High risk newborn 1

1. HIGH RISK
NEWBORN- PART-I
Mrs. U SREEVIDYA Msc.
NURSING,
Associate Professor,
Apollo college of nursing,
CHITTOOR

2. INTRODUCTION
• A newborn, regardless of gestational age or birth
weight, who has a greater than average chance of
morbidity or mortality because of conditions or
circumstances superimposed on the normal course of
events associated with birth and the adjustment to
extra uterine existence… is termed as High-risk Newborn.

3. FACTORS –TO DEFINE HIGH RISK NEWBORN
• A) Demographic social factors
• B) Past medical history
• C) Previous pregnancy
• D) Present Pregnancy
• E)Labor and delivery
• F)Neonate

4. A) Demographic social factors
• Maternal age <16 or >40yr
• Poverty
• Unmarried
• Emotional or physical stress
• Illicit drug, alcohol, cigarette use

5. B) Past medical history
• Genetic disorders
• Diabetes mellitus
• Hypertension
• Asymptomatic bacteriuria
• Rheumatologic illness
• Immune –mediated disease
• Long-term medication

6. C) Previous pregnancy
• Intrauterine fetal demise
• Neonatal death
• Prematurity
• Intrauterine growth restriction
• Congenital malformation
• Incompetent cervix
• Blood group sensitization
• Neonatal thrombocytopenia
• Hydrops fetalis

7. D) Present Pregnancy
• Vaginal bleeding
• Sexually transmitted infections
• Multiple gestation
• Preeclampsia
• PROM
• Short interpregnancy time
• Poly-/ oligohydramnios
• Acute medical or surgical illness
• Inadequate prenatal care
• Familial or acquired hypercoagulable states
• Abnormal fetal USG findings
• Treatment of infertility

8. E)Labor: and delivery
• Premature labor (<37wk)
• Postdates pregnancy(≥42wk)
• Fetal distress
• Immature lecithin: spingomylin ratio; absence of
phosphatidyleglycerol
• Breech presentation
• Meconium –stained fluid
• Nuchal cord abnormalities
• Cesarean section delivery
• Forceps delivery
• Apgar score <4 at 1 min

9. F)Neonate:
• Birth weight ≤2500 or ≥4000g
• Birth <37 or ≥42wk of gestation
• Small or large for gestational age
• Respiratory distress, cyanosis
• Congenital malformation
• Pallor, plethora, petechiae

11. Causes of Neonatal Mortality
Infection
32%
Other
5%
Congenital
Anomalies
10%
Birth Asphyxia
29%
Complications
of Prematurity
24%

12. DEFINITION
S
Low Birth Weight Baby:
Live born baby weighing 2500 gram or less at birth.
(VLBW: <1500 gm, ELBW:<1000 gm). ‐
Preterm baby:
When the baby is born before term. i.e.: before 38 weeks
of gestation.
Premature baby:
When the baby is born before 37 weeks of gestation.

13. Full term Newborn:
When the baby is born between 38 – 42 weeks of
gestation.
Post term baby:
When the baby is born after 42 weeks of gestation.
DEFINITIONS

14. POST TERM NEWBORN CHARACTERISTICS
 Newborn emaciated
 Meconium stained
 Hair and nails long
▪ dry peeling skin
▪ Creases cover soles
▪ Limited vernix & lanugo

15. Major problems in preterm babies and those with IUGR
PRETERM
■ Hypothermia
■ Perinatal asphyxia
■ Respiratory distress
syndrome
■ Bacterial sepsis
■ Apnea of prematurity
■ Metabolic problems
■ Hematologic problems
■ feeding problems
and Poor wt gain
IUGR
 Perinatal asphyxia
 Meconium
aspiration
 Hypothermia
 Hypoglycemia
 Feed intolerance
 Polycythemia
 Poor wt gain

16. Low birth
weight baby

17. DEFINITION
LOW BIRTH WEIGHT:
LBW infant is defined as one
whose birth weight is less than 2500gms
irrespective of the gestational age.
WHO/D.C.Dutta

18. LBW
Very low birth weight infants
weighs 1500gms or less and
extremely low birth weight
infants weighs 1000gms or
less.

19. CLASSIFICATION OF LBW
INFANTS
Low birth weight babies are again
classified after correlating both the
birth weight and gestational age into
two groups.
1. Preterm
2. Small for gestation age(SGA)

20. Cont..
Preterm-The growth potential is normal
and is appropriate for the gestational
period (10 to 90 th percentile)
Small for gestational age(SGA)-The term is
to designate the newborn with birth
weight less than 10th percentile or less
than gestational age.

22. Preterm infant
DEFINITION:
A baby born before 37 completed
weeks of gestation calculating from the first
day of last menstrual period is arbitrarily
defined as preterm baby
Babies born before 37 completed
weeks usually weighing 2500gms or less.

23. INCIDENCE
• Preterm baby constitutes 2/3 rd of low birth
weight babies.
• The incidence of low birth weight baby is
about 30-40% in the developing countries as
such the incidence of preterm baby is about
20-25%.

24. ETIOLOGY
•Spontaneous
•Induced

25. SPONTANEOUS
• Health status of the mother
• Multiple pregnancy
• Advanced parental age
• Placental problems
• Preterm labour and premature rupture of membrane
• Low maternal weight
• Chronic and acute systemic maternal disease
• Ante partum haemorrhage
• Cervical incompetence
• Maternal genital colonization and infections
• Cigarette smoking during pregnancy
• Acute emotional stress
• Physical exertion
• Sexual activity
• Trauma
• Bicornuate uterus
• Congenital malformations

26. INDUCED
• Maternal diabetes mellitus
• Placental dysfunction as indicated by unsatisfactory
fetal growth
• Eclampsia
• Fetal hypoxia
• Severe rhesus iso immunization

27. CLINICAL FEATURES
• Measurements:
• Size is small with relatively large head
• Crown- heel length is less than 47cm
• Head circumference is less than 33 cm
• But exceeds the chest circumference by more
than 3 cm(normally 1.5cm)

28. • Activity and posture:
• General activity is poor
• Automatic reflex response suchas, Moro
response, sucking and swallowing are sluggish
or incomplete
• Baby assumes an extended posture due to
poor tone

29. • Face and head:
• Face appears small
• large head size
• Sutures are widely separated
• Fontanels are large
• Small chin
• Protruding eyes
• Optic nerve is usually unmyelinated
• Ear cartilage is deficient or absent with poor recoil
• Hair appears woolly, and fuzzy and individual hair fibres can
be seen separately

30. • Skin and subcutaneous tissues:
• Skin is thin, gelatinous, Shiny and excessively pink
• Abundant lanugo
• Plentiful vernix caseosa
• Edema may be present
• Subcutaneous fat is deficient
• Breast nodule is small or absent

31. • Genitals:
• MALE:
• testes undescended
• scrotum poorly developed
• FEMALES :
• labia majora widely separated exposing labia
minora
• hypertrophied clitoris

32. CHARACTERISTICS OF
PRETERM INFANTS
• Skin
• Bright pink, often translucent, depending on
the degree of maturity
• Smooth and shiny ( may be oedematous)
• Small blood vessels clearly visible underneath
the thin epidermis
• Fine lanugo hair is abundant

33. • Ear cartilage
Soft and pliable
• Soles and palms
Minimal creases
Smooth appearance
• Scarf sign
Elbow may be easily brought across the
chest with little or no resistance

34. • Male genitalia
 Male infant’s scrotum is undeveloped and not
pendulous
 Minimal rugae are present
 Testes may be in the inguinal canal or in the
abdominal wall
• Female genitalia
 Clitoris is prominent
 Labia majora are poorly developed and gaping

35. COMPLICATIONS OF
PRETERM BIRTH
Central nervous system:
oImmaturity of central nervous system
oPoor cough reflex
oUncoordinated sucking and swallowing
oRetrolental fibroplasias
oIntra ventricular and periventricular
haemorrhage

36. Respiratory system
• Resuscitation difficulties at birth
• Hyaline membrane disease
• Breathing is periodic and associated with intercostal
recessions due to soft rib
• Pulmonary aspiration
• Atelectasis
• Broncho pulmonary dysplasia

37. Cardio vascular system
• The closure of ductus arteriosus is delayed among
preterm infants
G I system
• Regurgitations and aspirations
• Abdominal distension and functional
• intestinal obstruction
• Enter colitis
• Hyperbilirubinemia
• Hypoglycaemia

38. Thermo-regulation
• Excess heat loss
Infections
Renal immaturity
• The blood urea nitrogen is high
• Acidosis
• Edema
Toxicity of drug
Nutritional problems
• anemia
• Deficiencies of folic acid and Vit E
• osteopenia and rickets
Biochemical disturbance
• hypoglycaemia, hypocalcemia, hypoxia

39. MANAGEMENT
• Care of preterm infant
• Intensive care protocol

40. IMMEDIATE CARE OF NEWBORN
• Cord is clamped immediately to prevent hypovolemia.
• Cord length is kept 10-12 cms in case of exchange
transfusion
• Airway is cleared
• Adequate oxygen is given
• Baby is wrapped including head with sterile towel
• Administer inj .vitamin k

41. Intensive care protocol
Special care is needed incase of
• Inability to suckle the breast and to swallow
• Incapacity to regulate the temperature within
limited range from 96-99F
• Inability to control the cardio- respiratory function
without cyanotic attacks

42. PRINCIPLES OF SPECIAL CARE
• Tomaintain body temperature
• Adequate humidification to counter balance
increased water loss
• Oxygen therapy and adequate ventilation
• Toprevent infection
• Tomaintain nutrition and adequate nursing care

43. Management
• Prepare for high risk of need for resucsitation
• Gentle resuscitation using small bags for PPV (Positive
pressure ventilation), use of CPAP (Continuous positive airway
pressure)
• Take extra care to avoid hypothermia
• Special attention to maintain of warm chain
• KMC
• Strict adherence to asepsis, hand hygiene
• Management of metabolic, hematologic abnormality
• Management of immature organ systems in preterm

45. Choosing initial methods of feeding
>34 weeks
Initiate breast feeding
Observe if, positioning & Attachment
are good, able to suck
Effectively and long enough (10-15min)
yes
Breast feeding
Start feeds by spoon
Or paladai
no
Yes,spoon/
Paladai feeding
No, start feeds by OG or NG tube
No vomiting/abd distension
Gastric tube feeding
32-34weeks
28-31 weeks
Observe if accepting well
Without spilling/coughing
<28wks
Vomiting/abd distension
Start IV fluid

46. Progression of oral feeding in preterm, LBW
neonates & Infant on IV fluids
Start trophic feeding by OGT
And monitor for feed intolerence
If accepting well
Newborn with OGT feeds
Gradually increase the feed volume
Taper & stop IV fluids
Try spoon feeds once or twice a day
Put on mother’s breast and allow non nutritive
suck
Gradually ↑ the frequency & amount
↓OGT feeds
Put the baby on mother’s breast before each
feed, if good attachment and effective sucking
Taper and stop spoon feeds
Once the mother is confident

47. Nutritional supplements for infants with birth wt
between 1500-2499g
Nutrition Method of
supplementation
Dose Duration
Vitamin D Multivitamin
drops
400IU/day 2wks to 1yr
Iron Iron drops 2mg/kg/day 6-8wks to 1yr

48. Supplementation inVLBW neonates
1) Calcium & phosphorus (140-160mg/kg/Day & 70-
80mg/kg/Day for infants on EBM-Expressed breast
milk)
2) Vitamin D, B complex, Zinc
3) Folate (50 µg/kg/D)
4) Iron- Supplementation should be added at different times in
the day to avoid abnormal ↑ in osmolarity

49. Management of inadequate wt gain
• Proper counselling of mothers, assessment of
positioning/attachment & managing sore ,flat
nipples.
• Frequency & timing of both breast feeding and
spoon or paladai feeding
• EBM by spoon or paladai feeding (preterm)
• Initiating fortification of breast milk when indicated

50. NURSING CARE
• Cushioned bed
• Avoid excessive light ,sound ,rough handling and
painful procedures
• Use effective analgesia and sedation for procedures
• Provide warmth
• Ensure strict asepsis
• Cover the baby approximately

51. CONT…
• Provide effective and safe oxygenation
• Nutrition
• Tactile and kinesthetic stimulation
• Prone position or side lying with head lifted
• Phototherapy if needed
• Prevention of nosocomial infection
• Weight record daily
• Immunizations
• Family support

53. HYPOTHERMIA

56. DEFINITION AND CLASSIFICATION
It is a condition characterized by lowering of body
temperature than 36°C.
Types of Hypothermia:
Could be classified according to Causes and
according to Severity.

58. CLASSIFICATION BASED ON CAUSE
• Primary Hypothermia:
– Seen immediately after delivery
– Normal term infant delivered into a warm environment may
drop its rectal temperature by 1 – 2°C shortly after birth and
may not achieve a normal stable body temperature until the
age of 4 – 8hours.
– In low birth weight infants, the decrease of body
temperature may be much greater and more rapid unless
special precautions are taken immediately after birth. (loss
at least 0.25 °C/ min.)

59. • Secondary Hypothermia:
– This occurs due to factors other than those
immediately associated with delivery.
– Important contributory factors are:
e.g.: Acute infection especially Septicemia.
CLASSIFICATION BASED ON CAUSE

60. CLASSIFICATION BASED ON SEVERITY
II) According to Severity:
(1) Mild Hypothermia: < 36°C
(2) Moderate Hypothermia: < 35.5°C.
(3) Severe Hypothermia: < 35°C.

62. CLINICAL FEATURES
• Decrease in body temperature
• Cold skin on trunk and extremities
• Poor feeding in the form of poor suckling
• Shallow respiration
• Cyanosis
• Decrease activity, e.g. Weak cry

65. FOUR MODALITIES OF HEAT LOSS IN
NEONATES
1. Evaporation:
Heat loss that resulted from expenditure of internal thermal energy to
convert liquid on an exposed surface to gases, e.g.: amniotic fluid, sweat.
Prevention: Carefully dry the infant after delivery or after bathing.
2. Conduction:
Heat loss occurred from direct contact between body surface and cooler
solid object.
Prevention:
Warm all objects before the infant comes into contact with them.

67. 3. Radiation:
It occurred from body surface to relatively distant objects that are cooler than
skin temperature.
4. Convection:
Heat loss is resulted from exposure of an infant to direct source of air
draft.
Prevention:
· Keep infant out of drafts.
· Close one end of heat shield in incubator to reduce velocity of
air.

69. MANAGEMENT
• Infant should be warmed quickly by wrapping in a warm towel.
• Use extra clothes or blankets to keep the baby warm.
• If the infant is in incubator, increase the incubator’s
temperature.
• Avoid exposure to direct source of air drafts.
• Check body temperature frequently.
• Give antibiotics if infection is present.

80. HYPERTHERMIA

81. DEFINITION
It is a condition characterized by an elevation in body
temperature more than 37.5°C.
Causes:
1.Disturbance in Heat Regulating Center caused by
intracranial hemorrhage.
2. Incubator temperature is set too high.

82. MANAGEMENT
• Undress the infant. If at home; keep light clothes, cover that
containing light sheet, Or only a diaper if the infant is inside an
incubator.
• Reduction of incubator temperature.
• Provide Tepid sponge bath.
• If available; fill the water mattress with cold water, and keep it
in contact with the infant’s skin.
• Increase fluid intake in the form of 5cc of Glucose 5%
between feeds to prevent dehydration.

84. IQ Question

85. The first letters are in alphabetical order with a letter skipped
in between each segment: C, E, G, I, K. The second and third
letters are repeated; they are also in order with a skipped
letter: M, O, Q, S, U.

86. HYPOGLYCEMIA

88. DEFINITION:
Neonatal hypoglycemia is usually defined as a serum
glucose value of < 40‐45 mg/dl.
For the preterm infant a value of < 30 mg/dl is
considered abnormal (hypoglycemia).

90. 1- The main cause may be maternal malnutrition during pregnancy
which leads to fetal malnutrition and of course a low birth weight.
2‐ Those infants, who are Small for gestational age (SGA),
manifested by decrease in their birth weight and subcutaneous fat
and hepatic glycogen.
3‐ Those infants’ of diabetic mothers (IDM) or those named as
large for gestational age (LGA).
NEONATES AT RISK FOR DEVELOPING
HYPOGLYCEMIA:

91. 4‐ Those whom placentas were abnormal,
e.g. placenta Previa.
5‐ Those whom their mothers had toxemia during
pregnancy,
e.g. eclampsia or pre‐eclampsia induction of labor
preterm infant.
6‐ Those very ill or stressed neonates whom their
metabolic needs were increased due to hypothermia,
infection, respiratory distress syndrome, or cardiac failure.

93. Fetus receives glucose from the mother
Cord cut
Glucose level falls from 70 – 80 mg/dl to 50 mg/dl
Hepatic glucose is released into the blood
Cold extra‐uterine one,
Beginning the respiratory cycles,
Muscular activity
Suckling effort
High risk infant
Risk for developing hypoglycemia.
PATHOPHYSIOLOGY

94. CLINICAL
MANIFESTATIONS:1‐ Hypotonia
2‐ Poor Feeding
3‐ Tremors
4‐ Cyanotic spells
5‐ Lethargy
6‐ Seizures

95. CLINICAL MANIFESTATIONS CONTD:
7‐ Hypothermia.
8‐ Irregular respiratory pattern (Apnea).
9‐ Irritability.
10‐ High pitched cry followed by weak cry.
11‐ poor reflexes, especially sucking reflex.

98. Infants who develop hypoglycemia should immediately
be given 2 cc/kg of 10% dextrose over 1 minute,
repeated as needed.
MANAGEMENT OF THE NEONATE
WITH HYPOGLYCEMIA:

99. • A continuous infusion of 10% glucose at a rate of
8-10 mg/kg/min should be started to keep
glucose values normal (NOTE: 10 mg/kg/min of
10 % dextrose = 144 cc/kg/day).
• Frequent bedside glucose monitoring is
necessary.
• When feedings are tolerated and frequent
bedside glucose monitoring values are normal,
the infusion can be tapered gradually.

103. INFANT OF DIABETIC
MOTHER

104. INFANT OF DIABETIC MOTHER

105. INFANT OF DIABETIC MOTHER

106. Maternal hyperglycemia
Fetal hyperglycemia in‐utero
Fetal hyperinsulinemia‐ increased fat and
glycogen synthesis‐ Macrosomic infant
Cord clamped
Interrupts the transplacental glucose supply
Inspite of which Hyperinsulinemia persists,
this leads to hypoglycemia
PATHOPHYSIOLOGY

107. DISORDERS IN INFANTS OF DIABETIC MOTHERS
• Hypoglycemia.
• Hypocalcemia.
• Hypomagnesemia.
• Cardio‐respiratory disorders
• Hyperbilirubinemia (Unconjugated)

108. MANAGEMENT:
• For the mother:
Good antenatal care for proper control of maternal
diabetes
• For an infant:
 All IDMs should receive continuous observation and
intensive care.
 Serum glucose levels should be checked at birth and at
half an hour, 1, 2, 4, 8, 12, 24, 36 and 48 hours of age

109. • If clinically well and normoglycemia; oral or gavage feeding should be
started and continued with 2 hours intervals.
• If hypoglycemic; give 2 – 4 ml/kg of 10% dextrose over 5 minutes,
repeated as needed.
• A continuous infusion of 10% glucose at a rate of 8‐10 mg/kg/min.
Start enteral feeding as soon as possible. Give Corticosteroids in
persistent hypoglycemia.
• Oxygen therapy for RDS, Calcium gluconate 10% for
hypocalcemia, phototherapy for hyperbilirubinemia
MANAGEMENT cont:

113. NEONATAL INFECTIONS

115. NEONATAL INFECTIONS
• Infection is still one of the leading causes of neonatal
death in developing countries.
• The neonates are more susceptible to infection as they are
deficient in natural immunity and acquired immunity.
• Preterm infants are at high risk for perinatal infections.
• Neonates that survive from sepsis often suffer from
severe neurological as well as severe parenchymal lung
diseases.
NEONATAL SEPSIS
INTRODUCTION

116. • The newborn infant is uniquely susceptible to acquire
infection, whether bacterial, viral or fungal.
• Bacterial sepsis and meningitis continue to be major
causes of morbidity and mortality in the newborn.
• The mortality rate due to sepsis ranges from 20% to as high
as 80% among neonates. Surviving infants can have
significant neurologic squeal because of CNS involvement.

117. DEFINITION
Neonatal sepsis is a disease of neonates (who
are younger than 1 month) in which they are
clinically ill and have a positive blood culture.

119. RISK FACTORS FOR NEONATAL
INFECTION
• Rupture of membranes > 18 hours
• Maternal intrapartum fever > 100.4˚F
• Low birth weight infant (< 2500 g)
• Prematurity (< 37 weeks)
• Chorioamnionitis
• Mother with (Group-B Streptococcus) infection
• Repeated vaginal examinations in labour
• Invasive procedures of monitoring

120. MOST COMMON RISK FACTORS
• Maternal risk factors:
‐ e.g.: Premature/prolonged rupture of membranes.
• Neonatal risk factors:
‐e.g.: Prematurity (less immunologic ability to resist
infection + more liable to penetrate their defensive
barriers).

121. MODE OF INFECTION
Antenatal
• Transplacental : maternal infection that can affect the fetus
through transplacental route are predominantely the viruses,
they are rubella, cytomegalovirus, herpes virus, HIV, chicken
pox and hepatitis – B virus.
• Other infections are syphilis, toxoplasmosis and
tuberculosis.
• Aminonitis : Following premature rupture of the
membranes can affect the baby following aspiration or
ingestion of infected amniotic fluid.

122. INTRANATA
L• Aspiration of infected liquor or meconium following early
rupture of the membranes or repeated internal examination.
This may lead to neonatal sepsis, pneumonia and meningitis.
• while the fetus is passing through the infected vagina –
(a) eyes are infected – opthalmia neonatorum or
(b) oral thrush with candid albican
• Improper asepsis while caring the umbilical cord.

123. POSTNATAL – NOSOCOMIAL INFECTIONS
• Transmission due to human contact – infected mother,
relatives or staff of the nursery.
• Cross infection from an infected baby in the nursery.
• Infection through feeding, bathing, clothing or air-borne.
• Infection in environment of neonatal intensive care (NICU)
or invasive monitoring.

124. COMMON ROUTES OF TRANSMISSION
• Through the maternal blood, through placenta as rubella,
toxoplasma, and syphilis.
• From the vagina or cervix, as groups B streptococci.
• The newborn may be, come in contact as it passes through the birth
canal with gram negative organisms.
• The newborn may come in contact in its environment after birth
(Coagulate positive or negative staphylococci).
• When a susceptible host acquires the pathogenic organism, and the
organism proliferates and overcomes the host defense, infection
results.

125. THE COMMON PATHOGENS
• Group b streptococcus (GBS),
• Staphylococcus aureus,
• E. Coli,
• Klebsiella and pseudomonas,
• Fungus(candida) and anaerobes.

126. THE PRIMARY SITES OF INFECTION
• Skin,
• Nasopharynx,
• Oropharynx,
• Conjunctiva and
• Umbilical cord.

127. COMMON SITES OF INFECTION
• Eyes – opthalmia neonatorum
• Skin
• Umbilicus
• Oral thrush
Severe systematic :
• Respiratory tract
• Septicaemia
• Meningitis
• Intra – abdominal infections

130. CLASSIFICATION OF NEONATAL SEPSIS
• Early onset Sepsis
• Late onset Sepsis
 Newborns with early‐onset infection present within 24
hours till 72 hours.
 Early‐onset sepsis is associated with acquisition of
microorganisms from the mother during pregnancy
(transplacental infection), or during labor (an ascending
infection from the cervix).
 Late‐onset sepsis occurs beyond the first 72 hours of life
(most common after the 3rd day till the 7th day after birth)
and is acquired from the care giving environment
(Nosocomial infection).

131. CLINICAL FEATURES
• Decreased activity
• Excessive crying
• Apnea
• Jaundice
• Hypo/Hyperthermia
• Bulging or full fontanel
• Seizures
• Hypotonia

134. LABORATORY FINDINGS
• Raised Total leukocyte count (WBC count)
• Raised C – reactive Protein (CRP)
• Increased Erythrocyte Sedimentation Rate (ESR)
• Cultures positive

136. MANAGEMENT
• Prevention: through proper application to infection
control practices.
• Early onset sepsis; give intrapartum antimicrobial
prophylaxis (IAP) to the mother.

137. PREVENTION
• Demonstrate the effect of hand washing upon the prevention of the
nosocomial infections.
• Standard precautions should be applied in the nursery for infection
prevention.
• Instillation of antibiotics into newborn’s eye 1‐2 hours after birth is
done to prevent the infection.
• Skin care should be done using warm water & may use mild soap for
removal of blood or meconium.
• Cord care should be given regularly using alcohol or an
antimicrobial agent.

140. MANAGEMENT (CONT..)
• Neonates with clinically suspected sepsis:
– Culture should be obtained first.
– The recommended antibiotics are ampicillin and
gentamicin.
– Third generation cephalosporins (Cefotaxime) may replace
gentamicin if meningitis is clinically suspected
• Late onset neonatal sepsis:
– Vancomycin in combination with either gentamicin or
cephalosporins should be considered in penicillin resistant cases.

141. Antibiotic therapy – broad spectrum
are given to cover the germ positive and
anaerobes. Inj. Ampicillin
negative organisms as well as the
150
mg/kg/every 12 hours, gentamycin 3-4
mg/kg/every 24 hours, usually are
started. In a severely ill patient,
cefotaxime or ceftazidime is also added.

143. CONT…
• Supportive therapy and management of
complications as needed.
• E.g. mechanical ventilation for RDS, dopamine
for hypotension, anti convulsion therpy for
seizures, sodium bicarbonate for metabolic
acidosis and Immunotherapy with hyper
immune globulins.

148. GENERAL AND NURSING MANAGEMENT
cont..
•Encourage breast feeding from the mother.
• Adequate fluid and caloric intake should be administered by
gavage feeding or intravenous fluid as ordered.
• Extra‐measures for hypothermia or hyperthermia that may be
taken to the newborn.
• Administering medications as doctor order.
• Follow the isolation precautions.
• Monitoring intravenous infusion rate and antibiotics are the
Nurses responsibility.

149. •Administer the medication in the prescribed dose, route, and time
within hour after it is prepared to avoid the loss of drug stability.
•Care must be taken in suctioning secretions from the newborn as it may be
infected.
•Isolation procedures are implemented according to the isolation protocols
of the hospital.
•Observe for the complications e.g. meningitis and septic shock.
•Encourage in‐service programs and continuing education of nurses
regarding the infI
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151. HEMOLYTIC
DISEASES OF
NEWBORN

152. Hemolytic Disease
 The term hemolytic disease is limited to
conditions in which the rate of RBCs
destruction is accelerated and the ability of
bone marrow to respond is unimpaired.

153. Causes:
 Rh incompatibility
 Autoimmune HemolyticAnemia
 Hereditary Spherocytosis
 Sickle Cell Disease
 Thalassemia

154. Rh incompatibility:
 Rh incompatibility is a condition which
develops when an Rh negative mother
conceives a fetus which is Rh positive.
Isoimmunization:
 When the mother produces Antibodies directed
against fetus RBC surfaceAg.

155. THE MOST COMMON….
 Cause of Maternal Isoimmunization
 Feto- maternal Bleed
Risk Factors of Feto-maternal Bleed:
 Amniocentesis
Ectopic pregnancy

156.  RBC Rh Antigen :
 Rh “ D ’’Ag
 Mother produces:
 Anti Rh (D)Abs
THE MOST COMMON….

161. Rh Incompatibilty
Rh (-) woman + Rh (+) man = Rh (+) children
Rh positive fetus cross the placental barrier
and enter into Rh negative mother’s blood
stream.
mother’s immue system reacts fetal Rh
antigen stimulus by producing a large number
of anti-Rh antibodies.
 mother’s antibodies + feotus RBCs=hemolysis

163. Mother
must be
Rh -
Dad must
be Rh +
Coombs
test must
be positive
Abs must
be
associated
with
Hemolysis
Ab titer
must be
above 1:8
Is the baby at risk?
• Anti Lewis
Abs
Non-Hemolytic
ABS
• Anti KELLAbs
• Anti RH(D)Abs
Hemolytic
ABS

169. Erythroblastosis Fetalis
• Hemolytic anemia and it occurs during
transplacental transmission of maternal
antibodies to fetal RBCs.
• The disorder usually results from
incompatibility between maternal
and fetal blood groups.

170.  Mother’s antibodies destroy baby's RBCs and the
baby develops anemia.
 The baby's body tries to compensate for the
anemia by releasing immature RBCs called
erythroblasts from the bone marrow.
 Liver and spleen to become enlarged potentially
causing liver damage or a ruptured spleen.

173. Jaundice (Icterus gravis neonatorum)
 Infants have high levels of bilirubin in their blood,
which leads to jaundice. (hyperbillirubinemia)
 Shorter life span of RBCs
 Unconjugated billirubin binds to albumin and
travels to liver.
 Increased reabsorption of conjugated billirubin
from GI tract.

177. Kernicterus
• Free bilirubin is lipid soluble.
• Deposited in brain.
• It causes a condition known as
Kernicterus.

181. Diagnostic features of Hydrops fetalis-
■ Mother is rh –ve
■ Serological examination reveals presence of rh antibodies
■ May be presence of poly hydramnios
■ sonography- to detect oedema in the skin, scalp and pleural/pericardial
effusion.
■ Straight X-Ray abdomen showing ‘Budha’ position of the fetus.
■ The baby at birth looks pale and oedematous with an enlarged abdomen due
to ascites.
■ There is enlargement of liver and spleen.
■ Placenta is large, pale , oedematous with fluid oozing from it.
Fetal death occurs sooner or later due to cardiac failure. The baby
is either stillborn or macerated and even if born alive, dies soon after.

182. Diagnosis of Haemolytic diseases
Routine blood Test
Fetus Blood Test
Indirect Coombs Test
Direct Coombs Test

183. DirectCoombs test or DAT
RBCs wash to remove plasma
RBCs are incubated with anti-
hemoglobulin.
Antihemoglobulin binds to patient’s
antibodies that are attached with RBCs
Agglutation indicates positive DAT.

184. Indirect coombs test or IDT
• The IDT deals with extracted plasma.
• Unbound antibodies remains in blood
• Plasma is then incubated with reagent RBCs.
• Antibodies binds to reagent RBCs.
• Positivr IDT indicates presence of antibodies in
blood.

185. Treatment
Rho-Gamma Globulin
Administered at 28th week of
pregnancy
After 72 hours of Delivery.

186. RhoGam vaccination
• Contains antibodies
to RH (+)
• But not harmfull
enough
• Mother’s body
react to these
antibodies and
never reacts to fetal
antigens.

187. Intrauterine blood transfusion
• Given to replace fetal RBCs that are being
destroyed by mother’s allo antibodies.
• Keep the fetus healthy until he or she is
mature enough to be delivered.

188. Procedure
position of placenta through
ultrasound image.
Antiseptic solution to clean mother’s abdomen
Anesthetic injection to make
abdominal region insensitive
 Needle is inserted

189. From mother's abdomen into the
fetus's abdomen or an umbilical cord
vein.
A compatible blood type is delivered
into the fetus's umbilical cord vessel.

191. Management after delivery:
Phototherapy for neonate
with mild jaundice
Exchange transfusion in
Severe cases

192. HYPERBILIRUBINEMIA
(NEONATAL
JAUNDICE)

194. DEFINITION
• Hyperbilirubinemia is an elevation in the neonatal serum bilirubin
≥ 12.9 mg/dl in Full‐term, Formula feed infant OR ≥ 15 mg/dl in
Preterm, Breast feed infant
• Characterized by JAUNDICE, which is defined as “yellowish
discoloration of skin and mucous membranes”.
• In the neonate, clinical jaundice is diagnosed if the total
serum bilirubin is ≥ 7 mg/dl.

195. The following are possible causes of hyperbilirubinemia
in the newly born infants:
1. Over production of bilirubin.
2. Under excretion of bilirubin.
3. Combined over production and under excretion.
4. Physiological jaundice.
5. Breast milk associated jaundice.
CAUSES

200. CAUSE

209. PHOTOTHERAPY: PRINCIPLES
1.Cover the infant’s eyes and genital organs.
2.The infant must be turned frequently to expose all body
surface areas to the light.
3.Continued until the Serum bilirubin level must be
10mg%.
4.In each shift, eyes are checked for evidence of discharge
or excessive pressure on the lids and eye care should be
done using warm water, then apply eye drops or ointment.

210. 5.Eye cover should be removed during feeding, and this
opportunity is taken to provide visual and sensory stimuli.
6. Avoid oily lubricants or lotion on the infant’s exposed
skin, because this can act as a barrier that prevent
penetration of light through the skin.
7.Increase feeds in volume and calories. Add 20%
additional fluid volume to compensate for insensible and
intestinal water loss.
8. Maintain Intake and output chart.
PHOTOTHERAPY cont..:

215. OBJECTIVES:
■ To correct anaemia.
■ To remove the circulatory antibodies.
■ To eliminate the circulatory bilirubin.
PROCEDURE:
■ The route of transfusion should preferably be through the umbilical vein.
A plastic catheter of 1 mm diameter is passed about 7 cm beyond the
umbilicus, so as to place it in the inferior vena cava.
■ Blood should be warmed to 370 C.
■ 15 ml of fetal blood is withdrawn first followed by 10 ml to be pushed in-
return slowly. (PUSH-PULL METHOD)
■ For every 100ml of blood transfused, 1meq of sodium bicarbonate is
given to combat metabolic acidosis and 1 ml of 10% calcium gluconate to
prevent tetany due to transfusion of citrated blood.

216. COMPLICATIONS OF
HYPERBILIRUBINAEMIA
• The most common complication of hyperbilirubinemia is
Kernicterus (Bilirubin Encephalopathy), which usually occurs
when the unconjugated serum bilirubin level exceeds than
20 mg/dl.
• In small, sick preterm infants, even a bilirubin level in a
low range may cause Kernicterus.

219. Clinical Presentation:
Kernicterus progresses through 4 stages:
Stage I: Poor Moro reflex, poor feeding, vomiting, high‐pitched cry,
decreased tone and lethargy.
Stage II: Spasticity, seizures, fever. Neonatal mortality is high at this
stage (80%).
Stage III: Asymptomatic (Spasticity decreases and all remaining
clinical signs and symptoms may disappear).
Stage IV: Appears after the neonatal period. Long‐term sequelae can
include: spasticity quadriplegia, deafness and mental retardation (for the
20%).

220. ■ Hypoxia, acidosis, hypoglycaemia, hypothermia or sepsis enhance the
pathogenesis, so that affection may occur even at a low levels of
bilirubin.
■ It is clinically characterised by lethargy, hypotonia, poor feeding and
loss of moro reflex.
■ Gradually, hypertonia, severe illness is manifested by respiratory
distress and opisthotonous, hyperpyrexia, convulsions, enlarged liver
and spleen.
PREVENTION & MANAGEMENT:
■ Regular and periodic estimation of blood bilirubin level.
■ In susceptible cases, treat with exchange transfusion.
■ Use of barbiturates and photherapy also treat the condition.

221. • Neonates with overt neurologic features usually die (75%).Those who
survive often suffer from MR and cerebral palsy.