BABY AT RISK:

New Born Unit (NBU)

Koros E.K., BSc.N, UoN,

Lecturer, AIC Litein MTC
 Complications of the Neonate
 Preterm baby, Low Birth Weight (LBW), Small for
gestational age (SGA) and large for gestational age (LGA)
baby
 Asphyxia Neonatorum
 Respiratory Distress Syndrome
 Meconium Aspiration Syndrome
 Neonatal Jaundice
 Neonatal Sepsis
 Hypothermia Neonatorum
 Ophthalmia Neonatorum
 Birth Injuries
 Hemorrhagic Disease of the Newborn
 Content Outline
1. Introduction
 Admission Criteria into NBU
 Infection Control in the NBU
 First Examination of the Newborn Baby
 Characteristics of a Normal Neonate
2. Preterm Baby
3. Small for Gestational Age (SGA)
4. Asphyxia Neonatorum
5. Respiratory Distress Syndrome (RDS)
6. Hypoglycemia
7. Neonatal Hypothermia
8. Ophthalmia Neonatorum
9. Neonatal Jaundice
10. Haemorrhagic Disease of the Newborn (HDN)
11. Birth Injuries
12. Hydrocephalus
REFERENCES
1. INTRODUCTION
ADMISSION CRITERIA INTO THE NEWBORN UNIT
The new born unit does not only admit babies at risk but also offers
accommodation to normal neonates due to unstable condition or death of
the mother.
Reasons for admitting a baby into the nursery include the following:
 Pre-maturity
 Asphyxia neonatorum
 Haemorrhagic disease of the new born
 Ophalmia neonatorum
 Birth injuries
 Congenital abnormalities e.g hydrocephalus
 Respiratory distress syndrome
 Infants of diabetic mothers(risk of hypoglycaemia)
 Maternal death
 Unstable maternal condition
INFECTION CONTROL IN NEW BORN UNIT
Due to low immunity of the babies in the NBU,
infection control is critical to protect the babies
from infection during their stay in the unit. This is
necessitates high infection control measures within
the unit.
The following are some ways of ensuring infection
control in the nursery.
 Keep the unit clean, free from dust. The windows should
remain closed at all times to prevent flowing in of dusty
air.
 Daily dump dusting and cleaning of the incubator and
cots
 Isolation of infected babies for barrier nursing.
 Restriction of visitors to ensure adequate control of human traffic
into the nursery. Visitors should see the babies through the window
glass.
 Washing hand before and after handling the baby for any procedure.
 Strictly observing aseptic technique while performing procedures.
 Feeding utensils should be rinsed, decontaminated, cleaned
thoroughly in soapy water and kept in presept till the next feed.
 Staff working in isolation room should not move into other
nurseries
 Cleaning of incubators upon discharge or death of a baby, before the
next baby is put.
 Mothers changing clothes whenever they come to feed the babies
 Health educating the mothers on the importance of personal hygiene
and care of the baby.
 FIRST EXAMINATION OF THE BABY
This is a routine procedure done after third stage of labour in
labour ward but is also done in the nursery as part of admission
procedure.
The main aims of first exam are;
1. To rule out congenital abnormalities
2. To rule out birth injuries
3. To assess maturity of the baby
Head
Measure the head circumference (average is 35 cm)
Check for the moulding of the foetal skull
Width of the fontanelles and sutures; bulging of fontanelles and
wide sutures may indicate hydrocephalus
Depression on the skull may imply a fracture
Injuries e.g. caput succadenium and cephalohaematoma
Eyes
Absence of eyebrows
Conjunctival haemorrhage / bleeding
Any discharge and squint

Nose
Check for any deformities e.g. well formed septum
Bleeding from the nose
Check for nasal flaring which is a sign of respiratory
distress
Check for blocked nostrils
Mouth
Bleeding from the mouth
Check for tongue tie
Abnormalities e.g. cleft palate or cleft lip
Frothing of the mouth

Ears
Bleeding from the ears
Leakage of CSF through the ears (otorrhoea)
Shape of the lobes to rule out malformations
Extra lobe of the ears
Neck
Check out for abnormalities e.g. congenital goiter
Check for meningocele

Chest
Shape of the chest for symmetry
Chest movement during respiration
Take apex beat (at level of 5th ICS, LMCL).
 Check breast for swelling and discharge
Abdomen
Check for skin colour and presence of rashes
Check whether the cord is well ligated
Bleeding from the umbilical cord
Abdominal abnormalities e.g. hernia

Genitalia
For males check for the testis to rule out undescended
testis
Female check for vaginal discharge, labia should be well
formed; check size of a clitoris
Hip joint
Rule out congenital hip dislocation

Limbs
Check if arms and hands are moving freely
Rule out dislocation, fractures and Erb’s paralysis
Check for equality of the arms and to rule out
abnormalities
Fingers for webbed and extra digits
Legs for equality, abnormalities and movement
Rule out talipes and club foot
Back
Abnormalities of the back e.g. spina bifida,
myelomeningocele
Check for skin colour and septic spots

Anus
While taking rectal temperature, check for imperforate
anus
Bruises on the skin or rashes
Check for the following reflexes:
Sucking reflexes – full term infant sucks the small finger
Moro reflex – tested by gently lifting the baby up by its
fingers from a flat surface and suddenly releasing it. It
will respond by spreading its hands then move them
together as though hugging.
Rooting reflex – the baby turns in search of the nipple
Grasping reflex – it will grasp your finger if you put it in
its palm.
Stepping reflex – when held on a flat surface in standing
position, it makes stepping movement.
 NORMAL NEONATE
This refers to a baby born at term or as near term
as possible after 37 weeks of gestation and has no
complications.
Upon birth the infant has to undergo
physiological changes in order to adapt to life
outside the uterus to have independent existence.
 PHYSIOLOGICAL CHANGES AT BIRTH
1. Respiration occurs due to:
 Low oxygen and high carbon- dioxide stimulates
respiratory center and respiration begins
 Compression of the chest wall during second stage
creates a vacuum and aid respiration
 External stimuli e.g. handling the baby, cold extra
uterine environment makes the baby gasp and respiration
starts
 Baby is encouraged to cry initially by flicking the sole of
the foot for it allows complete aeration of the lungs
 Presence of surfactant factor aids expansion of the lungs
(Lecithin : Sphingomyelin = 2 :1 and is an indicator of
lung maturity detectable on amniocentesis)
The normal respiration rate at birth is 40-50/min
Irregular breathing may be due to the following
factors:
i. Prematurity (inadequate surfactant factor)
ii. Depression of the respiratory centre by drugs e.g.
pethidine or strong uterine contractions
iii. Excessive carbon dioxide (hyperpnoea)
iv. Lack of oxygen (hypoxia)
2. Circulatory system
 Extra-uterine circulation is established and the baby is
able to divert deoxygenated blood to the lung for de-
oxygenation. This accounts for the pink colour of an
infant.
 In utero the Hb is high 18-20g/dl and high RBC to
transport sufficient oxygen to the foetus. After birth the
Hb drops to 14g/dl and some of the RBC are broken
down by the liver cells to bilirubin and may lead to
physiological jaundice.
 Normal heart rate in utero is 120 -160 beats/minute but
upon birth it drops to 100 -120 beats /min
3. Temperature regulation
 Temperature in utero is 38oC but the baby’s rectal
temperature is 37oC. The temperature drops due to
evaporation, conduction, convection and radiation.

 Temperature is not adequately regulated due to low

metabolic rate and insufficient heat regulating center in the
hypothalamus. They are at risk of overheating as well as
chilling.
 They have thin subcutaneous layer which provides poor
insulation and heat is lost. They have brown adipose tissue
to mobilize heat resources.
4. Digestive system
 Sucking and swallowing reflexes are present and they
feed on colostrums and pass meconium (initially green
then turns yellow)
 They open bowels 3-4 times a day.
5. Liver
 Stars functioning in utero although negligible.
 Its function remains depressed for a few days yet it has
to handle excess Hb thus there is accumulation of
bilirubin leading to physiological jaundice.
6. Urinary system
 A kidney start functioning in utero and the foetus passes
urine but has no ability to concentrate urine thus excretes
chlorides and phosphates.
 The baby should pass urine within the first 48 hours after
birth.
7. Weight
 Average birth weight is 2.5 -3.5 kg but is affected by factors
such as period of gestation, placental function, nutritional
status of the mother, size of the parents, type of pregnancy
i.e. single or multiple and sex of the baby.
 In the first three days the baby looses 1/10 of its weight
(physiological weight loss) due to limited intake, loss of
meconium and loss of tissue fluid. The weight is gained
within 7-10 days then it gains 250-500g weekly.
 CHARACTERISTIC OF NORMAL NEONATE 
Weight is 2.5 -3.5 kg.
Length from vertex to heel is 45-52 cm
Head circumference is 35 cm and increases by 1-2 cm during the
first month
Fontanelles and sutures are patent. Anterior fontanel closes at 18 -24
months while the posterior closes at 6-8 weeks.
Skin is covered by vernix caseosa, a secretion of the sebaceous
gland that helps in heat retention and acts as a lubricant during
delivery.
Umbilical cord shrivels by necrosis and falls off in 7 days. The
remaining part forms abdominal ligaments. Hernia may develop but
usually disappears spontaneously.
Reflexes are fully developed.
Senses are developing.
 2. PRE TERM BABY
This refers to a baby born before 37 complete weeks of
pregnancy.
Some of them may have growth retardation and
therefore be small while others may be excessively
large for gestational age (macrosomia)
Low birth weight baby is one with less than 2500g

Categories of Low Birth Weights;

 Low birth weight < 2500g
 Very low birth weight < 1500g
 Extremely low birth weight < 1000g
 Predisposing factors to Prematurity
I. Maternal factors – maternal age e.g. Primigravida below
17 years or above 35 years; Maternal disease in
pregnancy such as anaemia, hypertension, pre-
eclampsia.
II. Foetal factors – congenital abnormalities; multiple
pregnancy and polyhydramnios due to over distension of
the uterus; rhesus incompatibility interfering with foetal
viability
III. Placental factors – APH due to placenta praevia and
placenta abruption
IV. Social factors – strenuous exercises, excessive drinking
of alcohol and smoking, previous history of miscarriage,
physiological stress.
 Clinical Features 
 Small stature with low birth weighs less than 2500g
 Thin and sparsely distributed hair on the head.
 Skin is reddish with plenty of lanugo
 Widely open sutures
 Eyes are closed most of the time
 Pinnae of the ears are soft and fold easily on pressure
and slow to uncoil
 Narrow sinuses and the nose a bit flat
 Swallowing and sucking reflexes absent or very weak
 Weak cry and there are no tears
 Chest is small, soft with underdeveloped breast tissue
Clinical Features Cont’…
 Poor muscle tone and the baby lies inactive most of the
time
 In females, labia majora are widely separated and labia
minora is protruding in between
 In males, scrotal muscles are smooth and testis are
undescended
 Palmer and planter creases are absent
 Grasp reflexes are absent
 Physiology of the Preterm Baby
1. Immunity is low due to:
 Low gamma globulins responsible for immunity.
 Delicate skin that is vulnerable to injuries and infection
 Lack of passive immunity which usually develops around
38 weeks gestation
2. Blood system
 Has poor peripheral circulation with high tendency to
hemorrhage because of weak vascular walls.
 Prone to hemorrhage due to lack of clotting factors (vitamin
K is administered to promote clotting)
 Unable to store iron hence at risk of iron deficiency anemia.
 They have very few blood cells and may develop non
pitting anemia
3. Weight;
 Initially they lose up to 10% of their birth weight and
start gaining and reach birth weight 2-3 weeks post
delivery.
4. Temperature regulation is poor due to:
 Immature heat regulatory centre
 Limited food intake and low metabolic rate
 Inability to shiver and generate heat
 Excessive heat loss due to little or no subcutaneous fat.
The brown fat is usually in baby’s body by 36 weeks
gestation.
 
5. Respiratory system
 Under developed respiratory centre leading to difficulty in
initiation of respiration.
 Frequent apnoeic attacks with irregular respiration.
 Abdominal movements more than chest movements.
6. Renal system
 Immature kidneys are unable to concentrate urine hence they
excrete chlorides and phosphates.
7. Digestive system
 Absence of swallowing and sucking reflexes lead to poor feeding
 Regurgitation after feeds due to underdeveloped cardiac
sphincter
8. Nervous system
 All regulatory centres are under developed.
 NURSING MANAGEMENT
OF PRETERM BABY
Delivery of a preterm baby should be conducted in a
warm room and subsequently nursed in a preterm
incubator.
Temperatures of the incubator should be maintained
within normal range of about 36 – 37oC
Perform first examination of the baby to assess
maturity.
Fix NG tube and the baby with breast milk and
substitute only where breast milk is not available.
Feed the baby using the oral feeding regime as
follows:
 Baby is given 60 - 65 mls per kg of body weight in 24
hrs in 8 divided doses e.g. 2.5 kg baby will have 2.5 x
60/8 =18.99 mls per feeding thus should be fed 3
hourly.
 If the baby tolerates, the feed can be increased
 If the baby can’t tolerate the oral feeds, give IV fluids
e.g. 10% dextrose
 Introduce cup and spoon feeding gradually as the baby
gains weight
 Aspirate the gastric content to rule out indigestion.
Close observation to include:
 Vital signs Temp, Pulse, Resp.
 Respiratory rhythm to note apnoeic attack
 Umbilical stump for signs of infection
 Vomiting or retaining food
 General activity and emotional status
Provide care of IV line i.e. securing, cleaning and
dressing.
Give nutritional supplements e.g. iron, folic acids,
vitamin from the second week.
Administer broad spectrum antibiotic
prophylactically for prevention of infection
Take weight on alternate days to monitor the
progress.
Discharge the baby at 2000 – 2500g
Give BCG vaccine on discharge or advice the
mother to go for it.
Advice mother on family planning so that she
gets another baby by choice and not by chance
i.e. when stress has reduced.
 Complications of Prematurity
 Hypothermia neonatorum
 Haemorrhagic disease of the newborn
 Respiratory distress syndrome
 Retrolental fibroplasias
 Failure to thrive
 Jaundice
 Infections
 Anaemia
 Rickets
 3. SMALL FOR GESTATIONAL AGE (SGA)
This term refers to a baby whose birth weight is
below 10th percentile of his gestational age;
commonly referred to as low birth weight but this
includes preterm babies.
SGA babies are susceptible to various problems
including:
 Congenital abnormalities
 Foetal hypoxia that may lead to intrapartal death
 Birth asphyxia due to inadequate perfusion, meconium
aspiration leading to airway obstruction.
 Hypothermia due to little subcutaneous tissues
 Apnoeic attacks
 Hypoglycemia
 Signs and Symptoms of SGA
 Mostly they are born after 37 weeks gestation.
 Pale, dry loose skin with wrinkles and have little or no lanugo
 Subcutaneous fat is minimal
 Shows features of retarded growth
 The abdomen appears sunken
 Sutures and fontanel appear normal
 Eyes are alert and has mature facial expression
 Skull bones are hard and allow little mobility
 Have strong cry
 Umbilical cord is thin
 Swallowing and sucking reflexes are present so they feed well
 Normal muscle tone are active
 NURSING MANAGEMENT of SGA Babies
The baby is predisposed to the risks similar to those of
preterm baby thus the management principles are the
same.
Management should start in labour by closely
monitoring foetal condition for signs of foetal distress.
In case of foetal distress in the first stage, administer
oxygen to the mother and start IV drip of 10% dextrose
as you prepare the mother for emergency caesarian
section. If in second stage, the delivery is hastened by
giving generous episiotomy.
Since the baby is prone to hypoglycaemia, it should be
stared on breastfeeding as soon as possible.
Gastric lavage should be done with warm dextrose
before breastfeeding.
Substitutes are given if there is no breast milk. The
feed is calculated at 90 mls/kg of body weight in
24 hrs in 8 divided doses i.e. 3 hourly feeding.
Closely observe vital signs; TPR and signs of
infection.
The baby should be nursed in a warm environment
to prevent hypothermia although it has temperature
regulating mechanism.
Closely monitor blood sugar to rule out
hypoglycemia.
Weigh the baby on alternate days to monitor the
progress. Usually weight loss is minimal and it
gains weight more rapidly and steadily than
preterm.
Teach the mother how to take care of the delicate
skin that may be dry, cracked or peeling
COMPLICATIONS of SGA
 Hypoglycaemia
 Respiratory distress syndrome
 Aspiration pneumonia
 Brain damage
ANY QUESTIONS SO FAR?
 4. ASPHYXIA NEONATORUM
This is a term which refers to a condition in which
the baby fails to breath at birth.
Types of Asphyxia
The degree of asphyxia is determined by APGAR
score in which the following features are observed
and score 0-2;
 Appearance (colour of the body)
 Pulse (heart rate)
 Grimace (response to stimuli)
 Activity (muscle tone)
 Respiration /respiratory effort
A score between 8-10 does not show asphyxia.
There are three types of asphyxia namely:
1. Mild asphyxia – Apgar score is 6-7. It
requires clearing of the airway and application
of external stimuli to in initiate breathing
2. Moderate asphyxia – Apgar score is 4-5. It
requires resuscitation, administration of
oxygen and drugs to initiate breathing.
3. Severe asphyxia – Apgar score is 0-3. It
requires intensive resuscitative measures and
intubation to survive.
 Predisposing Factors to Asphyxia Neonatorum
Any condition causing foetal distress e.g.
 cord prolapse,
 prolonged labour,
 APH,
 intrauterine hypoxia due to placental insufficiency,
 post maturity,
 placenta abruption.
 anaemia,
 pre-eclampsia
Pre-maturity due to under development of the respiratory centre.
Blockage of the airway by mucus or liquor amnii at birth.
Birth injuries e.g. intracranial injury
Severe maternal disease in pregnancy e.g. sickle cell anaemia,
cardiac disease
Depression of respiratory center due to drugs e.g. GA and narcotics
 Signs and Symptoms
a) Mild and Moderate Asphyxia
 Apex beat (pulse rate) 100/min or less
 Skin colour is pink with blue extremities
 Response to stimuli may be present
 Cry may be weak or strong
 Makes effort to breath and may gasp with
irregular respiration
b) Severe Asphyxia
 No attempt to breath and may gasp periodically
 Baby does not cry
 Entire body skin is blue i.e. cyanosed-central.
 No response to stimuli
 Pulse rate very low or absent
 Poor muscle tone
 NURSING MANAGEMENT
Clear the airway as soon as possible.
Nurse the baby in an incubator for at least 48 hrs to
keep it warm at body temperature.
Resuscitation may be needed to promote ventilation
and ensure effective circulation to prevent acidosis,
hypoglycaemia and intracranial hemorrhage
Do suctioning whenever necessary
Closely observe the baby for skin colour, TPR.
Administer oxygen by mask, ambu bag or nasal
catheter whenever there is an apnoeic attack
Give IV fluids for rehydration.
Aspirate mucus to unblock the airway or may
intubate the baby.
Give fluids with electrolytes to maintain fluid –
electrolyte balance.
If the mother was given narcotics during labour,
administer its antidote naloxone thro the umbilical
vein.
Give anticonvulsants to control convulsions if present
Administer the following drugs:
 Sodium bi-carbonate 1-2 mls to combat acidosis.
 Vitamin K 0.5 -1 mg i.m to prevent haemorrhagic disorders.
 Aminophylline (with caution) to improve respiration.
 Calcium gluconate to strengthen heart muscles.
Maintain accurate input output chart to prevent
over hydration and under hydration
When the baby is stable pass NG tube and start
feeding.
Observe aseptic technique to prevent cross
infection.
 Administer broad spectrum antibiotic
prophylactically.
 Prevention of Asphyxia 
Proper screening of mothers to detect those mothers at
risk and advice on hospital delivery for proper
management.
Pelvic assessment should be done at 36 weeks gestation to
rule out pelvic inadequacy e.g. CPD.
Proper management of maternal diseases in pregnancy.
Drugs that depress respiratory center e.g. sedatives, GA
and narcotics should be avoided in late first stage.
Early detection and management of foetal distress.
Clearing baby’s airway as soon as the head is born.
Avoiding instrumental deliveries but rather prepare for
caeserian section.
 Complications of Asphyxia Neonatorum
 Brain damage
 Cardiac arrest
 Respiratory acidosis.
 Respiratory distress syndrome
 5. Respiratory Distress Syndrome (RDS)
This is a condition that occurs due to lack of or
inadequate surfactant in the lung tissue.
Mature lungs have adequate surfactant factor that
lower the surface tension in the alveoli, stabilizes the
alveoli and prevents them from adhering together and
collapse. This leads to breathing with ease. Surfactant
is produced slowly from 20 weeks gestation and
reaches a surge at 30-34 weeks gestation and another
surge at onset of labour.
The premature infant lack this function thus the alveoli
walls pressure rise as s/he breaths out and alveoli
collapse leading to severe difficulty in breathing.
NB: Other names for RDS are:
 Hyaline membrane disease
 Pulmonary syndrome of the newborn
 Developmental respiratory distress
RDS is a disease of prematurity and self limiting
with recovery phase or death.
 Predisposing Factors to RDS
RDS may be a complication of asphyxia and
develops within 4hrs of birth
Prematurity due to inadequate surfactant factor
Prenatal hypoxia e.g due to APH which reduces
surfactant synthesis
Perinatal hypoxia
Trauma to CNS due to difficult delivery or
precipitate labour
Profound hypothermia – leads to injury of cells
that produces surfactant
Congenital heart disease
 Clinical Features of RDS
Difficulty in breathing - dyspnoea
Flaring of the alae nasi (ala of the nose)
Tachypnoea with respiration of above 60/min
Hypothermia
Generalized cyanosis
Costal and sternal retraction
Grunting expiration (prevent atelectasis)
Reduced or increased heart rate
Chest X-ray shows collapsed alveoli
The baby has poor muscle tone and is motionless
Poor digestion due to diminished bowel movement
Resolves or death occurs within 3-5 days
 Nursing Management of RDS
Management is symptomatic until the disease resolves.
If RDS is anticipated, inform the pediatrician to
resuscitate the baby.
Nurse the baby in an incubator to prevent hypothermia
by controlling the body temperature.
Administer oxygen or do artificial ventilation to
prevent hypoxia.
Closely monitor the blood PH to prevent acidosis and
support pulmonary circulation because high carbon
dioxide level leads to constriction of pulmonary
arterioles leading to poor pulmonary blood flow.
In case there is acidosis, Sodium Bicarbonate is
added to 10 % dextrose drip.
Keep the baby nil per oral till the distress
resolves.
Administer IV fluids eg.10% dextrose and add
Calcium Gluconate to strengthen heart muscles;
Sodium Bicarbonate to ensure fluid electrolyte
balance.
Check haematocrit (PCV) and if less than 40%
transfuse with blood.
Maintain the normal BP with volume expanders
e.g. n/saline.
Position the baby to provide greatest air
entry(prone position with extended head)
Suction and do postural drainage to remove
secretion and keep the airway patent.
Close observation to monitor the progress whether
improving or deteriorating i.e. the heart rate,
respiration, chest in- drawing, grunting respiration
and cyanosis.
When the condition resolves, introduce oral feeds.
In case the baby develops abdominal distention
due to ingestion, stop the oral feeds and start IV
fluids.
NB: Principles followed during care of babies with
respiratory problems are;
 observation,
 oxygenation,
 positioning,
 nutrition and
 hydration.
Prevention of RDS
Early detection and management of high risk
pregnancies to prevent premature delivery
Conditions such as diabetes mellitus should be
properly managed so that delivery can be
prolonged to 36 -38 weeks.
The mother is then given Dexamethasone 4mg tds
48 hrs before c/s to stimulate lung maturity.
Prevent prenatal hypoxia by ensuring there is no
intracranial injury at birth.
Effective resuscitation at birth of high-risk babies.
Assessment of gestational age and lungs maturity
through amniocentesis so that elective c/s or
delivery can be delayed if lungs are not mature
enough.
 Complications of RDS
Retrolental fibroplasia
Hypothermia
Hypoglycaemia
Patent ductus arteriosus
Abdominal distension
Hypocalcaemia
Intracranial haemorrhage
Infection
6. HYPOGLYCAEMIA
This is a metabolic disorder in which the blood
glucose level falls below 2.6 mmol/L.
At term, the baby’s glucose level is almost equal
to that of the mother but gradually drops within 3-
4 hrs after birth. This is why the baby has to be
fed within I hour of life.
The baby’s blood glucose rises steadily following
feeds to 2.8-4.5mmol/l in 6-12 hours
Term babies can maintain their energy
requirements as long as they are kept warm.
Hypoglycemia is common in infants of diabetic
mothers. Due to excess glucose, the fetus
produces more insulin which increases its body fat
and muscle mass leading to large babies
(macrosomia).
At birth, the glucose level falls rapidly while
insulin levels remain relatively high so the baby is
at risk of hypoglycemia. This is why such babies
are admitted into the NBU.
Prolonged hypoglycaemia can lead to mental
retardation, permanent neurological damage and
death due to respiratory and metabolic acidosis.
 Predisposing Factors to Hypoglycemia
Low birth weight
Prematurity
Birth injuries
Maternal diabetes mellitus
Asphyxia
Septicaemia
Respiratory distress syndrome
 Clinical Features of Hypoglycemia
Low blood glucose less than 2.6 mmol/L
Poor feeding
High pitched cry
Lethargy
Irritability
Hypotonic muscle activity
Hypothermia
Apnoea
Nursing Management of Hypoglycemia
Give 10% dextrose infusion until normal glucose
levels are achieved.
Encourage the mother to breastfeed the baby
Feed through NG tube or cup and spoon
expressed breast milk.
If the hypoglycemia is severe, put up 10%
dextrose infusion and give 65-85 mls/kg of body
weight in 24hrs.
Give a bolus dose of 25% dextrose 2mls/kg body
weight i.v slowly for 30 min.
Closely monitor the glucose levels 1 hourly until
the general condition is stable or normal levels
have been achieved.
Once the normal levels have been achieved, wean
off the dextrose and observe closely for changes in
the condition.
 Prevention of Hypoglycemia
Taking blood glucose levels at birth and
introducing glucose feeds e.g. dextrose or
breastfeeding within 1hr of life.
Prevent hypothermia.
Monitoring glucose level 2hrly for the first 6-8
hours.
Infants of diabetic mothers should be admitted
into NBU and blood glucose levels regularly
checked.
 Complications of Hypoglycemia
Hypothermia
Convulsions
Braindamage
Neonatal death as an outcome.
 
 7. NEONATAL HYPOTHERMIA
This is a condition in which the neonate’s body
temperature falls below 36oC.
The baby losses heat through radiation,
conduction, convection and evaporation.
Predisposing Factors
 Prematurity
 Asphyxia Neonatorum
 Maternal diabetes mellitus
 Respiratory Distress Syndrome
 Cold environment
 Clinical Features of Neonatal Hypothermia
Rectal temperatures is below 36oC
Baby feels cold on touch
Paleness of extremities and face
Very weak cry
Low respiration rate
Baby not eager to feed (poor feeding)
Nursing Management of Neonatal Hypothermia
Nurse the baby in a warm environment in a
resuscitaire or wrap it in warm clothings
Feed the baby with expressed breast milk via
NGT
Give the baby extra glucose e.g. dextrose
Closely observe the baby for signs of
hypoglycaemia and if present, give 10% dextrose
Check for and treat convulsions with
anticonvulsants
 Prevention of Neonatal Hypothermia
Delivery should be conducted in a room with
controlled temperature,
Put the baby on resuscitaire or in incubator to
compensate heat loss to the environment.
Baby should not be bathed within 1hr of life but
top-tailing can be done after one hour.
Encourage skin to skin contact (kangaroo
method) when carrying the baby.
 Complications of Neonatal Hypothermia
Convulsions
Hypoglycaemia
Brain damage
 8. OPTHALMIA NEONATORUM
This is a condition that occurs in neonates within
21 days of life and is characterized by purulent
discharge from the eyes.
It is common in infants of mothers who had
vaginal discharge e.g. Gonorrhoea during
pregnancy.
NB: Syphilis does not predispose an infant to
Opthalmia Neonatorum but it causes congenital
syphilis that is characterized by gross congenital
malformation.
 Causative Organisms of Ophthalmia
Neonatorum
Neisseria gonorrhoeae
Chlamydia trachomatis
Staphylococcus aureus
Escherichia coli
Haemophilus influenza
Streptococcus pneumoniae
Pseudomonas spp
Klebsiella
 Clinical Features
Eyes have sticky watery discharge
Eyes are slightly red
Oedematus eyelids
Yellow purulent discharge if the infection is by
Neisseria gonorrhoeae
Inflamed conjunctiva
 Nursing Management
All perinatal mothers presenting with vaginal
discharge suggestive of gonorrhoae should be
treated before delivery.
Correctly swab the baby’s eye at birth.
Instill 1% tetracycline ointment (TEO) to all
babies at birth prophylactically.
All infected babies should be isolated
Take eye swab for culture and sensitivity
Administer drugs such as;
 Gentamycin eye drops
 TEO but not systemic tetracycline
 Penicillin eye drops
 Kanamycin eye drops
Swab the eyes with warm saline 3 times a day
from inside outwards
Administer some broad–spectrum systemic
antibiotic but not tetracycline because it deposits in
bone leading to depressed bone growth.
Complications of Opthalmia Neonatorum
 Partial or permanent blindness
ANY QUESTIONS SO FAR ?
 9. NEONATAL JAUNDICE
This is condition in neonates characterized by
yellow discoloration of the skin, sclera and
mucous membrane.
It develops when there is an excessive bilirubin
level in the blood stream.
When there is increased rate of haemolysis of
RBC or decreased conjugation of bilirubin,
there are high amounts of free bilirubin in
circulation leading to jaundice.
 Bilirubin Metabolism
When RBC’s are broken down by haemolysis, they
produce haeme and globulin.
The haeme part produces bilirubin and iron.
Unconjugated (indirect) bilirubin is fat soluble hence
has to be converted to water soluble form
(conjugated/direct bilirubin) by process of
conjugation for it to be excreted.
Conjugation of bilirubin occurs in the liver and thus it
has to be transported to the liver by binding to
transport protein, albumin.
On arrival to the liver, bilirubin detaches itself from
the albumin.
Conjugation is done by glucoronyl transferase in which
bilirubin is added to glucoronic acid to become bilirubin
diglucoronide that is water soluble.
Excretion of the bilirubin is done through the biliary system
into the intestine. While in the intestine, it is converted to
stercobilinogen by the gut normal flora and excreted in
stool. Some of it is absorbed from the gut and becomes
urobilinogen which is excreted in urine.
If conjugation process is interfered with, there will be
accumulation of unconjugated bilirubin leading to
hyperbilirubinaemia and jaundice. This bilirubin may cross
the blood brain barrier (BBB) and cause brain damage, a
condition known as kernicterus that is characterized by
seizure, hyper-tonicity, lethargy, and stiff neck with hyper
extended head.
 Types of Jaundice
a) Physiological Jaundice
This type of jaundice affects both preterm and
term babies in the first few days of life. It is
apparent with the signs on the third day when the
unconjugated bilirubin levels in serum is 25-125
mmol/L.
In term babies, it never appears before 24 hrs
of life but it can be in preterms and the serum
levels never exceeds 200mmol/L.
It is also self limiting in term babies.
 Causes of Physiological Jaundice
Excessive haemolysis of RBCs greater than
conjugation rate.
Glucoronyl transferase enzyme deficiency
Increased enterohepatic reabsorption
Decreased albumin binding capacity thus less
bilirubin is transported to the liver for
conjugation.
 Nursing Management of Physiological Jaundice
Admit the baby into the NBU and assess the general
condition.
Start early and frequent breastfeeding for it provides
glucose to the liver cells and also encourages bowel
colonization with normal flora which is important in
formation of stercobilinogen for excretion in stool and also
leads to increased gut motility leading to faster excretion of
bilirubin.
Feeding also enhances enzyme production and conjugation.
Closely monitor serum bilirubin levels at 12 -24 hrs
interval.
If bilirubin levels takes time to clear, put the baby on
phototherapy.
 b) Pathological Jaundice
This type of jaundice appears within 24-48hrs of
life and is not self- limiting thus may persist for
long (14-21 days if untreated).
There is rapid rise in serum bilirubin.
It includes both obstructive and hemolytic
jaundice.
Causes of Pathological Jaundice
They include pathological disorders that increase
bilirubin production, reduces transportation to and
fro the liver or reduced rate of conjugation. These
are;
1. Increased haemolysis
 Rhesus and ABO incompatibility,
 G6PD enzyme deficiency,
 Bacterial septicaemia.
2. Non-haemolytic causes of increased
unconjugated bilirubin
 CNS hemorrhage,
 Cephalo-haematoma,
 Polycythaemia,
 Exaggerated entero-hepatic circulation of bilirubin
due to functional ileus.
3. Decreased rate of conjugation;
 Criggler Nagar syndrome,
 Gilbert’s syndrome
4. Hepatotoxic drugs
5. Billiary obstruction that prevents transport of
conjugated bilirubin to GIT for excretion
6. Reduced bilirubin binding sites to the albumin.
7. Malnutrition
8. Increased reconversion of conjugated to
unconjugated bilirubin if it stays in the GIT for
long.
 Nursing Management of Pathological Jaundice
Assess the baby to determine the degree of jaundice.
Do investigations on serum bilirubin levels and Hb.
Start the baby on phototherapy.
Order for blood exchange transfusion if necessary.

Complication of neonatal jaundice

Retinal damage due to light used in treatment
Anemia
Hyperthermia associated with phototherapy.
Hypocalcaemia
Kernicterus

NB: Read more on obstructive and haemolytic jaundice

 Treatment Modalities of Neonatal Jaundice
There are three main modalities namely;
I. Phototherapy
II. Blood exchange transfusion
III. Protoporphyrins
I. Phototherapy
Phototherapy prevents bilirubin levels from going
high enough to cross BBB and cause kernicterus
Mechanism of action
Blue florescent light at a given wave length is
absorbed by the unconjugated bilirubin in the
skin and superficial capillary and is converted into
conjugated bilirubin which is water soluble and
can be excreted in stool and urine.
 Indications for Phototherapy
Pre term with jaundice appearing after 48 hrs and
bilirubin levels are 260-265 mmol/L
Pre term with weight less than 1500g and
bilirubin levels are 85 -114 mmol/L
Pre term with weight more than 1500g and
bilirubin levels are 114-165 mmol/L
 Care of the baby on Phototherapy
Expose the whole body of the baby to increase surface
area exposed to light
Keep turning the baby 2hrly to expose all parts to the
fluorescent light.
Ensure the airway of the baby is patent by extending
the head.
Cover the eyes of the baby to prevent damage by direct
ray of lights.
When breastfeeding the eyes are unpadded to
encourage eye contact with the mother.
Provide intermittent phototherapy i.e. 6 hours on and 6
hours off but may be continuous.
Give phototherapy for 2-3days and assess the serum
bilirubin levels twice or three times a day
NB: Greatest reduction in bilirubin levels will be in the
first 24 hrs of phototherapy.
Observe the eyes for weeping or discharge.
If phototherapy is continuous, give extra fluids to prevent
dehydration and maintain accurate input output charts.
Change linen frequently because opening of bowels is
increased(loose stool)
Observe the feeding and sleeping behavior of the baby.
Observations e.g. temperature to rule out hyperthermia
and skin colour to monitor the progress.
Top tail the baby to maintain hygiene.
 Side effects of Phototherapy
Loose stool due to rapid intestinal transit
Dehydration
Hyperthermia
Visual deprivation
Poor feeding
Fragility
Lethargy
Irritability
Hypocalcaemia
 Nursing Diagnosis of children undergoing
Phototherapy
Deficient fluid volume
Imbalanced nutrition less than body requirements
Impaired skin integrity
Risk for injury
Ineffective thermoregulation
 II. Blood Exchange Transfusion
This is a treatment in which the baby’s blood is
gradually removed and replaced by donor’s blood.
It is used as a definitive treatment when bilirubin
concentrations are approaching toxic levels.
The baby has haemolytic disease or low Hb.
The blood exchange transfusion has the following
benefits;
 It helps in increasing the baby’s Hb
 Excessive bilirubin and unwanted antibodies are
washed from the baby’s circulation.
The donor’s blood used for the transfusion
should be Rhesus negative so that it does not alter
the baby’s blood group and to ensure that no
antigen is introduced into the baby’s circulation
that may lead to antibodies production.
It should also be fresh and ABO compatible.
 Indications for Blood Exchange
Transfusion
Infants with haemolytic disease.
Preterms with bilirubin levels of 300-400 mol/l
Babies whose birth weight was less than 1500g
and have bilirubin levels of 255mol/l
Term babies with bilirubin levels above 100 mol/l
at birth or later 400-500 mol/l
 Care of the baby Post Transfusion
Put the baby back to phototherapy to continue with it.
Closely observe the baby for bleeding from the
umbilical cord.
If the baby was on infusion, continue for some time.
Reassure the mother and involve her in the care of the
baby.
Complications of Blood Exchange Transfusion
Circulatorycollapse
Incompatibility reactions
Acquired infections e.g. HIV, Hepatitis B.
III. Protoporphyrins
These are haeme oxygenase inhibitors which are
administered to inhibit the breakdown of haeme
thus reduce bilirubin production.
They are usually used in combination with
phototherapy and/or blood exchange transfusion.
 10. HAEMORRHAGIC DISEASE OF THE
NEWBORN (HDN)
This refers to bleeding that occurs during the first
few days of life due to vitamin K deficiency.
Vitamin K is synthesized by the bowel normal
flora and its role is to convert clotting factors such
as prothombin, thrombokinase, thromboplastin.
To prevent HDN, all neonates are given Vitamin K
0.5mg - 1mg i.m at birth
 (Vit. K 0.5mg for Preterm babies and 1 mg for term
babies).
 Predisposing factors to HDN
Hereditary factors; clotting factor defect e.g.
haemophilia
Prematurity
Birth trauma
Treatment with antibiotics
Respiratory Distress Syndrome
Disseminated intravascular coagulopathy (DIC)
Birth asphyxia
Mothers who are on drug such as warfarin,
heparin and phenobarbital
 Clinical features of HDN
Continuous oozing of blood from the umbilical cord
There is spontaneous bleeding from various parts of
the body
Bleeding in the mucous membrane of GIT and may
present with maleana stool or haematemesis
Continuous bleeding from any punctured blood
vessel or injection site thus when looking for venous
access avoid puncturing femoral or jugular veins
which are the largest veins in the body
Haematuria or omphalorrhagia
 Nursing Management of HDN
Upon admission into NBU, administer vitamin K 0.5mg-
1mg I.M,
Preserve all linen soiled by blood for estimation of blood
loss
Administer vitamin K 1-2 mg to arrest bleeding
immediately
Observe vital signs TPR ¼ hrly
If bleeding is severe, transfuse fresh blood or frozen plasma
at 20mls/kg of body weight
Observe for signs of shock and if present transfuse with
packed cells and fresh whole blood at 75 -100mls/kg of
body weight if the baby is term
General management is like any other baby in the unit
 Complications of HDN
Anaemia
Hypovolaemic shock
Brain damage
 11. BIRTH INJURIES
Birth injuries refer to trauma that a foetus sustains
during birth. The structures commonly involved are
muscles, nerves, bones, visceral organs and skin.
Types of Birth Injuries 
1) Internal organ injuries – spleen, liver, adrenal glands
2) Nerve injury–mostly brachial plexus leading to Erb’s
palsy
3) Soft tissue injury-genitalia, eyes.
4) Intracranial injuries e.g. haemorrhages, skull fractures
5) Extracranial injuries e.g. cephalo-haematoma, caput
succedaneum.
 Predisposing factors to Birth Injuries
Prematurity
Large for dates babies
Cephalo pelvic disproportion
Malpresentation
Congenital malformation e.g. hydrocephalus
a) Caput Succadenium and Cephalohaematoma
Caput succadenium is an oedematous swelling due to
accumulation of serum fluid under the foetal scalp. It
results from pressure between the foetal skull and
pelvic bones during delivery that leads to reduced
venous blood and lymphatic drainage and part of the
serum escapes into the tissues. The swelling is self-
limiting and disappears within 36hours of life.
Cephalohaematoma is accumulation of blood
between the periosternum and the skull bone. It is
caused by friction between the foetal skull bones and
the pelvic bones e.g. in CPD
Caput succadenium Cephalohaematoma
Present at birth Appears after 12 hrs of life
Disappears within 36 hours May persist for weeks
Diffuse and pits on pressure Circumscribed; doesn’t pit
on pressure
May cross a suture line Never crosses a suture line
Double caput is unilateral Double cephalohaematoma is
bilateral
Tends to grow less with Tends to grow larger with
time time
b) Intracranial Injuries And Haemorrhage
This refer to the damage of structures within the
cerebral hemispheres of the brain.
Various structures may be injured leading to
different types of haemorrhage e.g.;
 Cerebral tissue–injury to cerebrum leading to cerebral
haemorrhage
 Cerebral hemisphere and basal ganglia–supra
tentorial haemorrhage
 Veins of gallen and tentorium–subarachnoid
haemorrhage
 Falx cerebri (fold of dura mater and tentorium
cerebelli)–subdural haemorrhage
 Predisposing Factors to Birth Injuries
Prematurity
Excessive moulding
Instrumental delivery
Hypoxia that leads to engorgement of blood
vessels
Precipitate labour
Prolonged labour
Large babies
 Clinical Features of Birth Injuries
Dyspnoea
Asphyxia
Rolling of the eyes
Pallor of the skin and mucous membranes
Bulging of the anterior fontanelle due to increased ICP
Shock due to circulatory collapse
Twitching of the facial muscles if facial nerve is affected
Cyanosis
Grunting respirations
High pitched cry
Rigidity of limbs
 General Management of Birth Injuries
Intrapartally, predisposing factors should be
diagnosed and managed early e.g. preterm labour,
malpresentation, prolonged labour.
Observe the baby closely for skin colour,
twitching, rolling of the eyes, convulsions
Keep the baby warm
Administer Vitamin K 0.5 -1 mg i.m for they are
predisposed to haemorrhage
Maintain 2 hrly turning of the baby
Provide intermittent oxygen therapy PRN
Give IV fluids e.g. 10% dextrose for the first 24
hours then introduce oral feeds if the condition
improves
Give symptomatic management
Have resuscitative equipment ready in case of an
emergency
Administer anticonvulsants e.g. Phenobarbital
prophylactically
 Complications of Birth Injuries
Musculoskeletal deformities
Brain damage
Respiratory distress
Hyperbilirubineamia (jaundice)
Hypoglycaemia
 12. HYDROCEPHALUS
This is a condition where there is accumulation of
CSF within the ventricles of the brain with
resultant increased ICP and enlargement of the
cerebral ventricles.
It can be detected prenatally by ultrasound and in
labour they present by breech, fontanelles and
sutures are very wide on VE
 Formation and flow of CSF
CSF is secreted by the choroid plexus into the
lateral ventricles. It then passes to the third
ventricle from where it flows to the fourth
ventricle through the aqueduct. From the fourth
ventricle, it flows through the median and lateral
foramina of the fourth ventricle into the
subarachnoid space. It is then absorbed into the
venous sinuses of dura matter through arachnoid
granulations.
Hydrocephalus occurs when there is increased
formation or decreased absorption of CSF.
 Causes of Hydrocephalus
Congenital Malformations
Infections e.g. meningitis
Cerebral trauma
Space occupying lesions
Intracranial haemorrhage
Haematomas
 Types of Hydrocephalus
Communicating Hydrocephalus – occurs when CSF
is inadequately absorbed into subarachnoid space due
to aqueductal stenosis or chiari malformation
(brainstem, cerebellum and the fourth ventricle are
displaced downwards into foramen magnum).
Non-communicating Hydrocephalus – occurs when
there is obstruction of CSF outflow from the fourth
ventricle due to atresia of the foramina
Post-inflammatory Hydrocephalus – occurs
secondary to meningeal inflammation or subarachnoid
haemorrhage which cause ventricular obstruction or
formation of fibrous tissue in subarachnoid space.
 Clinical Features of Hydrocephalus
Prominent forehead Headache
Bulging fontanelles High pitched cry
Distended scalp veins Lethargy
Setting sun eyes (downward Poor feeding
rotation) Irritability
Failure of muscle co- Papilloedema
ordination (ataxia) Seizures
Separated cranial sutures Vomiting
Increased head circumference
Alteration in consciousness
 Management of Hydrocephalus
a) Treatment;
Surgery to remove the lesion, mass, adhesion,
within CSF system
Creating a divert (shunt) from the ventricles to
another body compartment e.g. into the right
atrium of the heart via the superior vena cava (VA
shunt) or into peritoneum (VP shunt)
Diuretics e.g. acetazolamide and furosemide are
occasionally used to control the head
enlargement.
 Nursing Management
Take head circumference daily to know the progress
Palpate for cranial suture’s separation
Observe fontanels for bulging
Monitor neurological status to detect signs of
Increased ICP
Administer analgesics to relieve pain
Postoperatively, pay more attention to the shunt
Observe the operation site for bleeding and draining
Give the baby small frequent feeds for it has feeding
difficulty
Observe for swelling which may indicate
obstruction of the shunt
Monitor the vitals signs quarter hourly until the
baby stabilizes
Administer antibiotics prophylactically to combat
infection
Maintain fluid input output charts to avoid
overhydration
Reassure the mother and family
REFERENCES
Barbara F. Weller (2000) Bailliere’s Nurses
Dictionary, 23rd edition.
Myles Margaret Textbook for Midwifery
Odanga O. A, (2004). Baby at Risk. Covering
Conditions in the Newborn Unit, Nambale, Kenya.
Waugh A. and Grant A. (2001). Ross and Wilson
Anatomy and Physiology in health and illness, 12th
edition.
WHO (2000) Integrated Management of Pregnancy
and Child birth, guidelines for midwives and doctors.
MOPHS and MOMS (2012). National Guidelines for
Quality Obstetrics and Perinatal Care.
FURTHER READING/RESEARCH

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