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Chapter 26. Liver Failure

Ruchir Gupta, MD

  • ETOH
  • Hepatitis B, C, and D
  • Hemochromatosis, Wilson disease
  • Autoimmune, inherited (biliary atresia, alpha-1 antitrypsin deficiency, etc.)

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Assessment of Systemic Manifestations of Liver Disease
SystemFeatures
CVIncreased CO, increased TBW but relative hypovolemia, decreased SVR
Metabolic
  • Hypokalemia, hyponatremia, hypoalbuminemia, hypoglycemia
  • Skeletal muscle wasting, poor skin turgor, loss of adipose tissue
Respiratory
  • Increased A-V shunts, decreased FRC, pleural effusions
  • Hepatopulmonary syndrome—marked pulmonary HTN with prominence of A-V shunts. Orthodeoxia and platypnea (desaturation and dyspnea when upright)
GI
  • Ascites, portal HTN, esophageal varices, hypersplenism
  • Spontaneous bacterial peritonitis—gram positive in asymptomatic patients but usually gram negative in symptomatic patients (E. coli, Klebsiella)
RenalHepatorenal syndrome—oliguric deterioration in renal function in patients with liver failure:
  • Cause unknown (may be caused by nephrotoxins not cleared by liver)
  • Resolves with liver transplantation
  • Intraoperative/postoperative dialysis may be necessary
HematologicAnemia, coagulopathy (decreased factors II, V, VII, X, increased PT), decreased platelets
Neurologic

Encephalopathy—etiology multifactorial: false neurotransmitters, inflammation

Tx: lactulose (accelerates GI transit to reduce absorption of false neurotransmitters), neomycin (eliminates ammonia-producing bacteria), low-protein diet (lowers ammonia produced by protein breakdown)

West Haven criteria:

  • Grade 1—trivial lack of awareness, euphoria or anxiety, shortened attention span, impaired performance of addition or subtraction
  • Grade 2—lethargy or apathy, minimal disorientation for time or place, subtle personality change, inappropriate behavior
  • Grade 3—somnolence to semistupor, but responsive to verbal stimuli; confusion; gross disorientation
  • Grade 4—coma (unresponsive to verbal or noxious stimuli)
    • Transition from grade 1 to 2/3 may occur over a period of hours. Treatment should focus on relieving causes of increased ICP (head elevation, hyperventilation, osmotic diuretics)

Pharmacokinetic and pharmacodynamic
  • Increased Vd for most drugs
  • Decreased protein binding with increased free drug fraction

  • Assess overall severity of liver disease
  • If elective surgery, optimize patient:
    • Reduce ascites
    • Correct electrolyte abnormalities (hypokalemia and hyponatremia)
    • Look for prerenal renal insufficiency (may need to have dialysis equipment intraoperatively/postoperatively if hepatorenal syndrome present)
    • Improve nutritional status:
      • If patient on TPN/feeds, continue intraoperatively and postoperatively
    • In patient with hemochromatosis or alcoholic dilated cardiomyopathy:
      • Assess cardiac function (TTE)
      • Possible conduction abnormalities
  • Preoperative therapies:
    • Continue beta-blockers (if portal hypertension)
    • If premedication needed, prefer hydroxyzine to benzodiazepines; no premedication if encephalopathy

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Child–Pugh Classification of Severity of Liver Disease
VariableAbsent (1 point)Slight (2 points)Moderate (3 points)
AscitesNoneMildModerate
Bilirubin<22–3>3
Albumin>3.52.8–3.5<2.8
PT<44–6>6
EncephalopathyNoneMildSevere
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Score2-year survival (%)Mortality risk of major abdominal surgery (excluding liver transplantation) (%)
5–685–10010
7–960–8030
10–1535–4550–70

GA preferred but regional can be considered in the absence of coagulation abnormalities. Superficial nerve blocks in “compressible” compartments (not infraclavicular, psoas compartment, or sciatic blocks) can be performed by an experienced practitioner even if coagulation abnormal.

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