Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Heparin-induced thrombocytopenia and thrombosis syndrome (HITTS) is an immune-mediated response to the administration of heparin that results in life-threatening thrombosis. The pathophysiology of HITTS remains controversial. The onset of clinical symptoms and laboratory changes is usually delayed 1-2 weeks after exposure to heparin. Thrombosis occurs in both the arterial and venous circulation with significant morbidity and mortality. Complications include deep venous thrombosis, pulmonary embolus, stroke, myocardial infarction, chronic venous insufficiency, extremity ischemia, gangrene, and death. Diagnostic criteria for HITTS include thrombocytopenia during heparin exposure, exclusion of other causes such as sepsis or medications, resolution of thrombocytopenia after withdrawal of heparin, demonstration of in vitro heparin-dependent platelet antibodies, and development of vascular thrombosis. Despite having several disadvantages, the carbon-14-serotonin release assay is the most sensitive and specific test for HITTS. Angiography as an adjunct to other imaging modalities can document the presence, location, and extent of thrombus. Optimal treatment has not yet been defined but should include immediate discontinuation of use of all heparin products and heparin-coated catheters. In addition, alternate methods of antithrombotic therapy should be considered. In severe cases, thrombolysis or thrombectomy may be warranted. Familiarity with the pathophysiology, clinical manifestations, complications, diagnostic criteria, and treatment options associated with HITTS will enable timely recognition and facilitate prompt and effective treatment.
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PMID:Heparin-induced thrombocytopenia and thrombosis syndrome. 946 Jan 12

Heparin-induced thrombocytopenia, an increasingly recognized aspect of heparin therapy, occurs in 0.6% to 30% of patients receiving heparin. Approximately 1% of those patients develop the more severe heparin-induced thrombocytopenia II, also called white clot syndrome, in which synchronous venous and arterial thrombi impede blood flow in central vessels. Mortality (as high as 25%) and morbidity are related to the site and extent of thrombi formation. Following vascular surgery, one patient manifested an unusual consequence of heparin-induced thrombocytopenia II when thrombotic blockage of the vessels supplying the bilateral gluteus maximus and minimus muscles resulted in tissue ischemia and death. Supporting the patient through numerous complications and managing the extensive wound healing process required multidisciplinary skills and innovative technology, including use of vacuum-assisted closure therapy, platelet-derived growth factors, parenteral and enteral nutritional support, and spirit-restoring favorite foods. This article describes the patient's life-threatening and long-lasting effects from an allergic reaction to heparin therapy. In addition to information about the diagnosis of heparin-induced thrombocytopenia, this article also describes management of the wound and other aspects of care and comforting that occurred over a 9-month hospitalization.
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PMID:Heparin-induced thrombocytopenia as the cause of gluteus muscle necrosis: a case study describing the benefits of multidisciplinary physical and psychosocial interventions. 1188 19

Heparin-induced thrombocytopenia (HIT) is of special interest to vascular surgeons as heparin is the predominant anticoagulant used before, during, and after vascular surgery. Further, the prothrombotic nature of this antibody-mediated disorder leads to a high frequency of limb ischemia due to large arterial occlusion by platelet-rich ("white") clots or because of extensive venous thrombosis involving large veins and small venules. This latter syndrome has been associated with coumarin anticoagulation of HIT-associated deep-vein thrombosis (coumarin-induced venous limb gangrene). Non-heparin anticoagulants, such as the direct thrombin inhibitors (lepirudin, argatroban), may be needed for intraoperative management of a patient with suspected acute HIT who requires vascular surgery. The transience of HIT antibodies provides a rationale for intraoperative use of heparin in a patient who has recovered from HIT and in whom HIT antibodies are no longer detectable.
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PMID:Heparin-induced thrombocytopenia and vascular surgery. 1528 34

Heparin-induced thrombocytopenia HIT is a potentially devastating complication of heparin therapy. The severe form of HIT has been associated with both venous and arterial thrombosis manifested by myocardial infarction, cerebrovascular occlusion, skin necrosis or limb ischemia. Several agents are now available as alternatives to heparin in patients with suspected HIT, including the thrombin specific inhibitors lepirudin and argatroban as well as the low molecular weight heparinoid known as danaparoid. When lacking these agents, here we report the use of plasmapheresis to create an artificial state of anticoagulation; exchanging patient's plasma with albumin rather than fresh frozen plasma, to allow the safe introduction of warfarin.
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PMID:Treating heparin-induced thrombocytopenia. The unconventional way! 1544 79

Although heparin/protamine has been the standard anticoagulation regimen in cardiac surgery for decades, it induces negative reactions within the vasculature. Heparin-induced thrombocytopenia (HIT) is a highly prothrombotic immune reaction to heparin that may result in death, limb ischemia leading to amputation, graft occlusion, and other severe thrombotic events. Patients undergoing cardiac surgery are at high risk for HIT antibody seroconversion and at risk for clinical HIT. For patients with acute or subacute HIT and needing urgent cardiac surgery, accepted protocols for alternative, non-heparin anticoagulation are needed. The direct thrombin inhibitor bivalirudin offers promise in this area and is currently being evaluated in multicenter trials as an alternative for heparin/protamine in patients with HIT undergoing cardiac surgery.
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PMID:Update on heparin-induced thrombocytopenia and cardiovascular interventions. 1610 55

Heparin-induced thrombocytopenia, or HIT, can present in many ways, ranging from common-isolated thrombocytopenia, venous thromboembolism, acute limb ischemia-to less common but specific presentations-necrotizing skin lesions at heparin injection sites, post-bolus acute systemic reactions, and adrenal hemorrhagic necrosis (secondary to adrenal vein thrombosis). Many patients with HIT have mild or moderate thrombocytopenia: the median platelet count nadir is 60 x 10(9)/L, and ranges from 15 to 150 x 10(9)/L in 90% of patients, most of whom evince a 50% or greater fall in the platelet count. HIT that begins after stopping heparin ("delayed-onset HIT") is increasingly recognized. Factors influencing risk of HIT include type of heparin (unfractionated heparin > low-molecular-weight heparin), type of patient (surgical > medical), and gender (female > male). Since timely diagnosis and treatment of HIT may reduce the risk of adverse outcomes, this review focuses on those clinical circumstances that should prompt the clinician to "think of HIT." Coumarin anticoagulants such as warfarin are ineffective in acute HIT and can even be deleterious by predisposing to micro-thrombosis via protein C depletion (venous limb gangrene and skin necrosis syndromes). Thus, it is important to avoid or postpone coumarin while managing HIT hypercoagulability, focusing on agents that inhibit thrombin directly (lepirudin, argatroban) or that inhibit its generation (danaparoid, fondaparinux). Post-marketing experience suggests that standard dosing of lepirudin is too high; current recommendations are to avoid the initial lepirudin bolus and to begin with lower infusion rates, even in patients without overt renal dysfunction.
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PMID:Think of HIT. 1712 91

Heparin-induced thrombocytopenia (HIT) is an underdiagnosed problem, and the optimal treatment of arterial thrombosis in patients with HIT remains controversial. There are many angiographic procedures which require heparin as an adjunctive agent; however, some of the heparin-related complications and their management remains unclear. We are presenting a 77-year-old male patient with HIT, who developed acute lower extremity limb threatening ischemia due to arterial thrombosis. In our case, the patient has been successfully treated with percutaneous catheter-directed thrombolysis with tissue plasminogen activator and a direct thrombin inhibitor argatroban.
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PMID:Catheter-directed thrombolysis of acute lower extremity arterial thrombosis in a patient with heparin-induced thrombocytopenia. 1804 75

Heparin-induced thrombocytopenia (HIT) is caused by platelet-activating antiplatelet factor 4/heparin antibodies. However, clinical HIT (thrombocytopenia or thrombosis, or both) develops in only a minority of patients who form antibodies. It is difficult to distinguish HIT from non-HIT thrombocytopenia in patients after ventricular assist device (VAD) implantation. Further, the risks of heparin-induced immunization and clinical HIT approach 65% and 10%, respectively, in this patient population, with a particularly high risk of cerebrovascular ischemia/infarction. Given the apparent high risk of HIT and its complications, and the diagnostic challenges, we suggest that the VAD patient population be evaluated using alternative, nonheparin agents for routine postimplantation anticoagulation.
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PMID:Heparin-induced thrombocytopenia in patients with ventricular assist devices: are new prevention strategies required? 1937 37

Heparin-induced thrombocytopenia (HIT) and heparin-induced thrombocytopenia with thrombosis (HITT) syndromes are the result of an adverse reaction to heparin that results in a spectrum of laboratory and end-organ manifestations secondary to thrombosis of both arterial and venous small and large vessels. HITT most often manifests in the extremities as acral ischemia and necrosis, with a spectrum of severity. The lower extremity surgical patient is at risk for deep venous thrombosis, and when exposed to heparin products, is also at risk for the development of a heparin-induced thrombocytopenic syndrome. This article reports on a cohort of patients from a tertiary referral lower extremity reconstruction practice with the HIT/HITT syndromes, with an analysis of the frequency, medical characteristics, clinical settings, lower extremity manifestations, management, and outcomes of patients with HIT/HITT.).
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PMID:Lower extremity manifestations and treatment of heparin-induced thrombocytopenia syndromes: a cohort study. 2105 74

Heparin-induced thrombocytopenia (HIT) is an immune-mediated thrombocytopenia resulting from prior heparin exposure. It can be associated with limb- or life-threatening thrombotic events. Patients undergoing any vascular procedures including endovascular procedures that require heparin administration are at risk. There is very little reported in the literature with regards to thrombosis associated with HIT after endovascular aortic aneurysm repair. All reported cases of HIT thrombosis presented as acute arterial lower limb ischemia or deep vein thrombosis. In this report, we present a case of HIT complicated by stent graft thrombosis and bowel ischemia.
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PMID:Heparin-induced thrombocytopenia causing graft thrombosis and bowel ischemia postendovascular aneurysm repair. 2413 22


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