Cases reported "Pulmonary Edema"

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1/86. hydrochlorothiazide-induced pulmonary edema and associated immunologic changes.

    OBJECTIVE: To describe a patient with noncardiogenic acute pulmonary edema induced by hydrochlorothiazide and to investigate the possible involvement of an immunologic mechanism in this adverse reaction. CASE SUMMARY: A 66-year-old Hispanic woman developed acute pulmonary edema 30 minutes after the ingestion of one tablet of triamterene 75 mg/hydrochlorothiazide 50 mg. The reaction was associated with hemoconcentration; a decreased white blood cell count with a shift to a predominance of polymorphonuclear cells; decreased serum immunoglobulin (Ig) G, IgG1, and IgG4; and increased serum IgM and complement 3 concentrations. DISCUSSION: Although there have been 35 reports of cases of hydrochlorothiazide-induced pulmonary edema, the etiology of this adverse reaction remains unknown. The observations presented in this case report, along with commonalities with previously reported cases, suggest that granulocytic infiltration into the lungs and IgG deposition in alveolar membranes may play a role in hydrochlorothiazide-induced pulmonary edema. CONCLUSIONS: Noncardiogenic pulmonary edema may be an immunologically mediated rare idiosyncratic reaction to hydrochlorothiazide.
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2/86. Negative pressure pulmonary hemorrhage.

    Negative pressure pulmonary edema, a well-recognized phenomenon, is the formation of pulmonary edema following an acute upper airway obstruction (UAO). To our knowledge, diffuse alveolar hemorrhage has not been reported previously as a complication of an UAO. We describe a case of negative pressure pulmonary hemorrhage, and we propose that its etiology is stress failure, the mechanical disruption of the alveolar-capillary membrane.
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3/86. Haemoptysis after breath-hold diving.

    Pulmonary oedema has been described in swimmers and self-contained underwater breathing apparatus (Scuba) divers. This study reports three cases of haemoptysis secondary to alveolar haemorrhage in breath-hold divers. Contributory factors, such as haemodynamic modifications secondary to immersion, cold exposure, exercise and exposure to an increase in ambient pressure, could explain this type of accident. Furthermore, these divers had taken aspirin, which may have aggravated the bleeding.
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4/86. The pathology of transfusion-related acute lung injury.

    Transfusion-related acute lung injury is an uncommon condition characterized by the rapid onset of respiratory distress soon after transfusion. Our understanding of its pathophysiology is based on animal models of complement (C5a) and antibody-induced lung injury and a limited number of autopsies. These models suggest that transfusion-related acute lung injury is induced by granulocytes that aggregate in the pulmonary microvasculature after activation by transfusion-derived antibodies or biologically active lipids. The published autopsy reports provide little support for this model, as they are invariably confounded by underlying pulmonary infection, preexisting disease, and resuscitation injury. We report the case of a previously well 58-year-old man who died of transfusion-related acute lung injury within 2 hours of the onset of pulmonary distress; autopsy showed evidence of massive pulmonary edema with granulocyte aggregation within the pulmonary microvasculature and extravasation into alveoli. Electron microscopy revealed capillary endothelial damage with activated granulocytes in contact with the alveolar basement membranes. These findings provide direct support for the proposed model of transfusion-related acute lung injury pathogenesis.
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keywords = alveolar
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5/86. Alveolar haemorrhage in a case of high altitude pulmonary oedema.

    A case of high altitude pulmonary oedema (HAPE) in a climber who made a rapid ascent on Mt McKinley (Denali), alaska is described. The bronchoalveolar lavage (BAL) fluid contained increased numbers of red blood cells and an abundance of haemosiderin laden macrophages consistent with alveolar haemorrhage. The timing of this finding indicates that alveolar haemorrhage began early during the ascent, well before the onset of symptoms. Although evidence of alveolar haemorrhage has been reported at necropsy in individuals dying of HAPE, previous reports have not shown the same abundance of haemosiderin laden macrophages in the BAL fluid. These findings suggest that alveolar haemorrhage is an early event in HAPE.
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ranking = 5
keywords = alveolar
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6/86. Biting the laryngeal mask: an unusual cause of negative pressure pulmonary edema.

    PURPOSE: To describe negative pressure pulmonary edema due to biting of the laryngeal mask tube at emergence from general anesthesia. CLINICAL FEATURES: A healthy patient underwent general anesthesia using a laryngeal mask airway and mechanical ventilation. During recovery, the patient strongly bit the laryngeal mask and made very forceful inspiratory efforts until the mask was removed. Five minutes later, the patient developed dyspnea and had an hemoptysis of 50 ml fresh blood. Chest radiograph showed bilateral alveolar infiltrates. Pharyngo-laryngeal examination was normal. bronchoscopy revealed no injury but diffuse pink frothy edema fluid. Clinical examination and chest radiograph became normal after 12 hr of nasal oxygen therapy confirming airway obstruction as the most available cause of this pulmonary edema. CONCLUSION: airway obstruction due to biting of a laryngeal mask tube may result in negative pressure pulmonary edema.
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7/86. An autopsy case of ovarian hyperstimulation syndrome with massive pulmonary edema and pleural effusion.

    ovarian hyperstimulation syndrome (OHSS) is the most serious complication of ovulation induction with exogenous gonadotropins, such as human menopausal gonadotropin and follicle-stimulating hormone. These hormones are considered to increase capillary permeability and cause third space fluid shift. We report an autopsy case of severe OHSS in a 28-year-old Japanese female. The patient developed bilateral chest pain and progressive dyspnea during the course of administration of human gonadotropins. pleural effusion and hypouresis clinically disappeared 4 days after the onset of the symptoms, but the patient died suddenly of rapid respiratory insufficiency. autopsy examination revealed massive pulmonary edema, intra-alveolar hemorrhage and pleural effusion without any evidence of pulmonary thromboembolism. Histopathological examination of the ovary demonstrated multiple well-developed follicle formations, consistent with OHSS. It is very important to recognize that massive pulmonary edema can occur in a patient with OHSS. To the best of our knowledge, this is the first autopsy report of a patient with severe OHSS.
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8/86. Protein concentration in pulmonary oedema fluid for negative pressure pulmonary oedema in children.

    We report a case of acute pulmonary oedema following upper airway obstruction in a 1-year-old patient. We discuss the pathophysiology of this infrequent complication of upper airway obstruction and the interest of alveolar protein/blood protein ratio measurement to determine the mechanism of pulmonary oedema.
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9/86. Unilateral high-altitude pulmonary edema (HAPE): a case report and discussion of pathophysiology.

    High-altitude pulmonary edema (HAPE), a potentially life-threatening altitude adaptation disorder, is considered to be caused by an exaggerated increase in pulmonary blood pressure and a non-cardiogenic rise in pulmonary vascular permeability subsequent to alveolar hypoxia. A 40-year-old male mountaineer was affected by an advanced stage of HAPE at high altitude (Monte rosa plateau, 4000 m). The symptoms abated immediately after the patient descended from the altitude. However, six hours after the symptoms had resolved, radiographic signs of pulmonary edema, confined to the right lung, were seen. This rarely described unilateral radiological pattern of HAPE resolved completely within two days. We suggest that aspiration events of nasal secretion, the right sleeping position at night and an elevated right diaphragm reduced the patient's compensatory hyperventilation capacity of the right lung. The resulting increased alveolar hypoxia in the right lung was responsible for unilateral edema. The pathophysiological mechanism underlying unilateral HAPE is discussed.
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ranking = 2
keywords = alveolar
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10/86. Complications of ultrarapid opioid detoxification with subcutaneous naltrexone pellets.

    Rapid and ultrarapid opioid detoxification (ROD and UROD) centers promise quick, painless, same-day detoxification treatment for patients with opioid addiction. The goal of ROD and UROD is to provide a rapid transition from opioid dependency to oral naltrexone therapy. The patient is given general anesthesia and high-dose opioid antagonists. This induces a severe withdrawal but spares the patient the experience. In theory, the process is complete within four to five hours. The patient awakens without opioid dependency and is started on oral naltrexone. Any subsequent, persistent withdrawal symptoms are treated symptomatically. A novel, unapproved approach is to compound a pellet of naltrexone and implant it in the subcutaneous tissue. In theory, this should result in continuous therapeutic levels for this drug, and avoid issues with noncompliance. CASE SERIES: This article reports six cases of complications from the same detoxification center that performed UROD with naltrexone pellet implantation, including pulmonary edema, prolonged withdrawal, drug toxicity, withdrawal from cross-addiction to alcohol and benzodiazepines, variceal rupture, aspiration pneumonia, and death. CONCLUSIONS: The risks of this procedure are great and further studies should assess its safety and the novel use of naltrexone.
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