Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019079 (hemoptysis)
 6,129 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 58-year-old female was admitted with an abrupt onset of chest and back pain. The CT scan of the chest showed aortic dissection of the ascending aorta and proximal aortic arch, but the false lumen of the aortic dissection had already been occluded by a blood clot. After admission, she complained of chest pain with hemoptysis and presented facial edema and the distention of the neck veins. The pulmonary angiogram showed complete occlusion of the right pulmonary artery at the proximal segment. These findings were interpreted as pulmonary embolism. She was treated with intravenous heparin and urokinase, but these treatments did not demonstrate any improvement. She underwent a surgical exploration on the fourth hospital day. During surgery, the right pulmonary artery was discovered to be compressed and occluded by the large dissecting aneurysm of the ascending aorta. In addition, hematoma was seen between the right pulmonary artery. The ascending aorta and pulmonary trunk, which was injured in the operative procedure, were replaced with an artificial graft successfully. Postoperative pulmonary angiogram showed no stenosis of right pulmonary artery. The occlusion of the pulmonary artery by an acute dissecting aneurysm is an extremely rare complication and it is often wrongly diagnosed as pulmonary embolism. In such cases, the correct diagnosis and prompt surgical treatment is essential and antithrombolytic and anticoagulant therapy should be avoided.
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PMID:[Occlusion of the right pulmonary artery due to acute dissecting aortic aneurysm]. 194 May 29

The history and physical examination were assessed in 215 patients with acute pulmonary embolism uncomplicated by preexisting cardiac or pulmonary disease. The patients had been included in the Urokinase Pulmonary Embolism Trial or the Urokinase-Streptokinase Embolism Trial. Presenting syndromes were (1) circulatory collapse with shock (10 percent) or syncope (9 percent); (2) pulmonary infarction with hemoptysis (25 percent) or pleuritic pain and no hemoptysis (41 percent); (3) uncomplicated embolism characterized by dyspnea (12 percent) or nonpleuritic pain usually with tachypnea (3 percent) or deep venous thrombosis with tachypnea (0.5 percent). The most frequent symptoms were dyspnea (84 percent), pleuritic pain (74 percent), apprehension (63 percent) and cough (50 percent). Hemoptysis occurred in only 28 percent. Dyspnea, hemoptysis or pleuritic pain occurred separately or in combination in 94 percent. All three occurred in only 22 percent. The most frequent signs were tachypnea (respiration ate 20/min or more) (85 percent), tachycardia (heart rate 100 beats/min or more) (58 percent), accentuated pulmonary component of the second heart sound (57 percent) and rales (56 percent). Signs of deep venous thrombosis were present in only 41 percent and a pleural friction rub was present in only 18 percent. Either dyspnea or tachypnea occurred in 96 percent. Dyspnea, tachypnea or deep venous thrombosis occurred in 99 percent. As a group, the identified clinical manifestations, although nonspecific, are strongly suggestive of acute pulmonary embolism. Conversely, acute pulmonary embolism was rarely identified in the absence of dyspnea, tachypnea or deep venous thrombosis.
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PMID:History and physical examination in acute pulmonary embolism in patients without preexisting cardiac or pulmonary disease. 746 69

Endobronchial streptokinase has been used previously to dissolve blood clots caused by massive spontaneous hemoptysis, in settings including sarcoidosis, cavitary histoplasmosis, and multiple myeloma. To our knowledge, however, the use of thrombolytic agents to dissolve clots following transbronchial biopsy has not been reported previously. We describe a patient in whom endobronchial urokinase was used for successful dissolution of clots secondary to massive bleeding after transbronchial biopsy.
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PMID:Endobronchial urokinase for dissolution of massive clot following transbronchial biopsy. 813 76

Patients with nephrotic syndrome carry a high risk of pulmonary embolism due to the abnormalities in coagulation and fibrinolysis. Thrombolytic therapy for critical pulmonary embolism in nephrotic syndrome patients was rarely reported and remains controversial in the regimen selection so far. We reported a case of fatal pulmonary embolism, complicating in hepatitis B virus-associated nephrotic syndrome. The patient presented with chest pain, hemoptysis and shortness of breath on admission and his initial vital signs showed a high risk of developing hypotension. Urgent radiological examinations confirmed massive embolisms in bilateral pulmonary arteries. Prompt thrombolytic therapy was performed right after the diagnosis of pulmonary embolism with an intravenous infusion of urokinase (20 000 U/kg) in 2 h. Complete resolution of pulmonary embolism was achieved after urokinase administration and the patient was discharged in good conditions. This report highlighted the efficacy and safety of prompt thrombolytic therapy with urokinase for nephrotic syndrome patients presented with massive pulmonary embolism. In this study, we also briefly discuss the recent findings on the current state of urokinase in the clinical practice of thrombolysis.
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PMID:High dose urokinase against massive pulmonary embolism in nephrotic syndrome. 2338 77

A 75-year-old woman who had been treated for pulmonary Mycobacterium intracellulare infection was admitted to a nearby hospital because of hemoptysis, right pneumothorax, and empyema. She had been treated by thoracic drainage and pleural lavage, but was reffered to our hospital because of refractory empyema. Her chest radiograph and chest computed tomography( CT) showed right chronic empyema of which pleural aspirate was smear positive for acid-fast bacilli and positive for the polymerase chain reaction method(PCR)-Mycobacterium intracellulare. Serum levels of white blood cell and C-reactive protein(CRP) were found to be slightly elevated. She was treated with combined use of ethambutol, rifampicin, clarithromycin, and kanamycin and with pleural curettage by thoracoscopic surgery. After surgery additional treatment was done using urokinase which was administered into the thoracic cavity via an thoracic tube. Chronic empyema gradually improved with the treatment and the pleural effusion became bacterial free, enabling the patient to discharge from hospital without thoracic drainage.
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PMID:[Pulmonary mycobacterium intracellulare infection complicated with pneumothorax and chronic empyema]. 2391 30