Anesthetic Management for Patients with Hyperbilirubinemia

Abstract

The liver is the largest internal organ in the body and it plays a critical role in the homeostasis of many physiologic systems, including nutrient and drug metabolism, synthesis of plasma proteins and hemostatic factors, and detoxification and elimination of many endogenous and exogenous substances. Bilirubin metabolism is one of the biochemical and physiologic functions of the liver. The main source of serum bilirubin is heme metabolism. The normal total serum bilirubin levels is less than 1.5mg/dl (<25 mmol/L) and reflects the balance between bilirubin production and excretion. Hyperbilirubinemia is usually clinically obvious when total bilirubin exceeds 3mg/dl. In the form of jaundices. A predominantly conjugated hyperbilirubinemia (>50% of total bilirubin) is associated with increased urinary urobilinogen and may reflect hepatocellular dysfunction, congenital (Dubin-Johnson or Rotor Syndrome) or acquired intrahepatic cholestasis, or extrahepatic biliary obstruction. Hyperbilirubinemia that is primarily unconjugated may be seen with hemolysis or with congenital (Gilbert or Crigler-Najjar syndrome) or acquired defects in bilirubin conjugation. Unconjugated bilirubin is neurotoxic, and high levels may produce encephalopathy or “Kernicterus”. A good anesthetic technique include the awareness of different systemic changes in various organs due to liver dysfunction as well as the effect of anesthesia on hepatic function. Hepatic blood flow usually decreases during regional and general anesthesia, and multiple factors are responsible, including both direct and indirect effects of anesthetic agents, the type of ventilation employed, and the type of surgery being performed. Patients with hyperbilirubinemia are at increased risk of deterioration of liver function because of their decreased functional reserve. All volatile anesthetics decrease hepatic blood flow, but Desflurane and Sevoflurane have the least significant effect on total hepatic blood flow and hepatic oxygen delivery, whereas Halothane induces the most profound reductions in hepatic blood flow. Advanced liver disease may impair the elimination, prolong the half life, and potentiate the clinical effects of several drugs, including Morphine, Alfentanil, Vecuronium, Rocuronium, Mivacurium and Benzodiazepines. These drugs should be used cautioualy in patients with cirrhosis or end stage liver disease from any cause and their dosage and administration should be adjusted accordingly. Based on large retrospective studies, patients with cirrhosis who are undergoing abdominal surgery, especially those in CPT class C, appear to have an increased risk of perioperative death. Elective surgery in these individuals should be avoided, if possible, in favor of less invasive procedures. Post operative pain relief can be challenging. The role of regional techniques is very much restricted by the high incidence of coagulation defects. Non-steroidal anti-inflammatory medications and their association with increased risk of GI bleeding, platelet dysfunction and nephrotoxicity.Paracetamol is sometimes used.