9.1 Coagulopathies & Transfusion Therapy

Disseminated Intravascular Coagulation (DIC)

Disseminated intravascular coagulation (DIC) is a consumptive coagulopathy: an underlying insult triggers uncontrolled, systemic activation of the clotting cascade. Circulating tissue factor and inflammatory cytokines drive fibrin generation throughout the microvasculature, so the patient forms microthrombi (causing ischemic organ injury) while simultaneously consuming platelets and clotting factors faster than the marrow and liver can replace them. The paradox the CCRN loves to test is that the patient clots and bleeds at the same time. Common triggers are sepsis (the most frequent ICU cause), major trauma, burns, obstetric catastrophes (abruption, amniotic fluid embolism), acute promyelocytic leukemia, and severe hemolytic transfusion reactions.

Recognition and laboratory pattern

Clinically you see diffuse oozing from IV sites, incisions, gums, and suction catheters together with petechiae, purpura, and evidence of end-organ hypoperfusion (oliguria, delirium, acral cyanosis). Memorize the lab signature as a set:

A rising D-dimer with a falling fibrinogen and platelet count in a septic or post-trauma patient is DIC until proven otherwise.

Management

The single most important intervention is to treat the precipitating cause - antibiotics and source control for sepsis, delivery for obstetric DIC, ATRA for acute promyelocytic leukemia. DIC never resolves while the trigger burns. Blood-product support is guided by active bleeding plus labs, not numbers in isolation: give fresh frozen plasma (FFP) to replace consumed factors when PT/aPTT are prolonged, cryoprecipitate when fibrinogen falls below roughly 100-150 mg/dL, and platelets for counts under 20,000-50,000/uL when the patient is bleeding or facing a procedure. Heparin has a narrow role limited to thrombosis-predominant DIC (for example purpura fulminans) and is generally avoided when bleeding dominates.

Heparin-Induced Thrombocytopenia (HIT)

Heparin-induced thrombocytopenia (HIT) is an immune, prothrombotic drug reaction: IgG antibodies form against the heparin-platelet factor 4 (PF4) complex, activating platelets and coagulation. Despite the falling platelet count, the danger is thrombosis, not bleeding - venous and arterial clots, limb ischemia, and pulmonary embolism.

Use the 4Ts to gauge probability: Thrombocytopenia (typically a >50% drop), Timing (day 5-10 of exposure, or faster with prior heparin), Thrombosis (new clot), and aTternate cause absent. A platelet drop from 250,000 to 80,000/uL on day 6 of a heparin infusion with a new arterial thrombus is a textbook picture.

The two non-negotiable steps

1. Stop ALL heparin immediately - infusions, subcutaneous prophylaxis, low-molecular-weight heparin, and even heparin-coated catheter flushes.
2. Start a non-heparin anticoagulant - a direct thrombin inhibitor such as argatroban (hepatically cleared, useful in renal disease) or bivalirudin.

Do not transfuse platelets prophylactically (adds fuel to thrombosis) and do not start warfarin until the platelet count recovers above roughly 150,000/uL, because early warfarin can precipitate venous limb gangrene. Send a HIT antibody/serotonin-release assay, but treat empirically when clinical probability is high.

Thrombocytopenia in the ICU

Beyond HIT and DIC, ICU thrombocytopenia stems from dilution (massive transfusion), sepsis, TTP/HUS, drugs, and devices (IABP, ECMO, CRRT). The spontaneous bleeding risk rises steeply below 10,000-20,000/uL; most procedures need >50,000, and neuraxial or neurosurgical procedures need about 100,000. Avoid IM injections, apply pressure at puncture sites, and hold offending drugs.

Transfusion Therapy

Each product corrects a specific deficit:

Massive transfusion protocol (MTP)

For life-threatening hemorrhage, resuscitate with a balanced 1:1:1 ratio of PRBCs:FFP:platelets that approximates whole blood, limit crystalloid, and give tranexamic acid early in trauma. Watch the lethal triad - hypothermia, acidosis, and coagulopathy - which worsens bleeding; warm all products and the patient.

Transfusion reactions

For any acute reaction the first action is stop the transfusion and maintain the line with normal saline. Citrate/hypocalcemia is a tested favorite: stored blood is anticoagulated with citrate, which chelates calcium during rapid transfusion, producing perioral tingling, a prolonged QT interval, and a low ionized calcium - treated with IV calcium (chloride or gluconate).

TRALI versus TACO

These two are the highest-yield discriminators on the exam because both cause dyspnea and hypoxemia soon after transfusion but demand opposite treatment. Transfusion-related acute lung injury (TRALI) is an immune, non-cardiogenic injury: within 6 hours the patient develops bilateral pulmonary infiltrates and hypoxemia with normal filling pressures and a normal or low CVP - fluid overload is absent, so diuretics do NOT help and management is supportive respiratory care and often intubation. Transfusion-associated circulatory overload (TACO) is volume overload: hypertension, jugular venous distention, an S3, and a rising CVP - the correct response is to slow or stop the transfusion and diurese. When in doubt, the blood pressure and filling pressures separate them: high with TACO, normal or low with TRALI.

Reversal beyond FFP

For urgent reversal of warfarin with life-threatening bleeding, four-factor prothrombin complex concentrate (PCC) plus IV vitamin K is faster and lower-volume than FFP and is preferred when available. Recognizing that DIC, dilution, and vitamin-K deficiency each demand a different product is exactly the reasoning the CCRN tests: match the deficit to the correct component rather than transfusing reflexively.