​NEONATAL JAUNDICE

Congratulations to all new mums and dads! 
So, your baby was born, looking all fresh, pink and healthy. However, on your arrival at home, having been discharged from the hospital, you found that he is as yellow as saffron. “Oh Dear! What’s wrong with my cutie pie”, you’re worried. Should you be worried? 

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Jaundice is defined as the yellowish discoloration of the skin and sclera (white of the eyes) due to excessive amount of a pigment called BILIRUBIN. 
Bilirubin is produced normally, following the recycling and breakdown of red blood cells. It is excreted in the urine and faeces, to maintain a tight balance and normal concentration in the body. Therefore, anything that increases the rate of breakdown of the red cells, or impedes the excretion of bilirubin, will result in jaundice. 

In fetal life, red cells are much more than in adults. Once the baby is born, he sheds this excess red cells as they are no longer needed. This results in a mild form of jaundice known as PHYSIOLOGICAL JAUNDICE. This form of jaundice is transient and self-limiting. If you worry, it will go. If you don’t worry, it will go! 
There are two things you can do to speed up the clearance of physiological jaundice :

1. Breastfeeding 

2. Exposure to sunlight 

Of the numerous benefits of human breast milk is that it helps to prevent and treat jaundice. There’s a tendency to think that breast milk is the cause of physiological jaundice because it is commoner in breastfed infants. But the truth is, breastfeeding provides a better chance at recovery from jaundice than not breastfeeding. 
Once you have checked with your paediatrician, and they tell you that the jaundice is mild or physiological,   try to expose him to early morning sunlight until the jaundice clears. A plus to this practice is that your baby also gets loads of vitamin D *winks. 

Remember to cover his eyes and genitals before exposure (too much UV rays can damage those organs), and do not expose to midday sunlight (to avoid sunburn)… 

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So, we have talked about physiological jaundice. What about pathological jaundice? Basically, neonatal jaundice is physiological until proven otherwise. Pathological jaundice is just an extension of physiological jaundice, ie. when the latter fails to go away or when there are superimposed factors complicating the former. 

Now, let’s break it down. As mentioned earlier, jaundice can be caused by excessive breakdown of red cells or decreased clearance of bilirubin from the blood due to – 
*Haemolytic anaemias (immune and non immune) 

*Polycythaemia (pathologically high red cell count) 

*Extravasation of blood during delivery (eg. Cephal haematoma) 

*Bruising during delivery 

*Genetic/Familial anomalies in the enzymes required for red haemoglobin and bilirubin metabolisms (eg. G6PD deficiency) 

*Infections (congenital or acquired) eg. Malaria, pneumonia, etc. 

*Some drugs, if taken in late pregnancy or given to the infant (especially sulfur-containing drugs, eg. Fansidar) 

*Congenital malformations of the liver and biliary tract

***In a Nigerian study, 13% of babies with clinical jaundice tested positive for G6PD deficiency. 

 

This list is not exhaustive; it’s just a rough overview. 
Let’s zoom in a little on Haemolytic anaemias. The commonest causes include blood group incompatibility (ABO & RHESUS) and infections (sepsis). Rhesus incompatibility is particularly important. When a baby’s blood group is different from that of the mother (mother Rhesus negative, baby positive), the mother produces some substances called ANTIBODIES. These antibodies may not affect the triggering baby, but subsequent babies are affected. 
These antibodies travel from the mother’s blood, through the placenta and attack the baby’s red blood cells which are seen as “aliens”. The cells break down at a faster rate than the baby’s liver can clear. The resultant hyperbilirubinaemia manifests as jaundice. In severe cases, anaemia or death may occur even before the baby is born (stillbirth) 

There are two components of bilirubin: the conjugated (coupled with a plasma protein) and the unconjugated. When the unconjugated bilirubin exceeds a threshold level, it crosses the blood-brain barrier resulting in a condition called KERNICTERUS. Early signs include muscle weakness, failure to feed and convulsions. This is a neurological disorder that can result in severe intellectual disability or death.

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So that I don’t bore you with too much details, let’s discuss the clinical features and management of neonatal jaundice. 
Of course, jaundice itself is a symptom, but in subtle cases, parents may not be able to detect it easily. It starts with a yellowish tinge in the sclera (white of the eye). You need to be very observant to detect a jaundiced eye because the neonatal eyes consists of more dark than white; plus, they usually sleep for the most part of the day! 

As bilirubin level rises, the skin gradually becomes yellow. In dark-skinned babies, you need to indent the skin gently to see the yellowness. You may also notice changes in the colour of the urine and faeces. 
Other signs and symptoms are related to the underlying cause and resultant effect (complications) of jaundice…

*fever

*irritability (excessive crying) 

*inability to feed

*failure to thrive (loss of weight or failure to gain weight) 

*vomiting 

*muscle weakness

*convulsions

*sudden death

The best way to manage jaundice successfully is to detect it early. As mentioned earlier, unattended jaundice can lead to permanent brain injury and severe handicap or death. Parents should be able to recognise red flags and know when to seek help. Never underrate any sign and never resort to self-medication. 
Treatment modalities include:

1. PHOTOTHERAPY – The baby is placed under a specialised kind of light. This light converts bilirubin into a form that can be easily excreted from the body. The eyes and genitals are protected while extra breastmilk or iv drips are given to replace the fluid loss due to heat. 

2. INTRAVENOUS IMMUNOGLOBULIN – In hemolytic jaundice due to blood group incompatibility, maternal antibodies can be wiped out of the baby’s blood by infusion of IVIG. This therapy is highly effective, faster and more preferable to other invasive treatments. However, IVIG is very expensive and often unavailable in developing countries. 

3. EXCHANGE BLOOD TRANSFUSION – This is a form of blood transfusion that involves gradual withdrawal of the “jaundiced” blood and replacement with normal, compatible, screened blood. The procedure is performed in the special baby care unit and there are potential risks such as infection and transfusion reactions. 

4. ADJUNCT MANAGEMENT – The cause should be determined and treated as appropriate. Breastfeeding should be continued as tolerated. Serial bilirubin levels are checked until normal. Psychosocial support should be offered to parents as they are often in distress due to the prolonged hospital stay. 

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