A 62-year-old hospitalized man is evaluated for new-onset, right lower extremity pain. The patient underwent bypass surgery for 3-vessel coronary artery disease 2 months ago. He arrived at the emergency department 2 nights ago due to recurrent chest pains. At that time, ECG showed sinus rhythm with no ST-segment changes, but cardiac troponin I levels were elevated. The patient was initiated on unfractionated heparin, antiplatelet agents, a beta blocker, and a nitrate. A coronary angiogram was performed via the radial artery; it revealed graft insertion site stenosis and was treated with stenting. Postintervention echocardiography revealed left ventricular ejection fraction of 50% with no regional wall motion abnormalities. This morning, the patient had new, sudden-onset, right lower extremity pain. He has never had pain in that extremity before. The patient has a history of hypertension, hyperlipidemia, and type 2 diabetes mellitus. Current medications include aspirin, clopidogrel, rosuvastatin, metoprolol, losartan, isosorbide mononitrate, basal-bolus insulins, and subcutaneous heparin at a prophylactic dose. The patient is a former smoker with a 30-pack-year history. Temperature is 37.6 C (99.7 F), blood pressure is 138/84 mm Hg, pulse is 96/min, and respirations are 18/min. Physical examination reveals normal jugular venous pressure, clear lungs, no heart murmurs, and a soft, nontender abdomen. The right leg is tender and cool to the touch when compared to the left leg. Right lower extremity distal pulses are diminished, but capillary refill is intact. Left leg examination is normal with the exception of healed scars from previous saphenous vein harvesting. Neurological examination is normal. Laboratory results are as follows:

Which of the following is the most likely cause of this patient's leg pain?

Question

A 62-year-old hospitalized man is evaluated for new-onset, right lower extremity pain.  The patient underwent bypass surgery for 3-vessel coronary artery disease 2 months ago.  He arrived at the emergency department 2 nights ago due to recurrent chest pains.  At that time, ECG showed sinus rhythm with no ST-segment changes, but cardiac troponin I levels were elevated.  The patient was initiated on unfractionated heparin, antiplatelet agents, a beta blocker, and a nitrate.  A coronary angiogram was performed via the radial artery; it revealed graft insertion site stenosis and was treated with stenting.  Postintervention echocardiography revealed left ventricular ejection fraction of 50% with no regional wall motion abnormalities.  This morning, the patient had new, sudden-onset, right lower extremity pain.  He has never had pain in that extremity before.  The patient has a history of hypertension, hyperlipidemia, and type 2 diabetes mellitus.  Current medications include aspirin, clopidogrel, rosuvastatin, metoprolol, losartan, isosorbide mononitrate, basal-bolus insulins, and subcutaneous heparin at a prophylactic dose.  The patient is a former smoker with a 30-pack-year history.  Temperature is 37.6 C (99.7 F), blood pressure is 138/84 mm Hg, pulse is 96/min, and respirations are 18/min.  Physical examination reveals normal jugular venous pressure, clear lungs, no heart murmurs, and a soft, nontender abdomen.  The right leg is tender and cool to the touch when compared to the left leg.  Right lower extremity distal pulses are diminished, but capillary refill is intact.  Left leg examination is normal with the exception of healed scars from previous saphenous vein harvesting.  Neurological examination is normal.  Laboratory results are as follows:

Which of the following is the most likely cause of this patient's leg pain?

Quizplus · Accepted Answer

Explanation: 11ec2b69_bf5d_ab36_8f63_ff2f23fcbd24_MD0005_00 This patient developed sudden-onset right leg pain associated with diminished pulses, coolness to the touch, and normal capillary refill, suggesting viable acute leg ischemia. As he also has new-onset thrombocytopenia in the setting of heparin administration, the most likely underlying etiology is an arterial thrombus due to type 2 heparin induced thrombocytopenia (HIT). viable acute leg ischemia Type 2 HIT is a life-threatening condition that affects 5% of patients exposed to heparin. Risk is greatest with unfractionated heparin, particularly when used in the perioperative setting. Manifestations arise due to the formation of autoantibodies against heparin-platelet factor 4 complexes, which leads to thrombocytopenia (due to platelet removal by the reticuloendothelial system) and arterial/venous thrombosis (due to platelet activation). autoantibodies against heparin-platelet factor 4 complexes The likelihood of type 2 HIT is calculated using the 4 Ts score, which includes the following: Thrombocytopenia - platelets typically decline >30%-50% Timing - onset 5-10 days after heparin initiation or ≤1 day with prior, recent heparin exposure Thrombosis - new thrombosis, progressive thrombosis, or skin necrosis Alternate causes - no other sources for thrombocytopenia are present or likely This patient with a platelet decline >50% and evidence of limb ischemia (new thrombosis) has a 4 Ts score of ≥4, indicating at least an intermediate probability of type 2 HIT, which necessitates HIT antibody testing and presumptive treatment. Type 2 HIT likely developed rapidly due to recent heparin exposure during coronary artery bypass surgery. Unlike type 2 HIT, type 1 HIT is nonimmune-mediated and caused by heparin-induced platelet clumping. Type 1 HIT usually arises within 2 days of heparin exposure, results in platelet nadirs >100,000 mm³, and resolves spontaneously over several days without intervention. (Choice A) Rupture of an atherosclerotic plaque is a common cause of acute leg ischemia but usually occurs in patients with a history of symptomatic peripheral artery disease (eg, claudication). Type 2 HIT is more likely in this patient with no previous claudication and new-onset thrombocytopenia following recent heparin administration. (Choice B) Left ventricular thrombus most commonly occurs following large myocardial infarction complicated by aneurysm and reduced ejection fraction. This patient had a recent echocardiogram demonstrating an ejection fraction of 50% and no evidence of wall motion abnormality, making thrombus unlikely. (Choice D) Atheroemboli are more likely to cause digital ischemia and ischemia of the arterioles of the skin (eg, livedo reticularis); acute limb ischemia is less common. (Choice E) Disseminated intravascular coagulation can also cause thrombocytopenia and thrombosis but is usually associated with oozing from mucosal sites and abnormal coagulation studies (eg, prolonged PT and activated PTT, low fibrinogen, elevated d-dimer). Educational objective: Type 2 heparin-induced thrombocytopenia occurs in approximately 5% of individuals who receive heparin. It is an immune-mediated condition due to the formation of autoantibodies against heparin-platelet factor 4 complexes, which leads to thrombocytopenia and arterial/venous thrombosis. References: Heparin-induced thrombocytopenia. (http://www.ncbi.nlm.nih.gov/pubmed/24319250)

A 62-Year-Old Hospitalized Man Is Evaluated for New-Onset, Right Lower