Hematologic Emergencies (DIC, TTP/HUS, HIT)
<200
Low Fibrinogen
DIC hallmark finding
>50%
Platelet Drop
HIT diagnostic threshold
5-10 days
HIT Onset
After heparin initiation
DIC (Consumptive Coagulopathy)
DIC is a paradox. Widespread clotting consumes all available clotting factors and platelets, which then causes uncontrolled bleeding. Labs show elevated D-dimer, prolonged PT/PTT, low fibrinogen, low platelets, and schistocytes on smear.
In TTP, do NOT transfuse platelets. It adds fuel to the fire. DIC treatment is always directed at the underlying cause. Blood products are supportive only.
TTP/HUS and HIT
TTP presents with the classic pentad of thrombocytopenia, microangiopathic hemolytic anemia, renal dysfunction, neurological changes, and fever. Treatment is urgent plasma exchange. HIT is an immune-mediated reaction to heparin causing platelet activation and paradoxical thrombosis.
TTP Treatment
Plasma exchange (plasmapheresis)
HIT Treatment
Stop ALL heparin, start direct thrombin inhibitor
Key Values to Memorize
Fibrinogen <200 = DIC
D-dimer elevated in DIC
Platelet drop >50% = HIT
HIT onset 5-10 days
TTP = plasma exchange
No warfarin until plts >150k
hematologic emergencies are high-yield CCRN territory
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TTP equals plasma exchange, NEVER platelets
Transfusing platelets in TTP feeds the pathologic microthrombi. It is like throwing gasoline on a fire. Treatment is urgent plasma exchange to remove the defective vWF multimers and replenish ADAMTS13.
HIT means stop ALL heparin including flushes
Every source of heparin must be discontinued. This includes IV drips, subcutaneous prophylaxis, heparin-coated catheters, and heparin flushes for IV lines. Even trace exposure can perpetuate the immune response.
DIC treatment is treating the CAUSE
There is no DIC drug. The coagulopathy resolves only when the underlying trigger (sepsis, trauma, malignancy, obstetric complication) is treated. Supportive blood product replacement addresses symptoms, not the disease.
No warfarin in HIT until platelets recover above 150,000
Starting warfarin during active HIT causes a transient drop in Protein C before Protein S, creating a hypercoagulable window. This can trigger limb-threatening venous limb gangrene or skin necrosis. Use a direct thrombin inhibitor (argatroban or bivalirudin) first.
TTP Platelet Rule
Platelets in TTP add fuel to the fire. The answer is ALWAYS plasma exchange, never transfusion.
HIT Heparin Sweep
When HIT is suspected, do a full heparin sweep. IV lines, flushes, coated catheters, subQ prophylaxis. Every last drop must go.
DIC is like dozens of small fires breaking out all over the building simultaneously. The body uses up all its fire extinguishers (clotting factors, platelets, fibrinogen) trying to fight them. Eventually, there is nothing left to stop the bleeding. The solution is to find WHO set the fires (the underlying cause).
In TTP, tiny clots are forming in small blood vessels, chewing up platelets. Giving more platelets is like pumping oxygen into a burning room. It makes everything worse. Plasma exchange removes the toxic fuel and replaces it with clean plasma.
Heparin was supposed to prevent clots. Instead, the immune system forms antibodies against heparin-platelet complexes, causing MASSIVE clotting. The fire extinguisher itself started the fire. Stop the extinguisher. Switch to a completely different agent.
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