respiratory distress syndrome...“respiratory development and respiratory distress syndrome”....
TRANSCRIPT
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RESPIRATORY DISTRESS SYNDROME
5 Stages of Lung Development
Embryonic
Pseudoglandular
Canalicular
Saccular (Terminal Sac)
Alveolar
STAGES OF LUNG DEVELOPMENT
The more premature, the higher the RDS risk
Estimated to cause 30% of neonatal deaths
As many as 70% of all preterm deaths are also attributed to RDS
RESPIRATORY DISTRESS SYNDROME Statistics
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Surfactant Deficiency Surfactant is composed of:
Phospholipids Dipalmitoyl phosphatidylcholine (DPPC) (Lecithin)
Peaks at around 35 wks
Phosphatidylglycerol (PG) Sphingomyelin
Formed at around 18 wks Stable throughout gestation Immature surfactant
Neutral lipids (cholesterol) Surfactant proteins
Produced by Type II pneumocytes
RESPIRATORY DISTRESS SYNDROME
L/S RATIO
Reduces alveolar surface tension
Enhances alveolar expansion
Optimizes compliance
Lessens WOB
Helps to maintain FRC
Allows optimal gas exchange
SURFACTANT FUNCTION
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SURFACTANT
Hypoxia Hypercapnea Acidosis Shock Pulmonary edema Smaller of twins IDM
Underinflation Overdistention Mechanical ventilation
SURFACTANT INTERUPTION/INHIBITION
WHY DO BELLY FLOPS HURT?
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SURFACE TENSION!!!!
Decreased compliance
Increased incidence of atelectasis
Intrapulmonary shunting – V/Q mismatch
Hypoxemia
Hypercarbia
Acidosis
RESPIRATORY DISTRESS SYNDROMEPhysiology
Hypoxemia and Acidosis leads to:
Pulmonary vasoconstriction
Increased PVR
Intracardiac shunting (Right to left)
PFO
PDA
Cascade of events intensifying V/Q mismatch
RESPIRATORY DISTRESS SYNDROMEPhysiology (cont’d)
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Immaturity of terminal air sacs/vasculature
Chest wall immaturity/non-ossified bone
Poor stability during inspiration
Immaturity of diaphragm and other respiratory muscles
CNS immaturity leading to apnea
RESPIRATORY DISTRESS SYNDROMEPhysiology (cont’d)
Neonates at greatest risk:
Born before 35 wks (especially 28)
IDM
History of RDS in siblings
Male
C-section without labor
Poor Apgar scores
RESPIRATORY DISTRESS SYNDROME
Symptoms arise to compensate for increasing atelectasis
Tachypnea
Retractions
Nasal flaring
Grunting
Diminished breath sounds
Inspiratory crackles
Cyanosis
Pallor
RESPIRATORY DISTRESS SYNDROMEClinical Symptoms
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Goal of treatment:
Maintain alveolar ventilation and support the respiratory system while minimizing damage and minimizing complications.
Easy to envision, difficult to accomplish.
MANAGEMENT
Prevent pre-term deliveries
Antenatal corticosteroids (betamethasone or dexamethasone)
Thermoregulation
Fluid management
Optimizing nutrition
Early institution of CPAP
Avoidance of mechanical ventilation
Selective surfactant administration
MANAGEMENT (cont’d)
CPAP Stents airways
Establishes and maintains functional residual capacity (FRC)
Increases pharyngeal cross-sectional area
Improves pulmonary compliance
Decreases airway resistance
Increases tidal volumes
Improves diaphragmatic activity
Prevents further alveolar collapse
Reduces labored breathing
CPAP
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Promotes surfactant production
Improves oxygenation via enhanced diffusion
Increases V/Q matching
Decreases shunting (intrapulmonary and intracardiac)
Stabilizes the compliant chest wall
Reduces obstructive apnea
May decrease central apnea by promoting a regular breathing pattern
CPAP (cont’d)
Functional residual capacity Resting volume of the lung at end-expiration
Expiratory reserve volume (ERV) + residual volume (RV)
Approximately 20% of total lung volume
Infants with RDS have an abnormally low FRC Poor compliance, lung volumes and increased WOB
Severe RDS requires positive end-expiratory pressure to establish FRC
Decreases the risk of developing BPD
IMPORTANCE OF FUNCTIONAL RESIDUAL CAPACITY (FRC) IN RDS
FRC
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FRC (cont’d)
Give every baby an opportunity to succeed on CPAP
Start CPAP in delivery (T-piece)
Use “liberal” definition of CPAP failure
Deliver an appropriate level of support (5-8 cm H2O)
Routine monitoring of pressures/positioning
Choose appropriate interface and fixation
MAXIMIZE CPAP SUCCESS
Chinstraps and pacifiers
Avoiding gastric distention
Maximizing positioning
Nipple feeding
Skin-to-skin
Weaning properly (according to guidelines)
Identifying and managing weaning failure
MAXIMIZE CPAP SUCCESS (cont’d)
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Duration of CPAP (3 clinical considerations)
When does the infant meet “weaning” criteria?
Deciding which is the preferred method to cease CPAP
Toleration of “weaning”
Worsening apnea
Increased FiO2 to maintain sats
Increase WOB
Return to previous CPAP level if not tolerated
MAXIMIZE CPAP SUCCESS (cont’d)
Implications for Clinical Practice
Columbia approach towards weaning
The more premature the infant at birth, the later the typical PMA at successful CPAP discontinuation
Premature infants vs more mature infants at the same PMA
There may be a trade-off between CPAP support and O2
MAXIMIZE CPAP SUCCESS (cont’d)
Prolonged ventilation is a leading factor for development of BPD and poor neurodevelopmental outcomes
Lung injury is minimized by non-invasive ventilation
Mechanical ventilation is a last resort
MECHANICAL VENTILATION
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Effects of mechanical ventilation Volutrauma
Barotrauma
Atelectotrauma
Rheotrauma
Biotrauma
Increased MAP needed to expand collapsed alveoli
Cytokine release - inflammation
Alveolar endothelial lining damage
Leakage of proteins – hyaline membrane formation
MECHANICAL VENTILATION (cont’d)
“New approaches” to invasive ventilation have not panned out
High frequency DOES NOT reduce BPD incidence in the smallest patients
MECHANICAL VENTILATION (cont’d)
In the 1990s, CPAP as an initial modality went out of favor
ET intubation and surfactant was believed superior
Improved survival
Decreased air leaks
There were problems:
None of the trials had a control group randomized to CPAP
The widely-accepted intubate and surf didn’t lead to a decrease in BPD
SELECTIVE SURFACTANT ADMINISTRATION
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Jump to 2008
5 large RCTs examined: Meta-analysis of those trials have recently been published
Compared early CPAP use with routine intubation and surfactant administration
Infants <30 wks gestation at birth
2 trials:
infants randomized to either CPAP or surfactant
Remaining 3 trials:
Infant’s assessed at birth before randomization
SELECTIVE SURFACTANT ADMINISTRATION (cont’d)
Results of those analysis:
Initial CPAP decreased the incidence of BPD or death
Furthermore:
The authors concluded that one additional infant could survive to 36 wks without BPD for every 25 babies treated with NCPAP in DR.
SELECTIVE SURFACTANT ADMINISTRATION (cont’d)
Cochrane review:
Intubation and prophylactic surfactant administration was associated with a higher BPD and death than infants on CPAP as an initial therapy with selective surfactant delivery
SELECTIVE SURFACTANT ADMINISTRATION (cont’d)
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1. Clyde J. Wright, MD; Richard A. Polin, MD; Haresh Kirpalani, BM, MSc. “Continuous Positive Airway Pressure to Prevent Neonatal Lung Injury: How Did We Get here, and How Do We Improve?”. The Journal of Pediatrics. 2016.
2. Nicolas Bamat; Erik A. Jensen, Haresh Kirpalani. “Duration of Continuous Positive Airway Pressure in Premature Infants”. Seminars in Fetal and Neonatal Medicine. 2016: vol 21(189-195).
3. Rakesh Sahni; Maria Schiaratura; Richard A. Polin. “Strategies for the Prevention of Continuous Positive Airway Pressure Failure”. Seminars in Fetal and neonatal medicine. 2016: vol. 21(196-203).
4. Rubarth, Lori, PhD, NNP-BC; Quinn, Jenny, MSN, NNP-BC, MHA. “Respiratory Development and Respiratory Distress Syndrome”. Neonatal Network. July/August 2015: vol . 34, no. 4.
5. Samir Gupta; Steven M. Donn. “Continuous Positive Airway Pressure: Physiology and Comparison of Devices”. Seminars in Fetal and Neonatal Medicine. 2016: vol. 21(204-211).
References
6. Walsh, Brian K. Perinatal and Pediatric Respiratory Care (pg. 248). St. Louis, Missouri: Saunders, 2010.
7. Whitaker, Kent. Comprehensive Perinatal and Pediatric Respiratory Care (pg. 203). Stamford, Connecticut: Cengage Learning, 2015.
References (cont’d)