A CBC is performed with Hgb 60 g/L, Hct 0.290/L, RBC 3.0 x 10^12/L, WBC 18.0 x 10^9/L, PLT 40 x 10^9/L, MCV 91 fL, MCH 29 pg, MCHC 329 g/L, RETIC 10%, Peripheral Smear: Schistocytes, helmet cells, burr cells. Coagulation Testing: PT 40 sec, APTT 65 sec, TT 35 sec, D-dimer >500 ng/mL. Additional Testing: uBIL 80 μmol/L, LDH 700 U/L. What is the presumptive diagnosis?

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Multiple Choice

A CBC is performed with Hgb 60 g/L, Hct 0.290/L, RBC 3.0 x 10^12/L, WBC 18.0 x 10^9/L, PLT 40 x 10^9/L, MCV 91 fL, MCH 29 pg, MCHC 329 g/L, RETIC 10%, Peripheral Smear: Schistocytes, helmet cells, burr cells. Coagulation Testing: PT 40 sec, APTT 65 sec, TT 35 sec, D-dimer >500 ng/mL. Additional Testing: uBIL 80 μmol/L, LDH 700 U/L. What is the presumptive diagnosis?

Disseminated intravascular coagulation is a consumptive coagulopathy where widespread activation of coagulation causes microthrombi formation and simultaneous consumption of platelets and clotting factors, leading to both thrombosis and bleeding. Here, several findings line up with that process. The blood smear shows schistocytes, helmet and burr cells—typical of microangiopathic hemolysis from intravascular fibrin strands. The patient has marked thrombocytopenia (low platelets) and a severe anemia with reticulocytosis, LDH elevation, and unconjugated bilirubin rise, all pointing to ongoing hemolysis from intravascular clots. Coagulation tests are markedly abnormal: prolonged PT and aPTT indicate consumption of clotting factors, and the thrombin time is extended, consistent with a defective coagulation cascade due to factor consumption. An elevated D-dimer reflects fibrin degradation from widespread clot formation, which is a hallmark of DIC. Taken together, these features—MAHA with schistocytes, thrombocytopenia, prolonged coagulation times, and high D-dimer—most strongly support disseminated intravascular coagulation rather than other microangiopathies where coagulation tests are typically normal.

Disseminated intravascular coagulation is a consumptive coagulopathy where widespread activation of coagulation causes microthrombi formation and simultaneous consumption of platelets and clotting factors, leading to both thrombosis and bleeding.

Here, several findings line up with that process. The blood smear shows schistocytes, helmet and burr cells—typical of microangiopathic hemolysis from intravascular fibrin strands. The patient has marked thrombocytopenia (low platelets) and a severe anemia with reticulocytosis, LDH elevation, and unconjugated bilirubin rise, all pointing to ongoing hemolysis from intravascular clots.

Coagulation tests are markedly abnormal: prolonged PT and aPTT indicate consumption of clotting factors, and the thrombin time is extended, consistent with a defective coagulation cascade due to factor consumption. An elevated D-dimer reflects fibrin degradation from widespread clot formation, which is a hallmark of DIC. Taken together, these features—MAHA with schistocytes, thrombocytopenia, prolonged coagulation times, and high D-dimer—most strongly support disseminated intravascular coagulation rather than other microangiopathies where coagulation tests are typically normal.

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