respiratory distress syndrome...“respiratory development and respiratory distress syndrome”....

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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


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


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


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


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.


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


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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)

respiratory distress syndrome...“respiratory development and respiratory distress syndrome”....

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