Amniotic fluid and meconium aspiration syndrome (aspiration of amniotic fluid and meconium syndrome) occurs in 0.3% to 2.0% of live births and is more common in full-term and post-term infants. It primarily results from the fetus inhaling meconium-stained amniotic fluid during birth, leading to a series of symptoms such as asphyxia and respiratory distress. Severe cases may progress to respiratory failure or death. The medical history often includes fetal distress, prolonged labor, placental insufficiency, difficult delivery, etc. Meconium-stained amniotic fluid usually indicates fetal hypoxia, but full-term or post-term infants may physiologically pass small amounts of meconium into the amniotic fluid.

bubble_chart Pathogenesis

Fetal hypoxia can trigger mass reflexes, leading to the expulsion of meconium and the onset of true respiration, which causes the inhalation of meconium, amniotic fluid, and keratinized cells. The inhalation of large amounts of thick meconium can result in complete tracheal obstruction, atelectasis, and acute asphyxial hypoxia. If the inhaled meconium-amniotic fluid is thin or the amount is small, it may cause partial obstruction, leading to subsegmental atelectasis and obstructive {|###|} lung qi distension. If alveoli rupture, it can result in interstitial emphysema or pneumothorax. When gas spreads along blood vessel walls and lymphatic vessels to the mediastinum, it can cause mediastinal emphysema.

The stimulation of respiratory tract mucous {|###|} membranes by meconium-amniotic fluid or secondary infections can lead to pneumonia. During the recovery phase, the inhaled material is absorbed or phagocytized, but in severe cases, fibrosis may develop, resulting in pathological changes such as {|###|} lung qi distension.

At birth, the entire body is contaminated with meconium. If the fetus is immersed in meconium-stained amniotic fluid for 4–6 hours, the fingernails and toenails may turn yellow-green. After 10–12 hours, the umbilical cord, vernix caseosa, and placental membranes can also be stained with meconium. The newborn's breathing is severely suppressed, exhibiting bradycardia, low muscle tone, and shock. After spontaneous breathing begins, rapid breathing may be observed, gradually progressing to dyspnea, intercostal retractions, expiratory grunting, and cyanosis. If cyanosis is severe and does not improve with oxygen therapy, persistent pulmonary hypertension of the newborn (PPHN) should be considered. The lung signs depend on the amount and thickness of the meconium aspirated. If pneumothorax occurs, respiratory movements and breath sounds may be asymmetrical on both sides.

Severe asphyxia and hypoxia can lead to cardiovascular adaptation disorders, right-to-left shunting, cardiomegaly with poor peripheral circulation congestion, and occasional spasms. Blood gas analysis shows decreased PO₂, increased PCO₂, and reduced pH. Severe cases may die within minutes to hours after birth, while survivors may experience a prolonged course. In general cases, significant improvement occurs within 2 days, with complete recovery after 10 days or longer. Mild cases may only develop dyspnea several hours after birth, with slight thickening of lung markings, grade I pulmonary emphysema, and grade I diaphragmatic depression on X-ray. For those with significant meconium aspiration, the lungs may show dense patchy or nodular infiltrates, hyperinflation, occasional small pleural effusions, interstitial emphysema, pneumomediastinum, or pneumothorax.

1. Blood Gas Analysis Hypoxemia is a characteristic manifestation. Grade I infants may present with respiratory alkalosis due to hyperventilation. Severe cases often exhibit increased PaCO₂ and respiratory acidosis due to airway obstruction. If the infant experiences asphyxia, the blood gas may show mixed acidosis.

2. Chest X-ray Inhaled meconium typically reaches the alveoli 4 hours after birth, at which point specific radiographic findings become apparent. Approximately 85% of MAS infants show the most pronounced X-ray signs at 48 hours post-birth, but about 70% may exhibit discrepancies between chest X-ray findings and clinical manifestations. Based on chest X-ray findings, MAS is classified as:

- Grade I: Increased lung markings, Grade I lung qi swelling, diaphragmatic Grade I depression, normal cardiac silhouette;

- Grade II: Coarse granular or patchy opacities with increased density in the lung fields, cloud-like shadows or segmental atelectasis, accompanied by hyperlucent cystic emphysema and a relatively small cardiac silhouette;

- Grade III: In addition to the Grade II findings, features such as interstitial emphysema, pneumomediastinum, or pneumothorax (gas fistula disease) may be present.

bubble_chart Diagnosis

(1) Medical History

The following factors are risk factors for MAS:

1. The mother has pregnancy toxemia, preeclampsia, diabetes, etc.;

2. The mother has obstetric complications, prolonged labor, and meconium-stained amniotic fluid;

3. Post-term infants, small-for-gestational-age infants; abnormal fetal heart rate, intrauterine distress; birth asphyxia and meconium suction from the trachea.

The clinical manifestations of MAS vary depending on the severity of hypoxic damage and the amount and viscosity of meconium-stained amniotic fluid inhaled.

1. If the infant is exposed to meconium-stained amniotic fluid in utero for >4–6 hours, the skin, fingernails, toenails, and umbilical cord will be stained yellow-green or dark green at birth. _{2. Respiratory Distress} Main manifestations include tachypnea (>60 breaths/min), nasal flaring, retractions, and cyanosis. Due to varying degrees of meconium contamination, the severity of respiratory distress can range from mild to severe. Most cases appear within 4 hours after birth. Grade I cases only exhibit transient dyspnea and often recover spontaneously. More severe cases involve dyspnea and cyanosis but can maintain normal PaO₂ and PaCO

2

with 40% oxygen inhalation. The most severe cases may die within minutes after birth or develop severe dyspnea and cyanosis within hours, requiring mechanical ventilation and comprehensive treatment as conventional oxygen therapy is ineffective. Some infants may initially present with only Grade I respiratory distress but worsen within hours due to chemical pneumonia.

3. Barrel Chest {|114|} Thick meconium-stained amniotic fluid inhalation can cause partial or complete airway obstruction. Acute airway obstruction manifests as wheezing, cyanosis, and requires immediate tracheal suction. Infants with partial obstruction may develop gas trapping, leading to an increased anteroposterior chest diameter (barrel chest), shallow and rapid breathing, diminished breath sounds, rales, or wheezing. If pneumothorax occurs, sudden cyanosis and worsened dyspnea may appear. {|115|} 4. Some infants may develop persistent pulmonary stirred pulse hypertension (see persistent pulmonary stirred pulse hypertension). {|116|} (3) Laboratory Tests (Refer to Laboratory Tests)

bubble_chart Treatment Measures

For cases with meconium-stained amniotic fluid, after clearing the meconium mucus from the oropharynx and nose, a neonatal laryngoscope must be used for examination, and endotracheal intubation should be performed to suction until the airway is completely cleared. Positive pressure ventilation should not be initiated before complete suctioning. Gastric contents should also be suctioned to avoid vomiting and re-aspiration, as well as the occurrence of meconium gastritis and anorexia.

After admission to the neonatal unit, intensive monitoring is required. Ultrasonic nebulization should be administered every 4–6 hours to achieve dilution. Following nebulization, postural drainage, percussion, and vibration should be performed according to the bronchial pathways of the affected lung segments to facilitate the removal of obstructions and improve atelectasis. The nebulization solution may include antibiotics, bronchodilators, and mucolytics as needed. For severe cases with abnormal blood gases and progressively rising PaCO₂, 1–2 ml of sterile saline can be instilled into the trachea via the endotracheal tube, followed by ventilation for 1–2 minutes before suctioning. This lavage and suction process should be repeated until the secretions are clear. If spontaneous breathing is strong after lavage, the endotracheal tube can be removed, and the patient should be closely monitored. If the infant can maintain PaO₂ at 5.33–6.67 kPa (40–50 mmHg) with high-concentration oxygen inhalation and spontaneous breathing, mechanical ventilation may not be necessary, and the vasodilator tolazoline can be administered instead.

Mechanical ventilation may drive meconium particles deeper into the lungs and should therefore be used cautiously. The principle of parameter adjustment is to use higher oxygen concentration, faster frequency, shorter inspiratory time, longer expiratory time, and the lowest possible pressure to reduce the risk of pulmonary overinflation and fistula disease. If agitation occurs, sedatives and muscle relaxants may be used. During oxygen therapy, transcutaneous oxygen monitoring should be employed to precisely guide oxygen concentration adjustments.

Maintain warmth and a neutral thermal environment, closely monitor heart rate, respiration, and blood pressure, and regularly measure blood gases and fluid intake/output. Broad-spectrum antibiotics should be routinely administered to prevent infection. Symptomatic treatment should be provided for conditions such as hypoglycemia, hypocalcemia, or pneumothorax.

bubble_chart Prevention

Proper management of fetal distress during the prenatal and intrapartum periods should be implemented to minimize and prevent aspiration. It is crucial to clear the oropharynx and nasal mucus by suction or using a disposable suction tube before the first breath occurs after the fetal head is delivered, as this is key to reducing the incidence. It is essential for perinatal medical and nursing staff to undergo qualified resuscitation training before assuming their duties.

bubble_chart Complications

Simple amniotic fluid aspiration is easier to absorb and less likely to lead to secondary pneumonia. Meconium-stained amniotic fluid aspiration may result in complications such as atelectasis, pulmonary emphysema, pneumomediastinum, and pneumothorax, depending on the degree of obstruction. Severe hypoxic acidosis can cause intracranial hemorrhage and pulmonary hemorrhage. Prolonged cases often develop interstitial pneumonia and pulmonary fibrosis.