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)

Diagnosis of clinically suspected deep venous thrombosis is based on a clinical score, serial compression ultrasonography and D-dimer assay. For the diagnosis of pulmonary embolism perfusion scintigraphy, ventilation scintigraphy, echography of the leg veins and pulmonary angiography in that order lead to the lowest mortality, morbidity and costs. Diagnostics with spiral CT followed by pulmonary angiography leads to equal mortality and fewer angiography procedures. Decision rules based on anamnesis, physical examination, blood gas analysis and chest radiograph have proved to be insufficiently reliable. The present D-dimer assays have too little sensitivity and too much variability. Thrombo-prophylaxis with low-molecular-weight heparin is indicated for general surgery, joint replacement of the knee or hip, cranial and spinal surgery, subarachnoid haemorrhage after surgical treatment of an aneurysm, acute myocardial infarction, ischaemic stroke or spinal cord lesion, intensive care patients, patients with acute paralysis due to a neuromuscular disorder, and bedridden patients with a risk factor. Prophylaxis has to be continued as long as the indication exists. In the acute phase of deep venous thrombosis or pulmonary embolism treatment with (low-molecular-weight) heparin in an adequate dose is necessary. When started at the same time as coumarin derivatives the treatment with heparin has to be continued for at least 5 days. The risk of postthrombotic syndrome after deep venous thrombosis will be lowered by carrying compression stockings for at least 2 years after the event.
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PMID:[CBO guideline 'Deep venous thrombosis and pulmonary embolism; revision of the earlier guidelines. Dutch Organization for Quality Assurance in Hospitals]. 1152 95

Akinetic crisis (AC) is a life-threatening complication of parkinsonism characterized by an acute severe akinetic-hypertonic state, consciousness disturbance, hyperthermia, and muscle enzymes elevation. Injectable dopaminomimetic drugs, high-dose methylprednisolone, and dantrolene are advocated as putative specific treatments. The course of the illness is frequently complicated by infections, pulmonary embolism, renal failure, disseminated intravascular coagulation, and cardiac arrhythmias. Critical illness neuromyopathy (CINM) is an acquired neuromuscular disorder characterized by flaccid quadriparesis and muscle enzyme elevation, often occurring in intensive care units and primarily associated with inactivity, sepsis, multiorgan failure, neuromuscular blocking agents, and steroid treatment. In 3 parkinsonian patients, during the course of AC we observed disappearance of rigidity but persistent hypoactivity. In all, neurological examination showed quadriparesis with loss of tendon reflexes and laboratory investigation disclosed a second peak of muscle enzymes elevation, following the first increment due to AC. Electrophysiological studies showed absent or reduced sensory nerve action potentials and compound muscular action potentials, myopathic changes, and fibrillation potentials at electromyography recordings, and reduced excitability or inexcitability of tibialis anterior at direct muscle stimulation, leading to a diagnosis of CINM in all 3 patients. In 1 patient, the diagnosis was also confirmed by muscle biopsy. Outcome was fatal in 2 of the 3 patients. Although AC is associated with most of the known risk factors for CINM, the cooccurrence of the 2 disorders may be difficult to recognize and has never been reported. We found that CINM can occur as a severe complication of AC, and should be suspected when hypertonia-rigidity subsides despite persistent akinesia. Strict monitoring of muscle enzyme levels may help diagnosis. This finding addresses possible caveats in the use of putative treatments for AC.
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PMID:Critical Illness Neuromyopathy Complicating Akinetic Crisis in Parkinsonism: Report of 3 Cases. 2618 47