RESPIRATORY DISEASES OF THE NEWBORN By: dr Ismah, Paeds department 1
RESPIRATORY DISEASES
OF THE NEWBORN
By: dr Ismah, Paeds department
1
2
Respiratory diseases
of the newborn
Respiratory distress syndrome - RDS
(hyaline membrane disease)
Transient tachypnea of the newborn (TTN)
Meconium aspiration syndrome (MAS)
Primary pulmonary hypertension of the newborn
(PPHN)
Apnea of prematurity
Congenital pneumonia
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Preterm infant Term infant Both
• RDS
• Erythroblastosis
fetalis
• Nonimmune
hydrops
• Pulmonary
hemorrhage
• PPHN
• MAS
• Polycythemia
• Amniotic fluid
aspiration
• Bacterial sepsis e.g. GBS
• TTN
• Spontaneous pneumothorax
• Congenital anomalies e.g.
congenital lobar
emphysema, diaphragmatic
hernia
• Congenital heart disease
• Pulmonary hypoplasia
• Viral infection e.g. CMV,
herpes
• Inborn metabolic errors
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1. Respiratory distress
syndrome
- RDS
(hyaline membrane
disease)
Occurred after the onset of breathing
and is associated with an insufficiency
of pulmonary surfactant
Incidence of RDS increase with decrease gestational
age
RDS develops in 30-60% in infant 28-32 W
Others risk factors: delivery of previous preterm infant
with RDS, maternal DM, male sex, 2nd born of twins, c
sec not in labor
May develop immediately in extremely immature infant
or 3-4 hrs after birth in 34W infant 5
LUNG DEVELOPMENT
Lining of alveolus consists 90% type 1 and 10% types
II cells
The surfactant production depends on the fetal
cortisol, begins between 32-34 W of gestation
Surfactant produced by type II cells sufficiently by 34-
36 W
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Contents of surfactant are 90% lipids (lecithin,
phosphatidylglycerol) and proteins SP-A, SP-B, SP-C
and SP-D
Surfactant prevents atelectasis and contributes to the
lung recoil by manipulates the surface tension of the
lungs
Lecithin/Sphingomyelin ratio 2:1 in amniotic fluid
usually indicate fetal lung maturity or the presence of
minor phospholipids e.g. phosphatidylglycerol
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CLINICAL MANIFESTATION
Tachypnea
Nasal flaring
Intercostal, sternal recession
Grunting; closure of glottis during expiration
Cyanosis
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CXR
Shows air bronchogramsand reticulonodularshadowing throughout the lung fields (often termed ‘ground glass’ appearance)
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PREVENTION AND TREATMENT
Prevent preterm birth; treatment of infections, cervical
cerclage
Prevention of neonatal cold stress, birth asphyxia,
hypovolemia reduces risk of RDS
Administration of corticosteroid before delivery for lung
maturity
Surfactant usage
Aim SPO2 ≥ 90%, PaO2 60-70 mmHg, pH> 7.25
Start antibiotic for 48-72 hrs (difficult to differentiate
sepsis, pneumonia from RDS)
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SURFACTANT
Surfactant therapy reduces mortality rates most
effectively in infants <30 weeks and those of birth weight
<1250 gm
12
WHO TO GIVE?
Depressed preterm infants who have no spontaneous respiration
after 30 seconds of ventilation that require positive pressure
ventilation (PPV)
Preterm infants below 28 weeks gestation who are given only
CPAP from birth in delivery room, i.e. the infant has spontaneous
respiration and good tone at birth. Surfactant to be given within
30 minutes after birth
Preterm infants between 28-32 weeks – to have CPAP from birth
in delivery room. To assess requirement for surfactant in NICU
based on oxygen requirement of FiO2 > 30% and respiratory
distress
More mature or larger infants should also be given surfactant if
the RDS is severe13
TIMING OF SURFACTANT
THERAPY
The first dose has to be given as early as possible to the
preterm infants requiring mechanical ventilation for RDS but
not in 1st minute OL
The repeat dose is given 4-6 hours later if FiO2 is still >
0.30 with optimal tidal volume settings for those below 32
weeks;
And if FiO2 > 0.40 and CXR still shows moderate to severe
RDS (“white” CXR) for those infants > 32 weeks gestational
age.
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TYPES OF SURFACTANT
Survanta , a natural surfactant, bovine derived
Dose : 4 ml/kg per dose.
Curosurf , a natural surfactant, porcine derived
Dose: 1.25 mls/kg per dose.
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COMPLICATIONS
PDAPulmonary air
leaks
Bronchopulmonarydysplasia
(chronic lung disease)
ROP
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RDS
increased
pulmonary
pressure
prevent
closure of
ductus
arteriosus
Associated
with
ventilation
that may
lead to
ruptured
alveolar
O2 dependent ≥
CGA 36W
Excessive
O2
developing
blood
vessels of
premature
infant retina
blindness
Tachypnea, mild retraction, hypoxia, occasional
grunting, rarely cyanosis which may persist for up to
48 hrs
Caused by retained lung fluid or slow resorption of
lung fluid
Associated in larger premature infant or term infant in
precipitate delivery (not in labor), infant DM mother or
use of analgesia intrapartum
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2. TTN
PATHOPHYSIOLOGY
The lungs in utero are constantly secreting fluid to aid lung
growth and development
However the rate of lung fluid production and volume of foetal
lung lumen decreases before birth, most during labour
The mechanism for fluid absorption is triggered by
neuroendocrine hormones, which cause lymphatic vessel
dilatation
As the lung pulmonary circulation increases following the first
breath, the fluid in the lungs is cleared thus interruption of this
process of clearing fluid from the lungs may result in
respiratory distress. 18
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MANAGEMENT
It is often managed conservatively by a period of close
observation on the postnatal ward or in the neonatal unit
but must be weighed against other differential diagnoses
including RDS and pneumonia which may progress rapidly
in newborn infants
Oxygen therapy
Antibiotics may be used if persistent (consider other
associated condition e.g. sepsis)
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3. MAS
Term and post term delivery
Tachypnea, hypoxia, hypercapnia, small airway obstruction,
air trapping, overdistention and extra alveolar air leaks
Meconium stained liquor suggest utero distress with
asphyxia, hypoxia and acidosis
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The inhaled meconium can cause:
• Mechanical obstruction of the airways leading to
mismatched ventilation/ perfusion
• Chemical pneumonitis (in 24-48 hrs)
• Infection which inhibit surfactant function and leads to
inflammation and swelling, which also can obstruct small
airways
• The combination of ventilation/perfusion mismatch and
pulmonary inflammatory can trigger vasoconstriction of
the pulmonary vasculature leading to PPHN
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MANAGEMENT
Mostly supportive therapy
Most cases of MAS will recover within 2–3 days
However, some infants will progress to develop severe
MAS requiring intubation and ventilation
Start on antibiotic in view of distinguishing MAS from
pneumonia can be difficult
• The initial chest radiograph is often similar to findings
associated with pneumonia with bilateral patchy infiltrates and
possible pleural effusion
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CXR
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Bilateral diffuse
grossly patchy
opacities
4. PPHN
Term, post term
Defined as a failure of normal pulmonary vasculature
relaxation at or shortly after birth, resulting in
impedance to pulmonary blood flow which exceeds
systemic vascular resistance, such that unoxygenated
blood is shunted to the systemic circulation
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PPHN can be:
• Idiopathic - 20%
• Associated with a variety of lung diseases:
Meconium aspiration syndrome (50%)
Pneumonia/sepsis (20%)
RDS (5%)
Congenital diaphragmatic hernia (CDH)
Others: Asphyxia, Maternal diabetes, Polycythemia
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DIAGNOSIS
History
- Precipitating factors during antenatal, intrapartum, postnatal
periods
Respiratory signs
- Signs of respiratory distress
- Onset at birth or within the first 4 to 8 hours of life
- Marked lability in pulse oximetry
Cardiac signs
- Central cyanosis
- Prominent precordial impulse
- Murmur27
Radiography
- Lung fields: normal, parenchymal lesions if lung disease is
present, or oligaemia
- Cardiac shadow: normal sized-heart, or cardiomegaly (usually
right atrial or ventricular enlargement)
Echocardiography
- Exclude congenital heart disease
- To look for pulmonary artery pressure
- Define the presence, degree, direction of shunt through the
duct / foramen ovale
- Define the ventricular output.
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Differentiate PPHN from Congenital
Cyanotic Cardiac diseases.
Differentiating points between the two are:
• Infants with PPHN usually had some perinatal hypoxia
• Bradycardia is almost always due to hypoxia, not a
primary cardiac problem
• Babies with congenital cyanotic heart diseases are
seldom critically ill at delivery
• Infants with cyanotic lesions usually do not have
respiratory distress
• The cyanosed cardiac baby is usually pretty happy, but
blue
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MANAGEMENT
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• Preventing and treating; hypothermia, hypoglycaemia, hypocalcaemia, hypovolemia, anaemia
General measures
• Morphine, midazolamSedation
Ventilation
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• Aim MAP>50 mmHg
• Inotropes to increase COCirculatory
• Inhaled NOVasodilators
• Extracorporeal membrane oxygenation
ECMO
5. APNEA OF PREMATURITY
Defined as sudden cessation of breathing that lasts for
at least 20 seconds or is accompanied by bradycardia
or oxygen desaturation (cyanosis) in an infant less
than 37 weeks’ gestational age
Incidence increase with decrease gestational age
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CLASSIFICATION
Central
Complete cessation of airflow and respiratory efforts with
no chest wall movement with no evidence of obstruction
Obstructive
Absence of noticeable airflow but with continuation of
chest wall movement
Mixed apnea – most common
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ETIOLOGY
Symptomatic of underlying problems, commoner ones
of which are:
• Respiratory conditions (RDS, pulmonary haemorrhage,
pneumothorax,
upper airway obstruction, respiratory depression due to drugs).
• Sepsis
• Hypoxemia
• Hypothermia
• CNS abnormality (e.g. IVH, asphyxia, increased ICP, seizures)
• Metabolic disturbances (hypoglycaemia, hyponatraemia,
hypocalcaemia)
• Cardiac failure, congenital heart disease, anaemia
• Aspiration/ Gastro-oesophageal reflux
• Vagal reflex: Nasogastric tube insertion, suctioning, feeding
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Differentiate from Periodic
breathing
Regular sequence of respiratory pauses of 10-20 sec
interspersed with periods of hyperventilation (4-15 sec) and
occurring at least 3x/ minute, not associated with cyanosis
or bradycardia
Benign respiratory pattern for which no treatment is
required
Respiratory pauses appear self-limited, and ventilation
continues cyclically
Periodic breathing typically does not occur in neonates in
the first 2 days of life35
MANAGEMENT Immediate resuscitation.
36Pediatrics Protocol 3rd ed
Review possible underlying causes and institute specific
therapy, e.g. septic workup if sepsis suspected and
commence antibiotics
Remember to check blood glucose via glucometer
Management to prevent recurrence
- Nurse baby in thermoneutral environment
- Nursing prone can improve thoraco-abdominal wall synchrony and
reduce apnoea
Monitoring:
- Pulse Oximeter, cardio-respiratory monitor
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Drug therapy
- Methylxanthine compounds:
Caffeine citrate (preferred if available)
IV Aminophylline or Theophylline
• Start methylxanthines prophylactically for babies < 32
weeks gestation
• For those > 32 weeks of gestation, give methylxanthines if
babies have apnoea
• To stop methylxanthines if
- Gestation > 34 weeks
- Apnoea free for 1 week when the patient is no longer on CPAP
- Monitor for at least 1 week once the methylxanthines are stopped
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After discharge, parents should be given advice
- Supine sleep position
- Elimination of exposure to tobacco smoke
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6. CONGENITAL PNEUMONIA
Acquired through the birth passages especially after
prolonged rupture of membranes
Pneumonia in newborn infants is often difficult to
diagnose and often difficult to distinguish from other
causes of respiratory distress including RDS and TTN
Investigations including blood white cell counts, blood
cultures, C-reactive protein, CXR
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PATHOPHYSIOLOGY
Pneumonia may be acquired due to ascending
infection especially when chorioamnionitis is
present
Common pathogens include • Bacteria, such as group B Streptococci (GBS), Streptococcus
pneumonia, Staphylococcus aureus, Listeria and gram-
negative enteric rods (e.g. E.Coli)
• Viruses, such as Herpes simplex virus, Respiratory syncytial
virus and Influenza A & B viruses
• Atypical organisms such as chlamydia
• Fungi such as Candida albicans.
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RISK FACTORS
Prolonged rupture of membranes (PROM)
Prematurity
Maternal infection (maternal fever or raised
white cell count) e.g. GBS
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MANAGEMENT
Blood gases and pulse oximetry monitoring will guide
the respiratory support required by the infant
Antibiotic; Penicillin and gentamicin
Supportive care such as oxygen, thermoregulation,
prevention of hypoglycaemia and parenteral nutrition
or nasogastric tube feeding
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CXR
A chest radiograph may show bilateral patchy
shadowing with or without pleural effusion.
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TAKE HOME MESSAGE
Gestation age
Risk factors
Recognize signs of respiratory distress
Early intervention, consultation and close monitoring
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THANK YOU
Ref:
1. Nelson Essential of Pediatrics 6th ed
2. Pediatrics Protocol 3rd ed
3. http://www.learningradiology.com
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