3. History
• Greek philosopher Aristotle (350-370 BC) first described the
condition meconium stained amniotic fluid derived from the Greek
word “meconium-arion” literally meaning “opium-like”.
• He believed that MSAF induced fetal sleep and that it was also
associated with fetal deaths and neonatal depression, or because
meconium resembled the black, tarry consistency of processed
opium.
• Several publications from the 1600s reported MSAF as a sign of
fetal death.
• The first description of in-utero aspiration of meconium and MAS
was published in 1918.
4. Meconium
• sterile, thick, black-green, odorless matter that is first found in the fetal ileum by
the 10th-16th week of gestation gradually increasing to reach about 200g at birth as
the first intestinal discharge within 24-48hrs after birth.
• Composition:
o 72-80% water
o desquamated cells from skin and intestine
o bile and drug metabolites
o gastrointestinal mucin
o lanugo
o vernix caseosa
o amniotic fluid
o cholesterol, pancreatic enzymes, blood group specific glycoproteins
5. • 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 weeks.
6. 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.”
7. Epidemiology
• Meconium stained amniotic fluid occurs in about 10-25% of childbirths
after 34 weeks of gestation.
• Meconium aspiration syndrome develops in about 4-10% of the infants
born with MSAF.
• Neonates with MAS, 1/3 will need ventilatory support, 10% develop air
leaks and 5-10% have a definite fatal outcome and 5-6 % develop
persistent pulmonary hypertension of the newborn.
• Mortality rate vary 4-12% depending on the severity of the complication
and the effectiveness of treatment.
• Changes in obstetrical and neonatal practices appear to be decreasing the
incidence of meconium aspiration syndrome.
• In developing countries with less availability of prenatal care and where
home births are common, incidence of meconium aspiration syndrome is
thought to be higher and is associated with a greater mortality rate.
8. Etiology
• Risk factors that promote meconium passage in-utero:
o Placental insufficiency
o Maternal hypertension and diabetes mellitus
o Pre-eclampsia/Eclampsia
o Oligohydramnios
o Maternal drug abuse especially tobacco and cocaine
o Maternal infection/chorioamnionitis
o Fetal gasping secondary to hypoxia
9. • Causes of meconium passage:
o Distressed Fetus-Hypoxia and acidosis
stimulates vagal pathway causing peristalsis
and relaxes anal sphincter
o Mature fetus (Post-term)-increased
parasympathetic tone, increased motilin, vagal
stimulation produced by cord or head
compression causing in-utero distress
11. Clinical Features
• History
o The presence of meconium in amniotic fluid but not all
neonates with MSAF develop MAS.
o Green urine may be observed in newborns less than 24
hours after birth. Meconium pigments can be absorbed
by the lung and excreted in urine.
o Post term delivery
12. • Physical Examination
Severe respiratory distress may be present. Symptoms include the following:
o Cyanosis
o End-expiratory grunting
o Alar nasal flaring
o Intercostal retractions
o Tachypnea
o Barrel chest (increased anteroposterior diameter) due to the presence of air
trapping
o Auscultated rales and rhonchi (in some cases)
Yellow-green staining of fingernails, umbilical cord, skin or under the vocal cords.
Signs of cerebral irritation resulting from cerebral edema and hypoxia may appear
later after birth i.e. seizures or jitteriness
13. Differential Diagnosis
• Aspiration Syndromes
• Neonatal Pneumonia
• Transient Tachypnea of the Newborn
• Respiratory Distress Syndrome
• Neonatal Congenital Diaphragmatic
Hernia
• Persistent Pulmonary Hypertension
of the Newborn
• Surfactant Deficiency
• Transposition of the Great Arteries
• Neonatal Sepsis
• Congenital Heart Disease with
Pulmonary Hypertension
14. Diagnosis
Lab Investigations
Acid-base status
• V-Q mismatch and perinatal stress
• Arterial Blood Gases
• Metabolic acidosis from perinatal stress is
complicated by respiratory acidosis from
parenchymal disease and persistent
pulmonary hypertension of the newborn.
• Continuous measurement of oxygenation
by pulse oximetry are necessary for
appropriate management
Serum Electrolytes
• Na, Ca, K concentrations at 24 hours of life
to detect MAS because SIADH and ARF are
frequent complications of perinatal stress.
Full Blood Count
• Low Hemoglobin and Hematocrit
Hypoxia
• Thrombocytopenia neonatal
hemorrhage.
• Neutropenia or neutrophilia with left shift
of the differential perinatal bacterial
infection.
• Polycythemia chronic fetal hypoxia
• Polycythemia is associated with decreased
pulmonary blood flow and may worsen
the hypoxia associated with MAS and
PPHN.
15. • Imaging
Chest X-Ray
o Confirm the diagnosis of MAS and see the extent of intra-
thoracic pathology
o Identify atelectasis
o Ensure appropriate positioning of the ETT and umbilical
catheters
• Classic CXR Findings:
o Diffuse asymmetric patchy infiltration and consolidation
o Air trapping and hyper-expansion from airway
obstruction.
o Acute atelectasis
o Pneumomediastinum from gas trapping and air leak.
o Left pneumothorax with depressed diaphragm and
minimal mediastinal shift because of noncompliant
lungs.
o Diffuse chemical pneumonitis from constituents of
meconium.
• Echocardiography
o ensure normal cardiac structure and assess cardiac
function, determine the severity of pulmonary
hypertension and right-to-left shunting.
• Brain Imaging
o Later in the course of meconium aspiration syndrome,
when the infant is stable, imaging studies of the brain
(e.g. MRI, CT scanning, cranial ultrasonography) are
indicated, if the infant's neurologic examination is
abnormal.
16. • Classification of MAS:
o Mild MAS
<40% pO2 for <48hrs
o Moderate MAS
>40% pO2 for >48hrs without air leak
o Severe MAS
Assisted ventilation for >48hrs often
associated with PPHN
• Complications of MAS
o Severe Parenchymal Pulmonary
Disease
o Pulmonary HTN
o Air block syndromes
pneumothorax,
pneumomediastinum
pneumopericardium
o Pulmonary interstitial emphysema
Anticipate the worst!
Be prepared!
17. Immediate Management
The American Academy of Pediatrics Neonatal
Resuscitation Program Steering Committee guidelines are
as follows
If the baby is not vigorous:
• Suction the trachea immediately after delivery
• Suction for no longer than 5 seconds
• If no meconium is retrieved, do not repeat intubation and
suction
• If meconium is retrieved and no bradycardia is present,
reintubate and suction
• If the heart rate is low, administer positive pressure
ventilation and consider suctioning again later.
If the baby is vigorous:
• Do not electively intubate
• Clear secretions and meconium from the mouth and nose
with a bulb syringe or a large-bore suction catheter.
Dry, stimulate, reposition, and administer oxygen as
necessary.
Transfer ill newborns with respiratory distress to NICU
18. General Management
Continued care in the neonatal ICU (NICU)
Maintain an optimal thermal environment
Minimal handling to reduce agitation thus
pulmonary hypertension and right-to-left shunting
causing hypoxia and acidosis
Insert umbilical artery to monitor blood pH and
blood gases without agitating the infant.
Continue respiratory care.
o Oxygen therapy via hood or positive.
o Conventional Mechanical ventilation
• High flow rate
• minimize mean airway pressure
• short inspiratory time (0.4-0.5 secs)
• Adequate expiratory time to prevent air trapping
o Oxygen saturations should be maintained at 90-
95%.
Broad spectrum antibiotics
Supportive treatment
o IV Dextrose to prevent hypoglycemia.
o Fluid restriction (60-70 mL/kg/d) to prevent
cerebral and pulmonary edema
o Electrolytes to correct metabolic acidosis
o Protein, lipids, and vitamins to prevent deficiencies
Conventional Mechanical Ventilation Support
o Continuous Positive Airway Pressure
If FiO2 is >0.4
CPAP with pressures 2-6 cm of H20 before
mechanical ventilation
o Indications of CMV
PaO2 <50 mm of Hg
PaC02 >60 mm of Hg
pH <7.25
Sleep Apnea
20. Volume and Pressure Support
o Inhaled nitric oxide has replaced the use of most IV
pulmonary vasodilators
o Maintain systemic BP higher than pulmonary BP by
decreasing R-L shunt through the PDA by:
• Volume expansion
• Transfusion therapy
• Systemic vasopressors e.g. dopamine
Albumin/Bile Acid Blockers
o Bile acid blockers such as cholestyramine and serum
bovine albumin that binds to lipids and free fatty
acids are administered into the trachea and
reducing lung toxicity
o Maybe coupled with surfactant administration
• Surfactant Therapy
• replace displaced or inactivated surfactant and as a
detergent to remove meconium
• may reduce the severity of disease, progression to
extracorporeal membrane oxygenation and
decrease length of hospital stay
• May decrease respiratory failure with MAS within 6
hrs of 3 doses
ECMO
• Extracorporeal membrane oxygenation is the last
option
• focused on the function of oxygenation and CO2
removal
• Effective but associated with a high incidence of
poor neurologic outcomes
• ECMO is done using only cervical cannulation,
which can be performed under local anesthesia
• used for longer-term support ranging from 3-10
days
• allow time for intrinsic recovery of the lungs and
heart
• Survival rate 93-100%
21. Prevention of MAS
• Obstetricians should monitor mothers at risk
for uro-placental insufficiency and fetal
distress with repeated CTG
• Timing of delivery in post due date, induction
as early as 41 weeks may help prevent MAS
• Upon delivery of the head of baby careful
suctioning of the posterior pharynx
decreases potential for MAS
Prognosis
• Most complete recovery of pulmonary
function.
• Severely affected infants have about a 50%
risk of developing reactive airway disease in
the first 6 months of life.
• May cause the infant to have long-term
neurologic deficits, including CNS damage,
seizures, mental retardation, and cerebral
palsy.
22. References
• Manual of Neonatal Care 6th edition John P. Cloherty
• Essential Pediatrics 6th edition, O.P Ghai
• Neonatal Resuscitation Manual
• Clarke, M.B. and Rosenkrantz, T. (2016) Meconium aspiration syndrome:
Background, Pathophysiology, prognosis. Available at:
http://emedicine.medscape.com/article/974110-overview#a5 (Accessed:
5 July 2016)
• Fanaroff, A.A. (2008) ‘Meconium aspiration syndrome: Historical aspects’,
Journal of Perinatology, 28, pp. S3–S7. doi: 10.1038/jp.2008.162.
• Raju, U., Sondhi, V. and Patnaik, S. (2010) ‘Meconium aspiration syndrome:
An insight’, Medical Journal Armed Forces India, 66(2), pp. 152–157. doi:
10.1016/s0377-1237(10)80131-5.
