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

Pulmonary edema occurring in divers using a self-contained underwater breathing apparatus (scuba) is an uncommon, probably under-reported, but potentially life-threatening and recurrent condition. We report six episodes of pulmonary edema in five scuba divers seen during a period of 15 months. The four men and one woman ranged in age from 37 to 56 years and two were treated for hypertension. Symptoms were mostly dyspnea onset at depth, cough, hemoptysis and hypoxemia, which in the recurrent case led to cardiac arrest and death. All cases occurred in rather cold water. Findings on thoracic computed tomography (CT) scanning ranged from pleural effusion to ground-glass opacities restricted to a few areas of the lung. The complex underlying mechanisms that would contribute to a raised transalveolar pressure or to a disruption of the blood-gas barrier are discussed. It is important for emergency care providers to be aware of this syndrome for prompt recognition and optimal treatment.
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PMID:Pulmonary edema in scuba divers: recurrence and fatal outcome. 1579 13

We treated a 59-year-old woman presenting with hemoptysis, a rare symptom of pheochromocytoma. Multiple factors including hypertension caused by sudden catecholamine release may result in pulmonary edema. It should be noted that the increased activation of coagulation cascade, which was demonstrated by increased thrombin-antithrombin III complex (TAT) and prothrombin fragment factor 1 and 2 (F1 + 2), as well as endothelial or platelet stimulation evidenced by the increased plasma von Willebrand factor, may have contributed to hemoptysis. These abnormalities were normalized after adrenalectomy. Our case indicates the important role of catecholamine in coagulopathy and possibly in vasculopathy.
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PMID:A pheochromocytoma causing limited coagulopathy with hemoptysis. 1595 97

An unusual case of fibrosing mediastinitis with obstruction of the inferior and superior left pulmonary veins and severe narrowing of the right pulmonary artery, disclosed after unilateral pulmonary edema, is described. The 18-year-old male patient had a long history of cough, progressive dyspnea and recurrent hemoptysis and the possible diagnosis of "interstitial fibrosis" from a previous lung biopsy. The diagnosis and the pulmonary vessels involvement were suspected after right heart catheterization combined with transesophageal echocardiography and confirmed during urgent thoracotomy and at postmortem examination.
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PMID:Unilateral pulmonary edema due to pulmonary venous obstruction from fibrosing mediastinitis. 1652 Jan 36

Medical observations are reported from an eight-day world championship breath-hold diving competition involving 57 participants. The deepest dive was to 75 metres, and the longest breath-hold time exceeded 9 minutes. There were 35 diving-related adverse events witnessed or reported, including transient loss of motor control due to hypoxia, syncope during ascent, hemoptysis, and pulmonary edema. All events occurred in healthy individuals, and resolved without apparent sequelae. There was no relationship between symptoms and depth. The medical implications of these adverse events are discussed. Despite the inherent risks of the sport, established organizational procedures for competitive breath-hold diving maintain a high degree of safety.
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PMID:Adverse events in competitive breath-hold diving. 1660 57

Postobstructive pulmonary oedema is a complication after extubation that occurs rarely . It can be associated with haemoptysis. We report two cases of haemoptysis occuring in ASA 1 otherwise healthy patients who underwent uncomplicated anaesthesia. Understanding of the mechanism and prompt treatment lead to rapid recovery of this dramatic complication.
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PMID:[Haemoptysis after anesthesia]. 1685 78

Almost one mountain trekker or climber out of two develops several symptoms of high altitude illness after a rapid ascent (> 300 m/day) to an altitude above 4000 m. Individual susceptibility is the most important determinant for the occurrence of high altitude pulmonary oedema (HAPE). Symptoms associated with HAPE are incapacitating fatigue, chest tightness, dyspnoea at the slightest effort, orthopnoea, and cough with due to haemoptysis in an advanced stage of the disease pink frothy sputum. The hallmark of HAPE is an excessively elevated pulmonary artery pressure (mean pressures of 35 and 55 mm Hg), which precedes the development of pulmonary oedema. Elevated pulmonary capillary pressure and protein- as well as red blood cell-rich oedema fluid without signs of inflammation in its early stage are characteristic findings. Furthermore, decreased fluid clearance from the alveoli may contribute to this non-cardiogenic pulmonary oedema. Immediate descent or supplemental oxygen and nifedipine are recommended until descent is possible. Susceptible individuals can prevent HAPE by slow ascent: an average gain of altitude not exceeding 400 m/day above an altitude of 2500 m. If progressive high altitude acclimatization is not possible, a prophylaxis with nifedipine should be recommended.
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PMID:High altitude-induced pulmonary oedema. 1690 89

Ischemic mitral regurgitation is a complication of coronary artery disease specifically in the settings of prior myocardial infarction. It is a dynamic lesion and its severity may increase with different forms of exercise leading to flash pulmonary edema. We present the case of an 81-year-old man with ischemic mitral regurgitation who presented with long standing history of hemoptysis limited to sexual intercourse only. After a thorough negative work-up for the usual causes of hemoptysis, comprehensive right and left cardiac catheterization studies revealed marked increase in baseline mitral regurgitation and pulmonary capillary wedge pressure with isometric exercise. This case illustrates that sexual intercourse, a form of isometric exercise, can cause severe increase in ischemic mitral regurgitation and more so compared to other forms of exercise due to heightened sympathetic activity, leading to flash pulmonary edema and hemoptysis.
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PMID:Post coital hemoptysis. 1805 33

To simulate pressure effects and experience thoracic compression while breath-hold diving in a relatively safe environment, competitive breath-hold divers exhale to residual volume before diving in a swimming pool, thus compressing the chest even at depth of only 3-6 m. The study was undertaken to investigate whether such diving could cause pulmonary edema and hemoptysis. Eleven volunteer breath-hold divers who regularly dive on full exhalation performed repeated dives to 6 m during a 20-min period. The subjects were studied with dynamic spirometry, video-fibernasolaryngoscopy, and single-breath diffusion capacity of carbon monoxide (Dl(CO)). The duration of dives with empty lungs ranged from 30 to 120 s. Postdiving forced vital capacity (FVC) was reduced from mean (SD) 6.57 +/- 0.88 to 6.23 +/- 1.02 liters (P < 0.05), and forced expiratory volume during the first second (FEV(1.0)) was reduced from 5.09 +/- 0.64 to 4.59 +/- 0.72 liters (P < 0.001) (n = 11). FEV(1.0)/FVC was 0.78 +/- 0.05 prediving and 0.74 +/- 0.05 postdiving (P < 0.001) (n = 11). All subjects reported a (reversible) change in their voice after diving, irritation, and slight congestion in the larynx. Fresh blood that originated from somewhere below the vocal cords was found by laryngoscopy in two subjects. Dl(CO)/alveolar ventilation (Va) was 1.56 +/- 0.17 mmol.kPa(-1).min(-1).l(-1) before diving. After diving, the Dl(CO)/Va increased to 1.72 +/- 0.24 (P = 0.001), but 20 min later it was indistinguishable from the predive value: 1.57 +/- 0.20 (n = 11). Breath-hold diving with empty lungs to shallow depths can induce hemoptysis in healthy subjects. Edema was possibly present in the lower airways, as suggested by reduced dynamic spirometry.
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PMID:Pulmonary edema and hemoptysis after breath-hold diving at residual volume. 1823 82

During an international breath-hold diving competition, 19 of the participating divers volunteered for the present study, aimed at elucidating possible symptoms and signs of pulmonary edema after deep dives. Measurements included dynamic spirometry and pulse oximetry, and chest auscultation was performed on those with the most severe symptoms. After deep dives (25-75 m), 12 of the divers had signs of pulmonary edema. None had any symptoms or signs after shallow pool dives. For the whole group of 19 divers, average reductions in forced vital capacity (FVC) and forced expiratory volume in the first second (FEV(1)) were -9 and -12%, respectively, after deep dives compared with after pool dives. In addition, the average reduction in arterial oxygen saturation (Sa(O(2))) was -4% after the deep dives. In six divers, respiratory symptoms (including dyspnea, cough, fatigue, substernal chest pain or discomfort, and hemoptysis) were associated with aggravated deteriorations in the physiological variables (FVC: -16%; FEV(1): -27%; Sa(O(2)): -11%). This is the first study showing reduced spirometric performance and arterial hypoxemia as consequences of deep breath-hold diving, and we suggest that the observed changes are caused by diving-induced pulmonary edema. From the results of the present study, it must be concluded that the great depths reached by these elite apnea divers are associated with a risk of pulmonary edema.
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PMID:Pulmonary edema after competitive breath-hold diving. 1821 6

Following an international consensus conference held in Chapel Hill, North Carolina, USA, vasculitides have been divided based on the size of the vessel involved in the inflammatory process. Thus, the terms large, medium and small vessel vasculitis emerged. Wegener's granulomatosis, microscopic polyangitis and Churg-Strauss syndrome are described as small vessel vasculitides. Pulmonary involvement is a characteristic feature of both Wegener's granulomatosis and Churg-Strauss syndrome, less so in microscopic polyangitis. A pathognomonic feature is alveolar haemorrhage, which encompasses the trias: 1) bilateral acinar pulmonary infiltrates reminiscent of pulmonary edema, 2) anemia and 3) haemoptysis, which however may be absent. Bronchoalveolar lavage typically returns lavage fluid that remains hemorrhagic even after sequential sampling. The discovery that antineutrophil cytoplasmic antibodies (ANCA) are strongly associated with vasculitic disorders and their subsequent characterisation has led to improved understanding of the pathogenic mechanisms underlying vasculitis. This paper will review clinical aspects of pulmonary involvement in the systemic vasculitides.
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PMID:[Pulmonary vasculitis]. 1862 34


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