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

A variety of clinical diseases are associated with diffuse alveolar hemorrhage. Although mitral valve disease can cause hemoptysis, it rarely is associated with diffuse alveolar hemorrhage at presentation. A 49-year-old woman was admitted to the hospital with the abrupt onset of fever, anemia, dyspnea, azotemia, and diffuse alveolar infiltrates. Two-dimensional echocardiography done several months earlier to evaluate atypical chest pain had been unremarkable. Fiberoptic bronchoscopy 2 days after admission to the hospital revealed fresh blood throughout the tracheobronchial tree. The infiltrates resolved rapidly and completely during systemic steroid therapy only to reappear as the steroids were tapered, suggesting a beneficial therapeutic response. Results of serologic evaluation were negative. Transbronchial biopsies showed inflammation and hemosiderin-laden macrophages; no specific diagnosis was established. The patient was scheduled for open lung biopsy. The surgeon was concerned about the history of chest pain and requested placement of a pulmonary artery catheter, which revealed severe pulmonary hypertension. Transesophageal echocardiography and subsequent cardiac catheterization showed severe mitral regurgitation. Mitral valve replacement resulted in complete elimination of symptoms.
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PMID:Diffuse alveolar hemorrhage syndrome due to 'silent' mitral valve regurgitation. 1065 69

A 71-year-old man who had been suffering from slowly progressive dyspnea on exertion for 16 years was admitted because of hemoptysis and severe dyspnea in 1997. His medical history included respiratory failure in 1986. At that time, chest X-ray films showed cardiomegaly and striking enlargement of hilar pulmonary arteries, while a lung perfusion scan revealed segmental defects. A diagnosis of chronic thromboembolic pulmonary hypertension (CTPH) was made on the basis of multiple filling defects detected by pulmonary angiography and marked pulmonary hypertension (104/29 mmHg) measured by right heart catheterization. The patient died unexpectedly 1 month later. Autopsy revealed a large new thrombotic lesion straddling the organizing thrombotic lesion in the right pulmonary artery. It is important to keep CTPH in mind when examining and treating patients with unexplained dyspnea. In this respect, our case was considered of value to an understanding of the natural course of CTPH.
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PMID:[An autopsy case of chronic thromboembolic pulmonary hypertension with long-term progressive dyspnea]. 1097 84

Authors described a case of 26-year old patient with history of progressing dyspnea and repetitive syncopes. In history is intermittent hemoptysis and dyspnea from 1990. Diagnosis of thromboembolic disease was suspected. Clinical picture was dominated by dyspnea, central cyanosis, sinus tachycardia without pulmonary signs of hearth failure. On ecg there is right heart hypertrophy. Echocardiographic examination shows dilatation of right heart, systolic pressure in a. pulmonalis about 90 mmHg and tricuspidal regurgitation of the III. degree. Phlebothrombosis was not found. Complete hemocoagulation examination excluded a primary procoagulating hematologic disease. Pulmonary angiography did not confirm thromboembolic disease but found a high grade pulmonary hypertension--mean pulmonary arterial pressure of 93 mmHg. After complex pneumological examination, including HRCT, and other examinations the diagnosis of primary pulmonary hypertension was made. Patient is indicated to lung transplantation. (Fig. 4, Ref. 9.)
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PMID:[Primary pulmonary hypertension]. 1103 5

A 44-year-old woman with recurrent pulmonary infections developed severe hemoptysis. Chest radiography revealed a hypoplastic right lung. Absence of the right pulmonary artery, a very rare congenital anomaly, was demonstrated by computed tomography and cardiac catheterization. Severe pulmonary hypertension in the contralateral lung precluded right pneumonectomy but percutaneous embolization of a large systemic arterial collateral to the right lung provided palliative relief of hemoptysis.
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PMID:Congenital agenesis of the right pulmonary artery. 1110 81

Pulmonary embolism is nearly always a complication of deep venous thrombosis. The evaluation of risk factors for venous thromboembolism not only aids diagnosis but also guides decisions about the intensity of prophylactic measures. As both the extent and chronicity of pulmonary vascular obstruction vary widely, pulmonary embolism can produce widely differing clinical pictures. From the clinical, pathophysiological and therapeutical point of view, it is convenient to classify pulmonary embolism into four types: acute minor embolism (dyspnoea with or without pleuritic pain or haemoptysis), acute massive embolism (hemodynamic instability), subacute massive embolism (mimicking heart failure or indolent pneumonia), and chronic thromboembolic pulmonary hypertension (slowly progressing dyspnoea). This classification is of importance not only for the rational diagnosis and differential diagnosis, but also for the institution of adequate therapy. Because the disease has many nonspecific manifestations but no pathognomonic symptoms or signs, it is impossible to prove the diagnosis of pulmonary embolism alone on the basis of clinical presentation.
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PMID:[Clinical characteristics of pulmonary embolism]. 1121 69

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

Hemoptysis, the expectoration of blood or bloody mucus from the respiratory tract at or below the larynx, was retrospectively evaluated in 36 dogs. Cough, tachypnea, and dyspnea were common historical and physical examination signs. Anemia was documented in 11 dogs, but was severe in only one dog. Other clinicopathological findings reflected the underlying diseases. All thoracic radiographs obtained were abnormal; alveolar and interstitial patterns were most common. Diseases predisposing to hemoptysis included bacterial bronchopneumonia (n=7), neoplasia (n=5), trauma (n=5), immune-mediated thrombocytopenia (n=4), heartworm disease (n=4), rodenticide poisoning (n=3), lung-lobe torsion (n=1), left-sided congestive heart failure (n=1), pulmonary hypertension (n=1), and foreign-body pneumonia (n=1). Four additional dogs had more than one underlying disease process. Nine dogs were either euthanized or died in the hospital during the initial visit. While at least half of the 27 dogs discharged went on to completely recover, five dogs discharged were known to have either died or been euthanized as a result of their disease in <6 months.
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PMID:Clinical signs, clinicopathological findings, etiology, and outcome associated with hemoptysis in dogs: 36 cases (1990-1999). 1190 30

A 28-year-old male was referred to our hospital because of hemoptysis. A chest X-ray revealed an increase of vascular marking in the left lower field and a partial defect in the lateral line of the descending thoracic aorta. An aortogram and pulmonary arteriogram showed a large artery arising from the descending thoracic aorta and supplying the left basal segment, which had no normal pulmonary arteries. A bronchoscopy showed no abnormal findings in the bronchial tree. A clinical diagnosis of systemic arterial supply to the basal segment of the left lower lung was made, and a left lower lobectomy and closure of the anomalous systemic artery by video-assisted thoracic surgery (VATS) were successfully performed. Vascular marking of the visceral pleura of left lower basal segment was observed and the anomalous arterial pressure was 84 mmHg, as high as systemic arterial pressure, during the procedure. The histopathological examination revealed normal alveolar structure, and sclerosis and hypertrophy of pulmonary arteries of the lesion (Heath-Edwards V, which means irreversible vascular changes due to pulmonary hypertension). The patient had an uneventful postoperative course and was discharged on postoperative day 8. The VATS procedure is a more useful and less invasive method for cases of systemic arterial supply to the basal segment of the left lower lung than an open thoracotomy.
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PMID:[Anomalous systemic arterial supply to normal basal segment of the left lower lobe; report of a case]. 1217 32

Hemoptysis can be caused by either pulmonary or extrapulmonary causes. Congenital heart disease should be considered as a possible cause in patients who have no obvious evidence of pulmonary disease. We report on an 8-year-old girl who presented with recurrent hemoptysis without other cardiopulmonary signs, except for mild tachypnea and a prominent pulmonic component of the second heart sound, suggesting pulmonary hypertension. A chest X-ray revealed pulmonary venous congestion without other parenchymal disease. An echocardiogram revealed classical cor triatriatum, with a 6-mm orifice in the anomalous septum. Cardiac evaluation should be considered in patients with hemoptysis unexplained by pulmonary causes, even in the absence of overt cardiac symptoms.
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PMID:Cor triatriatum: a cause of hemoptysis. 1235 91

Pulmonary vein (PV) stenosis has emerged recently as an important issue in patients who received radiofrequency (RF) ablation of atrial fibrillation (AF). Serial pathophysiological responses, including thrombosis, metaplasia, proliferation and neovascularization, may lead to PV stenosis after RF energy application around or inside the PV ostia. The clinical manifestations of PV stenosis consist of chest pain, dyspnea, cough, hemoptysis, recurrent lung infection and pulmonary hypertension. Although PV stenosis can be asymptomatic, its severity may be related to the numbers of stenotic PVs, the degree and chronicity of PV stenosis. The incidence of PV stenosis (defined as luminal diameter reduction >50%) detected by spiral computer tomography scan or three dimensional magnetic resonance angiography was from 0 to 7% per PV after isolation of PVs from left atria. Furthermore, some patients may show late progression of PV stenosis during follow-up. The first choice of treatment for symptomatic PV stenosis is PV angioplasty with stenting; however, restenosis were reported occasionally. Several studies have analyzed the predictors of PV stenosis, and the results are controversial. However, the consensus for prevention of PV stenosis should include less energy application and the ablation site more close to the atrial site.
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PMID:Evaluation of pulmonary vein stenosis after catheter ablation of atrial fibrillation. 1243 19


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