New Thrombocytopenia & Coagulopathy in the ICU

1. Disseminated Intravascular Coagulation (DIC):

• Labs are dynamic rather than a single required phenotype: a falling/low platelet count and elevated fibrin-related markers are common; PT is often prolonged, aPTT is variable, and fibrinogen may be low but can remain normal or elevated early in inflammatory/sepsis-associated DIC. Interpret serial trends with a validated disease-appropriate scoring framework rather than fixed cutoffs.
• Mechanism: systemic coagulation activation with consumption and phenotype-dependent fibrinolytic disturbance.
• Management: Treat the underlying cause and use targeted component therapy for clinically important bleeding/procedures rather than correcting numbers alone.

2. Thrombotic Thrombocytopenic Purpura (TTP):

• Suspect with thrombocytopenia plus microangiopathic hemolytic anemia (schistocytes, elevated LDH, low haptoglobin) when an alternative explanation is not more likely. Severe thrombocytopenia and >1% schistocytes may occur but are not mandatory diagnostic cutoffs. PT/aPTT are often normal. Use a validated pretest tool such as PLASMIC while urgent ADAMTS13 testing is pending.
• Mechanism: severe ADAMTS13 deficiency (<10%) in immune TTP.
• Emergency Therapy: When immune TTP is strongly suspected, do not delay TTP-directed therapy while awaiting ADAMTS13; therapeutic plasma exchange, corticosteroids and caplacizumab are core contemporary treatments when appropriate. Avoid routine prophylactic platelet transfusion; consider platelets for life-threatening bleeding or an urgent high-risk procedure after specialist assessment.

3. Heparin-Induced Thrombocytopenia (HIT):

• Typical pattern: a platelet fall >50% beginning around days 5–10 after heparin, or rapid onset with recent heparin exposure; use the 4Ts score before laboratory testing.
• If clinical probability is intermediate/high, stop heparin and start an appropriate non-heparin anticoagulant while testing proceeds unless bleeding risk changes the plan. Options include argatroban or bivalirudin and, in selected clinically stable patients, fondaparinux or a DOAC; choose according to organ function, bleeding/procedure needs, and guideline/local protocol.

4. Hemolytic Uremic Syndrome (STEC-HUS / aHUS):

• Labs: Thrombocytopenia, prominent schistocytes, acute anuric renal failure, normal coagulation factors; complement-mediated aHUS treated with C5 inhibitors (Eculizumab/Ravulizumab).

DIC: ISTH scoring, fibrinolytic phenotypes, and targeted replacement.

HIT: 4T score calculation, PF4 antibodies, and argatroban dosing.

Transfusion: Restrictive triggers, component therapy, and platelet refractoriness.

Anticoagulation: Non-heparin anticoagulation and reversal strategies.

Sepsis: Sepsis-induced coagulopathy and endothelial dysfunction.

AKI: Uremic platelet dysfunction and thrombotic microangiopathy in renal failure.