Managemen of Meconium Aspiration Syndrome

Meconium aspiration syndrome is a common problem will be encountered in the delivery room. Meconium aspiration primarily affects term and postmature infants. The meconium-stained amniotic fluid may be aspirated by the fetus when fetal gasping or deep breathing movements are stimulated by hypoxia and vagal reflex. Meconium aspiration syndrome must be considered in any infant born through meconium-stained amniotic fluid who develops symptoms of respiratory distress. There is no specific treatment of meconium aspiration syndrome. The key to manage meconium aspiration lies in prevention during the prenatal period. The oropharynx and nasopharynx of all meconium exposed neonates should be cleared before delivery of the shoulders. Immediate tracheal intubation and suctioning is recommended only if the infant is depressed. Positive pressure ventilation should be avoided, if possible, until tracheal suctioning is accomplished. Conventional therapy for meconium aspiration syndrome is aimed at increasing oxygenation while minimizing the barotrauma that may lead to air leak syndromes. The amount of ventilatory support depends on the amount of respiratory distress. The optimal ventilatory modes in meconium aspiration syndrome are not known. Optimal dose, method, and timing of instillation of surfactant in meconium aspiration syndrome remain to be determined. The optimal time for initiation of inhaled nitric oxide remain to be determined. Inhaled nitric oxide should be instituted only at centers with extracorporeal membrane oxygenation availability. These patients may have suffered perinatal asphyxia, surveillance for any end-organ damage is essential. Complications are common and are associated with significant mortality.

INTRODUCTION

Meconium aspiration syndrome (MAS) is a common problem will be encountered in the delivery room (1,2). Meconium aspiration primarily affects term and postmature infants (1-8). Intrauterine stress may cause in utero passage of meconium into the amniotic fluid. The meconium-stained amniotic fluid may be aspirated by the fetus when fetal gasping or deep breathing movements are stimulated by hypoxia and vagal stimulation (3-8). MAS must be considered in any infant born through meconium-stained amniotic fluid who develops symtoms of respiratory distress (2-4). Clinical diagnosis of MAS defined by found meconium below the vocal cords (6). The presence of meconium in the trachea may cause airway obstruction as well as an inflammatory response, resulting in severe respiratory distress. The presence of meconium in amniotic fluid can be a warning sign of fetal distress (3,4). The meconium present in amniotic fluid varies in appearance and viscosity, ranging from thin, green-stained fluid to a thick, “pea soup” consistency (3). Mothers with meconiumstained amniotic fluid should be carefully monitored during labor (1-8). The incidence of meconium-stained amniotic fluid varies from 8 to 20% of all deliveries (3). Suctioning of the mouth and oropharynx before delivery of the shoulders and direct suctioning of meconium from the trachea in depressed infants favorably affect the clinical course (1,2,9). Adequate airway management, however, cannot prevent meconium aspiration altogether, since meconium may be aspirated by the fetus prior to delivery (1,3,4). Of infants delivered through meconium-stained amniotic fluid, 5 to 33% develop respiratory symptoms and radiographic changes of MAS (4). Up to 50% of these infants require mechanical ventilation. Approximately one-third develop persistent pulmonary hypertension (PPHN), which contributes to the mortality associated with this syndrome. Approximately 5% of survivors require supplemental oxygen at 1 month of age, and a substantial proportion may have abnormal pulmonary function, including increased functional residual capacity, airway reactivity, and higher incidence of pneumonia (3).

PATHOPHYSIOLOGY

In utero control of passage of meconium is dependent on hormonal and parasympathetic neural maturation (6). Meconium-stained fluid is rarely seen prior to 37 weeks’ gestation but may occur in more than 30% of pregnancies that continue past 42 weeks’ gestation (3-8). Meconium first appears in the fetal ileum between 10 and 16 weeks of gestation as a viscous, green liquid composed of gastrointestinal secretions, cellular debris, bile and pancreatic juice, mucus, blood, lanugo, vernix and approximately 72% to 80% water. The dry weight composition consists primarily of mucopolysaccharides, with less protein and lipid (6). The exact mechanisms for in utero passage of meconium remain unclear, but fetal distress and vagal stimulation are two probable factors (3,4). Vagal stimulation produced by cord or head compression (1,6). The increased incidence meconium-stained amniotic fluid advancing gestational age probably reflects the maturation peristalsis in the fetal intestine. Motilin, an intestinal peptide that stimulates contraction of the intestinal muscle is in lower concentrations in the intestine of premature versus postterm infants. Intestinal parasympathetic innervation and myelination also increase throughout gestation and may play a role in the increased incidence of passage of meconium in late gestation. Infants born through meconium-stained amniotic fluid frequently have had antepartum or intrapartum asphyxia (6). The timing of the insult maybe suggested by the color of the fluid; yellow meconium is usually old, whereas green meconium suggests a more recent insult (3). After intrauterine passage of meconium, deep irregular respiration or gasping, either in utero or during labor and delivery can cause aspiration of the meconium-stained amniotic fluid. Before delivery, the progression of the aspirated meconium is, as a rule, impeded by the presence of the viscous liquid that normally fills the fetal lung and airways. Therefore, the distal progression occurs mostly after birth in conjunction with the reabsorption of lung fluid. Early consequences of meconium aspiration include airway obstruction, decreased lung compliance, and increased expiratory large airway resistance (3-6). Thick, meconium-stained amniotic fluid can result in acute upper airway obstruction. As the aspirated meconium progresses distally, total or partial airway obstruction may occure. In areas of total obstruction atelectasis develops, but in areas of partial obstruction a ball-valve phenomenon occurs, resulting in air trapping and alveolar hyperexpansion, Air trapping increases the risk of air leak. With distal progression of meconium, chemical pneumonitis develops, with resulting bronchiolar edema and narrowing of the small airways (3,5). Meconium at the alveolar level may inactivate existing surfactant. Uneven ventilation resulting from areas of partial obstruction, atelectasis, and superimposed pneumonitis causes carbon dioxide retention and hypoxemia. Pulmonary vascular resistance increases as a direct result of alveolar hypoxia, acidosis, and hyperinflation of the lungs. The increase in pulmonary vascular resistance may lead to atrial and ductal right-to-left shunting and further hypoxemia (3-8).

CLINICAL MANIFESTATION

The presentation of an infant who has aspirated meconium-stained amniotic fluid is variable (1-8). Symptoms depend on the severity of the hypoxic insult and the amount and viscosity of the meconium aspirated. Infants with meconium aspiration syndrome often exhibit signs of postmaturity: They heavily stained on the nails, hair, and umbilical cord with meconium. Infants with severe MAS often have an increased anteriorposterior dimension of the thorax, a “barrel” chest. If there has been significant perinatal asphyxia, they may have respiratory depression with poor respiratory effort, heart rate less than 100 beats per minute and decreased muscle tone (1-8). The infant who has aspirated meconium into the distal airways but does not have total airway obstruction manifests signs of respiratory distress (ie., tachypnea, nasal flaring, intercostal retractions, increased anterior posterior diameter of the chest, and cyanosis). Some infants may have a delayed presentation, with only mild initial respiratory distress, which becomes more severe hours after delivery as atelectasis and chemical pneumonitis develop. If air trapping develops, there may be a noticeable increase in anteriorposterior diameter of the chest. Auscultation often reveals, decreased air exchange, rales, rhonchi, or wheezing (3-6).

MANAGEMENT

There is no specific treatment of MAS (6). The key to manage meconium aspiration lies in prevention during the prenatal period (4).

Prenatal Management.

1. Identification of high-risk pregnancies (3,4,8). The approach to prevention begins with recognition of predisposing maternal factors that may cause uteroplacental insufficiency and subsequent fetal hypoxia during labor Mothers at risk for uteroplacental insufficiency include those with preeclampsia-eclampsia, increased blood pressure, chronic respiratory, cardiovascular disease, post-term pregnancy, heavy smokers, maternal diabetes mellitus, intrauterine growth retardation, abnormal fetal heart rate pattern, and oligohydramnios (3,4).

2. Monitoring. During labor, careful observation and fetal monitoring should be performed. Any signs of fetal distress (eg., appearance of meconium-stained fluid with membrane rupture, loss of beat-to-beat variability, fetal tachycardia, or deceleration patterns) warrant assessment of fetal well-being by scrutiny of fetal heart pattern (1-8). If the assessment identifies a compromised fetus, corrective measures should be undertaken or the infant should be delivered in a timely manner (3, 4) 3. Amnioinfusion. During this procedure a sterile isotonic solution (either normal saline or ringers lactate) is infused into the amniotic cavity through a catheter. By adding volume into the cavity, not only is the meconium diluted, but the cord compression may be decreased, relieving hypoxia and therefore decreasing fetal gasping (2). There is evidence that amnioinfusion reduces the consistency of meconium (2,10). Routine amnioinfusion in the presence meconium stained amniotic fluid to prevent MAS is not recommended (1). There are several reports of relatively common adverse events associated with amnioinfusion, including uterine hypertonus, fetal bradycardia, and fetal tachycardia that may be mitigated by adjustment of infusion. Although the procedure seems to be relatively safe, rare complications reported included uterine rupture, cord prolapse, abruption, pulmonary edema, and amniotic fluid embolus (1,2,11). Systematic reviews concluded that amnioinfusion was effective in reducing the incidence of MAS, particularly when performed in settings where facilities for perinatal surveillance are limited (1).

Delivery Room Management.

American Academy of Pediatrics and American College of Obstetrics and Gynecology guidelines recommend that when meconium of any consistency is present intrapartum, the obstetrician should clear the infant’s nose and oropharynx before delivery of the shoulders (9). This can be done with either a bulb syringe or a De Lee suction catheter, which are equally effective (1,2,11,12). Although some studies suggested that intrapartum suctioning might be effective for decreasing the risk of aspiration syndrome, subsequent evidence from a large multicenter randomized trial does not show such an effect. There is evidence to support discontinuation of the recommendation of routinely performing intrapartum oropharyngeal and nasopharyngeal suctioning for infants born to mothers with meconium staining of amniotic fluid (1). During assessment at a delivery complicated by meconium, the pediatrician should determine whether the infant is vigorous, demonstrated by heart rate >100 beats per minute, spontaneous respirations, and good tone (spontaneous movement or some degree of flexion) (9). If the infant appears vigorous, routine care should be provided (1). In questionable cases, it is safer to intubate and suction, as MAS can occur in infants delivered through thinly stained amniotic fluid (3,12). If respiratory distress develops or the infant becomes depressed, the trachea should be intubated under direct laryngoscopy and intratracheal suctioning performed by using a meconium aspirator before inspiratory efforts have been initiated (1,2,9,11).

The tube is attached to wall suction at a negative pressure of 80 to 100 mm Hg (3,4,6). Continuous suction is applied as the tube is being withdrawn; the procedure is repeated until the trachea is cleared or resuscitation needs to be initiated (9). Visualization of the cords without suctioning is not adequate because significant meconium may be present below the cords (1,2). Although complication rates of this procedure are low, the infant’s general condition must not be ignored in persistent attempts to clear the trachea. This procedure should be accomplished rapidly, and ventilation with oxygen should be initiated before significant bradycardia occurs (1,9). Because a few inspiratory efforts by the infant will move the meconium from the trachea to the smaller airways, exhaustive attempts to remove it are unwise. Positive pressure ventilation should be avoided, if possible, until tracheal suctioning is accomplished (9). Emptying of any gastric contents should also be postponed until the infant has stabilized (1, 3). Routine gastric lavage prior to feeding,however,did not decrease the incidence of MAS in babies born through meconium-stained amniotic fluid (5).

Management of the newborn with meconium aspiration.

Respiratory Management a. Pulmonary toilet.

Chest physiotherapy and suctioning of particulate meconium useful if there is airway obstruction. In the severity affected baby who is intubated and paralysed, chest percussion and endo tracheal suctioning may be helpful, but should be continued anly as long as this prosedur significant amount of secrete material (1,2,11). Discontinue this prosedur if the infant become irritable, restless and hypoxemia. Chest physiotherapy may be not recommended in labile infants with significant persistent pulmonary hypertension (5). b. Arterial blood gas levels.

On admission to the NICU, arterial blood gas measurements to assess ventilatory compromise and supplemental oxygen requirements should be obtained. c. Oxygen monitoring.

A pulse oximeter will provide important information regarding the severity of the child’s respiratory status and will also assist in preventing hypoxemia. Comparing oxygen saturation values from a probe placed on the right arm to those from a probe placed on the lower extremities may help to identify those infants with right-to-left ductal shunting secondary to pulmonary hypertension (3,4).

d. Chest x-ray films should be obtained after delivery if the infant is in distress.

Radiologic studies. A chest radiograph typically reveals hyperinflation of the lung fields and flattened diaphragms. There are coarse, irregular patchy infiltrates (3,4). Pneumothorax or pneumomediastinum may be present. Because of the diverse mechanisms that cause disease, various radiographic findings may be present (1,6). However, the radiograph often poorly correlates with the clinical presentation (1,5,6).

e. Antibiotic coverage.

Meconium inhibits the normally bacteriostatic quality of amniotic fluid. Because it is difficult to differentiate meconium aspiration from pneumonia radiographically, infants with infiltrates on chest x-ray film should be started on broad-spectrum antibiotics (eg., ampicillin and gentamicin) after appropriate cultures have been obtained (3-8). f. Supplemental oxygen.

A major goal is to prevent episodes of alveolar hypoxia leading to hypoxic pulmonary vasoconstriction and the development of persistent pulmonary hypertension of the newborn. For that purpose, supplemental oxygen is provided “generously,” such that arterial oxygen tension is maintained at least in the range of 80—90 mm Hg (3). Some clinicians may elect to maintain PaO2 at a higher level because the risk of retinopathy should be negligible among full- term infants (4). The same goal of preventing alveolar hypoxia requires cautious weaning from oxygen therapy. Many of the patients are very labile, and weaning from oxygen should be made slowly, sometimes at a pace of 1% at a time (3). The prevention of alveolar hypoxia includes a high index of suspicion for the diagnosis of air leak as well as efforts to minimize handling of the child (3-8). g. Mechanical ventilation.

Patients with severe disease who are in impending respiratory failure with hypercapnia and persistent hypoxemia require mechanical ventilation (3,4,8). The approach to ventilation must be directed at preventing hypoxemia and providing adequate ventilation at the lowest mean airway pressure possible to reduce the risk of catastrophic air leak (6). Those infants who do not respond to conventional ventilation should be given a trial high frequency ventilation (HFV) . Rate settings of ventilation must be tailored to the individual patient. These patients typically require higher inspiratory pressures and faster rates than those with hyaline membrane disease (HMD). Relatively short inspiratory time allows for adequate expiration in patients with preexisting air trapping. Both high frequency jet ventilation (HFJV) and high frequency oscillatory ventilation (HFOV) have been shown to be efficacious in infants in whom adequate ventilation cannot be maintained on conventional ventilation without using excessive ventilatory pressures (3,4). No prospective, randomized, controlled trials have compared conventional ventilation versus high-frequency ventilation in MAS (11). The optimal ventilatory modes in MAS are not known (2).h. Surfactant.

Endogenous surfactant activity may he inhibited by meconium (3,4,6). Surfactant treatment of MAS may improve oxygenation and reduce pulmonary complications and the need for ECMO (3,4). Infants with severe meconium aspiration syndrome who require mechanical ventilation and have radiologic evidence of parenchymal lung disease are likely to benefit from early surfactant therapy (4). Because of the frequently associated pulmonary hypertension, close monitoring at the time of the surfactant therapy will be required to prevent the consequences of transient airway obstruction that may develop during the tracheal instillation of surfactant (3,4,6). Lavage with surfactant may be a particularly effective method of improving gas exchange by washing out meconium and the products of inflammation, as well as diluting the meconium (2,5,11). This is an exciting area of investigation, however, and additional trials are warranted (11). Optimal dose, method, and timing of instillation of surfactant in MAS remain to be determined (1).i. Extracorporeal membrane oxygenation (ECMO).

Patients who cannot be ventilated by the just-mentioned therapies may be candidates for ECMO. Since the introduction of treatment of persistent pulmonary hypertension with inhaled nitric oxide, the need for ECMO has decreased (1,3,5,6).

Cardiovascular Management

Persistent pulmonary hypertension is frequently associated with meconium aspiration (1-8). The development of pulmonary hypertension may be a result of hypoxic pulmonary vasoconstriction, abnormal muscularization of the pulmonary microcirculation, or both (3,6). To minimize the risk of persistent pulmonary hypertension, aggressive resuscitation and stabilization are essential. Consider nitric oxide therapy if pulmonary hypertension is associated with meconium aspiration. In such event the use of high-frequency oscillation may further optimize the response to nitric oxide (6). Inhaled nitric oxide causes selective pulmonary vasodilation by acting directly on the vascular smooth muscle with minimal effects on other body systems (11). The lack of efficacy of early iNO is accompanied by increased expenses, as has been shown in several analyses of the cost-effective-ness of iNO. This multicenter trial answers the question of the optimal time for initiation of iNO (2). Inhaled nitric oxide should be instituted only at centers with ECMO availability because ECMO may need to be started emergently should all other treatment modalities fail. The use of oral sildenafil may be effective in Persistent Pulmonary Hyperternsion of the Newborn (13).

General Management

The thermal environment of all infants at risk for MAS should be watched closely. Tactile stimulation should be minimized. The use of sedation and muscle relaxation may be warranted in those who require mechanical ventilation. Blood glucose and calcium levels should be assessed and corrected if necessary. In addition, severely depressed infants may have significant metabolic acidosis that should be corrected. These infants may also require specific therapy for hypotension and poor cardiac output, including cardiotonic medications such as dopamine. Fluids should be restricted as much as possible to prevent cerebral and pulmonary edema (3). Because these patients may have suffered perinatal asphyxia, surveillance for any end-organ damage is essential (4).

PROGNOSIS

Complications are common and are associated with significant mortality (1,3-8). The clinician must maintain a high index of suspicion for air leak. For any unexplained deterioration of clinical status, the possibility of a pneumothorax should be considered and appropriate evaluation undertaken (3,6). With the development of atelectasis, air trapping, and decreased lung compliance, high mean airway pressures may be required in a patient who is at risk for air leak (3,4). New modalities of therapy such as administration of exogenous surfactant, high-frequency ventilation, inhaled nitric oxide, and ECMO have reduced the mortality to <5%. In patients surviving severe meconium aspiration, broncho pulmonary dysplasia or chronic lung disease may result from prolonged mechanical ventilation. Those with a significant asphyxial insult may demonstrate neurologic sequelae (4).

SUMMARY

Like many aspect of the perinatal period, optimal care of an infant born through meconium-stained amniotic fluid involves collaboration between obstetrician, anesthesiologist and pediatrician, each with separate but important roles. As always, effective communication and advanced preparation and anticipation of potential problems from the cornerstone of this partnership. Together the health of infants may be improved.

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