Scleral icterus is the medical term for yellowing in the whites of the eyes, a visible sign of an underlying medical issue. This discoloration occurs due to the abnormal accumulation of bilirubin, a yellow pigment, in the bloodstream—a condition known as jaundice. Yellowing becomes noticeable when serum bilirubin levels rise above approximately 3 milligrams per deciliter (mg/dL). Scleral icterus is a symptom, not a disease, and always warrants prompt medical evaluation to identify and address the root cause.
The Biological Origin of Yellowing
Bilirubin is a natural byproduct of the body’s constant process of recycling old red blood cells. Red blood cells live for about 120 days, and when they break down, the hemoglobin they contain is converted into unconjugated bilirubin. This initial form of bilirubin is insoluble in water, meaning it cannot be easily excreted by the kidneys.
The unconjugated bilirubin is then transported through the blood, bound to a protein called albumin, to the liver for further processing. Once inside the liver cells, it undergoes a chemical transformation known as conjugation, which makes the bilirubin water-soluble. This newly formed conjugated bilirubin can now be excreted from the body.
The final stage of this metabolic process involves the conjugated bilirubin being secreted from the liver into the small bile ducts, which eventually merge into the common bile duct. From there, it moves into the small intestine, where it is metabolized by bacteria and largely eliminated in the stool, giving feces its characteristic brown color. Any disruption at any point in this three-part pathway—before, during, or after the liver—causes bilirubin to back up into the bloodstream, leading to the visible yellowing of the eyes.
Categorizing the Underlying Causes
The causes of scleral icterus are grouped based on where they interfere with bilirubin metabolism. This structure helps medical professionals narrow down diagnostic possibilities.
Pre-Hepatic Causes
Pre-hepatic causes involve conditions that lead to the excessive breakdown of red blood cells, a process called hemolysis. The liver is healthy but cannot keep up with the overwhelming quantity of unconjugated bilirubin being produced. The rapid destruction of red blood cells releases bilirubin faster than the liver can process it.
Common examples include hemolytic anemia, where red blood cells are destroyed prematurely, and genetic blood disorders like sickle cell disease. Malaria also accelerates unconjugated bilirubin production by destroying red blood cells. In these scenarios, the excess pigment remains unconjugated, a specific finding on blood tests.
Hepatic Causes
Hepatic causes stem from dysfunction or damage within the liver itself, compromising its ability to properly conjugate or secrete bilirubin. The liver’s cellular machinery is impaired, hindering the conjugation step and leading to a buildup of both unconjugated and conjugated bilirubin in the blood.
Frequent causes include acute or chronic liver infections, such as viral hepatitis A, B, or C, which inflame and injure liver cells. Long-term damage from conditions like cirrhosis, often related to alcohol misuse or non-alcoholic fatty liver disease, also limits processing capacity. Gilbert’s syndrome is a relatively benign inherited condition where the liver has a reduced ability to conjugate bilirubin, often causing mild and intermittent yellowing.
Post-Hepatic Causes
Post-hepatic causes, often called obstructive jaundice, occur when bilirubin excretion is physically blocked after processing by the liver. The problem lies in the drainage system, preventing conjugated, bile-rich bilirubin from flowing into the intestines. This blockage causes the water-soluble bilirubin to reflux back into the bloodstream.
The most frequent culprit is gallstones that have migrated from the gallbladder to lodge in the common bile duct. Other causes include tumors or inflammation in the pancreas, such as pancreatic cancer, which can compress the common bile duct. Any physical obstruction in the biliary tree prevents the final elimination of bilirubin, forcing it to accumulate.
Accompanying Signs and Symptom Differentiation
Observing other physical changes alongside yellow eyes provides important clues to differentiate the underlying cause. The color of the urine and stool are particularly useful indicators of where the metabolic process has failed. Normal bilirubin breakdown results in a product that colors the stool brown, and water-soluble bilirubin in the urine makes it dark.
In post-hepatic obstruction, the lack of bile flow results in stools that appear pale, clay-colored, or putty-like due to the absence of pigment. Since the conjugated bilirubin is blocked from leaving the body through the digestive tract, it spills into the urine. This makes the urine appear unusually dark, often described as tea or cola-colored. The presence of dark urine and pale stools together strongly points toward a blockage.
Pre-hepatic causes, involving unconjugated bilirubin, do not typically result in dark urine because unconjugated bilirubin is not water-soluble and cannot be filtered by the kidneys. Severe abdominal pain, particularly in the upper right quadrant, suggests an acute condition like a migrating gallstone or an inflamed gallbladder. Systemic symptoms such as fever and chills often suggest an underlying infection, such as acute hepatitis or a blocked and infected bile duct (cholangitis).
Diagnosis and Urgent Care Indicators
Medical evaluation for yellow eyes typically begins with a physical examination and a detailed review of the patient’s medical history. The initial diagnostic step involves blood tests to measure the total bilirubin level and to determine the ratio of unconjugated (indirect) to conjugated (direct) bilirubin. This ratio is crucial as it indicates the stage of the bilirubin pathway where the failure is occurring.
Blood work also includes a liver function panel, measuring enzymes like alanine aminotransferase (ALT) and aspartate aminotransferase (AST) to assess the degree of liver cell damage. If a blockage is suspected, tests for alkaline phosphatase (ALP) and gamma-glutamyl transferase (GGT) are often elevated, further supporting a diagnosis of bile duct obstruction. Following blood tests, imaging studies, such as an abdominal ultrasound, are used to visualize the liver, gallbladder, and bile ducts to check for physical obstructions.
While any case of yellow eyes warrants medical attention, certain signs indicate the need for immediate emergency care. A sudden onset of yellowing accompanied by severe, unrelenting abdominal pain requires urgent evaluation to rule out acute obstruction or infection. Yellowing combined with confusion, unusual sleepiness, or disorientation suggests the possibility of hepatic encephalopathy, a serious complication of advanced liver failure. High fever paired with chills and yellowing is another indicator of a potentially life-threatening infection requiring prompt hospital treatment.