Inhalation syndrome

Introduction Inhalation syndrome is divided into amniocentesis, meconium inhalation and milk inhalation according to the different people. Here is a summary of meconium aspiration syndrome. Meconium aspiration syndrome refers to the inhalation of amniotic fluid contaminated by meconium during intrauterine or delivery, resulting in airway obstruction, intrapulmonary inflammation and a series of systemic symptoms. In recent years, studies have shown that MAS can cause pulmonary vascular endothelial damage, and can damage alveolar type II cells, reduce pulmonary surfactant, and cause acute lung injury such as alveolar collapse and clear film formation, forming pulmonary edema and pulmonary hemorrhage. Hypoxia is aggravated.

Cause

(1) Causes of the disease

1. Intrauterine distress: a large amount of amniotic fluid meconium inhalation can be initiated and delivered during the unsuccessful period of labor. It is generally believed that MAS is associated with intrauterine distress. When the fetus undergoes asphyxia and acute or chronic hypoxemia during intrauterine or childbirth, body blood flow is redistributed, intestinal and skin blood flow is reduced, resulting in intestinal wall ischemia. The anus and anal sphincter relax and excrete meconium. The incidence of meconium-contaminated amniotic fluid in live births is about 12% to 21.9%. Hypoxia stimulates the fetal respiratory center, causing a strong wheezing of respiratory movements from irregularities, inhaling meconium into the nasopharynx and trachea; and effective breathing after delivery of the fetus, inhaling meconium from the upper respiratory tract into the lungs Inside. Expired births due to increased intestinal maternal system and intestinal peptide levels and placental dysfunction, the possibility of MAS increased compared with full-term children.

2. Fetal maturation: The current data does not fully support the correlation between MAS and intrauterine distress. The changes in fetal heart rate, Apgar score, fetal scalp blood pH and other factors are not related to amniotic fluid meconium contamination. However, according to the increased risk of MAS with gestational age, it suggests that intrauterine meconium discharge is related to fetal parasympathetic development and reflex regulation after umbilical cord compression, and meconium discharge also reflects the development of fetal digestive tract. natural phenomenon. When the fetus is stimulated (extrusion, umbilical cord knot, asphyxia, acidosis, etc.), the fetal anal sphincter relaxes and excretes meconium into the amniotic fluid, while the reflex begins deep breathing, inhaling contaminated amniotic fluid and meconium into the airway and lungs. Inside.

3. Fetal distress in the labor process: Under normal circumstances, the lung endocrine fluid keeps the lung fluid flowing to the amniotic sac. The actual amplitude of intrauterine respiratory movement is very small. Even if a small amount of meconium enters the amniotic fluid, it will not be inhaled into the lungs. However, factors such as decreased amniotic fluid and stimulating the fetus during the late pregnancy may be manifested as signs of distress in the fetus and inhaled into the lungs.

(two) pathogenesis

1. Airway obstruction and intrapulmonary inflammation: Viscous meconium particles entering the airway can completely block the bronchi, causing mechanical obstruction, resulting in atelectasis of the lungs or segments of the lungs. Alveolar ventilation - imbalance of blood perfusion; valvular occlusion in small airways is more likely to cause pneumothorax, interstitial emphysema or mediastinal emphysema, aggravation of ventilatory disorders, and acute respiratory failure. Stimulating effects of meconium, bile salts, biliverdin, trypsin, enteric acid, etc., and subsequent secondary infections can cause chemical and infectious inflammatory reactions in the lungs, resulting in hypoxemia and acidosis. . When the airway is partially blocked, the airway pressure is high, so that the gas enters the peripheral alveoli easily, and the pressure of the exhaust gas is low, so that the airway is partially blocked and becomes completely blocked, and the peripheral alveolar gas retention causes emphysema. When the lung tissue is over-expanded, it shows signs such as full intercostal space and lower pressure. Meconium in large and small airways can stimulate the mucous membranes, produce inflammatory reactions and chemical pneumonia.

2. Ventilation and ventilation dysfunction: If the meconium in the airway is not absorbed and removed in time after resuscitation, it will gradually move into the small airway and peripheral lung tissue, and the meconium entering the alveoli can inhibit the pulmonary surfactant. Causes local alveolar collapse. Under the combined influence of the above reasons, the lungs have obstacles in ventilation and ventilation, which are characterized by persistent hypoxemia, hypercapnia and acidosis, and pulmonary hypertension occurs in severe cases. Meconium particles that enter the alveoli can be immediately engulfed and digested by alveolar macrophages.

3. Transparent membrane formation: Because MAS is often associated with prenatal, intrapartum, and postpartum hypoxia, it may have a greater impact on the pathological damage of the lungs in the early postnatal period. Airway and alveolar epithelial cells can be degenerated, necrotic, and shedding due to hypoxia, and there is a large amount of exudation and transparent membrane formation in the alveoli.

4. Pulmonary hypertension and acute lung injury intrauterine hypoxemia can lead to pulmonary vascular muscle hypertrophy, which is the cause of increased pulmonary vascular resistance - perinatal asphyxia, acidosis, hypercapnia and hypoxemia Pulmonary vasoconstriction, persistent pulmonary hypertension (PPH), right-to-left shunt at the level of atrial or catheter, further aggravating the condition. In recent years, studies have shown that MAS can cause pulmonary vascular endothelial damage, and can damage alveolar type II cells, reduce pulmonary surfactant, and cause acute lung injury such as alveolar collapse and clear film formation, forming pulmonary edema and pulmonary hemorrhage. Hypoxia is aggravated.

an examination

Related inspection

Chest MRI

Inspection diagnosis

1. History of intrauterine distress: If there is intrauterine distress or suffocation at birth, Apgar score can be performed at 1, 5, and 10 minutes after birth, less than 3 points, which may be a serious asphyxia. However, the Apgar score of severe MAS may be 3 to 6 points, which is not proportional to the degree of clinical respiratory distress.

2. Meconium-contaminated amniotic fluid during childbirth: This is an important clinical diagnosis basis for respiratory distress. If a large amount of meconium is contaminated in the baby's skin, nails, umbilical cord, or meconium is sucked from the mouth and airway during childbirth, the cause of respiratory distress can be determined.

3. Clinical symptoms of dyspnea: generally manifested as progressive dyspnea, with intercostal depression. At 12 to 24 hours after birth, the meconium enters the peripheral lung and shows increased difficulty in breathing. The airway attracts fluid contaminated by meconium. The cause of dyspnea may be that airway obstruction makes the alveolar expansion difficult, but it is also due to asphyxia that the fetal lung fluid cannot be discharged and hypoxic pulmonary vasospasm. Physical examination can be found that the thorax is full, etc., is due to emphysema.

4. Radiological examination: signs of meconium granules, atelectasis and emphysema.

5. Blood gas examination: severe MAS blood gas examination showed hypoxemia and hypercapnia, may have severe mixed acidosis, must rely on airway intubation and mechanical ventilation.

Differential diagnosis

Differential diagnosis:

Amphoteric and amniotic fluid and meconium syndrome accounts for 0.3% to 2.0% of live births in both full-term and expired children. It is mainly caused by the inhalation of amniotic fluid contaminated with meconium during the birth of the fetus, causing a series of symptoms such as suffocation and dyspnea. Severe cases develop into respiratory failure or death. In the medical history, there are often fetal distress prolonged labor, placental insufficiency, dystocia and other amniotic fluid stained meconium often expressed as fetal hypoxia, but full-term or expired children can have a small amount of physiological meconium discharged into amniotic fluid.

Diagnosis: The severity of the disease varies greatly, depending on the severity of the hypoxic damage and the amount and viscosity of meconium-stained amniotic fluid. Less inhalation can be asymptomatic at birth; large inhalation of meconium can cause stillbirth or die shortly after birth.

1. Meconium pollution: Meconium-contaminated amniotic fluid, if the child is exposed to meconium-contaminated amniotic fluid in the uterus for >4-6 hours, the whole body skin, nails and umbilical cord are dyed yellow-green or dark green at birth.

2. Respiratory distress: Most children often have shortness of breath (breathing frequency > 60 beats / min), difficulty breathing, cyanosis, nasal fan, sputum, and triconcae. Due to the severity of meconium-contaminated amniotic fluid, the degree of respiratory distress can vary, and general cases often occur within 4 hours after birth. Mild people only show temporary dyspnea and often self-heal. Heavier people have difficulty breathing and bruising, but they need to inhale 40% oxygen to maintain normal PaO2 and PaCO2. Severe cases may die within a few minutes after birth or severe dyspnea and bruising within a few hours after birth. Generally, oxygen therapy is ineffective and requires comprehensive treatment such as mechanical ventilation. Some children may only show mild respiratory distress at the beginning, but after a few hours, the condition may worsen due to chemical pneumonia.

3. Airway obstruction to barrel chest: thick amniotic fluid contaminated amniotic fluid can cause airway obstruction or semi-blocking after inhalation of airway. The two lungs often have a voice, a thick wet sound, and a medium, fine wet sound. The clinical manifestations of acute airway obstruction are wheezing breathing, cyanosis, and must be immediately recruited by the trachea. In children with airway obstruction, due to gas retention, the anteroposterior diameter of the thorax increases with barrel chest, shallow breathing, decreased breathing sound or wet sound and wheezing. If the clinical symptoms suddenly deteriorate, the pneumothorax should be suspected, and the incidence rate is 20% to 50%. When the pneumothorax occurs, the cyanosis and dyspnea may increase suddenly.

4. Continuous pulmonary hypertension: some children may have persistent pulmonary hypertension (see continuous pulmonary hypertension), because there are a large number of right to left shunt, in addition to causing severe blue ultraviolet, heart enlargement, liver enlargement and other heart failure.

5. Others: Children with severe meconium aspiration and acute hypoxia often have central nervous system symptoms such as dysfunction, increased intracranial pressure, convulsions, and polycythemia, hypoglycemia, hypocalcemia, and pulmonary hemorrhage.

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