Meconium Aspiration Syndrome



Meconium aspiration syndrome (MAS) is the aspiration of stained amniotic fluid, which can occur before, during, or immediately after birth. Meconium is the first intestinal discharge from newborns, a viscous, dark-green substance composed of intestinal epithelial cells, lanugo, mucus, and intestinal secretions (eg, bile. Water is the major liquid constituent, comprising 85-95% of meconium; the remaining 5-15% of ingredients consists of solid constituents, primarily intestinal secretions, mucosal cells, and solid elements of swallowed amniotic fluid, such as proteins and lipids.

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. Factors that promote the passage in utero include placental insufficiency, maternal hypertension, preeclampsia, oligohydramnios, infection, acidosis, and maternal drug abuse, especially use of tobacco and cocaine.

As noted above, 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 primarily affects infants born at term and postterm.


In utero meconium passage results from neural stimulation of a maturing gastrointestinal (GI) tract, usually due to fetal hypoxic stress. As the fetus approaches term, the GI tract matures, and vagal stimulation from head or spinal 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. In addition, meconium is irritating to fetal skin, thus increasing the incidence of erythema toxicum. However, the most severe complication of meconium passage in utero is perinatal aspiration of stained amniotic fluid (before, during, or immediately after birth)—ie, meconium aspiration syndrome (MAS). Aspiration of meconium-stained amniotic fluid may occur if the fetus is in distress, leading to a gasping breathing pattern. This aspiration induces hypoxia via four major pulmonary effects: airway obstruction, surfactant dysfunction, chemical pneumonitis, and pulmonary hypertension.[1]

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)-1β, IL-6, 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.


Factors that promote the passage of meconium in utero include the following:


United States data

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 (MAS). However, changes in obstetric and neonatal practices appear to be decreasing its incidence.[6]  MAS was the admission diagnosis for 1.8% of term neonates in one large retrospective study from 1997-2007.[1]

International data

In developing countries with less availability of prenatal care and where home births are common, the incidence of MAS is thought to be higher and is associated with a greater mortality rate.

Age-, sex-, and race-related demographics

MAS is exclusively a disease of newborns, especially those delivered at or beyond the mother's estimated due date.[1]  MAS affects both sexes equally.

A study of 499,096 singleton live births in London, England, reported the rates of meconium-stained amniotic fluid varied by ethnicity: It was 22.6% in the black population, 16.8% in south Asian groups, and 15.7% in the white population.[7] The study also demonstrated that meconium-stained amniotic fluid occurred more often in later-gestational-age pregnancies and in babies in the breech presentation.


Most infants with meconium aspiration syndrome (MAS) have complete recovery of pulmonary function; however, MAS infants have a slightly increased incidence of respiratory infections in the first year of life because the lungs are still in recovery. Severely affected infants have an increased risk of developing reactive airway disease (RAD) in the first 6 months of life.[8]

Children with MAS may develop chronic lung disease from intense pulmonary intervention.

Prenatal and intrapartum events that initiate the meconium passage may cause the infant to have long-term neurologic deficits, including central nervous system (CNS) damage, seizures, mental retardation, and cerebral palsy.


A large retrospective analysis demonstrated the overall mortality rate for MAS to be 1.2% in the United States.The mortality rate for MAS resulting from severe parenchymal pulmonary disease and pulmonary hypertension is as high as 20%. Other complications include air leak syndromes (eg, pneumothorax, pneumomediastinum, pneumopericardium), which occur in 10-30% of infants with MAS. 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.

A large retrospective analysis demonstrated the overall mortality rate for MAS to be 1.2% in the United States.[1]  The mortality for MAS resulting from severe parenchymal pulmonary disease and pulmonary hypertension is as high as 20%. Other complications include air-leak syndromes (eg, pneumothorax, pneumomediastinum, pneumopericardium) and pulmonary interstitial emphysema, which occur in 10-30% of infants who have MAS. The neurologic disabilities of survivors are not due primarily to the aspiration of meconium, but rather owing to in utero pathophysiology, including chronic hypoxia and acidosis.[9]


The presence of meconium in amniotic fluid is required to cause meconium aspiration syndrome (MAS), but not all neonates with meconium-stained fluid develop this condition. The diagnosis of MAS requires the presence of meconium-stained amniotic fluid or neonatal respiratory distress, as well as characteristic radiographic abnormalities.

Historically, efforts to reduce the development of MAS included oropharyngeal suctioning at the perineum, followed by intubation and tracheal suction of meconium immediately following delivery. This universal practice was abandoned over a decade ago when studies showed that infants who were vigorous at birth did not benefit from this intervention. Following this practice change, the Neonatal Resuscitation Program (NRP) recommended intubation and tracheal suctioning only for nonvigorous infants born through meconium-stained fluid.

However, in 2015, these recommendations changed again: It is no longer recommended to intubate and suction nonvigorous infants born through meconium-stained fluid due to a lack of evidence to support this practice.[10, 11] Instead, in this setting, the NRP now recommends having a practitioner skilled at endotracheal intubation be present at the time of birth, and they should begin with the initial steps of resuscitation (ie, provide warmth, position the head and neck to open the airway, clear secretions with a bulb syringe, dry, and stimulate the infant).[10, 11]  The 2017 American College of Obstetricians and Gynecologists (ACOG) opinion number 689 indicates that, regardless of whether infants with meconium-stained amniotic fluid are vigorous or nonvigorous, do not routinely administer intrapartum suctioning.[11]

In a 2015 developing nation retrospective study (2008-2009) that evaluated the effect of intrapartum oropharyngeal suction on MAS in 509 meconium-stained, term singleton neonates without major congenital malformations, investigators found that outcomes in those who received suctioning were similar to those in the control group (who did not undergo suctioning).[12] The incidence and severity of MAS, as well as oxygen requirements longer than 48 hours, were comparable between the groups.

Physical Examination

Severe respiratory distress may be present. Symptoms include the following:

Yellow-green staining of fingernails, umbilical cord, and skin may be also observed.

Green urine may be noted in newborns with MAS less than 24 hours after birth. Meconium pigments can be absorbed by the lung and can be excreted in urine.

Laboratory Studies

Acid-base status

Ventilation-perfusion (V/Q) mismatch and perinatal stress are prevalent in meconium aspiration syndrome (MAS); therefore, assessment of the infant's acid-base status is crucial.

Metabolic acidosis from perinatal stress is complicated by respiratory acidosis from parenchymal disease and persistent pulmonary hypertension of the newborn (PPHN).

Measurement of arterial blood gas (ABG) pH, partial pressure of carbon dioxide (pCO2), and partial pressure of oxygen (pO2), as well as continuous monitoring of oxygenation by pulse oximetry are necessary for appropriate management. The calculation of an oxygenation index (OI) can be helpful when considering advanced treatment modalities, such as extracorporeal membrane oxygenation (ECMO). 

Serum electrolytes

Obtain sodium, potassium, and calcium concentrations at 24 hours of life in infants with MAS, because syndrome of inappropriate secretion of antidiuretic hormone (SIADH) and acute renal failure are frequent complications of perinatal stress.

Complete blood cell (CBC) count

Note the following:

Fetal scalp blood lactate sampling has not been shown to reduce the risk of respiratory distress syndrome in infants with meconium-stained amniotic fluid.[13]

Imaging Studies

Chest radiography

Chest radiography is essential in order to achieve the following:

See the images below.

View Image

Air trapping and hyperexpansion from airway obstruction.

View Image

Acute atelectasis.

View Image

Pneumomediastinum from gas trapping and air leak.

View Image

Left pneumothorax with depressed diaphragm and minimal mediastinal shift because of noncompliant lungs.

View Image

Diffuse chemical pneumonitis from constituents of meconium.



Echocardiography is necessary to ensure normal cardiac structure and for assessment of cardiac function, as well as to determine the severity of pulmonary hypertension and right-to-left shunting.

A prospective observational study of 117 newborns with MAS (and 100 controls) demonstrated that pulmonary ultrasonography may be a convenient, noninvasive, and accurate imaging modality for the diagnosis of MAS.[14] The primary features of MAS noted on sonograms included the following[14] :

Brain imaging studings

Later in the course of MAS, when the infant is stable and if the infant's neurologic examination is abnormal, imaging studies of the brain (eg, magnetic resonance imaging [MRI], computed tomography [CT] scanning, cranial ultrasonography) are indicated.

Medical Care

The American College of Obstetricians and Gynecologists (ACOG) continues to provide guidance regarding the appropriate indications for delivery to prevent neonatal complications of a prolonged pregnancy, as well as for avoiding the unnecessary delivery of a preterm baby.[15, 16]

In patients with meconium aspiration syndrome (MAS), a thorough cardiac examination and echocardiography are necessary to evaluate for congenital heart disease and persistent pulmonary hypertension of the newborn (PPHN).

Quantifying the degree of pulmonary hypertension, prior to instituting therapy, is essential.

Prevention of MAS

Prevention of MAS is paramount. Obstetricians should closely monitor fetal status in an attempt to identify fetal distress.

When meconium is detected, amnioinfusion with warm, sterile saline is theoretically beneficial to dilute the meconium in the amniotic fluid, thereby minimizing the severity of the aspiration. However, current evidence does not support routine amnioinfusion to prevent MAS.[17, 18, 19] One large, multicenter study determined that amnioinfusion did not reduce the risk of moderate or severe MAS or MAS-related death.[20]

As noted earlier under Presentation, current recommendations no longer advise routine intrapartum suctioning for infants born to mothers with meconium staining of the amniotic fluid.[10, 11, 21, 22, 23]

No clinical trials justify suctioning on the basis of the meconium consistency. Do NOT perform the following harmful techniques in an attempt to prevent aspiration of meconium-stained amniotic fluid:

The American Academy of Pediatrics (AAP) Neonatal Resuscitation Program Steering Committee and the American Heart Association (AHA) have promulgated guidelines for management of babies exposed to meconium.[10] The guidelines are under continuous review and are revised as new evidence-based research becomes available. The seventh edition of the Neonatal Resuscitation Program modified its previous recommendations regarding endotracheal suctioning for the nonvigorous infant. The most recent guidelines are as follows[10, 11] :

Continued care in the neonatal intensive care unit (NICU)

Maintain an optimal thermal environment to minimize oxygen consumption.

Minimal handling is essential because these infants are easily agitated. Agitation can increase pulmonary hypertension and right-to-left shunting, leading to additional hypoxia and acidosis. Sedation may be necessary to reduce agitation.

An umbilical artery catheter should be inserted to monitor blood pH and blood gases without agitating the infant.

Continue respiratory care includes oxygen therapy via hood or positive pressure, and it is crucial in maintaining adequate arterial oxygenation. Mechanical ventilation is required by approximately 30% of infants with MAS.[5] Make concerted efforts to minimize the mean airway pressure and to use as short an inspiratory time as possible. Oxygen saturations should be maintained at 90-95%.

Surfactant therapy is commonly used to replace displaced or inactivated surfactant and as a detergent to remove meconium.[24, 25, 26] Although surfactant use does not appear to affect mortality rates, it may reduce the severity of disease, progression to extracorporeal membrane oxygenation (ECMO) utilization,[27] and decrease the length of hospital stay.

Although conventional ventilation is commonly used as initial management, high-frequency oscillation and jet ventilation are alternative effective therapies. Hyperventilation to induce hypocapnia and compensate for metabolic acidosis is no longer a primary therapy for pulmonary hypertension, because hypocarbia often results in decreased cerebral perfusion (partial pressure of carbon dioxide [PaCO2] <30 mm Hg). Prolonged alkalosis has been shown to cause neuronal injury in animals and humans, providing another reason to avoid alkalosis in these patients.[28]

Jet ventilator therapy aimed at minimizing mean airway pressure and tidal volume should be used if pulmonary interstitial emphysema or a pneumothorax is present.

For treatment of persistent pulmonary hypertension of the newborn (PPHN), inhaled nitric oxide is the pulmonary vasodilator of choice.[29] Oxygen is also a potent pulmonary vasculature vasodilator. Phosphodiesterase inhibitors, including sildenafil and milrinone, are being increasingly used as adjunctive therapies for PPHN.

Pay careful attention to systemic blood volume and blood pressure. Volume expansion, transfusion therapy, and systemic vasopressors are critical in maintaining systemic blood pressure greater than pulmonary blood pressure, thereby decreasing the right-to-left shunt through the patent ductus arteriosus. Dopamine is often the first-line vasopressor for neonates with MAS requiring vasopressor support.

Ensure adequate oxygen carrying capacity by maintaining the hemoglobin concentration at a minimum of 13 g/dL.

Corticosteroids are not recommended. Evidence supporting the use of steroids in the management of MAS is insufficient.[30]

Neonates with MAS have historically been routinely treated with empiric broad-spectrum antibiotics, but this practice is being increasingly called into question. No studies have shown prophylactic antibiotics to reduce the incidence of sepsis in neonates born through meconium-stained amniotic fluid; thus, antibiotic use may be reserved for suspected or documented infections.

ECMO is used if all other therapeutic options have been exhausted. Although it is effective in treating MAS, note that ECMO is associated with a high incidence of poor neurologic outcomes.


Evaluation by a pediatric cardiologist is necessary for echocardiographic assessment of the cardiac structures and to assess the severity of pulmonary hypertension and right-to-left shunting.

Evaluation by a pediatric neurologist is helpful in the presence of neonatal encephalopathy or seizure activity.


Although initial stabilization is necessary at community hospitals, infants with MAS frequently require high-frequency ventilation, inhaled nitric oxide (NO), or ECMO. Therefore, infants with a significant aspiration should be transferred to a regional NICU as soon as possible.


Perinatal distress and severe respiratory distress preclude feeding at the early stages of the disease.

Intravenous fluid therapy begins with adequate dextrose infusion to prevent hypoglycemia. Intravenous fluids should be provided at mildly restricted rates (60-70 mL/kg/day).

Progressively add electrolytes, protein, lipids, and vitamins to ensure adequate nutrition and to prevent deficiencies of essential amino acids and essential fatty acids.

Outpatient care

Infants with MAS are at increased risk for adverse developmental outcomes and should be referred for developmental assessment as an outpatient.

Surgical Care

Although primary management of air leak syndromes (pneumothorax or pneumopericardium) is achieved by thoracic drainage tubes inserted by a neonatologist, a pediatric surgical consultation may be necessary in severe cases. Therapy with fibrin glue has been shown to be effective in patients with a persistent air leak.[31]

Medication Summary

In addition to the treatments discussed earlier and the medications listed below, surfactant replacement therapy is frequently used in infants with meconium aspiration syndrome (MAS). Natural lung extract is administered to replace the surfactant that has been stripped. Surfactant also acts as a detergent to break up residual meconium, thereby decreasing the severity of lung disease. Surfactant is used in patients with MAS; however, its efficacy, dosage regimen, and most effective product are not yet established.

Nitric oxide, inhaled

Clinical Context:  Endogenously produced from the action of the enzyme NO synthetase on arginine. Exogenously inhaled NO is used in an attempt to decrease pulmonary vascular resistance and improve lung blood flow. It relaxes vascular smooth muscle by binding to the heme moiety of cytosolic guanylate cyclase, activating guanylate cyclase and increasing intracellular levels of cGMP, which then leads to vasodilation.

Class Summary

Inhaled nitric oxide (NO) has the direct effect of pulmonary vasodilatation without the adverse effect of systemic hypotension. It is approved for use, if concomitant hypoxemic respiratory failure occurs.


Clinical Context:  At lower doses, dopamine stimulates beta1-adrenergic and dopaminergic receptors (renal vasodilation, positive inotropism); at higher doses, it stimulates alpha-adrenergic receptors (renal vasoconstriction).


Clinical Context:  Increases blood pressure primarily via stimulation of beta1-adrenergic receptors. This drug appears to have a more prominent effect on cardiac output than on blood pressure.


Clinical Context:  Used for severe bronchoconstriction, especially in patients with underlying reactive airway disease. Alpha-agonist effects include increased peripheral vascular resistance, reversed peripheral vasodilatation, systemic hypotension, and vascular permeability. Beta2-agonist effects include bronchodilatation, chronotropic cardiac activity, and positive inotropic effects.

Class Summary

These agents are used to prevent right-to-left shunting by raising systemic pressure above pulmonary pressure. Systemic vasoconstrictors include dopamine, dobutamine, and epinephrine. Dopamine is the most commonly used.


Clinical Context:  Used for analgesia and sedation.


Clinical Context:  Potent opioid used for analgesia, sedation, and anesthesia. Has a shorter duration of action than morphine.


Clinical Context:  An anticonvulsant that may be used as a sedative. Suppresses the CNS from the reticular activating system (ie, presynaptic, postsynaptic).

Phenobarbital remains a first-line therapy for neonatal seizures, which may occur in the setting of perinatal depression.

Class Summary

These agents maximize efficiency of mechanical ventilation, minimize oxygen consumption, and treat the discomfort of invasive therapies. However, some controversy exists around the unknown long-term effect(s) of analgesics and sedatives on the developing brain.

Pancuronium or vecuronium

Clinical Context:  Neuromuscular blocker whose effects are reversed by neostigmine and atropine.

Class Summary

These agents are used for skeletal muscle paralysis to maximize ventilation by improving oxygenation and ventilation. They are also used to reduce barotrauma and minimize oxygen consumption.

The use of paralytics remains controversial and should be considered in newborns whose management with sedatives alone is failing.


Gina M Geis, MD, Attending Neonatologist, Associate Director, Neonatal-Perinatal Medicine Fellowship Program, Albany Medical Center; Assistant Professor, Department of Pediatrics, Albany Medical College

Disclosure: Nothing to disclose.


David A Clark, MD, Professor and Martha Lepow Chairman of Pediatrics, Professor of Obstetrics and Gynecology, Albany Medical College; Director, Children's Hospital at Albany Medical Center

Disclosure: Nothing to disclose.

Specialty Editors

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

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

Disclosure: Nothing to disclose.

Additional Contributors

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

Disclosure: Nothing to disclose.


  1. Singh BS, Clark RH, Powers RJ, Spitzer AR. Meconium aspiration syndrome remains a significant problem in the NICU: outcomes and treatment patterns in term neonates admitted for intensive care during a ten-year period. J Perinatol. 2009 Jul. 29 (7):497-503. [View Abstract]
  2. Janssen DJ, Carnielli VP, Cogo P, et al. Surfactant phosphatidylcholine metabolism in neonates with meconium aspiration syndrome. J Pediatr. 2006 Nov. 149 (5):634-9. [View Abstract]
  3. Clark DA, Nieman GF, Thompson JE, Paskanik AM, Rokhar JE, Bredenberg CE. Surfactant displacement by meconium free fatty acids: an alternative explanation for atelectasis in meconium aspiration syndrome. J Pediatr. 1987 May. 110 (5):765-70. [View Abstract]
  4. Terasaka D, Clark DA, Singh BN, Rokahr J. Free fatty acids of human meconium. Biol Neonate. 1986. 50 (1):16-20. [View Abstract]
  5. Wiswell TE, Tuggle JM, Turner BS. Meconium aspiration syndrome: have we made a difference?. Pediatrics. 1990 May. 85 (5):715-21. [View Abstract]
  6. Yoder BA, Kirsch EA, Barth WH, Gordon MC. Changing obstetric practices associated with decreasing incidence of meconium aspiration syndrome. Obstet Gynecol. 2002 May. 99 (5 pt 1):731-9. [View Abstract]
  7. Balchin I, Whittaker JC, Lamont RF, Steer PJ. Maternal and fetal characteristics associated with meconium-stained amniotic fluid. Obstet Gynecol. 2011 Apr. 117 (4):828-35. [View Abstract]
  8. Macfarlane PI, Heaf DP. Pulmonary function in children after neonatal meconium aspiration syndrome. Arch Dis Child. 1988 Apr. 63 (4):368-72. [View Abstract]
  9. Ghidini A, Spong CY. Severe meconium aspiration syndrome is not caused by aspiration of meconium. Am J Obstet Gynecol. 2001 Oct. 185 (4):931-8. [View Abstract]
  10. [Guideline] Wyckoff MH, Aziz K, Escobedo MB, et al. Part 13: Neonatal resuscitation: 2015 American Heart Association guidelines update for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation. 2015 Nov 3. 132 (18 suppl 2):S543-60. [View Abstract]
  11. American College of Obstetricians and Gynecologists. ACOG Committee opinion no. 689 summary: delivery of a newborn with meconium-stained amniotic fluid. Obstet Gynecol. 2017 Mar. 129 (3):593-4. [View Abstract]
  12. Nangia S, Pal MM, Saili A, Gupta U. Effect of intrapartum oropharyngeal (IP-OP) suction on meconium aspiration syndrome (MAS) in developing country: A RCT. Resuscitation. 2015 Dec. 97:83-7. [View Abstract]
  13. Boujenah J, Oliveira J, De La Hosseraye C, Benbara A, Tigaizin A, Bricou A, et al. Should fetal scalp blood sampling be performed in the case of meconium-stained amniotic fluid?. J Matern Fetal Neonatal Med. 2016 Dec. 29 (23):3875-8. [View Abstract]
  14. Liu J, Cao HY, Fu W. Lung ultrasonography to diagnose meconium aspiration syndrome of the newborn. J Int Med Res. 2016 Nov 1. [View Abstract]
  15. American College of Obstetricians and Gynecologists. ACOG Committee opinion no 579: definition of term pregnancy. Obstet Gynecol. 2013 Nov. 122 (5):1139-40. [View Abstract]
  16. American College of Obstetricians and Gynecologists. ACOG Committee opinion no. 561: nonmedically indicated early-term deliveries. Obstet Gynecol. 2013 Apr. 121 (4):911-5. [View Abstract]
  17. ACOG Committee Obstetric Practice. ACOG Committee opinion number 346, October 2006: amnioninfusion does not prevent meconium aspiration syndrome. Obstet Gynecol. 2006 Oct. 108 (4):1053. [View Abstract]
  18. Velaphi S, Vidyasagar D. Intrapartum and postdelivery management of infants born to mothers with meconium-stained amniotic fluid: evidence-based recommendations. Clin Perinatol. 2006 Mar. 33 (1):29-42, v-vi. [View Abstract]
  19. Hofmeyr GJ, Xu H. Amnioinfusion for meconium-stained liquor in labour. Cochrane Database Syst Rev. 2010 Jan 20. CD000014. [View Abstract]
  20. Fraser WD, Hofmeyr J, Lede R, et al, for the Amnioinfusion Trial Group. Amnioinfusion for the prevention of the meconium aspiration syndrome. N Engl J Med. 2005 Sep 1. 353 (9):909-17. [View Abstract]
  21. Committee on Obstetric Practice, American College of Obstetricians and Gynecologists. ACOG Committee opinion no. 379: management of delivery of a newborn with meconium-stained amniotic fluid. Obstet Gynecol. 2007 Sep. 110 (3):739. [View Abstract]
  22. Vain NE, Szyld EG, Prudent LM, Wiswell TE, Aguilar AM, Vivas NI. Oropharyngeal and nasopharyngeal suctioning of meconium-stained neonates before delivery of their shoulders: multicentre, randomised controlled trial. Lancet. 2004 Aug 14-20. 364 (9434):597-602. [View Abstract]
  23. Chettri S, Bhat BV, Adhisivam B. Current concepts in the management of meconium aspiration syndrome. Indian J Pediatr. 2016 Oct. 83 (10):1125-30. [View Abstract]
  24. Wiswell TE, Knight GR, Finer NN, et al. A multicenter, randomized, controlled trial comparing Surfaxin (Lucinactant) lavage with standard care for treatment of meconium aspiration syndrome. Pediatrics. 2002 Jun. 109 (6):1081-7. [View Abstract]
  25. Dargaville PA, Mills JF. Surfactant therapy for meconium aspiration syndrome: current status. Drugs. 2005. 65 (18):2569-91. [View Abstract]
  26. Dargaville PA. Innovation in surfactant therapy I: surfactant lavage and surfactant administration by fluid bolus using minimally invasive techniques. Neonatology. 2012. 101 (4):326-36. [View Abstract]
  27. El Shahed AI, Dargaville PA, Ohlsson A, Soll R. Surfactant for meconium aspiration syndrome in term and late preterm infants. Cochrane Database Syst Rev. 2014 Dec 14. CD002054. [View Abstract]
  28. Collins MP, Lorenz JM, Jetton JR, Paneth N. Hypocapnia and other ventilation-related risk factors for cerebral palsy in low birth weight infants. Pediatr Res. 2001 Dec. 50 (6):712-9. [View Abstract]
  29. Abman SH, Kinsella JP. Inhaled nitric oxide therapy for pulmonary disease in pediatrics. Curr Opin Pediatr. 1998 Jun. 10 (3):236-42. [View Abstract]
  30. Ward M, Sinn J. Steroid therapy for meconium aspiration syndrome in newborn infants. Cochrane Database Syst Rev. 2003. CD003485. [View Abstract]
  31. Sarkar S, Hussain N, Herson V. Fibrin glue for persistent pneumothorax in neonates. J Perinatol. 2003 Jan. 23 (1):82-4. [View Abstract]
  32. El Shahed AI, Dargaville P, Ohlsson A, Soll RF. Surfactant for meconium aspiration syndrome in full term/near term infants. Cochrane Database Syst Rev. 2007 Jul 18. 2:CD002054. [View Abstract]
  33. [Guideline] American Heart Association, American Academy of Pediatrics. 2005 American Heart Association (AHA) guidelines for cardiopulmonary resuscitation (CPR) and emergency cardiovascular care (ECC) of pediatric and neonatal patients: neonatal resuscitation guidelines. Pediatrics. 2006 May. 117 (5):e1029-38. [View Abstract]
  34. Cialone PR, Sherer DM, Ryan RM, Sinkin RA, Abramowicz JS. Amnioinfusion during labor complicated by particulate meconium-stained amniotic fluid decreases neonatal morbidity. Am J Obstet Gynecol. 1994 Mar. 170 (3):842-9. [View Abstract]
  35. Dargaville PA, Copnell B, and the Australian and New Zealand Neonatal Network. The epidemiology of meconium aspiration syndrome: incidence, risk factors, therapies, and outcome. Pediatrics. 2006 May. 117 (5):1712-21. [View Abstract]
  36. Dargaville PA, South M, McDougall PN. Surfactant and surfactant inhibitors in meconium aspiration syndrome. J Pediatr. 2001 Jan. 138 (1):113-5. [View Abstract]
  37. Glantz JC, Woods JR. Significance of amniotic fluid meconium. In: Creasy RK, Resnick R, eds. Maternal-Fetal Medicine. 4th ed. Philadelphia, Pa: WB Saunders; 1999. 393-403.
  38. Kattwinkel J, Niermeyer S, Denson SE, eds. Textbook of Neonatal Resuscitation. 4th ed. Chicago, Ill: American Academy of Pediatrics; 2000.
  39. Kinsella JP. Meconium aspiration syndrome: is surfactant lavage the answer?. Am J Respir Crit Care Med. 2003 Aug 15. 168 (4):413-4. [View Abstract]
  40. Korones SB, Bada-Ellzey HS. Meconium aspiration. Neonatal Decision Making (Clinical Decision Making). St Louis, Mo: Mosby-Year Book; 1993. 128-9.
  41. Kugelman A, Gangitano E, Taschuk R, et al. Extracorporeal membrane oxygenation in infants with meconium aspiration syndrome: a decade of experience with venovenous ECMO. J Pediatr Surg. 2005 Jul. 40 (7):1082-9. [View Abstract]
  42. Lo KW, Rogers M. A controlled trial of amnioinfusion: the prevention of meconium aspiration in labour. Aust N Z J Obstet Gynaecol. 1993 Feb. 33 (1):51-4. [View Abstract]
  43. Ranzini AC, Chan L. Meconium and fetal-neonatal compromise. In: Spitzer AR, ed. Intensive Care of the Fetus and Neonate. St Louis, Mo: Mosby; 1996. 297-303.
  44. Roberton NRC. Aspiration syndromes. In: Greenough A, Robertson NRC, Milner AD, eds. Neonatal Respiratory Disorders. London, UK: Arnold Publication; 1996. 313-33.
  45. Soll RF, Dargaville P. Surfactant for meconium aspiration syndrome in full term infants. Cochrane Database Syst Rev. 2000. CD002054. [View Abstract]
  46. Usta IM, Mercer BM, Aswad NK, Sibai BM. The impact of a policy of amnioinfusion for meconium-stained amniotic fluid. Obstet Gynecol. 1995 Feb. 85 (2):237-41. [View Abstract]
  47. Whitsett JA, Pryhuber GS, Rice WR, Warner BB, Wert SE. Acute respiratory disorders. In: Avery GB, Fletcher MA, MacDonald MG, eds. Neonatology: Pathophysiology and Management of the Newborn. 5th ed. Philadelphia, Pa: Lippincott Williams & Wilkins; 1999. 494-508.
  48. Wiswell TE, Gannon CM, Jacob J, et al. Delivery room management of the apparently vigorous meconium-stained neonate: results of the multicenter, international collaborative trial. Pediatrics. 2000 Jan. 105 (1 pt 1):1-7. [View Abstract]
  49. Yeh TF. Core concepts: meconium aspiration syndrome: pathogenesis and current management. NeoReviews. Sep 2010. 11(9):e503-12.
  50. Young TE, Mangum OB. Neofax: A Manual of Drugs Used in Neonatal Care. 11th ed. Bethesda, M: American Society of Health-System Pharmacists; 1998.
  51. Boet A, Brat R, Aguilera SS, Tissieres P, De Luca D. Surfactant from neonatal to pediatric ICU: bench and bedside evidence. Minerva Anestesiol. 2014 Dec. 80 (12):1345-56. [View Abstract]
  52. Hermansen CL, Mahajan A. Newborn respiratory distress. Am Fam Physician. 2015 Dec 1. 92 (11):994-1002. [View Abstract]
  53. von Bahr V, Hultman J, Eksborg S, et al. Long-term survival and causes of late death in children treated with extracorporeal membrane oxygenation. Pediatr Crit Care Med. 2017 Mar. 18 (3):272-80. [View Abstract]

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.

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.