eMedicine Specialties > Pediatrics: Cardiac Disease and Critical Care Medicine > Neonatology

Meconium Aspiration Syndrome

Author: Melinda B Clark, MD, Assistant Professor of Pediatrics, Department of Pediatrics, Albany Medical College
Coauthor(s): David A Clark, MD, Chairman, Professor, Department of Pediatrics, Albany Medical College
Contributor Information and Disclosures

Updated: Dec 2, 2008

Introduction

Background

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. 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 during labor and delivery, causing neonatal respiratory distress. Because meconium is rarely found in the amniotic fluid prior to 34 weeks' gestation, meconium aspiration chiefly affects infants at term and postterm.

Pathophysiology

In utero meconium passage results from neural stimulation of a mature 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. 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 4 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

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.

Chemical pneumonitis

Enzymes, bile salts, and fats 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) and resulting in a diffuse pneumonia that may begin within a few hours of aspiration.

Persistent pulmonary hypertension of the newborn

All of these pulmonary effects can produce gross ventilation-perfusion (V/Q) mismatch. 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. Finally, although meconium is sterile, its presence in the air passages can predispose the infant to pulmonary infection.

Frequency

United States

In the industrialized world, meconium in the amniotic fluid can be detected in 8-25% of all births after 34 weeks' gestation. Of those newborns with meconium-stained amniotic fluid, approximately 10% develop meconium aspiration syndrome.

International

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.

Mortality/Morbidity

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.

Race

No racial predilection is known.

Sex

Meconium aspiration syndrome equally affects both sexes.

Age

Meconium aspiration syndrome is exclusively a disease of newborns.

Clinical

History

  • Presence of meconium in amniotic fluid is required to cause meconium aspiration syndrome (MAS), but not all neonates with meconium-stained fluid develop meconium aspiration syndrome. The presence of thick particulate meconium in the amnionic fluid increases the likelihood of prenatal aspiration.
  • Green urine may be observed in newborns with meconium aspiration syndrome less than 24 hours after birth. Meconium pigments can be absorbed by the lung and can be excreted in urine.

Physical

  • Severe respiratory distress may be present. Symptoms include the following:
    • Cyanosis
    • End-expiratory grunting
    • Alar flaring
    • Intercostal retractions
    • Tachypnea
    • Barrel chest in the presence of air trapping
    • Auscultated rales and rhonchi (in some cases)
  • Yellow-green staining of fingernails, umbilical cord, and skin may be observed.

Causes

  • Factors that promote the passage of meconium in utero include the following:
    • Placental insufficiency
    • Maternal hypertension
    • Preeclampsia
    • Oligohydramnios
    • Maternal drug abuse, especially of tobacco and cocaine
    • Maternal infection/chorioamnionitis
    • Fetal gasping secondary to hypoxia
    • Inadequate removal of meconium from the airway prior to the first breath
    • Use of positive pressure ventilation (PPV) prior to clearing the airway of meconium

More on Meconium Aspiration Syndrome

Overview: Meconium Aspiration Syndrome
Differential Diagnoses & Workup: Meconium Aspiration Syndrome
Treatment & Medication: Meconium Aspiration Syndrome
Follow-up: Meconium Aspiration Syndrome
Multimedia: Meconium Aspiration Syndrome
References
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References

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Further Reading

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Keywords

meconium aspiration syndrome, MAS, meconium-stained amniotic fluid, fetal hypoxic distress, intrauterine distress, placental insufficiency, maternal hypertension, preeclampsia, oligohydramnios, maternal drug abuse, neonatal respiratory distress, airway obstruction, surfactant dysfunction, chemical pneumonitis, pulmonary hypertension, atelectasis, persistent pulmonary hypertension of the newborn, PPHN, pneumothorax, pneumomediastinum, pneumopericardium, pulmonary interstitial emphysema, respiratory acidosis, metabolic acidosis, syndrome of inappropriate secretion of antidiuretic hormone, SIADH

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Contributor Information and Disclosures

Author

Melinda B Clark, MD, Assistant Professor of Pediatrics, Department of Pediatrics, Albany Medical College
Melinda B Clark, MD is a member of the following medical societies: Alpha Omega Alpha, Ambulatory Pediatric Association, American Academy of Pediatrics, and Medical Society of the State of New York
Disclosure: Nothing to disclose.

Coauthor(s)

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 & Dental Society, Medical Society of the State of New York, New York Academy of Sciences, and Society for Pediatric Research
Disclosure: Nothing to disclose.

Medical Editor

Steven M Donn, MD, Professor of Pediatrics, Director, Neonatal-Perinatal Medicine, Department of Pediatrics, University of Michigan Health System
Steven M Donn, MD is a member of the following medical societies: American Pediatric Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from broker recommendation; Avanir Pharma Stock Investment from broker recommendation

Managing Editor

Brian S Carter, MD, FAAP, Professor of Pediatrics (Neonatology), Vanderbilt University School of Medicine; Co-director, Pediatric Advance Comfort Team, Monroe Carell Jr Children's Hospital at Vanderbilt
Brian S Carter, MD, FAAP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, National Hospice and Palliative Care Organization, and National Perinatal Association
Disclosure: Nothing to disclose.

CME Editor

Carol L Wagner, MD, Professor of Pediatrics, Medical University of South Carolina
Carol L Wagner, MD is a member of the following medical societies: American Academy of Pediatrics, American Chemical Society, American Medical Women's Association, American Public Health Association, American Society for Bone and Mineral Research, American Society for Clinical Nutrition, Massachusetts Medical Society, National Perinatal Association, and Society for Pediatric Research
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 Medical Association, American Pediatric Society, Connecticut State Medical Society, Eastern Society for Pediatric Research, and Society for Pediatric Research
Disclosure: Nothing to disclose.

 
 
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