmonary edema.

    PubMed

    Xu, Chunyang; Jiang, Lei; Zou, Yuxia; Xing, Jingjing; Sun, Hao; Zhu, Baoli; Zhang, Hengdong; Wang, Jun; Zhang, Jinsong

    2017-01-01

    Acute exposure to hydrogen sulfide (H2S) poses a significant threat to life, and the lung is one of the primary target organs of H2S. However, the mechanisms involved in H2S-induced acute pulmonary edema are poorly understood. This study aims to investigate the effects of H2S on the expression of water channel aquaporin 5 (AQP5) and to elucidate the signaling pathways involved in AQP5 regulation. In an in vivo study, C57BL6 mice were exposed to sub-lethal concentrations of inhaled H2S, and histological injury of the lungs and ultrastructure injury of the epithelial cells were evaluated. With real-time PCR and western blot assays, we found that H2S exposure contributed to a significant decrease in AQP5 expression both in murine lung tissue and the A549 cell line, and the ERK1/2 and p38 MAPK signaling pathways were demonstrated to be implicated in AQP5 regulation. Therefore, adjusting AQP5 protein levels could be considered a therapeutic strategy for the treatment of APE induced by H2S and other hazardous gases.

  13. Angiotensin II receptor 1 gene variants are associated with high-altitude pulmonary edema risk.

    PubMed

    Jin, Tianbo; Ren, Yongchao; Zhu, Xikai; Li, Xun; Ouyang, Yongri; He, Xue; Zhang, Zhiying; Zhang, Yuan; Kang, Longli; Yuan, Dongya

    2016-11-22

    Previous studies demonstrated that Angiotensin II Receptor 1 (AGTR1) may play an important role in the development of high-altitude pulmonary edema. We envisaged a role for AGTR1 gene variants in the pathogenesis of HAPE and investigated their potential associations with HAPE in a Han Chinese population. We genotyped seven AGTR1 polymorphisms in 267 patients with diagnosed HAPE and 304 controls and evaluated their association with risk of HAPE. Statistically significant associations were found for the single nucleotide polymorphisms (SNPs) rs275651 (p = 0.017; odds ratio [OR] = 0.65) and rs275652 (p = 0.016; OR = 0.64). Another SNP rs10941679 showed a marginally significant association after adjusting for age and sex in the additive genetic model (adjusted OR = 1.44, 95% CI = 1.01-2.04, p = 0.040). Haplotype analysis confirmed that the haplotype "AG" was associated with a 35% reduction in the risk of developing HAPE, while the haplotype "AA" increased the risk of developing HAPE by 44%. These results provide the first evidence linking genetic variations in AGTR1 with HAPE risk in Han Chinese individuals.

  14. An analysis of and new risk factors for reexpansion pulmonary edema following spontaneous pneumothorax

    PubMed Central

    Kawabata, Tsutomu; Ichi, Takaharu; Yohena, Tomofumi; Kawasaki, Hidenori; Ishikawa, Kiyoshi

    2014-01-01

    Background The major risk factor for reexpansion pulmonary edema (RPE) following the treatment of spontaneous pneumothorax is thought to be chronic lung collapse. However, a long-term collapsed lung does not always cause RPE. The purpose of this study was to define other risk factors for RPE among patients undergoing drainage for the treatment of spontaneous pneumothorax. Methods We retrospectively reviewed all the patients with spontaneous pneumothorax who had been treated at our hospital during a 5-year period. The duration of symptoms, location and size of the pneumothorax, size of the chest tube, and pleural effusion, which can occur coincidentally with pneumothorax, were compared in patients who did and did not experience RPE. Results Forty patients were underwent drainage for the treatment of a spontaneous pneumothorax between January 2007 and December 2012. RPE developed in 13 of the 40 (32.5%) patients. In the multivariate analysis, the presence of pleural effusion coincident with pneumothorax contributed to the risk for RPE [odds ratios (OR), 1.557; 95% confidence intervals (CI), 1.290-1.880]. The duration of symptoms, location and size of the pneumothorax and size of the chest tube were similar between the groups. Symptomatic RPE was associated with a larger pneumothorax size. Conclusions The rate of RPE following spontaneous pneumothorax is higher than was previously reported. Our findings suggest the presence of pleural effusion coincidentally with pneumothorax may therefore be a new risk factor for RPE. PMID:25276359

  15. Causes and correlates of anemia in 200 patients with acute cardiogenic pulmonary edema.

    PubMed

    Rovellini, Angelo; Graziadei, Giovanna; Folli, Christian; Brambilla, Anna Maria; Cosentini, Roberto; Canetta, Ciro; Monzani, Valter

    2012-12-01

    Acute heart failure has a poor prognosis and the presence of anemia may increase the risk of adverse outcomes. However, the clinical and laboratory characteristics of anemia in acute heart failure are poorly known. We aimed to assess the causes and the clinical and laboratory correlates of anemia in patients with acute cardiogenic pulmonary edema (ACPE). This observational study, performed in an Emergency Unit, enrolled 200 patients treated with medical therapy and continuous positive airway pressure. Anemia was found in 36% of patients (38.5% of females and 32.5% of males) and was severe (hemoglobin <9 g/dL) in 6.9% of cases. The most frequent causes of anemia were chronic renal failure (27.8%), chronic inflammatory states (27.8%) and the clustering of multiple factors (18.1%). A wider spectrum of etiological factors was found in females than in males. Microcytic anemia was observed only in females (20% of those anemic), mainly due to iron deficiency/chronic blood loss. Glomerular filtration rate, serum iron, serum albumin, total cholesterol and diastolic blood pressure were independently associated with hemoglobin levels. The etiology of anemia in ACPE is heterogeneous, with several causal factors besides impaired renal function. The pattern of anemia is different between genders, suggesting that sex-specific diagnostic and therapeutic targets should be implemented. Copyright © 2012 European Federation of Internal Medicine. Published by Elsevier B.V. All rights reserved.

  16. Genome-wide association study of high-altitude pulmonary edema in a Han Chinese population.

    PubMed

    Li, Xun; Jin, Tianbo; Zhang, Mingxia; Yang, Hua; Huang, Xuewen; Zhou, Xiaobo; Huang, Wenchao; Qin, Lipeng; Kang, Longli; Fan, Ming; Li, Suzhi

    2017-05-09

    A two-stage genome-wide association study (GWAS) was performed to identify and analyze genes and single nucleotide polymorphisms (SNPs) associated with high-altitude pulmonary edema (HAPE) in a Han Chinese patient population. In the first stage, DNA samples from 68 patients with recurrent HAPE were scanned using Affymetrix SNP Array 6.0 Chips, and allele frequencies were compared to those of 84 HapMap CHB samples to identify candidate SNPs. In the second stage, the 77 identified candidate SNPs were examined in an independent cohort of samples from 199 HAPE patients and 304 controls. Associations between SNPs and HAPE risk were tested using various genetic models. Of the 77 original SNPs, 7 were found to be associated with HAPE susceptibility in the second stage of the study. GO and pathway enrichment analysis of the 7 SNPs revealed 5 adjacent genes involved in various processes, including regulation of nucleoside diphosphate metabolism, thyroid hormone catabolism, and low-density lipoprotein receptor activity. These results suggest the identified SNPs and genes may contribute to the physiopathology of HAPE.

  17. ROCK2 and MYLK variants under hypobaric hypoxic environment of high altitude associate with high altitude pulmonary edema and adaptation

    PubMed Central

    Pandey, Priyanka; Mohammad, Ghulam; Singh, Yogendra; Qadar Pasha, MA

    2015-01-01

    Objective To date, a major class of kinases, serine–threonine kinase, has been scantly investigated in stress-induced rare, fatal (if not treated early), and morbid disorder, high altitude pulmonary edema (HAPE). This study examined three major serine–threonine kinases, ROCK2, MYLK, and JNK1, along with six other genes, tyrosine hydroxylase, G-protein subunits GNA11 and GNB3, and alpha1 adrenergic receptor isoforms 1A, 1B, and 1D as candidate gene markers of HAPE and adaptation. Methods For this, 57 variants across these nine genes were genotyped in HAPE patients (n=225), HAPE controls (n=210), and highlanders (n=259) by Sequenom MS (TOF)-based MassARRAY® platform using iPLEX™ Gold technology. In addition, to study the gene expression, quantitative real-time polymerase chain reaction was performed in human peripheral blood mononuclear cells of the three study groups. Results A significant association was observed for C allele (ROCK2 single-nucleotide polymorphism, rs10929728) with HAPE (P=0.03) and C, T, and A alleles (MYLK single-nucleotide polymorphisms, rs11717814, rs40305, and rs820336) with both HAPE and adaptation (P=0.001, P=0.006, and P=0.02, respectively). ROCK2 88 kb GGGTTGGT haplotype was associated with lower risk of HAPE (P=0.0009). MYLK 7 kb haplotype CTA, composed of variant alleles, was associated with higher risk of HAPE (P=0.0006) and lower association with adaptation (P=1E–06), whereas haplotype GCG, composed of wild-type alleles, was associated with lower risk of HAPE (P=0.001) and higher association with adaptation (P=1E–06). Haplotype–haplotype and gene–gene interactions demonstrated a correlation in working of ROCK2 and MYLK. Conclusion The data suggest the association of ROCK2 with HAPE and MYLK with HAPE and adaptation in Indian population. The outcome has provided new insights into the physiology of HAPE and adaptation. PMID:26586960

  18. Novel Peptide for Attenuation of Hyperoxia-induced Disruption of Lung Endothelial Barrier and Pulmonary Edema via Modulating Peroxynitrite Formation*

    PubMed Central

    Kondrikov, Dmitry; Gross, Christine; Black, Stephen M.; Su, Yunchao

    2014-01-01

    Pulmonary damages of oxygen toxicity include vascular leakage and pulmonary edema. We have previously reported that hyperoxia increases the formation of NO and peroxynitrite in lung endothelial cells via increased interaction of endothelial nitric oxide (eNOS) with β-actin. A peptide (P326TAT) with amino acid sequence corresponding to the actin binding region of eNOS residues 326–333 has been shown to reduce the hyperoxia-induced formation of NO and peroxynitrite in lung endothelial cells. In the present study, we found that exposure of pulmonary artery endothelial cells to hyperoxia (95% oxygen and 5% CO2) for 48 h resulted in disruption of monolayer barrier integrity in two phases, and apoptosis occurred in the second phase. NOS inhibitor NG-nitro-l-arginine methyl ester attenuated the endothelial barrier disruption in both phases. Peroxynitrite scavenger uric acid did not affect the first phase but ameliorated the second phase of endothelial barrier disruption and apoptosis. P326TAT inhibited hyperoxia-induced disruption of monolayer barrier integrity in two phases and apoptosis in the second phase. More importantly, injection of P326TAT attenuated vascular leakage, pulmonary edema, and endothelial apoptosis in the lungs of mice exposed to hyperoxia. P326TAT also significantly reduced the increase in eNOS-β-actin association and protein tyrosine nitration. Together, these results indicate that peptide P326TAT ameliorates barrier dysfunction of hyperoxic lung endothelial monolayer and attenuates eNOS-β-actin association, peroxynitrite formation, endothelial apoptosis, and pulmonary edema in lungs of hyperoxic mice. P326TAT can be a novel therapeutic agent to treat or prevent acute lung injury in oxygen toxicity. PMID:25315770

  19. Bolus intravenous 0.9% saline, but not 4% albumin or 5% glucose, causes interstitial pulmonary edema in healthy subjects.

    PubMed

    Bihari, Shailesh; Wiersema, Ubbo F; Schembri, David; De Pasquale, Carmine G; Dixon, Dani-Louise; Prakash, Shivesh; Lawrence, Mark D; Bowden, Jeffrey J; Bersten, Andrew D

    2015-10-01

    Rapid intravenous (iv) infusion of 0.9% saline alters respiratory mechanics in healthy subjects. However, the relative cardiovascular and respiratory effects of bolus iv crystalloid vs. colloid are unknown. Six healthy male volunteers were given 30 ml/kg iv 0.9% saline, 4% albumin, and 5% glucose at a rate of 100 ml/min on 3 separate days in a double-blinded, randomized crossover study. Impulse oscillometry, spirometry, lung volumes, diffusing capacity (DLCO), and blood samples were measured before and after fluid administration. Lung ultrasound B-line score (indicating interstitial pulmonary edema) and Doppler echocardiography indices of cardiac preload were measured before, midway, immediately after, and 1 h after fluid administration. Infusion of 0.9% saline increased small airway resistance at 5 Hz (P = 0.04) and lung ultrasound B-line score (P = 0.01) without changes in Doppler echocardiography measures of preload. In contrast, 4% albumin increased DLCO, decreased lung volumes, and increased the Doppler echocardiography mitral E velocity (P = 0.001) and E-to-lateral/septal e' ratio, estimated blood volume, and N-terminal pro B-type natriuretic peptide (P = 0.01) but not lung ultrasound B-line score, consistent with increased pulmonary blood volume without interstitial pulmonary edema. There were no significant changes with 5% glucose. Plasma angiopoietin-2 concentration increased only after 0.9% saline (P = 0.001), suggesting an inflammatory mechanism associated with edema formation. In healthy subjects, 0.9% saline and 4% albumin have differential pulmonary effects not attributable to passive fluid filtration. This may reflect either different effects of these fluids on active signaling in the pulmonary circulation or a protective effect of albumin.

  20. Fatal Pulmonary Embolism in the Setting of Immune Reconstitution Inflammatory Syndrome Attributed to Ovarian Tuberculosis.

    PubMed

    Ugalde, Israel; Pirela, Daniela; Lo Presti, Saberio; Bilderback, Molly; Pirela, Andrés; Chan, Joseph

    2017-01-01

    In developed countries, tuberculosis remains a health care challenge due to human immunodeficiency virus (HIV) and immigration from endemic regions. The Centers for Disease Control and Prevention reported 9557 new cases in 2015, with extrapulmonary involvement in 20.2% of the cases. We present a 33-year-old woman from Cape Town, South Africa, who developed abdominal pain and fever while working on a cruise ship. She sought medical where she underwent computed tomography of her chest, abdomen, and pelvis with findings suggestive of pulmonary tuberculosis and an 8.9-cm pelvic mass. HIV testing was positive and the patient was started on antiretroviral therapy. Bronchoscopy confirmed the presence of acid-fast bacilli, and she was started on rifampin, isoniazid, pyrazinamide, and ethambutol. She remained persistently febrile, raising suspicion for immune reconstitution inflammatory syndrome. However, despite empiric antibiotics, the patient remained persistently febrile, tachycardic, and on day 10 of admission she went into ventricular fibrillation and expired. Autopsy revealed an occlusive thrombus in the left main pulmonary artery in addition to necrotizing granulomata in multiple organs and bilateral tubo-ovarian abscesses. Postmortem cultures for were positive for Mycobacterium tuberculosis, all consistent with disseminated Mycobacterium tuberculosis. Although previous reports underscore the association between tuberculosis and hypercoagulability, the exact mechanism remains unknown. In this article, we report a case of disseminated tuberculosis complicated by bilateral tubo-ovarian abscesses with fatal pulmonary thrombus formation.

  1. Fatal postoperative systemic pulmonary hypertension in benfluorex-induced valvular heart disease surgery

    PubMed Central

    Baufreton, Christophe; Bruneval, Patrick; Rousselet, Marie-Christine; Ennezat, Pierre-Vladimir; Fouquet, Olivier; Giraud, Raphael; Banfi, Carlo

    2017-01-01

    Abstract Rationale: Drug-induced valvular heart disease (DI-VHD) remains an under-recognized entity. Patient concerns: This report describes a heart valve replacement which was complicated by intractable systemic pulmonary arterial hypertension in a 61-year-old female with severe restrictive mitral and aortic disease. The diagnosis of valvular disease was preceded by a history of unexplained respiratory distress. The patient had been exposed to benfluorex for 6.5 years. Diagnoses: The diagnostic procedure documented specific drug-induced valvular fibrosis. Interventions: Surgical mitral and aortic valve replacement was performed. Outcomes: Heart valve replacement was postoperatively complicated by unanticipated disproportionate pulmonary hypertension. This issue was fatal despite intensive care including prolonged extracorporeal life support. Lessons: Benfluorex is a fenfluramine derivative which has been marketed between 1976 and 2009. Although norfenfluramine is the common active and toxic metabolite of all fenfluramine derivatives, the valvular and pulmonary arterial toxicity of benfluorex was much less known than that of fenfluramine and dexfenfluramine. The vast majority of benfluorex-induced valvular heart disease remains misdiagnosed as hypothetical rheumatic fever due to similarities between both etiologies. Better recognition of DI-VHD is likely to improve patient outcome. PMID:28079786

  2. Neurogenic pulmonary edema in patients with nontraumatic intracerebral hemorrhage: predictors and association with outcome.

    PubMed

    Junttila, Eija; Ala-Kokko, Tero; Ohtonen, Pasi; Vaarala, Anne; Karttunen, Ari; Vuolteenaho, Olli; Salo, Tuula; Sutinen, Meeri; Karhu, Toni; Herzig, Karl-Heinz; Koskenkari, Juha

    2013-04-01

    Neurogenic pulmonary edema (NPE) is a well-recognized phenomenon after intracranial insult. In this study, we evaluated the predictors for NPE and its association with outcome in patients with intensive care unit-treated nontraumatic intracranial hemorrhage. This was a prospective, observational clinical study in a university-level intensive care unit. Clinical characteristics, level of consciousness, and Acute Physiology and Chronic Health Evaluation (APACHE) II score were recorded on admission and the findings of primary head computed tomography were reviewed. A chest radiograph and arterial blood gas analysis were taken serially and NPE was determined as acute bilateral infiltrates in chest radiograph and hypoxemia. Echocardiography and cardiac and inflammatory markers were recorded. The 1-year outcome was assessed using the Glasgow Outcome Scale. NPE developed in 38 (35%) of the 108 patients included. Predictors for NPE were higher APACHE II score (≥20, odds ratio 6.17, P = 0.003) and higher interleukin-6 plasma concentration (>40 pg/mL, odds ratio 5.62, P = 0.003). Of patients with 0, 1, or 2 predictors mentioned above, 4%, 37%, and 65% had NPE, respectively. NPE was associated with a higher 1-year mortality (37% vs 14%, P = 0.007, respectively), but with an unchanged functional outcome after 1 year (Glasgow Outcome Scale score 1-3, 53% vs 51%, P > 0.9). Predictors for NPE are the severity of disease defined by APACHE II scores and higher levels of systemic inflammatory mediators. NPE is associated with a higher 1-year mortality, but not with a poorer 1-year functional outcome.

  3. Prevention of recurrent pulmonary edema in patients with bilateral renovascular disease through renal artery stent placement.

    PubMed

    Bloch, M J; Trost, D W; Pickering, T G; Sos, T A; August, P

    1999-01-01

    Pulmonary edema and congestive heart failure (both referred to here as PE) have been reported to be complications of bilateral renal artery stenosis or unilateral stenosis in a solitary functioning kidney (both referred to as BRAS). The goals of this study were to determine whether a history of PE was more common in patients with BRAS than in those with unilateral stenosis and a normal contralateral kidney (URAS), and whether recurrent PE could be prevented by renal artery stent placement. We evaluated 90 consecutive patients with renovascular disease who were treated with percutaneous renal artery stent placement. History and clinical follow-up were obtained through chart review and phone contact with referring physicians. Mean follow-up was 18.4 months after stent placement. Twenty-three of 56 (41%) subjects with BRAS had a history of PE before revascularization, compared with four of 34 (12%) subjects with URAS (P = .05). Twenty-five of the 27 patients with history of PE had adequate clinical follow-up. Seventeen of the 22 (77%) subjects with BRAS and history of PE had no further PE after stent placement in one or both renal arteries. The five BRAS subjects with recurrent PE after stent placement had evidence of stent thrombosis or restenosis. In contrast, only one of three (33%) URAS subjects with a history of PE remained free of PE after stent placement. We conclude that PE is a common complication of BRAS, but not of URAS. In patients with BRAS, recurrent PE can be prevented by successful stent placement in one or both renal arteries.

  4. Pulmonary edema following generalized tonic clonic seizures is directly associated with seizure duration

    PubMed Central

    Kennedy, Jeffrey D.; Hardin, Kimberly A.; Parikh, Palak; Li, Chin-Shang; Seyal, Masud

    2015-01-01

    Purpose Postictal pulmonary edema (PPE) is almost invariably present in human and animal cases of sudden unexpected death in epilepsy (SUDEP) coming to autopsy. PPE may be a contributing factor in SUDEP. The incidence of postictal PPE is unknown. We retrospectively investigated PPE following generalized tonic clonic seizures (GTCS) in the epilepsy monitoring unit. Methods Chest X-Rays (CXR) following each GTCS were obtained in 24 consecutive patients. Relationship of CXR abnormality to seizure duration, ictal/postictal oxygen desaturation (SpO2), apnea and presence of postictal generalized EEG suppression (PGES) was investigated using logistic regression. Results Eleven of 24 patients had CXR abnormalities following a GTCS. In these 11 patients, 22 CXR were obtained and abnormalities were present in 15 CXR. Abnormalities included PPE in 7 patients, of which 2 also had focal infiltrates. In 4 patients focal infiltrates were present without PPE. There was no significant difference in mean time to CXR (225 min) following GTCS in the abnormal CXR group versus the normal group of patients (196 min). Mean preceding seizure duration was longer (p=0.002) in GTCS with abnormal CXR (259.7 sec) versus GTCS with normal CXR (101.2 sec). Odds-ratio for CXR abnormality was 20.46 (p=0.006) with seizure duration greater than 100 sec versus less than 100 sec. On multivariable analysis, only the seizure duration was a significant predictor of CXR abnormality (p=0.015). Conclusions Radiographic abnormalities are not uncommon following GTCS. The presence of CXR abnormality is significantly associated with the duration of the preceding GTCS. Severe, untreated PPE may be relevant to the pathophysiology of SUDEP. PMID:25844030

  5. Negative-pressure pulmonary edema complicated by acute respiratory distress syndrome in an orangutan (Pongo pygmaeus abelii).

    PubMed

    Kenny, David E; Knightly, Felicia; Haas, Bradley; Hergott, Lawrence; Kutinsky, Ilana; Eller, Jimmie L

    2003-12-01

    A 22-yr-old, 86-kg, morbidly obese female orangutan (Pongo pygmaeus abelii) was immobilized and transported to the Denver Zoological Gardens hospital for a routine physical examination. Immediately after arriving at the hospital, cyanosis and apparent inadequate ventilatory efforts were noted. Clinically significant hypoxia occurred despite attempts to ventilate the orangutan through face mask, and attempts to place an endotracheal tube began. A large volume of pink-tinged frothy fluid flowed from the trachea when the laryngoscope was inserted into the oropharynx. Severe pulmonary edema due to negative-pressure pulmonary edema, precipitating life-threatening hypoxia was suspected. The orangutan was maintained on a mechanical ventilator using the neuromuscular blocking agent cisatracurium besylate and sedation with periodic doses of isoflurane and midazolam for 48 hr. Positive end-expiratory pressure was used while the orangutan was ventilated mechanically to improve respiratory function. The edema and hypoxia improved, but respiratory arrest ensued 30 min after extubation, when the orangutan was removed from mechanical ventilation. Necropsy and histopathology demonstrated that serious lung injury had led to acute respiratory distress syndrome.

  6. Fatal pulmonary complication during induction therapy in a patient with ANCA-associated vasculitis

    PubMed Central

    Brigita, Jonaitytė; Rūta, Kibarskytė; Edvardas, Danila; Marius, Miglinas; Dmitrij, Šeinin; Rokas, Stulpinas; Jurgita, Mitrikevičienė; Vygantas, Gruslys; Virginija, Šileikienė; Rolandas, Zablockis

    2016-01-01

    ANCA-associated vasculitis (AAV) is an inflammatory systemic disorder affecting small to medium sized vessels and likely leading to any organ dysfunction. Adequate treatment is important to avoid mortality or severe organ damage. In most cases initial treatment (induction therapy) allows to achieve remission. Induction therapy leads to immunosuppression and may cause severe infections. However, in vasculitis patients even an intensive immunosuppressive therapy is rarely complicated by an invasive fungal infection. We present a case in a 29-year old male patient with newly diagnosed AAV. He suffered a fatal pulmonary complication of the induction immunosuppressive treatment. Pathological (infectious) changes in the lungs were misinterpreted as progression of the vasculitis and he died due to disseminated angioinvasive aspergillosis. A clinical course, imaging and histopathology of this case are described and discussed. PMID:28356801

  7. [Acute pulmonary edema occurred during tocolytic treatment using nicardipine in a twin pregnancy. Report of three cases].

    PubMed

    Philippe, H-J; Le Trong, A; Pigeau, H; Demeure, D; Desjars, P; Esbelin, J; Caroit, Y; Winer, N

    2009-02-01

    We report three cases of acute pulmonary edema that occurred during treatment by intravenous tocolysis using nicardipine in twin pregnancy patients with no previous heart problems. The three patients were admitted into our unit on account of the risk of premature birth after 29 to 32 weeks of amenorrhea. The treatment by intravenous tocolysis using nicardipine combined with glucocorticoids therapy had been undertaken in the previous maternity ward. The three patients presented symptoms of acute dyspnea 48 hours after the beginning of the treatment. Paraclinical examinations eliminated the diagnosis of pulmonary embolism. The patients'condition improved rapidly with appropriate diuretic treatment and by modifying the tocolysis. There are currently few studies proving the benefits of nicardipine in tocolysis treatment. Few similar cases of acute pulmonary edema have been noted in twin pregnancy patients treated with nicardipine. Haemodynamic modifications specific to twin pregnancy, intravenous hydratation and glucocorticoid maturation may explain a part of this complication. Therefore, it is appropriated to limit the use of intravenous nicardipine in the sole indication of tocolysis in twin pregnancy, and to prefer the use of nifedipine and atosiban, that have proven their effectiveness in this indication.

  8. The critical roles of platelet activation and reduced NO bioavailability in fatal pulmonary arterial hypertension in a murine hemolysis model

    PubMed Central

    Hu, Weiguo; Jin, Richard; Zhang, Jinyan; You, Tao; Peng, Zhihai; Ge, Xiaowen; Bronson, Roderick T.; Halperin, Jose A.; Loscalzo, Joseph

    2010-01-01

    Pulmonary arterial hypertension (PAH) is suspected to be a strong mortality determinant of hemolytic disorders. However, direct contribution of acute intravascular hemolysis to fatal PAH has not been investigated. The roles of nitric oxide (NO) insufficiency and platelet activation in hemolysis-associated fatal PAH have been suspected but not been experimentally studied. We recently generated a unique intravascular hemolysis mouse model in which the membrane toxin, intermedilysin (ILY), exclusively lyses the erythrocytes of transgenically expressing human CD59 mice (ThCD59RBC), thereby inducing ILY-dose–dependent massive hemolysis. Using this murine hemolysis model, we found that the acute increase in pulmonary arterial pressure leading to right ventricle failure caused sudden death. Reduced NO bioavailability and massive platelet activation/aggregation leading to the formation of massive thrombosis specifically in the pulmonary microvasculature played the critical roles in pathogenesis of acute hemolysis-associated fatal PAH. Therapeutic interventions enhancing NO bioactivity or inhibiting platelet activation prevented sudden death or prolonged survival time via the suppression of the acute increase in pulmonary arterial pressure and improvement of right ventricle function. These findings further highlight the importance of the inhibition of platelet activation and the enhancement of NO bioavailability for the treatment and prevention of hemolysis-associated (fatal) PAH. PMID:20511540

  9. Risk factors for intubation as a guide for noninvasive ventilation in patients with severe acute cardiogenic pulmonary edema.

    PubMed

    Masip, Josep; Páez, Joaquim; Merino, Montserrat; Parejo, Sandra; Vecilla, Francisco; Riera, Clara; Ríos, Araceli; Sabater, Joan; Ballús, Josep; Padró, J

    2003-11-01

    Noninvasive ventilation may reduce the endotracheal intubation rate in patients with acute cardiogenic pulmonary edema. However, criteria for selecting candidates for this technique are not well established. We analyzed a cohort of patients with severe acute cardiogenic pulmonary edema managed by conventional therapy to identify risk factors for intubation. These factors were used as guide for indications for noninvasive ventilation. Observational cohort registry in the ICU and emergency and cardiology departments in a community teaching hospital. . 110 consecutive patients with acute cardiogenic pulmonary edema, 80 of whom received conventional oxygen therapy. Physiological measurements and blood gas samples registered upon admission. Twenty-one patients (26%) treated with conventional oxygen therapy needed intubation. Acute myocardial infarction, pH below 7.25, low ejection fraction (<30%), hypercapnia, and systolic blood pressure below 140 mmHg were independent predictors for intubation. Conversely, systolic blood pressure of 180 mmHg or higher showed to be a protective factor since only two patients with this blood pressure value required intubation (8%)], both presenting with a pH lower than 7.25. Considering systolic blood pressure lower than 180 mmHg, patients who showed hypercapnia presented a high intubation rate (13/21, 62%) whereas the rate of intubation in patients with normocapnia was intermediate (6/23, 26%). All normocapnic patients with pH less than 7.25 required intubation. No patient with hypocapnia was intubated regardless the level of blood pressure. Patients with pH less than 7.25 or systolic blood pressure less than 180 mmHg associated with hypercapnia should be promptly considered for noninvasive ventilation. With this strategy about 40% of the patients would be initially treated with this technique, which would involve nearly 90% of the patients that require intubation.

  10. Exogenous interleukin-6, interleukin-13, and interferon-γ provoke pulmonary abnormality with mild edema in enterovirus 71-infected mice.

    PubMed

    Huang, Szu-Wei; Lee, Yi-Ping; Hung, Yu-Ting; Lin, Chun-Hung; Chuang, Jih-Ing; Lei, Huan-Yao; Su, Ih-Jen; Yu, Chun-Keung

    2011-11-06

    Neonatal mice developed neurological disease and pulmonary dysfunction after an infection with a mouse-adapted human Enterovirus 71 (EV71) strain MP4. However, the hallmark of severe human EV71 infection, pulmonary edema (PE), was not evident. To test whether EV71-induced PE required a proinflammatory cytokine response, exogenous pro-inflammatory cytokines were administered to EV71-infected mice during the late stage of infection. After intracranial infection of EV71/MP4, 7-day-old mice developed hind-limb paralysis, pulmonary dysfunction, and emphysema. A transient increase was observed in serum IL-6, IL-10, IL-13, and IFN-γ, but not noradrenaline. At day 3 post infection, treatment with IL-6, IL-13, and IFN-γ provoked mild PE and severe emphysema that were accompanied by pulmonary dysfunction in EV71-infected, but not herpes simplex virus-1 (HSV-1)-infected control mice. Adult mice did not develop PE after an intracerebral microinjection of EV71 into the nucleus tractus solitarii (NTS). While viral antigen accumulated in the ventral medulla and the NTS of intracerebrally injected mice, neuronal loss was observed in the ventral medulla only. Exogenous IL-6, IL-13, and IFN-γ treatment could induce mild PE and exacerbate pulmonary abnormality of EV71-infected mice. However, other factors such as over-activation of the sympathetic nervous system may also be required for the development of classic PE symptoms.

  11. Exogenous interleukin-6, interleukin-13, and interferon-gamma provoke pulmonary abnormality with mild edema in enterovirus 71-infected mice

    PubMed Central

    2011-01-01

    Background Neonatal mice developed neurological disease and pulmonary dysfunction after an infection with a mouse-adapted human Enterovirus 71 (EV71) strain MP4. However, the hallmark of severe human EV71 infection, pulmonary edema (PE), was not evident. Methods To test whether EV71-induced PE required a proinflammatory cytokine response, exogenous pro-inflammatory cytokines were administered to EV71-infected mice during the late stage of infection. Results After intracranial infection of EV71/MP4, 7-day-old mice developed hind-limb paralysis, pulmonary dysfunction, and emphysema. A transient increase was observed in serum IL-6, IL-10, IL-13, and IFN-γ, but not noradrenaline. At day 3 post infection, treatment with IL-6, IL-13, and IFN-γ provoked mild PE and severe emphysema that were accompanied by pulmonary dysfunction in EV71-infected, but not herpes simplex virus-1 (HSV-1)-infected control mice. Adult mice did not develop PE after an intracerebral microinjection of EV71 into the nucleus tractus solitarii (NTS). While viral antigen accumulated in the ventral medulla and the NTS of intracerebrally injected mice, neuronal loss was observed in the ventral medulla only. Conclusions Exogenous IL-6, IL-13, and IFN-γ treatment could induce mild PE and exacerbate pulmonary abnormality of EV71-infected mice. However, other factors such as over-activation of the sympathetic nervous system may also be required for the development of classic PE symptoms. PMID:22054060

  12. Association between serum lactate levels and early neurogenic pulmonary edema after nontraumatic subarachnoid hemorrhage.

    PubMed

    Satoh, Etsuko; Tagami, Takashi; Watanabe, Akihiro; Matsumoto, Gaku; Suzuki, Go; Onda, Hidetaka; Fuse, Akira; Gemma, Akihiko; Yokota, Hiroyuki

    2014-01-01

    Few studies have described the risk factors associated with the development of neurological pulmonary edema (NPE) after subarachnoid hemorrhage (SAH). We have hypothesized that acute-phase increases in serum lactate levels are associated with the early development of NPE following SAH. The aim of this study was to clarify the association between lactic acidosis and NPE in patients with nontraumatic SAH. We retrospectively evaluated 140 patients with nontraumatic SAH who were directly transported to the Nippon Medical School Hospital emergency room by the emergency medical services. We compared patients in whom NPE developed (NPE group) and those in whom it did not (non-NPE group). The median (quartiles 1-3) arrival time at the hospital was 32 minutes (28-38 minutes) after the emergency call was received. Although the characteristics of the NPE and non-NPE groups, including mean arterial pressure (121.3 [109.0-144.5] and 124.6 [108.7-142.6] mm Hg, respectively; P=0.96), were similar, the median pH and the bicarbonate ion (HCO3(-)) concentrations were significantly lower in the NPE group than in the non-NPE group (pH, 7.33 [7.28-7.37] vs. 7.39 [7.35-7.43]); P=0.002; HCO3(-), 20.8 [18.6-22.6] vs. 22.8 [20.9-24.7] mmol/L; P=0.01). The lactate concentration was significantly higher in the NPE group (54.0 [40.3-61.0] mg/dL) than in the non-NPE group (28.0 [17.0-37.5] mg/dL; P<0.001). Multivariable regression analysis indicated that younger age and higher glucose and lactate levels were significantly associated with the early onset of NPE in patients with SAH. The present findings indicate that an increased serum lactate level, occurring within 1 hour of the ictus, is an independent factor associated with the early onset of NPE. Multicenter prospective studies are required to confirm our results.

  13. Acute lyme infection presenting with amyopathic dermatomyositis and rapidly fatal interstitial pulmonary fibrosis: a case report.

    PubMed

    Nguyen, Hien; Le, Connie; Nguyen, Hanh

    2010-06-21

    Dermatomyositis has been described in the setting of lyme infection in only nine previous case reports. Although lyme disease is known to induce typical clinical findings that are observed in various collagen vascular diseases, to our knowledge, we believe that our case is the first presentation of acute lyme disease associated with amyopathic dermatomyositis, which was then followed by severe and fatal interstitial pulmonary fibrosis only two months later. We present a case of a 64-year-old African-American man with multiple medical problems who was diagnosed with acute lyme infection after presenting with the pathognomonic rash and confirmatory serology. In spite of appropriate antimicrobial therapy for lyme infection, he developed unexpected amyopathic dermatomyositis and then interstitial lung disease. This case illustrates a potential for lyme disease to produce clinical syndromes that may be indistinguishable from primary connective tissue diseases. An atypical and sequential presentation (dermatomyositis and interstitial lung disease) of a common disease (lyme infection) is discussed. This case illustrates that in patients who are diagnosed with lyme infection who subsequently develop atypical muscular, respiratory or other systemic complaints, the possibility of severe rheumatological and pulmonary complications should be considered.

  14. Inhibition of secretory phospholipase A2 activity attenuates acute cardiogenic pulmonary edema induced by isoproterenol infusion in mice after myocardial infarction.

    PubMed

    Kawabata, Kenichi; Fujioka, Daisuke; Kobayashi, Tsuyoshi; Saito, Yukio; Obata, Jun-Ei; Nakamura, Takamitsu; Yano, Toshiaki; Watanabe, Kazuhiro; Watanabe, Yosuke; Mishina, Hideto; Kugiyama, Kiyotaka

    2010-10-01

    Several types of secretory phospholipase A2 (sPLA2) are expressed in lung tissue, yielding various eicosanoids that might cause pulmonary edema. This study examined whether inhibition of sPLA2 activity attenuates acute cardiogenic pulmonary edema in mice. Acute cardiogenic pulmonary edema was induced in C57BL/6J male mice by an increase in heart rate with continuous intravenous infusion of isoproterenol (ISP) (10 mg/kg/h) at 2 weeks after the creation of myocardial infarction by left coronary artery ligation. Just before ISP infusion, a single intraperitoneal injection of 100 mg/kg LY374388, a prodrug of LY329722 that inhibits sPLA2 activity, or vehicle was administered. The ISP infusion after myocardial infarction induced interstitial and alveolar edema on lung histology. Furthermore, it increased the lung-to-body weight ratio, pulmonary vascular permeability evaluated by the Evans blue extravasation method, lung activity of sPLA2, and lung content of thromboxane A2 and leukotriene B4. These changes were significantly attenuated by LY374388 treatment. In Kaplan-Meier analysis, the survival rate during the ISP infusion after myocardial infarction was significantly higher in LY374388- than in vehicle-treated mice. Similar results were obtained with another inhibitor of sPLA2 activity, para-bromophenacyl bromide. In conclusion, inhibition of sPLA2 activity suppressed acute cardiogenic pulmonary edema.

  15. Fatal pulmonary microthrombi during surgical therapy for end-stage heart failure: possible association with antifibrinolytic therapy.

    PubMed

    Cooper, John R; Abrams, Jacki; Frazier, O H; Radovancevic, Rajko; Radovancevic, Branislav; Bracey, Arthur W; Kindo, Michel J; Gregoric, Igor D

    2006-05-01

    Maintaining hemostasis in patients with end-stage heart failure undergoing cardiac surgery is always challenging. These patients have chronic hepatic insufficiency, resulting in derangement of coagulation. In addition, they are commonly receiving both systemic anticoagulation (warfarin or heparin) and antiplatelet therapy. The introduction of antifibrinolytics has had a significant effect on postoperative coagulopathy. We report fatal pulmonary microthrombi in patients receiving antifibrinolytics who developed suprasystemic pulmonary artery pressures and right heart failure that was impossible to overcome despite insertion of a right ventricular assist device. We reviewed the surgical procedure and autopsy reports to identify patients with high pulmonary artery pressures caused by pulmonary microthrombi after a cardiac surgical procedure for end-stage heart failure. Patient demographics and preoperative, intraoperative, and postoperative variables were collected from a retrospective review of the patients' medical records. We identified 9 patients (7 men and 2 women; mean age, 45 +/- 16 years) who died of pulmonary microthrombi after cardiac surgery between January 1997 and January 2004. Surgical procedures included 5 left ventricular assist device implantations, 2 heart transplantations, and 2 left ventricular reconstructions with mitral valve repair or replacement. Eight patients received aprotinin, and 1 patient received epsilon-aminocaproic acid immediately before and during cardiopulmonary bypass. All patients had severe suprasystemic pulmonary artery pressures after protamine administration for heparin reversal, a complication that proved fatal in all cases. Intraoperative wedge biopsy of the lungs revealed multiple microthrombi within capillaries and in the small- and medium-sized pulmonary arterioles. We report 9 cases for which fatal pulmonary microthrombi might be associated with the use of prophylactic antifibrinolytic therapy. Mortally ill patients with

  16. The characteristic of Indonesia's pre-eclampsia: From obstetric intensive care with ventilator until epidemiologic and its molecular biology profile of pulmonary edema in severe pre-eclampsia.

    PubMed

    Hermanto; Adityawarman; Sulistyono; Ardian, M; Dachlan, E G

    2014-07-01

    Pulmonary edema is among the least frequently diagnosed criteria for severe pre-eclampsia. A higher incidence of pulmonary edema was noted in older patients, multigravidas, and patients with underlying chronic hypertension that developed prior to delivery. The development of pulmonary edema was also associated with the administration of excess colloid or crystaloid infusion. Two hundreds and thirty millions people occupying Indonesia as tropical and coastal country gave rise the problem of highly maternal mortality rate of 225/100,000 deliveries where pre-eclampsia and eclampsia as most possible cause. Over 5years from the year 2005 through 2009 our 160 eclampsia study observed about significantly correlation between typical estafet referred case and maternal mortality (Odds ratio 19.1 and P=0.065). Specifically those referred eclampsia cases arriving lately to our tertiary hospital, complication of pulmonary edema also apparently became determinant factor to uphold the increased maternal mortality (Odds ratio 6.1 and P=0.083) We found at our teaching hospital Dr. Soetomo Surabaya as referral center along the year 2012, 477 pre-eclampsia-eclampsia cases which complicated by 27 cases of pulmonary from which we apply obstetric intensive care unit for tightly monitoring treatment. The majority use of ventilator were applied on 22 cases (81.4%), that most approximately 16 cases (72%) need 48h under ventilator use and the remaining 6 cases was not untill 5days of extubation. The etiology of pulmonary edema in preeclamptic patients involves multi-factors; abnormal COP-PWCP gradient, increased pulmonary capillary permeability, and left ventricular failure were identified causes. It has been well known that the pathogenesis of pulmonary edema in severe pre-eclampsia-eclampsia initiated by capillary alveolar leakage that leading increased capillary permeability and extravascular fluid oncotic as well as decreased plasma oncotic pressure. In severe pre-eclampsia appear that

  17. Postoperative negative pressure pulmonary edema following repetitive laryngospasm even after reversal of neuromuscular blockade by sugammadex: a case report

    PubMed Central

    Lee, Jae Ho; Lee, Min Hyun; Cho, Hyun Oh; Park, Soon Eun

    2017-01-01

    Laryngospasm, an occlusion of the glottis, can occur at any time during anesthesia, and is associated with serious perioperative complications such as hypoxia, hypercabia, aspiration, bronchospasm, arrhythmia, prolonged recovery, cardiac collapse, and eventually catastrophic death. Importantly, postoperative negative pressure pulmonary edema (NPPE) is a rare, but well described life-threatening complication related to acute and chronic upper airway obstruction. Sugammadex well known for affirmatively reducing the postoperative pulmonary complications associated with residual neuromuscular blockade may have an indirect role in triggering the negative intrathoracic pressure by raising a rapid and efficacious respiratory muscle strength in acute upper airway obstruction. Herein, we report a case of postoperative NPPE following repetitive laryngospasm even after reversal of rocuronium-induced neuromuscular blockade using sugammadex. PMID:28184275

  18. Postoperative negative pressure pulmonary edema following repetitive laryngospasm even after reversal of neuromuscular blockade by sugammadex: a case report.

    PubMed

    Lee, Ji Hyeon; Lee, Jae Ho; Lee, Min Hyun; Cho, Hyun Oh; Park, Soon Eun

    2017-02-01

    Laryngospasm, an occlusion of the glottis, can occur at any time during anesthesia, and is associated with serious perioperative complications such as hypoxia, hypercabia, aspiration, bronchospasm, arrhythmia, prolonged recovery, cardiac collapse, and eventually catastrophic death. Importantly, postoperative negative pressure pulmonary edema (NPPE) is a rare, but well described life-threatening complication related to acute and chronic upper airway obstruction. Sugammadex well known for affirmatively reducing the postoperative pulmonary complications associated with residual neuromuscular blockade may have an indirect role in triggering the negative intrathoracic pressure by raising a rapid and efficacious respiratory muscle strength in acute upper airway obstruction. Herein, we report a case of postoperative NPPE following repetitive laryngospasm even after reversal of rocuronium-induced neuromuscular blockade using sugammadex.

  19. Frequent subclinical high-altitude pulmonary edema detected by chest sonography as ultrasound lung comets in recreational climbers.

    PubMed

    Pratali, Lorenza; Cavana, Marco; Sicari, Rosa; Picano, Eugenio

    2010-09-01

    The ultrasound lung comets detected by chest sonography are a simple, noninvasive, semiquantitative sign of increased extravascular lung water. The aim of this study was to evaluate, by chest sonography, the incidence of interstitial pulmonary edema in recreational high-altitude climbers. Observational study. Eighteen healthy subjects (mean age 45 +/- 10 yrs, ten males) participating in a high-altitude trek in Nepal. Chest and cardiac sonography at sea level and at different altitudes during ascent. Ultrasound lung comets were evaluated on anterior chest at 28 predefined scanning sites. At individual patient analysis, ultrasound lung comets during ascent appeared in 15 of 18 subjects (83%) at 3440 m above sea level and in 18 of 18 subjects (100%) at 4790 m above sea level in the presence of normal left and right ventricular function and pulmonary artery systolic pressure rise (sea level = 24 +/- 5 mm Hg vs. peak ascent = 42 +/- 11 mm Hg, p < .001). Ultrasound lung comets were absent at baseline (day 2, altitude 1350 m, 1.06 +/- 1.3), increased progressively during the ascent (day 14, altitude 5130 m: 16.5 +/- 8; p < .001 vs. previous steps), and decreased at descent (day 20, altitude 1355 m: 2.9 +/- 1.7; p = nonsignificant vs. baseline). An ultrasound lung comet score showed a negative correlation with O(2) saturation (R = -.7; p < .0001). In recreational climbers, chest sonography revealed a high prevalence of clinically silent interstitial pulmonary edema mirrored by decreased O(2) saturation, whereas no statistically significant relationship with pulmonary artery systolic pressure was observed during ascent.

  20. Pathophysiological and diagnostic implications of cardiac biomarkers and antidiuretic hormone release in distinguishing immersion pulmonary edema from decompression sickness

    PubMed Central

    Louge, Pierre; Coulange, Mathieu; Beneton, Frederic; Gempp, Emmanuel; Le Pennetier, Olivier; Algoud, Maxime; Dubourg, Lorene; Naibo, Pierre; Marlinge, Marion; Michelet, Pierre; Vairo, Donato; Kipson, Nathalie; Kerbaul, François; Jammes, Yves; Jones, Ian M.; Steinberg, Jean-Guillaume; Ruf, Jean; Guieu, Régis; Boussuges, Alain; Fenouillet, Emmanuel

    2016-01-01

    Abstract Immersion pulmonary edema (IPE) is a misdiagnosed environmental illness caused by water immersion, cold, and exertion. IPE occurs typically during SCUBA diving, snorkeling, and swimming. IPE is sometimes associated with myocardial injury and/or loss of consciousness in water, which may be fatal. IPE is thought to involve hemodynamic and cardiovascular disturbances, but its pathophysiology remains largely unclear, which makes IPE prevention difficult. This observational study aimed to document IPE pathogenesis and improve diagnostic reliability, including distinguishing in some conditions IPE from decompression sickness (DCS), another diving-related disorder. Thirty-one patients (19 IPE, 12 DCS) treated at the Hyperbaric Medicine Department (Ste-Anne hospital, Toulon, France; July 2013–June 2014) were recruited into the study. Ten healthy divers were recruited as controls. We tested: (i) copeptin, a surrogate marker for antidiuretic hormone and a stress marker; (ii) ischemia-modified albumin, an ischemia/hypoxia marker; (iii) brain-natriuretic peptide (BNP), a marker of heart failure, and (iv) ultrasensitive-cardiac troponin-I (cTnI), a marker of myocardial ischemia. We found that copeptin and cardiac biomarkers were higher in IPE versus DCS and controls: (i) copeptin: 68% of IPE patients had a high level versus 25% of DCS patients (P < 0.05) (mean ± standard-deviation: IPE: 53 ± 61 pmol/L; DCS: 15 ± 17; controls: 6 ± 3; IPE versus DCS or controls: P < 0.05); (ii) ischemia-modified albumin: 68% of IPE patients had a high level versus 16% of DCS patients (P < 0.05) (IPE: 123 ± 25 arbitrary-units; DCS: 84 ± 25; controls: 94 ± 7; IPE versus DCS or controls: P < 0.05); (iii) BNP: 53% of IPE patients had a high level, DCS patients having normal values (P < 0.05) (IPE: 383 ± 394 ng/L; DCS: 37 ± 28; controls: 19 ± 15; IPE versus DCS or controls: P < 0.01); (iv) cTnI: 63% of IPE

  1. Pathophysiological and diagnostic implications of cardiac biomarkers and antidiuretic hormone release in distinguishing immersion pulmonary edema from decompression sickness.

    PubMed

    Louge, Pierre; Coulange, Mathieu; Beneton, Frederic; Gempp, Emmanuel; Le Pennetier, Olivier; Algoud, Maxime; Dubourg, Lorene; Naibo, Pierre; Marlinge, Marion; Michelet, Pierre; Vairo, Donato; Kipson, Nathalie; Kerbaul, François; Jammes, Yves; Jones, Ian M; Steinberg, Jean-Guillaume; Ruf, Jean; Guieu, Régis; Boussuges, Alain; Fenouillet, Emmanuel

    2016-06-01

    Immersion pulmonary edema (IPE) is a misdiagnosed environmental illness caused by water immersion, cold, and exertion. IPE occurs typically during SCUBA diving, snorkeling, and swimming. IPE is sometimes associated with myocardial injury and/or loss of consciousness in water, which may be fatal. IPE is thought to involve hemodynamic and cardiovascular disturbances, but its pathophysiology remains largely unclear, which makes IPE prevention difficult. This observational study aimed to document IPE pathogenesis and improve diagnostic reliability, including distinguishing in some conditions IPE from decompression sickness (DCS), another diving-related disorder.Thirty-one patients (19 IPE, 12 DCS) treated at the Hyperbaric Medicine Department (Ste-Anne hospital, Toulon, France; July 2013-June 2014) were recruited into the study. Ten healthy divers were recruited as controls. We tested: (i) copeptin, a surrogate marker for antidiuretic hormone and a stress marker; (ii) ischemia-modified albumin, an ischemia/hypoxia marker; (iii) brain-natriuretic peptide (BNP), a marker of heart failure, and (iv) ultrasensitive-cardiac troponin-I (cTnI), a marker of myocardial ischemia.We found that copeptin and cardiac biomarkers were higher in IPE versus DCS and controls: (i) copeptin: 68% of IPE patients had a high level versus 25% of DCS patients (P < 0.05) (mean ± standard-deviation: IPE: 53 ± 61 pmol/L; DCS: 15 ± 17; controls: 6 ± 3; IPE versus DCS or controls: P < 0.05); (ii) ischemia-modified albumin: 68% of IPE patients had a high level versus 16% of DCS patients (P < 0.05) (IPE: 123 ± 25 arbitrary-units; DCS: 84 ± 25; controls: 94 ± 7; IPE versus DCS or controls: P < 0.05); (iii) BNP: 53% of IPE patients had a high level, DCS patients having normal values (P < 0.05) (IPE: 383 ± 394 ng/L; DCS: 37 ± 28; controls: 19 ± 15; IPE versus DCS or controls: P < 0.01); (iv) cTnI: 63% of IPE patients had a high

  2. Estimates of cost-effectiveness of prehospital continuous positive airway pressure in the management of acute pulmonary edema.

    PubMed

    Hubble, Michael W; Richards, Michael E; Wilfong, Denise A

    2008-01-01

    To estimate the cost-effectiveness of continuous positive airway pressure (CPAP) in managing prehospital acute pulmonary edema in an urban EMS system. Using estimates from published reports on prehospital and emergency department CPAP, a cost-effectiveness model of implementing CPAP in a typical urban EMS system was derived from the societal perspective as well as the perspective of the implementing EMS system. To assess the robustness of the model, a series of univariate and multivariate sensitivity analyses was performed on the input variables. The cost of consumables, equipment, and training yielded a total cost of $89 per CPAP application. The theoretical system would be expected to use CPAP 4 times per 1000 EMS patients and is expected to save 0.75 additional lives per 1000 EMS patients at a cost of $490 per life saved. CPAP is also expected to result in approximately one less intubation per 6 CPAP applications and reduce hospitalization costs by $4075 per year for each CPAP application. Through sensitivity analyses the model was verified to be robust across a wide range of input variable assumptions. Previous studies have demonstrated the clinical effectiveness of CPAP in the management of acute pulmonary edema. Through a theoretical analysis which modeled the costs and clinical benefits of implementing CPAP in an urban EMS system, prehospital CPAP appears to be a cost-effective treatment.

  3. Essential roles of sphingosine-1–phosphate receptor 2 in human mast cell activation, anaphylaxis, and pulmonary edema

    PubMed Central

    Price, Megan M.; Hait, Nitai C.; Kapitonov, Dmitri; Falanga, Yves T.; Morales, Johanna K.; Ryan, John J.; Milstien, Sheldon; Spiegel, Sarah

    2010-01-01

    Systemic exacerbation of allergic responses, in which mast cells play a critical role, results in life-threatening anaphylactic shock. Sphingosine-1–phosphate (S1P), a ligand for a family of G protein–coupled receptors, is a new addition to the repertoire of bioactive lipids secreted by activated mast cells. Yet little is known of its role in human mast cell functions and in anaphylaxis. We show that S1P2 receptors play a critical role in regulating human mast cell functions, including degranulation and cytokine and chemokine release. Immunoglobulin E–triggered anaphylactic responses, including elevation of circulating histamine and associated pulmonary edema in mice, were significantly attenuated by the S1P2 antagonist JTE-013 and in S1P2-deficient mice, in contrast to anaphylaxis induced by administration of histamine or platelet-activating factor. Hence, S1P and S1P2 on mast cells are determinants of systemic anaphylaxis and associated pulmonary edema and might be beneficial targets for anaphylaxis attenuation and prophylaxis. PMID:20194630

  4. Donor smoking is associated with pulmonary edema, inflammation and epithelial dysfunction in ex vivo human donor lungs

    PubMed Central

    Ware, Lorraine B.; Lee, Jae W.; Wickersham, Nancy; Nguyen, John; Matthay, Michael A.; Calfee, Carolyn S.

    2014-01-01

    Although recipients of donor lungs from smokers have worse clinical outcomes, the underlying mechanisms are unknown. We tested the association between donor smoking and the degree of pulmonary edema (as estimated by lung weight), the rate of alveolar fluid clearance (measured by airspace instillation of 5% albumin) and biomarkers of lung epithelial injury and inflammation (bronchoalveolar lavage surfactant protein-D and IL-8) in ex vivo lungs recovered from 298 organ donors. The extent of pulmonary edema was higher in current smokers (n=127) compared to non-smokers (median 408g, IQR 364-500 vs. 385g, IQR 340 - 460, p=0.009). Oxygenation at study enrollment was worse in current smokers versus non-smokers (median PaO2/FiO2 214 mmHg, IQR 126-323 vs. 266 mmHg, IQR 154-370, p=0.02). Current smokers with the highest exposure (≥20 pack-years) had significantly lower rates of alveolar fluid clearance, suggesting that the effects of cigarette smoke on alveolar epithelial fluid transport function may be dose related. BAL IL-8 was significantly higher in smokers while surfactant protein-D was lower. These findings indicate that chronic exposure to cigarette smoke has important effects on inflammation, gas exchange, lung epithelial function and lung fluid balance in the organ donor that could influence lung function in the lung transplant recipient. PMID:25146497

  5. A Randomized Trial of the Effects of Nebulized Albuterol on Pulmonary Edema in Brain Dead Organ Donors

    PubMed Central

    Ware, Lorraine B.; Landeck, Megan; Koyama, Tatsuki; Zhao, Zhiguo; Singer, Jonathan; Kern, Ryan; Neidlinger, Nikole; Nguyen, John; Johnson, Elizabeth; Janz, David R.; Bernard, Gordon R.; Lee, Jae W.; Matthay, Michael A.

    2013-01-01

    Donor lung utilization rates are persistently low primarily due to donor lung dysfunction. We hypothesized that a treatment that enhances the resolution of pulmonary edema by stimulating the rate of alveolar fluid clearance would improve donor oxygenation and increase donor lung utilization. We conducted a randomized, blinded, placebo-controlled trial of aerosolized albuterol (5 mg q4h) versus saline placebo during active donor management in 506 organ donors. The primary outcome was change in oxygenation (PaO2/FiO2) from enrollment to organ procurement. The albuterol (n=260) and placebo (n=246) groups were well matched for age, gender, ethnicity, smoking, and cause of brain death. The change in PaO2/FiO2 from enrollment to organ procurement did not differ between treatment groups (p=0.54) nor did donor lung utilization (albuterol 29% vs. placebo 32%, p=0.44). Donors in the albuterol vs. placebo group were more likely to have the study drug dose reduced (13% vs. 1%, p<0.001) or stopped (8% vs. 0%, p<0.001) for tachycardia. In summary, treatment with high dose inhaled albuterol during the donor management period did not improve donor oxygenation or increase donor lung utilization but did cause tachycardia. High dose aerosolized albuterol should not be used in donors to enhance the resolution of pulmonary edema. PMID:24730050

  6. [Anesthetic Management of a Parturient with Eclampsia, Posterior Reversible Encephalopathy Syndrome and Pulmonary Edema due to Pregnancy-induced Hypertension].

    PubMed

    Aida, Junko; Okutani, Hiroai; Oda, Yutaka; Okutani, Ryu

    2015-08-01

    A 27-year-old woman with mental retardation was admitted to a nearby hospital for an abrupt onset of seizure. Physical examination revealed remarkable hypertension and pregnancy with estimated gestational age of 28th week. Severe pulmonary edema and hypoxia led to a diagnosis of pregnancy-induced hypertension (PIH) accompanied by eclampsia. She was orotracheally intubated because of refractory seizure and hypoxemia, and transferred to our hospital for further treatment. Besides severe hypoxia and hypercapnea, an enhanced lesion was detected in the left posterior cerebrum by brain MRI. No abnormal findings were detected in the fetus, with heart rate of 150 beats x min. She was diagnosed with posterior reversible encephalopathy syndrome (PRES) caused by PIH and emergency cesarean section under general anesthesia was scheduled. A male newborn was delivered with Apgar score of 1/4 (1/5 min), followed by starting continuous infusion of nicardipine for controlling hypertension. Chest X-P on completion of surgery revealed remarkably alleviated pulmonary edema. She received intensive treatment and continued positive pressure ventilation for four days after delivery. She recovered with no neurological deficits and her child was well without any complications.

  7. Levels of interleukin-6, superoxide dismutase and malondialdehyde in the lung tissue of a rat model of hypoxia-induced acute pulmonary edema

    PubMed Central

    GAO, HENGBO; TIAN, YINGPING; WANG, WEI; YAO, DONGQI; ZHENG, TUOKANG; MENG, QINGBING

    2016-01-01

    The present study aimed to investigate the levels of malondialdehyde (MDA), superoxide dismutase (SOD) and interleukin (IL)-6 in the lung tissue of a rat model of acute pulmonary edema induced by acute hypoxia, and its pathophysiological significance. A total of 48 adult Wistar rats were randomly divided into group A, a normal group; group B, a model of acute pulmonary edema induced by hypoxia for 24 h; group C, a model of acute pulmonary edema induced by hypoxia for 48 h; and group D, a model of acute pulmonary edema induced by hypoxia for 72 h. The rats in groups B-D were intraperitoneally injected with 6% ammonium chloride to establish the model of acute pulmonary edema, and were subsequently sacrificed following successful modeling for 24, 48 and 72 h. The plasma of rats was isolated and the lungs of the rats were removed. Subsequently, a 10% lung homogenate was prepared and the contents and the activities of MDA, SOD and IL-6 in the lung tissue and IL-6 in the plasma were detected by enzyme-linked immunosorbent assay. MDA and IL-6 expression levels increased and SOD activity decreased in the lung tissue in group B as compared with group A; however the difference did not reach significance (P>0.05). MDA, IL-6 and SOD levels in the lung tissue of rats were significantly altered following the increased duration of pulmonary edema in groups C and D, as compared group A (P<0.05). The plasma IL-6 levels of the rats in groups B-D significantly increased, as compared with those in group A (P<0.05). In conclusion, the results of the present study demonstrated that the incidence of acute pulmonary edema may be associated with oxidative stress. Furthermore, decreased antioxidant capacity and increased free radical levels may be associated with pulmonary edema, as in the present study the levels of IL-6, SOD and MDA in the lung tissue were observed to be associated with the pathological changes of the disease. PMID:26998026

  8. Receptor for advanced glycation end products and neuronal deficit in the fatal brain edema of diabetic ketoacidosis.

    PubMed

    Hoffman, William H; Artlett, Carol M; Zhang, Weixian; Kreipke, Christian W; Passmore, Gregory G; Rafols, Jose A; Sima, Anders A F

    2008-10-31

    Radiologic and neuropsychologic studies suggest that diabetes mellitus causes structural changes in the brain and adversely effects cognitive development. Experimental animal models of type 1 diabetes mellitus (T1DM) have advanced these findings by demonstrating duration-related neuronal and cognitive deficits in T1DM BB/Wor rats. We studied the expression of receptor for advanced glycation end products (RAGE) and neuronal densities in the brains of two patients who died as the result of clinical brain edema(BE)that developed during the treatment of severe diabetic ketoacidosis (DKA). RAGE was markedly and diffusely expressed in blood vessels, neurons, and the choroid plexus and co-localized with glial fibrillary acidic protein (GFAP) in astrocytes. Significant neuronal loss was seen in the hippocampus and frontal cortex. Astrocytosis was present and white matter was atrophied in both cases when compared to age-matched controls. Our data supports that a neuroinflammatory response occurs in the BE associated with DKA, and that even after a relatively short duration of poorly controlled T1DM, the pathogenesis of primary diabetic encephalopathy can be initiated.

  9. Natural History of Tuberculosis: Duration and Fatality of Untreated Pulmonary Tuberculosis in HIV Negative Patients: A Systematic Review

    PubMed Central

    Tiemersma, Edine W.; van der Werf, Marieke J.; Borgdorff, Martien W.; Williams, Brian G.; Nagelkerke, Nico J. D.

    2011-01-01

    Background The prognosis, specifically the case fatality and duration, of untreated tuberculosis is important as many patients are not correctly diagnosed and therefore receive inadequate or no treatment. Furthermore, duration and case fatality of tuberculosis are key parameters in interpreting epidemiological data. Methodology and Principal Findings To estimate the duration and case fatality of untreated pulmonary tuberculosis in HIV negative patients we reviewed studies from the pre-chemotherapy era. Untreated smear-positive tuberculosis among HIV negative individuals has a 10-year case fatality variously reported between 53% and 86%, with a weighted mean of 70%. Ten-year case fatality of culture-positive smear-negative tuberculosis was nowhere reported directly but can be indirectly estimated to be approximately 20%. The duration of tuberculosis from onset to cure or death is approximately 3 years and appears to be similar for smear-positive and smear-negative tuberculosis. Conclusions Current models of untreated tuberculosis that assume a total duration of 2 years until self-cure or death underestimate the duration of disease by about one year, but their case fatality estimates of 70% for smear-positive and 20% for culture-positive smear-negative tuberculosis appear to be satisfactory. PMID:21483732

  10. Fatal right ventricular failure and pulmonary hypertension after protamine administration during cardiac transplantation.

    PubMed

    Pannu, Bibek S; Sanghavi, Devang K; Guru, Pramod K; Reddy, Dereddi Raja; Iyer, Vivek N

    2016-03-01

    Protamine sulfate is the only Food and Drug administration approved medication for reversal of intraoperative heparin-induced anticoagulation during cardiac and vascular surgeries. One of the rare side effects of protamine sulfate is an idiosyncratic reaction resulting in acute pulmonary hypertension (APH) and right ventricular (RV) failure occurring after protamine administration. These reactions are rare but catastrophic with high mortality. A 36-year-old female with severe congestive heart failure was undergoing cardiac transplant surgery. After successful implantation of the donor heart, the patient was weaned off cardiopulmonary bypass. Protamine was then administered to reverse the heparin anticoagulation. She immediately developed APH and RV failure immediately after protamine infusion. The patient required immediate administration of inotropic agents, nitric oxide (NO), and subsequently required a number of mechanical support devices including an RV assist device (RVAD) and ultimately full veno-arterial extracorporeal membrane oxygenation (VA-ECMO). Despite heroic efforts, the patient developed refractory multi-organ failure in the Intensive Care Unit and died after family requested discontinuation of resuscitative efforts. This case probably represents the first reported occurrence of fatal protamine-induced APH and ventricular failure in the setting of cardiac transplantation surgery. A number of interventions including inhaled NO, systemic vasopressors, RVAD, and ultimately VA-ECMO failed to reverse the situation, and the patient died of multi-organ failure.

  11. Role of Survival Time and Injury Severity in Fatal Pulmonary Fat Embolism.

    PubMed

    Jarmer, Juliane; Ampanozi, Garyfalia; Thali, Michael J; Bolliger, Stephan A

    2017-03-01

    Pulmonary fat embolism (PFE) is frequent in blunt trauma and may occasionally lead to death. A correlation between fracture grade and severity and PFE grade has been described before, but no correlation between PFE and survival time, fat crushing extent, fat crush grade, or number of body regions with fractures could be noted in this small study. To further examine this, we decided to examine the aforementioned points in a far larger study group.Autopsy protocols of 188 nonresuscitated fatalities with blunt trauma and without right heart injury, which underwent whole body dissection, were retrospectively reviewed concerning the presence and the severity of PFE, injuries, survival time, age, sex, and the body mass index.The fracture grade, the fracture severity, and the number of the fractured regions correlated very well with the grade of PFE, but the crushed regions, crush grade, and crush severity did not. We observed a time correlation between survival time and PFE only in the sense that very rapid deaths were often PFE negative. High-grade PFE was observed most often in patients having died less than 6 hours after the incident, and PFE grades of 2 or more were occasionally noted even after 48 hours.

  12. Which patients with venous thromboembolism are at risk for fatal pulmonary embolism?

    PubMed

    Gallus, Alexander

    2008-10-01

    In a registry of 15,520 patients treated for symptomatic deep vein thrombosis or pulmonary embolism (PE), the 90-day mortality was 8.65% and death was attributed to PE in 1.68% of patients (19.4% of all deaths). Multivariate analysis defined five simple predictors of death from PE during the first 3 months after presentation. The odds ratio for fatal PE was raised to 5.4 by initially nonmassive symptomatic PE (compared with deep vein thrombosis and no symptoms of PE), to 17.5 by initially massive PE (systolic blood pressure below 90 mmHg), 4.9 by immobility as a result of neurological disease, 2.5 by age over 75 years, and 2.0 by the presence of cancer. Of all the deaths from PE, 75% occurred within 12 days of presentation and 50% occurred within 5 days. These results reinforce previous observations that also linked symptomatic PE, massive PE, old age, and cancer to a raised likelihood of death from PE despite appropriate therapy.

  13. Fatal pulmonary cysticercosis caused by Cysticercus longicollis in a captive ring-tailed lemur (Lemur catta).

    PubMed

    Alić, Amer; Hodžić, Adnan; Škapur, Vedad; Alić, Alma Šeho; Prašović, Senad; Duscher, Georg G

    2017-07-15

    Here we describe fatal pulmonary cysticercosis caused by Cysticercus longicollis, the larval stage of Taenia crassiceps in a 15-year-old female ring-tailed lemur (Lemur catta) from Sarajevo Zoo. After sudden death, the lemur was subjected to necropsy and large multicystic structure, subdivided with fibrous septa and filled with numerous translucent, oval to ellipsoid bladder-like cysts (cysticerci), almost completely replacing right lung lobe was observed. In addition, numerous free and encysted cysticerci were found in the thoracic cavity. Histopathology revealed connective tissue outlined cavities that compress lung parenchyma. Each cavity contained several thin walled cysticerci with single inverted protoscolex, one or more suckers and rostelum with two rows of hooks. In many of the cysticerci one or several exogenous buds of daughter cysticerci were observed. Based on morphology and microscopic appearance the parasite was identified as C. longicollis. Subsequent molecular analysis and sequencing confirmed presumptive diagnosis. To our knowledge, this case represents the first report of T. crassiceps and cysticercosis caused by C. longicollis in Bosnia and Herzegovina. Copyright © 2017 Elsevier B.V. All rights reserved.

  14. Role of PiCCO monitoring for the integrated management of neurogenic pulmonary edema following traumatic brain injury: A case report and literature review.

    PubMed

    Lin, Xiaoping; Xu, Zhijun; Wang, Pengfei; Xu, Yan; Zhang, Gensheng

    2016-10-01

    Neurogenic pulmonary edema (NPE) is occasionally observed in patients with traumatic brain injury (TBI); however, this condition is often underappreciated. NPE is frequently misdiagnosed due to its atypical clinical performance, thus delaying appropriate treatment. A comprehensive management protocol of NPE in patients with TBI has yet to be established. The current study reported the case of a 67-year-old man with severe TBI who was transferred to our intensive care unit (ICU). On day 7 after hospitalization, the patient suddenly suffered tachypnea, tachycardia, systemic hypertension and hypoxemia during lumbar cistern drainage. Intravenous diuretics, tranquilizer and glucocorticoid were administered due to suspected left heart failure attack. Chest radiography examination supported the diagnosis of pulmonary edema; however, hypotension and hypovolemia were subsequently observed. Pulse index continuous cardiac output (PiCCO) hemodynamic monitoring and bedside echocardiography were performed, which excluded the diagnosis of cardiac pulmonary edema, and thus the diagnosis of NPE was confirmed. Goal-directed therapy by dynamic PiCCO monitoring was then implemented. In addition, levosimendan, an inotropic agent, was introduced to improve cardiac output. The patient had complete recovered from pulmonary edema and regained consciousness on day 11 of hospitalization. The current case demonstrated that PiCCO monitoring may serve a central role in the integrated management of NPE in patients with TBI. Levosimendan may be a potential medicine in treating cardiac dysfunction, along with its benefit from improving neurological function in NPE patients.

  15. Role of PiCCO monitoring for the integrated management of neurogenic pulmonary edema following traumatic brain injury: A case report and literature review

    PubMed Central

    Lin, Xiaoping; Xu, Zhijun; Wang, Pengfei; Xu, Yan; Zhang, Gensheng

    2016-01-01

    Neurogenic pulmonary edema (NPE) is occasionally observed in patients with traumatic brain injury (TBI); however, this condition is often underappreciated. NPE is frequently misdiagnosed due to its atypical clinical performance, thus delaying appropriate treatment. A comprehensive management protocol of NPE in patients with TBI has yet to be established. The current study reported the case of a 67-year-old man with severe TBI who was transferred to our intensive care unit (ICU). On day 7 after hospitalization, the patient suddenly suffered tachypnea, tachycardia, systemic hypertension and hypoxemia during lumbar cistern drainage. Intravenous diuretics, tranquilizer and glucocorticoid were administered due to suspected left heart failure attack. Chest radiography examination supported the diagnosis of pulmonary edema; however, hypotension and hypovolemia were subsequently observed. Pulse index continuous cardiac output (PiCCO) hemodynamic monitoring and bedside echocardiography were performed, which excluded the diagnosis of cardiac pulmonary edema, and thus the diagnosis of NPE was confirmed. Goal-directed therapy by dynamic PiCCO monitoring was then implemented. In addition, levosimendan, an inotropic agent, was introduced to improve cardiac output. The patient had complete recovered from pulmonary edema and regained consciousness on day 11 of hospitalization. The current case demonstrated that PiCCO monitoring may serve a central role in the integrated management of NPE in patients with TBI. Levosimendan may be a potential medicine in treating cardiac dysfunction, along with its benefit from improving neurological function in NPE patients. PMID:27698733

  16. Inhaled nitric oxide for the brain dead donor with neurogenic pulmonary edema during anesthesia for organ donation: a case report

    PubMed Central

    Park, Eun Sun; Lee, A-Ran; Lee, Sang Hyun; Kim, An Suk; Park, Soon Eun; Cho, Young Woo

    2014-01-01

    Neurogenic pulmonary edema (NPE) in brain dead organ donors occurring after an acute central nervous system insult threatens organ preservation of potential organ donors and the outcome of organ donation. Hence the active and immediate management of NPE is critical. In this case, a 50-year-old male was admitted to the intensive care unit (ICU) for organ donation. He was hypoxic due to NPE induced by spontaneous intracerebral hemorrhage and intraventricular hemorrhage. Protective ventilatory management, intermittent recruitment maneuvers, and supportive treatment were maintained in the ICU and the operating room (OR). Despite this management, the hypoxemia worsened after the OR admission. So inhaled nitric oxide (NO) therapy was performed during the operation, and the hypoxic phenomena showed remarkable improvement. The organ retrieval was successfully completed. Therefore, NO inhalation can be helpful in the improvement of hypoxemia caused by NPE in brain dead organ donors during anesthesia for the organ donation. PMID:25237451

  17. An uncommon complication of a common clinical scenario: exploring reexpansion pulmonary edema with a case report and literature review

    PubMed Central

    Meeker, Jared W.; Jaeger, Amy L.; Tillis, William P.

    2016-01-01

    Reexpansion pulmonary edema (RPE) is a rare complication that can occur after rapid reinflation of the lung following thoracentesis of a pleural effusion or chest tube drainage of pneumothorax. The severity in clinical presentation can be widely varied from radiographic changes only to rapidly progressive respiratory failure requiring mechanical ventilation. The quick nature of onset and potential for serious decline in a previously stable patient makes it important to prepare, recognize, diagnose, and appropriately manage patients who develop RPE. The standard treatment for RPE consists of supportive care, and there are certain measures that may be taken to reduce the risk, including limiting the amount drained and avoiding excessive negative pleural pressure. Exactly how to prevent RPE remains unclear, however, and varying recommendations exist. This is a case report of RPE after thoracentesis for a pleural effusion and a brief review of literature to date, including potential preventative strategies. PMID:27406463

  18. An uncommon complication of a common clinical scenario: exploring reexpansion pulmonary edema with a case report and literature review.

    PubMed

    Meeker, Jared W; Jaeger, Amy L; Tillis, William P

    2016-01-01

    Reexpansion pulmonary edema (RPE) is a rare complication that can occur after rapid reinflation of the lung following thoracentesis of a pleural effusion or chest tube drainage of pneumothorax. The severity in clinical presentation can be widely varied from radiographic changes only to rapidly progressive respiratory failure requiring mechanical ventilation. The quick nature of onset and potential for serious decline in a previously stable patient makes it important to prepare, recognize, diagnose, and appropriately manage patients who develop RPE. The standard treatment for RPE consists of supportive care, and there are certain measures that may be taken to reduce the risk, including limiting the amount drained and avoiding excessive negative pleural pressure. Exactly how to prevent RPE remains unclear, however, and varying recommendations exist. This is a case report of RPE after thoracentesis for a pleural effusion and a brief review of literature to date, including potential preventative strategies.

  19. Hydrothorax with alveolar-pleural fistula mimicking re-expansion pulmonary edema during liver transplantation: a case report

    PubMed Central

    2015-01-01

    We present a case of an alveolar-pleural fistula with hepatic hydrothorax in a patient undergoing orthotropic liver transplantation, which was detected by drainage of transudate through an endotracheal tube during operation. A standard endotracheal tube was changed to a double-lumen tube to provide differential lung ventilation. The patient was diagnosed with an alveolar-pleural fistula by direct vision of an air leak during positive-pressure ventilation through a diaphragmatic incision. There was still a concern about worsening his ventilation due to persistent aspiration of pleural effusion towards the ipsilateral lung during the remaining operation period. Surgeon repaired the defect on the exposed lung surface via diaphragmatic opening. Anesthesiologists should consider an alveolar-pleural fistula as a possible differential diagnosis with re-expansion pulmonary edema when transudate emanating from the endotracheal tube is obtained in patients with massive hydrothorax. PMID:25844139

  20. Early Endovascular Treatment of Aneurysmal Subarachnoid Hemorrhage Complicated by Neurogenic Pulmonary Edema and Takotsubo-Like Cardiomyopathy

    PubMed Central

    Manto, Andrea; De Gennaro, Angela; Manzo, Gaetana; Serino, Antonietta; Quaranta, Gaetano; Cancella, Claudia

    2014-01-01

    Summary Aneurysmal subarachnoid hemorrhage (SAH) may be associated with acute cardiopulmonary complications, like neurogenic pulmonary edema (NPE) and Takotsubo-like cardiomyopathy (TCM). These dysfunctions seem to result from a neurogenically induced overstimulation of the sympathetic nervous system through the brain-heart connection and often complicate poor grade aneurysmal SAH. The optimal treatment modality and timing of intervention in this clinical setting have not been established yet. Early endovascular therapy seems to be the fitting treatment in this particular group of patients, in which surgical clipping is often contraindicated due to the added risk of craniotomy. Herein we describe the case of a woman admitted to the emergency department with aneurysmal SAH complicated by NPE-TCM, in which early endovascular coiling was successfully performed. Our case, characterized by a favorable outcome, further supports the evidence that early endovascular treatment should be preferred in this peculiar clinical scenario. PMID:24976204

  1. Early endovascular treatment of aneurysmal subarachnoid hemorrhage complicated by neurogenic pulmonary edema and Takotsubo-like cardiomyopathy.

    PubMed

    Manto, Andrea; De Gennaro, Angela; Manzo, Gaetana; Serino, Antonietta; Quaranta, Gaetano; Cancella, Claudia

    2014-06-01

    Aneurysmal subarachnoid hemorrhage (SAH) may be associated with acute cardiopulmonary complications, like neurogenic pulmonary edema (NPE) and Takotsubo-like cardiomyopathy (TCM). These dysfunctions seem to result from a neurogenically induced overstimulation of the sympathetic nervous system through the brain-heart connection and often complicate poor grade aneurysmal SAH. The optimal treatment modality and timing of intervention in this clinical setting have not been established yet. Early endovascular therapy seems to be the fitting treatment in this particular group of patients, in which surgical clipping is often contraindicated due to the added risk of craniotomy. Herein we describe the case of a woman admitted to the emergency department with aneurysmal SAH complicated by NPE-TCM, in which early endovascular coiling was successfully performed. Our case, characterized by a favorable outcome, further supports the evidence that early endovascular treatment should be preferred in this peculiar clinical scenario.

  2. Coagulation factor V Leiden mutation in sudden fatal pulmonary embolism and in a general northern European population sample.

    PubMed

    Kuismanen, K; Savontaus, M L; Kozlov, A; Vuorio, A F; Sajantila, A

    1999-12-06

    The R506Q point mutation in the gene coding for coagulation factor V (Leiden mutation) is the major underlying defect in resistance to activated protein C (APC), which predisposes to venous thrombosis. The risk of deep vein thrombosis is clearly elevated in carriers of the mutation, but the risk for pulmonary embolism has not been demonstrated to be as high. The aim of our study was to determine the frequency of the Leiden mutation in an autopsy series of sudden fatal pulmonary embolism cases. PCR and subsequent restriction enzyme digestion were applied for genotyping 164 cases of pulmonary embolism. According to our data, the allele frequency of the Leiden mutation is not higher in sudden fatal pulmonary embolism cases (0.8%, 95% CI 0-1.9%) than in the general Finnish population (1.5%, 95% CI 0-3.3%). In addition to the 97 Finns, we determined the frequency of the Leiden mutation in 255 individuals from the neighbouring populations (Saami, Komi, and Karelians from Russia and Estonians), and found the Saami to have the highest frequency of the Leiden mutation (6.3%, 95% CI 3.2-9.2) in the general northern European population sample studied here.

  3. Benzo(a)pyrene-induced pulmonary inflammation, edema, surfactant dysfunction, and injuries in rats: alleviation by farnesol.

    PubMed

    Qamar, Wajhul; Khan, Abdul Quaiyoom; Khan, Rehan; Lateef, Abdul; Tahir, Mir; Rehman, Muneeb U; Ali, Farrah; Sultana, Sarwat

    2012-02-01

    Benzo(a)pyrene (B(a)P) is a well-known environmental contaminant and carcinogen. Its sources include tobacco smoke, automobile exhaust, forest fire, and other combustion processes. Farnesol, an active principle of Vachellia farnesiana and other aromatic plants, possesses preventive properties against various toxicities. Present study was designed to estimate chemopreventive effects of farnesol against B(a)P-induced pulmonary injuries. To determine the protective effects of farnesol, it was administered orally at 2 doses (100 and 200 mg/kg body weight [b.w.]) once daily for 14 days. Rats were exposed intratracheally to B(a)P, 5 mg/kg b.w. on days 12 and 14, thereafter assessed for pulmonary toxicities 24 hours post last dose of B(a)P. B(a)P-induced edema, inflammation, oxidative stress, and consequent damages in lungs were assessed in terms of total protein, total cell count, nitric oxide (NO), lactate dehydrogenase (LDH), alkaline phosphatase, and in bronchoalveolar lavage fluid (BALF). B(a)P also reduced the levels of phospholipids (lung surfactants) in BALF. However, pretreatment with farnesol at both the doses significantly reduced the lung injuries and inflammatory responses. Farnesol also protected the levels of phospholipids to normal when compared with control. It also modified the activities of B(a)P metabolizing enzymes NADPH-cytochrome P450 reductase, microsomal epoxide hydrolase (mEH), and glutathione S-transferase (GST) in lung tissue of rats. Present findings suggest a prominent role of farnesol against B(a)P-induced lung inflammation, edema, surfactant dysfunction, and epithelial damages in Wistar rats. In conclusion, farnesol shows lung protection against B(a)P toxicities in Wistar rats.

  4. Selective HDAC6 inhibition prevents TNF-α-induced lung endothelial cell barrier disruption and endotoxin-induced pulmonary edema.

    PubMed

    Yu, Jinyan; Ma, Zhongsen; Shetty, Sreerama; Ma, Mengshi; Fu, Jian

    2016-07-01

    Lung endothelial damage contributes to the pathogenesis of acute lung injury. New strategies against lung endothelial barrier dysfunction may provide therapeutic benefits against lung vascular injury. Cell-cell junctions and microtubule cytoskeleton are basic components in maintaining endothelial barrier integrity. HDAC6, a deacetylase primarily localized in the cytoplasm, has been reported to modulate nonnuclear protein function through deacetylation. Both α-tubulin and β-catenin are substrates for HDAC6. Here, we examined the effects of tubastatin A, a highly selective HDAC6 inhibitor, on TNF-α induced lung endothelial cell barrier disruption and endotoxin-induced pulmonary edema. Selective HDAC6 inhibition by tubastatin A blocked TNF-α-induced lung endothelial cell hyperpermeability, which was associated with increased α-tubulin acetylation and microtubule stability. Tubastatin A pretreatment inhibited TNF-α-induced endothelial cell contraction and actin stress fiber formation with reduced myosin light chain phosphorylation. Selective HDAC6 inhibition by tubastatin A also induced β-catenin acetylation in human lung endothelial cells, which was associated with increased membrane localization of β-catenin and stabilization of adherens junctions. HDAC6 knockdown by small interfering RNA also prevented TNF-α-induced barrier dysfunction and increased α-tubulin and β-catenin acetylation in endothelial cells. Furthermore, in a mouse model of endotoxemia, tubastatin A was able to prevent endotoxin-induced deacetylation of α-tubulin and β-catenin in lung tissues, which was associated with reduced pulmonary edema. Collectively, our data indicate that selective HDAC6 inhibition by tubastatin A is a potent approach against lung endothelial barrier dysfunction.

  5. Clara Cell Protein (CC16), a Marker of Lung Epithelial Injury, Is Decreased in Plasma and Pulmonary Edema Fluid From Patients With Acute Lung Injury

    PubMed Central

    Kropski, Jonathan A.; Fremont, Richard D.; Calfee, Carolyn S.; Ware, Lorraine B.

    2009-01-01

    Background: Acute lung injury (ALI) and ARDS are common clinical syndromes that are underdiagnosed. Clara cell secretory protein (CC16) is an antiinflammatory protein secreted by the Clara cells of the distal respiratory epithelium that has been proposed as a biomarker of lung epithelial injury. We tested the diagnostic and prognostic utility of CC16 in patients with non–trauma-related ALI/ARDS compared to a control group of patients with acute cardiogenic pulmonary edema (CPE). Methods: Plasma and pulmonary edema fluid samples were obtained from medical and surgical patients with ALI/ARDS or CPE requiring intubation for mechanical ventilation. The etiology of pulmonary edema was determined using consensus clinical criteria for ALI/ARDS and CPE and the edema fluid-to-plasma protein ratio. Plasma and edema fluid CC16 levels were measured by sandwich enzyme-linked immunosorbent assay. CC16 levels were log transformed for analysis, and comparisons were made by the Student t test or χ2 as appropriate. Results: Compared to patients with CPE (n = 9), patients with ALI/ARDS (n = 23) had lower median CC16 levels in plasma (22 ng/mL [interquartile range (IQR), 9 to 44 ng/mL] vs 55 ng/mL [IQR, 18 to 123 ng/mL], respectively; p = 0.053) and pulmonary edema fluid (1,950 ng/mL [IQR, 1,780 to 4,024 ng/mL] vs 4,835 ng/mL [IQR, 2,006 to 6,350 ng/mL], respectively; p = 0.044). Relative to total pulmonary edema fluid protein concentration, the median CC16 level was significantly lower in patients with ALI/ARDS (45 ng CC16/mg total protein [IQR, 4 to 64 ng CC16/mg total protein] vs 120 ng CC16/mg total protein [IQR, 87 to 257 ng CC16/mg total protein], respectively; p = 0.005). Neither plasma nor edema fluid CC16 levels predicted mortality, the number of days of unassisted ventilation, or ICU length of stay. Conclusion: CC16 is a promising diagnostic biomarker for helping to discriminate ALI from CPE. Larger scale validation is warranted to better characterize the utility of CC16

  6. A Peptide to Reduce Pulmonary Edema in a Rat Model of Lung Transplantation

    PubMed Central

    Finsterwalder, Richard; Friedl, Heinz P.; Rauscher, Sabine; Gröger, Marion; Kocher, Alfred; Wagner, Christine; Wagner, Stephan N.; Fischer, Gottfried; Schultz, Marcus J.; Wiedemann, Dominik; Petzelbauer, Peter

    2015-01-01

    Background Despite significant advances in organ preservation, surgical techniques and perioperative care, primary graft dysfunction is a serious medical problem in transplantation medicine in general and a specific problem in patients undergoing lung transplantation. As a result, patients develop lung edema, causing reduced tissue oxygenation capacity, reduced lung compliance and increased requirements for mechanical ventilatory support. Yet, there is no effective strategy available to protect the grafted organ from stress reactions induced by ischemia/reperfusion and by the surgical procedure itself. Methods We assessed the effect of a cingulin-derived peptide, XIB13 or a random peptide in an established rat model of allogeneic lung transplantation. Donor lungs and recipients received therapeutic peptide at the time of transplantation and outcome was analyzed 100min and 28 days post grafting. Results XIB13 improved blood oxygenation and reduced vascular leak 100min post grafting. Even after 28 days, lung edema was significantly reduced by XIB13 and lungs had reduced fibrotic or necrotic zones. Moreover, the induction of an allogeneic T cell response was delayed indicating a reduced antigen exchange between the donor and the host. Conclusions In summary, we provide a new tool to strengthen endothelial barrier function thereby improving outcomes in lung transplantation. PMID:26536466

  7. [Acute pulmonary edema from inhalation of the bite-block after anesthesia with a laryngeal mask].

    PubMed

    Banchereau, F; Marié, S; Pez, H; Boully-Balihaut, A; Tueux, O

    2001-12-01

    We report a case of acute pulmonary oedema, consecutive to upper airway obstruction due to the inhalation of the laryngeal mask airway (LMA) bite block during recovery. The LMA was used for general anaesthesia with the bite-block provided in France. No trouble occurred during LMA insertion and anaesthesia. Symptomatic treatment provided complete resolution within a few days.

  8. A patient with possible TRALI who developed pulmonary hypertensive crisis and acute pulmonary edema during cardiac surgery.

    PubMed

    Kojima, Taiki; Nishisako, Ryo; Sato, Hideo

    2012-06-01

    There are very few case reports of transfusion-related acute lung injury (TRALI) under close hemodynamic monitoring. We encountered a case of possible TRALI during on-pump coronary artery bypass grafting (CABG). A 66-year-old man who had undergone on-pump CABG was administered fresh frozen plasma (FFP). One hour after FFP transfusion, pulmonary hypertensive crisis and subsequent hypoxic decompensation occurred. A second cardiopulmonary bypass (CPB) was needed for circulatory and respiratory deterioration. Extracorporeal life support (ECLS), intraaortic balloon pumping (IABP), and nitric oxide therapy were required after the surgery. Despite the severity of the initial state, his recovery was comparatively smooth. ECLS and IABP were removed on postoperative day (POD)1; the patient was extubated and discharged from the ICU on POD7 and POD12, respectively. The diagnosis of TRALI was confirmed by human leukocyte antigen antibody detection in the administered FFP. In addition, lymphocytic immunofluorescence test showed that a cross-match of the plasma from the pooled FFP against the recipient leukocytes was positive. The clinical course of the pulmonary artery hypertension was followed by a decrease in dynamic lung compliance. The mechanism of this phenomenon is unclear. However, it might suggest the possibility of vasoconstriction or obstruction of the peripheral pulmonary artery preceding lung damage, as in the case in animal models reported previously.

  9. Lower extremity deep venous thrombosis with fatal pulmonary thromboembolism caused by benign pelvic space-occupying lesions--an overview.

    PubMed

    Rosenfeld, Hannah; Byard, Roger W

    2012-05-01

    Venous stasis predisposes to thrombosis. One hundred and sixty cases of fatal pulmonary thromboembolism were reviewed to determine how many cases had deep venous thromboses associated with venous blood flow reduction caused by external pressure from benign pelvic masses. Three cases were identified, representing 2% of cases overall (3/160): a 44-year-old woman with a large uterine leiomyoma (1048 g); a 74-year-old man with prostatomegaly and bladder distension (containing 1 L of urine); and a 70-year-old man with prostatomegaly and bladder distension (containing 3 L of urine). Although a rare cause of fatal deep venous thrombosis and pulmonary thromboembolism, space-occupying pelvic lesions can lead to extrinsic pressure on adjacent veins reducing blood flow and causing stasis and thrombosis. Individuals with large pelvic masses may, therefore, be at increased risk of pulmonary thromboembolism from deep venous thrombosis, particularly in the presence of concurrent risk factors such as immobility, thrombophilias, malignancy, and significant cardiopulmonary disease.

  10. Fatal pulmonary embolism following elective total knee replacement using aspirin in multi-modal prophylaxis - A 12year study.

    PubMed

    Quah, C; Bayley, E; Bhamber, N; Howard, P

    2017-10-01

    The National Institute for Health and Clinical Excellence (NICE) has issued guidelines on which thromboprophylaxis regimens are suitable following lower limb arthroplasty. Aspirin is not a recommended agent despite being accepted in orthopaedic guidelines elsewhere. We assessed the incidence of fatal pulmonary embolism (PE) and all-cause mortality following elective primary total knee replacement (TKR) with a standardised multi-modal prophylaxis regime in a large teaching district general hospital. We utilised a prospective audit database to identify those that had died within 42 and 90days postoperatively. Data from April 2000 to 2012 were analysed for 42 and 90day mortality rates. There were a total of 8277 elective primary TKR performed over the 12year period. The multi-modal prophylaxis regimen used unless contraindicated for all patients included 75mg aspirin once daily for four weeks. Case note review ascertained the causes of death. Where a patient had been referred to the coroner, they were contacted for post mortem results. The mortality rates at 42 and 90days were 0.36 and 0.46%. There was one fatal PE within 42days of surgery (0.01%) who was taking enoxaparin because of aspirin intolerance. Two fatal PE's occurred at 48 and 57days post-operatively (0.02%). The leading cause of death was myocardial infarction (0.13%). Fatal PE following elective TKR with a multi-modal prophylaxis regime is a very rare cause of mortality. Copyright © 2017 Elsevier B.V. All rights reserved.

  11. Intratracheal dopamine attenuates pulmonary edema and improves survival after ventilator-induced lung injury in rats

    PubMed Central

    Chamorro-Marín, Virginia; García-Delgado, Manuel; Touma-Fernández, Angel; Aguilar-Alonso, Eduardo; Fernández-Mondejar, Enrique

    2008-01-01

    Intoduction Clearance of alveolar oedema depends on active transport of sodium across the alveolar-epithelial barrier. β-Adrenergic agonists increase clearance of pulmonary oedema, but it has not been established whether β-agonist stimulation achieves sufficient oedema clearance to improve survival in animals. The objective of this study was to determine whether the increased pulmonary oedema clearance produced by intratracheal dopamine improves the survival of rats after mechanical ventilation with high tidal volume (HVT). Methods This was a randomized, controlled, experimental study. One hundred and thirty-two Wistar-Kyoto rats, weighing 250 to 300 g, were anaesthetized and cannulated via endotracheal tube. Pulmonary oedema was induced by endotracheal instillation of saline solution and mechanical ventilation with HVT. Two types of experiment were carried out. The first was an analysis of pulmonary oedema conducted in six groups of 10 rats ventilated with low (8 ml/kg) or high (25 ml/kg) tidal volume for 30 or 60 minutes with or without intratracheally instilled dopamine. At the end of the experiment the animals were exsanguinated and pulmonary oedema analysis performed. The second experiment was a survival analysis, which was conducted in two groups of 36 animals ventilated with HVT for 60 minutes with or without intratracheal dopamine; survival of the animals was monitored for up to 7 days after extubation. Results In animals ventilated at HVT with or without intratracheal dopamine, oxygen saturation deteriorated over time and was significantly higher at 30 minutes than at 60 minutes. After 60 minutes, a lower wet weight/dry weight ratio was observed in rats ventilated with HVT and instilled with dopamine than in rats ventilated with HVT without dopamine (3.9 ± 0.27 versus 4.9 ± 0.29; P = 0.014). Survival was significantly (P = 0.013) higher in animals receiving intratracheal dopamine and ventilated with HVT, especially at 15 minutes after extubation, when

  12. Acute pulmonary edema in patients with reduced left ventricular ejection fraction is associated with concentric left ventricular geometry.

    PubMed

    Imanishi, Junichi; Kaihotsu, Kenji; Yoshikawa, Sachiko; Nishimori, Makoto; Sone, Naohiko; Honjo, Tomoyuki; Iwahashi, Masanori

    2017-08-02

    Although acute pulmonary edema (APE) is common in patients with heart failure (HF) with preserved ejection fraction (EF), its pathogenesis in patients with HF with reduced EF (HFrEF) is not completely understood. The purpose of our study was to explore the contributions of left ventricular (LV) geometry to understand the difference between HFrEF patients with or without APE. We studied 122 consecutive acute decompensated HF patients with HFrEF (≤40%). APE was defined as acute-onset dyspnea and radiographic alveolar edema requiring immediate airway intervention. LV geometry was determined from a combination of the LV mass index and relative wall thickness (RWT). Long-term unfavorable outcome events were tracked during a follow-up of a median of 21 months (interquartile range, 10-28 months), during which APE was observed in 29 patients (24%). Compared to those without APE, hospitalized patients with APE had a higher systolic blood pressure, RWT, and LVEF and lower end-diastolic dimension. Among echocardiographic variables, a multivariate logistic regression analysis identified RWT as the only independent determinant of APE (hazard ratio: 2.46, p < 0.001). Those with concentric geometry (n = 25; RWT > 0.42) had a higher incidence of APE relative to those with non-concentric geometry. Furthermore, among patients with APE, mortality was significantly higher among those with concentric geometry (log-rank, p = 0.008). Compared with non-concentric geometry, concentric geometry (increased RWT, not LV mass) was strongly associated with APE onset and a poorer outcome among APE patients. An easily obtained echocardiographic RWT index may facilitate the risk stratification of patients.

  13. Intravenous administration of hyperoxygenated solution attenuates pulmonary edema formation in phosgene-induced acute lung injury in rabbits.

    PubMed

    Wang, Ling; Liu, Chunran; Zhang, Hui; Gao, Changjun; Chai, Wei; Xu, Ruifen; Wang, Hui-xia; Xu, Lixian

    2010-11-01

    The aim of this study was to investigate the post-treatment effect of intravenous hyperoxygenated solution (HOS) on pulmonary parameters in rabbits whole-body-exposed to the toxic gas phosgene. Twenty-four New Zealand rabbits were divided into four groups randomly: rabbits were exposed whole-body to either filtered room air or 539 ppm phosgene for 5 minutes followed by room air washout for 5 minutes. Phosgene-exposed group (exposed to phosgene without treatment, PH group); Control group (exposed to air, Control group); Lactate Ringer's solution (LRS)-treated group (intravenous infusion of LRS by 30 ml·kg-1 after phosgene exposure, LRS group); Hyperoxygenated solution (HOS)-treated group (intravenous infusion of HOS after phosgene exposure by 30 mL·kg-1, HOS group). Arterial blood was collected for blood gas analysis at 1, 3, 8, and 12 hours after phosgene or air exposure. Rabbits were put to death 12 hours after exposure. Lung edema was assessed gravimetrically by measuring tissue wet/dry weight ratio (W/D) and lung coefficient (LC). Bronchoalveolar lavage (BAL) was performed and fluid was analyzed for total maloaldehyde (MDA), glutathione peroxidase (GSH-Px), and protein concentration. Lungs were perfused with saline to remove blood, snap-frozen in liquid nitrogen (N2), analyzed for tissue reduced glutathione (GSH) and oxidized glutathione (GSSG). Parts of lung tissues were reserved for histopathology examination. In the PH, LRS, and HOS groups, phosgene inhalation caused serious lung edema, W/D and LC, lung tissue GSSG, BALF MDA, and protein content increased significantly. Meanwhile, PaO2, lung tissue GSH, and BALF GSH-Px decreased markedly. However, after HOS treatment in the HOS group, PaO2 was clearly higher than that in the PH group and LRS group at 3, 8, 12 hours (P < 0.01). W/D and LC, lung tissue GSSG, BALF MDA, and protein content in the HOS group were apparently lower than that in the PH group and LRS group (P < 0.01). In the HOS group, lung tissue

  14. Effects of hyperoxia on ventilation and pulmonary hemodynamics during immersed prone exercise at 4.7 ATA: possible implications for immersion pulmonary edema

    PubMed Central

    Peacher, Dionne F.; Pecorella, Shelly R. H.; Freiberger, John J.; Natoli, Michael J.; Schinazi, Eric A.; Doar, P. Owen; Boso, Albert E.; Walker, Aaron J.; Gill, Matthew; Kernagis, Dawn; Uguccioni, Donna

    2010-01-01

    Immersion pulmonary edema (IPE) can occur in otherwise healthy swimmers and divers, likely because of stress failure of pulmonary capillaries secondary to increased pulmonary vascular pressures. Prior studies have revealed progressive increase in ventilation [minute ventilation (V̇e)] during prolonged immersed exercise. We hypothesized that this increase occurs because of development of metabolic acidosis with concomitant rise in mean pulmonary artery pressure (MPAP) and that hyperoxia attenuates this increase. Ten subjects were studied at rest and during 16 min of exercise submersed at 1 atm absolute (ATA) breathing air and at 4.7 ATA in normoxia and hyperoxia [inspired PO2 (PiO2) 1.75 ATA]. V̇e increased from early (E, 6th minute) to late (L, 16th minute) exercise at 1 ATA (64.1 ± 8.6 to 71.7 ± 10.9 l/min BTPS; P < 0.001), with no change in arterial pH or Pco2. MPAP decreased from E to L at 1 ATA (26.7 ± 5.8 to 22.7 ± 5.2 mmHg; P = 0.003). V̇e and MPAP did not change from E to L at 4.7 ATA. Hyperoxia reduced V̇e (62.6 ± 10.5 to 53.1 ± 6.1 l/min BTPS; P < 0.0001) and MPAP (29.7 ± 7.4 to 25.1 ± 5.7 mmHg, P = 0.002). Variability in MPAP among subjects was wide (range 14.1–42.1 mmHg during surface and depth exercise). Alveolar-arterial Po2 difference increased from E to L in normoxia, consistent with increased lung water. We conclude that increased V̇e at 1 ATA is not due to acidosis and is more consistent with respiratory muscle fatigue and that progressive pulmonary vascular hypertension does not occur during prolonged immersed exercise. Wide variation in MPAP among healthy subjects is consistent with variable individual susceptibility to IPE. PMID:20431020

  15. Ruptured Mycotic Common Femoral Artery Pseudoaneurysm: Fatal Pulmonary Embolism after Emergency Stent-Grafting in a Drug Abuser

    PubMed Central

    Kalogirou, Thomas E.; Giagtzidis, Ioakeim T.; Papazoglou, Konstantinos O.

    2014-01-01

    The rupture of a mycotic femoral artery pseudoaneurysm in an intravenous drug abuser is a limb- and life-threatening condition that necessitates emergency intervention. Emergency stent-grafting appears to be a viable, minimally invasive alternative, or a bridge, to subsequent open surgery. Caution is required in cases of suspected concomitant deep vein thrombosis in order to minimize the possibility of massive pulmonary embolism during stent-grafting, perhaps by omitting stent-graft postdilation or by inserting an inferior vena cava filter first. We describe the emergency endovascular management, in a 60-year-old male intravenous drug abuser, of a ruptured mycotic femoral artery pseudoaneurysm, which was complicated by a fatal pulmonary embolism. PMID:25593530

  16. Genetic differences and aberrant methylation in the apelin system predict the risk of high-altitude pulmonary edema

    PubMed Central

    Mishra, Aastha; Kohli, Samantha; Dua, Sanchi; Thinlas, Tashi; Mohammad, Ghulam; Pasha, M. A. Qadar

    2015-01-01

    Hypoxia-inducible factor stimulates the expression of apelin, a potent vasodilator, in response to reduced blood arterial oxygen saturation. However, aberrations in the apelin system impair pulmonary vascular function, potentially resulting in the development of high-altitude (HA)-related disorders. This study aimed to elucidate the genetic and epigenetic regulation of apelin, apelin receptor (APLNR), and endothelial nitric oxide synthase (NOS3) in HA adaptation and HA pulmonary edema (HAPE). A genome-wide association study and sequencing identified variants of apelin, APLNR, and NOS3 that were validated in a larger sample size of HAPE-patients (HAPE-p), HAPE-free controls (HAPE-f), and healthy highland natives (HLs). Apelin-13 and nitrite levels and apelin and NOS3 expression were down-regulated in HAPE-p (P < 0.001). Among the several studied polymorphisms, apelin rs3761581, rs2235312, and rs3115757; APLNR rs11544374 and rs2282623; and NOS3 4b/4a, rs1799983, and rs7830 were associated with HAPE (P < 0.03). The risk allele rs3761581G was associated with a 58.6% reduction in gene expression (P = 0.017), and the risk alleles rs3761581G and rs2235312T were associated with low levels of apelin-13 and nitrite (P < 0.05). The latter two levels decreased further when both of these risk alleles were present in the patients (P < 0.05). Methylation of the apelin CpG island was significantly higher in HAPE-p at 11.92% than in HAPE-f and HLs at ≤7.1% (P < 0.05). Moreover, the methylation effect was 9% stronger in the 5′ UTR and was associated with decreased apelin expression and apelin-13 levels. The rs3761581 and rs2235312 polymorphisms and methylation of the CpG island influence the expression of apelin in HAPE. PMID:25918383

  17. Genetic differences and aberrant methylation in the apelin system predict the risk of high-altitude pulmonary edema.

    PubMed

    Mishra, Aastha; Kohli, Samantha; Dua, Sanchi; Thinlas, Tashi; Mohammad, Ghulam; Pasha, M A Qadar

    2015-05-12

    Hypoxia-inducible factor stimulates the expression of apelin, a potent vasodilator, in response to reduced blood arterial oxygen saturation. However, aberrations in the apelin system impair pulmonary vascular function, potentially resulting in the development of high-altitude (HA)-related disorders. This study aimed to elucidate the genetic and epigenetic regulation of apelin, apelin receptor (APLNR), and endothelial nitric oxide synthase (NOS3) in HA adaptation and HA pulmonary edema (HAPE). A genome-wide association study and sequencing identified variants of apelin, APLNR, and NOS3 that were validated in a larger sample size of HAPE-patients (HAPE-p), HAPE-free controls (HAPE-f), and healthy highland natives (HLs). Apelin-13 and nitrite levels and apelin and NOS3 expression were down-regulated in HAPE-p (P < 0.001). Among the several studied polymorphisms, apelin rs3761581, rs2235312, and rs3115757; APLNR rs11544374 and rs2282623; and NOS3 4b/4a, rs1799983, and rs7830 were associated with HAPE (P < 0.03). The risk allele rs3761581G was associated with a 58.6% reduction in gene expression (P = 0.017), and the risk alleles rs3761581G and rs2235312T were associated with low levels of apelin-13 and nitrite (P < 0.05). The latter two levels decreased further when both of these risk alleles were present in the patients (P < 0.05). Methylation of the apelin CpG island was significantly higher in HAPE-p at 11.92% than in HAPE-f and HLs at ≤ 7.1% (P < 0.05). Moreover, the methylation effect was 9% stronger in the 5' UTR and was associated with decreased apelin expression and apelin-13 levels. The rs3761581 and rs2235312 polymorphisms and methylation of the CpG island influence the expression of apelin in HAPE.

  18. Incidence of high altitude pulmonary edema in low-landers during re-exposure to high altitude after a sojourn in the plains.

    PubMed

    Apte, C V; Tomar, R K S; Sharma, D

    2015-07-01

    There is uncertainty whether acclimatized low-landers who return to high altitude after a sojourn at low altitude have a higher incidence of pulmonary edema than during the first exposure to high altitude. This was a prospective cohort study consisting of men ascending to 3400 m by road (N = 1003) or by air (N = 4178). The study compared the incidence of high altitude pulmonary edema during first exposure vs the incidence during re-exposure in each of these cohorts. Pulmonary edema occurred in 13 of the 4178 entries by air (Incidence: 0.31%, 95% CI: 0.18%-0.53%). The incidence during first exposure was 0.18% (0.05%-0.66%) and 0.36% (0.2%-0.64%) during re-exposure (Fisher Exact Test for differences in the incidence (two-tailed) p = 0.534). The relative risk for the re-exposure cohort was 1.95 (95% CI, 0.43%-8.80%). Pulmonary edema occurred in 3 of the 1003 road entrants (Incidence: 0.30%, 95% CI: 0.08%-0.95%). All three cases occurred in the re-exposure cohort. The large overlap of confidence intervals between incidence during first exposure and re-exposure; the nature of the confidence interval of the relative risk; and the result of the Fisher exact test, all suggest that this difference in incidence could have occurred purely by chance. We did not find evidence for a significantly higher incidence of HAPE during re-entry to HA after a sojourn in the plains.

  19. Incidence of high altitude pulmonary edema in low-landers during re-exposure to high altitude after a sojourn in the plains

    PubMed Central

    Apte, C.V.; Tomar, R.K.S.; Sharma, D.

    2015-01-01

    Background There is uncertainty whether acclimatized low-landers who return to high altitude after a sojourn at low altitude have a higher incidence of pulmonary edema than during the first exposure to high altitude. Methods This was a prospective cohort study consisting of men ascending to 3400 m by road (N = 1003) or by air (N = 4178). The study compared the incidence of high altitude pulmonary edema during first exposure vs the incidence during re-exposure in each of these cohorts. Results Pulmonary edema occurred in 13 of the 4178 entries by air (Incidence: 0.31%, 95% CI: 0.18%–0.53%). The incidence during first exposure was 0.18% (0.05%–0.66%) and 0.36% (0.2%–0.64%) during re-exposure (Fisher Exact Test for differences in the incidence (two-tailed) p = 0.534). The relative risk for the re-exposure cohort was 1.95 (95% CI, 0.43%–8.80%). Pulmonary edema occurred in 3 of the 1003 road entrants (Incidence: 0.30%, 95% CI: 0.08%–0.95%). All three cases occurred in the re-exposure cohort. Conclusion The large overlap of confidence intervals between incidence during first exposure and re-exposure; the nature of the confidence interval of the relative risk; and the result of the Fisher exact test, all suggest that this difference in incidence could have occurred purely by chance. We did not find evidence for a significantly higher incidence of HAPE during re-entry to HA after a sojourn in the plains. PMID:26288488

  20. High-Flow Nasal Cannula Versus Conventional Oxygen Therapy in Emergency Department Patients With Cardiogenic Pulmonary Edema: A Randomized Controlled Trial.

    PubMed

    Makdee, Onlak; Monsomboon, Apichaya; Surabenjawong, Usapan; Praphruetkit, Nattakarn; Chaisirin, Wansiri; Chakorn, Tipa; Permpikul, Chairat; Thiravit, Phakphoom; Nakornchai, Tanyaporn

    2017-10-01

    High-flow nasal cannula is a new method for delivering high-flow supplemental oxygen for victims of respiratory failure. This randomized controlled trial compares high-flow nasal cannula with conventional oxygen therapy in emergency department (ED) patients with cardiogenic pulmonary edema. We conducted an open-label randomized controlled trial in the ED of Siriraj Hospital, Bangkok, Thailand. Patients aged 18 years or older with cardiogenic pulmonary edema were randomly assigned to receive either conventional oxygen therapy or high-flow nasal cannula. The primary outcome was the respiratory rate 60 minutes postintervention. We enrolled 128 participants (65 in the conventional oxygen therapy and 63 in the high-flow nasal cannula groups). Baseline high-flow nasal cannula and conventional oxygen therapy mean respiratory rates were 28.7 breaths/min (SD 3.2) and 28.6 breaths/min (SD 3.5). Mean respiratory rates at 60 minutes postintervention were lower in the high-flow nasal cannula group (21.8 versus 25.1 breaths/min; difference 3.3; 95% confidence interval 1.9 to 4.6). No significant differences were found in the admission rate, ED and hospital lengths of stay, noninvasive ventilation, intubation, or mortality. In patients with cardiogenic pulmonary edema in the ED, high-flow nasal cannula therapy may decrease the severity of dyspnea during the first hour of treatment. Copyright © 2017 American College of Emergency Physicians. Published by Elsevier Inc. All rights reserved.

  1. A fatal case of Nocardia otitidiscaviarum pulmonary infection and brain abscess: taxonomic characterization by molecular techniques

    PubMed Central

    Pelaez, Ana Isabel; del Mar Garcia-Suarez, Maria; Manteca, Angel; Melon, Ovidio; Aranaz, Carlos; Cimadevilla, Rafael; Mendez, Francisco Javier; Vazquez, Fernando

    2009-01-01

    We report on a rare case of pulmonary Nocardiosis and brain abscess caused by Nocardia otitidiscaviarum in an elderly woman with chronic obstructive pulmonary disease. Taxonomic identification involved phenotypic testing, restriction fragment length polymorphism (RFLP), and complete 16S rRNA gene sequencing. PMID:19366439

  2. [Fatal Klippel-Trénaunay syndrome in a child with pulmonary embolism].

    PubMed

    Pedersen, Rie S; Hedelund, Lene; Poulsen, Lone H; Bach, Arne; Keller, Johnny

    2013-09-16

    Klippel-Trénaunay syndrome is characterized by the venous varicosities, ipsilateral cutaneous capillary malformations, and bony/soft-tissue overgrowth. Potential complications such as hypercoagulability, thrombosis and pulmonary embolism have been casuistically reported. Here, we describe a child with Klippel-Trénaunay syndrome complicated by a pulmonary embolism leading to sudden death.

  3. A fatal case of Nocardia otitidiscaviarum pulmonary infection and brain abscess: taxonomic characterization by molecular techniques.

    PubMed

    Pelaez, Ana Isabel; Garcia-Suarez, Maria del Mar; Manteca, Angel; Melon, Ovidio; Aranaz, Carlos; Cimadevilla, Rafael; Mendez, Francisco Javier; Vazquez, Fernando

    2009-04-14

    We report on a rare case of pulmonary Nocardiosis and brain abscess caused by Nocardia otitidiscaviarum in an elderly woman with chronic obstructive pulmonary disease. Taxonomic identification involved phenotypic testing, restriction fragment length polymorphism (RFLP), and complete 16S rRNA gene sequencing.

  4. 2009 H1N1 fatalities: the New Mexico experience.

    PubMed

    Brooks, Erin G; Bryce, Clare H; Avery, Catherine; Smelser, Chad; Thompson, Deborah; Nolte, Kurt B

    2012-11-01

    Histopathologic features of New Mexico 2009 H1N1 fatalities have not been representative of those reported nationwide. We retrospectively reviewed medical records of all New Mexico 2009 pandemic influenza A (pH1N1) fatalities (n = 50). In cases in which autopsy was performed (n = 12), histologic sections and culture results were examined. In contrast to previously published studies, the majority of our fatalities did not have diffuse alveolar damage (DAD) (2/12; 16.7%). Common findings included pulmonary interstitial inflammation and edema, tracheobronchitis, and pneumonia. Two cases had significant extra-pulmonary manifestations: myocarditis and cerebral edema with herniation. The majority had a rapid disease course: range from 1 to 12 days (median, 2 days), and Native Americans were disproportionately represented among fatalities. These findings suggest that New Mexico H1N1 fatalities generally did not survive long enough to develop the classic picture of DAD. Pathologists should be aware that H1N1 may cause extra-pulmonary pathology and perform postmortem cultures and histologic sampling accordingly.

  5. Enhanced expression of Fas and FasL modulates apoptosis in the lungs of severe P. falciparum malaria patients with pulmonary edema

    PubMed Central

    Punsawad, Chuchard; Viriyavejakul, Parnpen; Setthapramote, Chayanee; Palipoch, Sarawoot

    2015-01-01

    Apoptosis mediated by Fas/FasL has been implicated in pulmonary disorders. However, little is known about the relationship between Fas and FasL in the process of lung injury during malaria infection. Paraffin-embedded lung tissues from malaria patients were divided into two groups: those with pulmonary edema (PE) and those without pulmonary edema (non-PE). Normal lung tissues were used as the control group. Cellular expression of Fas, FasL, and the markers of apoptotic caspases, including cleaved caspase-3 and cleaved caspase-8 in the lung tissues were investigated by the immunohistochemistry (IHC) method. Semi-quantitative analysis of IHC staining revealed that cellular expression of Fas, FasL, cleaved caspase-8, and cleaved caspase-3 were significantly increased in the lungs of patients with PE compared with the lungs of patients with non-PE and control groups (all P < 0.05). In addition, significant positive correlations were obtained between Fas and apoptosis (rs = 0.937, P < 0.001) and FasL and apoptosis (rs = 0.808, P < 0.001). Significant positive correlations were found between Fas and FasL expression (rs = 0.827, P < 0.001) and between cleaved caspase-8 and cleaved caspase-3 expression (rs = 0.823, P < 0.001), which suggests that Fas-dependent initiator and effector caspases, including cleaved caspase-8 and caspase-3, are necessary for inducing apoptosis in the lungs of patients with severe P. falciparum malaria. The Fas/FasL system and downstream activation of caspases are important mediators of apoptosis and may be involved in the pathogenesis of pulmonary edema in severe P. falciparum malaria patients. The proper regulation of the Fas/FasL pathway can be a potential treatment for pulmonary complications in falciparum malaria patients. PMID:26617708

  6. [Alveolar capillary dysplasia with misalignment of pulmonary veins: a fatal cause of refractory neonatal cyanosis].

    PubMed

    Savey, B; Jeanne-Pasquier, C; Dupont-Chauvet, P; Maragnes, P; Bellot, A; Guillois, B

    2015-02-01

    Alveolar capillary dysplasia with misalignment of pulmonary veins (ACD/MPV) is a rare neonatal pathology that combines refractory hypoxemia with severe pulmonary arterial hypertension, and leads to death every time. Histologic examination of lung tissue confirms the diagnosis and is characterized by a decreased number of pulmonary capillaries, immature lobular development, and abnormal proximity between pulmonary arteries and veins. This abnormal proximity is responsible for an arteriovenous shunt. We report five cases confirmed by postmortem histology, which occurred over 14 years in Lower Normandy (France). The cumulative incidence is therefore of 1.8 for 100,000 births. In these five cases, the first symptoms appeared during the first hour of life and death occurred before 24h in four of five cases. The patient with the longest survival had mild histological lesions and delayed emergence of the first symptoms. Genitourinary and gastrointestinal anomalies were associated with ACD/MPV in two cases, and bilateral pulmonary hypoplasia in three cases. Optimized invasive ventilation, pulmonary vasodilators, vasoactive drugs, and pulmonary surfactant did not improve survival. Extracorporeal membrane oxygenation (ECMO) was not used. We present a review of the literature on ACD/MPV, a clinical and histological entity little known to both clinicians and pathologists, whereas a premortem diagnosis is possible and genetic counseling in affected families can be suggested.

  7. Fatal water intoxication of an Army trainee during urine drug testing.

    PubMed

    Gutmann, Frank D; Gardner, John W

    2002-05-01

    An Army trainee developed acute water intoxication, hyponatremia, pulmonary edema, and fatal cerebral edema. This is the first report of a fatality related to urine drug testing. This resulted from supervised excessive water ingestion in an attempt to induce a sufficient urine specimen for substance abuse testing. To avoid a similar preventable death in the future, we make several recommendations. These include limiting the volume of ingested fluid to eight ounces every 30 to 45 minutes, not to exceed 40 ounces, and providing a relaxed, reassuring environment when obtaining urine specimens for substance abuse detection.

  8. Fatal pulmonary hemorrhage associated with RTX toxin producing Actinobacillus equuli subspecies haemolyticus infection in an adult horse.

    PubMed

    Pusterla, Nicola; Jones, Megan E B; Mohr, F Charles; Higgins, Jamie K; Mapes, Samantha; Jang, Spencer S; Samitz, Eileen M; Byrne, Barbara A

    2008-01-01

    A case of fatal pulmonary hemorrhage in a 6-year-old American Paint mare with a 2-week history of intermittent coughing, fever, and epistaxis is described. Significant macroscopic abnormalities at postmortem examination were restricted to the respiratory system, and microscopically, severe pulmonary hemorrhage with suppurative bronchopneumonia was found. Actinobacillus equuli subsp. haemolyticus was cultured from a transtracheal wash performed antemortem as well as from the lungs at necropsy. The presence of airway-associated hemorrhage in conjunction with bacterial bronchopneumonia suggested endothelial damage caused by a locally elaborated bacterial toxin, possibly produced by the A. equuli strain isolated from the lungs. The objective of this report was to indirectly document the presence of hemolysin repeat in structural toxin (RTX) in the lungs of the reported mare. A real-time polymerase chain reaction (PCR) assay targeting the recently described aqx gene of A. equuli subsp. haemolyticus was established and validated. Transcriptional activity of the aqx gene was used as a surrogate method to document toxin production. Real-time PCR analysis of the transtracheal fluid and lung tissue of the affected mare confirmed the presence and the transcriptional activity of the aqx gene at the genomic (gDNA) and complementary DNA (cDNA) levels, respectively. The presence of pneumonia associated with hemorrhagic pulmonary fluid and the culture of large numbers of hemolytic A. equuli should prompt the clinician to consider endothelial damage caused by bacterial toxins.

  9. Surfactant protein A (SP-A) and angiotensin converting enzyme (ACE) as early biomarkers for pulmonary edema formation in ventilated human lung lobes.

    PubMed

    Gnadt, Mirjam; Kardziev, Boris; Schmidt, Michael; Högger, Petra

    2012-08-01

    Ex vivo perfused and ventilated lung lobes frequently develop pulmonary edema. We were looking for a suitable and early detectable biomarker in the perfusion fluid indicating lung cell damage and loss of tissue integrity in ventilated human lung lobes. Therefore, we elucidated whether surfactant protein A (SP-A) and angiotensin-converting enzyme (ACE) were measurable in the perfusion fluid and whether they were suitable indicators for edema formation occurring within the experimental time frame of 1-2 h. Patients (n = 39) undergoing a lobectomy, bilobectomy or pneumonectomy due to primary bronchial cell carcinoma were included in the studies. Lung lobes were extracorporally ventilated and perfused for up to 2 h. Two different perfusion fluids were used, plain perfusion buffer and perfusion buffer containing packed erythrocytes or buffy coats. Perfusion fluid samples were analyzed for SP-A and ACE using immunoassays served as perfusion fluids. SP-A and ACE concentrations were analyzed in fluid sample sets of 39 and 33 perfusion experiments, respectively. Degrees of edema formation were arbitrarily classified into three groups (≤ 29, 30-59, ≥ 60 % weight gain). The maximum increase of SP-A and ACE concentrations in the perfusate was significantly higher for more pronounced edemas in case of perfusions using a mixture of blood components and buffer. Interestingly, the time courses of ACE and SP-A were highly similar. We suggest that SP-A and ACE are promising early biochemical markers for the development for pulmonary edema formation in the ex vivo lung lobe perfusion.

  10. Management of high altitude pulmonary edema in the Himalaya: a review of 56 cases presenting at Pheriche medical aid post (4240 m).

    PubMed

    Jones, Barbara E; Stokes, Suzy; McKenzie, Suzi; Nilles, Eric; Stoddard, Gregory J

    2013-03-01

    The purpose of this study was to review the patient characteristics and management of 56 cases of high altitude pulmonary edema at the Pheriche Himalayan Rescue Association Medical Aid Post, and to measure the use of medications in addition to descent and oxygen. In a retrospective case series, we reviewed all patients diagnosed clinically with high altitude pulmonary edema during the 2010 Spring and Fall seasons. Nationality, altitude at onset of symptoms, physical examination findings, therapies administered, and evacuation methods were evaluated. Of all patients, 23% were Nepalese, with no difference in clinical features compared with non-Nepalese patients; 28% of all patients were also suspected of having high altitude cerebral edema. Symptoms developed in 91% of all patients at an altitude higher than the aid post (median altitude of onset of 4834 m); 83% received oxygen therapy, and 87% received nifedipine, 44% sildenafil, 32% dexamethasone, and 39% acetazolamide. Patients who were administered sildenafil, dexamethasone, or acetazolamide had presented with significantly lower initial oxygen saturations (P ≤ .05). After treatment, 93% of all patients descended; 38% descended on foot without a supply of oxygen. A significant number of patients presenting to the Pheriche medical aid post with high altitude pulmonary edema were given dexamethasone, sildenafil, or acetazolamide in addition to oxygen, nifedipine, and descent. This finding may be related to perceived severity of illness and evacuation limitations. Although no adverse effects were observed, the use of multiple medications is not supported by current evidence and should not be widely adopted without further study. Copyright © 2013 Wilderness Medical Society. Published by Elsevier Inc. All rights reserved.

  11. Using a Caesalpinia echinata Lam. protease inhibitor as a tool for studying the roles of neutrophil elastase, cathepsin G and proteinase 3 in pulmonary edema.

    PubMed

    Cruz-Silva, Ilana; Neuhof, Christiane; Gozzo, Andrezza Justino; Nunes, Viviane Abreu; Hirata, Izaura Yoshico; Sampaio, Misako Uemura; Figueiredo-Ribeiro, Rita de Cássia; Neuhof, Heinz; Araújo, Mariana da Silva

    2013-12-01

    Acute lung injury (ALI) is characterized by neutrophil infiltration and the release of proteases, mainly elastase (NE), cathepsin G (Cat G) and proteinase 3 (PR3), which can be controlled by specific endogenous inhibitors. However, inhibitors of these proteases have been isolated from different sources, including plants. For this study, CeEI, or Caesalpinia echinata elastase inhibitor, was purified from C. echinata (Brazil-wood) seeds after acetone fractionation, followed by ion exchange and reversed phase chromatographic steps. Characterization with SDS-PAGE, stability assays, amino acid sequencing and alignment with other protein sequences confirmed that CeEI is a member of the soybean Kunitz trypsin inhibitor family. Like other members of this family, CeEI is a 20 kDa monomeric protein; it is stable within a large pH and temperature range, with four cysteine residues forming two disulfide bridges, conserved amino acid residues and leucine-isoleucine residues in the reactive site. CeEI was able to inhibit NE and Cat G at a nanomolar range (with K(i)s of 1.9 and 3.6 nM, respectively) and inhibited PR3 within a micromolar range (K(i) 3.7 μM), leading to hydrolysis of specific synthetic substrates. In a lung edema model, CeEI reduced the lung weight and pulmonary artery pressure until 180 min after the injection of zymosan-activated polymorphonuclear neutrophils. In experiments performed in the presence of a Cat G and PR3, but not an NE inhibitor, lung edema was reduced only until 150 min and pulmonary artery pressure was similar to that of the control. These results confirm that NE action is crucial to edema establishment and progression. Additionally, CeEI appears to be a useful tool for studying the physiology of pulmonary edema and provides a template for molecular engineering and drug design for ALI therapy.

  12. Acidemia in severe acute cardiogenic pulmonary edema treated with noninvasive pressure support ventilation: a single-center experience.

    PubMed

    Lazzeri, Chiara; Gensini, Gian F; Picariello, Claudio; Attanà, Paola; Mattesini, Alessio; Chiostri, Marco; Valente, Serafina

    2015-09-01

    In clinical practice, acidotic patients with acute cardiogenic pulmonary edema (ACPE) are commonly considered more severe in comparison with nonacidotic patients, and data on the outcome of these patients treated with noninvasive pressure support ventilation (NIV) are lacking.The present investigation was aimed at assessing whether acidosis on admission (pH < 7.35) was associated with adverse outcome in 65 consecutive patients with ACPE treated with NIV and admitted to our Intensive Cardiac Care Unit (ICCU).In our population, 28 patients were acidotic (28 of 65, 43.1%), whereas 41 patients were not (37 of 65, 56.9%). According to the Repeated Measures General Linear Model, pCO2 values significantly changed throughout the 2-h NIV treatment (P = 0.019) in both groups (P = 0001). In acidotic patients, pCO2 significantly decreased (51.9 ± 15.3 → 47.0 ± 12.8 → 44.8 ± 12.7), whereas they increased in the nonacidotic subgroup (36.8 ± 6.5 → 36.9 ± 7.2 → 37.6 ± 6.4). No difference was observed in intubation rate between acidotic (eight patients, 28.6%) and nonacidotic patients (12 patients, 32.4%) (P = 0.738). In-ICCU mortality rate did not differ between (13 patients, 35.1%) and nonacidotic patients (nine patients, 32.1%) (P = 0.801).Our data strongly suggest that in patients with severe ACPE treated with NIV, the presence of acidosis is not associated with adverse outcomes (early mortality and intubation rates) in these patients.

  13. Non-Invasive Mechanical Ventilation Versus Continuous Positive Airway Pressure Relating to Cardiogenic Pulmonary Edema in an Intensive Care Unit.

    PubMed

    Belenguer-Muncharaz, Alberto; Mateu-Campos, Lidón; González-Luís, Rubén; Vidal-Tegedor, Bárbara; Ferrándiz-Sellés, Amparo; Árguedas-Cervera, Joaquín; Altaba-Tena, Susana; Casero-Roig, Patricia; Moreno-Clarí, Ester

    2017-10-01

    To compare the application of non-invasive ventilation (NIV) versus continuous positive airway pressure (CPAP) in the treatment of patients with cardiogenic pulmonary edema (CPE) admitted to an intensive care unit (ICU). In a prospective, randomized, controlled study performed in an ICU, patients with CPE were assigned to NIV (n=56) or CPAP (n=54). Primary outcome was intubation rate. Secondary outcomes included duration of ventilation, length of ICU and hospital stay, improvement of gas exchange, complications, ICU and hospital mortality, and 28-day mortality. The outcomes were analyzed in hypercapnic patients (PaCO2>45mmHg) with no underlying chronic lung disease. Both devices led to similar clinical and gas exchange improvement; however, in the first 60min of treatment a higher PaO2/FiO2 ratio was observed in the NIV group (205±112 in NIV vs. 150±84 in CPAP, P=.02). The rate of intubation was similar in both groups (9% in NIV vs. 9% in CPAP, P=1.0). There were no differences in duration of ventilation, ICU and length of hospital stay. There were no significant differences in ICU, hospital and 28-d mortality between groups. In the hypercapnic group, there were no differences between NIV and CPAP. Either NIV or CPAP are recommended in patients with CPE in the ICU. Outcomes in the hypercapnic group with no chronic lung disease were similar using NIV or CPAP. Copyright © 2017 SEPAR. Publicado por Elsevier España, S.L.U. All rights reserved.

  14. Brain Natriuretic Peptide Levels and the Occurrence of Subclinical Pulmonary Edema in Healthy Lowlanders at High Altitude.

    PubMed

    Pagé, Maude; Henri, Christine; Pagé, Pierre; Sauvé, Claude; Schampaert, Erick

    2015-08-01

    High altitude (HA) pulmonary edema (PE) results from complex and misunderstood interactions between adaptation mechanisms. We assessed the occurrence of subclinical PE and brain natriuretic peptide (BNP) levels among nonacclimatized individuals during an expedition on Mount Elbrus (5642 m). Seven subjects underwent assessment of vital signs, Lake Louise Score, ultrasound lung comets using handheld echography and circulating BNP using capillary testing at different stages of ascension, in addition to baseline echocardiography. Friedman tests were used to compare serial measurements. Heart rate, Lake Louise Score (P < 0.0001) and blood pressure (P = 0.037) increased during ascension; oxygen saturation decreased (P < 0.0001). BNP increased (40.7 ± 16.8 vs 19.7 ± 3.04 pg/mL; P < 0.01) after the summit, as did ultrasound lung comet count throughout ascension (P < 0.0001), but both parameters were not correlated (r = 0.36; P = 0.42). Post-summit peak BNP correlated with baseline left ventricular mass index (r = -0.79; P = 0.033). This study confirms the high incidence of subclinical PE during subacute exposure to hypobaric hypoxia and enhancement of this phenomenon after exertion. Although not correlated with the degree of PE, BNP levels increased after sustained effort at HA, but not at rest. Further investigation is needed to determine the mechanisms underlying the BNP response at HA and its usefulness as a monitoring tool during expeditions. Copyright © 2015 Canadian Cardiovascular Society. Published by Elsevier Inc. All rights reserved.

  15. The Frequency of Reexpansion Pulmonary Edema after Trocar and Hemostat Assisted Thoracostomy in Patients with Spontaneous Pneumothorax

    PubMed Central

    Cha, Kyoung Chul; Ji, Ho Jin; Kwon, Woo Cheol; Shin, Hyung Jin; Cha, Yong Sung; Lee, Kang Hyun; Hwang, Sung Oh; Lee, Christopher C.; Singer, Adam J.

    2013-01-01

    Purpose Several risk factors for development of reexpansion pulmonary edema (REPE) after drainage of pneumothoraces have been reported, but the association between the method of thoracostomy and the development of REPE is unknown. The aim of this study was to compare the frequency of REPE after treatment of spontaneous pneumothorax with trocar or hemostat assisted closed thoracostomy. Materials and Methods We performed a prospective, observational study including 173 patients with spontaneous pneumothorax who visited the emergency department from January 2007 to December 2008. In 2007, patients were treated with hemostat-assisted drainage, whereas patients in 2008 were treated with trocar-assisted drainage. The main outcome was the development of REPE, determined by computed tomography of the chest 8 hours after closed thoracostomy. Outcomes in both groups were compared using univariate and multivariate analyses. Results Ninety-two patients were included, 48 (42 males) of which underwent hemostat-assisted drainage and 44 (41 males) underwent trocar-assisted drainage. The groups were similar in mean age (24±10 vs. 26±14 respectively). The frequencies of REPE after hemostat- and trocar-assisted drainage were 63% (30 patients) and 86% (38 patients) respectively (p=0.009). In multivariate analysis, trocar-assisted drainage was the major contributing factor for developing REPE (odds ratio=5.7, 95% confidence interval, 1.5-21). Age, gender, size of pneumothorax, symptom duration and laboratory results were similar between the groups. Conclusion Closed thoracostomy using a trocar is associated with an increased risk of REPE compared with hemostat-assisted drainage in patients with spontaneous pneumothorax. PMID:23225814

  16. The frequency of reexpansion pulmonary edema after trocar and hemostat assisted thoracostomy in patients with spontaneous pneumothorax.

    PubMed

    Cha, Kyoung Chul; Kim, Hyun; Ji, Ho Jin; Kwon, Woo Cheol; Shin, Hyung Jin; Cha, Yong Sung; Lee, Kang Hyun; Hwang, Sung Oh; Lee, Christopher C; Singer, Adam J

    2013-01-01

    Several risk factors for development of reexpansion pulmonary edema (REPE) after drainage of pneumothoraces have been reported, but the association between the method of thoracostomy and the development of REPE is unknown. The aim of this study was to compare the frequency of REPE after treatment of spontaneous pneumothorax with trocar or hemostat assisted closed thoracostomy. We performed a prospective, observational study including 173 patients with spontaneous pneumothorax who visited the emergency department from January 2007 to December 2008. In 2007, patients were treated with hemostat-assisted drainage, whereas patients in 2008 were treated with trocar-assisted drainage. The main outcome was the development of REPE, determined by computed tomography of the chest 8 hours after closed thoracostomy. Outcomes in both groups were compared using univariate and multivariate analyses. Ninety-two patients were included, 48 (42 males) of which underwent hemostat-assisted drainage and 44 (41 males) underwent trocar-assisted drainage. The groups were similar in mean age (24 ± 10 vs. 26 ± 14 respectively). The frequencies of REPE after hemostat- and trocar-assisted drainage were 63% (30 patients) and 86% (38 patients) respectively (p=0.009). In multivariate analysis, trocar-assisted drainage was the major contributing factor for developing REPE (odds ratio=5.7, 95% confidence interval, 1.5-21). Age, gender, size of pneumothorax, symptom duration and laboratory results were similar between the groups. Closed thoracostomy using a trocar is associated with an increased risk of REPE compared with hemostat- assisted drainage in patients with spontaneous pneumothorax.

  17. The susceptibility gene screening in a Chinese high-altitude pulmonary edema family by whole-exome sequencing.

    PubMed

    Yingzhong, Yang; Yaping, Wang; Jin, Xu; Rili, Ge

    2017-02-20

    High-altitude pulmonary edema (HAPE) is one of idiopathic mountain sicknesses that occur in healthy lowlanders when they quickly ascend to altitudes exceeding 2500 m above sea levels within 1-7 days. Growing evidence suggests that genetics plays an important role in the risk of HAPE. In this study, we recruited a Chinese HAPE family and screened genetic variations in the 7 family members (including 6 family members with a medical history of HAPE and the propositus's mother) by whole-exome sequencing. The results showed 18 genetic variations (9 SNVs and 9 Indels) were related to HAPE. Two SNV sites (CFHR4 (p.L85F) and OXER1 (p.R176C)) were predicted to be damaging and alter protein functions by SIFT, PolyPhen-2 and PROVEAN software. The biological function of OXER1 was highly related to the hypoxia-inducible factor pathway. Therefore, those two sites were identified as candidate pathological variations. Moreover, other SNVs (NMB p.S150P, APOB p.I4194T, EIF4ENIF1 p.Q763P) and Indels (KCNJ12 p.EE333-334E, ANKRD31 p.LMN251-253LN, OR2A14 p.HFFC175-178HFC) were also predicted to be damaging as well, which also might be considered as potential candidate pathological variations related to HAPE. Collectively we firstly screened the susceptibility genes in a Chinese HAPE family by whole-exome sequencing, which will provide new clues for further mechanistic studies of HAPE.

  18. Hospital and 4-Year Mortality Predictors in Patients With Acute Pulmonary Edema With and Without Coronary Artery Disease.

    PubMed

    Figueras, Jaume; Bañeras, Jordi; Peña-Gil, Carlos; Barrabés, José A; Rodriguez Palomares, Jose; Garcia Dorado, David

    2016-02-16

    Long-term prognosis of acute pulmonary edema (APE) remains ill defined. We evaluated demographic, echocardiographic, and angiographic data of 806 consecutive patients with APE with (CAD) and without coronary artery disease (non-CAD) admitted from 2000 to 2010. Differences between hospital and long-term mortality and its predictors were also assessed. CAD patients (n=638) were older and had higher incidence of diabetes and peripheral vascular disease than non-CAD (n=168), and lower ejection fraction. Hospital mortality was similar in both groups (26.5% vs 31.5%; P=0.169) but APE recurrence was higher in CAD patients (17.3% vs 6.5%; P<0.001). Age, admission systolic blood pressure, recurrence of APE, and need for inotropics or endotracheal intubation were the main independent predictors of hospital mortality. In contrast, overall mortality (70.0% vs 57.1%; P=0.002) and readmission for nonfatal heart failure after a 45-month follow-up (10-140; 17.3% vs 7.6%; P=0.009) were higher in CAD than in non-CAD patients. Age, peripheral vascular disease, and peak creatine kinase MB during index hospitalization, but not ejection fraction, were the main independent predictors of overall mortality, whereas coronary revascularization or valvular surgery were protective. These interventions were mostly performed during hospitalization index (294 of 307; 96%) and not intervened patients showed a higher risk profile. Long-term mortality in APE is high and higher in CAD than in non-CAD patients. Considering the different in-hospital and long-term mortality predictors herein described, which do not necessarily involve systolic function, it is conceivable that a more aggressive interventional program might improve survival in high-risk patients. © 2016 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell.

  19. Clinical predictors for fatal pulmonary embolism in 15,520 patients with venous thromboembolism: findings from the Registro Informatizado de la Enfermedad TromboEmbolica venosa (RIETE) Registry.

    PubMed

    Laporte, Silvy; Mismetti, Patrick; Décousus, Hervé; Uresandi, Fernando; Otero, Remedios; Lobo, Jose Luis; Monreal, Manuel

    2008-04-01

    Clinical predictors for fatal pulmonary embolism (PE) in patients with venous thromboembolism have never been studied. Using data from the international prospective Registro Informatizado de la Enfermedad TromboEmbolica venosa (RIETE) registry about patients with objectively confirmed symptomatic acute venous thromboembolism, we determined independent predictive factors for fatal PE. Between March 2001 and July 2006, 15 520 consecutive patients (mean age+/-SD, 66.3+/-16.9 years; 49.7% men) with acute venous thromboembolism were included. Symptomatic deep-vein thrombosis without symptomatic PE was observed in 58.0% (n=9008) of patients, symptomatic nonmassive PE in 40.4% (n=6264), and symptomatic massive PE in 1.6% (n=248). At 3 months, the cumulative rates of overall mortality and fatal PE were 8.65% and 1.68%, respectively. On multivariable analysis, patients with symptomatic nonmassive PE at presentation exhibited a 5.42-fold higher risk of fatal PE compared with patients with deep-vein thrombosis without symptomatic PE (P<0.001). The risk of fatal PE was multiplied by 17.5 in patients presenting with a symptomatic massive PE. Other clinical factors independently associated with an increased risk of fatal PE were immobilization for neurological disease, age >75 years, and cancer. PE remains a potentially fatal disease. The clinical predictors identified in the present study should be included in any clinical risk stratification scheme to optimally adapt the treatment of PE to the risk of the fatal outcome.

  20. Pulmonary bullet embolism – a safe treatment strategy of a potentially fatal injury: a case report

    PubMed Central

    Hassan, Ali M; Cooley, Roger S; Papadimos, Thomas J; Fath, John J; Schwann, Thomas A; Elsamaloty, Haitham

    2009-01-01

    Background Vascular embolization of a projectile discharged from a weapon is a rare event. In this report a hunter's errant gunshot struck a farmer in the left chest. Case report The projectile was lodged between the apex of the heart and the diaphragm. The patient was treated non-operatively and was discharged home only to return to the emergency department with chest pain and subsequent identification of the projectile in the left inferior pulmonary vein. Operative management consisted of a median sternotomy, cardiopulmonary bypass, and a pulmonary venectomy. Conclusion He was subsequently discharged home and recovered uneventfully. PMID:19545380

  1. Spontaneous tension pneumothorax and CO₂ narcosis in a near fatal episode of chronic obstructive pulmonary disease exacerbation.

    PubMed

    Spindelboeck, Walter; Moser, Adrian

    2012-10-01

    Exacerbation of chronic obstructive pulmonary disease (COPD) is a disease pattern frequently seen in emergency medical services and intensive care units. Usually, exacerbations of COPD are of infectious origin, and an acute vital threat may take several days to develop. Tension pneumothorax in patients with COPD is a rare and often unexpected cause of acute vital threat. To the best of our knowledge, this is a unique case of CO2 narcosis after spontaneous tension pneumothorax in a patient with COPD. We describe the rapid development of respiratory insufficiency and near fatal pulmonary failure in a 65-year-old female patient with COPD due to spontaneous tension pneumothorax. The patient was in respiratory failure and comatose upon arrival of the emergency service. Before mechanical ventilation, coma could be confirmed to be due to CO2 narcosis caused by exorbitant arterial hypercapnia (PCO2, 193 mm Hg). Pneumothorax was diagnosed in the hospital by chest x-ray and resolved after pleural drainage. The patient could be extubated early and discharged without sequelae. In conclusion, we want to report the occurrence of a tension pneumothorax as an important and potentially overseen condition in patients with COPD with acute respiratory failure. Copyright © 2012 Elsevier Inc. All rights reserved.

  2. Extravascular lung water index measurement in critically ill children does not correlate with a chest x-ray score of pulmonary edema

    PubMed Central

    2010-01-01

    Introduction Extravascular lung water index (EVLWI) can be measured at the bedside using the transpulmonary thermodilution technique (TPTD). The goal of this study was to compare EVLWI values with a chest x-ray score of pulmonary edema and markers of oxygenation in critically ill children. Methods This was a prospective observational study in a pediatric intensive care unit of a university hospital. We included 27 critically ill children with an indication for advanced invasive hemodynamic monitoring. No specific interventions for the purpose of the study were carried out. Measurements included EVLWI and other relevant hemodynamic variables. Blood gas analysis, ventilator parameters, chest x-ray and TPTD measurements were obtained within a three-hour time frame. Two radiologists assessed the chest x-ray and determined a score for pulmonary edema. Results A total of 103 measurements from 24 patients were eligible for final analysis. Mean age was two years (range: two months to eight years). Median cardiac index was 4.00 (range: 1.65 to 10.85) l/min/m2. Median EVLWI was 16 (range: 6 to 31) ml/kg. The weighted kappa between the chest x-ray scores of the two radiologists was 0.53. There was no significant correlation between EVLWI or chest x-ray score and the number of ventilator days, severity of illness or markers of oxygenation. There was no correlation between EVLWI and the chest x-ray score. EVLWI was significantly correlated with age and length (r2 of 0.47 and 0.67 respectively). Conclusions The extravascular lung water index in critically ill children does not correlate with a chest x-ray score of pulmonary edema, nor with markers of oxygenation. PMID:20529308

  3. [Fatal pulmonary embolism after embolization of a hepatocellular carcinoma using microspheres].

    PubMed

    Noguera, J J; Martínez-Cuesta, A; Sangro, B; Bilbao, J I

    2008-01-01

    Intra-arterial treatment has become a first-line alternative in the therapeutic arsenal against primary and metastatic hepatic tumors. Despite its proven safety and efficacy, intra-arterial treatment with lipiodol, chemotherapy, and particles carries the risk of complications, some of which can be lethal. We present the case of a 32-year-old woman with multifocal hepatocellular carcinoma treated with microsphere embolization. After the second session, the patient died of a pulmonary embolism composed of particles and tumor cells.

  4. Post splenectomy fatal pulmonary embolism in a patient with moderate hemophilia a.

    PubMed

    Davoodabadi, Abdolhossein; Adib, Mohammad Mahdi; Keleidari, Behrooz

    2011-06-01

    Hemophilia A is a bleeding disorder caused by defective production of factor VIII. The main concern associated with the disease is bleeding, especially after trauma and surgeries. Factor VIII replacement therapy is associated with substantial decrease of bleeding events during surgery. However, there have been a number of reports of thromboemblic events in this situation. The present report describes a case of moderate hemophilia A in which splenectomy did lead to pulmonary embolism and subsequent death.The patient was a 25-year-old man with hemophilia A admitted after a car accident and trauma to left lower chest and abdomen. He received factor VIII concentrates for replacement therapy. He was hemodynamically stable on the first day, but on the second day his hemoglobin declined and he showed signs of abdominal tenderness. He, therefore, was subjected to laparatomy and splenectomy. After the operation, he suddenly developed dyspnea and decline in blood pressure, and death afterwards. Autopsy of the patient revealed massive pulmonary thromboembolism. The symptoms and outcome of the present case indicate that although pulmonary thromboembolism in the early postoperative period in patients with hemophilia A undergoing splenectomy and receiving factor VIII concentrate for replacement is rare, it should not be assumed a far-fetched event, and prophylactic measures to prevent thromboemboly must be considered.

  5. Hemorrhagic onset of hemangioblastoma located in the dorsal medulla oblongata presenting with tako-tsubo cardiomyopathy and neurogenic pulmonary edema: a case report.

    PubMed

    Gekka, Masayuki; Yamaguchi, Shigeru; Kazumata, Ken; Kobayashi, Hiroyuki; Motegi, Hiroaki; Terasaka, Shunsuke; Houkin, Kiyohiro

    2014-01-01

    Here, we present a case of dorsal medulla oblongata hemangioblastoma with fourth ventricular hemorrhage. A 23-year-old female developed sudden consciousness disturbance, and CT revealed hemorrhage in all cerebral ventricles and a hyperdense mass in the cisterna magna. Although the reddish tumor located in the dorsal medulla oblongata was successfully removed, she suffered from severe tako-tsubo cardiomyopathy (TTC) and neurogenic pulmonary edema (NPE) because of baroreflex failure and damage to the solitary tract nuclei. After intensive care for 12 weeks following surgery, she was discharged without any neurological or radiological deficits. Pathogenesis of TTC/NPE is discussed in this paper.

  6. The clinical usefulness of extravascular lung water and pulmonary vascular permeability index to diagnose and characterize pulmonary edema: a prospective multicenter study on the quantitative differential diagnostic definition for acute lung injury/acute respiratory distress syndrome

    PubMed Central

    2012-01-01

    Introduction Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is characterized by features other than increased pulmonary vascular permeability. Pulmonary vascular permeability combined with increased extravascular lung water content has been considered a quantitative diagnostic criterion of ALI/ARDS. This prospective, multi-institutional, observational study aimed to clarify the clinical pathophysiological features of ALI/ARDS and establish its quantitative diagnostic criteria. Methods The extravascular lung water index (EVLWI) and the pulmonary vascular permeability index (PVPI) were measured using the transpulmonary thermodilution method in 266 patients with PaO2/FiO2 ratio ≤ 300 mmHg and bilateral infiltration on chest radiography, in 23 ICUs of academic tertiary referral hospitals. Pulmonary edema was defined as EVLWI ≥ 10 ml/kg. Three experts retrospectively determined the pathophysiological features of respiratory insufficiency by considering the patients' history, clinical presentation, chest computed tomography and radiography, echocardiography, EVLWI and brain natriuretic peptide level, and the time course of all preceding findings under systemic and respiratory therapy. Results Patients were divided into the following three categories on the basis of the pathophysiological diagnostic differentiation of respiratory insufficiency: ALI/ARDS, cardiogenic edema, and pleural effusion with atelectasis, which were noted in 207 patients, 26 patients, and 33 patients, respectively. EVLWI was greater in ALI/ARDS and cardiogenic edema patients than in patients with pleural effusion with atelectasis (18.5 ± 6.8, 14.4 ± 4.0, and 8.3 ± 2.1, respectively; P < 0.01). PVPI was higher in ALI/ARDS patients than in cardiogenic edema or pleural effusion with atelectasis patients (3.2 ± 1.4, 2.0 ± 0.8, and 1.6 ± 0.5; P < 0.01). In ALI/ARDS patients, EVLWI increased with increasing pulmonary vascular permeability (r = 0.729, P < 0.01) and was weakly

  7. Soluble Urokinase-Type Plasminogen Activator Receptor Plasma Concentration May Predict Susceptibility to High Altitude Pulmonary Edema

    PubMed Central

    Zügel, Stefanie; Schoeb, Michele; Auinger, Katja; Dehnert, Christoph; Maggiorini, Marco

    2016-01-01

    Introduction. Acute exposure to high altitude induces inflammation. However, the relationship between inflammation and high altitude related illness such as high altitude pulmonary edema (HAPE) and acute mountain sickness (AMS) is poorly understood. We tested if soluble urokinase-type plasminogen activator receptor (suPAR) plasma concentration, a prognostic factor for cardiovascular disease and marker for low grade activation of leukocytes, will predict susceptibility to HAPE and AMS. Methods. 41 healthy mountaineers were examined at sea level (SL, 446 m) and 24 h after rapid ascent to 4559 m (HA). 24/41 subjects had a history of HAPE and were thus considered HAPE-susceptible (HAPE-s). Out of the latter, 10/24 HAPE-s subjects were randomly chosen to suppress the inflammatory cascade with dexamethasone 8 mg bid 24 h prior to ascent. Results. Acute hypoxic exposure led to an acute inflammatory reaction represented by an increase in suPAR (1.9 ± 0.4 at SL versus 2.3 ± 0.5 at HA, p < 0.01), CRP (0.7 ± 0.5 at SL versus 3.6 ± 4.6 at HA, p < 0.01), and IL-6 (0.8 ± 0.4 at SL versus 3.3 ± 4.9 at HA, p < 0.01) in all subjects except those receiving dexamethasone. The ascent associated decrease in PaO2 correlated with the increase in IL-6 (r = 0.46, p < 0.001), but not suPAR (r = 0.27, p = 0.08); the increase in IL-6 was not correlated with suPAR (r = 0.16, p = 0.24). Baseline suPAR plasma concentration was higher in the HAPE-s group (2.0 ± 0.4 versus 1.8 ± 0.4, p = 0.04); no difference was found for CRP and IL-6 and for subjects developing AMS. Conclusion. High altitude exposure leads to an increase in suPAR plasma concentration, with the missing correlation between suPAR and IL-6 suggesting a cytokine independent, leukocyte mediated mechanism of low grade inflammation. The correlation between IL-6 and PaO2 suggests a direct effect of hypoxia, which is not the case for suPAR. However, suPAR plasma concentration measured before hypoxic exposure may predict

  8. Fatal intoxication as a consequence of intranasal administration (snorting) or pulmonary inhalation (smoking) of heroin.

    PubMed

    Thiblin, I; Eksborg, S; Petersson, A; Fugelstad, A; Rajs, J

    2004-01-28

    In recent years we have noticed an increasing proportion of mortalities resulting from an overdose of heroin that involve routes of administration other than injection. Of 239 cases of fatal heroin intoxication examined at our department during the period 1997-2000, 18 deaths were associated with non-parental administration. Seven of these fatalities were experienced heroin users who had begun to use more sporadically, seven were recreational "party-users", while the remaining four persons had relapsed into heroin use following long periods of abstinence. The median blood morphine concentration of these non-injectors was 0.095 microg/g (range: 0.02-0.67 microg/g), significantly lower than that of the injectors. Concurrent use of alcohol, other illicit drugs and/or pharmaceutical preparations was observed in 17 of the 18 cases. However, there were no statistically significant differences between the victims of heroin intoxication by injection or by other routes with respect to the proportion who had simultaneously consumed alcohol or benzodiazepines. Pathological alterations like lung fibrosis, liver cirrhosis, endocarditis, etc. were not found to play a significant role in any of the 18 mortalities. We conclude that snorting or smoking heroin probably involves a reduced risk of obtaining high blood concentrations of morphine but still constitutes a considerable risk of lethal outcome due to high variability in blood concentrations. Furthermore, decreased tolerance resulting from periods of reduced or sporadic use appears to be an important risk factor in connection with heroin overdosing by snorting or smoking, which indicate that some heroin addicts may inaccurately assume that these routes of administration are safe when resuming their use of heroin after a period of abstinence.

  9. Successful management of severe unilateral re-expansion pulmonary edema after mitral valve repair with mini-thoracotomy using extracorporeal membrane oxygenation.

    PubMed

    Kitahara, Hiroto; Okamoto, Kazuma; Kudo, Mikihiko; Yoshitake, Akihiro; Hayashi, Kanako; Inaba, Yu; Ai, Kimiaki; Suzuki, Takeshi; Morisaki, Hiroshi; Shimizu, Hideyuki

    2017-03-01

    A 60-year-old man received mitral valve repair via right mini-thoracotomy, which was followed by unilateral re-expansion pulmonary edema on the right side and severe hemoptysis just after the surgery. Despite differential lung ventilation with unilateral high positive end expiratory pressure was initiated for the affected right lung, respiratory function did not improved and hemodynamics was collapsed in the next day. Veno-venous extracorporeal membrane oxygenation was initiated by cannulation of the right jugular and the left femoral vein. After pulmonary function recovered gradually, veno-venous extracorporeal membrane oxygenation was terminated on the fifth postoperative day. He was discharged in ambulatory condition on postoperative day 52.

  10. Andes Virus and First Case Report of Bermejo Virus Causing Fatal Pulmonary Syndrome

    PubMed Central

    Della Valle, Marcelo González; Alai, María Garcia; Cortada, Pedro; Villagra, Mario; Gianella, Alberto

    2002-01-01

    Two suspected hantavirus pulmonary syndrome (HPS) cases from Bolivia were confirmed by enzyme-linked immunosorbent assay. (ELISA)-ANDES was performed using N-Andes recombinant antigen serology in May and July 2000. Clot RNAs from the two patients were subjected to reverse transcription–polymerase chain reaction (PCR) amplification and sequencing. We describe two characterized cases of HPS. One was caused by infection with Bermejo virus and the other with Andes Nort viral lineage, both previously obtained from Oligoryzomys species. This is the first report of molecular identification of a human hantavirus associated with Bermejo virus. PMID:11971782

  11. Fatal bilateral lower-limb deep vein thrombosis and pulmonary embolism following single digit replantation.

    PubMed

    Leung, Anderson S M; Fok, Margaret W M; Fung, Boris K K

    2015-06-01

    Venous thromboembolism in hand surgery is rare. There is no report in the literature on postoperative mortality from venous thromboembolism following microsurgery in upper limbs. We report the case of a 56-year-old Chinese man who died from pulmonary embolism as a result of bilateral lower-limb deep vein thrombosis following prolonged surgery under general anaesthesia after replantation of a finger. This case raises awareness of the need for precautions against venous thromboembolism following prolonged microsurgery and identification of high-risk patients.

  12. Non-cardiogenic pulmonary edema and life-threatening shock due to calcium channel blocker overdose: a case report and clinical review.

    PubMed

    Siddiqi, Tauseef Afaq; Hill, Jennifer; Huckleberry, Yvonne; Parthasarathy, Sairam

    2014-02-01

    Calcium channel blockers (CCBs) overdose can be life-threatening when manifest as catastrophic shock and non-cardiogenic pulmonary edema. We describe a case of massive overdose of multiple medications, including sustained-release verapamil, which was resistant to conventional support. Initial treatment for CCB overdose is primarily supportive, and includes fluid resuscitation. The mechanism of non-cardiogenic pulmonary edema is not well known, and reported cases have been successfully treated with mechanical ventilation. Circulatory shock may fail to respond to atropine, glucagon, and calcium in severely poisoned patients, and vasopressors are usually required. Attempting to overcome calcium-channel antagonism with the supra-therapeutic doses of calcium salts is clinically indicated to reverse hypotension and bradycardia. There is evidence that hyperinsulinemia-euglycemia therapy is superior to other therapies for CCB poisoning, and the mechanism is thought to be the insulin-mediated active transport of glucose into the cells, which counters the CCB-induced intra-cellular carbohydrate-deficient state. Conventional decontamination measures are ineffective in accelerating clearance of CCB. Experience with intravenous lipid emulsion for lipophilic drug overdose, such as verapamil, is limited, but has been proposed as a rescue therapy and might improve cardiac inotropy through intravascular sequestration of the lipophilic CCB.

  13. Fatal diffuse alveolar haemorrhage mimicking acute exacerbation in idiopathic pulmonary fibrosis treated with nintedanib.

    PubMed

    Sugino, Keishi; Nakamura, Yasuhiko; Sekiya, Muneyuki; Kobayashi, Hiroshi; Shibuya, Kazutoshi; Homma, Sakae

    2017-11-01

    A 75-year-old man was referred to our hospital with a 1-year history of persistent dry cough and progressive dyspnoea on exertion. He was treated with aspirin due to thrombosis of internal carotid artery. He was diagnosed with idiopathic pulmonary fibrosis (IPF)/usual interstitial pneumonia (UIP), and started on inhaled N-acetylcysteine therapy and pirfenidone. Since his clinical condition progressively deteriorated after 6 months, he was switched from pirfenidone to nintedanib. As a result, his general condition worsened rapidly. He was diagnosed with acute exacerbation (AE) of IPF, and was treated with methylprednisolone pulse and recombinant human soluble thrombomodulin. Despite the administration of these treatments, he died of severe haemoptysis four days after the onset of AE. Autopsied lungs revealed significantly dark red-brown appearance corresponding to diffuse alveolar haemorrhage (DAH) histopathogically with a background pattern of UIP with fibrotic change. Notably, there was no evidence of diffuse alveolar damage suggesting IPF-AE.

  14. Endomyocardial fibrosis as a cause of Budd-Chiari syndrome and fatal pulmonary embolism.

    PubMed

    Bestetti, Reinaldo B; Silva, Carolina M P D C; Ardito, Sabrina Q; Theodoropoulos, Tatiana A D; Cury, Patrícia M; Corbucci, Hélio A R

    2010-01-01

    A 24-year-old-man had right-sided heart failure of 3 months' duration. A Doppler echocardiogram revealed atrium and right ventricular enlargement, obliteration of the right ventricular apex, and a mass with an echolucent center measuring 20x21 mm in the right ventricular outlet. He died of pulmonary embolism. At autopsy, a huge organized thrombus obliterating the right ventricular apex passing through the tricuspid valve to the right atrium and then extending to the inferior vena cava up to the suprahepatic veins was seen. Histologically, an intense fibrotic thickening of the endomyocardium extending into the myocardium was observed. Cardiac thrombosis associated with endomyocardial fibrosis should be added to the list of causes of Budd-Chiari syndrome.

  15. Fatal systemic adenoviral infection superimposed on pulmonary mucormycosis in a child with acute leukemia

    PubMed Central

    Seo, Yu Mi; Hwang-Bo, Seok; Kim, Seong koo; Han, Seung Beom; Chung, Nack-Gyun; Kang, Jin Han

    2016-01-01

    Abstract Background: Although adenovirus (ADV) infection usually causes self-limiting respiratory disorders in immune competent children; severe and systemic ADV infection in children undergoing chemotherapy for leukemia has been continuously reported. Nevertheless, there has been no consensus on risk factors and treatment strategies for severe ADV infection in children undergoing chemotherapy. Case summary: We report a case of a 15-year-old boy with a fatal systemic ADV infection. He had received reinduction chemotherapy for relapsed acute lymphoblastic leukemia under continuing antifungal therapy for previously diagnosed fungal pneumonia. He complained of fever and right shoulder pain 4 days after completing the reinduction chemotherapy. In spite of appropriate antibiotic and antifungal therapy, pneumonia was aggravated and gross hematuria was accompanied. A multiplex polymerase chain reaction test for respiratory viruses was positive for ADV in a blood sample, and a urine culture was positive for ADV. He received oral ribavirin, intravenous immunoglobulin, and intravenous cidofovir therapy; however, he eventually died. Relapsed leukemia, concurrent fungal pneumonia, and delayed cidofovir administration were considered the cause of the grave outcome in this patient. Conclusion: ADV may cause severe infections not only in allogeneic hematopoietic cell transplant recipients, but also in patients undergoing chemotherapy for acute leukemia. The risk factors for severe ADV infection in patients undergoing chemotherapy should be determined in the future studies, and early antiviral therapy should be administered to immune compromised patients with systemic ADV infection. PMID:27749571

  16. Intralipid prevents and rescues fatal pulmonary arterial hypertension and right ventricular failure in rats.

    PubMed

    Umar, Soban; Nadadur, Rangarajan D; Li, Jingyuan; Maltese, Federica; Partownavid, Parisa; van der Laarse, Arnoud; Eghbali, Mansoureh

    2011-09-01

    Pulmonary arterial hypertension (PAH) is characterized by pulmonary vascular remodeling leading to right ventricular (RV) hypertrophy and failure. Intralipid (ILP), a source of parenteral nutrition for patients, contains γ-linolenic acid and soy-derived phytoestrogens that are protective for lungs and heart. We, therefore, investigated the therapeutic potential of ILP in preventing and rescuing monocrotaline-induced PAH and RV dysfunction. PAH was induced in male rats with monocrotaline (60 mg/kg). Rats then received daily ILP (1 mL of 20% ILP per day IP) from day 1 to day 30 for prevention protocol or from day 21 to day 30 for rescue protocol. Other monocrotaline-injected rats were left untreated to develop severe PAH by day 21 or RV failure by approximately day 30. Saline or ILP-treated rats served as controls. Significant increase in RV pressure and decrease in RV ejection fraction in the RV failure group resulted in high mortality. Therapy with ILP resulted in 100% survival and prevented PAH-induced RV failure by preserving RV pressure and RV ejection fraction and preventing RV hypertrophy and lung remodeling. In preexisting severe PAH, ILP attenuated most lung and RV abnormalities. The beneficial effects of ILP in PAH seem to result from the interplay of various factors, among which preservation and/or stimulation of angiogenesis, suppression and/or reversal of inflammation, fibrosis and hypertrophy, in both lung and RV, appear to be major contributors. In conclusion, ILP not only prevents the development of PAH and RV failure but also rescues preexisting severe PAH.

  17. Pulmonary artery perforation and coronary air embolism-two fatal outcomes in percutaneous left atrial appendage occlusion.

    PubMed

    Zwirner, J; Bayer, R; Hädrich, C; Bollmann, A; Klein, N; Dreßler, J; Ondruschka, B

    2017-01-01

    Percutaneous left atrial appendage (LAA) closure is a routinely performed method to reduce the risk of stroke in patients suffering from atrial fibrillation, when an oral anticoagulation is no longer indicated due to relevant bleeding complications. Currently, the Amplatzer Amulet and the Watchman system are two equally used systems. While there is an acute success rate of more than 95 per cent for this intervention, several minor and major complications such as pericardial effusions, air embolism, vascular lesions in proximity to the heart or even death can occur. Here, we report two cases of very rare fatal outcomes in percutaneous LAA occlusion. Eight hours after deployment of an Amplatzer Amulet a patient died, after the pulmonary trunk was perforated by a hook of the occluder device causing pericardial tamponade. In the second case during final radiological position control of the deployed Watchman occluder air was injected accidentally. The patient immediately died due to coronary air embolism. Forensic autopsies are necessary to solve the cause and manner of death, to evaluate and develop medical devices and to rule out medical malpractice. Thus, a close collaboration of legal medicine and the various cardiologic departments is proposed.

  18. Coexistence of dynamic mitral regurgitation and dynamic left ventricular dyssynchrony in a patient with repeated episodes of acute pulmonary edema: improvement with cardiac resynchronization therapy.

    PubMed

    Carvalho, Maria Salomé; Andrade, Maria João; Reis, Carla; Brito, João; Trabulo, Marisa; Mendes, Miguel

    2013-12-01

    A 69-year-old woman with idiopathic dilated cardiomyopathy and chronic heart failure experienced repeated hospital admissions for acute pulmonary edema with no recognizable precipitating factor. Worsening mitral regurgitation was triggered by exercise echocardiography and significant intraventricular dyssynchrony was elicited by low-dose dobutamine stress echocardiography. After cardiac resynchronization therapy she remained free of hospitalizations for 12 months. This case highlights the dynamic nature of both functional mitral regurgitation and left ventricular dyssynchrony and illustrates how in some patients stress echocardiography can help to clarify clinical scenarios and help with the challenging task of selecting patients who will benefit from cardiac resynchronization therapy. Copyright © 2013 Sociedade Portuguesa de Cardiologia. Published by Elsevier España. All rights reserved.

  19. Mouse-Passaged Severe Acute Respiratory Syndrome-Associated Coronavirus Leads to Lethal Pulmonary Edema and Diffuse Alveolar Damage in Adult but Not Young Mice

    PubMed Central

    Nagata, Noriyo; Iwata, Naoko; Hasegawa, Hideki; Fukushi, Shuetsu; Harashima, Ayako; Sato, Yuko; Saijo, Masayuki; Taguchi, Fumihiro; Morikawa, Shigeru; Sata, Tetsutaro

    2008-01-01

    Advanced age is a risk factor of severe acute respiratory syndrome (SARS) in humans. To understand its pathogenesis, we developed an animal model using BALB/c mice and the mouse-passaged Frankfurt 1 isolate of SARS coronavirus (SARS-CoV). We examined the immune responses to SARS-CoV in both young and adult mice. SARS-CoV induced severe respiratory illness in all adult, but not young, mice on day 2 after inoculation with a mortality rate of 30 to 50%. Moribund adult mice showed severe pulmonary edema and diffuse alveolar damage accompanied by virus replication. Adult murine lungs, which had significantly higher interleukin (IL)-4 and lower IL-10 and IL-13 levels before infection than young murine lungs, rapidly produced high levels of proinflammatory chemokines and cytokines known to induce macrophage and neutrophil infiltration and activation (eg, tumor necrosis factor-α). On day 2 after inoculation, young murine lungs produced not only proinflammatory cytokines but also IL-2, interferon-γ, IL-10, and IL-13. Adult mice showed early and acute excessive proinflammatory responses (ie, cytokine storm) in the lungs after SARS-CoV infection, which led to severe pulmonary edema and diffuse alveolar damage. Intravenous injection with anti-tumor necrosis factor-α antibody 3 hours after infection had no effect on SARS-CoV infection. However, intraperitoneal interferon-γ injection protected adult mice from the lethal respiratory illness. The experimental model described here may be useful for elucidating the pathophysiology of SARS and for evaluating therapies to treat SARS-CoV infection. PMID:18467696

  20. [Case report of re-expansion pulmonary edema in a patient with anorexia nervosa after removal of a huge ovarian tumor].

    PubMed

    Hari, Junko; Arai, Masayasu; Kosaka, Yasuharu; Toda, Masaya; Kuroiwa, Masayuki; Okamoto, Hirotsugu

    2014-04-01

    We described a case of 19-year-old female who developed re-expansion pulmonary edema (RPE) after removal of a huge ovarian tumor. Altered lung volume after the surgery was observed by chest X-ray. Preoperatively, the lung was highly compressed by the tumor. Patient was intubated under general anesthesia and was ventilated by pressure controlled mode with only 5 cmH2O of positive end-expiratory pressure (PEEP). P/F ratio was changed from 163 to 444 after removal of the tumor. At the end of the surgery, P/F ratio decreased to 263 with yellow frothy sputum in the endotracheal tube and we diagnosed re-expansion pulmonary edema based on appearing yellow frothy sputum and chest X-ray. No recruitment procedure was carried out through the course except positive pressure ventilation with 5 cmH2O of PEEP in the intensive care unit after surgery. Twelve hours after the surgery, we could not confirm the recovery of lung volume on chest X-ray; however the patient was extubated because of P/F ratio increasing to 507. After 8 days of the surgery, the chest X-ray showed recovery of the lung volume to almost normal size. In this case, the compressed lung needed almost 1 week to recover the lung volume. This change in chest X-ray might indicate inadequate recovery of lung volume by recruitment maneuver and this should be avoided in order not to allow development of unfavorable clinical course of RPE.

  1. Dexmedetomidine alleviates pulmonary edema by upregulating AQP1 and AQP5 expression in rats with acute lung injury induced by lipopolysaccharide.

    PubMed

    Jiang, Yuan-xu; Dai, Zhong-liang; Zhang, Xue-ping; Zhao, Wei; Huang, Qiang; Gao, Li-kun

    2015-10-01

    This study aims to elucidate the mechanisms by which dexmedetomidine alleviates pulmonary edema in rats with acute lung injury induced by lipopolysaccharide (LPS). Male Wistar rats were randomly divided into five groups: normal saline control (NS) group, receiving intravenous 0.9% normal saline (5 mL/kg); LPS group, receiving intravenous LPS (10 mg/kg); small-dose dexmedetomidine (S) group, treated with a small dose of dexmedetomidine (0.5 μg · kg(-1) · h(-1)); medium-dose dexmedetomidine (M) group, treated with a medium dose of dexmedetomidine (2.5 μg · kg(-1) · h(-1)); high-dose dexmedetomidine (H) group, treated with a high dose of dexmedetomidine (5 μg · kg(-1) · h(-1)). The rats were sacrificed 6 h after intravenous injection of LPS or NS, and the lungs were removed for evaluating histological characteristics and determining the lung wet/dry weight ratio (W/D). The levels of tumor necrosis factor-alpha (TNF-α) and interleukin-1β (IL-1β) in the lung tissues were assessed by enzyme- linked immunosorbent assay (ELISA). The mRNA and protein expression levels of aquaporin-1 (AQP1) and aquaporin-5 (AQP5) were detected by RT-PCR, immunohistochemistry, and Western blotting. The lung tissues from the LPS groups were significantly damaged, which were less pronounced in the H group but not in the small-dose dexmedetomidine group or medium-dose dexmedetomidine group. The W/D and the concentrations of TNF-α and IL-1β in the pulmonary tissues were increased in the LPS group as compared with those in NS group, which were reduced in the H group but not in S group or M group (P<0.01). The expression of AQP1 and AQP5 was lower in the LPS group than in the NS group, and significantly increased in the H group but not in the S group or M group (P<0.01). Our findings suggest that dexmedetomidine may alleviate pulmonary edema by increasing the expression of AQP-1 and AQP-5.

  2. Lipopolysaccharide-induced pulmonary endothelial barrier disruption and lung edema: critical role for bicarbonate stimulation of AC10.

    PubMed

    Nickols, Jordan; Obiako, Boniface; Ramila, K C; Putinta, Kevin; Schilling, Sarah; Sayner, Sarah L

    2015-12-15

    Bacteria-induced sepsis is a common cause of pulmonary endothelial barrier dysfunction and can progress toward acute respiratory distress syndrome. Elevations in intracellular cAMP tightly regulate pulmonary endothelial barrier integrity; however, cAMP signals are highly compartmentalized: whether cAMP is barrier-protective or -disruptive depends on the compartment (plasma membrane or cytosol, respectively) in which the signal is generated. The mammalian soluble adenylyl cyclase isoform 10 (AC10) is uniquely stimulated by bicarbonate and is expressed in pulmonary microvascular endothelial cells (PMVECs). Elevated extracellular bicarbonate increases cAMP in PMVECs to disrupt the endothelial barrier and increase the filtration coefficient (Kf) in the isolated lung. We tested the hypothesis that sepsis-induced endothelial barrier disruption and increased permeability are dependent on extracellular bicarbonate and activation of AC10. Our findings reveal that LPS-induced endothelial barrier disruption is dependent on extracellular bicarbonate: LPS-induced barrier failure and increased permeability are exacerbated in elevated bicarbonate compared with low extracellular bicarbonate. The AC10 inhibitor KH7 attenuated the bicarbonate-dependent LPS-induced barrier disruption. In the isolated lung, LPS failed to increase Kf in the presence of minimal perfusate bicarbonate. An increase in perfusate bicarbonate to the physiological range (24 mM) revealed the LPS-induced increase in Kf, which was attenuated by KH7. Furthermore, in PMVECs treated with LPS for 6 h, there was a dose-dependent increase in AC10 expression. Thus these findings reveal that LPS-induced pulmonary endothelial barrier failure requires bicarbonate activation of AC10. Copyright © 2015 the American Physiological Society.

  3. Lipopolysaccharide-induced pulmonary endothelial barrier disruption and lung edema: critical role for bicarbonate stimulation of AC10

    PubMed Central

    Nickols, Jordan; Obiako, Boniface; Ramila, K. C.; Putinta, Kevin; Schilling, Sarah

    2015-01-01

    Bacteria-induced sepsis is a common cause of pulmonary endothelial barrier dysfunction and can progress toward acute respiratory distress syndrome. Elevations in intracellular cAMP tightly regulate pulmonary endothelial barrier integrity; however, cAMP signals are highly compartmentalized: whether cAMP is barrier-protective or -disruptive depends on the compartment (plasma membrane or cytosol, respectively) in which the signal is generated. The mammalian soluble adenylyl cyclase isoform 10 (AC10) is uniquely stimulated by bicarbonate and is expressed in pulmonary microvascular endothelial cells (PMVECs). Elevated extracellular bicarbonate increases cAMP in PMVECs to disrupt the endothelial barrier and increase the filtration coefficient (Kf) in the isolated lung. We tested the hypothesis that sepsis-induced endothelial barrier disruption and increased permeability are dependent on extracellular bicarbonate and activation of AC10. Our findings reveal that LPS-induced endothelial barrier disruption is dependent on extracellular bicarbonate: LPS-induced barrier failure and increased permeability are exacerbated in elevated bicarbonate compared with low extracellular bicarbonate. The AC10 inhibitor KH7 attenuated the bicarbonate-dependent LPS-induced barrier disruption. In the isolated lung, LPS failed to increase Kf in the presence of minimal perfusate bicarbonate. An increase in perfusate bicarbonate to the physiological range (24 mM) revealed the LPS-induced increase in Kf, which was attenuated by KH7. Furthermore, in PMVECs treated with LPS for 6 h, there was a dose-dependent increase in AC10 expression. Thus these findings reveal that LPS-induced pulmonary endothelial barrier failure requires bicarbonate activation of AC10. PMID:26475732

  4. Severe Tumor Lysis Syndrome and Acute Pulmonary Edema Requiring Extracorporeal Membrane Oxygenation Following Initiation of Chemotherapy for Metastatic Alveolar Rhabdomyosarcoma.

    PubMed

    Sanford, Ethan; Wolbrink, Traci; Mack, Jennifer; Rowe, R Grant

    2016-05-01

    We present an 8-year-old male with metastatic alveolar rhabdomyosarcoma (ARMS) who developed precipitous cardiopulmonary collapse with severe tumor lysis syndrome (TLS) 48 hr after initiation of chemotherapy. Despite no detectable pulmonary metastases, acute hypoxemic respiratory failure developed, requiring extracorporeal membrane oxygenation (ECMO). Although TLS has been reported in disseminated ARMS, this singular case of life-threatening respiratory deterioration developing after initiation of chemotherapy presented unique therapeutic dilemmas. We review the clinical aspects of this case, including possible mechanisms of respiratory failure, and discuss the role of ECMO utilization in pediatric oncology.

  5. TRPV4 inhibition counteracts edema and inflammation and improves pulmonary function and oxygen saturation in chemically induced acute lung injury

    PubMed Central

    Balakrishna, Shrilatha; Song, Weifeng; Achanta, Satyanarayana; Doran, Stephen F.; Liu, Boyi; Kaelberer, Melanie M.; Yu, Zhihong; Sui, Aiwei; Cheung, Mui; Leishman, Emma; Eidam, Hilary S.; Ye, Guosen; Willette, Robert N.; Thorneloe, Kevin S.; Bradshaw, Heather B.; Matalon, Sadis

    2014-01-01

    The treatment of acute lung injury caused by exposure to reactive chemicals remains challenging because of the lack of mechanism-based therapeutic approaches. Recent studies have shown that transient receptor potential vanilloid 4 (TRPV4), an ion channel expressed in pulmonary tissues, is a crucial mediator of pressure-induced damage associated with ventilator-induced lung injury, heart failure, and infarction. Here, we examined the effects of two novel TRPV4 inhibitors in mice exposed to hydrochloric acid, mimicking acid exposure and acid aspiration injury, and to chlorine gas, a severe chemical threat with frequent exposures in domestic and occupational environments and in transportation accidents. Postexposure treatment with a TRPV4 inhibitor suppressed acid-induced pulmonary inflammation by diminishing neutrophils, macrophages, and associated chemokines and cytokines, while improving tissue pathology. These effects were recapitulated in TRPV4-deficient mice. TRPV4 inhibitors had similar anti-inflammatory effects in chlorine-exposed mice and inhibited vascular leakage, airway hyperreactivity, and increase in elastance, while improving blood oxygen saturation. In both models of lung injury we detected increased concentrations of N-acylamides, a class of endogenous TRP channel agonists. Taken together, we demonstrate that TRPV4 inhibitors are potent and efficacious countermeasures against severe chemical exposures, acting against exaggerated inflammatory responses, and protecting tissue barriers and cardiovascular function. PMID:24838754

  6. TRPV4 inhibition counteracts edema and inflammation and improves pulmonary function and oxygen saturation in chemically induced acute lung injury.

    PubMed

    Balakrishna, Shrilatha; Song, Weifeng; Achanta, Satyanarayana; Doran, Stephen F; Liu, Boyi; Kaelberer, Melanie M; Yu, Zhihong; Sui, Aiwei; Cheung, Mui; Leishman, Emma; Eidam, Hilary S; Ye, Guosen; Willette, Robert N; Thorneloe, Kevin S; Bradshaw, Heather B; Matalon, Sadis; Jordt, Sven-Eric

    2014-07-15

    The treatment of acute lung injury caused by exposure to reactive chemicals remains challenging because of the lack of mechanism-based therapeutic approaches. Recent studies have shown that transient receptor potential vanilloid 4 (TRPV4), an ion channel expressed in pulmonary tissues, is a crucial mediator of pressure-induced damage associated with ventilator-induced lung injury, heart failure, and infarction. Here, we examined the effects of two novel TRPV4 inhibitors in mice exposed to hydrochloric acid, mimicking acid exposure and acid aspiration injury, and to chlorine gas, a severe chemical threat with frequent exposures in domestic and occupational environments and in transportation accidents. Postexposure treatment with a TRPV4 inhibitor suppressed acid-induced pulmonary inflammation by diminishing neutrophils, macrophages, and associated chemokines and cytokines, while improving tissue pathology. These effects were recapitulated in TRPV4-deficient mice. TRPV4 inhibitors had similar anti-inflammatory effects in chlorine-exposed mice and inhibited vascular leakage, airway hyperreactivity, and increase in elastance, while improving blood oxygen saturation. In both models of lung injury we detected increased concentrations of N-acylamides, a class of endogenous TRP channel agonists. Taken together, we demonstrate that TRPV4 inhibitors are potent and efficacious countermeasures against severe chemical exposures, acting against exaggerated inflammatory responses, and protecting tissue barriers and cardiovascular function. Copyright © 2014 the American Physiological Society.

  7. Mitochondrial haplogroup D4 confers resistance and haplogroup B is a genetic risk factor for high-altitude pulmonary edema among Han Chinese.

    PubMed

    Luo, Y J; Gao, W X; Li, S Z; Huang, X W; Chen, Y; Liu, F Y; Huang, Q Y; Gao, Y Q

    2012-10-09

    High-altitude pulmonary edema (HAPE) is a life-threatening condition caused by acute exposure to high altitude. Accumulating evidence suggests that genetic factors play an important role in the etiology of HAPE. However, conclusions from association studies have been hindered by limited sample size due to the rareness of this disease. It is known that mitochondria are critical for hypoxic adaptation, and mitochondrial malfunction can be an important factor in HAPE development. Therefore, we tested the hypothesis that mitochondrial DNA haplotypes and polymorphisms affect HAPE susceptibility. We recruited 204 HAPE patients and 174 healthy controls in Tibet (3658 m above sea level), all Han Chinese, constituting the largest sample size of all HAPE vulnerability studies. Among mtDNA haplogroups, we found that haplogroup D4 is associated with resistance to HAPE, while haplogroup B is a genetic risk factor for this condition. Haplogroup D4 (tagged by 3010A) may enhance the stability of 16S rRNA, resulting in reduced oxidative stress and protection against HAPE. Within haplogroup B, subhaplogroup B4c (tagged by 15436A and 1119C) was associated with increased risk for HAPE, while subhaplogroup B4b may protect against HAPE. We indicate that there are differences in HAPE susceptibility among mtDNA haplogroups. We conclude that mitochondria are involved in adverse reactions to acute hypoxic exposure; our finding of differences in susceptibility as a function of mitochondrial DNA haplotype may shed light on the pathogenesis of other disorders associated with hypoxia, such as chronic obstructive pulmonary disease.

  8. Association between single nucleotide polymorphisms in ADRB2, GNB3 and GSTP1 genes and high-altitude pulmonary edema (HAPE) in the Chinese Han population.

    PubMed

    He, Yongjun; Liu, Lijun; Xu, Pengcheng; He, Na; Yuan, Dongya; Kang, Longli; Jin, Tianbo

    2017-03-14

    High altitude pulmonary edema (HAPE) occurs mainly under conditions such as high altitude, rapid ascent, or hypoxia. Previous studies suggest that ADRB2, GNB3, TH, and GSTP1 polymorphisms are associated with various lung diseases. We evaluated whether those polymorphisms are associated with the risk of HAPE in a Chinese Han population. ADRB2, GNB3, TH and GSTP1 polymorphisms were genotyped using a Sequenom MassARRAY. Logistic regression, adjusted for age and gender, was used to evaluate the association between the genotypes and the risk of HAPE by computing odds ratios (ORs) and 95% confidence intervals (95% CIs). The results revealed that GNB3 rs4963516 allele ''G'' (G vs T: OR = 0.70, 95% CI = 0.55-0.90, p = 0.006) was associated with HAPE risk. The ADRB2 rs1042718 alleles had a 1.29-fold (95%CI = 1.00-1.66; p = 0.045) increased risk of HAPE, and the GSTP1 rs749174 alleles had a 0.71-fold (95%CI = 0.52-0.99; p = 0.042) decreased risk of HAPE. Co-dominant and dominant models of GNB3 rs4963516 decreased the risk of HAPE (p = 0.023 and p = 0.008, respectively). Our results indicate GNB3 and GSTP1 polymorphisms may protect against HAPE progression, while ADRB2 polymorphisms are associated with an increased risk of HAPE.

  9. Therapeutic implications of melatonin in cerebral edema.

    PubMed

    Rathnasamy, Gurugirijha; Ling, Eng-Ang; Kaur, Charanjit

    2014-12-01

    Cerebral edema/brain edema refers to the accumulation of fluid in the brain and is one of the fatal conditions that require immediate medical attention. Cerebral edema develops as a consequence of cerebral trauma, cerebral infarction, hemorrhages, abscess, tumor, hypoxia, and other toxic or metabolic factors. Based on the causative factors cerebral edema is differentiated into cytotoxic cerebral edema, vasogenic cerebral edema, osmotic and interstitial cerebral edema. Treatment of cerebral edema depends on timely diagnosis and medical assistance. Pragmatic treatment strategies such as antihypertensive medications, nonsteroidal anti-inflammatory drugs, barbiturates, steroids, glutamate and N-methyl-D-aspartate receptor antagonists and trometamol are used in clinical practice. Although the above mentioned treatment approaches are being used, owing to the complexity of the mechanisms involved in cerebral edema, a single therapeutic strategy which could ameliorate cerebral edema is yet to be identified. However, recent experimental studies have suggested that melatonin, a neurohormone produced by the pineal gland, could be an effective alternative for treating cerebral edema. In animal models of stroke, melatonin was not only shown to reduce cerebral edema but also preserved the blood brain barrier. Melatonin's beneficial effects were attributed to its properties, such as being a potent anti-oxidant, and its ability to cross the blood brain barrier within minutes after its administration. This review summarizes the beneficial effects of melatonin when used for treating cerebral edema.

  10. Drug-induced pulmonary disease

    MedlinePlus

    ... mediastinitis ) Abnormal buildup of fluid in the lungs ( pulmonary edema ) Buildup of fluid between the layers of tissue ... reactions Cardiovascular Chemotherapy Interstitial lung disease Pleural effusion Pulmonary edema Respiratory Systemic lupus erythematosus Patient Instructions Interstitial lung ...

  11. Fatal course of pulmonary Absidia sp. infection in a 4-year-old girl undergoing treatment for acute lymphoblastic leukemia.

    PubMed

    Krauze, Agnieszka; Krenke, Katarzyna; Matysiak, Michal; Kulus, Marek

    2005-07-01

    Absidia sp. is a rare etiologic agent responsible for infectious complications in immunosuppressed patients. The authors describe a 4-year-old girl with acute lymphoblastic leukemia complicated with pleuropneumonia caused by an Absidia infection during the induction of remission. A review of the published reports in current literature is included for comparison. To the authors' knowledge only six cases of primary pulmonary absidiomycosis have been published. Despite its uncommon pulmonary presentation, mucormycosis should be considered in patients with an immunosuppressing illness and positive risk factors and when a pulmonary lesion is not responding to appropriate antibiotic therapy.

  12. Familial Thoracic Aortic Aneurysm with Dissection Presenting as Flash Pulmonary Edema in a 26-Year-Old Man

    PubMed Central

    Omar, Sabry; Moore, Tyler; Payne, Drew; Momeni, Parastoo; Mulkey, Zachary; Nugent, Kenneth

    2014-01-01

    We are reporting a case of familial thoracic aortic aneurysm and dissection in a 26-year-old man with no significant past medical history and a family history of dissecting aortic aneurysm in his mother at the age of 40. The patient presented with cough, shortness of breath, and chest pain. Chest X-ray showed bilateral pulmonary infiltrates. CT scan of the chest showed a dissection of the ascending aorta. The patient underwent aortic dissection repair and three months later he returned to our hospital with new complaints of back pain. CT angiography showed a new aortic dissection extending from the left carotid artery through the bifurcation and into the iliac arteries. The patient underwent replacement of the aortic root, ascending aorta, total aortic arch, and aortic valve. The patient recovered well postoperatively. Genetic studies of the patient and his children revealed no mutations in ACTA2, TGFBR1, TGFBR2, TGFB2, MYH11, MYLK, SMAD3, or FBN1. This case report focuses on a patient with familial TAAD and discusses the associated genetic loci and available screening methods. It is important to recognize potential cases of familial TAAD and understand the available screening methods since early diagnosis allows appropriate management of risk factors and treatment when necessary. PMID:25104961

  13. Hantavirus Pulmonary Syndrome

    PubMed Central

    Zaki, Sherif R.; Greer, Patricia w.; Coffield, Lisa M.; Goldsmith, Cynthia S.; Nolte, Kurt B.; Foucar, Kathy; Feddersen, Richard M.; Zumwalt, Ross E.; Miller, Gayle L.; Khan, Ali S.; Rollin, Pierre E.; Ksiazek, Thomas G.; Nichol, Stuart T.; Mahy, Brian W.J.; Peters, Clarence J.

    1995-01-01

    A recent outbreak of a severe pulmonary disease in the southwestern United States was etiologically linked to a previously unrecognized bantavirus. The virus has been isolated from its majorreservoir, the deer mouse, Peromyscus maniculatus,and recently named Sin Nombre virus. Clinically, the disease has become known as the bantavirus pulmonary syndrome (HPS). Since May 1993, 44 fatal cases of HPS have been identified through clinicopathological review and immunobistochemical(IHC) testing of tissues from 273 patients who died of an unexplained noncardiogenic pulmonary edema. In 158 cases for which suitable specimens were available, serologicaltesting and/or reverse transcription-polymerase chain reaction (RT-PCR) amplification of extracted RNA was also performed. IHC, serological, and PCR results were concordant for virtually all HPS and non-HPS patients when more than one assay was performed. The prodromal ilness of HPS is similar to that of many other viral diseases. Consistent bematological features include thrombocytopenia, bemoconcentration, neutropbilic leukocytosis with a left shift, and reactivel lymphocytes. Pulmonary bistopatbological features were similar in most of the fatal HPS cases (40/44) and consisted of an interstitial pneumonitis with a variable mononuclear cell infiltrate, edema, and focal byaline membranes. In four cases, bowever, pulmonary features were significantly different and included diffuse alveolar damage and variable degrees of severe air space disorganization. IHC analysis showed widespread presence of bantaviral antigens in endothelial cells of the microvasculature, particularly in the lung. Hantaviral antigens were also observed within follicular dendritic cells, macrophages, and lymphocytes. Hantaviral inclusions were observed in endothelial cells of lungs by thinsection electron microscopy, and their identity was verified by immunogold labeling. Virus-like particles were seen in pulmonary endothelial cells and macropbages. HPS is

  14. Postmortem pulmonary CT in hypothermia.

    PubMed

    Schweitzer, Wolf; Thali, Michael; Giugni, Giannina; Winklhofer, Sebastian

    2014-12-01

    Fatal hypothermia has been associated with pulmonary edema. With postmortem full body computed tomography scanning (PMCT), the lungs can also be examined for CT attenuation. In fatal hypothermia cases low CT attenuation appeared to prevail in the lungs. We compared 14 cases of fatal hypothermia with an age-sex matched control group. Additionally, 4 cases of carbon monoxide (CO) poisoning were examined. Furthermore, 10 test cases were examined to test predictability based on PMCT. Two readers measured CT attenuation on four different axial slices across the lungs (blinded to case group and other reader's results). Hypothermia was associated with statistically significantly lower lung PMCT attenuation and lower lung weights than controls, and there was a dose-effect relationship at an environmental temperature cutoff of 2 °C. CO poisoning yielded low pulmonary attenuation but higher lung weights. General model based prediction yielded a 94% probability for fatal hypothermia deaths and a 21% probability for non-hypothermia deaths in the test group. Increased breathing rate is known to accompany both CO poisoning and hypothermia, so this could partly explain the low PMCT lung attenuation due to an oxygen dissociation curve left shift. A more marked distension in fatal hypothermia, compared to CO poisoning, indicates that further, possibly different mechanisms, are involved in these cases. Increased dead space and increased stiffness to deflation (but not inflation) appear to be effects of inhaling cold air (but not CO) that may explain the difference in low PMCT attenuation seen in hypothermia cases.

  15. Hantavirus pulmonary syndrome.

    PubMed

    Macneil, Adam; Nichol, Stuart T; Spiropoulou, Christina F

    2011-12-01

    Hantavirus pulmonary syndrome (HPS) is a severe disease characterized by a rapid onset of pulmonary edema followed by respiratory failure and cardiogenic shock. The HPS associated viruses are members of the genus Hantavirus, family Bunyaviridae. Hantaviruses have a worldwide distribution and are broadly split into the New World hantaviruses, which includes those causing HPS, and the Old World hantaviruses [including the prototype Hantaan virus (HTNV)], which are associated with a different disease, hemorrhagic fever with renal syndrome (HFRS). Sin Nombre virus (SNV) and Andes virus (ANDV) are the most common causes of HPS in North and South America, respectively. Case fatality of HPS is approximately 40%. Pathogenic New World hantaviruses infect the lung microvascular endothelium without causing any virus induced cytopathic effect. However, virus infection results in microvascular leakage, which is the hallmark of HPS. This article briefly reviews the knowledge on HPS-associated hantaviruses accumulated since their discovery, less than 20 years ago.

  16. Accuracy of point-of-care lung ultrasonography for the diagnosis of cardiogenic pulmonary edema in dogs and cats with acute dyspnea.

    PubMed

    Ward, Jessica L; Lisciandro, Gregory R; Keene, Bruce W; Tou, Sandra P; DeFrancesco, Teresa C

    2017-03-15

    OBJECTIVE To determine the accuracy of a point-of-care lung ultrasonography (LUS) protocol designed to diagnose cardiogenic pulmonary edema (CPE) in dyspneic dogs and cats. DESIGN Diagnostic test evaluation. ANIMALS 76 dogs and 24 cats evaluated for dyspnea. PROCEDURES Dogs and cats were evaluated by LUS; B lines were counted at 4 anatomic sites on each hemithorax. A site was scored as positive when > 3 B lines were identified. Animals with ≥ 2 positive sites identified on each hemithorax were considered positive for CPE. Medical records were evaluated to obtain a final diagnosis (reference standard) for calculation of the sensitivity and specificity of LUS and thoracic radiography for the diagnosis of CPE. RESULTS Dogs and cats with a final diagnosis of CPE had a higher number of positive LUS sites than did those with noncardiac causes of dyspnea. Overall sensitivity and specificity of LUS for the diagnosis of CPE were 84% and 74%, respectively, and these values were similar to those of thoracic radiography (85% and 87%, respectively). Use of LUS generally led to the misdiagnosis of CPE (ie, a false-positive result) in animals with diffuse interstitial or alveolar disease. Interobserver agreement on LUS results was high (κ > 0.85). CONCLUSIONS AND CLINICAL RELEVANCE LUS was useful for predicting CPE as the cause of dyspnea in dogs and cats, although this technique could not be used to differentiate CPE from other causes of diffuse interstitial or alveolar disease. Point-of-care LUS has promise as a diagnostic tool for dyspneic dogs and cats.

  17. Objective criteria for diagnosing high altitude pulmonary edema in acclimatized patients at altitudes between 2700 m and 3500 m

    PubMed Central

    Chawla, Anuj; Tripathi, K.K.

    2015-01-01

    Background The criteria used for diagnosing high altitude illnesses are largely based on Western literature. This study was undertaken to define objective, simple and reliable diagnostic criteria for high altitude pulmonary edema (HAPE) in Indian soldiers at altitudes between 2700 m and 3500 m. Methods Clinical data of 235 cases of HAPE that occurred between 2700 m and 3500 m were analysed. Receiver operator characteristic (ROC) curve analysis was used to select simple clinical parameters suitable for the diagnosis of HAPE at peripheral medical facilities. Cut-off values and their reliability for the diagnosis of HAPE were defined. Results HAPE occurred 2.8 ± 2.2 days after arrival at altitudes between 2700 m and 3500 m. Breathlessness, cough, chest discomfort and headache were the commonest symptoms. Low pulse oximetry (SPO2) values than normal for this altitude were seen in 89% of patients. ROC analysis of clinical parameters identified a heart rate more than 95 beats per minute (bpm), respiratory rate more than 21 per minute and SPO2 less than 86% while breathing ambient air at this altitude as diagnostic of HAPE. The sensitivity and specificity of these cut-offs was 0.66, 0.83 and 0.82 and 0.94, 0.95 and 0.93 respectively. Conclusion A heart rate of more than 95 bpm, respiratory rate more than 21 per minute and SPO2 less than 86% breathing room air in individuals complaining of breathlessness, cough, chest discomfort or headache within the first 5 days of arrival at altitudes between 2700 m and 3500 m is highly suggestive of HAPE. PMID:26663962

  18. Airway surface liquid volume expansion induces rapid changes in amiloride-sensitive Na+ transport across upper airway epithelium-Implications concerning the resolution of pulmonary edema

    PubMed Central

    Azizi, Fouad; Arredouani, Abdelilah; Mohammad, Ramzi M

    2015-01-01

    During airway inflammation, airway surface liquid volume (ASLV) expansion may result from the movement of plasma proteins and excess liquid into the airway lumen due to extravasation and elevation of subepithelial hydrostatic pressure. We previously demonstrated that elevation of submucosal hydrostatic pressure increases airway epithelium permeability resulting in ASLV expansion by 500 μL cm−2 h−1. Liquid reabsorption by healthy airway epithelium is regulated by active Na+ transport at a rate of 5 μL cm−2 h−1. Thus, during inflammation the airway epithelium may be submerged by a large volume of luminal liquid. Here, we have investigated the mechanism by which ASLV expansion alters active epithelial Na+ transport, and we have characterized the time course of the change. We used primary cultures of tracheal airway epithelium maintained under air interface (basal ASLV, depth is 7 ± 0.5 μm). To mimic airway flooding, ASLV was expanded to a depth of 5 mm. On switching from basal to expanded ASLV conditions, short-circuit current (Isc, a measure of total transepithelial active ion transport) declined by 90% with a half-time (t1/2) of 1 h. 24 h after the switch, there was no significant change in ATP concentration nor in the number of functional sodium pumps as revealed by [3H]-ouabain binding. However, amiloride-sensitive uptake of 22Na+ was reduced by 70% upon ASLV expansion. This process is reversible since after returning cells back to air interface, Isc recovered with a t1/2 of 5–10 h. These results may have important clinical implications concerning the development of Na+ channels activators and resolution of pulmonary edema. PMID:26333829

  19. Fatal Intoxication with Acetyl Fentanyl.

    PubMed

    Cunningham, Susan M; Haikal, Nabila A; Kraner, James C

    2016-01-01

    Among the new psychoactive substances encountered in forensic investigations is the opioid, acetyl fentanyl. The death of a 28-year-old man from recreational use of this compound is reported. The decedent was found in the bathroom of his residence with a tourniquet secured around his arm and a syringe nearby. Postmortem examination findings included marked pulmonary and cerebral edema and needle track marks. Toxicological analysis revealed acetyl fentanyl in subclavian blood, liver, vitreous fluid, and urine at concentrations of 235 ng/mL, 2400 ng/g, 131 ng/mL, and 234 ng/mL, respectively. Acetyl fentanyl was also detected in the accompanying syringe. Death was attributed to recreational acetyl fentanyl abuse, likely through intravenous administration. The blood acetyl fentanyl concentration is considerably higher than typically found in fatal fentanyl intoxications. Analysis of this case underscores the need for consideration of a wide range of compounds with potential opioid-agonist activity when investigating apparent recreational drug-related deaths. © 2015 American Academy of Forensic Sciences.

  20. Pathogenesis of Brain Edema and Investigation into Anti-Edema Drugs

    PubMed Central

    Michinaga, Shotaro; Koyama, Yutaka

    2015-01-01

    Brain edema is a potentially fatal pathological state that occurs after brain injuries such as stroke and head trauma. In the edematous brain, excess accumulation of extracellular fluid results in elevation of intracranial pressure, leading to impaired nerve function. Despite the seriousness of brain edema, only symptomatic treatments to remove edema fluid are currently available. Thus, the development of novel anti-edema drugs is required. The pathogenesis of brain edema is classified as vasogenic or cytotoxic edema. Vasogenic edema is defined as extracellular accumulation of fluid resulting from disruption of the blood-brain barrier (BBB) and extravasations of serum proteins, while cytotoxic edema is characterized by cell swelling caused by intracellular accumulation of fluid. Various experimental animal models are often used to investigate mechanisms underlying brain edema. Many soluble factors and functional molecules have been confirmed to induce BBB disruption or cell swelling and drugs targeted to these factors are expected to have anti-edema effects. In this review, we discuss the mechanisms and involvement of factors that induce brain edema formation, and the possibility of anti-edema drugs targeting them. PMID:25941935

  1. Elevated blood plasma levels of epinephrine, norepinephrine, tyrosine hydroxylase, TGFβ1, and TNFα associated with high-altitude pulmonary edema in an Indian population

    PubMed Central

    Pandey, Priyanka; Ali, Zahara; Mohammad, Ghulam; Pasha, M A Qadar

    2016-01-01

    Biomarkers are essential to unravel the locked pathophysiology of any disease. This study investigated the role of biomarkers and their interactions with each other and with the clinical parameters to study the physiology of high-altitude pulmonary edema (HAPE) in HAPE-patients (HAPE-p) against adapted highlanders (HLs) and healthy sojourners, HAPE-controls (HAPE-c). For this, seven circulatory biomarkers, namely, epinephrine, norepinephrine, tyrosine hydroxylase, transforming growth factor beta 1, tumor necrosis factor alpha (TNFα), platelet-derived growth factor beta beta, and C-reactive protein (CRP), were measured in blood plasma of the three study groups. All the subjects were recruited at ~3,500 m, and clinical features such as arterial oxygen saturation (SaO2), body mass index, and mean arterial pressure were measured. Increased levels of epinephrine, norepinephrine, tyrosine hydroxylase, transforming growth factor-beta 1, and TNFα were observed in HAPE-p against the healthy groups, HAPE-c, and HLs (P<0.0001). CRP levels were decreased in HAPE-p against HAPE-c and HLs (P<0.0001). There was no significant difference or very marginal difference in the levels of these biomarkers in HAPE-c and HLs (P>0.01). Correlation analysis revealed a negative correlation between epinephrine and norepinephrine (P=4.6E−06) in HAPE-p and positive correlation in HAPE-c (P=0.004) and HLs (P=9.78E−07). A positive correlation was observed between TNFα and CRP (P=0.004) in HAPE-p and a negative correlation in HAPE-c (P=4.6E−06). SaO2 correlated negatively with platelet-derived growth factor beta beta (HAPE-p; P=0.05), norepinephrine (P=0.01), and TNFα (P=0.005) and positively with CRP (HAPE-c; P=0.02) and norepinephrine (HLs; P=0.04). Body mass index correlated negatively with epinephrine (HAPE-p; P=0.001) and positively with norepinephrine and tyrosine hydroxylase in HAPE-c (P<0.05). Mean arterial pressure correlated positively with TNFα in HAPE-p and norepinephrine in

  2. Elevated blood plasma levels of epinephrine, norepinephrine, tyrosine hydroxylase, TGFβ1, and TNFα associated with high-altitude pulmonary edema in an Indian population.

    PubMed

    Pandey, Priyanka; Ali, Zahara; Mohammad, Ghulam; Pasha, M A Qadar

    2016-01-01

    Biomarkers are essential to unravel the locked pathophysiology of any disease. This study investigated the role of biomarkers and their interactions with each other and with the clinical parameters to study the physiology of high-altitude pulmonary edema (HAPE) in HAPE-patients (HAPE-p) against adapted highlanders (HLs) and healthy sojourners, HAPE-controls (HAPE-c). For this, seven circulatory biomarkers, namely, epinephrine, norepinephrine, tyrosine hydroxylase, transforming growth factor beta 1, tumor necrosis factor alpha (TNFα), platelet-derived growth factor beta beta, and C-reactive protein (CRP), were measured in blood plasma of the three study groups. All the subjects were recruited at ~3,500 m, and clinical features such as arterial oxygen saturation (SaO2), body mass index, and mean arterial pressure were measured. Increased levels of epinephrine, norepinephrine, tyrosine hydroxylase, transforming growth factor-beta 1, and TNFα were observed in HAPE-p against the healthy groups, HAPE-c, and HLs (P<0.0001). CRP levels were decreased in HAPE-p against HAPE-c and HLs (P<0.0001). There was no significant difference or very marginal difference in the levels of these biomarkers in HAPE-c and HLs (P>0.01). Correlation analysis revealed a negative correlation between epinephrine and norepinephrine (P=4.6E-06) in HAPE-p and positive correlation in HAPE-c (P=0.004) and HLs (P=9.78E-07). A positive correlation was observed between TNFα and CRP (P=0.004) in HAPE-p and a negative correlation in HAPE-c (P=4.6E-06). SaO2 correlated negatively with platelet-derived growth factor beta beta (HAPE-p; P=0.05), norepinephrine (P=0.01), and TNFα (P=0.005) and positively with CRP (HAPE-c; P=0.02) and norepinephrine (HLs; P=0.04). Body mass index correlated negatively with epinephrine (HAPE-p; P=0.001) and positively with norepinephrine and tyrosine hydroxylase in HAPE-c (P<0.05). Mean arterial pressure correlated positively with TNFα in HAPE-p and norepinephrine in HLs (P

  3. Agents Which Mediate Pulmonary Edema

    DTIC Science & Technology

    1990-12-01

    varying fractions of the LD50 and the plate was incubated at 370C for 4 hours. Control wells of endothelial cells plhs medium/ diluent were established. All...measured by incubation of the targets in culture medium/ diluent without challenge. Specific cytolysis was calculated by: Experimental Counts - Spontaneous...and is an important bactericidal mechanism employed by the AM. In Figures 3 and 4, production of SOA (as measured by ferricytochrome C reduction) by

  4. Proceedings of the Workshop on Acute Lung Injury and Pulmonary Edema Held in Aberdeen Proving Ground, Maryland on 4-5 May 1989

    DTIC Science & Technology

    1989-11-01

    to the 14 Moore Materials Presented cellularity of the perivascular inflammatory exudate. Acute alveolitis , first apparent at 24 hours, was...of alveoli. Fibrin and eosinophilic amorphous material (edema) were usually present in the inflamed alveoli. Subacute alveolitis was usually

  5. Diagnostic features in 10 naturally occurring cases of acute fatal canine leptospirosis.

    PubMed

    Rissi, Daniel R; Brown, Cathy A

    2014-11-01

    The current report describes the diagnostic features in 10 cases of acute fatal canine leptospirosis with minimal renal and hepatic changes that may present a diagnostic challenge for the pathologist. Most affected dogs were less than 6 months of age and had a biochemical profile consistent with hepatorenal dysfunction. Clinical signs consisted of vomiting, depression, icterus, dehydration, diarrhea, and anorexia. All dogs died or were humanely euthanized within 3-7 days after the onset of clinical disease. Necropsy findings included pulmonary edema with hemorrhages, icterus, renal and hepatic pallor and swelling, and gastric edema with hemorrhage. Despite severe azotemia, histological changes in the kidneys were subtle in all dogs, and included mild renal tubular simplification, with single-cell necrosis and attenuation, along with minimal interstitial lymphoplasmacytic inflammation, edema, and hemorrhage. Hepatic lesions included scattered hepatocellular single-cell necrosis and hepatocellular dissociation. Prominent extrarenal lesions typically associated with uremia including vascular fibrinoid necrosis in multiple organs, pulmonary mineralization with occasional fibrinosuppurative exudation, and gastric mineralization were also present. Postmortem diagnostic confirmation was based on the detection of leptospiral antigen on fresh renal samples by fluorescent antibody test and on the demonstration of intact spirochetes in sections of kidneys using immunohistochemical staining. Acute fatal canine leptospirosis occurred as a fulminant hepatorenal disease affecting mainly young dogs, and the diagnosis was dependent on the recognition of the subtle renal changes with confirmation via fluorescent antibody testing or immunohistochemical staining. © 2014 The Author(s).

  6. Fulminant Laryngeal-tracheobronchial-pulmonary Aspergillosis: A Rare and Fatal Complication in Allogeneic Hematopoietic Stem Cell Transplantation Recipients

    PubMed Central

    Tao, Tao; Zhang, Ying-Hui; Xue, Sheng-Li; Wu, De-Pei; Chen, Feng

    2017-01-01

    A 23-year-old man who had previously undergone allogeneic hematopoietic stem cell transplantation (allo-HSCT) for severe aplastic anemia was diagnosed with invasive laryngeal-tracheobronchial-pulmonary aspergillosis after presenting with a persistent dry cough at six months post-transplantation based on the findings of laryngoscopy and fiberoptic bronchoscopy. A fiberoptic bronchoscope was used to remove the obstructive material from the patient's airway and posaconazole plus caspofungin were administered to successfully to treat the patient. Our report suggests that laryngoscopy and fiberoptic bronchoscopy should be considered as alternative approaches to the diagnosis and treatment of allo-HSCT recipients with persistent respiratory symptoms when invasive laryngeal aspergillosis and invasive tracheobronchial aspergillosis are suspected. PMID:28154281

  7. A Fatal Hantavirus Pulmonary Syndrome Misdiagnosed as Dengue: An Investigation into the First Reported Case in Rio de Janeiro State, Brazil.

    PubMed

    de Oliveira, Renata Carvalho; Guterres, Alexandro; Teixeira, Bernardo Rodrigues; Fernandes, Jorlan; Júnior, João Marcos Penna; de Jesus Oliveira Júnior, Reynaldo; Pereira, Liana Strecht; Júnior, João Bosco; Meneguete, Patrícia Soares; Dias, Cristina Maria Giordano; Bonvicino, Cibele Rodrigues; D'Andrea, Paulo Sérgio; de Lemos, Elba Regina Sampaio

    2017-07-01

    We report the results of an investigation into a fatal case of hantavirus pulmonary syndrome (HPS) in Rio de Janeiro State, Brazil, where the disease had not been reported previous to 2015. Following the notification of an HPS case, serum samples were collected from the household members and work contacts of the HPS patient and tested for antibody to hantaviruses. Seroprevalence of 22% (10/45) was indicated for hantavirus out of 45 human samples tested. Blood and tissue samples were collected from 72 rodents during fieldwork to evaluate the prevalence of hantavirus infection, by using enzyme-linked immunosorbent assay IgG, and to characterize the rodent hantavirus reservoir(s), by reverse transcription polymerase chain reaction and sequencing. Antibody prevalence was 6.9%. The circulation of a single genotype, the Juquitiba hantavirus, carried by two rodent species, black-footed pigmy rice rat (Oligoryzomys nigripes) and cursor grass mouse (Akodon cursor), was shown by analysis of the nucleotide sequences of the S segment. Juquitiba hantavirus circulates in rodents of various species, but mainly in the black-footed pigmy rice rat. HPS is a newly recognized clinical entity in Rio de Janeiro State and should be considered in patients with febrile illness and acute respiratory distress.

  8. Reperfusion edema after thromboendarterectomy: radiographic patterns of disease.

    PubMed

    Miller, W T; Osiason, A W; Langlotz, C P; Palevsky, H I

    1998-07-01

    In patients with chronic pulmonary embolism, pulmonary thromboendarterectomy may result in a unique form of noncardiogenic pulmonary edema termed reperfusion edema. This report reviews the authors' experience after pulmonary thromboendarterectomy with particular emphasis on the radiographic manifestations of reperfusion edema. The clinical and radiographic record of 25 patients who underwent pulmonary thromboendarterectomy at the University of Pennsylvania from 1985 through 1995 were reviewed. The zonal distribution of radiographic opacity, time to maximal opacity, and the time to clearance of reperfusion edema were determined. The relationship of these radiographic manifestations to clinical severity of disease and clinical outcome was examined. Reperfusion edema, characterized by patchy bilateral perihilar alveolar opacities, occurred in all but one patient. There is a lower lung zone predominance of opacities, but in individual cases, striking unilateral or haphazard arrangements of opacities may be seen. In this small sample of patients, no association between preoperative pulmonary arterial pressures and radiographic appearance or clinical outcome was found. However, severity of radiographic opacities, as measured by the extent of involved lung, correlated with disease severity, as measured by time to extubation and time to discharge. Pneumonia, defined as a radiographic opacity that evolves discordantly with the reperfusion edema opacities, occurred in 20% of cases. Reperfusion edema is a common consequence of pulmonary thromboendarterectomy. The severity of radiographic manifestations and clinical severity of disease are related. This characteristically appears as perihilar alveolar opacities.

  9. Polymorphisms of the tissue inhibitor of metalloproteinase 3 gene are associated with resistance to high-altitude pulmonary edema (HAPE) in a Japanese population: a case control study using polymorphic microsatellite markers.

    PubMed

    Kobayashi, Nobumitsu; Hanaoka, Masayuki; Droma, Yunden; Ito, Michiko; Katsuyama, Yoshihiko; Kubo, Keishi; Ota, Masao

    2013-01-01

    High-altitude pulmonary edema (HAPE) is a hypoxia-induced, life-threatening, high permeability type of edema attributable to pulmonary capillary stress failure. Genome-wide association analysis is necessary to better understand how genetics influence the outcome of HAPE. DNA samples were collected from 53 subjects susceptible to HAPE (HAPE-s) and 67 elite Alpinists resistant to HAPE (HAPE-r). The genome scan was carried out using 400 polymorphic microsatellite markers throughout the whole genome in all subjects. In addition, six single nucleotide polymorphisms (SNPs) of the gene encoding the tissue inhibitor of metalloproteinase 3 (TIMP3) were genotyped by Taqman® SNP Genotyping Assays. The results were analyzed using case-control comparisons. Whole genome scanning revealed that allele frequencies in nine markers were statistically different between HAPE-s and HAPE-r subjects. The SNP genotyping of the TIMP3 gene revealed that the derived allele C of rs130293 was associated with resistance to HAPE [odds ratio (OR) = 0.21, P = 0.0012) and recessive inheritance of the phenotype of HAPE-s (P = 0.0012). A haplotype CAC carrying allele C of rs130293 was associated with resistance to HAPE. This genome-wide association study revealed several novel candidate genes associated with susceptibility or resistance to HAPE in a Japanese population. Among those, the minor allele C of rs130293 (C/T) in the TIMP3 gene was linked to resistance to HAPE; while, the ancestral allele T was associated with susceptibility to HAPE.

  10. FATAL EPISTAXIS

    PubMed Central

    Quinn, Francis Berchmans

    1961-01-01

    The instances in which nosebleed is potentially fatal are those in which there is a history of recent head injury, severe arteriosclerotic cardiovascular disease or an underlying vascular tumor in the nasal chambers. Fatal nasal bleeding has not been reported in children. An awareness on the part of the physician of the potentially fatal significance of his patient's nosebleed is the very best insurance against such an event. Intelligent history-taking, careful physical and x-ray examination, generous sedation, precise local cauterization and packing, estimation of hemoglobin mass and a search for bleeding and clotting disorders are the best weapons of the physician called to treat epistaxis. These procedures, coupled with adequate blood replacement and an informed attitude toward surgical interruption of the blood supply to the bleeding region should forestall death from fatal nosebleed. PMID:13738727

  11. Scintigraphy for Pulmonary Capillary Protein Leak

    DTIC Science & Technology

    1983-09-01

    det,,rmine the severity and duration of non- cardiogenic pulmonary edema (17). C. Approach to the Problem The anim-als were anesthetize,, intubated and...pulmonary lymphatics. If the leak exceeds the lymphatic capacity, which can increase flow by a factor of 20, pulmonary interstitial edema occurs. When...therefore, does not appear to cause permeability pulmonary edema in either the sheep or dog. The ARDS seen in patients following sclerotherapy of esophageal

  12. Fatal cocaine intoxication in a body packer.

    PubMed

    Brajković, Gordana; Babić, Gordana; Stosić, Jasna Jović; Tomasević, Gordana; Rancić, Dragana; Kilibarda, Vesna

    2016-02-01

    'Body packer' syndrome with severe intoxication or sudden death may happen in persons who smuggle drugs in their body cavities. In case of lethal outcome when carrying cocaine, it is important, but sometimes difficult to determine whether death was due to intoxication or due to other causes. Therefore, it is necessary not only to quantify cocaine and its metabolites in biological material, but also based on their distribution in body fluids and tissues to conclude whether it is acute intoxication. We described a well-documented case of fatal poisoning in a body packer and post mortem distribution of the drug in biological samples. A 26-year-old man was brought to hospital with no vital signs. Resuscitation measures started at once, but with no success. Autopsy revealed 66 packets of cocaine in his digestive tract, one of which was ruptured. Hyperemia of the most of all internal organs and pulmonary and brain edema were found. High concentrations of cocaine, its metabolites benzoylecgonine and ecgonine methyl ester, as well as cocaine adulteration levamisole were proven in the post mortem blood and tissues by liquid chromatography-mass spectrometry (LC-MC) method with selective-ion monitoring. The ratio of cocaine and its metabolites concentrations in the brain and blood obtained by LC-MS method can be used for forensic confirmation of acute intoxication with cocaine.

  13. Complete Heart Block with Diastolic Heart Failure and Pulmonary Edema Secondary to Enlarging Previously Diagnosed Thrombosed Aneurysm of Sinus of Valsalva in a Patient with History of Autosomal Dominant Polycystic Kidney Disease

    PubMed Central

    Eltawansy, Sherif Ali; Thomas, Maria Joana; Daniels, Jeffrey

    2015-01-01

    Autosomal dominant polycystic kidney disease (ADPKD) is associated with vascular aneurysms that can affect any part of the vascular tree, like ascending aorta or coronary arteries. Sinus of Valsalva is known as an anatomical dilation at the root of aorta above the aortic valve and very few cases show aneurysm at that site in patients with ADPKD. Sinus of Valsalva aneurysm (SVA) can present with rupture and acute heart failure and infective endocarditis or could be asymptomatic accidentally discovered during cardiac catheterization. We report a case of a 76-year-old male with a unique constellation of cardiovascular anomalies associated with ADPKD. Patient was previously diagnosed with aneurysms affecting ascending aorta, sinus of Valsalva, and coronary arteries. Several years later, he came with complete heart block which was discovered later to be secondary to enlargement of his previously diagnosed thrombosed SVA. His case was complicated with acute heart failure and pulmonary edema. Conclusion. Patients with ADPKD can present with extrarenal manifestations. In our case, aneurysm at sinus of Valsalva was progressively enlarging and presented with complete heart block. PMID:25861484

  14. Histochemical analyses and quantum dot imaging of microvascular blood flow with pulmonary edema in living mouse lungs by "in vivo cryotechnique".

    PubMed

    Saitoh, Yurika; Terada, Nobuo; Saitoh, Sei; Ohno, Nobuhiko; Jin, Takashi; Ohno, Shinichi

    2012-02-01

    Light microscopic imaging of blood vessels and distribution of serum proteins is essential to analyze hemodynamics in living animal lungs under normal respiration or respiratory diseases. In this study, to demonstrate dynamically changing morphology and immunohistochemical images of their living states, "in vivo cryotechnique" (IVCT) combined with freeze-substitution fixation was applied to anesthetized mouse lungs. By hematoxylin-eosin staining, morphological features, such as shapes of alveolar septum and sizes of alveolar lumen, reflected their respiratory conditions in vivo, and alveolar capillaries were filled with variously shaped erythrocytes. Albumin was usually immunolocalized in the capillaries, which was confirmed by double-immunostaining for aquaporin-1 of endothelium. To capture accurate time-courses of blood flow in peripheral pulmonary alveoli, glutathione-coated quantum dots (QDs) were injected into right ventricles, and then IVCT was performed at different time-points after the QD injection. QDs were localized in most arterioles and some alveolar capillaries at 1 s, and later in venules at 2 s, reflecting a typical blood flow direction in vivo. Three-dimensional QD images of microvascular networks were reconstructed by confocal laser scanning microscopy. It was also applied to lungs of acute pulmonary hypertension mouse model. Erythrocytes were crammed in blood vessels, and some serum components leaked into alveolar lumens, as confirmed by mouse albumin immunostaining. Some separated collagen fibers and connecting elastic fibers were still detected in edematous tunica adventitia near terminal bronchioles. Thus, IVCT combined with histochemical approaches enabled us to capture native images of dynamically changing structures and microvascular hemodynamics of living mouse lungs.

  15. Postmortem diagnosis of acute myocardial infarction in patients with acute respiratory failure - demographics, etiologic and pulmonary histologic analysis

    PubMed Central

    de Matos Soeiro, Alexandre; Ruppert, Aline D; Canzian, Mauro; Capelozzi, Vera L; Serrano, Carlos V

    2012-01-01

    OBJECTIVES: Acute respiratory failure is present in 5% of patients with acute myocardial infarction and is responsible for 20% to 30% of the fatal post-acute myocardial infarction. The role of inflammation associated with pulmonary edema as a cause of acute respiratory failure post-acute myocardial infarction remains to be determined. We aimed to describe the demographics, etiologic data and histological pulmonary findings obtained through autopsies of patients who died during the period from 1990 to 2008 due to acute respiratory failure with no diagnosis of acute myocardial infarction during life. METHODS: This study considers 4,223 autopsies of patients who died of acute respiratory failure that was not preceded by any particular diagnosis while they were alive. The diagnosis of acute myocardial infarction was given in 218 (4.63%) patients. The age, sex and major associated diseases were recorded for each patient. Pulmonary histopathology was categorized as follows: diffuse alveolar damage, pulmonary edema, alveolar hemorrhage and lymphoplasmacytic interstitial pneumonia. The odds ratio of acute myocardial infarction associated with specific histopathology was determined by logistic regression. RESULTS: In total, 147 men were included in the study. The mean age at the time of death was 64 years. Pulmonary histopathology revealed pulmonary edema as well as the presence of diffuse alveolar damage in 72.9% of patients. Bacterial bronchopneumonia was present in 11.9% of patients, systemic arterial hypertension in 10.1% and dilated cardiomyopathy in 6.9%. A multivariate analysis demonstrated a significant positive association between acute myocardial infarction with diffuse alveolar damage and pulmonary edema. CONCLUSIONS: For the first time, we demonstrated that in autopsies of patients with acute respiratory failure as the cause of death, 5% were diagnosed with acute myocardial infarction. Pulmonary histology revealed a significant inflammatory response, which has

  16. Scintigraphy for Pulmonary Capillary Protein Leak.

    DTIC Science & Technology

    1986-06-01

    duration of non- cardiogenic pulmonary edema (17). C. Approach to the Problem The animals were anesthetized, intubated and placed beneath a Pho-ajiui: I...capacity, which can increase flow 1w a K factor of 20, pulmonary interstitial edema occurs. ien the interstitial Compartment reaches a critical volume and...of sheep is the accepted model for the study of pulmonary permeability edema (18). It is, therefore, necessary to compare our scintigraphic technique

  17. Fatal acute pulmonary oedema and acute renal failure following multiple wasp/hornet (Vespa affinis) stings in Sri Lanka: two case reports.

    PubMed

    Kularatne, Keerthi; Kannangare, Thamara; Jayasena, Ajith; Jayasekera, Aruni; Waduge, Roshitha; Weerakoon, Kosala; Kularatne, Senanayake A M

    2014-06-13

    Vespa affinis is a hornet widely distributed in Sri Lanka and it is responsible for the highest number of deaths related to Hymenoptera stings. Apart from the early reactions, victims often die in hospital many hours later due to complications such as myocardial infarction and multiple organ failure. Increased microvascular permeability and acute pulmonary oedema as the primary pathology is less known in hornet envenoming. Here, we report clinical and postmortem findings of two Sinhalese patients, a 48-year-old husband and his 46-year-old wife, who both died following a massive attack by hornets 32 hours and 9 hours after the incidence respectively. At postmortem examination, both patients had pleural effusions, acute pulmonary oedema and red cell casts in their urine. Their coronary arteries and histology of myocardium were normal. Early recognition of acute pulmonary oedema in hornet stings is needed with implementation of crucial treatments to avert deaths.

  18. Fatal acute pulmonary oedema and acute renal failure following multiple wasp/hornet (Vespa affinis) stings in Sri Lanka: two case reports

    PubMed Central

    2014-01-01

    Introduction Vespa affinis is a hornet widely distributed in Sri Lanka and it is responsible for the highest number of deaths related to Hymenoptera stings. Apart from the early reactions, victims often die in hospital many hours later due to complications such as myocardial infarction and multiple organ failure. Increased microvascular permeability and acute pulmonary oedema as the primary pathology is less known in hornet envenoming. Case presentation Here, we report clinical and postmortem findings of two Sinhalese patients, a 48-year-old husband and his 46-year-old wife, who both died following a massive attack by hornets 32 hours and 9 hours after the incidence respectively. At postmortem examination, both patients had pleural effusions, acute pulmonary oedema and red cell casts in their urine. Their coronary arteries and histology of myocardium were normal. Conclusion Early recognition of acute pulmonary oedema in hornet stings is needed with implementation of crucial treatments to avert deaths. PMID:24929921

  19. Fatal foreign-body granulomatous pulmonary embolization due to microcrystalline cellulose in a patient receiving total parenteral nutrition: all crystals are not what they seem.

    PubMed

    Strickland, Sarah; Pena, Elena; Walker, Alfredo E

    2015-06-01

    Pulmonary foreign-body granulomatous embolization has been described secondary to crystal precipitation in total parenteral nutrition (TPN) as well as when pharmaceutical tablets are crushed and injected intravenously. Extensive granulomatous embolization may cause pulmonary hypertension and death due to acute cor pulmonale. We report the case of a 34-year old woman who had been receiving TPN post-operatively secondary to complications of a paraesophageal hernia repair. During and following receiving TPN, she experienced episodes of hypoxia, tachycardia, fever, and hypotension. Computed tomography scans of the thorax showed centrilobular nodules, tree-in-bud and ground-glass opacities, as well as findings of pulmonary hypertension. Following an episode of hypoxia she was found unresponsive and died despite resuscitative efforts. Microscopic examination of the lungs following post-mortem examination revealed occlusive granulomatous inflammation of the pulmonary arterial vasculature by crystalline material. The morphologic and histochemical patterns of the crystals were suggestive of microcrystalline cellulose, a finding that was confirmed by energy dispersive X-spectroscopy and infrared spectroscopy. Ancillary tests did not support that the crystalline material was the result of TPN precipitation. Foreign-body granulomatous embolization leading to acute core pulmonale may occur as a complication of both intravenous injection of oral medications as well as of TPN crystallization. The source of crystalline material may be difficult to discern based solely on morphological assessment or by histochemical staining. Ancillary studies such as energy dispersive X-spectroscopy or infrared spectroscopy should be performed to definitively discern the two entities.

  20. Side Effects: Edema

    Cancer.gov

    Edema, a condition in which fluid builds up in your body’s tissues, may be caused by chemotherapy, cancer, and conditions not related to cancer. Learn about signs of edema, including swelling in your feet, ankles, and legs. Learn how prevent swelling.

  1. LUNG EDEMA FOLLOWING BILATERAL VAGOTOMY

    PubMed Central

    Lorber, Victor

    1939-01-01

    1. Small animals (rat and guinea pig) vagotomized in the neck die within a period of hours, the lungs showing extensive congestion and edema. 2. Tracheotomy permits appreciably longer survival with minimal lung changes approximating those seen in the control animals. 3. Intrathoracic vagotomy (sparing the recurrent laryngeal nerve) on one side, and cervical vagotomy on the other, permits almost indefinite survival (guinea pig and rabbit), unless laryngeal paralysis from the unilateral denervation produces respiratory obstruction (rat, guinea pig, and rabbit). 4. Pulmonary edema following bilateral vagotomy probably results primarily from respiratory obstruction. It is suggested that circulatory failure may also be a factor of some importance. The rôle of vagotomy itself is considered in relationship to these two phenomena. 5. The reaction of smaller animals to bilateral vagotomy, with regard to lung changes, apparently differs in no way from that of the larger animals, but is less readily demonstrated because of the smaller diameters of the air passages. PMID:19870894

  2. Pulmonary pathology in pediatric cerebral malaria.

    PubMed

    Milner, Danny; Factor, Rachel; Whitten, Rich; Carr, Richard A; Kamiza, Steve; Pinkus, Geraldine; Molyneux, Malcolm; Taylor, Terrie

    2013-12-01

    Respiratory signs are common in African children where malaria is highly endemic, and thus, parsing the role of pulmonary pathology in illness is challenging. We examined the lungs of 100 children from an autopsy series in Blantyre, Malawi, many of whom death was attributed to Plasmodium falciparum malaria. Our aim was to describe the pathologic manifestations of fatal malaria; to understand the role of parasites, pigment, and macrophages; and to catalog comorbidities. From available patients, which included 55 patients with cerebral malaria and 45 controls, we obtained 4 cores of lung tissue for immunohistochemistry and morphological evaluation. We found that, in patients with cerebral malaria, large numbers of malaria parasites were present in pulmonary alveolar capillaries, together with extensive deposits of malaria pigment (hemozoin). The number of pulmonary macrophages in this vascular bed did not differ between patients with cerebral malaria, noncerebral malaria, and nonmalarial diagnoses. Comorbidities found in some cerebral malaria patients included pneumonia, pulmonary edema, hemorrhage, and systemic activation of coagulation. We conclude that the respiratory distress seen in patients with cerebral malaria does not appear to be anatomic in origin but that increasing malaria pigment is strongly associated with cerebral malaria at autopsy. © 2013.

  3. Pulmonary pathology in pediatric cerebral malaria

    PubMed Central

    Milner, Danny; Factor, Rachel; Whitten, Rich; Carr, Richard A.; Kamiza, Steve; Pinkus, Geraldine; Molyneux, Malcolm; Taylor, Terrie

    2013-01-01

    Respiratory signs are common in African children where malaria is highly endemic and, thus, parsing the role of pulmonary pathology in illness is challenging. We examined the lungs of 100 children from an autopsy series in Blantyre, Malawi, in many of whom death was attributed to P falciparum malaria. Our aim was to describe the pathological manifestations of fatal malaria, to understand the role of parasites, pigment, and macrophages, and to catalogue co-morbidities. From available patients which included 55 patients with cerebral malaria and 45 controls, we obtained 4 cores of lung tissue for immunohistochemistry and morphological evaluation. We found that in patients with cerebral malaria, large numbers of malaria parasites were present in pulmonary alveolar capillaries, together with extensive deposits of malaria pigment (hemozoin). The number of pulmonary macrophages in this vascular bed did not differ between patients with cerebral malaria, non-cerebral malaria and non-malarial diagnoses. Co-morbidities found in some cerebral malaria patients included pneumonia, pulmonary edema, hemorrhage, and systemic activation of coagulation. We conclude that the respiratory distress seen in patients with cerebral malaria does not appear to be anatomic in origin but that increasing malaria pigment is strongly associated with cerebral malaria at autopsy. PMID:24074535

  4. Pulmonary blastomycosis.

    PubMed

    Bariola, J Ryan; Vyas, Keyur S

    2011-12-01

    Blastomyces dermatitidis is acquired in almost all cases via inhalation, and pulmonary disease is the most frequent clinical manifestation of blastomycosis. Pulmonary disease can range from asymptomatic infection to rapidly severe and fatal disease. Most cases will present as pneumonia, either acute or chronic, or as a lung mass. In rare cases pulmonary blastomycosis is associated with the acute respiratory distress syndrome. Blastomycosis can present as isolated pulmonary disease or along with coexisting extrapulmonary disease that usually will involve the skin, bony structures, genitourinary tract, or central nervous system. Diagnosis is largely based on isolation of the organism via culture or visualization of the organism in clinical specimens. Detection of urinary Blastomyces antigen is a recent addition to diagnostic options. Itraconazole is the drug of choice for most forms of the disease; amphotericin B is reserved for the more severe forms. Newer azoles such as voriconazole and posaconazole have a limited role in the treatment of pulmonary blastomycosis. © Thieme Medical Publishers.

  5. Handbook of pulmonary emergencies

    SciTech Connect

    Spaquolo, S.V.; Medinger, A

    1986-01-01

    This book presents information on the following topics: clinical assessment of the patient with pulmonary disease; interpretation of arterial blood gases in the emergency patient; life-threatening pneumonia; extrapulmonic ventilatory failure; acute inhalation lung disease; pulmonary edema; near drowning; chest trauma; upper airway emergencies; chronic lung disease with acute respiratory decompensation; acute respiratory failure in the patient with chronic airflow obstruction; asthma; hemoptysis; embolic pulmonary disease; superior vena cava syndrome; catastrophic pleural disease; ventilatory assistance and its complications; and ventilator emergencies.

  6. Isolation and Characterization of Two Novel Bacteria Afipia cberi and Mesorhizobium hominis from Blood of a Patient Afflicted with Fatal Pulmonary Illness

    PubMed Central

    Lo, Shyh-Ching; Li, Bingjie; Hung, Guo-Chiuan; Lei, Haiyan; Li, Tianwei; Zhang, Jing; Nagamine, Kenjiro; Tsai, Shien; Zucker, Mark J.; Olesnicky, Ludmilla

    2013-01-01

    We recently isolated and discovered new Bradyrhizobiaceae microbes from the cryopreserved culture broth of blood samples from 3 patients with poorly defined illnesses using modified SP4 media and culture conditions coupled with genomic sequencing. Using a similar protocol, we studied a previously cryopreserved culture broth of blood sample from a patient who had succumbed to an acute onset of fulminant pulmonary illness. We report that two phases of microbial growth were observed in the re-initiated culture. Biochemical and genomic characterization revealed microbes isolated from the first phase of growth were new Afipia species of Bradyrhizobiaceae, tentatively named A. cberi with a ~ 5 MB chromosome that was different from those of all previously known Afipia microbes including the newly discovered A. septicemium. The microbes isolated from the second phase of growth were prominent sugar assimilators, novel Phyllobacteriaceae, phylogenetically most closely related to Mesorhizobium and tentatively named M. hominis with a ~ 5.5 MB chromosome. All A. cberi isolates carry a circular ~ 140 KB plasmid. Some M. hominis isolates possess a circular ~ 412 KB plasmid that can be lost in prolonged culture or passage. No antibiotics resistant genes could be identified in both of the A. cberi and M. hominis plasmids. Antibiotic susceptibility studies using broth culture systems revealed isolates of A. cberi could be sensitive to some antibiotics, but all isolates of M. hominis were resistant to essentially all tested antibiotics. However, the cell-free antibiotics susceptibility test results may not be applicable to clinical treatment against the microbes that are known to be capable of intracellular growth. It remains to be determined if the 2 previously unknown Rhizobiales were indeed pathogenic and played a role in the pulmonary disease process in this patient. Specific probes and methods will be developed to re-examine the diseased lungs from patient's autopsy. PMID

  7. Diabetic macular edema.

    PubMed

    Stefánsson, Einar

    2009-07-01

    A variety of treatment options are available for the treatment of diabetic macular edema. They include laser photocoagulation, anti-VEGF drugs, intravitreal steroids, and vitrectomy with or without release of vitreoretinal traction. A full understanding of the physiological mechanisms of these treatment modalities allows sensible combination of treatment options. Retinal photocoagulation has repeatedly been shown to improve retinal oxygenation, as does vitrectomy. Oxygen naturally reduces VEGF production and thereby decreases leakage of plasma proteins from capillaries into the tissue. In addition, vitrectomy allows faster clearance of cytokines, such as VEGF, from the retina into the vitreous cavity. The VEGF-lowering effect of photocoagulation and vitrectomy can be augmented with anti-VEGF drugs and corticosteroids reduce the effect of VEGF on capillary permeability. Starling's law explains vasogenic edema, which is controlled by osmotic and hydrostatic gradients between vessel and tissue. It explains how VEGF-induced vascular permeability causes plasma protein to leak into the tissue interstitial space, thus decreasing the osmotic pressure gradient between vessel and tissue, resulting in water accumulation, i.e. edema. This is reversed by reducing VEGF production, which is achieved with laser treatment; or by removing VEGF with antibodies or vitrectomy; or by reducing the permeability effect with steroids. At the same time, Starling's law takes into account hemodynamic changes that affect the hydrostatic gradient. High arterial blood pressure and hypoxic vasodilatation increase the hydrostatic pressure in the microcirculation, which increases water flux from vessel to tissue and induce edema. Treatment of arterial hypertension or reversal of retinal hypoxia with laser reverses this pathophysiology and reduces edema. Newton's third law explains, that vitreoretinal traction decreases hydrostatic tissue pressure in the retina, increases the pressure gradient

  8. Critical Care Management of Cerebral Edema in Brain Tumors.

    PubMed

    Esquenazi, Yoshua; Lo, Victor P; Lee, Kiwon

    2017-01-01

    Cerebral edema associated with brain tumors is extremely common and can occur in both primary and metastatic tumors. The edema surrounding brain tumors results from leakage of plasma across the vessel wall into the parenchyma secondary to disruption of the blood-brain barrier. The clinical signs of brain tumor edema depend on the location of the tumor as well as the extent of the edema, which often exceeds the mass effect induced by the tumor itself. Uncontrolled cerebral edema may result in increased intracranial pressure and acute herniation syndromes that can result in permanent neurological dysfunction and potentially fatal herniation. Treatment strategies for elevated intracranial pressure consist of general measures, medical interventions, and surgery. Alhough the definitive treatment for the edema may ultimately be surgical resection of the tumor, the impact of the critical care management cannot be underestimated and thus patients must be vigilantly monitored in the intensive care unit. In this review, we discuss the pathology, pathophysiology, and clinical features of patients presenting with cerebral edema. Imaging findings and treatment modalities used in the intensive care unit are also discussed.

  9. A Fatal Case of Pentedrone and α-Pyrrolidinovalerophenone Poisoning.

    PubMed

    Sykutera, Marzena; Cychowska, Magdalena; Bloch-Boguslawska, Elżbieta

    2015-05-01

    We report a fatal case of combined α-pyrrolidinovalerophenone (α-PVP) and 2-(methylamino)-1-phenylpentan-1-one (pentedrone) poisoning. A 28-year-old man was taken to hospital in asystole. Despite resuscitation efforts over 30 min, he died. The forensic autopsy showed pulmonary edema and moderately advanced atherosclerotic lesions of the arteries. Microscopic observation revealed chronic changes in the heart. Confirmation of the presence of pentedrone, α-PVP, and its metabolite 1-phenyl-2-(pyrrolidin-1-yl)pentan-1-ol (OH-α-PVP) in tissues and fluids were achieved using gas chromatography-mass spectrometry analysis after liquid-liquid extraction. A quantitative validated liquid chromatography-mass spectrometry method was used to determine the concentrations of the above designer drugs in postmortem samples. Pentedrone, α-PVP, and OH-α-PVP concentrations were 8,794, 901 and 185 ng/mL in whole blood, respectively; 100,044, 2,610 and 2,264 ng/g in the liver, respectively; 22,102, 462 and 294 ng/g in the kidney, respectively; 13,248, 120 and 91 ng/g in the brain, respectively and 500,534, 4,190 and 47 ng/g in the stomach contents, respectively. This is the first known reported death attributed to the combined use of α-PVP and pentedrone. Additionally, this article is the first to report the distribution of pentedrone in postmortem human samples.

  10. [Secondary prophylaxis of venous thromboembolism: analysis of 49 fatal cases].

    PubMed

    Wawrzyńska, L; Hajduk, B; Vertun-Baranowska, B; Kober, J; Filipecki, S

    1998-01-01

    The analysis of 49 fatal cases of venous thromboembolism--VTE (15% of total ambulatory patients number during long observation was performed. The advanced age of patients, multiple risk factors, underlying circulatory and respiratory tract diseases, malignancies, previous episodes of VTE especially with secondary pulmonary hypertension were the most important factors determining fatal prognoses in those patients.

  11. [Limb edema and lymphoscintigraphy].

    PubMed

    Bourgeois, P; Munck, D; Belgrado, J P; Leduc, O; Leduc, A

    2003-02-01

    Lymphoscintigraphic investigations represent techniques of nuclear medicine very contributive for the management and treatment of the limb edemas, either primary or secundary. Their principle is presented and methodologies proposed in the literature are reviewed. Their diagnostic contributions are detailed. The sensitivities and specificities of several protocols of investigation are reported. Some limitations of these examinations are analyzed and discussed. Clinical indications for their use are proposed and their interest with regard to the various treatments that can be applied to these limb edemas is discussed.

  12. Pulmonary Artery Sarcoma - Multimodality Imaging.

    PubMed

    Jeong, Nari; Seol, Sang-Hoon; Kim, Il Hwan; Kim, Ji Yeon

    2016-01-01

    Pulmonary artery sarcoma (PAS) is a rare and fatal disease. PAS can often be misdiagnosed as pulmonary thromboembolism. Moreover, the correct diagnosis is frequently delayed due to nonspecific signs and symptoms. The prognosis of patients with PAS is poor. We report a case of a woman with a primary PAS who was initially diagnosed with pulmonary thromboembolism.

  13. Pulmonary Artery Sarcoma - Multimodality Imaging

    PubMed Central

    Jeong, Nari; Seol, Sang-Hoon; Kim, Il Hwan; Kim, Ji Yeon

    2016-01-01

    Pulmonary artery sarcoma (PAS) is a rare and fatal disease. PAS can often be misdiagnosed as pulmonary thromboembolism. Moreover, the correct diagnosis is frequently delayed due to nonspecific signs and symptoms. The prognosis of patients with PAS is poor. We report a case of a woman with a primary PAS who was initially diagnosed with pulmonary thromboembolism. PMID:27833785

  14. Latest advances in edema

    NASA Technical Reports Server (NTRS)

    Villavicencio, J. L.; Hargens, A. R.; Pikoulicz, E.

    1996-01-01

    Basic concepts in the physiopathology of edema are reviewed. The mechanisms of fluid exchange across the capillary endothelium are explained. Interstitial flow and lymph formation are examined. Clinical disorders of tissue and lymphatic transport, microcirculatory derangements in venous disorders, protein disorders, and lymphatic system disorders are explored. Techniques for investigational imaging of the lymphatic system are explained.

  15. A fatal case of n-butane poisoning after inhaling anti-perspiration aerosol deodorant.

    PubMed

    Ago, Mihoko; Ago, Kazutoshi; Ogata, Mamoru

    2002-06-01

    We report a case of sudden death due to n-butane poisoning after the inhalation of anti-perspiration aerosol deodorant. The deceased was a 15-year-old boy who was found unresponsive on the road, and was pronounced dead after 1.25h. A spray can of anti-perspiration deodorant and vinyl bags were found in a thicket near the scene. An autopsy revealed pulmonary edema, cerebral edema and congestion of the organs. Using qualitative gas chromatography/mass spectrometry, the existence of n-butane was ascertained. The concentration of n-butane (in microl/ml or microl/g) was estimated to be 15.3 in the blood, 13.3 in the brain, 26.6 in the liver, 7.5 in the lung, and 13.6 in the kidney. These n-butane levels in the blood and in the tissues were higher than those of previous reports of death associated with n-butane inhalation. We concluded that the cause of death was n-butane poisoning and presumed that n-butane in the can of anti-perspiration aerosol deodorant induced fatal cardiac arrhythmia.

  16. Fatality due to gamma-hydroxybutyric acid (GHB) and heroin intoxication.

    PubMed

    Ferrara, S D; Tedeschi, L; Frison, G; Rossi, A

    1995-05-01

    The first case of fatal intoxication due to ingestion of gamma-hydroxybutyric acid (GHB) and intravenous use of heroin is reported. A 42-year-old man, known to have been a heroin addict and to have taken other psychoactive substances, who had been in treatment with GHB for several months, was found dead. Anatomohistopathologic examination showed generalized visceral congestion, edema and pulmonary anthracosis, chronic bronchitis and chronic active hepatitis. Toxicological findings included fluid and tissue distributions of GHB, morphine and 6-monoacetylmorphine. GHB and morphine concentrations were respectively 11.5 and 0.77 micrograms/mL (blood), 84.3 and 0.3 micrograms/mL (vitreous humor), 258.3 and 1.35 micrograms/mL (urine), 57.0 and 14.3 micrograms/mL (bile), 40.0 and 0.43 micrograms/g (brain), 43.0 and 0.60 micrograms/g (liver), 47.0 and 0.68 micrograms/g (kidney). Blood and urine levels of 6-monoacetylmorphine were 28.5 and 12.1 ng/mL respectively. The presumed mechanism of action and pharmacokinetics of GHB are briefly reviewed, with reference to its therapeutic use and to reports of non-fatal GHB intoxication.

  17. Transient Idiopathic Primary Penoscrotal Edema

    PubMed Central

    Namir, Sody A; Trattner, Akiva

    2013-01-01

    We present the case of a male born prematurely at 32 weeks gestation by cesarean section following overt symptoms of maternal preeclampsia. He developed severe penoscrotal edema anew one month from birth. No remarkable exposure or trauma was identified. This unexplained swelling remained uniform till 4 months of age, while the penile edema resolved spontaneously. A small benign hydrocele remained unchanged, since onset of the edema and continued after the edema subsided. This is the first report of persistent, but transient penoscrotal edema resolving in a 3 months course, without any apparent explanation, a possible pathogenetic mechanism was suggested. PMID:24082210

  18. Mechanics of the left ventricular myocardial interstitium: effects of acute and chronic myocardial edema.

    PubMed

    Desai, Ketaki V; Laine, Glen A; Stewart, Randolph H; Cox, Charles S; Quick, Christopher M; Allen, Steven J; Fischer, Uwe M

    2008-06-01

    Myocardial interstitial edema forms as a result of several disease states and clinical interventions. Acute myocardial interstitial edema is associated with compromised systolic and diastolic cardiac function and increased stiffness of the left ventricular chamber. Formation of chronic myocardial interstitial edema results in deposition of interstitial collagen, which causes interstitial fibrosis. To assess the effect of myocardial interstitial edema on the mechanical properties of the left ventricle and the myocardial interstitium, we induced acute and chronic interstitial edema in dogs. Acute myocardial edema was generated by coronary sinus pressure elevation, while chronic myocardial edema was generated by chronic pulmonary artery banding. The pressure-volume relationships of the left ventricular myocardial interstitium and left ventricular chamber for control animals were compared with acutely and chronically edematous animals. Collagen content of nonedematous and chronically edematous animals was also compared. Generating acute myocardial interstitial edema resulted in decreased left ventricular chamber compliance compared with nonedematous animals. With chronic edema, the primary form of collagen changed from type I to III. Left ventricular chamber compliance in animals made chronically edematous was significantly higher than nonedematous animals. The change in primary collagen type secondary to chronic left ventricular myocardial interstitial edema provides direct evidence for structural remodeling. The resulting functional adaptation allows the chronically edematous heart to maintain left ventricular chamber compliance when challenged with acute edema, thus preserving cardiac function over a wide range of interstitial fluid pressures.

  19. Pulmonary hypertension

    MedlinePlus

    Pulmonary arterial hypertension; Sporadic primary pulmonary hypertension; Familial primary pulmonary hypertension; Idiopathic pulmonary arterial hypertension; Primary pulmonary hypertension; PPH; Secondary pulmonary ...

  20. Fatal pulmonary hemorrhage after taking anticoagulation medication.

    PubMed

    Hammar, Samuel P

    2015-01-01

    We describe a 64-year-old man with extensive diffuse acute lung hemorrhage, presumably as a result of anticoagulation therapy. We evaluated reports in the literature concerning acute exacerbation (acute lung injury of unknown cause) in UIP and other forms of fibrotic interstitial pneumonias. We also evaluated autopsy tissue in this case in order to determine the cause of death in this 64-year-old man, who was initially thought to have an asbestos-related disease. Based on the autopsy findings, this man died as a result of anticoagulation therapy; specifically, the use of Xarelto(®) (rivaroxaban).

  1. Fatal pulmonary hemorrhage after taking anticoagulation medication

    PubMed Central

    Hammar, Samuel P.

    2015-01-01

    We describe a 64-year-old man with extensive diffuse acute lung hemorrhage, presumably as a result of anticoagulation therapy. We evaluated reports in the literature concerning acute exacerbation (acute lung injury of unknown cause) in UIP and other forms of fibrotic interstitial pneumonias. We also evaluated autopsy tissue in this case in order to determine the cause of death in this 64-year-old man, who was initially thought to have an asbestos-related disease. Based on the autopsy findings, this man died as a result of anticoagulation therapy; specifically, the use of Xarelto® (rivaroxaban). PMID:26236607

  2. Diabetic Macular Edema

    NASA Astrophysics Data System (ADS)

    Lobo, Conceição; Pires, Isabel; Cunha-Vaz, José

    The optical coherence tomography (OCT), a noninvasive and noncontact diagnostic method, was introduced in 1995 for imaging macular diseases. In diabetic macular edema (DME), OCT scans show hyporeflectivity, due to intraretinal and/or subretinal fluid accumulation, related to inner and/or outer blood-retinal barrier breakdown. OCT tomograms may also reveal the presence of hard exudates, as hyperreflective spots with a shadow, in the outer retinal layers, among others. In conclusion, OCT is a particularly valuable diagnostic tool in DME, helpful both in the diagnosis and follow-up procedure.

  3. Postoperative Acute Pulmonary Embolism Following Pulmonary Resections.

    PubMed

    Shonyela, Felix Samuel; Yang, Shuangqiang; Liu, Bo; Jiao, Jia

    2015-01-01

    Postoperative acute pulmonary embolism after pulmonary resections is highly fatal complication. Many literatures have documented cancer to be the highest risk factor for acute pulmonary embolism after pulmonary resections. Early diagnosis of acute pulmonary embolism is highly recommended and computed tomographic pulmonary angiography is the gold standard in diagnosis of acute pulmonary embolism. Anticoagulants and thrombolytic therapy have shown a great success in treatment of acute pulmonary embolism. Surgical therapies (embolectomy and inferior vena cava filter replacement) proved to be lifesaving but many literatures favored medical therapy as the first choice. Prophylaxis pre and post operation is highly recommended, because there were statistical significant results in different studies which supported the use of prophylaxis in prevention of acute pulmonary embolism. Having reviewed satisfactory number of literatures, it is suggested that thoroughly preoperative assessment of patient conditions, determining their risk factors complicating to pulmonary embolism and the use of appropriate prophylaxis measures are the key options to the successful minimization or eradication of acute pulmonary embolism after lung resections.

  4. Pulmonary Aspects of Exercise and Sports

    PubMed Central

    Bove, Alfred A.

    2016-01-01

    Although the lungs are a critical component of exercise performance, their response to exercise and other environmental stresses is often overlooked when evaluating pulmonary performance during high workloads. Exercise can produce capillary leakage, particularly when left atrial pressure increases related to left ventricular (LV) systolic or diastolic failure. Diastolic LV dysfunction that results in elevated left atrial pressure during exercise is particularly likely to result in pulmonary edema and capillary hemorrhage. Data from race horses, endurance athletes, and triathletes support the concept that the lungs can react to exercise and immersion stress with pulmonary edema and pulmonary hemorrhage. Immersion in water by swimmers and divers can also increase stress on pulmonary capillaries and result in pulmonary edema. Swimming-induced pulmonary edema and immersion pulmonary edema in scuba divers are well-documented events caused by the fluid shifts that occur with immersion, elevated pulmonary venous pressure during extreme exercise, and negative alveolar pressure due to inhalation resistance. Prevention strategies include avoiding extreme exercise, avoiding over hydration, and assuring that inspiratory resistance is minimized. PMID:27486491

  5. Pulmonary Aspects of Exercise and Sports.

    PubMed

    Bove, Alfred A

    2016-01-01

    Although the lungs are a critical component of exercise performance, their response to exercise and other environmental stresses is often overlooked when evaluating pulmonary performance during high workloads. Exercise can produce capillary leakage, particularly when left atrial pressure increases related to left ventricular (LV) systolic or diastolic failure. Diastolic LV dysfunction that results in elevated left atrial pressure during exercise is particularly likely to result in pulmonary edema and capillary hemorrhage. Data from race horses, endurance athletes, and triathletes support the concept that the lungs can react to exercise and immersion stress with pulmonary edema and pulmonary hemorrhage. Immersion in water by swimmers and divers can also increase stress on pulmonary capillaries and result in pulmonary edema. Swimming-induced pulmonary edema and immersion pulmonary edema in scuba divers are well-documented events caused by the fluid shifts that occur with immersion, elevated pulmonary venous pressure during extreme exercise, and negative alveolar pressure due to inhalation resistance. Prevention strategies include avoiding extreme exercise, avoiding over hydration, and assuring that inspiratory resistance is minimized.

  6. Death by band-aid: fatal misuse of transdermal fentanyl patch.

    PubMed

    Bakovic, Marija; Nestic, Marina; Mayer, Davor

    2015-11-01

    We present a case of fatal intoxication by the application of a transdermal fentanyl patch upon a superficial bleeding abrasion of a 2-year-old girl. The grandmother discovered the body of the child in bed at approximately 7 a.m. External examination revealed a properly developed, nourished, and hydrated child, with some vomit in the nostrils and inside the mouth. There was no evidence of trauma besides small contusions and abrasions on the knees, with a patch placed over the largest abrasion. Closer inspection revealed that this was transdermal fentanyl patch. Internal examination and microscopic analysis revealed regurgitation of stomach content, cerebral and pulmonary edema, and liver congestion. Toxicology analysis revealed trace levels of fentanyl in the blood just above the limit of detection (2 ng/mL), while concentrations in the urine, liver, and kidney were approximately 102, 28, and 10 ng/mL, respectively. Investigation discovered that the child injured her knee while playing the evening before. The grandmother applied the patch to cover the injury, unaware that she had used a fentanyl transdermal patch instead of simple band-aid. Although fatal intoxications are uncommon among young children in high-income countries, it is of major interest to raise awareness of such events especially since a great majority of these are preventable. The presented case points at the need for more thorough education of users and more strict rules in prescribing and handling of this potent medicine. As well, we find this case to be a useful contribution to the evaluation of postmortem fentanyl concentrations in fatal intoxication in a small child.

  7. Molecular pathophysiology of cerebral edema

    PubMed Central

    Gerzanich, Volodymyr; Simard, J Marc

    2015-01-01

    Advancements in molecular biology have led to a greater understanding of the individual proteins responsible for generating cerebral edema. In large part, the study of cerebral edema is the study of maladaptive ion transport. Following acute CNS injury, cells of the neurovascular unit, particularly brain endothelial cells and astrocytes, undergo a program of pre- and post-transcriptional changes in the activity of ion channels and transporters. These changes can result in maladaptive ion transport and the generation of abnormal osmotic forces that, ultimately, manifest as cerebral edema. This review discusses past models and current knowledge regarding the molecular and cellular pathophysiology of cerebral edema. PMID:26661240

  8. Molecular pathophysiology of cerebral edema.

    PubMed

    Stokum, Jesse A; Gerzanich, Volodymyr; Simard, J Marc

    2016-03-01

    Advancements in molecular biology have led to a greater understanding of the individual proteins responsible for generating cerebral edema. In large part, the study of cerebral edema is the study of maladaptive ion transport. Following acute CNS injury, cells of the neurovascular unit, particularly brain endothelial cells and astrocytes, undergo a program of pre- and post-transcriptional changes in the activity of ion channels and transporters. These changes can result in maladaptive ion transport and the generation of abnormal osmotic forces that, ultimately, manifest as cerebral edema. This review discusses past models and current knowledge regarding the molecular and cellular pathophysiology of cerebral edema.

  9. [Pathopshysiological mechanisms in macular edema].

    PubMed

    Turlea, Cristian; Zolog, Ileana; Blăjan, Codruta; Roşca, C; Turlea, Magdalena; Munteanu, Mihnea; Boruga, Ovidiu

    2014-01-01

    The treatment of diabetic macular edema has known a fast development in the last 5 years where the transition from laser monotherapy to intravitreal pharmacotherapy is becoming standard practice. Intravitreal injections therapy is in a continuous development with promising positive results. The use of intratvitreal devices in the treatment of macular edema of vascular cause has become a viable alternative also in treating diabetic macular edema. Several clinical studies have revealed the superiority of intravitreal treatment versus laser monotherapy. This article is evaluating and reviewing present and future treatments used to combat diabetic macular edema. [corrected].

  10. Occupational injury fatalities--1994.

    PubMed

    Toscano, G; Jack, T

    1996-01-01

    Factory workers caught in machinery and construction workers falling or struck by huge beams are images that typically come to mind when considering serious hazards in the workplace. But these types of events account for only a small portion of job-related fatalities each year. Transportation-related fatalities, along with assaults and violent acts during work, made up almost two-thirds of the 6,588 fatal work injuries recorded in 1994. The majority of job-related fatal work events occurred on the streets and highways and in public buildings and in areas such as grocery stores and parking lots. Today the most deadly jobs are found in outdoor occupations such as fishing and timber cutting. In fact, in all 10 jobs studied that have high fatality rates, most workers are affected by severe weather conditions while driving on highways, performing farm chores and working at construction sites. Highway crashes are the primary cause of trucker fatalities; falls are the leading cause of death for roofers, construction laborers and structural metal workers, while tractor rollovers account for a third of farm worker fatalities. Another deadly contributing factor for some workers is homicide, which accounted for 16 percent of job-related fatalities in 1994. Workers most at risk are those who work alone, work late at night and handle varying sums of money. Taxicab drivers are the most susceptible and have a work injury fatality rate nine times higher than the national rate of 5 deaths per 100,000 workers. Others at high risk of homicide include gas station cashiers, grocery store employees and workers in retail eating and drinking establishments. Although the risk of a fatal injury at work varies greatly by occupation and industry, no one is immune. For prevention, workers and employers need to know what jobs are risky, what equipment is dangerous and what activities are hazardous. They also should understand that a fatal incident can happen to anyone.

  11. Fatalities in Swedish skydiving.

    PubMed

    Westman, Anton; Björnstig, Ulf

    2005-11-01

    Exact risk patterns in skydiving fatalities are not well known, but incomplete world injury data indicate that many are preventable. A comprehensive national material for Sweden of 37 skydiving fatalities 1964-2003 were reviewed to identify risk factors. In relation to jump volume, the period 1994-2003 had a fatality rate 11 times lower than 1964-1973. Student skydivers had the highest risk of fatal outcome, often caused by instability in freefall leading to unstable parachute activation with subsequent line entanglement, or parachute activation failure. Unintentional water landings also contributed to student fatality, with life jacket malfunctions, neglect to use life jackets, and automatic reserve parachute activation devices activated by water as aggravating factors. One-third of all fatalities had an inflated and operational parachute at some point prior to injury. A drastic worldwide increase in fatal landing incidents with fast wing parachutes during the 1990s did not occur in Sweden. Every fourth fatality caused by rapid deceleration against ground or water survived impact and died during transports or in hospitals. Rescue units and health care providers can improve management of skydiving incidents from knowledge about the incident and injury mechanisms we have described, and the skydiving community can target risk factors in preventive safety work.

  12. Brain Edema After Ischaemic Stroke

    PubMed Central

    Dostovic, Zikrija; Dostovic, Ernestina; Smajlovic, Dzevdet; Ibrahimagic, Omer C.; Avdic, Leila

    2016-01-01

    Objectives: To determine the incidence of brain edema after ischaemic stroke and its impact on the outcome of patients in the acute phase of ischaemic stroke. Patients and Methods: We retrospectively analyzed 114 patients. Ischaemic stroke and brain edema are verified by computed tomography. The severity of stroke was determined by National Institutes of Health Stroke Scale. Laboratory findings were made during the first four days of hospitalization, and complications were verified by clinical examination and additional tests. Results: In 9 (7.9%) patients developed brain edema. Pneumonia was the most common complication (12.3%). Brain edema had a higher incidence in women, patients with hypertension and elevated serum creatinine values, and patients who are suffering from diabetes. There was no significant correlation between brain edema and survival in patients after acute ischaemic stroke. Patients with brain edema had a significantly higher degree of neurological deficit as at admission, and at discharge (p = 0.04, p = 0.004). Conclusion: The cerebral edema is common after acute ischaemic stroke and no effect on survival in the acute phase. The existence of brain edema in acute ischaemic stroke significantly influence the degree of neurological deficit. PMID:27994292

  13. The Impact of Moderate-Altitude Staging on Pulmonary Arterial Hemodynamics after Ascent to High Altitude

    DTIC Science & Technology

    2010-01-01

    et al., 1956; Sime et al., 1974). The magnitude of the PAP in- crease plays an important role in the development of high altitude pulmonary edema ...implications for travelers to high altitude. High altitude pulmonary edema (HAPE) is an important cause of high altitude morbidity and mortality, and...P., and Oelz O. (1991). Prevention of high-altitude pulmonary edema by nifedipine. N. Engl. J. Med. 325:1284–1289. Beidleman B.A., Fulco C.S., Muza

  14. PULMONARY CIRCULATION AT EXERCISE

    PubMed Central

    NAEIJE, R; CHESLER, N

    2012-01-01

    The pulmonary circulation is a high flow and low pressure circuit, with an average resistance of 1 mmHg.min.L−1 in young adults, increasing to 2.5 mmHg.min.L−1 over 4–6 decades of life. Pulmonary vascular mechanics at exercise are best described by distensible models. Exercise does not appear to affect the time constant of the pulmonary circulation or the longitudinal distribution of resistances. Very high flows are associated with high capillary pressures, up to a 20–25 mmHg threshold associated with interstitial lung edema and altered ventilation/perfusion relationships. Pulmonary artery pressures of 40–50 mmHg, which can be achieved at maximal exercise, may correspond to the extreme of tolerable right ventricular afterload. Distension of capillaries that decrease resistance may be of adaptative value during exercise, but this is limited by hypoxemia from altered diffusion/perfusion relationships. Exercise in hypoxia is associated with higher pulmonary vascular pressures and lower maximal cardiac output, with increased likelihood of right ventricular function limitation and altered gas exchange by interstitial lung edema. Pharmacological interventions aimed at the reduction of pulmonary vascular tone have little effect on pulmonary vascular pressure-flow relationships in normoxia, but may decrease resistance in hypoxia, unloading the right ventricle and thereby improving exercise capacity. Exercise in patients with pulmonary hypertension is associated with sharp increases in pulmonary artery pressure and a right ventricular limitation of aerobic capacity. Exercise stress testing to determine multipoint pulmonary vascular pressures-flow relationships may uncover early stage pulmonary vascular disease. PMID:23105961

  15. Pulmonary circulation at exercise.

    PubMed

    Naeije, Robert; Chesler, N

    2012-01-01

    The pulmonary circulation is a high-flow and low-pressure circuit, with an average resistance of 1 mmHg/min/L in young adults, increasing to 2.5 mmHg/min/L over four to six decades of life. Pulmonary vascular mechanics at exercise are best described by distensible models. Exercise does not appear to affect the time constant of the pulmonary circulation or the longitudinal distribution of resistances. Very high flows are associated with high capillary pressures, up to a 20 to 25 mmHg threshold associated with interstitial lung edema and altered ventilation/perfusion relationships. Pulmonary artery pressures of 40 to 50 mmHg, which can be achieved at maximal exercise, may correspond to the extreme of tolerable right ventricular afterload. Distension of capillaries that decrease resistance may be of adaptative value during exercise, but this is limited by hypoxemia from altered diffusion/perfusion relationships. Exercise in hypoxia is associated with higher pulmonary vascular pressures and lower maximal cardiac output, with increased likelihood of right ventricular function limitation and altered gas exchange by interstitial lung edema. Pharmacological interventions aimed at the reduction of pulmonary vascular tone have little effect on pulmonary vascular pressure-flow relationships in normoxia, but may decrease resistance in hypoxia, unloading the right ventricle and thereby improving exercise capacity. Exercise in patients with pulmonary hypertension is associated with sharp increases in pulmonary artery pressure and a right ventricular limitation of aerobic capacity. Exercise stress testing to determine multipoint pulmonary vascular pressures-flow relationships may uncover early stage pulmonary vascular disease.

  16. Aluminum phosphide fatalities at mild exertion in asymptomatic children: a clue to understand the variations of the autopsy findings.

    PubMed

    Abder-Rahman, Hasan A

    2009-08-01

    Fatalities resulted from aluminium phosphide (ALP) intoxication in completely healthy children with no preceded clinical sings or symptoms were presented. Data regarding circumstances, autopsy reports, histopathological examination, toxicological investigation, and police enquiries were also collected and evaluated. The affected children were females, and 6-16 years old. They were completely healthy and died suddenly in relation to some physical activities such as running, walking, and bathing, without any prior complain. The viscera showed intense congestion with moderate to severe pulmonary edema. The cause of the sudden termination of life in the reported cases is mostly cardiac ones. Physical exertion may precipitate death due to increased cardiac stress, increased oxygen demand, and by aggravating metabolic acidosis. The absence of clinical symptoms before death may be due to the low level ALP, or due to the occurrence of death in the early stages after exposure to poison. Death due to ALP could result in cases of mild, moderate, or severe ALP intoxication. This may explain partly the differences encountered in clinical, autopsy, and histopathology findings of ALP intoxication. Fatalities are not the mere consequences of the dose of the poison, but factors such as physical activity and low oxygen level may be quite important.

  17. Letter to the Editor Reply to commentary by G. Sikri and S. Dua on the article "Correlation between single nucleotide polymorphisms in hypoxia-related genes and susceptibility to acute high-altitude pulmonary edema" published in Genetics and Molecular Research 14 (3): 11562-11572 to the letter published in Genet. Mol. Res. 14 (4): 15904-15905.

    PubMed

    Wu, L J

    2016-03-24

    The object in this study was a Han Chinese population in Lhasa, with 3658 m in altitude from Chengdu, which has 505 m in altitude by air. Within 24 to 48 h before the subjects arrived in the plateau, they completed a basic situation questionnaire, under the guidance of medical staff. Within 24 to 48 h after they reached the plateau, the subjects completed an acute plateau disease questionnaire. The diagnostic standard of HAPE and the diagnosis of acute plateau disease were adopted by the Lake Louise diagnostic standards in 1991 and the Chinese Medical Association promulgated the domestic diagnostic criteria on the Third National Plateau Medical Academic Seminar. Other diseases that cause acute symptoms of altitude sickness, such as plateau pulmonary edema, plateau cerebral edema, acute respiratory infections and neurosis, were excluded. According to the Lake Louise standard, questionnaire and symptom score values >3 points were diagnosed as HAPE. According to the national standard, the questionnaire and symptom score values >5 points were diagnosed as HAPE. At the present, morbidity of HAPE remains relatively high in China. The research shows that usually in the case of not taking preventive measures, according to the factors such as altitude, speed, and time of arrival, the incidence of HAPE is 30% to 90%. Epidemiological survey shows that HAPE happens at an altitude of 2500 m above the plateau. And an altitude of 3000 m above the plateau of China is occupied 1/6 of the total land area, the population of permanent residents is more than sixty million. We detected the 200 cases who adapted to plateau and the 106 cases of patients with HAPE susceptibility genes SNP locus, and got the key SNP loci of HAPE susceptibility genes. We maked the corresponding gene chip diagnostic kits.

  18. Approach to Lower Extremity Edema.

    PubMed

    Ratchford, Elizabeth V; Evans, Natalie S

    2017-03-01

    Lower extremity edema is extremely common among patients seen across multiple specialties. The differential diagnosis is broad and ranges from simple dependent edema to more complex conditions such as chronic venous disease and lymphedema. Several key features from the history and physical exam can assist with the diagnosis. Imaging is rarely necessary at the initial visit unless venous thromboembolism is suspected. Treatment is specific to the etiology of the edema, but compression stockings, elevation, exercise, and weight loss remain the cornerstone in most cases.

  19. Fatal big cat attacks.

    PubMed

    Cohle, S D; Harlan, C W; Harlan, G

    1990-09-01

    Two cases of fatal attacks by large cats are presented. In the first case, a 30-year-old female zoo worker was attacked by a jaguar that had escaped its cage. In the second case, a 2-year-old girl was fatally injured by her father's pet leopard. The pattern of injuries in these cases is nearly identical to those of these cats' prey in the wild.

  20. Mountaineering fatalities on Denali.

    PubMed

    McIntosh, Scott E; Campbell, Aaron D; Dow, Jennifer; Grissom, Colin K

    2008-01-01

    Mount McKinley, or Denali, is the tallest mountain in North America and attracts over 1,000 climbers annually from around the world. Since Denali is located within a national park, the National Park Service (NPS) manages mountaineering activities and attempts to maintain a balance of an adventurous experience while promoting safety. We retrospectively reviewed the fatalities on Denali from 1903 to 2006 to assist the NPS, medical personnel, and mountaineers improve safety and reduce fatalities on the mountain. Historical records and the NPS climber database were reviewed. Demographics, mechanisms, and circumstances surrounding each fatality were examined. Fatality rates and odds ratios for country of origin were calculated. From 1903 through the end of the 2006 climbing season, 96 individuals died on Denali. The fatality rate is declining and is 3.08/1,000 summit attempts. Of the 96 deaths, 92% were male, 51% occurred on the West Buttress route, and 45% were due to injuries sustained from falls. Sixty-one percent occurred on the descent and the largest number of deaths in 1 year occurred in 1992. Climbers from Asia had the highest odds of dying on the mountain. Fatalities were decreased by 53% after a NPS registration system was established in 1995. Although mountaineering remains a high-risk activity, safety on Denali is improving. Certain groups have a significantly higher chance of dying. Registration systems and screening methods provide ways to target at-risk groups and improve safety on high altitude mountains such as Denali.

  1. Near fatal asthma: treatment and prevention.

    PubMed

    D'Amato, G; Vitale, C; Lanza, M; Sanduzzi, A; Molino, A; Mormile, M; Vatrella, A; Bilò, M B; Antonicelli, L; Bresciani, M; Micheletto, C; Vaghi, A; D'Amato, M

    2016-07-01

    Near-fatal asthma (NFA) is described as acute asthma associated with a respiratory arrest or arterial carbon dioxide tension greater than 50 mmHg, with or without altered consciousness, requiring mechanical ventilation. Risk factors for near fatal asthma have not been fully elucidated. In 80-85% of all fatal events, a phenotype, characterized by eosinophilic inflammation associated with gradual deterioration occurring in patients with severe and poorly controlled asthma, has been identified. Regarding to the management, acute severe asthma remains a significant clinical problem, which needs to be identified to facilitate early and appropriate therapeutic interventions. The assessment relies on clinical signs, but additional information might be obtained from chest radiography or blood gas analysis. No investigation should delay the initiation of appropriate therapy. The goals of therapy are the maintenance of oxygenation, relief of airflow obstruction, reduction of airways edema and mucus plugging (with Increased use of medications such as beta-agonists via metered dose inhalers and nebulizers, oral and/or intravenous (other than by inhalation) corticosteroids and oral or intravenous theophylline) whereas supporting ventilation as clinically indicated. Of course, the emergency physician needs to consider the wide range of potential complications, as attention to these problems when managing severe acute asthma might significantly improve outcome. An understanding of the available agents and potential pitfalls in the management of NFA is mandatory for the emergency physician.

  2. Diuretics in cardiac edema--1969.

    PubMed

    Shanoff, H M

    1969-10-04

    New and powerful diuretics have made it possible for the physician to control cardiac edema in most patients. At the same time their potentially dangerous side effects make it mandatory for the physician to be knowledgeable and judicious in their use. The appreciation of a few simplified facts about cardiac edema and renal reabsorption of sodium makes the clinical pharmacology of the diuretics much easier to understand, remember and apply.

  3. Excitotoxicity in the Lung: N-Methyl-D-Aspartate-Induced, Nitric Oxide-Dependent, Pulmonary Edema is Attenuated by Vasoactive Intestinal Peptide and by Inhibitors of Poly(ADP-Ribose) Polymerase

    NASA Astrophysics Data System (ADS)

    Said, Sami I.; Berisha, Hasan I.; Pakbaz, Hedayatollah

    1996-05-01

    Excitatory amino acid toxicity, resulting from overactivation of N-methyl-D-aspartate (NMDA) glutamate receptors, is a major mechanism of neuronal cell death in acute and chronic neurological diseases. We have investigated whether excitotoxicity may occur in peripheral organs, causing tissue injury, and report that NMDA receptor activation in perfused, ventilated rat lungs triggered acute injury, marked by increased pressures needed to ventilate and perfuse the lung, and by high-permeability edema. The injury was prevented by competitive NMDA receptor antagonists or by channel-blocker MK-801, and was reduced in the presence of Mg2+. As with NMDA toxicity to central neurons, the lung injury was nitric oxide (NO) dependent: it required L-arginine, was associated with increased production of NO, and was attenuated by either of two NO synthase inhibitors. The neuropeptide vasoactive intestinal peptide and inhibitors of poly(ADP-ribose) polymerase also prevented this injury, but without inhibiting NO synthesis, both acting by inhibiting a toxic action of NO that is critical to tissue injury. The findings indicate that: (i) NMDA receptors exist in the lung (and probably elsewhere outside the central nervous system), (ii) excessive activation of these receptors may provoke acute edematous lung injury as seen in the ``adult respiratory distress syndrome,'' and (iii) this injury can be modulated by blockade of one of three critical steps: NMDA receptor binding, inhibition of NO synthesis, or activation of poly(ADP-ribose) polymerase.

  4. A fatal cytokine-induced systemic inflammatory response reveals a critical role for NK cells.

    PubMed

    Carson, W E; Yu, H; Dierksheide, J; Pfeffer, K; Bouchard, P; Clark, R; Durbin, J; Baldwin, A S; Peschon, J; Johnson, P R; Ku, G; Baumann, H; Caligiuri, M A

    1999-04-15

    The mechanism of cytokine-induced shock remains poorly understood. The combination of IL-2 and IL-12 has synergistic antitumor activity in vivo, yet has been associated with significant toxicity. We examined the effects of IL-2 plus IL-12 in a murine model and found that the daily, simultaneous administration of IL-2 and IL-12 resulted in shock and 100% mortality within 4 to 12 days depending on the strain employed. Mice treated with IL-2 plus IL-12 exhibited NK cell apoptosis, pulmonary edema, degenerative lesions of the gastrointestinal tract, and elevated serum levels of proinflammatory cytokines and acute phase reactants. The actions of TNF-alpha, IFN-gamma, macrophage-inflammatory protein-1alpha, IL-1, IL-1-converting enzyme, Fas, perforin, inducible nitric oxide synthase, and STAT1 did not contribute to the observed toxicity, nor did B or T cells. However, toxicity and death from treatment with IL-2 plus IL-12 could be completely abrogated by elimination of NK cells. These results suggest that the fatal systemic inflammatory response induced by this cytokine treatment is critically dependent upon NK cells, but does not appear to be mediated by the known effector molecules of this cellular compartment. These data may provide insight into the pathogenesis of cytokine-induced shock in humans.

  5. Dosimetric Predictors of Laryngeal Edema

    SciTech Connect

    Sanguineti, Giuseppe . E-mail: gisangui@utmb.edu; Adapala, Prashanth; Endres, Eugene J. C; Brack, Collin; Fiorino, Claudio; Sormani, Maria Pia; Parker, Brent

    2007-07-01

    Purpose: To investigate dosimetric predictors of laryngeal edema after radiotherapy (RT). Methods and Materials: A total of 66 patients were selected who had squamous cell carcinoma of the head and neck with grossly uninvolved larynx at the time of RT, no prior major surgical operation except for neck dissection and tonsillectomy, treatment planning data available for analysis, and at least one fiberoptic examination of the larynx within 2 years from RT performed by a single observer. Both the biologically equivalent mean dose at 2 Gy per fraction and the cumulative biologic dose-volume histogram of the larynx were extracted for each patient. Laryngeal edema was prospectively scored after treatment. Time to endpoint, moderate or worse laryngeal edema (Radiation Therapy Oncology Group Grade 2+), was calculated with log rank test from the date of treatment end. Results: At a median follow-up of 17.1 months (range, 0.4- 50.0 months), the risk of Grade 2+ edema was 58.9% {+-} 7%. Mean dose to the larynx, V30, V40, V50, V60, and V70 were significantly correlated with Grade 2+ edema at univariate analysis. At multivariate analysis, mean laryngeal dose (continuum, hazard ratio, 1.11; 95% confidence interval, 1.06-1.15; p < 0.001), and positive neck stage at RT (N0-x vs. N +, hazard ratio, 3.66; 95% confidence interval, 1.40-9.58; p = 0.008) were the only independent predictors. Further stratification showed that, to minimize the risk of Grade 2+ edema, the mean dose to the larynx has to be kept {<=}43.5 Gy at 2 Gy per fraction. Conclusion: Laryngeal edema is strictly correlated with various dosimetric parameters; mean dose to the larynx should be kept {<=}43.5 Gy.

  6. Effectiveness of CT for clinical stratification of occupational lung edema.

    PubMed

    Masaki, Yoshinori; Sugiyama, Keisaku; Tanaka, Hiroyuki; Uwabe, Yasuhide; Takayama, Masanori; Sakai, Masao; Hayashi, Takuya; Otsuka, Masayuki; Suzuki, Shinya

    2007-01-01

    We treated two occupational lung diseases in different situations during military training. The purpose of this study is to investigate the availability of CT scanning for the evaluation of inhalation pulmonary edema. Two soldiers suffered severe lung edema after using a spray for the daily maintenance of their firearms. Four soldiers suffered severe dyspnea after undertaking drills in a narrow zone where numerous smoke bombs had been used. We evaluated these patients from several aspects. CT scans of the chest of spray-induced patients revealed bilateral infiltration predominantly in the upper lung fields. The patients received steroid pulse treatment and gradually recovered. CT scans of the chest of smoke-induced patients revealed bilateral ground-glass attenuation with peripheral lung sparing. The patients gradually recovered with steroid therapy. In accordance with previous studies, CT scans of the chest in our patients demonstrated that the periphery of the lungs remained normal, except in cases of serious injury. When differential diagnosis is required, we consider that CT scans of the chest are particularly useful; CT findings are useful in determining the severity of lung injury as well as the diagnosis of inhalation pulmonary edema.

  7. Laguna Negra Virus Infection Causes Hantavirus Pulmonary Syndrome in Turkish Hamsters (Mesocricetus brandti).

    PubMed

    Hardcastle, K; Scott, D; Safronetz, D; Brining, D L; Ebihara, H; Feldmann, H; LaCasse, R A

    2016-01-01

    Laguna Negra virus (LNV) is a New World hantavirus associated with severe and often fatal cardiopulmonary disease in humans, known as hantavirus pulmonary syndrome (HPS). Five hamster species were evaluated for clinical and serologic responses following inoculation with 4 hantaviruses. Of the 5 hamster species, only Turkish hamsters infected with LNV demonstrated signs consistent with HPS and a fatality rate of 43%. Clinical manifestations in infected animals that succumbed to disease included severe and rapid onset of dyspnea, weight loss, leukopenia, and reduced thrombocyte numbers as compared to uninfected controls. Histopathologic examination revealed lung lesions that resemble the hallmarks of HPS in humans, including interstitial pneumonia and pulmonary edema, as well as generalized infection of endothelial cells and macrophages in major organ tissues. Histologic lesions corresponded to the presence of viral antigen in affected tissues. To date, there have been no small animal models available to study LNV infection and pathogenesis. The Turkish hamster model of LNV infection may be important in the study of LNV-induced HPS pathogenesis and development of disease treatment and prevention strategies.

  8. Understanding Fatal Child Abuse.

    ERIC Educational Resources Information Center

    Hicks, Ralph A.; Gaughan, Daniel C.

    1995-01-01

    Medical, social service, and coroner reports were reviewed for 14 cases of fatal child abuse and neglect identified at a children's hospital from 1988 to 1992. Median age was 6.5 months. Six families had prior protective service involvement (though four of these had involved a sibling). The cause of death in all cases was blunt impact head injury.…

  9. Acute Hemorrhagic Edema of Infancy.

    PubMed

    Serra E Moura Garcia, C; Sokolova, A; Torre, M L; Amaro, C

    2016-01-01

    Acute Hemorrhagic Edema of Infancy is a small vessel leucocytoclastic vasculitis affecting young infants. It is characterized by large, target-like, macular to purpuric plaques predominantly affecting the face, ear lobes and extremities. Non-pitting edema of the distal extremities and low-grade fever may also be present. Extra-cutaneous involvement is very rare. Although the lesions have a dramatic onset in a twenty-four to forty-eight hour period, usually the child has a non-toxic appearance. In most cases there are no changes in laboratory parameters. The cutaneous biopsy reveals an inflammatory perivascular infiltrate. It is a benign and auto-limited disease, with complete resolution within two to three weeks leaving no sequelae in the majority of cases. No recurrences are described. We report a case of a 42-day old girl admitted at our hospital with Acute Hemorrhagic Edema of Infancy.

  10. Chronic fatal pneumocystosis in nude mice.

    PubMed

    Ueda, K; Goto, Y; Yamazaki, S; Fujiwara, K

    1977-12-01

    A chronic pulmonary disease was encountered in nude mice of a barrier sustained colony, and Pneumocystis carinii was identified as the causative agent histopathologically as well as on impression smear preparations in the affected lungs. Fatal infection was seen only in old nude mice aged more than 6 months, while focal pulmonary lesions were developed without clinical signs in young adult nudes 2 to 3 months of age. The lesions produced in aged nude mice were characterized by propagation of mononuclear cells with the presence of foamy masses of P. carinii. Heterozygous littermates were much less susceptible to the infection but pneumocystic lesions could be produced readily by multiple treatment with immunosuppressants. The infection could be transmitted without immunosuppressant to non-infected nudes but not to heterozygous littermates after intranasal inoculation of affected tissue emulsion or by cage mating with severely affected nudes.

  11. Maporal viral infection in the Syrian golden hamster: a model of hantavirus pulmonary syndrome.

    PubMed

    Milazzo, Mary Louise; Eyzaguirre, Eduardo J; Molina, Claudia P; Fulhorst, Charles F

    2002-11-15

    Hantavirus pulmonary syndrome (HPS) is a severe and often fatal rodent-borne zoonosis. Maporal (MAP) virus is a newly discovered hantavirus that originally was isolated from an arboreal rice rat captured in central Venezuela. The results of this study indicate that MAP virus in the Syrian golden hamster (Mesocricetus auratus) can cause a disease that is clinically and pathologically remarkably similar to HPS. The similarities include the time course of clinical disease, presence of virus-specific IgG at the onset of clinical disease, subacute pneumonitis, rapid onset of diffuse alveolar edema in the absence of necrosis, hepatic-portal triaditis, mononuclear-cellular infiltrate in lung and liver, widespread distribution of hantaviral antigen in endothelial cells of the microvasculature of lung and other tissues, and variable lethality. These similarities suggest that the MAP virus-hamster system is a useful model for studies of the pathogenesis of HPS and for the evaluation of potential therapeutic agents.

  12. Pulmonary embolism caused by intimal sarcoma of the pulmonary artery.

    PubMed

    Yamamoto, Kei; Nozue, Tsuyoshi; Tsuchida, Masayuki; Iwaki, Taku; Nagamine, Hiroshi; Yasuda, Tamotsu; Kawase, Hiroshi; Matsushita, Kazuhiko; Michishita, Ichiro

    2012-01-01

    We herein report the case of a 39-year-old woman with a pulmonary embolism caused by intimal sarcoma of the pulmonary artery. She presented with shortness of breath and leg edema. Computed tomography showed a low density area that extended from the main pulmonary artery to the bilateral pulmonary arteries. We diagnosed her to have a pulmonary thromboembolism. The thrombosis did not decrease after the administration of anti-coagulant therapy, and she underwent resection of the thrombotic tissue. Histopathologically, the surgical specimen was not found to be thrombotic tissue but rather an intimal sarcoma of the pulmonary artery. After undergoing surgery, she received radiation therapy and chemotherapy; however, she died 31 months after being diagnosed.

  13. [Concealed and simulated trauma fatalities(II)].

    PubMed

    Klotzbach, H; Püschel, K

    2001-12-01

    A careful investigation of fatal accidents is required due to the relevant financial consequences for the insured as well as for the insurance company. An evaluation of post-mortem cases handled by our institute from 1988 to 1998 showed that 16% of all fatal accidents were not initially classified as such; it was only possible to determine the cause by post-mortem and criminal investigation. The frequency of a relevant alcoholization varied with different types of accidents. Furthermore, of all fatal accidents, 3% were revealed to be deceptive. Those 42 cases in total, presenting themselves as fatal accidents at first glance, were later determined either to be natural deaths (n = 27), homicide (n = 11) or suicide (n = 4). In addition to this, autopsies showed 83 cases of death to be sequelae to accidents. Particularly in cases of a victim plunging out of the window or into water, it can be difficult to make the distinction between natural death--e.g. as a reason for falling--and suicide or homicide. Further difficulties can result from interpretations of the findings in cases of putrefaction, mauling by animals, defects caused by burning or severely deformed corpses. In these cases, the importance of patho-morphological findings from the autopsy must be emphasized. Indirect sequelae of accidents may be pulmonary embolism or pneumonia. The cause of death has to be classified as accidental if the chain of events is of traumatic origin. Mistakes can be avoided if the medical history is taken conscientiously. If no facts are available, the cause of death should be certificated as undetermined. Our evaluation only included autopsy cases from our institute. The concealed fatal accidents which were incorrectly certified as natural deaths or the cases dismissed by the police and the public prosecutor without performing an autopsy were not evaluated.

  14. Occupational fatalities in Jordan.

    PubMed

    Al-Abdallat, Emad M; Oqailan, Ahmad Mohammad A; Al Ali, Rayyan; Hudaib, Arwa A; Salameh, Ghada A M

    2015-01-01

    Occupational fatalities are a worldwide problem. Certain occupations pose a greater risk than others. Recent statistics on global occupational injuries and diseases that might lead to temporary or permanent disability and even worse might lead to death, are staggering. The purpose of this study was to estimate the death rates from occupational injuries in Jordan over a period of four years; to estimate occupational fatality rate that results from accidental injuries and identify the most risky concurrent occupations with the type of injuries, the age and nationality of the victims. A total of 88 work related fatalities were admitted to three hospitals in Amman through 2008-2012 and were examined by a forensic (occupational) physician at the time. They were categorized according to, age, nationality, occupation, type of injury and were all tested for toxic substances. The occupation with the most fatalities was construction (44%); falling from a height was the commonest type of accident (44%) and head injuries were the leading injury type (21.6%); 9.1% of the deaths were positive for alcohol. Moreover, 22.7% of deaths were between ages of 25-29. Consequently, the mean occupational fatality rate was 2 per 100.000 workers during 2008-2012. Constructions and other types of occupations are more extensive problems than what is usually anticipated, especially when safety precautions are not effective or implemented. They may cause injuries and death, which will have a socioeconomic burden on families, society, governments and industries. Not to mention the grief that is associated with the death of a worker at his work site to all concerned parties. Copyright © 2014 Elsevier Ltd and Faculty of Forensic and Legal Medicine. All rights reserved.

  15. A fatal case of acute interstitial pneumonia (AIP) in a woman affected by glioblastoma.

    PubMed

    Balzarini, Laura; Mancini, Chiara; Marvisi, Maurizio

    2014-03-01

    This report presents the case of a 67-year-old woman affected by glioblastoma. After a few days of adjuvant therapy with temozolomide and prophylaxis with trimetrophin-sulfamethoxazolo to prevent Pneumocystis Jiroveci, she had progressive and rapid worsening of symptoms with weakness, dyspnea and orthopnea. She had peripheral edema and proximal hyposthenia of the lower limbs. Chest CT showed bilateral ground-glass opacities and laboratory exams revealed hypoxemia and hypocapnia, an initial reduction in platelet and white blood cells, and an elevation of LDH, AST, ALT, and active urinary sediment. Blood cultures, bronchoalveolar lavage (BAL) data and transbronchial biopsy showed no infections, and in particular no evidence of Pneumocystis Jiroveci pneumonia. Histological examination revealed a typical pattern of AIP. She was treated with broad-spectrum antibiotics and high-dose steroids. The symptoms worsened and respiratory failure required mechanical ventilation. The pneumonia was not responsive to medical or invasive care. She died after ten days of hospitalization. At present very little can be found in the literature about lung toxicity caused by temozolomide. This case can be added as a new report describing this risk. The combination therapy with temozolamide and trimetophin-sulfamethoxazolo could have a synergistic action inducing various forms of pulmonary toxicity. ESTABLISHED FACTS: Acute interstitial pneumonia is a common manifestation of lung toxicity caused by drugs. The clinical course is favorable with a good response to corticosteroids. NOVEL INSIGHT: This is the first fatal case of lung toxicity caused by Temozolomide. Clinicians must be aware that a combination therapy including trimetophin-sulfamethoxazolo could have a synergistic action in inducing pulmonary toxicity.

  16. Lung edema due to hydrogen peroxide is independent of cyclooxygenase products

    SciTech Connect

    Burghuber, O.; Mathias, M.M.; McMurtry, I.F.; Reeves, J.T.; Voelkel, N.F.

    1984-01-01

    Active oxygen species can cause lung injury. Although a direct action on endothelial cells is proposed, the possibility exists that they might cause injury via mediators. We considered that active oxygen species would stimulate the generation of cyclooxygenase metabolites, which then alter pulmonary vasoreactivity and cause edema. We chemically produced hydrogen peroxide by adding glucose oxidase to a plasma- and cell-free, but ..beta..-D-glucose-containing, solution, which perfused isolated rat lungs. Addition of glucose oxidase to the perfusate caused a marked decrease in pulmonary vasoreactivity, accompanied by an increase in the concentrations of prostacyclin, thromboxane A/sub 2/, and prostaglandin F/sub 2..cap alpha../. Pretreatment with catalase, a specific scavenger of hydrogen peroxide, preserved pulomonary vasoreactivity, inhibited the increase of the concentration of the measured prostaglandins, and prevented edema formation. Indomethacin effectively blocked lung prostaglandin production but neither prevented the decrease in vasoreactivity nor inhibited edema formation. From these data we conclude the hydrogen peroxide impaired pulmonary vasoreactivity and subsequently caused edema. Depsite the fact that hydrogen peroxide stimulated lung prostaglandin production, cyclooxygenase-derived products neither caused the decrease in vasoreactivity nor the development of edema.

  17. Surgical management of pulmonary tuberculosis.

    PubMed

    Picciocchi, A; Granone, P; Margaritora, S; Cesario, A; Galetta, D

    1998-01-01

    Surgery for pulmonary tubercolosis (PTB) is now the second place treatment. Among the surgical indications the most debated is the multi-drug resistance of a focal pulmonary tuberculous disease. Other indications are: bronchiectasis, hemoptysis and the presence of a broncho-pleural fistula. Pulmonary Aspergilloma is a frequent indication for surgery; it is commonly a PTB sequela and causes severe complications. The presence of an unknown pulmonary mass or nodule is a surgical criterion because it might signal a cancer. Surgery therefore now constitutes a valid option for the treatment of clinical patterns of PTB unresponsive to medical treatment in severe, potentially fatal clinical conditions.

  18. Edema: a silent but important factor.

    PubMed

    Villeco, June P

    2012-01-01

    Edema is a normal response to injury. Even the smallest injury is associated with some inflammation, and initial edema is part of the normal inflammatory process. However, edema becomes a concern when it persists beyond the inflammatory phase. Once we have progressed into the rebuilding, or fibroplastic phase of healing, edema will delay healing and contribute to complications such as pain and stiffness. Early prevention and management to prevent this progression are therefore critical. This article discusses edema in relation to stages of healing and presents the research behind techniques available to the clinician to manage localized extracellular upper extremity edema in the patient with an intact lymphatic system.

  19. Uveitic Macular Edema: Treatment Update

    PubMed Central

    Goldhardt, Raquel; Rosen, Bradley Simon

    2016-01-01

    The aim of this review is to summarize recent developments in the treatment of uveitic macular edema (ME). ME represent a major cause of visual loss in uveitis and adequate management is crucial for the maintenance of useful vision in patients with chronic uveitis. PMID:27347446

  20. Retrograde pulmonary perfusion as an adjunct to standard pulmonary embolectomy for acute pulmonary embolism.

    PubMed

    Spagnolo, Salvatore; Barbato, Luciano; Grasso, Maria Antonia; Tesler, Ugo Filippo

    2014-01-01

    Mortality rates for pulmonary embolectomy in patients with acute massive pulmonary embolism have decreased in recent years. However, it still ranges from 30 to 45% when surgery is performed on critically ill patients, and the mortality rates reach 60% in patients who have experienced a cardiac arrest before the procedure. The causes of death in these patients are generally attributed to right heart failure due to persistent pulmonary hypertension, intractable pulmonary oedema, and massive parenchymal and intrabronchial haemorrhage. Clinical and experimental findings indicate that venous air embolism causes severe or even lethal damage to the pulmonary microvasculature and the lung parenchyma consequent to the release of endothelium-derived cytokines. These findings are similar to those observed when severely compromised patients undergo pulmonary embolectomy for air entrapped in the pulmonary artery during embolectomy, which may lead to fatal outcomes. Retrograde pulmonary perfusion (RPP), besides enabling the removal of residual thrombotic material from the peripheral branches of the pulmonary artery, fills the pulmonary artery with blood and prevents pulmonary air embolism. We believe that the use of RPP as an adjunct to conventional pulmonary embolectomy decreases the morbidity and mortality rates associated with pulmonary embolectomy in critically ill patients.

  1. Bosentan for pulmonary hypertension secondary to idiopathic pulmonary fibrosis.

    PubMed

    Onda, Naomi; Tanaka, Yosuke; Hino, Mitsunori; Gemma, Akihiko

    2015-01-01

    Pulmonary hypertension is a poor prognostic factor in patients with interstitial lung disease. No established treatment exists for pulmonary hypertension secondary to interstitial pneumonia. We describe the case of an 81-year-old woman with idiopathic pulmonary fibrosis (IPF), who was admitted to our hospital due to aggravation of dyspnea and decreased oxygen saturation, as well as onset of orthopnea and rapidly progressing edema. The transthoracic echocardiography and right heart catheterization showed the mean pulmonary artery pressure was 39 mmHg and the mean pulmonary capillary wedge pressure was 9 mmHg. After various examinations, the diagnoses of pulmonary hypertension (PH) due to IPF and of congestive heart failure secondary to PH were established. Diuretic therapy was started, but the patient's condition showed poor improvement. Subsequent initiation of oral bosentan therapy led to improvement in symptoms and findings. At the follow-up assessment one year later her pulmonary function showed no significant changes and no apparent worsening of arterial blood gases, with evident improvement of PH, WHO functional class, maximum exercise tolerance on treadmill exercise testing, right heart catheterization, and transthoracic echocardiography. This report describes a case of successful treatment with bosentan for severe pulmonary hypertension in a patient with idiopathic pulmonary fibrosis. We also present a review of the literature on treatment of pulmonary hypertension in patients with chronic lung disease. Bosentan appears to be efficacious in some patients with pulmonary hypertension secondary to idiopathic interstitial pneumonitis.

  2. Bladder irrigation and urothelium disruption: a reminder apropos of a case of fatal fluid absorption.

    PubMed

    Di Paolo, Marco; Bugelli, Valentina; Di Luca, Alessandro; Turillazzi, Emanuela

    2014-11-20

    Irrigation or washouts of the bladder are usually performed in various clinical settings. In the 1980s Elliot and colleagues argued that urothelial damage could occur after washouts and irrigations of the bladder. The exact mechanism underlying urothelial damage has not yet been discovered. To our knowledge, this is the first report of fatal fluid overload and pulmonary edema, due to urothelium disruption occurring during bladder irrigation, approached performing complete histological and immunohistochemical investigation on bladder specimens. The exposed case deserves attention since it demonstrates that, although very rarely, irrigation or washouts of the bladder may have unexpected serious clinical consequences. An 85 year-old Caucasian man, unable to eat independently and whose fluid intake was controlled, underwent continuous bladder irrigation with a 3-way catheter due to a severe episode of macrohematuria. During the third day of hospitalization, while still undergoing bladder irrigati