Heparin-induced thrombocytopenia (HIT) is a life-threatening disorder that follows exposure to unfractionated heparin or (less commonly) low-molecular-weight heparin (LMWH). Patients classically present with a low platelet count (< 150,000 cells/mm3) or a relative decrease of 50% or more from baseline, although the fall may be less (eg, 30%–40%) in some patients. Thrombotic complications develop in approximately 20%–50% of patients.

HIT is caused by antibodies against complexes of platelet factor 4 and heparin. These antibodies are present in nearly all patients who receive a clinical diagnosis of the disorder and are also known to cause disease in animals. However, they are also present in many patients who have been exposed to heparin in various clinical settings but who do not develop clinical manifestations. It is uncertain why complications occur in some patients but not in others.1 We present a 73-yearold man who developed thrombocytopenia after starting LMWH and who has newly diagnosed adenocarcinoma of the lungs with extensive arterial and venous thrombosis and a negative serology for HIT.

Case presentation

A 73-year-old man presented to the emergency department after waking up in the morning with rightsided vague weakness and an inability to get out of bed. He had a history of right parietal stroke 1 month before the current presentation, when he was diagnosed with an aortic arch atheroma and started on warfarin. (At that time, CT scan of the head showed a right posterior temporoparietal lobe infarct in the posterior right middle cerebral artery distribution, and MRI of the brain and magnetic resonance angiography showed acute or subacute infarction in the distribution of the posterior division of the right middle cerebral artery, likely embolic, and tiny acute infarctions in the left frontal lobe.) This patient had been admitted 5 days prior to the current presentation for right lower extremity deep vein thrombosis (DVT) and was discharged after being prescribed enoxaparin (60 mg subcutaneously every 12 hours) and warfarin as per international normalized ratio (INR) daily

Also included in the medical history was supraventricular tachycardia status post ablation, non–ST elevation myocardial infarction (NSTEMI), hypertension, hyperlipidemia, and macular degeneration. He had no surgical history. The patient had a family history of coronary artery disease. He had an extensive smoking history up until the day of admission. His medications on admission included atorvastatin (Lipitor; 20 mg daily), warfarin daily as per INR, enoxaparin (60 mg subcutaneously every 12 hours), amlodipine (5 mg daily), and aspirin (81 mg daily).

Pertinent initial laboratory results on admission were as follows: hemoglobin, 12.9 g/dL; white blood cell count, 8.6 ×109/L; platelet count, 183,000 cells/ mm3; INR, 1.2; and initial troponin level, negative. His admission chest x-ray showed a 4.5 cm × 5.5 cm lobulated density in the right hilum, suspicious for a hilar or subcarinal mass. Initial peripheral blood smear showed an isolated platelet decrease with increased size and no schistocytes. Initial CT of the head on admission showed no evidence of acute transcortical infarction and no definite evidence of acute intracranial hemorrhage but did show interval evolution of the right middle cerebral artery and left watershed distribution infarctions, with a probable small region of laminar necrosis in the right parietal lobe.

Clinical course

The patient was initially thought to have had a transient ischemic attack causing aphasia, confusion, and rightsided weakness. He was started on therapeutic anticoagulation with dalteparin (Fragmin; 12,000 U subcutaneously daily), and enoxaparin was discontinued. The following day, his platelet count was 86,000 cells/mm3, down from an admission platelet count of 183,000 cells/mm3. A subsequent MRI of the brain showed a new hemorrhagic area in the right parietal infarct (Figure 1). The decision was made to stop anticoagulation, even though he had an embolic source from his aortic arch atheroma and lower extremity DVT.