A CBC is performed with Hgb 78 g/L, Hct 0.290/L, RBC 4.0 x 10^12/L, WBC 15.0 x 10^9/L, PLT 85 x 10^9/L, MCV 91 fL, MCH 29 pg, MCHC 329 g/L, RETIC 11%, Peripheral Smear: Schistocytes, helmet cells. Additional Testing: uBIL 42 μmol/L, LDH 1800 U/L, CREA 290 μmol/L. Microbiology isolated E. coli O157:H7. What is the presumptive diagnosis?

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Multiple Choice

A CBC is performed with Hgb 78 g/L, Hct 0.290/L, RBC 4.0 x 10^12/L, WBC 15.0 x 10^9/L, PLT 85 x 10^9/L, MCV 91 fL, MCH 29 pg, MCHC 329 g/L, RETIC 11%, Peripheral Smear: Schistocytes, helmet cells. Additional Testing: uBIL 42 μmol/L, LDH 1800 U/L, CREA 290 μmol/L. Microbiology isolated E. coli O157:H7. What is the presumptive diagnosis?

Shiga toxin–producing E. coli infection leading to hemolytic uremic syndrome (HUS) fits this picture best. The key clues are microangiopathic hemolytic anemia signs — schistocytes on the smear, reticulocytosis, and markedly elevated LDH — plus thrombocytopenia and acute kidney injury (elevated creatinine). The unconjugated bilirubin is up from hemolysis, supporting MAHA. The isolation of E. coli O157:H7 after a diarrheal illness is a classic trigger for HUS, where endothelial injury in small vessels—especially in the kidneys—causes microthrombi, leading to red cell fragmentation, platelet consumption, and renal dysfunction. Thrombotic thrombocytopenic purpura can present with MAHA and thrombocytopenia as well, but it typically features more pronounced neurologic symptoms and less dominant kidney injury; the postdiarrheal context and the prominent renal involvement here point toward HUS rather than TTP.

Shiga toxin–producing E. coli infection leading to hemolytic uremic syndrome (HUS) fits this picture best. The key clues are microangiopathic hemolytic anemia signs — schistocytes on the smear, reticulocytosis, and markedly elevated LDH — plus thrombocytopenia and acute kidney injury (elevated creatinine). The unconjugated bilirubin is up from hemolysis, supporting MAHA. The isolation of E. coli O157:H7 after a diarrheal illness is a classic trigger for HUS, where endothelial injury in small vessels—especially in the kidneys—causes microthrombi, leading to red cell fragmentation, platelet consumption, and renal dysfunction.

Thrombotic thrombocytopenic purpura can present with MAHA and thrombocytopenia as well, but it typically features more pronounced neurologic symptoms and less dominant kidney injury; the postdiarrheal context and the prominent renal involvement here point toward HUS rather than TTP.

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