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Query: UMLS:C0019079 (hemoptysis)
 6,129 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Almost every second trekker or climber develops two to three symptoms of the high altitude illness after a rapid ascent (> 300 m/day) to an altitude above 4000 m. We distinguish two forms of high altitude illness, a cerebral form called acute mountain sickness and a pulmonary form called high altitude pulmonary edema. Essentially, acute mountain sickness is self-limiting and benign. Its symptoms are mild to moderate headache, loss of appetite, nausea, dizziness and insomnia. Nausea rarely progresses to vomiting, but if it does, this may anticipate a progression of the disease into the severe form of acute mountain sickness, called high altitude cerebral edema. Symptoms and signs of high altitude cerebral edema are severe headache, which is not relieved by acetaminophen, loss of movement coordination, ataxia and mental deterioration ending in coma. The mechanisms leading to acute mountain sickness are not very well understood; the loss of cerebral autoregulation and a vasogenic type of cerebral edema are being discussed. High altitude pulmonary edema presents in roughly twenty percent of the cases with mild symptoms of acute mountain sickness or even without any symptoms at all. Symptoms associated with high altitude pulmonary edema are incapacitating fatigue, chest tightness, dyspnoe at the minimal effort that advances to dyspnoe at rest and orthopnoe, and a dry non-productive cough that progresses to cough with pink frothy sputum due to hemoptysis. The hallmark of high altitude pulmonary edema is an exaggerated hypoxic pulmonary vasoconstriction. Successful prophylaxis and treatment of high altitude pulmonary edema using nifedipine, a pulmonary vasodilator, indicates that pulmonary hypertension is crucial for the development of high altitude pulmonary edema. The primary treatment of high altitude illness consists in improving hypoxemia and acclimatization. For prophylaxis a slow ascent at a rate of 300 m/day is recommended, if symptoms persist, acetazolamide at a dose of 500 mg/day is effective. Mild acute mountain sickness may also be treated with the same dose acetazolamide. Glucocorticoids are the first line treatment of the malignant form of acute mountain sickness. Nifedipine is effective only for the prophylaxis and treatment of high altitude pulmonary edema.
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PMID:[Mountaineering and altitude sickness]. 1144 1

A 38-year-old woman presented with massive hemoptysis (>200 mL/ 24 hours) occurring abruptly after generalized tonic clonic seizure. She experienced similar episodes of hemoptysis on three later occasions. Although the coexistence of hemoptysis and seizure has been reported, albeit rarely, as a clinical manifestation of postictal neurogenic pulmonary edema, massive hemoptysis after seizure is an extremely rare event with no recurrent cases of such episodes having ever been reported. The coexistence of hemoptysis and seizure increases the difficulty in diagnosis for the clinician. We describe the differential diagnosis among the diseases capable of causing seizure and hemoptysis.
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PMID:Massive hemoptysis after generalized tonic clonic seizure requiring mechanical ventilation. 1220 46

Pulmonary capillary hemangiomatosis (PCH) is a rare cause of primary pulmonary hypertension characterized by thin-walled microvessels infiltrating the peribronchial and perivascular interstitium, the lung parenchyma, and the pleura. These proliferating microvessels are prone to bleeding, resulting in accumulation of hemosiderin-laden macrophages in alveolar spaces. Here we report 2 cases of PCH with pulmonary hypertension, 1 of them associated with mechanical intravascular hemolysis, a feature previously reported in other hemangiomatous diseases, but not in PCH. Case 2 was diagnosed by pulmonary biopsy; to our knowledge the patient is the second adult to be treated with interferon alpha-2a. Review of the literature identified 35 patients with PCH and pulmonary hypertension. The prognosis is poor and median survival was 3 years from the first clinical manifestation. Dyspnea and right heart failure are the most common findings of the disease. Hemoptysis, pleural effusion, acropachy, and signs of pulmonary capillary hypertension are less common. Chest X-ray or computed tomography scan usually shows evidence of interstitial infiltrates, pulmonary nodules, or pleural effusion. Hemodynamic features include normal wedge pressures. Radiologic and hemodynamic findings are undifferentiated from those of pulmonary veno-occlusive disease but differ from other causes of primary pulmonary hypertension. Epoprostenol therapy, considered the treatment of choice in patients with primary pulmonary hypertension, may produce pulmonary edema and is contraindicated in patients with PCH. Regression of lesions was reported in 1 patient treated with interferon therapy and 2 other patients stabilized, including our second patient. PCH was treated successfully by lung transplantation in 5 cases. Early recognition of PCH in patients with suspected primary pulmonary hypertension is possible based on clinical and radiologic characteristics. Diagnosis by pulmonary biopsy is essential for allowing appropriate treatment.
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PMID:Pulmonary capillary hemangiomatosis associated with primary pulmonary hypertension: report of 2 new cases and review of 35 cases from the literature. 1244 98

A 45-year-old patient developed shortness of breath, intensive cough, hemoptysis, chest pain and acute bilateral pulmonary infiltrates following the inhalation of crack-cocaine. The bronchoalveolar lavage and transbronchial biopsy revealed infiltrations of polymorphonuclear neutrophils and the formation of foreign body granulomas. The diagnosis of a crack-syndrome was made and the patient rapidly improved under temporary discontinuation of cocaine inhalation and symptomatic therapy. Crack-cocaine is the free-base of cocaine-hydrochloride and its chemical properties allows it to be inhaled tobacco-like. Therefore the lungs become the principal organs exposed and affected. In addition to our findings, diffuse damage of the alveolar wall and capillary injury due to vasoconstriction and toxic action were reported, in some cases rapidly progressing into pulmonary oedema and ARDS. As the consumption of crack cocaine in Germany has markedly increased over the past decade, a higher prevalence of the reported syndrome has to be assumed.
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PMID:[Crack-syndrome: the pulmonary complications of inhaled cocaine. A review a propos a case report]. 1244 9

Pulmonary edema of water immersion, which is not associated with aspiration or a closed glottis, is infrequently described in the literature. Swimming-induced pulmonary edema is a syndrome whose pathophysiologic characteristics have not been fully elucidated. Immersion alone has marked effects on central vascular volume, redistribution of pulmonary blood flow, and lung volumes. These changes are more prominent in cold water. These changes, coupled with an elevated cardiac output, may expose regions of the capillary bed to high pressures that favor the extravasation of fluid by hydrostatic forces and potential stress failure of the capillaries. Patients with swimming-induced pulmonary edema present with dyspnea, cough, hypoxemia, and occasionally hemoptysis. Physical examination and chest radiographs usually reveal evidence of pulmonary edema. Treatment is symptomatic and conservative. Improvement and resolution of symptoms are usually rapid, with radiographic normalization in 24 to 48 hours. We describe here 3 cases of swimming-induced pulmonary edema.
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PMID:Swimming-induced pulmonary edema. 1254 77

A 64-year-old man complained of irritable cough of 3 months' duration and 1 episode of hemoptysis and dyspnea related to effort. The radiograph revealed a mass in the upper right lobe. Adenocarcinoma of the lung was diagnosed by mediastinoscopy. After removal of the right lung, the patient was admitted to the recovery unit for 36 hours and transferred out without complications. The clinical course in 48 hours on the ward included increasing dyspnea, tachypnea and greater respiratory effort with hypoxemia in spite of increased FiO2. A radiograph showed pulmonary edema and the patient was readmitted to the recovery unit. We describe this case of postpneumonectomy edema and discuss the possible origins of the clinical picture, differential diagnosis, preventive measures and possible treatments.
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PMID:[Post-pneumonectomy edema]. 1270 11

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.
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PMID:Pulmonary edema following closed-circuit oxygen diving and strenuous swimming. 1462 Apr 79

A 33 years old woman was admitted to the hospital after four days with cough, dyspnea, orthopnea and hemoptysis. Blood pressure was 170/90 mmHg, pulse was 112 and temperature was normal. She had cyanosis and a left ventricular gallop, without heart murmurs. A chest radiograph revealed pulmonary edema and echocardiogram showed a global left ventricular systolic disfunction. Oxygen and furosemide were started, but cardiopulmonary collapse ensued. The patient was supported with mechanical ventilation and treated with inotropic drugs. A right sided cardiac catheterization showed pulmonary wedge pressure of 18 mmHg and a cardiac index of 3 l/min/m2. The levels of creatinine and urea nitrogen were elevated and a urine protein was 97 mg/dl. Coagulation tests were normal except by a positive lupic anticoagulant. Markers of connective tissue diseases or vasculitis were negatives. The clinical evolution suggested that a catastrophic antiphospholipid syndrome was ongoing. Intravenous corticoids, gammaglobulin and cyclophosphamide were administered with transient improvement. On her fourth day of treatment, the patient presented sudden pulmonary bleeding and embolism. A plasmapheresis was performed with improvement of renal, cardiac and pulmonary function. After this episode, the patient has been treated with prednisone and oral anticoagulants treatment for the last two years, without further clinical events.
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PMID:[Catastrophic antiphospholipid syndrome and acute heart failure. Report of a case]. 1463 91

A 29-year-old woman was admitted to our hospital with a 7-day history of elevated temperature to 39.5 degrees C associated with headache and nausea. She had been diagnosed with tuberous sclerosis complex 10 years earlier. Her unconsciousness progressed, and she was diagnosed as having aseptic meningoencephalitis. The next day, she had a generalized seizure with severe hemoptysis, and she suddenly fell into severe respiratory failure (PaO2/FiO2 = 76.9). Transbronchial lung biopsy revealed the findings of lymphangioleiomyomatosis. It was suggested that neurogenic pulmonary edema accompanied with venous flow obstruction by lymphangioleiomyomatosis lesions resulted in diffuse pulmonary hemorrhage with resultant gross hemoptysis accelerating to severe hypoxemia.
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PMID:Acute respiratory failure with gross hemoptysis in a patient with lymphangioleiomyomatosis as part of tuberous sclerosis complex. 1546 81

Acute pulmonary oedema has been described in individuals participating in three aquatic activities: (i) scuba diving; (ii) breath-hold diving; and (iii) endurance swimming. In this review, 60 published cases have been compiled for comparison. Variables considered included: age; past medical history; activity; water depth, type (salt or fresh) and temperature; clinical presentation; investigations; management; and outcome. From these data, we conclude that a similar phenomenon is occurring among scuba, breath-hold divers and swimmers. The pathophysiology is likely a pulmonary overperfusion mechanism. High pulmonary capillary pressures lead to extravasation of fluid into the interstitium. This overperfusion is caused by the increase in ambient pressure, peripheral vasoconstriction from ambient cold, and increased pulmonary blood flow resulting from exercise. Affected individuals are typically healthy males and females. Older individuals may be at higher risk. The most common symptoms are cough and dyspnoea, with haemoptysis also a frequent occurrence. Chest pain has never been reported. Radiography is the investigation of choice, demonstrating typical findings for pulmonary oedema. Management is supportive, with oxygen the mainstay of treatment. Cases usually resolve within 24 hours. In some cases, diuretics have been used, but there are no data as to their efficacy. Nifedipine has been used to prevent recurrence, but there is only anecdotal evidence to support its use.
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PMID:Pulmonary oedema of immersion. 1573 Mar 35


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