The yellowing of the white part of the eye, medically known as scleral icterus, is often the first visible indicator of jaundice. This discoloration is a physical sign of an abnormal accumulation of a yellow-orange pigment in the bloodstream. Scleral icterus suggests a disturbance in the body’s natural waste processing system, specifically involving the liver and the breakdown of blood components. Because this symptom points to potential dysfunctions ranging from minor to severe, any noticeable yellowing requires prompt medical investigation.
Understanding Bilirubin
The yellow color that stains the eyes and skin originates from bilirubin, a byproduct of the normal breakdown of red blood cells. When old or damaged red blood cells are disassembled in the spleen and liver, the hemoglobin molecule is converted into unconjugated bilirubin, which is not water-soluble. This unconjugated bilirubin must be transported through the bloodstream bound to a protein called albumin to reach the liver cells. Once inside the liver, an enzyme process called conjugation converts the bilirubin into a water-soluble form, known as conjugated bilirubin.
This conversion allows the pigment to be excreted from the body. The conjugated bilirubin is then secreted by the liver into the small bile ducts, becoming a primary component of bile. Bile travels from the liver through the main bile duct to the small intestine, where it aids in digestion. Finally, the bilirubin is metabolized by intestinal bacteria before being eliminated, giving stool its characteristic brown color.
Hyperbilirubinemia, the medical term for elevated bilirubin in the blood, occurs when this process is overwhelmed or interrupted. When serum bilirubin levels exceed the normal range of under 1.0 mg/dL, the pigment begins to deposit in tissues. Yellowing of the eyes typically becomes noticeable when the total bilirubin concentration reaches approximately 2 to 3 mg/dL.
Causes of Yellow Eyes by Location of Dysfunction
Conditions that cause yellow eyes are categorized by where the failure occurs within the bilirubin pathway: before the liver (pre-hepatic), within the liver (intra-hepatic), or after the liver (post-hepatic). This categorization helps pinpoint the specific underlying mechanism causing the bilirubin buildup.
Pre-hepatic Dysfunction
Pre-hepatic dysfunction occurs before the bilirubin reaches the liver, meaning the problem lies in the sheer volume of pigment produced. This is caused by an accelerated breakdown of red blood cells, a process called hemolysis. Conditions like hemolytic anemia, where red blood cells are destroyed prematurely, or the resorption of a large hematoma can lead to this rapid increase. Genetic disorders such as Gilbert’s syndrome also fall into this category, resulting in impaired liver enzyme function that cannot keep pace with even normal bilirubin production. In these cases, the elevated bilirubin is predominantly the unconjugated type.
Intra-hepatic Dysfunction
Intra-hepatic dysfunction refers to damage or disease within the liver cells themselves, impairing their ability to process and excrete bilirubin. The liver tissue is compromised, leading to a failure in converting unconjugated bilirubin to its conjugated form. This results in an elevation of both unconjugated and conjugated bilirubin in the bloodstream, known as a mixed picture. Common causes include viral hepatitis (A, B, or C), which causes inflammation and injury, or chronic conditions like cirrhosis, where scarring permanently disrupts liver function. Drug-induced liver injury or chronic, excessive alcohol consumption can also directly damage the cells responsible for bilirubin conjugation.
Post-hepatic Dysfunction
Post-hepatic dysfunction, often called obstructive jaundice, happens after the liver has successfully processed the bilirubin. This involves a physical blockage that prevents the conjugated, water-soluble bilirubin from draining out of the liver and into the intestine. Because the flow is obstructed, the conjugated bilirubin backs up into the liver and re-enters the bloodstream. The most frequent cause of this obstruction is choledocholithiasis, which is the presence of gallstones lodged in the common bile duct. Other serious causes include inflammation of the pancreas (pancreatitis) or the growth of tumors in the pancreas or bile ducts.
Associated Symptoms and When to Seek Immediate Care
Jaundice is often accompanied by other symptoms that provide important clues about the underlying cause, particularly changes in the color of bodily waste products. Since conjugated bilirubin is meant to exit the body via the digestive tract, an obstruction causes its diversion into the urine, resulting in a noticeably dark, tea-colored appearance. Conversely, the lack of bilirubin reaching the intestines means that the stool loses its color, often appearing pale, gray, or clay-colored. Other common symptoms include generalized fatigue, loss of appetite, and pruritus, an intense itching caused by the deposition of bile salts in the skin.
Certain combinations of symptoms necessitate immediate medical attention, as they can signal a rapidly progressing or life-threatening condition.
- The sudden onset of jaundice accompanied by a high fever and chills may indicate ascending cholangitis, a severe infection of the bile duct.
- Severe, unremitting abdominal pain, especially in the upper right quadrant, can point to acute inflammation or a complete obstruction.
- Any change in mental status, such as confusion, disorientation, or excessive sleepiness, is a red flag for hepatic encephalopathy, which occurs when the failing liver allows toxins to build up in the brain.
- Acute, persistent vomiting or the presence of unexplained bleeding or bruising alongside the yellowing should prompt an emergency department visit.
Medical Diagnosis and Treatment Approaches
A medical evaluation begins with a thorough physical examination and detailed patient history, focusing on potential exposures, medications, and the onset of associated symptoms. The initial diagnostic step is a blood test to measure the levels of bilirubin, separating the total amount into conjugated and unconjugated fractions. This ratio helps determine whether the problem is pre-hepatic, intra-hepatic, or post-hepatic.
Blood work also includes a liver function panel, which measures enzymes like alanine aminotransferase (ALT) and aspartate aminotransferase (AST) that are released when liver cells are damaged. High levels of these enzymes usually point toward an intra-hepatic cause, such as hepatitis or drug toxicity. Further blood tests may check for viral markers or autoimmune antibodies to identify specific infectious or inflammatory conditions.
If blood tests suggest a post-hepatic, obstructive cause, imaging studies are performed next to visualize the liver and bile ducts. An abdominal ultrasound is a common first-line test that can non-invasively detect gallstones or dilation of the bile ducts, indicating a blockage. In some cases, a computed tomography (CT) scan or magnetic resonance cholangiopancreatography (MRCP) may be used to provide more detailed images of the biliary system and surrounding organs, like the pancreas.
Treatment for jaundice is always directed at resolving the underlying cause of the hyperbilirubinemia. For pre-hepatic causes like hemolytic anemia, treatment involves managing the red blood cell destruction. If the cause is a post-hepatic obstruction, such as a gallstone, a procedure like endoscopic retrograde cholangiopancreatography (ERCP) may be used to remove the blockage. Intra-hepatic conditions, like viral hepatitis, are often treated with antiviral medications or supportive care, while conditions caused by alcohol or drugs require immediate discontinuation of the offending substance.