Neonatal Resuscitation

 Neonatal resuscitation is defined as the set of

interventions at the time of birth to support the
establishment of breathing and circulation
◦ Transition to EU (Extra uterine)life is the most
important period in neonatology
◦ 5 to 10 % require resuscitation.
◦ Failure to initiate and maintain effective respiration is
the most common delivery room emergency for
neonates.
Goals of neonatal resuscitation

1. Prevent the morbidity and mortality associated with

hypoxic-ischemic tissue injury.
2. Reestablish adequate spontaneous respiration and
cardiac output.
3. Improve the likelihood of preventing brain damage.
◦ In order to achieve this goal high-risk situations should be
anticipated during
 Pregnancy, labor, and delivery history and
 Identification of signs of fetal distress.
Neonatal resuscitation supplies and
equipment.
Suction equipment
 Bulb syringe
 Mechanical suction, tubing, and catheters
 Meconium aspirator
 8F feeding tube and 20 cc syringe

Intubation equipment
 Laryngoscope with straight blades (Number 0 and 1
for preterm and term infants, respectively)
 Face masks (preterm and term infant sizes)
 Oxygen source with flowmeter ….
When anticipating resuscitation
1. The radiant warmer is turned on and is heating.
2. The oxygen source is open with adequate flow
through the tubing.
3. The suctioning apparatus is tested and is functioning
properly.
4. The laryngoscope is functional with a bright light.
5. Testing of resuscitation bag and mask demonstrates an
adequate seal and generation of pressure.
How we can determine the need for
resuscitation?
 APGAR score
 The is a practical method of systematically assessing newborn
infants immediately after birth to help identify those requiring
resuscitation and to predict survival in the neonatal period.
 The 1-min APGAR score may signal the need for immediate
resuscitation, and 5-, 10-, 15-, and 20-min scores may
indicate the probability of successfully resuscitating an
infant.
 Evaluation of Newborn Infants
(The APGAR score)

SIGN 0 1 2
Color (Appearance) Blue, pale Body pink, Completely pink
extremities blue

Heart rate(Pulse) Absent Below 100 Over 100

Response to catheter in No response Grimace Cough or sneeze

nostril (Grimace)

Muscle tone (Activity) Limp Some flexion of Active motion

extremities

Respiratory effort Absent Slow, irregular Good, crying

• A total score of 10 indicates an infant is in the best possible condition.
• An infant with a score of 0–3 requires immediate resuscitation.
 Neonatal Resuscitation flow algorism
Time frame Birth ROUTINE CARE
 Keep warm(Skin to skin
_____ contact)
 Term gestation?
 Clear amniotic fluid? Yes  Clear air way if needed
 Breathing/crying?  Dry neonate
 Good muscle tone?  Assess color
30 sec

 Medication (Vit K and

NO TTC eye ointment
A Provide warmth  Initiate breast feeding
Position, Clear air way
Dry, Stimulate and reposition

Observational
Evaluate RR,HR Breathing,
_____ care
and color HR >100 ,Pink
Breathing& HR
>100 but Pink
30 sec

Supplementary
Cyanosed
Apnea oxygen
/HR<100
Persistent cyanosis
 Apnea Persistent cyanosis
/HR<100 Post resuscitation
Effective ventilation
Positive pressure Observation/care
HR>100 and Pink
B ventilation*
HR<60 HR>60
HR 60 -80 and
not responding
_____
Continue PPV*
C
Administer chest compression
30 sec

HR<60

D
Administer epinephrine
_____ Volume expansion
? Sodium bicarbonate

* Endotracheal intubation
 Ineffective bag and mask ventilation
 If tracheal suctioning is required (MAS)
 Diaphragmatic hernia is suspected
 Prolonged PPV is required
 Neonatal resuscitation…
 Rate of chest compression to ventilation is 3 to 1
 Medications
◦ Epinephrine :- 0.1–0.3 mL/kg of a 1 : 10,000 solution
:- Intravenously or intratracheally
◦ volume expansion :- 10–20 mL/kg of an isotonic solution
◦ Sodium bicarbonate :- 2 mEq/kg, 0.5 mEq/mL of a 4.2% solution
slowly (1 mEq/kg/min) if metabolic acidosis
◦ Make sure ventilation is adequate before giving
Bicarbonate.

◦ NB: Restoration of oxygenation and tissue perfusion

is the main treatment of metabolic acidosis
associated with asphyxia
 Severe asphyxia may also depress myocardial function
and cause cardiogenic shock despite the recovery of
heart and respiratory rates.
◦ Poor peripheral perfusion, weak pulses, hypotension,
tachycardia, and poor urine output.
◦ Dopamine or dobutamine administered as a continuous infusion
(5–20 μg/kg/min) and fluids should be started after the initial
resuscitation effort to improve cardiac output
◦ Epinephrine (0.1–1.0 μg/kg/min) may be indicated for infants
in severe shock who do not respond to dopamine or dobutamine
Hypoxic-ischemic encephalopathy

13
Hypoxic-ischemic encephalopathy/HIE
 The most common consequence of perinatal asphyxia
 Is an important cause of permanent damage to CNS
tissues that may result in neonatal death or manifest later
as cerebral palsy or developmental delay.
◦ 15 - 20% of infants with hypoxic-ischemic encephalopathy
(HIE) die in the neonatal period,
◦ 25–30% of survivors are left with permanent neuro-
developmental abnormalities (cerebral palsy, mental
retardation).
05/21/2024 14
 The greatest risk of adverse outcome is seen in infants
with fetal
◦ acidosis (pH <7.0),
◦ a 5-min Apgar score of 0–3,
◦ hypoxic-ischemic encephalopathy (altered tone, depressed
level of consciousness, seizures)
May be due to:
1. impaired maternal oxygenation.
2. Decreased blood flow from the mother to placenta or
from placenta to the fetus.
3. Impaired gas exchange across the placenta
4. Increase fetal O2 requirements.

15
Such situations may interact in cases of :

• Maternal: hypertension, vascular disease,

D.M. Hypotension, infections
• Hyperstimulation with oxytocic agents
• Placental: infarction, fibrosis, abruption
• Cord Accidents: ( prolapsed, knotting ,
compression )
• Fetal : anemia , hydrops, infection, and
post maturity.

16
Perinatal asphyxia
Respiratory depression Circulatory depression

Low cardiac output

Hypoxemia Decreased tissue perfusion
Hypercarbia Ischemia
Respiratory acidosis Metabolic acidosis
Capillary leak, edema

Multi-organ dysfunction

17
 Pathophysiology:HIE
 Hypoxia  Stimulation of anaerobic glycolysis and
increased local tissue lactate and fall of PH.
• Decrease cardiac function  hypotension, loss of
cerebral blood flow auto regulation, irreversible tissue
ischemia.
• Release of Excitatory and toxic amino acids,
particularly glutamate, accumulate in the damaged
tissue.
• Increased amounts of intracellular sodium and calcium may
result in tissue swelling and cerebral edema.
• There is also increased production of free radicals and nitric
oxide in these tissues.
18
CLINICAL MANIFESTATIONS OF HIE

 Depends on the organ/organs affected

◦ Altered consciousness
◦ Tone problems
◦ Seizure activity
◦ Autonomic disturbances
◦ Abnormalities of peripheral reflexes

05/21/2024 19
Sarnat staging of hypoxic-ischemic
encephalopathy.
Grade 3 Grade2 Grade 1
(severe) (moderate) (mild)
Coma Lethargy Irritable/ hyper alert Level of
consciousness
Flaccid Hypotonia Normal or Muscle tone
hypertonia
Depressed or absent Increased Increased Tendon reflexes

Frequent Frequent Absent Seizures

Absent weak Normal Complex
reflexes
High mortality and Variable Good Prognosis
neurological disability (80% )
(50% Death Normal (100%) Normal
50% major sequelae)
21
 Diagnosis
 There is no clear diagnostic test for HIE
◦ Abnormal findings on the neurologic exam in the first few days after
birth is the single most useful predictor that brain insult has occurred in
the perinatal period
 Essential Criteria for Diagnosis of HIE:
◦ Metabolic acidosis (cord pH <7)
◦ Early onset of encephalopathy
◦ Multisystem organ dysfunction
Investigations:
EEG  to determine severity and presence of seizures.
1. Cranial U/S : to determine presence of IC Hemorrhage or
brain edema.
2. CT scan :

22
Systemic Complications

 Acute renal failure in up to 20% of asphyxiated term

infants
 Myocardial dysfunction and hypotension in 28-50%

of term infants
 Elevated LFTs in 80-85% of term infants
 Coagulation impairment is relatively common in

severely asphyxiated infants

05/21/2024 23
Management of HIE
Treatment is supportive.
 appropriate ventilators support

 IV fluid 2/3 of maintenance

 avoid BP fluctuation

 Correct metabolic abnormalities

 Anti convulsant

 Maintain temperature, perfusion, oxygénations & ventilation

 Correct & maintain normal metabolic & acid base

 Prompt management of complications

 May need total parenteral nutrition (TPN)

24
Thermoregulation
 The newborn cannot regulate its temperature well ; needs to be
protected from cold and heat.
 •A newborn is at risk of Heat loss/Hypothermia:
 High Body surface area : body weight ratio.
 Poor Insulation from the coat/ little subcutaneous fat
 Large head in proportion to the body
 Less stores of brown fat & glycogen (preterm, SGA)
 Inability to take enough calories
 Limited ability to shiver

05/21/2024 25
 Goal of Thermoregulation
 To maintain correct body temperature range in order to:
– Maximize metabolic efficiency
– Reduce oxygen use
– Protect enzyme function
– Reduce calorie expenditure
Non shivering Thermogenesis
 Brown fat is an energy source for infants
 It can be found: Near Kidneys and adrenals, Neck,
mediastinum, scapular and the axilla areas.
 Can not be replaced once used
◦ When the air temperature around the baby is cool, thermo
receptors in the skin are stimulated.
◦ Non-shivering thermogenesis is initiated and brown fat is
burned for energy to keep the body temperature stable. This
is the infant’s initial response.
Cont’d
 The primary mechanism of heat production in the neonate is
through metabolism of brown fat or non-shivering thermogenesis
 Thermo neutral environment
 The temperature range during which:
◦ the basal metabolic rate of the baby is at a minimum
◦ oxygen utilization is least and baby thrives well
 Thermoneutral Environment- narrow range of environmental
temperature at which a given baby can maintain normal body
temperature with minimal O2 & fuel consumption
Cont..
 The normal range for axillary temperature is 36.5 –

37.5°C

 When heat loss exceeds the baby's ability to produce heat,

its body temperature drops below the normal range and it

becomes hypothermic.

05/21/2024 29
CONT’D
How the neonate looses heat?
Hypothermia < 36.5˚C
Classification of hypothermia is based on core
temperature
◦ NORMAL – 36.5 to 37.5˚C
◦ Cold Stress 36.0 to 36.4˚C
 Cause for concern
◦ Moderate hypothermia 32 –35.9˚C
 Danger, warm the newborn
◦ Severe hypothermia – below 32˚C
 Outlook grave, skilled care urgently needed
Physiologic consequences of cold stress
Cold stress
Metabolism Oxygen consumption

Brown adipose
use of tissue Respiratory rate
glucose metabolism
Release of FAs
Hypoxia
use of Glycogen
stores Anaerobic metabolism
Lactic acidosis
Hypoglycemia Metabolic
PH acidosis
Surfactant production
Failure to gain weight Pulmonary vasoconstriction

Further hyopxia

Respiratory distress
 Signs and Symptoms

Vasoconstriction
 Peripheral vasoconstriction occurs in an effort to
limit heat loss via blood vessels close to the skin
surface.
◦ Pallor and cool skin may be noted, due to poor peripheral
perfusion
Increased Respiratory Rate
 Pulmonary vasoconstriction occurs secondary to

metabolic acidosis.
◦ Increasing Respiratory Distress related to decreased surfactant
production , hypoxia , & acidosis
Restlessness
 Restlessness may be a type of behavioral thermoregulation
 The first sign may be an alteration in sleep patterns.
 Restlessness also indicates a change in mental status as cerebral
blood flow diminishes, due to vasoconstriction
Lethargy
 If thermo-instability goes unrecognized, the infant will become
more lethargic, as cerebral blood flow continues to diminish and
hypoxemia and hypoglycemia become more pronounced.
Cont…
Cardiac
 As central blood volume increases, initially the heart

rate and blood pressure increase.

Arrhythmias
 May result from depressed myocardial contractility

and irritability caused by hypothermia

Poor Feeding/Weight Loss
 Poor weight gain occurs when:

◦ calories consumed
◦ brown fat stores are used to make body heat.
Prevention of Hypothermia
 Hypothermia can be prevented by maintaining a
neutral thermal environment and reducing heat loss.
 A neonate is in a neutral thermal environment when
the axillary temperature remains at 36.5° - 37.5°C
(97.7° - 99.2° F) with minimal oxygen and calorie
consumption
Interventions for at Risk Infants
 Pre-warmed radiant warmer bed
 Pre-warmed incubator
 Do not leave a warmer bed or incubator in the manual
mode
 Heated water pad
 Warm and humidify inspired gases
Rewarming the Hypothermic Infant
 Always be prepared to intervene
 Rewarm slowly (0.5˚C per hour)
 Monitor closely (vital signs every 15 – 30min)
◦ Core temp
◦ Skin temp will be higher than axillary
◦ Blood pressure
 Rewarming may lead to vasodilation - hypotension
◦ Heart rate and rhythm
 Bradycardia & arrhythmias common with hypothermia
 Jaundice and
Hyperbilirubinemia in the
Newborn
Neonatal jaundice
 Is a yellowish discoloration of the skin and /or sclera due
to bilirubin deposition.
 Hyperbilirubinemia is a common and, in most cases,

benign problem in neonates.

 However, untreated, severe indirect hyperbilirubinemia

is potentially neurotoxic
 Conjugated-direct hyperbilirubinemia often signifies a

serious hepatic or systemic illness.

 It could be physiologic or pathologic
Neonatal Jaundice—yellowish skin
Bilirubin occurs in plasma in four forms

1. Unconjugated bilirubin tightly bound to albumin;

2. Free or unbound bilirubin (the form responsible for
kernicterus, because it can cross cell membranes);
3. Conjugated bilirubin (only fraction to appear in urine)
4. Delta (d) fraction (bilirubin covalently bound to albumin),
which appears in serum when hepatic excretion of conjugated
bilirubin is impaired in patients with hepatobiliary disease.
Physiology of bilirubin metabolism

Introduction
 Hemoglobin----Bilivervdin-----Bilirubin---Uptake in
the liver---Conjugation----Excretion
◦ Unconjugated bilirubin (indirect) is toxic to the brain
◦ Unconugated bilirubin cross blood brain barrier
◦ Conjugated bilirubin (direct bilirubin) is non toxic to the brain
and not cross blood brain barrier
 Comparison b/n physiological from
Pathological Jaundice
No Features Physiologic Pathological Jaundice
Jaundice

1 Clinical onset of jaundice (after >24 hrs <24 hrs

birth)

2 Jaundice still clinically visible Term < 8 days Term ≥8 days

(day after birth) Preterm < 14 days Preterm > 14 days

3 Peak Total Serum Bilirubin Term < 12 mg/dl Term > 12 mg/dl
(TSB)
Preterm < 15 mg/dl Preterm > 15 mg/dl

4 Rise in TSB < 5mg/dl/24 hrs > 5mg/dl/24 hrs

5 Conjugated serum bilirubin <2mg/dl >2mg/dl or 15 % of

level TB
Clinical assessment of jaundice
 Jaundice in the newborn progresses in cephalocaudal
direction.

Area of the body bilirubin level(mg/dl)

◦ Face 5-7
◦ Chest 10
◦ Abdomen/thigh 12
◦ Soles >15
Cont’d
History
 Age of onset
 Family history of Jaundice, pallor, splenectomy
 Previous sibling with Jaundice
 Maternal illness during pregnancy
 Delivery Hx eg. PROM →sepsis
prolonged labor →cephalhematoma
Cont’d
Physical Examination
 Proper classification of the newborn
according to GA, weight and both.
 Clolor , Pallor,
 Bruises and cephalhematoma
 Dark urine and clay colored stool
Investigations
 TSB with conjugated fraction
 CBC with RBC morphology
 Blood group of the baby with coomb’s test
 Specific investigations for suspected specific problems
Kernicterus

 Kernicterus, or bilirubin encephalopathy, is a neurologic

syndrome resulting from the deposition of unconjugated
bilirubin in the basal ganglia and brainstem nuclei

 In previously healthy, predominantly breast-fed term infants,

kernicterus has developed when bilirubin levels exceed 30
mg/dL.
Clinical Manifestations

 Phase 1 (1st 1–2 days): poor sucking, stupor,

hypotonia, seizures
 Phase 2 (middle of 1st wk) hypertonia of extensor
muscles, opisthotonos, fever
 Phase 3 (after the 1st wk): hypertonia
Management

Lower serum Bilirubin level

 Phototherapy
 Exchange transfusion

 Drugs
◦ phenobarbitone
Butanic curve
Principles of treatment

Phototherapy
The mechanisms by which phototherapy works are:-
1. Photoisomerization
◦ It will convert the toxic bilirubin to non toxic
molecule.
2. Intramolecular cyclization of bilirubin to lumirubin.
3. Photoxidation:- Conversion of bilirubin to polar,
colorless product
◦ Bilirubin absorbs light maximally in the blue range
(420-470 nm).
4. Bilirubin in the skin absorbs light energy, causing
Several photochemical reactions.
While baby is under phototherapy:

◦ Babies eye should be securely covered

◦ Take baby of phototherapy every 2 to 3 hours
◦ Monitor fluid and electrolyte status
◦ Increase fluid intake by 20 ml/kg
◦ Monitor temperature regularly
 Increase fluid intake by 25 %
Radiant phototherapy
Blanket phototherapy
Complications of phototherapy
 Increased insensible water loss
 Sterility if tests not well covered
 Retinal damage
 Erythematous skin rash
 Bronze baby syndrome-is the dark grey-brown
pigmentation of skin, mucous membrane and
urine following phototherapy
 Hypo or hyperthermia
Exchange Transfusion
 Most effective and reliable method of reducing
bilirubin level there by reduce the risk of brain damage
and kernicterus
 Can also help treat sever anemia
 One double volume exchange transfusion lowers serum

bilirubin to half pre exchange value

Indication of exchange transfusion
Indications
1. Hydrops fetalis
2. History of previous sibiling requiring an exchange
transfusion because of Rh isoimmunization in a baby
born with pallor and +ve direct coombs test
3. Cord Hgb < 11gm
4. Cord TSB >5 mg
5. Rate of rise of TSB > 5mg /24hrs despite
phototherapy
6. Rate of rise of TSB > 0.5mg/hr despite phototherapy
7. Any TSB > 12 mg in the 1st 24 hrs
8. Any TSB >20 mg in the neonatal period
 Complications of ET
1. Catheter related
◦ Infection
◦ Hemorrhage
◦ Portal and splenic vein thrombosis
◦ Air embolism
2. Hemodynamic problems
◦ Overload cardiac failure
◦ Hypovolaemic shock
◦ Arrhythmia (Catheter tip near sinus node in Rt Atria)
3. Electrolyte imbalance
 Hyperkalemia (old blood)
 Tissue hypoxia (old blood )
 Hypocalcaemia
 Increase or decrease Blood glucose
 Acidosis (sometimes late alkalosis due to breakdown of

citrate)
Other treatment modalities
 Phenobarbital 5 mg/kg to stimulate liver enzyme in
Crigler – Najjar syndrome.
 In case of Breast milk jaundice discontinuation of

breast milk for 1-3days

 Follow-up

 Follow up of Serum bilirubin level till discharge and

then 2 days after discharge
 For infant who had exchange transfusion, follow-up
for 2 years.
◦ Assess every time for the late complications

 Signs of deafness
 Cerebral palsy and
 Mental retardation
Summary
 Jaundice is yellowish discoloration of mucus
membranes and skin
 Isoimmune Hemolytic disease is the leading cause of

pathologic jaundice
 The feared complication of hyper biluribinemia is

kernicturus.
 Management is mainly by phototherapy and sometimes

double volume exchange transfusion.

Prematurity
Objectives
 Describe possible causes of preterm
 What health challenges do preterm neonates face?
 Discuss the complications of preterm birth
Key facts
 Every year, an estimated 15 million babies are born
preterm.

 In almost all countries of reliable data, preterm birth

rates are increasing.
 The possible explanations for the rise are?

 Globally, prematurity is the leading cause of death in

children under the age of 5 years.

 Three-quarters of them could be saved with current, cost

effective interventions if they had access to it.
The possible explanations for the rise are..

◦ Better measurement
◦ Increase in maternal age,
◦ Underlying maternal health problems
◦ Greater use of infertility treatment and increase rate of
multiple pregnancies.
◦ Changes in obstetrics procedures, increase in c/s.
 More than 60% of preterm births occur in Africa
and South Asia, but preterm birth is a global
problem.
 In the lower income countries , on average, 12% of
babies are born too early compared with 9% in
higher income countries.

05/21/2024 78
Definition
 Prematurity is defined as a birth that occurs
before 37 completed weeks (less than 259
days) of gestation.

 There are sub-categories of preterm birth,

based on the gestational age:
◦ Extremely preterm (<28 weeks)
◦ Very preterm (28-32 weeks)
◦ Moderate to late preterm (32-37 weeks)
Why does preterm birth happen?
 The etiology of preterm birth is multifactor
and involves a complex interaction between
fetal, placental, uterine and maternal factors.

◦ Approximately 70 to 80% of preterm births occur

spontaneously.

◦ The remaining 20 to 30% of preterm births are

medically indicated because of maternal or fetal
issues.
Cont’d
Fetal Uterine
 Fetal distress
 Multiple gestation
 Bicornuate uterus
 Erythroblastosis
 Incompetent cervix
(premature dilatation)
Placental
 Placenta previa
Other -
 Abruptio placentae
Premature rupture of
membranes
Maternal
 Preeclampsia Polyhydramnios
 Chronic medical illness Iatrogenic
 Infections
What health challenges do preterm neonates face?

 The ability to suck, swallow, and breath in a

coordinated fashion is not achieved until 34-36wks
gestation.
 Decreased ability to maintain body temperature
 Pulmonary immaturity
 Immature control respirations
 Immature cerebral vasculature
 Immature immune system.
 Common neonatal problems associated with
premature newborn
 Respiratory

◦ RDS
◦ Apnea
 CVS
◦ PDA
◦ Bradycardia ( with apnea
 Hematological
◦ Subcutaneous, organ( liver, cranial, adrenal) hemorrhage
 GI
◦ Poor GI function- poor motility, NEC
◦ Increased bilirubin level- direct and indirect
 Metabolic and endocrine
◦ Hypoglycemia
◦ Hypocalcaemia
◦ Hypothermia
 CNS
◦ IVH
◦ Hypothermia
 Renal
◦ Hypernatremia
◦ Hyponatremia
◦ Hyperkalemia
 Other
◦ Infection (congenital, perinatal, nosocomial
bacterial, viral, fungal and protozoa)
Management
 Standard care in the delivery room to prevent
hypothermia includes:
 Maintaining the delivery room temperature at a minimum of
26ºC
 Drying the baby thoroughly immediately after birth
 Removal of any wet blankets
 Use of prewarmed radiant heaters if resuscitation is necessary
Cont’d
Cont’d
 under a radiant heater;
 in an incubator, at 35-36°C

(95-96.8°F);
 by using a heated water-filled

mattress;
 in a warm room: the

temperature of the room should

be 32-34°C/89.6-93.2°F
 Breast-feeding
 Bathing and weighing
 postponed
Kangaroo mother care !
Necrotizing Enterocolitis
 It is a disorder characterized by ischemic necrosis of the
intestinal mucosa, which is associated with inflammation,
invasion of enteric gas forming organisms, and dissection
of gas into the muscularis and portal venous system.
◦ Occurs in 2 to 10% of VLBW infants.
◦ NEC is associated with an increase in mortality.
◦ Survivors are at increased risk for growth delay and
neurodevelopmental disabilities.
Clinical Manifestations
 Systemic signs are nonspecific and include apnea,
respiratory failure, lethargy, poor feeding, or
temperature instability.

 Hypotension resulting from septic shock may be

present in the most severe cases.

 Twenty to 30% of infants with NEC have associated

bacteremia, which may contribute to these
findings.
Cont’d
 Abdominal signs include distention, gastric retention
(residual milk in the stomach before a feeding),
tenderness, vomiting, diarrhea, rectal bleeding and
bilious drainage from enteral feeding tubes
Diagnosis
Abdominal radiography
 Free intraperitonial fluid -----perforation
 Pneumatosis intestinalis ------intramural

gas
Retinopathy of prematurity

 Developmental vascular proliferative disorder occurs in the

incompletely vascularized retina of premature infants.
◦ Incidence & severity of ROP increases with decreasing gestational age
or birth weight.
◦ Typically begins about 34 weeks, but may be seen as early as 30 to 32
weeks.
◦ Next to cortical blindness, ROP is the most common cause of childhood
blindness in the USA.
What are the consequences of preterm birth
later in life?

 Neurodevelopmental outcome: Impaired cognitive skills

 Motor deficits including mild fine or gross motor delay,
and cerebral palsy
 Sensory impairment including vision and hearing losses
 Behavioral and psychological problems
 Poor growth compared to those born full-term
 Impairment of lung function
THANK YOU!