Review Question - QID 212488

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Heparin-Induced Thrombocytopenia (HIT) Introduction Type II HIT QID: 212488 (M1.OMB.18.1)

QID 212488 (Type "212488" in App Search)

A 45-year-old man presents to the emergency department for worsening shortness of breath with exertion, mild chest pain, and lower extremity swelling. The patient reports increasing his alcohol intake and has been consuming a diet rich in salt over the past few days. Physical examination is significant for bilateral crackles in the lung bases, jugular venous distension, and pitting edema up to the knees. An electrocardiogram is unremarkable. He is admitted to the cardiac step-down unit. In the unit, he is started on his home anti-hypertensive medications, intravenous furosemide every 6 hours, and prophylactic enoxaparin. His initial labs on the day of admission are remarkable for the following:

Hemoglobin: 12 g/dL
Hematocrit: 37%
Leukocyte count: 8,500 /mm^3 with normal differential
Platelet count: 150,000 /mm^3

Serum:
Na+: 138 mEq/L
Cl-: 102 mEq/L
K+: 4.1 mEq/L
HCO3-: 25 mEq/L

On hospital day 5, routine laboratory testing is demonstrated below:

Hemoglobin: 12.5 g/dL
Hematocrit: 38%
Leukocyte count: 8,550 /mm^3 with normal differential
Platelet count: 60,000 /mm^3

Serum:
Na+: 140 mEq/L
Cl-: 100 mEq/L
K+: 3.9 mEq/L
HCO3-: 24 mEq/L

Physical examination is unremarkable for any bleeding and the patient denies any lower extremity pain. There is an erythematous and necrotic skin lesion in the left abdomen.

Which of the following best explains this patient’s current presentation?

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ADAMTS13 protease deficiency

11%

18/164

Antibodies to heparin-platelet factor 4 complex

60%

98/164

Non-immune platelet aggregation

9/164

Protein C deficiency

9/164

Vitamin K epoxide reductase inhibitor

13%

21/164

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This patient's severe drop in platelets 5 days after receiving prophylactic enoxaparin and an erythematous/necrotic lesion in the abdomen (where the enoxaparin was placed) is suggestive of heparin-induced thrombocytopenia type II.

Heparin-induced thrombocytopenia (HIT) can be divided into type I and type II. HIT type I is due to a non-immune effect of heparin leading to platelet aggregation. This typically occurs 1-4 days after administration of heparin therapy, platelet count usually nadirs around 100,000, and it is not associated with thrombosis. HIT type II results from an immune-mediated phenomenon, where IgG antibodies act on a neoantigen formed between heparin and the platelet factor 4 (PF4) complex. This binding ultimately leads to platelet activation (leading to thrombosis) and removal of IgG-PF4 platelets by splenic macrophages (leading to thrombocytopenia). HIT type II typically occurs 5-10 days after heparin administration.

Incorrect Answers:
Answer 1: ADAMTS13 protease deficiency is seen in thrombocytopenic purpura, which presents with fever, anemia, microangiopathic hemolytic thrombocytopenia, renal failure, and neurologic symptoms.

Answer 3: Non-immune platelet aggregation is seen in HIT type I, which causes a less severe thrombocytopenia that HIT type II.

Answer 4: Protein C deficiency presents with thrombotic skin necrosis and hemorrhage after warfarin administration.

Answer 5: Vitamin K epoxide reductase inhibitor is the mechanism of action of warfarin, which has not been administered to this patient.

Bullet Summary:
HIT type II is caused by the production of antibodies against heparin-platelet factor 4 complex.

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