Meconium Aspiration Syndrome: Walter Otieno Consultant Paediatrician

Meconium Aspiration Syndrome
Walter Otieno
Consultant Paediatrician
Background
• Composition of meconium:
– Water,
– Mucopolysaccharides,
– Cholesterol and sterol precursor,
– Protein,
– Lipid,
– Bile acids and salts,
– Enzymes,
– Blood group substances,
– Squamous cell,
– Vernix caseosa
• No bacteria!
Pathophysiology
• The passage of meconium from the fetus into
amnion is prevented by:
– lack of peristalsis (low motilin level),
– tonic contraction of the anal sphincter,
– terminal cap of viscous meconium.
• Meconium Stained Amniotic Fluid may be a natural
phenomenon that doesn’t indicate fetal distress but
mature GI tract in post term fetus with increased
motilin level.
• Vagal stimulation by cord or head compression may
be associated with passage of meconium in the
absence of fetal distress.
Pathophysiology
• The pathophysiology of MAS is complex.
• Intrauterine fetal gasping, mechanical airway
obstruction, pneumonitis, surfactant
inactivation, and damage of umbilical vessels: all
play roles in the pathophysiology of meconium
aspiration.
• There is also a strong association between MAS
and persistent pulmonary hypertension of the
newborn (PPHN).
Risk factors associated with in utero passage of
meconium:
– Post term pregnancy

– Little/no amniotic fluid at amniotomy
– Oligohydramnion by US
– IUGR/ placental insufficiency
– Maternal HTN
– Preeclampsia
– Maternal drug abuse (tobacco, cocaine).
Pathophysiology
• As the GI tract matures:

vagal stimulation  peristalsis+ rectal
sphincter relaxation  meconium
• Etiology not well understood:
– Fetal response to intra-uterine stress: hypoxia 
increased vagal tone
– Transient compression of umbilical cord/head 
increased vagal tone
– Maturation of fetal intestinal function
Pathophysiology
• Airway obstruction:
• Chemical pneumonitis:
• Surfactant dysfunction:
• Umbilical vessel damage
• Persistent pulmonary hypertension of the
newborn
Mechanism of injury
1.Mechanical Obstruction of the Airway
• It is commonly thought that the initial and

most important problem of the infant with
MAS is obstruction caused by meconium in
the airways.
• Complete obstruction of large airways by thick

meconium is an uncommon occurrence.
Pathophysiology
• Usually, small amounts of meconium migrate
slowly to the peripheral airways.
• This mechanism can create a ball valve
phenomenon, in which air flows past the
meconium during inspiration but is trapped
distally during expiration, leading to increases
in expiratory lung resistance, functional
residual capacity, and anterior posterior
diameter of the chest.
Airway obstruction
• Immediate : obstruction of large airways: (volume

dependent ):
hypoventilation => hypoxemia, hypercapnea, acidosis
• Central clearing – obstruction of small airways:
– Complete  atelectasis
– Partial  air trapping (ball valve phenomenon)  hyperdistention of
alveoli  increaesed lung resistance during exhalation
– pneumothorax, pneumomediastinum , pneumopericardium.
Pneumonitis
• Pneumonitis is a usual feature of MAS,

occurring in about ½ of the cases.
• Meconium has a direct toxic effect mediated
by inflammation.
• An intense inflammatory response in the
bronchi and alveoli can occur within hours of
aspiration of meconium.
Pathophysiology
• The airways and lung parenchyma become
infiltrated with large numbers of
polymorphonuclear leukocytes and
macrophages.
• Produce direct local injury by release of
inflammatory mediators-cytokines (TNF-α, IL-1β,
IL-8) and reactive oxygen species.
• Lead to vascular leakage, which may cause toxic
pneumonitis with hemorrhagic pulmonary
edema.
Pulmonary vasoconstriction
• The release of vasoactive mediators, such as

eicosanoids, endothelin-1 and prostaglandin
E2 as a result of injury from meconium seems
to play role in the development of persistent
PH.
• The pulmonary vasoconstriction is, in part, the
result of the underlying in utero stressors.
Pathophysiology
Other effects of meconium
• Reduce antibacterial activity (perinatal
bacterial infection)
• Irritating to fetal skin ( erythema
toxicum)
Clinical features
• Evidence of postmaturity: peeling skin, long fingernails, and
decreased vernix.
• The vernix, umbilical cord, and nails may be meconium-
stained, depending upon how long the infant has been
exposed in utero.
• In general, nails will become stained after 6 hours and vernix
after 12 to 14 hours of exposure.
• respiratory distress with tachypnea and cyanosis.
• Reduced pulmonary compliance and use of accessory muscles
of respiration are evidenced by intercostal and subcostal
retractions and abdominal (paradoxical) breathing, often with
grunting and nasal flaring.
Clinical features
• The chest typically appears barrel-shaped, with an
increased anterior-posterior diameter caused by
overinflation.
• Auscultation reveals rales and rhonchi -immediately
after birth.
• Some patients are asymptomatic at birth and
develop worsening signs of respiratory distress as
the meconium moves from the large airways into the
lower tracheobronchial tree.
Diagnosis
• The diagnosis of MAS is confirmed by chest
radiograph.
• The initial CXR may show streaky, linear
densities similar in appearance to transient
tachypnea of the newborn (TTN).
• As the disease progresses, the lungs typically
appear hyperinflated with flattening of the
diaphragms.
• Diffuse patchy densities may alternate with
areas of expansion.
Coarse focal consolidation with emphysema.
Hyperinflation and patchy asymmetric
airspace disease that is typical of MAS.
Coarse interstitial infiltrates +L side pneumothorax
Management
Management
• Skilled resuscitation team should be present at all
deliveries that involve MSAF.
• Pediatric intervention depends on whether the
infant is vigorous.
• Vigorous infant is if has:
1. Strong resp. efforts
2. Good muscle tone
3. Heart rate >100b/m
• When this is a case-no need for tracheal suctioning,
only routine management.
Management
• When the infant is not vigorous:
-Clear airways as quickly as possible.
-Give oxygen
-keep dry and warm.
-Direct laryngoscopy with suction of the mouth and
hypopharynx under direct visualization, followed by
intubation and then suction directly to the ET tube as it is
slowly withdrawn.
-The process is repeated until either ‘‘little additional
meconium is recovered, or until the baby’s heart rate
indicates that resuscitation must proceed without delay’’.
Postnatal Management
Approach to the ill newborns:
• Transfer to NICU.
• Monitor closely.
• Full range of respiratory support should be
available.
• Sepsis w/up and ABx indicated.
• Transfer to ECMO center may be necessary.
Other modalities of management
• Inhaled NO and Surfactants tried with poor
results
• ECMO good outcome
Prognosis
• Depends on severity and complications.

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Meconium Aspiration Syndrome

– Post term pregnancy

• As the GI tract matures:

• It is commonly thought that the initial and

• Complete obstruction of large airways by thick

• Immediate : obstruction of large airways: (volume

hypoventilation => hypoxemia, hypercapnea, acidosis

• Central clearing – obstruction of small airways:

• Pneumonitis is a usual feature of MAS,

• The release of vasoactive mediators, such as

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