Abstract

Heparin-induced thrombocytopenia (HIT) is a major health problem, especially in cardiac surgery theaters, cardiac catheterization labs, and intensive care units. Some patients with HIT develop serious thrombotic complications like limb ischemia and gangrene, while others may not develop such complications and have only mild thrombocytopenia. Current laboratory diagnostic tools incur significant time delays before confirming HIT, therefore upon clinical suspicion, treatment of HIT should start immediately while awaiting laboratory results. This is a review of the types, phases, pathophysiology, clinical presentation and diagnosis of HIT, and its current management strategies.

Highlights

  • Heparin is a proven effective anticoagulant therapy in many thrombotic conditions such as acute coronary syndrome and deep venous thrombosis, where heparin therapy is recommended after administration of thrombolytic agent to reduce mortality[1]

  • It is vital to differentiate between heparin induced thrombocytopenia (HIT) where Heparin-induced thrombocytopenia (HIT) antibodies develop upon heparin exposure, and heparin induced thrombocytopenia with thrombosis (HITT) - where serious complications occur

  • HIT type-1 is a mild transient asymptomatic thrombocytopenia that develops 2–3 days after heparin exposure and disappears quickly, patients remain asymptomatic without thrombosis[21,22]

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Summary

INTRODUCTION

Heparin is a proven effective anticoagulant therapy in many thrombotic conditions such as acute coronary syndrome and deep venous thrombosis, where heparin therapy is recommended after administration of thrombolytic agent to reduce mortality[1]. Combining heparin with Aspirin reduces the risk of thrombosis by 75%2. Heparin is highly successful in reducing morbidity and mortality associated with thrombotic conditions, there are significant problems associated with its use. HIT is a severe prothrombotic condition, occurring with fractionated and unfractionated heparin (UFH), and low-molecular weight heparins (LMWHs). It was discovered in the 1950s by Weisman and Tobin[3]. The mortality rate is approximately 20%, and approximately 10% of patients suffer from major morbidity like amputation[4,5]

TYPES OF HIT
PHASES OF HIT
INCIDENCE AND RISK FACTORS
Other causes of Thrombocytopenia
LABORATORY CONFIRMATION
TRANSITION TO ORAL ANTICOAGULATION
HIT AND CARDIOVASCULAR INTERVENTIONS
Findings
CONCLUSION
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