Hepatic physiology and preoperative evaluation

Published on 13/02/2015 by admin

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Last modified 13/02/2015

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Hepatic physiology and preoperative evaluation

Frank D. Crowl, MD

Patients with preexisting severe hepatic dysfunction are known to be at significant risk for experiencing perioperative death. Patients with mild to moderate hepatic dysfunction are at increased risk for death.

Some patients develop unexpected hepatic dysfunction (jaundice) in the postoperative period. The reported incidence of postoperative hepatic dysfunction, as demonstrated by abnormalities in liver function tests, is between 1 in 239 and 1 in 1091 anesthetics delivered. Interestingly, some of these patients had preexisting hepatic dysfunction that was not clinically apparent. One study found that 1 in 700 healthy asymptomatic ASA class I and II patients admitted for elective operations had unexplained abnormalities on preoperative liver function tests. After cancellation of their operations, one third of these patients developed clinical jaundice.

Metabolic function

Glucose homeostasis

The liver maintains glucose homeostasis through a combination of mechanisms: the conversion of fats and proteins to glucose by gluconeogenesis, glycogenesis (glucose → glycogen, 75 g stored in liver ∼ 24-h supply), and the release of glucose from glycogen by glycogenolysis. Insulin stimulates glycogenesis and inhibits gluconeogenesis and the oxidation of fatty acids. Glucagon and epinephrine have the opposite effect by inhibiting glycogenesis and stimulating gluconeogenesis.

Fat metabolism

Beta oxidation of fatty acids between meals provides a large proportion of body energy requirements and reduces the need for gluconeogenesis.

Protein synthesis

All plasma proteins are produced in the liver, except gamma globulins, which are synthesized in the reticuloendothelial system, and antihemophiliac factor VIII, which is produced by vascular and glomerular endothelium and sinusoidal cells of the liver. Most drugs administered by anesthesia providers are metabolized by the liver, and many of the metabolites are excreted through the biliary system.

Hepatic blood flow

Total hepatic blood flow (HBF) is approximately 100 mL·100 g⁻¹·min⁻¹, 75% of which flows through the portal vein, which is rich in nutrients from the gut but is partially deoxygenated, and can therefore supply 50% to 55% of hepatic O₂ requirements. The hepatic artery supplies 25% of HBF and 45% to 50% of hepatic O₂ requirements.

Splanchnic vessels supplying the portal vein receive sympathetic innervation from T3 through T11. Hypoxemia, hypercarbia, and catecholamines produce hepatic artery and portal vein vasoconstriction and decrease HBF. β-Adrenergic blockade, positive end-expiratory pressure, positive-pressure ventilation (increased intrathoracic pressure increases hepatic vein pressure, which in turn decreases HBF), inhalation anesthetic agents, regional anesthesia with a sensory level above T5, and surgical stimulation (proximity of surgery to the liver determines the degree of HBF reduction) can all cause a reduction in HBF.

Preoperative hepatic assessment

Two indices are used to assess preoperative risk in patients with underlying advanced liver disease. The Child-Pugh score, the first scoring system used to stratify the severity of end-stage hepatic dysfunction, comprises five criteria: ascites, hepatic encephalopathy, INR (international normalized ratio), serum albumin, and bilirubin concentration. Patients are then stratified into three risk categories: A, minimal; B, moderate; C, severe.

The Model for End-stage Liver Disease (MELD) score, developed at the Mayo Clinic, uses only three laboratory values in its assessment of end-stage liver disease: INR, serum creatinine, and serum bilirubin concentration:

< ?xml:namespace prefix = "mml" />MELD = 3.78 [ln bilirubin] + 11.2 [ln INR] + 9.57 [ln creatinine] + 6.43

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