Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034065 (pulmonary embolism)
 14,979 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Streptokinase, urokinase, tissue plasminogen activator and similar drugs can all cause lysis of venous thrombi and pulmonary emboli, but there is small evidence that accelerated lysis achieves a significantly better clinical outcome, on average, in the shorter or longer term, than heparin alone. Thrombolytic therapy for deep leg vein thrombosis aims to restore flow and to preserve venous valves, and so to prevent chronic post-phlebitic disability, but no trial has convincingly demonstrated that the last can be achieved in more than a few patients. Only a small minority of people with extensive proximal thrombosis develop disabling post-phlebitic venous insufficiency, and there are no good clinical predictors of this outcome. As a result, any widespread use of thrombolytics would bring an immediate risk of major bleeding to many people who will never be destined to develop a clinically important problem. Thrombolytic therapy after venous thrombosis should be avoided except, perhaps, in a few carefully selected patients with severe obstruction. The case for using thrombolytics after recent pulmonary embolism is strongest in the limited number of patients with ongoing hypoxia, respiratory distress, pulmonary hypertension and right heart failure, because thrombolytic therapy often achieves an impressive and almost immediate clinical benefit in this clinical setting. Whether early relief from pulmonary artery obstruction translates into longer-term advantage over heparin remains uncertain, however, because no comparative trial has ever shown these drugs to reduce mortality after pulmonary embolism. In all cases, both the physician and the patient must balance the certainty of an immediate bleeding risk against the uncertainty of a better than marginal real benefit.
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PMID:Thrombolytic therapy for venous thrombosis and pulmonary embolism. 1033 Oct 98

We report a case of bilateral chylothorax revealing diffuse tuberculosis. The clinical presentation was complicated by the apparition of a massive acute pulmonary embolism and an acute respiratory distress syndrome. Mycobacterium tuberculosis was isolated from the cultures of the bronchi aspiration of the bronchoscopic examination. With antituberculous chemotherapy, the course of the chylothorax was satisfactory.
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PMID:[Spontaneous bilateral chylothorax revealing disseminated tuberculosis complicated by massive pulmonary embolism]. 1061 55

A thirty-eight-year old immunosuppressed woman presented with respiratory distress and was diagnosed with Pneumocystis Carinii Pneumonia. Pulmonary embolism was also suspected on clinical grounds. A Ventilation-Perfusion Scan was indeterminate. Contrast-enhanced spiral computed tomography of the chest confirmed the presence of a central pulmonary embolus and helped to avoid pulmonary angiography in this critically ill patient.
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PMID:Diagnosis of pulmonary embolus by spiral CT: a case study. 1065 Jul 76

The diagnosis of major pulmonary embolism should be considered in case of acute respiratory distress, particularly when there is high thromboembolic risk. Although clinical symptoms are not specific, some are suggestive: syncope or dizziness with cyanosis and polypnoea, and especially arterial hypotension and cardiogenic shock. Diagnostic workup should be rapid and straight forward. Transthoracic echography is particularly useful to detect right heart thrombi and right ventricular overload. More information could be provided by helical computed tomography or perfusion lung scan or less commonly now by pulmonary angiography, depending on the patient's clinical condition and the available equipment. The mortality rate can reach 20 to 30%, and up to 65% after resuscitated cardiac arrest. Rapid desobstruction is justified through surgical embolectomy or intravenous thrombolysis favouring short duration protocols (alteplase over 2 h), in spite of the bleeding risk.
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PMID:[Major pulmonary embolism]. 1073 26

We report three cases of pleural effusion in the context of ovarian stimulation for in vitro fertilization. The ovarian hyperstimulation syndrome usually causes pleural effusion and ascites. When the latter is lacking, an isolated pleural effusion in a pregnant patient can be mistaken for pulmonary embolism. Early recognition of the condition should allow for an appropriate diagnostic and therapeutic management. Except for some rare but life-threatening complications, such as major hypovolemia or respiratory distress syndrome, the spontaneous outcome is usually favorable. The pathogenesis of this condition may involve an increase of capillary permeability due to the release of vasoactive mediators.
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PMID:An uncommon etiology of isolated pleural effusion. The ovarian hyperstimulation syndrome. 1089 91

A 30-year-old HBsAg-positive woman was admitted to the hospital because of 6 days of progressive shortness of breath. She was in severe respiratory distress with circulatory collapse. She had an enlarged liver but no stigmata of chronic liver disease or signs of cirrhosis. She had rapidly developed respiratory arrest and was transferred to intensive care unit. Heart ultrasonography and Doppler scan showed right heart straining and high pulmonary artery pressure. Despite cardiovascular and respiratory support she died a few hours after admission. Autopsy revealed combined hepatocellular-cholangiocarcinoma infiltrating the entire liver, metastatic invasion of lung blood vessels and absence of right ventricular hypertrophy. The incidence of hepatocellular-cholangiocarcinoma, a variant of hepatocellular carcinoma, is roughly 2-3% and the presenting symptoms are abdominal pain, weight loss, jaundice, fever or decompensation of liver disease. Associated HBsAg positivity and cirrhosis are reported in 20-30% and 60% of patients, respectively. Metastases to lungs are relatively frequent but this is the first report of hepatocellular-cholangiocarcinoma presented with acute respiratory distress due to massive pulmonary embolism.
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PMID:Combined hepatocellular-cholangiocarcinoma presented with massive pulmonary embolism. 1102 Aug 95

Although 3D MRA has been shown to provide excellent depiction of the pulmonary arterial tree, its clinical use has been limited due to lengthy breath-holding requirements. Employing the newest gradient generation (1.5 T MR system, amplitude of 40 mT/m and a slew rate of 200 mT/m/msec), we evaluated a technique permitting the dynamic acquisition of 3D data sets of the entire pulmonary tree in under 4 seconds. Coronal image sets were collected using a repetition time of 1.64 msec and an echo time of 0.6 msec, resulting in an acquisition time of 3.74 seconds. Three volunteers and eight dyspneic patients with known or suspected pulmonary embolism underwent MRI of the pulmonary arteries. The pulmonary arterial tree was visible to a subsegmental level in all examined subjects. Regarding the presence of pulmonary emboli in four patients, there was complete concordance between MR angiographic findings and those of corroborative studies. We conclude that diagnostic MRA of the pulmonary vasculature can be obtained even in patients with severe respiratory distress.
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PMID:Dynamic 3D MR angiography of the pulmonary arteries in under four seconds. 1124 9

We present the case of a 69-year-old man with a history of hypertension and a recent pelvic fracture who presented with acute chest pain, shortness of breath, and severe hypotension. The history of recent pelvic fracture and the clinical manifestations, including the sudden onset of acute respiratory distress, hypotension, and hypoxemia, indicated pulmonary embolism; however, at surgery the patient was found to have an acute dissection of the ascending aorta with obstruction and thrombosis of the right pulmonary artery. This case emphasizes the need to consider such a diagnosis in patients who have unilateral absence of perfusion to the right lung.
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PMID:Acute dissecting aneurysm of the ascending thoracic aorta causing obstruction and thrombosis of the right pulmonary artery. 1145 30

Dental treatment is usually conducted in the oral cavity and in very close proximity to the upper respiratory airway. The possibility of unintentionally compromising this airway is high in the dental environment. The accumulation of fluid (water or blood) near to the upper respiratory airway or the loosening of teeth fragmentations and fallen dental instruments can occur. Also, some of the drugs prescribed in the dental practice are central nervous system depressants and some are direct respiratory drive depressors. For this reason, awareness of the respiratory status of the dental patient is of paramount importance. This article focuses on several of the more common causes of respiratory distress, including airway obstruction, hyperventilation, asthma, bronchospasm, pulmonary edema, pulmonary embolism and cardiac insufficiency. The common denominator to all these conditions described here is that in most instances the patient is conscious. Therefore, on the one hand, valuable information can be retrieved from the patient making diagnosis easier than when the patient is unconscious. On the other hand, the conscious patient is under extreme apprehension and stress under such situations. Respiratory depression which occurs during conscious sedation or following narcotic analgesic medication will not be dealt with in this article. Advanced pain and anxiety control techniques such as conscious sedation and general anesthesia should be confined only to operators who undergo special extended training.
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PMID:[Respiratory distress]. 1185 48

We report the case of a 13-year-old male presenting with recurrent symptoms of respiratory distress after a trauma of the lower limb. Pulmonary symptoms had been misinterpreted for several weeks and only marked symptoms of deep venous (DVT) and caval vein thrombosis later prompted the correct diagnosis of DVT and embolic events and subsequently a successful thrombolytic therapy. The case reported here shows a diagnostic pitfall of pulmonary embolism in an adolescent. It emphasizes the need to consider the possibility of thromboembolic events also in young children and adolescents presenting with atypical pulmonary symptoms and suffering from pulmonary diseases not responding to antibiotic therapy. In addition, although the homozygous PT A20210A gene mutation is a rare defect and its relevance as a risk factor on its own remains to be elucidated, this case suggests that a complete thrombophilia laboratory workup should be performed in young patients with a first symptomatic thromboembolic onset.
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PMID:Recurrent pulmonary embolism in a 13-year-old male homozygous for the prothrombin G20210A mutation combined with protein S deficiency and increased lipoprotein (a). 1186 7


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