MECONIUM ASPIRATION SYNDROME

Meconium Aspiration Syndrome :
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, such as 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, making up 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:
Meconium may be passed in utero secondary to a hypoxic stress; alternatively, evidence exists suggesting that meconium passage results from neural stimulation of a mature GI tract. 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.

Although the etiology is not well understood, effects of meconium 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 3 major pulmonary effects, which are airway obstruction, surfactant dysfunction, and chemical pneumonitis.

Airway obstruction
Complete obstruction of the airways results in atelectasis. Partial obstruction causes air trapping and hyperdistention of the alveoli. 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 diffuse pneumonia that may begin within a few hours of aspiration.

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

Frequency:
• In the US: In the industrialized world, meconium in the amniotic fluid can be detected in 8-20% of all births after 34 weeks' gestation. Of those newborns with meconium-stained amniotic fluid, 1-9% may develop MAS.
• Internationally: In developing countries with less availability of prenatal care and where home births are common, incidence of MAS is thought to be higher and is associated with a greater mortality rate.

Mortality/Morbidity:
• The mortality rate for MAS 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. Race: No racial predilection exists. Sex: MAS affects both sexes equally. Age: MAS is exclusively a disease of newborns.

History:
• Severe respiratory distress may be present. Symptoms include the following:
o Cyanosis
o End-expiratory grunting
o Alar flaring
o Intercostal retractions
o Tachypnea
o Barrel chest in the presence of air trapping

• Green urine may be observed in newborns with meconium aspiration syndrome (MAS) less than 24 hours after birth. Meconium pigments can be absorbed by the lung and excreted in urine.

Physical:
• Presence of meconium in amniotic fluid is essential to the initiation of the pathogenesis.

Causes:
• Factors that promote the passage of meconium in utero include the following:
o Placental insufficiency
o Maternal hypertension
o Preeclampsia
o Oligohydramnios
o Maternal drug abuse, especially of tobacco and cocaine

Lab Studies:
• Acid-base status
o Because V-Q mismatch and perinatal stress are prevalent, assessment of acid-base status is crucial.
o Metabolic acidosis from perinatal stress is complicated by respiratory acidosis from parenchymal disease and PPHN.
o Arterial blood gases that measure 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 is aged 24 hours because the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) and acute renal failure are frequent complications of perinatal stress.

• CBC
o In utero or perinatal blood loss may contribute to perinatal stress, and infection also may be the source of the stress.
o Hemoglobin and hematocrit levels must be sufficient to ensure adequate oxygen-carrying capacity.
o Thrombocytopenia increases the risk for neonatal hemorrhage.
o Neutropenia or neutrophilia with left shift of the differential may indicate perinatal bacterial infection.

Imaging Studies:
• A chest radiograph is essential to do the following:
o Determine the extent of intrathoracic pathology
o Identify areas of atelectasis and air block syndromes
o Assure appropriate positioning of an endotracheal tube and umbilical arterial catheter

• Later in the course of MAS when the infant is stable, imaging procedures of the brain, such as MRI, CT scan, or cranial ultrasound, are indicated if findings of the infant's neurologic examination are abnormal.

Other Tests: An echocardiogram ensures normal cardiac structure and assesses the severity of pulmonary hypertension and right-to-left shunting.

Further Inpatient Care:
• Thorough cardiac examination is necessary to eliminate the possibility of cyanotic heart disease.
• Confirming the degree of pulmonary hypertension, prior to instituting therapy, is extremely important.

Transfer:
• Although stabilization is possible at community hospitals, infants with MAS frequently require high-frequency ventilation, inhaled nitric oxide, or ECMO. Therefore, in the event of significant aspiration, transfer these infants in community hospitals to regional NICUs.

Complications:
• A few infants with MAS have increased incidence of infections in the first year of life because the lungs are still recovering.
• Children with MAS may develop chronic lung disease as a result of intense pulmonary intervention.

Prognosis:
• Nearly all infants with MAS have complete recovery of pulmonary function.
• Events initiating the meconium passage may cause the infant to have long-term neurologic deficits, including CNS damage, seizures, mental retardation, and cerebral palsy.

Medical/Legal Pitfalls:
• Many infants who have experienced 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 rarely are the basis of legal action.