Respiratory Distress Syndrome

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Common Respiratory

Conditions in the
Newborn
Gianina M. Aparato
2nd year resident
How to evaluate an infant in
respiratory distress?

• Signs and symptoms


• Retractions
• Tachypnea (>60 breaths/min)
• Nasal flaring
• Grunting
• Cyanosis
Respiratory
Distress
Syndrome
“Hyaline Membrane Disease”
RECALL!

• Pulmonary surfactant Pulmonary Surfactants


DEFICIENCY - Reduce surface tension
- Maintain alveolar stability
- Prevent collapse of small air
spaces at end expiration
• Increased surface tension

• Alveoli collapse

Kliegman, R. (2016). Nelson textbook of pediatrics (Edition 20)


Risk Factors
1. Prematurity
• 28 – 32 weeks AOG – appears in amniotic fluid
• >35 weeks AOG - mature levels of pulmonary surfactant
2. Male
• Circulating weak fetal androgens that inhibit production of
surfactant phospholipids
3. Race: White > African
• Genetic polymorphism
Risk factors
4. Maternal Diabetes
• Enhanced production of fetal insulin à inhibits production of proteins

5. Mutations in surfactant related proteins (SP-B & ABCA3)


• Dysfunctional surfactant or severely limited production

6. Perinatal asphyxia & cold stress


• Inactivation of surfactant
Pathophysiology
Tachypnea
Retractions
Clinical
Manifestation
Nasal flaring
Grunting
Cyanosis
Diagnosis
• Clinical Manifestation

• Radiographic findings:
Reticulogranular, ground
glass appearance

• Blood gas: Hypoxemia,


Hypercapnia & variable
metabolic acidosis
Management

Assisted Ventilation Pharmacologic


Surfactant Therapy Supportive care
Techniques Therapies
1. Assisted Ventilation
techniques

• CPAP
• provide positive end-expiratory pressure (PEEP)
• more effective with lower mortality and
reduced risk of bronchopulmonary dysplasia
(BPD) compared with intubation with or without
surfactant administration
Assisted Ventilation
Techniques

• Caffeine
• increase respiratory drive for infants
Assisted
Ventilation
Techniques

• NIPPV
• augments nCPAP by delivering ventilator
breaths via nasal prongs (or nasal mask).
• Requires use of ventilator
Assisted Ventilation
Techniques

• High Flow nasal cannula


• Heated, humidified high-flow nasal cannulas
(HFNC)
• Pressure delivery is highly variable
Assistef Ventilation
Techniques
Endotracheal Intubation and Mechanical Ventilation

Indications:
1. Respiratory acidosis
• arterial pH <7.2 & PaCO2 >60 to 65 mmHg.
2. Hypoxemia
• PaO2<50 mmHg despite oxygen supplementation

3. Severe apnea
Mechanical Ventilation
• Goal: Improve oxygenation and elimination of CO2 without
causing pulmonary injury or oxygen toxicity
• Initial ventilatory mode: volume-targeted ventilation
• Target tidal volumes at 4 to 6 mL/kg with permissive
hypercarbia (PaCO2 50 to 55 mmHg with pH ≥7.2)
• Target Oxygen Saturation: 91-95 %
• Target carbon dioxide levels : PaCO2 45 and 65 mmHg.

Kliegman, R. (2016). Nelson textbook of pediatrics (Edition 20)


Blood Gas
Monitoring
• Arterial blood gas
• should often be monitored
prevent episodes of
hypoxemia and hyperoxia and
to avoid the use of excessive
supplemental oxygen
2. Surfactant Therapy

United States Prescribing Information. National Library of


Medicine,
DailyMed. http://dailymed.nlm.nih.gov/dailymed/index.cfm
Surfactant Therapy
• Given to neonates who fail CPAP
• Administration:
• The ETT should be secured after intubation
• Administration via a sterile feeding tube inserted
into the ETT with the tip is at or above the end
of the ETT is preferable or via closed in-line
suction devices to enable continuous mechanical
ventilation
• Providing the dose in 2 to 4 aliquots and allowing
for recovery on mechanical ventilation between
aliquots
Surfactant Therapy
• Timing — it is most effective when given within the first 30 to 60
minutes of life.
• However, the potential benefits of timely administration of surfactant must be
balanced with adequate time for an initial trial of nCPAP

• Complications of Surfactant Therapy:


• Transient hypoxia
• Hypercapnia
• Bradycardia
• Hypotension
• Blockage of endotracheal tube
• Pulmonary hemorrhage

Kliegman, R. (2016). Nelson textbook of pediatrics (Edition 20)


3. Pharmacologic Therapies
• Steroids
• Systemic Steroids
• Mortality/BPD at 36 weeks decrease with moderately early (7-14 days)
administration of steroids.
• Short term adverse effects (Hyperglycemia, HTN, GI bleeding, HOCM, poor
weight gain, poor growth of head, periventricular leukomalacia,
neurodedevelopmental delay, CP)
• NOT recommended by AAP and Canadian Pediatric Society

• Inhaled steroids
• reduced the need for systemic steroids
• decrease rates of death and or BPD at 36 weeks without increase in adverse
effects
3. Pharmacologic Therapies

• Inhaled Nitric Oxide


• NOT beneficial in preterm infants with RDS in reducing mortality or
the risk of BPD
• Pulmonary hypertension or hypoplasia

• Sodium Bicarbonate
• 1-2meq/Kg over 20 mins
• Metabolic Acidosis
Decrease complication rates

• Reducing oxygen consumption and caloric needs

4.
• Reducing concomitant risk factors for poor
outcome (fluid overload & systemic HTN)

Supportive Adequate nutrition à metabolic needs and


growth
Care
General supportive care includes:

• Thermoregulation
• Fluid management – slightly negative fluid balance
• Cardiovascular management – adequate perfusion
Management
approach
Prevention
• Antenatal Corticosteroids before 34 weeks
• Modifies surfactant readiness, lung structure and thinning of alveolar
walls
• Target population: Pregnant women 24-34 weeks AOG with preterm
labor
• Betamethasone at 12 mg intramuscular (IM) q24h × 2 doses
• Dexamethasone 6 mg IM q12h × 4 doses
Complications

Endotracheal tube Pulmonary air Bronchopulmonary


complications leak dysplasia
Endotracheal tube complications

• . Endotracheal tube placement into a main stem (typically


right-sided) bronchus
• hyperinflation of the ventilated lung and atelectasis of the
contralateral lung
• Subglottic stenosis
• Post-extubation atelectasis
Pulmonary air
leaks
• due to the rupture of an
overdistended alveolus
• occur spontaneously or arise
from positive pressure due to
mechanical ventilation
• Pneumomediastinum
• Pneumothorax
• Subcutaneous emphysema
• Pneumoperitoneum
Bronchopulmonary
Dysplasia

• AKA “Chronic lung disease of


prematurity”
• main chronic complication of RDS
• Inflammation, caused by
volutrauma, barotrauma, oxygen
toxicity, or infection
• Clinical S/Sx: Tachypnea,
retractions and baseline wheeze
or crackles
BPD treatment
• Nutritional support
• Added calories (24-30 calories/30 mL formula), protein (3-3.5 g/kg/24 hr), and fat (3 g/kg/24 hr)
is needed for growth
• Diuretic therapy
• Furosemide (1-2mkdose) BID
• decrease pulmonary interstitial emphysema and PVR
• improve pulmonary function
• facilitate weaning from mechanical ventilation and oxygen.
• Inhaled bronchodilators – decrease airway resistance
• Caffeine – increase respiratory drive
• Vitamin A (5000IU/IM) – provides epithelial repair and minimizes fibrosis
• Corticosteroids
Prognosis of RDS
• Antenatal steroids, postnatal surfactant use, and improved modes of ventilation have resulted in low mortality from RDS
(≈10%)
• Mortality increases with decreasing gestational age.
• The long-term prognosis for normal pulmonary function in most infants surviving RDS is excellent.

Kliegman, R. (2016). Nelson textbook of pediatrics (Edition 20)


Transient
Tachypnea of
the Newborn
Benign and self limited process

Definition Affects infants born late preterm or term


gestation

Early onset with signs of mild respiratory


distress (retractions, cyanosis) decreased O2
saturation relieved by minimal oxygen
supplementation <40%
Pathophysiology
Before birth: switch from
Lungs are constantly secretory mode to Adrenergic stimulation:
secreting fluid to aid absorptive mode to transport of fluid into the
growth and development accommodate transition to interstitium
breathe in air at birth

Any disruption/delay in
fetal lung fluid
clearance:
- Uneventful delivery at
or near term (CS As the lung pulmonary
Interstitial lung fluid is
circulation increases
without labor) cleared into pulmonary
following the first breath,
- Precipitous birth capillaries and lung
the fluid in the lungs is
- Preterm birth lymphatics
cleared
Clinical Manifestation
Tachypnea within
the first 6 hours Retractions Grunting
after birth

Mild Cyanosis
Nasal flaring • Responds with
supplemental
oxygen FiO2 <40%
Radiographic
Findings
• Prominent perihilar
streaking
• Hyperaeration (Widened
intercostal spaces)
• Small pleural effusions

* Resolve by 48 -72h
Treatment

SUPPLEMENTAL OXYGEN CPAP


Neonatal
Pneumonia
Routes of Infection

Early Onset Pneumonia Late Onset Pneumonia

• Within 48 hours to 6 days • During hospitalization or


of birth after discharge
• Intrauterine aspiration of • Organisms colonizing the
infected amniotic fluid hospitalized newborn or is
• Aspiration material during nosocomially acquired from
passage through the birth infected individuals
canal
Risk Factors

Early Onset Pneumonia Late Onset Pneumonia


• Prolonged rupture of • Assisted ventilation
membranes (>18 hours) • Prolonged hospitalization
• Maternal amnionitis • Poor handwashing and
• Preterm delivery overcrowding
Pathogens

Early Onset Pneumonia Late Onset Pneumonia


• Group B Streptococcus • Staphylococcus aureus
• E Coli • Staphylococcus epidermidis
• Listeria Monocytogenes • GBS
• Mycobacterium tuberculosis • Klebsiella pneumoniae
• E Coli
• Pseudomonas aeruginosa
Tachypnea
Retractions
Cyanosis

Clinical Lethargy

Manifestation Poor suck


Apneic spells
Thermal instability (Hypo/hyperthermia)
Jaundice
Clinical Findings

Laboratories

• CBC with differential and platelet count

Diagnosis
• Blood culture
• Tracheal aspirate culture

Chest X ray

• Streaky densities (usually in lower lung)


• Diffusely granular appearance with air
bronchogram
Treatment
Early Onset Late onset

• Ampicillin + Gentamicin Ampicillin or Vancomycin +


Aminoglycoside or 3rd gen
OR
Cephalosporin
• Ampicillin + Cefotaxime

Duration of therapy: 10-14 days


In Summary
• RDS is a disease affecting preterm infants caused by insufficient
pulmonary surfactant
• TTN is benign and self limited. Symptoms resolve in 12 to 72 hours
• Pneumonia is an important cause of neonatal infection and is a
major contributor to infant mortality worldwide.
• Clinical signs/symptoms may be nonspecific hence a panel of
laboratories as well as imaging such as CXR may be requested
Thank You

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