Heparin-Induced Thrombocytopenia with Thrombosis

Heparin-induced thrombocytopenia type II (HIT II) is an immune-mediated adverse drug reaction to heparin and heparinoid compounds. Unlike other etiologies of thrombocytopenia, HIT II frequently manifests with arterial or venous thromboemboli, leading to significant morbidity and mortality. Diagnosis of HIT II requires a high clinical suspicion, pretest probability scoring, and laboratory confirmation through immunologic and functional assays. Moderate probability for HIT II should be met with discontinuation of the offending agent and initiation of an alternative anticoagulant. Key words: heparin-induced thrombocytopenia, heparin-induced thrombocytopenia with thrombosis, HIT II, HITT

Prophylaxis of Deep Vein Thrombosis and Pulmonary Embolism: Current Recommendations

Pulmonary embolism remains a major cause of death in high-risk medical and surgical patients. This is unfor tunate as effective measures for prevention of venous throm boembolism in such patients are now available. Based on Level 1 evidence from clincial trials and systematic reviews, recom mendations can be made for the prevention of venous throm boembolism in most situations. If such information is not avail able, recommendations based on extrapolation from similar risk situations or from consensus opinions must be used. Additional clinical trials are required to fill in such gaps in our knowledge and permit adequate protection against fatal pulmonary embo lism in most if not all medical and surgical patients. Key Words: Heparin—Low molecular weight heparin—Oral anti coagulants—Intermittent pneumatic compression—Graduated compression stockings—Deep vein thrombosis—Pulmonary embolism.

Orally Ingested Heparin Is Absorbed in, Humans

It has been accepted for many years that orally ingested heparin is not absorbed. Recent evidence has shown that heparin placed in the stomach of rats is very rapidly absorbed and that it also quickly and almost completely attaches to the vascular endothelium and prevents jugular vein thrombosis. Within 6 min, heparin was undetectable in the blood plasma. If a similar situation exists in humans, blood samples taken >15 min after heparin ingestion will lack evidence of anticoagulant activity. In this study, 45 individuals swallowed 20,000 units of heparin. Plasma activated partial thromboplastin time (APTT) levels were determined (in duplicate) before and at frequent intervals for 30 min after the heparin ingestion. There as a slightly prolonged APTT (range, 1-5 s) after swallowing the heparin. The average increase in the APTT was 2.3 s, which is statistically significant (p < 0.001), as the standard deviation of the method is .43 s. In several instances, frozen plasma aliquots, analyzed for heparin by a chromogenic method, showed its presence after ingestion. The preliminary results are important, although obviously oral heparin does not attain effective anticoagulant levels, as the many non-anticoagulant actions of heparin and the observation of its absorption after oral ingestion present numerous possibilities for new clinical applications. Key Words: Heparin—Oral absorption.