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

Meconium Aspiration Syndrome

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

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

Differential Diagnoses

Other Problems to Be Considered

Surfactant deficiency
Congenital heart disease with pulmonary hypertension

Workup

Laboratory Studies

The following studies are indicated in suspected meconium aspiration syndrome (MAS):

• Acid-base status
  • Ventilation-perfusion (V/Q) mismatch and perinatal stress are prevalent and assessment of 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).
  • ABG measurement of pH, partial pressure of carbon dioxide (pCO₂), partial pressure of oxygen (pO₂), and continuous measurement of oxygenation by pulse oximetry are necessary for appropriate management.
• Serum electrolytes: Obtain sodium, potassium, and calcium concentrations when the infant with MAS aged 24 hours because the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) and acute renal failure are frequent complications of perinatal stress.
• CBC count
  • In utero or perinatal blood loss, as well as infection, contributes to postnatal stress.
  • Hemoglobin and hematocrit levels must be sufficient to ensure adequate oxygen-carrying capacity.
  • Thrombocytopenia increases the risk for neonatal hemorrhage.
  • Neutropenia or neutrophilia with left shift of the differential may indicate perinatal bacterial infection.
  • Polycythemia may be present secondary to chronic or acute fetal hypoxia. Polycythemia is associated with decreased pulmonary blood flow and may exacerbate the hypoxia associated with meconium aspiration syndrome and PPHN.

Imaging Studies

• Chest radiography is essential for the following:
  • To confirm the diagnosis of meconium aspiration syndrome and determine the extent of intrathoracic pathology
  • To identify areas of atelectasis and air block syndromes
  • To assure appropriate positioning of the endotracheal tube and umbilical catheters
• Later in the course of meconium aspiration syndrome, when the infant is stable, imaging procedures of the brain (eg, MRI, CT scanning, cranial ultrasonography) are indicated, if the infant's neurologic examination findings are abnormal.

Other Tests

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

Treatment

Medical Care

• Prevention of meconium aspiration syndrome (MAS)
  • Prevention is paramount.
  • Obstetricians should monitor fetal status in an attempt to identify fetal stress.
  • When meconium is detected, administering amnioinfusion with warm, sterile saline is theoretically beneficial; it dilutes the meconium in the amniotic fluid, thereby minimizing the severity of the aspiration. However, routine amnioinfusion to prevent meconium aspiration syndrome is not well-supported by current evidence.
  • Current recommendations no longer advise routine intrapartum suctioning for infants born to mothers with meconium staining of the amniotic fluid.¹
  • When aspiration occurs, intubation and immediate suctioning of the airway can remove much of the aspirated meconium.
  • No clinical trials justify suctioning based on the consistency of meconium. Do not perform the following harmful techniques in an attempt to prevent aspiration of meconium-stained amniotic fluid:
    • Squeezing the chest of the baby
    • Inserting a finger into the mouth of the baby
  • The American Academy of Pediatrics Neonatal Resuscitation Program Steering Committee has promulgated guidelines for management of the baby exposed to meconium. The guidelines are under continuous review and are revised as new evidence-based research becomes available. The current guidelines are as follows:²
    • If the baby is not vigorous (defined as minimal or absent respiratory effort, poor muscle tone, or heart rate <100 beats/min): Use direct laryngoscopy, intubate, and 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 (defined as good respiratory effort, crying, good muscle tone, and heart rate >100 beats/min): Do not electively intubate. Clear secretions and meconium from the mouth and nose with a bulb syringe or a large-bore suction catheter.
    • In either case: The remainder of the initial resuscitation steps should ensue and include drying, stimulating, repositioning, and administering oxygen as necessary.
• Continued care in the neonatal ICU (NICU)
  • Maintain an optimal thermal environment to minimize oxygen consumption.
  • Minimal handling is necessary because these infants are easily agitated, which causes right-to-left shunting, leading to hypoxia and acidosis.
  • Sedation is often necessary to decrease agitation.
  • Continue respiratory care. Oxygen therapy via hood or positive pressure is crucial in maintaining adequate arterial oxygenation. If mechanical ventilation is required, 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 now commonly used to replace displaced or inactivated surfactant and as a detergent to remove meconium. Although surfactant use does not appear to affect mortality rates, it appears to reduce the severity of disease and progression to extracorporeal membrane oxygenation (ECMO).³ Studies are ongoing to evaluate the potential role of pulmonary lavage with surfactant.
  • Although conventional ventilation commonly is initially used, 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 may result in decreased cerebral perfusion (PaCO ₂ <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.⁴
  • 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.
  • 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.
  • ECMO is used if all other therapeutic options have been exhausted. Although effective in treating meconium aspiration syndrome, ECMO is associated with a high incidence of poor neurologic outcomes.

Surgical Care

• Although primary management of air block 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.

Consultations

• Evaluation with a pediatric cardiologist is necessary for echocardiographic assessment. This imaging technique ensures normal cardiac structure and assesses the severity of pulmonary hypertension and right-to-left shunting.
• Evaluation with a pediatric neurologist is helpful in the presence of neonatal encephalopathy or seizure activity.

Diet

• Perinatal distress and severe respiratory distress preclude feeding.
• Intravenous fluid therapy begins with adequate dextrose infusion to prevent hypoglycemia.
• Intravenous fluids should be provided at mildly restricted rates (60-70 mL/kg/d).
• Progressively add electrolytes, protein, lipids, and vitamins to ensure adequate nutrition and prevent essential amino acid and essential fatty acid deficiencies.

Medication

In addition to the treatments listed below, surfactant replacement therapy is frequently used. 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 meconium aspiration syndrome (MAS); however, its efficacy, dosage regimen, and most effective product are not yet established.

Respiratory gases

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.

Nitric oxide, inhaled (INOmax)

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.

Dosing

Adult

Pediatric

20 ppm inhaled via respirator initially; not to exceed 80 ppm; most children respond at 20 ppm and can be weaned to lower doses; effect of pulmonary vasodilatation may still be observed at 5 ppm
Must be delivered by a system that measures concentrations of NO in the breathing gas, with a constant concentration throughout the respiratory cycle and that does not cause generation of excessive inhaled nitrogen dioxide

Interactions

Nitric oxide donor compounds (eg, nitroprusside, nitroglycerin) may increase risk of developing methemoglobinemia

Contraindications

Right to left shunting of blood; methemoglobin reductase deficiency

Precautions

Pregnancy

Precautions

Toxic effects include methemoglobinemia and pulmonary inflammation resulting from reactive nitrogen intermediates; caution in thrombocytopenia, anemia, leukopenia, or bleeding disorders; monitor for PaO₂, methemoglobin, and NO₂; abrupt withdrawal causes rebound pulmonary hypertension

Systemic vasoconstrictors

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.

Dopamine (Intropin)

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

Dosing

Adult

Pediatric

5-20 mcg/kg/min IV

Interactions

Incompatible when admixed with acyclovir, amphotericin B, indomethacin, insulin, and sodium bicarbonate
Phenytoin, alpha-adrenergic and beta-adrenergic blockers, general anesthesia, and MAOIs increase and prolong effects of dopamine

Contraindications

Documented hypersensitivity (rare in neonatal population); outflow tract obstructions such as subaortic stenosis

Precautions

Pregnancy

Precautions

Adverse effects include tachycardia and arrhythmia; treat hypovolemia before infusion; promptly treat extravasation with SC phentolamine; administration through a central vein is recommended; do not use a systemic or umbilical artery for infusion; if dosages >20 mcg/kg/min are required, consider a different agent (eg, epinephrine, dobutamine)
Monitor closely urine flow, cardiac output, pulmonary wedge pressure, and blood pressure during the infusion; before infusion, correct hypovolemia as indicated; monitoring central venous pressure or left ventricular filling pressure may be helpful in detecting and treating hypovolemia

Dobutamine (Dobutrex)

Increases blood pressure primarily via stimulation of beta1-adrenergic receptors. Drug appears to have more prominent effect on cardiac output than on blood pressure.

Dosing

Adult

Pediatric

2-25 mcg/kg/min IV continuous infusion; initiate at low dose and titrate while monitoring effects

Interactions

Beta-adrenergic blockers antagonize effects of dobutamine; general anesthetics may increase toxicity

Contraindications

Documented hypersensitivity; idiopathic hypertrophic subaortic stenosis and atrial fibrillation or flutter

Precautions

Pregnancy

Precautions

Following a myocardial infarction use with extreme caution; hypovolemic state should be corrected before using this drug

Epinephrine

Used for severe bronchoconstriction, especially in patients with underlying reactive airways 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.

Dosing

Adult

Pediatric

0.1 mcg/kg/min IV initially; gradually titrate dose; not to exceed 1 mcg/kg/min

Interactions

Increases toxicity of beta-blocking and alpha-blocking agents and that of halogenated inhalational anesthetics

Contraindications

Documented hypersensitivity; cardiac arrhythmias, angle-closure glaucoma; local anesthesia in areas such as fingers or toes because vasoconstriction may produce sloughing of tissue; during labor (may delay second stage of labor)

Precautions

Pregnancy

Precautions

Caution in elderly, prostatic hypertrophy, hypertension, cardiovascular disease, diabetes mellitus, hyperthyroidism, and cerebrovascular insufficiency; rapid IV infusions may cause death from cerebrovascular hemorrhage or cardiac arrhythmias

Sedatives

These agents maximize efficiency of mechanical ventilation, minimize oxygen consumption, and treat the discomfort of invasive therapies.

Morphine

Used for analgesia and sedation.

Dosing

Adult

Pediatric

0.05-0.2 mg/kg/dose IV over 5 min q2-4h prn

Interactions

Any CNS depressant; phenothiazines may antagonize analgesic effects of opiate agonists; tricyclic antidepressants, MAOIs, and other CNS depressants may potentiate adverse effects of morphine; incompatible when admixed with furosemide, pentobarbital, phenobarbital, or phenytoin (forms precipitant)

Contraindications

Documented hypersensitivity (rare in neonates); severe respiratory depression

Precautions

Pregnancy

Precautions

Caution in hypotension, respiratory depression, nausea, emesis, constipation, urinary retention, atrial flutter, and other supraventricular tachycardias; has vagolytic action and may increase ventricular response rate; may cause histamine release

Fentanyl (Sublimaze)

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

Dosing

Adult

Pediatric

1-4 mcg/kg/dose IV slow push
Infusion rate: 1-5 mcg/kg/h IV

Interactions

Barbiturates (eg, pentobarbital, thiopental) or other CNS depressants may have additive effects; phenothiazines may antagonize analgesic effects of opiate agonists; tricyclic antidepressants may potentiate adverse effects of fentanyl when both drugs are used concurrently

Contraindications

Documented hypersensitivity (rare in neonates); hypotension or potentially compromised airway in which establishing rapid airway control is difficult

Precautions

Pregnancy

Precautions

May cause marked respiratory depression and hypotension; exercise caution with patients diagnosed with emesis, constipation, or urinary retention; idiosyncratic reaction (ie, chest wall rigidity syndrome) may require neuromuscular blockade to increase ventilation

Phenobarbital (Luminal)

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

Dosing

Adult

Pediatric

20 mg/kg IV as a single loading dose, administer slowly over 10-15 min. Maintenance dose is 3-5 mg/kg/day

Interactions

Incompatible when admixed with clindamycin, hydralazine, insulin, methadone, midazolam, morphine, ranitidine, and vancomycin; may cause respiratory depression if concurrently on CNS depressants (eg, benzodiazepines); decreases effectiveness of corticosteroids, theophylline, and beta-blockers

Contraindications

Documented hypersensitivity (rare in neonates); severe uncontrolled pain

Precautions

Pregnancy

Precautions

Rarely causes respiratory depression at this dose; do not administer IV administration faster than 50 mg/min; carefully monitor upon administration for hypotension, bradycardia, and arrhythmias because parental product contains 68% propylene glycol; paradoxical excitement and delirium may occur in infants experiencing pain

Pentobarbital (Nembutal)

CNS sedative and hypnotic that acts primarily on the cerebral cortex and reticular formation through decreased neuronal synaptic activity.

Dosing

Adult

Pediatric

2-6 mg/kg IV slow push

Interactions

Incompatible when admixed with cefazolin, cimetidine, clindamycin, fentanyl, hydrocortisone, insulin, midazolam, morphine, pancuronium bromide, phenytoin, ranitidine, or vancomycin; may cause respiratory depression with concurrent use of CNS depressants (eg, benzodiazepines); increased toxicity with CNS depressants and possibly phenobarbital

Contraindications

Documented hypersensitivity (rare in neonates); severe uncontrolled pain

Precautions

Pregnancy

Precautions

Caution with hypovolemic shock, CHF, hepatic impairment, chronic or acute pain, or renal dysfunction; may cause respiratory and cardiovascular depression; carefully monitor upon administration for hypotension, bradycardia, and arrhythmias because parental product contains 68% propylene glycol; paradoxical excitement and delirium may occur in infants experiencing pain

Neuromuscular blocking agents

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.

Pancuronium (Pavulon)

Neuromuscular blocker whose effects are reversed by neostigmine and atropine.

Dosing

Adult

Pediatric

Initial dose: 0.1 mg/kg (0.04-0.15 mg/kg) IV push
Maintenance dose: 0.02-0.1 mg/kg/dose q30min to q3h prn

Interactions

Dose-dependent increased toxicity with magnesium sulfate and furosemide (increase or decrease neuromuscular blockade); caution with coadministration with drugs that increase neuromuscular blockade (eg, aminoglycosides, inhaled anesthetics); avoid drugs that antagonize neuromuscular blockade or prolong muscular weakness (eg, corticosteroids, amphotericin B, phenytoin, verapamil)

Contraindications

Documented hypersensitivity (rare in neonates)

Precautions

Pregnancy

Precautions

May cause hypoxemia (unlikely in a ventilated patient), tachycardia, BP changes, and excessive salivation; exercise caution in patients with preexisting pulmonary, hepatic, or renal disease; prolonged use may result in muscle delayed recovery of paralysis

Follow-up

Further Inpatient Care

• In patients with meconium aspiration syndrome (MAS), thorough cardiac examination and echocardiography are necessary to evaluate for congenital heart disease and persistent pulmonary hypertension of the newborn (PPHN).
• Confirming the degree of pulmonary hypertension, prior to instituting therapy, is extremely important.

Further Outpatient Care

• Infants with meconium aspiration syndrome are at increased risk for adverse developmental outcomes and should be referred for developmental assessment as an outpatient.

Transfer

• Although initial stabilization is necessary at community hospitals, infants with meconium aspiration syndrome frequently require high-frequency ventilation, inhaled nitric oxide (NO), or extracorporeal membrane oxygenation (ECMO). Therefore, in the event of significant aspiration, transferring these infants to a regional neonatal ICU (NICU) as soon as possible is important.

Complications

• Children with meconium aspiration syndrome may develop chronic lung disease as a result of intense pulmonary intervention.
• Infants with meconium aspiration syndrome have a slightly increased incidence of infections in the first year of life because the lungs are still in recovery.

Prognosis

• Most infants with meconium aspiration syndrome have complete recovery of pulmonary function.
• 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.

Miscellaneous

Medicolegal Pitfalls

• Many infants who have experienced meconium aspiration syndrome (MAS) have had prenatal and postnatal periods of hypoxia and acidosis; therefore, these individuals are at increased risk of significant CNS damage.
• Typically, medicolegal action is initiated by parents whose newborn develops long-term sequelae from significant perinatal hypoxia. Although the delivering physician is the primary focus of such a lawsuit, additional liability to other healthcare professionals may ensue from a poorly planned and executed resuscitation.
• Commonly, the providers of the tertiary intensive care are included in these lawsuits, which are usually due to complications of necessary complex and aggressive care. Although other organ systems may be damaged by the initial insult and subsequent therapy, they are rarely the basis of legal action.

Multimedia

Media file 1: Air trapping and hyperexpansion from airway obstruction.

Media file 2: Acute atelectasis.

Media file 3: Pneumomediastinum from gas trapping and air leak.

Media file 4: Left pneumothorax with depressed diaphragm and minimal mediastinal shift because of noncompliant lungs.

Media file 5: Diffuse chemical pneumonitis from constituents of meconium.

References

1. 2005 American Heart Association (AHA) guidelines for cardiopulmonary resuscitation (CPR) and emergency cardiovascular care (ECC) of pediatric and neonatal patients: neonatal resuscitation guidelines. Pediatrics. May 2006;117(5):e1029-38. [Medline].

2. American Academy of Pediatrics, American Heart Association. Neonatal Resuscitation Program. 4^th ed. 2000.

3. El Shahed AI, Dargaville P, Ohlsson A, Soll RF. Surfactant for meconium aspiration syndrome in full term/near term infants. Cochrane Database of Systematic Reviews [serial online]. 2007;2:Accessed 6/30/2008. [Medline]. Available at www.cochrane.org/reviews/en/ab002054.html.

4. 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. Dec 2001;50(6):712-9. [Medline].

5. Abman SH, Kinsella JP. Inhaled nitric oxide therapy for pulmonary disease in pediatrics. Curr Opin Pediatr. Jun 1998;10(3):236-42. [Medline].

6. Cialone PR, Sherer DM, Ryan RM, et al. Amnioinfusion during labor complicated by particulate meconium-stained amniotic fluid decreases neonatal morbidity. Am J Obstet Gynecol. Mar 1994;170(3):842-9. [Medline].

7. Clark DA, Nieman GF, Thompson JE, et al. Surfactant displacement by meconium free fatty acids: an alternative explanation for atelectasis in meconium aspiration syndrome. J Pediatr. May 1987;110(5):765-70. [Medline].

8. Dargaville PA, South M, McDougall PN. Surfactant and surfactant inhibitors in meconium aspiration syndrome. J Pediatr. Jan 2001;138(1):113-5. [Medline].

9. Glantz JC, Woods JR. Significance of amniotic fluid meconium. In: Maternal-Fetal Medicine. 1999:393-403.

10. Kattwinkel J, Niermeyer S, Denson SE. Textbook of Neonatal Resuscitation. 2000.

11. Kinsella JP. Meconium aspiration syndrome: is surfactant lavage the answer?. Am J Respir Crit Care Med. Aug 15 2003;168(4):413-4. [Medline].

12. Korones SB, Bada-Ellzey HS. Meconium aspiration. In: Neonatal Decision Making. 1993:128-9.

13. 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. Jul 2005;40(7):1082-9. [Medline].

14. Lo KW, Rogers M. A controlled trial of amnioinfusion: the prevention of meconium aspiration in labour. Aust N Z J Obstet Gynaecol. Feb 1993;33(1):51-4. [Medline].

15. Ranzini AC, Chan L. Meconium and fetal-neonatal compromise. In: Intensive Care of the Fetus and Neonate. 1996: 297-303.

16. Roberton NRC. Aspiration syndromes. In: Neonatal Respiratory Disorders. 1996:313-33.

17. Soll RF, Dargaville P. Surfactant for meconium aspiration syndrome in full term infants. Cochrane Database Syst Rev. 2000;CD002054. [Medline].

18. Terasaka D, Clark DA, Singh BN, Rokahr J. Free fatty acids of human meconium. Biol Neonate. 1986;50(1):16-20. [Medline].

19. Usta IM, Mercer BM, Aswad NK, Sibai BM. The impact of a policy of amnioinfusion for meconium-stained amniotic fluid. Obstet Gynecol. Feb 1995;85(2):237-41. [Medline].

20. Whitsett JA, Pryhuber GS, Rice WR, Warner BB, Wert SE. Acute respiratory disorders. In: Neonatology: Pathophysiology and Management of the Newborn. 1999:494-508.

21. 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. Jan 2000;105(1 Pt 1):1-7. [Medline]. [Full Text].

22. Yoder BA, Kirsch EA, Barth WH, Gordon MC. Changing obstetric practices associated with decreasing incidence of meconium aspiration syndrome. Obstet Gynecol. May 2002;99(5 Pt 1):731-9. [Medline].

23. Young TE, Mangum OB. Neofax: A Manual of Drugs Used in Neonatal Care. 1998.

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

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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