NEONATAL JAUNDICE

  
NEONATAL
NEONATALJAUNDICE
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 .
• It occurs when abnormal amounts of fluid buildup in
two or more body areas of a fetus or newborn. It is a
symptom of underlying problems
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.
Hydrops fetalis
 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 cross 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 treat 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 of neonatal jaundice
• 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
cardiac failure.
• 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.

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