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ICU Corner HIT, HITT and DIC

ICU Corner HIT, HITT and DIC. Raymond W Pryor III, M.D. Aug 21, 2008. Heparin-Induced Thrombocytopenia (HIT). Heparin combines with a heparin-binding protein (platelet factor 4) to form antigenic complex Induces formation of IgG antibodies ( IgG PF4)

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ICU Corner HIT, HITT and DIC

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  1. ICU CornerHIT, HITT and DIC Raymond W Pryor III, M.D. Aug 21, 2008

  2. Heparin-Induced Thrombocytopenia (HIT) • Heparin combines with a heparin-binding protein (platelet factor 4) to form antigenic complex • Induces formation of IgG antibodies (IgG PF4) • Bind to platelets and form cross-bridges • Platelets aggregate & causes a consumptive thrombocytopenia

  3. HIT: Clinical Features • 50% or greater reduction in platelet count • Typically begins 5-10 days after the FIRST exposure to heparin • Can be within 24 hours if pt exposed to heparin before • 5-10% will develop erythematous lesions around injection site • 25% of pt’s w/HIT from IV heparin will develop systemic reactions • Fever, chills, tachypnea, tachycardia, SOB • Risks vary with different types of Heparin • Unfractionated Heparin (UFH) • 3-5% after orthopedic surgery, 1-3% after cardiac surgery, 1% all other • LMWH (Lovenox) • 1% in orthopedic surgery, <1% in all others • Can even come from heparin flushes or heparin-coated catheters

  4. HIT: Diagnosis • Mostly on high-probability clinical scenario combined with serologic evidence of IgG PF4 antibodies • Assay is 92% sensitive, 81% specific • 75% of HIT cases accompanied by symptomatic thrombosis • AKA: HITT • LE DVT 50%, UE DVT 10%, Acute PE 25%, Arterial thrombosis of limb 5-10%, Thrombotic stroke 3-5%, MI 3-5%

  5. HIT: Treatment • Stop the heparin • Remove any heparin-coated catheters • Stop the heparin • If anticoagulation is necessary: • Argatroban • Direct thrombin inhibitor • Hepatically cleared • Adjust dose based on PTT • Lepirudin • Direct thrombin inhibitor • Recombinant form of leech saliva • Renally cleared • Stop the heparin

  6. Disseminated Intravascular Coagulation (DIC) • Widespread endothelial damage releases protein called Tissue Factor (TF) • TF activates endogenous coagulation cascade & fibrinolytic system • Causes widespread microvascular thrombosis, dpeletion of platelets & procoagulant proteins • Most commonly caused by sepsis, trauma, & OB emergencies

  7. DIC: Clinical Features • Microvascular thrombosis produces multiorgan dysfunction • Lungs commonly involved—resembles ARDS • Oliguric renal failure • Progressive hepatocellular injury • Bleeding from any injury site & GI tract • Symmetrical necrosis & ecchymosis involving limbs • Purpurafulminans(most common with meningococcemia)

  8. DIC: Diagnosis • Clinical presence of a predisposing condition (e.g., sepsis, trauma, OB, ect) • Labarotory evidence of widespread coagulation deficits • International Society on Thrombosis & Haemostasis scoring system • Score of 5 or greater consistent with DIC

  9. DIC: Management • Advanced cases have mortality of >80% • Treatment directed at predisposing conditions • Replacement of platelets & coagulation factors • Cryoprecipitate • Often can aggravate the thrombosis • Heparin ineffective at slowing thrombosis due to depletion of antithrombin-III • Some early trials of giving AT-III with heparin

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