When a pathological process interferes with the normal functioning of the metabolism and excretion of bilirubin just described, jaundice may be the result.
Jaundice is classified into three categories, depending on which part of the physiological mechanism the pathology affects. The three categories are:
||The pathology is occurring prior to the liver.
||The pathology is located within the liver.
||The pathology is located after the conjugation of bilirubin in the liver.
Laboratory findings include:
- Urine: no bilirubin present, urobilirubin > 2 units (except in infants where gut flora has not developed).
- Serum: increased unconjugated bilirubin.
- Kernicterus is associated with increased bilirubin
Hepatic jaundice causes include acute hepatitis, hepatotoxicity and alcoholic liver disease, whereby cell necrosis reduces the liver's ability to metabolize and excrete bilirubin leading to a buildup in the blood.
Less common causes include primary biliary cirrhosis, Gilbert's syndrome (a genetic disorder of bilirubin metabolism which can result in mild jaundice, which is found in about 5% of the population), Crigler-Najjar syndrome, metastatic carcinoma and Niemann-Pick disease.
Jaundice seen in the newborn, known as neonatal jaundice, is common, occurring in almost every newborn as hepatic machinery for the conjugation and excretion of bilirubin does not fully mature until approximately two weeks of age.
Laboratory findings include:
- Urine: Conjugated bilirubin present, urobilirubin > 2 units but variable (except in children). Kernicterus is a condition not associated with increased bilirubin.
Post-hepatic jaundice, also called obstructive jaundice, is caused by an interruption to the drainage of bile in the biliary system.
The most common causes are gallstones in the common bile duct, and pancreatic cancer in the head of the pancreas. Also, a group of parasites known as "liver flukes" can live in the common bile duct, causing obstructive jaundice.
Other causes include strictures of the common bile duct, biliary atresia, ductal carcinoma, pancreatitis and pancreatic pseudocysts. A rare cause of obstructive jaundice is Mirizzi's syndrome.
The presence of pale stools and dark urine suggests an obstructive or post-hepatic cause as normal feces get their color from bile pigments.
Patients also can present with elevated serum cholesterol, and often complain of severe itching or "pruritus".
Not one test can differentiate between various classifications of jaundice. A combination of liver function tests is essential to arrive at a diagnosis.
Table of diagnostic tests
||Normal / Increased
||Normal / Increased
||Normal / Increased
||Decreased / Negative
|Alkaline phosphatase levels
|Alanine transferase and Aspartate transferase levels
|Conjugated Bilirubin in Urine
Neonatal jaundice is usually harmless: this condition is often seen in infants around the second day after birth, lasting until day 8 in normal births, or to around day 14 in premature births.
Serum bilirubin normally drops to a low level without any intervention required: the jaundice is presumably a consequence of metabolic and physiological adjustments after birth. In extreme cases, a brain-damaging condition known as kernicterus can occur, leading to significant lifelong disability; there are concerns that this condition has been rising in recent years due to inadequate detection and treatment of neonatal hyperbilirubinemia.
A Bili light is often the tool used for early treatment, which often consists of exposing the baby to intensive phototherapy. Bilirubin count is lowered through bowel movements and urination so regular and proper feedings are especially important.
Most patients presenting with jaundice will have various
predictable patterns of liver panel abnormalities, though significant
variation does exist.
The typical liver panel will include blood levels
of enzymes found primarily from the liver, such as the
aminotransferases (ALT, AST), and alkaline phosphatase (ALP); bilirubin
(which causes the jaundice); and protein levels, specifically, total
protein and albumin. Other primary lab tests for liver function include
GGT and prothrombin time (PT).
Some bone and heart disorders can lead to an increase in ALP
and the aminotransferases, so the first step in differentiating these
from liver problems is to compare the levels of GGT, which will only be
elevated in liver-specific conditions.
The second step is
distinguishing from biliary (cholestatic) or liver (hepatic) causes of
jaundice and altered lab results. The former typically indicates a
surgical response, while the latter typically leans toward a medical
ALP and GGT levels will typically rise with one pattern while
AST and ALT rise in a separate pattern. If the ALP (10–45) and GGT
(18–85) levels rise proportionately about as high as the AST (12–38) and
ALT (10–45) levels, this indicates a cholestatic problem.
On the other
hand, if the AST and ALT rise is significantly higher than the ALP and
GGT rise, this indicates an hepatic problem.
between hepatic causes of jaundice, comparing levels of AST and ALT can
prove useful. AST levels will typically be higher than ALT.
remains the case in most hepatic disorders except for hepatitis (viral
or hepatotoxic). Alcoholic liver damage may see fairly normal ALT
levels, with AST 10x higher than ALT.
On the other hand, if ALT is
higher than AST, this is indicative of hepatitis. Levels of ALT and AST
are not well correlated to the extent of liver damage, although rapid
drops in these levels from very high levels can indicate severe
necrosis. Low levels of albumin tend to indicate a chronic condition,
while it is normal in hepatitis and cholestasis.
Lab results for liver panels are frequently compared by the
magnitude of their differences, not the pure number, as well as by their
The AST:ALT ratio can be a good indicator of whether the
disorder is alcoholic liver damage (10), some other form of liver damage
(above 1), or hepatitis (less than 1).
Bilirubin levels greater than
10x normal could indicate neoplastic or intrahepatic cholestasis.
Levels lower than this tend to indicate hepatocellular causes.
levels greater than 15x tends to indicate acute hepatocellular damage.
Less than this tend to indicate obstructive causes. ALP levels greater
than 5x normal tend to indicate obstruction, while levels greater than
10x normal can indicate drug (toxic) induced cholestatic hepatitis or
Both of these conditions can also have ALT and AST
greater than 20× normal. GGT levels greater than 10x normal typically
indicate cholestasis. Levels 5–10× tend to indicate viral hepatitis.
Levels less than 5× normal tend to indicate drug toxicity. Acute
hepatitis will typically have ALT and AST levels rising 20–30× normal
(above 1000), and may remain significantly elevated for several weeks.
Acetaminophen toxicity can result in ALT and AST levels greater than 50x
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