High risk newborn is a chapter under OBG for 4 th yr BSc nursing students. this helps them to understand about the classification of high risk newborn, KMC, problems associated with LBW babies, management of LBW babies.

2. High risk neonate is a newborn, regardless of GA or
BW, who has a greater than average chance of
morbidity, mortality because of conditions or
circumstances associated with birth & adjustments
to extrauterine existence.
1. LBW <2.5kg
2. SGA, weight <10th percentile ( IUGR)
3. LGA, weight >90th percentile
4. PRETERM, delivered before 37 weeks

3. LOW BIRTH WEIGHT BABY
● LBW babies are those weighing below 2500 g at birth
● VERY LOW BIRTHWEIGHT (VLBW) babies are those
weighing below 1500 g at birth
● EXTREMELY LOW BIRTHWEIGHT (ELBW) babies are
those who weigh below 1000 g at birth
● The definitions of LBW is based upon weight alone & do
not consider the gestational age.

5. PHYSICAL ASSESSMENT
1. SKIN
● Pallor
● Plethora - beetroot appearance in babies due to
polycythemia
● Cyanosis
● Jaundice
● Skin rashes
● Milia
● Miliaria
● Petechiae or purpura rash

6. ● Bruising
● Erythema toxicum
● Infectious lesions - thrush, herpes simplex virus, umbilical
sepsis, staphylococcal infection
GENERAL ASSESSMENT WARNING SIGNS
pallor Central
cyanosis
Apnoea
lasting
longer
than 20 s
HR<110
or >180
Beats/mn

7. RR<30
or >60
breaths/
mn
Skin T
<36.2C
or
>37.2C
Lack of
spontaneous
movement &
responsiveness
Abnormal
lying
position
either
hypotonic
or
hypertonic
Lack of
interest in
surroundings
jaundice

8. ● Infant is small & limp
● Thin skin, blood vessels beneath the
epidermis
● Wrinkled skin with lanugo, little or no vernix
caseosa
● No subcutaneous fat
● Head larger than the body ( cephalocaudal
growth )
● Prominent eyes
● Male genitalia - few scrotal rage,

9. Undescended testes
● Female genitalia - labia & clitoris are
prominent
● Protruded abdomen
● Thin muscles
● Minimal creases on palm & soles
● Regurgitation
● Cyanosis, pallor, plethora
● Inactive, extended arms & legs

10. ● Poor reflexes
● Absence of sucking reflex
● Barrel or concave shaped chest
● Hypothermia, hypotonia, apnea, poor colour
● Nasal flaring, suprasternarnal , substernal
retractions
● Grieving, stridor breath sound.

11. NURSING MANAGEMENT
1. Maintenance of controlled thermal
environment
2. Monitoring HR,RR, & BP
3. Collection of specimen ( blood glucose,
haematocrit,Calcium,bilirubin, ABG)

12. Thermo
regulation
Infection
& injury
prevention
Nutrition
&
hydration
Prevention
of Cx
Respira
tory
support
Skin
care
Energy
conservation

13. KANGAROO MOTHER CARE

14. Kangaroo mother care (KMC) is used to promote
closeness between a baby & mother & involves
placing the nappy-clad baby upright between the
maternal breasts for
Skin to skin contact

15. COMPONENTS OF KMC
Skin to
skin
contact
Exclusive
breastfeeding
Support
to mother
& baby
Discharge of
baby

17. BENEFITS OF KMC
● Better adaptation to the environment
● Helps baby to sleep better
● Aids better mental development
● Makes breastfeeding convenient
● Promote healthy weight gain
● Reduces baby’s stress level
● Promotes increased lactation
● Helps mother to fight postpartum depression

18. ● Helps in bonding with father & mother
● It endorses the notion of togetherness
● Promotion of early tactile, audio visual &
emotional contact for both, & the baby is given
the opportunity to further his familiarity with
the mother’s voice, smell & heart beat
● It provides a sense of containment &
closeness that is reminiscent of the uterus

20. RESPIRATORY PROBLEMS

21. Neonates are susceptible to respiratory
compromise, for a reasons like lack of
maturation in other body systems & as a result of
their stage of lung development, diseases like
Hyaline Membrane Disease (HMD), where
surfactant production is inhibited.

22. STAGES OF LUNG DEVELOPMENT
1. EMBRYONIC PHASE - this lasts until 5th week
of gestation, in this stage the proximal
airways develop
2. PSEUDOGLANDULAR PHASE - this lasts from
5th to the 16th week of gestation. During this
phase there is development of the lower
conducting airways, bronchi & large
bronchioles

23. 3. CANALICULAR PHASE - lasts from 17th to the
24th week of gestation. It’s the period for the
development of the gas exchanging bronchioles
4. TERMINAL SAC PHASE - this takes place
between the 24th week & 36th week of gestation.
Surfactant production begins with increasing
efficiency as the alveolar ducts develop.
5. ALVEOLAR PHASE -this is ongoing from the
37th week of gestation until the 8th year of age

24. During this phase alveoli increase in number &
there is maturation of the surfactant production.
SIGNS OF RESPIRATORY COMPROMISE
1. GRUNTING - audible sound heard on
expiration
2. RETRACTIONS - occurs due to an increase in
the need to create higher inspiratory pressure
3. ASYNCHRONY - breathing has a SEE- SAW
pattern as the abdominal & diaphragm

25. movements works out of unison
4. TACHYPNOEA - RR above 60 breaths/mn, &
aims to remove hypercarbia & prevent hypoxia
5. NASAL FLARING
6. APNOEA - absence of breathing for more than
20 seconds, occurs due to increasing respiratory
fatigue in baby

26. COMMON RESPIRATORY PROBLEMS
1. Pneumothorax
2. Transient tachypnoea of the newborn (TTN)
3. Infection/Pneumonia
4. Meconium Aspiration Syndrome
5. Respiratory Distress Syndrome (RDS)
6. Cardiac disease

27. MECONIUM ASPIRATION SYNDROME

28. ● Fetal asphyxia causes the passage of
meconium into the liquor. This meconium is
unproblematic unless the baby gasps or
breathes in amniotic fluid, potentially inhaling
meconium simultaneously
● The passage of meconium into the liquor is
rarely seen prior to 34 weeks, which suggests
this is due to immaturity of the pre-term GI
● The baby may present with initial respiratory
distress with cyanosis, increased work of

29. Breathing & a barrel shaped chest
● The meconium becomes trapped in the
airways & causes a ball- valve effect, the
meconium then blocks the airway during
expiration so that air accumulates behind the
blockage.
● This can leads to rupture of alveoli & cause
the baby to develop a pneumothorax & causes
pneumonitis too

30. ● The concentration of meconium is directly
related to the volume of AF.
● Assessment of AF by doing meconium crit,
hematocrit readings
● <4gm/dl ml = thin = dilute brownish fluid
● 4 - 9gm/dl ml = moderate, yellowish brown
fluid,not clear
● >9gm/dl ml = thick = pea soup consistency

31. ● These babies need full intensive care &
ventilation to prevent further deterioration
● Use of EXTRACORPOREAL MEMBRANE
OXYGENATION (ECMO) where prolonged
cardiac & respiratory support is given. This
system provides heart lung bypass support
outside of the baby.
● Symptomatic treatment

34. ● RDS or Hyaline Membrane Disease
● The diagnosis of HMD is derived from the
presence of hyaline membranes in the airways
resulting from the damaged epithelium.
● This occurs as a result of the insufficient
production of surfactant & is more commonly
seen in preterm babies, maternal diabetes also
can inhibit surfactant production
● The introduction of surfactant therapy into
neonatal care has significantly decreased the

35. Mortality & morbidity associated with RDS.
Surfactant consists of several different types
of proteins & phospholipids, which also help
to prevent infection & produce further
surfactant
● The X-ray has a ground glass appearance
across the lung fields, while severe distress is
represented by a “ white out”, the greater the
density of white out, that much severe the

36. Disease.
● The infant has an increasing respiratory
distress & work of breathing
● Baby requires NICU care for weeks

37. NEONATAL INFECTION

38. MODES OF ACQUIRING INFECTION
● Transplacental infection
● From amniotic fluid
● After birth from health care providers
● Contaminated objects or droplet infection
INFECTIONS ACQUIRED BEFORE or DURING
BIRTH
● rubella

39. ● Varicella zoster
● Toxoplasmosis
● Candida - oral candidiasis, cutaneous
candidiasis, disseminated candidiasis
● Ophthalmia neonatorum
● Meningitis
● Eye, skin, respiratory & GI infections
● Umbilical infection
● UTI

40. MANAGEMENT OF INFECTION
1. Prevention of infections in the mother
2. Prevention of infection in the newborn
● Provide a safe environment
● Handwashing
● Promote exclusive breastfeeding
● Maintaining skin integrity & pH balance to
increase immune function, avoiding irritation
or trauma of the baby’s skin

41. ● Restrict visitors
● Early diagnosis & Rx of infection
● Use individual equipment for each baby
● Isolate infected baby
● Adequate spacing of cots in hospital
● Health education infection control
3. Prevention of infection in midwife
● Follow universal precautions
● Use of PPE

42. ● Covering all skin lesions
● Changing gloves between patients & washing
hands after gloves are changed
● Disinfecting all blood splashes & spillage
● Follow safe biomedical waste Mx
● Appropriate vaccination. Eg; Hepatitis B
DIAGNOSIS OF INFECTION
Physical assessment may include observation
of :

43. ● Temperature instability
● Lethargy or poor feeding, dehydration,
starvation
● Acidosis or hypoxia
● Bradycardia or tachycardia or any apnoea
● Reduced urine output & any vomiting
● CNS signs
● Lab investigations include -
1. AF, placental tissue & cord blood for specific
organisms

44. 2. CBC
3. Specimens of urine & meconium for specific
organisms
4.swabs from nose, throat, umbilicus,skin
rashes, pustules or vesicles
5. MRI, CT scan, US & chest X ray
6. Comprehensive neurodevelopmental
examination

45. ● LP for CSF examination
TREATMENT OF INFECTION
● Caring of the baby in a warm thermoneutral
environment
● Good hydration & correction of electrolyte
imbalance, with demand feeding if possible &
intravenous fluids as required
● Maintaining skin integrity to increase
thermoregulation & to prevent fluid loss

46. ● Prompt systemic antibiotics or other drug
therapy & local Rx of infection
● Ongoing monitoring of neurobehavioural
status
● Reducing separation of mother & baby
● Encouraging breastfeeding
● Providing evidence based information, support
& reassurance to parents

47. HAEMOLYTIC DISORDERS

49. ● Life span of RBC is 120 days
● Breakdown of RBC takes place in
LIVER,SPLEEN & MACROPHAGES
● Normal bilirubin level in neonates - 5 mg/dL
● For adults - 0.1 to 1.2 mg/dL

50. HAEMOGLOBIN
HAEM GLOBIN IRON
BILIVERDIN
UNCONJUGATED
BILIRUBIN
AMINO ACIDS
PROTEIN
FORMATION
RBC
FORMATION

51. BILIRUBIN
UNCONJUGATED
BILIRUBIN
● Fat soluble
● Can’t excrete through
urine & faeces
● Deposits in fatty
tissues
CONJUGATED BILIRUBIN
● Water soluble
● Excreted in faeces &
urine
● Jaundice occurs as a
result of obstruction in
excretion

52. JAUNDICE
● Jaundice is caused by bilirubin deposits in the
skin. In term neonates it appears when serum
bilirubin concentrations reach 5-7 mg/dl
● Types :
1. Physiological jaundice
2. Pathological jaundice
3. Haemolytic jaundice`

53. PHYSIOLOGICAL JAUNDICE
● It occurs when unconjugated (fat soluble )
bilirubin is deposited in the skin instead of
being taken to the liver .
● It is a normal transition occurring in 50% of
term & 80% of preterm babies.

54. ● Jaundice usually appears on 2nd & 3rd day &
never before 24 hrs of life.
● Bilirubin level never exceed 200-215
micromol/L (12-13 mg/dL)
● For a preterm baby,bilirubin level is 165
micromol/L (10 mg/dL)
● Fades usually by 1 week of age.

55. CAUSES
● Increased RBC destruction due to shorter life
span of excess RBC, the neonatal had
acquired due to relative anoxia state during
intrauterine life.
● Decreased albumin binding capacity -
hypoxia,acidosis & hypothermia can interfere
with this.

56. ● Deficiency of UDP-GT enzyme. The level of
enzyme is low during first 24hrs of life causing
reduced bilirubin conjugation in liver.
● Increased enterohepatic reabsorption
-This process is increased as the newborn
bowel lacks the normal enteric bacteria that
break down conjugated bilirubin to
urobilinogen.

57. Mx
● Initiate breastfeeding within half an hour from
birth, & continue exclusive breastfeeding for
the neonate.
● Check for serum bilirubin level
● Provide phototherapy
● Monitor for pale stools & dark urine, this may
indicate cholestatic liver disease

58. PATHOLOGICAL JAUNDICE
● It appears within 24 hrs of birth,characterized
by rapid rise in serum bilirubin. Criteria for
diagnosing are:
1. Jaundice within the first 24 hrs of life
2. Rapid increase in total serum bilirubin >85
micromol/L (5 mg/dL) per day
3. Total serum bilirubin >200 micromol/L (12
mg/dL)

59. ● Conjugated bilirubin >25-35 micromol/L (1.5-
2 mg/dL)
● Persistence of clinical jaundice for 7-10 days
in term or 2 weeks in preterm babies.
CAUSES
● Interference in bilirubin
production,transport,conjugation or
excretion

60. 1. Production :
● Increased RBC destruction or haemolysis
causes increased bilirubin levels. Causes of
increased haemolysis are:
a. Blood type/group incompatibility
b. Extravasated blood - from cephalhematoma
c. Sepsis
d. Polycythemia
e. Spherocytosis - fragile red cell membranes

61. f. Haemoglobinopathies - sickle cell disease or
thalassaemia
g. Enzyme deficiencies - glucose-6-phosphate
dehydrogenase maintains the integrity of red cell
membrane.
2. Transport
● Factors that lower blood albumin levels or
decrease albumin binding capacity include;

62. a) Hypothermia,acidosis or hypoxia can interfere
with albumin binding capacity
b) Drugs that compete with bilirubin for albumin
binding sites (eg : aspirin,sulphonamides &
ampicillin)
3. Conjugation
● Immaturity of the neonate’s enzyme system
interferes with bilirubin conjugation in the
liver.other factors are ;

63. a)Dehydration,starvation,hypoxia & sepsis. (O2 &
glucose are required for conjugation)
b) TORCH infections
(toxoplasmosis,others,rubella,cytomegalovirus,h
erpes)
c) Other viral infections (eg; neonatal viral
hepatitis)
d) Other bacterial infections,particularly caused

64. e) Metabolic & endocrine disorders that alter
UDP-GT enzyme activity( eg; Crigler- Najjar
disease & Gilbert’s syndrome)
f) Other metabolic disorders such as
hypothyroidism & galactosaemia.
4. Excretion
● Hepatic obstruction caused by congenital
anomalies such as extrahepatic biliary atresia

65. ● Obstruction by bile plugs from increased bile
viscosity (eg: cystic fibrosis,TPN,haemolytic
disorders & dehydration)
● Infection,other congenital disorders &
idiopathic neonatal hepatitis,which can also
cause an excess of conjugated bilirubin
● Saturation of protein carriers needed to
excrete conjugated bilirubin into the biliary
system.

66. KERNICTERUS

67. ● Kernicterus ( bilirubin toxicity) is an
encephalopathy caused by deposits of
unconjugated bilirubin in the basal ganglia
of the brain,where bilirubin levels can be
>340 micromol/L (20mg/dL)
● Signs :
1. Lethargy
2. Changes in muscle tone
3. High pitched cry
4. irritability

68. RISK FACTORS
● Hypoxia
● Acidosis
● Infection
● Hypothermia
● Dehydration
● Preterm & sick babies

69. HAEMOLYTIC JAUNDICE

71. ● Reason for increased Hb destruction in the
fetus are Rhesus (RhD) isoimmunization or
ABO incompatibility
RhD INCOMPATIBILITY
● This occurs when a Rhesus positive baby
enter a Rhesus negative mother’s blood
stream.
● Mother’s blood treats the D antigen on
positive blood cells as a foreign substance

72. & produces antibodies
Patterns of Rhesus factor inheritance
MOTHER FATHER BABY
dd DD
(HOMOZYGOUS)
DD
dd Dd
(HETEROZYGOUS)
Dd,dd
dd dd dd

73. Causes
1. Fetomaternal haemorrhage - small amounts of
fetal Rh positive blood cross the placenta &
enter the Rh negative mother’s blood.
2. Any procedure or incident where +ve blood
leaks across the placenta
3. During any blood or platelet transfusion or
drug use

75. Prevention of RhD isoimmunization
Anti D Ig
● Administer Anti D Ig within 72 hrs of birth
● Anti D Ig is a human plasma based product
that is used to prevent women producing anti
D antibodies.
● It is not used when anti D antibodies are
already present in the maternal blood

76. ● It does not protect against the development of
other antibodies that cause haemolytic
disease of the newborn
Antenatal Prophylaxis Following Sensitizing
Events
● Anti D Ig should be administered within 72 hrs
of birth to all non sensitized Rh -ve mother inn
the following cases:

77. 1. Spontaneous miscarriage before 12 weeks
requiring Sx intervention
2. Any threatened,complete,incomplete or
missed abortion after 12 weeks of pregnancy
3. Termination of pregnancy by surgical or
medical methods regardless of gestational age
4. Ectopic pregnancy
5. Amniocentesis,cordocentesis,chorionic villi
sampling,fetal blood sampling or other
invasive intrauterine procedure such as

78. shunt insertion
● ECV
● Fetal death in utero or stillbirth
● Abdominal trauma or antepartum
haemorrhage
● Transfusion of Rh +ve blood or platelets or
drug use

79. Administration of Anti D Ig
● ABO grouping & Rh type, Rh -ve mother are
screened or Rh antibodies test (indirect
Coomb test). A negative test shows absence
of antibodies or sensitization
● Blood is retested at 28 weeks of pregnancy,if
antenatal prophylaxis is routine, the first dose
of anti D Ig is given
● Blood is retested at 34 weeks of GA, where

80. antenatal prophylaxis is not in place
● When anti D Ig prophylaxis is given at 28
weeks of GA,blood is not retested at 34 weeks
of GA as it is difficult to distinguish passive
anti D Ig from immune anti D.
● 2nd routine dose is given at 34 weeks of GA
● Following the birth cord blood is taken for the
confirmation of Rh type ,ABO
grouping,Hb,serum bilirubin & presence of

81. maternal antibodies
● A Kleihauer acid elution test is carried out on
an anticoagulated maternal blood sample
within 2 hrs of time to detect fetal Hb &
estimates the no. of fetal cells in a sample of
blood
● Anti D Ig is given into the deltoid
muscle,where absorption is optimal.

82. Dose of Anti D Ig
● IM dose of 500 IU of anti D Ig will suppress the
immunization that could occur following a
FMH of 4-5 ml of RhD positive red cells.
● 500 IU of anti D Ig at 28 & 34 weeks of GA for
women in their first pregnancy
● 250 IU following sensitizing events up to 20
weeks gestation.

83. Effects of RhD isoimmunization
● Anaemia
● Hypoxia
● Edema
● CCF
● Increased bilirubin levels in brain causes
neurological damage
● Haemolytic anaemia leads to hydrops fetalis &
death

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tftyyf
● Babies are pale, have
edema & ascites & may
be stillborn

86. Postnatal Rx of Isoimmunization
1. Prevent further haemolysis
2. Reduce bilirubin levels
3. Remove maternal RhD antibodies from the
baby’s circulation
4. Combat anaemia

87. ABO INCOMPATIBILITY
● Occurs when mother’s blood group is O & the
baby is group A or less often group B

88. Physical Assessment of a Baby with Jaundice
● Extent of changes in skin & scleral colour
● Head to toe progression of jaundice
● Lethargy & decreased eagerness to feed
● Dark urine or light stools
● Dehydration,starvation,hypothermia,acidosis
or hypoxia
● Vomiting,irritability or high pitched cry

89. Rx Modalities
PHOTOTHERAPY
1

90. ● Phototherapy or Light therapy is referred to as
Heliotherapy, where patient is exposed to
daylight or to a specific wavelength of light
using polychromatic polarised
light,fluorescent lamps,light emitting diodes &
fibreoptic mattresses.
● Phototherapy converts fat soluble
unconjugated bilirubin into water soluble
bilirubin & decreases the likelihood of
neurotoxicity or kernicterus

91. INDICATIONS FOR PHOTOTHERAPY
● For preterm infants <1500 g - between 85 &
140 micromol/L (5&8 mg/dL)
● For preterm infants >1500 g, sick infants &
those with haemolysis -

92. Between 140&165 micromol/L (8&10mg/dL)
● For healthy term infants jaundiced after 48hrs
- between 280 & 365 micromol/L (17 & 22
mg/dL)
TYPES OF PHOTOTHERAPY
1. Conventional phototherapy systems
Uses high intensity light from conventional
white & more recently blue,blue-green

93. & turquoise fluorescent lamps
2. Fibre optic light systems
These uses a woven fibre optic pad that delivers
high intensity light with no ultraviolet or infrared
radiation.
SIDE EFFECTS OF PHOTOTHERAPY
Side effects of conventional white & blue
fluorescent phototherapy are ;

94. ● Hyperthermia,increased fluid loss &
dehydration
● Damage to the retina from the high intensity
light
● Lethargy or irritability,decreased eagerness to
feed,loose stools
● Skin rashes & skin burns
● Alterations in a baby’s state &
neurobehavioral organization

95. ● Isolation & lack of usual sensory
experiences,including visual deprivation
● A decrease in calcium level leading to
hypocalcemia
● Low platelet counts & increased red cell
osmotic fragility
● BRONZE BABY SYNDROME,riboflavin
deficiency & DNA damage

96. CARE OF BABY UNDER PHOTOTHERAPY
● TEMPERATURE - maintain warm
thermoneutral environment,monitor for
hypo/hyperthermia
● EYES - eye shields or patches must cover the
eyes without occluding the nose,& not be too
tight or cause eye discharge or weeping
● SKIN - skin is cleaned with warm water &
observed for rashes,dryness & excoriation

97. ● HYDRATION- monitor I/O chart,demand
feeding is continued,extra fluids may require
for ill & dehydrated babies
● NEUROBEHAVIOURAL STATUS- includes
sleep & wake status,feeding
behaviours,responsiveness,response to
stress & interaction with parents & other
carers
● CALCIUM LEVELS- monitor for
hypocalcemia(7 mg/dL or <1.7 micromol/L

98. ● BILIRUBIN LEVELS - reducrd bilirubin level
appesrsto be greatest in the first 24hrs of
phototherapy
● PARENT SUPPORT

99. EXCHANGE TRANSFUSION
2

100. ● Assisting in withdrawing baby’s blood,which
contains high bilirubin & replacing with fresh
blood through umbilical vein.
● With HDN, sensitized erythrocytes are
replaced with blood compatible with both the
mother’s & the infant’s serum
● Helps to increase Hb level

101. ● Done for babies with:
1. 255 micromol/L(15 mg/dL) for preterm babies,
<1500 g
2. 300-400 micromol/L(17-23 mg/dL) for sick &
pre term babies > 1500 g, & with haemolysis
3. 400-500 micromol/L (23-29 mg/dL) for healthy
term babies

103. DRUG Rx
● Metalloporphyrins to
reduce the level of
unconjugated bilirubin
3

104. BIRTH INJURIES

105. Trauma during birth includes:
Trauma to skin &
superficial
tissues
Muscle
trauma
Nerve trauma Fractures

106. TRAUMA TO SKIN & SUPERFICIAL TISSUES
1. Skin - scalp abrasions,bruising or superficial
fat necrosis,puncture wound,lacerations
resulting from forceps blades, vacuum
extractor cups,scalp electrodes & scalpels
2. Superficial tissues - includes oedematous
swelling or bruising. Caput succedaneum is
the diffuse oedematous swelling under the
scalp & above the periosteum.

107. ● In face presentation,
cervical os may restrict
venous return & becomes
congested & causes bruising
of eyes & edematous lips
● In breech - bruised & edematous genitalia &
buttocks

108. MUSCLE TRAUMA
Injuries to muscle result from tearing or when the
blood supply is disrupted.
1. TORTICOLLIS
● The most commonly damaged muscle is the
sternocleidomastoid muscles
● Excessive traction or twisting causing tearing
to these muscles can occur during birth of the
anterior shoulder of a fetus with a cephalic

109. presentation or during rotation of the shoulders
when the fetus is being born by vaginal breech
or C section
● 1-3 cm, apparently painless,hard lump of
blood & fibrous tissue is felt on the affected
muscle,the muscle length is
shortened,therefore the neck is twisted to the
affected side; a torticollis or wry neck.
● Mx - passive muscle stretching exercise

111. NERVE TRAUMA
1. FACIAL NERVE
● On the affected side,has no nasolabial fold
● The eyelid remain open
● Mouth is drawn over to the unaffected side
● Excessive drooling
● Difficulty in feeding & swallowing
● Rx : if the eye is opened ,regular instillation of
methyl cellulose eye drops which can

112. lubricate the eyeball
● Cosmetic Sx interventions can be done

113. 2. Brachial plexus

114. ● Nerve roots exiting from the spine at the fifth
to eight cervical & the first thoracic vertebrae
form a matrix of nerves in the neck &
shoulder.
● Brachial plexus trauma results from excessive
laceration,rotation or traction of the head &
neck during vaginal breech birth or when
shoulder dystocia occurs.
● There are three main injuries;Erb’s
palsy,Klumpke’s palsy & total brachial plexus

115. ERB’S PALSY
● Paralysis of shoulder & the arm (not the
hands) due to damage of 5th & 6th cranial
nerves
● Baby’s affected arm is inwardly rotated,the
elbow extended,the wrist pronated & flexed &
the hand partially closed ( the waiter’s tip
position)
● Baby’s hand is limp

117. KLUMPKE’S PALSY
● The shoulder & upper arm are unaffected
● Lower arm,wrist & hand are paralyzed resulting
in wrist drop & no gasp reflex
● Occurs due to damage to the lower brachial
plexus involving the 7th & 8th cervical & 1st
thoracic nerve roots.

119. Total brachial plexus palsy
● There is complete paralysis of shoulder,arm &
hand,lack of sensation & circulatory problems
due to damage of all brachial plexus nerve
roots
INVESTIGATIONS
● X-ray
● US,MRI

120. FRACTURES
1. Clavicular # - occurs with shoulder
dystocia,vaginal breech birth or a macrosomic
baby
2. Humerus # - midshaft # occur with shoulder
dystocia,vaginal breech birth
3. Femur # - midshaft # due to vaginal breech
birth
4. Skull #

121. HAEMORRHAGE
● Blood volume in term baby = 80-100 ml/kg
● For a preterm = 90-105 ml/kg
● Haemorrhage can be due to :
1. Trauma
2. Disruptions in blood flow
Or can be due to related to:
1. Coagulopathies 2. Other causes

122. Haemorrhage due to trauma
1. Cephalhematoma
2. Subaponeurotic haemorrhage
3. Subdural haemorrhage
Haemorrhage due to disruptions in blood flow
1. Subarachnoid haemorrhage
2. Germinal matrix/intraventricular haemorrhage
& intraparenchymal lesions

123. Haemorrhage related to coagulopathies
1. Vitamin K deficiency bleeding (VKDB)
● This occur up to 12 months of age
● Commonly occurs between birth & 8 weeks of
life
● Forms of VKDB :
a) EARLY (0-24 hrs)
b) CLASSICAL (1-7 days)

124. c) LATE (1-12 months, although the peak onset
is before 8 weeks)
2. Thrombocytopenia
● Platelet count <1,50,000/ microlitre
● Severe thrombocytopenia <50,000/microlitre
● Babies at risk are :
a) A severe congenital or acquired infection ( eg:
syphilis,cytomegalovirus,rubella,toxoplasmosi
s,bacterial infection)

125. b) isoimmune thrombocytopenia
c) inherited thrombocytopenia
Or whose mother :
● Has idiopathic thrombocytopenia,purpura,SLE
or thyrotoxicosis
● Takes thiazide diuretics
3. Disseminated intravascular coagulation

126. Haemorrhage related to other causes
1. Umbilical haemorrhage
2. Vaginal bleeding
3. Haematemesis & melaena
4. Haematuria
5. Bleeding associated with IV access

127. CONVULSIONS

128. ● A convulsion is a sign of neurological
disturbance not a disease & its a medical
emergency
● Convulsive movements tend to be slower,less
equal,are not necessarily stimulated by
disturbance, cannot be stopped by restraint &
are always pathological

129. CAUSES OF CONVULSIONS IN NEWBORN ARE :
CATEGORY SELECTED CAUSES
CNS Intracranial haemorrhage,intracerebral
haemorrhage,hypoxic-ischemic
encephalopathy,kernicterus,congenital abnormalities
Metabolic Acquired disorders of metabolism,hypo &
hyperglycaemia,hypo & hypercalcaemia,hypo &
hypernatraemia,inborn errors of metabolism
Other Hypoxia,congenital infections,severe postnatally acquired
infections,neonatal abstinence syndrome,hyperthermia
Idiopathic unknown

130. TYPES ARE :
1. Subtle convulsions
2. Focal tonic convulsions
3. Clonic convulsions
4. Myoclonic convulsions

131. Treatment
● Clear airway
● Provide adequate ventilation
● Semi prone position,with the head in neutral
position
● Suctioning
● Administer O2 if required
● Active resuscitation
● Temperature regulation

132. ● Drug therapy - phenobarbitone &
phenytoin,topiramate,levetiracetam

133. CONGENITAL
MALFORMATIONS

134. ● A congenital abnormality is any defect in
form,structure or function
CAUSES OF CONGENITAL MALFORMATIONS
CHROMOSOMAL
ABNORMALITIES
SINGLE GENE
DEFECT
MITOCHONDRIAL
DNA DISORDERS
MULTIFACTORIAL
DISEASES
TERATOGENS

135. WHO IS AT RISK ??
● Women over 35 yrs
● Family history of neural tube defect or
previous history of NTD
● Previous child born with chromosomal
anomaly
● Parent carriers of sex linked or autosomal
traits
● History of recurrent abortion

136. DIAGNOSIS
● US
● Clinical evaluation at birth
● MRI
● Radiography

137. IMPERFORATED ANUS
● A condition in which partial or complete
obstruction of the anus,discovered at birth
due to failure of the anus to develop normally
in the embryo.
● More prevalent in males
● TYPES:
1. High imperforated anus : it is a condition
where rectum ends above the puborectalis

138. Sling.can be associated with rectourinary fistula
in males or recto vaginal fistula in females
2. Low imperforated anus : it is a condition
where rectum has transversed the rectalis sling
DIAGNOSIS
● Absence of meconium passage
● Failure to pass a rubber catheter
● Radiology to detect atresia

139. MANAGEMENT
● Perineal anoplasty
● Colostomy for high imperforated anus
MECONIUM ILEUS
● It is a manifestation of fibrocystic disease of
the pancreas.

140. Pathophysiology
Deficiency of pancreatic enzyme
Causes meconium in the intestine inspissated
This obstructs the lumen of lower ileum

141. DIAGNOSIS
● Obstruction of small gut
● Sweat test
● X ray
● Rectal mucosal biopsy to exclude
Hirschsprung’s disease

142. MANAGEMENT
● Transaction of gut containing inspissated
meconium
● anastomosis

143. FETAL ALCOHOL SYNDROME
● IUGR
● A growth restricted infant with
microcephaly,flat facies,close-set
eyes,epicanthic folds,small upturned nose,thin
upper lip & low set ears
● Child can have learning difficulties
● Experiences acute withdrawal symptoms

144. Mx :
● Supportive therapy
● Counselling for the mother

145. FEEDING OF HIGH RISK
NEONATE

146. ● EARLY FEEDING - initiate breastfeeding within
half an hour after birth
● BREASTFEEDING - exclusive breastfeeding
● CUP/ KATORI/PALADAI FEEDING
● NASO/ ORAL GASTRIC TUBE FEEDING
● FORMULA FEEDING(complementary
feeding/top-ups)
● SUPPLEMENTARY FEEDING

147. PALADAI/KATORI FEEDING

148. INFECTION CONTROL IN NICU