CHAPTER ONE

INTRODUCTION
DEFINITION
High Risk Neonates are infants with certain medical conditions, diseases, illness or difficulties as a
result of maternal, placental, fetal and delivery conditions regardless of birth weight or gestational age. It
can also be defined as a newborn that requires more than the standard monitoring and care offered to a
healthy term newborn baby. Any baby exposed to any condition that makes the survival rate difficult or
put the baby survival in danger is seen as high risk neonate. These babies require special test, care,
treatment and continuous monitoring as a result of the difficulties they face.
A newborn who has a potentially life-threatening problem is in an emergency situation requiring
immediate diagnosis and management. Delay in identification of the problem or providing the correct
management may be fatal.

CLASSIFICATION OF HIGH-RISK NEONATE

Newborns are classified based on two main criteria; birth weight/size and gestational age. (Length of
stay in utero). An infant may be at risk even if he or she has reached an acceptable maturation age.
1. BASED ON WEIGHT / SIZE
• Low birth weight (LBW). Birth weight less than / below 2.5kg.
• Very low birth weight (VLBW) refers to newborns weighing less than 1.5 kg
• Extremely low birth weight (ELBW) refers to newborns weighing less than 1.0 kg
2. BASED ON GESTATIONAL AGE
• Preterm: Neonates born before the completion of the 37th week of gestation/pregnancy.
(Before 259 days counting from the first day of the woman’s last normal menstrual period).
• Term: Neonates born from 37th week of gestation but before or on completion of the 41st
week of gestation. (260-294 days).
Term neonates can be further classified under
a. Early term. Baby born between 37weeks,0days and 38weeks 6days
b. Full Term. Baby born between39weeks,0days and 40weeks ,6days
c. Late term. baby born between 41weeks,0days and 41weeks,6days
• Post term: Neonates born after 42 weeks of completed gestation or pregnancies extending
beyond 42 weeks of gestation. (295 days or more).
The underlisted neonates are classified based on their weight size as well as taking into
consideration the gestational age. (Weight and gestational age)
• Large for gestational age (LGA)/Heavy for date babies: weight above the 90th percentile for
gestational age thus above 4kg.
• Average / Appropriate for gestational age (AGA): weight is between the 10th and 90th
percentile for gestational age thus Between 2.5 Kg and 4kg. Newborns whose weight falls
within standard norms are categorized as appropriate for gestational age (A G A)
• Small for gestational age (SGA)/Light for date babies: weight is below the 10th percentile for
gestational age.

GENERAL FACTORS / CAUSES ASSOCIATED WITH HIGH-RISK NEONATE.

The following factors are associated with high-risk newborn;

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A. MATERNAL FACTORS
1. AGE AT DELIVERY
A). Women over the age of 40years are prone to chromosomal abnormalities, macrosomia, intrauterine
growth retardation (IUGR).
B). under 16 years of age are prone to intrauterine growth retardation (IUGR), prematurity.

2. PERSONAL FACTORS
A). Poverty (low socio-economic level of mother): prematurity, intrauterine growth retardation (IUGR),
neonatal infections
B). Smoking: Increased perinatal mortality, intrauterine growth retardation (IUGR)
C). Drug / alcohol use: intrauterine growth retardation (IUGR), fetal alcohol syndrome, withdrawal
syndrome, sudden infant death syndrome.
D). Poor diet: Mild intrauterine growth retardation (IUGR) to fetal demise in severe malnutrition.
E). Trauma (acute, chronic), leading to Abruptio placentae: prematurity.

3. MEDICAL CONDITION
A). Diabetes mellitus: stillbirth, macrosomia / birth injury, respiratory distress syndrome (RDS),
hypoglycemia, congenital anomalies.
B). Thyroid disease; Goiter, hypothyroidism, hyperthyroidism.
C). Renal disease: stillbirth, intrauterine growth retardation (IUGR), prematurity
D). Urinary tract infection: prematurity, neonatal infections.
E). Heart and /or lung disease; stillbirth, intrauterine growth retardation (IUGR), prematurity.
(f). Hypertension (chronic or pregnancy – related): stillbirth, intrauterine growth retardation (IUGR),
prematurity, and asphyxia
(g). Anemia; Stillbirth, intrauterine growth retardation (IUGR), hydrops fetalis, prematurity, asphyxia
(h). Isoimmunization (Red cell antigens); stillbirth, hydrops fetalis, erythroblastosis fetalis/jaundice

4. OBSTETRICAL HISTORY
(a) Past history of infant with prematurity, Jaundice, Respiratory Distress Syndrome (RDS) or anomalies
(b). Maternal medication: jaundice, congenital anomalies
(c). Bleeding in early pregnancy: stillbirth, prematurity.
(d). Bleeding in third trimester: Stillbirth
(e). Premature rupture of membranes; infection / sepsis
(f). Trauma. Prematurity

B. FOETAL FACTORS
(a). Multiple gestation: intrauterine growth retardation (IUGR), Twin – twin transfusion syndrome,
prematurity, birth trauma, asphyxia
(b). Macrosomia: Congenital anomalies, birth trauma, hypoglycemia.
(c). Abnormal fetal position / presentation; congenital anomalies
(d). Abnormality of fetal heart rate or rhythm, congestive heart failure, heart block, asphyxia.
(e). Decreased activity: Fetal demise, asphyxia
(f). Polyhydramnios: Anencephaly, other central nervous system (CNS) disorders, neuromuscular
disorder, problems with swallowing (example, esophageal atresia), diaphragmatic hernia, omphalocele,
gastroschisis, trisomy, tumors, hydrops fetalis, iso-immunization, cardiac failure, intrauterine infection.

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(g). Oligohydramnios: Fetal demise, intrauterine growth retardation (IUGR), deformations, asphyxia
post term delivery.

C. CONDITIONS OF LABOUR AND DELIVERY

• Preterm delivery; respiratory distress syndrome, other issues of preterm birth
• Post term delivery (occurring more than 2 weeks after term): stillbirth, asphyxia, meconium
aspiration
• Maternal fever: Neonatal Infection / sepsis
• Maternal hypotension: Stillbirth, asphyxia
• Precipitate labour: Birth trauma, intracranial hemorrhage (ICH), transient tachypnea.
• Prolonged labour: Stillbirth, asphyxia, birth trauma.
• Abnormal presentation. Birth trauma, asphyxia
• Meconium-stained amniotic fluid. Stillbirth, asphyxia meconium aspiration syndrome, persistent
pulmonary hypertension.
• Prolapsed cord. Stillbirth, asphyxia
• Obstetric analgesics and anesthesia; Respiratory depression, hypothermia.
• Large placenta, maternal diabetes; large infant, hypoglycaemia

LOW BIRTH WEIGHT INFANT (LBW)

Definition:
Infant born weighting less than 2.5 kg (2500g) regardless of the gestational age. A low-birth-weight
baby may be healthy or may have serious health problems. Most LBW infants are preterm while some
are term or post term but small for gestational age. They are LBW because of the following reasons
1. Babies whose rate of intrauterine growth was normal at the moment of birth; they are small
because labour began before the end of 37th gestational week. These are preterm babies and they
are appropriately grown for their gestational age.
2. Babies whose rate of intrauterine growth was slowed and who were delivered at or later than
term; these term or post term babies are under grown for gestational age. They are light/small for
date.
3. Babies who at birth are malnourished or appears to have lost weight in the later part of
pregnancy. This is Intra-Uterine Growth Retardation (IUGR).
LBW infants can be further sub-classified as follows;
• Very low birth weight (VLBW). These infants are less than 1.5kg (1500g)
• Extremely low birth weight (ELBW). These are infants less than 1 kg(1000g).

CAUSES OF LOW BIRTH WEIGHT

MATERNAL FACTORS:
(a). Malnutrition: this happens when fetus does not get the required nutrients from maternal blood as a
results of mother’s poor diet or nutrition.
(b). maternal infection: A rise in mothers temperature affects the liqour aminii making the liquor too
warm hence unconducive for the survival of the baby. Hence the baby may have low birth weight. Other
infections include: malaria, urinary tract infection.
(c). Stress (Physical / psychological)

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Stress is common during pregnancy but too much stress can make you uncomfortable, have headaches,
trouble sleeping, lose appetite. High levels of stress for a long time may cause health problems which
results in low birth weight.

(e). Addiction to drugs, alcohol and smoking. Drugs, alcohol, heroine, cocaine, marijuana, cigarette.
For example, nicotine may limit blood flow through the placenta and this slow the baby’s growth
leading to low birth weight.

PLACENTAL FACTORS
Medical conditions such as hypertension, diabetes mellitus and asthma can bring about placental
insufficiency. Conditions such as Antepartum hemorrhage (APH) being placenta Previa or placenta
abruption can also lead to placenta inadequacy resulting in low birth weight.
Abnormal cord insertion, infarcted areas, placenta thrombosis, these placenta conditions will affect
circulation to the foetus which becomes deficient with increasing age.

FOETAL FACTORS
• Intra uterine factors or infections such as fibroids rubella, toxoplasmosis can affect growth in the
utero.
• Genetic abnormality can lead to some babies being small or low birth weight.
• Multiple gestations.
• Fetal developmental or chromosomal abnormalities
• Polyhydraminous
• Rhesus incompatibility

PREVENTION OF LOW BIRTH WEIGHT

• Education on the importance of good diet during pregnancy as soon as mother misses her
menses.
• Education of mother on the importance of taking antimalarial drugs as well as maintaining
good personal and environmental hygiene.
• Conditions such as hypertension, diabetes, asthma should be detected early and treated at the
antenatal clinic.
• Treatment of maternal infection such as rubella to prevent low birth weight.
• Preconception care before pregnancy to rule out any condition that can lead to low birth
weight of baby before conception or commencement of pregnancy.

PRETERM / PRE-MATURE / PREMIE / PREEMIE BABIES

Definition:
Preterm neonate is one whose birth occurs before the end of the 37th week following onset of the last
menstrual period. Prematurity is sub categorized or classified based on the weeks of gestation. These
are,
1. Severe prematurity/extremely prematurity is described as birth less than 28 weeks.
2. Very preterm (28 to less than 32 weeks)
3. Moderate to late prematurity is birth at 32 to less than 37 weeks.
a. Early moderate preterm: 32 to under 34 weeks
b. Late moderate preterm: 34 to under 37 weeks

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 The risk factors increase as the size and gestational age decrease.
Preterm can also be classified based on the birth weight
 Low birth weight (LBW). These infants are less than 2.5kg (2500g)BY WHO
 Very low birth weight (VLBW). These infants are less than 1.5kg (1500g)
 Extremely low birth weight (ELBW). These are infants less than 1 kg(1000g).
CAUSES / ETIOLOGY OF PRETERM
About 40% of the causes of preterm are unknown. But the following predisposing factors are associated
with preterm.
A). Multiple gestation; Over distention of the uterus. In causes such as polyhydraminous and uterine
fibroids can also lead to over distension of the uterus and early contraction in preterm delivery.
B). Obstetric history such as uterine malformations, uterine trauma, placenta Previa, abruption
placentae, cervical incompetence, previous cervical surgery also contribute to prematurity.
C). Low socio-economic status: Family income, educational level, geographic area, social class and
occupation has significant impact on preterm delivery.
D). Maternal infections: Acute infections associated with high temperature. Example Urinary Tract
Infection, malaria, rubella infections.
E). Psychological factors like stress, hearing of unpleasant news leading to shock may cause the foetus
to be born prematurely.
F). Elective causes of preterm delivery in case like congenital abnormality, PIH (pregnancy induced
hypertension), placenta Previa may cause babies to be born preterm
G) Addition to drugs, alcohol and tobacco smoking also contribute to preterm delivery due to the
presence of nicotine which may limit blood flow to the placenta
H) Lack of prenatal care
I) Age of mother; mothers who are younger than 16 and older than 35 years
J) Past obstetrical history of preterm delivery also contributes to the reoccurrence of preterm delivery.
Other causes include
• Congenital abnormality of baby (foetal developmental or chromosomal abnormalities)
• Rhesus incompatibility
The causes of preterm delivery can also be grouped under spontaneous and elective causes.
Spontaneous causes
• 40% unkown
• Multiple gestation – the higher the multiple the greater the chance
• Hyperpyrexia as a result of viral or bacterial infection, often urinary tract infections
• Premature rapture of the membranes caused by maternal infection, especially chorioamnionitis.
Also polyhydramnios
• Maternal short stature, age (<18or >35 years) and parity.
• Maternal uterine malformation; often bicornuate or significant fibroids
• Poor obstetric history of preterm labour
• Cervical incompetence, history of cone biopsy.
• Maternal substance abuse, particularly alcohol and cigarette smoking
Elective causes
• Pregnancy-induced hypertension, pre-eclampsia, chronic hypertension
• Maternal disease; renal or heart
• Placenta plaevia, abruptio placenta
• Rhesus incompatibility
• Congenital abnormality of the baby

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 • IUGR
Sources: Sinha et al 2012; Smith 2012

DIAGNOSIS
• Gestational age
• By the clinical manifestation or characteristics.
• Blood tests to check for glucose, calcium levels and bilirubin levels.
• Blood gas analysis to check oxygen levels in blood
• Chest X-ray
• Continuous cardiorespiratory monitoring
CHARACTERISTICS OR CLINICAL MANIFESTATION OF PRETERM BABIES
SKIN
• Baby presents with thin, smooth, shiny skin which is sometimes red and wrinkled.
• Little or no subcutaneous fat/less body fat.
• Surface veins are visible with Plenty of lanugo hair covering the shoulders, back thighs,
forehead and ears.
• Fragile and easily injured.
• Soles of the feet are smooth.
• If baby is born before 34 weeks, there may be absence of palmer and plantar creases.
HEAD
• Small body size with a disproportionately large head or proportionate head size based on
gestation..
• Have or present with soft skull bones with widely separated fontanelles and sutures.
FACE. The face looks triangular in shape and worried.
NOSE
• Nose is flattened or bruised.
EARS
• Soft, flexible ear cartilage with flat pinnae of ears which easily fold upon itself, does not
recoil.
EYES
• The eyes bulge and the orbital ridge are prominent
• The eyes are always closed
Chin. The chin recedes easily.
EYE BROW
• Baby lacks eyebrow at birth.
CHEST
• The chest is small and narrow and appears underdeveloped, the chest wall is not firm.
• The ribs are visible.
• The breast nodule is very small only about 2mm as compared to 7mm in a normal baby.
ABDOMEN
• The abdomen is prominent because the liver and spleen are larger and abdominal muscle tone is
poor. This makes the baby to assume the supine position/lies on its back.

GENETALIA

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Males: presents with small scrotum, smooth without ridges or no rugae. The testes may not have usually
descended and the scrotum has no rugae. The term for undescended testes is known as cryptorchidism.
In the male, descent of the testes from the abdomen to the scrotum begins at 28 to 30 weeks gestation.

 At 34 weeks gestation, the testes are palpable in the inguinal canal and the scrotal skin begins to
thicken and develop rugae.

Female: The labia major is not fully developed and smaller in size making the clitoris enlarged and the
vestibule more prominent (exposed). At term, the labia minora and the clitoris are completely covered
by the labia majora.

BEHAVIOUR / ACTIVITY.
• There is poor muscle tone (hypotonic and sluggish body movements with poor activity
compared to full term infants).
• Have weak and feeble or faint cry
• They sleep so deep and it’s difficult waking them up.
• Have poor reflexes / some reflexes may be absent. Example sucking and gagging reflex are
often absent until about 32nd to 34 weeks. Moro reflex may also be absent or weak

SUMMARY
1. Weight is usually less than 2.5kg 10. Short and soft nail
2. Length is usually 45 to 47cm 11. Small genital and undescended testes in
3. Prominent fontanelles and wild sutures males
4. Small chest, large abdomen and cord is 12. In females the majora fails to cover the
freshy minora
5. Plenty of lanugo 13. Pinnae of the ear is flat, soft and no
6. Lack subcutaneous tissue curves
7. Plenty venous caseosa 14. Usually weak, lethargic
8. Extremities appear soft 15. Failure to thrive
9. No eye brow and protruding eye 16. Weak cry

NOTE. The General Appearance Varies According to The Degree of Intra Uterine Growth.

PROBLEMS OF PRETERM BABIES

Preterm babies have problems or difficulties related to them in extra uterine adaptation due to
immaturity of their organ system.

RESPIRATORY
Preterm infant may experience the following.
• Perinatal depression in the delivery room due to poor transition to breathing.
• Apnea due to immaturity in mechanisms controlling breathing.
• Respiratory distress syndrome

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TEMPERATURE REGULATION.
Preterm infants are mostly susceptible to hypothermia and hyperthermia due to lack of brown fat.
NUTRITIONAL
Have poor sucking and swallowing reflex leading to hypoglycaemia
HEMATOLOGIC
Have poor blood vessels or immature vessels hence prone to bleeding when injured.
METABOLIC
Problems especially in glucose and calcium metabolism
INFECTION
There is no immunoglobin present a birth and there is no active immunity especially in severe
prematurity.

MANAGEMENT OF PRETERM INFANT

The basic objective for managing preterm babies is support to enable them overcome their related
complications. It is appropriate to keep them in the hospital till they attain an appropriate gestation and
maintain weight of 2.5kg or above.
It should be noted that preterm infant’s survival depends on quality of health care given.

ANTENATAL / PRENATAL MANAGEMENT

Management of prematurity should begin at ANC
• The midwife should educate client on causes of prematurity in individual basis.
• Conditions that predispose predisposed premature births should be detected and referred for
prompt treatment.
• Social /psychological factors should be detected and treated as soon as possible.
• Educate mothers on the need to take in good or nutritious diets.
• Mothers with previous history of preterm labour should be encouraged to deliver at the
hospital.
• Mothers having premature contractions should be admitted on strict bed rest and observation.
• There should be administration of tocolytic drug such as salbutamol / ventolin 10mg given
either subcutaneously or intravenously when contractions ceases or oral ventolin 6 hourly
should be given and continued till the 37th week.
• Pregnant women with premature delivery prior to the 32nd week are administered
glucocorticoid which is a steroid that crossed the placenta barrier to stimulate the production
of surfactant

MANAGEMENT DURING DELIVERY

This is a very stressful moment for the women with anticipation of delivering a preterm baby hence
needs to be reassured and continuous encouragement given. Caution should be taken if administering
narcotic analgesics. For example, pethidine should be given in the latent phase of labour. Avoid heavy
sedation especially in the active stage of labour to prevent respiratory distress.
Delivery should be in an appropriate equipped and staffed hospital. Risks to the very premature or sick
preterm infant are greatly increased by delays in initiating necessary specialized care.
• Resuscitation and stabilization require the immediate availability of qualified personnel and
equipment. Resuscitation of the newborn at delivery should be in accordance with standard.

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 The midwife should prepare to receive an asphyxiated baby. All equipment for resuscitation
should be ready to give episiotomy because the cranial bones are soft and may lead to head
injury hence more room needed for delivery of baby’s head.
Care at Birth
i. As soon as the baby is born ensure that the air passages are cleared
ii. Quickly clamp and cut the cord
iii. Wrap the baby warmly and take him/her to the resuscitation table and continue to clear airway
iv. Oxygen is given where necessary about 1 litre per minute initially and gradually reduced
when condition improves to minimize the risk of retrolental fibroplasia (vasoconstriction of
the retinal capillaries)
v. Give injection vitamin K 0.5mg to check bleeding and improve blood clotting.
vi. Allow baby to rest and during this period minimize handling.
vii. Provide warmth adequately as heat regulatory centre is not well matured so that chilling is
prevented.
viii. If on the district and baby’s weight is less than 2.5kg, the midwife should refer the baby to the
hospital where baby may be nursed in an incubator if available.
ix. Covered or protected hot water bottles can be used to keep the baby warm in places where
there are no incubators or on the district before ready to refer.
• As soon as delivery is eminent, the midwife should be concerned / aim at initiating respiration
and maintenance of proper body temperature which is the immediate postnatal goal.
• Immediately the head is delivered suction oropharynx before nasopharynx.
• Dry baby off liquour and receive baby into a warm sheet
• Clamp and cut cord
• Assess first minute APGAR SCORE

POSTNATAL CARE / MANAGEMENT

Postnatal management aims at
• Maintenance of Respiration
• Temperature Regulation / maintenance / provision of warmth.
• Prevention of infection
• Feeding (nutrition) of baby
• Psychological support of mother during admission and before discharge.

MAINTENANCE OF RESPIRATION
• Position baby at the side so as to ensure drainage of mucus and prevent backflow of mucus
into the lungs as well as prevent mucus aspiration.
• Continually suction baby as the need arises, when necessary, administer oxygen through
ambubag or from the cylinder through mask. The normal oxygen can be given as 30 L/h or30-
40% or 1½ - 2L/minutes. If baby’s condition stabilizes, you can maintain O2 at 0.5 L/min at
every 8 – 12 hours. Excess administration of oxygen may lead to brain damage or result in
Retro-lental fibroplasia / retinopathy of predatory.
• Transfer baby to the resuscitation area and assess baby’s fifth (5th) minutes Apgar score
• Give or administer vitamin K to prevent bleeding and improve blood clotting.
• Procedure like weight taking, full length should be delayed until baby’s condition improves.

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MAINTENANCE OF BODY TEMPERATURE
Provision of warmth / Temperature regulation.
• Due to the immaturity of their heat regulating center or lack of brown fat to produce heat,
premature babies tend to lose heat easily,
• For this reason, the baby should be wipe off liquour and receive in a warm towel and where
baby is to be nursed should be reheated. The baby is nursed in a warm environment to
improve their survival at an environment temperature of 36-370CThis can be achieved by
placing baby near source of light (round bulb) at reasonable centimeters.
• Using hot water bottles; In the village, advise mother to smear baby’s body with shear butter /
palm kernel oil and baby well covered.
• If baby’s weight is 2.0kg or less incubator care is necessary to provide adequate warmth but
those with birth weight above 2.0 can be cared for in a warm cot with a room temperature of
37.
• The mother is made or advised to practice Kangaroo mother care to provide warmth and it
associated benefits explained to her.
• The nursing area or room should be well ventilated to prevent draught
• Baby hats and cloths should be worn to prevent heat loss and keep baby warm.

PREVENTION OF INFECTION
The midwife should employ aseptic technique in the care of the baby.
• Practicing of hand washing technique before and after handling of baby.
• Nurse baby in a separate cot
• One incubator /cot to each baby.
• Space one cot / incubator from another, spacing should be about 90cm.
• There should be daily cleaning of cot/incubator
• Limit the number of visitors
• Any care provider with upper respiratory tract infection should not be allowed to care for
these babies.
• Teach mother simple hand washing technique with soap and water before and after handling
baby
• Educate mothers to refrain from using their handkerchief in cleaning babies’ eyes
• Educate mother to desist from sucking the baby’s nose with their mouth.
• As soon as babies are discharged, decontaminate cot for next use.
• Advocate an individual bathing article.
• Cord dressing should be done aseptically.

PSYCHOLOGICAL SUPPORT OF THE MOTHER

A preterm baby’s mother goes through numerous psychological stresses such as
• Fear about baby’s condition and the ability to care for the baby.
• Disappointed with the small and skinny nature of her baby. May be upset to strange
surroundings and sophisticated gadgets used. It is therefore necessary to help mother
establish bond.
• Allow mothers who have been through such situation to share their experience and ideas.
• Keep photos of babies at birth who were born preterm to mothers to relieve fear and anxiety.
• Explain the equipment /gadgets used on the baby to mum.
• Make time for her to come out with her problems.

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 • Involve mother in the care of her baby.

FEEDING OF BABY
The main aim is to feed the baby to obtain or maintain an adequate growth weight before discharge.
Most preterm infants will need assistance with feeding and method of feeding depends on the weight
and condition of baby.
• The first feed should be given within 4 hours of delivery.
• If the baby’s condition is not critical put baby to breast that is infants weighing 2kg or more
with good sucking and swallowing reflexes can be given direct breast feeding and those who
are unable to suckle directly but can swallow may be fed with expressed breast milk in a cup
with spoon under supervision
• If condition does not permit breastfeeding IV 10% dextrose is set up.
• If baby is born before 32 weeks or if condition does not allow for breast feeding. Baby will
need to be fed through Nasogastric tube on regular basis.
• Keep detailed records of feeding and weigh baby every day.
DRUGS
Vitamin K, prophylaxis antibiotics and chloramphenicol eye drop
OBSERVATION
This is keen because babies’ condition can change anytime.
• Observe respiratory rate and pattern, Rate should be 40bpm.
• Observe skin colour; colour should be pink
• Observe heartbeat and check using the apex heartbeat. Heart rate should be between 120 –
160bpm
• Any bradycardia / tachycardia should be reported.
• Check body temperature, overheating and hypothermia, overchilling, if everything is normal,
temperature should be 36 ֯ C, check temperature of incubator.
• Check baby’s blood glucose level because glucose level should be assessed every 4-6hrs at
least should be for 3 days. The midwife can check.
Check baby’s blood glucose level because they are prone hypoglycaemia. Blood glucose level
should be assessed every 4-6 hour / by action.
• Observe if baby has passed urine within the 1st 24 hours.
• observe and report any abnormalities.
• Bowel action, observe if baby has passed meconium and the nature of for abnormalities.

EDUCATION TO MOTHER DURING ADMISSION

Explain baby’s condition to the mother. This should be during admission of baby and jeered towards
discharge. They include;
• Maintenance of respiration in the baby. Tell woman the changing nature of the baby’s
respiration that can cease anytime and hence should observe and report any slight change in
respiration.
• Education on how to provide warmth for the baby.
• Education on how to prevent infection and how to maintain personal hygiene practicing hand
washing or not using majority sponge and towel for the baby.
• Discuss feeding with the baby been fed on the breast, teach her to express milk to top it up for
the baby.

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 • Educate her to handle baby gently because baby is fragile.
• If all has been discussed with woman allow her to demonstrate some of the education to you
the midwife.
• It is therefore necessary to help mother bond with baby.
• Infant, bonding by: allowing mothers to touch baby, cuddle baby and feed baby.
• Allow mothers who have been through such situation to share their experience and ideas.
• Keep photos of babies at birth who were born preterm to mothers to relieve fear and anxiety.
• Explain the equipment / gadgets used on the baby to mum.
• Make time for her to come of her problems.
• Involve mother in the care of her baby.
• Continue the education till baby attain birth weight of 2.5kg or above.
• Teach mother to prevent the re-occurrence premature delivery using the causes.
EDUCATION BEFORE DISCHARGE
• Ask her to prevent people from coming into contact with the baby.
• The need to change diapers, napkins frequently to prevent sore buttocks and heat loss.
• Educate on exclusive breastfeeding and its importance (demand feeding).
• Ask mother to prevent the occurrence of malaria by weeding around the compound and use of
insecticide treated nets.
• Should not apply herbs and hot compress on sutures and fontanelles.
• Due to weak jaw, babies suckle small and get tired hence should express milk and top up.
• Mothers should attend post-natal often to check baby’s well-being and weight.
• Educate mothers to avoid use of herbs on the cord, fontanelles and genitalia.
• Discus with mother on some of the complications of preterm baby so as to report as early as
possible.
Favorable signs of thriving (signs of improvement) in a preterm baby
i. The baby’s colour remains pink without cyanosis
ii. Infant moves rigorously with good muscle tone
iii. Eagerness to feed
iv. Baby gains weight steadily
v. Oedema becomes less
vi. Audible cry in small babies and lusty cry in bigger babies
vii. Normal weight gain
Less favorable signs
i. Cyanosis and pallor, this may be due to respiratory distress syndrome, intracranial injuries etc.
ii. Jaundice
iii. Signs of infections like pyrexia
iv. Weight loss or abnormal weight gain
v. Refusal to feed
vi. Repeated signs of respiratory distress.

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PREVENTION OF PREMATURITY

Preconceptual Level Prevention

 Raising public awareness about the scope of the problem, its causes and prevention.
 Establishment of specific programmes to protect women especially those at risk and protecting
pregnant women from hazardous work schedule, especially night sift, providing time for prenatal
visit. Research has come out that preterm delivery has related to prolong work, standing and
exposure to potential hazards such as chemicals, extreme heat and cold.
 Pregnancy planning and identification of barriers to care.
 Adjustment of prescribed and over-the-counter medications that may pose a threat to the developing
fetus.
 Avoidance of weight extremes
 Vitamins supplement before getting pregnant especially folic acid and vitamin B12
 Various investigations can be conducted VDRL, HIV/AIDS test
 Genetic counseling as indicated.

During Pregnancy

 Nutritional adjustment the use of vitamins, folic acid etc

 Avoidance/cessation of drug or substance abuse eg. Alcohol, smoking
 Asymptomatic disease screening
 Routine ultrasound examination for both mother and foetus
 Avoidance of stress
 Early seeking of medical care for existing condition and early recognition and prevention of preterm
labour and preterm birth [ evidence of regular uterine contraction and with accompanying
effacement and dilatation of the cervix between 37th week of gestation]
Early therapy options include bed rest, hydration, and abstention from intercourse and orgasm;
effectiveness of each method is uncertain.
Onset of contractions (intrapartum)
Tocolytic Therapy
If antepartum therapy is not successful, tocolytic therapy may be instituted. These drugs should be used
only when the potential benefit to the fetus outweighs the potential risk.
1. Betamimetic—Terbutaline (Brethine): acts on β2 receptor cells located in smooth muscle, which
decreases or stops uterine contractions.
2. Mg2SO4—interferes with smooth-muscle contractility, although its exact mechanism of action is
unknown.
3. Prostaglandin inhibitors—Indomethacin (Indocin): inhibits prostaglandin stimulation of contractions.
4. Calcium channel blocker—Nifedipine (Procardia): relaxes smooth muscle by inhibiting the transport
of calcium, hence negating contraction formation.
5. Antibiotic therapy to treat existing infection that can trigger pre-term contractions.
6. Progesterone, often given in the form of 17-hydroxyprogesterone caproate, relaxes the uterine
musculature, maintains cervical length, and has anti-inflammatory properties, and thus exerts activities
expected to be beneficial in reducing preterm birth.
7. Cervical cerclage is a surgical intervention that places a suture around the cervix to prevent its
shortening and widening.

13
Complications of preterm babies
• Hypoglycemia • Infections
• Respiratory Distress Syndrome
• Necrotizing enterocolitis • Retinopathy of prematurity
• Jaundice • Cerebral palsy
• Hyperthermia • Patant ductus arteriosus
• Hypothermia

SMALL FOR GESTATIONAL AGE / LIGHT FOR DATE BABIES (SGA)

These are infants born at any gestational age whose birth weight falls below the 10th percentile on the
growth chart. They have a birth weight usually below 2.5 kg and usually looks smaller compared to their
gestation. Their small gestational age can be the results of intrauterine growth restriction.
These infants are small because they suffer a nutritional or oxygenation deficit due to the following
causes;
Maternal causes
• Drugs addicts (alcoholism/ smokers)
• Pregnancy induced hypertension, asthmatic or sickle cell mothers are predisposed to giving birth
to small gestational age babies
• Effects of certain drugs such as mother on anticonvulsants/ steroids.
• Malnutrition/ anaemia
• Infections; malaria, syphilis
• Socio-economic background
• Genetic predisposition. Small mothers may give birth to small babies

Foetal causes
• Multiple gestation
• Chromosomal or genetic abnormality
• Intra uterine infection; example, syphilis

Placental causes
• Abruption placenta
• Previa
• Abnormal cord insertion
DIAGNOSIS
• Ultrasounds
• Mother’s weight gain during pregnancy
• Clinical features during postnatal

CHARACTERISTICS OF SMALL GESTATIONAL AGE

They are normally born at term (37 weeks) or even post-term (42 weeks). Their low birth weight is as a
result of prolong inter uterine malnutrition. They have birth weight of less than 2.5 kg
HEAD
Have large head compared to the rest of the body but skull bones are hard
EYE

14
Have eyebrow
EAR
Pinna of ear (cartilage) is well developed
SKIN
• Looks dry, cracked and peeling
• Skin looks thin and wasted making it easy for ribs to show and may present with old man’s face
• Have plenty lanugo hair/ may be absent
• Scanty or absent vernix caseosa
• Have both palmar and plantar creases which are well developed
• Have shallow chest compared with abdomen
GENITALIA
• Testicles are descended into scrotum and vulva is well developed in the male in the female
respectively
BEHAVIOUR/ACTIVITY
• Have good muscle tone
• They are very active or present with active movement which is vigorous
• Sucks strongly and cries a lot as an indication of hunger
• All reflexes are well developed

MANAGEMENT OF SMALL GESTATIONAL AGE

1. Pregnancy
• Attempt to determine the cause of small gestational age by searching for relevant factors or
causes through history, laboratory and ultrasonic examination.
• Treat any underlying cause example, hypertension when possible.
• Monitor fetal well-being including biophysical profile, fetal movement count, amniotic fluid
volume evaluation and serial ultrasonic examination.
• Use of Doppler evaluation of placental flow may be used to evaluate or check the fetal well-
being
2. Delivery
• Early delivery is necessary if the risk to the fetus of remaining in utero is considered greater than
the risk of prematurity.
• Indication for delivery is arrest of fetal growth and fetal distress.
• When there is poor placental blood flow, the fetus may not tolerate labour ad may require
cesarean delivery.
• Infants with extreme small gestational age are at risk for perinatal problems and often require
specialized care in the first few days of life. Therefore, if possible delivery should occur at a
center with a NICU or special care nursery. The delivery team should be prepared to manage
fetal distress, perinatal depression, meconium aspiration, hypoxia, hypoglycemia and heat loss.
3. Postpartum Management of Small for Gestational Age Baby / Light for Date Baby
• Initiation and maintenance of • Observation
respiration • Psychological support
• Provision of warmth • Education on admission
• Feeding • Education before discharge
• Prevention of infection

Prevention of heat loss:

15
SGA are at risk of hypothermia due to limited stores of fat and liver glycogen which helps to prevent
heat loss. Heat loss is increased in SGA as a result of Large Surface area in relation to body mass and
lack of adipose tissue.
• Nurse baby in a warm but well-ventilated room. Teach mother Kangaroo mother care and
encourage her to practice to prevent heat loss.
• The cot should be warm to prevent heat loss. (by either convectional or conduction) place
away from windows.
• Warm hands before handling baby.
• Always place a cap on infants’ head as the head size makes 25% of the total body size.

FEEDING / NUTRITION: Initiate exclusive breastfeeding as soon as mother and baby condition
allows and cup feed if there is poor sucking reflex. Feed every 3- hours or feed on demand.
OBSERVATION
• Observe for any abnormality due to baby suffering from intrauterine malnutrition.
• Elimination (all voids and stool • Daily weighing/ weight monitoring
colour) • Activity and sleep pattern
• Breathing pattern • Reflexes
• V/S (Temperature pulse) • Cord for bleeding

COMPLICATIONS OF SMALL GESTATIONAL AGE

• Meconium Aspiration/aspiration • Hypothermia
syndrome • Hypoglycaemia
• Birth Asphyxia/perinatal asphyxia • Hypocalcemia
• Infection

16
 KANGAROO MOTHER CARE

INTRODUCTION
In 1978, due to increasing morbidity and mortality rates in the ‘instituto materno infantal’ NICU in
Bogota, Colombia. Dr Edgar Rey Sanabria, professor of neonatology. Introduce a method to alleviate
the shortage of caregivers and lack of resources.
He suggested that mothers should have continuous skin – skin contact with their low-birth-weight
babies to keep them warm and to give exclusive breastfeeding as needed.
1979 Dr. Rey and Martinez started the programme in Bogota, Colombia, In response to shortage of
incubators and severe hospital infections. In 1983 UNICEF brought attention to the programme in
Spanish. The international kangaroo care awareness day has been celebrated worldwide on may15 th
since 2011. The name is derived from the similarities it bears to care given in which infant kangaroo
always born premature is guided into the maternal poach where it is kept warm contained and close to
the breast for unlimited feeding opportunities until matured.
Knowledge about the animal Kangaroo
Pinky→ smooth, non-hairy Kangaroo just delivered.
Joey →Baby Kangaroo.
When it is born, the Kangaroo baby has no hair, and is called PINKY. It is the size of a peanut yet must
crawl into pouch by itself. Baby Kangaroo are born very immature – as in premature babies.
It is extremely premature and very tiny.
This means that the pinky’s skin can be in direct contact with the inside pouch, which is mostly skin
with very few hairs hence skin to skin contact. They smell their way from the birth canal using their
front crawls to crawl all the way to the mother’s pouch.
They hold unto the nipple and do not let go. The nipple ejects milk into their mouth. In the pouch, they
are kept warm, safe and protected and feed as they continue their gestation. The pouch can close tightly
to protect the baby. The baby comes out of the pouch for the first time when is a quarter of the mother’s
weight.
The (Joey) Baby Kangaroo continues to feed even when it is too big to fit in the pouch.
The pouch covers the baby with skin, and this does not only protect the very immature baby, but also
provides it with a total environment which is essential for development. The baby is cared for all this
time without interruption.

Definition
Kangaroo Mother Care (KMC) is a special way of caring of low-birth-weight babies .It involves placing
the baby in diapers upright between the maternal breast and abdomen for skin to skin contact. It fosters
their health and well-being by promoting effective thermal control, breastfeeding, infection prevention
and bonding.

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 COMPONENTS OF KMC
I. Skin-to-skin contact: Early, continuous and prolonged skin-to-skin contact between the mother and
her baby is the basic component of KMC. The infant is placed on her mother's chest between the breasts.
II. Exclusive breastfeeding: The baby on KMC is breastfed exclusively. Skin to-skin contact promotes
lactation and facilitate the feeding interaction. KMC is initiated in the hospital and continued at home.
III. Early Discharge: when mothers are confident in practicing KMC, and baby is doing well, they can
go home and continue this at home. The more involved the mother is in caring for her baby at the
facility, the more likely she will be able to care for the baby at home.
IV. Follow up care after discharge: this is a critical part of KMC. After the mother and baby leave the
facility, they must be actively followed up to ensure the baby remains well.
TYPES OF KMC
There are two main types of KMC, namely continuous KMC and intermittent KMC.
CONTINUOUS KMC: The LBW baby is kept and carried in skin to skin contact with his/her mother
or other caregivers for as close to 24 hours as possible but not less than 20 hours a day. Other family
members or caregivers may be involved to ensure the maximum duration of skin-to-skin contact. All
other aspects of KMC such as feeding and monitoring of the baby should continue as normal.

INTERMITTENT KMC: This is recurrent but not continuous skin to skin contact between mother and
baby, with the same support from health workers as is given in continuous KMC. It is recommended that
this should be done for not less than 8 hours a day. Intermittent KMC is practiced where the facility set
up does not support continuous KMC or where there is a reason why either caregiver or baby is unable
to do continuous KMC in a health facility if, for example, the baby becomes stable. In some cases,
continuous KMC will not be possible until the baby goes home because of the health facility’s set up.

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PRE-REQUISITES OF KMC

i. Support to the mother in hospital and at home

A mother cannot successfully provide KMC all alone. She would require counseling along with
supervision from care-providers, and assistance and cooperation from her family members.
ii. Post-discharge follow-up
KMC is continued at home after early discharge from the hospital. A regular follow up and access to
health providers for solving problem are crucial to ensure safe and successful KMC at home.
BENEFITS OF KANGAROO MOTHER CARE
• Breastfeeding: Studies have revealed that KMC results in increased breastfeeding rates as well as
increased duration of breastfeeding. Even when initiated late and for a limited time during day
and night, KMC has been shown to exert a beneficial effect on breastfeeding.
• Thermal control: Prolonged skin-to-skin contact between the mother and her preterm/ LBW
infant provides effective thermal control with a reduced risk of hypothermia. For stable babies,
KMC is at least equivalent to conventional care with incubators in terms of safety and thermal
protection.
• Early discharge: Studies have shown that KMC cared LBW infants could be discharged from the
hospital earlier than the conventionally managed babies. The babies gained more weight on
KMC than on conventional care.
• Less morbidity: Babies receiving KMC have more regular breathing and less predisposition to
apnea. KMC protects against nosocomial infections. Even after discharge from the hospital, the
morbidity amongst babies managed by KMC is less. KMC is associated with reduced incidence
of severe illness including pneumonia during infancy
• Decreases the occurrence of apneic episodes and irregular breathing
• Associated with fewer and less severe infections
• Improves bonding between mother and baby
• Increases mother’s confidence in handling her small baby
Benefits For Health System:
• Reduces the length of hospital stay
• Reduces the number of staff needed to care for babies
• Reduces the equipment need for the care of LBWs
• Reduces the cost of treating a small baby
The Practice of KMC (Criteria and when to Start)
Criteria and when to start
• All babies below 2.5 kg are eligible
• Started when baby is stable
Contraindications (Baby)
• severe respiratory distress
• Apnoiec episodes requiring intervention to re-establish breathing
• Any acute condition which requires close direct visual observation
Contraindication (Mother)
• Acute medical condition, especially one that impairs consciousness
• Severe mental condition that will cause her to pose a risk to her baby

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KMC PROCEDURE
Positioning
• The baby should be placed between the mother’s breasts in an upright position.
• The head should be turned to one side and in as lightly extended position. This slightly extended head
position keeps the airway open and allows eye to eye contact between the mother and her baby.
• The hips should be flexed and abducted in a "frog “position; the arms should also be flexed.
• Baby's abdomen should be at the level of the mother’s epigastrium. Mother's breathing stimulates the
baby, thus reducing the occurrence of apnea.
• Support the baby’s bottom with a sling/binder.

LARGE GESTATIONAL AGE BABY / HEAVY FOR DATE BABY/MACROSOMIC BABY

A new born baby whether delivered preterm or term whose birth weight is above 90th percentiles is
considered Large for gestational age. Birth weight of 4.5kg or more (sometimes ranges between 4kg to
4.5kg or more) is usually recorded for the large for gestational age baby. There are two reasons why
newborns may grow to a large than average size in utero. They can be genetically large or more
commonly, they are exposed to an imbalance of nutrients in utero. The most common energy and growth
source in utero is glucose. It is easily transported by diffusion across the placental barrier. If the
maternal circulation contains excessive glucose levels, the fetus circulation will have a higher-than-
normal glucose level too. Infants of diabetic mothers are often Large Gestational Age (LGA).

CAUSES OF LGA /RISK FACTORS CONTRIBUTING TO LGA NEWBORNS

• Genetics: women or parents who are big or large you are likely to give birth to big baby.
• History of other LGA newborns or • Excessive weight gain in
macrosomic babies pregnancy
• Multiparity / Increase Parity • Increase maternal age.
• Women who are obese/maternal obesity • Increased pregnancy weight gain
• Prolong pregnancy • Maternal glucose intolerance (mostly
seen in diabetic women)
DIAGNOSIS
• Ultrasound scan to know the weight
• Symphysiofundal height greater than the average length.
• Test for glucose in urine.
• Mother’s weight gain during pregnancy.

CHARACTERISTICS
• Have exaggerated or greatest birth weight of 4.5 kg or above.
• Their skin is flabby and edematous
• In some cases the odema subsides within 24hours/drastic reduction in weight.
 They are hypotonic and lethargic

 Blood sugar level that falls below 4mmol/l

 They look handsome and plumpy due to increase subcutaneous fat
 Their face appears round and puffy
 They look lethargic and weak

20
  Their size makes them look healthy but this is deceitful as they often have serious developmental
defects.

MANAGEMENT
ANTENATAL CLINIC
Plan for delivery, when they are identified by planning an elective caesarian section. When they are
delivered it should not be vaginal delivery to prevent birth injuries and shoulder dystocia.

POSTALNATAL MANAGEMENT
1. Initiation of respiration
2. Prevention of infection
3. Maintenance of adequate nutrition: Feeding baby as frequently as possible to prevent
hypoglycemia by feeding 2-4 hours.
4. Initiate breastfeeding if baby and mother’s condition allows.
5. Monitoring feeding tolerance and asses functioning of sucking reflex.
6. Check blood glucose level.

MAINTENANCE OF RESPIRATION
1. Assess condition to see if baby needs resuscitation
2. Position baby at the side so as to ensure drainage of mucus and prevent backflow of mucus
into the lungs as well as prevent mucus aspiration.
3. Continue suction baby as the need arises, when necessary, administer oxygen through
ambubag or from the cylinder through mask.
4. Transfer baby to the resuscitation area and assess baby’s fifty (5th) minutes Apgar score
5. Give or administer vitamin K to prevent bleeding and improve blood clotting.
6. Procedure like weight taking, full length should be deferred until baby’s condition improves
or allows.
MAINTENANCE OF BODY TEMPERATURE
Provision of warmth (Temperature/regulation)
• Baby should be dress in warmth cotton clothing
• Wrap baby as this prevents jittery movements and help keep baby warm
• Frequent changing of diapers to prevent heat loss
PREVENTION OF INFECTION
The midwife should employ aseptic technique in the care of the baby.
• Practicing of hand washing technique before and after handling of baby.
• Use of alcohol hand sanitizers
• Nurse baby in a separate cot
• One incubator /cot to each baby.
• Space one cot / incubate form another, spacing should be about 90cm.
• There should be daily cleaning of cot/incubator
• Limit the number of visitors
• Any care provider with upper respiratory tract infection should not be allowed to care for
these babies.
• Teach mother simple hand washing technique with soap and water before and after handling
baby

21
 • Educate mothers to refrain from using their handkerchief in cleaning babies’ eyes
• Educate mother to desist from sucking the baby’s nose with their mouth.
• As soon as babes are discharged decontaminate cot for next use.
• Advocate an individual bathing articles.

PSYCHOLOGICAL SUPPORT OF THE MOTHER

• Discuss the drastic reduction in weight of baby to the mother to allay anxiety. When it
happens since not all LGA babies experience sudden weight reduction within the first 48
hours,
• Explain baby’s condition – reason been given
- Encourage parents to ask questions.
FEEDING OF BABY
• Initiate feeding as soon as mother and baby’s condition will allow.
• Encourage mother to feed every 3-4 hours
• Monitor feeding tolerance and assess for suckling reflex
OBSERVATION
• Carefully examine for any birth injuries
• Check blood glucose level every 3 hours to be sure baby is not diabetic. This is done to
determine hypoglycaemia.

COMPLICATIONS
• Brachial nerve plexus injury. • Brain damage
• Hypoglycaemia. • Shoulder dystocia at delivery
• Hyperglycaemia • Fractures
• Asphyxia. • Hypocalcemia

POST TERM /POST DATE/ POST DATISM

A baby who is born after 42 weeks completed gestation OR A baby who remains in utero from 1-3
weeks or more after the expected date of delivery.
CAUSES (PRE– DISPOSING FACTORS)
The actual cause is unknown, but predisposing causes include;
• Wrong date of last menstrual period. • Irregular menses.
• Wrong calculation of expected date of • High Multiparity example. 5 or
delivery more pregnancies.
• Previous history of post term birth. • Primiparity
DIAGNOSIS
• Ultrasound scan
• Last menstrual period.
• Decreased liquor amnii.
• In post –natal, clinical manifestations of the baby.
CHARACTERISTICS / FEATURES
• Skin desquamation or peeling which is often dry and cracked.
• Their fingers appear long often peeling or over grown nails.
• Absence of lanugo and scanty vernix caseosa, or limited vernix and lanugo.

22
 • Abundant hair on the scalp.
• Long nails
• Creases in the baby’s palms and soles of the feet planter creases are present
• Long thin extremities
• Minimal subcutaneous fat.
• Thin umbilical cord
• Skin is wrinkled.
• Meconium-stained skin and fingernails
• On the head, they have hard skull small fontanelles and narrow sutures.

• Reduction of soft cutaneous fat.

• Baby always look alert

MANAGEMENT
Post-term newborns are susceptible to several challenges secondary to placental dysfunction that place
them at risk for asphyxia, hypoglycaemia, and respiratory distress. The nurse must therefore be vigilant
for complications when managing these newborns.
DURING ANTENATAL
• Induction of labour.
• Caesarean section (C/S) can be done if foetus is distressed.
POST NATAL MANAGEMENT
• Provision of warmth.
• Maintenance of respiration.
• Good nutrition – monitoring glucose level and initiate early feeding.
• Psychological support; explain all procedures to the parents and include them in the care of
their baby
• Prevention of infection

OBSERVATION
• Observe for elimination. • Observe the cord for bleeding.
• Monitor daily weighing. • The skin colour.
DRUGS
• Give Vitamin K
• Prophylactics antibiotics are given to prevent infection.
COMPLICATIONS
• Asphyxia • Meconium Aspiration.
• Hypoglycaemia. • Birth trauma or injury.

INDICATIONS FOR INDUCTION OF LABOUR IN A POST TERM BABY

 Placental degeneration
 Risk of Foetal distress
 Oligohydramnios
 Medical conditions of the mother (PIH)
 Risk of meconium aspiration in the baby.

23
 CHAPTER TWO

ASPHYXIA NEONATORIUM
Definition
Also called Birth or Newborn Asphyxia: This is the failure of the new born to start or initiate regular
respiration due to high level of carbon dioxide (CO2) and low level of oxygen (O2) in blood. Mostly
within the first minute of birth.

CAUSES / PREDISPOSING FACTORS

The causes of asphyxia are in groups under 3 headings;
1. Causes during pregnancy:.
 Conditions of mother that may lead to placental insufficiency. Example; APH, PIH,
Hypertension, cardiac respiratory disease, anaemia, maternal malnutrition, eclampsia.
 low socioeconomic status of mother
 alcohol abuse and smoking
 lack of prenatal care
 maternal age of less than sixteen (16) years old or over 40 years old
2. Causes during labor;
• Prolong first (1st) and second (2nd) stages
• Hypertonic uterine action
• Prolapse of cord
• Tight cord around neck
• True knots of the cord
• Administration of narcotic within 2 – 4 hours to 2nd stage of labour
• Anaesthetic drugs (depresses respiratory center of baby
• Other causes like mal presentation e.g. Breech presentation.
• Difficult labour
• Obstruction of air way by either mucus or blood.

NB. CAUSES OF ASPHYXIA NEONATORIUM CAN ALSO BE GROUPED UNDER

MATERNAL AND FOETAL CAUSES:
 Maternal and
 Foetal causes
A. Maternal causes
 Prolonged labour
 Conditions which lead to placenta insufficiency e.g. eclampsia, chronic nephritis, Severe
anemia, Respiratory disease e.g. TB
 Premature separation of the placenta as in ante partum haemorrhage e.g. Placenta
abruption.
 Prolonged intra-uterine hypoxia
 APH: Placenta praevia and abrutio
 Severe hemorrhage and shock
 Hypertonic uterine contractions
 Maternal age – Elderly primigravidae – due to ossification of the pelvic bones.
 Drugs given to mother in late first stage of labour e.g., Pethidine and morphine, valium
etc.

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 B. Foetal causes
 Depression of the baby’s respiratory center by narcotics and anaesthetic drugs given to
mother during labour. e.g. pethidine
 Immaturity of the baby’s respiratory center as found in preterm baby.
 Blockage of the airway by thick mucus, blood or meconium.
 Cord prolapse
 Congenital abnormality as in tracheal atresia
 Rhesus incompatibility
 True knot in the cord/ tight cord around the neck.
 Cerebral damage (intracranial injury) during labour or delivery e.g. in excessive
moulding.
 After coming head of the breech /breech presentation.
 Multiple pregnancy
 Macrosomic baby with Cephalo pelvic disproportion (CPD).

SIGNS OF ASPHYXIA IN UTERO

There are basically 3 main signs
• Fetal Heart rate, if it is less than 120bpm and more than 160bpm, it signifies fetal distress.
• Meconium-stained liquor with cephalic presentation i.e. Hypoxia
• Delay recovery of fetal heart rate that is late decelerations

CLASSIFICATION OF ASPHYXIA
There are 2 main types of asphyxia; based on the ratings of the APGAR score
SIGN 0 1 2

Heart rate Absent Slow (Less than 100) More than 100

Respiratory effort Absent Irregular, slow, weak cry Good, strong cry

Muscle tone Limp Some flexion of extremities Well flexed

Reflex Irritability No response Grimace Cry, sneeze

Color Blue, pale Body pink, extremities blues Completely pink

• Mild / blue plus asphyxia or asphyxia livida

• Severe/ white asphyxia or asphyxia pallida (pale).

25
These can be classified using APGAR score
MILD ASPHYXIA
The main cause is blockage or obstruction of the airway by either, mucus, meconium, liquor or blood.
Apgar Score between 5-7 with moderate depression of their vital signs

APPEARANCE OF BABY / CLINICAL MANIFESTATION / CHARACTERISTICS

• A – appearance: Here baby looks cyanosed with skin colour of bluish–red
• Pulse – There is strong and firm pulsation in baby’s cord and heart rate is above 100bpm
• G-grimace: There is response to skin stimulant.
• A- activity: there is good muscle tone
• R- respiration: There is short period of Apnoea (ceasation of breathing and baby may attempt to
breath.
• Anal sphincter: The anal sphincter is intact meaning there is no meconium-stained liquor in
utero. APGAR score is between 5-7.
MANAGEMENT
Management should start from ANC and all conditions identified should be treated urgently to
prevent the occurrence of asphyxia. If asphyxia becomes inevitable, then we prepare to receive
an asphyxiated baby. Here, all equipment for resuscitation should be ready.
CARE AT BIRTH
As soon as head is out, clear mouth and nose. Wipe liquor, then clamp and cut cord
• Assess 1st min APGAR score. Here, caution should be taken not to turn baby upside
down. This creates tension in the brain and may lead to intracranial haemorrhage.
• Transfer baby from delivery site to resuscitation area which should be pre-heated.
• Put baby on a firm flat with workable height and continue to wipe liquor as source of
stimulation such babies do not normally need O2 by ambubag
• Check 5th minutes APGAR score.
• Give drugs, Vitamin K and antibiotics
• Provide warmth and put baby to breast. After all these, you prevent infection, provide
psychological support, education and maintenance of respiration and observation.

SEVERE ASPHYXIA
APGAR score is below or less than 5 and presents with severely depressed vital signs and are at risk of
dying unless actively resuscitated.
A- appearance: Colour is bluish grey
P- pulse: There is slow and weak pulsation of the cord and cord look flabby.
G- grimace: there is no response to skin stimulant
A- activity: there is poor muscle tone and baby lies limp.
R- respiration: Baby is always in profound shock and does not make the attempt to breath but
sometimes, baby gasp.
Anal sphincter: This relaxes hence the passage of meconium liquor in utero.

MANAGEMENT
Same as for mild asphyxia with respect to initiation of respiration to the 5th minutes APGAR score.
Then;
• Re- position baby and then do further suctioning

26
 • Continue to provide warmth and give oxygen (O2) by ambubag. If after 10minutes, baby is not
breathing, colour is blue and Heart Rate is less than100bpm, then administer the resuscitation
drugs (dextrose, vitamin K, Na, dexametazone, Ca etc.
• If after this, baby does not breathe.
• And condition does not improve, call in the obstetrician to pass the endotracheal tube.
• Explain all procedures to the mother about the baby’s condition after calling in the obstetrician.
• If condition improves, send baby into the incubator
• Set IV dextrose H2O to counteract hypoglycemia 250mls slowly 24 hours
• Show baby to mother when condition improves.

NB:// follow the steps under newborn resuscitation

PSYCHOLOGICAL SUPPORT
• Explain baby’s condition to mother • Involve parents when condition arouse.
• Equipment - support person. • Record & report findings.
• Reassure mother.
TABLE SHOWING THE SIGNS AND SYMPTOMS OF MILD AND SEVERE
ASPHYXIA
SIGN MILD ASPHYXIA SEVERE ASPHYXIA
A (Appearance) Bluish red (deeply cyanotic) Pale, grey
P (Pulse) The cord pulsates strongly, The cord pulsates flabby,
firm and is 60-80bpm feeble and is less than
40bpm

G (Grimace) Responsive to stimuli; baby Limp, unresponsive to

squeezes its face stimuli

A (Activity) Good muscle tone Poor muscle tone

R (Respiration) Makes an attempt to breath; No attempt to breath; may

cries weakly; apnoeic. not cry; in profound shock;
gasps
APGAR SCORE 5-7 Less than 5

NEWBORN RESUSCITATION
It is the process of helping to initiate or sustain breathing or respiration after birth in the
newborn.
AIMS
• Establish and maintain clear airway for ventilation & oxygenation
• To correct acidosis
• To ensure effective circulation
• To prevent hypothermia, hypoglycaemia and intra –cranial hemorrhage.
• This is the action that is taken to revive the newborn and return to normal heart rate, colour,
activity and blood pressure. Newborns at birth who are blue, limp make little respiratory effort or
heart rate less than 100bpm.

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CONDITIONS THAT MAY REQUIRE RESUSCITATION (PREGNANCY)
PREGNANCY
• Maternal diabetes • Post term gestation
• High Blood Pressure (PH or chronic) • Multiple fetal gestation
• Chronic mental illness • No pre- natal care
• Anaemia • Diminished fetal activity
• Previous fetal death / neonatal death • Maternal age below 16 & above 35
• Polyhydraminous / oligohydraminous • Maternal substance abuse
• Premature rupture of membranes
LABOUR
• Breech delivery • Prolonged second (2nd) stage of labour
• Premature labour • Fetal bradycardia
• Precipitous labour • Uterine Tetany
• Chorio amnionitis • Meconium-stained amniotic fluid
• Premature rupture of membranes greater • Cord Prolapse
than18 hours. • Placenta Abrutio
• Prolonged labour greater than 24 hours. • Placenta Praevia

RESUSCITATE IF
• Heart rate is less than 100bpm
• Deep, gasping respirations/ absence of breathing
• Blue, grey mottled in colour
• Limp with little / no response to stimuli

IMMEDIATELY AFTER DELIVERY, THESE FIVE (5) IMPORTANT QUESTIONS MAY BE

ASKED
• Is the amniotic fluid clear & is the skin clear of meconium?
• Is the newborn breathing / crying?
• Is there good muscle tone?
• Is the colour pink?
• Is the new born term gestation?
If answers are yes to all questions, then baby needs no resuscitation.

INITIAL STEPS
Airway
• Provide warmth
• Position to open airway
• Clear airway

Breathing
• Stimulate
Circulation
• Assess heart rate and colour.
Drugs
• Use of resuscitation drugs

28
If the baby’s response is slow or he remains hypotonic after ventilation is achieved, consideration will
be given to the use of drugs.
 a. Naloxone hydrochloride: it is a powerful antiopioid drug used to reverse the effects of
maternal narcotic drugs given in the preceding 3 hours. Ventilation should be established prior to
its use. A dose of up to 0.1-0.2 mg/KBW may be administered intramuscularly.

 b. Sodium bicarbonate- if the heart rate is less than 60bpm despite effective ventilation, chest
compression and two intravenous doses of adrenaline then sodium bicarbonate 4.2% solution can
be administered using 2-4 ml/kg by slow intravenous injection at a rate of 1 ml/min to correct
acidosis.
 Ventilation should be established prior to its use.
c. Adrenaline (epinephrine)- this is indicated if the heart rate is less than 60 despite 1 minute of effective
ventilation and chest compression.
 An initial dose of 0.1-0.3ml/kg of 1 :10000 solution can be given intravenously.
d. Calcium gluconate- a dose of 100mg/KBW and isoprenaline 0.1-0.5mg/kg/min may be used for
severe bradycardia or cardiopulmonary arrest.
 e. Human albumin- if pulmonary haemorrhage or sign of shock persists despite adequate
resuscitation then 4.5% human albumin 10-20 ml/kg as a volume expander should administered
as quickly as possible.
 f. Dextrose- 10% 3ml/kg may be given intravenously to correct hypoglycaemia.
 g. Konakion (Vit K)- up to 1mg may be given intramuscularly to reduce risks associated
haemorrhage.
 h. Dexamethasone- 1=2mg may be given intravenously or intramuscularly to minimise the risk
of cerebral oedema if severe asphyxia is present.

Newborn respiratory assessment

• Normal respiration is 40- 60 bpm
• Newborns breath irregularly and at varying depth
• Respiration is relaxed
• Newborns may have periodic breathing episodes of 5- 10 seconds without breathing followed by
rapid, shallow breaths (Apnoea)
• Chest should be round & symmetrical. Asymmetrical of the chest may be caused by long/
cardiac abnormalities, skeletal disorders, masses, or nerve damage.
• Abdomen rises (because diaphragm is the source of primary respiration)

SIGNS OF RESPIRATORY DISTRESS IN NEWBORN

• Tachypnea, respiratory rate greater than • Absence of breathing greater /equal to
40 breath per minutes 20 seconds in duration and the skin
• Retractions colour from pink to cyanotic.
• Grunting on expiration • Grasping
• Cyanosis • Occasional breaths with long pauses
• Nasal flaring between.
• Apnoea

STIMULATION (METHODS)
• Drying

29
 • Suctioning (if after suctioning and baby does not cry, then stimulate)
• Rub the back of shoulders or extremities or ‘trunk’.

INAPPROPRIATE METHODS OF STIMULATION

• Slapping the newborn’s back, bruises and spinal cord complications.
• Soaking the newborn in cold/ Hot water, result in temperature instability
• Forcing thighs onto abdomen; damage to liver and spleen
• squeezing rib cage, Fracture, death
• Dilating anal sphincter, tearing
• Milking the cord
• Using onion juice
• After everything, (stimulation) evaluate, Respiration, heart rate and colour (pink) after 30
seconds. If after stimulation and baby is showing no sign of breathing / crying, then baby will
need pressure ventilation (O2 administration).
• To ascertain/ evaluate count the apex beat for 60 seconds. Heat is produced in the baby
by two (2) main mechanism (shivering) and voluntary muscle activity (restlessness and crying)

WAYS OF ADMINISTERING O2 TO BABY.

• Mouth to mouth and nose resuscitation where oxygen (O2) is blown to the baby. The babies.
Mouth should be covered with a layer of gauze before starting.
• Giving oxygen (O2) from oxygen (O2) cylinder
• The use of the ambubag. There are 2. That is the round mask & the anatomical mask and this is
known as positive Pressure Ventilation.

ADVANTAGES OF AMBUBAG/SELF INFLATING BAG

• It fills on its own
• Does not require gas source
• Less possibility of over- inflating because of pressure release value /popped up value

DISADVANTAGES
• It inflates even in the absence of adequate seal
• Requires a reservoir to deliver -100% oxygen (O2)
• Not reliable way to deliver free flow of oxygen (O2)

THE RESERVOIR
• Maintains 50% oxygen (O2)
ALWAYS TEST EQUIPMENT
• From a seal in the palm
• Squeeze the bag, feeling for pressure
• Check for a crack/ leak presence
• Listen for pressure release value
• Is the pressure release value stock or not?

FACE MASK
• Avoid excessive pressure
• Mask should cover the chin, mouth & nose

30
 • Use the right Mask.
• Too big of the mask can cause eye damage

SIGNS OF IMPROVEMENT
• Improvement in colour and heart rate
• Respiration should be spontaneous. When the heart rate is consistently above 100, slowly stop
assisted ventilation.
NB. If positive pressure ventilation (PPV) is needed for more than 2 minutes, then, an oro-gastric
tube is inserted.
External cardiac massage/ chest compression
 If bradycardia persists.

NEW BORN RESUSCITATION COMPONENT TASK

GETTING READY
1. Quickly wrap or cover the newborn and place on a clean, warm surface
2. Tell the woman (and her support person) what is going to be done and encourage them to
ask questions.
3. provide continual emotional support and reassurance as feasible

RESUSCITATION USING BAG AND MASK

[Link] the head in a slightly extended position to open the airway
2. Clear the airway by suctioning the mouth and nose
3. Position the newborn’s neck and place the mask on the newborn’s face so that it covers the
chin, mouth and nose. Form a seal between mask and newborn’s face
4. ventilate at a rate of 40 breaths /minute and then stop and quickly assess if the newborn is
breathing spontaneously.
5. if breathing is normal and there is no indrawing of the chest and no grunting put in skin-to
–skin contact with mother
6. If new born is not breathing, breathing is less than 30 breaths / minute or severe chest
indrawing is present, ventilate with oxygen if available. Arrange immediate transfer for
special care.

7. If there is no gasping or breathing at all after 20 minute of ventilation, stop ventilating

POST PROCEDURE TASKS

1. Place disposable suction catheters and mucus extractor in a leak-proof container or
plastic bag. Place reusable catheter and mucus extractors in 0.5 % chlorine solution for
decontamination. Then, clean and process.
2. clean and decontaminate the valve and mask and check for damage
3. wash hands thoroughly
4. Record pertinent information on the mother’s /newborn’s record.

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External Cardiac Massage/Chest Compression
 If bradycardia persists or the heart beat is less than 40 beats per minute, then external cardiac
massage or chest compression is done. This is achieved by encircling the baby’s chest with two
hands so that the thumbs meet on the sternum below the line between the nipples (see 80e).
Compress chest by one third of its depth – three times for each inflation. It follows a rhythm like
1, 2, 3, breath (inflate the bag). Carried out with caution and expertise.
 Discontinue chest compression when the heart rate is above 60 beats per minute and there is
progressive increase in the rate. This can be done in conjunction with mouth-to-mouth
respiration.
If the baby’s breathing is normal (40 – 60 breaths/minute) and there is no in drawing of the chest and no
grunting:
a) Give baby to mother and maintain skin to skin contact.
b) Observe breathing at frequent intervals that is every 15 minutes
c) Encourage mother to begin breastfeeding.
d) Monitor baby’s vital signs and evaluate at least the first 90 minutes
e) Give essential care (eye care, cord care vit K, check temperature, weight and do examination:
head to toe and assess the following
i. Heart rate : more than 100 beats/minute
ii. Breathing: 40 – 60 bpm
iii. Colour: pink
iv. Cord appearance: no bleeding
v. Movement and tone: active and should have spontaneous movement of the arms and legs
vi. Entire body for abnormalities
f) Explain what happened to the mother.

NOTE:
 If there is no gasping or breathing at all after 20 minutes of ventilation, or gasping but no
breathing after 30 minutes of ventilation, stop ventilating.
 Provide emotional support to the family.

POINTS TO NOTE DURING RESUSCITATION OF THE BABY

Never:
a) Slap, blow on, or pour cold water on the baby
b) Hold the baby upside down or rub methylated spirit on the body
c) Routinely suction the mouth and nose of a well-baby
d) Use heavy suctioning of the back of the throat of any baby.
e) Give injections of respiratory stimulants or routine sodium bicarbonate injections.

Intubation
Where facilities are available, the midwife must prepare to intubate, but in most hospitals, intubation is
done by the doctor.
The doctor passes a small endotracheal tube into the glottis after clearing the airway.
Oxygen is administered at intermittent positive pressure ventilation (IPPV). This is given to a baby who
fails to breathe at all.
Requirement for intubation

32
 1) Resuscitaire with radiant heaters and light.
2) Pipe oxygen, manometer, suction and clock time
3) The shelf provides a firm surface and enables a 150 head tilt to be achieved.
4) Straight infant blade laryngoscopes with spare batteries and bulb
5) Neonatal endotracheal tubes 2.5mm and 3.0mm and connectors.
6) Neonatal airways sizes 0, 00, 000
7) Mucous extractor
8) End hole suction catheters sizes 6, 8, 10
9) Neonatal bag and mask and face mask of assorted sizes
10) Syringes 5ml and 2ml and assorted needles
Drugs
a) Sodium bicarbonate 5ml of 4.2% or 8.4% given IV to correct acidosis
b) Dextrose 5mls of 10% or 5% given intravenously to correct hypoglycemia
c) Vitamin K/Konakion (0.5mg- 1mg) given IM to prevent hemorrhage
d) Normal saline
e) Naloxone Hydrochloride (narcotic antagonists) 100 micrograms/kg body weight (IV or IM) to
reverse the effects of pethidine given to the mother to relieve pain. In addition to resuscitation
with oxygen via face mask or endotracheal tube. Caution: should only be given when
respiration is effective.
f) Dexamethasone to minimize the risk of cerebral oedema if severe asphyxia is present. 1- 2mg
may be given IV or IM.
Summary of New-Born Resuscitation
1) Position: place the baby on his back with the head slightly extended
2) Clear the airway:
a) Clear the airway and dry the baby’s mouth with a gauze
b) Suction the baby nose and mouth
c) Reassess the baby
3) Ventilate
 Use neonatal bags and mask e.g. Ambo bag (mouth to mouth if the former is not
available).
 Assess the baby after one (1) minute and the 5 minutes.
4) Monitor
i. Keep the baby warm by wrapping and covering the read.
ii. Delay first bath.
iii. Watch for signs of difficulty in breathing: rapid, labored, poor colour.

Care after successful Resuscitation

1. Reassure the mother and explain whatever happened and what was also done for the baby to her.
2. Provide warm especially skin to skin contact
3. Prevent heat loss by wrapping the baby.
4. Observe the colour, activity, and respiration of the baby.
5. Examine for malformation and birth injuries.
6. Observe critically for the first 24 hours
7. If condition permit start breastfeeding
8. Decontaminate all equipment used using bleach solution as by standard protocols of infection
prevention.

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 9. Document all findings.
COMPLICATIONS OF ASPHYXIA
 Hypothermia
 Hypoglycaemia
 Cerebral haemorrhage
 Retinopathy
 Intracranial haemorrhage
 Mental retardation
 Learning difficulties.
 Seizure Disorders
 Paralysis
 Developmental delay
 Cerebral palsy

34
 CHAPTER THREE

NEONATAL JAUNDICE/ICTERUS

It is a yellowish discoloration or yellow coloration of the skin, sclera and mucus membranes due to an
accumulation of bilirubin in the blood and tissue (hyperbilirubinaemia).

CONJUGATION OF BILIRUBIN
The breakdown of aged malformed and immature red blood cell (RBC) from circulation results in by-
product of haemoglobin and iron (from haemoglobin breakdown)
• Heam is converted to biliverdin and then to unconjugated bilirubin
• Globin is broken down into Amino acids which are reused by the body to make proteins
• Iron is stored in the body or used for new red blood cells.
• Two main forms of bilirubin are found in the body
Conjugated bilirubin and
Unconjugated bilirubin
• Unconjugated bilirubin is fat soluble and cannot be excreted easily either in bile or urine
• Conjugated bilirubin has been made water soluble in the liver and can be excreted either in
feaces or urine.

STAGES OF BILIRUBIN CONJUGATION

There are three stages involved in the process of bilirubin Conjugation.
 Transport
 Conjugation
 Excretion

1. The transport stage;

At this stage, unconjugated bilirubin is transported in plasma to the liver bound to albumin which does
not move out from the circulating blood but bilirubin that is not bound to albumin (free bilirubin) moves
from circulation into tissues such as skin and brain.

2. Conjugation stage
Unconjugated bilirubin is transported by intracellular protein Y and Z to the smooth endoplasmic
reticulum of the liver where it detaches itself from albumin and combines with glucose and glucuronic
acid to form Conjugated bile (Conjugated bilirubin) in the presence of oxygen using an enzyme called
uridine diphosphgluronyl transferase (UDP-GT) or glucuronlytransferase. The Conjugated bilirubin is
now water soluble and available for excretion.
3. Excretion
The Conjugated (water soluble) bilirubin is excreted through the biliary system into the small intestine
and act on by intestinal / normal flora bacterial to form urobilinogen which is the oxidized to form
urobilin (orange coloured) and excreted in feaces and urine (stercobilinogen excretion in feaces makes
the colour brown)

35
TYPES OF JAUNDICE IN THE NEWBORN
There are basically Two main types of jaundice
• Physiological jaundice and
• Pathological jaundice

PHYSIOLOGICAL JAUNDICE
This is common problem seen in both term and preterm babies. This results from physiological breaking
down of red blood cell.

CAUSES OF PHYSIOLOGICAL JAUNDICE

• Excessive/Increased Red Blood Cell breakdown
The foetus in utero relies on haemoglobin F (foetal haemoglobin) and this has a great affinity for oxygen
than haemoglobin A (adult haemoglobin or primary haemoglobin after birth). This greater affinity
ensures that the foetus obtains sufficient oxygen through the placenta from maternal blood. Following
birth, as haemoglobin A replaces haemoglobin F. The latter is broken down into bilirubin and other
products. Also the newborn red blood cells have a shorter life span (100 days in infants and 60-80 days
in preterm infants as opposed 120 days in adults.
• Liver immaturity
Neonatal liver cannot produce enough enzyme glucuronyl transferase to cope with the large amount of
bilirubin to be conjugated and so the excessive unconjugated bilirubin get into the tissues.
• Increase Entero-hepatic reabsorption:
Entero-hepatic reabsorption of bilirubin is increased in neonates because they lack the normal enteric
bacteria that break down bilirubin to urobilinogen (the gut is sterile and lack the enzymes needed). In
addition, there is increased Beta glucuronidase enzyme activity in the bowel of the newborn which
hydrolyses conjugated bilirubin back into the unconjugated state which reabsorbed back into circulation.
If feeding is delayed, bowel motility is also decreased aiding in reabsorption.
• Low Plasma-Binding Capacity
Newborns have poor albumin binding capacity for bilirubin because of reduced albumin concentrations.

SIGNS OF PHYSIOLOGICAL JAUNDICE

• Occurs 2-3 days after delivery
• Fades by the end of the 7th day and completely disappears by the second week.
• The discoloration may appear only as faint thing or orange –pink colour.
• The baby is not anaemic
• The baby’s general condition is good.
• The serum bilirubin level never exceeds 250mmol/L.
• The highest serum bilirubin level occurs on the 3rd and 4th day of life.

MANAGEMENT OF PHYSIOLOGICAL JAUNDICE

1. Reassure the mother and explain to her that, it is common with most babies and that it will resolve by
itself. This will allay her fear in anxiety.
2. Early breastfeeding should be encouraged because;
a. It increase the GIT motility thereby helping with the excretion of the conjugated bilirubin.
b. It also help the GIT to be colonized by bacteria
c. The liver will also be supplied with glucose to manufacture the enzymes.

36
3. The degree of jaundice must also be observed. If the serum level is above normal, then the causes
should be investigated.
4. Phototherapy may be given continuously/ intermittently (6 hours on, then 6 hours off)
5. Protect the eye and genitals
6. Extra fluid may be given when necessary.
7. Provide warmth
8. Avoid chilling and overheating of baby
9. Put baby on early morning sun.
10. Observe stool and urine of baby (green stools in this case is due to excretion of bilirubin)
11. Careful observation will help to distinguish between healthy babies with a normal physiological
response (needing no active treatment) and those who need serum bilirubin testing or active treatment.

PHOTOTHERAPY
This is the application of intense fluorescent light on the infant’s exposed skin. The blue light enhances
bilirubin excretion by the process of photoisomerization.
The effectiveness of phototherapy is determined by a decrease in the bilirubin levels usually a fall of 3-
4mg/daily after 8-12 hours of treatment. The child’s physical status should also be assessed because
suppression of jaundice can mask the signs of sepsis, hepatitis etc. The baby is exposed with the eye
covered with early Moring sunlight for about 45mins or a high-density fluorescent light (blue / white).
This may reduce the serum bilirubin level. Photo therapy may be done with a baby in a cot or exposed in
an incubator with the eyes covered to prevent damage.

INDICATIONS OF PHOTOTHERAPY
1. Serum bilirubin exceeding 250mmol/L in a full-term baby or level determined by the baby’s gestation
e.g. Preterm.
2. Jaundice appearing before 24 hours of life
3. It depends on serum bilirubin level.
a. In pre-term babies who weigh 1500 g; 85 -140umol/ L (5- 8 mg/d l).
b. The pre-term infants greater than 1500 g, sick infants those with haemolysis between 140- 165 mg/dl
c. For healthy term infant’s jaundice between 250- 365umol /L (17-22mg /d l).

N/B: Visible jaundice anywhere on the body on day 1or on the hand and feet in addition to the arms and
legs on day 2 is very serious and needs to be treated with phototherapy immediately. Do not wait to
begin phototherapy until serum bilirubin level is known

PRECAUTIONS USED DURING PHOTO THERAPY

The infant receiving phototherapy requires special attention to avoid complications like the
following;
• The infant’s eye should be covered with opaque mask to prevent exposure to ultraviolent rays
that can cause retinal damage. The shield should be properly sized and positioned to prevent
any occlusion of the nares.
• The eye lids are closed before the masks are applied; the corneas may become excoriated if
they come into contact with the dressing.
• The eye lids should be removed periodically (15mins) every 3hours for inspection of
inflammation or excessive pressure. If the shields allow light to enter, the area of jaundice
around the eyes will begin disappearing indicating the need for better eye protection.

37
 • The child is placed nude under the fluorescent light and turned frequently because areas that
are protective from light retained their jaundiced appearance and must be turned.
• Extra fluid must be given to the baby because fluid may be lost by insensible perspiration
from the skin due to heat and loose stools resulting from the photo therapy. Signs of
dehydration should also be watched for; intake and output should be monitored accurately.
• The temperature should be checked every 4hours, because the baby may become too cold,
from being uncovered or too hot as a result of the produced by the light.
• The therapy can disrupt the attachment bond between the child and his parents. This can be
minimized by removing the child from the light and removing the eye shield every 8hours for
the parents to feed and cuddle.
• Parents should be encouraged to touch and speak to the baby during breast feeding periods
and also while lying in phototherapy apparatus.
• There should be accurate charting on times phototherapy started and stopped including
internal lights off.
• As with any other electrical equipment in the nursery safety of unity must be ensured.
• If the child does not response to phototherapy and the unconjugated bilirubin rises above
350mmo1/dl in a normal term infant, an exchange blood transfusion should be done.
• It is also recommended that the new born genital area should be shielded to protect the
testicles.
• Frequent stool occurs with rapid decrease in bilirubin and can lead to perineal excoriation,
carefully and frequent cleansing of the new born is essential.
• Ointments should not be used because it could burn the skin during the phototherapy.
• Urine specific gravity is assessed for dehydration
• A new born temperature is monitored frequently and position is change a minimum of every
2hours.

FAMILY SUPPORT DURING PHOTOTHERAPY

1. The queer part of the therapy should be explained to the parents. This includes the nakedness of the
baby, blind folds etc. Efforts that they try to put towards the child’s recovery should be praised.
2. The parents may also feel guilty for causing blood incompatibility. Hence, they should be made to
express their feelings.
3. Tell the parents that, the discolouration may disappear within 2-3days.

DURATION OF PHOTOTHERAPY
It may be given continuously interrupted only for care and feeding or intermittently for periods of 6hrs
on and 6hrs off.

MANAGEMENT OF BABY RECEIVING PHOTOTHERAPY

A high intensity fluorescent light either white or blue is used.
It can be placed on top of the incubator or baby’s cot.
The baby is exposed naked to light, but the eyes are covered to prevent retinal damage.
If it’s a male, the scrotum is covered with gauze to prevent too much heat to the testes.

NB: The full term could be managed in a cot, but the pre-term in an incubator to prevent hypothermia.

38
1. Temperature control is important because the baby may become too cold from being uncovered or too
hot as a result of radiant heat.
2. Fluid may be lost by perspiration from the skin and intestinal injury due to the effect of the
phototherapy hence extra fluid may be given either by IV infusion or encourage frequent breastfeeding.
3. Mother should be encouraged to touch or speak to baby during treatment period, to lift baby and feed
baby as often as possible.
4. The treatment should be given continuously, interrupted only for care and feeding or intermittently for
period of 6hrs on and 6hrs off.
5. Close monitoring is needed to observe the colour, temperature of the cot or incubator and the baby
and increase fluid intake.
6. The baby should be changed regularly and keep proper records on everything.
Check colour of urine and faeces and consistence.
7. DRUGS: Phonobarbitone 4mg / Kilo per day may be prescribed for the enzyme.
8. Physical assessment which includes observation on;
a. The extent of changes in skin and sclera / colour.
b. Head to toe regression of jaundice
c. Other clinical signs such as lethargy and decrease eagerness to feed.
d. Dark urine or light stools
e. Dehydration, hypothermia, starvation, acidosis or hypoxia, vomiting, irritability or high pitch
cry.

MIDWIFERY CARE DURING PHOTOTHERAPY

1. TEMPERATURE; Baby is maintained in a warm thermo neutral environment and observe for
hyperthermia or hypothermia.
2. EYE: Eye shields or patches must cover the eyes without occluding the nose and not to be too tight to
cause eye discharge or weeping.
3. SKIN: Skin is cleaned with warm water and observed for rashes, dryness and excoriation.
4. HYDRATION: Fluid intake and output are monitored and demand feeding is continued.
- Extra fluid may be needed for ill / dehydrated babies.
5. NEUROBEHAVIORAL STATUS: This includes sleep and wake state, feeding behavior,
responsiveness, response to stress and interaction with parents and other carriers.
6. CALCIUM LEVELS: In neonate, hypocalcaemia is defined as total serum of less than 1 .7umol/L (7
mg / dl). Symptoms include jitteriness, irritability, rash loose stools, fever dehydration and convulsion.
The need to assess and observe for the above-mentioned signs.
7. BILIRUBIN LEVELS: The reduction in bilirubin levels appears be greatest in the 1st 24 hours of
phototherapy hence bilirubin levels are usually estimated daily.
8. PARENTS SUPPORT: In most cases, parents will be caring for their infants and need adequate
information and support to help them in this role. To give informed consent, parents must know the side
effect of phototherapy and the possible risk of not treating their baby.

COMPLICATIONS OF PHOTOTHERAPY
 Bronze baby syndrome, in this syndrome the baby’s urine and skin become blackish – brown.
This condition occurs mostly with those who have elevated conjugated bilirubin.
 Retinal damage  Passage of loose green stools
 Skin rash and burns  Dehydration

39
  Hyporthermia  Separation from the mother
 Hypoglycaemia  Hypocalcemia

NB: Physiological Jaundice can sometimes occur within the first 24 hours of life and last about five (5)
days.

PATHOLOGICAL JAUNDICE
This is also known as unconjugated pathological hyperbilirubinaemia.
Pathological Jaundice in the new born usually appears within 24hours at birth or less than 24 hours of
age and last longer than the first week of life. It is characterized by a rapid rise in serum bilirubin. This
jaundice is called pathological because it poses a risk to the baby due to its degree or its cause.

CRITERIA OR CHARACTERISTICS
• Jaundice within the first 24hours of life or earlier.
• Rapid rise in total serum bilirubin greater than 85umol/L (5mg/dl) per day.
• Total serum bilirubin greater than 200umol/L (12mg/dl)
• Conjugated bilirubin greater than 25 – 35mmol (1.5 – 2 mg /dl)
• Persistent of clinical jaundice for 7 – 10 days in term babies or 2 weeks in preterm babies.

CAUSES OF PATHOLOGICAL JAUNDICE

The underlying causes of pathological jaundice is any interference in bilirubin production, transport,
conjugation and excretion.
Underlying causes of pathological jaundice include;
 Blood incompatibility
 Blood diseases
 Genetic syndromes
 Hepatic Cirrhosis
 Bile diet blockage
 Other liver diseases
 Infections or medications (antimalarial in G6PD deficiency)
General Causes of Pathological Jaundice as Discussed under the Following Headings (Production,
Transport, Conjugation and Excretion)

A. PRODUCTION:
Increased red cell destruction or haemolysis cause increase bilirubin level and this is caused by:
• Blood type/group incompatibility; Rhesus and ABO incompatibility.
• Extravasated blood from cephal haematoma and bruising.
• Sepsis can lead to increased haemolysis
• Haemoglobinopathies such as sickle cell and thalassaemia (recessively inherited
haemoglobinopathuy prevent normal haemoglobin production.
• Spherocytosis: fragile red cell membrane
• Polycythemia: too many red blood cells as in materno-foetal / twin-to – twin transfusion.
• Enzyme deficiency: glucose 6 phosphate dehydrogenase (G6PD) maintain the integrity of the
cell membrane of the red blood cell, therefore a deficiency result in increased
breakdown of Haemoglobin. The deficiency can be as a result of certain drugs Example, Anti
malaria drugs.

40
B. TRANSPORT
This deals with factors that lower blood albumin levels or decrease albumin binding capacity.
• Hypothermia, acidosis or hypoxia can interfere with albumin binding capacity.
• Drugs that compete with bilirubin for albumin binding site (aspirin, sulphonamides and
ampicillin).

C. CONJUGATION:
Immaturity of the neonate enzyme system interferes with bilirubin conjugation in the liver.
However, other factors such as
• Dehydration, starvation, hypoxia and sepsis (Oxygen and glucose are required for conjugation.
• Torch infection (Toxoplasmosis others are rubella, cytomegalovirus, herpes).
• Other viral infections (eg. Neonatal viral hepatitis)
• Other bacterial infection, particularly those caused by [Link].
Metabolic and endocrine disorders that alter UDPT-GT enzyme activity. Such as hypothyroidism and
galactosaemia.

D. EXCRETION
Condition interfering with bilirubin excretion include the following
I. Hepatic obstruction caused by congenital anomalies example; Extra hepatic biliary atresia
ii. Obstruction by bile plugs from increased bile viscosity (example; Cystic fibrosis, total parenteral
nutrition, haemolytic disorders, dehydration.).
iii. infection, other congenital disorders and idiopathic neonatal hepatitis which can also cause excess of
unconjugation bilirubin.
iv. Saturation of protein carries needed to excrete conjugated bilirubin into biliary system.

TYPES OF PATHOLOGICAL JAUNDICE

1. Haemolytic jaundice
2. Obstructive Jaundice
3. Infective Jaundice

HAEMOLYTIC JAUNDICE / ERYTHROBLASTOSIS

This is also referred to as Erythroblastosis fetalis or haemolytic disease of the new born. It is the most
destructive among all the jaundice. It is most commonly caused by Rhesus factor or ABO blood
grouping incompatibility between the mother and the fetus or by G6PD deficiency in the baby.

CAUSES
• Rhesus incompatibility that is between mother and fetus
• ABO incompatibility.
Other causes include;
• G6PD
• Polycythermia and
• Septicaemia
All pregnant women who are Rhesus negative who have blood type ‘O’ (possible ABO incompatibility)
should be asked about outcome of any previous pregnancies including abortions and their history of
blood transfusion.

41
RHESUS INCOMPATIBILITY
The Rh factor is named after the Rhesus monkey, because while using monkey blood to develop an
antiserum that would differentiate between blood types, some of the blood began to clot. Your blood is
said to be Rh+ if it clots when exposed to the antiserum. If not, you have Rh- blood.

Rhesus (Rh) factor is an inherited trait that refers to a specific protein found on the surface of red blood
cells. If your blood has the protein, you are Rh positive + the most common Rh factor (85%). If your
blood lacks the protein, you are Rh negative. Although Rh factor does not affect health, it can affect
pregnancy. Pregnancy needs special care if one (woman) is Rh – and the husband is Rh+.
Rhesus incompatibility is a condition that develops when a pregnant woman has Rh- blood and the baby
in her womb has Rh+ blood.

Causes:
During pregnancy, red blood cells from the unborn baby can cross into the mother's bloodstream
through the placenta.
If the mother is Rh (-) negative, her immune system treats Rh-positive fetal cells as if they were a
foreign substance and makes antibodies against the fetal blood cells. These anti- Rh antibodies may
cross back through the placenta into the developing baby and destroy the baby's circulating red blood
cells.
When red blood cells are broken down, they make bilirubin. This causes an infant to become yellow
(jaundiced). The level of bilirubin in the infant's bloodstream may range from mild to dangerously high.
Because it takes time for the mother to develop antibodies, first born infants are often not affected
unless the mother had past miscarriages or abortions that sensitized her immune system. However, all
children she has afterwards who are also Rh-positive may be affected.

42
SIGNS AND SYMPTOMS:
 Anemia (low red blood cell count)
 Problems with blood circulation and fast heart rate, which may lead to heart failure
 Hydrops fetalis (the baby’s whole body becomes swollen)
 Jaundice (yellow coloring of skin and sometimes eyes) resulting from high bilirubin
 Enlarged organs (liver, spleen, and/or heart)
 Small red/brown spots, or purple patches of the skin
 Trouble breathing
 Dark, amber colored urine
 Fatigue
Diagnostic findings:
• A positive direct Coombs test result
• Higher-than-normal levels of bilirubin in the baby's umbilical cord blood
• Signs of red blood cell destruction in the infant's blood

Treatment:
• Because Rh incompatibility is preventable with the use of anti-D, prevention remains the best
treatment.
• Treatment of an infant who is already affected depends on the severity of the condition.
• Infants with mild Rh incompatibility may be treated with phototherapy using bilirubin lights. IV
immunoglobulin may be used.

Prevention:
• Rh incompatibility is almost completely preventable. Rh-negative mothers should be followed
closely by their obstetricians during pregnancy.

43
 • Special immunoglobulins, called anti-D, are now used to prevent RH incompatibility in mothers
who are Rh-negative.
• If the father of the infant is Rh-positive or if his blood type cannot be confirmed, the mother is
given an injection of anti-D during the second trimester. If the baby is Rh-positive, the mother
will get a second injection within a few days after delivery. (72 hours)
• These injections prevent the development of antibodies against Rh-positive blood. However,
women with Rh-negative blood type must receive injections:
• During every pregnancy
• If they have a miscarriage or abortion
• After prenatal tests such as amniocentesis and chorionic villus biopsy
• After injury to the abdomen during pregnancy

MANIFESTATION OR FEATURES OF SUCH BABIES

Babies present basically with three (3) features
1. Haemolytic anaemia
2. Icterus gravis Neonatorium
3. Hydrops fetalis.

1. HAEMOLYTIC ANAEMIA
This is anaemia that starts right at birth and is noticed between the third (3rd) and tenth (10th) day after
birth or between third (3rd) to fourth (4th) week of birth. That is Anaemia is present at birth. Jaundice is
slight and on set of anaemia is slow.

SIGNS/SYMPTOMS
• Liver and spleen are enlarged
• Baby looks pale after delivery
• Haemoglobin level is low (about 6g/dl or 40%)
TREATMENT
Exchange transfusion to restore haemoglolin level, reduce the bilirubin and remove maternal rhesus
antibodies. Blood transfusion is of packed cells and the amount of blood is 30mls.
NB: Give all nursing care.

2. HYDROPS FETALIS
This is the most serious form of the haemolytic disease of new born. In this type both the placenta and
the fetus are oedematous which may be associated with hydramninos and toxaemia. Congestive heart
failure occurs due to severity of anaemia. Most of the time the fetus dies in utero after 28 weeks of
pregnancy and it is still born or dies soon after birth.
SYMPTOM
1. Baby is extremely pale at birth.
2. Red Blood cells breakdown
3. Severe oedema and ascites
4. Mother may present with polyhydraminous in pregnancy and labour.
5. Placenta is large and bulky with fluid oozing from it.
6. Baby is usually still born or die soon after birth
NB: There is no treatment

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 ICTERUS GRAVIS NEONATORIUM
This starts right from the utero and it is the severest form of jaundice (Haemolytic Jaundice) in new born
baby. The baby is deeply jaundiced and develops anaemia quickly or progressively within few hours of
birth. The spleen and liver are enlarged upon examination and the cord is yellowish due to the presence
of bilirubin in the liquor aminii.

SYMPTOM
1. baby has low haemoglobin level 5. Decreased respiratory movement
2. Umbilical cord at birth is bile stained. 6. Baby is lethargic
3. Liquor ammi is also bile stained. 7. Baby is pale
4. Frosty mucus in baby’s mouth. 8. Liver and spleen are enlarged
TREATMENT
• Blood transfusion of packed cells.
• Give all nursing care.

PREVENTION OF RHESUS INCOMPATIBILITY

• Avoid transfusion of Rhesus positive blood to Rhesus negative women
• Placental localization by ultrasound should be undertaken before amniocentesis.
• There should be proper management of second and third of labour
• External cephalic version or manual removal of placenta should be done with gentleness
• Reduce abnormal palpation in the cases of APH.
• Administration of anti “D” (RhOGAM) immunoglobulin after amniocentesis or Rhesus
immunoglobulin (RhoGAM) can also be given in abortions before 20th week of pregnancy;
250mmol. Dosage is 500 iv after abortion after 20th weeks. After delivery, dosage is 500 IV given in
72 hours.

DIAGNOSIS
Kleihauer’s test: This is done to determine the number of fetal cells in maternal circulation.
Coomb’s test: This measures the number of antibodies in the maternal blood (direct and indirect).

ANC MANAGEMENT OF ISOIMMUNIZATION

• Estimation of blood group for all pregnant women. Women with Rhesus negative blood group are
screened for antibodies with indirect coomb’s test. Blood is tested at 28 and 34weeks of pregnancy.
If antibody is present, depending on the level, amniocentesis is done.
• Spectrophotometric Scanning is done to determine the amount of bilirubin excretion.
• Intrauterine transfusion to the foetus. Amniocentesis: in some cases amniocentesis between 30 and
36weeks of pregnancy adds great accuracy of prediction and helps to assess the severity of the
disease. The degree of staining of the liquor with bile pigment and the actual quantity of the antibody
is estimated. PROCEDURE FOR INTRAUTERINE TRANSFUSION
Blood group O- packed cells are given through fetoscopy depending on gestational age or antibody
level. The level of transfusion is giving two weeks interval until delivery and only a specialist must
carry out the procedure. Premature induction of labour – this is based on previous history of
maternal antibody level and bilirubin content of amniotic fluid.
• As prophylasis Rhogam is given during antenatal

45
 CARE AT BIRTH
Clamp cord immediately baby is born.
Cord blood sample is taken using syringes and needle.
Wet saline dressing is applied to the umbilical cord to keep the vessels patent.

INVESTIGATION DONE ON CORD BLOOD

• ABO and Rhesus type.
• Direct coomb’s test
• Haemoglobin estimation
• Serum bilirubin level (exchange blood transfusion if serum bilirubin level is above 340mmol)
• Kleihauer’s test

POSTPARTUM MANAGEMENT
The goals of postpartum care are to prevent sensitization in the as-yet-unsensitized woman and to treat
the isoimmune haemolytic disease in the new born.
The Rhesus mother who has no titer (in – direct coomb’s test negative) and who has given birth to a
Rhesus positive baby (direct coomb’s test negative) is given in Rhogam 500mg 72hours so that she does
not have time to produce antibodies to fetal cells that entered bloodstream when the placenta was
separated.
RhoGAM works to destroy fetal cells in the maternal circulation before sensitization occurs.

ABO IMCOMPATIBILITY
A, B, and O are the three major blood types. The types are based on small substances (molecules) on the
surface of the blood cells.
When people who have one blood type receive blood from someone with a different blood type, it may
cause their immune system to react. This is called ABO incompatibility.
• If you have type A blood, you can receive type A & O blood.
• If you have type B blood, you can receive type B & O blood.
• If you have type AB blood, you can receive type A, B, AB & O blood.
• If you have type O blood, you can receive type O blood
• NB: Type O blood can be given to anybody with any blood group. This is why people with type
O blood are called universal blood donors. Blood type AB can receive blood from all the blood
types, they are called universal blood recipients. People who have one blood type may form
proteins (antibodies) that cause their immune system to react against one or more of the other
blood types.

FOR EXAMPLE
• Being exposed to another type of blood can cause a reaction. This is important when a patient
needs to receive blood (transfusion) or have an organ transplant. The blood types must be
matched to avoid an ABO incompatibility reaction.
• A patient with type A blood will react against type B or type AB blood.
• A patient with type B blood will react against type A or type AB blood.
• A patient with type O blood will react against type A, type B, or type AB blood.
• A patient with type AB blood will NOT react against type A, type B, or type AB blood.

46
COMPATIBLE AND INCOMPATIBLE BLOOD GROUPS
Patient Antibodies Antigens in the red blood cell of donor
(recipient present in A B AB O
blood serum
group)
A anti-b • X X •
B anti-a X • X •
AB Non • • • •
O anti-a & -b X X X •
Key:
• -compatible recipient’s blood
X -incompatible with recipient’s blood

SYMPTOMS
The following are symptoms of ABO incompatible transfusion reactions:
1. Back pain 4. Feeling of "impending doom"
2. Blood in urine 5. Fever
3. Chills 6. Yellow skin (jaundice)

DIAGNOSTIC FINDINGS
• The health care provider will perform a • Complete blood count (CBC) shows
physical exam. Blood tests will usually damage to red blood cells or anemia
show: • The patient's and donor's blood are not
• Bilirubin level is high compatible

TREATMENT
• Treatment may include:
• Drugs used to treat allergic reactions (antihistamines)
• Drugs used to treat swelling and allergies (steroids)
• Fluids given through a vein (intravenously)
• Medicines to raise blood pressure if it drops too low

OUTLOOK (PROGNOSIS)
• ABO incompatibility can be a very serious problem that can even result in death. With the right
treatment, a full recovery is likely.
COMPLICATIONS
• Kidney failure
• Low blood pressure needing intensive care

ABO INCOMPATIBILITY IN RELATION TO NEONATAL JAUNDICE

Haemolytic disease of the newborn can also result from maternal blood group O. The condition usually
affects first born baby and subsequent ones. It is usually seen in infants with blood group A and B whose
mothers are of O.

47
This incompatibility occurs as a result of the maternal antibodies present in her serum and interaction
between the antigen sites on the foetal red blood cells. The high maternal serum anti A and B crosses the
placenta and produces haemolysis of the foetal red blood cells. Once haemolysis occurs, Bilirubin levels
goes up and subsequently jaundice.

SIGNS / RECOGNITION
ABO should be suspected in the following cases
1. Jaundice developing within 24 – 36 hrs of birth.
2. Bromeline test that is the presence of A or B haemolysis or antibodies.
3. Haemolysis in the maternal blood.
4. Negative coomb’s test is found in jaundice developing 24hrs after birth.
5. Jaundice is mild.
6. Spleen and liver enlargement

MANAGEMENT OF ABO AND RH FACTOR INCOMPATIBILITY

ANC
• Find out proper history from mother at antenatal clinic. Questions like any anaemia, jaundice,
transfusions etc in her previous pregnancies
• Find out if she had APA, abortions or Manuel removal of placenta before
• Check blood for Rhesus factor and ABO. This test uses two forms. Coombs test (direct and
indirect)
• Couples should be counselled as to the dangers of the baby’s health when born for them to make
an informed choice or terminate pregnancy
• In advanced countries, intrauterine blood transfusion can be given to support the baby till term.
Packed cells between 40-120mls.

CARE DURING LABOUR

• Clamp and cut cord immediately baby is born
• Coombs test can be done here also, few drops of blood from baby’s cord when cut can be used
• Take blood for Haemoglobin estimation and serum bilirubin level.
• Caution should be taken to avoid milking the cord before clamping

POSTNATAL CARE
• Nurse baby in the NICU whiles waiting for blood results to come with ABO /RHESUS factors
• Main treatment is EXCHANGE BLOOD TRANSFUSION to correct anaemia t, remove
maternal Rhesus factor, reduce serum bilirubin level, and remove the breakdown red blood cells.
Blood transfusion should aim at exchanging 80-90percent of foetal blood
• Phototherapy is ensured after delivery
• All other nursing care included.

EXCHANGE BLOOD TRANSFUSION

Exchange transfusion is a potentially life-saving procedure that is done to counteract the effects of
serious jaundice or changes in the blood due to diseases such as sickle cell anemia.
The procedure involves slowly removing the patient's blood and replacing it with fresh donor blood or
plasma.

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DESCRIPTION
An exchange transfusion requires that the patient's blood be removed and replaced. In most cases, this
involves placing one or more thin tubes, called catheters, into a blood vessel. The exchange transfusion
is done in cycles; each one usually lasts a few minutes.
The infant’s blood is slowly withdrawn (usually about 5 to 10 mL within 15 to 20 seconds and the same
volume of donor’s blood is infused over 60 to 90 seconds, depending on the infant’s body weight and
the severity of illness). An equal amount of fresh, pre warmed blood or plasma flows into the patient's
body. This cycle is repeated until the correct volume of blood has been replaced.
After the exchange transfusion, catheters may be left in place in case the procedure needs to be repeated.
If the blood has been citrated (addition of citrate phosphate adenine to prevent coagulation), calcium
gluconate may be given after the infusion of each 100mls if donor’s blood, to prevent hypocalcaemia
In diseases such as sickle cell anemia, blood is removed and replaced with donor blood.
In conditions such as neonatal polycythemia, a specific amount of the child’s blood is removed and
replaced with a normal saline solution, plasma (the clear liquid part of blood), or albumin (a solution of
blood proteins). This decreases the total number of red blood cells in the body and makes it easier for
blood to flow through the body.

INDICATIONS
An exchange transfusion may be needed to treat the following conditions:
• Neonatal polycythemia (dangerously high red blood cell count in a newborn)
• Rh-induced hemolytic disease of the newborn/Rh isoimmunization
• Severe newborn jaundice that does not respond to phototherapy.
• Severe sickle cell crisis
• Toxic effects of certain drugs
• ABO incompatibility
TECHNIQUE
PREPARATION FOR EXCHANGE TRANSFUSION
Inform the parents of the baby’s condition. Explain the procedure to them and obtain permission by
helping them, sign consent form. A trolley is prepared with required equipment.

REQUIREMENT
TOP SHELF
20mls syringe A probe
2 or 3way catheter. A plain dissecting forceps.
A gallipot for containing methylated spirit. A pair of scissors
A gallipot with saline. A needle holder
2 small towels drape pulse oximeter Suture silk
An overhead radiant heater.

BOTTOM SHELF
Calcium gluconate (10 %) Padded Cruciform
Methylated spirit 2 well label specimen bottles
Bandage

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MANAGEMENT BEFORE EXCHANGE TRANSFUSION
• Signing of consent form and explanation of procedure to parents as well as possible complications of
the procedure.
• Infants should be kept under a servo- controlled radiant/warmer with cardiac, Blood pressure and
oxygen saturation monitoring in place.
• Ensure equipment and personal for resuscitation are readily available.
• Ensure intravenous line in place for administration of glucose and other medications.
• The infant’s arms and legs should be restrained
• Ensure blood is warmed to 37c before use.
• Sterile technique should be used .old umbilical cords can be softened with saline soaked gauze
facilitate locating the vein and inserting the catheter. If an umbilical line is placed in an infant more
than 1 or 2 days of age, or if there was a break in sterile technique you treat with oxacillin and
gentamycin for 2 to 3 days.
• Ensure the baby is fed before the procedure. Thus four (4) hours before the procedure
NB. The transfusion is given through the umbilical vein. 10mls of blood is withdrawn and used for
determining the levels of serum bilirubin, haemoglobin and glucose before transfusion in order to
avoid overloading the heart of the baby. The fetal blood is removed and discarded and immediately
replaced with a similar amount of fresh blood. Due to this 190mls of blood withdrawn and 180mls
replaced. At the end, the last syringe full of blood withdrawn is preserved for post transfusion test.

OBSERVATION DURING EXCHANGE TRANSFUSION

• Accurate recording of input and output of blood / volume of blood.
• The heart rate is monitored with electrocardiogram. Any changes are reported and recorded.
• The baby’s temperature is monitored in order to avoid the development of hypothermia or
hyperthermia.
• Any cyanosis, greyness or pallor is noted as these could indicate heart failure or collapse.
• Respirations are recorded and any sign of tarchypnoea, rib recession or grunting expirations are
reported.
• Abnormal movements such as jitteriness or twitching may indicate hypoglycaemia or
hypocalcaemia.

THE MIDWIFE RESPONSIBILITY AFTER EXCHANGE TRANSFUSION

a. When the exchange is finished a silk purse – sutre string suture should be placed around the vein.
The tails of the suture. Material should be left. This localization of vein will facilitate the next
exchange transfusion.
b. When the catheter is removed, the tie around the cord should be tightened snugly for
approximately 1 hour. It is important to loosen the tie after one hour to avoid necrosis around the
skin.
• The baby is returned to a warm cot or an incubation and observed closely for 6 – 8 hours.
• The umbilicus is inspected for bleeding every 15 minutes for the first few hours, 30 minutes, 1
hourly, 4 hourly after the procedure.
• Blood sample is taken for bilirubin estimation.
• The slow calcium infusions continue for a while in order to counteract any hypoglycaemia.
• After exchange transfusion, phototherapy is continued and bilirubin levels measured every 4 hours.
• Phototherapy may be given because the serum bilirubin level will rebound as antibodies in the
tissues return to the circulation and haemolyse further red blood cell.

50
• Parents are encouraged to visit their babies.
• Cease exchange transfusion if infant’s condition suddenly deteriorates. Sudden deterioration in
infant condition may be related to the procedure, underlying condition an adverse reaction report
should be made.

TECHNIQUE
1. Most exchange is done by the push-pull technique through the umbilical vein inserted only as far
as required to permit free blood exchange. (A catheter in the heart may cause arrhythmias).
2. Isovolumetric .ET. (Simultaneously pulling blood out of the umbilical artery and pushing new
blood in the umbilical vein). This is much tolerated better in small, sick or hydropic infants.
NB:// if it’s not possible to insert catheter in the umbilical vein, exchange transfusion can be
accomplished through central venous catheter placed in the antecubital fossa. (or into the
femoral vein through their saphrenous vein).

COMPLICATION
• Catheter related complications such as air embolism, thrombosis, haemorrhage.
• Haemodynamic (related to excess removal of infection of blood); hypotension or hypertension,
intraventricular haemorrhage (preterm)
• Hypoglcaemia or hyperqlycaemia, hypercalcaemia, hyperkalaemia acidaemia.
• Arrhythmia, bradycardia, neutropenia, feed intolerance, necrotizing, enterocolitis, septicaemia,
hypothermia or hyperthermia.

OBSTRUCTIVE JAUNDICE
This is the type of jaundice in which there is an obstruction within the liver or a blockage in the
extrahepatic bile duct. Here the liver is not diseased or immature but the channels are blocked which
leads to the accumulation of unconjugated bilirubin in the blood.
CAUSE
1. Biliary atresia
2. Biliary duct compression
3. Cystic fibrosis

SIGNS AND SYMPTOM

 Seen within the second week of life. It becomes deep, more severe and persistent for weeks.
 Fat digestion is impaired
 Stools are grey in colour
 Urine is bile stain making it darker in colour.
 There is sign of cerebral irritation, because some of the unconjugated bilirubin may stain the
brain cells.
 Spleen and liver may be enlarged.

MANAGEMENT
Treatment is surgical due to blockage in the biliary duct /extra hepatic duct. The surgery is done as
early as the 8th week of life.
General prognosis is poor, but if surgery is done in time, there is chances of baby’s recovery. All
other nursing care, both Pre-operative and post-operative is ensured.
Maintenance of body temperature, drugs and infection prevention is ensured.

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 INFECTIVE JAUNDICE
This is caused by either viral infection / bacterial infection. Examples are viral infection include
rubella, syphilis, cytomegalovirus and toxoplasmosis (touch).
Bacterial infection includes staphylococcus, streptococcus, (though the umbilical cord)

SIGNS/SYMPTOMS
• Hepato –Splenomegaly (enlargement • Drowsiness
of spleen and liver) • Fever
• Thrombocytopaemia (low platelet) • Baby may refuse to feed
• Diarrhoea and vomiting • Occurs within 1st week of life.

MANAGEMENT
1. In addition to the nursing care of infants, treatment for this is, isolation of organism through
Blood culture and sensitivity test. Administration of appropriate drugs based on causative organism.
2. Phototherapy is done.

KERNICTERUS (BILIRUBIN TOXICITY, BILIRUBIN ENCEPHALOPATHY)

This is a type of jaundice where there are high levels of unconjugated bilirubin on the brain cell/ basal
ganglion which stains it. This occurs when there is accumulation of fats soluble bilirubin (unconjugated
bilirubin) in circulation. The bilirubin level is as high as 340mmol/dl and can cause an irreversible
damage to the brain.
CAUSES
• High levels of bilirubin (icterus gravis Neonatorium).
• Overdose /indiscriminate use of Vitamin K.
• Infections (viral or bacterial)
• Prematurity
SYMPTOMS
1. There may be abnormal Moro reflex. 5. Neck rigidity when there is head
2. Signs of cerebral irritation example retraction (Opisthotonos)
(convulsions, retracted neck/signs of 6. Rolling of the eye ball.
hypotonic movement of limbs) 7. High pitch cry
3. Severe jaundice. 8. Floppiness
4. Baby shows signs of cerebral irritation 9. Baby may be lethargic and reluctant to
such as convulsion. feed.
PROGNOSIS
Prognosis is very poor but if the baby survive may have severe motor impairment.

MANAGEMENT
• The objective of care here is to prevent convulsion; therefore, stimuli should be avoided. If
convulsion is present manage.
• Handle baby gently when care is been giving.
• Tube feeding is encouraged due to difficulty in swallowing.
• If serum bilirubin is at the level requiring phototherapy continue it.
• Exchange blood transfusion is done and repeated if necessary.

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PREVENTION OF KERNICTERUS
• Carefully watch on bilirubin levels even if jaundice is slight (serum bilirubin level should be
monitored twice daily).
• Drugs likely to cause jaundice such as sulphonamides in the neonate should be avoided.
• Phototherapy both in the hospital and at home when levels are high.

COMPLICATIONS
• Mental Retardation. • Motor impairment.
• Deafness • Cerebral palsy

BREASTFEEDING JAUNDICE (EARLY-ONSET JAUNDICE)

Breastfeeding jaundice is a condition that occurs when there is a decreased intake of breast milk and a
decreased passage of meconium. Breastfed infants tend to have higher bilirubin levels than bottle-fed
infants.
Breastfeeding jaundice generally occurs between the 2nd and 4th days of life.
The total serum bilirubin levels peak at 15 mg to 19 mg/dL by 72 hours of life. Breastfeeding jaundice is
believed to be associated with poor feeding practices and is not related to the composition of the breast
milk.
Management
Early and frequent feedings with avoidance of formula and glucose supplementation constitutes the
primary therapy for breastfeeding jaundice

Breastmilk Jaundice (Late-Onset Jaundice)

This type of jaundice is called late-onset, or breast milk jaundice. This type of jaundice shows up during
the second week of life, and peaks around the tenth day or later. It affects a very small percentage of
infants between 2% and 3%.
The bilirubin count can remain elevated for weeks or even months, but will eventually level out at adult
level of 1mg/dl.
The diagnosis is usually made in a healthy. Thriving infant and only after all the pathologic causes of
jaundice have been ruled out. Often this type of jaundice runs in families and breastfed siblings are
likely to be jaundiced as well.
It may be due to a substance in the mother’s milk that increases the reabsorption of bilirubin, or
decreases the liver processing of bilirubin. When the baby is temporarily given formula, either as a
substitute for or along with mother's milk, the levels drop quickly, rising again as the baby returns to
breastfeeding.
Management
 It is managed by increasing frequency of breastfeeding.
 Sometimes babies are taken off breast for 24 hours just to make the diagnosis of breast milk
jaundice, though this is seldom necessary.
 Home phototherapy without discontinuation of breastfeeding may also be instituted.

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 CHAPTER FOUR

BLEEDING DISORDERS OF THE NEWBORN

This is also referred to as haemorrhagic disorders of the new born. Bleeding disorders in neonates are
associated with a traumatic birth or hemophilia. Bleeding disorders of the newborn, also known as
vitamin K deficiency bleeding (VKDB), is a coagulation disturbance in newborn infants due to vitamin
K deficiency. As a consequence of vitamin K deficiency there is an impaired production of coagulation
factors II, VII, IX, X, protein C and protein S by the liver, resulting in excessive bleeding (hemorrhage).
NOTE:
Vitamin K is necessary for the production of clotting factors. The production takes place in the liver, so
when the liver is damaged, production cannot take place. The intestinal flora also synthesis vitamin K
with peristalsis, so if there is delay in feeding vitamin K, cannot be produced. The breast milk contains
just a small quantity of this vitamin. Therefore, breast feeding babies also suffer from this condition. The
general causes of haemorrhage disorder of the newborn is deficient of vitamin K and its’ dependent
clotting factors (II, VII, IX)

CLASSIFICATIONS

1. Early-onset vitamin K deficiency bleeding in the newborn

Early-onset vitamin K deficiency bleeding usually occurs during first 24 hours after birth. It is seen in
infants born to mothers taking anticonvulsant or antituberculosis medication. Serious hemorrhagic
complications can occur in this type of hemorrhage.

The mechanisms by which anticonvulsant and antituberculosis medications cause vitamin K deficiency
bleeding in neonates is not clearly understood, but limited studies suggest that vitamin K deficiency
bleeding is a result of vitamin K deficiency and can be prevented by administration of vitamin K to the
mother during the last 2-4 weeks of pregnancy. Vitamin K supplementation given after the birth for
early onset vitamin K deficiency bleeding may be too late to prevent this disease, especially if vitamin K
supplementation was not provided during pregnancy.

Numerous maternal medications and/or exposure to toxins during pregnancy are associated with vitamin
K deficiency bleeding in neonates (eg, anticonvulsants [eg, phenytoin, barbiturates, carbamazepine],
antitubercular drugs [eg, rifampin, isoniazid], vitamin K antagonists [eg, warfarin, phenprocoumon]).

2. Classic vitamin K deficiency bleeding in the newborn

Classic vitamin K deficiency bleeding usually occurs after 24 hours and as late as the first week of life.
Classic vitamin K deficiency bleeding is observed in infants who have not received prophylactic vitamin
K at birth.

The incidence of classic vitamin K deficiency bleeding ranges from 0.25-1.7 cases per 100 births.

54
Usually the disease occurs from the second day of life to the end of the first week; however, it can occur
during first month and sometimes overlaps with late-onset vitamin K deficiency bleeding.

Infants who have classic vitamin K deficiency bleeding are often ill, have delayed feeding, or both.
Bleeding commonly occurs in the umbilicus, GI tract (ie, melena), skin, nose, surgical sites (ie,
circumcision), and, uncommonly, in the brain.

3. Late-onset vitamin K deficiency bleeding in the newborn

This usually occurs between age 2-12 weeks; however, late-onset vitamin K deficiency bleeding can be
seen as long as 6 months after birth.

This disease is most common in breastfed infants who did not receive vitamin K prophylaxis at birth.
Vitamin K content is low in mature human milk and ranges from 1-4 mcg/L.

Industrial contaminants in breast milk have been implicated in promoting vitamin K deficiency bleeding.

More than half of these infants present with acute intracranial hemorrhages

CAUSES

Newborns are relatively vitamin K deficient for a variety of reasons:

1. They have low vitamin K stores at birth, because vitamin K passes the placenta poorly
2. The levels of vitamin K in breast milk are low
3. The gut flora has not yet been developed (vitamin K is normally produced by intestinal
bacteria).
4. Maternal medications that interfere with vitamin K stores or function (eg, carbamazepine,
phenytoin, barbiturates, some cephalosporins, rifampin, isoniazid, warfarin or warfarinlike
drugs) can result in vitamin K deficiency bleeding in the infant.
5. In addition to breastfeeding, clinical states that are risk factors for late-onset vitamin K
deficiency bleeding include the following:
 Diarrhea  Short bowel syndrome
 Hepatitis  Intestinal bacterial overgrowth
 Cystic fibrosis  Chronic exposure to broad
 Celiac disease spectrum antimicrobials
 Alpha1-antitrypin deficiency

SIGNS AND SYMPTOMPS

Most newborn infants are healthy upon examination, even if early onset bleeding is present; however,
intracranial hemorrhage can occur during the birthing process and can lead to severe complications.

Signs of intracranial hemorrhage include apnea with or without seizures and a shock-like syndrome.

55
Internal hemorrhage of organs other than the brain may be difficult to detect; however, if they are
suspected, careful physical monitoring and serial imaging after birth are indicated.

Soft tissue hemorrhage is easier to recognize, but sequential measurements of the bleeding into soft
tissues or muscle are mandatory. The disease causes an increased risk of bleeding. The most common
sites of bleeding are:

1. Umbilicus,
2. Mucous membranes,
3. Gastrointestinal tract,
4. Circumcision sites
5. Venepunctures sites

DIAGNOSIS

Coagulations studies

A prothrombin time (PT), activated partial thromboplastin time (aPTT), fibrinogen levels, and a platelet
count should be included in the initial workup for vitamin K deficiency bleeding (VKDB) in a newborn.
A thrombin clotting time (TCT) is optional.

Note the following:

 A prolonged PT is usually the first laboratory test result to be abnormal in vitamin K deficiency
bleeding; however, no laboratory test result can confirm the diagnosis of vitamin K deficiency
bleeding.
 A direct blood measurement of vitamin K is not useful because levels normally are low in
newborns.
 Levels of protein induced by vitamin K antagonism (PIVKA II) are increased in vitamin K
deficiency bleeding, but this test is generally not available outside of research laboratories.
 Infants with vitamin K deficiency bleeding typically have a prolonged PT with platelet counts
and fibrinogen levels within the normal range for newborns. Thrombocytopenia or a prolonged
aPTT should prompt workup for other causes of bleeding during the neonatal period. For
example, maternal transfer of antiplatelet antibodies in mothers with immune thrombocytopenia
via breastfeeding may be associated with persistent neonatal thrombocytopenia.

The diagnosis of vitamin K deficiency bleeding is confirmed if administration of vitamin K halts the
bleeding and reduces the PT value.

Median platelet count and platelet mass have been reported to be significantly associated with
intracranial hemorrhage in neonates at days 1, 2, and 3 after diagnosis of gram-negative sepsis.

Other tests

A full coagulopathy work-up and hematology consultation are required if clinical and laboratory
findings are suggestive of non–vitamin K deficiency bleeding.

56
A work-up that includes functional tests and imaging are mandatory if liver disease is suspected.

Hereditary defects in the coagulation system must always be considered among the differential
diagnoses.

Differential Diagnoses

 Alloimmune Thrombocytopenia
 Consumption Coagulopathy
 Hepatobiliary Disease
 Maternal Isoimmune Thrombocytopenia
 Pediatric Von Willebrand Disease
 Uncommon Ccoagulopathies

NURSING MANAGEMENT

During acute bleeding, the infant with vitamin K deficiency bleeding should be handled with caution
until the coagulation profile returns to normal after vitamin K supplementation.

Immediately administer vitamin K subcutaneously (hold pressure on the site) for any infant in whom
vitamin K deficiency bleeding is suspected or who has serious, unexplained neonatal bleeding. Note the
following:

 IM administration can result in a hematoma because of the coagulopathy.

 Intravenous (IV) administration of vitamin K has been associated with anaphylactoid-like
reactions.
 Fresh frozen plasma may be considered for moderate-to-severe bleeding.
 Life-threatening bleeding may also be treated with prothrombin complex concentrates (PCC).
 Because the bleeding in classic vitamin K deficiency bleeding usually is not life threatening, a
single dose of parenteral vitamin K is sufficient to stop the bleeding and return prothrombin time
(PT) values to the reference range.

 In patients with vitamin K deficiency bleeding (VKDB), follow-up for continued bleeding after
vitamin K administration is indicated because other causes may be present.
 Hematocrit levels should be obtained serially and before discharge
 Ensure neurologic complications are stable or resolved before discharge.
 Infants with evidence of intracranial bleeding may require transfer to a level III nursery after
stabilization with subcutaneous vitamin K and other aspects of supportive care.
 Advice on best sources of vitamin K: green leafy vegetables, legumes, soybean and olive oils.
 Breastfed infants should receive vitamin K supplementation; if mothers refuse prophylaxis, they
should be counselled. Because breast milk is not a good source of vitamin K, infants of mothers
who refuse prophylaxis and who exclusively breastfeed should have receive oral
supplementation of vitamin K.

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DETERRENCE/PREVENTION

1. Intramuscular (IM) vitamin K prophylaxis at birth

2. Supplemental vitamin K in commercial infant formulas
3. Mothers should be encouraged to take diet in vitamin K to build up their vitamin K stores since
the baby would depend on the mother for its source of vitamin K

Forms of vitamin K

The following 3 forms of vitamin K are known:

 K 1: Phylloquinone is predominantly found in green leafy vegetables, vegetable oils, and dairy
products. Vitamin K given to neonates as a prophylactic agent is an aqueous, colloidal solution
of vitamin K 1.
 K 2: Menaquinone is synthesized by gut flora.
 K 3: Menadione is a synthetic, water-soluble form that is no longer used medically because of its
ability to produce hemolytic anemia.

COMPLICATIONS

Intracranial hemorrhage is the primary serious complication of vitamin K deficiency bleeding.

 Complications of treatment include anaphylactoid-like reactions during intravenous (IV) vitamin

K administration, hyperbilirubinemia or hemolytic anemia after high doses of vitamin K, and
hematomas at the site of injection, if administered IM.
 Neonatal mortality and long-term neurologic morbidity are severe consequences of vitamin K
deficiency bleeding.

CLOTTING DEFICIENCIES / DEFICIENT CLOTTING FACTORS

HYPOPROPTHROMBINAEMIA (FACTOR II DEFICIENCY)
This is where thromboplastin cannot be converted to prothrombin leading to low level of prothrombin in
the blood. It is a blood disorder in which a deficiency of prothrombin (factor 2) result in impaired blood
clotting leading to increased physiological risk for bleeding especially in the gastro intestinal system,
cranial vault and superficial integumentary system.

INCIDENCE
Congenital factor two deficiency is really very rare as only 100 cases are known worldwide. It affects
both male and female as well as people of all races and ethnic origin.

CAUSES
• Vitamin K deficiency: Prothrombin is produced in the presence of Vitamin K and its deficient
in the new born
• Liver Immaturity or Disorders can cause a reduction of factor two since this organ sensitized

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PREDISPOSING FACTORS
• Anoxia: This causes engorgement of the blood vessels leading to bleeding into organs. It can
occur in conditions such as Asphyxia, hypoxia, liver damage etc.
• Use of anticoagulant or Anti-Convulsant.
• Poor breastfeeding Vitamin K is also derived from breast milk especially colostrum.

SIGNS AND SYMPTOM

The effect of the infant will depend on the severity and the amount of haemorrhage that has occurred.
• Bleeding from umbilical cord at birth. Bleeding is seen between the second (2nd) and forth (4th)
day of birth without any apparent cause.
• Bleeding may start like a petechial rash spot. Site of bleeding can be from any of the mucus
that is retina, scalp of head, nose and conjunctiva.
• Bleeding is observed from punctured site or after using forceps on any part of the body.

DIAGNOSIS
Blood is taken for clotting time which reveals prothrombin time and partial thrombin time while
platelets remain normal.

MANAGEMENT
1. In addition to all nursing care, if the condition is mild give 0.5-1 mg Vitamin K
intramuscularly (IM) start and closely observe the baby.
2. If condition is severe, fresh frozen plasma transfusion may be given in addition to Vitamin K.
3. If baby shows any signs of shock, and or baby is grossly anaemic transfuse blood with red cell
concentrate.
4. Nurse baby in an incubator to allow close observation, warmth and carefully monitoring.
5. Expressed breast milk is given by nasogastric tube.
6. Sometimes Vitamin K is given to the mother to raise prothrombin level during pregnancy.

PREVENTION
1. If signs are detected earlier, Vitamin K intravenous or intramuscular or oral should be given
to the mother to raise infant prothrombin level before labour.
2. Direct administration of Vitamin K to infants immediately at birth
3. Encourage an early breastfeeding to help in the colonization intestines to help in the
production of Vitamin K.
4. Procedures like bathing of the baby should be prost pond for some time to prevent trauma or
injury to the skin.
THROMBOCYTOPENIA
This is a condition whereby there is reduced low count of circulating platelets, less than100, micro liter.
It results from either.
1. Decreased rate of producing / forming platelets.
2. Increase rate of consumption

INCIDENCE
It is a rare (0.7%) but occurs in 20-35% of preterm infants when sick.

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 CAUSES
1. Severe infection acquired /congenital example syphilis/rubella.
2. Maternal causes example idiopathic thrombocypenia, thyrotoxicosis, and herpes.
3. Inherited thrombocypenia
a. B 12 /folate deficiency, heavy alcohol use
b. Blood cancers (leukemia)radiation therapy
c. Viral infection (chicken pox, HIV, Hepatitis C).
4. Pre-eclampsia (HELLP Syndrome) in pregnant women
5. DIC.

BABIES AT RISK OF DEVELOPING THROMBOCYTOPENIA.

1. Severe congenital / acquired infection.
2. Mother takes thiazide diuretics
3. Who have iso-immune thrombocytopenia
4. Who have inherited thrombocytopenia

SYMPTOM
• A petechial rash appears soon after birth
• Presenting in a mild case localized petechial
• In severe case wide spread when serious haemorrhage from multiple sites.
DIAGNOSIS
• Based on history
• Clinical examination
• Presence of reduced platelets count during blood investigation

MANAGEMENT
Conditions resolves on its own.
• In severe cases, transfusion is done with platelets.

INHERITED COAGULATION FACTOR DEFFICIENCY

A. X-linked A/recessive
• Haemophilia (factor VIII deficiency)
• Haemophilia B - Christmas disease (factor IX deficiency): These are x-linked recessive
conditions which rarely cause problem in the neonatal period, but may present with excessive
bleeding after birth trauma or surgical interventions example circumcision

HAEMOPHILIA A (FACTOR VIII DEFICIENCY)

This is also known as classic haemophilia or haemophilia A and it is an inherited bleeding disease found
mainly in males and transmitted through carrier females
INCIDENCE
Males are predominantly affected with the disease and females are carries of this genetic illness. In rare
instances, a female may be affected with the disease when a man with haemophilia produces an
offspring with a woman who is a carrier of this disorder.
It accounts for about 7.5 % of all cases.

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HAEMOPHILIA B (FACTOR IX /CHRISTMAS DISEASE)
It is called Christmas disease because it was named after Stephen Christmas, the first patient described
with the disease and the first report of its identification was published in the Christmas edition of the
British Medical Journal. Haemophilia B is a blood clotting disorder caused by deficiency of factor IX.
GENETICS: The factor IX gene is located on the 21 chromosomes. It is an x-linked recessive trait
which explains why as in haemophilia A, usually only males are affected.
HAEMOPHILIA C
It is a mild form of haemophilia affecting both sexes. However, it predominantly occurs among Jews of
Ashkenazi descent. It is caused by a deficiency of coagulation factor XI and its distinguished from
haemophilia A and B by the facts that it does not lead to bleed into joint (Haemarthosis).

SYMPTOMS
• It severe, moderate or mild depending on clotting factor I, VIII, IX and XI level.
• The hallmark of severe disease is recurrent simultaneous bleeding into joints and muscles.
• Intracranial haemorrhage.
• Bleeding in post circumcision
• Prolong oozing from heel stick and vein puncture site.
• Warmth, swelling and severe pain

DIAGNOSIS
• Factor VIII and IX assays
• Partial thromboplastin time test

MANAGEMENT
There are three (3) reasons available to control bleeding
• Fresh frozen plasma.
• Factor VIII concentrate
• Desmopressin (a synthetic hormone which rises factor VIII in cases of mild deficiency) with
or without the use of blood product.
DISSEMINATED INTRACASCULAR COAGULATION
It occurs as a result of coagulation defect leading to deposition of fibrin in the blood vessels. They are
abnormally low platelets and coagulation factors.
In DIC, the body’s natural ability to regulate clotting does not function properly. This causes the blood
clotting cells (platelets) to clump together and block small blood vessels throughout the body reducing
blood flow. This excessive clotting damages organs, destroys blood cells, and depletes the supply of
platelets, fibrinogen and other clotting factors like V, VIII and X so that the blood is no longer able to
clot normally thereby causing widespread bleeding, both internally and externally.

Predisposing factors
 Severe birth asphyxia  Severe hypoxia
 Severe infections. Eg septiceamia  Thrombocytopaenia

Signs and symptoms

 Excessive bleeding (haemorrhage) occurs throughout the body. The severity of bleeding can
range from red dots and bruises under the skin to heavy bleeding from punctured sites, umbilical
stump or body openings, such as the mouth, nose, rectum, or vagina.

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  Shortness of breath from lung damage
 Low urine output from kidney damage
 Shock
 Pallor

Diagnostic measures
 Clinical signs and symptoms  Platelet count
 Full blood count  Clotting test

Treatment
 Transfuse fresh frozen plasma or whole blood in severe cases or anaemia.
 Occasionally exchange blood transfusion
 In persistent cases, heparin treatment is given.

LOCAL TRAUMAS/ CAUSES OF HAEMORRHAGE

• Umbilical cord; ligation of cord
• Vagina bleeding; pseudomenstruation
• Vomiting (haematemasis)
 swallowing of blood during birth
 Congenital malformation of the GIT
 If baby feeds on cracked or sore nipple
• Malaena stool swallowing of blood during birth
 meconium ileus
 Severe constipation
• Haematemia – during delivery if there is any trauma to the urinary tract, baby may bleed.

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 CHAPTER FIVE
METABOLIC DISORDERS (INBORN ERRORS OF METABOLISM)

Metabolism refers to all the chemical reactions taking place in the body to convert or use energy. A few
major examples of metabolism include:

 Breaking down the carbohydrates, proteins, and fats in food to release energy.
 Transforming excess nitrogen into waste products excreted in urine.
 Breaking down or converting chemicals into other substances and transporting them inside cells.

Metabolism is an organized but chaotic chemical assembly line. Raw materials, half-finished products,
and waste materials are constantly being used, produced, transported, and excreted. The "workers" on
the assembly line are enzymes and other proteins that make chemical reactions happen.

INBORN ERRORS OF METABOLISM (INHERITED)

Inherited Metabolic Disorders are genetic conditions that result in metabolism problems. Most people
with inherited metabolic disorders have a defective gene that results in an enzyme deficiency. There are
hundreds of different genetic metabolic disorders, and their symptoms, treatments, and prognoses vary
widely.

CAUSES
In most inherited metabolic disorders, a single enzyme is either not produced by the body at all or is
produced in a form that doesn't work. The missing enzyme is like an absentee worker on the assembly
line. Depending on that enzyme's job, its absence means toxic chemicals may build up, or an essential
product may not be produced.

The code or blueprint to produce an enzyme is usually contained on a pair of genes. Most people with
inherited metabolic disorders inherit two defective copies of the gene -- one from each parent. Both
parents are "carriers" of the bad gene, meaning they carry one defective copy and one normal copy.

In the parents, the normal gene copy compensates for the bad copy. Their enzyme levels are usually
adequate, so they may have no symptoms of a genetic metabolic disorder. However, the child who
inherits two defective gene copies cannot produce enough effective enzyme and develops the genetic
metabolic disorder. This form of genetic transmission is called autosomal recessive inheritance.

The original cause of most genetic metabolic disorders is a gene mutation that occurred many, many
generations ago. The gene mutation is passed along through the generations, ensuring its preservation.

Each inherited metabolic disorder is quite rare in the general population. Considered all together,
inherited metabolic disorders may affect about 1 in 1,000 to 2,500 newborns. In certain ethnic
populations, such as Ashkenazi Jews (Jews of central and eastern European ancestry), the rate of
inherited metabolic disorders is higher.

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TYPES OF INHERITED METABOLIC DISORDERS

Hundreds of inherited metabolic disorders have been identified, and new ones continue to be discovered.
Some of the more common and important genetic metabolic disorders include:

GALACTTOSAEMIA
This disorder of carbohydrate metabolism that is autosomal recessive in inheritance and has an incidence
of, 1:60,000. This is caused by the absence of the enzyme galactose – phosphate uridytransferase which
is responsible for converting galactose into glucose. This leads to increase galactose and reduced levels
of glucose in the blood. The metabolite that builds up is harmful galactose -1 phosphate.
Note; Galactose is a monosaccharide resulting from the digestion of lactose which the liver converts to
glucose

CLINICAL FEATURES
• Normally at birth, the baby’s condition is normal.
• Since milk’s main sugar, lactose is a disaccharide containing glucose and galatose, infant with
this condition gets deterioration when fed with either breast milk or cow’s milk formulae.
• Feels reluctant to eat
• Present with vomiting
• Diarrhea
• Hypoglycaemia
• Jaundice
• Acidosis
• Failure to gain weight
• Haemolysis and deficient clothing factors leading to anaemia
• Affected babies present with septicaemia by damage to intestinal mucosa from the high levels
of galactose in the gut.
• Cataracts may be present.
• Enlargement of the liver

DIAGNOSIS
• A blood test using Guthrie inhibition assay method.
• Test or galactose in urine
• Estimation of galactose
• Phosphate in the red cells

NURSING MANAGEMENT
• Admit baby and reassure mother
• Feed baby frequently
• Since there is diarrhea, observe baby for signs of sore buttocks.
• Frequently changing of Baby’s napkins / underwear.
• Give IV fluids
• Observe Vital signs
• Observe for neurological changes such as irritability, convulsions.
• Keep baby warm.

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MEDICAL MANAGEMENT
• This is by giving them lactose free milk formula which must be commenced as soon as it is
diagnosed. Thus Galactomine 17 milk has been developed for these babies.
• All soya milk preparations may be used
• As the child grows, specially prepared low galactose food stuffs are used.
• With the removal of galactose from the diet the disease connects itself but damage to organs
which has already been sustained cannot be connected.

PROGNOSIS
A lifelong galactose free diet is indicated for those infants affected. So if the mother is able to adhere to
the baby, the prognosis will be good.

COMPLICATIONS
• Mental retardation
• Liver failure
• Renal impairment
• Toxic by – products of galactose can damage the lens of the liver and the kidneys.
• In severe cases, death will occur.

PHENYLKTONURIA (INBORN)
This is an inherited genetic disorder in which the body cannot breakdown the essential amino acid due to
deficiency of an enzyme called phenylalanine hydroxylase which convert amino acid to tyrosine in the
liver. As a result, there is an accumulation of phenylalanine in the blood tissue. Because it cannot be
converted, it builds up to a poisonous substance known as phenylpuruvic acid which is toxic to the brain
and may cause brain damage. The risk of phenylalanine in the blood is found within few days after the
baby is subjected to dietary problem on breast milk.

CAUSES
• Accumulation of amino acid in the blood
• It occurs though inheritance (phenylalanine deficiency)
• Accumulation of phenypuruvic acid in the body
SIGNS
• Vomiting
• The baby looks normal at birth but will present the signs.
• There is peculiar odour and rashes like eczema.
• Baby feels reluctant to feed or difficult to feed.
• Cyanosis (blue eyes)
• Fair skin and hair.
DIAGNOSIS
• Blood sample to screen for phenylketonuria (from the heel of the baby).
• Guthre test is the cheapest test performed on baby of 7 days of age. This test is carried out
between the 6th – 14days of life been the baby has taking milk feeds for several days.
• Serive test: This is a more accurate biochemical test used to diagnosis whole range of inborn
errors of metabolism including phenylketonuria about 725mol/L or 12mg or 100mol must be
seek.
• Urine test for the presence of phenylpyruvic acid

65
 • By sign and symptom
NURSING MANAGEMENT
• Admit and reassure mother
• Oral hygiene should be cared for.
• Monitor Vital signs and sleeping patterns.
• Check blood sample regularly for phenylalanine level.
• Keep baby warm throughout
• Frequent before since the child since the child is having feeding difficulty.
• Frequent of napkins and give IVF as ordered.

MEDICAL MANAGEMENT
A low phenylalanine diet is prescribed and milk substitute such as minuferi, analogy lofenalae milks will
be used with iron and vitamin supplements.

PROGNOSIS
It is good if parents adhere to the instructions given. In female, a return to the diet is essential prior to
conception and during pregnancy. Fetal damage may be causes by exposure to high concentrates of
menylalaine and its metabolites in the mother.

COMPLICATIONS
• Fetal damage • Asphyxia
• Mental retardation • Central Nervous System (CNS)
• Growth retardation damage.
• Hypothermia

Glycogen storage diseases: Problems with sugar storage lead to low blood sugar levels, muscle pain,
and weakness.

Symptoms of Inherited Metabolic Disorders

The symptoms of genetic metabolic disorders vary widely depending on the metabolism problem
present. Some symptoms of inherited metabolic disorders include:
 Lethargy  Failure to gain weight or grow
 Poor appetite  Developmental delay
 Abdominal pain  Seizures
 Vomiting  Coma
 Weight loss  Abnormal odor of urine, breath, sweat,
 Jaundice or saliva

The symptoms may come on suddenly or progress slowly. Symptoms may be brought on by foods,
medications, dehydration, minor illnesses, or other factors. Symptoms appear within a few weeks after
birth in many conditions. Other inherited metabolic disorders may take years for symptoms to develop.

o For inborn errors of metabolism (IEMs) of energy deficiency, symptoms usually develop
within 24 hours of birth and are often present at birth. Neonates with inborn errors that

66
 result in defects in energy production and use often have dysmorphic features, skeletal
malformations, cardiopulmonary compromise, organomegaly, and severe generalized
hypotonia.

Diagnosis of Inherited Metabolic Disorders

Inherited metabolic disorders are present at birth, and some are detected by routine screening. Improved
testing technology is leading to expand newborn screening for genetic metabolic disorders.

If an inherited metabolic disorder is not detected at birth, it is often not diagnosed until symptoms
appear. Once symptoms develop, specific blood or DNA tests are available to diagnose most genetic
metabolic disorders. Referral to a specialized center (usually at a university) increases the chances of a
correct diagnosis.

Management of Inherited Metabolic Disorders

Limited treatments are available for inherited metabolic disorders. The essential genetic defect causing
the condition can't be corrected with current technology. Instead, treatments try to work around the
problem with metabolism.

Treatments for genetic metabolic disorders follow a few general principles:

 Reduce or eliminate intake of any food or drug that can't be metabolized properly.
 Replace the enzyme or other chemical that is missing or inactive, to restore metabolism to as
close to normal as possible.
 Remove toxic products of metabolism that accumulate due to the metabolic disorder.

Treatment may include such measures as:

 Special diets that eliminate certain nutrients

 Taking enzyme replacements, or other supplements that support metabolism
 Treating the blood with chemicals to detoxify dangerous metabolic by-products
 Whenever possible, a person with an inherited metabolic disorder should receive care at a
medical center with experience with these rare conditions.
Children and adults with inherited metabolic disorders can become quite ill, requiring hospitalization
and sometimes life support. Treatment during these episodes focuses on emergency care and improving
organ function

Provide education regarding disease and patient care (manifestations, course of disease, treatment,
psychosocial support) as appropriate.

Provide genetic counseling to discuss recurrence risks, screening of other family members, and prenatal
diagnosis.
Provide information regarding support groups

Deterrence/Prevention

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Strict adherence to dietary and pharmacologic regimen is recommended for patients diagnosed with an
inborn error of metabolism.

Early treatment symptoms and recognition that physiologic stressors, including intercurrent illness,
trauma, surgery, and changes in diet may precipitate symptoms, is important in avoiding metabolic
decompensation.

Complications

Complications of metabolic diseases may include the following:

 Significant neurologic impairment

 Death

METABOLIC DISTURBANCES IN THE NEWBORN(ACQUIRED):

Preterm and growth restricted infants are usually at risk. The most common of these disturbances is
hypoglycaemia.

Hypoglycaemia

Definition: Blood glucose concentration < 2.6mml/L

Causes:
 Increased or impaired glucose utilization
 Hyperinsulinism (e.g. born to mothers with diabetes)
 Increased demand: cold stress, sepsis, after resuscitation, enzymatic or endocrine defects
 Decreased glucose stores
 Preterm, low birth weight, or growth-restricted infants
 Signs and symptoms:CNS: jitteriness, tremours, twitching, weak or high-pitched cry, lethargy,
limpness, apathy, convulsions, coma
 Other: cyanosis, apnea, rapid irregular respirations, sweating, eye rolling, poor feeding
signs are often vague, may be transient but generally reoccur.

Diagnosis:
 Bedside monitoring of blood glucose should be done for:
 LBW (<2.5kg) or premature infants
 Small for gestational age, intra-uterine growth restricted
 >4kg
 Infants with low apgar, resuscitation
 Postdates infants
 All infants exhibiting any of the symptoms
 Lab diagnosis
 Serum glucose <2.8mmol/L in any newborn
Infants at risk of the neurological sequelae of hypoglycaemia
 Preterm infant and growth restricted infants
 Infants of diabetic mothers
 Sick term infants

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  Infants with Inborn Errors of Metabolism
Management:
 If the blood glucose < 2.6, then feed should be given at increased volume and decreased
frequency. This may require supplementary feeding with formula milk in infants who
are breastfed or naso-gastric tube (NGT) feeding, or both. Breast milk can also be
expressed to give via an NGT.
If the blood glucose remains low despite these measures and there’s adequate feed volume
intake, then IV treatment with dextrose (10%) is required. Enteral feeding should continue, as it
contains more energy, promotes ketone body production and metabolic adaptation.
In infants contra-indicated, 10% Dextrose 60ml/Kg/day administered intravenously is
recommended.

Prevention:
 Early initiation of breastfeeding (within 30minutes after birth)
 Adequate temperature control by keeping baby warm
 Frequent feeding

Hyperglycaemia
Definition: Blood glucose concentration > 2.8mmol/L.
It occurs predominately in preterm and severely growth restricted infants, as well as term infants
in response to stress such following perinatal hypoxia-ischaemia, surgery or drugs (esp.
corticosteroids). In preterm infants, this transient phenomenon is as a result of the infant’s
inability to deal with excessive glucose intake (immature glucoregulation).

Management:
No treatment is usually required unless there is significant loss of glucose in urine, which may
cause an osmotic dieresis. In this situation, if the infant is on glucose infusion, then the rate has
to be decreased. Giving insulin infusion also has an advantage of allowing glucose input to
continue and sufficient calories to be given and may result in better weight gain.

Hyponatraemia
In other words, reduced sodium concentration in the blood. Normal sodium requirements are 1-
2mmol/kg/day for term infants and 3-4mmol/kg/day for preterm infants. Hypponataemia in the
presence of weight gain is as a result of fluid overload. But hyponatraemia in the presence of
weight loss is due sodium depletion. The normal serum sodium concentration is 133-146mmol/L.
Thus, Hyponataemia is serum sodium concentration < 133mmol/L. It is commonly seen in
infants receiving intravenous fluids or in infants with oliguric renal failure.

Causes:
Related to fluid overload
 Excessive intravenous fluid administration
 Oliguric renal failure
 Drugs (eg. indometacin) given to preterm infants
Related to sodium depletion

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  Renal loss in preterm infants
 Loss into the bowel due to ileus or severe vomiting
 Drugs eg. Diuresis
 Adrenocortical failure
Management:
The objective is to reduce the fluid intake whilst maintaining normal sodium intake with appropriate
intravenous fluid.

Hypernatraemia
Increased sodium concentration is almost always due to water depletion and loss of extracellular fluid
but can also be rarely be due to an excessive sodium intake. These causes can easily be differentiated by
weighing the infant to assess changes since birth.
Causes:
Related to water depletion
 Transepidermal water loss in preterm infants
 Excessive urine output in preterm infants during recovery from respiratory distress syndrome
 High rates of fluid loss through vomiting, diarrhea or bowel obstruction
 Inadequate lactation
Related to excessive sodium intake
 Incorrect fluid prescription
 Excessive administration sodium bicarbonate
 Incorrectly formulated powdered feeds
 Munchausen’s syndrome by proxy-intentional administration of salt to an infant
Management:
Provide sufficient assistance and supervision of feeding. However, as feeding continues, intravenous
administration with dextrose saline may be required.
Hyperkalaemia
Any abnormality in serum potassium concentration is of significance since it can cause arrhythmias.
Potassium concentration can be affected by measurement technique; any haemolysis of the blood
sample, especially from capillary sampling is likely to lead to a falsely high value > 8mmol/L, or
evidence by abnormal ECG/arrhythmias or both.
Causes:
 Acidosis
 Acute renal failure
 Congenital adrenal hyperplasia
Management:
Objective of treatment is to remove all potassium supplements from intravenous fluids.
To consider rectal administration of calcium resonium, sodium bicarbonate to increase pH and
intravenous glucose and insulin

HYPOKALAEMIA
Itis caused by
 Inadequate intake of potassium
 Bowel losses through vomiting and dirrhoea
 Diuretic therapy

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  Hyperaldosteronism
Management:
Add potassium to IV fluids or administer orally, not exceeding the daily requirement of 2mmol/kg/day

Hypocalcaemia
Serum calcium concentration <1.95-2.0mmol/L in term infants
Types:
 Early onset: Appears in first 48hrs, preterm infants who experienced perinatal hypoxia;
sometimes in infant of diabetic mother
 Late onset: cow’s milk-induced hypocalcaeima; apparent after first 3-4 days (high
phosphorus/calcium ratio of cow’s milk depresses parathyroid activity, reducing serum calcium
levels); infants with intestinal malabsorption, hypoparathyroidism or hypogagnesaeima.
Causes:
 Prematurity
 Significant hypoxia-ischaemia
 Renal failure
 Maternal diabetes mellitus
Signs and symptoms
 Early onset: jitteriness, apnea, cyanotic episodes, oedema, high pitched cry, abdominal distention
 Late onset: twitching, tremours, seizures
Management
 Early onset: increased formula feedings, administration of calcium supplements
 Late onset: administration of calcium gluconate orally or intravenously; vitamin D; correct
hypoparathyroidism

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 CHAPTER SIX

BIRTH INJURIES

Definition:
Birth injuries refer to injuries sustained during the birthing process. This usually occurs during transit
through the birth canal. Birth injury can be minor of which majority resolve spontaneously in few days.
There can also be a major injury which is serious and even fatal. The responsibility of the nurse is to
identify the problem early for appropriate intervention.

RISK FACTORS / BABIES AT RISK

• Large for date infants
• Instrumental deliveries especially forceps or vacuum delivery.
• Vaginal breech deliveries
• Abnormal or excessive traction (Shoulder dystocia)
• Mal – presentation and abnormal position.
• Prematurity/primiparity
• Rigid perineum
• Twin delivery

INCIDENCE
• It accounts for less than 2% of neonatal death and still birth where these conditions are well
documented.
• In USA incidence is 6 to 8 birth injuries per 1000 live births.
• Generally large infants are more susceptible to birth traumas especially those greater than 4.5 kg.
Many infants have minor injuries, damaged nerves, broken bones which resolve with or without
treatment.

HEAD AND BRAIN INJURY

In most births, the head is the first part to enter the birth canal and experiences much of the pressure
during the delivery.
CAPUT SUCCEDANEUM
It is defined as oedema or swelling on the skull. It involves swelling below or under the scalp and above
the periosteum (outer covering of the skull bone). It is also a neonatal condition involving a
serosanguinous subcutaneous, extra periosteal fluid collection. Bruising usually occurs on the top of the
scalp.

CAUSES
1. Pressure from the cervix
2. It occurs in many cases of prolonged labour.

CLINICAL FEATURES / CLINICAL MANIFESTATION

1. Swelling is present at birth
2. May extend across Suture lines
3. Caput succedaneum does not usually cause complications and usually resolves over the first few days.
4. Turns to grow larger at birth but gradually subsides within a day.

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5. The swelling feels soft and spongy mass.

MANAGEMENT
• Treatment is usually not required.
• Reassure mother that swelling will heal after blood is absorbed.
• Gentle handling of the abrasions is appropriate.
• It heals rapidly if the area is kept clean, dry and is not irritated.
• Condition is resolved few days to weeks.

CEPHAL HAEMATOMA
It is defined as swelling on the head of the newborn infant due to collection of blood from damaged
capillaries under the periosteum of the cranial bone.

CAUSES
• It usually occurs when there is friction between the fetal skull and the maternal pelvic (as in the case
of CPD)
• Prolonged second stage of labour
• Instrumental delivery, particularly ventouse (vacuum).

CLINICAL FEATURES
• It does not cross the suture line
• It has defined margins
• If severe the child may develop jaundice or anaemia
• The swelling of a cephalhaematoma takes weeks to resolve as the blood clot is slowly absorbed from
the periphery boards the Centre.
• It does not pit on pressure
• Swelling is usually noticed after 24 hours or few days after birth about 2-3 days.
• The head is usually more red and bruised in appearance than with caput succedanneum

MANAGEMENT
• No active treatment is required
• Mothers should be reassured that swelling will disappear with time and not interfere with baby’s
normal development.
• Assess haemoglobin level and treat anaemia if any.

DIFFERENCES BETWEEN CAPUT SUCCEDENEUM AND CEPHAL HAEMATOMA

CAPUT SUCCENEUM CEPHAL HAEMATOMA
1. Present at birth on the vagina delivery 1. Appears within a few days or hours after
birth on forceps or normal delivery.
2. Crosses suture line 2. Does not cross suture line
3. Soft, pits on pressure 3. Soft, elastic but does not pit on pressure.
4. Large size at birth but gradually subsides 4. Become largest after birth and then
within a day. disappears within 6 – 8 weeks to a few
months.
5. No treatment is required. 5. No treatment unless there is neurological

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 symptoms
6. Swelling feels soft and spongy 6. Swelling hardens (calcified)

INTRACRANIAL HAEMORRHAGE / INJURY

Bleeding in the brain (intracranial haemorrhage) is caused by the rupture of a blood vessel within the
skull. It affects the deep structures of the fetal head during delivery or from 1ack of oxygen. Structures
include falx cerebelli, falx cerebri, tentorium, cerebella, galen and straight sinus.

INCIDENCE
More common among very premature infants (very low birth weight).

TYPES OF INTRACRANIAL HAEMORRHAGE / INJURY

The types of intracranial haemorrhage / injury include:
a. Subdural
b. Subarachnoid
c. Periventricular haemorrhage or intraventricular haemorrhage

A) Subdural haemorrhages: This occurs between the outer and the inner layers of brain covering the
dura and arachnoid mater. A subdural haemorrhage can put increased pressure on the surface of the
brain. Infants with Subdural haemorrhage may develop problems such as seizures or high levels of
bilirubin in the blood.

B) Subarachnoid haemorrhages: This occurs below the innermost of the two membranes that cover
the brain namely arachnoid and pia meter

C) Periventriculas or intraventricular harmorrhage: This occurs between the ventricles of the brain.
This condition is very common in low-birth-weight babies.

CAUSES
• Prolong labour associated with abnormal moulding.
• Diminished amount of oxygen in the blood (hypoxia)
• Injudicious mechanical interference example vacuum extraction.
• Precipitate delivery / labour
• Excessive moulding associated with CPD in obstructed labour or contracted pelvis.

DIAGNOSIS
• Ultrasound / MRI
• By clinical manifestation or signs symptoms.

CLINICAL MANIFESTATION
• There is Restlessness and irritability • Moro reflex is absent or diminished
• There may be twitching of facial muscles • Opistothonos may be present
• High pitched cry and shrill • Convulsions may occur
• Suckling and swallowing reflexes are poor • Temperature may be subnormal or high
• The eyes roll upward and sideways • Poor muscle tone

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 NURSING MANAGEMENT
Maintaining Respiration
• Baby is resuscitated and oxygen administered when cyanosis is present
• Maintain clear airway by removing of secretions through suction.

Provision of warmth
• Baby is kept warm by wrapping baby with warm clothes – Bathing delayed till there is
improvement.
• Baby is nursed in an incubator or NICU.

Infection Prevention
• Minimal handling and measurements are avoided until condition improves.
• Hand washing before and after handling baby.

Maintaining Adequate Nutrition:

• Baby is fed with care.
• All nursing care and feeding is done in a cot
• Place baby in the recumbent position and on side after feeding.
• Tube feeding if condition permits or as ordered.
• Iv infusions as prescribed

Observation
• Skin colour, muscle bone, respiration, temperature, sleep pattern and general condition
• Any twitching is noted as well as duration
• Urinary output and bowel movement
• Strict intake and output chart usage.

MEDICAL MANAGEMENT / TREATMENT

• Seizures are treated with anticonvulsants (Phenobard) 5 – 10g
• Administer vitamin K to prevent further bleeding
• Antibiotics like ampicillin can also be prescribed

PROGNOSIS
• Majority of babies die within 24 hours of delivery in massive bleeds.

PREVENTION
Antenatally
• Early detection and treatment of maternal conditions that may predispose the fetus to
intrauterine hypoxia
• Cesarean section done in cases of malpresentation
• Pelvic assessment to rule out any disproportion

LABOUR

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• Prolong 1st and 2nd stage should be avoided
• Skilled management of 2nd stage of Labour
• Experience midwives to conduct deliveries like breech, preterm labour etc.

COMPLICATIONS
Mental retardation
Convulsions
Cerebral atrophy

NERVE INJURIES
The most common nerves affected or traumatized are the facial and brachial plexus nerves

FACIAL NERVE INJURY / FACIAL PALSY

Otherwise known as Bell's palsy, is a common birth injury affecting newborn babies. The facial nerve
also known as the seventh cranial nerve controls the face muscles and causes them to contract. It has a
complex route from the brain stem to the face muscles it controls, which lift the eyebrows, close the
eyelids and move the cheek muscles. Facial palsy results from pressures over the facial nerve.

NB: It may be unrelated to trauma. The condition may have no obvious cause. Many of the patients who
present with facial palsy have it in association with malformation like hydrocephalus and spinal bifida.
Facial nerve injury leads to facial palsy or paralysis.

CAUSES
• Forceps delivery: damage to facial nerves may be due to compression of the ramus of the mandible
by forceps blade resulting in unilateral facial palsy.
• Spontaneous delivery, when pressure is exerted on the facial nerve.
• Fetus head lying against the mother’s pelvis’ resulting in weaken of the superficial nerves on the side
of the face.

CLINICAL MANIFESTATION
1. Diminished movement on the affected side.
2. Unilateral facial weakness with eyelid on the affected side remaining open.
3. The mouth is drawn to the unaffected side
4. Initially there may be feeding difficulty if the baby cannot form an effective seal on the nipple.
5. Milk dribbles out on the affected side of the mouth when feeding.

MANAGEMENT
• There is no specific treatment
• Give psychological support to mother
• Spontaneous resolution usually occurs with a mouth
• Alternative feeding positions can be adapted.
• Regular instillation of methyl cellulose eye drops to lubricate the eye ball if the eyelids remain open.

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 BRACHIAL PLEXUS INJURY
The Brachial plexus is a network of nerve root existing from the spine at the level of the fifth, sixth,
seventh and eighth cervical vertebrae and the thoracic vertebra. (C5 – C8, T1) the Brachial plexus passes
the neck, the axilla and into the arm.
CAUSES
1. Excessive lateral flexion, rotation or traction of head and neck in vertex presentation.
2. Damage may occur during delivery of the after coming head of the breech.
3. Shoulder dystocia

RISK FACTORS
• Big babies (3.5 plus) are at risk
• Prolonged labour increases risk
• Breech deliveries
• Fetal distress
• A mother with a history of previous brachial plexus injured infant

TYPES OF BRACHIAL PLEXUS INJURIES

1. Erb’s palsy
2. Klumpke’s
3. Total brachial plexus palsy

ERB’S PALSY
This involves damage to the upper brachial plexus involving the fifth and sixth cervical nerve roots.
SIGN AND SYMTPOM
• “Water’s / Porter’s tip” position: adducted and internal rotation of the arm with pronation of the
forearm.
• The forearm is extended and pronated.
• The arm hangs down limp from the shoulders although some movement of fingers and arm is
possible.
• The wrist is pronated and flexed and hand is partially closed.

MANAGEMENT
• Complete recovery occurs in mild cases but permanent paralysis may accompany a severe case.
• Treatment involves splinting the arm in correct position that is a position that allows for relaxation of
affected muscles.

KLUMPKE’S PALSY
This occurs when there is a damage to the lower brachial plexus involving the seventh, eight cervical
roots and the first thoracic nerve roots.

SIGNS AND SYMPTOM

• The upper arm has a normal movement but the lower arm wrist and hand are affected.
• There is drop of wrist
• Flaccid paralysis of the hand with no grasp reflex.
• The infant may also have dropping eyelid on the opposite side of the affected hand.

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TREATMENT
1. Provide psychological support to the mother
2. Nerve regeneration may occur spontaneously.

TOTAL BRACHIAL PALSY

This occurs when there is damage to all the brachial plexus nerve roots. (5 th, 6th, 7th, 8th and 1st thoracic
nerve (C5 – C8 and T1)

SIGNS AND SYMPTOMS

• There is complete paralysis of arm and hand.
• Lack of sensation and circulatory problems
• Spinal injury should be suspected when there is bilateral paralysis.

TREATMENT
• Provide mother with psychological support. Nerve generation in new born usually heal on their own
leading to complete recovery.
• However, many children with brachial palsy require treatment
• Surgery may be indicated in some cases.
• Specialist who may become involved in child’s treatment include
Physical therapist
Occupational therapist
• Neurologist
• Paediatric neurosurgeon
Plastic surgeons

DIAGNOSIS
• X- ray
• Ultrasound
• Electromyography (EMG) measures muscle response
• A nerve condition velocity text (NCV) to detect nerve damage

NURSING MANAGEMENT
• Admit and reassure mother
• Advice to move shoulder gently
• The affected arm is rested for 7 – 10 days followed by
• Physiotherapy to avoid contractions
• Splinting of the affected arm
• Passive exercise with parents.
• Provision of warmth
• Prevention of infection
• Breast feed baby well
• Continuous observation for any other complication.

PROGNOSIS
• It depends on the location, severely and extent of the damage and may be difficult to predict.
• In general damage to the nerve sheath (outer covering) alone has good prognosis.

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• In severe cases, permanent paralysis may occur.
• Stress injuries heal on their own with about 90% - 100 percent of function returning within one to two
years.
MUSCLE INJURY
Injuries to muscle result from tearing or disrupted blood supply.

TORTICOLIS (WRY NECK)

• Birth trauma or intrauterine malposition is also considered to cause damage to the
sternocleidomastoid muscles run which from the respective sides of the sternum, along the right or
left side of the neck and is inserted into the mastoid process of the right and temporal bone.
• When contracted simultaneously, these muscles allow the head to flex.
• When contracted separately, each turns the head to the opposite side.

CAUSES
• Excessive traction or twisting causing tearing to one of these muscles can occur during the
birth of anterior shoulder of a foetus with cephalic presentation.
• During rotation of the shoulders when the foetus is being born by vaginal breech or caesarean
section.

CLINICAL MANIFESTATION
• Painless, hard lump of blood and fibrous tissue is felt on the affected sternomastoid muscle.
• The muscle length is shortened; therefore, the neck is twisted to the affected side.

MANAGEMENT
Management involves caregivers and parents performing passive muscle stretching, exercises under
the guidance of physiotherapist, actively ensuring baby moves the neck.
• The swelling usually resolves over several weeks to months.
• Surgical intervention is required if there is no resolution by one year.
• Follow up to ensure achievement of normal/movement is recommended.

FRACTURES
A fracture occurs when there is break in the continuity of a bone. Fractures are rare but the most
commonly affected bones are the clavicle, humerus, and femur, and with the mentioned fractures a
‘crack’ may be heard during birth.

FRACTURED CLAVICLE
It is the most fractured bone during delivery mostly during delivery of the shoulder in vertex and of the
extended arms in breech. The affected clavicle is usually the one that was nearest the maternal
symphysis pubis.
SIGNS AND SYMPTOMS
• No free movement on affected side.
• Callus formation during examination.
• Moro reflex may be absent.

TREATMENT
This usually does not require treatment and stable union occurs within 7- 10 days.

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LONG BONES
Humerus: Midshaft humeral fractures can occur during vaginal breech birth if the extended arm is
forced down and born with shoulder dystocia.

SIGNS AND SYMPTOM

• Considerable deformity is evident on examination.
• Baby is reluctant to move the arm owing to pain.
TREATMENT
• Two weeks of immobilization and splinting the arm to the chest by placing a pad in the axilla.
• Application should not disturb respiration and should be firm.
• Give analgesic to relieve pain.
Femur
Midshaft femoral fractures can occur during vaginal breech birth if extended leg is brought down and
born.
DIAGNOSIS
• X- ray
• Clinical manifestation with most fractures distortion, deformity, swelling or bruising are
present on examination.

SIGNS AND SYMPTOM

• Deformity
• Reluctant to move leg due to pain.
TREATMENT
• Administer analgesic to relieve pain.
• Gentle handling to avoid further pain.
• Immobilize a fractured femur using a splint and bandage.
• Traction and plaster casting may be required.
N/B: Stable union of a fractured clavicle usually occurs in 7 -10 days, while numerous and femur take 2-
4 weeks.

FRACTURED SKULL
Although this condition rare, these fractures, linear or depressed may occur during prolonged or difficult
instrumental births.
CAUSES
• This is usually caused by sacral promontory in contracted pelvis.
• The blade of a forceps in difficult delivery in and after coming head in breech presentation.
DIAGNOSIS
• X- ray
• Ultrasound to detect level of haemorrhage

SIGNS AND SYMPTOMS

• There may be cephalhaematoma
• Intracranial haemorrhage
• Raised intracranial pressure
• Leakage of cerebrospinal fluid

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TREATMENT
• A simple linear fracture usually requires no treatment and heals quickly.
• Treatment of a depressed fracture depends on the depth of the concavity.
• Shallow depressions in asymptomatic babies usually resolves spontaneously
• With a deeper depression or where there are signs of complications, the fracture requires no
surgical repair.
• Contamination or evidence of cerebrospinal fluid (CSF) leakage via the ear or nose require
antibiotic therapy.
• Treatment of associated complication is necessary.

SKIN INJURIES
These include Abrasions and Lacerations. Damage to the skin is often latrogenic usually from forceps
blades, vacuum extractor cups, scapel blades etc. Occasionally, during incision of the uterus at
caesarean section, laceration of the baby’s skin can occur.

MANAGEMENT:
Abrasions and lacerations should be kept clean and dry. If there are signs of infection, medical advice
should be sought. Antibiotics may be prescribed. Deeper Lacerations may require closure with butterfly
strips or sutures.

INTRA-ABDOMINAL INJURIES
Intra –abdominal birth trauma is uncommon.
(a). HEPATIC/ LIVER INJURY
The liver is the most commonly injured solid organ during birth. Macrosomia, hepatomegaly and breech
presentation are risk factors for hepatic hematoma and or rupture. The etiology is thought to be a direct
pressure on the liver.
(b). SPLENIC INJURY
Risk factors for splenic injury include macrosomia, breech delivery and splenomegaly.

SIGNS AND SYMPTOMS

Similar to hepatic rupture which includes
• Pallor • Tachypnea
• Poor feeding • Tachycardia

DIAGNOSIS
• It is sometimes palpable in the left upper quadrant stomach which may be displaced medially
on abdominal radiography.
• Differential diagnosis includes injury to other abdominal organs.

MANAGEMENT
Includes volume replacement and correction of coagulation disorders. Surgical consultation should be
obtained. Especially management with close observation is appropriate if stabilized. If Laparotomy is
necessary salvage of the spleen is attempted to minimize the risk of sepsis.

NOTE: Other Intra –abdominal organs that may be affected include the kidney, lungs and intestines.

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 CHAPTER SEVEN

CONGENITAL ABNORMALITIES /MALFORMATION OR ANORMALIES OR BIRTH

DEFECTS
Definition:
Congenital abnormalities or malformations is any defect in form, structure or function present at birth. It
can also be defined as structural or functional anomalies that occur during intrauterine life and can be
identified prenatally at birth or later in life.
Congenital anomalies can be divided into major or minor anomalies/ malformations.
• Major malformations are structural abnormalities that have medical and cosmetic consequence.
They may require surgical intervention. Examples include; cleft palate and congenital heart
disease. Such as tetralogy of Fallot.
• Minor Malformations; are anomalies with no medical or cosmetic significance. They are used in
the diagnosis or recognition of a specific syndrome. Most of the minor abnormalities are limited
to the head and neck region. Infants with three or more minor malformations are at high risk for
having a major malformation (20% - 25% or a syndrome).
INCIDENCE
The center for Disease Control and Prevention (CDC) monitors rates of birth defects in the United
States. Approximately ,1 of 33 children has a major birth defect. Infants with birth defects accounts
for 20 % of infant deaths.
ETIOLOGY /CAUSES OF CONGENITAL ANOMALIES/ ABNORMALITIES
/MALFORMATIONS OR BIRTH DEFFECTS
The cause / etiology is approximately 50% of birth defects is unknown of the remainder, etiology is
attributed 6 % to 10% chromosomes, 3% to 7.5% single gene disorders 20% to 30% multifactorial
and 4% to 5% environmental exposures (teratogens)
• Unknown causes
• Single gene defects / Genetic factors
• Chromosomal abnormities
• Environmental exposure /teratogens
• Multifactorial

• Unknown Causes: The specific cause of around 50% OF Abnormalities remains unknown.
• Multifactorial Causes: These are due to a genetic defect in addition to one or more teratogenic
or environmental factors or influences.
• Genetic Factors: In this case, the defective gene is inherited from parents which could be single
or multiple (dominant or recessive) dominant – if the child acquire defect gene from either
parent, it will produce its effect even though it is single. E.g. Huntington disease recessive – if
only one defect gene is inherited from one parent, she is a carrier. He must inherit the defective
gene from both parents before the defect can be shown. cystic fibrosis, Phenylhetonuria.
• Chromosomal Defect: This could result from;
• Non disjunction - failure of the chromosome to separate during meiosis.
• Trisomy – When there is an extra chromosome added to the normal complete chromosome,
resulting in a particular chromosome being represented three times in the nucleus. E.g. Down
syndrome or Mongolism, klinefelters syndrome (XXY), (Tri 21), Polydactyl – extra digits,
Hare lip and cleft palate.

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 • Deletions – Breaking of or loss of part of the chromosome eg. Fragile x-syndrome (breaking
of the tip of the chromosome)
• Environmental Factors
Internal Environment
External Environment

INTERNAL ENVIRONMENT
What happens within the uterus?
In maternal infection where virus crosses the placental barrier or attack the developing embryo.
e.g. virus, rubella, syphilis
Occurring within the first trimester may cause congenital cataract, deafness, microcephaly and cardiac
conditions.

EXTERNAL ENVIRONMENT
• Maternal Disease: severe anemia, diabetes, anoxia state of the mother and cardiac disease may
cause congenital defects. Iodine deficiency in the mother may result in mental retardation.
• Maternal Malnutrition: Dietary deficiencies in the mother such as folic acid deficiency can
cause neural tube defects. The mother needs adequate nutrients such as protein and vitamins in
the body to help in the growth and development of the brain. Lack of good nutrition results in
abnormalities such as microcephaly.
• Radiation: Exposure to radioactive substances in industrial setting and x-ray may lead to
skeletal deformity. e.g. talipes.
• Drugs: Heavy smoking or excessive of alcohol, drugs such as thalidomide which is administered
to pregnant women causes deformities like Phocomelia (absence of long bones), Amelia
(armless).
Streptomycin: is known to cause deafness in the body
Maternal age and Health: The older the mother the more likely it is for her to have abnormal
children.
Down Syndrome is associated with maternal age e.g. over 40 year.
• Paternal Factors : These factors too can transit environmentally caused defect , a man’s
exposure to lead , marijuana and tobacco smoking ,large amounts of alcohol , radiation, certain
pesticides and drugs may result in the production of abnormal sperm .A study revealed that
children of men who are electrical or electronic workers , auto mechanic , miners , printers or
paper mill workers are more likely to develop tumours in the nervous system . According to
another study, fathers whose diet is low in vitamin c are more likely to have children with birth
defect and certain types of cancer.

PREVENTION OF CONGENITAL ABNORMALITIES

• Before pregnancy (preconception care) ideally all women should be screened before
pregnancy begins.
• Any disease or infection identified should be treated.
• The midwife should advice the woman against the intake of excessive amount of alcohol
intake
• Educate on personal hygiene to prevent infection, also the importance of environmental
hygiene.
• Educate mother on intake of well adequate nutritious food.

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 • Encourage woman to avoid taking unprescribed drugs.
• All mothers should undergo genetic counselling before, during and after pregnancy.

CONGENITAL ABNORMALTIES UNDER VARIOUS SYSTEMS

 Gastro-Intestinal tract (GTI) /Digestive system/Alimentary tract

• Cleft up and cleft palate • Hirschsprung’s disease
• Malrotation • Gastroschisis
• Volvulus • Exomphalos
• Pierre Robin Sequence • Meconium ileus (cystic fibrosis)
• Atresias: • Imperforate Anus
• Oesophageal atresia • Pyloric stenosis
• Duodenal atresia

 Central Nervous System

• Anencephaly • Hydrocephalus
• Spinal bifida • Microcephaly

 Musculoskeletal System
• Polydactyly • Developmental hip dysplasia.
• Syndactyly • Achondroplasia
• Talipes • Osteogenesis Imperfecta
• Limb reduction deficiencies /
Anomalies
 Genitourinary system
• polycystic kidneys • Cryptorchidism
• Hypospadias • Posterior urethral valves
• Epispadias • Potter’s syndrome

 Cardiovascular system
• Congenital cardiac defects
• Cyanotic
• Acyanotic
• Chromosomal defect
• Trisomy 21
• Trisomy 18
• Trisomy 13
• Turners syndrome
• Klinefelter’s syndrome

 Respiratory system
• Diaphragmatic hernia
• Choanal atresia
• Laryngeal stridor

 Integumentary System (Skin Abnormalities)

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 • Vascular Naevi
• Capillary malformation
• Capillary haemangomata (strawberry marks)
• Pigmented (melanocytic) Naevi

CONGENITAL ABNORMALITIES OF THE DIGESTIVE SYSTEM

CLEFT LIP AND PALATE
• Cleft lip is a congenital unilateral or bilateral defect resulting from the failure of fusion of the
nasal and maxillary process in the embryo.
• Cleft palate is a congenital defect in which there is a split or cleft in the palate either centrally or
on one side only, which interferes with sucking and speech and requires corrective surgery that is
usually very successful.
• The most severe form is complete cleft of the palate accompanied by bilateral cleft lip.
• Cleft palate or lip can occur singly or together and each may be unilateral or bilateral. they occur
as a result of the failure of the frontonasal palate to unit.

TYPES OF CLEFT PALATE

• Bilateral cleft lip
• Unilateral cleft lip

INCIDENCE OF CLEFT LIP

• The incidence is 1: 1000 per live birth babies.
• It occurs more often in males than females
• Combination of cleft lip and palate occurs approximately 50% of cases.
• Cleft lip alone occurs in about 25% of cases.

INCIDENCE OF CLEFT PALATE

• Incidence is 1: 700 live birth babies.
• It is common in females than males.

CLINICAL FEATURES
A split in the lip and roof of the mouth can affect one or both sides of the face.
A split in the lip can only appear as only a small notch in the lip.
A split can appear in the roof of the mouth that does not affect the appeal of the face.

CAUSES
• Failure of embryonic development
• Chromosomal abnormalities
• Hereditary factors
• Effects of drugs
• Radiations from x-rays and other machines can also cause cleft palate and lip.

Health related problems of the cleft lip and cleft palate include the following;
• Difficulty in breathing
• Failure to gain weight

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 • Repeated ear infection
• Poor growth
• Flow of milk through nasal passage during feeding
MANAGEMENT
General management is by surgery. The cleft lip is generally repaired before the palate defect Immediate
repair is done several hours to several weeks after birth. Late repair is when infant is 6-12 weeks old and
has gain weight steadily.
Cleft palate repair may be done anytime between 6 months and 5 years .it is based on the degree of
deformity, width of oropharynx neuromuscular function of palate and pharynx and surgeons preference.

NURSING MANAGEMENT
Preventing aspiration and airway obstructions; When the feeding the baby, he should be in a vertical and
slightly forward. Feed slowly.
Suction naso-pharynx as needed so as to prevent respiratory obstruction. In mild cases the baby may
feed normally, but in severe cases a special nipple may be used or it may be fed by spoon until problem
is solved. There may be breathing difficulties, observe respiration.
Administer tube feeding if nipple feeding is been delayed.
Feeding is easier if nipple is angled to the side of the mouth away from the cleft so the baby’s tongue
can press the nipple against the upper gum.
Feed slowly over approximately 18-30 minutes.

INEFFECTIVE SUCKLING
DESCRIPTION
If suckling is ineffective, use squeezable bottle by applying rhythmic pressure along infant normal
suckling and swallowing.
Encourage mother to begin feeding the baby as soon as possible to enhance bondage and to strengthen
the oral structure needed later for mastication and speech production.
Assist and support the mother with breastfeeding if necessary.
PREVENTION OF INFECTION
Protect the baby from infection so that surgery will not be delayed. Educate mother on good
handwashing practices.
Avoid baby coming into contact with anyone who has infection.
Change baby’s position frequently. Clean the cleft after each feeding with water and a cotton.
Observation
• Observe for fever, irritability, redness or drainage around cleft and report promptly
• Monitor temperature
• Monitor pulse
• Monitor respiration

PROMOTE ACCEPTANCE AND ADJUSTMENT

• Reassure parents and explain condition and treatment plan for baby to them.
• Show acceptance of the baby, maintain composure and do not show negative motion when
handling the baby.
• The manner in which the nurse handles the baby can make lasting impression on the parents.
• Offer information and answer any question in a simple manner

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 • Give information that will let family see the baby a normal physical defect which can be
repaired.
• Encourage parents involvement in baby’s care, frequent holding, cuddling and playing with the
baby
• Show pictures of babies with success stories of the parent.

PRE-OPERATIVE CARE
All kind of cares should be taken in to consideration.
• Socio Economic preparation
• Spiritual preparation
• Physical preparation
• Psychological preparation
Prepare the parents to be with baby especially when awaking from anesthesia,to offer security and
comfort.

POST OPERATIVE CARE

Diet after surgery may be; breastfeeding, bottle feeding and cup-feeding after the surgery.
OBSERVATION
• Observe for signs of infection
• Observe for cyanotic attacks

PREVENTION OF INFECTION AT THE INCISION SITE

Small amount of water should be offered after feeding to clean the incision site.
Rinse the incision site gently with water several time a day if necessary.

GASTROSCHISIS
Gastroschisis is a congenital defect characterized by a defect in the anterior abdominal wall through
which the abdominal content freely protrudes.
There is no overlying sac and the size of the defect is usually less than 4cm.
The abdominal wall defect is located at the junction of the umbilicus and normal skin is almost always
to the umbilicus.
The defect occurs 5-8 weeks after conception most likely due to disruption of the blood supply to the
developing abdominal wall.

EMBRYOLOGY
During the fourth week of development, the lateral body folds move centrally and fuse in the midline to
form the anterior body wall. incomplete fusion result in a defect that allows abdominal vescera to
protrude through the abdominal wall
The bowels typically herniate through the rectus muscle, lying to the right of the umbilicus.
INCIDENCE
The incidence is 1: 1000 live birth and usually detected before birth.

CLINICAL FEATURES
• The protruding gut mostly flamed from irritation by amniotic fluid.
• The baby often has peritonitis at birth.
• The bowel is edematous, thickened and often appears blue due to infection with blood supply.

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RISK FACTORS
The exact cause is unknown, but what we know is there is disruption of blood supply to the developing
abdominal wall from the eight weeks of gestation by omphalomesenteric duct artery.

Those at risk are;

• Users of Aspirin
• Those who change paternity during child bearing ages.
• Young mothers.
• Mothers who smoke.
• Mothers who consume alcohol.
• Mothers with low body mass index.
• Mothers with genitourinary infection.
• Mothers who use recreational drugs.

DIAGNOSIS.
• Ultrasound scan.
• Maternal serum alphafeto protein screen in the second trimester.

MANAGEMENT
Gastrischisis is a surgical emergency. Patient frequency require more than one surgery. Only 10% of
cases can be closed in a single surgery. Immediate treatment is aimed at preventing hypothermia,
dehydration, drying of the organs and infection.
This can be done the following;
Cover the baby from legs to the thorax with an insulating clothing.
Example Vaseline gauze or sterile gauze soaked in normal saline. Inform doctor immediately. If at the
district level, refer.
PROGNOSIS
The survival rate is 90%. In adequate sittings, when a client is diagnose, pregnancy can be induced or
caesarean section can be done preferably within two weeks of term, and allow the immediate surgery to
be perform on the newborn.

EXOMPHALOS
This is the protrusion of the abdominal content through the umbilical cord so that the cord is inserted
into part of the hernia sac. Mostly occurs in macrosomia babies.
INTRODUCTION
Early in pregnancy, the intestine develops inside the umbilical cord and usually moves inside the
abdomen a few weeks later. In Exomphalos, the intestine and sometimes other organs such as liver
remain inside umbilical cord but outside the abdomen.

INCIDENCE
Incidence is 2:5000 birth

CAUSES
The cause is unknown.

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SIGNS AND SYMPTOMS
Exomphalos is immediately recognize because the child intestine are outside the body and covered in a
membrane, the size if the bulging membrane containing the intestine and other organs varies from small
protrusion to quiet a large lump.

TYPES
There are two types; namely:
• Exomphalos major: where the opening is greater than 4cm and or with the liver inside the cord.
• Exomphalos minor: where the opening is less than 4cm and only contain the intestine.
DIAGNOSIS
By the use of ultrasound scan

MANAGEMENT
The management and treatment is the same as gastroschisis.

MALROTATION AND VULVULUS

MALROTATION
Malrotation occurs when the intestine does not make the turns as it should. Intestinal malrotation is an
abnormality that occurs while a fetus is forming in its mother’s uterus.

VOLVULUS
A volvulus is a problem that can occur after birth as a result of the intestinal malrotation. The intestine
becomes twisted, causing an intestinal blockage. The twisting can also cut off the blood flow to the
intestine, and the intestine can be damaged.
This will cause an obstruction, preventing food from being digested normally.

THOSE AT RISK
Malrotation occurs equally in boys and girls. However, more boys have symptoms by the first
month of life than girls. The majority of children with malrotation develop symptoms within the
first year of life. Intestinal malrotation is most often recognized in infancy , as most infants
develop symptoms of acute bowel obstruction within the first week of life . Malrotation is rarely
seen in older children, and when it does occur, symptoms may be absent or intermirrent.

SYMPTOMS
• Vomiting bile (green digestive fluid) • Rectal bleeding
• Drawing up the legs • Failure to thrive
• Abdominal pain • Rapid heart rate
• Swollen abdomen • Rapid breathing
• Diarrhea • Bloody stools
• Constipation

DIAGNOSIS
Blood test. Test to check electrolytes
Stool R/E. A test to detect blood in stool
Computed tomography scan (CT Scan)
Abdominal X-ray. A diagnostic test which may show intestinal obstructions

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TREATMENT
The treatment depends on;
• The extent of the problem
• The child’s age and the overall health
• The opinion of the surgeon and other doctors involved in the child’s care.
• Expectations for the course of the problem
• The parents’ opinion and preference
• A volvulus is usually surgically repaired as soon as possible. The intestine is untwisted and
checked for drainage. Ideally, the circulation to the intestine will be restored after it is unwound,
and it will turn pink.
• If the intestine is healthy, it is replaced in the abdomen
• If the blood supply to the intestine is in question, the intestine may be untwisted and placed back
into the abdomen. Another operation will be done in 24 to 28 hours to check the health of the
intestine. If it appears the intestine has been damaged, the injured section may be removed.
• If the injured section of the intestine is large a significant amount of intestine, may be removed.
in this case, the parts of the intestine that remain after the damaged section is removed cannot be
attached to each other surgically. A colostomy may be done so that the digestive process
continues.

CENTRAL NERVOUS SYSTEM

• Spina Bifida (aperta)
It is a malformation of the spine in which the posterior portion of the laminae / the neural arches of the
vertebrae fails to close leaving an opening to which the spinal meninges and spinal cord may protrude. It
may occur at any area of the spine but most common in the lumbosacral region.
INCIDENCE
It’s the common defect of the nervous system occurring in about 1:1000 newborn. There are 3 types of
spina bifida discussed (degree of severity).
• Spina bifida oculta
• Meningocele
• Myelomeningocele

SPINA BIFIDA OCULTA

In this, the spinal cord and meninges are normal, the defect being only of the vertebrae.
SIGNS AND SYMPTOMS OF BIFIDA OCULTA
In most instances, it is asymptomatic and presents no problem. Some may have a dimple in the skin or
growth of hair over the malformed vertebrae site.
DIAGNOSIS
• Ultrasonography
• Roentgenogram (x-ray)
• By signs. that is by observation and examination
TREATMENT
No need for treatment unless neurologic symptoms indicate that the defect is greater than thought. If
there us the possibility that the spinal cord may be involved in the defect, surgical treatment is involved.

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NB: Parents who have a baby with a neural tube defect should be offered genetic counselling since the
risk of occurrence is 1:25.
MENINGOCELE
When a portion of the spinal meninges protrudes out of the bony defect and form a systic sac, the
condition is termed spina bifida with meningocele. Hence, it’s a hemiation of the meninges and it may
be closed /open i.e. covered with skin or open.

SIGNS AND SYMPTOMS

On examination, the newborn is found to have a defect in the spinal column large enough for the
meninges to protrude to the opening.
• Defect is usually in the centre line
• No evidence of weakness of the legs. The infant stretched and kicks in a normal manner.
• There is lack of sphincter control
PROGNOSIS: Excellent but majority die
TREATMENT: The sac may rupture /perforate thus introducing infection into the spinal fluid and
causing meningitis. For this reason, surgical removal of the sac and with closure of the skin is indicated.

MYELOMENINGOCELE
(Meningo myelocele): In this condition, there is a protrusion of both meninges and spinal cord

Manifestation
The defect may vary in severity from sensory loss or partial paralysis below the lesion to complete
flaccid of all muscles below the lesion.
There may be minimal weakness of a complete paralysis of the lower trunk and legs as well as bowel
and bladder sphincters.
The feet may be webbed.

Nursing Care
Objective: It is to prevent infection of the sac and to help restore function; orthopaedically and
urologically.

Pre-operative care
• Talk to parent to make an informed choice whether they want their baby to have surgery or not.
• Until operation is performed, the newborn should be kept flat on his abdomen with a single layer
of sterile petrolation gauze/ a telfa pad, saturated with varidase(saline) solution over the lesion.
• No diaper should be applied. The objective of care is to prevent bleeding from the meningocele
sac therefore no pressure is to be put on it.
• If the neurosurgeon for some reason delay the operation of lesion, pre-operative nursing care is
that of a normal infant and to protect the sac from pressure, injury or infection.
• To decrease danger of infection of the area from urine and faeces. The genitalia and buttocks
should be kept clean.
• To prevent deformity of the feet when the infant is placed on his abdomen, the ankles are
supported with foam, rubber pads so that, the legs do not rest on the bed.
• Antibiotics may be used if infections is suspected.
• If the baby is to be transferred home before operation, parents would be taught how to hold and
care for the baby at home without causing pressure of the sac.

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 • The most important nursing care is observation and accurate reporting of the behavior of these
infants as well as solutions directly connected to their condition.
• Record degree of incontinence and note whether there is retension of urine and faeces
• Vital signs are taken

NOTE: talk to parents to make an informed choice whether they want their baby to have
surgery or not.
POST–OPERATIVE CARE
• Observation of vital signs
• Symptoms of shock and incubator in readiness for use.
• Oxygen should be kept near the bed.
• Any abdominal distention of bladder follows most spinal cord surgery and should be repaired
immediately.
• Head circumference may be required to know if hydrocephalus follows repair of
meningomyelocele.
• Surgical dressing should be kept clean and dry by use of a meningocele apron.
• Nutrition is important
• If feed in bed, head should be elevated.
• Breast withdrawn to allow rest and release of air.

Habilitation
Habilitation of the child is necessary. Functional improvement of the legs and bowel and bladder
function is will require long time and diligent care .
• Parent learn to accept the help if normal borns are not met.
• Follow-ups by the urologist, pediatrician or orthopedic specialists, physical therapists, nurse is
necessary.
• Although, half of the leg may be paralyzed, the infant must be put in stroller and later learn how
to use wheelchair.

HYDROCEPHALUS
It is a condition in which there is excessive and abdominal accumulation of C.S.F. in the cerebral
ventricles which then becomes enlarged. Due to increased amount of C.S.F. and intracranial
pressure, ventricles become dialated and brain substance is compressed against the bony cranium.

INDICATION
Its common in the group from birth to two days

CAUSES
• Excessive secretion of the C.S.F.
• Obstruction in the C.S.F. pathway to prevent the C.S.F from getting into the subarachnoid space.

CLINICAL FEATURES
• Anterior fontanelle is tense, bulging, enlarged and non-pulsating.
• Scalp veins may be prominent and dilated when baby cries.
• An excessive large skill with separated sutures which can even be seen in 3 years of age.
• Eyes have sun set sign.

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• There is high pitch cry, restlessness and irritability.
• There is alteration in vital signs such as increased BP, decreased pulse and respiration.
• Vomiting, serious and squirt eyes are common.

DIAGNOSIS
• By clinical features
• X-ray showing the widening fontanelle and sutures
• Transillumination which is the illumination of a translucent body structure by a strong light can
also be used to visualize the accumulated fluid.
• Percussion of the skull may produce a typical cracked pot (massive sign)

TREATMENT
Surgical intervention is the only effective means of relieving brain pressure and preventing further
damage to the brain tissue.
The surgical intervention may remove the cause of the obstruction such as neoplasm, a cyst or
heamatoma but for most children, the procedure that must be done is installation of shunting device
that by passes the point of obstruction and drains the C.S.F. from the ventricles to the atrium of the
heart which in turn absorbs into the blood stream.
This is termed as ventriculo-atrial shunting.

PRE-OPERATING CARE
• Reassure the mother and seek her comfort for the operation to be done.
• The head circumference should be checked
• The vital signs must be checked
• Baby is then sent for the surgery

POST-OPERATIVE MANAGEMENT
• The vital signs must be checked and recorded every 30 mins. till the child recovers from the
anaesthesia.
• The mucous and secretions should be cleared from the airway to enhance respiration.
• Oral hygiene should be maintained to prevent infections and dryness of the mouth.
• Pressure sore must be prevented by taking care of the skin and changing the patients’ position
every 2 hours. While turning these children, the head and body should be rotated at the same
time to prevent a strain on the neck. A film pillow may be kept under the head and the shoulder
for support while lifting the child.
• Avoid positioning the child on the incisional site until the incision is healed.
• Fluid and electrolyte balance can be maintained by encouraging frequent breastfeeding.

COMPLICATION
• Increased intracranial tension occurs if the shunt malfunctions.
• Dehydration should be expected if the fontanelle is sunken.

ANENCEPHALY
It’s the absence of the vault of the skull and the cerebrum. It’s a condition that is incompatible
with sustained life but occasionally. Such babies are born alive. Malpresentation such as face
presentation are common

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 SIGNS AND SYMPTOMS
• Absence of the vault of skull and cerebrum.
• Abnormally small head

DIAGNOSIS
• Clinical features
• X-ray to confirm the absence of the vault

NURSING MANAGEMENT
• Since its incompatible with life, when diagnosis is confirmed by the x-ray examination, labour is
terminated prematurely.
• If undiagnosed and baby is born alive, he should be wrapped nicely by the midwife and showed
to the mother. It’s recognized that, seeing the whole body will help them to accept the reality of
the situation and prevent imagination of any horrible picture.
• Counselling should be done.

MICRO-CEPHALY
This is an abnormality in which the fetus possesses an abnormally small head. The vault of the
skull is very small. There are two (2) types, one in which the brain has failed to grow and the
other in which the sutures have ossified prematurely and constricted the growth of the brain. If
the child survives, its mentally retarded.

CAUSES
• Intra-uterine infection such as rubella, cytomegalovirus /toxoplasmosis.

SIGNS AND SYMPTOMS

• The infant has small brain and miniature head.
• The head circumference is less than 28 am
• The forehead is shallow and recedes the fontanelles.
• The child would be mentally retarded.

DIAGNOSIS
It’s difficult to diagnose by ultrasound, hence series of measurements of the HO and comparing
them with the fetal length and abdominal girth.
NOTE: not all babies with small head than normal are micro-cephalic even though mentally
retarded.

MANAGEMENT
• Admit baby and reassure mother
• Treatment is not instituted quickly since diagnosis is difficult with the type in which the sutures
could be separated by surgical means.
• Encourage the mother on breastfeeding since the baby wouldn’t cry for food.
• Ensure personal hygiene by changing nappies frequently.
• Monitor and record vital signs
• Prevent other infections

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• Pre and post operative care are followed as accepted when an incision is involved in the
treatment.

ATRESIA
This is the absence of a natural operation in tubular structure.

OESOPHAGEAL ATRESIA
This is a congenital abnormality which is associated with failure of the oesophagus to develop as
a continuous canal with or without a tracheo-oesophageal fistula (an oesopgeal abnormality).
There is complete canalization of the oesophagus in early intra-uterine development or during
the 4th and 5th weeks. Usually, the oesophagus ends kblindly in the upper chest, i.e. the lower end
communicates normally with the stomach and has a proximal fistula into the trachea.

CLASSIFICATION
• The blind pouch at the upper end and lower end or segment of the upper of the oesophagus
and there is no communication with the trachea.
• The proximal segment of the oesophagus connects with the fistula, to the trachea and the
distal end if the oesophagus is blind.
• The proximal segment of the oesophagus has a bling pouch and the distal segment of the
oesophagus connects near its bifurcation.
• This rare defect consists of a fistula, from the trachea to the lower segment of the oesophagus
(H-type)
INCIDENCE
90% of cases are due to faulty development of these structures.

PREDISPOSING CAUSES
Babies born to mothers with polyhydraminios

SIGNS
• At birth, the baby has copious of mucous amount from the mouth.
• The baby is unable to swallow normally.
• Continually dribbles mucous from the mouth.
• There may be cyanotic attacks due to feeds which leads to laryngospasm.
• Sneezing, choking and coughing are common.
• Abdominal distention, if air enters the stand.

DIAGNOSIS
• x-ray (radiography) showing the tip of the catheter in the blind.
• Passing a soft radio-opaque catheter into the oesophagus until the obstruction on is felt.
• A film catheter is passed into the oesophagus to check whether the passage is continuous. If it
passes no further than 4 inches, it’s likely that, the baby is suffering from atrexia.

NURSING MANAGEMENT
• Transfer the baby immediately to the paediatric surgical unit.

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• Feeding should be held to prevent inhalation into the lungs or prevent aspiration minimize reflux.
• Place the infant in a semi-upright position or if possible on its abdomen with the head down
position or suction to prevent gastric juice from entering the trachea.
• The infant should be given nothing per os. Hence IV fluids may be commenced.
• Treat infant in an incubator to maintain their temperature and oxygenation.

SURGICAL INTERVENTION
• Through a right thoracotomy where the fistula is closed by joining the two ends of the
oesophagus.
• If they are two for apart, primary anastomosis should be done/transplant will be needed at a later
date. Hence, the baby should be fed through a gastratomy.

DUODENAL ATRESIA
This is the commonest intestinal abnormality occurring at any level of the bowel but duodenum is
the most common site. volvulus, fibro bands or adhesions may also occlude the bowel.

INCIDENCE
30% of cases occur in children with Down’s syndrome.

SIGNS AND SYMPTOMS

• Persistent vomiting occurring within 24-36 hours of birth.
• Abdominal distention
• Following the passage of meconium, no further stools are passed.
• Vomitus may be milky at first, later bile stained and then green.

DIAGNOSIS
Radiation to detect the obstruction

MANAGEMENT
• Replace fluid and electrolyte balance
SURGICAL MANAGEMENT
• Immediate operation is often successful.
RECTAL ATRESIA/IMPERFORATE ANUS
The anal sphincter may be closed by aa membrane in which it can be reconstruction operatively.

SIGNS AND SYMPTOMS

• Small amount of meconium may be passed because a fistula from the intestine opens between
the forchette and the vagina orifice in baby girls and on the perineum (urethra) in boys.
• Rectal temperature is contra-indicated since there will be anus.
DIAGNOSIS
• Radiography

MANAGEMENT
• Operation is done immediately to restore patency of the bowel and any fistula closed.
• Colostomy is sometimes performed.

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 COMPLICATIONS
• Recto-urethral fistula in boys.
• Recto-vaginal fistula in girls.

MECONIUM ILEUS
This is a form of intestinal obstruction in newborn due to blockage of the bowel by a plug of
meconium in a neonate with cystic fibrosis. Babies with the meconium ileus almost always
develop other symptoms of cystic fibrosis later.

SIGNS AND SYMPTOMS

• This meconium which is passed slowly than normal.
• Abdominal distension
• Dehydration
• Bile-stained vomitus
• Growth is slow despite normal diet
• Poor weight gain
• Frequent, bulk, foul-smelling oily stool
• Flabby muscles.

DIAGNOSIS
• By signs and symptoms
• Presence of raised immune active trypsin levels
• History of any removed bowel
• Definite diagnosis is not usually possible until a sweat test has been carried –out at 4-6 weeks of
age.

MANAGEMENT
• Admit for observation and reassure mother
• Monitor daily weighing of the baby.
• Nappies should be Aed daily.
• Ensure frequency breastfeeding.
• Rectal tube may be passed if necessary
• Ensure proper mouthcare of the infant.
• IV fluids should be commenced to relieve the obstruction.
• Regular intake of drugs that draw fluid into the intestines (Eg. Lactose) may be served as ordered
by medical officer to prevent the stools from obstructing the intestinal tract.

COMPLICATIONS
• Rectal prolapse
• Anaemia
• Night blindness due to malabsorption of vitamin A.

PIERRE ROBIN’S SYNDROME

A child with this syndrome has a central cleft palate and micrognathia (undeveloped mandibular
process /lower jaw).

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 Cleft normally occur due to failure of union in the development of the face and mouth. This
syndrome normally affects the soft palate. There is an abnormal attachment of muscles
controlling the tongue which allows it to fall back and occlude the airway.

SIGNS AND SYMPTOMS

• The receding jaw leads to further difficulties in feeding.
• There is difficulty in breathing.
• Chocking and cyanotic attacks may occur at feeding time and milk is returned down the nose.
• There is a wide gap between the nostrils with a piece of bone projecting through it.

NURSING MANAGEMENT
• In order to miss this type of defect, the mouth of the newborn should be inspected with a good
light source for earlier detection.
• The baby should be admitted.
• The mother has to be reassured.
• The baby with this defect should not be shown instantly to the parents to avoid unconsciousness.
• Mothers should be told that, there is hope in the future hence should be shown pictures of babies
before and after a successful surgery.
• A flanged spoon may be used for feeding until a suitable palate is made.
• It is a prominent management to keep the airway clear.
• It may be sufficient to nurse the infant in the prone position with the head slightly suspended to
prevent the tongue from protruding into the cleft to obstruct the airway.
• Insertion of oral airway can be alone.
• Since there’s high risk of aspiration occurring, suction catheter and oxygen equipment should be
ready after feeds.
• The action of sucking will encourage the development of the mandible so mothers should be
encouraged to breastfeeding but if it’s not possible, should be expressed for the baby.
• The parents should have adequate instructions and explanation into feeding their babies and
cleaning the mouth before they are discharged.
• The baby is discharged when lower jaw has developed or parents feels comfortable to take him
home.
• At times, endotracheal tube is passed to ensure a patent nasopharyngeal airway where its
required to replace the tube every 2 weeks until adequate mandibular development.

SURGICAL TREATMENT
Plastic surgery is required to correct the central cleft palate. An operation to close the cleft palate is
usually carried out 12-15 months old.
Surgeons wait until this time so that, the infant will have no respiratory infection and level will
also be high.

COMPLICATIONS
• Mental retardation
• If palate repair is delayed beyond the 5th year of its life, there will be defects in hearing and
speech.

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 PYLORIC STENOSIS
This is the narrowing or hardening of the pyloric orifice which may be due to:
• Hypertrophy: when there is thickening of the normal tissue, this is congenital
• Cicatrical: when there is ulceration or malignant growth near the pylories. Shortly after birth, the
average affected infant does not show the symptoms until about the 3rd week of life.
CAUSES
The main cause is unknown but if affects infants between a narrow age range of 3-8 weeks. Most
theories has been propounded but the most acceptable being that , the condition is due to
achalasia ( primary failure of the pyloric to relax).
INCIDENCE
It occurs 3-4 times in every 1000 births. Babies with affected parents have 1:5 chance of having
the above condition.
SIGNS AND SYMPTOMS
• During the 1st week of life, the infant often eats well and gains more weight.
• They have projective vomiting mostly after feeds.
• A palpable pyloric tumor at the upper right quadrant of the abdomen.
• The peak incidence is within 3-6 weeks of life night across the abdomen are visible after each
feeding.
• Infants became hungry, irritable as the condition worsens
• There is loss of fluid intake which may result in dehydration.

CARDINAL SIGNS AND SYMPTOMS

• Projectile vomiting - constipation
• Visible peristalsis - loss of weight

DIAGNOSIS
• By signs and symptoms
• Through history taking, where information are gathered about the nature and type of vomiting,
palpable pyloric mass.
• X-ray with barium meal, shows a narrow pyloric canal, delayed emplying and enlarged stomach.
• Breastfeeding for PH and breastfeeding gas studies.
• Serum electrolytes balance.

TREATMENT
Surgery is the best treatment for this condition by a surgical procedure known as pylomyotomy
also known as Fred et Ramsted operation.

MEDICAL MANAGEMENT
• Gastric lavage can be ordered.
• Order antipasmadic (comychin drop 0.6% solution) of atropine melromitrate in alcohol is given
15-30 minutes before feeds.
• Toxic symptoms (erythemia and hyperpyrexia) though less common and when atropine is used
with eumydrin and the the effects are such that, the dose should be reduced or the drug
discontinued, it should be observed as such.
• Correct fluid and electrolyte imbalance by IV therapy
• Where gastritis is eminent, then stomach washout should be ordered.

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PRE –OPERATIVE MANAGEMENT
• Treat dehydration and alkalosis
• Administration of saline should be commenced when Na2CO3 has been given.
• Record should, urine and vomits output.
• Monitor vital signs
• If muscle relaxants have been ordered, they should be served by feeding.
• Prescribed atropine should be administered 30 minutes before the surgery.
• Nasogastric tube should be maintained.

POST-OPERATIVE MANAGEMENT
• During recovery from anaesthesia, vital signs and behavior of the body should be monitored.
• The patient should be observed for abdominal distention which may be due to accumulation of
gas or infection.
• Commence IV fluid to enhance adequate nutrition.
• Start feeding 4-6 hours after the surgery, beginning 5% dextrose.
• The amount and consistency of the feeds should gradually be changed.

PARENTAL ADVICE
• The parents should be explained to adopt the proper feeding techniques; the types of feed and
position of the baby before and after feeds.
• Educate parents on frequent follow-ups after discharge of their children.

DIAPHRAGMATIC HERNIA
This is the hemiation of the abdominal content into the thoracic cavity. Occurs as a result of a
defect in the diaphragm.

INCIDENCE
• Mothers with polyhydraminios
• Infants with defect in the diaphragm.

SIGNS
• Respiratory distress
• Cyanosis
• Respiratory movement and heat sounds displaced.
• Abdomen is concave
• Chest appears distended.

NURSING MANAGMENT
• Admit and reassure mother
• Explain every procedure you will do to the mother.
• Observe vital signs and record.
• Gastric suction should be chartered to prevent further distention.
• Provide warmth
• A gastric tube should be passed to decompress the bowels.
• Polyhydraminios should be treatment at ANC.

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MEDICAL MANAGEMENT
• Endotracheal tube is passed
• Radiographie is needed.
• Surgery is recommended and it’s the only life saving measure.

COMPLICATION
• Coma
• Death because of under development of the lungs.

GENITO-URINARY SYSTEM
POSTERIOR URETHRAL VALVES OR IMPERFORATE URETHRA
It’s the presence of valves in the posterior urethra which prevents the normal outflow of urine. The
urethral is a card or tube that drains urine from the bladder. This abnormality mostly affects boys.

SIGNS AND SYMPTOMS

• The bladder distends due to difficulty in the flow of urine.
• There is stasis of urine causing back pressure on the ureters and to the kidneys. This leads to
hydronephrosis (accumulation of urine in the pelvis of the kidney structure).
• Urine dribbles –out rather than being passed forcefully.
• Failure to pass urine within the 1st 4-10 hours after birth.
• Urine output is less than 2-4 mls/hr
• Lethargy
• Poor feeding
• Vomiting
• Increasing jaundice.

DIAGNOSIS
• By signs and symptoms
• Urinalysis using reagent strips
• Ultrasound to detect abnormalities.

MANAGEMENT
• Intra-uterine fetal bladder catheterization.
• Baby should be admitted and mom reassured.
• Baby should be nursed in the lateral position to help in drainage of vomitus.
• Phototherapy in cases of jaundice
• Frequent breastfeeding to fasten the maturation on process of the organs.

AMBIGIOUS GENITALIA
Difficulty in determining the sex of the newborn. Parents are usually invited to identify the baby’s sex
for themselves at delivery. On some occasions, the midwife may be asked to clarify this and if there is
any doubt should decline to assign a gender to the baby.
Examination of the baby may reveal any of the following;

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 • A small hypoplastic penis
• Bifid serotom
• Undescended testes (careful examination should be made to detect undescended testes in the
inguinal canal)
• Enlarged clitoris, incompletely separated or poorly differentiated tibia.
• Chordee (downward curcature of the penis)
There are a number of causes of this which needs expert classification.
• Some of the reasons for this ambiguous genitalia is autosomal recessive condition called
congenital adrenal hyperplasia .in this condition, the adrenal gland stimulated to over produce
androgens because a deficiency of enzyme called 21- hydrocylase which is necessary for normal
production of steroid from cholesterol.
So far the diagnosis of this, a 24 hour urine collection may be requested. It’s necessary to ensure
that, the urine bay is avoided of fetal contamination. Treatment is by cosmetic surgery. This
condition is not commonly seen in male neonates.
• INTERSEX: this is where the internal reproductive organs are at variance with the external
appearance of the geniatalia. To detect this, ultrasound examination will help to identify the
nature of the internal reproductive organ. True hermaphrodite is very rare. The decision of
gender attribution is made following chromosomal studies to determine the genetic make-up.
Treatment is by cosmetic make –up.

RESPONSIBILITIES OF THE MIDWIFE

After the 4th stage where the condition of the woman is well, she is counselled with the husband before
the exposure of the baby. The parents are invited to identify the sex of the baby. The nurse should help
to clear any doubt of the parents and reassure them or she can refer the case to the psychologist.

HYPOSPADIASIS AND EPISPADIASIS

Hypospadiasis : It’s a congenital condition of a male child in which the urethral meatus opens onto the
inferior aspect of the penis instead of the tip . A cord like anomaly called a chordee extends from the
scrotum to the penis pulling the penis downwards in an arc. The foreskin is only present on the side of
the penis.
Urination is not interfered but the boy is unable to void while. in a normal male fashion.

MANAGEMENT
The boy is not circumcised because the foreskin is needed for the repair.
Surgical repair is desirable between the ages of 6months and 18 months before the boy reaches school
going age.

Epispadiasis: In Epispadias, the opening is on the superior aspect of the penis. This condition is
extremely rare and its often associated with complete pelvis abnormality.
In this too. Surgical repair is indicated.

POLYCYSTIC KIDNEYS
It’s a congenital disorder in which many cyst less functioning. The cyst gradually enlarges and destroys
most of the normal tissues in the kidneys making the kidney tissue lose its function.

SIGNS AND SYMPTOMS

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 • The fetus is difficult to deliver due to increase abdominal girth.
• The kidneys are palpable on abdominal examination.
• There is increasing renal insufficiency and as a result, hypertension and signs of congestive
cardiac failure may occur.
• Severely affected fetus may die in utero or may die immediately or shortly after birth.

DIAGNOSIS
• By signs and symptoms
• Radiological or ultrasound investigations will reveal enlargement of the kidneys and deformity
of the calices and pelvis.
• Urine test reveal proteinuria, haematuria, bacteruria and elevated blood non-protein nitrogen
level.
NURSING MANAGEMENT
• Admit baby and reassure mother
• Advice mother to ensure proper breastfeeding habit.
• Ensure good personal hygiene by frequent changing of nappies.
• Keep baby warm
• Monitor vital signs
MEDICAL MANAGEMENT
• There is no specific reason for it. How even supportive and palliative measures may be used to
combat renal acidosis and insufficiency.
• Urine infections will be treated to help prolong life.
SURGICAL RX
• Kidney transplantation
• Surgical drainage of large cyst may be done when they interfere with renal function.
Prognosis is poor.
PREVENTION
• Genetic counselling can help people with polycystic kidney disorder understand the probability
of their children also inheriting it.
COMPLICATIONS
• Renal failure
• Cardiac failure
• Fetus may die in utero.

MUSCULOSKELETAL SYSTEM

SYNDACTLY AND POLYDACTYLY

Syndactyly is the webbing of the webbing of the fingers or toes that is fusion of the digits which
may be in the form of webbing between the fingers or toes.
It can appear as an independent anomaly or as a feature of a syndrome such as Apert’s syndrome.
This is genetically inherited condition in which there is premature fusion of suture of the vault of the
skull, cleft palate and complete syndactyly of both hands and effect.
• Surgery can be done depending on the degree of webbing or fusion.

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 Polydactyly is the extra digits which may be fully formed or simply extra tissue attached by a
peddicle.
• Reassure mother and encourage her to breastfeeding baby frequently.
• The midwife should tie-off the extra digits if no bony structure is involved.
• The hand must be opened to find any digit folded on the fist.
• Pediatrician should be informed and decision made or rx. If bones are present, surgery can be
done.

TALIPES
It’s a congenital deformity in which the foot has developed at an abnormal angle of the leg. The
cause is not fully understood. In some cases, notably in patients with oligohydramios, the child
has been cramped in uterus. and is born with mild position talipes.

TYPES
• Talipes Equinus: The toes points downwards and inwards.
• Talipes Calcaneus: the heel is downwards.
• Talipes Varos: the foot is turned inwards.
• Talipes Valgus: foot is turned outwards.
• Talipes Equinovarus: in this condition, the foot is bent downwards and inwards.
It may affect one or both feet and its often a positional defect due to pressure from the uterus.
• Talipes Calcaneovalgus: Here, the foot end turns upward and outward. Its opposite to the
talipes equinovanus.

CAUSES
• Family history of defect.
• When the intra-uterine space has been minimized. Examples in multiple pregnancy,
macrosomic fetus, oligohydramnios causing pressure on the uterus.
INCIDENCE
Particularly in males

MANAGEMENT
• In mild cases, the physiotherapy, starting on the day of birth, can gently manipulate the
foot to quickly correct the deformity.
• In severe cases, stretching, massaging or splitting of the foot may be of good help. Care
should be taken to ensure that, the babies who have splints applied and strappings are not
too tight.
• Operative treatment may be needed.

ACHONDROPLASIA
This is a rare condition in which the limbs are short due to failure in the ossification of
the long bones during early fetal life but the body is of normal length that is, the trunk has
a normal development. The children are dwarfed permanently but will have normal
mental development.
AETIOLOGY
• Achondroplasia tends to run in families and there’s no treatment for it.

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CHARACTERISTICS
• They have large head, normal trunk and very short limbs.

NURSING MANAGEMENT
• Reassure mum and keep baby warm.
• Baby should be fed frequently
• Frequent changing of napkins.

OSTEOGENESIS IMPERDECTA
This is recessive inherited condition of extreme fragility of the bones with numerous
spontaneous fractures. Fractures may occur in utero or during the process of birth . Many of
these children are warned because of multiple fractures of long bones and compression of the
vertebral columns.

SIGNS
Multiple fractures of the long bones
NURSING CARE
• The child should be kept in state of good nutrition. e.g. breastfeeding
• The child should be handled gently in order to prevent further fractures.
• Keep baby warm.
• Change baby’s napkins frequently.
• Reassure mother.

TREATMENT
Orthopedic management may help these children but the condition can’t be treated.

LIMB REDUCTION ANOMALLY

This is a congenital abnormality in which the hand or foot may be completely missing of birth or in
some, normal hand or foot will be present on the end of a shortened limb. (This is known as
Longitudinal Arrest).

CAUSES
• Amniotic band syndrome
• Arrested development that is failure of formation.
• Tetrogenic cause : inflicted at the time of chorionic villus sampling.
• The use of drugs like thalidomide to treat pregnant mothers. Some instances too are unexplained.

INCIDENCE
It can affect all category of infants

SIGNS
• A hand or foot may be completely missing
• A normal hand or foot will be present on the end of a shortened limb.
• The baby is not ill and will not be upset by the defect.

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DIAGNOSIS
• By signs
• By ultrasound scan

MANAGEMENT
Although, as to any deviation from normal, the parents of the child with limb defect will grieve for the
loss of their perfect child so as a midwife;
• You reassure and counsel them to accept the child.
• Prepare them psychologically. let them know a, children usually prove themselves to be most
adaptable to cope.
• The midwife can be helpful in the early day of parental adjustment is to offer them address of
support group such as reach.

TREATMENT
The only treatment is surgical for parents or children who require them, different kinds of prosthesis are
early as 3 months. Again, innovative surgical techniques such as the transferring of toes to hand to serve
as substitute fingers are proving successful for some children

CONGENITAL HIP DYSPLASIA

Congenital hip dysplasia results from different development of the acetabulum with or without
dislocation. The malformed acetabulum permits dislocation, the head of the femur becoming displaced
upward and backward and it can be bilateral or unilateral.

CAUSES
• Breech presentations
• Oligohydramnios with fetal malfunction
• In primigrivada pregnancies
• Multiple pregnancy
• Genetic origin

INCIDENCE
Its more common in female babies and mostly in the hip than the right.
SIGNS
• When the baby is examined lying on his back, the thighs are fixed at the hips and the knees
rotated outwards at right angles.
• There is apparent shortening of the affected limb.
• Limitation of abduction of the affected hip
• There is an additional transverse fold on the thigh

DIAGNOSIS
• By the signs
• X-ray
• By examination after birth. i.e. Barlow’s test ortolanis test.
Procedure: (is done by experienced personnel). Put the baby on a firm surface with the legs pointed
towards the examiner. Then flex the hip to get on an angle 90˚, then flex the knee with the middle finger
behind over the greater trochanter and the thumb on the inner thigh with the thigh, In mild abduction.

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The head of the femur is then lifted gently. If there is a clink sounding noise, it means there is a
dislocation.

MANAGEMENT
The treatment is done by an orthopaedic surgeon. There are several accepted ways of keeping the hip
joint in place. E.g.
• Van Dansum splint
• Abendeen’s splint
• Marlow’s splint
• Barlow’s splint
• Parlik harness
• An open reduction of the lip

NURSING MANAGEMENT OF AN INFANT

In a cast or orthopaedic device . The main aim is to prevent drying of the cast,effective
circulation and movement , sign of pressure or irritation ,sign of shock and bleeding if operation
chain has been perfomed.
Personal hygiene and elimination.
• Admit the infant, reassure the parent to give their cooperation in the care of the infant.
• For the 1st 24-48 hours after application of cast, the infant should be placed on a firm mattress
and support by firm pillows.
• The infant may be irritable because of restriction of movement caused by the device or cast, so
soothing methods such as stroking, cuddling and crooning should be done.
• The skin around the cast edges should be carefully inspected for signs of irritation, redness or
oedema and carefully massage to promote circulation.
• The cast should be kept dry always so bathing should be done by top and tail and frequent
changing of wet napkins.
• Care should be taken to prevent any small particles of food or toys from being pushed down in
the east.
• Position should be changed frequently if infants is confined to bed and passive exercise carried
out.
• Baby may suck the breast if condition allow. If not the breast milk should be expressed and used
to feed the infant.

EDUCATION ON DISCHARGE
• Educate the mother on the importance of the cast
• Care of the cast at home
• The need for review or return visit to have the cast checked.
• The curve of the infant at home.

PROGNOSIS: Early recognition and treatment before an infant starts to stand or walk have a
good prognosis.

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 RESPIRATORY SYSTEM
CHOANAL ATRESIA
It is a unilateral or bilateral narrowing of the nasal passage(s) with web of tissue or bone
occluding the nasopharynx.

INCIDENCE
1:8000 meaning it hardly occurs

CAUSES
The cause is not known but it has something to do with the malformation of the nasal bone.

SIGNS
• The infant breathes through the mouth and finds feeding impossible.
• On attempt to pass nasal catheter, it cannot enter pharynx.
• Vapour cannot be collected when a mirror or cold spoon is held under the nose.
• At birth, the baby’s colour will improve by cry.
• Unilateral defect may not be noticed until the baby feeds for the 1st time.
• There are tachypnea and dyspnea
• There may be cyanosis.

DIAGNOSIS
• Signs
• X-ray

NURSING CARE
• The midwife should bear in mind the possibility of respiration difficulty and cyanosis and
therefore should position baby to help breath through the mouth.
• Oral feeding is suspended
• Give IV fluids
• Keep baby warm
• Refer to doctor immediately this is detected
• Mother and relatives are educated on the condition and reassured.
• Continues observation of vital signs is necessary
• Surgical intervention is needed to remove the obstruction.

PROGNOSIS: It is good, if surgical intervention is as early as possible.

COMPLICATION
• It is associated with ‘charge’ syndrome
A syndrome in which there are defects found in the eye (coloboma) the heart, the ear and
occasionally oesophageal atresia.
• Growth retardation
• Asphyxia

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 LARYNGEAL STRIDOR
This is a noise made by the baby usually on inspiration and exacerbated. i.e. an increase in the
severity of the symptoms of a disease by crying.
CAUSE
It is most commonly caused by laryngomalacia which is due to laxity or softening of the
laryngeal cartilage.

NURSING MANAGEMENT
• Although it sounds distressing, the body generally is not at all upset. But it’s the parents who
need to be reassured and made comfortable often or repeatedly.
• It should be explained to them that the stridor may take sometimes to resolve, perhaps up to 2
years.
• If however, the stridor is accompanied by signs of dyspnea i.e. (difficulty in breathing) or
feeding problems, further investigation on such as bronchoscopy examination of the bronchi or
laryngoscopy would become necessary to rule out a more serious cause,
• Keep the baby warm.
• Prevent infection.
NB: the larynx is the organ of the voice situated at the upper end of the trachea.

CHROMOSOMAL ABNORMALITIES (COMMON OCCURING)

These are the abnormalities that develop in utero by mutation of chromosomes. The most common ones
include ;
• Trisomy 21/ Down syndrome /Mongolism
• Trisomy 18/ Edward’s syndrome
• Trisomy 13/ Patau syndrome
• Tunner’s syndrome
• Klinefelter’s syndrome
General causes
• Advance maternal age over 35
• Hereditary
Diagnosis of chromosomal abnormalities
• Ultrasound
• C.T. scan
• By signs and symptoms
• X-ray
• Amniocentesis

Trisomy 21/ Down syndrome /Mongolism

It is the most common chromosomal related syndrome. It is usually due to the presence of extra
chromosome instead of 46 chromosomes . It is the 47 chromosomes with 21 being repeated three
times rather than two times. As a result of the non-disjunction of the first meiotic division usually
associated with maternal age over 35 years.
Incidence
The estimated incidence of Down syndrome is between 1 to 1000 to 1100 live births. It mostly
affects males more than females.
Clinical features

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• Broad flat nose
• Slanting eyes
• Short neck with loose skin
• Thick protruding tongue
• Short hands with single Palma crease
• Flat occiput
• Small head
• Wider space between the thumb and index finger
• The palate of the mouth is narrow
• There is a wide space between the first and the second toe
• General softness of the body
• Severe mental retardation

Other health related problems are

• Congenital heart disease • Hearing problems
• Duodenal Atresia • Delay in sexual development
• Eye problems like cataract • Acute leukemia: cancer of the blood
Trisomy 18/Edward’s Syndrome
It is rare than Trisomy 21 and it is due to the defect on the 18th pair of chromosomes. In this case
there is an extra chromosome on the 18th pair of chromosomes making it three instead of two.
Most affected individuals are females and it arises as a result of parent non-disjunction at the second
meiotic division.
Incidence
It is the second most common autosomal Trisomy after Down syndrome.
1: 6,000, 80% of those affected are females.
Prognosis
They mostly die in utero and, those who are born alive, approximately 50% die within 1 week and
90% within 5 months.

Clinical Features
• Low set malformed ears • Delayed brain development
• Low birth weight • Small narrow cranium
• Prominent occiput • Mental retardation
• Narrow pelvis • Small mouth
• Umbilical and inguinal hernia Short sternum
• Micrognathia: small lower jaw • Short nails
• Microcephaly • Physical malformation
• Abnormal flexion of fingers, index over • Small wide set ears
the third finger • Cleft lip and palate
• Rocker bottom feet – prominent heels • Failure to thrive

Trisony 13/Patau Syndrome

Trisomy 13 is a congenital abnormality which occurs when there is an extra copy of the 13 th
chromosome. The children have short life.
Incidence

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 Is the least common and most severe of the viable automal trisomies? 1:8,00-12,000 live births.
Mostly affecting males than females. only 5% live beyond 3 years.
Prognosis
Prognosis is generally poor for the neonate identified with Patau syndrome. Median survival is fewer
than 3 days ,81% die within 1 month and 95 % die within 6 months. Only 5% live beyond 3 years.
Some end in spontaneous abortion, fetal demise and stillbirth
Clinical features
• Small infant
• Microcephaly • Flexed /overlapping fingers
• Cleft lip and palate are normally • Polydactyl (webbed fingers and toes)
common • Eye deformities (blindness)
• Limb abnormalities present • Umblilical /inguinal hern
• Slopping forehead • Scalp defect
• Rocker-bottom feet (protruding heels) • Low set ears
• Micrognathia ( small lower jaw ) • Hernias
• Seizures • Close set eyes
• Urinary tract anomalies • Mental retardation
• Deafness

Tunner’s syndrome /Gonadal Dysgenesis/Xogonosomal Monosomu (XO)

Chromosomal defect where only one sex chromosome exists an X. the absent chromosome is
indicated by ‘O’. Is being diagnosed in puberty .
Incidence
• Normally affect female body
• It occurs 1:3000 life female births
Clinical features
• Short webbed neck • Nail abnormalities: deep set nails bed
• Widely spaced nipple • Congenital cardiac defect
• Oedematous feet • Mental development is usually normal
• Undeveloped genitalia

Klinefelter’s syndrome
This is an abnormality affecting boys but it is not normally diagnosed until puberty changes fail to
occur. This is a syndrome caused by additional X-chromosome in males occurring in approximately in
1:500 to 1:1000 male births. They have male genotype. Abnormal sperm X & Y fertilized normal X egg.
XXY
Clinical feature
• Features appear in puberty
• Taller than average (long arms and legs)
• Hypogonadism (under developed testes)
• Sterile but there may be gynaecomastia (increased breast tissue)
• Female type pubic hair pattern
• Frontal baldness absent
• Narrowed shoulders
• Wide hips
• Poor beard growth

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General management
Nursing management
• Manage the baby as normal neonate such as provision of warmth, infection prevention, nutrition
and protection (immunization).
• Observe pre and post-operative care if necessary.
Psychological management /support
• Reassure the mother that the health team are there to support her in caring for the child.
• Explain and educate the mother on the condition especially it’s causes to clear and remove any
misconception and superstition
• Involve the mother and the family members during the care of the baby
• Assessing the condition of the baby, pictures of successful babies who have the same condition
can be shown to the mother to allay any anxiety.
• Encourage the mother to ask questions concerning the care of her child and the health provider
who answers her must have an in-depth knowledge on birth defect to clear the mother’s mind.
• Encourage mother to consider a range of supportive options in order to help her built a strong
support network as this will help her and baby now and in the future.
• Encourage the mother to discuss the condition with family and friends by informing her loved
ones about the nature of her baby’s condition which will help others know what to expect and
how to safely interact with her child.
• Encourage mother to talk about her feelings and emotions with regard to her baby’s condition
which will help her cope by releasing stress and emotions.

GENITOURINARY SYSTEM
Potter’s syndrome / renal agenesis
This is a defect whereby there is an absent of the kidneys. It is suspected in olihydraminios due to
compressive effects of longstanding, mostly from 13-14 weeks of generation .
It can also be as a result of severe hypoplasia (imperfect development).
Can be unilateral or bilateral
Incidence
• 1: 1000 mostly present is the unilateral
• 1: 3000 mostly present is the bilateral
• mostly occurring from mothers or parents with malformed or absent kidney
• Males are mostly affected
• Such babies mostly do not live beyond 4 years
Causes
• When the kidney bud fails to develop at early stage during fetal growth.
• Genetic mutation is also thought to be a cause.
Clinical features
• Widely separated eyes with epicanthal folds
• Oligohydramnios
• Abnormal limbs and position
• Under developed lungs
• Dypnoea (difficulty in breathing)
• Low set ears
• Broad nasal bridge.

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 ABNORMALITIES OF THE SKIN
NAEVI OOR BIRTHMARK
This is a congenital blemish token of the skin due to the dilation of small blood vessels or pigmented
area of the skin caused by excess skin pigment cells such as melanocytes.
They vary in size and can affect any part of the skin surfaces, it may also be seen on eye lids.
These are brown, sometimes hairy, marks on the skin that vary in size and maybe flat or raised.
A percentage of this type of birth mark may become malignant.
Surgical excision may be recommended to pre-empt this.
It is unlikely that treatment for any pf this birth-mark will be carried out in immediate neonatal
period except in case of large pigmented naevi. The responsibilities of the midwives is to reassure
parents and notify appropriate medical staff for intervention.

CAPILLARY HAEMANGIOMA (STRAWBERRY MARKS):

They are benign swelling or growth of endothelial cells, the cells that line blood vessels.
INCIDENCE
Capillary haemangioma are not usually noticeable at birth but appear as red raise lesions in the first
few weeks of life. They are common in girls than boys and also common in preterm infants. They
can appear anywhere in the body but cause particular distress to the parents when appear on the face.
However, parents may be reassured that, although the lesion will grow bigger for the first few
months but it will regress and disappear completely by the age of 5-6 years.

TREATMENT
No treatment is normally required unless the haemangioma is situated in an awkward area where it is
likely to be subjected to abrasion, such as on the lip, or around the eye where it may interfere with
vision. Treatment with steroids or pulsed laser therapy is possible.

PORTWINE STAIN
These are capillary malformation affecting the face. It is characterized by purple-blue pigment of the
affected part. Usually occur on the face and neck.
INCIDENCE
• It occurs in 1 in 3000 births
• Its twice as common in girls than in boys
CAUSES
When blood vessels remain dilated due to fault nerve supply to affected vessels this means the nerve
impulses needed to make the blood vessels narrow are absent.
MANAGEMENT
• Reassure the mother
• Laser treatment can be given as the condition does not appear with time. This is given ten times
at 8 weeks interval before the child reaches 5 years .
• Cosmetic preparation can be used to camouflage the affected skin area.
MONGOLIAN BLUE SPOTS
These are bluish-black or bluish grey discoloration (pigmented) of the skin usually seen on
the back and buttocks of babies at birth. It may cover a large area of the skin.
CLINICAL MANIFESTATION
• Blue or bluish –grey spot on the back, base of spine or shoulders.

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• Flat area with irregular shape and unclear edges.
• The spots are usually 2-8 centimeters wide.
TREATMENT
• Some go away on their own
• Compression and massaging can be done if they are small
• Steroids can be given or either surgery, laser therapy or cryotherapy (freezing) is done.

CONGENITAL CARDIAC DEFECT

DEFINITION: congenital heart defects are anatomical and physiological abnormalities in the
heart that are present at birth.
Abnormalities in the heart at birth may be due to intrauterine development errors or to the failure
of the heart and blood vessels to adapt to extra uterine life. Sometimes, there are no symptoms in
early life and the abnormality is reorganized only when complications appear.

TERMINOLOGIES
• Stenosis: narrowing due to scar or abnormal growth
• Atresia: occlusion or blockage of lumen
• Coarctation: narrowing of the aorta
• Tetra: four
• Valve: folds of membrane passage or tube, so placed as to permit passage of fluid in one
direction only.
• Cyanosis: bluish appearance
• Acyanosis: absence of bluish appearance
• Regurgitate: backward flow
• Transposition: displacement of any of the viscera to the opposite
• Septum: division or partition

TYPES:
 Cardiac defect presenting with cyanosis
• Transposition of the great arteries • Tetralogy of fallot
• Pulmonary atresia • Tricuspid atresia
 Acynotic cardiac defect
• Patent / persistent ductus arteriosus • Coarctation of the aorta
• Ventricular Septal defect (VSD) • Aortic stenosis
• Atrial Septal defect (ASD) • Pulmonary stenosis
•
Transposition of the great arteries: this is a condition wherein the aorta arises from the
right ventricle and pulmonary artery from the left. Or it is the defect that occurs from birth
where the two major vessels (aorta and pulmonary artery) that carry blood away from the
heart are switched (transposed)
Patent/ persistent ductus arteriosus: if it remains patent, blood regurgitate from the aorta to
the pulmonary artery where the pressure is lower, reducing the volume entering the systemic
circulation and increasing the volume of blood in the pulmonary circulation. This leads to
pulmonary congestion and eventually cardiac failure.

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 Ventricular Septal defect (VSD): it is an abnormal opening between the right and the left
ventricles. Due to higher pressure in the left ventricle shunting blood from the right to the left
ventricles during systolic. Correction of this is done by surgery.
Coarctation of the aorta: this is the narrowing of the lumen of the aorta. This leads to high
blood pressure in the upper body. Increase force of contraction of the heart is needed to push
the blood to the coarctation which eventually causes hypotension in the rest of the body.
Aortic stenosis: narrowing of the aortic orifice of the heart due to malformation.
Pulmonary stenosis: narrowing of the pulmonary lumen of the heart due to malformation.
Tetralogy of fallot: it is a combination of congenital cardiac defect of pulmonary stenosis,
ventricular septal defect, destroposition of aorta and hypertrophy of right ventricle
Atrial Septal defect (ASD): there is communication between the two atria

SIGNS AND SYMPTOMS OF THE ACYANOTIC CARDIAC DEFECT

• Tachypnoea
• Tachycardia COMPLICATION
• Low pulse • Mental retardation
• Heart failure • Asphyxia
• Growth retardation
• Brain damage

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 CHAPTER EIGHT
CARE OF THE BABY TO AN HIV POSITIVE MOTHER

DEFINITION OF HIV AND AIDS

HIV: HIV stands for human immunodeficiency virus

H: Human
I: Immunodeficiency
V: Virus
HIV breaks down the body’s defenses against infection and disease by infecting specific blood cells,
leading to a weakened immune system.
When the immune system becomes weak, the body loses its protection against illness. With time, the
immune system is unable to fight the HIV infection and individuals may develop serious diseases
including other infections and some types of cancers.

Definition OF AIDS.
AIDS is an acronym for Acquired Immune Deficiency syndrome and refers to the most advance stage of
HIV infection.
It is referred to as a group of serious illnesses and opportunistic infections that develop after being
infected with HIV for a long period of time.
A: Acquired
I: Immune
D: Deficiency
S: Syndrome
HIV is the virus that causes infections.
A person who is HIV infected may have no signs of illness but can still infect others.

TYPES OF HIV
HIV 1 and HIV 2 are types of HIV. Both are transmitted the same way.
In GHANA HIV 1 is the most prevalent constituting about 95% of all HIV infections.

EPIDEMIOLOGY
HIV is transmitted by sexual contact, through exposure to blood and blood components prenatally from
an infected mother to the child and through breast feeding from an infected mother to her infant.
Perinatal transmission can be in utero, intra partum or postpartum (through breast milk).
Most perinatal transmission probably occurs late in pregnancy or during birth.
An HIV infected mother can have a child who is also infected.

PATHOPHYSIOLOGY AND AETIOLOGY

• The causative agent is a retrovirus that damages the immune system by infecting and
depleting the CD4 lymphocytes (t4-helper cells).
• These CD4 lymphocytes play central role in the regulation of the immune system.
Progressive destruction of the immune system leads to:
Increase incidence of serious bacterial infection such as bacteremia, bacteria pneumonias and
osteomyelitis

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 • Opportunistic infections which commonly include pneumocystis proumonia (PCP), oesophageal
candidacies.
• More aggressive forms of the viral infections such as severe vermicelli, disseminated zoster,
cytomegalovirus pnoumonitis.
• Cancers, especially lymphomas.
• Washing syndromes and encephalopathy
• Multisystem, gastro-intestinal dysfunction, dermatologic manifestation, musculoskeletal
abnormalities, ocular impairments, car, nose and throat problems and hematologic.,

CLINICAL MANIFESTATIONS
• Generalized lymphadenophathies
• Persistent, recurrent oral candidiasis
• Failure to thrive
• Developmental delays or loss of previously acquire milestone
• Hapatomegaly
• Splenomegally
• Persistent diarrhea
• Parotids
• Unexplained anemia, thrombocytopenia
• Unexplained cardiac or kidney diseases
• Recurrent serious bacterial infection

DIAGNOSTIC EVALUATION
• Neonatal testing with enzyme-linked immune-sorbent assay (ELISA)
• Complete blood count (CBC) used to monitor anemia and neutropenia and lymphocytes
• Polymerase chain (PCR) and virus culture are the most sensitive and specific assays for detecting
HIV infection in children.

MANAGEMENT FOR HIV BABIES: NURSING INTERVENTION

When caring for a baby of an HIV- positive mother, always
-Respect the confidentiality of the mother and family
-Care for the baby as for any other baby, paying particular attention to infection prevention
procedure
-Give the baby all routine immunization
• Emphasize to the mother the importance of condom use to prevent infection of her partner (s)
and transmission of other sexually transmitted infections.
• Provide emotional support
• Administer or teach caretaker to administer drugs that may help prevent serious bacterial
infections, prevent opportunistic infections that occurs.
• Maintain cleanliness of the environment and family members that essentials of
environmental sanitations.
• Use aseptic techniques when performing invasive procedures.
• Administer and teach the family good skin care.
• Advice families of the need to complete all recommended childhood immunizations.

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MAINTAINING ADEQUATE NUTRITION
• Advice the mother regarding her feeding options and respect and support the mother’s choice.
• Allow the mother to make an informed choice about the best feeding option for her baby.
• Explain to the mother that breastfeeding carries an increased risk of transmitting HIV to the
baby after birth.
• Inform the mother about her options for feeding, the advantages and the risk. The mother can
choose to;
- Give replacement feeding if this is acceptable, affordable, feasible, sustainable and safe. Explain to the
mother that replacement feeding often carries a higher risk of infant mortality than breastfeeding,
especially if it cannot be prepared safely, is not continuously available and affordable to the family and
there are limited facilities and water for preparation.
- Exclusively breastfeed until replacement feeding is feasible. It is important that the mother stops
breastfeeding once replacement feeding is introduced.
-Exclusively breastfeed for six (6) months, then continue breastfeeding while starting complementary
feed (e.g. mashed solid foods) after six months of age.
• Help the mother to assess her situation. Help her decide whether to breastfeed or give
replacement feeding.

MOTHER CHOOSES TO BREASTFEED

• Support the mother’s choice.
• Advice the mother against mixed feeding (e.g. feeding anything other than breast milk, such as
commercial breast-milk substitute, animal milks, local porridge, tea, water etc.). Mixed feeding
may increase the risk of both HIV transmission and illness or death from diarrhea or other
illnesses.
• Ensure correct positioning and attachment to prevent mastitis and damage of the mother’s
nipples;
- Advice the mother to return immediately if she has any problem with her breast or nipples, or if the
baby has difficulty feeding.
- If there are no other problems requiring hospitalization, discharge the baby.
- Ensure a follow-up visit during the first week after discharge to assess attachment and positioning and
the condition of the mother’s breast.
- Ensure that the baby receives regular follow-up visit with an appropriate child care provide
- Arrange for further counselling to prepare the mother for the possibility of stopping breastfeeding
early.

MOTHER CHOOSES REPLACEMENT FEEDING

• Support mother’s choice
• Ensure the mother understands the if she chooses replacement feeding, she should begin
complementary feeding at six months of age while continuing to provide milk.
• Review the guidelines for preparing and feeding breast-milk substitutes.
• Allow the mother to begin preparing feed as soon as she is able to and teach her how to feed the
baby using cup, cup and spoon or other device e.g. paladai.
• Encourage the mother to feed the baby at least eight times daily. Teach her to be flexible and
respond to the baby’s demand
• Give the mother written instruction on safe preparation of the replacement feed.
• Explain the risk of replacement feeding and how to avoid them.

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 -The baby may get diarrhea if the mother’s hands, water or utensils are not clean, or if the milk
stands too long before being used
-The baby may not grow well if;
*too little substitute is given at each feed
*too few feeds are given
* the substitute contains too much water
*the baby has diarrhea
• Advice the mother to seek care if the baby has any problem, such as;
-Feeding less than six times daily
-Diarrhea
-Poor weight gain
• If there are no other problems requiring hospitalization, discharge the baby
• Ensure a follow-up visit during the first week after discharge to assess how the mother is coping
with replacement feeding and ensure that she receives support to provide safe replacement
feeding.
• Ensure that the baby receives regular follow-up visits with an appropriate child care provider.

MAINTAINING ORAL MUCOS INTEGRITY

• Examine mouth regularly to rule out fungal infections
• Administer presented antifungal and anti viral therapy
• Offer fluids and blended food to minimize chewing and facilitate swallowing.
• Avoid high seasoned, spicy or acidic foods.

DETECTING AND CONTROLLING FEVER

Monitor for fever and report any temperature over 101 ⁰ F (38.4 ⁰ C)
Teach the family to promptly report any febrile episode
Administer prescribe antipyretics.

PROMOTING EFFECTIVE FAMILY COPING

Provide emotional support to the family
Refer the family to the appropriate community resources for grief counseling
Maintain non-judgmental attitude and non-prejudicial approach.
Allow the family to use denial as a protective mechanism. This gives them some sense of control.
Explain all care and treatment plans to the family.
Involve the family in planning for the care and management of their child
FAMILY EDUCATION AND HEALTH MAINTANANCE
• Teach families and other care takers of the child universal precautions. In caring for HIV
infected infants and children, gloves are recommended when handling potentially contaminated
body fluids (such as blood) but are not considered necessary for routine diaper chaining unless
bloody diarrhon haomaturia exist,
• Facilitate supply of adequate numbers of latex gloves to families to use as indicated.
• All fevers should be reported as well as adverse experience with medications
• Assess whether parents are receiving care for themselves, often time’s parents will neglect their
own care to provide for the child. As a result, the parent immune status may become quickly
compromised.

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PROMOTING DEVELOPMENTAL GOALS
• Assess the child’s development status on a regular basis.
• Report any delay in achieving development milestones.
DRUG MANAGEMENT
ANTIRETROVIRAL THERAPY
Without antiretroviral therapy, 15% to 30% of babies born to HIV-positive mothers will be infected
during pregnancy and birth, and 5% to 20% may be infected by breastfeeding.
• Determine if the mother is receiving or has received antiretroviral treatment for HIV to prevent
mother-to-child transmission.
• Treat the baby according to the protocol used for the mother per national policy. E.g.
- If zidovudine (AZT) was given to the mother for four weeks before birth, continue to give AZT
to the baby for six weeks after birth (2mg/kg body weight by mouth every six hours.)
- If the mother received a single dose of nevirapine during labour and the baby is less than three
days old, immediately give the baby nevirapine in suspension 2mg/kg body weight by mouth.
- schedule a follow-up examination in 10 days to assess feeding and growth.
All infants born to HIV-infected woman should be started on Pneumocystis Pneumonia (PCP)
prophylaxis at 4-6 weeks of age regardless of CD4 count.
• The first drug of choice is Trimethroprim-Sulfamethoxozole.(saptrin)
• Pentamdine and Dapsone are alternative choices.
• In all infants infected with HIV regardless of clinical manifestations or viral load.

Aggressive antiretroviral therapy should be initiated

DRUG REGIMEN FOR BABY
ZDV(Zidovudine) 4mg/kg body weight of ZDV daily for 6
weeks
EFC (efavirenz) (600mg) Or NVP 2mg/kg daily for 6 weeks if infants
is anaemic

• Use intravenous immune globulin (IVIG) in infected children who have two or more serious
bacterial infections within one year or for the treatment of HIM-related thrombocytopenia.
• Use of antifungal drugs such as nystatin, Nzoral, fluconazole, (Difluean) and clotrimazole for
persistent or recurrent oral candidiasis
• Aggressive, prompt assessment and treatment of febrile illness.
• Nutritional support.
• Adequate pain management in advance or each stage of disease.

COMPLICATIONS
• Repeated, overwhelming infection and certain cancers particularly lymphomas.
• Hearing loss, tooth and gum diseases, acute and chronic ENT infections
• Drug related toxicities.
• Opportunistic infections
• Cardiomyopathy
• Failure to thrive
• Chronic atopic dermatitis and other skin reactions
• Nephropathy.
• Developmental delay.

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• Neuropathy, myopathy.
• Anaemia, thrombocytopenia, neutropenia
• Death.

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 CHAPTER NINE

INTENSIVE CARE OF THE NEONATE

THE NEONATAL INTENSIVE CARE UNIT (NICU)

A neonatal intensive care unit (NICU), also known as an intensive care nursery (ICN), is a special
department of a hospital or health care facility that provides a special care of ill or premature newborn
infants.

Newborn babies who need intensive medical attention are often admitted into a special area of the
hospital called the Neonatal Intensive Care Unit (NICU). The NICU combines advanced technology and
trained health care professionals to provide specialized care for the tiniest patients. NICUs may also
have intermediate or continuing care areas for babies who are not as sick but do need specialized nursing
care. Some hospitals do not have the personnel or a NICU and babies must be transferred to another
hospital.

Some newborn babies will require care in a NICU, and giving birth to a sick or premature baby can be
quite unexpected for any parent. Unfamiliar sights, sounds, and equipment in the NICU can be
overwhelming. This information is provided to help you understand some of the problems of sick and
premature babies. You will also find out about some of the procedures that may be needed for the care
of your baby.

Before birth, breathing, eating, elimination of waste, and immunologic protection all came from the
mother. When a baby enters the world, many body systems change dramatically from the way they
functioned during fetal life:

 The lungs must breathe air.

 The cardiac and pulmonary circulation changes.
 The digestive system must begin to process food and excrete waste.
 The kidneys must begin working to balance fluids and chemicals in the body and excrete waste.
 The liver and immunologic systems must begin functioning independently.

Sometimes, a baby has difficulty making the transition to the world. Being born prematurely, having a
difficult delivery or birth defects can make these changes more challenging. Fortunately for these babies,
special newborn care is available. (NICU).

FACTORS THAT MAY REQUIRE CARE OF THE BABY AT NICU INCLUDE THE
FOLLOWING:

 Maternal factors:
o Age younger than 16 or older than 40 years
o Drug or alcohol exposure
o Diabetes
o Hypertension (high blood pressure)
o Bleeding

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 oSexually transmitted diseases
oMultiple pregnancy (twins, triplets, or more)
oToo little or too much amniotic fluid
oPremature rupture of membranes
 Delivery factors:
o Fetal distress/birth asphyxia (changes in organ systems due to lack of oxygen)
o Breech delivery presentation (buttocks delivered first) or other abnormal presentation
o Meconium (the baby's first stool passed during pregnancy into the amniotic fluid)
o Nuchal cord (cord around the baby's neck)
o Forceps or cesarean delivery
 Baby factors:
o Birth at gestational age less than 37 weeks or more than 42 weeks
o Birth weight less than 2,500 grams (5 pounds, 8 ounces) or over 4,000 grams (8 pounds,
13 ounces)
o Small for gestational age
o Medication or resuscitation in the delivery room
o Birth defects
o Respiratory distress including rapid breathing, grunting, or apnea (stopping breathing)
o Infection such as herpes, group B streptococcus, chlamydia
o Seizures
o Hypoglycemia (low blood sugar)
o Need for extra oxygen or monitoring, intravenous (IV) therapy, or medications
o Need for special treatment or procedures such as a blood transfusion
BABIES WHO NEED INTENSIVE CARE OR BABIES WHO ARE NURSED IN AN
INCUBATOR
 Preterm or extremely immature babies of very low birth weight
 Respiratory disorders: Babies with severe respiratory distress syndrome.
 Cerebral disorders
 Certain severe infections; septicaemia, meningitis
 After major neonate surgery: e.g. Congenital heart diseases.
 Haemolytic disease of the new born requiring exchange transfusion.
 Babies with birth defects

HEALTH CARE PROFESSIONALS AT THE NICU

The following are some of the specially trained health care professionals who will be involved in the
care of your baby:

 Neonatologist. A pediatrician with additional training in the care of sick and premature babies.
The neonatologist supervises pediatric fellows and residents, nurse practitioners, and nurses who
care for babies in the NICU.
 Respiratory therapists
 Occupational therapists
 Dietitians
 Lactation consultants
 Pharmacists

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  Social workers
 Hospital chaplains

The members of the NICU team work together with parents to develop a plan of care for high-risk
newborns.

INCUBATOR PARTS AND CARE

The term incubation was derived from a latin word “incubare” that means “lie on”. Incubation is the
process of providing an environment to keep neonate warm and suitable for their development. A
neonate incubator is a rigid box – liked enclosure in which an infant can be kept in a controlled
environment for observation and care.

TYPES OF INCUBATORS
• Portable and non-portable.
• Open box type / Amstrong
• Close type
• Double wall type
• Servo control incubator – automatic
THE INCUBATOR

PARTS OF INCUBATOR
• Main switch • A heater within
• Control panel • Humidification Control (water tank)

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 • Oxygen fix • Exhaust pipe
• Entry points (Access parts doors) • Alarm and Safety control
• Copper board to radiate ice heat to main • Filter and bacteria’s filter
chamber • Mattress
• Baby’s trail • Cot sheet
• Canopy • Incubator drip stand

CARE OF THE INCUBATOR

• The incubator should be handled properly when moving it around the neonate unit and should be
well maintained to ensure efficiency
• Daily dump dusting of the side should be carried out every morning and total cleaning done
every week with mild detergent.
• Incubator should be totally disinfected after discharged of an infant
• If Humidified Chamber must be emptied and cleaned daily, fill with fresh distilled water.
• After use the incubator should be switched off, if not in used.
• The cleaning of the incubator should be done according to manufacturer’s direction.

EMOTIONAL SUPPORT TO THE MOTHER/FATHER DURING ADMISSION.

• Orient parents to the unit and its waiting areas.
• Clarify visiting policies and hospital expectations;
• Familiarize the parent with the unit before admission.
• If admission is unexpected and sudden the family care to reduce fear, stress and anxiety is of
prime importance for the family.
• Assure parents that everything possible is being done for their baby.
• Whenever possible encourage parent to see their child touch and cuddle to facilitate bonding.
• Explain special equipment and changes in nursing management to the parent.
• Provide opportunities for parents to ask questions and have them answered.
• Encourage parent not to compare progress to other babies to their child. It can set them up to be
quickly disappointed.
• Help minimize guilt feelings by providing adequate specific information and clarify any
misconception.

RESPIRATORY NEEDS
• To determine respiratory needs of the sick baby an accurate hourly assessment of the neonate is
made.
• This includes the chest shape, e.g concave shape and colour of the baby, e.g cyanoses.
• The rate and regularity of respiration together with breathing sounds e.g. wheezing or grunting
respiration.
• Depending on these findings, the need for suction can be determined.
• In all babies with breathing difficulties, gentle suction of the oropharynx and oral cavity will
remove secretions.
• To maintain respiration, the most suitable position for nursing babies with the respiratory
problems is usually supine, alternating to the left and right sides.
• The tray of the incubator is slightly tilted upwards at the head end in order to prevent abdominal
organs from pressing on the diaphragm.

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 • A small neck roll or piece of cloth can be rolled and inserted and the nape of the neck to help
maintain alignment of the airway.

CARDIOVASCULAR NEEDS
• These are assessed by ascertaining the heart rate and rhythm.
• Colour is also noted.
• Maintenance of correct blood volume is vital to the neonate.
• The circulating blood volume of the baby weighing 1000g is only 85ml and any reduction
may be critical to the baby.
• Therefore, extreme care is required in sustaining it.
• Samples of blood taken are carefully done to prevent any leakage.
• Babies who have intravenous or intra- arterial lines should be observed critically for possible
haemorrhage from loose connections.
• Top-up blood transfusions are fairly regular requirement in babies who are critically ill.
• Likewise, all fluid intakes require diligent calculation and administration to avoid
compromising the cardiovascular system.

TEMPERATURE CONTROL
Infants loose heat rapidly through the mechanism of heat loss to the objects been in touched, through
convection that is heating the surrounding air, radiation and evaporation of fluid from the skin.
• Sick newborn babies are at a greater risk of heat loss due many interventions which they
have to withstand.
• Axillary temperature is taken regularly according to the baby’s individual needs.
• To obtain true reading the thermometer must remain in the axilla for 5 minutes.
• Rectal thermometer should not be used because there is a risk of trauma and it is
distressing for the baby.
• Babies whether in incubators or cots should not be placed near outside walls or draughts
from doors, passage or air conditioning vents nor should they be in position which is
direct sunlight.
• Care also needs to be exercised when taking babies out of incubators or cots for feeding
or cuddling.
• Such practices are emotionally beneficially to the baby but it is critical to check that baby
is well wrapped.
NUTRITIONAL NEEDS
• The nutritional needs of sick neonate somewhat different from his healthy counterparts
since he does not only require the nutrient necessary for growth and development but
also some for tissue repair and sustenance throughout physiological difficulties.
• Preterm infants have virtual no reserves of tissues and require urgent attention to their
caloric needs if they are to avoid hypoglycaemia.
• Healthy, low birth weight infants should be feed or orogastrically with expressed breast
milk or preterm formula milk.
• A preterm baby nursed under a radiant heater requires an extra 40ml per kg day to
compensate for water loss.
• A very sick baby may need to be adjusted more slowly in accordance with their
physiological status.
• The route, frequency and method of feeding are largely based on clinical judgment.

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 • Amendments are made accordingly to the level of tolerance in the individual baby.
• A baby weighing below 1000g has a small gastric capacity and cannot tolerate feeds
less frequently than hourly.
• Preterm infants have poor muscle tone in the cardiac sphincter and regulation with
possible aspiration must be avoided.
• For the feeding methods, babies who are below 34 weeks of gestation cannot
breastfeed since their sucking and swallowing mechanism are under developed.
• Even babies above this gestation are often too ill to attempt sucking.
• However, if a baby is able to suck and swallow without becoming exhausted, the
mother should be encouraged to breastfeeding.
SKIN CARE
Prevention of latrogenic (brought about by surgical or medical treatment) skin problems in the low birth
weight baby is an important nursing responsibility.
• Particular vigilance is therefore called for in the early weeks of life when the use of
monitoring and medical interventions tends to be at its peak.
• Problems include epidermal stripping caused by the application of tape or plaster.
• Thermal injuries associated with application of hot water bottles.
• Isehaemia naves caused by improperly secured endotracheal tubes and improper
secured canula.
INFECTION PREVENTION AT THE NEONATAL INTENSIVE CARE UNIT
 Proper handwashing before every procedure
 Daily cleaning of the unit
 Separating of infected babies from the uninfected.
 Practice of barrier nursing
 Use of separate cot and incubators for each baby.
 Daily cleaning of the incubators and cots
EDUCATION DURING DISCHARGE
Advice to parents taking their baby home from neonatal intensive care. Parents need
reassurance that whatever the baby’s previous problems were they are not going to recur.
They are advised on the following:
WARMTH
• Parents should be advised to keep the baby’s environment heated.
• During every cold weather it is not necessary to bath a baby every day at this may cause
rapid cooling. The baby can be topped and tail.
• Advice mother to add extra clothing but make sure they do not over heat the baby as they
try to maintain or generate heat.
CLOTHING
• Disposable diapers may be desirable.
• Wet or solid diaper should be changed frequently to avoid excoriation of the skin.
• They are also advised to dress baby with appropriate clothing.
• Cotton should be choice of clothing.
• Clothing should not be tight on baby.
FEEDING
• The mother will be educated on importance of breastfeeding
• Advice will be given with regard to the amount of milk to be offered at each feed time.
The amount is gradually increased according to the baby’s need.

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 • Mother who is supplementing breastfeeds with artificial should be educated on
preparation and how to keep the equipment sterile.

NURSING A BABY IN AN INCUBATOR /INTENSIVE CARE UNIT

Receiving a baby to the intensive care unit
Procedure
• Warm and oxygenate the incubator as you receive the message of the expected arrival of neonate
generally 10 – 15 minute early.
• Check the physicians order.
• Explain the need of incubator care to the parents of neonate.
• Adjust the incubator parameters and maintain flow chart.
• Remove clothes of neonate and put into incubator.
• Provide meticulous care as long as neonate remains inside the incubator.
• Continue care through the incubator port hole.
• Report to the doctor if baby is not maintaining the temperature generally after two (2) abnormal
readings.
• Do not bring neonate out of the incubator without any justifiable cause.
Babies who need intensive care or babies who are nursed in an incubator
• Preterm or extremely immature babies of very low birth weight
• Respiratory disorder; babies with severe respiratory distress syndrome.
• Cerebral disorder:
• Certain server infections: septicaemia, meningitis.
• After major neonatal surgery: eg. Congenital heart disease.
• Haemolytic disease of the new born requiring exchange transfusion

COMPLICATIONS OF INTENSIVE CARE.

• Retinopathy of prematurity.
• Necrotizing enterocolitis.
• Nasocomial infections
• Separation from parents or lack of bonding
• Electric shock or burns.
NB:// other complications based on the type of babies being nursed at the unit.

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 CHAPTER TEN

MANAGEMENT OF NEONATAL INFECTION

INTRODUCTION
Newborn babies’ especially premature and artificial fed babies are particularly susceptible to infection
Newborn infections are also referred to as sepsis neonatorum. The neonatal infections are caused by
micro-organism like staphylococcus aureus, streptococcus, tetanus bacillus etc. Once any infection
occurs in the newborns, it can spread rapidly through the blood stream, regardless of its primary site.

FACTORS PREDISPOSING NEWBORNS TO INFECTIONS

• Prematurity.
• Premature babies are susceptible to infections as a result of their immature immunological
system and have a low body resistance against infecting organism.
• They also lack the complex factors involved in effective phagocytosis and the ability to localize
infection or to respond with a well-defined recognizable inflammatory response.(also apply to
full term babies)
• Early rupture of membranes
• Prolonged labour
• Prolonged resuscitation at birth.
• Operations for surgical correction of congenital abnormalities.
• Infants born by mothers who have diabetes, toxemia of pregnancy and chronic anemia
• Babies whose mothers have active tuberculosis, STI and rubella
• Babies delivered in unhygienic surroundings
• Bottle fed babies

SITE OF ENTRY
• The skin, if there is a break
• The umbilicus
• The gastro intestinal tract
• The eyes
• Any other part of the body.

SOURCES OF INFECTION
• The mother
• The attendants
• Equipment used
• Visitors

NURSING ASSESSMENT AND DIAGNOSIS OF INFECTION

• Symptoms of infections are most often noticed by the midwife during daily care of the newborn.
• Onset of sepsis may be rapid or gradual with subtler signs and symptoms.
• The infant may deteriorate rapidly in the first 12 to 24 hours after birth if infection is present.
With signs and symptoms mimicking respiratory distress syndrome.
• Nursing diagnosis that may apply to the infant with suspected infection and the family include
the following:
• Risk for infection related to immature immunologic system

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 • Fluid Volume Deficit related to feeding intolerance
• Ineffective Family Coping: Compromised related to present illness resulting in prolonged
hospital stay for the newborn

NURSING PLAN AND IMPLEMENTATION

• In the nursery; the neonatal nurse has to control the environment and prevent acquired infections.
• The midwife must promote strict hand washing technique for all who enter the nursery, including
nursing colleagues, physicians, parents, etc.
• Scrupulous care of equipment
• Changing and cleaning incubators
• Removing and sterilizing wet equipment every 24 hours
• Preventing cross-use of linen and other equipment
• cleaning sink
• unnecessary visits by personnel and parents should be discouraged.
EVALUATION
• Expected outcomes of nursing care include the following;
• The risks for development of infection are identified early, and immediate action is taken to
minimize the development of the illness.
• Appropriate use of aseptic technique protects the new born from further exposure to illness.
• The baby’s symptoms are relieved, and the infections treated.
• The parents verbalize their concerns about their baby’s illness and understand the rational behind
the management of their newborn.

GENERAL MANAGEMENT OF NEONATAL INFECTION

PRENATAL
• Before conception couple must be in good health, vaccination can be given to women who are
not immune to rubella
• During pregnancy, all infections must be treated before delivery. Sometimes caesarean section is
performed to avoid passage through the infected vulva.
• Antenatal period, tetanus toxoid vaccination for mothers and screening and treatment of maternal
infection such as syphilis or any of the touch infection.
INTRAPATUM
• Infection prevention can be achieved through proper hand washing technique. Use of gloves and
goggles during procedure.
• Minimization of vagina examinations and as well as avoidance of vagina examination during
every shift
• Use of partograph during labour
• Prompt diagnosis and treatment of prolonged labour
• Infected health care providers should not be allowed to handle baby during labour
• Use of sterile instruments in cutting the cord
• The delivery surface should be cleaned with 0.5% solution of chlorine after use
• Prompt diagnosis and treatment of chorioamionitis

POSTPATUM
• Appropriate hand washing by mother and caregivers (before and after handling infants)

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 • Exclusive breastfeeding
• Umbilical cord should be kept clean and dry
• Timely identification of infection and prompt treatment with appropriate antibiotics
• All immunization must be given. E.g. BCG, polio etc.
• Provision of safe environment free from all infection
• Isolation of infected babies at the hospital
• Use individual equipment or articles for each baby

SPECIFIC INFECTIONS
MOUTH; oral thrush
SKIN;
Pemphigus neonatorum
UMBILICAL CORD;
Cord sepsis/ omphalitis
GASTRO-INTESTINAL TRACT;
Gastroenteristis
EYE;
Ophthalmic neonatorum
NOSE/RESPIRATORY;
Common cold, neonatal pneumonia, bronchitis, sinusitis
EAR
Otitis media

PEMPHIGUS NEONATORUM (BULLOUS IMPETIGO)

Definition: is a highly infection and contagious skin disease characterized by watery blisters.
CAUSES
• Caused by streptococcus or staphylococcus aureus

SIGNS AND SYMPTOMS

• It is characterized by watery blisters.
• The lesion may be smaller or larger.
• The lesions are usually pink or dull-white in appearance
• Within a few hours of appearing, they come to contain fluid known are vesicles
• Later, the watery blisters contain pus
• When they have broken down, the underlying skin is raw and red and the remaining part are
covered by tags of skin
• The fluid is infectious (when one blister breaks, the infection spreads to the surrounding
skin).

NURSING CARE AND MANAGEMENT

• Baby must be examined by the midwife or doctor
• The lesions are usually pink or dull-white in appearance
• Within a few hours of appearing, they come to contain fluid known are vesicles
• Later, the watery blisters contain pus
• In severe cases, the baby is admitted into a separate ward and given a specialized care to avoid
the spread of the disease

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 • Do laboratory investigations (A swab of the blister is taken for diagnostic test)
MEDICAL TREATMENT
In severe case penicillin intramuscularly; lubricate erosion 1-2 % alcoholic solution of aniline dyes
(gentian violet). 2% aqueous solution of silver nitrate. Dusting powder with 10% white streptocid or
xeroform.
PREVENTION AND TREATMENT
• During the warm weather, baby must be worn light clothing.
• Bath baby with antiseptic in warm water (once a day)
• The skin must be cleaned with mild antibiotic ointment after baby’s bath
• The baby may also be given syrup antibiotic ordered by a doctor.
• If the baby is admitted, isolate baby from uninfected or new babies
• Neonatal Intensive Care Unit (NICU) must be disinfected properly.
• Strict aseptic technique must be observed by health personnel and mothers.
• Avoid visitors into NICU.

CORD SEPSIS
It is an inflammation or infections of the umbilical cord. It is common with babies born at home. It is
also known as omphalitis
Pathology
Staphylococcus aureus or Escherichia coli ([Link]) are the most common bacteria that causes omphalitis.
The organism gets into the body through a direct contact with the umbilical cord and the surrounding
skin that result in a marginal erythema. This may or may not be accompanied by drainage from the cord.
The cord falls off between two to three days that releases a small amount of opaque yellowish discharge.
Predisposing Factors
• Dressing baby with dirty clothing
• Cutting the cord with unsterile instruments
• Untreated vaginal infections of the mother
• Application of herbs on the cord
• Making the cord wet with water and shear butter
• Normal infants who had prolong birth with placenta complication.

CAUSES
• Staphylococcus aureus
• E. coli
• Clostridium tetany
• Streptococcus pneumoniae
• Klebsiella pneumoniae

SIGNS AND SYMPTOMS

• There may be periodical inflammation and redness of the umbilical cord.
• Surrounding skin of the umbilical cord looks red and edematous
• There may be pus from the umbilical cord indicating the presence of an infection
• There may also be an offensive odour and greenish discharge from the umbilicus
• Child may also have a slight fever
• Child may fail to suck and will therefore gain poor weight

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 • The infant appears restless
• Evidence of dehydration and emaciation
• Vomiting and diarrhoea may be present
• Reddening and moistening of the stump of the cord
• There may also be hepatosplenomegaly
• Jaundice
DIAGNOSES
• From the health history and clinical presentation
• Full blood count that shows an elevated white blood cells
• A swab from the drainage for culture and sensitivity
MEDICAL MANAGEMENT
• Oral or parenteral antibiotics such as Cloxacline 62.5mg and ampicillin 62.5mg may be ordered
6hrly to treat the infection
• Antipyretic such as Paracetamol may also be given for the fever
• 1% GV in spirit, mercurocream may also be applied to the stamp
NURSING MANAGEMENT
• Admit the child to the ward and reassure the mother.
• Educate and encourage the mother to breast feed the baby.
• Isolate baby from uninfected babies to prevent the spread of the disease.
• Monitor vital signs especially temperature and tepid sponge the child when temperature is high.
• The cord should be dressed and kept dry with a prescribed solution (alcohol).
• The cord should be left open after dressing
• Observe and record bleeding of stump if any.
• Administer oxygen when necessary and observe baby closely.
• Serve prescribed IV Fluid in case of severe diarrhoea and vomiting.
• Transfusion blood if necessary.

PREVENTIONS
• There must be aseptic technique applied during delivery
• Educate mother on simple hand washing to prevent infection to the cord
• Cord should be dressed aseptically with sterile instruments
• Educate mother on personal hygiene
• Educate mother to avoid the use of herbs and other items on the cord
• Educate mother to keep diaper/napkin from cord

COMPLICATIONS
• Hepatitis, Septicaemia and jaundice may occur as a results of infection travelling to the liver
• Cellulitis at the skin around the base of the cord
• Portal vein thrombosis may occur
• Septicaemia
• Haemorrhage
• Tetanus

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 Ophthalmic Neonatorium
Definition: it is defined as any purulent discharge from the eyes of an infant within 21 days of [Link] a
bilateral purulent conjuctivitis occurring in the newborn with the first 3 weeks of life
CAUSATIVE ORGANISMS
• Gonococcus
• Escherichia coli
• Pneumococcus
• Staphylococcus aureus
• Streptococcus haemolyticus
• Chlamydia tracomatis
• Haemophilus influenza
• Streptococcus pneumonia
• Klebsiella pseudomonas
• Neisseria gonorrhoeae

MODE OF TRANSMISSION
• During birth- contamination from the vagina passage
• After birth- formites
SIGNS AND SYMPTOMS
• conjuctivitis appear bright red, chemosed and inflamed
• The discharge is first watery-yellowish-purulent-thick
• swollen /oedamatus eyelid
• Exudate may coagulate on the surface of the conjuctival to form psedomembrane.

DIAGNOSIS
• Swab for culture and sensitivity test

TREATMENT
• Antibiotics eg, ceftriaxone 50mg/kg
• Erythromycin oral 12.5mg/kg

NURSING MANAGEMENT
• Isolation and barrier nursing
• Positioning-if unilateral should lie on the affected side
• Frequent irrigation 2hourly with N/S

COMPLICATIONS
• cornea ulcerations
• Blindness
• speticaemia

PREVENTION
• efficient hand hygiene before handling child especially mother
• ANC treatment of vaginal infections
• Cleaning of babies eyes as soon as the head is born from inside outwards
• Prophlaxis of silver nitrate 1% solution and erythromycin of o.5% opthalmic ointment

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COMMON COLD / ACUTE RHINCTIS / CATRRH
It is a viral infection of the upper respiratory tract (nose and throat) OR It is the inflammation of the
mucous membrane of the nose.
CAUSATIVE ORGANISMS
Viral by rhinovirus and coronavirus and bacteria such as staphylococcus aureus
DIAGNOSIS
• By signs / Clinical features
• Nose swab for culture at sensitively.
DIFFERENTIAL DIAGNOSIS
Influenza

PREDISPOSING CAUSES
• Infections from attendant / mother
• Cold weather
• Allergies
• Overcrowding
SIGNS & SYMPTOMS
• Running nose / stuffy nose
• Nasal discharge that may be clear at first usually becomes thicker
• Sneezing
• Coughing
• Irritability
• Difficulty in sleeping
• High temperature
MODE OF TRANSMISSION
• Air borne
• Direct Contact
MANAGEMENT
• There is no known cure for common cold
• Antibiotics do not work on viral causes
• Best care is to suction mucus from his / her nose and keeping air moist
• Fever can be managed by fever reducing medications prescribed by Physician
• Offer plenty fluids (Breast milk) to prevent dehydration. Breast milk offer extra protection from
cold easily virus.
• Saline drops may be recommended to loosen thick nasal mucus or ephedrine nasal drop 0.1%
may be instilled as well.
• Vital signs.

PREVENTION
• Keep baby away from anyone who is sick of common cold or respiratory infections
• Avoid public gathering if possible with your newborn baby.

COMPLICATION
• Sinusitis
• Acute ear infection (Otitis media)

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ORAL CANDIDIASIS (ORAL THRUSH, MONILIIASIS)
It is an infection of the mucus membrane mostly common in the mouth and throat from bottle feeding.
That is the tongue, tonsils, soft palate, buccal mucosa and other surfaces. This condition is common in
newborns. It is benign (it does not spread) and always confined to the area affected.
CAUSATIVE AGENT
Candida Albicans
Mode of transmissiom
• From maternal vagina infection
• cross infection from the nursery
• contaminated articles or formite
RISK FACTORS
• Exposure to antibiotics / Oral flora alteration by antibiotics
• In preterm babies (immune system immaturity)
• Contaminated hands from mother nurses or other attendance
• The neonate acquires it through the mother’s infected vagina.
• It can also be acquired from contaminated hands of mother and other alternatives during delivery
• From contaminated articles used for the child like drinking cups, towels ect.

INCUBATION PERIOD
2 to 5 days
PATHOPHYSIOLOGY
When one comes into contact with any of the risk factors such as intake of certain oral antibiotics, the
drugs destroy the mucus membrane and the normal flora present. This pave way for the Candida
albicans to dominate so that they gain power enough to cause infection.

DIAGNOSIS
• By sign and symptoms
• Swabs from the mouth for culture
• Biopsy for hyphen of Candida
SIGNS AND SYMPTOMS
• Creamy white patches on the tongue, palate and the inner part of the cheek which bleeds
in attempt to remove
• It is characterized by soft, milky-looking patches which may grow on any part of the
mouth.
• Attempt to remove the patches mas result in bleeding
• Feeding difficulty
• Irritability
• Pain
• Fever
• Difficulty in swallowing
• Erythematous (Redness of the skin)
• Dehydration leading to sunken fontanelles
• diarrhoae
• Baby may refuse to suck
• Appearance of white patches(which looks like milk stains in the mouth
• The baby is lethargic (depends on the severity of the infections)

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 •Feeding tolerance evidenced by a decreased in total intake, abdominal distention,
vomiting, poor sucking (because the spreading lesions cause pain) and lack of interest in
feeding.
• The baby passes stool(i.e. when the alimentary canal is infected)
• The signs appear a few weeks after birth (usually after the fourth day)
MEDICATION
• 0.5% gention violet is applied 2times daily if lesion persist/nystatin mouth rinse
500000units tid held in the mouth and then swallowed
• Saline solution for mouth rinsing every 2 hours
• Oral nystatin suspension is given 2times daily 4-7days
• Topical application of 1ml of nystatin
• Miconazole IV or oral
• Clotrimazole IV or Oral
• Have the mother put nystatin cream or 0.5 %gentian violet on her breast after
breastfeeding for as long as the baby is being treated
NURSING MANAGEMENT
• Serve nutritious diet
• Ensure enough rest.
• After feeding the child’s mouth should be rinsed.
Put patient in the prone position after applying the gentian violet.
• Mouth care at least twice daily.
• Infection prevention
• Infants hands is covered or elbow restrains to prevent scratching of lesions
• Inform the doctor about the baby’s condition
• Clean baby’s mouth with oral antibiotics as ordered by the doctor

PREVENTION
• Mothers who have vaginal thrush should treat before delivery.
• Delivery equipment should be sterilized at all times
• Mothers should be educated to boil the cups, spoons and plates used in feeding.
• Nursing mothers and staff at labour and delivery unit must practice personal hygiene
• Proper hand washing among staff
• All pregnant mothers with vaginal discharges must be treated.
• Early detection and isolation of infected babies
• Proper sterilization of feeding utensils
• Educate mothers on good personal and environmental hygiene
• Feeding bottles of an infected baby must not be given to other babies(especially in the
NICU)
• Daily inspection of baby’s mouth must be done.
• Clean baby’s mouth after each feed.
• Disinfect the babies clothing after use.
• Employ good nursery techniques
COMPLICATION
• Lymphadenopathy • Poor Feeding
• Stomatitis • Malnutrition

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 • Dehydration • Oesophagitis
• Anaemia • Systemic candidiasis

TETANUS (LOCKJAW)
• Is an acute preventable and fatal disease caused by exotoxin produce by the anaerobic spore
forming bacteria clostridium tetani.
• Tetanus, also called lockjaw, is a medical condition characterized by a prolonged contraction of
skeletal muscle fibres.
• Tetanus is a very dangerous infectious disease caused by Clostridium tetani (a gram-positive
anaerobic spore-forming bacterium).
• These bacteria live predominantly in the soil, so that it is easy to get this infection whenever a
break in the skin is not cleaned properly.
• Neonatal tetanusis tetanus that affects a newborn. Infection is usually via the umbilicus if it is
not kept clean or if unsterile instruments or dressings are used.
• Neonatal tetanus – tetanus occurring in new born children under one month of age.
• Incubation period:children – 3 -14 days. Dependent on extend of injury.
Requirement for tetanus development
• Presence of tetanus spore bacillus
• Cut or injury to the tissues
• Susceptible host
• The organism enters the body through. Wounds, burns, crushed injuries
CAUSES
The babymight acquire the infection through any of the following means:
• Cutting the umbilical cord with unsterile instrument
• Circumcision with unsterile instrument
• The use of cow dung or infected powder
• Stepped on a rusted metal/nail.
• Not taking tetanus injection after a cut
• Through an open wound which comes in contact with infected soil.
• Cut on leg with contaminated cutlass or hoe.
• Mother not vaccinated during the last five years (placental in utero)
• Application of cow dung or herbs on umbilical cord
• Aspiration of capput succudanum and subsequent application of herbs
• Birth/tribal makes with unsterile instruments, tattoos.
• Not using aseptic techniques in caring for and dressing the cord.
Pathophysiology
• The organisms (clostridium tetani) on entering the wound and condition favours, they proliferate
and release exotoxin (tetanospasmin) which is potent and affects the CNS to produce the clinical
manifestation of the condition.
• The exotoxins reach the CNS by the neuron axons. They fix onto the nerve cells of the anterior
horn of the spinal cord and brain stem. They then act on the myoneural junction to produce the
muscular stiffness and also lower the threshold for reflex excitability.
SIGNS AND SYMPTOMS
In Infants:
• Baby cannot suck. • Umbilicus is infected.

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 • Stiff body. • Constipation.
• Irritability. • Tongue and lips become blue (cyanosed)
• Spasms. during spasms.
In Adults and older children;
• Sardonic smile (mocking smile).
• Lockjaw/Trismus (cannot open the mouth);- that is locking of the jaw.
• Opisthotonos (i.e. stiff arched back); - muscle spasm causing the back to be arched and the head
retracted with great rigidity of the muscle of the neck and back.
• Muscle spasms that result by noise, bright light, touching the body or moving part of the body.
• Photophobia – cannot stand bright light and it triggers muscle spasms.
• Phonophobia
• Confusion.
• Fever
• Rigid abdomen – no movement in the abdomen.
• Stiff neck
• Severe headache.
• Difficulty in urinating
• Profuse sweating
• Restlessness and irritability
• Muscle spasm – movement of the body (fitting) or muscles.
• Sensitive to touch, when patient is touched he has spasms.
• Difficulty in swallowing.
• Positive Kerning’s sign(inability to extend the leg at the knee when the thigh is flexed because of
stiffness in the hamstrings).
• Respiratory distress.
• Fit is present.
• Fever.
• Cyanosis.
• Rhizus sardonicus (Sardonic smile); thus, contraction of the frontal muscle which leaves a
smiling expression on the patient’s face.
• In tetanus, noise, bright light, touching the body or moving part of the body will trigger muscle
spasms.

MANAGEMENT/MEDICAL TREATMENT
1. Sedatives and muscle relaxant medications (Diazepam, Chlorpromazine);-large doses may be
necessary.
2. Neuromuscular blockage (vecuronium; pancuronium, metocurine.);-for treatment of severe,
uncontrolled general spasms.
3. Cardiac Monitoring.
4. Sympathetic blocking agents for management of persistent hypertension and tachycardia due to
autonomic nervous system dysfunction.
[Link] medications used;
• Benzylpenicillin, IV. • Human Tetanus Immunoglobulin.
• Gentamicin.
• Erythromycin • Anti tetanus serum.
• Tetanus toxoid.

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 • Antibiotic e.g. penicillin. • Anticonvulsants e.g. Diazepam;
• Sedatives e.g. diazepam. phenobarbitone
6. Tracheostomy – in very severe cases. Done before severe respiratory distress
COMPLICATIONS
• Cardiac arrest.
• Autonomic disturbances; dysrhythmias.
• Bacterial shock.
NURSING MANAGEMENT OF THE PATIENT UNDER THE FOLLOWING HEADINGS.
• Control of Spasms:
• In tetanus, noise, bright light, touching the body or moving part of the body triggers muscle
spasms like convulsions for that reason they should be avoided if possible or minimized.
• Nurse patient in a quiet environment with minimal disturbance.
• Nurse patient in a darkened room.
• Before touching patient inform him and warm hands by rubbing hands together before touching
him.
• Group nursing activities in order to minimize disturbance to patient.
• Provide patient with warmth.
• Lock bed/cot of patient in order to prevent movement of bed as this moves the body.
• Serve prescribed medication such as sedatives and muscle relaxant e.g. Diazepam,
chlorpromazine or largactil.
• Neuromuscular blockage e.g. vecuronium, pancuronium.
• Plan nursing care or activities during periods when sedatives have maximum effect for minimal
patient disturbance.
• Maintain adequate airway.
• Initiate intubations and mechanical ventilation as quickly as possible if spasms are interfering
with respiration function.
• Observations:
• Observe patient’s vital signs (i.e. TPR & BP).
• Observe intake and output by maintaining intake and output chart.
• Observe and chart frequency and length of spasms (if any) as a guide to management
• Maintenance of Fluid and Electrolyte Balance or Nutrition:
• Check skin for elasticity, if skin is inelastic prepare tray for I V infusion
• Administer prescribed IV fluids
• Give fluid orally if the jaw is not locked.
• If the jaw is locked, pass an NG tube, & set IV line and administer prescribed amount of fluid.

• Maintenance of Fluid and Electrolyte Balance or Nutrition

• Check for over hydration by maintaining strict intake and output chart.
• Check for worsening dehydration
• Encourage the intake of copious fluid.
• Pass an NG tube and feed patient (remember patient has difficulty with swallowing).
• Health Education in the Hospital:
• Educate patient and relatives on the nature of the condition and the treatment procedure.
• Educate patient on the need for him to adhere to his treatment regimen.
• Educate relatives to avoid unnecessary touching of the patient.
• Educate them not to make noise when they come to visit the patient.

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 • Educate patient on the need to maintain personal hygiene.
• Allow patient and relatives to ask questions and their questions should be answered tactfully.
• The most important step in the prevention of tetanus is the thorough washing and cleansing of
the wound, with removal of all foreign material and devitalized tissue.
• Encourage the patient to keep an up-to-date record of his immunization status.
• Immunization with TT and ATS.
• Consider every break in the skin as a potential portal of entry for C. tetani.
• Health Education To Prevent Tetanus In The Community:
• Reporting for early treatment.
• Immunization of women in reproductive years.
• Avoiding road traffic accident.
• Should always wear slippers and avoid walking bear footed to prevent a cut or needle prick.
• Women in child bearing age (or pregnant women) should be immunized with tetanus toxoid.
• Delivery should be done under aseptic condition; using sterile instrument for cutting and legating
of umbilical cord.
• Cord dressing should be done aseptically using sterile items and avoiding the use of cow dung
and herbal preparations.
• Expectant mothers should receive the expected dose of tetanus vaccines to protect themselves
and the unborn child.
• Traditional birth attendants should be taught to do deliveries aseptically using sterile instruments.
• People who perform (“wanzam” -traditional circumciser) should be taught how to sterile their
instruments for circumcision.

TREATMENT
• Tetanus immune globulin - tetanus toxoid
• Antibiotics – penicillin G (risk of increasing spasm and so not used anymore)/gentamycin (now
used)
• Muscle relaxant – diazepam
• Anticonvulsant – phenytoin
• Sedatives – diazepam
• Antipyretic – paracetamol
• Neuromuscular blocking agent – metocurine iodide

GENERAL NURSING CARE

• Reassure patient and relatives that the health team will do their best for him/her.
• Nurse in a low bed, quiet and darkened environment to prevent photophobia.
• Isolation and barrier nursing is also employed.
• Draw curtains down.
• Use bed cradle to lift the top sheet.
• Touch patient with warmed hands.
• Coordinate Nursing activities, so as not to disturb the patient unduly.
• Observe level of consciousness, mental state, and neurological state.
• Observe vital signs such as TPR & BP.
• Observe seizures by keeping fit chart.
• Pass NG tube to feed
• Touch patient or perform personal hygiene when sedatives are at their maximum effect.

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 • Patient is catheterized because urine can sensitize them.
• Prescribed drugs are administered such as sedatives and anti convulsants e.g diazepam.

OTHER NURSING INTERVENTIONS

A. Preventing Respiratory and Cardiovascular complications;
• Monitor for dysphagia.
• Initiate intubation and mechanical ventilation as quickly as possible if spasms are interfering
with respiratory function.
• Maintain an adequate airway.
• Provide cardiac monitoring
B. Providing ongoing Assessment and support:
• Support the patient during titanic spasm and convulsions.
• Plan nursing management during periods when sedation has maximum effect for minimal patient
disturbance.
• Maintain fluid and electrolyte balance.
• Avoid contractures and pressure sores.
• Watch for urinary retention.
• Monitor for faecal impaction.

GASTROENTERITIS
This is inflammation of the linning of the stomach and intestine (digestive tract). It is sometimes
referred to as infective diarrhea or stomach flu.
CAUSATIVE ORGANISMS
The most common virus causing this condition include;
• Rotavirus
• Adenovirus
• Calicinovirus
It can also be caused by a potentially serious bacterial infection such as;
• Salmonella
• Shigella
• Staphylococcus
• [Link]
PREDISPOSING FACTORS
• Allergic reaction to milk formula
• Unhygienic habits of the mother
SIGNS AND SYMPTOMS
• Diarrhoea • Respiration is deep and rapid
• Profuse vomiting • Sunken fontanelle
• Abdominal pains • Wrinkled skin
• Watery offensive stool • Sunken eyes
• Weight loss • Extreme thirst
• Dehydration with its association • Dry lips
• Decreased urination • Crying without tears
• Excessive sleepiness • Irritability
DIAGNOSIS

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 • By signs and symptoms
• Culture for sensitivity to rule out causative organism
• Blood for estimation of electrolyte balance
• Stool test to rule out rotavirus
MANAGEMENT
• Admit baby
• Reassure mother
• Isolation of baby since the organism that causes this condition is contagious
• IV fluid to rehydrate baby
• Incase baby is dehydrated ORS/zinc tablets can also be given
• Frequent changing of baby’s napkins
• Application of protective soothing preparation such as barrier cream, baby oil
• Expose buttocks for air circulation and observations
• Monitor vital signs
• Observe baby’s urine, stool, vomit
• Monitor for signs of dehydration
• Intake and output
• Encourage mother to breastfeed when vomiting stops
MEDICAL MANAGEMENT
Course of antibiotics may also be given when blood or stool test reveals that there is bacterial infection
PREVENTION
• Proper hand washing with soap and warm water after every diaper change
• Immunization of babies with three dose rotavirus vaccination
• Articles used in the care of baby should be sterile
COMPLICATION
• Dehydration
• Anaemia
• Convulsion
• Kidney failure

NEONATAL PNEUMONIA
Is a term the refers to infections or inflammation of the lungs in the neonate with formation of fluid
CAUSATIVE ORGANISMS
• Group B haemolytic streptococcus
• E. coli
• Streptococcus pneumonia
• Staph. Aureus
SOURCES OF INFECTION
• Acquired prior to birth by an ascending route/ transplacental route. Group B streptococcus in the
mother’s vagina which passes to infant during birth. In case of prolonged rupture of membranes
or prolonged labour
• Infections acquired by aspiration during delivery (meconium aspiration/ secretions from
mother’s vagina)
• Complication of endotracheal intubation
INCIDECE
Common in low birth weight especially preterm babies.

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SIGNS AND SYMPTOMS
• This is similar to respiratory distress syndrome
• Baby is cyanosed
• Yellow or green airway secretions
• Fluctuating temperature
• Irregular heart rate and distended abdomen
• Nasal flaring
DIAGNOSIS
• Chest X-ray
• Culture and sensitivity of nose and throat swab
• Culture and sensitivity of gastric aspirate
TREATMENT
Medically, aentamycin and ampicillin are commonly used until specific causative organism are
identified.
NURSING MANAGEMENT
• Admit and reassure
• Monitor vital signs
• Resuscitate if baby is cyanosed
• All other nursing care included
PREVENTION
• Identify the presence of B streptococcal infection in the mother and begin prenatal treatment,
helps prevent this infection in the newborn
• Careful feeding to prevent aspiration
• Lower baby’s head to one side to allow free flow of feed and regurgitation
COMPLICATIONS
• Respiratory failure
• Meningitis
• Endocordoritis
• Perccardetis
• Septicaemia
• Lung abscess

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 CHAPTER ELEVEN

CONCEPT OF PAIN IN THE NEONATE

Definition: Pain is a feeling of distress, suffering or agony, caused by stimulation of specialized nerve
endings. Its purpose is chiefly protective. It acts as a warming that tissues are being damaged.
TYPES OF PAIN
Acute pain and chronic pain
• ACUTE PAIN may be caused by
• Tissue damage example burns or trauma.
• Specific diseases process, eg. Sickle cell crisis
• Medical intervention i.e investigation or procedures
• Surgery
• CHRONIC PAIN
In children, chronic severe pain sometimes occurs as a result of disease such as malignant disease.
Intermittent pain of mild or moderate severity example headache or recurrent abdominal pain is more
common.
PAIN ASSESSMENT AND DOCUMENTATION IN THE NEONATE
Neonates cannot verbalize their pain experience and depends on others to recognize, assess and manage
their pain. Even if not expressed through conscious memory, neonate may suffer immediate or long term
consequences, if exposed to painful stimuli for prolonged period. Neonates and infants perceive pain and
have memory of these painful experiences. Selecting the most appropriate tool for evaluating neonatal
pain is essential to its management.

Documentation of pain is essential and it’s based on the results from the assessment scale used.
Pain can be measured by the use of appropriate pain scales.
Pain assessment by scale has become the 5th vital sings in hospital settings and is documented at least as
frequently as the heart rate or blood pressure (every 1-2 hours). Many tools exist and a few of the more
common ones are shown below:
PAIN AGE ASSESSMENT ASSESSMENT INDICATIONS
MANAGEMENT ITEMS
CRIES Neonates from 32-60 Crying Post-operative
weeks Requires increased oxygen
Increased vital signs
Expression
Sleeplessness
PREMATURE Tested in infants Gestational age Procedural post-
INFANT PAIN 27weeks to term Behavioral age operative up to 24
PROFILE (PIPP) Heart rate hours
Oxygen saturation
Brow bulge
Eye squeeze
Nasolabial furrow
NEONATAL 28 – 38weeks Facial expression Procedural
INFANT PAIN Crying
SACLE (NIPS) Breathing pattern

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 Arm movement
Leg movement
State of arousal
NB: The cries scale is more applicable to the neonate.
ANOTHER EXAMPLE IS THE WONG BAKER FACES SCALE FOR CHILDREN

Explanation into detail: (The various scales).

CRIES
Cries scale is an acronym of five physiological and behavioral variable previously shown to be
associated with neonatal pain.
It is 10 point scale like the Apgar score.
INTERPRETATION OF THE ACRONYM
C – Crying: The characteristic cry of pain is high pitched.
If no cry or cry which is not high pitched score 0
If cry high pitched but baby is easily consoled score 1
If cry is high pitched and baby is inconsolable score 2

R – Required O2: Look for changes in the oxygenation. Babies experiencing pain decreases in
oxygenation as measured by oxygen saturation which is 95%
If no oxygen is required (95%) score 0
If < 30% O2is required score 1
If > 30 % is required score 2

I – Increase vital signs: Multiply baseline Heart rate (HR) X 0.2 then add this to baseline HR to
determine the HR which is 20% over baseline.
If HR less than baseline score 0
If HR < 20% of baseline score 1
If HR > 20% of baseline score 2

E – Expression: The facial expression most often associated with pain is a grimace. This may be
characterized by: Brow Lowering, eyes squeezed shut, deepening of the naso-labial furrow, open lips
and mouth.
If no grimace score 0
If grimace alone present score 1
If grimace and non-cry vocalization grunt is present score 2

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S – Sleepless: This parameter is scored based upon the infant’s state during the hour preceding this
recorded score.
If child has been continuously asleep score 0
If he/she has awakened at frequent intervals score 1
If he/she has been awake constantly score 2.

TABLE 2: PREMATURE INFANT PAIN PROFILE (PIPP)

SN PARAMETERS SCORE
1 What is gestation of infants 0 1 2 3
> 36 wks 32-35 28-31 < 28 wks
2 Score behavioral state Active awake Quite awaken Active sleep Quite/sleep
before the procedure (15sec) Eyes-open Eyes-open Eyes closed Eyes closed
Facial No facial Facial No facial
Movement + movements movements+ movements
3 Record baseline HR and 0-4/min increase 5-14/min 15-24/min >25/min
find out maximum HR
during the procedure
4 Record baseline SO2% and 0-4% fall 2.5-4.9% fall 5-7.4% fall >7.5% fall
find out minimum SO2%
during the procedure
5 Observe the infant for 30 None Min Moderate Maximum
sec immediately after the (0-9% of time) (10-39% of (40-69% of (> 70% of
procedure 9for brow bulge, time) time) time)
eye squeeze and nasolabial
furrow).

Health professionals should record PIPP score of all babies during/nursing shift end before the
procedures. The issue as pain should be discussed on the rounds. The minimum score is 0 and is 21.
Higher is the score greater than the pain. The minimum score is maximum is 21. Higher is the score
greater than the pain. Score < 5: no pain; 6-10; moderate pain; and >10: severe pain.
MANAGEMENT STRATEGIES OR APPROACHES TO PAIN
Explanation and Information
• Psychological by the parents, doctor, nurse or play specialist
• Behavioral
• Distraction
• Hypnosis
MEDICAL
Local: Anesthetic cream, local anesthetic infiltration, nerve blocks
Analgesics: Mild – Paracetamol,
Moderate – Codeine,
Strong – Morphine
Sedatives or anaesthetics agents
• Anti-epileptic and antidepressant drugs for neuropathic pain.
CONSEQUENCES OF PAIN IN THE NEONATES
In adequate treatment of pain in the neonate produces not only physiological pain problems, but also
psychological, behavioral and social challenges.

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In addition, pain has lasting bad effects on infant’s brain development which manifests later as abnormal
pain perception abnormalities, cognitive defects and learning disabilities. .
Hence routine assessment and management of pain, forms an important part of the developmental
supportive care.

PREVENTING OR REDUCING PAIN

General Measures
Pain is managed most effectively by preventing, limiting or avoiding noxious stimuli. The following
measures in combination are followed to minimize pain:
• Avoid bright light. Loud noise
• Limit the number of painful procedures and handling
• Bundling of investigation and nursing interventions
• Swaddling facilitated tucking, distraction measures like talking, music etc.
• Tactile stimulation like stroking, caressing, massaging.
NON-PHARMACOLOGICAL MEASURES
The environmental and behavioural interventions that do not use pharmacological agents are collectively
called non-pharmacological measures. These include:
• Sucrose/glucose solution induced analgesia
• Breastfeeding/ breastmilk supplementation
• Skin to skin care (kangaroo mother care)
• Non-nutritive sucking using pacifiers
The non-pharmacological measures are thought to alleviate pain by activating gate control mechanism,
secretion of endogenous endorphins, diversion of attention and by pre-emptying hypersensitivity.

SUCROSE ANALGESIA
Sucrose administration is particularly useful for short procedures like, heel prick etc. Oral administration
of concentrated sucrose solution (24-50%) acts by release of endogenous opiods like beta-endorphin.
Analgesic effect lasts for 5-8 min and should be combined with other non-pharmacological measures for
maximum benefit. Alternative to sucrose is dextrose, which is less widely used.

TABLE 3 Dose of sucrose/dextrose for analgesia

Concentration For babies who are Preterm (<32 weeks) Late PT/Term
NPO
24% sucrose/25% 0.1-0.2mL 0.1-0.5Ml 0.2-1mL
dextrose
The sucrose solution is given orally by a syringe 2-3 min before procedure and may be
repeated 1-2 min after the procedure. Intragastric administration has no analgesic effect.

Breast Feeding and breast milk supplementation

Almost as effective as sucrose analgesia in reducing pain in newborns undergoing single painful
procedure.

PHARMACOLOGICAL MEASURES
The pharmacological measures can be broadly divided into:
• Local anaesthetic agents
• Systematic agents: opiods, acetaminophen.

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