[Hypereosinophilic syndrome complicated by disseminated intravascular coagulation (DIC), deep venous thrombosis and pulmonary embolism].
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Thromboembolic prophylaxis remains a significant problem and is obviously incompletely understood. It would appear, however, that at present the information available implies several points. First, administration of low-dose heparin is efficacious in preventing deep vein thrombosis and pulmonary emboli in most general surgical patients who are at risk for thromboembolic complications. Second, low-dose heparin probably works by augmenting the effect of the naturally occurring inhibitor to Factor Xa. Third, patients in whom surgical operations are done and extensive tissue dissection or postoperative immobilization (such as hip arthroplasties) is required are probably not protected by low-dose heparin administration; full anticoagulation with warfarin or treatment with one of the platelet antiaggregating agents should be carried out. Fourth, any form of anticoagulation carries some risk of bleeding complications, but it appears that the incidence of major bleeding complications is not significantly greater in the treatment groups.
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Twenty-one patients with acute traumatic spinal cord lesions who were admitted to our Spinal Unit during 1974 have been treated with Calcium Heparin, using a dosage of 5000-7500 i.u. at 12-hourly intervals from the first days after the lesion until the use of a wheelchair, as a prophylactic measure in order to prevent venous thromboembolism. Of these 21 patients 18 received this treatment continuously, with a resulting 0 per cent of venous thrombosis and 0 per cent of pulmonary embolisms. In the three remaining cases, treatment had to be temporarily interrupted and in one case clinical thrombo-phlebitis was clearly evident. No case of pulmonary embolism was registered. We consider this technique to be very useful in the prophylaxis of thrombo-embolic complications in this type of patient. The use of this type of prophylactic therapy, results and conclusions are discussed.
Twenty-one patients with acute traumatic spinal cord lesions, who were admitted to our spinal unit during 1974, have been treated with calcium heparin, using a dosage of 5000-7500 i.u. at 12-hourly intervals from the first days after the lesion until the use of a wheelchair, as a prophylactic measure in order to prevent venous thromboembolism. Of these 21 patients 18 received this treatment continuously, with a resulting 0 per cent of venous thrombosis and 0 per cent of pulmonary embolisms. In the three remaining cases, treatment had to be temporarily interrupted and in one case clinical thrombo-phlebitis was clearly evident. No case of pulmonary embolism was registered. We consider this technique to be very useful in the prophylaxis of thrombo-embolic complications in this type of patient. The use of this type of prophylactic therapy, results and conclusions are discussed.
BACKGROUND: Venous thromboembolism has been recognized as a potentially life-threatening complication following major thoracic trauma. Little or no attention has been directed at the difference in rates of venous thromboembolism in subjects with penetrating and nonpenetrating chest trauma. METHODS: The reported experience with venous thromboembolism in subjects with chest trauma has not segregated the effect penetrating vs. closed chest trauma. The influence of long-term hospitalization to the formation deep vein thrombosis, pulmonary embolism or subsequent death. The present study evaluated the causes of early death occurring within 96 hours of hospitalization for penetrating chest trauma. The clinical records and autopsy reports of 32 individuals, who died within 96 hours of admission to hospital for penetrating chest trauma, were evaluated for the presence of deep vein thrombosis and pulmonary embolism. RESULTS: All 32 subjects were male with an average age of 31 years. Eighty percent were successfully resuscitated in the emergency room. Forty percent (40%) required an emergency or operating room thoracotomy. The initial revised trauma score (RTS) was below 4 in each case. Thirty-two percent (32%) of the patients died on the fourth day; 48% died between 1 and 3 days of admission and 20% died in the emergency room. None of the patients had any clinical signs or evidence of deep vein thrombosis or pulmonary embolism. Moreover, the autopsy findings were negative for deep vein thrombosis and pulmonary embolism. CONCLUSION: Deep vein thrombosis and pulmonary embolism is rarely a cause of death within the initial 96 hours of hospitalization in individuals sustaining penetrating chest trauma.
BACKGROUND: As would be expected with a hypercoagulable state, pulmonary embolism (PE) occurs in sickle cell disease (SCD). Its frequency, however, is undetermined, largely because of difficulties in distinguishing it from thrombosis in situ. The prevalence of deep venous thrombosis (DVT) is also undetermined in patients with SCD. Knowing the prevalence of DVT would be an important step in the overall assessment of the risk of PE in these patients. METHODS: Data from the National Hospital Discharge Survey were assessed. RESULTS: In patients <age 40 years, 7000 of 1,581,000 (0.44%) with SCD had a discharge diagnosis of PE compared with 59,000 of 48,611,000 (0.12%) of African Americans without SCD. The prevalence of DVT was similar in patients < age 40 with SCD, 7000 of 1,581,000 (0.44%) and in African Americans who did not have SCD, 193,000 of 48,611,000 (0.40%). CONCLUSION: The high prevalence of apparent PE in patients with SCD, compared with non-SCD African-American patients of the same age and the comparable prevalence of DVT in both groups are compatible with the concept that thrombosis in situ might be present in many. On the other hand, the data suggest that PE is not rare in patients with SCD. This suggests that PE might be an etiologic factor in patients with SCD who develop respiratory symptoms. In such patients, an imaging procedure might be appropriate.
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