Thrombotic complications heparins

Heparin-induced thrombocytopenia (platelet count <150,000/ml or a 50% decrease from the pretreatment value) occurs in about 0.5% of medical patients 5 to 10 days after initiation of therapy with standard heparin. The incidence of thrombocytopenia is lower with low-molecular-weight heparin. Thrombotic complications that can be life threatening or lead to amputation occur in about one-half of the affected heparin-treated patients and may precede the onset of thrombocytopenia. The incidence of heparin-induced thrombocytopenia and thrombosis is higher in surgical patients. Venous thromboembolism occurs most commonly, but arterial thromboses causing limb ischemia, myocardial infarction, and stroke also occur. Bilateral adrenal hemorrhage, skin lesions at the site of subcutaneous heparin injection, and a variety of systemic reactions may accompany heparin-induced thrombocytopenia. The development of IgG antibodies against complexes of heparin with... 

Epoprostenol is the natural occurring prostacyclin which is formed in vascular endothelial cells. It increases cyclic AMP in the thrombocyte and is a strong platelet aggregation inhibitor. It is used to prevent thrombotic complications during hemodialysis when heparin is contraindicated. As its duration of action is no longer than 30 minutes it has to be given as an intravenous infusion. 

Deficiency of antithrombin predisposes the patient to thrombotic complications. Antithrombin deficiencies can be the result of low protein levels or due to functionally abnormal molecules. Low protein levels can be brought about by reduced synthesis or an increased turnover of the molecule, Functional deficiencies can be brought about by mutations in either the reactive site or heparin binding sites, A number of such mutations have been documented (81,86,87),... 

Some patients with acute myocardial infarction (AMI) are found to have HIT antibodies career state of HIT antibodies regardless of previous heparin usage. In those patients, early-onset HIT has been observed, which occurs within a very short period after UFH administration during PCI even if it is the initial exposure to UFH (10). Once HIT antibodies are generated after the exposure to UFH, the antibodies do not disappear for approximately 100 days after the cessation of UFH. If UFH intervention is resumed while the antibodies remain, HIT may readily develop as rapid-onset type of HIT (II). Thrombotic complications are highly anticipated following the abrupt onset of HIT in patients who have been exposed recently to UFH. 

Optimal stent implantation and new antiplatelet therapy have reduced the thrombotic complication after stent implantation, dramatically. However, thrombosis remains a challenge in some lesions and patient subgroups. As an initial and unavoidable event during stent implantation, thrombosis and platelet activation are also involved in the development of neointimal hyperplasia. Stents coated with heparin and other antithrombotic drugs have been demonstrated to decrease thrombotic complications, although their effect on neointimal hyperplasia remains uncertain. As heparin is attached to the stent surface, we divide thromboresistant stents as heparin-coated stents and drug-eluting thromboresistant stents. 

Two forms of heparin-induced thrombocytopenia (HIT) have been observed. The first (HIT I) is a transient, mild, and benign thrombocytopenia seen soon after initiation of heparin therapy (normally within 2 days) and is felt to be due to inherent plateletaggregating properties of heparin. A second, more severe form of HIT (HIT II) is typically seen later and is immune-mediated. The incidence of HIT II is estimated at 3-5%. The onset is generally 3-14 days after initiation of heparin therapy but may occur sooner with repeat exposure. HIT II may occur with any dose and type of heparin, but the frequency is highest with continuous intravenous infusions of unfractionated heparin. HIT with subsequent thrombosis is a feared complication. These thrombi can form in the venous or arterial circulation. Thrombotic complications include necrotic skin lesions, myocardial infarction, stroke, and gangrene. Hyperkalemia may be seen with heparin therapy due to aldosterone synthesis inhibition. 

Platelet counts should be carefully monitored for any decline. If thrombocytopenia develops, the time course and severity should help differentiate which type of HIT exists. If HIT I is suspected, heparin may be continued with caution. If HIT II is suspected, heparin therapy should be discontinued and an alternate form of anticoagulation therapy begun. If a low platelet count is encountered with a thrombotic complication, heparin should be discontinued immediately. Thrombolytic therapy or embolectomy may be necessary. Lepirudin (recombinant hirudin) is... 

A large percentage of patients develop asymptomatic VTE. PE occurs in 25% of patients with thrombotic complications and contributes significantly to mortality. Arterial thrombosis occurs less commonly. Limb artery occlusion, stroke, and myocardial infarction are the most commonly reported arterial events. Heparin-induced skin lesions occur in 10% to 20% of patients with HIT. Lesions range from painful, localized erythematous plaques to widespread dermal necrosis. Amputation in such cases frequently is required. Mortality from HIT may be as high as 36% in patients with acute thrombosis. The relatively high frequency of thrombotic complications and poor outcomes... 

Rostoker G, Durand-Zaleski 1, Petit-Phar M, et al. Prevention of thrombotic complications of the nephrotic syndrome by the low-molecular-weight heparin enoxaparin. Nephron 1995 69 20-28. 

Heparin has been associated with priapism (90). The frequency and severity of iatrogenic priapism as a result of heparin therapy seems to be greater than with any other type of medical treatment (91). However, it is uncertain whether it is heparin or the underlying thrombotic condition that causes the complication. 

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