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Jaundice (Icterus): causes, signs, diagnosis and management

Jaundice (icterus) is yellowing of the skin and eyes due to raised bilirubin. This article explains causes, how bilirubin metabolism is altered, common presentations, diagnosis, treatment, and special considerations in newborns.

Author: Leandro Alegsa Creation date: November 13, 2022 Last updated: May 21, 2026

simple.wikipedia.org · CC BY 3.0

Overview

Jaundice, also called icterus, is the yellow discoloration of the skin, mucous membranes and the whites of the eyes caused by accumulation of bilirubin in the body. The condition reflects an imbalance between bilirubin production and elimination. The visible change is most obvious on the skin and the sclera, but laboratory tests that measure bilirubin in the blood are used to confirm a diagnosis.

How bilirubin and bile relate to jaundice

Bilirubin is produced when the heme part of hemoglobin is broken down during red blood cell turnover. The liver plays a central role in taking up, chemically changing and excreting bilirubin into bile. When the liver cannot remove bilirubin efficiently or when bile flow is obstructed, bilirubin rises and causes yellowing. Bile itself is a digestive fluid made by the liver; it aids fat absorption and carries waste products into the intestines for elimination. Interruption of bile flow alters digestion and can contribute to jaundice of obstructive origin.

Common causes and types

Pre-hepatic (increased production): excessive breakdown of red blood cells raises unconjugated bilirubin.
Hepatic (liver dysfunction): disorders that affect hepatic uptake, conjugation or excretion of bilirubin, such as viral hepatitis or inherited enzyme defects.
Post-hepatic (obstructive): blockage of bile ducts by gallstones or tumors prevents bile entering the intestinal tract and causes conjugated bilirubin to build up.

Infectious diseases such as malaria can also cause jaundice through hemolysis or liver involvement.

Presentation, diagnosis and special populations

Typical signs include yellowing of the skin and eyes, dark urine and pale stools when bile flow is reduced. Laboratory evaluation distinguishes unconjugated from conjugated hyperbilirubinemia and includes liver enzymes and imaging when obstruction is suspected. Jaundice is very common in newborns; physiologic neonatal jaundice usually appears on the second or third day after birth and is often self-limited, though some infants need monitoring or treatment (newborn care).

Treatment and prognosis

Treatment targets the cause: treating infections, relieving biliary obstruction, or supporting liver disease.
Supportive measures can include hydration and nutritional support; in newborns phototherapy increases bilirubin breakdown.
Prognosis depends on severity and underlying illness; isolated physiologic neonatal jaundice typically resolves, while jaundice from severe liver failure requires specialist care.

Notable facts and prevention

Because many different processes can produce jaundice, the pattern of laboratory results and imaging helps identify whether the problem originates before, in, or after the liver. Maintaining vaccination against hepatitis, prompt treatment of hemolytic conditions, and timely management of gallstones can reduce the risk of jaundice related to those causes. For more general information about liver function and digestion see material on digestive physiology and bile metabolism, or consult clinical resources on bilirubin chemistry and visible signs used in examination. For clinical guidance and resources follow specialist summaries and local health authority advice (liver health, intestinal health).

Marked yellowing of the sclerae and facial skin, in this case caused by hepatitis A

Hemolytic icterus (prehepatic)

In prehepatic jaundice, the greatly increased decay of red blood cells (erythrocytes) in the context of hemolysis leads to an increased accumulation of unconjugated bilirubin. The same mechanism occurs physiologically in neonatal icterus (haemolytic neonatorum). Shortly after birth, the erythrocytes loaded with fetal hemoglobin are increasingly broken down and replaced by newly formed red blood cells. Neonatal icterus is a sign of this ongoing reaction and is usually harmless. In the case of massively elevated bilirubin levels shortly after birth (e.g. due to an existing rhesus incompatibility (erythroblastosis) or in premature births), however, there is a risk of kernicterus, damage to important centres of the central nervous system with a poor prognosis.

Prehepatic icterus can also occur in blood transfusion complications (loss of blood cells), as a result of a pulmonary infarction and in the case of large haematomas.

Hepatocellular jaundice (intrahepatic)

Since several steps of bilirubin metabolism take place in the liver, there are accordingly also different possibilities for the development of (intra)hepatic icterus. Essentially, the following processes can be disturbed:

hepatocellular bilirubin uptake
Bilirubin conjugation (conversion of water-insoluble, unconjugated bilirubin into water-soluble, conjugated bilirubin with the aid of glucuronic acid)
Transport of conjugated bilirubin out of the liver cell
Outflow from the bile ducts of the liver into the intrahepatic bile ducts

bilirubin imbalance

Insufficient uptake of unconjugated bilirubin may be due to liver cell damage, for example in the context of viral hepatitis or acute liver failure, or to an overload of the cell's own transport system. Some drugs (some antibiotics, for example) have to be excreted via the same transport pathways and may compete with bilirubin.

bilirubin conjugation disorder

It is usually triggered by genetic defects in the enzymes involved (especially UDP-glucuronyltransferase). The best-known diseases in this context are Gilbert-Meulengracht syndrome and Crigler-Najjar syndrome.

bilirubin imbalance

In addition to liver cell damage of various causes, hereditary disorders of the necessary structures can also be triggering. These include the Dubin-Johnson syndrome or the rotor syndrome. In the case of inanitional icterus, mobilized fatty acids displace bilirubin from the transport proteins.

bile duct obstruction

Similar to posthepatic jaundice, several other substances are affected by the lack of excretion in addition to bilirubin. Therefore, we speak of an intrahepatic cholestasis.

Questions and Answers

Q: What is jaundice?

A: Jaundice is a medical condition where the skin and the whites of the eyes turn yellow.

Q: What causes jaundice?

A: Jaundice is caused by problems with the liver not being able to remove heme properly. Heme changes into a chemical called bilirubin after red blood cells die, and bilirubin causes the yellow coloration of the skin.

Q: When is jaundice common?

A: Jaundice is common in newly born babies, usually starting on the second day after birth.

Q: What other diseases can cause jaundice?

A: Other diseases that can cause jaundice include malaria, hepatitis, and gallstones.

Q: What is the most common liver problem?

A: Jaundice is the most common liver problem.

Q: What is bile?

A: Bile is a digestive fluid made by the liver that is necessary for proper nutrition, and it also prevents decaying changes in food.

Q: What happens if bile is unable to enter the intestines?

A: If bile is unable to enter the intestines, then there will be an increase in gases and other byproducts. Normally, the production of bile and its flow is constant.