Morning Report 11/17 – Hepatorenal syndrome

Teaching Pearls:

  • Pathophysiology
    • Involves excessive splanchnic vasodilation due to production of nitric oxide, causing increased decreased flow to the renal circulation.
    • MAP = CO x SVR
      • In patients with HRS, SVR is decreased due to the splanchnic vasodilation. Hence treatment is geared towards improving SVP and MAP.
  • Diagnosis of Exclusion
    • Normal urinary sediment
    • No nephrotoxic meds
    • No hypotension
    • Urine studies similar to pre-renal AKI
      • UNa low, elevated FENa or FEUrea
    • Cannot distinguish between HRS and and pre-renal AKI
  • Requires fluid challenge with albumin to distinguish between HRS and pre-renal AKI
    • 1g/kg albumin (max 100g) daily x 2 days
    • If renal function improves, suggestive of pre-renal AKI
    • If renal function continues to worsen, suggestive of HRS
  • Types
    • Type I
      • Two-fold increase in Cr to Cr>2.5 within two weeks
      • Very poor prognosis
    • Type II
      • Less severe disease, associated with diuretic resistance
  • Treatment of Choice
    • Liver Transplantation
    • Medical Management
      • If in ICU
        • Treat with norepinephrine and albumin
      • If non-ICU
        • Treat with midodrine, octreotide, and albumin

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