Jaundice is the yellow or greenish discolouration of the skin, whites of the eyes (scleral icterus), and other tissues caused by elevated bilirubin in the blood. Bilirubin is a yellow pigment produced when the body breaks down the haemoglobin from old red blood cells, which are renewed approximately every 120 days. The liver normally processes bilirubin and excretes it via bile into the faeces; when this process is overwhelmed or disrupted, bilirubin accumulates in the tissues.
Jaundice has three main mechanisms. Pre-hepatic jaundice occurs when red blood cells are broken down too rapidly (haemolysis), overwhelming the liver’s capacity. Hepatic jaundice occurs when the liver itself is damaged or diseased (as in hepatitis, cirrhosis, or drug toxicity). Post-hepatic (obstructive) jaundice occurs when the flow of bile from the liver is blocked by gallstones, a tumour, or inflammation.
In the context of critical illness following cardiac arrest, jaundice may develop as a complication of post-cardiac arrest syndrome. Hepatic ischaemia (reduced liver blood flow during the arrest) can cause ischaemic hepatitis (shock liver), leading to elevated liver enzymes and, in severe cases, jaundice. Prolonged haemodynamic instability and blood transfusions can also contribute.
Jaundice is assessed by blood tests (bilirubin levels, liver function tests, haemolytic screen) and imaging (ultrasound and CT) to identify the underlying cause. Treatment depends on the cause, ranging from managing haemolysis to treating liver disease or relieving biliary obstruction.
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