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Meconium Aspiration Syndrome

  • Author: Melinda B Clark, MD; Chief Editor: Ted Rosenkrantz, MD  more...
Updated: Jan 14, 2014


The first intestinal discharge from newborns is meconium, which is a viscous, dark-green substance composed of intestinal epithelial cells, lanugo, mucus, and intestinal secretions (eg, bile). Intestinal secretions, mucosal cells, and solid elements of swallowed amniotic fluid are the 3 major solid constituents of meconium. Water is the major liquid constituent, comprising 85-95% of meconium. Meconium is sterile and does not contain bacteria, the primary factor that differentiates it from stool. Intrauterine distress can cause passage into the amniotic fluid. Factors that promote the passage in utero include placental insufficiency, maternal hypertension, preeclampsia, oligohydramnios, and maternal drug abuse, especially of tobacco and cocaine.

Meconium-stained amniotic fluid may be aspirated before or during labor and delivery. Because meconium is rarely found in the amniotic fluid prior to 34 weeks' gestation, meconium aspiration chiefly affects infants born at term and postterm.



In utero meconium passage results from neural stimulation of a maturing GI tract and usually results from fetal hypoxic stress. As the fetus approaches term, the GI tract matures, and vagal stimulation from head or cord compression may cause peristalsis and relaxation of the rectal sphincter leading to meconium passage.

The effects of meconium in amniotic fluid are well documented.[1] Meconium directly alters the amniotic fluid, reducing antibacterial activity and subsequently increasing the risk of perinatal bacterial infection. Additionally, meconium is irritating to fetal skin, thus increasing the incidence of erythema toxicum. However, the most severe complication of meconium passage in utero is aspiration of stained amniotic fluid before, during, and after birth. Aspiration induces hypoxia via four major pulmonary effects: airway obstruction, surfactant dysfunction, chemical pneumonitis, and pulmonary hypertension.

Airway obstruction

Complete obstruction of the airways by meconium results in atelectasis. Partial obstruction causes air trapping and hyperdistention of the alveoli, commonly termed the ball-valve effect. Hyperdistention of the alveoli occurs from airway expansion during inhalation and airway collapse around inspissated meconium in the airway, causing increased resistance during exhalation. The gas that is trapped (hyperinflating the lung) may rupture into the pleura (pneumothorax), mediastinum (pneumomediastinum), or pericardium (pneumopericardium).

Surfactant dysfunction

Meconium deactivates surfactant and may also inhibit surfactant synthesis.[2, 3] Several constituents of meconium, especially the free fatty acids (eg, palmitic, stearic, oleic), have a higher minimal surface tension than surfactant and strip it from the alveolar surface, resulting in diffuse atelectasis.[4]

Chemical pneumonitis

Enzymes, bile salts, and free fatty acids in meconium irritate the airways and parenchyma, causing a release of cytokines (including tumor necrosis factor (TNF-α, interleukin (IL)-1ß, I-L6, IL-8, IL-13), which initiate a diffuse pneumonitis that may begin within a few hours of aspiration.

All of these pulmonary effects can produce a gross ventilation-perfusion (V/Q) mismatch.

Persistent pulmonary hypertension of the newborn

To complicate matters further, many infants with meconium aspiration syndrome (MAS) have primary or secondary persistent pulmonary hypertension of the newborn (PPHN) as a result of chronic in utero stress and thickening of the pulmonary vessels. PPHN further contributes to the hypoxemia caused by meconium aspiration syndrome.[5]

Finally, although meconium is sterile, its presence in the air passages can predispose the infant to pulmonary infection.



Most infants with meconium aspiration syndrome (MAS) have complete recovery of pulmonary function. Severely affected infants have approximately a 50% risk of developing reactive airway disease in the first 6 months of life.

Prenatal and intrapartum events initiating the meconium passage may cause the infant to have long-term neurologic deficits, including CNS damage, seizures, mental retardation, and cerebral palsy.


A large retrospective analysis demonstrated the overall mortality rate for meconium aspiration syndrome to be 1.2% in the United States.[7] The mortality rate for meconium aspiration syndrome resulting from severe parenchymal pulmonary disease and pulmonary hypertension is as high as 20%. Other complications include air block syndromes (eg, pneumothorax, pneumomediastinum, pneumopericardium) and pulmonary interstitial emphysema, which occur in 10-30% of infants with meconium aspiration syndrome. The neurologic disabilities of survivors are not due primarily to the aspiration of meconium, but rather by in-utero pathophysiology, including chronic hypoxia and acidosis.[8]


Children with meconium aspiration syndrome may develop chronic lung disease from intense pulmonary intervention.

Infants with meconium aspiration syndrome have a slightly increased incidence of respiratory infections in the first year of life because the lungs are still in recovery.


A study of 499,096 singleton live births in London, England reported the rates of meconium-stained amniotic fluid varied by ethnicity: blacks (22.6%), south Asian (16.8%), and whites (15.7%). The study also demonstrated that later-gestational-age pregnancies and babies in the breach presentation more often had meconium-stained amniotic fluid.[9]


Meconium aspiration syndrome equally affects both sexes.


Meconium aspiration syndrome is exclusively a disease of newborns, especially those that are delivered at or beyond the mother's estimated due date.[1]




United States

In the industrialized world, meconium in the amniotic fluid can be detected in 8-25% of all births after 34 weeks' gestation. Historically, approximately 10% of newborns born through meconium-stained amniotic fluid developed meconium aspiration syndrome. Changes in obstetrical and neonatal practices appear to be decreasing the incidence of meconium aspiration syndrome.[6] Meconium aspiration syndrome was the admission diagnosis for 1.8% of term neonates in one large retrospective study from 1997-2007.[7]


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.

Contributor Information and Disclosures

Melinda B Clark, MD Associate Professor of Pediatrics, Department of Pediatrics, Albany Medical College

Melinda B Clark, MD is a member of the following medical societies: Alpha Omega Alpha, Academic Pediatric Association, American Academy of Pediatrics, Medical Society of the State of New York

Disclosure: Nothing to disclose.


David A Clark, MD Chairman, Professor, Department of Pediatrics, Albany Medical College

David A Clark, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American Pediatric Society, Christian Medical and Dental Associations, Medical Society of the State of New York, New York Academy of Sciences, Society for Pediatric Research

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Brian S Carter, MD, FAAP Professor of Pediatrics, University of Missouri-Kansas City School of Medicine; Attending Physician, Division of Neonatology, Children's Mercy Hospital and Clinics; Faculty, Children's Mercy Bioethics Center

Brian S Carter, MD, FAAP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Hospice and Palliative Medicine, American Academy of Pediatrics, American Pediatric Society, American Society for Bioethics and Humanities, American Society of Law, Medicine & Ethics, Society for Pediatric Research, National Hospice and Palliative Care Organization

Disclosure: Nothing to disclose.

Chief Editor

Ted Rosenkrantz, MD Professor, Departments of Pediatrics and Obstetrics/Gynecology, Division of Neonatal-Perinatal Medicine, University of Connecticut School of Medicine

Ted Rosenkrantz, MD is a member of the following medical societies: American Academy of Pediatrics, American Pediatric Society, Eastern Society for Pediatric Research, American Medical Association, Connecticut State Medical Society, Society for Pediatric Research

Disclosure: Nothing to disclose.

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Air trapping and hyperexpansion from airway obstruction.
Acute atelectasis.
Pneumomediastinum from gas trapping and air leak.
Left pneumothorax with depressed diaphragm and minimal mediastinal shift because of noncompliant lungs.
Diffuse chemical pneumonitis from constituents of meconium.
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