AM Report 11/30/2016: Hepatorenal Syndrome

Some common physical exam findings of liver disease:

  • Fetor hepaticus (breath smells like a freshly opened corpse)
  • Spider nevi
  • Gynecomastia
  • Jaundice / Scleral icterus
  • Ascites
  • Caput medusae (dilated abdominal veins)
  • Rectal varices
  • Testicular atrophy
  • Palmar erythema
  • Dupuytren’s contracture

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MELD Score:

  • Predicts 3-month survival in patients with cirrhosis.  In cirrhotic patients, an increasing MELD is associated with increasing severity of hepatic dysfunction and increased 3-month mortality.

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Factors that go into MELD: serum bilirubin, serum creatinine, INR, sodium (added 1/2016), +/- hemodialysis > 2 in the past week

MELD Interpretation:

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Maddrey Discriminant Function:

DF = (4.6 x [prothrombin time] – [control prothrombin time]) + (serum bilirubin)

  • DF > 32 indicates SEVERE alcoholic hepatitis
  • High short term mortality (20-30% within 1 month; 30-40% within 6 months)
  • Patient may benefit from glucocorticoids
  • Prednisone requires hepatic conversion to the active form (prednisolone)
  • Multiple trials have showed a reduced short term mortality in patients with a DF >32 (NNT 3-68); no effect in patients <32

STOPAH Trial:

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  • Multicenter, double blinded, RTC
  • 1103 patients with DF >32 and TBili > 4.7
  • 4 treatment groups: (placebo, pentoxifylline + placebo, prednisolone + placebo, pentoxifylline + prednisolone)
  • Prednisolone had a significant 28 day mortality benefit (after adjusting factors), but the benefit was lost at 90 days and 1 year
  • Pentoxifylline did not improve survival compared to placebo

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Hepatorenal Syndrome:

Characteristics of HRS:

  • Clinically evidence acute or chronic liver disease
  • Progressive rise in serum creatinine
  • Normal urine sediment
  • Absent/Minimal proteinuria
  • Low urine sodium (often < 10 mEq/L)
  • Oliguria

Types of HRS:

Type 1: more serious; at least a 2 fold increase in serum creatinine to >2.5 mg/dL in less than 2 weeks

Type 2: less severe; major clinical feature is ascites resistant to diuretics

Etiology:

  • Splanchnic vasodilation ⇒ reduced effective circulating volume ⇒ renal failure
  • MAP = CO x SVR; In patients with HRS, SVR is decreased (from splanchnic vasodilation); hence treatment is aimed at improving SVR and MAP.

Diagnosis of HRS is one of exclusion:

  • Normal urinary sediment
  • Absence of nephrotoxic meds
  • No hypotension
  • Urine studies similar to pre-renal AKI

Fluid challenge with albumin: 1 g/kg albumin (max 100 g) daily for 2 days

  • If renal function IMPROVES, suggestive of pre-renal AKI
  • If renal function continues to DECLINES, suggestive of HRS

Treatment of HRS:

  • Liver transplantation – TREATMENT OF CHOICE
  • Medical Management:
    • ICU: treat with norepinephrine and albumin
    • Non-ICU: treat with midodrine, octreotide, and albumin

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