NEONATAL
INTRODUCTION
Bilirubin
is a yellow pigment that arises from the break down of red blood cells
haemoglobin. Jaundice’s the yellow
discolouration of the skin and mucous membrane, due to accumulation of
bilirubin in the serum. Neonatal
jaundice become apparent at serum bilirubin concentration of 5-7 mg/d.
1. DEFINITION:
Jaundice
is yellow discolouration of skin and mucosa is caused by accumulation of excess
bilirubin in the tissues and the plasma conjugated. Neonatal jaundice becomes apparent at serum bilirubin
concentrations of 5-7 mg/dl. (Bilirubin level should be in excess 2mg/dl).
2. INCIDENCE
Neonatal
jaundice is observed during first week of life.
More than 50% of full term infants and 80% preterm neonates.
3. TYPES
Neonatal
jaundice is divided into two groups.
a.
Physiological
jaundice
b.
Pathological
jaundice
a) Physiological Jaundice
The
jaundice usually appears on 2nd and 3rd day and
disappears by 7th -10th day a little later in premature
neonates. In a term infant the level may
be 6-8 mg/dl on 3rd day. A
rise of uncongugated serum bilirubin to 12mg/dl is in the physiological range
in a fulterm well baby, physiological jaundice never appears before 24 hrs of
age.
Causes
1. Increased red cell break down
The
newborns red blood cells have a shorter life span (100 days in term infants and
60-80 days in preterm infants as opposed to 120 days in adults). The average concentration of serum conjugated
bilirubin in neonates is three to seven times higher than that of adults. Whereas the concentration of unconjugated
bilirubin is four to 24 times higher.
2.
Demand albumin binding capacity
The
ability of neonates to actively transport bilirubin to the lives for
conjugation is reduced because of lower albumin concentration, decreased
albumin capacity.
3.
Enzyme deficiency
New
born infants have low levels of uride diphospho Glucuronyl transferance
(UDP-GT) enzyme activity during the first 24 hours of life.
4. Increased entro hepatic reabsorption
Increased
enterhepatic circulation due to decreased gut motility.
MANAGEMENT
No
specific treatment is generally required
a.
Adequate
feeding
Early frequent feeding
helps newborns deal with their increased bilirubin load. Demand feeding ensures adequate volume of
colostrums and milk in the intestine.
b.
Careful
observation of newborn
It will help to
distinguish between healthy babies with normal, physiological response and
those for whom serum bilirubin is required.
c.
In
premature babies:
Rising bilirubin level
to critical level require use of phototherapy or phenobarbitone administration.
b) PATHOLOGICAL
JAUNDICE
Pathological
jaundice usually appears within 24 hours of birth, and is characterized by a
rapid rise in serum bilirubin and prolonged jaundice.
FEATURES
OF PATHOLOGICAL JAUNDICE
a)
Clinical
jaundice appears within the first 24 hours of life.
b)
Increase
in bilirubin > 5mg/dl pr day.
c)
Total
bilirubin > 13 mg/dl
d)
Persistence
of clinical jaundice for 7-10 days in full term infants and two weeks in
premature infants
CAUSES
OF PATHOLOGICAL JAUNDICE
1)
Excessive
red cell haemolysis
a.
Haemolytic
disease of the newborn Feto – maternal blood group incompatibilities Rh
incompatibility, ABO incompatibility immunization against kell antigen
i.
Increased
red cell fragility – congenital sphirocytosis.
ii.
Deficient
red cell enzyme (Glucose 6-phosphate) dehydrogenase)
b.
Neonatal
sepsis specially with E.coli
c.
Polycythemia,
delayed cord clamping and infants of diabetic mothers.
d.
Extravasated
blood, such as incephal haematoma and bruising
2)
Defective
conjugation
a.
Congenital
deficiency of gluconyl transferase
i.
Immature
liver cells as in premature babies.
ii.
Dehydration,
starvation, hypoxia and sepsis because oxygen and glucose are required for
conjuation.
3)
Breast
Milk jaundice: The enzyme – cluclaronyl transferase activity of the liver is
inhibited by a specific steroid 3a, 20b pregnaediol and
increased fatty acids of breast milk.
4)
Metabolic
disorders: Galactosemia, hypothyrodism may be associated with unconjugated
hyper bilirubinemia
5)
Transport
and excretion failure
a.
Hepatic
obstruction caused by congenital anomalies such as biliary atresia, bile plugs
or absence of common bile duct
b.
Excess
conjugated bilieubin caused by infection or idiopathic neonatal jaundice.
c.
Umbilicas
cord sepsis leading to ascending thrombophlebitis, obstruction of biliary
cancaliculi and destruction of liver cells.
CLINICAL
MANIFESTATIONS
a.
Urine
become yellow
b.
Stool
are often pace or clay coloured peuritis
c.
Fatigue
d.
Lethargy
e.
Scleral
appearance yellow
f.
Refusal
of feed
g.
Presence
of dehydration, starvation hypothermia, acidosis, hypoxia.
h.
Presence
of irritability, a high pitched cry, dark urine or light stools
DIAGNOSTIC
EVALUATION
a)
History collection
i. Maternal history of
infection or administration of drugs during pregnancy.
ii. Previous sibling
affected by jaundice and anemia.
iii. Ethnic groups of
the parents and ancestors.
iv. Time of onset of
jaundice
v. General condition
of the infant, whether healthy having no feeding difficulty, no fever no
rash.
b)
Laboratory
Investigation
i. Haemoglobin
ii. Serum bilirubin
iii. Direct coomb’s test
iv.Indirect coomb’s
test.
v. Reticulocyte count.
vi. ABO blood group
and Rhesus type for possible incompatibility.
vii. Peripheral blood
smear
viii.White cell count
ix. Glucose
6-phosphate dehydrogen are assay
MANAGEMENT
Three methods of treatment are used to reduce
the level of unconjugated bilirubin.
1.
Phototherapy
2.
Pharmacologic
therapy
3.
Exchange
transfusion
1) Phototherapy
During
phototherapy the neonates skin surface is exposed to high intensity light,
which photochemically converts fat soluble, unconjugated bilirubin into water
soluble bilirubin, which can be exerted in bile and urine.
Indications
a)
Who
are smaller or preterm
b)
Who
are sick particularly with hemolysis
c)
In
whom jaundice appears within 12-24 hrs.
d)
17-22
mg / dl for teem infants who become jaundiced after 48 hrs.
e)
8-10
mg/dl for preterm infants > 1,500 gm.
f)
5-8 mg / dl for
preterm babies < 1500 gm
Length Of Phototherapy
Just 24-28 hours exposure is generally long
enough to bring down serum bilirubin levle to safe limit.
Special
Precuation
Male baby: Protect the eyes and genetalia from
exposure to phototherapy.
Female baby – Protect the eyes using mask
Types Of Phototherapy
1. Conventional systems
Flurescent lamps are used deliver high
intensity light.
2. Fiberoptic light systems
Side effects
a.
Lethargy
b.
Hyperthermia
c.
Dehydration
d.
Fluid
losses
e.
Skin
rashes
f.
Retinal
haemorrhage
g.
Skin
Malignancy
h.
Delayed
puberty
Care of
the baby undergoing phototherapy
a.
Observing
any visible side effects.
b.
Check
the baby’s temperature
c.
Apply
eye pads. The infant is also observed
for any eye discharge or weeping.
d.
Estimation
of bilirubin level.
e.
Undress
the baby
f.
Apply
genital pads
g.
Put
on the photo therapy machine
h.
Fluid
intake and urine output are to be monitored
i.
Neurobehavioural
status
j.
Sensory
deprivation
To
reduce the effects of isolation when feeding
the eye patches are to be taken off and the infant is removed from
lights.
a.
Place
on each side small pillow or a rolled sheet for safely.
b.
Turn
the baby frequently to exposure all the body parts.
c.
Check
the serum bilirubin level as per order.
d.
Maintain
intake and output chart.
e.
Remove
the eye pads when mother is feeding.
f.
Check
in weight twice daily
g.
Hypocalcemia.
Serum
calcium level decreases in some babies and a level < 7 mg / dl is considered
hypocalcaemia in neonates.
After
Care
Ø Switch of the
phototheraphy machine.
Ø Remove the eye pad
from the baby.
Ø Inspect the baby for
any sign of complication.
Ø Give the baby to the
mother for feeding.
Complications
Ø Watery diarrhoae
Ø Skin rashes
Ø Dehydration
Ø Bronze baby syndrome
Ø Retinal damage
2. Pharmacological Therapy
Ø Phenobarbital therapy
induces hepatic microsomal enzymes and increase bilirubin conjugation and
excretion. A dore of 5-8 mg / kg every
24 hrs is used it takes 3-7 days to be effective.
Ø Metalloporphyrins
decrease bilirubin production by inhibiting heme oxygenace.
Salt
free albumin
It
may be prescribed about one gram per kg of the body weight. The salt free albumin increases bilirubin
binding capacity.
3. Exchange blood transfusion
It
is necessary to remove the excess serum bilirubin mechanically by exchange
blood transfusion.
Indications
a.
Progressive
rise of bilirubin > 1mg / dl / hr inspite of phototherapy.
b.
Cord
blood bilirubin level > 5mg / dl and haemoglobin level < 12 gm / dl
c.
Total
bilirubin 20 mg / dl or more
Objectives
a.
To
remove circulatory antibodies.
b.
To
correct the anaemia by replacing the Rh positive sensitized red cells.
c.
To
eliminate the circulating bilirubin
Complications
a.
Air
embolism
b.
Cardiac
failure
c.
Sepsis
d.
Hyperkalaemia
e.
Coagulopathesis
due to thrombocytopenia
NURSING
MANAGEMENT
a.
Constant
observation is necessary to detect early changes.
b.
Skin
color is observe for increase or decrease yellowness.
c.
Urination
is checked for frequency amount of colour.
d.
Vital
Signs should bechecked.
e.
Maintain
the body temperature specially when the baby is under phototherapy.
f.
Any
behavioural changes, convulsion or sluggishness should be noted and reported.
g.
Enough
fluid intake is necessary to help in the excretion of bile to prevent
dehydration.
h.
Eye
of the baby should be covered with eye pads to protect from high intensity
light in the care of the baby under phototherapy.
i.
Check
the weight twice daily.
j.
Check
the serum bilirubin level
k.
Maintain
intake and output chart.
l.
Advice
mother to give lactore free milk feeding for the baby suffering from
Glactosemia.
CONCLUSION
Jaundice
results from deposition of bilirubin in the skin premature infants are also
more likely to develop jaundice. Asian
and native American babies tend to have higher bilirubin levels than white
babies who in turn have higher level than black infants.
BIBLIOGRAPHY
1.
D.C.
Dutta “Text Book of Obstetric Including Perinatology and contraception”.
Sixth edition 2004,
New Central Book Agency (P) Ltd., Page.No.447-481.
2.
Annamma
Jacob “A comprehensive Text Book of Midwifery”, Second Edition Jaypee brothers
Medical Publishers Page.No.588-594.
3.
V.Ruth
Benet and Linda K. Brown Myles Text Book for Midwives Thirteenth Edition,
Page.No.816-822, 827-830.
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