Pathological Jaundice in Newborn

Pathophysiological jaundice in newborns is defined as the appearance of jaundice at birth or within the first 24 hours of life.

Or,

• When clinical jaundice appears within the first 24 hours of life, it is considered abnormal.
• Serum bilirubin levels greater than 12 mg/dl in a term newborn and greater than 15 mg/dl in a preterm baby.
• Every hour, bilirubin levels rise by more than 0.5 mg/dl.
• Jaundice that worsens after it had improved initially.
• More than 2 mg/dl direct serum bilirubin.

Clinical estimation of Severity of Jaundice

Day 1 – Jaundice appears in the face

Day 2 – Jaundice appears in the arms and legs

Day 3 onwards - hands and feet. Then on palm and soles

Causes

• Fetomaternal blood group incompatibility; ABO and Rh factors
• Hereditary spherocytosis
• Deficiency of red cell enzymes such as glucose-6 phosphate dehydrogenase
• Increased enterohepatic circulation
• Congenital defect of liver
• Infections
• Drugs such as oxytocin to a mother, salicylates to a baby.
• Hemolytic diseases

Hemolytic Jaundice

When a mother and fetus have Rh-incompatibility and ABO incompatibility, a newborn baby will develop hemolytic jaundice.

Rh- Incompatibility

Occurs when the mother is Rh-negative and the infant is Rh-positive, having received the Rhesus factor gene from his or her parents.

ABO Incompatibility

If a mother has blood group O and her baby has blood group A or B, the mother produces anti-A and anti-B type antibodies of the IgG class, which cross the placenta and destroy the baby's red blood cells. This disease can impact both the firstborn and subsequent children.

Rh- iso- Immunization

If the mother is Rh- negative and the infant is Rh + positive on the RBC, and a little amount of Rh- positive blood containing D- antigen enters the maternal circulation during pregnancy, antibody production against antigen D occurs in the Rh- negative recipient mother1. Sensitization develops when it is combined with maternal circulation, and a lower dosage of antigen might promote an increase in IgG antibody, which quickly crosses the placenta to agglutinate the infant's RBC, causing hemolytic symptoms. Because of the high bilirubin load and the inability of the liver to deal with it, the infant develops acute jaundice soon after birth. RBC damage is more likely in successive pregnancies. The baby is born with widespread edema, ascites, and hydrops fetalis in extreme cases.

Clinical Presentation

• Jaundice appears within first 24 hours of life with pallor and anemia

Kernicterus

Kernicterus is a yellow-wise staining of brain cells caused by the accumulation of unconjugated bilirubin. If unconjugated bilirubin enters the brain's basa1l ganglia, it can cause irreversible damage, resulting in lethargy, poor sucking, hypotonia, aberrant more-reflex, cerebral inflammation, and cerebral palsy in the newborn.

Severe Jaundice ( Bilirubin Encephalopathy)1

Bilirubin Encephalopathy, often known as severe jaundice, is a disorder characterized by severe brain damage caused by bilirubin buildup in brain cells.

Diagnosis of Hyperbilirubinemia

• Previous newborns with jaundice, positive family history of jaundice and a1nemia
• A family history of neonatal or early infant fatalities caused by liver disorders, which suggests galactosemia.
• Maternal pharmaceuticals, such as sulphonamides or anti-malarial medications, cause hemolysis in the newborn yellow presence- desire to color sclera, skin, and mucous membrane
• Serum 1bilirubin direct and indirect tests, cell count, Hb, Tc, DC, LFT, PT, BT, CT, Com1bs test11 are all blood tests.
• Urine and stool analysis1
• Li1ver, gallbladder, and biliary tract ultrasound1
• Endoscopic retrograde cholangiopancreatography (ERCP)