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

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.

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

MELD Interpretation:

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:

• 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

  

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