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Pedia 2

Module 1 - Jaundice Neonatology




ABO incompatability - Indirect (Unconjugated) Hyperbilirubinemia.(NEONATAL

Objectives :-

1. To know the mechanis of bilirubin formation.

 Bilirubin is a yellow compound that occurs in the normal catabolic pathway that breaks
down heme in vertebrates. This catabolism is a necessary process in the body's clearance of
waste products that arise from the destruction of aged red blood cells. First the hemoglobingets
stripped of the heme molecule which thereafter passes through various processes
of porphyrin catabolism, depending on the part of the body in which the breakdown occurs.
For example, the molecules excreted in the urine differ from those in the feces. The production
of biliverdin from heme is the first major step in the catabolic pathway, after which
the enzymebiliverdin reductase performs the second step, producing bilirubin from biliverdin.

2. To differentiat pathologic from physiologic jaundice.

 Physiological hyperbilirubinemia (jaundice is just a symptom) is a build-up of bilirubin due

to the normal hemolyisis of red blood cells that were needed for fetal circulation before birth
and discarded afterward. Normally, the liver processes the bilirubin and converts it to a form
that can be excreted in stool. In a newborn, the immature liver is just ramping up to function on
its own apart from mom. The imbalance of an overabundance of bilirubin to process and a liver
that is not at top speed yet allows the yellow pigment from hemolyzed red cells to accumulate
in the blood and give the skin and sclera (whites of the eyes) the yellow tone we call jaundice.

 Pathological hyperbilirubinemia (notice the similarity to "pathology") is related to a

condition other than normal newborn bilirubin being processed slowly by an immature liver.
Such conditions include an incompatibility between the baby's and the mother's blood types,
incompatibility of additional blood factors, or liver problems. There is actual pathology
involved that might require more aggressive and lengthier intervention than physiological
bilirubin problems.

3. To identify different etiologies of jaundice in the newborn.

 Neonatal jaundice can be seen in cases of maternal-fetal blood type incompatibility. The
mother's body will actually produce antibodies that attack the fetus's blood cells. This causes a
breakdown of the red blood cells and thus an increased release of bilirubin from the red cells.

 A large scalp bruise called a cephalohematoma can occur during the birthing process. Such a
bruise is really a collection of clotted blood just beneath the skin surface. As the body naturally
breaks down this clotted blood, a large amount of bilirubin is released at once. This sudden
excess in serum bilirubin may be too much for the baby's liver to handle, and jaundice will

 Sometimes a baby swallows blood during birth. This swallowed blood is broken down in the
baby's intestinesand absorbed into the bloodstream. Just as the excess blood from a blood
clot will cause a rise in serum bilirubin, so will this.

 A mother who has diabetes may cause a baby to develop neonatal jaundice.

 Crigler-Najjar syndrome and Lucey-Driscoll syndrome are also conditions that can cause

 Breast-fed babies, particularly those who have difficulty nursing or getting enough nutrition
from breast-feeding, are at higher risk of jaundice. Dehydration or a low calorie intake may
contribute to the onset of jaundice.

4. To know the basic laboratory examinations needed to work-up neonatal jaundice.

 Blood type and Rh determination in mother and infant,Direct antiglobulin test (DAT) in the
infant (direct Coombs test), Hemoglobin and hematocrit values, Serum albumin levels,
Peripheral blood film for erythrocyte morphology, reticulocyte count, conjugated bilirubin
levels, Ultrasonography and Radionuclide scanning

5. To discuss treatment options of neonatal jaundice and its complications.

 Light therapy (phototherapy) :-

Your baby may be placed under special lighting that emits light in
the blue-green spectrum. The light changes the shape and structure of bilirubin molecules in such a
way that they can be excreted in the urine and stool. The light isn't an ultraviolet light, and a
protective plastic shield filters out any ultraviolet light that may be emitted.During treatment, your
baby will wear only a diaper and protective eye patches. The light therapy may be supplemented
with the use of a light-emitting pad or mattress.

 Intravenous immunoglobulin (IVIg):-

Jaundice may be related to blood type differences between

mother and baby. This condition results in the baby carrying antibodies from the mother that
contribute to the breakdown of blood cells in the baby. Intravenous transfusion of an
immunoglobulin — a blood protein that can reduce levels of antibodies — may decrease jaundice
and lessen the need for an exchange blood transfusion.

 Exchange transfusion:-

Rarely, when severe jaundice doesn't respond to other treatments, a baby

may need an exchange transfusion of blood. This involves repeatedly withdrawing small amounts of
blood, diluting the bilirubin and maternal antibodies, and then transferring blood back into the baby
— a procedure that's performed in a newborn intensive care unit.

6. To explain the complications and prognosis of hyperbilirubinemia.

 Acute bilirubin encephalopathy :-

Bilirubin is toxic to cells of the brain. If a baby has severe

jaundice, there's a risk of bilirubin passing into the brain, a condition called acute bilirubin
encephalopathy. Prompt treatment may prevent significant lasting damage.

 Listlessness or difficulty waking

 High-pitched crying

 Poor sucking or feeding

 Backward arching of the neck and body

 Fever
 Vomiting

 Kernicterus :-

Kernicterus is the syndrome that occurs if acute bilirubin encephalopathy causes

permanent damage to the brain. Kernicterus may result in:

 Involuntary and uncontrolled movements (athetoid cerebral palsy)

 Permanent upward gaze

 Hearing loss

 Improper development of tooth enamel

Diagnosis : jaundice