Jaundice

Jaundice is a yellowish discoloration of the skin and deep tissues

results from abnormally high levels of bilirubin in the blood.
Jaundice occurs when there is an imbalance between the synthesis
of bilirubin and the clearance of bilirubin. Jaundice becomes evident
when the serum bilirubin levels rise above 2 to 2.5 mg/dL (34.2 to
42.8 mol). Because normal skin has a yellow cast, the early signs
of jaundice often are difficult to detect, especially in persons with
dark skin. Bilirubin has a special affinity for elastic tissue. The sclera
of the eye, which contains a high proportion of elastic fibers, usually
is one of the first structures in which jaundice can be detected.
The five major causes of jaundice are
1).
Excessive destruction of red blood cells
2).
Impaired uptake of bilirubin by the liver cells
3).
Decreased conjugation of bilirubin
4).
Obstruction of bile flow in the canaliculi of the hepatic
lobules or in the intrahepatic or extrahepatic bile ducts,
5).
Excessive extrahepatic production of bilirubin
Jaundice can be categorized as prehepatic, intrahepatic, and
posthepatic.
A). Prehepatic (Excessive Red Blood Cell Destruction): There
is mild jaundice, the unconjugated bilirubin is elevated, the stools
are of normal color, and there is no bilirubin in the urine.
Causes:
1). Hemolytic blood transfusion reaction
2). Hereditary disorders of the red blood cell
i).Sickle cell disease
ii).Thalassemia
iii). Spherocytosis
3). Acquired hemolytic disorders
4). Hemolytic disease of the newborn
5). Autoimmune hemolytic anemias
B). Intrahepatic: Intrahepatic or hepatocellular jaundice is caused
by disorders that directly affect the ability of the liver to remove
bilirubin from the blood or conjugate it so it can be eliminated in the
bile. This type of jaundice usually interferes with all phases of
bilirubin metabolism uptake, conjugation, and excretion. Both
conjugated and unconjugated bilirubin are elevated, the urine often
is dark because of bilirubin in the urine, and the serum alkaline
phosphatase is slightly elevated.

Causes:
1).
2).
3).
4).
5).
6).

Decreased bilirubin uptake by the liver

Decreased conjugation of bilirubin
Hepatocellular liver damage
Hepatitis Cirrhosis
Cancer of the liver
Drug-induced cholestasis

C). Posthepatic (Obstruction of Bile Flow): Posthepatic or

obstructive jaundice, also called cholestatic jaundice, occurs when
bile flow is obstructed between the liver and the intestine, with the
obstruction located at any point between the junction of the right or
left hepatic duct and the point where the bile duct opens into the
intestine. Conjugated bilirubin levels usually are elevated; the stools
are clay colored because of the lack of bilirubin in the bile; the urine
is dark; the levels of serum alkaline phosphatase are markedly
elevated; and the aminotransferase levels are slightly increased.
Blood levels of bile acids often are elevated in obstructive jaundice.
As the bile acids accumulate in the blood, pruritus develops.
Causes:
1).
Structural disorders of the bile duct
2).
Cholelithiasis
3).
Congenital atresia of the extrahepatic bile ducts
4).
Bile duct obstruction caused by tumors
Chart 46.1

Physiologic jaundice (hyperbilirubinemia) of the newborn is

usually a transient, benign icterus that occurs during the first week
of life in otherwise healthy full-term infants. It is caused by mild
unconjugated (indirect-reacting) hyperbilirubinemia.
Pathologic jaundice appears within 24 hours after birth with total
serum bilirubin level greater than 20 mg/dl or an indirect bilirubin
level greater than 15 mg/dl. Risk factors include fetal-maternal
blood type incompatibility (ABO and Rh incompatibility),
prematurity, exclusive breast-feeding, maternal age greater than or
equal to 25 years, an infant of male gender, delayed meconium
passage, and excessive birth trauma such as bruising or
cephalhematomas. It causes (1) increased bilirubin production, (2)
impaired hepatic uptake or excretion of unconjugated bilirubin, and
(3) delayed maturation of liver conjugating mechanisms.
Clinical Manifestation
Physiologic jaundice develops during the second or third day after
birth and usually subsides in 1 to 2 weeks in full-term infants and in

2 to 4 weeks in premature infants. After this, increasing bilirubin

values and persistent jaundice indicate pathologic
hyperbilirubinemia. Manifestations include yellowing skin, dark
urine, light-colored stools, and weight loss. Premature infants with
respiratory distress, acidosis, or sepsis are at greater risk for
encephalopathy. The resulting disabilities include athetoid cerebral
palsy and speech and hearing impairment.
Evaluation and Treatment
Total and direct (conjugated) bilirubin levels are monitored and the
bilirubin/albumin ratio is being evaluated as a corollary to unbound
serum bilirubin level for predicting neurotoxicity. Pathologic jaundice
should be suspected with serum bilirubin values that increase
greater than 5 mg/dl per day, persistent jaundice (more than 7 to
10 days in the full-term infant), or conjugated bilirubin values
greater than 2 mg/dl. Other causes of jaundice must be eliminated
to confirm physiologic jaundice.
Treatment depends on the degree of hyperbilirubinemia. Physiologic
jaundice is usually treated by phototherapy (ultraviolet light) with
good eye protection. Phototherapy produces isomers of bilirubin
that are water soluble, can be more rapidly excreted in the stools
and urine, and do not cross the blood-brain barrier. Pathologic
jaundice requires high-intensity phototherapy, exchange
transfusion, and treatment of the underlying cause. Advances are
being made to improve transcutaneous bilirubin monitoring and use
of drugs to reduce serum bilirubin levels.