Critical Care Express Report

Based on Data Presented at a Satellite Symposium during the Society of Critical Care Medicine 34^th Critical Care Congress, January 15-19, 2005, Phoenix, Arizona

Publication date: 2005-03-07

Recognizing and Treating Heparin-induced Thrombocytopenia in the Critical Care Setting

This report was reviewed for medical and scientific accuracy by John R. Bartholomew, MD, Section Head and Program Director, Section of Vascular Medicine, and Member of the Department of Cardiovascular Medicine and Hematology/Oncology, The Cleveland Clinic Foundation, Cleveland, Ohio.

Expert Commentary

Provided by Lou Guzzi, MD, FCCM, Section Chief, Critical Care Medicine, Florida Hospital, Orlando, Florida; Associate Professor of Anesthesiology, Florida State University, Tallahassee, Florida

Data presented at the Society of Critical Care Medicine 34^th Critical Care Congress provide new insight on the optimal management of heparin-induced thrombocytopenia (HIT),¹ an immune-mediated adverse drug reaction of heparin therapy.,² Importantly, HIT remains an under-recognized and under-diagnosed immunohematologic disease in the critical care setting. The incidence of heparin-dependent antibodies varies depending on the patient population, ranging from 6.6% in orthopedic patients³ to as high as 50% in post-cardiac surgery patients.⁴ Up to 3% of heparin-exposed patients develop HIT (approximately 180,000 patients per year).^5-10 It is estimated that approximately 50% of patients with HIT will develop a thromboembolic event,¹¹ of which approximately 20% will require amputation and 30% will die.¹² Serious thromboembolic complications include deep vein thrombosis, pulmonary embolism, myocardial infarction, occlusion of limb arteries, skin necrosis, cerebrovascular accident, end organ damage, or death.^11,13 An understanding of the diagnosis and risk factors for HIT, as well as early clinical intervention with a direct thrombin inhibitor, such as argatroban or lepirudin, is critical in avoiding the devastating sequelae associated with HIT.

The consequences of inappropriate management of HIT can result in significant morbidity and mortality. Successful outcomes for HIT can be achieved with early recognition, diagnosis, and aggressive treatment. Optimal treatment includes immediate discontinuation of heparin therapy and initiation of alternative anticoagulation therapy. Clinical guidelines issued by the American College of Chest Physicians on the recognition, treatment, and prevention of HIT recommend direct thrombin inhibitors (ie, argatroban, lepirudin, bivalirudin) as treatment for HIT.¹⁴ However, only argatroban and lepirudin are approved by the Food and Drug Administration (FDA) for this indication.^15,16 Additionally, argatroban is the only FDA-approved direct thrombin inhibitor for use in patients at risk for HIT undergoing percutaneous coronary intervention (PCI).¹⁵ Favorable pharmacologic properties of argatroban include a short half-life, rapid achievement and maintenance of steady state with little or no dosage adjustments, and safe use in patients with renal insufficiency; caution should be exercised in patients with hepatic disease.¹⁵

This Critical Care Medicine Express Report^TM reviews the data presented at the satellite symposium and focuses on increasing physician awareness of HIT, improving diagnostic accuracy, and enhancing treatment efficacy. By instituting protocols such as those described in this report, physicians can do much to prevent the significant morbidity and mortality associated with HIT.

Recognizing HIT and Related Complications

According to Susan M. Begelman, MD, RVT, Medical Director, Noninvasive Vascular Laboratory, Department of Cardiovascular Medicine, The Cleveland Clinic Foundation, Cleveland, Ohio,¹⁷ HIT is an acquired hypercoaguable disorder with increased in vivo thrombin generation that greatly heightens the risk for arterial and venous thrombosis.¹⁸ Indeed, the presence of HIT significantly increases the risk of developing thrombosis by nearly 37-fold.¹⁹ By comparison, patients with heterozygous factor V Leiden have a 7-fold increased risk of thrombo