Hemolytic Uremic Syndrome (HUS)

Labs before induction - CBC with peripheral smear (schistocytes, hemoglobin often under 10 g/dL, low platelets), a metabolic panel for creatinine, potassium, and sodium, and LDH with indirect bilirubin to gauge ongoing hemolysis. Urinalysis shows hematuria and proteinuria.

Volume status - They arrive dry from vomiting and diarrhea and usually need fluid, but oliguric renal failure turns generous resuscitation into overload. Titrate to urine output; sustained output under 0.5 mL/kg/hr for 72 hours is the threshold that sends them to dialysis.

Platelets - Don't reflexively transfuse. Consumption continues and transfusion may worsen thrombosis, so the accepted exceptions are active bleeding and immediately before a surgical procedure. Settle the count with the surgical team rather than chasing a number.

Uremic bleeding - Uremic toxins impair platelet adhesion to endothelium on top of the thrombocytopenia, so expect oozing out of proportion to the coags. Have blood crossmatched for anything beyond a minor case.

Succinylcholine - Off the table once potassium is climbing. Hyperkalemia and hyponatremia both develop as they enter renal failure, so check a potassium the day of surgery.

Full stomach - Active colitis with vomiting and bloody diarrhea makes this an RSI.

Renal drug handling - Avoid NSAIDs, aminoglycosides, and IV contrast where an alternative exists; favor drugs that don't depend on renal elimination and dose to the reduced GFR.

Neurologic baseline - Seizures and encephalopathy appear late, driven by uremia and electrolyte derangement. Document mental status preoperatively so you can read a slow emergence correctly.

Blood pressure - Hypertension can be severe and drug-resistant when the kidneys are the main site of disease, and it is one of the things followed long term after recovery.

The emergency laparotomy - Severe colitis can progress to intestinal necrosis and perforation. That patient comes to you volume depleted, thrombocytopenic, and in renal failure, so plan invasive monitoring and products in the room.

Ongoing therapies - Familial atypical HUS is managed with repeated plasma exchange and the pregnancy-associated complement-driven form with eculizumab. Both mean indwelling large-bore access, a line-infection history, and a patient who may hit the OR between treatments.

Hemolytic uremic syndrome (HUS) is a thrombotic microangiopathy defined by the triad of thrombocytopenia, microangiopathic hemolytic anemia, and acute kidney injury. Platelet microthrombi form in arterioles and capillaries, consuming platelets and shearing red cells as they pass, so the anemia is Coombs negative and the smear shows schistocytes. Typical HUS follows Shiga toxin-producing E. coli O157:H7 or Shigella dysenteriae; the toxin binds the Gb3 receptor on glomerular endothelium and tubular cells, producing glomerular necrosis, apoptosis, and microangiopathic thrombosis. Atypical HUS comes from complement dysregulation, Streptococcus pneumoniae, or drugs such as mitomycin C, cyclosporine, cisplatin, and quinine. It is a leading cause of acute renal injury in children under five. As renal failure sets in, hyponatremia and hyperkalemia follow, and uremia brings seizures and encephalopathy.