• Meconium is a sterile, thick, black-green, odorless material that
results from the accumulation of debris in the fetal intestine starting
in the third month of gestation.
• Meconium is sterile and does not contain bacteria, which is the
primary factor that differentiates it from stool. Intrauterine distress
can cause passage of meconium into the amniotic fluid.
• In the fetus, passage of meconium first occurs physiologically in the
10th-16th week of gestation, when it contributes to alkaline phosphatase
in amniotic ﬂuid.
• Fetal defecation reduces after 16 weeks and stops by 20 weeks,
concurrent with innervation of the anal sphincter.
• In-utero meconium passage is uncommon till term due to:
o lack of strong peristalsis
o good anal sphincter tone
o low levels of motilin
o cap of viscous meconium in the rectum
• Because meconium is rarely found in the amniotic fluid before 34 weeks
gestation, MAS mainly affects infants at term and post-term beyond 42
• Meconium-stained amniotic fluid (MSAF)
complicates approximately 10% to 15% of deliveries.
• The incidence of MSAF in preterm infants is very low. Most babies with
MSAF are 37 weeks or older, and many meconium-stained infants are
post mature and small for gestational age.
• Approximately 3% to 4% of neonates born through MSAF develop
meconium aspiration syndrome (MAS), and
• Approximately 30% to 50% of these infants require continuous positive
airway pressure (CPAP) or mechanical ventilation.
Meconium Aspiration Syndrome:
“Respiratory distress in newborn infants from inhalation of meconium
stained amniotic fluid into the tracheobronchial tree with compatible
radiological findings which cannot be otherwise explained.”
• Thick and viscous meconium lead to Complete or partial airway
With onset of respiration – meconium migrates from central to peripheral
• Complete obstruction – atelectasis
• Partial obstruction –Ball-valve – air trapping.
Risk of pneumothorax - 15 – 33%
• Aspiration of meconium causes airway irritation.
• The enzymes and bile salts of meconium may cause a release of cytokines
(eg, tumor necrosis factor-1-alpha and interleukins-1B, -6, -8, -13), which
can result in diffuse toxic pneumonitis.
• With distal progressing of meconium, chemical pneumonitis develop
resulting bronchiolar edema and narrowing of the small airway.
2. Chemical pneumonitis:
3. Surfactant inactivation:
• Meconium has cytotoxic effect on type II pneumocytes and decreased levels of
surfactant protein A and B (SP-A and SP-B).
• Bilirubin, fatty acid, triglycerides, cholesterol content of meconium causes
alterations in phospholipid structure.
• Bile salts in meconium may inhibit surfactant synthesis.
• Several constituents of meconium, especially the free fatty acids (eg, palmitic,
stearic, and oleic acid), have a higher minimal surface tension than surfactant.
• These may displace it from the alveolar surface, resulting in diffuse atelectasis,
with decreased lung volume, compliance, and oxygenation.
• The effect of MAS on surfactant dysfunction usually occurs in the subacute and late
phase of the disease.
4. Persistent pulmonary hypertension
• Persistent pulmonary hypertension of the newborn (PPHN) frequently
accompanies MAS, with right-to-left shunting caused by increased
pulmonary vascular resistance.
• PPHN usually presents in the subacute phase and as persistent
hypoxemia at 6 to 24 hours after birth.
• Significant pulmonary hypertension with right-to-left shunting occurs in
about 20% to 40% of infants who have MAS.
• PPHN in infants who have MAS could be due to:
1) hypertrophy or neomuscularization of post-acinar capillaries as a
result of chronic intrauterine hypoxia.
2) pulmonary vasoconstriction as a result of hypoxia, hypercarbia,
3) pulmonary vasoconstriction as a result of lung inflammation
Symptoms include the following:
o End-expiratory grunting
o Alar nasal flaring
o Intercostal retractions
o Barrel chest (increased anteroposterior diameter) due to the presence of air
o Auscultated rales and rhonchi (in some cases)
Yellow-green staining of fingernails, umbilical cord, skin or under the vocal
Signs of cerebral irritation resulting from cerebral edema and hypoxia may
appear later after birth i.e. seizures or jitteriness