Infant
jaundice is a yellow discolouration in a newborn baby’s skin and eyes. It occurs
because the baby’s blood cells contain an excess of bilirubin, a
yellow-coloured pigment of red blood cells. And also because a baby’s liver
isn’t mature enough to get rid of bilirubin in the blood stream. Neonatal
jaundice can make the newborn sleepy and interfere with feeding. Extreme
jaundice can cause permanent brain damage from kernicterus (Mayo, 2015).
jaundice is a yellow discolouration in a newborn baby’s skin and eyes. It occurs
because the baby’s blood cells contain an excess of bilirubin, a
yellow-coloured pigment of red blood cells. And also because a baby’s liver
isn’t mature enough to get rid of bilirubin in the blood stream. Neonatal
jaundice can make the newborn sleepy and interfere with feeding. Extreme
jaundice can cause permanent brain damage from kernicterus (Mayo, 2015).
Bilirubin
Bilirubin
is a by-product of the breakdown of haemoglobin (the oxygen-carrying substance
in red blood cells) in the blood. Newborn babies’ red blood cells have a
shorter lifespan than those of adult. The concentration of red blood cells in
the circulation is also higher than it is in adults, so bilirubin levels are
higher than they are later in life. Before birth, an infant get rid of bilirubin
through the mother’s blood and liver system. After birth, the baby’s liver has
to take over processing bilirubin on its own. Unconjugated bilirubin is
metabolised in the liver to produce conjugated (or direct) bilirubin which then
passes through the gut and is excreted in the stool. Bilirubin can be reabsorbed
again from stool remaining in the gut which is known as entero-hepatic
circulation of bilirubin.
is a by-product of the breakdown of haemoglobin (the oxygen-carrying substance
in red blood cells) in the blood. Newborn babies’ red blood cells have a
shorter lifespan than those of adult. The concentration of red blood cells in
the circulation is also higher than it is in adults, so bilirubin levels are
higher than they are later in life. Before birth, an infant get rid of bilirubin
through the mother’s blood and liver system. After birth, the baby’s liver has
to take over processing bilirubin on its own. Unconjugated bilirubin is
metabolised in the liver to produce conjugated (or direct) bilirubin which then
passes through the gut and is excreted in the stool. Bilirubin can be reabsorbed
again from stool remaining in the gut which is known as entero-hepatic
circulation of bilirubin.
Hyper-bilirubinaemia
is a condition particularly common in the blood. In young babies unconjugated
bilirubin can penetrate the membrane that lies between the brain and the blood
(the blood-brain barrier). Unconjugated bilirubin is potentially toxic to
neural tissue (brain and spinal cord). Entry of unconjugated bilirubin into the
brain can cause both short-term and long-term neurological dysfunction. Acute
features include lethargy, irritability, abnormal muscle tone and posture,
temporary cessation of breathing (apnoea) and convulsion. This is known as
acute bilirubin encephalopathy. Factor that increase the risk of acute
bilirubin encephalopathy include preterm birth, sepsis, hypoxia, seizures,
acidosis and hypoalbuminaemia. (NCBI, 2014).
is a condition particularly common in the blood. In young babies unconjugated
bilirubin can penetrate the membrane that lies between the brain and the blood
(the blood-brain barrier). Unconjugated bilirubin is potentially toxic to
neural tissue (brain and spinal cord). Entry of unconjugated bilirubin into the
brain can cause both short-term and long-term neurological dysfunction. Acute
features include lethargy, irritability, abnormal muscle tone and posture,
temporary cessation of breathing (apnoea) and convulsion. This is known as
acute bilirubin encephalopathy. Factor that increase the risk of acute
bilirubin encephalopathy include preterm birth, sepsis, hypoxia, seizures,
acidosis and hypoalbuminaemia. (NCBI, 2014).
Kernicterus
This
is a pathogenic diagnosis characterised by bilirubin deposited particularly in
a part of the brain known as the globus pallidus, part of the deep grey matter
of the brain. On pathological examination of the brain, this produces yellow
staining; this staining is referred to as kernicterus. The term kernicterus is
also used to denote the clinical features of chronic bilirubin encephalopathy.
Features of the latter include athetoid cerebral palsy, hearing loss, visual
and dental problems. The level of bilirubin that is likely to cause neurotoxicity
in any individual baby varies and depends on the interplay of multiple factors
which acidosis, gestational and postnatal age, rate of rise of serum bilirubin,
serum albumin concentration, and concurrent illness (including infection)
(NCBI, 2014).
is a pathogenic diagnosis characterised by bilirubin deposited particularly in
a part of the brain known as the globus pallidus, part of the deep grey matter
of the brain. On pathological examination of the brain, this produces yellow
staining; this staining is referred to as kernicterus. The term kernicterus is
also used to denote the clinical features of chronic bilirubin encephalopathy.
Features of the latter include athetoid cerebral palsy, hearing loss, visual
and dental problems. The level of bilirubin that is likely to cause neurotoxicity
in any individual baby varies and depends on the interplay of multiple factors
which acidosis, gestational and postnatal age, rate of rise of serum bilirubin,
serum albumin concentration, and concurrent illness (including infection)
(NCBI, 2014).
