REPRODUCTIVE MODULE

Paediatrics

Academic Circle
MFSU Ragama
REPRO-PEAD
 contents
1.Respiratory distress in neonate.
2.Birth asphyxia
3.Neonatal resuscitation
4.Neonal infection
5.Neonatal sepsis
6.Neonatal seizure
7.Preterm Laboure and prematurity
8.Rh isoimmunization
9.Neonatal jaundice
10.Pubertal abnormalities
11.Breast feeding
12.Complementary feeding
13.Immediatw care of the newborn
14.Transpotation of the sick new born
15.Introdution to clinical genetics
16.Common congenital abnormalities
17.Small for gestational age and intrauterine growth retardation
1.Respiratory distress in neonates
• Characterized by
• Tachypnoea (RR>60/min)
• Recessions
• Grunting (expiratory)
• Cyanosis

• Causes
1. Surfactant deficient lung disease (Respiratory distress syndrome)
2. Transient tachypnea of the newborn
3. Congenital pneumonia
4. Meconium aspiration syndrome
5. Pneumothorax
6. Congenital diaphragmatic hernia

Surfactant Deficient Lung Disease

• Primarily in premature infants.

Risk Factors Protective factors (Risk Reducing factors)

1. Prematurity 1.Maternal PIH/ hypertension
2. Maternal diabetes 2.Maternal heroin use
3. Birth asphyxia 3.Maternal heroin use
4. LSCS 4.Antenatal steroid prophylaxis
5. Multiple births
6. Precipitous delivery

Clinical features
• Respiratory distress – within minutes of birth
• If untreated
• Gradual worsening – peak 3 days
• Respiratory failure – hypoxia and hypercapnia
• Mixed respiratory and metabolic acidosis

Diagnose
• Mainly clinical
• Confirmatory by chest X-Ray (4hrs after birth)
Pathogenesis

Lesser Severe Severe

Homogenous bilateral opacities No cardiac margins
Ground glass appearance
Management (Aim – PaO2 around 50-70; SpO2 between 91%-95%)

• Thermoneutral environment- incubator

• Respiratory support
• Continuous positive airway pressure (CPAP)
• Non-invasive / invasive ventilation
• Surfactant replacement
• Intra-tracheal (if intubation is necessary)
• 4mL/kg
• Other measures
• Fluid management
• Nutrition
• Inotropes
• Antibiotics

Complications
• ET tube complications (tube block, Accidental removal)
• Pneumothorax (Due to high pressure)
• Patent ductus arteriosus (Hypoxia)
• Chronic lung disease / bronchopulmonary dysplasia
• Requirement of >21% O2 for over 28 days

Prevention
• Antenatal steroids
• Dexamethasone/betamethasone
• 2 doses
• All mothers who are threatened to deliver before 34 weeks of gestation
• Also decreases the incidence of Intraventricular haemorrhages, Necrotizing
encephalitis and neurodevelopmental impairment
 Transient tachypnoea Congenital pneumonia Meconium aspiration syndrome Pneumothorax

Pathogenesis secondary to slow absorption of Suspect in every newborn with Airway obstruction
fetal lung fluid, resulting in respiratory distress Chemical pneumonitis
decreased pulmonary Aetiology – same as for Causes- Hypoxia
compliance neonatal sepsis Hypercapnia
(eg: Group B streptococcus) Acidosis
Risk factors Term PROM In term and post-term infants
Following LSCS Chorioamnionitis
Clinical Respiratory distress soon after Features of respiratory distress Respiratory distress - soon after Sudden/gradual onset
features birth (onset variable) – gradually birth In the affected side
tachypnea worsening Over-distension of chest Reduced chest
expiratory grunting Other non-specific features of Pneumothorax, movements
recessions (mild) sepsis pneumomediastinum Hyperresonance
Chest auscultation – normal Poor feeding, lethargy, Persistent pulmonary Diminished/ absent breath
SpO2 and blood gas – mild irritability, unwell hypertension sounds
hypoxia/NL Auscultation – difficult to Mediastinal deviation
appreciate Transillumination
CXR prominent pulmonary vascular New infiltrates/opacities,
markings effusions
fluid in the intralobar fissures
Management Supportive- Thermoneutral environment At delivery Asymptomatic-
Thermoneutral enviornment Antibiotics Routine newborn care or Observation
Oxygen (low oxygen Penicillin/ampicillin + neonatal resuscitation 100% oxygen (in term
requirement <40%) Gentamicin / cefotaxime Respiratory supportive care babies)
iv fluids Supplemental O2
Antibiotics – until the possibility Respiratory support (oxygen, Assisted ventilation Severe/symptomatic-
of sepsis/pneumonia excluded CPAP, non-invasive or invasive Extracorporeal membrane Needle thoracocentisis
Resolves within 1-3 days ventilation) oxygenation (ECMO) and Intercostal tube
Fluids (iv/oral) Sedation - Morphine or Fentanyl
Surfactant- in severe disease
Pulmonary vasodilators
Circulatory support – inotropes
Antibiotics
Congenital Diaphragmatic Hernia

• Herniation of abdominal contents through a defect in the diaphragm

• Associated with pulmonary hypoplasia – major determinant of outcome
• Defect can be
• Posterolateral – Bochdalek
(90%)
• 80-90% in the left side
• Retrosternal – Morgagni
• Paraoesophageal
• Hiatal

Clinical presentation
• Antenatal
• Ultrasound scan between 16-24 weeks
• Postnatal
• Respiratory distress (onset variable)
• Scaphoid abdomen
• Displaced apex beat
• Diminished breath sounds
• Bowel sounds in chest

Management
• Aggressive respiratory support
• Immediate intubation (avoid bag and mask ventilation)
• Ventilation – SIMV, HFOV, ECMO
Other causes
• Cyanotic congenital heart disease
• Persistent pulmonary hypertension of newborn
• Congenital malformations of the lungs
• Pulmonary hemorrhage

Congenital heart disease

• Some are diagnosed antenatally
• Postnatal presentations
• Cyanosis – cyanotic CHD
• Respiratory distress – TAPVD, left ventricular outflow tract obstruction
• Hyperoxia test
• Check PaO2 in the right radial artery before and after 100 percent oxygen for 10
min.
• Rise in PaO2 to a level >150 mmHg suggests pulmonary disease

Persistent Pulmonary Hypertension of Newborn (MCQ)*

• Causes
• Meconium aspiration syndrome
• Congenital pneumonia
• SDLD
• Congenital diaphragmatic hernia
• Pulmonary hypoplasia
 2. Birth Asphyxia
Effect on the body which occurs as a result of hypoxia or inadequate oxygenated blood, ‘suffocation’ ,
lead to unconsciousness and death if left untreated

Foetal / neonatal Hypoxia Causes

Maternal factors Placental and umbilical cord

Foetal or neonatal factors
factors

1. Poor placental blood flow

1. Inadequate
2. Premature separation of
oxygenation of
the placenta 1. Anaemia
maternal blood
3. Placental insufficiency due 2. Heart disease
2. Low maternal
to other reasons eg: 3. Infections
blood pressure
infarction 4. Congenital
eg: sepsis
4. Cord : knots, prolapse, anomalies
3. Maternal
compression, etc
vascular disease
Hypoxic ischaemic encephalopathy:
Hypoxia induced brain damage which occurs during perinatal period
• About 30 – 50 % babies are left with permanent neurodisability
(Cerebral palsy, low IQ, learning disability)
• One of the best predictors of mortality is foetal PH (<6.7)
• Multi-organ failure is the final pathway causing death

International Classification of Diseases (ICD)– 10

Severe birth asphyxia (White asphyxia) Mild and moderate birth asphyxia (Blue
asphyxia)

Pulse < 100 / min at birth and falling or steady heart rate ≥100/min
respiration absent or gasping Normal respiration not established within one
minute
colour poor some response to stimulation
tone absent some muscle tone present
Asphyxia with 1-minute Apgar score 0-3 Asphyxia with 1-minute Apgar score 4-7

Pathogenesis

• Hypoxia -> anaerobic metabolism -> increased lactate and inorganic phosphate -> accumulation
of excitatory and toxic metabolites eg: glutamate damages tissue -> overactivation of NMDA,
AMPA & kainite receptors
• This overactivation increases the cellular permeability to Na and Ca
• Intracellular accumulation of Ca and Na causes cytotoxic oedema and neuronal death, apoptic
cell death
• Increased free radicals and NO in these tissues
• Prolonged hypoxia -> affect periventricular white matter -> Periventricular leucomalacia
Clinical features
Seizures : hypoxia, brain damage already happened, electrolyte abnormalities, structural, vascular
events , genetic disorders

Differential diagnosis
• Non-ketotic hyperglycaemia
• Vitamin dependent epilepsies
• Channelopathies
• Congenital myopathies
• Congenital myotonic dystrophy, Spinal muscular atrophy

Other organ involvement (MCQ)*

• Depends on the affected organ and the severity of the injury

• Circulation is shifted in a way to prioritize the blood flow to the brain, heart and
adrenals in compromise of perfusion to the other organs , so organ injury may be
evident in these organs
• Congestion, fluid leak from increased capillary permeability, endothelial cell swelling ->
coagulation necrosis and cell death
• Congestion and petechiae in multiple organs
• Hypoxia -> pulmonary arteriole smooth muscle hyperplasia -> pulmonary hypertension
• Hypoxia -> gasping -> aspiration of meconium : pneumonia, pulmonary hypertension,
pneumothorax
Investigations
• MRI brain
• CT brain – to help finding complications
• USS brain
• EEG
• Other organ functions : FBC, liver functions , renal functions

Management
• Effective resuscitation and stabilization
• Ventilatory support – neuroprotective
• Circulatory support to avoid hypotension
• Fluid restriction provided no hypotension
• Control seizures: Phenobarbitone , Levatiracetam
• Maintain normal glucose and electrolytes
• Support coagulation
• Assess & monitor other organ function

• Therapeutic cooling
Head cooling / whole body cooling
While core-temperature is controlled
Minimise secondary neuronal injury
Should avoid overcooling and cold injury syndrome

• Developmental care

Outcome
• Foetal demise
• Neonatal death
• Neurological disability
• Epilepsy
• Behavioural disorders
• Near normal or complete recovery
3. NEONATAL RESUSCITATION

Physiologic changes occur at birth

• Intrauterine life-nutrition and oxygen is through the placenta
• Placenta- less effective respirator membrane compared to lungs, therefore fetal
haemoglobin has higher affinity for oxygen and fetus has higher haemoglobin level.
• Lungs – not aerated during intrauterine life and filled with amniotic fluid, therefore
pulmonary vascular resistance is high
• At delivery- umbilical cord is clamped and arterial oxygen level goes down and carbon
dioxide level goes up. This stimulates respiratory center to initiate breathing and baby
starts cry.
• At birth- Have 30ml/kg lung fluid. Certain proportion absorbed through birth process
• First few breaths- create a higher negative pressure (>100cm H2O) ,the fluid in the
alveolar get absorbed to the lymphatics and allow the alveolar to expand
• With aeration of lungs- oxygenation of pulmonary arterial blood begins. High oxygen
and low carbon dioxide in pulmonary circulation causes vasodilatation. Vasodilatation
in the pulmonary circulation results in drop of pulmonary arterial pressure
• This event causes reversal of blood flow in the ductus arteriosus and results closure of
ductus arteriosus
• Stimuli for the first breath - Cord obstruction, Cold air & Physical discomfort

Primary apnoea
• If baby is still inside the uterus or delivered but airway is obstructed, no air will enter the
lungs to establish gas exchange
• This will further aggravate hypoxia, hypercarbia, and acidosis
• After a while the respiratory centre will be temporally malfunction due to deteriorating
blood gases and stop firing
• Thus, baby will stop breathing
• This is called primary apnoea
 • Due to myocardial suppression stroke volume is reduced
• To compensate, heart rate increases initially to maintain cardiac output, but latter will
start to drop
• Blood pressure will be reasonably maintained
• But blood gases will continue to deteriorate

Gasping
• After been in primary apnoea for while, baby will start to breathe again
• This respiration is initiated from spinal cord, not brain stem
• These movements are irregular, jerky, and forceful
• If by this time the airway is patent air will enter lungs and breathing will be established

Secondary apnoea / Terminal apnoea

• If gasping fails to bring in air to establish gas exchange, deteriorating blood gases will
stop functioning of spinal centres as well
• And baby will stop breathing again. This is called terminal apnoea
• During this period heart rate drops and cardiac output reduces significantly, resulting in
low BP
• Blood gases continue to deteriorate and with each second in terminal apnoea the risk of
permanent brain damage increases
• Without intervention baby will die within next couple of minutes
 Primary apnoea Secondary apnoea

Breathing Starts quickly with Poor response to

stimulation stimulation

Heart rate Around 60/minute Below 60/minute

Blood pressure Normal Low

Colour Blue Mottled and pale

Tone Mildly reduced Floppy

➢ A baby in primary apnoea can be stimulated to breath by tactile stimulation, but not a
baby in terminal apnoea
➢ The only way to save a baby in terminal apnoea is to establish artificial ventilation

Preparation for resuscitation

• Arrive at the place of delivery at least 5 minutes before delivery
• Introduce your self to staff and the mother ( if not yet anaesthetized)
• Wash your hands
• Check all equipment required for resuscitation
• Check availability of medication required for resuscitation
• Go through the patient record for any relevant information
• Make changes to the surroundings, to minimize hypothermia in the baby
➢ Resuscitation should ideally take place in a warm, well-lit area with a flat resuscitation surface placed
below a radiant heater together with other resuscitation equipment being immediately available.
➢ All equipment must be checked frequently and a record of this maintained

Initiation of resuscitation
• Keep the baby under a radiant warmer or 100W electric bulb. Give special attention to the head as it is
relatively large and a major part of heat loss can occur through it.
• In most instances the baby will cry soon after birth and will need no resuscitation
• Irrespective of the condition of the baby the first step is to wipe the baby of all fluid with
one warm towel and cover the baby with the second warm towel.
• If the baby is crying wrap and hand over the baby to mother.
• Babies who are not breathing after drying needs assessment and immediate action.
 • A more practical assessment which is recommended for use during resuscitation is
denoted by the abbreviation ‘CTBH’ (colour, tone, breathing and heart rate).
• After CTBH assessment if the baby is not crying do tactile stimulation

CTBH Assessment
➢ Colour – pink, pale or cyanosed
➢ Tone – good tone, some tone or floppy
➢ Breathing – good cry, some cry or no cry
➢ Heart rate - >100 bpm, <100 bpm or no heartbeat
❖ If baby is centrally pink, good muscle tone, crying vigorously with a heart rate >100 he is in
good condition
❖ Do a quick head to toe examination for gross abnormalities
❖ If everything if fine hand over the baby to the mother for a cuddle and a feed
❖ No Oxygen or suctioning upper airway, in such babies

Getting alveoli expanded

• Alveoli are filled with fluid and never expanded before
• Initials breaths will allow fluid to get absorbed to blood and lymphatics
• After that alveoli will expand
• Alveoli are like balloons which need higher pressure for inflation initially
• Therefore special method is used to ventilate apnoeic babies at birth
• This is called inflation breaths

Airway positioning

1. Head tilt & chin lift / Neutral position

• Airway can be opened by lifting the chin until face
becomes parallel to the surface on which the baby
is lying.
• This is called the neutral position of the head
• In a baby with poor tone it will also be necessary to
support the chin using a finger on the bony part of
the chin near the tip, in order to maintain neutral
position

2. Jaw thrust
• Push the jaw up and the tongue with it
• Any pressure on the soft tissues under
the jaw should be avoided as it may
worsen the situation by pushing the
tongue base backwards.
• If the baby is very floppy it may be
necessary to use one or two fingers under each side of the lower jaw, at the angle of the
jaw, to push the jaw forwards and outwards

Breathing
• You need a method of supplying positive pressure ventilation
➢ Self inflation bag – Mask- Valve system
➢ Neo-puff
➢ Via endotracheal tube (used if diaphragmatic hernia is suspected- not routinely
employed to provide inflation breaths)

Selecting the mask

• You should be ready with different sizes of

masks
• Correct size is the one that covers both
nostrils and mouth, but not go beyond the
chin below and infra-orbital ridge below
• Idea is to have a tight seal between the mask
and the face
• If not air will leak and if goes over eyes can
damage eyes due to pressure

Holding the mask (C & E method)

• Hold the mask by the firm neck, not the rim

 • Press down firmly on the face for tight fit
• Use thumb and index finger like ‘C’ to hold the
mask and use the middle finger to extend the
neck up to neutral position

Inflation breaths
• The main difference is when providing these breaths you provide a higher pressure for
longer duration (2-3 seconds)
• Here you count as 1-2-3 release, 2-2-3 release, 3- 2-3 release 4- 2-3 release, 5- 2-3 release
• Thus you give altogether 5 inflation breaths
• Counting is to keep track on duration of inspiration and expiration
• Release is for expiration
• Remember expiration is as important as inspiration
• If you don’t allow time for expiration air will build up inside alveoli and cause
pneumothorax

Ventilatory breaths
• These are given to provide ventilation to an expanded alveoli
• The rhythm here goes as squeeze one, squeeze two ……
• Squeeze is for inspiration and number for expiration
• Advantage is this will automatically indicate the number of breaths given
• 30 breaths per minute

External chest compressions

• Goal of chest compressions is to mimic normal systole and diastole of the heart
• Compression of the chest wall will compress the ventricles causing blood to be pumped out
of ventricles
• Relaxation will allow filling of ventricles as in diastole
• Idea of chest compressions during neonatal resuscitation is to provide the myocardium
with oxygenated blood
• Oxygen will bump start a heart that has stopped to contract temporally
• Therefore it is mandatory that ventilation is established before commencing chest
compressions

Technique of External Chest Compressions

• Technique of chest compressions vary with age
• In neonates it is totally different from adults
• This is due to anatomical’ physiological variations in chest wall and heart
• There are two techniques of chest compressions in neonates – two finger method and
encircling method - But principals are same in both
• Location is at inter-nipple line in midline
• Force applied is to compress 1/3 of chest wall
• Sequence is 3 chest compressions to one breath, to achieve 90 compressions and 30
breaths/min
a. Encircling method
➢ Need both hands to encircle the thorax
➢ Fingers at the back and thumbs in front
➢ Thumbs slightly angulated upwards to meet each
other at the centre
➢ This is the preferred method as it is more effective
and less likely to cause injury to chest wall
➢ But not possible if only one person is resuscitating,
short fingers or if other procedure like umbilical
catheterization is in progress

b. Two finger method

➢ If encircling method is not possible this method is
used
➢ Place your middle and index fingers over sternum
at inter-nipple line and apply compressions as in
encircling method
➢ In both methods make sure you relax the chest wall
at the time when ventilation given
➢ Otherwise, Air entry will be compromised by
external pressure
After chest compressions
• After one cycle reassess CTBH
• If baby is responding proceed according to the situation
• If not responding, baby must have been in longer duration in terminal apnea
• Now is the time for drugs

Drugs usage in resuscitation

• Drugs used in neonatal resuscitation should be administered through an umbilical catheter
• Drugs given through a peripheral line will not reach the heart
• Direct injection drugs in to umbilical vein is not effective as there is no circulation through
umbilical vessels after cord is clamped and is dangerous as they might enter umbilical
artery

Drugs used in resuscitation

• Adrenalin 1: 10,000 – 0.1 ml/kg
• 4.2% Sodium bicarbonate – 2 - 3 ml/kg
• Normal Saline
• 10% dextrose
• Note – Naloxone is not needed for resuscitation, but is needed to reverse pethidine
induced respiratory suppression
• Atropine and steroids have no place

Adrenalin
• First drug to use is 0.1 ml/kg, of 1:10,000 adrenalin via umbilical catheter
• Follow this with a 1 ml of normal saline push, so that adrenalin will reach the circulation
• Adrenalin is available as 1 : 1000 Preparation
• To make 1:10,000 use 10 ml syringe. Take 1ml of adrenaline and draw 9ml of 0.9% NaCl
(normal saline) and mix = 1:10,000
• Draw 1ml of this solution to a 1ml syringe & label it
• Dose through endo tracheal tube (ETT) 1ml/kg of 1: 10,000 0.1ml/kg of 1: 1000
• Role of adrenaline
➢ Adrenalin has positive chronotropic, inotropic, dromotropic and bathmotropic action
via beta receptors in the heart
➢ But most important effect of adrenalin during resuscitation is peripheral
vasoconstriction leading to increased diastolic pressure
 ➢ Myocardial perfusion occurs mainly during diastole
➢ Therefore main action of adrenalin during resuscitation is improving myocardial
oxygenation

After adrenalin
• Continue another cycle and reassess CTBH
• If still no response try 4.2% bolus dose of 2- 3 ml/kg sodium bicarbonate
• What we have in the ward is 8.4%, dilute it with 5% dextrose equal volume
• Rationale for bicarbonate is that, adrenalin binding to its receptors is inhibited by acidosis
• However in some countries it is used only at very late stage of resuscitation

After that
• If child is still responding give a second dose of adrenalin and continue CPR
• You can repeat adrenalin if required

When to stop
• You can stop resuscitation after 10 minutes of any sign of life observed in the baby
• Inform the most senior member before discontinuing resuscitation

Record keeping
• This is a very important aspect
• Make a note that “ notes are written in retrospect” and note down the entire procedure
that was carried out
• Make sure you put down the date and time
• Print your name at the end of the notes with your designation and initial it

Post resuscitation care

• If you managed to resuscitate the baby you got to decide where to manage him
• For a baby who needed only inflation breaths postnatal ward is adequate with little bit of
additional observation
• But any baby needing chest compressions and above need to go to a NICU or a SCBU, as
there can be complication during next 24 – 48 hours
• Birth asphyxia is a multisystem disorder, where each an every system having problems

SEQ26th proper Question no 1

 4.Neonatal infections

• Neonatal infections are the infections occur in the newborn during the neonatal period (the first
28 days of life)
• Up to 10% of infants have infections in the 1st month of life.
• Newborn infection is more common in areas with limited access to healthcare than in areas
with well-established healthcare infrastructure

Factors influencing the balance between health and disease in neonates

exposed to a potential pathogen

Neonatal infections classified by their timing relative to birth,

• Early-onset infection
• Occurs in the 1st week of life
• Organisms acquired during the perinatal period
• ( In most cases, the fetus or neonate is not exposed to potentially pathogenic bacteria until the
membranes rupture and the infant passes through the birth canal and/or enters the
extrauterine environment)
• Ways of acquiring Early onset infections: During passage through birth canal, Resuscitation at
birth, endotracheal intubation, Insertion of an umbilical vessel catheter

• Late-onset infection
Occurs between 7 and 30 days of life
Include bacteria, viruses, or other organisms that are typically acquired in the
postnatal period.

Ways of acquiring late onset infections:

Hand contamination of healthcare personnel (The most common source)
Hematogenous dissemination (Most cases of meningitis)
Contiguous spread (contamination of open neural tube defects, congenital sinus tracts, or
penetrating wounds from fetal scalp sampling)

Pathways of ascending or intrapartum infection

Ascending or intrapartum infection

 Chorioamnionitis
o Results from microbial invasion of amniotic fluid
o Often as a result of prolonged rupture of the chorioamniotic
membrane
o At 18 hr of membrane rupture, the incidence of early-onset disease
with group B streptococcus (GBS) increases significantly
▪ 18 hr is the appropriate cutoff for increased risk of neonatal
infection

Organisms causing Neonatal Infection

1. Bacteria (mneonic -My urea GEL)
• Group B streptococcus
• Escherichia coli
• Listeria monocytogenes
• Mycoplasma hominis
• Ureaplasma urealyticum

2. VIRUSES (mnemonic- PACE TORCH)

• Adenovirus
• Cytomegalovirus (CMV)
• Enteroviruses
• Hepatitis B and C viruses
• Herpes simplex virus (HSV)
• Human immunodeficiency virus (HIV)
• Parvovirus
• Rubella virus
• Varicella-zoster virus (VZV)

3. Fungi
• Candida spp.
• Malassezia spp.
Relative importance of neonatal viral infections related to the timing of acquisition of infection.

Neonatal sepsis
The overall incidence of neonatal sepsis ranges from 1 to 5 cases per 1,000 live births
Attack rates of neonatal sepsis increase significantly in LBW infants in the presence of
- maternal chorioamnionitis
- congenital immune defects
- mutations of genes involved in the innate immune system,
- asplenia
- galactosemia (E. coli)
- malformations leading to high inocula of bacteria
Eg: obstructive uropathy

The neonate is at risk for sepsis caused by pathogens that are uncommon in older
children.
The organisms include
Group B streptococcus
Escherichia coli
Listeria monocytogenes

Neonatal meningitis

• Bacterial meningitis is more common in the first month of life than at any other
time.
• An estimated 5-10% of neonates with early onset group B streptococcal (GBS)
sepsis have concurrent meningitis

Bacterial causes
• GBS
• E. coli
• L. monocytogenes
• S. pneumoniae
• other streptococci
• nontypable H. influenzae
• staphylococci (coagulase-positive and coagulase-negative)
• Klebsiella, Enterobacter,
• Pseudomonas
• Treponema pallidum
• Mycobacterium tuberculosis
Neonatal Pneumonia
• The progression of neonatal pneumonia can be variable.
• Fulminant infection is most frequently associated with pyogenic organisms such as GBS
• Onset may occur during the 1st hours or days of life, with the infant often manifesting
rapidly progressive circulatory collapse and respiratory failure.

Etiologic Agents - According to Timing of Acquisition

TRANSPLACENTAL
• Cytomegalovirus (CMV)
• Herpes simplex virus (HSV)
• Mycobacterium tuberculosis
• Rubella virus
• Treponema pallidum
• Varicella-zoster virus (VZV)
• Listeria monocytogenes

PERINATAL
• Anaerobic bacteria
• Chlamydia
• CMV
• Enteric bacteria
• Group B streptococci
• Haemophilus influenzae
• HSV
• Listeria monocytogenes
• Mycoplasma

POSTNATAL

• Adenovirus
• Candida spp
• Coagulase-negative staphylococci
• CMV
• Enteric bacteria
• Enteroviruses
• Influenza viruses A, B
• Parainfluenza
• Pseudomonas
• Respiratory syncytial virus (RSV)
• Staphylococcus aureus
• Mycobacterium tuberculosis

Conjunctivitis

• Relatively common
• Caused by a variety of organisms.
• Presentation includes periorbital swelling, conjunctival injection,
and purulent conjunctival drainage.
• Common causes
C. Trachomatis
Neisseria gonorrhoeae
• Pseudomonas aeruginosa
important pathogen in hospitalized VLBW infants
precursor to invasive disease

Skin and Soft Tissue Infections

• Include omphalitis, cellulitis, mastitis, and subcutaneous abscesses.

• Pustules, likely indicate the presence of staphylococcal infection but must be
distinguished from the vesicular rash of HSV infection.
• Staphylococcal pustulosis results in larger, pus-filled lesions 1 mm in diameter and
often scattered around the umbilicus

Skin and Soft Tissue Infections

• Ecthyma gangrenosum
infection with Pseudomonas spp.
 rare except in VLBW infants.
• Presence of small, salmon-pink papules
Suggests L. monocytogenes infection
• Mucocutaneous lesions
Suggest Candida spp.

Omphalitis
• The umbilical stump - colonized by bacteria from the maternal genital tract and the
environment.
• The necrotic tissue of the umbilical cord - excellent medium for bacterial growth.
• May remain a localized infection or spread to the abdominal wall, the peritoneum, the
umbilical or portal vessels, and the liver.
• Abdominal wall cellulitis or necrotizing fasciitis, with associated sepsis and a high
mortality rate, may develop in infants with omphalitis.
• Common pathogens
Staphylococcus aureus
Gram negatives

Tetanus
• Results from unclean delivery and unhygienic management of the umbilical cord in an
infant born to a mother who has not been immunized against tetanus.

• Typically occurs in infants 5-7 days after Birth

• Prevented by immunizing mothers before or during pregnancy and by ensuring a clean
delivery, sterile cutting of the umbilical cord and proper cord care after birth
 Neonatal Listeria
▪ Causative organism - Listeria monocytogenes (small, Gram-positive bacillus)
▪ Causes stillbirths, abortions, sepsis
▪ Transmitted vertically or horizontally, ascending or intrauterine placental infection
▪ Sources of Listeria include dairy products, cattle, sheep
▪ Newborn presents with sepsis, granulomatosis infantisepticum

Granulomatosis infantisepticum
• Intrauterine Listeria infection with a high fetal or neonatal mortality

• In the fetus the infection is generalized but is characterized by extensive focal necrosis
with a monocytic infiltration of the liver, spleen, and more rarely of the lungs and
intestines.

• There is associated meningitis in some cases

Laboratory Findings
• Signs of systemic infection in newborn infants may be unrevealing, so laboratory
investigation plays a particularly important role in diagnosis.

• Cultures and cell counts are obtained from blood and urine.

• CSF should be sent for Gram stain, routine culture, cell count with differential, and
protein/glucose concentrations.

• Surface swabs, blood, and CSF are often obtained for HSV testing.

• Except for culture and directed pathogen testing, no single laboratory test is completely
reliable for diagnosis of invasive infection in the newborn.

Limitations
• Even when laboratory tests are available, diagnostic tools to guide are limited.
• Traditional blood culture methods lack sensitivity, particularly in neonates where only
small samples can be obtained.
• This leads to a high number of negative results, leaving a large percentage of bacterial
infections microbiologically unconfirmed

• An immature-to-total phagocyte count (I/T ratio) (≥0.2) has the best sensitivity of the
neutrophil indices for predicting neonatal sepsis.

• After the newborn period, serum C-reactive protein (CRP) and procalcitonin have
demonstrated reasonable sensitivity and specificity for SBI.

• CRP may be monitored in newborn infants to assess response to therapy.

Antibiotic therapy

Antibiotic therapy
• An empirical regimen should be started after sampling for culture and ABST

• Definitive therapy is based on identification and susceptibility of the offending

organism.

• Duration of therapy depends on the organism and the site of infection.

In neonates with culture-proven sepsis, - Treat for 10 days.
Longer treatment courses may be warranted if a specific focus of infection is identified
(e.g., meningitis, osteomyelitis, septic arthritis).

• In neonatal sepsis - Antibiotics are chosen to cover the organisms typically causing
neonatal sepsis, including GBS, gram-negative organisms, Listeria, and Enterococcus.

• Since the latter 2 organisms are intrinsically resistant to cephalosporins, ampicillin is

generally included in the empirical treatment of infants with presumed neonatal infection

Prevention
Focuses on maternal health
• HIV testing at the first prenatal visit

• A serologic test for syphilis at the first prenatal visit.

• Serologic testing for hepatitis B surface antigen (HBsAg) at the first prenatal visit
 • Screening for rectovaginal GBS colonization of all pregnant women at 35-37 wk
gestation and a screening-based approach to selective intrapartum antibiotic
prophylaxis against GBS

GBS
• Intrapartum antibiotics are used to reduce vertical transmission of GBS

• Intrapartum chemoprophylaxis does not reduce the rates of late-onset

GBS Disease

• Aggressive management of suspected maternal chorioamnionitis with antibiotic

therapy during labor

• Neonatal infection with Chlamydia can be prevented by identification and treatment of

infected pregnant women

• Mother-to-child transmission of HIV is significantly reduced by maternal antiretroviral

therapy during pregnancy, labor, and delivery, by cesarean delivery before rupture of
membranes, and by antiretroviral treatment of the infant after birth
 1. Neonatal sepsis
Why are the neonates more susceptible for sepsis?
1. Small in age and small in size
2. Immature immune system
3. Naive to the environment
4. Skin is very delicate, and the external barrier is not optimum
5. Susceptible for hypothermia
6.

Why is it important to identify neonatal sepsis early?

1. Delay in minutes could cost a life!
2. Once the infection has set in difficult to control and develop multi-organ effects
3. Simple interventions could halt the progression of sepsis
4. Consequences of neonatal sepsis might result in long term disability

Sepsis

Early onset sepsis Late onset sepsis

• Timing : Sepsis which occurs within 48 – 72 • Timing : onset of sepsis after 48 – 72
hours of birth hours following birth
• Source of pathogen : maternal genital tract, • Source of pathogen : environment (home
deliver environment or hospital)
• Commonest pathogens: Group B • Commonest organisms: Staphylococcus
Streptococci , E Coli, Listeria aureus , coagulase negative Staphylococci
Monocytogenes , E Coli, Pseudomonas
• Commonest type of infection: congenital
pneumonia Common type of infections: septicaemia,
• meningitis
Risk factors for early onset sepsis Risk factors for late onset sepsis

• Maternal pyrexia >38°C or other evidence of Very low birth weight, prematurity
infection Lack of breastfeeding
• Prolonged rupture of membranes (ROM Delayed enteral feeding
>18hrs) Frequent handling/extensive
• Foul smelling liquor resuscitation with or without invasive
• Spontaneous preterm delivery (<37 weeks) procedures
• Very low birth weight (<1500g) Disruption of skin integrity with needle
pricks and use of intravenous fluids
• Prolonged or difficult delivery with
Poor hygiene
instrumentation or ≥3 vaginal examinations in
Poor maintenance of asepsis in neonatal
24 hours or presence / removal of cervical
unit including improper hand washing
suture.
techniques
• Maternal UTI in the third trimesterProlonged
Superficial infections (eg; skin and
or difficult delivery with instrumentation or
umbilical sepsis)
≥3 vaginal examinations in 24 hours or
Previous or prolonged hospitalization
presence / removal of cervical suture.
• Maternal UTI in the third trimester
•

Different infections Clinical features of neonatal sepsis

• Pneumonia • Respiratory distress
• Septicaemia • Grunting • Purulent umbilical
• Meningitis • Apnoea discharge / peri-
• Skin sepsis • Less activity / lethargy umbilical erythema
• Omphalitis • Hypothermia – • Crying on
• Urosepsis commoner micturition
• Necrotizing enterocolitis • Hyperthermia • Paucity of limb
• movements
Septic arthritis • Jaundice - unexplained
• • Bleeding tendency,
Acute osteomyelitis • Seizures
petechiae
• Tachycardia
Clinical features of neonatal sepsis • Loose stools or
• Hypotension
• Subtle , non-specific blood in stools
• Low SPO2
• May be just the feeling of • Skin mottling
• Poor feeding
‘not right’ • Conjunctival
• Instability of blood
• Could be reported by the redness, eye
sugar : high or low
mother , nursing officer or discharge
• Bulging fontanelle
the doctor.
• High pitched cry
• Vomiting
• Abdominal distention
• Skin pustules, vesicles
Skin mottling Pustules

Skin vesicles

Investigations for neonatal sepsis – to look for the cause

• Blood: FBC (neutropenia may be present instead of neutrophilia), CRP (serial values
more helpful), Blood culture, blood picture
• Urine: UFR, urine culture
• Imaging: Chest X-ray, abdominal X-ray
• CSF: CSF full report, CSF culture, CSF for bacterial antigen, CSF for viral PCR
• Swabs: skin, umbilicus, vesicles
Full septic screen vs partial septic screen

Full septic screen Partial septic screen

• Full blood count • All the components of the full septic

• CRP screen except CSF examination
• Blood culture
• Chest X ray
• Urine culture
• CSF examination
Might include – swabs, pus for culture
depending on the clinical scenario

Investigations for neonatal sepsis – to look for the secondary effects

• Platelet count
• Coagulation: PT/APTT
• Liver functions: AST, ALT, GGT, ALP, bilirubin
• Renal functions: S Creatinine, Blood Urea, electrolytes
• Metabolic: Blood sugar, calcium, magnesium, phosphate
• Blood gas: acid – base disturbances

Management
• Initial assessment & stabilization: A, B,C …..
- Fluid resuscitation
- Check blood sugar and correct if needed
- Manage hypothermia
 • Antibiotics, Intravenous route
Initially empirical, later altered as per response and ABST

Early onset sepsis:

First line medications: Penicillin, gentamycin, replace gentamycin with Cefotaxime if meningitis
is suspected or no response
Late onset sepsis:

First line: Flucloxacillin & Gentamycin

Second line medications: Flucoloxacillin, Amikacin (for E Coli)
Third line medications: Meropenum, Vancomycin
Duration of the antibiotics:

14 days for septicaemia, 21 days for meningitis, 7 – 14 days for other scenarios depending on
the clinical circumstances

If the sepsis was presumed and later all the parameters in the septic screen negative –
antibiotics should be stopped as early as possible provided the child is well, to avoid
antibiotic resistance

• Monitoring
Monitoring for the response to treatment, complications, drug adverse effects

• Other supportive care

Ventilation and oxygenation as required

Other organ support – inotropes, maintenance of normothermia, normoglycaemia
Ensure good hydration & nutrition - best through enteral feeding
Blood and blood products transfusion

Manage seizures if any

IVIG infusion
Neonatal meningitis

• Clinical features are just same as other

systemic sepsis, non- specific

• Convulsions may be present, bulging

fontanelle
• Irritability, high pitched cry
• Focal neurological signs, posturing, bulging fontanelle should be looked in to

Complications:
Short term – SIADH, Hydrocephalus, cerebral oedema, subdural effussion

Long term – developmental delay, hearing and visual assessment, seizures

Neonatal meningitis – ctd

Interpretation of the CSF results

Type of infant White cell count Protein g/l Glucose mmol/l

(count/mm3)

Pre-term 9 (0-30) 1 (0.5 – 2.5) 3 (1.5 – 5.5)

Term 6 (0-21) 0.6 (0.3 – 2.0) 3 (1.5 – 5.5)

Courtesy: Roberton Textbook of Neonatology 5th Edition; 2013

Management: Long term assessment:

IV antibiotics Penicillin & Cefotaxime
Monitor development
for 21 days
Hearing assessment
Monitor OFC Visual assessment
Cranial USS / CT Referral for early intervention and developmental
care
Complications of neonatal sepsis
• Septic shock
• Multi-organ dysfunction
• Meningitis: developmental delay, seizures, visual and hearing impairment, cognitive
defects
• Necrotizing enterocolitis: bowel obstruction, bowel resection, short gut syndrome
• Pneumonia: Requirement for prolonged ventilation, chronic lung disease
• UTI: renal scarring, hypertension, chronic kidney disease
• Septic arthritis: joint destruction, deformity
• Conjunctivitis: visual impairment

Prevention of neonatal sepsis

• Minimise risk factors

• Hand washing!!
• Minimal blood sampling
• Strict aseptic procedures
• Treat maternal sepsis
• Prophylactic antibiotics to the baby if indicated
• Meticulous monitoring of at-risk groups
• Rational antibiotic use to avoid antibiotic resistance
 6. Neonatal seizures

▪ Introduction
• Immature CNS is very susceptible to seizures
• If not controlled promptly lead to Progressive cerebral hypoxia and oedema and
Permanent brain damage.
▪ Incidence
• Seizures occur more often in the neonatal period than at any other time of life
• Higher in premature neonates
• Risk increases with decreasing gestational age and weight
• They most often occur within the first week of life

▪ Types of Seizures

1. Subtle seizures
a. Abnormal eye movements
b. Lip smacking
c. Swimming or pedaling movements
d. Apnea
2. Tonic (Focal/multi-focal/generalizes)
3. Clonic (Focal/ Generalized)
4. Myoclonic (Focal/generalized)
5. Epileptic spasms
6. Autonomic manifestations

Generalized Tonic Clonic Seizures tend not to occur

Differential diagnosis

• Seizures are difficult to diagnose during neonatal period

Seizure mimickers

I. Jitteriness
II. Motor automatisms
III. Benign neonatal sleep myoclonus
 Aeitiology
• 85% are symptomatic
• Therefore, must find the cause for seizure

• Intracranial pathologies

• Hypoxic ischemic encephalopathy • Benign neonatal seizure syndromes

• Intracranial hemorrhages • Benign idiopathic neonatal seizures
• Cerebral infarction (Fifth day fits)
• Structural brain abnormalities • Benign familial neonatal seizures
• Infections • Neonatal onset epilepsy
• Meningitis • Early myoclonic encephalopathy
• Encephalitis • Early infantile epileptic encephalopathy
• Congenital infections (TORCH]
• Neuro-Cutaneous Syndrome
• Metabolic causes
• Drug withdrawal
• Hypoglycemia
• Hypocalcemia
• Hypomagnesaemia
• Hypo/hypernatremia
• Pyridoxine dependent seizures
• Inborn errors of metabolism
• (Galactosemia, Hyperglycemia, Urea cycle
disorders)
History Examination
Birth History
• Maturity/ birth weight • Head – OFC
• Type of delivery • Skin – Vesicular lesions/ neuro cutaneous
• APGAR manifestations
• Eyes – Cataract/ chorioretinitis/ optic
atrophy/ hypotelorism
Maternal antenatal history
• Dysmorphism
• GDM • Neurological examination
• Risk factors for sepsis/ congenital • Tone/ power
infections • Cranial nerves
• Bleeding disorders

Family history
• Consanguinity
• Epilepsy/ neonatal seizures

Investigations
All neonates with seizures should be investigated to find the cause
• FBC • S. calcium
• CRP • Blood gas
• Blood culture •Ammonium lactate
• RBS
• SE
• Lumbar puncture
Indicated in all neonates with seizures unless the cause is obviously related to metabolic disorder

• TORCH screen
• Neuroimaging
• US Brain
• MRI Brain

• EEG/ Video EEG monitoring

• Genetic testing
Treatment
– Aetiologic Therapy
• Treatment directed at the cause of neonatal seizures

• Hyperglycemia – 10% Dextrose bolus and infusion

• Hypocalcemia – 10% Calcium gluconate
• Meningitis – IV antibiotics
• HSV – IV acyclovir

• HIE – Therapeutic hypothermia

• Pyridoxine dependent seizure – IV pyridoxine
Treatment
– Anti-Seizure drug therapy

• When to start
o Briefly seizures due to reversible causes do not require treatment
o Phenobarbitone is the treatment of choice
- IV 20mg/kg loading dose
- 5mg/kg/day maintenance dose

• Other drugs (phenytoin, midazolam, levetiracetam)

• Duration of anti-epileptic treatment
o If resolve n 2-3 days – stop immediately
o Wean off when no seizures and EEG has normalized
Prognosis
• Depends on the cause of the seizure
• Other predictors of outcome
• Seizure type
• Seizure burden, including the number of sites of seizure onset and seizure duration
• Status epilepticus
• Neurologic examination at the time of seizures
• Number of drugs required to treat seizures
• Findings on neuroimaging
• Gestational age (term vs. preterm)
• Birth weight
 7. Pre term labour and prematurity
Prematurity
• A baby born before 37 weeks of pregnancy from the 1st day of
last menstrual period is called a premature baby.
• Occurs due to preterm delivery of mother.
• Premature babies are of

Preterm labor

• Generally the etiology it is multi factorial

• Due to fetal, maternal, uterine, and placental factors
• Most of the preterm delivery occur spontaneously without a known
reason
• To prevent preterm birth tocolytics, antenatal steroids, Magnesium
Sulphate, cervical cerclage and progesterone can be given

Complication of baby due to prematurity:

Respiratory Metabolic –Endocrine
• SDLD • Osteopeia of prematurity
• BPD • Hypocalcaemia
• Pneumothorax • Hyoglycaemia

• Congenital pneumonia • Hyperglycaemia

• Apnoea of prematurity • Metabolic acidosis
CVS Renal
• PDA • Hyponatraemia

• Hypotension • Hypernatraemia
• Bradycardia (with apnoea) • Hyperkelaemia
• Renal tubular acidosis

CNS Other
 • IVH • Infections
• Periventricular leukomalacia • Anaemia of prematurity
• Seizures • Hypothermia

• ROP
• Deafness
GIT
• NEC

• Poor motility
• Jaundice

Some important complications and it’s management

Hypothermia
• Premature babies have increased surface/weight ratio, they have decreased epidermal
and dermal skin thickness
• They have reduced subcutaneous fat, brown fat, and energy store. They are also wet
• They suffer from heat loss through contact to cold surface (conduction), air currents
(convection), through cooler surface area movement (radiation) and evaporation

Management
• Plastic bags, kangaroo mother care method, radiant
warmers, clothing, incubators can be used to treat
hypothermia
• Asses need for incubator immediately, use transport
incubator with humidification if necessary.
• Minimize exposure time and handling
• Keep the baby dry and use dry drapes
• Maintain neutral thermal range
Bacterial infection
• Prematurity is a predisposing factor for bacterial infection because premature babies
have immature skin and not fully developed innate immune system.
• Baby is also predisposed if there is any antenatal exposure and use of devices (IV etc.)
• Infections can be prevented by

o Hand washing before touching the baby

o Meticulous skin care
o Surveilling for nosocomial infection
o Early enteral feeding
o Minimizing duration of device usage and contamination of devices like
catheters

Management
• Baby should be treated with IV antibiotics

Respiratory distress
• Respiratory distress is categorized by Tachypnoea, Intercostal recession, Sternal
recession, Paradoxical respiratory movement, Grunt, Oxygen requirement
• Surfactant deficient lung disease is the main cause of respiratory distress in a premature
baby
• This deficiency is more common in babies below 32 weeks of gestation
• Surfactant deficiency leads to increase of alveolar surface tension and lung alveoli
collapse.
• Distress can also be caused due to congenital pneumonia, congenital malformation,
pneumothorax and TTN “wet lung”

Management
• It is a medical emergency
• A.B.C. procedure is followed
• Minimal handling while management
• Minimal FiO2 to achieve 90-95% saturation (Avoid nasal
prong oxygen for preterm babies – unless for chronic lung
disease)
• Assess for infection – treat if indicated
• IV fluids: Avoid hypoglycaemia and electrolyte disturbance
• Consider need for invasive monitoring and is done if required
• Decide need for ventilatory support and is given if required
• Provide CPAP from time of birth
• Surfactant is given as “rescue” rather than “prophylactic”

Interventricular Hemorrhage
• It very rarely occurs in babies of >32/40, occurs mainly in babies
born <28/40
• Bleeding from the germinal matrix and blood moves into the
ventricles
• This blood can clot and obstruct the venous system
• This may cause periventricular infarction
• Seizures, hydrocephalus, cerebral palsy are some complications that can occur due to
IVH too
 Apnea of Prematurity

• Apnea -: Cessation of breathing for longer than 20 seconds or for any duration if
accompanied with bradycardia and cyanosis.
• There are 03 types of apnea based on the underlying mechanism.
o Central
o Obstructive
o Mixed – Majority
o
• Pathophysiology of central apnea:

Immature Attenuated Paradoxical

brainstem response to response to Apnoea
respiratory CO2 hypoxia
centers

Management
o Tactile stimulation
o Methylxanthines – Aminophylline (IV), Theophylline(orally)
o Caffeine – fewer side effects (not available in SL)
o Continuous positive pressure ventilation.

Jaundice of prematurity
• Pathophysiology:
Retinopathy of Prematurity
• Risk Factors:
o Less than 32 weeks.
o Lower gestational age, lower birth weight and sicker the infant – Greater the risk.
• Retinopathy of prematurity affects developing blood vessels at the junction pf the
vascularizes and non -vascularized retina.

Anemia of prematurity
• Hb levels may drop to 7-9g/dL by 3-6 weeks of life.
• Contributory factors:
o Shorter red blood cell life span
o Inadequate erythropoietin production
o Low iron stores
o Iatrogenic blood loss – venipuncture
o Rapid extrauterine growth
o Vitamin E deficiency leading to premature RBC break -down.

Osteopenia of prematurity
• Reduced bone mineral content in preterm babies.
• Due to post-natal nutrition being unable to match the intrauterine mineral delivery.
• 80% of calcium and phosphate mineral accretion takes place during the 3rd trimester.
• Can be treated with Calcium and phosphate supplements.

Approach to Small Baby

• Talk to parents antenatally. Give idea of what to expect. Find out any issues - liaison
with Obstetric team
• Preparation of resuscitation equipment
• ABC
• Minimal handling
• Neutral thermal environment
• Asses respiratory support needs: ? Vent ? CPAP ? Oxygen
• Consider and cover infection
• Nursery/incubator care preparation
Iatrogenic Complications of Prematurity
• Pneumothorax
• Bronchopulmonary Dysplasia
• Subglottic stenosis
• Retinopathy of prematurity
• Feed intolerance/orally aversive behaviour
• Nosocomial infection with resistant organisms
• “IV burns

Special treatment methods for Preterm babies:

”
Feeding
• Early parenteral or enteral nutritional support is essential.
• Preterm infants have a high nutritional requirement because of their rapid growth.
• Delayed starting of feeds will lead to poor growth and neurodevelopmental outcome.
• IV amino acids and dextrose should be started immediately after birth as early
parenteral nutrition.
• For enteral feeding expressed maternal milk is preferred.
• This will decrease the development of NEC, late onset sepsis , BPD and severe ROP.
• Feeding maternal milk is associated with superior neurodevelopmental outcomes.

IV Fluids
• Premature babies need more fluid as they lose more fluid.
• Fluid needed by premature babies on first 3 days of life:
o Day 1 – 75 – 80ml/Kg/day
o Day 2 – 90 – 95ml/Kg/day
o Day 3 – 105 – 110 ml/Kg/day
• st
1 Day of life – 10% Dextrose
• 2nd Day onwards – add electrolytes – Sodium, potassium, calcium.
•
Immaturity of drug metabolism
• The following features of preterm babies will slow down drug metabolism:
o Renal clearance is diminished
o GFR rises with gestational age
o Liver metabolism also not optimal
o Need to use smaller doses
o Drug dosing recommendations vary with age
Various supplements given to preterm babies
• Vit. K 0.5mg given at birth

Gestation <37 weeks and/or birth weight < 2000g:

• Iron from 2 weeks
• Multivitamin from 2 weeks of life

Gestation < 32weeks and/or 1500g

• Calcium & phosphorous
• Multivitamin
• Iron

Recommended supplements for infants 1500 - 2000g

• Iron - 2 mg elemental iron/kg/day (maximum 15 mg/day). From 2 weeks of age (if
tolerating full enteral feeds)
• Multivitamin (with folic acid) - For Vitamin D 200-400 IU/day. From 1 week of age until
12 months of age

Supplements for breast milk fed infants <1500g

• Phosphorus
o Enteral
o 100 mg/kg
o From time of tolerating full enteral feeds
o Until 40 weeks post-menstrual age
• Calcium
o Enteral
o 200 mg/kg/day
o From time of tolerating full enteral feeds
o Until 40 weeks post-menstrual age
Long term complications of
Outcome of preterm babies
< 22 weeks : minimal survival prematurity:
23 weeks : 30%
• Developmental disability – cerebral
24 weeks : 60%
palsy
28 weeks : 90%
• Sensory impairment – hearing, vision
30 weeks : 95%
• Learning disability
• Behavioral disorders
• Intellectual disability
• Chronic lung disease
Early intervention is very important !! • Increase risk of child abuse and
neglect
 8.Rh isoimmunisation
Pathophysiology of the Rh isoimmunisation
During the fetal maternal haemorrhage, the fetal RBC cross the placenta.
Maternal immune response recognizes the fetal RBC as a foreign antigen if fetus Rh positive
and mother Rh negative.
In maternal circulation, antibodies are formed against fetal antigen.
IgM is the first antigen that form follows the fetal maternal haemorrhage.
IgM can’t cross the placenta.
Initial IgM followed up by IgG in 2 weeks -6 months.it can cross the placenta.
In first pregnancy, the amount of antibody in maternal circulation is not enough to cross the
placenta.
Memory B cells activates immune response in subsequent pregnancy with Rh +ve fetus and
formed large amount of the antibody.
IgG antibody cross the placenta and attack the fetal RBC
The fetal RBC cell sequested by the macrophage of fetal spleen where they get haemolysed.
It forms fetal anaemia.
Sensitisation of mother is depend on the volume of fetal maternal haemorrhage (>4ml) and
magnitude of mother’s immune response.

Causes of fetal maternal RBS transfer

• At the time of placental delivery, the significant amount of fetal maternal RBC transfer
occurs.
Other causes

• Abortion, ectopic pregnancy, partial molar pregnancy.

• Antepartum haemorrhage- placenta previa, placental abruption
• External cephalic version
• Abdominal trauma
• Amniocentesis and cordocentesis
Large FMH is likely to be associated with:
Traumatic deliveries including caesarean section
Manual removal of the placenta
Stillbirths and fetal deaths
Abdominal trauma during the third trimester
Twin pregnancies (at delivery)
Unexplained hydrops fetalis.

(klihauer test shout be perform with in 2 hr of delivery to identify the Rh –ve mother with large
maternal haemorrhage)

Monitoring during the pregnancy

ABO and Rh status at booking visit
If Rh antigen negative – antibody screening is done at booking, 28 and 34 weeks of gestation.
If Rh antibodies are present, do parental blood phenotype (because the antibodies are from
previous pregnancy)
If Rh – ve
✓ assume Rh –ve fetus, require routine followup.
If Rh +ve determine paternal genotype
✓ If homozygous – fetus will be Rh+ve
✓ If heterozygous-50% baby will Rh +ve ( invasive testing for fetus Rh status or maternal
blood for fetal DNA)

If antibody present in maternal circulation

If anti D in maternal circulation <4IU –minimal risk
If anti D in maternal circulation >10IU at the beginning of pregnancy or sudden rise- need
further investigations
If anti D>4ml, Serial antibody levels once a month until 28 weeks, every fortnight thereafter
Prophylaxis
Anti-DIg should be given as soon as possible after the potentially sensitising event within 72
hours
Anti-D Ig dose given within 10 days may provide some protection.
Anti-D Ig 250 IU up to 19+6 weeks and 500 IU thereafter.
Klihauer test for the size of FMH should be performed when anti-D Ig is given at or after 20+0
weeks of gestation

Prophylaxis following sensitizing events before delivery

Invasive prenatal diagnosis (amniocentesis, chorion villus sampling, cordocentesis, intrauterine
transfusion)
Other intrauterine procedures (e.g. insertion of shunts, embryo reduction, laser)
Antepartum haemorrhage
External cephalic version of the fetus (including attempted)
Any abdominal trauma (direct/indirect, sharp/blunt, open/closed)
fetal death.

Screening of anemia of the fetus

• If mother had intrauterine transfusion and hydrop fetus in previous pregnancy
• Level of antibody in maternal circulation
✓ If anti D <5 IU/ml 3% anemia
✓ If antiD 5-14 IU/ml moderate anemia
✓ If antiD >15 IU/ml 30% anemia
• CTG Fetal heart rate monitoring
✓ sinusoidal pattern (severe anaemia)
• Invasive procedure
• Ultrasound Doppler scan- middle cerebral artery
✓ Peak systolic velocity
✓ Not reliable after 35 weeks
✓ Value >1.5 MoM
• Cordocentasis ( diagnostic/confirmatory )
Management of fetal anaemia
If Rh antibody present in mother
First identify the fetus blood group and Rh status by cell free DNA in maternal blood or by
cordocentasis
If fetus RH status is +ve then fetus have the risk to develop anaemia
If maternal antibody level >4IU, monitor the fetus middle cerebral artery viscosity
If it is >1.5 MoM, Intra uterine blood transfusion is the option to manage the anaemia.

Past CAT 6 Questions

23th Batch -21

24th Batch -21
25th Batch -37
 9. Neonatal Jaundice

Neonate – A new-born, following birth up to 28 days of life

Jaundice - Yellowish discoloration of the skin, sclera and other mucous membranes

It’s a common problem

o 60% of term and 80% of pre term infants develop jaundice within the first week
of life
o 10% of breast-fed babies are still jaundiced at one month of age

May leave a permanent disability - Such as bilirubin encephalopathy → kernicterus

Kernicterus
Kernicterus (bilirubin encephalopathy) – Occurs due to deposition of unconjugated
bilirubin in basal ganglia and brainstem nuclei which leads to neurological defects.
Conjugated bilirubin has no effect

Why is kernicterus problematic?

• Unconjugated bilirubin is lipophilic

• Neurons are more susceptible than glial cells
• Worse if blood-brain barrier is defective due to
o Concurrent infection
o Prematurity
o Acidosis, hyperoxia, hyperosmolality
• Toxicity is influenced by
o Duration of exposure of brain parenchyma to high bilirubin levels
o Level of bilirubin in brain tissue
o Bilirubin displacement from albumin

Clinical presentation – Poor feeding, Lethargy, High-pitched cry, Increased tone,

Opisthotonos, Seizures, Sensorineural hearing loss, Motor delay, extrapyramidal
disturbances, Upward gaze palsy, Dental dysplasia

Management - Transfer the child from primary/secondary to tertiary care center following
which early treatment through phototherapy and exchange transfusions can prevent
complications
Classification
There are different ways in which jaundice can be classified and commonly 3 criteria are used
for this purpose; state of conjugation, haemolysis and timing.

Conjugation

Unconjugated
Conjugated hyperbilirubinaemia hyperbilirubinaemia
Serum conjugated level of >25µmol/l or Majority of newborns have
2mg/dL unconjugated hyperbilirubinaemia

Haemolysis

Non-haemolytic
Haemolytic
Majority of newborns have non-
Usually appear within first 24-48 hours haemolytic jaundice

Timing

Within first 24 hours Within first week

This is mainly hemolytic Either hemolytic or non- Prolonged Jaundice
jaundice hemolytic
The above classifications are inter-related to one another and can be summarised as below

Jaundice

Unconjugated Conjugated

Physiological Pathological Pathological

Non-
Haemolytic Hepatic Post-hepatic
haemolytic

Intrinsic

Extrinsic

Keep in mind –
Physiological jaundice is the most common type of unconjugated hyperbilirubinemia

Conjugated / direct hyperbilirubinemia is only pathological (never physiological)

Types of jaundice based on the timing

Timing

Within first 24 hours Prolonged Jaundice

Within first week
(mostly pathological) (mostly pathological)
Clinical setting

History and examination of a baby presenting with jaundice -

Check naked baby in bright and preferably natural light – to identify jaundice

Examination of sclera, gums and blanched skin (exposing the face to sunlight and observing
blanching of the skin of the forehead) is useful across all skin tone
History Examination

Pregnancy / birth complications – twins, Degree of jaundice (Kramer’s rule: cephalo-

diabetes, viral infections, delivery mode caudal) – explained below

Family history/previous siblings/ethnicity Bruising, cephalhematoma, plethora / Pallor

Maternal blood group (If the mother is Rh Weight loss (as a % of birth weight), signs of
negative) and antibody status (During the dehydration
anti-natal period)

Gestational age / birth weight Temperature – low or high (to check for
sepsis)

When was jaundiced first noticed? Petechiae, hepatosplenomegaly (congenital

or acquired sepsis), cataract (congenital
Rubella infection along with galactosemia)

Waking for feeds / activity / irritability / Level of consciousness (whether the child is
vomiting - To see if the baby has sepsis septic or else having bilirubin
(activity) or to check for any clinical evidence encephalopathy)
of intestinal obstruction (vomiting)

Urine output (less) / frequency of stools (less) High pitched cry, irritability, activity level,
– in breastfeeding jaundice / their colours – feeding (whether the child is septic or else
urine →dark having bilirubin encephalopathy)

Type of feeds – breast milk (take longer to Fontanelle (bulging – in neonatal meningitis
clear physiological jaundice) / formula or sepsis/depressed - dehydration), tone,
posture

Previous phototherapy Head circumference Toxoplasmosis –

hydrocephalous (head is large). Congenital
Rubella infections - microcephaly

Weight loss?
Degree of jaundice (Kramer’s rule: cephalic-caudal)
Interpretation of the Kramer's rule –

• If the jaundice is present only in the head and neck →

100μmol
• Present in the hands and feet → >250μmol
And so on.

[Head & neck 100; Chest 150; lower body & thighs 200; arms & legs
below knees 200; hands & feet >250 in µmol/l]
The values are then added to get the final value

However, this method of determining the degree of jaundice is

unreliable
Why?
• The skin colour can vary due to tanning and it may be difficult to identify the jaundiced
areas

• The baby may have already undergone phototherapy

Details in to certain types of Jaundice will be discussed below -

• Physiological Jaundice (Unconjugated → physiological)
• Breast feeding jaundice (Unconjugated → pathological → non-haemolytic)
• Breast milk jaundice (Unconjugated → pathological → non-haemolytic)
 (01) Physiological Jaundice

✓ The commonest type of jaundice

✓ Jaundice appears usually after 48 hours (occasionally 24 – 48 hours)
✓ It never occurs in the first 24 hours (common MCQ)
✓ Usually lasts for 10 days in term infant with a peak SBR (serum bilirubin) of 12 mg/dl
(204 micmol/l)
✓ Reaches a peak at around 4-5 days
✓ In preterm infants it lasts for 14 days and reaches the peak at around 6-7 days (peak
SBR 15 mg/dl or 255 micmol/l)
✓ In exclusively breast-fed infants and in preterms clearance can take up to a month

Aetiology of physiological jaundice -

• Increase in RBC mass - Because the Hb concentration in newborns is, much higher than
normal child/adults → around 15-22g/dL
• Decrease in RBC lifespan (80-90 days)
• Increase in enterohepatic Circulation - Since it mainly contains fetal Hb
• Decrease in hepatic uptake
• Decrease in bilirubin conjugation

Treatment of physiological jaundice -

• Phototherapy If SBR high

• Talk to parents
• Re-assess if necessary

(02) Breast feeding jaundice

✓ Keep in mind that this is not the same as breast milk jaundice!
✓ It results from insufficient breast milk intake, resulting in inadequate quantities of bowel
movements to remove bilirubin from the body
✓ This leads to increased enterohepatic circulation, resulting in increased reabsorption of
bilirubin from the intestines (So it’s not only bile salts and urobilinogen that’s
reabsorbed. In special occasions such as this, bilirubin may be absorbed as well)
✓ Usually occurs during the first week of life
✓ Treatment -Most cases can be ameliorated by proper establishment of breastfeeding to
stimulate adequate milk production. Sometimes, initial correction of dehydration is
necessary (Sometimes intravenous fluid may be needed to correct this dehydration.)
 (03) Breast milk jaundice

✓ Commonest cause of prolonged jaundice

✓ The baby is otherwise normal and grows well (only feature is clinical evidence of
jaundice)
✓ Occurs due to inhibition of conjugation and increase in enterohepatic circulation (Due to
presence of some inhibitors in breast milk which deconjugate conjugated bilirubin in the
gut, which increases the enterohepatic circulation)
✓ Diagnosis is by exclusion
✓ Treatment - Explain about the condition to the parents and advise to bring the baby if
SBR is increasing, failure to gain weight or presence of pale stool and dark urine

When do you suspect that the cause for jaundice is pathological?

✓ Jaundice appearing within first 24 hours of life (usually haemolytic)
✓ Jaundice in a sick neonate
✓ Total serum bilirubin levels >250µmol/l by 48 hours or >300µmol/l by 72 hours of life
✓ Rapidly rising serum bilirubin (>100µmol/l in 24 hours)
✓ Jaundice that fails to respond to phototherapy
✓ Prolonged jaundice (>14 days in term infants; >21 days in preterm infants)
✓ Conjugated serum bilirubin >25µmol/l
✓ Pale stools and dark urine
Unconjugated (Indirect) hyperbilirubinemia

Heamolytic causes for unconjugated hyperbilirubinaemia - Intrinsic causes

• Red cell membrane defects e.g. spherocytosis & elliptocytosis

Hereditary spherocytosis –
➢ Family history (positive in 75%); autosomal dominant
➢ Spherocytes on blood film
➢ Incubated osmotic fragility testing, genetic testing
➢ Long term follow up and management

• Enzyme defects e.g., G6PD deficiency, Pyruvate kinase deficiency

G6PD deficiency -
➢ Mostly affects males (X-linked recessive disorder)
➢ G6PD level may be normal if reticulocyte count is high
➢ Advice on avoidance of precipitants – certain medications, fava beans, moth
balls

• Haemoglobinopathies e.g., sickle cell disease, HbH disease (type of alpha Thalassemia)

Heamolytic causes for unconjugated hyperbilirubinaemia - Extrinsic causes

• Alloimmune
➢ Rhesus incompatibility
➢ ABO incompatibility
➢ Rare blood group incompatibility (Such as Kell and Duffy)
• Systemic
➢ Sepsis

Non- Hemolytic causes for unconjugated hyperbilirubinaemia

• Cephalhematoma (excessive collection of blood below the aponeurotic layer and above
the skull) and excessive bruising (can be due to sub-aponeurotic hemorrhagic or trauma
during delivery → which causes lot of bruising)
• Polycythemia (infants of diabetic mothers and infants who are small for dates) → If
packed cell volume in more than 65%
 • Breast feeding jaundice
• Breast milk jaundice*
• UTI, sepsis*
• Hypothyroidism*
• Gilbert syndrome* Rare inherited congenital
• Crigler Najjar syndrome* abnormalities
• High GI obstruction* e.g., congenital hypertrophic pyloric stenosis (common MCQ)

* Causes prolonged or persistent jaundice (>14 days in a term baby and> 21 days in preterm)

Diagnostic procedures

1) Serum bilirubin total and fractional bilirubin levels

➢ Physiological: <100µmol/l
➢ Exaggerated (physiological) – breastfeeding or in preterm babies: 100-250/300µmol/l
➢ Pathological: >250µmol/l by 48 hours or >300µmol/l by 72 hours of life

2) Transcutaneous bilirubinometer for babies born > 35 weeks and > 24 hours of age (not
available in our hospitals)
- It’s a non-invasive method
Do NOT,

o Measure bilirubin levels routinely in babies who are not visibly jaundiced
o Use visual assessment to estimate level of bilirubin (check level)
o Use umbilical cord blood bilirubin level (Which we usually do in Rh group
incompatibility) and DAT test (direct agglutination test/Direct Coomb's test) to predict
significance of hyperbilirubinaemia

o Use end-tidal carbon monoxide (ETCOc) measurement to predict significance of

hyperbilirubinaemia

Apart from assessing the bilirubin levels you may need to order other investigations depending
on the cause –
✓ Haemolytic jaundice – FBC, blood group & Rh, Direct Coombs test (DAT), blood picture
(spherocytosis)
✓ Septic screen for suspected sepsis
✓ Blood sugar and serum electrolytes in dehydration
✓ If you’re suspecting a metabolic cause - Metabolic screening and blood gas analysis
Management of indirect hyperbilirubinaemia

Treatment modalities available –

 Phototherapy – single or multiple
 Exchange transfusion (carries a mortality rate of 1-5%)
 Manage dehydration (if required); provide lactation support
 Investigate and treat for sepsis (if clinically indicated)

 IV immunoglobulin – mainly in Rh isoimmune haemolytic disease to prevent need for

exchange transfusion (also used in ABO incompatibility)

Note -

 Albumin / FFP not recommended

 Use of sunlight – not advised

(01) Phototherapy

• Converts unconjugated bilirubin into more excretable non-toxic form

• Light wave length 450 – 470 nm

• Baby exposed, eyes covered and kept 18 inches away from the sources (maximum
distance)
 • Decreases SBR
2mg/hour
• Use total serum
bilirubin
measurement to
decide the necessity
for phototherapy

• Threshold graphs
are used according
to birth gestation
and chronological
age

While on single phototherapy –

o Place the baby in supine position provided other conditions of the baby permits

o Ensure treatment is applied to the maximum area of the skin

o Monitor temperature and maintain thermo-neutral environment
o Eye protection and routine eye care
o Monitor hydration by daily weighing and assessing wet nappies

o Support parents to interact

o Use tinted head boxes as an alternative to eye protection in term babies
o Do not give additional feeds or fluids routinely
o When additional feeds are needed maternal EBM is the choice

o Communication to parents
o Relieve anxiety
o Give idea about management plan
o Encourage breast feeding

o Breast feeding support where needed

o Can continue cuddling, nappy changing
 o Repeat serum bilirubin measurement 4–6 hours after initiating phototherapy
o Repeat serum bilirubin measurement every 6–12 hours when the serum bilirubin level is
stable or falling

When to stop phototherapy?

• Stop phototherapy once serum bilirubin has fallen to a level at least 50 micromol/liter
below the phototherapy threshold in treatment threshold graphs

• Check for rebound of significant hyperbilirubinaemia with a repeat serum bilirubin

measurement 12–18 hours after stopping phototherapy. Babies do not necessarily have
to remain in hospital for this to be done (for the re-assessment)

Continuous multiple phototherapy for term and preterm

Here, multiple phototherapy machines are used at the same time

Indications:
▪ Rapidly rising bilirubin – SBR> 8.5 micromol/l per hour
▪ SBR at a level within 50 micmol/l below exchange transfusion level in the threshold
graph

▪ SBR does not fall or continues to rise while on single phototherapy

Types of phototherapy machines

a) Conventional phototherapy machines - available in SL

Multiple
b) Fiberoptic phototherapy (Biliblankets, bilibeds and phototherapy
other products) – not machine
available in SL -
It’s preferred to conventional phototherapy in preterm babies

c) LED phototherapy - available in SL – The advantage is that there is minima l need of

additional fluids
However, more research is needed to compare the effectiveness of the above

Adverse effects of phototherapy

➢ Dehydration
➢ Hypo/hyperthermia
➢ Diarrhoea
➢ Erythematous skin rash
➢ Maternal anxiety
➢ ? Eye damage

However, keep in mind that side effects are usually uncommon

(02) Exchange transfusions

Indications -
▪ Serum Bilirubin above exchange transfusion in the threshold charts
▪ Clinical features of bilirubin encephalopathy

Preparation –

▪ Baby needs to be admitted to NNU

▪ Parental information and consent
Method of transfusion -
▪ Double Volume exchange 160ml/Kg – since normal babies have 80ml/kg of body weight
▪ Rh -ve blood sample of the same ABO blood group as that of the baby (best choice is O
negative blood in AB positive plasma)
▪ Should be compatible with mother’s blood group (therefore send a maternal sample) -
So if you’re transferring to a tertiary center/hospital for the procedure mother’s blood sample
should also be taken/sent
▪ Should be fresh blood that was obtained within 5 days
▪ Needs an assistant
▪ Utensils required → Exchange transfusion set/3-way tap, feeding tubes
▪ Continuous cardiac monitoring is needed during the process
▪ Umbilical venous catheter should be inserted – just to get continuous blood flow
▪ Pre-exchange & after exchange levels of Hb, SBR, RBS , SE should be measured (Hb –
Haemoglobin, SBR – serum bilirubin, RBS – Random blood sugar, SE – serum
electrolytes)
▪ Warm the blood before starting
▪ Either 10ml/20ml aliquots are done
▪ Always take out the blood
▪ The average time for exchange is 1-2 hours
▪ Prophylactic antibiotics should be given
▪ Monitor blood sugar

Do NOT do the following during an exchange transfusion –

▪ Stop, continues multiple phototherapy

▪ Perform a single volume exchange
▪ Use albumin priming
▪ Routinely administer IV calcium

After an exchange transfusion -

▪ Maintain multiple phototherapy (Until you reassess S. bilirubin levels)
▪ Measure s. bilirubin within 2 hours

Effect of double volume exchange transfusions –

o Removal of sensitized RBC > 85% (In Rh incompatibility)
o Removal of 55 – 60% Serum and free bilirubin (which can cross the BBB)
 o However, after few hours SBR can increase again due to rebound release of tissue
bilirubin in to the blood circulation

Complications -
Not common but very serious if it does occur
➢ Embolization (air/clots) - Since you catheterize the umbilical veins. In order to avoid
embolization you insert the catheter till you get a continuous flow of blood from the
umbilical vein
➢ Thrombosis of umbilical vein → later leading to portal hypertension
➢ Cardiac arrhythmias
➢ Hyper/hypovolaemia
➢ Hypothermia
➢ Increase in K+, Na+, decrease in Ca++, and acidosis (If old blood is used)
➢ Infection
➢ Hypoglycemia (Because the procedure itself takes 1 – 2 hours and anyway in Rh group
incompatibility hypoglycemia is a known complication)
➢ Necrotizing enterocolitis

(03) Intravenous immunoglobulins – IVIG

Role of IVIG and cost effectiveness on preventing exchange transfusions in Rh disease has been
proven but more studies needed for its effectiveness in ABO incompatibility
Recommendations: 0.5-1g/Kg over 4 hours in adjunct to multiple phototherapy in Rh or ABO
incompatibility with rapidly rising SBR
Haemolytic disease of the newborn - HDN

(A) Rhesus iso-immunisation

 Mother rhesus negative (5% in Sri Lanka) ; baby rhesus positive

Clinical features –
o First baby may not be affected
o Most severe form of haemolytic jaundice
o Starts in utero
o Stillbirths, hydrops fetalis due to severe anaemia, jaundice and anaemia

Prevention
o Maternal Anti D administration
o In-utero transfusions (for severe anaemia)

Treatment
o Neonatal administration of immunoglobulin
o Phototherapy, exchange transfusion
o Follow-up with full blood count; may require blood transfusions up to 6-8 weeks post
birth (if anaemia develops as a severe complication)

Factors influencing maternal Ab production

o No of sensitization (risk factor)
o Amount of blood in maternal circulation normally 0.3 – 5ml of foetal blood (risk factor)
o Co-existing ABO incompatibility – less risk (protective factor)
o Genetic predisposition for poor Ab production (protective factor)

Complications of Rh HDN

o Kernicterus
o Hypoglycaemia
o Infections
o DIC
 o Late anaemia
o Folate deficiency
o Obstructive jaundice

(B) ABO incompatibility

• Mother O +ve & baby A +ve commonly or B +ve

• About 90% of O +ve mothers have Ig M anti A & anti B
• 10% have Ig G anti A & anti B (IgG can cross the placenta!)
• 1st child can get affected (unlike in Rh incompatibility)
• Severe HDN is rare
• Direct Coombs test weekly +ve or it will be – ve
(In Rh incompatibility → strongly positive for Coomb’s test
Minor blood group incompatibility (Kell and Duffy) also strongly positive for Coomb’s)

Investigations - SBR, Blood group of mother & baby, Direct Coombs test, Hb%

Treatment - Phototherapy, Exchange transfusion

Conjugated (direct) hyperbilirubinemia

✓ Can be acquired or congenital

Causes -

Hepatic causes of conjugated (direct) hyperbilirubinemia

• Infections e.g., Sepsis, Hepatitis A, B and TORCH infections (acquired while in the womb)

T - Toxoplasma
O – Other infections
R - Rubella
C – Cytomegalo virus
H – Herpes simplex
• Metabolic e.g., galactosemic, tyrosinemia, Alfa 1 antitrypsin deficiency, cystic fibrosis,
Dubin-Johnson syndrome, Rotor syndrome
• Drugs e.g., Total parenteral nutrition
 • Idiopathic neonatal cholestasis

Post - hepatic causes of conjugated (direct) hyperbilirubinemia

• Biliary atresia (congenital)

• Extra hepatic biliary atresia (congenital or acquired during early neonatal period)
• Choledochal cyst

In conjugated hyperbilirubinaemia, additional investigations may be needed to investigate for

the above causes

Investigations to demonstrate biliary obstruction -

a. USS – to visualize gall bladder
- Triangular cord sign seen in USS in extrahepatic biliary atresia (A lump may
be felt in choledochal cyst but anyway it can be seen through an USS)
- 4 hours fasting needed for better visualization

If GB not visualized (Could mean that there is an extrahepatic biliary atresia)

b. Liver biopsy: closed / open

c. Per operative cholangiography (is the diagnostic test but now a days we do a liver biopsy
before that)

Other investigations –
o SGOT and SGPT
o Alk. Phosphatase
o S. protein → indicates hepatic damage
o TORCH screen and hepatitis B surface Ag
o VDRL
o Urine CMV
o Urine for reducing substances
Keep in mind that the above investigations are apart from the basic investigations given below
– (what you have to check first and foremost)
• Urine – positive for bile, negative for urobilinogen
• Serum conjugated bilirubin - Increased (CB is >25micmol/l)

Management of direct hyperbilirubinaemia

(1) Biliary atresia

• Early recognition is very important
• Kasai surgery (hepato-porto- enterostomy)
<8/52 (If you do it within 2 months) → bile drainage is good (80%)
>12/52 (If it takes more than 3 months) → bad prognosis, results in
• May lead to biliary cirrhosis - Might end up needing a liver transplant in this case

(2) Choledochal cyst - corrective sur

10.Abnormalitiesin puberty
Puberty
Period during which an individual attain sexual maturity and reproductive potential.
Females – onset is early and completes early
Over the years the age at onset of puberty has gradually decreased, which is called a secular
trend.

Endocrine basis of human puberty

GnRH
-Principle hormone that initiate puberty in both sexes. Increase in the frequency of pulsatile
release of GnRH will initiate puberty.
-Secreted even in pre pubertal children.

-Levels are very much higher in adolescents.

-GnRH stimulate LH and FSH secretion from the anterior pituitary.
-Lh and FSH has the same structure in both sexes but function differs.
FSH

Females- Stimulate ovarian follicles to grow and maturating ova.

-stimulate production of estrogen from graafian follicle
-Cyclical production of FSH continues after puberty to produce menstrual cycles.
Males- simulate testicular growth.
-Trophic to sertoli cells.

-Together with androgens it maintain the gematogenic function of the testis.

- Enhances the production of androgen binding protein by the sertoli cells.
-Inhibin cause feed back inhibition of FSH secretion.

LH
-In men LH secretion is noted during the transition period from juvenile to peripubertal stages
Stimulate production of Testosterone from intestinal cells (Leydig cells)
Testosterone is responsible the majority of changes seen internally and externally in boys
during puberty.

-In female LH surge observed just prior to ovulation.

LH needed for converting the Graafian follicle to corpus luteum, which will produce
progesterone
Estrogen

Naturally occurring types are 17 beta estradiol, estrone, estriol.

Primary sources are granulosa cells of ovarian follicles, corpus luteum and placenta.
Estrogen production depend on enzyme Aromatase. Fat, muscle, brain also can produce
estrone (from androstenedione)

- At onset of puberty – Development of female secondary sexual characteristics

-Development of breast – Mainly proliferation of mammary duct. Development of lobules
under the control of progesterone. Cause pigmentation of the areola.

-Estrogen increase cause increase in blood supply to uterus

-Increase amount of uterine muscle mass, thus the size of the uterus
-It stimulate the growth of vagina in length and width
-Changes of female body at puberty is partly to direct effect of estrogen and partly to absence of
androgens
-Narrow shoulders, broad hips, converging thighs, wide carrying angle, less body hair and more
scalp hair
-Fat distribution is mainly of breast and buttocks
-Larynx retains its prepubertal proportions, therefore have a high pitch voice
-Though estrogen play a role in axillary and pubic hair growth, it is primarily under androgens
from adrenals
 -Hence the name adrenarche
-Onset of pubic hair development is called pubarche

Comedones and Acne

-Common in both sexes during onset of puberty
-Mainly due sebaceous gland secretions becoming thick due to androgens
-Estrogens make secretions thin and counteract the action of androgens
Growth spurt during puberty

-Secondary (pubertal) growth spurt occurs with the on set of puberty

-However rate of pubertal growth spurt is slower than infantile growth spurt
-Female growth spurt start earlier and is almost complete by the time of menarche, which mark the
completion of period of puberty
-Only around 5 cm increase in height occur after menarche
-Growth spurt is associated with adrenarche/pubarche,andandrogens play thought to play an important
role
-Estrogens regulate effects of GH at many levels: secretion, clearance, and action
Consonance of female puberty

-Normal puberty initiated through Hypothalamo- pituitary – Gonadal axis follows a set pattern
-Breast development is the first external feature of on set of puberty
-Secondary (pubertal) growth spurt closely follow this
-Adrenarche which is externally seen as growth of pubic hair is seen just around the time of
breast development
-Axillary hair growth follow this
-Other body changers gradually follows
Menarche denotes the completion of pubertal process and indicate sexual maturity
Endocrine aspect of male sexual development
-First sign of puberty is testicular enlargement in response to FSH and LH
-Most of the changes seen during this time is due to effects of testosterone
Active form of testosterone is dihydroxy testosterone which is produced by 5ἀ reductase enzyme
-5ἀ reductase enzyme deficiency will result in female external genitalia with absent uterus and
bling vagina
*Testicular enlargement is closely associated with pubertal growth spurt.Unlike in females sexual
maturity in males occur at middle of the growth spurt
*Enlargement of penis and internal genitalia occurs in response to testosterone, scrotum
become pigmented and rugose
*Pubic hair, facial hair, axillary hair and total increase in body hair follows
*But in scalp temporal recession of hair is noted
*Vice become deep, with prominent larynx
*Broad shoulders
*Muscle mass increase
*More aggressive
*Attraction towards opposite sex
*Acne
*Unlike in females no definitive marker of sexual maturity like menarche
*First nocturnal emission may be taken as a sign

Pubertal disoders
• Delayed Puberty
• Precautious puberty
• Pubertal arrest
Delayed puberty
-Mean age at onset of puberty can vary from population to population, because of genetic and
environmental factors
-Delayed puberty is defined as failure to develop secondary sexual characteristics beyond 2
standard deviation from mean for the given population
-Generally absent breast development by 13 years of absent testicular development by 14 years

(but vary with different populations)

• Cause of delayed puberty can be central, where the delay is due to delayed
initiation of puberty by hypothalamic-pituitary axis
 • It can be due to a peripheral cause like abnormality in gonads, chronic
illness/malnutrition or target organ hormone insensitivity
• Delayed puberty due to a peripheral cause is commoner in boys and more likely to
be due to constitutional delay in growth & puberty
• Delayed puberty due to a peripheral cause in girls is more likely to be due to an
underlying abnormality
• Incidence of delayed puberty due to a central cause is equal among in both sexes
• Constitutional delay in growth and puberty

➢ Commoner in boys
➢ Apart from delayed onset of puberty no other abnormality on examination
➢ Shorter than their peers, but height projection is within the mid-parental height and compatible for the
age, stage of sexual maturation and bone age
➢ Usually there is a family history of delayed onset of puberty in parent and siblings, but not essential for
the diagnosis
➢ Reassurance and psychological support is often adequate, but pubertal induction is indicated if there is
significant psychological impact

• Chronic systemic disease

➢ Severe chronic uncontrolled medical conditions like chronic renal failure, severe persistent asthma,
cyanotic heart disease, chronic liver disease can result in delayed onset of puberty

➢ The delay may be attributable to direct effects of the disease, secondary hormonal changes, metabolic
derangements, nutritional problems, effects of long term medications
➢ However
• in manymalnutrition
Severe such cases the exact mechanism of pubertal delay is poorly understood

➢ Age at puberty has shown decreasing trend over the years, which is called a secular trend
➢ This is attributed to improved health status among children, and specifically the nutrition
➢ Onset of puberty is supposed to be signaled by achieving minimum amount of fat in the body
➢ This is to protect the individual, because sexual maturity means possibility of pregnancy, which will
further deteriorate her nutritional status, because fetus acts as a parasite
➢ Anorexia nervosa is a known cause for delayed puberty, where a secondary endocrine disturbance is
thought to be the cause
 • Intensive exercise
➢ Long distance runners, extensive physical training may delay the onset of puberty

➢ Puberty tend to occur without intervention in these girls when physical training is cut down

• Hypothalamo-pituitary disorders
➢ This is due failure of signaling puberty by increase in pulsatile release of GnRH

➢ This is called hypogonadotropic hypogonadism, because it is due to failure of gonadotrophins in initiating

puberty

➢ Craniopharyngiomas and other pituitary tumors of hypothalamus disorders will cause this

• Pseudo hermaphroditism
• Hypothyroidism
➢ Due to reduced metabolic activity of all tissues this can lead pubertal delay

➢ However hypothyroidism can be a cause for precocious puberty

• Gonadal dysgenesis – Turner, Klinefelter, Prader Willi
➢ Here the problem is with the ovaries or testicles
➢ It can be primary or secondary
➢ Classic example for primary gonadal
➢ dysgenesis is Turner syndrome (45 X0)
➢ Usually diagnosed before pubertal age due to presence of other clinical features of the syndrome
➢ Some may not have overt features other than short stature and pubertal delay
➢ Turner syndrome
There are normal germ cell numbers in ovaries up to second trimester, from when they start to regress
steadily
-Reduced growth velocity is a key feature including intrauterine growth due to reduced GH
➢ By the time of puberty there are no germ cells left in ovaries
secretion, as well as defective end organ responsiveness to growth factors at cartilage and
collagen level
-Mean IQ is around 95, and majority have majority of Tuner
children have IQ s within normal range
-Growth hormone therapy and inducing secondary sexual
characteristics with estrogen improves the appearance and growth
Estrogen is also important to prevent bone demineralization
-Results from chromosomal abnormality 45 X0
-Multiple abnormalities, including primary ovarian dysgenesis
-Streaky ovaries, infantile uterus

Klinefelter syndrome

-Results from karyotype 46 XXY

-Tall stature due to long legs - lack of androgens to close epiphysis
-Small testis and no spermatogenesis
-Puberty may initiate at correct age, but does not proceed normally
-Can be considered as a cause for pubertal arrest than pubertal delay
-IQ is low

Managing delayed puberty

1. Find the underlying cause and treat if treatable
2. Need counselling for both child and parents, especially when the condition is non
correctable like Turner syndrome
3. If relevant induce puberty, trying to mimic the normal physiological process
4. Too rapid induction will cause closure of epiphysis early hindering the maximum height
attainable
5. In girls induction is with estrogen
6. Add progesterone to avoid unopposed action of estrogen, which can promote
endometrial and breast cancer
Investigating a child with delayed puberty

1. In a boy testicular volume of 4 ml or above indicate puberty has been initiated- use a Prader
orchidometer for this
2. Testosterone level at 8 am will indicate whether puberty has been initiated
3. Raised Gonadotropin levels indicate primary gonadal failure
4. LH/FSH response to a dose of GnRH will help to identify whether puberty is imminent
5. If imminent there will be a significant rise in LH and FSH, and LH surge will be greater than FSH
6. US Scan to assess the internal organs
7. Do Karyotyping when indicated
 Precocious puberty

• When secondary sexual characteristics appear before 8 years in girls and before 9 years in boys, it is
considered precocious puberty
• It can be true precocious puberty or pseudo-precocious puberty
• True precocious puberty is when puberty is induced by hypothalamo-pituitary axis as usual
• This will result in secondary sexual characteristics and sexual maturity occur in the correct order,
which is called consonance
• Pseudo-precocious puberty occurs when secondary sexual characteristics are initiated via some
other mechanism, thus the consonance is lost
• Thus presence or absence of consonance is the most important feature
True precocious puberty - causes
Commoner in girls, with female: male ratio of 10:1

Thus an underlying cause should be actively sought in boys

Neuroimaging is indicated in boys with central precocious puberty

• Idiopathic > 80% in girls
• Intracranial tumors
• Cranial irradiation
• Raised intracranial pressure

Management
-Exclude an underlying cause if relevant
-If idiopathic delaying the onset of puberty can be done depending on circumstances
-Indications to suppression is more cultural and psychological than medical
-Puberty can be suppressed by cyproterone acetate and medroxyprogesterone
-Mainly used now adays is GnRH analogues (desensitize anterior pituitary to GnRH)
-Psychological and emotional support should be given to the child
-Advice regarding personal hygiene should be given

Pseudo- precocious puberty

Some secondary sexual characteristics occur without a sequence
Some features present and some are absent
Causes
• Premature thelarche
 Premature thelache

• Premature breast development without other features of puberty, may be

asymetrical
• Occasionally a vaginal bleeding may occur
• Onset is usually within first year and uncommon after two years
• There is waxing and waning breast enlargement with gradual disappearance over
several months
• Breast development regress completely and restart around the time of puberty at
usual time
• In thelarche variant breast enlargement may remain without regression to be
continued at puberty

Congenital Adrenal Hyperplasia

• Results from enzyme defect in adrenocortical hormonal synthesis

• Absent negative feedback cause excessive ACTH secretion
• Accumulated steroid precursors above the block are converted to androgens
• Female fetus will be virilized with varying degree of virilization, will be usually detected
• Male fetus may not have obvious external changes
• Salt looses will present during neonatal period
• Non salt loosing type congenital adrenal hyperplasia in males will present
• Loss
withof consonance
precocious is the characteristic feature
puberty
• Growth acceleration, penile enlargement and pubic and axillary hair
develop
• Bone age is advanced
• Testis remains prepubertal in size < 4 ml, because no GnRH to stimulate
• Replacement of glucocorticoid and mineralocorticoid replacement is
indicated
 Ovarian cysts, Ovarian/testicular tumors

• These will secrete estrogens, which will stimulate endometrial development

• It will overgrow the blood supply resulting in break through bleeding
• Breast development may be present, but no pubic and axillary hair growth
• If the cyst is a transient one it will stimulate endometrial development and a vaginal bleed, but there
would not be breast development
• A child having vaginal bleed without any other secondary sexual characteristic or without consonance is
not proper menarche, and need further investigations
• Accidental or purposeful ingestion of sex steroids will produce a similar picture

Arrest of puberty
-In this phenomenon onset of puberty will be denoted by appearance of secondary sexual
characteristics
-But normal pubertal process will not proceed and will get arrested at one point
-This can be due to a secondary event damaging Hypothalamo- pituitary- gonadal axis or may be
due to an underlying abnormality
-Testicular feminizing syndrome and Klinefelter syndrome are classic examples

Testicular feminization syndrome

• This is an autosomal recessive condition affecting males
• There is a defect in the androgen receptors, resulting in external genitalia appearing

like normal female

• External genitalia are designed to be female by default in the absence of androgenic

action

• Due to MIF, Mullerian structures regress, therefore child will have a blind vagina with

absent uterus or fallopian tubes

• At the time of puberty child will develop normal breast, scanty amont of axillary and
pubic hair, but no menstruation
• Gonads have features of testis but need removal due to increased risk of malignancy
11.Breastfeeding

Current policies in Sri Lanka

• BFHI from 1992 – with training from government

• Exclusive breast feeding for 6 months [implemented from late 2006]

• Continue breastfeeding together with complementary feeding up to 2 years or beyond

• Maternity leave in govt sector – fully paid 84 days

• Code of Marketing for Breast milk Substitutes

WHO definition

Only breast milk and no other liquids or solids except for drops or syrups consisting of vitamins,
mineral supplements or medicines if medically indicated

Early skin to skin contact and first feeding

 Every healthy term newborn, when placed on the mother's abdomen, soon after birth,
has the ability to find its mother's breast all on its own.
 Can decide when to take first breastfeed. (usually <60 mins)
 This is called the 'Breast Crawl'.
 Improves bonding as the baby is alert in the 1st 1-2 hours
 Enables colonization of the baby with maternal flora

Support mothers to maintain breastfeeding

 Teach correct method of expression

 Discuss with mother antenatally
 Need to start within 6 hours
 Express regularly – at least every 2-3 hours (overnight too)
 Build the mother’s confidence
✓ Colostrum - even for very sick babies

✓ Storage
✓ Opportunities for Kangaroo care; baby’s bedside / photo galactagogues

Expressed breast milk storage guidelines

Following guideline is for healthy term babies

Infant cues…
Parents and their infants have timely
access to ongoing support and care

• Lactation management centres

o Post discharge

o Self-referrals
o Referrals from other units
o Hotline

• Dedicated lactation nurses

o Who visit wards

• Public Health Midwives in the field

Nutritional, biochemical properties of breast milk
Breast milk
 Energy required by age and the amount supplied from breast milk

 The composition of breast milk is unique to each phase of breast milk production

 Composition of breast milk produced by the mother of a preterm infant is

biochemically and immunologically more suitable for such an infant than the milk
from the mother of a term newborn
Types of breast milk by stage of lactation

• Colostrum

• Transitional milk

• Mature milk

• Weaning milk

Colostrum

• Produced in the breast by 16th week of pregnancy

• Available for secretion when baby is born

• Yellow & thicker than mature milk

• Less volume – suitable for the baby’s small stomach and immature kidneys
 • More WBC, more IgA, more proteins, more whey proteins

• Rich in growth factors - matures the intestinal epithelium

• Laxative – helps to pass meconium

Mature milk

• From the second week (after day 9)

• Amount of milk produced is higher
• Less concentrated
• Whey:casein reduces from 90:10 to 60:40
Transitional milk
is the milk produced between transition from colostrum to

mature milk
Milk during weaning

• Volume gradually reduces

• Has higher concentration of immunoprotective factors

Variations in breast milk composition

• Breast milk composition changes from feed to
feed, day to day, month to month to meet the
baby’s needs.

• Also changes during the course of a feed.

• Fore milk - at beginning of a feed
grey and watery
rich in protein, lactose, vitamins, minerals
and water.
• Hind milk - towards an end of a feed Foremilk Hind milk
whiter than foremilk more fat

• Taste varies according to maternal food intake –

baby learns taste of family foods via breast milk

Why human breast milk (HBM) is better than cow’s milk(CM):

• Casein/whey (Lactalbumin) is low HBM– easy to digest
• No lysozyme / lactoferrin or growth factors in CM or formula
 • Essential amino acids (cystine, taurine) adequate in HBM
• Lactose important for brain development
• Lipase, cholesterol and DHAs not present in CM
• Fat content can vary from feed to feed; during a feed
• HBM rich in hormones, enzymes, live blood cells, Igs
Why is Breastfeeding important

Importance for baby Importance for mother

 Breast milk is the perfect food for the infant  Reduces risk of
hypercholesterolaemia, diabetes,
 Enhances brain development ; IQ upto 6-10
hypertension, cardiovascular disease
points higher
 Breast and ovarian cancer are reduced
 Thus has major beneficial effects
 Hip fractures and osteoporosis are
 Ideal composition biochemically /
reduced
nutritionally
 Faster return to pre-pregnancy weight
 Protects from infections – diarrhoea, otitis
media, UTI by,  Lactational amenorrhea –
contraception (partial)
• Immunoglobulins - SIgA
• Lactoferrins  Stops bleeding after birth of the baby
• Enzymes (Oxytocin)
• Hormones
• Cells – PNL, lymphocytes & macrophages
Importance
Stabilizes for family
endometriosis
 Optimises neurodevelopment
 Improves bonding with baby
 Protects from chronic diseases eg: diabetes
(type 1 & 2), childhood cancers, obesity,  No cost
inflammatory bowel disease
 Convenient (no preparation)
 Preterm – breastmilk reduces risk of sepsis,
NEC  Fresh

Disadvantages of formula feeding

• Contamination and infections
• Intolerance to proteins
• Allergies
• Obesity
• Inconvenience
• Cost
 Anatomy of breastfeeding

Maternal mammary gland Infant oral anatomy

• Embryologically develops as mammary ridges  Tongue, palate, facial muscles,
at 3-5 weeks gestation buccal fat pads

• At birth mammary ducts, areola and nipple are  Pharyngeal muscles and nerves
present
TONGUE TIE
• During puberty increased growth and
branching of ducts and alveolar buds –
oestrogen and progesterone
• Connective tissue and fatty tissue also increase
• During pregnancy – mammary epithelial cells
differentiate to lactocytes; alveoli proliferate

• Breast shapes and sizes vary greatly

• Milk production ability of the breast is not
dependant on the size.
• Nipple sizes and position can also vary
• True inversion of the nipple is rare
 Physiology of breastfeeding
Diferent stages
Lactogenesis I (colustrum) - endocrine

Lactogenesis II - endocrine
Lactogenesis III (mature milk) - autocrine
Involution
Maternal neuroendocrine reflexes

Milk ejection reflex

Infant reflexes

Oxytocin will provide a tranquilizing feeling to the

mother

Positioning baby for Breastfeeding

1.seated position
2.lying position

Basic positions for breastfeeding (seated)

1Craddle hold
2.Cross cradle
3.Clutch hold [football hold]
Suckling with a good attachment Suckling with a poor attachment

Suckling with a good positioning and attachment

• Positioning
- The baby’s whole body is facing his mother and close to her
- Face is close up to the breast
• Attachment
- Chin is touching the breast
- Mouth is wide open
- Lower lip is curled outwards
- More areola above baby’s upper lip & less areola below lower lip
• You can see the baby taking slow, deep sucks
• The baby is relaxed, happy and satisfied at the end of the feed
• The mother does not feel nipple pain
• You may be able to hear the baby swallowing
Signs of poor attachment

• Baby’s body turned away from mother’s and not close to it

• Chin is separated from the breast
• Mouth looks closed; Lips point forwards
 • You see too much areola, including below the lower lip

• Takes many quick, small sucks

• Cheeks may be pulled in as he sucks
• May fuss or refuse to feed because he does not get enough breast milk
• The mother may feel nipple pain
• The nipple may look flattened at the end of a feed and it may have a pale line across the
tip
After a feed

Burping
• After each feed
• Not essential if attachment is good
Positioning after a feed
• Supine or to a side
• Not prone

Advice to mothers

Pre-lacteal feeds;
• No formula, water, glucose in first 6 months
• Milk volume on day 1 very low; stomach size only 5ml
Colostrum is adequate
• No need of extra water even in a hot day.
• Demand feeding or unrestricted breastfeeding (on early hunger cues – taking hand to
mouth etc; crying is late)
For lengthen the period
• No fixed time period

• Most babies finish in 10 minutes

• Slow feeders finish in 20-30 min
• Feeding from one breast or both breasts?
• Night feeders
• Cleaning of breasts
• Teaching / supporting breast milk expression
Problems during breastfeeding

Maternal
• Normal breast fullness
• Breast engorgement
• Blocked duct
• Mastitis / abscess
• Sore / cracked nipples
• Inverted nipples
Not enough milk

Infant
• Breast refusal

Normal breast fullness Engorged breasts

when milk is coming-in ▪ Features

▪ breast may feel hot, heavy o Breasts feel hot, heavy and hard
and hard o Painful and tender
▪ There will be a free flow of o No free flow of milk from breasts
milk o May have maternal fever lasting less than
This is normal 48 hours
To relieve fullness: ▪ Causes
Feed frequently o Delay in starting to breast feed
Cool compresses between o Poor positioning and attachment, so that
feeds milk is not removed effectively
The breast will adjust milk o Infrequent feeding, not feeding at night
production to the baby’s need or short duration of feeds
▪ Prevention
o Optimal attachment / latch
Sore / cracked nipples o Early and frequent exclusive breastfeeds
o Feeding according to cue of baby
▪ Painful when sucking o Not restricting frequency or length of
▪ Skin may be normal feeds
▪ Pale lines (compression) on o Finishing first breast before offering
nipple immediately after second
suckling ▪ Treatment (above +)
▪ Treatment o Correct positioning and attachment
o Correct attachment o NO expression – other than small amount
o Wait to remove for comfort
▪ until baby takes off o Softening of areola by ‘reverse pressure
softening’
o Apply hind milk after
o NO hot compresses; only cold therapy in
a feed
between feeds if required
o Paracetamol / rest
 Mastitis and abscess Inverted nipples

▪ Part of breast becomes red, hot, swollen & ▪ Can BF, therefore reassure
tender.
▪ No antenatal discussion with
▪ Fever, chills & generalized unwell
mother required
▪ Fluctuant if an abscess is formed
o Most improve and when
▪ Symptoms are same for non-infective
baby sucks will evert
▪ & infective mastitis
▪ Breast feeding is not contraindicated
o Early initiation of
breastfeeding
▪ Extra support to establish
▪ Remove milk frequently by allowing baby to attachment
breast feed (if not, an abscess will formed) or by ▪ Once breasts are full – reverse
expression pressure softening / little hand
▪ Establish a good attachment expression
▪ Offer the baby the affected breast first (if not ▪ Draw nipple out by touch
too painful) ▪ Nipple-shield may help
▪ Wear a loose bra
▪ Rest with the baby, so that the baby can feed
often
▪ Paracetamol/ibuprofen for pain
▪ Antibiotics if fever >24 hours, infected cracked
nipple, not improving (or worsening) with above
measures within 24 hrs.
▪ Antibiotics for 10-14 days
▪ An abscess may need surgical drainage

Not enough milk

o Mostly perceived
o It might take 15-30 minutes of expression to produce 1 drop initially!

o First few days volume of milk is small

o Causes
o Poor technique of breastfeeding
o Prelacteals (feeds other than breast milk)
o Maternal ill health – physical (ask about excessive vaginal
• discharge) & mental
▪ Treatment
o Reassure if perceived
o Maintain maternal confidence
o -Find out the cause and correct
Adequacy of breastfeeds 25 proper SEQ
Is my baby getting enough milk?
• About 8 – 12 times a day (may not be regular intervals)
• Generally sleeps for about 2 hours after a feed
• Alert with bright eyes, good skin colour and tone
• Urine output – 6 wet cloth nappies/day (after day 5; pale inoffensive
• Stools
- Loose unformed bowel motions; yellow to
- greenish gold (about 3 initially; later less)

If weight gain is adequate baby is getting enough milk

Breastfeeding may need to be delayed in the following

• Sick babies
• Preterm babies
• Babies with a GI surgical problems
• Rarely for babies with metabolic problems

Contraindications to breastfeed

• Mother on certain medications

o Chemotherapeutic / antimetabolites
o Receiving radioisotopes / has received a substance which is still making the milk
radioactive
• Maternal medical conditions
o HIV if facilities for formula feeding is available
o Human T-cell lymphotrophic virus I-II
o Untreated brucellosis
o Untreated active pulmonary tuberculosis (can give EBM)

• Maternal street drug use of cocaine, marijuana, high dose opiates

• Infant with classic galactosaemia
• Herpetic lesion on areola – avoid feeding from that side
Methods of giving expressed breast milk

• Naso/orogastric tube – left insitu rather than gavage if required for every feed
• Spoon
• Cup
• Supplementer at the breast
12.COMPLEMENTARY FEEDING

• Complementary feeding is defined as the process starting when breast milk alone is no
longer sufficient to meet the nutritional requirements of infants, and therefore other
foods and liquids are needed, along with breast milk
• Covers the period from 6 months to 2 years – might vary in different children (WHO)

RIGHT FEEDING AT RIGHT TIME

Right time -
1. Standard recommendation is at 6 months

2. Co-ordinated swallowing, chewing and appropriate sensations

3. Could start at 4 months in selected scenarios

4. Might be late in children with neurodevelopmental disorders eg: cerebral palsy,

syndromes, neuromuscular disorders
5. NG/PEG/ jejunostomy or tube feeding could be used
6. Feeding according to Hunger cues, Adequate spacing between feeds , ‘Responsive
feeding’ are important.

Right Food-
Correct consistency of food is important for advancement of chewing & swallowing skills ,Food
variety and different tastes are important for neurodevelopment

The person who feeds the child should

- be confident in handling the child

- be fully attentive to the behaviour of the child
- minimal distractors
- carefully feed in small quantities

- allow the child to chew and or swallow

Children with feeding difficulties, neuro-developmental delay
- This group of children might not go through the standard feeding curve due to multiple
factors
- Additional feeding support and adjuncts may be needed
- Might start delay and progress slowly
- MDT approach

• Feeding during an inter-current illness

- Children might not have the normal appetite
- Continuing feeding during inter-current illness is important for quick recovery

- Use soft and palatable food types ex: yogurt, jelly which are easy to swallow
- Important to catch up with the nutrition once recovered from the illness
• Feeding children with chronic disorders
- Children might not have the normal appetite
- In contrast, the calorie need is more

- Might need especial feeds due to the underlying disease ex: children with liver disease
will require special feeds
 13.Immediate care of the newborn

Warmth Normal breathing

The basic needs

of a baby at
birth

Mother’s milk Protection from

infection

Basic Newborn Interventions – At birth

1. Skilled care at birth
2. Antenatal steroids
3. Prophylactic antibiotics for PROM
4. Delayed cord clamping & cord care
5. Skin to skin contact
6. First breast feed within 1 hour of birth
7. Prevention of hypothermia
8. Effective bag and mask ventilation
9. Vitamin K prophylaxis
10. Identifying major congenital anomalies

1. Skilled care at birth

• In Sri Lanka >98% of births attended by skilled health care worker
2. Antenatal steroids

Dexamethasone 8mg IM every 12 hours ( 2 doses)

• Prematurity: 10-12%
• For mothers at risk of giving birth at <35weeks gestation
• Complications of prematurity reduced – especially SDLS
• Optimal benefit when delivery occurs 24 hours after completing therapy.

3. Prophylactic antibiotics for PROM

Erythromycin / Ampicillin / Penicillin

• Antibiotics to the mother for prolonged rupture of membranes (>18hours)

• Prevents early onset sepsis in the newborn
• Prevents
Maternal temperature, FBC,early
CRP,onset
HR, sepsis in thevaginal
HVS (high newbornswabs) should be monitored.

Ten steps at birth (ENCC)

Drugs used: erythromycin / ampicillin /penicillin
1. Call out the time of birth
2. Dry baby with a warm clean towel or a piece of cloth; wipe eyes
Monitor : maternal temperature, FBC, CRP, HR, HVS (high
3. Assess the baby’s breathing while
vaginal drying
swabs)
4. Delayed cord clamping (change gloves before clamping)
5. Deliver baby on to mother’s abdomen after cord clamping
6. Cover mother and baby with warm cloth

7. Put a hat on the baby’s head

8. Baby remains between mother’s breasts skin to skin contact
9. Place an identity label on baby
10.Encourage first breastfeed within one hour of birth
4. Delayed cord clamping & cord care

Delay in umbilical cord clamping; Cord care

• for at least 1 minute for • Clamp & cut cord 2 to 5cm

• newborn infants not requiring from babies abdomen
resuscitation • Observe for oozing blood.
• Hold at or below placental • Put nothing on the stump
• Leave stump uncovered
level (if possible)
and dry

5. Skin to skin contact

• Naked baby between mother’s naked breasts,
• Cover them both

Advantages:
▪ Establish breastfeeding early
▪ Prevent hypothermia
▪ Bonding
▪ Colonise with maternal flora

6. First breastfeed within 1 hour of birth

• Facilitate immediate and uninterrupted skin-to-skin contact and support mothers to
initiate breastfeeding as soon as possible after birth( within 1 hour)
 Eye care
Skin care( prevent hypothermia)
• No special treatment
• Wipe amniotic fluid / meconium
/ blood at birth • Wipe with dry clean cloth
• Dry scalp and hair • Wash any maternal blood /
• Do not rub vigorously and wipe vernix
away vernix • with distilled water on
• Bathe only after 24 hours sterile cotton wool
• Further action only if sticky
Care / eye is red
after
birth
Nursing care
Umbilical care
• Baby with mother or under
• Cut between 1-2 inches from skin
warmer
• Wipe end with sterile gauze
• Check cord clamp
• Count number of vessels
• Check weight
• Observe for bleeding; leave stump
• Check & document temperature
uncovered
• Administer IM Vitamin K
• Do not apply any substance to
• Observe CTBH
stump

9. Vitamin K administration
1mg for term
0.5mg for preterm
• Routinely administered intramuscularly(1ml syringe with 23G needle)
• To prevent haemorrhagic disease of newborn

10. Identifying major congenital anomalies

By medical officer / nursing officer / By medical officer
midwife
• Dysmorphism • Heart sounds on both sides (by
• Excessive drooling MO)
• Cleft palate & hair lip • Femoral pulse (by MO)
• Eyes /ears /spine / limbs /scalp
swellings
• Anal/ urethral anomalies
14.TRANSPORTATION OF A SICK NEWBORN

PATHWAY

REFERRAL CENTRE (Initial referral to arrival of transport team)

TRANSPORT (From arrival at referring hospital to arrival at receiving hospital)

RECEIVING CENTRE (Departure from receiving unit following completion of transfer)

Stage 1: From initial referral up to arriving at the referring hospital

The ACCEPT approach

• A - assessment - Correct/accurate assessment of presenting problems and subsequent

actions. what is the problem, what is being done, what effect, what is needed now
• C - control - Control Staffing, appropriate documents, equipment and vehicle for transfer
• C - communication - Communication and documentation prior to arriving at the referring unit.
Speak to parents.
• E - evaluation - Prioritisation, assessment of urgency, appropriateness of transfer before
departing
• P - preparation, packaging, pre-departure checks. Preparation of equipment and vehicle
• T – transportation- During journey to the referring hospita

Counselling the family

• Stressful time for family - plans and hopes disrupted 

• Accept emotional outbursts calmly
• Explain baby’s condition thoroughly and need for transport as clearly as possible
• Provide assurance of best possible care and identity preservation
• Try to show the baby to the mother / father prior to transfer
• Obtain several contact phone numbers of parents and give to accepting hospital
• Provide direct updates to parents later or via referring hospital
 • Transfer mother to the hospital baby is being sent to or to a hospital in close proximity
as soon as possible Obtain mother’s blood sample – 5cc (more if anticipating exchange
transfusion etc) to plain clearly labelled bottle.
• Obtain consent for transfer and specifically for surgeries / procedures etc if anticipated
• Advice mother / staff of referring hospital regarding expression /storage and transport
of breast milk

Pre-transfer stabilization

• Assessment – vital signs, complete physical examination by transport team

• Establish genuine indication for transfer
• Stabilization of vital parameters:
• TOPS – temperature, oxygenation, perfusion, sugar
• DO NOT ATTEMPT TRANSFER OF UNSTABLE NEWBORNS
• Transport itself a high risk for destabilization
• Check tube / line positions by X-ray before setting out if feasible
• Secure endotracheal tubes, IV access. IC tubes
• CHECK LIST
• Vitamin k, antibiotics before the transfer

Preparation - On Arrival

• Introduce team
• Connect all rechargeable equipment to the mains
• History, examine baby, check investigation results
• Get copies / originals of X-rays and investigation results
• Identify priorities
• Make a plan – Communicate it

Packaging the Patient

1. Airway – position, security, fixation
2. Breathing – Monitoring SaO2, ETCO2, Tc PO2.
3. Circulation – ECG, iBP, check and secure all lines.
4. Dextrose – Maintenance fluids
5. Temperature – Trans warmer, Temp probe • Secure all access - chest drains to flutter
valves, ETT, NG tubes • Secure patient to trolley - Secure trolley to vehicle
Transportation
▪ Always check and utilize ambulance power and gas supplies
▪ Always ensure trolley, incubator, equipment and patient are secure before departure
▪ Nothing should be carried loose
▪ Staff must wear seatbelts – ambulance should stop if there is a need to unbuckle

Stage 3:

From arriving at the receiving hospital to completion of the transfer process

▪ Assessment Identifying previously unrecognized problems on arrival at the receiving
unit.
▪ Control Delegation of tasks, responsibilities.
▪ Communication Handover, communication and documentation
▪ Evaluation
▪ Preparation Preparing baby for care at the receiving unit, transfer between cot and
incubator, equipment.
▪ Transportation After leaving the receiving hospital
 15. INTRODUCTION TO CLINICAL GENETICS
Genetic diseases

Chromosomal Multifactorial
abnormalities inheritance

Single gene Mitochondrial

disorders inheritance

CHROMOSOMAL ABNORMALITIES

NUMERICAL ABNORMALITIES STRUCTURAL ABNORMALITIES

– change in chromosome number 1) DELETION
❖ Due to Non dysfunction during mitosis 1 or ❖ Part of chromosome is missing
2 • Cri-du-chat
• Velorcardiofacial xn
➢ ANEUPLOIDY – changes in single • Prada will xn
chromosome • Williams xn
o Trisomy – extra single chromosome
• Trisomy 21 – down Xn 2) DUPLICATION
• Trisomy 13 – patau Xn ❖ Part of chromosome get duplicated
• Trisomy 18 – Edward Xn
• 47,XXY – klinefelter Xn 3) INSERTION
❖ Part of chromosome get inverted
o Monosomy – absence of single and inserted in to same
chromosome chromosome
• 45,X - Turner Xn
4) Translocation
➢ POLYPLOIDY – change in pair of identical ❖ Part of chromosome get separated
chromosome and inserted into another
o Triploidy – addition of pair of chromosome chromosome
• Receprocal translocation
• Robertsonian translocation
Diagnosis –
Diagnosis–
▪ FLOURESECENCE IN SITU
▪ KARYOTYPING of Peripheral blood HYBRIDIZATION
lymphocytes/ skin fibroblasts ▪ Array comparative hybridization
▪ chromosomal micro array
 SINGLE GENE DISORDERS
1) SUBSTITUTION 2) INSERTION 3) DELETION

SUBSTITUTION – POINT MUTATION

• A single base of a codon is replaced by another type of base. Hence amino acid can be change.
• In substitution ,
1. altered codon encodes the same amino acid in previous sequence – SILENT MUTATION
2. altered codon encodes for another amino acid – MISSENSE MUTAION
3. altered codon encode for stopping codon – NONSENSE MUTATION

INSERTION – Addition of new base to a codon

DELETION – Loss of base from codon.

 PATTERN OF INHERITANCE OF SINGLE GENE MUTATIONS

PEDIGREE

AUTOSOMAL DOMINANT Y linked

PATTERN OF INHERITANCE

AUTOSOMAL RECESSIVE X- linked recessive

X-linked dominant
Red Ribbon For All Children

R – Rickets( vit D resistant)

R- Rett syndrome

F – fragile X syndrome

A -Alport syndrome

C -charcot-Marie-Tooth disease
Girls Do Come For CHAWAL

G - G6PD deficiency

Do – Duchene muscular dystrophy

Come – Red-Green color blindness

For -fabry disease ( alpha

galactosidase deficiency)

C – Chronic granulomatous disease

H – Haemophilia A and B, hunter

disease

A – Agammaglobulenemia

W -Wiskott Aldrich syndrome

A - Albinism

L – leisch nyhan syndrome

DIAGNOSIS OF SINGLE GENE DISORDERS

1. Array comparative genomic hybridization

2. Direct DNA based mutation testing
❖ Direct DNA sequencing of a gene
❖ Whole exome sequencing
❖ Whole genome sequencing
 16. Common Congenital Abnormalities.
Commonest congenital abnormalities are as follows,

1. Cleft lip/ palate

2. Absent red reflex
3. Sternocleidomastoid tumor
4. Other neck pathologies
5. Tongue tie

6. Preauricular skin tags

Congenital Abnormalities can be subdivided according to the systems that they are affecting.
1. Congenital abnormalities causing respiratory distress

 Congenital heart disease

 Choanal atresia
 Diaphragmatic hernia
 Tracheo oesophageal fistula
 Congenital lobar emphysema
 Congenital cystic adenomatous malformation of the
lung
2. Gastrointestinal tract abnormalities

Pyloric stenosis
Duodenal atresia/intestinal atresia
Malrotation/ volvulus
Hirschsprung disease
Anal atresia
Omphalocele
Gastroschisis
3. Orthopaedic abnormalities

 Talipes equinovarus
 Developmental dysplasia of the hip
4. Neurological abnormalities

 Encephalocele

 Anencephaly
 Spina bifida
 Meningomyelocele
5. Genitourinary abnormalities

Cryptorchidism
Hypospadias
Epispadias
Congenital hydrocele
Inguinal hernia
6. Umbilical abnormalities

7. Limb abnormalities
Now lets go through briefly about some common congenital abnormalities.

1. Cleft Lip
• Failure of the medial nasal and maxillary processes to join
• Incidence of cleft lip +/- cleft palate is 1 in 750
• Common in males
• Cleft lip can be unilateral or bilateral
• Surgical correction performed by 3 months

2. Cleft lip and palate

• Immediate problem is feeding

• Use of soft artificial nipples with large openings, a squeezable bottle and proper
instructions are important
• Can get problems with speech

3. Absent red reflex

• Leukocoria
• When light is shone through iris – retina appears red
• In leukocoria – retina is abnormally appears white
• Common etiologies
• Retinoblastoma
 • Retinopathy of prematurity
• Larval granulomatosis
• Posterior cataract
• Chorioretinitis
• Can be associated with microphthalmia

4. Sternocleidomastoid tumor

• Commonest cause of torticollis is childhood

• Present at 2-3 weeks of age
• Hard swelling within the muscle
• Treatment
• Physiotherapy
• surgery, if not responding

Other neck pathologies

• Thyroglossal cyst – anterior midline, moves with tongue protrusion

• Cystic hygroma – lymphatic origin, fluid filled lesion
• Branchial remnants – sinuses, fistulae, cysts

5. Tongue tie

• Short lingual frenulum

 • May have difficulty with feeding
• Not associated with speech problems

6. Diaphragmatic hernia

• Communication between the abdominal and thoracic cavities with or without

abdominal contents in the thorax

• 90% - Bochdalek hernia – defect in the posterolateral portion of the diaphragm

• Defect is more common in the left side

7. Esophageal atresia and Tracheo esophageal fistula

• Esophageal atresia is the most common congenital anomaly of esophagus

• >90% associated with trachea esophageal fistula
8. Congenital abnormalities of the lung
i. Congenital lobar emphysema

ii. Congenital cystic adenomatous malformation

9. Hypertrophic pyloric stenosis

• Approximately 1-3/1000 infants

 • Non-bilious vomiting is the initial symptom
• Vomiting may or may not be projectile
• But progressive
• Occurring immediately after a feed
• Usually starts after 3 weeks
• Hypochloremic metabolic alkalosis
• Hyperbilirubinaemia is the most common clinical association
• The surgical procedure of choice is pyloromyotomy

10. Duodenal atresia

• 1 in 10000 live births

• 25-40% of all intestinal atresia
• 50% of infants with duodenal atresia are premature
• Concomitant congenital anomalies are common
• Hallmark is bilious vomiting without abdominal distension
• Double bubble sign on plain radiograph

11. Omphalocele (Exomphalos)

• Herniation of abdominal organs through a central abdominal wall defect

 • Membrane is covering the abdominal contents
• Associated with major congenital anomalies or part of a syndrome
• Immediate care – cover with plastic wrap
• Decompensate the GI tract
• Maintain thermoregulation
• Keep NBM and give IV fluids

12. Gastroschisis

• Birth defect of the anterior abdominal wall

• Can be detected antenatally, usually around 18-20 weeks of gestation
• 2-5 cm opening within the umbilical ring
• Abdominal organs can extend outside the abdomen
• Surgery is needed to close the abdominal defect
• Keep NBM and continue IV fluids prior to surgery
13. Anorectal atresia

• Imperforated anus
• Incidence – 1 in 5000 live births
• Most are sporadic
• Can be associated with
• other atresia – esophageal atresia
• VACTERL association
• Caudal regression syndrome
• 2 broad categories – high ( supralevator) or low (infralevator)
• Low subtypes - treated with anoplasty
• High subtypes – treated with colostomy with subsequent potential repair

14. Talipes equinovarus (club foot)

• Postural or positional – not true club foot

• Congenital club foot
• Idiopathic
• Syndromic

• Deformity involving malalignment of the calcaneotalar – navicular complex

• Plantarflexion (cavus)and adduction of the forefoot/midfoot
• Hindfoot is in varus and equnius
• Occur commonly in males
• 50% bilateral
• 1 in 1000 births
• All patients exhibit calf atrophy
• Higher association with DDH than in general population

Management
• X-rays not recommended in idiopathic club foot
• Treatment should be initiated as soon as possible after birth – nonoperative
treatment
• Tapping and strapping, manipulation and serial casting
• Surgical release usually between 3-12 month of age
• Ponseti method – specific technique for manipulation and serial casting and surgery
• It is minimally invasive rather than noninvasive
15. Developmental dysplasia of the hip
• Spectrum of pathology in the development of the immature hip joint
• DDH is classified in to 2 major groups
• Typical DDH and tetrologic DDH
• Typical – DDH in otherwise normal patients
• Tetrologic – usually have identifiable cause, arthrogryposis or a genetic syndrome
• Etiology remains unknown
• Final pathway is increased joint laxity which fails to maintain a stable femoro-
acetabular articulation
• May have positive family history
• Common among girls (80%)/ breech presentation

Possible associated factors

• Hormonal influence – relaxin, which increases joint laxity
• First pregnancy
• Tighter intrauterine space
• Oligohydramnios
 • Large birth weight

Clinical features
Neonates
 Asymptomatic
 Screened by specific maneuvers
 Barlow – assess the potential for dislocation of an initially nondisplaced hip
 The examiner adducts the flexed hips and gently pushes the thigh posteriorly
 In positive test – the hip is felt to slide out of the acetabulum
 Ortolani test – reverse of the Barlow test
 The examiner attempts to reduce a hip that is dislocated at rest
 The examiner grasps the thigh between the thumb and index finger
 Lifts the trochanter while simultaneously abducting the hip
 In positive test – the femoral head slips into the socket with a cluck ( palpable not
audible)

Infants
 At2nd or 3rd
month of life – soft tissue begin to tighten
 Maneuvers are not reliable
 Physical signs
 Limited hip abduction – most reliable sign of a dislocated hip in this age group
 Apparent shortening of the thigh (Galeazzi sign)
 Proximal location of the greater trochanter
 Asymmetry of the gluteal or thigh folds
Walking child
 Limp
 Waddling gait
 Leg length discrepancy
 Affected side appear shorter than normal side
 Toe walking on the affected side
Limited hip abduction

Management
• Ultrasonography is superior to radiography
• Goals of management are to obtain and maintain a concentric reduction of the femoral
head within the acetabulum
• Newborns to 6 months
• Treat with Pavlik harness as soon as possible
• A significant proportion normalize with in 3-4weeks
• 6 months to 2 years
• Closed reduction under GA
• >2 years
• Open reduction
16. Neural tube defects
a. Spina bifida occulta
b. Meningocele
c. Meningomyelocele
d. Encephalocele
e. Anencephaly
17. Cryptorchidism

Absent of at least
1 testicle in scrotum
• 3% of term and 30% of preterm
• 80% descend by the third month of life
• Sequalae of cryptorchidism
1. Infertility
2. Psychological consequences
3. Risk of malignancy

• Ochidopexy

18. Hypospadias

• Urethral opening is ectopically located on the ventral aspect of the penis

• Affecting 1 in 250 male newborns
• Usually there is incomplete development of the prepuce – dorsal hood
• Circumcision should be avoided
• Because foreskin is used in the repair
• Ideally surgery done 6-12 months of age
19. Epispadias

• Both males and females can be affected

• Epispadias is in the spectrum of exstrophy anomalies
• Urethral meatus is on the dorsal aspect of the penis
• In females the clitoris is bifid and the urethra split dorsally
• In severely affected males and in all females with epispadias – there is total urinary
incontinence ( sphincter is incompletely formed )

20. Inguinal hernia

• 0.8-4.5% in term infants and nearly 30% in preterm, LBW infants

• Most commonly Indirect hernias – 99%
• More common in males
• 60% occur on right side, 30% on left side, 10% of them are bilateral
• Need surgical intervention
 21. Umbilical hernia

• Often associated with diastasis recti

• Caused by incomplete closure or weakness of the muscular umbilical ring
• LBW is a risk factor
• Consists of omentum or portion of small intestine
• Most appear before 6 months and disappear spontaneously by 1 year
• Strangulation of intestinal contents is extremely rare
• Defect - <1cm in diameter to as much as 5 cm
• Indications for surgery
A. Hernia persisting 4-5 years
B. Cause symptoms
C. Becomes strangulated
D. Progressively larger after age 1-2 years

Other umbilical abnormalities

Patent urachus
• Due to failure of closure of the allantoic duct
• Clear, light-yellow fluid discharge from umbilicus
• Can be associated with bladder outlet obstruction
22. Finger and toe abnormalities

Polydactyly ( extra digits)

Syndactyly ( webbing)

Clinodactyly – incurving of finger – usually 5 th finger

23. Absent radius

• Associated with syndromes

• TAR syndrome
• Holt oram syndrome
24. Skin abnormalities in newborn
a. Port wine stain

b. Capillary haemangioma
c. Erythema toxicum

d. Milia

e. Mongolian blue spots

f. Epstein pearls
 17.Small for gestational age and IUGR
WHO definitions
Low Birth Weight (LBW), defined as an infant
with a birth weight of less than 2500 g
regardless of gestational age at the time of
birth
Very low birth weight (VLBW) < 1500 g
Extremely low birth weight (ELBW) <1000 g

Small for gestational age Intrauterine growth

restriction(IUGR)
• Those who are smaller in size
than normal for • Refers to a condition in which
the gestational age a fetus is unable to achieve its
• Most commonly defined as a genetically determined
weight below the potential size as per the race
10th percentile for the and gender of the fetus
gestational age & gender • Not all newborns that are SGA
(Williams1982, WHO 1995) are pathologically growth
• Severe SGA - a length less restricted and, in fact, may be
than 2.5 SD below the mean constitutionally small

Symmetrical (from early Asymmetrical

pregnancy) Types of IUGR and • Uteroplacental insufficiency
• Congenital infections aetiology • Maternal malnutrition
• Chromosomal • Maternal hypertension
problems
 Aetiology of IUGR

IUGR

• Reduced maternal
vascular supply
• Constitutional
• (pre-eclampsia, • Undernutrition
• Genetic
hypertension, DM, • Maternal
syndromes,
• Chromosomal renal disease) hypoxia
chromosomal
• Expression of • Thrombosis, • Drugs /
• Structural
placental infarction substance abuse
malformations
growth factors • (Maternal LE, • Smoking (main
• Congenital
(e.g.IGF-1) antiphospholipid reason in
infections
syndrome, sickle western
(CMV, Rubella)
cell disease) countries)
• Sharing of uterine
vascularity(multipl
e gestation)

Pathophysiology Asymmetrical
Symmetrical • Growth failure with head growth relatively
preserved
• Growth failure affecting weight, length
• Utero-placental insufficiency-Reduced O2 transfer
and head to fetus (Fetus preserves blood supply to vital
• Caused by fetal factors organs (brain, myocardium, adrenal glands) at
• Chromosomal, infection, syndromes expense of kidney, GI tract, limbs and
• If swallowing affected, Mother will have subcutaneous tissues)
polyhydramnios • normal head growth BUT reduced abdominal
E.g. Trisomy 21 growth from reduced glycogen stores in the liver
• Infants likely to be small throughout • oligohydramnios from reduced urine production
childhood • If allowed to progress - fetal acidosis and death
 Clinical features

Consequences of progressive uteroplancental failure

Postnatal issues
Short term
• Perinatal asphyxia, meconium Long term
aspiration persistent pulmonary • Poor growth in about 10%, the
hypertension others will catch up growth by
• Hypothermia 2 years
• Hypoglycemia, hyperglycemia, • Poor neurodevelopment
hypocalcemia outcome at school-going age
• Polycythemia, jaundice and adulthood
• Feeding difficulties, feed • More susceptible to develop
intolerance adult-onset diseases e.g.
• Necrotizing enterocolitis, late- diabetes mellitus
onset sepsis, pulmonary
hemorrhage

Management

Antenatal care
• Intensive fetal surveillance to maximize Postnatal care
gestation without compromising the • Approach to small baby
fetus • Hypothermia-
o Reliable dating of pregnancy / thermoregulation
identify high risk mothers
• Kangaroo mother care (KMC)
o Fetal abdominal circumference as
• Hypoglycemia- feeding
screening (SFH unreliable)
• Nutritional supplements
o Fetal cause (anomaly scan,
karyotype)
o Monitor fetal growth and well –being
o (umbilical artery / middle cerebral
artery doppler blood flow velocity;
biophysical profile unreliable)
o Delivery when indicated
Postnatal care
Approach to small baby
• Talk to parents antenatally. Give idea of what to expect Find out any issues
• Careful liaison with Obstetric team
• Preparation of resuscitation equipment
• ABC
• Minimal handling
• Neutral thermal environment
• “Warm and Pink”
• Assess respiratory support needs: (Vent, CPAP, Oxygen)
• Consider possibility of infection
• Nursery/incubator care
• Venous access
• Consider context
• Local resources
• Screening for and management of known complications
• Hypoglycaemia, breast feeding/IV fluids
• GENTLE, minimalist approach
• Early consultation with transport team (intra-uterine preferred)
• EARLY re-discussion with parents

Hypothermia- Kangaroo mother care

thermoregulation
What is KMC?
WHO definition of hypothermia:
• Newborns / infants being carried
o mild 36.0°C– 36.4°C skin-to-skin
o moderate 32.0°C– 35.9°C • For babies <1800g
o severe < 32.0°C

How to prevent,
Advantages
• Warm delivery room
• Radiant warmer • Promotes exclusive breastfeeding
• ‘warm chain’ • Enhances parent-infant bonding
• Avoid early weighing, bathing • Earlier discharge from hospital
• Use hats / socks when • More stable vital signs; including
appropriate better thermal control
• Incubator if indicated
• Kangaroo mother care
 Nutritional supplements
Hypoglycemia-feeding
Vitamin D - All LBW infants who exclusively
• More common in asymmetrical IUGR breast feed should receive 400IU daily of
• Reduced glycogen stores vitamin D
• Need to monitor blood glucose Multivitamin drops - from the time the baby
• Breastfeeding ideal receives full enteral feeds
• Expressed breast milk – by cup
• Demand feeds as soon as possible Calcium and phosphorous - for all VLBW
• May rarely need intravenous fluids (1500g)

Iron supplementation from day 14

Postnatal growth
Symmetrical IUGR (because of less cell numbers at birth):

• are underdeveloped postnatally and

• remain small throughout life

Asymmetrical IUGR (normal cell numbers)

• good prognosis and

• good postnatal growth
• Lower strength and work capacity

Neurological problems
➢ Lower scores on cognitive testing
➢ Difficulties in schools or require special education
➢ Gross motor and minor neurologic dysfunction
➢ Behavioral problems (attention deficit hyperactivity syndrome)
➢ Cerebral palsy
➢ Low social competence
➢ Poor academic performance
➢ Lower levels of intelligence
➢ Poor perceptual performance
➢ Poor visuo-motor perception
THE END