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■ Consider cryoprecipitate infusion.
■ Provide blood transfusion and monitor for reactions.
■ Provide support to patient and family.
■ Assess for thrombotic and hemorrhagic conditions. Monitor for complica-
tions such as pulmonary embolism (PE), airway obstruction, acute tubular
necrosis, increased ICP, or multiple organ failure and shock.
Heparin-Induced Thrombocytopenia (HIT)
HIT is a transient disorder in which thrombocytopenia (>50% ↓ in platelet count)
appears 7–10 days after exposure to heparin. There is a strong association with
venous and arterial blood clot formation. HIT is a thrombotic, not a bleeding,
process.
Pathophysiology
After heparin is administered, an immune complex can form between heparin
and specific blood factor (platelet factor 4 [PF4]) that is released by platelets →
body viewing this “heparin-PF4” as a foreign body → formation of antibodies
against the heparin PF4 complex → antibodies binding to the complex →
platelet destruction → disruption of platelets → formation of new blood clot →
deep vein thrombosis (DVT) or arterial occlusion, PE, myocardial infarction (MI),
or cerebrovascular accident (CVA).
Clinical Presentation
■ Signs and symptoms of DVT (pain or tenderness, sudden swelling, discol-
oration of visible leg veins) or manifestation of venous thrombus
■ Signs and symptoms of PE (shortness of breath, change in HR, sharp chest
pain, dizziness, anxiety, excessive sweating)
■ Acute limb ischemia (from peripheral arterial occlusion)
■ Venous limb gangrene (distal ischemic necrosis following DVT)
■ Cerebral sinus thrombosis
■ Manifestation of arterial thrombosis (less common)
■ Stroke
■ MI
■ Organ infarction (kidney, mesentery)
■ Fall in platelet count of >50% 5–10 days after initiation of heparin therapy
■ Severe indicators:
■ Skin changes (bruising or blackening around injection site as well as on
fingers, toes, and nipples), ↑ gangrene
Diagnostic Tests
■ Serotonin release assay (SRA): remains gold standard among diagnostic
tests for HIT
■ PT/PTT
■ PF4 assay
HEMA/
ONCO