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Meconium Aspiration Syndrome

• Summary
• Introduction
• MAS Pathogenesis
• Clinical Features
• Complications
• Differential Diagnosis
• Management
• References

Summary

• Meconium aspiration syndrome (MAS) is characterised by early onset of respiratory distress and hypoxaemia in a meconium—stained term infant
• most babies with MAS require nothing more than oxygen therapy and general supportive care; oxygen should be used liberally in this condition
• ventilator support should be instituted where there is refractory hypoxaemia or respiratory acidosis; early consultation with NETS is advised  

Introduction

Meconium aspiration syndrome (MAS) is an important cause of respiratory distress in the term infant, with a local incidence of around 1.5 in 1000 live births. The prelude to MAS is the passage of meconium at or prior to delivery, a circumstance encountered in 10-20% of all deliveries at term, and more frequently beyond term. Meconium-stained amniotic fluid (MSAF) is rarely seen at preterm delivery; its presence raises the possibility of fetal infection (particularly Listeria). Delivery room management of the infant where liquor is meconium stained is described in a separate section.

MAS Pathogenesis

In an infant born through MSAF, the risk and severity of MAS is influenced by

• the severity of concurrent asphyxia
• the degree of contamination of the amniotic fluid with meconium
• the presence of meconium in the airways (nasopharynx, trachea) at delivery

Of these, asphyxia is the single most important risk factor for MAS, and is presumed to relate to the influx of MSAF into the lung during hypoxic fetal gasping. MAS can occur, however, in meconium-stained infants that are in good condition at birth. The perinatal events leading to the inhalation of meconium are outlined in Fig 1.

Figure 1. The pathogenesis of MAS (modified from ref 1)

NB: The MAS flowchart is available as a .pdf file for printing. If you do not have a copy of Acrobat Reader to view this file, the latest version is available for free download from www.adobe.com

Once in the lung, meconium quickly migrates down the tracheobronchial tree, inducing a complex lung disease that includes large and small airway obstruction, chemical pneumonitis, proteinaceous alveolar oedema, and surfactant dysfunction (Fig 1). The resultant impairment of gas exchange is often severe, and manifests as hypoxaemia with or without hypercarbia. Persistent pulmonary hypertension with right to left ductal and foramen ovale shunt frequently compounds the oxygenation difficulty.

Clinical Features

MAS is characterized by early onset of respiratory distress (within 2 hours) in a meconium-stained infant. Tachypnoea, cyanosis and variable hyperinflation are the main clinical findings. Ausculation reveals widespread "wet" inspiratory crackles, occasionally with expiratory noises suggesting ball-valve airway obstruction. Radiologically the typical progression is from global atelectasis in early X-rays to a widespread patchy opacification accompanied by areas of hyperinflation and/or atelectasis. Blood gas analysis invariably shows hypoxaemia, accompanied by hypercarbia in those infants with significant airway obstruction or severe respiratory failure.

Complications

• persistent pulmonary hypertension
• air leak — pneumomediastinum, pneumothorax , cystic lung disease
• pulmonary haemorrhage
• complications of asphyxia — encephalopathy, seizures, oliguria, coagulopathy and thrombocytopenia

Differential Diagnosis

• birth asphyxia with pulmonary hypertension and/or haemorrhagic pulmonary oedema
• transient tachypnoea of the newborn
• surfactant deficiency (especially after elective Caesarean delivery)
• sepsis/pneumonia
• pneumothorax
• congenital diaphragmatic hernia

Management

Respiratory care

Oxygen
It cannot be over-emphasised that administration of oxygen is critically important in infants with MAS, and in many infants is the only respiratory therapy needed. The pulmonary vasculature in the term infant is exquisitely sensitive to oxygen tension, and failure to overcome hypoxaemia almost inevitably will lead to progressive pulmonary hypertension. Oxygen should be administered early and liberally in any baby suspected of having inhaled meconium. The suggested target range for oxygen saturation is 94-98%; target PaO₂ 60 — 90 mm Hg. Oxygen toxicity is not an important consideration in the term infant.

Nasal CPAP
Consider as an interim measure in infants with MAS where there is moderate respiratory distress and hypoxaemia.


Intubation and positive pressure ventilation

Indications
Persistent hypoxaemia (SaO₂ < 90%, PaO₂ < 50) in 100% oxygen
Respiratory acidosis with pH < 7.20

Method
Other than in the delivery room, term infants with MAS require deep sedation and preferably muscle relaxation prior to intubation. Infants with MAS are frequently very difficult to manage once intubated, and often require high peak inspiratory pressures (30 — 35 cm H₂O) to achieve gas exchange. Most evidence favours a high positive end-expiratory pressure (6-8 cm H₂O), and a long expiratory time. The latter can be achieved using ventilator rates of 40 — 60 breaths per minute, with an inspiratory time of 0.5 — 0.6 secs. Particularly where there is concomitant pulmonary hypertension, deep sedation should be maintained after intubation, and muscle relaxation should be continued if the disease is severe.

Surfactant therapy
Available evidence does not suggest a consistent benefit from bolus surfactant therapy in MAS; many infants show no response, and some acutely deteriorate. Lung lavage using surfactant is currently being investigated in MAS, but cannot yet be recommended as a therapy for this disease.

Supportive therapy for pulmonary hypertension

Suctioning
All infants with MAS should have the stomach contents evacuated, and an in-dwelling nasogastric tube inserted. In those intubated, the trachea should be suctioned by small volume saline lavage if there is clinical evidence of build-up of meconium or secretions in the large airways.

General supportive care

• cardiovascular support — volume and inotrope therapy
• fluid restriction
• antibiotic therapy — should be continued until primary bacterial infection is excluded
• IV therapy and nil orally until the respiratory distress is resolving

References

Wiswell TE, Bent RC. Meconium staining and the meconium aspiration syndrome. Unresolved issues. Pediatr Clin North Am 1993; 40: 955-81.

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