HIGH RISK

NEWBORN
NEWBORN PRIORITIES IN THE FIRST
DAYS OF LIFE
 Initiation and maintenance of respirations
 Establishment of extrauterine circulation
 Maintenance of fluid and electrolyte balance
 Control of body temperature
 Intake of adequate nourishment
 Establishment of waste elimination
 Prevention of infection
 Establishment of an infant-parent/caregiver relationship
 Institution of developmental care or care that balance physiologic needs and
stimulation for best development.
INITIATING & MAINTAINING
REPIRATION
 An infant who has difficulty accomplishing effective breathing may experience
residual neurologic morbidities as a result of cerebral hypoxia.
 Most infant If respiratory activity does not begin immediately, it increases the
amount of blood pH and bicarbonate buffer system fail.
 Newborn defense mechanism, will do the effort of establishing respirations right
after birth so that it will not develop severe acidosis.
 Any infants who sustains any degree of asphyxia in utero, such as could occur
from cord compression, maternal anesthesia, placenta previa. IUGR, or premature
separation of the placenta, may already be experiencing acidosis at birth and may
have difficulty before the first minutes of life.
 Another concern that ineffective respirations creates is the failure of fetal
circulatory shunt, particularly the ductus arteriosus to close.
FACTORS PREDISPOSING INFANTS
TO RESPIRATORY DIFFICULTY:
 Low birth weight
 Intrauterine growth restriction
 Maternal history of diabetes
 Premature rupture of membranes
 Maternal use of barbiturates or narcotics close to birth
 Meconium staining
 Irregularities detected by fetal heart monitoring during labor
 Cord prolapse
 Lowered apgar scoring
 Postmaturity
 Small for gestational age
 Breech birth
 Multiple birth
 Chest, heart, or respiratory tract anomalies.

 10% of newborns require some assistance to begin breathing at birth.

 Resuscitation is important for both infants who fail to take first breath and for
those who have difficulty maintaining adequate respirations on their own.
THE NEWBORN AT RISK BECAUSE OF
ALTERED GESTATIONAL AGE OR
BIRTH WEIGHT
THE PRETERM INFANT

 Traditionally defined as a live-born infant born before the end of the week 37 of
gestation.
 Most preterm infants need infants need intensive care from the moment of birth
because they are prone to hypoglycaemia and intracranial haemorrhage.
 Extremely vulnerable to respiratory distress syndrome because they lack lung
surfactant. It does not form until about the 34th week of pregnancy.
 A preterm infant appears immature and has low birth weight.
COMMON FACTORS ASSOCIATED
WITH PRETERM BIRTH:
 Low socioeconomic level
 Poor nutritional staus
 Lack of prenatal care
 Multiple preganancy
 Previous early birth
 Race (non whites have higher incident)
 Cigarette smoking
 Age of the mother (younger mother less than 20 years old
 Order of birth
 Closely spaced pregnancies
 Abnormalities of the mother’s reproductive system, such as intrauterine septum
 Infections (UTI)
 Pregnancy complications (premature rupture of membranes)
 Early induction of labor
 Elective caesarean birth.
ASSESSMENT

 Preterm infant’s head appears disproportionately large.

 Skin is generally unusually ruddy because there is little subcutaneous fat beneath
it, making veins easily noticeable; higher degree of cyanosis.
 Vernix is lacking
 Lanugo is usually scant.
 Both anterior and posterior fontanelles is small
 Few or no crease on the soles of the feet
 Eyes appears small
 Has varying degrees of myopia because of lack of eye globe depth.
 The ears appear large in relation to head.
 The ear is immature and allows pinna to fall forward.
 RESTING POSTURE. The premature is characterized by very little, if any flexion
in the upper extremities and only partial flexion of the lower extremities.
 WRIST FLEXION. The wrist is flexed, applying enough pressure to get the hand
as close to forearm as possible.
 RECOIL OF EXTREMITIES. Place an infant supine. To test recoil of the legs (1)
flex the legs and knees fully and hold for 5 seconds, (2) extend the legs fully by
pulling on the feet, (3) release. To test the arms, flex forearms and follow same
procedure. In premature infant, response is minimal or basent.
 SCARF SIGN HOLD. Hold the baby, take the hand, and try to place it around the
neck and above the opposite shoulder as far posteriorly as possible. Assist the
manuever by lifting the elbow across the body.
 HEEL TO EAR. With the baby supine and the hips positioned flat on bed, draw
the baby’s foot as near to the ear as it will go without forcing it.
 BREAST TISSUE. the areola and nipple are barely visible (34 weeks)
 MALE GENITALIA. In the premature male, the testes are very high in the inguinal canal,
and there are very few rugae on the scrotum. The full-term infant’s testes are lower in the
scrotum and many rugae have developed.
 FEMALE GENITALIA. When the premature female is positioned on her back
with hips abducted, the clitoris is very prominent and the labia majora are very
small and widely separated. The labia minora and the clitoris are covered by the
labia majora in full term infant.
POTENTIAL COMPLICATIONS:

 Anemia of prematurity
 Acute bilirubin encephalopathy
 Persistent patent ductus arteriosus
ACUTE BILIRUBIN ENCEPALOPATHY

 Is the destruction of brain cells by invasion of indirect bilirubin.

 The invasion results from higher concentration of indirect bilirubin that forms in
the bloodstream from an excessive breakdown of red blood cells at birth.
 Preterms have less serum albumin available to bind indirect bilirubin and inactive
its effect.
 At the point that indirect bilirubin levels rises and jaundice occurs, phototherapy
or exchange transfusion can be initiated to prevent excessively high indirect
bilirubin levels.
PERSISTENT PATENT DUCTUS
ARTERIOSUS
 Because preterm lack surfactant, their lungs are noncompliant, so it is more
difficult for them to move blood from pulmonary artery into lungs.
 This condition leads to pulmonary artery hypertension, which then interferes with
closure of the ductus arteriosus.
PERIVENTRICULAR/
INTRAVENTICULAR HEMORHHAGE
 Preterm infants are prone to bleeding into the tissue surrounding the ventricles or
bleeding into the ventricles because of fragile cappilaries and immature cerebral
vascular development.
 Maintain a neutral thermal environment
 Monitor serum haematocrit (n is 45% to 65%)
 Assess the prenatal history for possible toxoplasmosis, rubella, CMV, and herpes
simplex infections during pregnancy. Assess maternal and infant antibody titers.
Use isolation precautions when congenital infections are suspected
 Provide education and emotional support
NURSING DIAGNOSIS:

 Impaired gas exchange related to immature pulmonary function.

 Risk for imbalanced nutrition, less than body requirements, related to additional
nutrients needed for maintenance of rapid growth, possible sucking difficulty, and
small stomach
 Ineffective thermoregulation related to immaturity.
 Risk for impaired parenting related to interference with patient-infant attachment
resulting from hospitalization of infant at birth.
 Deficient diversional activity (lack of stimualation) realted to preterm infant’srest
need.
 Risk for disorganized infant behavior related to prematurity and environmental
overstimulation.
SMALL-FOR-GESTATIONAL-AGE
INFANT
 Also called microsomia, if the birth weight is below the 10 th percentile on an
intrauterine growth curve for that age.
 SGA infants are small for their age because they have experienced IUGR.
ETIOLOGY

 Mother’s nutrition
 Partial placenta separation with bleeding
 Severe diabetes mellitus or gestational hypertension
 Women who smoke heavily
 Woman who use opiates
SIGNS & SYMPTOMS:

 Poor skin turgor

 Generally head appears large than the rest of the body
 Skull sutures may be widely separated
 Hair may be dull and lustreless
 Abdomen may be sunken
 Umbilical cord appears dry and maybe stained yellow
LABORATORY FINDINGS:

 High haematocrit level

 Increase in total number of red blood cells
 hypoglycemia
NURSING MANAGEMENT:
 Provide adequate fluid and electrolytes and nutrition
 Provide a high calorie formula for feeding to promote steady weight gain
 If the infant is breast feeding, add human milk fortifier to expressed breast milk
 Decrease metabolic demands when possible
 Provide small frequent feedings.
 Provide gavage feedings if the infant does not have a steady weight gain.
 Provide a neutral thermal environment.
 Decrease iatrogenic stimuli
 Prevent hypoglycaemia
 Monitor glucose screening
 Provide early feedings
 Provide frequent feedings (every to 3 hours)
 Administer IV glucose if blood sugar does not normalize with oral feedings.
NURSING DIAGNOSIS:

 Ineffective breathing pattern related to underdeveloped body systems at birth

 Risk for ineffective thermoregulation related to lack of subcutaneous fat.
 Risk for impaired parenting related to child’s high-risk status and possible
cognitive or neurologic impairment from lack of nutrients in the utero
THE LARGE-FOR-GESTATIONAL-
AGE INFANT
 is used to describe newborn babies who weigh more than usual for the number of
weeks of pregnancy.
 Babies may be called large for gestational age if they weigh more than 9 in 10
babies (90th percentile) or more than 97 of 100 babies (97th percentile) of the
same gestational age.
 It is important that LGA infants be identified immediately so they can be given
care appropriate to their gestational age rather than being treated as term
newborns.
What causes babies to be LGA?

 Large newborns may be normal babies who simply are large because the parents are large.
However, certain problems in the mother sometimes cause babies to be large for gestational
age.
 The most common cause of LGA newborns is
 Diabetes in the mother
 Other risk factors for having LGA newborns include
 Maternal obesity
 Having had previous LGA babies
 Genetic abnormalities or syndromes (for example, Beckwith-Wiedemann syndrome or Sotos
syndrome)
 Excessive weight gain during pregnancy (the fetus gets more calories as the mother gains more
weight)
What are the symptoms of LGA?

 Babies may be called large for gestational age if they weigh more than 9 in 10
babies or 97 of 100 babies of the same gestational age. In the U.S., this means
babies born at 40 weeks' gestation who weigh more than 8 pounds 13 ounces
(4,000 grams) or 9 pounds, 11 ounces (4,400 grams) at birth
Complications:

 Birth injuries
 Difficult delivery
 Low Apgar score
 Perinatal asphyxia
 Meconium aspiration
 Low blood sugar (glucose) levels (hypoglycemia)
 Lung problems
 Birth defects:
 Excess red blood cells (polycythemia)
How is LGA diagnosed?

 Before birth, measurement of the uterus and ultrasonography

 After birth, assessment of gestational age and size and weight of the baby
Appearance:

 Immature reflexes
 Low score on gestational exam
 Extensive bruising or birth injury
 Capput succedaneum
 Cephalhematoma
 molding
NURSING DIAGNOSIS:

 Ineffective breathing pattern related to possible birth trauma in the LGA newborn.
 Risk for imbalanced nutrition, less than body requirements, related to additional
nutrients needed to maintain weight and prevent hypoglycaemia.
 Risk for impaired parenting related to high risk status of LGA infant
THE POSTERM INFANT:

 Is one born after the 41st week of a pregnancy

 Infants who stay in utero past week 41 are at special risk because a placenta
appears to function effectively for only 40 weeks.
Characteristics of SGA:

 Dry, cracked, almost leather like skin from lack of fluid, and absence of vernix.
 Meconium stained
 Grown fingernails
 Demonstrates alertness
At birth:
 Difficulty establishing respiration
 Polycythemia
 Elevated haematocrit
 Hypoglycemia in the first hour of life
 Temperature regulation difficult
Complications

Postmature infants have higher morbidity and mortality than term infants due in large
part to:

 Perinatal asphyxia
 Meconium aspiration syndrome
RESPIRATORY DISTRESS
SYNDROME
 Formerly termed as “hyaline membrane disease“.
 is a common problem in premature babies. It causes babies to need extra oxygen
and help with breathing.
What causes RDS in premature babies?

 RDS occurs when there is not enough surfactant in the lungs. This liquid makes it
possible for babies to breathe in air after delivery.
 When there is not enough surfactant, the tiny alveoli collapse with each breath. As
the alveoli collapse, damaged cells collect in the airways. They further affect
breathing. The baby has to work harder and harder to breathe trying to reinflate
the collapsed airways.
 As the baby's lung function gets worse, the baby takes in less oxygen. More
carbon dioxide builds up in the blood. This can lead to increased acid in the blood
(acidosis). This condition can affect other body organs.
Which premature babies are at risk for
RDS?
 The baby is a boy or is white
 The baby has a sibling born with RDS
 C-section (Cesarean) delivery, especially without labor. Going through labor helps babies'
lungs become ready to breathe air.
 The baby doesn’t get enough oxygen just before, during, or after birth (perinatal asphyxia)
 The baby has trouble maintaining body temperature (cold stress)
 Infection
 The baby is a twin or other multiple (multiple birth babies are often premature)
 The mother has diabetes (a baby with too much insulin in his or her body can delay
making surfactant)
 The baby has a condition called patent ductus arteriosus (PDA)
What are the symptoms of RDS in
premature babies?
 Low body temperature
 Nasal flaring
 Sternal and subcostal retractions
 Tachypnea (more than 60lbreaths/min)
 Cyanotic mucous membrane

 Seesaw repiration
 Heart failure
 Pale gray skin
 Periods of apnea
 Bradycardia
 pneumothorax
How is RDS in premature babies
diagnosed?
 Baby’s appearance, color, and breathing efforts.
 Chest X-rays of the lungs.
 Blood gas tests.
 Echocardiography.
How is RDS in premature babies treated?

 Placing a breathing tube into your baby's windpipe (trachea)

 Having a ventilator breathe for the baby
 Extra oxygen (supplemental oxygen)
 Continuous positive airway pressure (CPAP). This is a breathing machine that
pushes a continuous flow of air or oxygen to the airways. It helps keep tiny air
passages in the lungs open.
 Artificial surfactant. This helps the most if it is started in the first 6 hours of birth.
Surfactant replacement may help make RDS less serious. It is given as preventive
treatment for some babies at very high risk for RDS. For others who become sick
after birth, it is used as a rescue method. Surfactant is a liquid given through the
breathing tube.

 Medicines to help calm the baby and ease pain during treatment
What are possible complications of RDS
in premature babies?
 Lungs leak air into the chest, the sac around the heart, or elsewhere in the chest

 Chronic lung disease (bronchopulmonary dysplasia)

How can RDS in premature babies be
prevented?
 Preventing a premature birth is the main way to prevent RDS. When a premature
birth can’t be prevented, you may be given corticosteroids before delivery. These
medicines may greatly lower the risk and severity of RDS in the baby. These
steroids are often given between 24 and 34 weeks of pregnancy to women at risk
of early delivery. They may sometimes be given up to 37 weeks. But if the
delivery is very quick or unexpected, there may not be time to give the steroids.
Or they may not have a chance to start working.
TRANSIENT TACHYPNEA OF THE
NEWBORN
 Transient tachypnea of the newborn is a mild breathing problem. It affects babies
during the first hours of life. Transient means it is short-lived.
 Tachypnea means fast breathing rate. The problem usually goes away without
treatment in 3 days or less.
What causes transient tachypnea of the
newborn?
 Before babies are born, they have fluid in their lungs.
 Babies reabsorb some of that fluid because of hormone changes that happen
before birth.
 More fluid gets reabsorbed as they pass through the birth canal during delivery.
The rest of the fluid is absorbed into the lungs after they are born and start
breathing on their own.
 If the fluid isn't absorbed fast enough or if they have too much fluid in the lungs,
they can't take in oxygen very well. Babies with this problem have to breathe
faster and harder to get enough oxygen into the lungs.
Who is at risk for transient tachypnea of
the newborn?
 Although premature babies can have it, most babies with this problem are full-
term.
 Babies delivered by C-section (without labor).
 Babies of moms with asthma and diabetes may also be more likely to have this
condition
What are the symptoms of transient tachypnea of the
newborn?

 Rapid breathing rate of more than 60 breaths per minute

 Grunting sounds with breathing
 Flaring of the nostrils
 Pulling in at the ribs with breathing
How is transient tachypnea of the newborn
diagnosed?
 On X-ray, the lungs look streaked and overinflated.
 The symptoms of this breathing problem may be similar to other more serious
respiratory problems. These include lung infection (pneumonia) or premature
lungs (respiratory distress syndrome).
 Often transient tachypnea of the newborn is diagnosed when symptoms go away
in the first few hours to days of life.
How is transient tachypnea of the newborn
treated?
 Supplemental oxygen.
 Blood tests.
 Continuous positive airway pressure.
 IV (intravenous) fluid.
 Tube feeding.
 MECONIUM ASPIRATION
SYNDROME
 is trouble breathing (respiratory distress) in a newborn who has breathed
(aspirated) a dark green, sterile fecal material called meconium into the lungs
before or around the time of birth.
 occurs when stress (such as infection or low oxygen levels) causes the fetus to
take forceful gasps, so that the amniotic fluid containing meconium is breathed
(aspirated) in and deposited into the lungs.
 After delivery, the aspirated meconium may block the newborn's airways and
cause regions of the lungs to collapse.
Symptoms:

 respiratory distress,
 grunt during breathing out.
 Their skin and/or lips may be bluish (a condition called cyanosis)
 They may also develop low blood pressure.
 The newborn's umbilical cord, nail beds, or skin may be covered in meconium,
giving them a greenish yellow color.
Diagnosis

 Meconium in the amniotic fluid

 Trouble breathing
 Chest x-ray
Treatment

 Amnioinfusion
 Sometimes suctioning of the airways
 Measures to support breathing
 Sometimes surfactant and antibiotics
 Treatment of any underlying disorder
Sudden Infant Death Syndrome (SIDS)

 is the unexplained death, usually during sleep, of a seemingly healthy baby less
than a year old.
 SIDS is sometimes known as crib death because the infants often die in their
cribs.
 The peak age of incidence is to 4 months of age
Risk factors:

 Infants with adolescent mothers

 Infants of closely spaced pregnancies
 Underweight and preterm infants
 Bronchopulmonary dysplasia
 Twins
 Native American infants
 Alaskan native infants
 Economically disadvantage black infants
 Infants of narcotic-dependent mothers
Other possible contributing factors:
 Sleeping prone rather than supine
 Viral respiratory or botulism infection
 Exposure to secondary smoke
 Pulmonary edema
 Brainstem abnormalities
 Neurotransmitter deficiencies
 Heart rate abnormalities
 Distorted familial breathing patterns
 Decreased arousal response
 Possible lack of surfactant in alveoli
 Sleeping in a room without moving air currents
Prevention

 Back to sleep.

 Keep the crib as bare as possible.

 Don't overheat your baby.

 Have your baby sleep in in your room..

 Adult beds aren't safe for infants.

 Breast-feed your baby, if possible.
 Don't use baby monitors and other commercial devices that claim to reduce the
risk of SIDS.
 Offer a pacifier.
 If your baby's not interested in the pacifier, don't force it.
 Immunize your baby.
HYPERBILIRUBINEMIA
 The term “hemolytic” is latin for “destruction” (lysis) of red blood cells.
 A certain degree of lysis of red blood cells in the newborn results from the
destruction of red blood cells by a normal physiologic process as the newborn
breaks down excess red blood cells formed in utero.
 Hemolytic disease is present when there is excessive destruction of red blood
cells, which leads to elevated bilirubin levels.
 Babies are not easily able to get rid of the bilirubin and it can build up in the
blood and other tissues and fluids of the baby’s body.
 Because bilirubin has a pigment or coloring, it causes a yellowing of the baby’s
skin, eyes and other tissues. This is called jaundice.
Several causes of hyperbilirubinemia and
jaundice:
 PHYSIOLOGIC JAUNDICE. Occurs as “normal” response to the baby’s limited
ability to excrete bilirubin in the first days of life.
 BREAST MILK JAUNDICE. A very small number of breastfed babies develop
jaundice when they are 2 to 12 weeks old. Babies who are born early may have
trouble breastfeeding at first and may also develop jaundice.
 JAINDICE FROM HEMOLYSIS. Jaundice may occur with the breakdown of red
blood cells due to haemolytic disease of the newborn (Rh disease), or from having
too many red blood cells that break down naturally and release bilirubin.
 JAUNDICE RELATED TO INADEQUATE LIVER FUNCTION. Jaundice may
be related to inadequate liver function due to infection or other factors. In this
condition, the direct bilirubin is increased.
At risk for hyperbilirubinemia:

 60% of term newborns and 80% of premature babies develop jaundice.

 Infants of diabetic mothers
 Mothers with Rh disease are more likely to develop hyperbilirubinemia and
jaundice.
Common symptoms:

 Yellow coloring of the baby’s skin and eyes (usually beginning on the face and
moving down the body).
 Poor feeding or lethargy
How is hyperbilirubinemia diagnosed?

 Jaundice appearing in the first 24 hours is quite serious and usually requires
immediate treatment.
 When jaundice appears on the 2nd or 3rd day, it usually “physiologic.
 When jaundice appears toward the end of the first week, it may due to an
infection.
 Later appearance of jaundice, in the second week, is often related to breast milk
feedings, but may have other serious causes, such as biliary atresia.
Diagnostics test:

 DIRECT & INDIRECT BILIRUBIN LEVELS. These reflect whether the

bilirubin is bound with other substances by the liver so that it can be excreted
(direct), or is circulating in the blood circulation (indirect).
 RED BLOOD CELLS
 BLOOD TYPE AND TESTING FOR Rh incompatibility ( Coomb’s test)
TREATMENT:

 PHOTOTHERAPY
 Since bilirubin absorbs light, jaundice and increased bilirubin levels usually decrease
when the baby is exposed to special blue spectrum lights.
 Phototherapy may take several hours to begin working and it is used throughout the
day and night.
 Different techniques may be used to allow all of the skin to be exposed to the light.
 The baby’s eyes must be protected and the temperature monitored during phototherapy.
 Blood levels of bilirubin are checked to monitor if the phototherapy is working.
 FIBEROPTIC BLANKET
 Another form of photo therapy placed under the baby.
 This may be used alone or in combination with regular phototherapy.
 EXCHANGE TRANSFUSION TO REPLACE THE BLOOD THAT HAS HIGH
BILIRUBIN LEVEL WITH FRESH BLOOD THAT HAS A NORMAL
BILIRUBIN LEVEL.
 Exchange transfusion helps increase the red blood cell count and lower the levels of
bilirubin.
 An exchange transfusions is done by alternating giving and withdrawing blood in
small amounts through a vein or artery.
 ADEQUATE HYDRATION WITH BREASTFEEDING OR PUMPED
BREASTMILK.
 Breastfed babies receiving phototherapy who are dehydrated or have excessive weight
loss can have supplementation with expressed breast milk or formula.
TWIN TO TWIN TRANSFUSION:

 Is a phenomenon that can occur if twins are monozygotic (identical; share the
same placenta) and abnormal arteriovenous shunt occurs that direct more blood to
one twin than the other.
 The result of this shift of blood leads anemia in the donor twin and polycythemia
in the receiving twin.
 The anemic twin may also be pale and SGA because of the lack of nutrients or
oxygen for growth as well as hypoglycemic from lack of glucose stores.
 The polycythemic twin is prone tp hyperbilirubinea as the excessive red blood cell
level is broken down.
HOW TTTS IS DIAGNOSED?

 Confirmed by ultrasound
 Hemoglobin determination
QUINTERO STAGING

 STAGE I. the ultrasound shows an imbalance of amniotic fluid around the twins,
but donor twin’s bladder is still visible. The visibility of the bladder indicates the
donor baby is receiving enough nutrients and fluid through the blood to produce
urine.
 STAGE II. The ultrasound shows an imbalance of amniotic fluid around the twins,
but the donor twin’s bladder is not visible. This finding indicates the bladder is
empty- a sign that the baby has stopped making urine.
 STAGE III. In addition to the stage I and II indicators, the ultrasound shows
significant abnormalities in the flow of blood within the twin’s umbilical cords.
 STAGE IV. In addition to the stage I-III indicators, the recipient twin shows signs
of heart failure (hydrops fetalis, or extra fluid within the baby).
TTTS TREATMENT BEFORE BIRTH

 Expectant management: continued close ultrasound surveillance throughout

pregnancy.
 Amnioreduction: removal of excess fluid in the recipient twin.
 Fetoscopic laser photocoagulation. Invasive surgery that uses a laser to ablate
(seal) blood vessels that are contributing to the abnormal flow of blood to the
babies.
 delivery: if TTTS is discovered later in the pregnancy, delivery of the babies may
be the best option.
RETINOPATHY OF PREMATURITY

 An acquired ocular disease that leads to partial or total blindness in children.

 Vasoconstriction of immature retinal blood vessels, caused by a higher
concentration of oxygen.
 Endothelial cells in the periphery of the retina then proliferate, causing retinal
detachment and possible blindness.
WHO IS AT RISK?

 A gestational age of 30 weeks or less

 A birth weight of 1,500 grams (3.3 pounds) or less
OTHER POSSIBLE RISK FACTORS
FOR ROP INCLUDE:
 Anemia
 Infection
 Transfusions
 Breathing difficulties
 Heart disease
 Ethnicity (Caucasian children)
 An infant with severe ROP might develop visible complications, such as
nystagmus (abnormal eye movements) and leukocoria (white pupils).
 However, these are also general signs of vision trouble.
HOW IS ROP TREATED?

 Mild ROP can be corrected by themselves.

 Severe type need ROP surgery to stop the growth of abnormal blood vessels.
 Treatment focuses on the peripheral retina (the sides of the retina) to preserve the
central retina (the most important part of the retina).
 Preserving the central retina causes some amount of the peripheral vision lost, but
can still do vital functions like seeing straight ahead, distinguishing colors,
reading, etc
TYPES OF ROP SURGERY:

 LASER SURGERY. Small laser beams scar the peripheral retina that lasts about
30-45 minutes for each eye.
 INJECTION. A medicine is injected into the eye.
Advance cases of ROP with retinal
detachment:
 SCLERAL BUCKLING. Placing a flexible silicone band around the
circumference of the eye. The band goes around the sclera, causing it to push in or
“buckle”. That pushes the torn retina closer to the outer wall of the eye, it takes 1-
2 hours .
 VITRECTOMY: A complex surgery that involves replacing the vitreous (the clear
gel in the center of the eye) with a saline (salt) solution. This allows for the
removal of a scar tissue and eases tugging on the retina, which stops it from
pulling away. It takes several hours.