INTRODUCTION — Meconium aspiration syndrome (MAS) is defined as respiratory distress in newborn infants born through meconium-stained amniotic fluid (MSAF) whose symptoms cannot be otherwise explained. MAS can present with varying degrees of severity from mild respiratory distress to life-threatening respiratory failure. Coordination of care between the obstetric and neonatal team is important to reduce the incidence of MAS and to identify and provide urgent therapy in those who develop MAS to reduce morbidity and mortality.
The prevention, management, and outcome of MAS will be reviewed here. The pathophysiology, clinical features, and diagnosis of MAS are discussed separately. (See "Meconium aspiration syndrome: Pathophysiology, clinical manifestations, and diagnosis".)
PREVENTION — Because of the potential for poor outcome, the best approach for managing MAS is prevention. Intrapartum care to reduce the incidence of MAS includes:
●Intrapartum fetal heart (FHR) monitoring – Continuous or periodic FHR monitoring has become a standard of care in the United States, particularly in pregnancies thought to be at higher risk for intrapartum fetal hypoxemia (eg, postterm pregnancy, intrauterine growth restriction, preeclampsia). The primary goal of FHR monitoring is to assess the adequacy of fetal oxygenation during labor. Evaluation and interventions are implemented in cases with abnormal tracings indicative of fetal stress to reduce the likelihood of perinatal asphyxia. Although the combination of a nonreassuring FHR tracing and thick meconium in amniotic fluid has been associated with an increased risk of MAS, the value of intrapartum fetal monitoring in preventing MAS has not been proven. Nevertheless, we agree that FHR monitoring identifies signs of hypoxemia and allows the caregivers to initiate prompt interventions in order to reduce the risk of MAS. (See "Intrapartum fetal heart rate monitoring: Overview" and "Meconium aspiration syndrome: Pathophysiology, clinical manifestations, and diagnosis", section on 'Pathophysiology'.)
●Prevention of postterm (>41 weeks gestation) delivery – Because the risk of MAS is greatest in infants with a gestational age (GA) greater than 41.0 weeks, preventing delivery after 41 weeks gestation reduces the incidence of MAS. To reduce the number of postterm births, induction of labor can be offered to women at 39 weeks gestation who have well-dated pregnancy and who have no contraindications for induction. (See "Induction of labor with oxytocin", section on 'Elective induction at ≥39 weeks' and "Meconium aspiration syndrome: Pathophysiology, clinical manifestations, and diagnosis", section on 'Epidemiology' and "Postterm infant" and "Postterm infant", section on 'Neonatal complications'.)
●Management of postterm delivery – For women greater than 41 weeks of gestation, induction of labor reduces the risk of MAS compared with expectant management. Evidence demonstrating a decreased incidence of MAS with induction of labor versus expectant management is discussed separately. (See "Postterm pregnancy", section on 'Our approach: Induction at 41+0 weeks'.)
DELIVERY ROOM MANAGEMENT OF INFANTS WITH MSAF
Obstetrical care — We concur with the guidelines of the American Heart Association (AHA), the American Academy of Pediatrics (AAP), and the American College of Obstetricians and Gynecologists (ACOG), which recommend against routine intrapartum nasopharyngeal suctioning of newborns with meconium-stained amniotic fluid (MSAF). Based on the available evidence, intrapartum oro/nasopharyngeal suctioning of newborns with MSAF does not appear to reduce the likelihood of developing MAS [1,2]. In a meta-analysis of two randomized trials involving 3032 infants with MSAF, mortality was higher among infants assigned to intrapartum suctioning compared with no suctioning; however, the finding was not statistically significant and the low number of events precludes drawing any conclusion (1.1 versus 0.46 percent, relative risk [RR] 2.29, 95% CI 0.94-5.53) [2]. Rates of MAS were not reported in the meta-analysis, but in the larger of the two trials (n = 2514), the incidence of MAS was similarly low in both groups (4 percent in each arm, RR 0.9, 95% CI 0.6-1.3) [1]. The need for mechanical ventilation, duration of respiratory support, and hospital length of stay were also similar in both groups.
Neonatal care
●Initial care – Based on the available evidence, the care of infants with MSAF should be guided by the general neonatal resuscitation principles for further intervention, including endotracheal intubation based on inadequate respiratory effort (gasping, labored breathing, or poor oxygenation) or heart rate (<100 bpm) (algorithm 1). As a result, our center does not routinely provide endotracheal suctioning for any infant with MSAF regardless of clinical status, which may delay resuscitation efforts without evidence of benefit. This approach is consistent with the guidelines from the International Liaison Committee on Resuscitation (ILCOR), AAP, and AHA for both vigorous and nonvigorous infants [3,4]. The care of infants with MSAF should be guided by the general neonatal resuscitation principles for further intervention, including endotracheal intubation based on inadequate respiratory effort (gasping, labored breathing, or poor oxygenation) or heart rate (<100 bpm) (algorithm 1). In addition, intubation and tracheal suction may be beneficial when there is evidence of airway obstruction in the nonvigorous neonate during positive pressure ventilation [3]. The risk of airway obstruction is likely higher in newborns delivered through MSAF and thus skilled caregivers who can address this possibility should be immediately available if needed. (See "Meconium aspiration syndrome: Pathophysiology, clinical manifestations, and diagnosis", section on 'Pulmonary disease' and "Neonatal resuscitation in the delivery room", section on 'Infants requiring delivery room resuscitation'.)
•Vigorous infant – Data from clinical trials in vigorous term infants with MSAF showed that suctioning in addition to routine delivery room care and resuscitation did not provide any additional improvement in outcome [5,6]. In a meta-analysis of 4 trials with 2884 infants, endotracheal intubation and suctioning versus no intubation did not reduce the risk of MAS (relative risk [RR] 1.29, 95% CI 0.80-2.08) [6]. However, the number of events were small (37 and 28, respectively).
•Nonvigorous infant – The recommendation not to perform routine endotracheal suction for nonvigorous infants with MSAF is based the principle of preventing harm (eg, delay in providing ventilation and preventing complications of intubation) and the lack of evidence that routine endotracheal suction is beneficial [3,4,7].
Data from non-blinded trials reported similar outcomes between non-vigorous infants randomly selected for no endotracheal suctioning versus those assigned with endotracheal suction [7-11]. In a meta-analysis of 4 trials with 581 infants, the two groups (no endotracheal and endotracheal suctioning) had similar risk of MAS (RR 1.00, 95% CI 0.80-1.25) and all-cause mortality (RR 1.24, 95% CI 0.76-2.02) [8]. But the quality of evidence is low due to the high risk of bias due to non-blinding of the personnel conducting the investigation as well as the small number of events.
Indirect support for no additional endotracheal intubation and suctioning was provided by a follow-up study from the California Perinatal Quality Care Collaborative and data from a single center that found no increase in the incidence or severity of MAS after implementation of the updated guideline [12,13].
However, one observational study reported that a higher proportion of nonvigorous infants were admitted to the neonatal intensive care unit (NICU) for respiratory issues following implementation of the revised 2015 guidelines of no endotracheal suctioning compared with a group of infants cared for in the previous year in which suctioning after endotracheal tracheal intubation for nonvigorous, meconium-stained infants was routine practice [14]. Of particular note, there was no increase in MAS in this cohort.
●Subsequent care and triage – Infants who develop MAS generally exhibit signs of respiratory distress immediately after birth [15]. Asymptomatic infants with Apgar scores ≥9 at five minutes can be admitted to the normal nursery without additional monitoring or intervention. In our practice, infants with MSAF with Apgar scores <9 at five minutes. are observed post-delivery in the NICU or Special Care Nursery for a minimum of four to six hours to ensure they transition successfully to extrauterine life. Those with evidence of persistent respiratory distress remain in a more intensive care setting and are evaluated for adequate oxygenation by pulse oximetry (or in more severe infants, arterial blood gas) and chest radiography to diagnose MAS. (See "Meconium aspiration syndrome: Pathophysiology, clinical manifestations, and diagnosis", section on 'Evaluation and initial management' and "Meconium aspiration syndrome: Pathophysiology, clinical manifestations, and diagnosis", section on 'Diagnosis'.)
MANAGEMENT
Approach — For the neonate with a suspected diagnosis of MAS, management of MAS is largely supportive (oxygen therapy, assisted ventilation, inhaled nitric oxide, extracorporeal membrane oxygenation [ECMO]) [16]. Prompt identification and care of affected patients decreases morbidity and mortality, especially in patients with severe disease. Coordination of care between the obstetric and neonatal team is crucial to initiate effective management of infants who develop MAS [17]. (See 'Outcome' below.)
The general approach to care includes:
●Maintenance of adequate oxygenation and ventilation
●Maintenance of adequate blood pressure (BP) and perfusion
●Correction of any metabolic abnormality including hypoglycemia and acidosis, which increase oxygen consumption
●Empirical antibiotic therapy
●Care in a neutral thermal environment (unless there are signs of hypoxemic ischemic encephalopathy, which is treated with hypothermia) (see "Clinical features, diagnosis, and treatment of neonatal encephalopathy", section on 'Therapeutic hypothermia')
●Minimal handling of the infant to avoid agitation, which exacerbates persistent pulmonary hypertension of the newborn (PPHN), if present (see "Persistent pulmonary hypertension of the newborn (PPHN): Clinical features and diagnosis")
Respiratory management — Respiratory management is focused on maintaining optimal oxygenation and ventilation, especially as hypoxemia, acidosis, and hypercapnia may increase pulmonary vascular resistance and contribute to the development of PPHN. Hyperventilation, respiratory alkalosis, and air-trapping should be avoided. (See "Persistent pulmonary hypertension of the newborn (PPHN): Management and outcome".)
Target oxygen saturation — Infants with MAS are typically born at term and the target pulse oximetry saturation (SpO2) is more liberal than for preterm infants who are at greater risk for pulmonary injury due to high concentrations of oxygen. As a result, while the term infant is undergoing diagnostic testing to determine the underlying cause of respiratory distress, we suggest that oxygen supplementation be given to keep the infant well saturated (SaO2 >99 percent). Once the diagnosis of MAS has been established, we suggest a range of preductal SaO2 95 to 98 percent [18] (arterial partial pressure of oxygen [PO2] between 55 and 90 mmHg) that provides adequate tissue oxygenation and avoids lung injury that may result from continued administration of high concentrations of oxygen [18]. Hypoxemia should be avoided because it contributes to pulmonary vasoconstriction and possibly PPHN. Pulse oximetry and arterial blood gases are used to monitor oxygenation.
Mild to moderate disease — For patients with mild or moderate disease, supplemental oxygen therapy that does not exceed an FiO2 (fraction of inspired oxygen) of 0.4 to 0.5 and without positive pressure is usually adequate to maintain SaO2 in the target range for patients with mild or moderate disease. In our center, the preferred initial method of oxygen delivery is via an oxygen hood, as the concentration of oxygen (FiO2) can be accurately determined. Administration of oxygen can also be given via nasal cannula, but the exact concentration of oxygen cannot accurately be measured and is determined by the size of the newborn infant and the infant's tidal volume and the liter flow administered (1/8 L/min to 1 L/min). (See "Respiratory support, oxygen delivery, and oxygen monitoring in the newborn", section on 'Choice of modality'.)
Severe disease — When an FiO2 of more than 0.5 is required to maintain target SaO2, it generally reflects worsening ventilation/perfusion (V/Q) mismatch. When this occurs, we suggest adding continuous positive airway pressure (CPAP) to improve oxygenation and avoid high concentrations of oxygen and need for mechanical ventilation [19]. However, CPAP should be used cautiously in infants with hyperinflation as it may exacerbate air trapping. If overinflation is noted on chest radiograph, pCO2 should be monitored, as well obtain subsequent chest radiographs to ensure that overinflation does not worsen.
Despite the use of CPAP, some infants with severe disease will require further intervention including mechanical ventilation, exogenous administration of surfactant, inhaled nitric oxide, and ECMO.
Mechanical ventilation — Approximately 30 percent of patients with MAS require mechanical ventilation due to respiratory failure [20,21]. The goal for assisted ventilation is to achieve optimal gas exchange with minimal respiratory trauma. In infants with MAS who receive mechanical ventilation, we suggest targeted arterial PO2 between 55 and 90 mmHg (SaO2 95 to 98 percent) and allow for permissive hypercapnia (partial pressure of carbon dioxide [PaCO2] 50 to 55 mmHg) as long as pH remains in the normal range (ie, pH 7.3 to 7.4). We consider using high-frequency oscillatory ventilation (HFOV) in infants who fail to respond to conventional mechanical ventilation, and in those who fail mechanical ventilation and pharmacologic treatment, ECMO therapy. (See 'Extracorporeal membrane oxygenation (ECMO)' below and "Overview of mechanical ventilation in neonates".)
In our practice, we use sedative therapy for infants who are mechanically ventilated and experience increased agitation due to asynchronous breathing. Agitation may be associated with catecholamine release, increased pulmonary vascular resistance, right-to-left shunting, and hypoxemia. The goal of sedative therapy is to maintain effective and safe sedation to achieve optimal gas exchange during the acute phase of the illness and allow for controlled weaning from assisted ventilation. In these patients, we use the following opioid analgesic for sedation and analgesia. (See "Prevention and treatment of neonatal pain".)
●Intravenous morphine sulfate (loading dose of 100 to 150 mcg/kg over one hour, followed by a continuous infusion of 10 to 20 mcg/kg per hour)
●Intravenous (IV) fentanyl (1 to 5 mcg/kg per hour)
If dyssynchronous breathing persists and a specific cause cannot be identified (eg, airway obstruction or air leak), we may use neuromuscular blockade with pancuronium (0.1 mg/kg IV push per dose). However, we limit this intervention as much as possible because of potential adverse effects.
Surfactant — We do not routinely administer surfactant to all patients with MAS. However, we will administer surfactant (150 mg/kg [6mL/kg]) to patients with severe disease who are mechanically ventilated and require high FiO2 (>0.5) and high mean airway pressure (>10 to 12 cm H2O) [16,22-25]. Meconium is thought to negatively impact the production of endogenous surfactant, and it is thought that administration of exogenous surfactant reduces V/Q mismatch as well as pulmonary vascular resistance. Limited data suggest that surfactant's beneficial effect on pulmonary function reduces the need for inhaled nitric oxide and/or ECMO in mechanically ventilated infants with MAS [24,25]. Surfactant may also be helpful in infants with radiographic evidence of surfactant dysfunction (eg, low lung volumes and homogeneous pulmonary parenchymal disease that is similar in appearance to respiratory distress syndrome [RDS]).
Inhaled nitric oxide — Inhaled nitric oxide (iNO) is a selective pulmonary vasodilator that may improve oxygenation in patients with associated PPHN. In our center, iNO is only administered after a trial of surfactant therapy to an infant with persistent severe respiratory disease based on continued high ventilatory settings of FiO2 and mean airway pressure and evidence of persistent pulmonary hypertension with right-to-left shunting based on echocardiography (if permissible) or postductal saturations. (See "Meconium aspiration syndrome: Pathophysiology, clinical manifestations, and diagnosis", section on 'Hypoxemia' and "Persistent pulmonary hypertension of the newborn (PPHN): Management and outcome", section on 'Inhaled nitric oxide (iNO)'.)
Another pulmonary vasodilator agent used in the treatment of PPHN is sildenafil, a phosphodiesterase inhibitor. We prefer the use of inhaled nitric oxide since it has localized effects in the lung versus sildenafil, which causes systemic vasodilation and can potentially lead to hypotension as a potential side effect. (See "Persistent pulmonary hypertension of the newborn (PPHN): Management and outcome", section on 'Sildenafil' and "Persistent pulmonary hypertension of the newborn (PPHN): Management and outcome", section on 'Pulmonary vasodilator therapy'.)
Extracorporeal membrane oxygenation (ECMO) — ECMO may be life saving in infants who do not respond to mechanical ventilation, surfactant therapy, and/or iNO [26-28]. ECMO provides cardiopulmonary support while awaiting resolution of the underlying pulmonary disease process without further risk of injury from volutrauma from mechanical ventilation and the use of high concentrations of supplemental oxygen.
Both venovenous and venoarterial ECMO have been used in infants with meconium aspiration [29]. Although both methods are invasive compared with the medical treatments for MAS, venoarterial ECMO requires ligation of the carotid artery and may be associated with complications of pulmonary emboli from the ECMO circuit and increased left ventricular afterload. The addition of other therapeutic modalities, such as surfactant and iNO, has allowed the successful use of venovenous ECMO in infants with MAS, thus avoiding the more invasive venoarterial procedure [29].
Circulatory support — Therapeutic measures that ensure adequate cardiac output and tissue perfusion include:
●Maintaining sufficient intravascular volume – Volume expansion using normal saline may be needed in infants with low BP (defined as a mean BP below the 5th percentile (figure 1)) and inadequate peripheral tissue perfusion (eg, cold extremities, acrocyanosis, and poor capillary refill). (See "Neonatal shock: Management".)
●Enteral feeds are not provided during severe respiratory illness – In patients with adequate circulation, parenteral fluid management during the first 24 hours of life is restricted to a volume of 65 mL/kg using a solution that consists of 5 percent dextrose without additional electrolytes. Subsequently, the volume is adjusted based on the needs of the infant, and sodium intake is limited to minimize peripheral and pulmonary edema. Parenteral nutrition is initiated if enteral feeding is contraindicated. (See "Fluid and electrolyte therapy in newborns", section on 'Fluid and electrolyte management' and "Parenteral nutrition in infants and children".)
●Transfusion of packed red blood cells may be required to optimize tissue oxygen delivery, especially in patients with marginal oxygenation – In our practice, hemoglobin concentration is maintained above 15 g/dL (hematocrit above 40 to 45 percent) in patients with severe MAS who are maintained on mechanical ventilation. (See "Red blood cell transfusions in the newborn".)
●Vasopressor support often is needed to maintain adequate BP– We begin with a continuous intravenous infusion of dopamine (2.5 to 10 mcg/kg per min IV) and increase the infusion rate as necessary to maintain normal mean arterial BP. BP may need to be higher in infants with PPHN to minimize right-to-left shunting. (See "Neonatal shock: Management", section on 'Vasoactive agents' and "Persistent pulmonary hypertension of the newborn (PPHN): Management and outcome".)
Antibiotics — Although it is uncertain whether antibiotic therapy is beneficial in infants with MAS [22,30,31], broad-spectrum antibiotics (ampicillin and gentamicin/amikacin) are administered while awaiting the results of blood cultures because of the difficulty of distinguishing MAS from serious bacterial infection (eg, sepsis and bacterial pneumonia). The presence of MSAF may also reflect a compromised intrauterine stress including an infectious process such as chorioamnionitis. (See "Meconium aspiration syndrome: Pathophysiology, clinical manifestations, and diagnosis", section on 'Differential diagnosis' and "Management and outcome of sepsis in term and late preterm neonates".)
Unproven therapy — Although corticosteroid therapy has been proposed to reduce the severity of MAS, there is no evidence of its effectiveness in infants with MAS [32,33]. As a result, we do not recommend the use of corticosteroid therapy in patients with MAS unless future control trials demonstrate significant benefit from its use.
OUTCOME — The overall outcome of MAS has improved with advances in neonatal care [20,21].
In a retrospective review from a multicenter study from the United States that included 162,075 term infants born between 1997 and 2007, 1.8 percent of patients developed MAS [21]. The following findings were noted:
●Of the 7518 infants with MAS, 82 percent were discharged home from a nonintensive care setting, 8 percent required transfer for intensive care, and 1.2 percent died (n = 88).
●Extracorporeal membrane oxygenation (ECMO) treatment was performed in 61 neonates (1.4 percent) including three infants who died.
●Multivariate analysis showed mortality was independently associated with an Apgar score <3 (odds ratio [OR] 7.5, 95% CI 4.6-12.2), need for ventilatory support within the first 48 hours of life (OR 4.1, 95% CI 2.1-8.1), repeated doses of vasopressive agents (OR 3.8, 95% CI 2.2-6.4), presence of a major congenital anomaly (OR 2.1, 95% CI 1.4-3.4), and the use of cefotaxime (OR 2.1, 95% CI 1.4-3.4).
●The short-term morbidity of survivors included oxygen supplementation at 28 days of life (5 percent) and seizures (5 percent), and four patients developed necrotizing enterocolitis.
In this study, the mortality rate of 1.2 percent was lower in comparison to 4.2 percent that was reported in a large retrospective study from the United States of 176,790 infants born between 1973 and 1987 [20].
Small follow-up studies suggest that long-term pulmonary morbidity, especially reactive airway disease, is a common finding in patients who had MAS [34-36]
Neurologic outcome — There are limited data on the neurodevelopmental outcome of patients with MAS. Small observational case series report that approximately 20 percent have significant neurodevelopmental impairment [37]. However, birth depression occurs in 20 to 30 percent of patients with MAS, and it is likely that intrauterine asphyxia and/or infection are underlying pathologic factors resulting in poor neurodevelopmental outcome. (See "Clinical features, diagnosis, and treatment of neonatal encephalopathy".)
SUMMARY AND RECOMMENDATIONS
●Definition – Meconium aspiration syndrome (MAS) is defined as respiratory distress in newborn infants born through meconium-stained amniotic fluid (MSAF) whose symptoms cannot be otherwise explained. In severe cases, MAS can be life threatening. As a result, it is important to reduce the incidence of MAS and provide urgent therapy to reduce mortality in those who develop MAS. (See "Meconium aspiration syndrome: Pathophysiology, clinical manifestations, and diagnosis".)
●Prevention of MAS includes:
•Routinely using intrapartum fetal heart rate (FHR) monitoring to detect and correct episodes of fetal hypoxia, which may be associated with MSAF. (See "Intrapartum fetal heart rate monitoring: Overview".)
•Avoiding delivery of postterm infants (gestational age [GA] >41 weeks) as the risk of MAS is greater in postterm infants compared with infants born at a GA ≤41 weeks. Induction of labor can be offered to women at 39 weeks gestation who have a well-dated pregnancy and who have no contraindications for induction to avoid postterm delivery. (See "Induction of labor with oxytocin", section on 'Elective induction at ≥39 weeks' and "Meconium aspiration syndrome: Pathophysiology, clinical manifestations, and diagnosis", section on 'Epidemiology'.)
●Delivery room care of newborns with MSAF:
•At delivery, we suggest not performing intrapartum nasopharyngeal suction for any newborn with MSAF (Grade 2C). The available evidence suggests that intrapartum suctioning does not reduce the risk of MAS. (See 'Obstetrical care' above.)
•After delivery, we recommend not to perform endotracheal suctioning for vigorous infants with MSAF (Grade 1B). For nonvigorous infants, we suggest not to perform endotracheal suctioning after delivery (Grade 2C). (See 'Neonatal care' above.)
•The care of infants with MSAF regardless of their level of activity is guided by the same general principles for further respiratory support, including endotracheal intubation based on inadequate respiratory effort (gasping, labored breathing, or poor oxygenation), heart rate (<100 bpm) or evidence of airway obstruction (algorithm 1). (See "Neonatal resuscitation in the delivery room", section on 'Infants requiring delivery room resuscitation'.)
•Patients who develop MAS typically exhibit signs of respiratory distress immediately after birth. (See 'Neonatal care' above.)
-Infants with MSAF who exhibit signs of respiratory distress in the delivery are observed in the neonatal intensive care unit (NICU) or Special Care Nursery for a minimum of four to six hours to ensure successful transition from intrauterine to extrauterine life. Those with evidence of persistent respiratory distress are evaluated for adequate oxygenation by pulse oximetry (or in more severe infants, arterial blood gas) and chest radiography to diagnose MAS.
-Asymptomatic infants are admitted to the normal nursery without additional monitoring or intervention.
●Management of MAS is supportive and includes the following:
•Respiratory management is focused on maintaining adequate oxygenation and ventilation, especially as hypoxemia, acidosis, and hypercapnia may increase pulmonary vascular resistance and contribute to the development of persistent pulmonary hypertension of the newborn (PPHN).
We suggest the use of respiratory support targeted at an oxygen saturation based upon preductal pulse oximetry (SpO2) of 95 to 98 percent to avoid hypoxemia (Grade 2C). (See 'Target oxygen saturation' above.)
-For patients with mild to moderate disease, supplemental oxygen without positive pressure administered via an oxygen hood or nasal cannulae is usually sufficient to maintain the targeted SpO2. (See 'Mild to moderate disease' above.)
-For patients with severe disease, interventions may include oxygen supplementation using continuous positive pressure support, mechanical ventilation, surfactant therapy, and/or inhaled nitric oxide (iNO) therapy to maintain targeted SpO2. In patients with respiratory failure who have failed to respond to other interventions, extracorporeal membrane oxygenation (ECMO) may be a life-saving intervention. (See 'Severe disease' above.)
•Maintenance of adequate blood pressure and perfusion with sufficient vascular volume, and in some patients, the use of vasopressor agents, such as dopamine. In our practice, hemoglobin concentration is maintained above 15 g/dL (hematocrit above 40 to 45 percent) in patients with severe MAS who are maintained on mechanical ventilation.(See 'Circulatory support' above.)
•Correction of any metabolic abnormality, including hypoglycemia, acidosis, and/or electrolyte derangements.
•Because it is difficult to differentiate MAS from bacterial pneumonia and sepsis, empiric antibiotic therapy is provided, pending culture results. (See 'Antibiotics' above and "Management and outcome of sepsis in term and late preterm neonates".)
•Care in a neutral thermal environment for infants without evidence of hypoxic-ischemic encephalopathy.
•Minimal handling of the infant to avoid agitation, which may exacerbate PPHN, if present. (See "Persistent pulmonary hypertension of the newborn (PPHN): Management and outcome".)
●Mortality – The mortality rate of MAS has improved because of advances in neonatal care. In survivors, long-term morbidity includes pulmonary sequelae, particularly reactive airway disease, and neurodevelopmental impairment. (See 'Outcome' above.)
