emDocs - October 14, 2019 - By Margus C and Beck-Esmay J
Edited by: Koyfman A; Montrief T and Brit Long B)
"Pearls & Pitfalls
- HRSis a high mortality complication of cirrhosis (1-7 month prognosis).
- HRS likely develops when portal hypertension leads to release of excess vasodilators, thereby triggering a compensatory restriction to kidney perfusion and function.
- HRS should be considered in all patients with cirrhosis + ascites + AKI refractory to volume resuscitation.
- HRS is a diagnosis of exclusion, after diuretics and nephrotoxic agents have been stopped and shock and intrinsic renal pathology ruled out.
- HRS evaluation is aided by ultrasound: to assess volume status, rule out obstructive nephropathy, and assist with paracentesis so as to exclude another big complication of cirrhosis, spontaneous bacterial peritonitis.
- HRS is a cirrhotic AKI that can be diagnosed and treated with intravenous albumin supplementation at 1g/kg/day.
- HRS vasoconstrictor therapy can be started in the ED with norepinephrine (0.5-3mg per hour IV infusion), but octreotide+ midodrine (octreotide 100-200mcg SQ every 8 hours; midodrine 7.5-12.5mg orally three times daily) is also an option, aiming for a MAP of 10 mmHg greater than the patient’s baseline.
- HRS doesn’t exclude other complications of cirrhosis like SBP and abdominal compartment syndrome, and paracentesis should be considered with a low threshold to start empiric antibiotics (typically a third-generation cephalosporin)."