HUS primarily affects children under 10 years old. It also affects the elderly.
HUS is associated with infectious gastroenteritis caused by E. coli strain O157:H7 and leading to bloody diarrhea. The Shiga-like toxin that is formed then enters the circulation through inflamed gastrointestinal mucosa.
Once in the circulation, the Shiga-like toxin interrupts endothelial cell function causing damage and leading to platelet activation and aggregation.
The thrombi formed in microcirculation shear blood cells as they travel through thus hemolyzing them. This results in the characteristic helmet cells. The word “microangiopathic” refers to small blood vessels.
Over-activation and aggregation of platelets leads to thrombocytopenia.
Thrombi deposit in glomeruli of kidneys and can lead to infarcts and necrosis and possible renal failure.
Sheared blood cells resemble helmets. Helmet cells are also known as schistocytes.
Elevated lactate dehydrogenase is characteristic in HUS as it is a chemical released from damaged cells.
Dialysis is indicated in patients with BUN>80 mg/dL, symptomatic uremia, and electrolyte overload.
Treatment for HUS is typically supportive consisting of IV hydration, monitoring of blood counts, monitoring of electrolyte counts and replenishing of electrolytes if needed. RBC and platelet transfusions are indicated if the hemoglobin drops to below 6 g/dL or if significant bleeding occurs, respectively.
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