NKANA COLLEGE OF APPLIED SCIENCES

AND EDUCATION

STUDENT NAME: MERCY CHUPA

STUDENT #: 722043
COURSE: PAEDIATRICS AND CHILD HEALTH
COURSE CODE: PEDG 2210
YEAR: COG13
DUE DATE: 08/08/2023
LECTURER: MR. KANGWA

ASIGNMENT QUESTIONS
 Neonatal jaundice (hyperbilirubinemia)

 Anatomy and physiology of billiry tree and metabolism of bilirubin

 Definition of hyperbilirubinemia, classification, causes, investigations, treatment,

complication and differential diagnosis of hyperbilirubinemia.

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Introduction
This assignment provides a comprehensive overview of neonatal jaundice (hyperbilirubinemia),

covering its pathophysiology, anatomical and physiological aspects of the biliary tree, and

bilirubin metabolism. It explores the definition, classification, causes, investigation, treatment,

complications, and differential diagnosis of neonatal jaundice, equipping healthcare

professionals with essential knowledge for managing this common condition in newborns

Neonatal Jaundice
Neonatal jaundice, also known as hyperbilirubinemia, is a common condition in newborns

characterized by the yellowish discoloration of the skin and sclera (the white part of the eyes)

due to elevated levels of bilirubin in the blood. Bilirubin is a yellow pigment produced when red

blood cells are broken down.

Causes

Neonatal jaundice can result from various factors, including the immature liver's limited capacity

to process bilirubin, increased breakdown of fetal red blood cells, delayed clearance of bilirubin

from the bloodstream, or certain underlying medical conditions affecting bilirubin metabolism.

Physiological Jaundice

The most common type of neonatal jaundice is physiological jaundice, which occurs in most

newborns due to the liver's immaturity in processing bilirubin. It typically appears a few days

after birth, peaks around the third to fifth day, and resolves without treatment within a week.

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Pathological Jaundice

Pathological jaundice is less common but may be more concerning as it can be a sign of an

underlying medical condition. It can be caused by factors such as ABO or Rh incompatibility,

blood group or enzyme deficiencies, infections, and liver diseases.

Risk Factors

Certain factors increase the risk of developing neonatal jaundice, including prematurity, bruising

during birth, a family history of jaundice or genetic disorders affecting bilirubin metabolism, and

blood group incompatibilities between the mother and baby.

Treatment

Mild cases of neonatal jaundice often do not require treatment, and the condition resolves on its

own. For moderate to severe cases, phototherapy is a common treatment method. During

phototherapy, the baby is exposed to special blue lights that help convert unconjugated bilirubin

into a water-soluble form that can be easily excreted. Exchange transfusion is a more invasive

treatment used in severe cases when phototherapy is insufficient or ineffective. It involves

replacing the baby's blood with donor blood to reduce bilirubin levels.

Monitoring

Regular monitoring of bilirubin levels is essential, especially for high-risk infants, to prevent the

development of severe hyperbilirubinemia and its potential complications.

Complications

Untreated or inadequately managed severe hyperbilirubinemia can lead to complications such as

kernicterus, a rare but serious neurological condition characterized by bilirubin accumulation in

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the brain. Kernicterus can result in permanent brain damage, developmental delays, hearing loss,

and movement disorders.

Neonatal jaundice is a common and usually benign condition in newborns. However, it requires

appropriate monitoring and, in some cases, treatment to prevent complications. Early detection

and management are crucial to ensure the well-being and healthy development of affected

newborns.

Anatomy and Physiology of the Biliary Tree

The biliary tree, also known as the bile duct system, is a network of ducts and organs involved in

the production, transportation, and storage of bile. It includes the liver, gallbladder, and a series

of bile ducts. The biliary tree's main functions are to produce, concentrate, and deliver bile to the

small intestine to aid in the digestion and absorption of fats.

The liver is a large organ located in the upper right abdomen. It consists of lobes, each

containing functional units called hepatocytes. Hepatocytes play a crucial role in the production

of bile, which contains bile salts, bilirubin, cholesterol, and phospholipids. Bile is continuously

produced by the hepatocytes and is secreted into tiny canals called bile canaliculi. Bile canaliculi

are small channels that collect bile produced by hepatocytes. They join to form larger bile ducts,

which eventually coalesce to form the left and right hepatic ducts. The left and right hepatic

ducts are larger bile ducts that carry bile out of the liver. They merge to form the common

hepatic duct. The Common Hepatic Duct is formed by the union of the left and right hepatic

ducts. It carries bile away from the liver and can either transport bile directly to the duodenum or

combine with the cystic duct to form the common bile duct. The gallbladder is a small, pear-

shaped sac located beneath the liver. Its primary function is to store and concentrate bile. When

food, especially fatty food, enters the duodenum, the gallbladder contracts, releasing

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concentrated bile into the duodenum through the cystic duct. The cystic duct connects the

gallbladder to the common hepatic duct, forming the common bile duct. The common bile duct is

formed by the union of the cystic duct and the common hepatic duct. It carries bile from the liver

and gallbladder to the small intestine (duodenum) through the ampulla of Vater. The ampulla of

Vater is a small opening located in the wall of the duodenum. It receives bile from the common

bile duct and pancreatic juices from the pancreatic duct, facilitating their entry into the

duodenum for digestion.

Metabolism of Bilirubin

Bilirubin is a yellow-orange pigment derived from the breakdown of heme, a component of

hemoglobin found in red blood cells. After the breakdown of old or damaged red blood cells,

heme is converted to biliverdin by the enzyme heme oxygenase. Biliverdin is then rapidly

converted to unconjugated bilirubin by biliverdin reductase. Unconjugated bilirubin is not water-

soluble and cannot be excreted directly. It binds to serum albumin and is transported to the liver,

where it undergoes further processing. In the liver, hepatocytes take up unconjugated bilirubin,

and inside the hepatocytes, it is conjugated with glucuronic acid by the enzyme uridine

diphosphate-glucuronosyltransferase (UGT). Conjugation makes bilirubin water-soluble,

allowing it to be excreted into the bile.

Conjugated bilirubin is then transported through the bile ducts to the gallbladder, where it is

stored and concentrated. When needed for digestion, bile is released from the gallbladder into the

duodenum through the common bile duct, where it aids in the emulsification and absorption of

fats.

Hyperbilirubinemia

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Hyperbilirubinemia is a common condition characterized by elevated bilirubin levels in the

blood, leading to jaundice and potential complications in affected individuals. Bilirubin is a

yellow-orange pigment produced during the breakdown of hemoglobin, the protein found in red

blood cells that carries oxygen. It is a natural byproduct of the normal recycling of old or

damaged red blood cells in the body. When the liver processes bilirubin, it becomes water-

soluble and is excreted from the body in the bile, a digestive fluid. However, in cases where there

is an excessive breakdown of red blood cells or when the liver's ability to process and excrete

bilirubin is compromised, bilirubin can accumulate in the bloodstream, leading to

hyperbilirubinemia. One of the most noticeable signs of hyperbilirubinemia is jaundice, a

yellowing of the skin and eyes. This occurs when the elevated bilirubin levels deposit in the skin

and sclera (the white part of the eyes). Jaundice is especially visible in newborns and is known as

neonatal jaundice.

Classifications
Hyperbilirubinemia can be classified as unconjugated (indirect) or conjugated (direct) depending

on the form of bilirubin present in the blood. Unconjugated bilirubin is not water-soluble and

cannot be excreted directly by the liver. Conjugated bilirubin, on the other hand, is water-soluble

and can be processed and excreted by the liver.

Causes
Hyperbilirubinemia can be caused by various factors, including hemolytic disorders (increased

breakdown of red blood cells), liver diseases, genetic conditions affecting bilirubin metabolism,

and certain infections.

Treatment

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Treatment for hyperbilirubinemia may involve phototherapy (exposing the baby's skin to special

lights that help break down bilirubin), exchange transfusion (a procedure that replaces the baby's

blood

with donor blood to reduce bilirubin levels), and managing the underlying cause of the condition.

It is essential to monitor and manage hyperbilirubinemia promptly to prevent potential

complications and ensure the well-being of the affected individual. If you or someone you know

exhibits symptoms of jaundice or hyperbilirubinemia, it is essential to seek medical evaluation

and guidance for appropriate diagnosis and management.

Complications of Hyperbilirubinemia
Kernicterus is a rare but severe neurological complication of untreated or poorly managed

hyperbilirubinemia, especially in newborns. It occurs when unconjugated bilirubin levels become

excessively high, leading to its deposition in the brain tissues. Kernicterus can cause permanent

damage to the central nervous system, resulting in developmental delays, intellectual disabilities,

hearing loss, movement disorders, and even death. Acute Bilirubin Encephalopathy: In severe

cases of hyperbilirubinemia, infants may develop acute bilirubin encephalopathy, a condition

characterized by bilirubin toxicity affecting the brain. Symptoms may include lethargy, poor

feeding, high-pitched crying, muscle rigidity, and decreased muscle tone. Prompt treatment is

essential to prevent progression to kernicterus. Cholelithiasis: Hyperbilirubinemia can lead to the

formation of gallstones in the gallbladder due to the precipitation of excess bilirubin.

Cholelithiasis may cause abdominal pain, inflammation of the gallbladder (cholecystitis), and, in

severe cases, obstruction of the bile ducts. Cholestasis: Prolonged or severe hyperbilirubinemia

can lead to cholestasis, a condition where there is a reduced flow of bile from the liver to the

intestines. Cholestasis can result in the accumulation of bile acids and bilirubin in the liver,

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leading to liver damage and impaired fat digestion. Biliary Sludge: Hyperbilirubinemia can

contribute to the formation of biliary sludge, a thick, gel-like mixture of bile components,

including bilirubin. Biliary sludge can lead to the obstruction of the bile ducts and increase the

risk of developing gallstones.

Differential Diagnosis (DD) of Hyperbilirubinemia

The differential diagnosis of hyperbilirubinemia involves considering various conditions that can

cause elevated bilirubin levels. It is essential to distinguish between different types of

hyperbilirubinemia to determine the underlying cause and appropriate treatment. Some common

differential diagnoses include:

Physiological Jaundice of Newborns

In newborns, mild jaundice is often a normal and transient condition due to the immature liver's

limited capacity to process bilirubin. Physiological jaundice typically appears a few days after

birth and resolves within the first week without intervention.

Hemolytic Disorders
Conditions that cause increased breakdown of red blood cells, such as hemolytic anemia and

hereditary spherocytosis, can lead to unconjugated hyperbilirubinemia.

Liver Diseases
Hepatitis, cirrhosis, and other liver diseases can impair the liver's ability to conjugate and excrete

bilirubin, resulting in elevated levels of both unconjugated and conjugated bilirubin.

Biliary Tract Disorders

Obstruction of the bile ducts due to gallstones, biliary atresia, or other biliary tract abnormalities

can cause elevated conjugated bilirubin levels.

Gilbert Syndrome

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Gilbert syndrome is a benign genetic condition characterized by mild unconjugated

hyperbilirubinemia. It results from a deficiency in the enzyme responsible for bilirubin

conjugation.

Crigler-Najjar Syndrome
Crigler-Najjar syndrome is a rare genetic disorder that leads to severe unconjugated

hyperbilirubinemia due to the absence or deficiency of the enzyme responsible for bilirubin

conjugation.

Accurate differential diagnosis is essential to guide appropriate management and treatment of

hyperbilirubinemia and to identify any underlying conditions that may require further evaluation

and intervention. A thorough medical history, physical examination, and laboratory tests are

crucial in differentiating the various causes of hyperbilirubinemia.

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Conclusion
Neonatal jaundice is a significant concern in newborn care, affecting a large number of infants

worldwide. It is primarily caused by an imbalance in bilirubin metabolism and clearance, leading

to elevated levels of the pigment in the bloodstream. While physiological jaundice is a common

and self-resolving condition in most infants, pathological jaundice requires close monitoring and

appropriate interventions to prevent complications such as kernicterus and other neurological

disorders. The biliary tree plays a crucial role in bilirubin metabolism and excretion, and any

disruption in its functioning can lead to hyperbilirubinemia. Early detection and management of

neonatal jaundice are vital to ensure the well-being and healthy development of affected

newborns. Healthcare professionals must be well-versed in the causes, investigations, and

treatment options for hyperbilirubinemia to provide optimal care and improve outcomes for

newborns affected by this condition. By understanding the complexities of neonatal jaundice and

its underlying physiology, healthcare providers can make informed decisions to safeguard the

health of these vulnerable infants.

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