Neonatal jaundice
Neonatal jaundice occurs in 50 – 80 %
of newborn babies (depending on maturity).
Most of the cases are due to an
exaggerated normal process; are not serious; resolve in two to three weeks; do
not need treatment and have no complications.
The bilirubin level is measured by
checking the serum bilirubin level (TSB)
There are many causes of neonatal
jaundice and it is the cause rather than the jaundice that is of importance.
One
of the most serious causes of neonatal jaundice is excessive breakdown of the
red blood cells as in haemolytic disease of the newborn due to blood group (Rh)
incompatibility between the mother and baby.
Treatment of neonatal jaundice is by
phototherapy that makes the bilirubin water-soluble and therefore able to be
excreted in the urine.
Breastmilk jaundice is NOT a reason to stop breastfeeding.
What is
neonatal jaundice?
Jaundice is the name given to the yellowish discoloration of the skin
and eyes by bilirubin that occurs in about 50 – 80 % of newborn babies
(depending whether term or preterm respectively). It usually only lasts for
about 10 to 14 days and no treatment is required.
Most of
the cases are not serious and are basically due to immature liver function. Some
are the result of disease causing excess breakdown (haemolysis) of the baby’s
red blood cells such as “haemolytic disease of the newborn”. Another reason is
hepatitis caused by either a viral or bacterial infection.
It is
also known as hyperbilirubinaemia.
It is
not so much the jaundice but rather the reason for the jaundice that is
important.
What
causes neonatal jaundice?
Normally red blood cells survive in the circulation for about 120
days before they are removed and broken down by the body. The haemoglobin
released is converted to bilirubin and carried to the liver where it is further
processed and excreted in the bile. In the uterus the baby has a large number of
extra red cells to help transport oxygen from the placenta to the baby. After
birth, when the baby starts to breathe and use the lungs, these extra cells are
no longer needed and are broken down. This means that the newborn baby will in
fact have a relatively increased load of bilirubin to clear.
Normally, the liver can cope with this bilirubin load. If the load becomes too
great, or the processes within the liver slow down, or there is some obstruction
to the outflow of the bile from the liver then bilirubin will accumulate in the
blood. Eventually it will reach a level where it is deposited in the skin to
cause the yellow colour.
Some of
the bilirubin in the bile in the intestine is normally re-absorbed. If there is
a significant delay in the passage of stools then a greater amount of bilirubin
will enter the circulation and add to the bilirubin levels.
Whilst
the baby is in the uterus the liver is assisted in its functions by the
placenta, including the processing of the bilirubin. At birth the liver is on
its own and suddenly has to cope with the bilirubin. It normally takes a few
days before the liver is fully functional. If it takes a longer period then the
bilirubin levels can become high enough to deposit out in the skin to give the
jaundice. Preterm babies are understandably more prone to this problem. This
form of neonatal jaundice is referred to as “physiological jaundice” because it
is essentially a prolongation of a normal process.
Breastmilk or breastfeeding jaundice is so called because the breastmilk of some
mothers appears to contain factors that cause jaundice. This is NOT a reason to
stop breastfeeding.
More
serious forms of jaundice are referred to as “pathological jaundice”. One very
important cause is excessive breakdown of the red cells and is known as
haemolytic disease of the newborn. This occurs when there is a difference
(incompatibility) between the mother and her baby’s blood groups.
The most
important of these causes is Rh incompatibility. The Rhesus (Rh) factor is one
of the blood group determinants. In this disease the mother is Rh negative but
her baby is Rh positive. The mother becomes sensitised and produces antibodies
that cross through the placenta and destroy the red blood cells of the baby. The
degree of haemolysis will depend on the stage of the pregnancy and the amount of
antibodies that cross over. The liver is overwhelmed by the bilirubin produced
and the baby becomes jaundiced. The destruction of large numbers of red blood
cells means that the baby also becomes anaemic which adds to the trouble.
This
rarely happens with the first pregnancy as it usually requires two or three
incompatible pregnancies for the mother to become sensitised. If the mother’s Rh
factor is known after her first pregnancy she can be given anti-D (Rh) immuno-globulin
immediately after delivery to try and prevent sensitisation whenever she carries
a Rh positive baby.
A second
situation where there may be incompatibility between mother and baby is with the
major blood groups – the ABO factors. This also leads to breakdown of the red
blood cells but is usually not as severe as the above.
There
are many other rarer causes of haemolysis. One of them is when there is a
deficiency of an enzyme necessary for the integrity of the red blood cells. This
enzyme is known as glucose-6-phosphate dehydrogenase (G-6-PD).
If the
baby has an infection resulting in hepatitis then jaundice may appear. This
happens because the inflamed liver cells are not able to process the bilirubin
as efficiently as usual. They also swell up and tend to block the very small
ducts in the liver that carry the processed bilirubin away to the larger bile
ducts. The bilirubin accumulates and eventually leaks back into the blood
stream. It is this obstructed bilirubin that accounts for most of the jaundice
and hence the name “obstructive jaundice”.
In very
rare instances a child may be born without functioning bile ducts. All the
bilirubin processed by the liver therefore can only escape by leaking back into
the blood. This condition is known as biliary atresia and the children have
severe obstructive jaundice.
What are
the signs and symptoms of neonatal jaundice?
The signs and symptoms will depend largely on the cause.
In the
physiological group the jaundice is only noted on the second or third day. The
baby feeds well, behaves normally and there is no enlarged liver or spleen on
examination. The urine may be dark but the stools are normal colour. The
bilirubin levels are not significantly raised, below 275 ěmol/l. The jaundice
resolves over two to three weeks.
Breastmilk jaundice becomes apparent after a few days; the TSB rarely exceeds
275 ěmol/l but it is a cause of prolonged jaundice; the baby remains completely
well and continues to thrive. It is not a reason to stop breastfeeding.
How is
neonatal jaundice diagnosed?
In the pathological group the jaundice occurs within the first 24
hours after birth. The baby may even be jaundiced at birth. The baby may be
unwell on examination; have an enlarged liver or spleen; have a rash; have pale
stools or be pale. The bilirubin level can be very high, well above 275 ěmol/l
in haemolytic disease. Jaundice lasting more than two weeks is considered to be
prolonged jaundice and requires further investigation.
The
majority of jaundiced babies will be managed simply by screening for the total
serum bilirubin (TSB). A sample of the baby’s blood is spun down and the colour
of the serum is measured in a machine – the darker the serum, the higher the
bilirubin level. Most delivery units will be able to do this screen.
The TSB
can be checked daily or more frequently if the baby is receiving phototherapy
until it shows a downward trend. It may have to be checked three-hourly if one
is monitoring haemolytic jaundice.
In some
cases it will be necessary to have the exact levels measured by a laboratory and
to distinguish between the bilirubin that has been processed by the liver
(conjugated bilirubin) and that which is still to be processed (unconjugated
bilirubin).
In
physiological as well as haemolytic jaundice the unconjugated fraction is much
greater than the conjugated, whereas in hepatitis the conjugated is higher
(obstructive jaundice). The two fractions added together are the TSB.
Routine
tests are the mother’s blood group and screening for syphilis (an important
cause of neonatal jaundice) and the baby’s blood group. In some places a screen
for hypothyroidism (also a cause of prolonged jaundice) is done.
Other
tests which may be considered if pathological neonatal jaundice is suspected
are: checking the baby’s blood for anaemia, a Coomb’s test (screening for
antibodies that may be causing haemolysis), assaying for G-6-PD, tests for liver
function or a “septic work-up” (screening the baby for common congenitally
acquired infections).
How is
neonatal jaundice treated?
Most cases will not require any treatment because the bilirubin
levels are usually below 275 ěmol/l and clear within two to three weeks.
Ensuring
that the baby feeds early and regularly will stimulate the intestine so that the
re-absorption of the bile is minimised.
Neonatal
jaundice is treated by means of phototherapy. When unconjugated bilirubin is
subjected to specific fluorescent light-waves its structure is changed and it
becomes water-soluble. This means that the excess can also be cleared in the
urine. Whilst undergoing phototherapy the baby’s eyes must be protected against
the light. The baby must be fed regularly to keep up a good urine output and to
prevent dehydration. The baby may have loose stools whilst undergoing
phototherapy and may also become “tanned”.
Charts
have been devised (one for term and one for preterm babies) to assist health
professionals as to how and when to intervene in the management. The course of
action depends on the baby’s age and the bilirubin level.
In
severe haemolytic disease if the uncongugated levels rise to >350 – >400 ěmol/l
it may be necessary to do an exchange transfusion. Here an attempt is made to
“wash-out” the baby’s own blood, the bilirubin, and the antibodies causing the
haemolysis, and to replace with donor blood. An exchange transfusion may be
performed in other circumstances where the unconjugated bilirubin is excessively
raised or there is severe anaemia.
This is
not a simple procedure. Not just the TSB level but many other factors have to be
considered such as the cause of the jaundice, the age of the baby, whether the
baby has other problems and so on before embarking on an exchange transfusion.
What is
the outcome of neonatal jaundice?
In by far the majority of cases there are no complications associated
with neonatal jaundice.
The
problem with unconjugated bilirubin is that if the levels are very high,
especially when caused by haemolytic disease, it can penetrate into the brain
and cause brain damage. This is known as “kernicterus”. It is rare because all
at-risk babies are treated early with phototherapy and, in the unlikely event of
that not reducing the TSB adequately, with an exchange transfusion.
Anaemia
can be a problem in some babies following heamolytic jaundice and they may need
one or two blood transfusions in the next few months until all the antibodies
have been cleared.
Can
neonatal jaundice be prevented?
The majority of cases cannot be prevented as they fall into the
physiological group.
As far
as pathological causes are concerned, the introduction of anti-D (Rh) immuno-globulin
has seen a significant decline in haemolytic disease due to Rh incompatibilty.
When to
seek advice?
The TSB is an easy investigation to perform on any newborn baby who
is becoming jaundiced.
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