Neonatal jaundice has no sexual predilection. Is found throughout the world but commoner in developing nations due to high rates of infections, poor antenatal care, and late presentation. It has a high prevalence rate in the hospital practice being the 4^th leading cause of admissions in the newborn units after prematurity, sepsis and perinatal asphyxia. As high as 80% of preterm and 60% of term newborns will develop jaundice. Most are physiologic and only 5-10% would require treatment.

Neonatal jaundice can be classified into two main categories:

1. Conjugated hyperbilirubinemia also referred to as direct hyperbilirubinemia.
2. Unconjugated hyperbilirubinemia also referred to as indirect hyperbilirubinemia. It is unconjugated bilirubin that can cross the blood brain barrier and cause brain damage.

Another classification groups Jaundice into Physiological and Pathological Jaundice. Physiologic jaundice is benign and requires no treatment while pathologic jaundice must be treated otherwise can lead to long-term severe and permanent sequelae. Most cases of hyperbilirubinemia are physiologic and lead to no serious complications. However, in rare cases of physiologic jaundice, bilirubin levels can reach toxic levels and cause neurodevelopmental abnormalities including intellectual impairment, athetosis and hearing loss. Physiologic jaundice usually appears between 24-48 hours of age, peaks in 4-5days in term neonates, by the 7^th day in preterm and resolves within 10-14days. Bilirubin is predominantly unconjugated, and levels do not usually exceed 12-15mg/dl. Physiologic jaundice is a diagnosis of exclusion.

Pathologic jaundice is characterized by

• Onset is usually before 24 to 36 hours of age.
• A rise in serum bilirubin levels of >0.5 mg/dL/hr or 5mg/dl/day
• Term infant with serum bilirubin > 12mg/dl.
• Preterm infant with serum bilirubin > 15mg/dl.
• Direct bilirubin > 2mg/dl or >10%
• Jaundice persisting after 10 -12 days in a term infant or after 14 days in a premature infant. (Prolong jaundice)
• Jaundice in a sick child

Physiologic jaundice is caused by a combination of the following:

1. Postnatal accelerated destruction of erythrocytes
2. Decreased excretory capacity of the hepatocytes due to low levels of ligandin
3. Reduced activity of the bilirubin conjugating enzyme uridine diphosphoglucuronyltransferase [UDPGT]

Pathologic Jaundice is due to additional factors accompanying the basic mechanisms described above.

1. Haemolytic anaemias including ABO Incompatibility [where mother is blood group O and baby is A/B/AB], Rhesus Isoimmunisation [where mother is Rh-ve and baby is Rh+ve].
2. Non-immune haemolytic disorders such as G6PD deficiency, Spherocytosis.
3. Neonatal infections such as sepsis, severe birth asphyxia, neonatal malaria.
4. Congenital conditions such as the Dubin Johnson syndrome, Crigler Najjar syndrome, Gilbert’s syndrome, Down syndrome
5. Polycythaemia
6. Presence of bruising or other extravasation of blood
7. Breastfeeding jaundice: here jaundice is due to poor lactation or inadequate feeding resulting in increased entero-hepatic circulation.
8. Breast milk jaundice: this results from the presence of icterogenic substances specifically B-gluconidase in breast milk. Treatment is by stopping breastfeeding for a few days and then recommencing, jaundice does not re-appear.
9. Congenital hypothyroidism, intestinal obstruction, pyloric stenosis, infant of diabetic mothers.
10. Biliary atresia which causes conjugated hyperbilirubinemia which is not toxic to the brain but requires treatment before 6 weeks of life.
11. Idiopathic

After birth, red blood cells undergo physiological breakdown, releasing haemoglobin which splits into heme and globin. Globin forms amino acids, while haeme releases iron into the body’s iron pool and converts to biliverdin, then to bilirubin. Bilirubin binds to albumin and is transported to the liver, where it’s conjugated with glucuronic acid to form conjugated bilirubin. This is excreted into bile ducts, reaching the gut where bacteria convert it into stercobilinogen and stercobilin, with some reabsorbed as urobilinogen, completing an enterohepatic circulation. Bilirubin acts as an antioxidant, but high levels of unconjugated bilirubin are neurotoxic.

1. Prematurity
2. Low birth weight
3. Mothers blood group type
4. Congenital anomalies and/or infections
5. Being a male
6. Genetics and familial risks: history of neonatal jaundice in siblings especially siblings treated for neonatal jaundice.
7. Race: higher in Asian descent and American Indians, lower in Africans and African Americans
8. Maternal factors like DM, use of some medications, herbal remedies
9. Nutrition: those who are breastfed or who receive inadequate nutrition are at higher risk.
10. Geography: Higher in populations living in high altitudes.

The baby will present with yellowness of the skin and eyes usually from the forehead, face and gradually spreads downwards to the body and extremities. There may be fever, poor suck, weakness, and seizures depending on the severity. A good history will help to determine the cause of the jaundice,

-Phototherapy

-Pharmacologic agents

-Intravenous immunoglobulins

-Exchange blood transfusion

-Surgery in cases of conjugated hyperbilirubinemia secondary to biliary atresia.

Steps in Evaluation

1. Determine if Jaundice is physiological or pathological.
2. The Kramer scale is used to determine the level of jaundice at the onset and hence the amount of bilirubin. Kramer scale not useful in babies that have already been exposed to phototherapy light.
3. Serum bilirubin is checked using biochemical methods, transcutaneous bilirubinometer or Bili meter.
4. Pointers to pathologic jaundice includes presentation within 24 hours of birth, presence of pallor, hydrops fetalis, hepatosplenomegaly, reticulocytosis, rapid bilirubin rise, haemolytic features on blood film, positive family history of jaundice.
5. Request for blood group, Rh type, packed cell volume, blood smear, red blood cells morphology, reticulocyte count and G6PD enzyme levels.
6. Determine if it is conjugated or unconjugated hyperbilirubinemia.

Double-surface phototherapy is more efficient than single-surface phototherapy. Continuous use is more efficient than intermittent use. There are two main types [i] Conventional phototherapy used for mild and non-haemolytic jaundice.

[ii] Intensive phototherapy is used in more severe cases, haemolytic jaundice and where the conventional type failed.

Includes the use of

1. Phenobarbitone: augments hepatic uptake of bilirubin and increases the activity of glucoronyl-transferase (UDPG-T) enzyme. Loading dose is 10mg/kg given within 6 hours of life and maintenance dose at 5mg/kg/day for 5days via the intravenous route.
2. Intravenous immunoglobulin [IVIG]: very useful in reducing the need for exchange blood transfusion in neonatal jaundice secondary to blood group incompatibilities. Used in conjunction with phototherapy at a dose of 0.5-1g/kg over 2 hours daily for 3 days.
3. Tin-mesoporphyrin [SnMP] and Tin-protoporphyrin [SnPP] inhibit the action of microsomal enzyme-heme oxygenase and prevents production of bilirubin. They may replace phototherapy in future. Administered as a single intramuscular dose of 6micromol/kg birthweight within 24-36 hours of life.

Other nonspecific medications include antibiotics where infection is suspected or confirmed.

Adequate hydration and nutrition of the neonate.

Critical values of serum bilirubin at which exchange blood transfusion is recommended include:

1. Total serum bilirubin of 10mg/dl on 1^st day, 15mg/dl on 2^nd day, 20mg/dl on any day.
2. Rate of rise of greater than or equal to 5mg/dl/day
3. Subtract 2mg/dl if any risk factor for acute bilirubin encephalopathy [ABE] is present
4. For preterms weighing <2000g; apply the rule of 10 if total serum bilirubin is ≥ 10mg/dl.

Monitor and follow up all babies managed for jaundice especially if their bilirubin levels were up to 20mg/dl or they had an exchange transfusion because they have an increased risk of developing permanent neurologic disorders. Screen them for hearing loss at 3 months using brainstem Evoked Response Audiometry.

1. Acute Bilirubin Encephalopathy
2. Kernicterus [Permanent brain damage]
3. Choreoathetoid cerebral palsy
4. Deafness

Neonatal jaundice is a common condition in newborns, particularly in low-income settings, where early detection and timely treatment are crucial to prevent complications like kernicterus. Limited access to healthcare and diagnostic tools can delay interventions, increasing the risk of severe outcomes. Promoting awareness among healthcare providers and caregivers, improving access to phototherapy, and encouraging breastfeeding can help manage and reduce the impact of neonatal jaundice in resource-limited environments.