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Meconium Aspiration Syndrome, Pediatric


Basics


Description


Meconium aspiration syndrome (MAS) is a clinical diagnosis defined as respiratory distress in a newborn delivered through meconium-stained amniotic fluid (MSAF) with no other explanation for clinical symptoms. Severity of MAS can be (a) mild: requiring <0.4 FiO2 for <48 hours; (b) moderate: requiring ≥0.4 FiO2 for >48 hours with no air leak; and (c) severe: requiring assisted ventilation or if associated with persistent pulmonary hypertension of the newborn (PPHN). ‚  

Epidemiology


  • Incidence of MSAF: 10 " “15% of all pregnancies
  • 2 " “9% infants born through MSAF develop MAS (0.1 " “1.8% of all live births).
  • MSAF is rare in premature infants and almost nonexistent before 31 weeks ' gestation.

Risk Factors


  • Postmature gestation
  • Small for gestational age (SGA)
  • Chorioamnionitis
  • Fetal hypoxia (in utero aspiration)
  • Thick consistency of meconium
  • 1 and 5 minutes Apgar <6
  • African American or South Asian ethnicity

Pathophysiology


Meconium aspiration creates ventilation/perfusion (V/Q) mismatch (by the following variable effects on the airways), leading to hypoxemia, hypercarbia, acidosis, and cardiopulmonary failure. ‚  
  • Mechanical obstruction of airways
    • Complete (atelectasis)
    • Partial (hyperinflation and air leaks due to ball and valve phenomenon)
  • Meconium-associated pulmonary inflammation
  • Inactivation of existing surfactant
  • Decreased production of surfactant
  • Meconium-induced lung apoptosis
  • Coexisting pulmonary hypertension

Diagnosis


History


  • Term or postterm gestation
  • Abnormal fetal tracing
  • Evidence of MSAF
  • Low Apgar score at 1 and 5 minutes
  • Respiratory distress at or shortly after birth

Physical Exam


  • Meconium staining (vocal cords, skin, nails, and umbilical cord)
  • Respiratory distress (tachypnea, retractions, grunting, cyanosis, and flaring)
  • Barrel-shaped chest (air trapping or air leak)
  • Rales and rhonchi
  • Systolic murmur (tricuspid regurgitation) due to pulmonary hypertension
  • Preductal oxygen saturation ≥10% higher than postductal value
  • Signs of encephalopathy, particularly if associated with perinatal asphyxia
  • Signs of hypoxemia (cyanosis, poor perfusion, hypotension)
  • Rarely, green color urine (meconium metabolites may appear in urine)

Diagnostic Tests & Interpretation


Lab
  • CBC with differential count
    • Leukocytosis with left shift can help to identify secondary infection or congenital pneumonia; however, a left shift is also common with MAS.
  • Peripheral blood culture
    • May help to identify secondary infection, sepsis, or congenital pneumonia
  • Arterial blood gas (ABG)
    • Can identify respiratory failure or hypoxemia and guide the need for respiratory support
    • The test is also used to calculate an oxygenation index if the infant is on mechanical ventilation.

Imaging
  • Initial chest radiograph
    • Radiographic appearance lags behind clinical symptoms.
    • Frequently, there is no significant association between the extent of radiographic abnormalities and the severity of disease.
    • Initial radiograph can be normal or may have some streaky, linear densities.
  • Follow-up chest radiograph
    • As the disease progresses, there can be diffuse patchy densities, hyperinflation, flattening of the diaphragm, pleural effusion, alternating areas of microatelectasis, hyperinflation, and consolidation.
    • Significant air leaks can be noted in 10 " “30% of infants with MAS.

Diagnostic Procedures/Other
  • Pre- and postductal Spo2 gradient
    • >10% may be associated with PPHN.
  • Oxygenation index (OI)
    • After optimizing mechanical ventilation, OI >40 on two serial ABGs performed 4 hours apart could be an indication for extracorporeal membrane oxygenation (ECMO).
    • OI = (FiO2 ƒ — mean airway pressure ƒ — 100) / Pao2
  • Echocardiography
    • To rule out congenital heart disease and to evaluate for PPHN

Differential Diagnosis


  • Congenital pneumonia
  • Transient tachypnea of newborn (TTN)
  • PPHN

Treatment


Medication


  • IV antibiotics
    • In the early stage of the disease, it is difficult to differentiate between MAS and congenital pneumonia. Many clinicians treat empirically while awaiting the results of cultures.
    • Prophylactic antibiotic treatment does not prevent secondary infection in MAS.
  • Surfactant bolus treatment
    • Although not specifically FDA approved for MAS, exogenous surfactant replacement may decrease the need for ECMO.
  • Steroid therapy
    • Not recommended for routine treatment of MAS
    • Systemic use of steroids has reportedly been associated with shorter duration of mechanical ventilation and with the improved pulmonary function.
  • Inhalational nitric oxide (iNO)
    • iNO is used to treat MAS that is associated with PPHN.

Additional Therapies


  • Oxygen therapy
    • The goal is to keep peripheral Spo2 between 92% and 98% or Pao2 between 60 and 80 torr (8 " “10.7 kPa).
    • Oxygen can be provided via oxyhood or nasal cannula. If >0.6 FiO2 is required to achieve the above-mentioned goal, consider additional respiratory support.
  • Continuous positive airway pressure (CPAP)
    • Due to the possible complications (i.e., air trapping, hyperinflation, and air leaks), many clinicians prefer to avoid CPAP. However, CPAP can be cautiously used if air trapping or air leak is not a major issue.
  • Conventional ventilation
    • Used to achieve optimal ventilation and oxygenation. No specific modes have been proven superior.
    • Most clinicians use low positive end-expiratory pressure (PEEP) and prolonged expiratory times in order to prevent hyperinflation, air trapping, and air leaks.
  • High-frequency ventilation (oscillator or jet):
    • High-frequency ventilation (HFV) is used as a rescue treatment. No clinical trial has demonstrated clear benefits of HFV over conventional modes in the initial management of MAS. However, in the presence of air trapping or air leaks, jet ventilation may help. Anecdotally, meconium clearance may be increased with high-frequency jet ventilation (HFJV).
  • ECMO
    • Indicated for severe respiratory failure manifested by an OI >40 on 2 serial ABGs performed 4 hours apart while on optimal mechanical ventilation
    • Veno-arterial or veno-venous ECMO can be considered in the absence of any vital organ failure, significant congenital anomaly, genetic syndrome, or intraventricular hemorrhage.
  • Broncho-alveolar lavage (BAL)
    • BAL with diluted surfactant is an experimental therapy that has been found to produce rapid and sustained improvement in oxygenation, a shorter ventilation course, and decreased need for ECMO.
    • Use of surfactant/dextran mixture for BAL is reportedly helpful in rapid clearance of meconium. However, none of these therapies have been approved for MAS.

General Measures


  • ICU care
    • For Spo2 and continuous cardiopulmonary monitoring, to provide optimal thermal environment, and to ensure minimal handling
  • Chest PT is generally not recommended.
  • IV fluids
    • Required for maintenance of hydration and prevention of hypoglycemia
    • IV fluid bolus may be required for hypovolemia or hypoperfusion.
  • Inotropic therapy
    • May be required to support the systemic perfusion especially if cardiac output is low due to left ventricular (LV) dysfunction (hypoxia or acidosis), severe PPHN, or decreased venous return
  • Sedation
    • May be helpful to decrease agitation, optimize ventilation, and minimize right-to-left shunting. However, routine use of muscle relaxants is controversial, as they may increase the risk for atelectasis and V/Q mismatch.
    • Paralysis is generally not recommended.
  • Feeding
    • During acute phase of severe illness, enteral feedings are discouraged to protect the underperfused gut from ischemic injury.
  • Sodium bicarbonate therapy: generally not recommended

Preventive Measures
  • Prevention of fetal hypoxia
    • Optimal obstetric care is the key for prevention of MAS. The decreased incidence of MAS in the last decade has been attributed to the reduction in postterm delivery and aggressive management of abnormal fetal heart tracings.
  • Amnioinfusion: not recommended
  • Intratracheal suctioning: recommended only for nonvigorous infants born through MSAF
  • Oropharyngeal suctioning: not recommended
  • Gastric suctioning: No clinical study had assessed this approach.
  • Contraindicated procedures:
    • Attempts to prevent deep inspiration prior to oropharyngeal or endotracheal suctioning by mechanical means (e.g., cricoid pressure, manual blockage of the airway, and thoracic compression)

Ongoing Care


Follow-up Recommendations


  • Long-term consequences include increased bronchial reactivity and wheezing among the survivors of MAS.
  • Infants with severe MAS are at risk for delayed development; they should be followed up in the developmental pediatrics clinic for 2 " “5 years.

Prognosis


  • Severity of lung injury is related to the consistency of meconium (thick meconium is high risk for severe disease) and to the degree of hypoxia and acidosis present at birth.
  • Generally, 1/3 of infants with MAS need mechanical ventilation, 15 " “20% develop PPHN, and 10 " “30% can have air leaks.
  • In spite of appropriate management and clinical care, up to 10% of infants with severe MAS may die.

Complications


  • Birth depression
    • Occurs in 20 " “33% of infants born through MSAF
    • These infants can have neurologic manifestations of hypoxic ischemic encephalopathy (HIE) and needs appropriate treatment.
  • SIADH
    • More likely to occur among infants with a history of perinatal asphyxia or air leaks
  • PPHN
    • Occurs in 15 " “20% of infants with MAS
    • PPHN in these infants may be caused by (a) pulmonary vasoconstriction secondary to pulmonary inflammation, hypoxia, hypercarbia, and acidosis and (b) pulmonary vascular remodeling as a result of chronic intrauterine hypoxia.
  • Secondary lung infection
    • Meconium provides an excellent growth medium for microorganisms. Meconium may also inhibit polymorphonuclear cells.
  • Reactive airway disease
    • Up to 50% of infants who survive severe MAS are at risk to develop reactive airway disease in the first 6 months of life.

Additional Reading


  • K ƒ € ƒ €p ƒ € ‚  PO. Meconium aspiration syndrome (MAS) " ”where do we go? Research perspectives. Early Hum Dev.  2009;85(10):627 " “629. ‚  [View Abstract]
  • Mokra ‚  D, Calkovska ‚  A. How to overcome surfactant dysfunction in meconium aspiration syndrome? Respir Physiol Neurobiol.  2013;187(1):58 " “63. ‚  [View Abstract]
  • Swarnam ‚  K, Soraisham ‚  AS, Sivanandan ‚  S. Advances in the management of meconium aspiration syndrome. Int J Pediatr.  2012;2012:359571. ‚  [View Abstract]

Codes


ICD09


  • 770.12 Meconium aspiration with respiratory symptoms
  • 770.11 Meconium aspiration without respiratory symptoms

ICD10


  • P24.01 Meconium aspiration with respiratory symptoms
  • P24.00 Meconium aspiration without respiratory symptoms

SNOMED


  • 206292002 Meconium aspiration syndrome (disorder)
  • 278927005 Neonatal aspiration of meconium (disorder)

FAQ


  • Q: What is the composition of meconium?
  • A: Meconium is a variable mixture of intestinal epithelial debris, gastrointestinal secretions, bile, mucus, pancreatic juice, blood, swallowed vernix caseosa, and lanugo.
  • Q: What are the recommendations for repeated intratracheal suctioning?
  • A: If no meconium is retrieved initially, repetitive suctioning is not required. However, if meconium is retrieved and in the absence of bradycardia, intratracheal suctioning can be repeated.
  • Q: How to manage vigorous infants born through MSAF?
  • A: Asymptomatic infants should be managed like normal newborns. It is important to clinically observe these infants for any signs of respiratory distress for at least 24 hours prior to discharge.
  • Q: What are current therapies being considered for the treatment of MAS?
  • A: Meconium-resistant surfactant enriched with high proteins, phospholipids, and polymers (e.g., dextran) is waiting for clinical trials. Research has shown potential benefits of the following drugs in the treatment of MAS; however, none of these treatments are approved for clinical use at this point: antioxidants: superoxide dismutase or N-acetylcysteine and angiotensin-converting enzyme (ACE) inhibitors (by suppressing apoptosis).
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