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A PREMATURE NEWBORN
Definition Liveborn infants delivered before 37 week from the 1st day of
the last menstrual period
Term : 37-42weeks
Prem : < 37weeks Gestation
Moderate Prem : 31/32 36weeks
Severe prem : 24-30weeks
Etiology FETAL
Fetal distress
Multiple gestation
Erythroblastosis
Nonimmune hydrops
PLACENTAL
Placental dysfunction
Placenta previa
Abruptio placentae
UTERINE
Bicornuate uterus
Incompetent cervix
(premature dilation)
CF Skull
may suggest hydrocephaly
Lung
high respiratory rate
Heart
higher resting heart rate, up
to about 160 beats/min
Skin
thin and delicate and tends
to be deep red
gelatinous and
translucent (extremely
premature)
Fine, soft, immature hair
called lanugo frequently
covers the scalp and brow
and may also cover the face
of premature infants.
Assessme Prenatal gestational age
nt Of assessment
Gestation Determined by
maternal history,
clinical examination,
and
ultrasound
MATERNAL
Preeclampsia
Chronic medical illness
(cyanotic heart disease,
renal disease)
Infection (Listeria
monocytogenes, group B
streptococcus,
urinary tract infection,
bacterial vaginosis,
chorioamnionitis)
Drug abuse (cocaine)
OTHER
Premature rupture of
membranes
Polyhydramnios
Iatrogenic
Trauma
Ear - Earlobe has no cartilage
Soles - One or two transverse
creases; posterior three fourths
of sole smooth
Breast - barely perceptible or,
flat, or small bud (2mm)
Genitalia -
Male: Smooth or faint rugae
of scrotum
Female: Prominent clitoris,
flat or small labia minora
Postnatal gestational age
assessment
-Usually done because prenatal
estimation are not always
accurate.
1. Rapid assessment of
gestational age in
FALAH 16/17

examination delivery room

2. New ballard score
The score span from 10
to 50
Best performed at <12
hours of age if the infant
is <26 weeks gestation

Criteria
For Rapid
Gestatio
nal Age
At
Delivery

NEW 1. Posture 4. Popliteal angle

BALLARD Score 0 if the arms and legs are
SCORE extended
Score +1 if infant has begining
flexion of knees and hips, with
arm extended.
2. Square window
Flex the hand on the forearm
between the thumb and index
finger of examiner.
Apply sufficient pressure to
achieve as much flexion as
possible.
Visually mmeasure the angle
between hypothenar eminence
and the ventral aspect of
forearm.
3. Arm recoil
Flex arm for 5 seconds then
grasp the hand
Fully extend the arm and release.
If arm returns to full flexion, give
score of +4
Hold thigh in knee-chest
position with left index
finger and the thumb
supporting the knee.
Then extend the leg by
gentle pressure from
right index finger behind
the ankle.
Scarf sign
Take infants hand and
try to put it around the
neck posteriorly as far as
possible over the
opposite shoulder.
6. Heel to ear
Keep the pelvis flat on
table
Take the infants foot
and try to pull it as close
to the head as possible
without forcing it.
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Direct allows for accurate determination of gestational age at 2734

opthalmos weeks only.
copy normal embryological process of the gradual disappearance of
the anterior lens capsule vascularity is between 27 and 34
weeks of gestation.
Before 27 weeks, the cornea is too opaque to allow
visualization
After 34 weeks, atrophy of the vessels of the lens occurs.
FALAH 16/17

Grade Description

4 (27- Vessels cover te entire anterior surface of the lens

38w) or the vessels meet in the centre of lens
3 (29- Vessels do not meet in the center buat are close.
30w) Central portion of the lens is not covered by
vessels
2 (31- Vessels reach only to the middle-outer part of the
32w) lens
1 (33- Vessels are seen only at the periphery of the lens.
34w)

Calculate Chronological age = Current date D.O.B

(7/11/2016-10/7/2016) =3months 27days
corrected age = Current Age - (preterm weeks)
= 3mo 27d (40wk-32wk)
= 3mo 27d 8week/ 2mo
= 1months 27days (8 weeks)
Compliatio CNS Intraventricular hemorrhage*
ns Periventricular leukomalacia
Seizures
Retinopathy of prematurity
Deafness
Hypotonia*
Respi Respiratory distress syndrome (hyaline membrane
disease)*
Bronchopulmonary dysplasia
Pneumothorax, pneumomediastinum; interstitial
emphysema
Congenital pneumonia
Apnea*
CVS Patent ductus arteriosus*
Hypotension
Bradycardia (with apnea)*
GIT Poor gastrointestinal functionpoor motility*
Necrotizing enterocolitis
Hyperbilirubinemiadirect and indirect*
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Spontaneous gastrointestinal isolated perforation

Renal Hyponatremia*
Hypernatremia*
Hyperkalemia*
Renal tubular acidosis
Renal glycosuria
Edema
Metabolic Hypocalcemia*
Hypoglycemia*
Hyperglycemia*
Late metabolic acidosis
Hypothermia*
Osteopenia
Hemato Anemia (early or late onset)
Others Infections* (congenital, perinatal,nosocomial:
bacterial, viral,fungal, protozoal)
Ix Routine bloods: FBC/LFT/RP/Ca/Mg/PO4
US Brain (< 32 weeks) : 1st week (IVH) and 28days (PVL)
ROP @ 36weeks / 4-6weeks ( if <1.5kg, < 32weeks, ventilated)
Hearing Assessment Indications:
Fhx of hearing loss
Ventilation >5days
Hyperbilirubinemia
Craniofacial abnormalities
Head Trauma
VLBW < 1.5kg
Ototoxic medication
Parental concern
In-Utero infections
Meningitis
Low Apgar Score
Mx 1)Before and during labour
Prewarmed incubator and appropriate equipment
2)Adequate Resuscitation
3)Transfer from Labour Room (LR) to NNU (Neonatal Unit)
Use prewarmed transport incubator if available. If not the
baby must be wiped dry and wrapped in dry linen before
transfer.
For ELBW infant, from birth, the infant should be wrapped
up to the neck with polyethylene plastic wrap or food plastic
bag to prevent evaporative heat loss.
If infants respiration is inadequate, keep the infant
intubated with manual bag ventilation with oxygen
during the transfer.
For those with mild respiratory distress, preferably initiate
CPAP in labour room, and if tolerated CPAP during transport.
Use a pulse oxymeter where available.
4) Admission Routine
Ensure thermoneutral temperature for infant.
Ventilation in NICU is often necessary if ventilated during
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transfer
Maintain SaO between 89-92% for ELBW; 90-94% for the
larger preterm
Bathing can be omitted.
Head circumference (OFC), length measurements, examine
and weigh the infant.
Assess the gestational age with Dubowitz or Ballard score
when stable
Monitor temp, HR, RR, BP and SaO.
5) Immediate Care for Symptomatic Infants
Investigations ( Blood gases, blood glucose, FBC, Blood
culture, CXR if respiratory signs and symptoms are present
Start on 10% dextrose drip
Correct anemia
Correct hypotension
Correct hypovolaemia
Start antibiotics after taking cultures
Start IV Aminophylline or caffeine in premature infants <32-
34weeks
Maintain SaO2 at 89-92% and PaO2 at 50-70mmHg
General Care of prem babies
1) Monitor temperature, Vital signs, DXT
2) I/O
3) Ventilation
4) IV line / Central Line
5) Feeding trickle feeding, multivitamin, folic acid, FAC (6wks) -
increase slowly, start 2.5cc/kg/feed, if tolerating x 2, increase
slowly, maximum 200cc/kg/day 6) strict hand hygiene
7) antibx
8) aminophyline (<34wks)
9) Immunization BCG (wt >1.8kg), Vit K (at birth)

Birthweigh 1. Micropreemie. <800 g or 1.8 lb.

t 2. Extremely low birthweight (ELBW). <1000 g
classificati 3. Very low birthweight (VLBW). <1500 g
on 4. Low birthweight (LBW). <2500 g
5. Normal birthweight (NBW). 2500 g to 4000 g
6. High birthweight (HBW). 4000 g to 4500 g
7. Very high birthweight (VHBW). >4500 g
Factors Low birth weight is due to
Related To 1. Prematurity
Low Birth 2. Poor intrauterine growth (IUGR)
Weight 3. Both prematurity and IUGR
Classificati 1. Appropriate for gestational age (AGA)
on by Defined as a birth weight between the 10 th and 90th
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birth percentiles for the infants gestational age.

weight 2. Small for gestational age (SGA)
and defined as below the 10th percentile
gestationa 3. Large for gestational age (LGA)
l age defined as above the 90th percentile
Viability refers to the gestational age when a fetus reaches an
anatomical threshold when critical organs, such as the lungs
and kidneys, can sustain life
Limit of viability has been defined as the age of fetal maturity
that ensures a reasonable chance of extrauterine survival given
technological support
Viability is the age at which the infant has a 50% chance of
long-term survival
Indication 1. Gestational age and
for 2. Other factors
resuscitati Infant's physiologic maturity at delivery
on Coexisting medical conditions (ie, presence of birth
defects or severe anomalies)
Probabilities of death
Severe disability
NOT PROVIDED
Gestational age of less than or equal to 22 weeks
Unless the "informed" parent requests it and clinicians agree it
is likely in the best interest of the infant
WITHHELD RESUSCITATION
Gestational age is less than 23 weeks
Birth weight is less than 400 grams
Anencephaly is present
Confirmed diagnosis of trisomy 13 or 18
ALLOW PARENTS TO CHOOSE
Gestational age is at 23 weeks
But the medical team is not required to resuscitate or provide
intensive care if they feel it does not benefit the infant
PROVIDED
Gestational age is at 24 weeks (maybe withheld based on
infants condition and both parents and medical team agree its
not in the infants best interest
Gestational age is at 25 weeks and more, recommended that
care is provided

Hypothermia
Thermoregul ability to balance heat production and heat loss in order to
ation maintain normal body temperature.
Normal skin temperature: 36.0-36.5
Normal rectal temperature: 36.5-37.5
Axillary temperature may be 0.5-1.0 lower.
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Mechanism of heat loss in newborn include:

Radiation- heat loss from the infant (warm object) to a
colder near by object (not in contact)
Conduction- direct heat loss from the infant to the surface
with which he or she in direct contact
Convection- heat loss from the infant to the surrounding
air
Evaporation- heat loss by water evaporation from the skin
of infant.
Preterm infants are predisposed to heat loss because:
High ratio of surface area to body weight (5x >than adult)
Little insulating subcutaneous fat
Reduce glycogen and brown fat store
Hypotonic (frog) posture limits their ability to curl up to
reduce the skin area exposed to the colder enviroment
Complications CONSEQUENCES OF CONSEQUENCES OF
EXCESSIVE HEAT LOSS HYPOTHERMIA
Insufficient ocygen supply Clotting disorder
and hypoxia Shock
Hypoglycemia Intraventricular
Metabolic acidosis hemorrhage
Decreased growth Severe sinus bradycardia
Apnea Increased neonatal
Pulmonary hypertension mortality

Management Rewarming by
Closed incubation
-usually used for infants who weight <1800g.
-convectively heated (heated airfow)
Radiant warmer
-used for very unstable infants or during performance of
medical procedure.
-heating is provided by radiation

Infant >2500g
Place the infant under a preheated radiant warmer
immediately after delivery
Dry the infant completely, cover the infants head
with a cap
Place the infant, wrapped the blankets, in a crib
Infant who weighs 1800-2500g with no medical problems,
Use crib,cap, and blanket
Infant who weighs 1000-1800g
A well infant should be placed in a closed incubator
with servo control
A sick infant should be placed under a radiant warmer with
servo-control
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Respiratory distress syndrome (hyaline membrane disease)

RF maternal diabetes, multiple births, caesarean delivery, precipitous
delivery, asphyxia, cold stress, maternal history of previous
affected infants
AETIOLOGY Surfactant deficiency exacerbated by:
Presence of overly compliant chest walls.
Decreased intra-thoracic pressure.
*surfactant deficiency - poor lung compliance due to high alveolar
surface tension atelectasis- decreased surface area for gas
exchange - hypoxia + acidosis- respiratory distress
*surfactant decreases alveolar surface tension, improves lung
compliance and maintain functional residual capacity
*Lungs mature at 35weeks

CF Usually appear within minutes of birth:

D/dx
Tachypnea Early-onset sepsis
Neonatal pneumonia
Prominent grunting Cyanotic heart disease (Total
Nasal flaring anomalous pulmonary return)
Transient tachynea of
Intercostal and subcostal retractions newborn (TTN)
Persistent pulmonary
Cyanosis hypertension
Diminished breath sounds Meconium aspiration
syndromes
Fine crackles on deep inspiration
Untreated child- mixed respiratory metabolic acidosis,
edema, ileus and oliguria
IX Chest x-ray fine reticular granularity of the parenchyma and
air bronchograms fine reticular granularity of the parenchyma
and air bronchograms
(ground glass appearance, larger airway outlined, no heart border,
diffuse granular)
Blood gas sampling
Sepsis work-up- including complete blood cell count and blood
culture.
Echocardiography to evaluate child for any possibility of patent
ductus arteriosus and other significant congenital Heart
disease.
Complicati Complications from tracheal intubation:
ons of Pneumothorax, pneumomediastinum
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HMD and Asphyxia from obstruction of airway

Intensive Bradycardia during intubation and suctioning
care Bleeding from trauma
Complications from umbilical arterial catheterization:
Vascular embolization
Thrombosis
Spasm
Vascular perforation
Delayed closure of patent ductus arteriosus.
Bronchopulmonary dysplasia result of lung injury from
mechanical ventilation and supplemental oxygen.
May lead to alveolar collapse
Worsen the respiratory distress and showing signs of
increased need of oxygen and respiratory support.
MX 1. Preventive managements:
Antenatal corticosteroids - use of antenatal
betamethasone to enhance fetal lung maturity.
Antenatal ultrasonography assess gestational age and
fetal well-being
Continuous fetal monitoring- to signal the need for
intervention in case of fetal respiratory distress.

2. Surfactant replacement
Surfactant prophylaxis (within 15 minutes of birth) to all
infants <27 weeks.
Consider prophylaxis if 27-29 weeks if baby was intubated
or mother did not get antenatal steroids
Repeated doses every 6-12 hours for a total of 3-4 doses.

3. Respiratory support
Endotracheal intubation and mechanical ventilation
Continuous positive airway pressure (CPAP) and Nasal
Synchronized Intermittent Mandatory Ventilation (SIMV).
4. Fluid & nutritional support
5. Antibx

Hypoglycemia (RBS < 2.6mmol in first 4 hours)

Neonatal glucose concentrations decrease after birth, to as low as 30 mg/dL
(1.7 mmol/dL) during the first 1 to 2 hours after birth, and then increase to
higher and relatively more stable concentrations, generally above 45 mg/dL
(2.5 mmol/L) by 12 hours after birth.
From birth to 4 hours, glucose level of above 25 mg/dL (1.5 mmol/L) is
acceptable if the infant is asymptomatic.

High Risk Infants

Infants of Diabetic Mothers.
Small for Gestational Age infants.
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Preterm infants including late preterm infants.

Macrosomic infants / Large for gestational age infants > 4.0kg.
Ill infants including those with:
Hypoxic-ischemic encephalopathy.
Rhesus disease.
Polycythaemia.
Sepsis.
Hypothermia.

Etiology
decreased carbohydrate stores (premature, IUGR)
infant of a diabetic mother (IDM): maternal hyperglycemia -+ fetal
hyperglycemia and
hyperinsulinism -+ hypoglycemia in the newborn infant because of high insulin
levels
sepsis
endocrine: hyperinsulinism due to islet cell hyperplasia (e.g. Beckwith-
Wiedemann syndrome),
panhypopituitarism
inborn errors of metabolism: fatty add oxidation defects, galactosemia

Clinical Findings
Jitteriness and irritability.
Apnoea and cyanosis.
Hypotonia and poor feeding.
Convulsions.

Management
identify and monitor infants at risk (pre-feed blood glucose checks)
begin oral feeds within first few hours of birth
if hypoglycemic, provide glucose IV (DlO, D12.5)
if persistent hypoglycemia (past day 3), hypoglycemia unresponsive to IV
glucose, and/or no
predisposing cause for hypoglycemia, send the following a critical bloodwork"
during an episode
of hypoglycemia:
insulin, cortisol, growth hormone (GH), beta-hydroxybutyrate, lactate,
ammonia
free fatty acids (FF.A's), ABG
treat hyperinsulinism with glucagon and diazoxide
Apnea of = pause of breathing > 20secs with brady or desaturation, HR
prematurit drop 30bpm from baseline
y 3 types
central: no chest wall movement
obstructive: chest wall movement continues
mixed: combination of central and obstructive apnea

cause: Immaturity of respiratory centre, lack of pharyngeal

muscle tone and collapsed upper airway - resolves at 36weeks
FALAH 16/17

Mx: tactile stimulation, Supportive O2, relieve obstruction (CPAP),

aminophyline to rinhibit adenosin receptor, mechanical ventilation
Hyponatremia dehydration/transepidermal h2o loss, immature kidney
Hypocalcemia Immature pancreas and reduced calcium from mother

Necrotizing Enterocolitis
Definition intestinal inflammation associated with focal or diffuse ulceration
and necrosis
primarily affecting terminal ileum and colon
affects 1-5% of preterm newborns admitted to NICU
Pathophysi postulated mechanism of bowel ischemia ->mucosal damage,
o and enteral feeding providing a substrate for bacterial growth
and mucosal invasion, leading to bowel necrosis or gangrene
and perforation
Risk prematurity (immature defenses)
Factors asphyxia, shock (poor bowel perfusion)
hyperosmolar feeds
enteral feeding with formula (breast milk can be protective)
sepsis
CF distended abdomen
increased amount of gastric aspirate/vomitus with bile staining
gross or occult blood in stool
feeding intolerance
diminished bowel sounds
signs of bowel perforation (sepsis, shock, peritonitis, DIC)
IX abdominal x-ray: pneumonitis intestinalis (intramural air,
hallmark ofNEC), free air, fixed loops, ileus, thickened bowel
wall, portal venous gas
CBC, ABG, blood culture
high or low WBC,low platelets, hyponatremia, acidosis,
hypoxia, hypercapnea
MX NPO (minimum 1 week), vigorous IV fluid resuscitation, NG
decompression, supportive therapy
total parenteral nutrition (TPN)
antibiotics (usually ampicillin, gentamicin metronidazole if risk
of perforation x 7-10 days)
serial abdominal x-rays detect early perforation
peritoneal drain/surgery if perforation
surgical resection of necrotic bowel and surgery for
FALAH 16/17

complications (e.g. perforation, strictures)

Complicati Early post-opt complications:
ons Wound infection
Dehiscence
Stomal problems (prolapse / necrosis)
Late complications:
Intestinal strictures
Short bowel syndrome
Complications related to central venous catheters
(sepsis, thrombosis)
Cholestatic jaundice

Intraventricular Haemorrhage (IVH) and periventricular leukomalacia (PVL)

Definition intracranial hemorrhage originating in the periventricular sub
ependymal germinal matrix ( GM)
Early IVH :diagnosed at <72 h after birth
Late IVH :diagnosed after 72 h of life.
Usually develops spontaneously
Less commonly, it may be caused by trauma or asphyxia,
Rarely, it occurs from a primary hemorrhagic disturbance or
congenital vascular anomaly.
RF extreme prematurity, need for vigorous resuscitation at birth,
pneumothorax, ventilated preterm infants, sudden increase in
arterial blood pressure with volume expansion, hypotensive event,
hypertension, RDS, fluctuating cerebral blood flow, coagulopathy
Pathogene IVH in preterm occurs in sub ependymal germinal matrix.
sis This area is highly vascularized and weakly supported. The
blood vessels in this area are immature and are prone to
hypoxic ischemic injury
Fluctuation in cerebral blood flow play an important role in
developing IVH. A sudden rise in systemic blood pressure may
result in an increase in cerebral circulation with subsequent
rupture of the germinal matrix vessels.
Decreases in cerebral blood flow can result in ischemic injury to
germinal matrix vessels, which rupture on re- perfusion.
Immature blood vessels in this highly vascular region of the
developing brain combined with poor tissue vascular support
predispose premature infants to haemorrhage.
Periventricular haemorrhagic infarction often develops after a
large IVH owing to venous congestion
CF many infants with IVH are asymptomatic
subtle signs: apnea. bradycardia, changes in tone or activity,
FALAH 16/17

altered level of consciousness

catastrophic presentation: bulging fontanelle, drop in
hematocrit. acidosis, seizures, hypotension
Grading The severity of hemorrhage may be defined on CT scans by the
location and degree of ventricular dilatation (Papile classification)

Grade I - bleeding is isolated to the subependymal area (germinal

matrix)
Grade II - IVH without ventricular dilatation
Grade III - IVH with ventricular dilatation
Grade IV - IVH with parenchymal extension
MX supportive care to maintain blood volume and add-base status
avoid fluctuations in blood pressure and cerebral blood flow
follow-up with serial imaging
symptomatic tx
o Seizures should be treated with anticonvulsant drugs
o Anemia and coagulopathy require transfusion with packed
red blood cells or fresh frozen plasma
o Shock and acidosis are treated with the judicious and slow
administration of sodium bicarbonate and fluid resuscitation
o Insertion of a ventriculoperitoneal shunt (preferred method)
to treat posthemorrhagic hydrocephalus
o prophylactic administration of low-dose indomethacin (0.1
mg/kg/day for 3 days) to VLBW preterm infants reduces the
incidence of severe IVH
Prognosis outcome depends on grade of IVH
short-term outcomes for severe IVH: mortality, posthemorrhagic
hydrocephalus (PHH), posthemorrhagic infarction
possible long-term major neurological sequelae: cerebral palsy;
cognitive deficits, motor deficits, visual, and hearing impairment
grades 1 and 2 hemorrhages have a relatively favourable
prognosis
greatest morbidity and mortality is seen with Grade 4
hemorrhage and PHH requiring ventriculoperitoneal shunt
placement
premature babies are also at risk of PVL (periventricular
leukomalacia) - radiologically seen as cysts or ischemic areas in
the periventricular white matter, also putting them at risk of
adverse neurological outcome
FALAH 16/17

RETINOPATHY OF PREMATURITY (ROP)

Definition A disorder of the developing retinal vasculature resulting from
interruption of normal progression of newly forming retinal vessels.
Pathogene *early vasoconstriction and obliteration of the capillary bed ->
sis repair response ->
neovascularisation
retinal detachment occurs in a small percentage

In the normally developing retina, there are no retinal vessels

until about 16 weeks gestation.
At 16 weeks, in response to a stimulus(experimental evidence
suggests relative hypoxia stimulating the release of angiogenic
factors as the retina thickens), cells derived from mesenchyme
travelling in the nerve fibre layer emanate from the optic nerve
head.
A fine capillary network advances through the retina to the ora
serrata, or retinal edge.
More mature vessels form behind this advancing network.
Vascularization on the nasal side of the ora serrata is complete
FALAH 16/17

at ~8monthsgestation, whereas that on the temporal side is

ordinarily complete at term.
Regulation of this process involves various factors including
vascular endothelial growth factor (VEGF) and insulin-like
growth factor 1 (IGF-1) working in combination.
Once the retinal vasculature is completely vascularised, it is no
longer susceptible to insults of the type that lead to ROP.
RF a) Extreme prematurity
b) Apnea
c) Sepsis
d) Hyper- and hypocapnia
e) Intraventricular hemorrhage
f) Anemia
g) Exchange transfusion
h) Hypoxia
i) Lactic acidosis
j) Possibly erythropoietin
CF ROP is classified by stage (I-V, with V being most severe)
Stage I:
A thin demarcation line develops between the vascularized
region of the retina and the avascular zone.
Stage II:
This line develops into a ridge protruding into the vitreous.
Stage III:
Extraretinal fibrovascular proliferation occurs with the ridge.
Neovascular tufts may be found just posterior to the ridge
(Figure 126-1).
Stage IV:
Fibrous and scarring occur as the neovscularization extends
into the vitreous.
Traction occurs on the retina, resulting in partial retinal
detachment.
Plus disease (eg, stage III+):
This may occur when vessels posterior to the ridge become
dilated and tortuous.
Plus disease has become a primary factor in
treatment decisions.
Pre-plus disease:
Dilatation and tortuosity of posterior pole vessels in zone 1;
less severe than plus disease.
* Sign: white pupil ( retinal detachment)
IX ophthalmoscopic examination
infants with birthweight <1500 g or <30 weeks GA: starting at 4-
6 weeks of chronologie age or at 32 weeks corrected age
(whichever is later) with examinations continue every 2-3 weeks
until retinal prematurity is reached, if no disease is present.
infants with ROP or very immature vessels: exams every l-2
weeks
Managem laser photocoagulation for severe prethreshold and threshold
ent ROP
FALAH 16/17

follow-up eye examinations for myopia, strabismus, amblyopia,

glaucoma, and late detachment
Prognosis stage I and II: 90% spontaneous regression
stage III+: -50% spontaneous regression
with treatment, incidence of poor visual outcome reduces by
-50%

PDA (patent sx: asymptomatic, brady/apnea, increased O2 requirment,

ductus Systolic murmur at 2nd Left ICS
arteriosus) Ix: CXR= cardiomegaly, pulmonary venous congestion

BPD Lung damage from pressure and volume trauma ( artificial

(bronchopnuemo ventilation/ O2 toxicity/ infection)
nary dysplasia) CXR: widespread opacity and cystic changes
Mx: prolonged artifical O2, Corticosteroids
Osteopenia of - rickets/chronic reduced Calcium
prem CXR: Bone deminieralization
Sx: Poor wt gain, fracture, respiratory distress
Anemia Anemia < 8 ( <12 if ventilated)|
Give hematinics, Folic Acid, appeton , FAC( ferrous amino
citrate, after 42/7)