NEONATAL

JAUNDICE

DN NDUNGE
NEONATAL JAUNDICE

DESCRIPTION
It’s a yellowish discolouration of the skin,sclera and
mucosal surface/mucous membranes, due to elevated
serum and tissue unconjugated bilirubin levels from
excessive haemolysis.
CAUSES
Physiological
Increased red cells breakdown, because of the high
number of fetal hemoglobin hence shorter life span.
Decreased albumin-binding capacity, due to lower albumin
concentration and competition for albumin binding sites.
Enzymes deficiency particularly lower levels of uridine
diphospho glucuronyl transferase (UDP-GT) within the first
24 hours . N- levels attained btwn 6-14 weeks.
Increased enterohepatic reabsorption due to lack of normal
enteric bacteria to further break down conjugated bilirubin
for excretion.
- Decreased bowel movement, in which high levels of beta-
glucuronidase enzyme hydrolyses conjugated bilirubin into
unconjugated.
 Pathological
-Results from interferences in; bilirubin production,
transport, Conjugation and excretion as follows:
Increased production of bilirubin levels factors
are:
Blood group and rhesus incompatibility.
Extravasated blood following traumatic deliveries,
accompanied large caput, cephalhaematoma or severe
subaponeurotic hemorrhage.
 contd
Polycythaemia results from increased numbers of
circulatory rbc due to either increased erythropoesis
associated with maternal diabetes mellitus or from
twin to twin transfusion.
Spherocytosis;it’s a congenital defects of the rbc shape
such that its round instead of being biconcave.
Haemoglobinopathies; in terms of sickle cell disease
and thalassaemia.
Enzymes deficiencies of glucose-6- phosphate
dehydrogenase (G6PD).it’s an x-linked genetic
disorder in which rbc cell membrane becomes fragile
and only affects male infants.
Transport interferences includes:
Hypothermia , acidosis & hypoxia can interfere with
albumin-binding capacity.
Drugs e.g. aspirin, sulphonamides, ampicillin among
others competes with bilirubin for albumin binding
sites.
Conjugation; interferences includes:
• Dehydration, starvation, hypoxia and sepsis because
oxygen and glucose are required for conjugation.
• Intrauterine infection either viral or bacterial ,
leading to damage of liver cells accompanied by
acidotic state hence low oxygen and glucose levels .
Metabolic and endocrine disorders e.g.. hypothyroidism and
galactoseamia which affects the glucose levels hence inhibit
conjugation process.
Excretion interferences includes:
Hepatic obstruction due to extra hepatic biliary atresia.
Increased bile viscosity hence formation of a bile plug.
Excess of conjugated bilirubin following idiopathic
neonatal hepatitis among other infections, such that the
excretion process is overwhelmed.
Saturation of protein carries required to excrete
conjugated bilirubin into the biliary system.
 CLASSIFICATION.
Based on the commonest causes during the
neonatal stage
1.PHYSIOLOGICAL SIMPLE JAUNDICE
Occurs due to discrepancy between the
normal haemolysis of the excess RBC, the
ability to transport ,conjugate and finally
excrete the conjugated bilirubin.
INCIDENCE
Term babies-occurs only to a few and its noted around
the 3rd to the 4th day. Resolves uneventfully by the 7th day if
all factors remain favorable.
Preterm babies –earliest occurrence is after the first 24
hrs postnatally and persists upto 10th day if all is well.
Rationales are:
Low levels of enzymes production generally.
Shorter life span of the rbc to 60 days.
Poor excretion of bilirubin due to poor guts colonization
High possibility of complications e.g.
acidosis ,hypothermia and hypoxia.
processing of conjugated bilirubin
The unconjugated bilirubin is also referred to as fat
soluble bilirubin or indirect reacting bilirubin.
It is harmful when accumulated in the circulation
because its deposited in fatty tissues causing jaundice.
 Processing stages are;
Transportation:-
 Following haemolysis, among the by product is haem.
-It is converted by some enzymes in to biliverdin
initially and later into unconjugated bilirubin.
So normally the unconjugated bilirubin molecule bind
onto the plasma albumin to be transported to the liver
cells.
NB :-If the albumin concentration is low or already
bound by others ,then the free unconjugated bilirubin
is deposited under the skin or at the nerve tissues of
the brain.
 contd
Conjugation;
 At the liver the unconjugated bilirubin molecules detach
from albumin.
-combines with glucose and glucoronic acid and
conjugation occurs in the presence of oxygen and uridine
diphosphogluronyl transferase enzyme.
The bilirubin is now water soluble or direct reacting
bilirubin.
Excretion
The excretion route is through biliary system into the
small intestine.
 contd
The normal flora/commensal changes the conjugated
bilirubin into urobilinogen initially, which is then
oxidized into orange coloured urobilin.
Finally most of it is excreted in feaces and the rest in
urine.
Therefore physiological jaundice occurs due to failure
of any of the above steps or excessive haemolysis such
that conjugation process is overwhelmed.
 SPECIFIC MANAGEMENT
MILD;
-commonest outcome and the care is basically conservative.
Remains in the postnatal ward with the mother
Daily monitor;colour change and areas involved,generally
behavior, feeding and sleeping pattern.
Vital signs 4hrly.
Serum bilirubin estimation stat and on alternate days.
Encourage frequent breastfeeding or 2hrly oral feeding
with recommended milk to supply liver cells with
adequate glucose and also to facilitate excretion of
conjugated bilirubin.
Exposure to ultra-violet sun rays daily for about 15
minutes between 9-10am, turn neonate for
effectiveness of treatment.
- These rays convert the fat soluble bilirubin into
water soluble bilirubin ready for excretion.
Evaluate the effectiveness of the treatment daily
through physical examination finding and
enquires.
Psychologically support the parents to allay
anxiety.
NB
Active management is only recommended in presence of:
 Fat soluble bilirubin levels ranging between
15-20mg/dl.
Rapid rise of unconjugated birilubin levels, by 0.3mg/dl
or more hourly , accompanied by positive clinical
features.
 MODERATE
Preterm are the commonly affected and the main mode
of treatment is phototherapy.
Sometimes phenobarbitone is also recommended in
conjunction with phototherapy because
-It activates the liver cells to release adequate levels of
glucuronyl transferase enzyme for the conjugation
process.
-Prolongs the neonates period of exposure to
treatment because of its sedative effects hence
jaundice clears fasts.
 Preparation for phototherapy
Following clinical diagnosis based on tissues
discolouration inform the doctor.
Blood specimen is sent to laboratory for serum bilirubin
estimation hence confirm diagnosis.
Briefly explain the condition to parent to include the
intended mode of treatment to allay anxiety.
Meanwhile get ready the photobox / incubator by
ensuring :
Cleanliness
 Correct light ,high intensity fluorescent light either
blue or white but the latter is better.However green light
can also be used.
With white light- Foil paper may be used in the
incubator to intensify the light such that the beam is
more direct on the neonatal body hence fast effective.
Wave length depends on the heat emitted by the
light .If low heat, then 15-30cm.If high heat then 45-
60cm.
 Admit baby in the NBU through:-
History taking
Parents blood group to asses for either ABO or Rhesus
incompatibility.
 H/O jaundice in other children
Antenatal profile, mainly illness and drugs given after 36
weeks gestation.
Labour process and conclusion.
Present complain in terms of when first noted, extent,
treatment taken and current situation.
 Perform physical examination in terms of :-
-Vital signs
-Extent of jaundice i.e.. areas involved
-State of the skin- whether dry or normal .
-General appearance and muscle toning /activity.
-Maintain record, interpret and consult prn
Label the baby- mother’s name i.e.. apply a name tag.
Have the infant feed in order to calm down and sleep.
Shield the eyes using an opaque mask immediately
he/she is deeply asleep to prevent retinal damage.
Prepare the relevant charts and place them within reach.
Lay the infant under phototherapy when completely nude
.Note time, position and document on the relevant charts
to serve as a guide.
Specific Care:
The eye shield to remain in place all through, so ensure
that it’s of correct size and well placed so that the nostrils
cannot be covered.
Regularly monitor the eyes for discharge and take
appropriate measures.
Encourage frequent feeds to prevent dehydration and
activate peristaltic movements hence excretion of
bilirubin.
During feeding session remove the shield to allow visual
stimulation and eye contact.
Simultaneously, encourage mother to perform tactile
stimulation regularly for development of human touch
and increase of the growth hormone levels hence growth
spurt.
Maintain a record of observations every 2 hourly.
Daily evaluation of state of jaundice and anaemia ,
muscle tone ,L.O.C, elimination ,feeding pattern and
general behavior.
Maintain high standards of hygiene to prevent cross
infection.
Regularly turn the neonate and limit time out of the
treatment daily because a total of 8-12hours of exposure
daily reduces unconjugated serum bilirubin level by a
range of 3-4mg/dl as long as other factors are favourable.
 Mode of action
The light (phototherapy) works through a process of
isomerization that changes unconjugated bilirubin under
the skin into water soluble bilirubin, ready for excretion.
NB: The photo – oxidation, occurs as the light causes
chemical alteration of bilirubin molecule under the skin.
Closely monitor the effectiveness of the treatment
through:
-Alternate days estimation of serum bilirubin.
 -Daily physical examination and weekly haemoglobin
level. Maintain records ,interpret and consult.
Prevent heat loss through maintaining room temperature
as well.
Encourage parents to visit and participate in the baby’s
care. Keep them informed on the baby’s progress to allay
anxiety .
As improvement occurs ,prepare mother for home care in
terms of :
-Nutrition – Exclusive breast feeding for 4-6months.
-Contraindicated, then 2 hourly artificial feeds and dilute
correctly.
Hygiene.
Sun- bathe the baby between 9-10a.m, until the yellowish
discoloration clears completely.
Follow-up for MCH/FP services and home visit prn
To seek medical attention if the condition relapses or
abnormal behavior is noted.
Types of phototherapy
Conventional systems:-Using the high intensity light,
commonly used in healthy facilities.
Fibreoptic light system uses a special blanket to deliver
the high intensity light. Fortunately this can be used at
home.
 CONCLUSION
This type of jaundice rarely progress to severe state. For
preterm particularly those who also get some form of sepsis
or conditions may have severe haemolysis. The exchange
transfusion is recommended as the main mode of
management
COMPLICATION
Side effects of conventional phototherapy.
Hypocalcaemia, due to persistent stress acquired in
prolonged period of treatment ie over 3wks, hence over
consumption of ionized calcium.
Skin burns and rashes due to shorter wave length and
inadequate turning of the infant.
Dehydration,hypothermia and increased fluid loss
leading to dehydration fever.
Retinal damage if shield is not maintained.
NB:Breast milk jaundice is rare and occurs to exclusively
b/fed babies whose mother milk contain a progesterone
metabolite known as 3-alpha-20 beta pregnanediol.
This substance inhibits the action of the enzyme uridine
diphosphoglucuronic transferase (UDP-GT)hence the
conjugation process.
11 HAEMOLYTIC JAUNDICE
Basically the haemolytic rate is higher leading to
overwhelming levels of birilubin, hence also referred to as
pathological jaundice.
1. RHESUS D INCOMPATIBILITY
Synonymes:
 Erythroblastosis foetalis , because fetal body releases
immature RBC
 Rhesus D isoimmunisation, refers to production of
anti-D antibodies following sensitisation of maternal
immune system by Rhesus positive antigen.
 Description
Refers to a situation where the mother’s &
fetus rhesus factors are different in that mother
is negative while fetus is positive.
For jaundice to occur, isoimmunisation must
have taken place, hence antibodies crosses the
placenta barrier leading to massive haemolysis
of the fetal RBC.
 Causes of Rh D Isoimmunisation
Normal 3rd stage of labour.
Antepartum haemmorhage.
Obstetrical manipulations e.g. cephalic version leading to
abruptio placenta.
Amniocentesis due to accidental pricking of the fetus.
Non-obstetrical events
Abortion after 12 weeks.
Tubal rupture .
Previous transfusion with rhesus positive blood.
 Pathophysiology
Rhesus positive means that antigen is present
in the RBC while Rh negative indicates absence
of antigen.
Alleles genetically produces 3 genotypes
denoted as; DD, Dd = rh positive and dd= Rh
negative.
Mother is always Rh –ve denoted as
dd(homozygous), while father is either Rh +ve
DD(homozygous) or Dd( heterozygous).
Fetus inherit rhesus factor from both parents.
-So if both parents are homozygous, all children are
positive.
-Father heterozygous, some children are Rh negative like
the mother.
-Both parents Rh –ve all children are Rh negative as well.
 Rh isoimmunised mother forms 2 types of anti-D
antibodies namely:
-Gamma M or 19(nineteen) S and they are large- size.
-Gamma G or 7(seven) S and are small in size
NB:They have no effect on her health.
If the next pregnancy is Rh +ve the
antibodies crosses the placenta barrier and
haemolysis the fetal RBC.
Severity depends on the size of the released
antibodies.
*Gamma M or 19s leads to mild-
moderate.
* Gamma G or 7s leads to severe
jaundice.
 Determiners of specific outcome
Refers to factors that leads to developing
jaundice or baby is born already jaundiced.
Birth order. The very first born is safe so
long as isoimmunisation has not occurred.
Actual status of the father’s rhesus factor.
Administration of anti-D immunoglobulin
at a dose of 500 IU intramuscularly within
72 hours of rhesus positive RBC entry to
the maternal circulation.
Mode of action:
 It destroys the fetal RBC in the maternal
circulation before the immune system realizes
their presence , hence anti-D antibodies are
not formed for future attack.
NB For evidence of fetal-maternal
haemorrhage ,antenatal dose is given within
the same period.
 Specific Management
Prenatally
Routine screening of all clients for group and rhesus
factor on booking visit.
For rhesus negative results, discuss them with client to
include the follow up schedule for:
*Indirect coomb’s test. To assesss for presence of
antibodies in the maternal circulation, irrespective of
history of isoimmunisation.
Positive results (indirect coomb’s test);
*Rhesus antibody titre is carried out, to estimate the
number of antibodies within a given volume of blood.
 * The test is repeated regularly to monitor the fate of the
fetus.
Positive titration results: Gestation is above 20 weeks
and findings are above a ratio of 1:8, amniocentasis is
indicated to estimate bilirubin level in the liquor.
Elevated results indicates that the fetus is in severe
danger.
* So due to prematurity, intra-uterine transfusion is
performed if facilities are available
*Donor blood is always group O negative and amount is
determined by gestation period.
NB For negative indirect coomb’s results; repeat is carried out at 28,
32 & 36 wks respectively.
Aim is to anticipate fate of the fetus.
For low titration results, follow up through non-invasive procedures
eg doppler ultrasonography, for the fetal well being.
Intrapartum ( During labour)
As 2nd approaches, have various specimen bottles and request forms
ready for cord blood investigations namely:-
*Direct coomb’s test, for Rhesus antibodies in the baby’s circulation.
*Rhesus factor & blood group.
*Haemoglobin level.
 *Serum bilirubin.
*Presence of immature red blood cell. High number
worsen the condition.
NB Specimen are collected from the cord with the baby.
Clamp and cut the cord immediately after delivery to
prevent more antibodies from entering the baby’s
circulation.
 Postnatally
Baby: routine examinations are performed as
usual.
Active management depends on the clinical
status and laboratory results.
Mother: Facilities available;
 kleihauser acid selution test is carried out
within the 1st 2 (two) hours of delivery to detect
fetal cells in the maternal circulation.
 contd
The aim is to determine the actual dose of anti-D to be
administered.
However standard dose of anti-D immunoglobin 1g is
500 IU stat.This should be discussed during prenatal
period so that it’s available, before delivery.
NB: The drug is effective for only 3 months .
*Therefore, exposure to antigen thereafter requires a
repeat dose to avoid isoimmunisation.
*For an abortion at a range of 12-20 weeks, the
recommended dose is 250 IU stat within 72 hours.
 OTHER ASSOCIATED HAEMOLYTIC
CONDITIONS.
Refers to those which occurs because of severe
haemolysis in rhesus incompatibility. They are:-
1.Congenital Haemolytic Anaemia
Indicates that the rate of intrauterine (fetal)
haemolysis was mild.
Clinical feature
Pallor of slow onset.
Slight jaundice at birth, because most of the bilirubin
has been excreted by mother’s body.
Hepatosleenomegally.
 Specific management
Admit in the special care baby unit(NBU) &
inform the DR.
Closely monitor vital signs and general
behaviour for features of neurotoxicity.
For the low HB, transfuse normally.
For the abnormal serum bilirubin levels ,
mode of treatment is phototherapy.
 2. Icterus Gravis Neonatorum
-Results from severe haemolysis prenatally, such that the
excretion of bilirubin through the mother is inefficient .
Clinical feature
Golden coloured liquor.
Severe jaundice at birth.
Bilirubin stained cord due to high levels in the liquor.
Haemoglobin level is below 10 gm/ dl.
Hepatospleenomegally and death of some liver cells is
noted through biopsy.
High probability of neurotoxicity, if immediate and
accurate interventions are delayed.
 Specific Management
Take cord blood for investigations and inform
the doctor promptly.
Resuscitate prn.
Admit in the special care baby unit and
commence phototherapy awaiting exchange
transfusion.
Prepare and participate in the latter procedure
as appropriate.
 3. Hydrops Fetalis
Results from very severe haemolysis prenatally, such that
at birth features of C.C.F are present hence the baby is
either severely asphyxiated or stillbirth .
Clinical features
Apgar score ranges between 1-3 due to very low HB.
Extreme pallor at birth –HB below 8 gm/dl
Gross oedema to include ascites due to low osmotic
pressure.
Large ,pale and marshy placenta.
Presence of either fresh or macerated stillbirth.
 contd
Specific Management
Prompt resuscitation and DR in attendance.
 Immediately after stabilisation admit in NBU for
subsequent care.
Commence phototherapy and transfuse with packed
cells to cure asphyxia.
Administer prophylactic antibiotics because of low
immunity.
Prepare & participate in exchange transfusion
procedure.
 ABO INCOMPATILITY
DESCRIPTION: the mother is always blood group O
while the fetus is any other ie A, B or AB.The mother
has natural antibodies against all the groups, and
hence all children are at risk of developing jaundice
irrespective of the birth order.
Pathophysiology/aetiology
The maternal immune system produces two types of
natural antibodies namely
1. Immunoglobulin g(1Gg)-small in size
2. Immunoglobulin m (igM) - large size.
If the system releases immunoglobulin M (IgM) jaundice
doesn’t occur because they cannot close the placenta
barrier although the fetal blood group is different from
the mothers.
Release of immunoglobulin G (IgG), they cross the
placenta barrier and haemolysis the fetal red blood cells
though not severely.
Clinical features
1. Baby’s blood groups is different from mothers.
2. Mild state of jaundice at birth, though mostly noted after
the 1st 24hrs.
 Specific management
Explain the condition and intended treatment to
parents to allay anxiety.
Inform the DR and admit to NBU for continuity of care.
Investigate- serum bilirubin, blood group, haemoglobin
level and coombs test to r/o rhesus D incompatility.
Mild to moderate cases- mode of treatment is
phototherapy.
Severe cases mode of exchange transfusion.
Specific feature for severe jaundice includes:-
*Unconjugated bilirubin level above 15mg/dl-preterm
and 25 mg/dl in term baby.
*Poor feeding pattern because of being sleepy most of
the time.
 *Dull looking, high pitched cry, tremors/ twitching
opisthotonous and spasticity.
 NB: palliative care continues if neurotoxicity
feature are present. They include:
* Upward rolling of the eyes.
* Excessive drowsiness-the infant is unrousable.
* Grunting and irregular breathing.
* Cyanotic attacks because of severe respiratory
distress.
* Convulsions/seizure.
 Explain the situation to parents so that they don’t cite
negligence
 EXCHANGE TRANSFUSION
It’s a sterile procedure carried out by a doctor specifically
neonatal/pediatrician due to severe neonatal jaundice
irrespective of the cause. The procedure involves slowly
removing the patient's blood and replacing it with fresh
donor blood or plasma.
Objectives
To restore hemoglobin level hence improves the oxygen
carrying capacity.
To reduce high levels of unconjugated bilirubin hence
prevent neurotoxicity.
 To remove the maternal antibodies from baby’s
circulation hence cure excessive haemolysis.
Indications
1. Unconjugated bilirubin levels of :-
*400-500µmol/litre (23-29mg/dl) for term babies.
* 300-400µmol/l, (17-23mg/dl) for sick term babies and
preterm whose wt is more than 1500gm.
* 255µmol/litre (15mg/dl) for preterm of less than 1500gm
accompanied by signs of severe jaundice.
2. Continuous rise of fat soluble bilirubin levels
irrespective of phototherapy
 Preparation
1)BABY
Thoroughly explain the mother/ parents the purpose
of the procedure and her/their role in order to obtain
verbal and written consent.
Ensure the infant is on intravenous fluid for 4(four)
hrs before the procedure hence well hydrated.
Maintain a record of the baby’s vital signs.
 11)REQUIREMENTS
Refers to what should be available to have the
procedure performed smoothly.
Fresh blood, preferably group O negative.
Exchange transfusion (tray) pack. Probe is the most
important instrument.
 Blood giving set
Specific drugs:
* Lasix (frusemide) to reduce cardiac work load.
* Heparin to prevent blockage of the umbilical
catheter.
* 10%calcium gluconate to prevent arrythmias.
2% sodium bicarbonate (NAHCO3) for treatment of
metabolic acidosis.
 10% dextrose to treat hypothermia and sooth the baby.
Steroids e.g.. hydrocortisone, dexamethasone for
resuscitation prn
Assorted syringes and needles
Antiseptic solution e.g. hibitane or betadine or
povidone iodine but not savlon.
Normal saline(sterile)1/2 L, for rinsing the syringe
occasionally.
Spirit swabs for sterilizing the cord area before
incision.
3 way stopcock or luer fitting or 3 way tap if
possible ,enables i.v extension tubing.
A cord catheter.
Drip stand.
Sterile gloves at least 4 pairs.
Big syringe at least 2 each to hold 20ml.
Surgical blade and suturing material
Sterile drums containing- caps, masks, cotton wool
gauze swabs and gowns
Specimen bottles in pairs
plain sequestrated and containing transport media for
pre and post procedure investigations
-serum bilirubin
-haemoglobin level
-blood cultures.
 N.B 1.The specimens should be clearly labeled and have
request forms respectively
2. Work out well before the procedure starts with
laboratory personnel to have the staff who will handle the
specimen for smoothing release of results.
111) ENVIRONMENT
Room & surface to be cleaned and disinfected.
Warmth room temperature to be at least 26 degrees
Celsius.
Have the near by windows closed for privacy and to
prevent excessive heat loss.
Provide for hand washing.
Have the sterile trolley within reach
Ensure the following accessories are available:
* Clean shoes and a mobile/flexible source light.
* A firm surface where a cross-splint is laid during the
procedure.
* Adequate warm baby wrappers to be used before and
after the procedure.
* A clean roll of cotton wool for keeping infant warm
during the procedure.
Writing materials/chart for:-
-Recording of the infants observation .
-Recording drugs used in terms of date and time.
given brand/ type, dose route, frequency & effects.
-Blood removed and given clearly indicated time and
amount.
-Duration the whole procedure takes and reported
regularly e.g.. every ½ hrly.
Clock, to account for the duration the whole
procedure takes.Normally ranges between 2-2½hrs
PERSONEL
Doctors-specialist, in terms of either a pediatrician or
neonatologist, not available, then general physician
Assistant
Qualified midwives to work closely with the dr.
Other 2 midwives either qualified staffs or a staff
and a student ,or students, a senior and a junior. Specific
roles are:-
 contd
One basically takes care of the baby in terms of:-
 observation-vital signs every 5-15 minutes intervals.
Record particularly the apical beat accurately.
 Appearance for abnormal colour e.g.. cyanosis/pallor.
 Signs of cerebral damage.
Report promptly to the dr
*Progressive tachycardia/bradycardia
*Respiratory distress.
*Tremosis/twitching at the angles mouth eyes.
*Cyanosis.
Prevention of hypothermia and hypoglycemia to the
neonate
*closely monitor room temperature and ensure that the
baby is adequately warm.
*stuffs some gauze with dextrose and the baby suckles
hence remain calm. May use a stuffed teat.
*If unable to suck then commence a dextrose drip.
The other one
Documentation , of drugs, blood removed and
replaced per session as well as the duration the
procedure has taken.
Is a runner around in the room and also liaise with the
outside respectively.
N.B the required amount of fresh bld for the procedure
is double the specific baby’s total volume. This is
based on the fact that the blood volume is about
85millilitres/kg body weight.
 Specific after care
Immediately after the procedure, nurse in the incubator
within NBU to prevent hypothermia.
* Hypothermia (cold stress) increases oxygen & glucose
consumption leading to metabolic acidosis hence
possibility of kernicterus.
on the other hand avoid hypothermia bcos it damages
the donor erythrocytes leading to high levels of free
potassium content hence cardiac arrest.
Phototherapy continues so as to control the
unconjugated serum bilirubin levels.
Closely monitor the progress through vital signs and
general behavior in order to early diagnose complications
e.g. C.C.F, respiratory distress and intracranial injury
respectively.
* Maintain records and consult as necessary.
For presence of a complication manage respectively.
 Also closely monitor elimination to assess excretion of the
conjugated bilirubin.
 Feed appropriately preferably using mother’s milk.
Monitor cord dressing for active bleeding and intervene
prn.
Evaluate the effectiveness of treatment through:-
*Daily estimation of serum bilirubin, physical exam findings.
*Weekly haemoglobin level recheck.
*Feeding /sleeping patterns, appearance and activity
respectively.
Administer prophylactic antibiotics of broad spectrum,
example X-pen 50,000 I.U/kg12 hrly &Gentamycin
2.5mg/kg 8hourly x5/7
*Haematinics for treatment of anaemia e.g. ferrous sulphate
syrup 2.5ml 8 hourly.
*Multivitamin-2.5ml to replenish vitamins stores.
Maintain high standards of hygiene, both personal
&environmental to prevent infection &promote comfort.
Emotionally support the parents all through and encourage
the mother to participate in the care as condition allows.
Finally nurse on the cot as condition improves greatly .Then
prepare mother for home care and share on:
Nutrition & hygiene.
Emphasis on hospital delivery in future. The facility should
have physical facilities &personel for jaundice management.
Follow up schedule –paediatric clinic ,MCH clinic &Home
visit services as appropriate.
 Prognosis
Good- early diagnosis and proper
management
Poor – If kernicterus have already
occurred before proper
management
Complication
kernicterus(encephalopathy);this is
an irreversible brain damage due
to deposition(accumulation) of
high levels of unconjugated
bilirubin at the basal ganglia(basal
nuclei of the brain.
 Severe anaemia due to excessive
haemolysis leading to congestive
Hepatospleenomegally; due to the extra tasks each these
structures is call upon to perform.
Mental retardation; its noted as growth and development
progresses and it means that the breakthrough of
unconjugated bilirubin to the basal ganglia was mild to
moderate, so, learning difficulties of varying degree is
experienced
Specific neurological defects such as, cerebral palpsy,
epilepsy, parasthesia, athetosis or physical defect like
deafness.
Shock- if not enough blood is replaced
Summary on causes of haemolytic jaundice
 Rhesus D compatibility.
 Abo incompatibly.
* These 2 are the commonest.
3. Haemoglobinopathies . Refers to sickle cell disease
and thalasaemia.
* Rarely causes jaundice during neonatal stage due to
presence of fetal haemoglobin.
4. Enzyme deficiency in terms of
* Glucose 6-phosphate dehydrogenase g6pd hence weak
cell membrane
* Spherocytosis ;RBC shape is round instead of concave.
Polycythermia ; because of either severe intrauterine
haemolysis or uncontrolled maternal diabetic
condition.

END
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