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Neonatal Diseases
common causes of respiratory
distress in the neonate are : 1.
2.
3.
4.
5.
Hyaline Membrane Disease (HMD)
Meconium Aspiration Syndrome (MAS)
Transient Tachypnoea of the Newborn (TTNB)
Congenital or acquired pneumonia
Persistent Pulmonary Hypertension of the Newborn
(PPHN)
6. Air leaks
Cont..
7. Congenital anomalies of upper airway (choanal
atresia), gut (tracheoesophageal fistula, congenital
diaphragmatic hernia) or lungs (lobar emphysema,
cysts)
8. Cardiac shock or Congenital Heart Disease
(CHD).
9. Haematological causes (severe anaemia,
polycythaemia)
10. Neurological ( seizures )
11. Metabolic causes- metabolic acidosis
Clinical Examination
Clues to the likely aetiology on examination of the
neonate :
1. A preterm baby weighing <1500 gms with retractions
and grunt is likely to have HMD.
2. A term baby born through meconium stained
amniotic fluid with an increase in the anteriorposterior
diameter of the chest (full chest) is likely
to be suffering from MAS.
3. A depressed baby with poor circulation is likely to
have neonatal sepsis with or without congenital
pneumonia.
4. A near term baby with no risk factors and mild
distress may have TTNB.
5. An asphyxiated baby may have PPHN.
Cont..
6.
A growth retarded baby with a plethoric look may
have polycythaemia.
7. A baby with respiratory distress should be checked
for an air leak by placing a cold light source over
the chest wall in a darkened room.
8. A baby presenting with tachypnoea and a cardiac
murmur may have a congenital heart disease.
9. Inability to pass catheter through the nostril
of a term baby is suggestive of choanal atresia.
Cont..
For babies presenting later with distress ask
for :
a) Is the distress associated with feed
refusal and lethargy? (sepsis, pneumonia)
b) Is there a family history of early neonatal
deaths?
(CHD).
Respiratory Distress Syndrome (RDS)
Synonym: hyaline membrane disease
• Caused by the inadequate production of surfactant in the lungs.
• produced by type II pneumocytes (reduce surface tension).
• surfactant is produced after 30 weeks gestation.
• Inadequate surfactant production causes air sacs to collapse
on expiration and greatly increases the energy required for
breathing.
• The development of interstitial oedema makes the lung less
compliant. This leads to hypoxia and retention of carbon
dioxide.
• Right-to-left shunting occurs: - in collapsed lung (intrapulmonary) or,
- if pulmonary hypertension is severe, across the ductus arteries
and the foramen ovale (extrapulmonary).
Risk factors
• Premature delivery
• Infants delivered via caesarian section
without maternal labour.
• Hypothermia
• Perinatal asphyxia
• Multiple pregnancy
• Family history of RD
Clinical features
. Usually preterm delivery.
- tachypnoea,
- expiratory grunting,
- subcostal and intercostal retractions
- diminished breath sounds,
- cyanosis and
- nasal flaring.
• May rapidly progress to fatigue, apnoea
and hypoxia
Investigations
• Blood gases: respiratory and metabolic acidosis
along with hypoxia.
• Pulse oximetry should be maintained at 90-95%.
• Chest x-ray (ground glass opacity )
• Monitor full blood count, electrolytes, renal and liver
function
• Echocardiogram
• diagnosing PDA
• determine the direction and degree of shunting,
• Cultures to rule out sepsis
Respiratory Distress
Syndrome
(RDS)
Also known as Hyaline Membrane
Disease
(HMD)
Occurrence
• 1-2% of all births
• 10% of all premature births
– Greatest occurrence is in the premature and
low birth weight infant
Etiology & Predisposing Factors
• Prematurity
– Immature lung architecture and surfactant
deficiency
• Fetal asphyxia & hypoxia
• Maternal diabetes
– Increased chance of premature birth
– Possible periods of reflex hypoglycemia in the
fetus causing impaired surfactant production
The cycle continues until
surfactant levels are adequate
to stabilize the lung
• Symptoms usually appear 2-6 hours
after birth
– Why not immediately?
• Disease peaks at 48-72 hours
• Recovery usually occurs 5-7 days after
birth
Clinical findings: Physical
• Tachypnea
(60 BPM or >)
• Retractions
• Nasal flaring
• Expiratory grunting
– Helps generate
autoPEEP
• Decreased breath
sounds with crackles
• Cyanosis on room air
• Hypothermia
• Hypotension
Clinical Findings: Lab
• ABGs: initially respiratory alkalosis and
hypoxemia that progresses to profound
hypoxemia and combined acidosis
• Increased Bilirubin
• Hypoglycemia
• Possibly decreased hematocrit
CXR: Normal
RDS CXR: Ground Glass Effect
RDS CXR: Air Bronchograms &
Hilar Densities
Time constant is decreased
since elastic resistance is so
high
Increased elastic resistance
means decreased compliance!
RDS Treatment: Primarily
supportive until lung stabilizes
• Maintain perfusion, maintain ventilation
and oxygenation
• O2 therapy, CPAP or mechanical
ventilation
– May require inverse I:E ratios if oxygenation
can not be achieved with normal I:E ratio
• Surfactant instillation!!!
– May cause a sudden drop in elastic
resistance!
Prognosis/Complications
Prognosis is good once infant makes it past
the peak (48-72 hours)
Complications possible are:
• Intracranial Bleed
• BPD (Bronchopulmonary Dysplasia)
• PDA (Patent Ductus Arteriosus)
Meconium Aspiration
Syndrome
-MASSyndrome of respiratory distress
that occurs when meconium is
aspirated prior to or during birth
Occurrence
• 10-20% of ALL births show meconium
staining
– 10-50% of stained babies may be
symptomatic
• More common in term and post-term
babies
Etiology & Predisposing Factors
• Intra-uterine hypoxic or asphyxic
episode
• Post-term
• Cord compression
Pathophysiology: Check Valve
Effect
Causes gas trapping
(obstruction)
If complete obstruction, then
eventually atelectasis occurs
Irritating to airways, so edema
and bronchospasm
Good culture ground for
bacteria, so pneumonia
possible
Pathophysiology (cont.)
• V/Q mismatch leads to hypoxia and
acidosis which increases PVR
• TC increases because it increases airway
resistance
• Meconium is usually absorbed in 24-48
hours; there are still many possible
complications
Clinical Signs
• Respiratory
depression or distress
at birth
• Hyperinflation
• Pallor
• Meconium stained
body
• Possible cyanosis on
room air
• Moist crackles
• ABGs – hypoxemia with
combined acidosis
• CXR – coarse, patchy
infiltrates with areas of
atelectasis and areas of
hyperinflation
– May see flattened
diaphragms if obstruction is
severe
Management
• Surfactant replacement therapy (endotracheal
tube).
• Oxygen: infants with mild RDS.
• Continuous positive airway pressure (CPAP).
• CPAP may be administered via an
endotracheal tube, nasal prongs, or
nasopharyngeal tubes.
• Assisted ventilation at fast rates (more than 40
breaths per minute)
Supportive therapy includes the following
:
.
. Temperature regulation:
prevent hypothermia.
• Fluids, metabolism, and nutrition:
monitor and maintain blood glucose, electrolytes,
acid balance, renal function, and hydration.
• Once the infant is stable, intravenous nutrition with
amino acids and lipid.
• After the respiratory status is stable, initiate small
volume gastric feeds (preferably breast milk) via a
tube to initially stimulate gut development.
Cont..
• Circulation and anaemia:
monitor heart rate, peripheral perfusion, and blood
pressure. Blood or volume expanders may be required.
• Antibiotics:
start antibiotics in all infants who present with
respiratory distress at birth after obtaining blood cultures.
Discontinue antibiotics after three to five days if blood
cultures are negative.
• Support of parents and family:
keep the parents well informed. Encourage parents to
frequently visit and stay with their baby.
Treatment schedule
• Inj. Betamethasone 12 mg IM every 24
hours , 2 doses
• Inj. Dexamethasone 6 mg IM every
12hours , 4 doses
Timing of effect :
• Opitimal effect occurs after 24 hours of
initiating treatment
• Effect of one course lasts for 7 days.
Prevention
• Antenatal corticosteroids (dexamethasone)
accelerate foetal surfactant production and lung
maturation. They have been shown to reduce
respiratory distress syndrome, intraventricular
haemorrhage and mortality by 40%.
• Delaying premature birth. Tocolytics,
e.g.nifedipine or ritodrine, may delay delivery by
48 hours and therefore enable time for antenatal
corticosteroids to be given.
• Avoid hypothermia in the neonate.
M.A.S. Treatment
Amnioinfusion – artificial
amniotic fluid infused
into uterus to dilute
meconium
Proper resuscitation at
birth(clear meconium
from trachea before
stimulating respiration)
Oro-gastric tube
NTE
O2
NaHCO3 if severe
metabolic acidosis
Broad spectrum antibiotics
Bronchial hygiene
May need mechanical
ventilation
– Slow rates and wide I:E
ratios because of increased
TC
– Low level of PEEP may
help prevent check valve
effect
– May need HFO
Prognosis & Complications
Good prognosis if there are no
complications
Complications:
Pneumonia
Pulmonary baro/volutrauma
Persistent Pulmonary Hypertension (PPHN)
CXR: Pneumothorax