neonatal jaundice power point presentation

1. Neonatal Jaundice
by Rose W.

2. Outline
• Definition
• Classification
• Causes
• Investigations
• Management

3. Definition
• It’s yellowish discolouration of the skin, sclera
and mucous membranes, due to elevated serum
and tissue bilirubin (hyperbilirubinaemia) levels
from excessive haemolysis.
• Serum billirubin is > 7mg/dl.
• A value > 15mg/dl is considered severe.
• About 80% of term newborn and most preterm
newborns develop clinical jaundice.

4. Neonatal jaundice is either:
1. Physiological
2. Pathological

5. Cont..
 Physiological jaundice- appears about 48
hours after birth and usually settles within 10-
12 days.
-It never appears before 24 hours of life.
 Pathological jaundice- appears within 24
hours of birth, and is characterized by a rapid
rise in serum bilirubin.

6. Causes of Physiological jaundice
1. Increased red cells breakdown, because of the
high number of fetal hemoglobin which has
shorter life span.
2. Decreased albumin-binding capacity, due to
lower albumin concentration and
competition for albumin binding sites.
3. Enzymes deficiency particularly lower levels of
uridine diphosphoglucuronyl transferase
(UDP-Gt or glucuronyl transferase) within the
first 24 hours. Normal levels attained
between 6-14 weeks.
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7. 4. Increased enterohepatic reabsorption due to lack
of normal enteric bacteria to further break
down conjugated bilirubin into urobilinogen
for excretion in faeces or urine.
- Decreased bowel movement, in which high
levels of beta-glucuronidase enzyme
hydrolyses conjugated bilirubin into
unconjugated.

8. Pathological Jaundice
Causes
Results from interferences in bilirubin;
i) Production
ii) Transport
iii) Conjugation
iv) Excretion

9. 1. Production
Increased production of bilirubin levels
factors are:
• Blood group and rhesus incompatibility.
Including ABO incompatibility.
• Extravasated blood following traumatic
deliveries, accompanied large caput,
cephalhaematoma or severe subaponeurotic
hemorrhage.

10. • 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.

11. 2. Transport
 Interference with binding of bilirubin to
albumin for transportation.
Factors that lower blood albumin levels or
decrease albumin binding capacity include:
• Hypothermia , acidosis & hypoxia.
• Drugs e.g. aspirin, sulphonamides, ampicillin
among others competes with bilirubin for
albumin binding sites.

12. 3. Conjugation
Interferences include:
Immaturity of the neonate’s enzyme system
interferes with bilirubin conjugation in the liver.
Other factors include:-
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.

13. Cont..
• Metabolic and endocrine disorders e.g..
hypothyroidism and galactoseamia which affects the
glucose levels hence inhibit conjugation process.

14. 4. Excretion
Interferences includes:
• Hepatic obstruction due to congenital
abnormalities like extra hepatic biliary atresia.
• Increased bile viscosity hence formation of a bile
plug thus obstruction of excretion.
• Excess of conjugated bilirubin following
idiopathic neonatal hepatitis among other
infections, such that the excretion process is
overwhelmed.
• Saturation of protein carriers required to excrete
conjugated bilirubin into the biliary system.

15. Classification Of Neonatal Jaundice
• 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 & onset is
after the 1st 24 hours after birth of the
neonate.

16. Incidence
• Term babies - Occurs only to a few and its
noted around the 3rd to the 4th day. Resolves
uneventfully by the 7th- 10 th 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.

17. - Poor excretion of bilirubin due to poor gut 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 it’s deposited in the extravascular fatty &
nerve tissues (skin and brain).
• Skin deposits of unconjugated/ fat soluble bilirubin
causes jaundice, while brain deposits can cause
bilirubin toxicity or kernicterus.

18. 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.

19. 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.

20. • 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.

21. Specific Management of Physiological Jaundice
Mild;
- Commonest outcome and care is basically
conservative.
• Neonate 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.

22. • 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
enquire.
• Psychologically support the parents to allay
anxiety.

23. 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.

24. 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.

26. 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 :

27. • 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.

28. Admit baby in the NBU through:-
History taking
• Parents blood group to asses for either ABO or
Rhesus incompatibility.
• History of 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.

29. 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.

30. • Prepare the relevant charts and place them
within reach.
• Lay the infant under phototherapy when
naked (put diaper only). 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.

32. • 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.

33. • 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.

35. Mode of action of phototherapy
• 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.

36. -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 .

37. • As improvement occurs ,prepare mother for
home care in terms of :
-Nutrition – Exclusive breast feeding for
6months.
-Contraindicated, then 2 hourly artificial feeds
and dilute correctly.
• Hygiene.
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38. • 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.

39. Types of phototherapy
1. Conventional systems:- Using the high
intensity light, commonly used in health
facilities.
2. Fibreoptic light system uses a special blanket
to deliver the high intensity light. Fortunately
this can be used at home.

40. Conclusion
• This type of jaundice rarely progress to severe
state.
• For preterm particularly those who also get
some form of sepsis or conditions, they may
have severe haemolysis.
- The exchange transfusion is recommended as
the main mode of management

41. Complications
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.

42. • Dehydration, hyperthermia and increased fluid
loss leading to dehydration fever.
• Retinal damage if shield is not maintained due
to high intensity light.
• Lethargy/ irritability, decreased eagerness to
feed, loose stools.

43. NB: Breast milk jaundice is rare and occurs to
exclusively breastfed 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 inhibit the conjugation process.

44. II. Pathological Jaundice / Haemolytic Jaundice
• Basically the haemolytic rate is higher leading
to overwhelming levels of unconjugated
birilubin, hence referred to as pathological
jaundice.
Causes
1. Rhesus D compatibility.
2. ABO incompatibly.
3. Haemoglobinopathies

45. 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.

46. 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.

47. Causes of Rh D Isoimmunisation
• 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

48. Pathophysiology of RhD incompatibility
• Rhesus positive means that antigen is
present in the RBC while Rh negative
indicates absence of antigen.
• Fetus inherit rhesus factor from both
parents.
• RhD incompatibility can occur when a
woman with Rh Negative blood type is
pregnant with a fetus with a Rh positive
blood type.

49.  The placenta usually acts as a barrier to fetal
blood entering the maternal circulation.
However, during pregnancy or birth,
fetalmaternal haemorrhge can occur (small
amounts of fetal Rh positive blood cross the
placenta and enter the circulation of the mother
with Rh negative blood).
 The woman’s immune system reacts by
producing anti-D antibodies that cause
sensitization.

50.  In subsequent pregnancies these maternal
antibodies can cross the placenta and destroy
fetal erythrocytes.
 This hemolytic disease of the fetus and
newborn caused by Rh isoimmunisation can
occur during the first pregnancy, but usually
sensitization during the first pregnancy or
birth leads to extensive destruction of fetal
red blood cells during subsequent
pregnancies.
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51. Determiners of specific outcome
These refers to factors that leads to
developing jaundice or baby is born already
jaundiced.
1. Birth order. The very first born is safe so long
as isoimmunisation has not occurred.
2. Actual status of the father’s rhesus factor.
3. Administration of anti-D immunoglobulin at a
dose of 500 IU intramuscularly within 72
hours of rhesus positive RBC entry to the
maternal circulation.

52. Mode of action of anti-D immunoglobin:
• 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.

55. Specific Management
Prenatally
• Routine screening of all clients for blood 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.

56. * 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.

57. 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.

58. Intrapartum ( During labour)
• As 2nd stage of labor 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

59. *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.

60. Postnatally
Baby: Routine examinations are performed as
usual.
• Active management depends on the clinical
status and laboratory results.
Mother: Facilities available;
• Kleihauser acid solution test is carried out
within the 1st 2 (two) hours of delivery to
detect fetal cells in the maternal circulation.

61. • The aim is to determine the actual dose of anti-
D to be administered.
• However standard dose of anti-D
immunoglobin is 500 IU stat within 72 hours.
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.

62. 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 features
• Pallor of slow onset.
• Slight jaundice at birth, because most of the
bilirubin has been excreted by mother’s body.
• Hepatospleenomegally.

63. Specific management
• Admit in the special care baby unit (NBU) &
inform the Doctor.
• 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.

64. 2. Icterus Gravis Neonatorum
Results from severe haemolysis prenatally, such
that the excretion of bilirubin through the mother
is inefficient .
Clinical features
• 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.

65. 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.

66. 3. Hydrops Fetalis
• Results from very severe haemolysis prenatally,
such that at birth features of congestive heart
failure (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.

67. 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.

68. Hydrops fetalis

69. 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.

70. 2. ABO Incompatibility
• 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.

71. • 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.

72. 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 treatment is exchange
transfusion.
• Specific features 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.

73. *Dull looking, high pitched cry, tremors/
twitching, opisthotonous and spasticity.
NB: Palliative care continues if neurotoxicity
features 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.

74. EXCHANGE TRANSFUSION

75. Description:
• 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.

76. 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 weight 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

77. Preparation
1)Baby
• Thoroughly explain to 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
hours before the procedure hence well
hydrated.
• Maintain a record of the baby’s vital signs.

78. 2) 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.

79. • 2% sodium bicarbonate (NAHCO3) for
treatment of metabolic acidosis.
• 10% dextrose to treat hypoglycemia 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.

80. • 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.

81. • 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.

82. N.B
• The specimens should be clearly labeled and
have request forms respectively
• Work out well before the procedure starts with
laboratory personnel to have the staff who will
handle the specimen for smoothing release of
results.
3. 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.

83. • 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.

84. • 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

85. 4. Personel
• Doctors-specialist, in terms of either a
pediatrician or neonatologist, not available,
then general physician
5. Assistant
• Qualified midwives to work closely with the
doctor
• Other 2 midwives

86. One midwife basically takes care of the baby
in terms of:-
• Observation-vital signs every 5-15 minutes
intervals. Record particularly the apical beat
accurately.
• Note appearance of abnormal colour e.g.
cyanosis/pallor.
• Signs of cerebral damage.
• Report promptly to the doctor
*Progressive tachycardia/bradycardia
*Respiratory distress.
*Tremosis/twitching at the angles mouth eyes.
*Cyanosis.

87. • 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.

88. Other nurse midwife
• 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 blood 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.

89. Documentation

90. Exchange transfusion items

91. 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
because 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.

92. • 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.

93. • 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/kg 12 hrly
& Gentamycin 2.5mg/kg 8hourly for 5 days
*Haematinics for treatment of anaemia e.g.
ferrous sulphate syrup 2.5ml 8 hourly.
*Multivitamin-2.5ml to replenish vitamins stores.

94. • 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.
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.

95. Prognosis of neonatal jaundice
• Good- early diagnosis and proper
management
• Poor – If kernicterus have already
occurred before proper
management
Complications
• 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.

96. • 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

97. Summary on causes of haemolytic jaundice
• Rhesus D compatibility.
• ABO incompatibly.
* These 2 are the commonest.
• Haemoglobinopathies . Refers to sickle cell
disease and thalasaemia.
* Rarely causes jaundice during neonatal stage
due to presence of fetal haemoglobin.

98. • 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.