ICTERUS

T U T O R : D R . Z U L F A H M I D A H M . K E S

DISUSUN OLEH : KELOMPOK 3B

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11020180155 SITTI AULIA RAMADHANI SUMARWAN
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CASE
SCENARIO 3:
A woman 18 years of giving birth in a complicated labor. In the first 2 days of birth, the baby looks
jaundiced light. On examination, there were no abnormalities in the morphology (shape) baby. Laboratory
results found bilirubin concentration of 4.9 mg / dL. In infants Coombs test result is positive RBC.
• How is the anatomy of the organ involved?
• How histology of the organ involved?
• Explain the physiology and biomechanics of the organ involved!
• Mention the etiology of jaundice!
• Describe the pathophysiology of the symptoms of jaundice!
 HARDWORD
1.Jaundice: Yellow discoloration that occurs in the
neonatal or newborn.
2.Tests cooms: Blood screening test to detect
antibodies to the surface of erythrocyte
KEY SENTENCE
1. Women 18 years old gave birth
2. The first 2 days of jaundice
3. Not found morphological abnormalities in
infants
4. The concentration of bilirubin in the baby
4,9mg / dl
5. Coombs test positive (+)
 QUESTION :
1. How anatomical images of organs involved! 7.Describe the various types of jaundice:

2. How histology of the organ involved! i. The etiology of jaundice

3. Explain and biomechanic organ physiology ii. Petogenesis over-production of bilirubin

involved! iii. The pathogenesis of declining
4. Mention the etiology of jaundice! conjugation of bilirubin

5. Describe the pathophysiology of the symptoms iv. Pathogenesis decrease hepatic uptake of
of jaundice! bilirubin conjugation

6. How normal bilirubin formation mechanism! v. Pathogenesis decreasing intracellular

transport of bilirubin
8.What is the relationship of all the symptoms
experienced!
9.Diseases whatever symptomatic yellow body!
10.Any treatment that can be done!
 ANSWER
1.ANATOMY
Liver (hepatic) is the largest intestinal organ weighing between 1.2 to 1.8 kg
or approximately 25% of the weight of adults who occupy most of the upper
right quadrant of the abdomen and is central to the body's metabolism to
function very complex. The upper limit of the liver are aligned with a right
intercostal space V and the lower limit of the upward diagonal ribs ribs VIII
IX right to left. Heart shaped concave posterior surface and there is a
transverse slit along the 5 cm of hepatic portal system. There are minor
omentum from the portal system containing the hepatic artery, portal vein
and common bile duct. Portal system located in front of the vena cava and
behind the gall bladder.

The convex anterior surface is divided into two lobes of the left lobe and
right lobe that is approximately 2 times the left lobe. In the area between
falsiform with gall bladder ligament in the right lobe can sometimes be found
quadrate lobe and caudate lobe which is normally covered by the inferior
vena cava and the ligament venosum the posterior surface. The liver is
divided into 8 segments with different functions. Basically, the line Cantile
contained from the vena cava to the heart of the gallbladder has been split
into two functional lobes, and in the presence of an area with relatively little
vascularization, sometimes used as a boundary resection. Further division
into eight segments based on the flow branch blood vessels and bile ducts
owned by each segment.

Intrahepatic bile ducts are slowly together to form larger ducts that can
channel the liver bile into eight segments. In the right liver segment,
combined these branches form a channel in the anterior and posterior are
then joined to form the right hepatic duct. In some people, the right hepatic
duct is approximately 1 cm outside the liver. The ducts are then joined by
three segments of the segment of the left heart (left hepatic duct) into hepatic
duct communists.
2.HISTOLOGY

Part of the liver, called lobules separated by connective tissue and

blood vessels. The blood vessels in the liver are at the corners of
the lobules, which eventually formed the so-called triangle of
Kiernan building or area of ​the portal. In the portal area can be
found hepatic artery branch, the branch portal vein and bile duct.
The structure of hepatic lobules in the transverse section will
appear as rows and radier structure, with its central veins,
separated by a gap or hepatic sinusoid. At the microscopic
appearance, in the hepatic sinusoid are Kupffer cells. These cells
have the function to fagocyt old erythrocytes, hemoglobin and
secrete cytokines. Can also be found liver cells or commonly
called hepatocytes. Polyhedral-shaped hepatocytes with the
surface 6 or more, has no clear boundaries, and have a round
nucleus in the middle. Colored eosinophilic cytoplasm in
hepatocytes, this was due to the hepatocytes have a lot of
mitochondria and smooth endoplasmic reticulum. In the cytoplasm
of hepatocytes are lysosomes, peroxisomes, glycogen granule and
can also be found that fat droplets will appear after fasting or after
eating fatty foods. The functional part of the liver is called lobules
portal, consisting of 3 classic lobule (the smallest unit of the liver
or liver lobules) and in the middle there interlobularis duct. In the
smallest functional unit of the liver are called hepatic acini. Liver
acini are part of the liver which is located between the central
vein. Acini hepatic artery hepatica has a terminal branch, duktuli
portal vein and biliary system.
3.PHYSIOLOGY
The liver has a very diverse functions. Circulation of the portal vein that supplies 75% of the supply of acini plays
an important role in the physiology of the heart, particularly in the metabolism of carbohydrates, proteins and fatty
acids.
The main function of the liver is the formation and excretion of bile. The liver excretes bile as much as one liter
per day into the small intestine. The main elements of the bile is water (97%), electrolytes, bile salts. Although
bilirubin (a bile pigment) is the end product of metabolism and physiological do not have an active role, but it is
important as an indicator of liver and biliary tract disease, because bilirubin can give color to the tissues and fluids
associated with it.
Results monosaccharide metabolism of the small intestine is converted into glycogen and stored in the liver
(glikogenesis). From glycogen depot is supplied constantly to the blood glucose (glycogenolysis) to meet the
body's needs. Most of the glucose is metabolized within the network to generate power and the rest is converted
into glycogen (stored in muscle) or fat (stored in the subcutaneous tissue).
Liver function in the metabolism of proteins is generating plasma proteins such as albumin (which is necessary to
maintain a colloid osmotic pressure), protombin, fibrinogen and other clotting factors.
Liver function in fat metabolism is generating lipoprotein, cholesterol, phospholipids and acetoacetic acid.
The main function is storage Fesica vellea bile, bile concentration and releases bile into the digestive tract.
landmark The normal Interpretation 4.BIOCHEMISTRY
value
Measurement of serum bilirubin,
aminotransferase, alkaline phosphatase,
bilirubin 5-18 umol / l Not specific to liver disease, increases also may hemolysis and
and albumin is often referred to as liver
biliary obstruction. By themselves, consider hereditary
function tests. In many cases, these tests
hyperbilirubinemia
can detect asymptomatic liver disease
SGOT 5-40 IU / I Corresponding increase inflammation and necrosis of
SGPT 5-35 IU / I hepatocytes.
biliary and before emergence of clinical
Usually not necessary to measure both, but the ratio of AST,
manifestations.
ALT> 2 refers to alcoholic hepatitis disease.
Some particular forms of hepatitis can
Alkaline 30-130 IU / I Usually increases with the cholestasis, hepatic biliary
cause varying degrees of cholestasis and,
phosphatase 5-50 IU / I obstruction or infiltration. Alkaline phosphatase are also
consequently, an increase in alkaline
ɣ-GT produced by the bone, gut, and placenta.
Sensitivity and low specificity in liver disease. Possible increases
phosphatase and ɣGT. Therefore,
240-524 IU / I in ischemic hepatitis. Levels also increased after bone damage or clinicians should work based on the
LDH hemolysis. existing pattern, and choose enzymes
which seems to be most dominant.
5.ETIOLOGY
Jaundice or jaundice is a yellowing of the skin, conjunctiva, and mucous membranes due to accumulation of bilirubin, whereas hyperbilirubinemia is
jaundice with serum bilirubin concentrations suggestive occurrence of kernicterus or bilirubin ensefalohepati when bilirubin levels are not controlled.
The etiology of jaundice divided into two based on physiology and patofiologi, while based fisiolognya:
In babies-newborns, changes in red blood cells in the womb into red blood cells outside the womb in large quantities so that the production of indirect
bilirubin is high. In newborn infants UDPGT capabilities within the heart to be able to change the entire indirect bilirubin into direct bilirubin is not
maximized. In addition, the intestines of newborns are still clean yet there are germs that can convert direct bilirubin that can be disposed of along
with bowel and movement or motility also not maximized so that direct bilirubin can be reabsorbed by the intestines and into the heart again. High
levels of indirect bilirubin can be dangerous because the bilirubin can enter and penetrate the brain barrier, causing kernicterus and life threatening.
In addition to the normal process of red blood cell changes in the womb into red blood cells outside the womb, neonatal jaundice can be pathological
because it is caused by:
1. Blood group incompatibility, rhesus incompatibility. This happens when there is a difference between the mother's blood type with baby rhesus
blood type or causing pernghancuran of the baby's red blood cells;
2. The shape of the red blood cells are not normal so easily broken or destroyed;
3. Disruption of enzyme in the red blood cells, for example, G6PD;
4. Extensive bruising on her head and a long labor process and the use of vacuum to aid delivery;
5. Severe infections;
6. Blockages in the digestive tract.
6.Pathophysiology
Increase of bilirubin levels can also be caused by the excessive production of bilirubin is derived largely from the destruction ekstrosit aging. In neonates 75%
bilitrubin derived from this mechanism. One gram of hemoglobin produced 34 mg of indirect bilirubin (free bilirubin) and the remaining 25% is called early labeled
bilirubin from the release of hemoglobin as eritropoeis ineffective in the bone marrow, tissue containing protein heme and heme-free.
Begins with the formation of bilirubin oxidation process that produces biliverdin. After experiencing a reduction of biliverdin to bilirubin-free, that is fat-soluble
substances which are lipophilic tough excretion and easily pass through biological membranes, such as the placenta and the brain barrier.
Four common mechanisms that cause hyperbilirubinemia and jaundice:
1. The formation of excessive bilirubin
2. Impaired decision unconjugated bilirubin by the liver
3. Impaired bilirubin conjugation
4. Decreased excretion of unconjugated bilirubin in the bile as a result of intrahepatic and extrahepatic factors that are functional or caused by mechanical
obstruction.
Bilirubinemia unconjugated hyper mainly due to the first three mechanisms, while the fourth mechanism mainly cause conjugated hyperbilirubinemia.
jaundice also can be caused by:
1. Inadequate intake of breast milk in the early days of breastfeeding because of low production resulting in increased direct bilirubin absorption in
the intestine;
2. In babies who were breastfed increased direct bilirubin absorption in the intestine because of the content contained in breast milk. If the baby looks
healthy, weight gain, and there are no signs of other disorders breastfeeding can be continued and harmless.
7.Bilirubin FORMATION OF NORMAL
Increased levels of bilirubin can be caused by excessive production. Most bilirubin comes from the destruction of
erythrocytes aging. In neonates 75% of bilirubin is derived from this mechanism. One gram of hemoglobin can
produce 35 mg of indirect bilirubin (free bilirubin) and this is the form that can enter the brain tissue and cause
kernicterus. Another likely source of the bone marrow and liver, which consists of two components, namely non-
erythrocyte components and components formed erythrocytes of erythropoiesis is not perfect.
The formation of bilirubin oxidation process begins with the yangmenghasilkan biliverdin. After
mengalamireduksi biliverdin into free bilirubin, a substance that is soluble in fat and are difficult to dissolve in
water. Bilirubin has a lipophilic nature are difficult excreted and easily pass through biological membranes such as
the placenta brain barrier. Free bilirubin in plasma is bound / bound with albumin and taken to the liver. In the case
of the liver uptake mechanisms so that bilirubin strain the liver cell membrane receptors and entry into hepatocytes.
Bilirubin in the cell will be tied and bound with ligandin (protein Y), protein Z and glutathione S-transferase bring
the bilirubin into the liver endoplasmic reticulum. In the liver cells due to their glukorinil transferase enzymes, a
process of conjugation of bilirubin produces direct bilirubin, which is bilirubin which is soluble in water and at
certain levels can be excreted through the kidneys. Most of the conjugated bilirubin is excreted via the hepatic duct
into the digestive tract. Further into urobilinogen and out with feces as sterkobilin. In the intestinal absorption
process occurs enterohepatik, that fraction is hydrolyzed to direct bilirubin and indirect bilirubin is reabsorbed back
by the intestinal mucosa,
8.TYPES JAUNDICE
A.Etiology
The cause of jaundice can be divided into three phases:
1.jaundice Prahepatik
Increased bilirubin production that occurs in red blood cell hemolysis. Increased formation of bilirubin can be caused by:
- Abnormalities of red blood cells
- Infections such as malaria, sepsis.
- Toxins come from outside the body such as: drugs - drugs, as well as from the body as occurs in transfusion reactions and
hemolytic disease of the newborn.
2.jaundice Pascahepatik
Dams in the bile duct will cause elevation of bilirubin conjugation of water-soluble. Consequently bilirubin experience will suffer
regurgitation back into the liver cells and continue to enter the bloodstream, enter
to the kidneys and in eksresikan by the kidney, so found bilirubin in urine.
On the contrary as there are dams expenditure bilirubin into the channel
digestion is reduced so that the stool will be colored putty because it contains no sterkobilin.
3.jaundice hepatocellular
Liver cell damage caused conjugation of bilirubin direct bilirubin impaired that will increase and also causes dam in the heart so
that blood bilirubin will hold regurgitation into liver cells which then leads to elevation of conjugation of bilirubin levels in the
blood stream. Liver cell damage occurs on the circumstances: hepatitis, hepatic cirrhosis, tumors, chemicals, etc.
 HIPERBILIRUBIN
Hyperbilirubinemia is one of the most common clinical
phenomenon in newborns. More than 85% of full-term babies
readmission within the first week of life disebab- right by this
situation. Infants with hyper bilirubinemia appear yellow due to
accumulation of yellow pigment bilirubin in the sclera and skin.
Bilirubin is produced in the reticuloendothelial system as an end
product of heme catabolism and formed through oxidation-
reduction reactions. In the first step of oxidation, biliverdin formed
from heme by heme oxygenase work, and the release of iron and
carbon monoksi- da. Iron can be reused, medium- right carbon
monoxide is excreted through the lungs. Water-soluble biliverdin is
reduced to bilirubin which is almost insoluble in water in the form
of isomeric (hence bond intramolecular hydro- gen). Bilirubin is the
hydrophobic terkonjuga- not be transported in the plasma, tightly
bound to albumin. When there is interference on countless bilirubin
binding to albumin conjugate either by endogenous or exogenous
factors (eg, drugs), bilirubin can freely pass Me- fat-containing
membrane (double lipid layer), including the blood-brain barrier,
which can lead to to neuro-toxicity.
T H E PAT H O G E N E S I S O F
D E C L I N I N G C O N J U G AT I O N
OF BILIRUBIN
Breakdown of heme metabolism process is very complex. After approximately
120 days, erythrocyte taken and degraded by the RES system mainly in the liver
and spleen. Approximately 85% of heme degraded derived from erythrocytes
and 15% comes from ekstraeritroid network. Bilirubin is formed due to the
carbon ring- terbukannya of heme originating from erythrocytes and
ekstraeritroid. The initial phase of the process of heme degradation is catalyzed
by the microsomal enzyme heme oxygenase in RE cells. With the presence of
NADPH and O2, this enzyme would add to the hydroxyl group methenyl bridge
between two pyrrole rings, together with the oxidation of ferrous ions (Fe) to
Fe solving the porphyrin ring. And ferric ions and CO in the release, resulting in
the formation of pigmented green biliverdin. Biliverdin is then reduced to form a
red-orange colored bilirubin. Bilirubin and derivatives together called bile
pigments.

Bilirubin is only slightly soluble in plasma, thus transported to the liver by

binding to the protein albumin in noncovalent. Bilirubin teruarai of carrier
molecules albumin and entry into hepatocytes, where bilirubin binds to the
intracellular protein, terutamaprotein liganin. In hepatocytes, the solubility of
bilirubin increased due to the addition of two molecules of glucuronic acid. This
reaction is catalyzed by bilirubin glukoniltransferase using UDP glucuronic acid
as glucuronic donor. Bilirubin diglukoronid actively transported by against a
concentration gradient into the bile canaliculi and then into the bile. This
process requires energy, the rate limiting stage and susceptible to disturbances
in liver disease. Unconjugated bilirubin is normally excreted. Bilirubin
diglukoronid hydrolyzed and reduced by bacteria in the gut to produce
urobilinogen, a substance that does not animate. Most urobilinogen is oxidized
by intestinal bacteria into sterkobilin, gives the brown color in the stool.
However, some of the urobilinogen is reabsorbed by the intestines and into the
portal circulation. Most urobilinogen is instrumental in intrahepatic urobilinogen
cycle that will be in the uptake by the liver and then excreted back into the bile.
The rest of the urobilinogen is transported by the blood to the kidneys, where
urobilinigen converted into urobilin yellow and excreted thus givinga distinctive
yellow color in urine.
D. T H E PAT H O G E N E S I S O F
H E PAT I C C O N J U G AT I O N O F
B I L I R U B I N D E C R E A S E U P TA K E
Liver uptake. Intake of bilirubin through active transport and running
quickly, but does not include making albumin.

• unconjugated hyperbilirubinemia / indirect

1. Over production

Increasing the amount of hemoglobin released from red blood cells that are
old or who have hemolysis will increase the production of bilirubin.
Destruction of erythrocytes cause hyperbilirubinemia most frequently due
to intravascular hemolysis (autoimmune disorders, microangiopathy or
hemoglobinopathies) or as a result of a large hematoma resorption.
Jaundice arising often called hemolytic jaundice.

Bilirubin conjugation and transfer take place normally, but

the supply of unconjugated bilirubin / indirect exceed the ability of liver
cells. As a result, increased indirect bilirubin in the blood. Because the
indirect bilirubin is not soluble in water it can not be excreted into the
urine and does not occur bilirubinuria. But the formation of urobilinogen
increased, resulting in increased urine excretion in feces (dark color). Some
of the causes of hemolytic jaundice: abnormal hemoglobin (cickle cell
anemia), abnormal erythrocytes (spherocytosis heriditer), antibody serum
(Rh. Incompatible transfusions), and severe tropical malaria.

2. Decreased hepatic uptake

Intake of unconjugated bilirubin is done by separating it

from binding to the protein albumin and receiver. Some medications such
as flavaspidat acid, novobiocin can affect the uptake of this.

3. Decreased hepatic conjugation

Conjugation of bilirubin interference occurs resulting in an

increase of unconjugated bilirubin. This is caused by a deficiency of the
enzyme glucuronyl transferase. Occurs in: Gilberth syndrome, Crigler
Najjar Syndrome I, Crigler Najjar Syndrome II.
E . PAT H O G E N E S I S D E C R E A S I N G
I N T R AC E L L U L A R T R A N S P O RT
OF BILIRUBIN
Most of the production of bilirubin is due to degradation of
hemoglobin in the reticuloendothelial system. The level of destruction
of hemoglobin in neonates is higher than older babies. Approximately 1
g of hemoglobin can produce 35 mg of indirect bilirubin, which is
bilirubin which dissolve in fat but not water soluble.

Indirect bilirubin transport by binding to albumin. Bilirubin is

transferred through the cell membrane into hepatocytes, while
albumin is not. Inside the cell, binds to ligandin bilirubin, as well as a
small portion at the other glutathione S-transferase and protein Z. This
process is a two-way process, depending on the konsentra- and affinity
plasma albumin and ligandin in hepatocytes. Most of conjugated
bilirubin entering hepatocytes and excreted into the bile. In the cytosol
of hepatocytes, ligandin biliru- bin while the albumin binding not.

In hepatocytes occurred conjugation of bilirubin into bilirubin up

diglukoronid. A small portion can be in the form of bilirubin most
monoglukoronid, which will be changed by glucuronyl-transferase
become diglukorinid. An enzyme involved in the synthesis of bilirubin
diglukorinid, the uridine diphosphate-glukoronid transferase (UDPG-T),
which mengatalisis establishment on an bilirubin monoglukoronid.
Synthesis and excretion of bile canaliculi diglukoronid happening.
Isomers of bilirubin can mem- form hydrogen bonds such as natural
bilirubin IX can be excreted directly into the bile without conjugation,
for example isomers occurring after light therapy. After conjugation of
bilirubin into

Bilirubin direct soluble in water, excretion occurs immediately to

the steering system dian bile into the intestine. In the gut, is not in the
direct bilirubin absorption; partially hydrolyzed into direct bilirubin and
indirect bilirubin is reabsorbed, this cycle called the enterohepatic
cycle.
9. RELATIONSHIP OF SYMPTOMS

Relationships of all the symptoms suffered namely, yellow urine for

Increased unconjugated bilirubin levels exceed the ability of the liver, this
results in increased levels of unconjugated bilirubin in the blood so that
the eyes and yellow skin.Yellow color of urine can also occur as a result
of consuming the substancecaroteneExcessive (this substance is most
abundant in tomatoes and carrots). An increase in the formation of
urobilinogen bilirubin load increases due to the liver and increased
conjugation and excretion in fases and urine.
While patients marasa limp because of excessive hemolysis so that the
red blood cells are supposed to be distributed throughout the body to
be reduced due to broken down into bilirubin. And the lack of appetite
caused by the passage in the liver distress syndrome and impaired nerve
center.
 10.JAUNDICE CAN CAUSE
C O M P L I C AT I O N S I N S O M E D I S E A S E S ,
N A M E LY :
Type Protozoa Symptoms caused
1.Malaria
Plasmodium vivax - Recurrence paroksisma shaking chills
Malaria is a disease caused by one of four
Plasmodium - High fever
types of protozoa: Plasmodium vivax
malariae - sweating wet
(malaria tertian benign), Plasmodium
- Sometimes cause jaundice
malariae (malaria kuartana benign),
Plasmodium ovale - High fever Plasmodium ovale (infrequent and similar to
- shiver benign tertian malaria), and Plasmodium
Plasmodium - High fever falciparum (malaria estivoautumna or
falciparum - shiver tertian ) which has a high mortality rate.
- Convulsions Each protozoa above shows the same
- Shock and death
symptoms, there is a different but very few.
- Occurred a few days sampi weeks
- Gag
- Urinary flow is dark red to black
- Dealing with massive hemolysis that causes jaundice, hemoglobinemi,
and hemoglobinuri.
2.Anemia hemolysis
Hemolytic anemia is divided into two, namely:
A.Hemolysis intravaskula: shown in red blood cells which undergo mechanical trauma, hemolytic
transfusion reactions and paroxysmal nocturnal hemoglobinuri. What pu cause, hemolysis can cause
hemoglobinemi intravaskula, hemoglobinuri, and hemosiderinuri. Conversion of heme into bilirubin
pigment can cause jaundice disease.
B.Hemolysis ekstravaskula: not followed by hemoglobinemi and hemoglobinuri, but can cause jaundice
disease and in cases of prolonged, resulting in the formation of gallstones.
3.Gallstones (cholelithiasis)
The disease is caused by a blockage of the bile ducts outside the liver, thus forming gallstones.
4.Hepatitis
This disease is also known as inflammation of the liver. The disease is caused by infection and virus.
Mothers with hepatitis virus can pass it to their children. Transmission can also be a blood transfusion,
sexual contact, cuts, and so on. Symptoms that can arise are nausea, decreased appetite, yellow eyes
and skin brwarna, fever, pain, and lethargy.
5.Liver cirrhosis
This is an advanced hepatitis, which for hepatitis late to be addressed, there will be stiffness and
swelling of the liver. This caused total obstruction of bile flow which causes the back pressure to the
entire system of bile. And this will lead to jaundice
11.TREATMENT
In infants who suffered neonatal physiological ikteris can be dried in the sun in the
morning between 7-9 am for 15 minutes. Sunlight contains blue-green light that can turn
into bilirubin indirect bilirubin is more easily discarded. In addition, the morning sun is
useful as a source of vitamin D.
In infants high bilirubin levels and pathological indireknya do phototherapy using blue light
- green. The light blue - green can change the order of indirect bilirubin into a form more
easily dispose of bilirubin up out of the body and is not harmful. In infants with high risk
factors early detection of neonatal jaundice phototherapy needs to be done and do it
early. In infants indirect bilirubin levels that remain high despite the application of photo
therapy, exchange transfusion can be done so that the bilirubin levels can be decreased.
If the pathological neonatal jaundice is not treated adequately can lead to kernicterus.
Indirect bilirubin can penetrate the brain barrier or lining of the brain, which can damage
nerve cells in the brain primarily because of the sheer numbers.The damage is permanent
and can lead to disability.