Jaundice

Jaundice (icterus) refers to the yellow or yellowish-green discoloration of the skin and visible mucous membranes. It results from elevated levels of the yellow pigment bilirubin in the blood, which accumulates in all tissues and bodily fluids but is most noticeable on the skin. Bilirubin is continuously produced from the breakdown of red blood cells.

Red blood cells carry oxygen, binding it to hemoglobin, a blood pigment. The average lifespan of a red blood cell is four months. Every minute, over 100 million red blood cells break down, and their hemoglobin is converted into bilirubin, most of which is processed by the liver and excreted into the intestines.

Bilirubin’s intense yellow color gives infant stools a golden hue. In adults, intestinal bacteria convert bilirubin into other compounds, giving stools their characteristic brown color. Some of these compounds are reabsorbed into the blood and excreted in urine.

Excessive bilirubin accumulation in the skin can cause severe itching, slow heart rate, and, due to tinted eye fluid, a yellow-tinted vision (xanthopsia).

Jaundice has many causes, but three primary types exist:

1. Hemolytic jaundice occurs in conditions causing excessive red blood cell breakdown. A healthy liver cannot process the sudden influx of bilirubin, leading to its accumulation in the blood and tissues. This results in mild, straw-yellow skin discoloration and is often accompanied by anemia due to reduced red blood cell counts. Causes include hereditary red blood cell fragility, bacterial toxins (e.g., sepsis), malaria, or poisoning with arsenic or arsine gas.
2. Obstructive jaundice, common in people over 40, results from blocked bile flow from the liver to the intestines, often due to gallstones lodged in bile ducts, causing sharp, cramp-like pain. Other causes include inflamed bile duct linings, parasites (e.g., roundworms), or tumors (benign or malignant) in the liver, gallbladder, pancreas, or surrounding tissues. Complete obstruction leads to clay-colored stools and greenish-yellow skin. Prolonged bile stasis damages the liver and impairs digestion, affecting other organs like the kidneys.
3. Hepatic jaundice, the most common, is caused by liver damage, often from viral hepatitis (spread via contaminated food/water), bacteria, or parasites. Alcohol is a major liver toxin, causing damage that varies by individual sensitivity. Other causes include medications (e.g., sulfonamides, antituberculosis drugs, diabetes medications, antibiotics) or hypersensitivity to contraceptives. Hepatitis-related jaundice may last days to weeks, while tropical yellow fever, transmitted by mosquitoes, also features jaundice.

Short-term jaundice can result from medications like sulfonamides, antituberculosis drugs, diabetes pills, antibiotics, or contraceptives in sensitive individuals. All jaundice cases must be reported to a doctor, and treatment often requires hospitalization.

Modern diagnostics allow doctors to quickly identify the type of jaundice. Treatment begins after diagnosing the underlying condition, sometimes requiring urgent surgery.

“False jaundice” refers to skin yellowing not caused by elevated bilirubin, often due to chemicals from medications or foods (e.g., atebrin, used for malaria, or high-carotene foods like carrots). Carotene, a vitamin A precursor, can yellow the palms, soles, and nose, but not the sclera, unlike true jaundice. Stopping the intake resolves the discoloration, though frequent occurrences may indicate liver damage or impaired vitamin A conversion.

Over 50% of newborns develop mild jaundice on day two or three post-birth, peaking by day five and fading gradually. This physiological jaundice is harmless, caused by increased red blood cell breakdown after birth, as newborns no longer need the high red blood cell count required in the womb. Immature liver cells cannot process the sudden bilirubin surge, leading to jaundice, which typically resolves within 10–12 days. Prolonged jaundice beyond 12 days requires hospital treatment.

Life-threatening jaundice in newborns appears within hours of birth, becoming severe within 24 hours. Despite appearing healthy, these infants need urgent hospitalization. Historically, over 80% died, and survivors often faced developmental delays. The primary cause is blood group incompatibility, especially Rh factor mismatch between an Rh-negative mother and Rh-positive fetus, leading to antibody-mediated red blood cell destruction. This is more common in later pregnancies or after prior Rh-positive blood transfusions. Hospital delivery is mandatory for Rh-negative mothers with Rh-positive partners. Modern treatments, like exchange transfusions, significantly reduce mortality and complications, sometimes even providing in-utero transfusions.