Avoid stress – stress aggravates the symptoms of Gilbert syndrome.

Drug preferences – Propofol is a good induction choice as it is metabolized by both liver and kidney. Fentanyl, as a single bolus dose, is generally considered safe as the effects are terminated by redistribution to muscle and fat. Remifentanil, however, is considered a safer option as it is very quickly metabolized by plasma esterases. Cisatracurium is generally considered the best option of the nondepolarizing muscle relaxants because it is eliminated by Hoffman degredation. Isoflurane is the inhaled anesthetic of choice because it is very lightly metabolized in the liver (less than 0.2%) and preserves hepatic blood flow. Acetaminophen and Morphine are avoided

Early case – Fasting can induce symptoms because fatty acids compete with unconjugated bilirubin in the liver. Therefore, these patients should ideally be scheduled for surgery as early as possible.

Gilbert syndrome is the most common form of congenital hyperbilirubinemia. Manifestation by signs and symptoms of the disorder is indication that the syndrome is an inherited autosomal dominant trait. However, the disorder can be autosomal recessive (typically no signs or symptoms), and passed to offspring. Dominant vs recessive is dependent on mutation differences of the UGT1A1 gene.

This syndrome is characterized by a buildup of unconjugated bilirubin in the absence of hemolysis or underlying liver disease. This buildup is due to a relative deficiency of glucuronyl transferase and insufficient uptake of unconjugated bilirubin by hepatocytes.

Gilbert syndrome has been recognized as a cause of postoperative jaundice. Jaundice will be visible only when the bilirubin is more than 3 mg/dL in the serum. Most patients will exhibit levels between 3-8 mg/dL

Signs and symptoms can be any of the following: clinical jaundice, nausea, malaise, discomfort in the right hypochondrium, and abdominal pain.