Hepatorenal Syndrome (HRS)

Perfusion pressure is the whole plan - These patients are vasodilated with a low SVR, and the actual treatment is splanchnic vasoconstriction to raise mean arterial pressure: terlipressin plus albumin in Europe, norepinephrine or midodrine plus octreotide in North America. Keep the vasopressor running through induction rather than letting pressure sag and finish the kidney off.

Invasive monitoring - Arterial line for anything beyond a brief case. You are titrating to a pressure target and drawing serial electrolytes and urine output, which is exactly what the medical team is following.

Know the triggers and don't be one - Spontaneous bacterial peritonitis, large-volume paracentesis without plasma expansion, and GI bleeding are the classic precipitants. If ascites is drained around the anesthetic, albumin replacement goes with it.

Stop the nephrotoxins - Establishing euvolemia and removing nephrotoxic agents is step one of treatment, not an afterthought. No NSAIDs or aminoglycosides, and find an alternative to IV contrast.

Coagulopathy - Synthetic failure means clotting factor deficiency and hypersplenism adds thrombocytopenia. Type and cross ahead of time and have products available.

Varices - Portal hypertension means gastroesophageal varices. Be deliberate with anything passed into the esophagus and be prepared for hemorrhage; variceal rupture is the bleeding emergency in this population.

Sepsis - Any infection reproduces the same vasoactive mediator release that drives HRS. Strict asepsis on lines and neuraxial procedures, and don't delay antibiotics.

Encephalopathy and drug handling - The failing liver isn't clearing toxic metabolites, and confusion is the late stage. Titrate sedatives and opioids to effect, expect a slow wake-up, and document baseline mentation so you can separate encephalopathy from residual drug.

Electrolytes and volume - Aim for euvolemia, not overload, and follow urine output and electrolytes intraoperatively. Hyponatremia and high plasma renin activity mark the highest-risk patients.

Where this ends - TIPS when medical therapy fails, liver transplant for the best long-term survival, and renal replacement therapy as a bridge rather than a treatment. Untreated type 1 HRS survives about two weeks, so these patients arrive sick and on a clock.

Hepatorenal syndrome (HRS) is functional acute kidney injury in advanced liver disease. The kidneys are histologically normal with no proteinuria, and function recovers after liver transplant. Cirrhosis and portal hypertension drive release of nitric oxide and prostaglandins, producing splanchnic and systemic vasodilation. The drop in circulating pressure trips carotid and aortic arch baroreceptors, activating the renin-angiotensin-aldosterone system, vasopressin release, and the sympathetic nervous system. Cardiac output falls as systemic vascular resistance falls, and the compensatory response clamps down on the renal circulation, so hypoperfusion feeds on itself until the kidney fails. Type 1 is a rapid doubling of creatinine past 2.5 mg/dL over two weeks with urine output under 500 mL/day and low urinary sodium; type 2 is slower, presenting with diuretic-resistant ascites.