A 62-year-old man comes to the hospital due to 2 days of bilateral lower extremity swelling and throbbing pain. Two weeks ago he was admitted to a different hospital with a non-ST elevation myocardial infarction. He initially received aspirin, metoprolol, nitrates, heparin, a statin, and a glycoprotein IIb/IIIa inhibitor. Cardiac catheterization showed 3-vessel coronary artery disease and a left ventricular ejection fraction of 40%. The patient underwent on-pump coronary artery bypass grafting. His postoperative course was uncomplicated, and he was discharged home with a normal blood count and serum creatinine levels. He also has a history of hypertension, hyperlipidemia, and type 2 diabetes mellitus. His current medications include aspirin, metoprolol, lisinopril, atorvastatin, metformin, insulin, and fish oil. The patient does not use tobacco, alcohol, or illicit drugs.
Blood pressure is 135/70 mm Hg, pulse is 78/min, and oxygen saturation is 98% on room air. Physical examination reveals clear lungs, normal heart sounds, and bilateral pitting edema. There is no jugular venous distension. The sternotomy scar is clean, dry, and intact. The remainder of the examination is unremarkable.
Laboratory results are as follows:
Lower extremity ultrasound reveals extensive, bilateral deep venous thrombosis extending into the superficial femoral veins.
Which of the following is the most appropriate next step in management of this patient?

Question

A 62-year-old man comes to the hospital due to 2 days of bilateral lower extremity swelling and throbbing pain.  Two weeks ago he was admitted to a different hospital with a non-ST elevation myocardial infarction.  He initially received aspirin, metoprolol, nitrates, heparin, a statin, and a glycoprotein IIb/IIIa inhibitor.  Cardiac catheterization showed 3-vessel coronary artery disease and a left ventricular ejection fraction of 40%.  The patient underwent on-pump coronary artery bypass grafting.  His postoperative course was uncomplicated, and he was discharged home with a normal blood count and serum creatinine levels.  He also has a history of hypertension, hyperlipidemia, and type 2 diabetes mellitus.  His current medications include aspirin, metoprolol, lisinopril, atorvastatin, metformin, insulin, and fish oil.  The patient does not use tobacco, alcohol, or illicit drugs.
Blood pressure is 135/70 mm Hg, pulse is 78/min, and oxygen saturation is 98% on room air.  Physical examination reveals clear lungs, normal heart sounds, and bilateral pitting edema.  There is no jugular venous distension.  The sternotomy scar is clean, dry, and intact.  The remainder of the examination is unremarkable.
Laboratory results are as follows:
 Lower extremity ultrasound reveals extensive, bilateral deep venous thrombosis extending into the superficial femoral veins.
Which of the following is the most appropriate next step in management of this patient?

Quizplus · Accepted Answer

This patient who recently underwent major thoracic surgery now has extensive deep venous thrombosis and thrombocytopenia. Although thrombosis can occasionally result in thrombocytopenia (due to platelet consumption), this patient's recent heparin exposure raises suspicion for delayed-onset heparin-induced thrombocytopenia (HIT). HIT is typically categorized as follows: Type 1 - nonimmune mediated due to heparin-induced platelet clumping. Typically presents with mild thrombocytopenia within the first 2 days of heparin exposure. Normalization occurs quickly, and no treatment changes are required.Type 2 - immune mediated due to antibodies against heparin-platelet factor 4 (PF4) complexes. Typically presents with mild or moderate thrombocytopenia with or without arterial/venous thrombus 5-10 days after heparin initiation (may occur earlier in patients previously exposed).Delayed-onset HIT - immune mediated due to high-titer antibodies against heparin-PF4 complexes in the absence of circulating heparin. Cases typically arise 5-19 days after heparin cessation; therefore, most patients present in the outpatient setting. Thrombocytopenia with or without life-threatening arterial or venous thrombosis are the norm. Type 1 - nonimmune mediated due to heparin-induced platelet clumping. Typically presents with mild thrombocytopenia within the first 2 days of heparin exposure. Normalization occurs quickly, and no treatment changes are required. Type 1 - nonimmune mediated due to heparin-induced platelet clumping. Typically presents with mild thrombocytopenia within the first 2 days of heparin exposure. Normalization occurs quickly, and no treatment changes are required. Type 2 - immune mediated due to antibodies against heparin-platelet factor 4 (PF4) complexes. Typically presents with mild or moderate thrombocytopenia with or without arterial/venous thrombus 5-10 days after heparin initiation (may occur earlier in patients previously exposed). Type 2 - immune mediated due to antibodies against heparin-platelet factor 4 (PF4) complexes. Typically presents with mild or moderate thrombocytopenia with or without arterial/venous thrombus 5-10 days after heparin initiation (may occur earlier in patients previously exposed). heparin-platelet factor 4 (PF4) complexes Delayed-onset HIT - immune mediated due to high-titer antibodies against heparin-PF4 complexes in the absence of circulating heparin. Cases typically arise 5-19 days after heparin cessation; therefore, most patients present in the outpatient setting. Thrombocytopenia with or without life-threatening arterial or venous thrombosis are the norm. Delayed-onset HIT - immune mediated due to high-titer antibodies against heparin-PF4 complexes in the absence of circulating heparin. Cases typically arise 5-19 days after heparin cessation; therefore, most patients present in the outpatient setting. Thrombocytopenia with or without life-threatening arterial or venous thrombosis are the norm. The diagnosis of immune-mediated (type 2 or delayed-onset) HIT is often suspected based on the 4 Ts score and is confirmed with HIT antibody testing. Empiric treatment with a nonheparin anticoagulant (eg, argatroban [a direct thrombin inhibitor]) and the avoidance of all heparin-containing products should be initiated while awaiting confirmation. Transition to warfarin can occur once the thrombocytopenia has resolved on alternate anticoagulation. Total treatment duration is unclear, but those with an active thrombus are usually treated for at least 6 months. 4 Ts score (Choices B and C) All forms of heparin must be stopped immediately in patients with suspected HIT while awaiting diagnostic confirmation. If HIT is confirmed, heparin should be flagged as an allergy, and patients should not receive it again. The use of inferior vena cava filters in patients with HIT has been associated with significant thrombotic complications and should be avoided. (Choice D) Disseminated intravascular coagulation (DIC) usually presents with bleeding, prolonged PT and PTT, and elevated fibrin split products. This patient's normal PT and PTT make DIC unlikely. (Choice E) Consumption of platelets and natural anticoagulants (eg, antithrombin, proteins C and S) can occur in patients with extensive thrombosis. As a result, testing for hypercoagulability is not generally done at diagnosis. Educational objective: Delayed-onset, heparin-induced thrombocytopenia is an immune-mediated condition that usually arises 5-19 days after heparin cessation. Most patients present in the outpatient setting with thrombocytopenia and arterial or venous thrombus. HIT antibody testing is required for confirmation, but empiric treatment with a nonheparin anticoagulation (eg, direct thrombin inhibitor) should be initiated with urgency to prevent life-threatening complications. __________ References: Evaluating heparin-induced thrombocytopenia: the old and the new. (http://www.ncbi.nlm.nih.gov/pubmed/22422328) Treatment and prevention of heparin-induced thrombocytopenia: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. (http://www.ncbi.nlm.nih.gov/pubmed/22315270) Delayed-onset heparin-induced thrombocytopenia. (http://www.ncbi.nlm.nih.gov/pubmed/11827497)

A 62-Year-Old Man Comes to the Hospital Due to 2