Thrombocytopenia with unfractionated heparin

Frequent control of coagulability is not necessary with low molecular weight heparin and incidence of side effects (bleeding, heparin-induced thrombocytopenia) is less frequent than with unfractionated heparin. 

Deep vein thrombosis prophylaxis is recommended for septic patients. Low-dose unfractionated heparin or low-molecular-weight heparin may be utilized. Graduated compression stockings or an intermittent compression device is recommended for patients with a contraindication to heparin products (thrombocytopenia, severe coagulopathy, active bleeding, or recent intracerebral hemorrhage).24... 

Heparin may also produce a decrease in platelets (thrombocytopenia) in some patients.13,84 This condition, known commonly as heparin-induced thrombocytopenia (HIT), is less common with LMWHs versus unfractionated heparin, but HIT can occur with any type of heparin treatment.101,145... 

Walenga JM, Prechel M, Jeske WP, Bakhos M. Unfractionated heparin compared with low-molecular-weight heparin as related to heparin-induced thrombocytopenia. Curr Opin Pulm Med. 2005 11 385-391. 

The recommendation for UFH is based on documented efficacy in many older mid-sized trials. Meta-analyses showed a clear reduction in Ml and death, but at the cost of an increase in major bleeding rates (35,36). The advantages of LMWH over unfractionated heparin include a better bioavailability, a stronger and longer anti-Xa activity, less platelet activation, and no need for monitoring. A major drawback of standard heparin therapy is the potential risk of heparin-induced thrombocytopenia, which is considerably reduced with LMWH (37). 

Warkentin TE, Levine MN, Hirsh J, Horsewood P, Roberts RS, Gent M, Kelton JG. Heparin-induced thrombocytopenia in patients treated with low-molecular-weight heparin or unfractionated heparin. N Engl J Med 1995 332(20) 1330-5. 

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. 

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