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Presented By
Dr. Hasen Ali Mia
2nd yr PGT ,NBMCH
Chairperson
Prof. Sankar Das
Dept. Pediatrics,NBMCH
1. What is surfactant ?
2. Composition of
surfactant
3. Functions & MOA of
surfactant
4. Types of surfactant
5. Timing of administration
6. How to administer ?
7. Complications of
surfactant therapy
8. Indications &
Contraindications
9. SRT in RDS
10. SRT beyond RDS
 Multicomponent complex of several phospholipids, neutral lipids, and
associated proteins.
 Synthesized and secreted by Type II epithelial cells (pneumocytes) within
the lung.
 Reduces collapsing force in the alveolus, conferring stability and
maintaining alveolar surface free of liquid.
 Production begins from 16 wks GA onwards ,appears in AF between 32-36
wks, optimum conc. in alveoli beyond 35 wks.
 Decrease the surface tension
 Promotes lung expansion during inspiration
 Prevents alveolar collapse and loss of lung volume at the end of expiration
 Molecular forces of the water molecules in the
alveolar lining result in high surface tension
 The hydrophilic and hydrophobic properties of
DPPC result in a head-to-tail orientation in the
air-liquid interface inside the alveolus.
 Decrease in surface tension of the liquid lining,
At risk baby born
Surfactant given at < 15
min age before respiratory
distress=
“Prophylactic”
Signs of RDS
develop
Nevertheless, if
baby develops
signs of RDS
Multiple doses
Described as part of
“prophylaxis” regime
If baby continues to have signs
of RDS
Multiple doses
Described as part of “rescue” regime
Surfactant given at
<2 hrs, after resp
distress starts but
before obvious HMD
=
“Early rescue”
Surfactant given at
>2 hrs, after obvious
HMD =
“Late rescue” or
“Selective”
 Prophylactic :
 Premature infants at high risk of developing RDS secondary to surfactant
deficiency (e.g., <32 weeks or LBW <1,300 g)
 Laboratory evidence of surfactant deficiency such as L/S ratio <2:1, bubble
stability test indicating lung immaturity, or the absence of
phosphatidylglycerol
 Rescue or therapeutic administration :
 Preterm or full-term Infants suspected of having surfactant deficiency
and
 Who require endotracheal intubation and mechanical ventilation secondary to
respiratory failure and
 Who require an FIO2) ≥0.40, and
 Clinical and radiographic evidence of neonatal RDS or MAS,
 Neonates with MAP >7 cm H2O to maintain an adequate PaO2, SpO2
 The presence of congenital anomalies incompatible with life beyond the
neonatal period.
 Respiratory distress in infants with laboratory evidence of lung maturity.
 Patient hemodynamically unstable.
 Active pulmonary haemorrhage.
 Administration of surfactant replacement therapy is strongly recommended
in a clinical setting where properly trained personnel and equipment for
intubation and resuscitation is readily available.
 Prophylactic surfactant administration is recommended for neonatal RDS in
which surfactant deficiency is suspected.
 Rescue or therapeutic administration of surfactant after the initiation of
mechanical ventilation in infants with clinically confirmed RDS is strongly
recommended.
 A multiple surfactant dose strategy is recommended over a single dose
strategy.
 Natural exogenous surfactant preparations are recommended over
laboratory derived synthetic suspensions at this time.
INSURE (Intubation, Surfactant, Extubation) technique:
Early surfactant replacement therapy with prompt extubation to nasal
CPAP.
A/w less need for mechanical ventilation,
lower incidence of BPD, and
fewer air leak syndromes,
when compared with later, selective surfactant replacement therapy,
mechanical ventilation, and extubation from lower ventilator settings.
 Pharyngeal instillation before first breath
 Laryngeal mask airway (LMA) administration
 Bronchoalveolar lavage
 Aerosolized surfactant
 Proper placement and position of delivery device and ETT
 FIO2 and ventilator settings
 Reflux of surfactant into ETT
 Chest-wall movement
 SpO2 by pulse oximetry
 Vital signs
 Pulmonary mechanics and tidal volumes
 Breath sounds
 ABG
 CXR
 Plugging of ETT by surfactant
 Hemoglobin desaturation and increased need for supplemental O2
 Bradycardia
 Tachycardia
 Pharyngeal deposition of surfactant
 Administration of surfactant to only one lung
 Administration of suboptimal dose
 Increase in pulmonary hemorrhage following surfactant treatment
 Extremely preterm infants with structural lung immaturity
 Pneumonia or pulmonary hypoplasia
 Perinatal asphyxia
 Pulmonary edema from lung damage or fluid overload
 Pulmonary edema from L-R shunting through PDA
 Congenital B protein deficiency
 What is RDS ?
 Respiratory distress in a preterm infant within first 6 hrs of life
 Biochemical markers of surfactant deficiency – L/S ratio < 1.5, negative
shake test of gastric aspirates
 Radiological evidence of HMD.
Systematic review of RCT confirmed that SRT in RDS reduces the mortality ,
decreases the incidence of pulmonary air leaks like pneumothorax, PIE and
lowers the risk of chronic lung diseases or death at 28 days of age.
 Meconium aspiration syndrome
 Pulmonary hemorrhage
 Pneumonia
 Congenital diaphragmatic hernia
 Early bronchopulmonary dysplasia
 Constituents of meconium can inactivate surfactant.
 Inflammatory mediators can also inhibit surfactant, as can the
protein that leaks into the alveolar spaces.
 Reduced pulmonary blood flow may cause pulmonary ischemia,
with damage to the type II cells and reduced surfactant production.
 Two approaches attempted: surfactant replacement and surfactant
lavage.
 Infants receiving surfactant-replacement therapy required less ECMO,
without a concomitant increase in complications.
 It appears that surfactant-replacement therapy for MAS consistently
improves gas exchange and short-term outcomes, especially avoidance of
air leaks and the need for ECMO.
 This takes advantage of the detergent-like property of pulmonary surfactant, in
which meconium might be solubilized and literally “washed” from the lung .
 In addition to repleting the lung with functional surfactant, lavage might
theoretically remove particulate meconium.
 Two 15-mL/kg aliquots of surfactant diluted in normal saline, with suctioning
performed after each.
 Pneumonia may be a/w surfactant inactivation
 Facco, et al. studied kinetics of surfactant’s major component, (DSPC), in
neonatal pneumonia and concluded that DSPC t1/2 and pool size were
markedly impaired in neonatal pneumonia, and that they inversely
correlated with the degree of respiratory failure.
 Improved oxygenation and a reduced need for ECMO compared with a
similar group of control infants.
 Improved gas exchange compared with infants without surfactant treatment
 Pulmonary hypoplasia and pulmonary hypertension--hallmarks of CDH.
 Morphologic and biochemical immaturity of the lung.
 Exogenous surfactant as adjuvant treatment for the severe
respiratory distress a/w this disease is an attractive concept..
 Lower rate of synthesis of SP-B and less SP-B in tracheal aspirates.
 Molecular components involved in pulmonary haemorrhage can
biophysically inactivate endogenous lung surfactant,
 Exogenous surfactant replacement - reverses this process even in the
continued presence of inhibitor molecules
1. Surfactant replacement, given as prophylaxis or rescue treatment, reduces the
incidence of RDS, air leaks, and mortality in preterm infants with RDS
2. Both animal-derived and newer synthetic surfactants with SP-B–like activity
decrease acute respiratory morbidity and mortality in preterm infants with RDS
3. Early rescue surfactant treatment (<2 hours of age) in infants with RDS
decreases the risk of mortality, air leak, and chronic lung disease in preterm infants
4. Early initiation of CPAP with subsequent selective surfactant administration in
extremely preterm infants results in lower rates of BPD/death when compared with
treatment with prophylactic surfactant therapy.
5. Surfactant replacement has not been shown to affect the incidence of
neurodevelopmental, behavioral, medical, or educational outcomes in preterm infants.
6. Surfactant treatment improves oxygenation and reduces the need for ECMO without an
increase in morbidity in neonates with MAS.
7. Antenatal steroids and postnatal surfactant replacement independently and additively
reduce mortality, the severity of RDS, and air leaks in preterm infants.
8. Evidence demonstrating the utility of surfactant replacement therapry across the varied
spectrum of neonatal respiratory disorders other than RDS exists, but there still remains a
paucity of high-quality RCTs to recommend routine incorporation into clinical practice .
Thank You

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Surfactant replacement therapy : RDS & beyond

  • 1. Presented By Dr. Hasen Ali Mia 2nd yr PGT ,NBMCH Chairperson Prof. Sankar Das Dept. Pediatrics,NBMCH
  • 2. 1. What is surfactant ? 2. Composition of surfactant 3. Functions & MOA of surfactant 4. Types of surfactant 5. Timing of administration 6. How to administer ? 7. Complications of surfactant therapy 8. Indications & Contraindications 9. SRT in RDS 10. SRT beyond RDS
  • 3.  Multicomponent complex of several phospholipids, neutral lipids, and associated proteins.  Synthesized and secreted by Type II epithelial cells (pneumocytes) within the lung.  Reduces collapsing force in the alveolus, conferring stability and maintaining alveolar surface free of liquid.  Production begins from 16 wks GA onwards ,appears in AF between 32-36 wks, optimum conc. in alveoli beyond 35 wks.
  • 4.
  • 5.
  • 6.  Decrease the surface tension  Promotes lung expansion during inspiration  Prevents alveolar collapse and loss of lung volume at the end of expiration
  • 7.  Molecular forces of the water molecules in the alveolar lining result in high surface tension  The hydrophilic and hydrophobic properties of DPPC result in a head-to-tail orientation in the air-liquid interface inside the alveolus.  Decrease in surface tension of the liquid lining,
  • 8.
  • 9.
  • 10. At risk baby born Surfactant given at < 15 min age before respiratory distress= “Prophylactic” Signs of RDS develop Nevertheless, if baby develops signs of RDS Multiple doses Described as part of “prophylaxis” regime If baby continues to have signs of RDS Multiple doses Described as part of “rescue” regime Surfactant given at <2 hrs, after resp distress starts but before obvious HMD = “Early rescue” Surfactant given at >2 hrs, after obvious HMD = “Late rescue” or “Selective”
  • 11.  Prophylactic :  Premature infants at high risk of developing RDS secondary to surfactant deficiency (e.g., <32 weeks or LBW <1,300 g)  Laboratory evidence of surfactant deficiency such as L/S ratio <2:1, bubble stability test indicating lung immaturity, or the absence of phosphatidylglycerol
  • 12.  Rescue or therapeutic administration :  Preterm or full-term Infants suspected of having surfactant deficiency and  Who require endotracheal intubation and mechanical ventilation secondary to respiratory failure and  Who require an FIO2) ≥0.40, and  Clinical and radiographic evidence of neonatal RDS or MAS,  Neonates with MAP >7 cm H2O to maintain an adequate PaO2, SpO2
  • 13.  The presence of congenital anomalies incompatible with life beyond the neonatal period.  Respiratory distress in infants with laboratory evidence of lung maturity.  Patient hemodynamically unstable.  Active pulmonary haemorrhage.
  • 14.  Administration of surfactant replacement therapy is strongly recommended in a clinical setting where properly trained personnel and equipment for intubation and resuscitation is readily available.  Prophylactic surfactant administration is recommended for neonatal RDS in which surfactant deficiency is suspected.  Rescue or therapeutic administration of surfactant after the initiation of mechanical ventilation in infants with clinically confirmed RDS is strongly recommended.  A multiple surfactant dose strategy is recommended over a single dose strategy.  Natural exogenous surfactant preparations are recommended over laboratory derived synthetic suspensions at this time.
  • 15. INSURE (Intubation, Surfactant, Extubation) technique: Early surfactant replacement therapy with prompt extubation to nasal CPAP. A/w less need for mechanical ventilation, lower incidence of BPD, and fewer air leak syndromes, when compared with later, selective surfactant replacement therapy, mechanical ventilation, and extubation from lower ventilator settings.
  • 16.
  • 17.  Pharyngeal instillation before first breath  Laryngeal mask airway (LMA) administration  Bronchoalveolar lavage  Aerosolized surfactant
  • 18.  Proper placement and position of delivery device and ETT  FIO2 and ventilator settings  Reflux of surfactant into ETT  Chest-wall movement  SpO2 by pulse oximetry  Vital signs  Pulmonary mechanics and tidal volumes  Breath sounds  ABG  CXR
  • 19.  Plugging of ETT by surfactant  Hemoglobin desaturation and increased need for supplemental O2  Bradycardia  Tachycardia  Pharyngeal deposition of surfactant  Administration of surfactant to only one lung  Administration of suboptimal dose  Increase in pulmonary hemorrhage following surfactant treatment
  • 20.  Extremely preterm infants with structural lung immaturity  Pneumonia or pulmonary hypoplasia  Perinatal asphyxia  Pulmonary edema from lung damage or fluid overload  Pulmonary edema from L-R shunting through PDA  Congenital B protein deficiency
  • 21.  What is RDS ?  Respiratory distress in a preterm infant within first 6 hrs of life  Biochemical markers of surfactant deficiency – L/S ratio < 1.5, negative shake test of gastric aspirates  Radiological evidence of HMD. Systematic review of RCT confirmed that SRT in RDS reduces the mortality , decreases the incidence of pulmonary air leaks like pneumothorax, PIE and lowers the risk of chronic lung diseases or death at 28 days of age.
  • 22.
  • 23.  Meconium aspiration syndrome  Pulmonary hemorrhage  Pneumonia  Congenital diaphragmatic hernia  Early bronchopulmonary dysplasia
  • 24.  Constituents of meconium can inactivate surfactant.  Inflammatory mediators can also inhibit surfactant, as can the protein that leaks into the alveolar spaces.  Reduced pulmonary blood flow may cause pulmonary ischemia, with damage to the type II cells and reduced surfactant production.  Two approaches attempted: surfactant replacement and surfactant lavage.
  • 25.  Infants receiving surfactant-replacement therapy required less ECMO, without a concomitant increase in complications.  It appears that surfactant-replacement therapy for MAS consistently improves gas exchange and short-term outcomes, especially avoidance of air leaks and the need for ECMO.
  • 26.  This takes advantage of the detergent-like property of pulmonary surfactant, in which meconium might be solubilized and literally “washed” from the lung .  In addition to repleting the lung with functional surfactant, lavage might theoretically remove particulate meconium.  Two 15-mL/kg aliquots of surfactant diluted in normal saline, with suctioning performed after each.
  • 27.
  • 28.  Pneumonia may be a/w surfactant inactivation  Facco, et al. studied kinetics of surfactant’s major component, (DSPC), in neonatal pneumonia and concluded that DSPC t1/2 and pool size were markedly impaired in neonatal pneumonia, and that they inversely correlated with the degree of respiratory failure.  Improved oxygenation and a reduced need for ECMO compared with a similar group of control infants.  Improved gas exchange compared with infants without surfactant treatment
  • 29.  Pulmonary hypoplasia and pulmonary hypertension--hallmarks of CDH.  Morphologic and biochemical immaturity of the lung.  Exogenous surfactant as adjuvant treatment for the severe respiratory distress a/w this disease is an attractive concept..  Lower rate of synthesis of SP-B and less SP-B in tracheal aspirates.
  • 30.  Molecular components involved in pulmonary haemorrhage can biophysically inactivate endogenous lung surfactant,  Exogenous surfactant replacement - reverses this process even in the continued presence of inhibitor molecules
  • 31. 1. Surfactant replacement, given as prophylaxis or rescue treatment, reduces the incidence of RDS, air leaks, and mortality in preterm infants with RDS 2. Both animal-derived and newer synthetic surfactants with SP-B–like activity decrease acute respiratory morbidity and mortality in preterm infants with RDS 3. Early rescue surfactant treatment (<2 hours of age) in infants with RDS decreases the risk of mortality, air leak, and chronic lung disease in preterm infants 4. Early initiation of CPAP with subsequent selective surfactant administration in extremely preterm infants results in lower rates of BPD/death when compared with treatment with prophylactic surfactant therapy.
  • 32. 5. Surfactant replacement has not been shown to affect the incidence of neurodevelopmental, behavioral, medical, or educational outcomes in preterm infants. 6. Surfactant treatment improves oxygenation and reduces the need for ECMO without an increase in morbidity in neonates with MAS. 7. Antenatal steroids and postnatal surfactant replacement independently and additively reduce mortality, the severity of RDS, and air leaks in preterm infants. 8. Evidence demonstrating the utility of surfactant replacement therapry across the varied spectrum of neonatal respiratory disorders other than RDS exists, but there still remains a paucity of high-quality RCTs to recommend routine incorporation into clinical practice .

Editor's Notes

  1. Prerequisites : Baby should be haemodynamically stabilized before administration. Sp O 2 should be normalized by short period of BMV. Surfactant should be brought to room temperature . Should not be shaken.
  2. Defined as : c/b tachypnea, retrations, grunting. .
  3. Meconium is a mixture of GI secretions, sloughed out GI epithelial cells, practically any compound that can appear in amniotic fluid.
  4. Surfactant administration may reduce the severity of respiratory illness , mortality and decreases number of infants with progressive respiratory failure requiring support of ECMO.
  5. BPD or CLD is a clinical entity characterized by requirement of oxygen beyond 28 days of life or beyond 36 wks of corrected age.
  6. In these infants, partial SP-B deficiency could contribute to the severity of respiratory failure and its correction might represent a therapeutic goal .