Respiratory Distress Syndrome

1
Respiratory Distress Syndrome

• PREPARED BY Dr. SALEH BANAT
• Moderator Dr. Y. ABU OSBA

2
Pathophysiology

• RDS is caused by A relative deficiency of
  surfactant.
• which leads to
• 1- a decrease in lung compliance and functional
  residual capacity with increased dead space.
• 2- large ventilation-perfusion mismatch.

3
Pathophysiology cont.

• Macroscopically the lungs appear airless and
  ruddy (i.e., liverlike).
• And so the lungs of these infants require a
  higher critical opening pressure to inflate.
• Microscopically Diffuse atelectasis of distal
  airspaces along with distension of some distal
  airways and perilymphatic areas.

4
Pathophysiology cont.

• With progressive atelectasis endothelial and
  epithelial cells lining these distal airways are
  damaged, resulting in exudation of fibrinous
  matrix derived from blood (Hyaline membranes).
• Hyaline Membranes that line the alveoli are
  formed within a half hour after birth.
• Hyaline membranes interstitial edema make the
  lungs less compliant so greater pressure is
  needed to expand the small alveoli.

5
Pathophysiology cont.

• ?? surfactant
• ? Atelectasis
• ? Hypoxia, Hypercapnia Acidosis
• ? Pulmonary arterial vasoconstriction ? Rt to
  Lt shunting through foramen ovale Ductus
  Arteriosus
• ? reduced pulmonary blood flow ischemic injury
  to surfactant-producing cells.

6
Surfactant

• Surfactant a complex lipoprotein comprised of 6
  phospholipids and 4 apoproteins.
• Functionally lecithin ( dipalmitoyl
  phosphatidylcholine), is the principle
  phospholipid (65).
• Apoproteins (SP-B SP-C) and other substances
  (e.g., nonionic detergent tyloxapol, C160
  alcohol hexadecanol Exosurf) facilitates
  adsorption and spreading of Lecithin as a
  monolayer.
• Lecithin lowers the surface tension at the
  alveolar air-fluid interface so maintain
  alveolar stability by preventing collapse of
  small airways at end expiration.

7
Surfactant cont.

• Surfactant is synthesized in the Golgi apparatus
  of the endoplasmic reticulum of the type II
  alveolar cell.
• It appears in amniotic fluid between 28 32 wks.
• Mature levels of pulmonary surfactant are present
  after 35 wks.

8
Surfactant cont.

• Factors that may impair surfactant production or
  secretion
• 1- Hypoxia.
• 2- Acidosis.
• 3- Hypothermia.
• 4- Hypotension.

9
Frequency

• The greatest risk factor for developing RDS is
  prematurity.
• RDS occur in as many as 60-80 of infants lt 28
  wks gestation.
• Approximately 50 of infants born at 28-32 wks
  gestation develop RDS.
• RDS affect 15-30 of those between 32 36 wks.
• Only 5 of infants are affected after 37 wks.

10
Frequency cont.

• Incidence of RDS increases with decreasing
  gestational age BW.
• Not all premature infants develop RDS.
• RDS has been reported in all races worldwide,
  however it occurs more often in premature infants
  of Caucasian ancestry.

11
Clinical Features

• RDS frequently occurs in the following
  individuals
• Male infants
• Infants of diabetic mothers
• Infants delivered via cesarean without maternal
  labor
• Second-born twins
• Infants with a family history of RDS
• Asphyxia cold stress.

12
Clinical Features cont.

• In contrast, the incidence of RDS decreases with
  the following
• Use of antenatal steroids
• Pregnancy-induced or chronic maternal HTN
• Prolonged rupture of membranes
• Maternal narcotic addiction

13
Clinical Features cont.

• Secondary surfactant deficiency may occur in
  infants with the following
• Intrapartum asphyxia
• Pulmonary infections
• Pulmonary hemorrhage
• Meconium aspiration pneumonia
• Oxygen toxicity along with barotrauma or
  volutrauma to the lungs

14
Physical Exam

• Physical findings are consistent with the
  infant's maturity assessed by The Ballard Scoring
  System.
• Progressive signs of respiratory distress are
  noted soon after birth and include the following
• Tachypnea
• Expiratory grunting (from partial closure of
  glottis)
• Subcostal and intercostal retractions
• Cyanosis
• Nasal flaring
• apnea and/or hypothermia in extremely immature
  infants.

15
Physical Exam cont.

• Breath sounds may be normal or diminished with a
  harsh tubular quality.
• On deep inspiration, fine rales may be heard,
  esp. over the lung bases posteriorly.
• If untreated progressive worsening of dyspnea,
  cyanosis, ? BP disappearance of grunting occur.
• Apnea is an ominous sign require immediate
  intervention.

16
Physical Exam cont.

• Patients with HMD may also have edema, ileus
  oliguria.
• Symptoms signs reach a peak within 3 days,
  after which improvement is gradual.
• Improvement is heralded by spontaneous diuresis
  the ability to oxygenate the infant at lower
  inspired O2 levels.
• Death usually occur between days 2-7, and usually
  associated with alveolar air leaks, pulmonary
  hemorrhage IVH.

17
Lab Studies

• Blood gases are usually obtained as clinically
  indicated from either an indwelling arterial
  (umbilical) catheter or an arterial puncture.
• Blood gases exhibit respiratory and metabolic
  acidosis along with hypoxia.
• Respiratory acidosis occurs because of alveolar
  atelectasis and/or overdistension of terminal
  airways.

18
Lab Studies cont.

• Metabolic acidosis is primarily lactic acidosis,
  which results from poor tissue perfusion and
  anaerobic metabolism.
• Hypoxia occurs from right-to-left shunting of
  blood through the pulmonary vessels, PDA, and/or
  foramen ovale.
• Pulse oximetry is used as a noninvasive tool to
  monitor oxygen saturation, which should be
  maintained at 90-95.

19
Imaging Studies

• Chest x-ray of an infant with RDS exhibit
• 1- bilateral diffuse reticular granular or
  ground glass appearance.
• 2- air bronchograms more prominent in Lt
  lower lobe because of superimposition of cardiac
  shadow.
• 3- poor lung expansion.
• The prominent air bronchograms represent aerated
  bronchioles superimposed on a background of
  collapsed alveoli.
• Typical x-ray pattern develops at 6-12 hrs.

20
Imaging Studies cont.

• The cardiac silhouette may be normal or enlarged.
• Cardiomegaly may be the result of
• prenatal asphyxia
• maternal diabetes
• PDA
• an associated congenital heart anomaly
• simply poor lung expansion.

21
Imaging Studies cont.

• These findings may be altered with either early
  surfactant therapy or indomethacin treatment with
  mechanical ventilation.
• The radiologic findings of RDS cannot be
  differentiated reliably from those of pneumonia,
  which is caused most commonly by GBBS.

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Imaging Studies cont.

• Echocardiography
• Performed in selected infants to
• 1- assist the clinician in diagnosing PDA and
  determine the direction and degree of shunting.
• 2- diagnose pulmonary hypertension.
• 3- excluding structural heart disease.

25
Pulmonary Mechanics Testing

• Newer ventilators are equipped with PMT
  capabilities to assist the neonatologist in
  adequately managing the changing pulmonary course
  of RDS.
• Constant PMT monitoring may be helpful in
• 1- Preventing volutrauma from alveolar and airway
  overdistension.
• 2- Facilitate weaning the infant from the
  ventilator after surfactant therapy or
  determining if the infant can be extubated.

26
PMT cont.

• Infants with RDS have significant decrease in
  lung compliance.
• And so the delivered tidal volume is reduced in
  infants with RDS.
• The airway resistance may be normal or increased.
• The anatomic dead space is increased and the
  functional residual capacity (FRC) is decreased.
  

27
Differential Diagnosis

• Pneumonia often caused by group B beta hemolytic
  streptococci (GBBS) and may coexists with RDS.
• X-ray may be identical to that for HMD.
• Factors that may suggest the diagnosis include
• 1- Maternal GBS colonization.
• 2- Organisms on Gram-stain of gastric or tracheal
  aspirates.
• 3- Marked neutropenia.

28
Differential Diagnosis cont.

• Transient tachypnea of the newborn (TTN)
• Usually occurs in term or near-term infants
  usually after C/S delivery.
• The chest x-ray of an infant with transient
  tachypnea exhibits good lung expansion and,
  often, fluid in the horizontal fissure.

29
Differential Diagnosis cont.

• Aspiration syndromes may result from aspiration
  of amniotic fluid, blood, or meconium.
• Congenital anomalies of the lungs (eg,
  diaphragmatic hernia, chylothorax, congenital
  cystic adenomatoid malformation of the lung,
  lobar emphysema, bronchogenic cyst, pulmonary
  sequestration) and heart (e.g., total anomalous
  pulmonary venous return) are rare in premature
  infants.

30
Differential Diagnosis cont.

• Congenital alveolar proteinosis (congenital
  surfactant protein B deficiency)
• Rare familial disease.
• Manifest as severe lethal RDS in both term
  premature infants.

31
Other Problems

• Other problems that may be associated with RDS
  include
• Metabolic problems (e.g., hypothermia,
  hypoglycemia).
• Hematologic problems (e.g., anemia,
  polycythemia).
• Pulmonary air leaks (e.g., pneumothorax,
  interstitial emphysema, pneumomediastinum,
  pneumopericardium). In premature infants, these
  complications may occur from excessive positive
  pressure ventilation, or they may be spontaneous.

32
Prevention

• Starts during Fetal Life
• Obstetricians with experience in fetal medicine
  should care for mothers whose infants are at an
  increased risk for developing RDS.
• Strategies to prevent premature birth including
• 1- bed rest
• 2- tocolytics
• 3- appropriate antibiotics
• 4- the use of antenatal steroids
• may decrease the incidence and severity of RDS.

33
Prevention cont.

• Fetal lung maturity can be predicted by
• Estimating the lecithin-to-sphingomyelin ratio
  (L/S Ratio).
• - The presence of phosphatidylglycerol in the
  amniotic fluid obtained via amniocentesis (used
  in cases of infants of diabetic mothers).

34
Prevention cont.

• Antenatal steroids
• - Betamethasone administered to women before
  delivery of fetuses between 24-34 wks
  significantly reduces the incidence mortality
  morbidity of RDS.
• Steroids also reduce the incidence of other
  prematurity complications IVH, PDA
  Pneumothorax.
• No effect on neonatal growth or the incidence of
  infection.

35
Prevention cont.

• It is suitable to give steroids to all pregnant
  women who are likely to deliver a fetus in 1 wk
  that is between 24-34 wks.
• Dexamethasone may be associated with a higher
  incidence of periventricular leukomalacia than
  betamethasone.

36
Thank You
37
Treatment Complications of Respiratory Distress
Syndrome.

• Prepared By Dr. Saleh Banat
• Directed By Dr. Y.Abu Osba

38
Medical Care

• Delivery and resuscitation
• - A neonatologist experienced in the
  resuscitation and care of premature infants
  should attend deliveries of fetuses when lt 28
  weeks' gestation.

39
Surfactant replacement therapy

• The mortality rate of RDS has decreased 50
  during the last decade with the advent of
  surfactant therapy.
• Indicated in Infants diagnosed with RDS who
  require assisted ventilation with (FIO2) of gt
  40.
• Should be given as soon as possible, preferably
  within 2 hours after birth.

40
Surfactant Therapy cont.

• Prophylactic use is recommended following
  resuscitation in extremely premature infants (lt27
  weeks' gestation).
• Rapid bolus administration of surfactant after
  adequate lung recruitment using a (PEEP) of 2-4
  cm adequate positive pressure may lead to a
  more homogenous distribution.

41
Surfactant Therapy cont.

• Following inhaled administration, surface tension
  is reduced and alveoli are stabilized, thus
  decreasing the work of breathing and increasing
  lung compliance.
• Most infants require 2 doses.
• However, as many as 4 doses at 6-12 hr intervals
  have been used in several clinical trials.
• If the infant improves rapidly after only 1 dose,
  the infant most likely does not have RDS.

42
Surfactant Therapy cont.

• Conversely, in infants who respond poorly or are
  nonresponders to surfactant, exclude
• PDA
• Pneumonia
• Complications of ventilation (air leak).
  especially prior to using 3rd and subsequent
  doses.

43
Surfactant Therapy cont.

• 2 Types
• 1- Natural e.g.
• A- Survanta (Beractant, Alveofact)
• Natural bovine lung extract.
• Composed of Dipalmitoyl phosphatidyl- choline
  (DPPC), tripalmitin SP (Blt0.5, C99 of TP)
• Given as 4 mL/kg (100 mg/kg) divided in 4
  aliquots administered at least 6 hrs apart for
  1-4 doses.

44
Surfactant Therapy cont.

• Survanta must be warmed to room temperature
  administered only under carefully supervised
  conditions because of risk of acute airway
  obstruction.
• Marked improvement in oxygenation may occur after
  administration and so a decrease in oxygen and
  ventilator pressures may be needed as suggested
  by blood gases, after administration.

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Surfactant Therapy cont.

• During administration
• - suction infant's ET tube (preferably using
  closed suction system) prior to administering
  surfactant because ET may rarely become
  occluded.
• - monitor HR BP.
• - Complications include
• 1- pulmonary hemorrhage(esp. in extremely
  premature infants).
• 2- apnea, cyanosis bradycardia,
• 3- nosocomial sepsis.

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Surfactant Therapy cont.

• B- Calfactant (Infasurf)
• A natural calf lung extract.
• Composed of phospholipids (DPPC, Tripalmitin),
  fatty acids and SP-B (260 mcg/mL) SP-C (390
  mcg/mL).
• Dose 3 mL/kg (105 mg/kg) q6-12h for 1-4 doses.

47
Surfactant Therapy cont.

• C- Curosurf (Poractant)
• Minced pig lung extract
• - Composed of DPPC, SP-B and SP-C (? amount)
• Dose 2.5 mL/kg (200 mg/kg) then 1.25 mL/kg (100
  mg/kg) at 12-h intervals prn in 2 subsequent
  doses.
• Complications of Curosurf Infasurf are similar
  to Survanta.

48
Surfactant Therapy cont.

• 2- Synthetic e.g.
• Colfosceril (Exosurf)
• Composed of 85 DPPC, 9 hexadecanol 6
  tyloxapol.
• Dose 5 mL/kg (67.5 mg/kg) q12h for 1-4 doses.
• Complications include pulmonary hemorrhage (esp.
  in infants weighing lt700 g), nosocomial sepsis
  apnea.

49
Surfactant Therapy cont.

• Clinical trials with protein-containing natural
  surfactants result in fewer complications and a
  more rapid improvement in the infant's
  respiratory status than synthetic ones.

50
Ventilation Therapy

• O2 Warm humidified Oxygen via hood or nasal
  cannula is used for treating infants with mild
  RDS.
• Given in a concentration sufficient to keep PaO2
  between 55-70 mm Hg (SpO2 gt 90).
• Mechanical Ventilation in the form of-
• 1- CPAP
• 2- SIMV
• 3- HFV.

51
CPAP

• Keeps the alveoli open at the end of expiration.
• May be administered via the endotracheal tube,
  nasal prongs, or nasopharyngeal tubes (in larger
  infants).
• It is an adjunct therapy following surfactant
  administration, if prolonged assisted ventilation
  is not required.

52
CPAP cont.

• Nasal CPAP is indicated if the PaO2 cannot be
  maintained above 50 mm Hg at inspired O2
  concentrations of 60 or greater.
• Nasal CPAP applied at a pressure of 6-10 cm H2O
  produce a rise in PaO2.
• May be used following extubation in individuals
  with RDS to prevent atelectasis and/or prevent
  apnea in premature infants.

53
SIMV

• Synchronous intermittent mandatory ventilation
• Is a technique wherein some of the patient's
  respirations are synchronized with breaths
  delivered by the ventilator.
• The incidence of BPD was reduced significantly
  when compared with standard intermittent
  mandatory ventilation (47 vs 72).

54
SIMV cont.

• Indications include
• 1- pH lt 7.20.
• 2- PCO2 gt 60 mm Hg.
• 3- PO2 lt 50 mm Hg at O2 concentrations of 70-100
  CPAP of 8-10 cm H2O.
• 4- Persistent Apnea.

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SIMV cont.

• The goal of therapy for patients with RDS is to
  maintain a
• pH of 7.25-7.4.
• - PaO2 of 50-70 mm Hg.
• PCO2 of 40-65 mm Hg.
• And so improving oxygenation eliminating CO2
  without causing barutrauma or oxygen toxicity.

56
SIMV cont.

• During Mechanical Ventilation, oxygenation is
  improved by
• 1- ? FiO2.
• 2- ? Mean Airway Pressure (MAP) which is
  achieved by
• Increasing PIP, gas flow, IE ratio or PEEP.

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SIMV cont.

• CO2 elimination is achieved by
• 1- ? PIP (tidal volume).
• 2- ? rate of ventilator.
• PEEP levels of 4-6 cm H2O are safe effective.
• Excessive PEEP may impede venous return so ?
  cardiac output O2 delivery.

58
HFV

• High-frequency ventilation (HFV)
• Is a technique wherein small tidal volumes (less
  than anatomic dead space) are usually delivered
  at rapid frequencies.
• HFV was originally designed to treat patients
  with air leak.

59
HFV cont.

• Numerous studies in animal models of RDS
  demonstrate that HFV
• promotes more uniform lung inflation.
• improves lung mechanics and gas exchange.
• reduces exudative alveolar edema, air leak, and
  lung inflammation.
• Some clinical trials demonstrated that HFV can
  reduce the occurrence of chronic lung disease.

60
Supportive Therapy

• Temperature regulation
• Hypothermia increases oxygen consumption.
• And so further compromising infants with RDS who
  are born prematurely.
• Hypothermia should be prevented in infants with
  RDS during delivery, resuscitation, and
  transport.
• Infants with RDS should be kept in a neutral
  thermal environment.

61
Supportive Therapy cont.

• Fluids, metabolism, and nutrition
• In infants with In infants with RDS, initially
  administer 5 or 10 dextrose intravenously at
  60-80 mL/kg/day.
• Closely monitor blood glucose level,
  electrolytes, Ca, PO4, renal function, and
  hydration (determined by body weight and urine
  output) to prevent any imbalance.
• Gradually increase the intake of fluid to 120-140
  mL/kg/day.

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Supportive Therapy cont.

• Excessive fluids should be avoided because it
  contribute to PDA BPD.
• - Once the infant is stable, intravenous
  nutrition with amino acids and lipid can be
  started.
• - After the respiratory status is stable,
  initiate a small volume of gastric feeds
  (preferably breast milk) via NGT to initially
  stimulate gut development.

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Supportive Therapy cont.

• Circulation and anemia
• Assess the baby's circulatory status by
  monitoring HR, peripheral perfusion, and BP.
• Administer blood or volume expanders, and use
  vasopressors to support circulation.
• Monitor blood withdrawn for laboratory tests
  closely in tiny infants and replace the blood by
  PRBCs when it has reached 10 of the infant's
  estimated blood volume or if the PCV level is lt
  40-45.

64
Supportive Therapy cont.

• Antibiotic administration
• Start antibiotics in all infants who present with
  respiratory distress at birth after obtaining
  blood cultures.
• Discontinue antibiotics after 3-5 days if blood
  cultures are negative.

65
Supportive Therapy cont.

• Exceptions to the use of antibiotics include
• 1- a recent negative maternal cervical
  culture for GBBS.
• 2- an infant delivered by a mother with intact
  amniotic membranes.
• 3- no clinical or laboratory findings suggestive
  of chorioamnionitis.
• 4- adequate antenatal care.

66
Supportive Therapy cont.

• Support of parents and family
• Often parents undergo much emotional and/or
  financial stress with the birth of a critically
  ill premature infant with RDS and the associated
  complications.
• The parents may feel guilty and be anxious about
  the prognosis for the infant.
• These factors interact to prevent maternal-infant
  bonding.

67
Supportive Therapy cont.

• Medical staff should provide adequate support for
  these parents and other family members to prevent
  or minimize these problems.
• The parents should be
• 1- Well-informed about the childs status.
• 2- Encouraged to touch, feed, and care for their
  infant as soon as possible.

68
Complications

• Divided into Acute Chronic.
• Acute Complications
• 1- Alveolar rupture
• pneumothorax
• pneumomediastinum
• pneumopericardium
• interstitial emphysema

69
Acute Complications

• Alveolar rupture should be suspected when an
  infant with RDS suddenly deteriorates with
  hypotension, apnea, or bradycardia.
• or when metabolic acidosis is persistent.

70
Acute Complications cont.

• 2- Infections
• may manifest in a variety of ways, including
• failure to improve, sudden deterioration, or a
  change in white blood cell count or
  thrombocytopenia.
• the use of invasive procedures (e.g.,
  venipunctures, catheter insertion, use of
  respiratory equipment) provide access for
  organisms that may invade the immunologically
  compromised host.

71
Acute Complications cont.

• With the advent of surfactant therapy, infants
  who are smaller and more ill are surviving with
  an increase in the incidence of septicemia
  secondary to staphylococcal epidermidis and/or
  infection by Candida species.
• When septicemia is suspected, we should obtain
  blood cultures from 2 sites and place the infant
  on appropriate antibiotics until the culture
  results are obtained.

72
Acute Complications cont.

• 3- Intracranial hemorrhage and periventricular
  leukomalacia
• Intraventricular hemorrhage (IVH) is observed in
  20-40 of premature infants with greater
  frequency in infants with RDS who require
  mechanical ventilation.
• Cranial ultrasound is performed within the first
  week and thereafter as indicated in premature
  infants younger than 32 weeks' gestation.

73
Acute Complications cont.

• Prophylactic indomethacin therapy and antenatal
  steroids have decreased the frequency of
  intracranial hemorrhage in these patients with
  RDS.
• Hypocarbia and chorioamnionitis are associated
  with an increase in periventricular leukomalacia.

74
Acute Complications cont.

• 4- PDA
• Should be suspected in any infant who
  deteriorates after initial improvement or has
  bloody tracheal secretions.
• Although helpful in the diagnosis of PDA, cardiac
  murmur and wide pulse pressure are not always
  apparent in critically ill infants.

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Acute Complications cont.

• An echocardiogram enables the clinician to
  confirm the diagnosis.
• Treat PDA with indomethacin, which can be
  repeated during the first 2 weeks if the PDA
  reopens.
• In refractory incidents of RDS or in infants in
  whom indomethacin is contraindicated, surgically
  close the PDA.

76
Acute Complications cont.

• 5- Pulmonary Hemorrhage
• Occurrence of pulmonary hemorrhage increases in
  tiny premature infants, especially following
  surfactant therapy.
• Pulmonary hemorrhage may be associated with PDA.
• Increasing PEEP on the ventilator and
  administering intratracheal epinephrine manages
  pulmonary hemorrhage.

77
Acute Complications cont.

• 6- Necrotizing enterocolitis and/or
  gastrointestinal perforation.
• Should be suspected in any infant with abnormal
  abdominal findings on physical examination.
• A radiograph of the abdomen assists in confirming
  the diagnosis.
• Spontaneous perforation may occasionally occur in
  critically ill premature infants and has been
  associated with the use of steroids and/or
  indomethacin.

78
Acute Complications cont.

• 7- Apnea of prematurity
• Its incidence has increased with surfactant
  therapy, possibly due to early extubation.
• Exclude septicemia, seizures, GER, and metabolic
  and other causes in infants with apnea of
  prematurity.
• Rx modalities include methylxanthines
  (theophylline, caffeine) and CPAP or assisted
  ventilation in refractory incidents.

79
Chronic Complications

• 1- Bronchopulmonary dysplasia (BPD)
• is a chronic lung disease and is defined as
  oxygen requirement at a corrected gestational age
  of 36 weeks.
• is related directly to high volume and/or
  pressures that are used in mechanical
  ventilation, infections, inflammation, and
  vitamin A deficiency.
• BPD increases with decreasing gestational age.

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Chronic Complications cont.

• Factors that decrease severity of BPD
• A- The postnatal use of surfactant therapy.
• B- Gentler ventilation.
• C- Vitamin A.
• D- Steroids.
• - The increased incidence of BPD, is attributed
  to an increase in the survival of smaller and
  more ill infants with RDS following the
  introduction of the above therapies.

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Chronic Complications cont.

• - BPD may also be associated with
  Gastroesophageal Reflux or Sudden Infant Death
  Syndrome and so these conditions should be
  considered in infants with unexplained apnea
  prior to discharge from the hospital.

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Chronic Complications cont.

• 2- Retinopathy of prematurity (ROP)
• - Infants with RDS and a PaO2 gt 100 mm Hg are at
  a greater risk of developing ROP.
• - And so PaO2 should be monitored closely and
  maintained at 50-70 mm Hg.
• - Eyes of all premature infants are examined at
  34 weeks' gestation by an ophthalmologist and
  thereafter as indicated.

83
Chronic Complications cont.

• If ROP progresses, laser therapy or cryotherapy
  is used to prevent retinal detachment and
  blindness.
• Monitor infants with ROP closely for refractive
  errors.

84
Chronic Complications cont.

• 3- Neurologic impairment
• Occurs in approximately 10-70 of infants.
• Related to
• A- The infant's gestational age.
• B- The extent and type of intracranial pathology.
• C- The presence of hypoxia.
• D- The presence of infections.

85
Chronic Complications cont.

• Hearing and visual handicaps may result further
  compromise the development of these infants.
• They may develop a specific learning disability
  and aberrant behavior.
• Therefore, these infants need to be followed-up
  to detect those with neurologic impairment, and
  to take appropriate interventions.

86
Chronic Complications cont.

• 4- Familial psychopathology
• Infants with RDS are at a greater risk of child
  abuse failure to thrive.
• To deal with these problems
• A- Encourage and document parental visits and the
  parent's interaction with the infant.
• B- Advise parents to spend time with their
  infants with RDS in a separate room prior to
  discharge.

87
Chronic Complications cont.

• C- Counsel parents because an increased risk of
  prematurity and RDS exists for subsequent
  pregnancies.