Meconium aspiration syndrome
Meconium aspiration syndrome (MAS) is a severe respiratory disorder in children due to meconium entering the lower respiratory tract.
Meconium is the original stool, a dark greenish substance that fills the large intestine. Meconium contains: glycoprotein, in particular sialomucopolysaccharide, gastrointestinal secretions, water, bilirubin, bile pigments, amniotic fluid and digested epithelium with hair.
The incidence of meconium aspiration syndrome varies between 2–3%, while meconium staining of amniotic fluid is observed in 9–15% of parturients. In post-term pregnancy, the incidence of meconium in amniotic fluid is 20–30%. The detection rate of meconium in amniotic fluid during premature pregnancy accounts for only 2–4%.
A special scale is used to evaluate meconium: the criteria are consistency and color.
Meconium score on a scale of 2B–3B is a prognostically unfavorable outcome, since the risk of MAS and cerebrovascular accident due to hypoxia increases.
The passage of meconium into the amniotic fluid usually occurs at 37 weeks, but cases of passage up to 34 weeks have been described in the literature. The frequency of occurrence directly correlates with gestational age, this is due to myelination of nerve fibers, increased parasympathetic tone and an increase in the concentration of motilin, which directly affects intestinal motility. Also, the passage of meconium is influenced by the weight of the fetus more than 3500 g; with a fetal weight of less than 2000 g, the passage of meconium is not typical.
There is no single pathogenetic theory of meconium passage; some authors, for example J. Neu, are of the opinion that the passage of meconium is an absolutely physiological process, which indicates the maturity of the gastrointestinal tract. In the FC Miller studies, hypoxia was analyzed in the presence of clear amniotic fluid and the absence of meconium impurities. The fetus influences the exchange of amniotic fluid through urination, secretion of the respiratory system and ingestion of amniotic fluid.
Some authors associate the passage of meconium with activation of the vagus during periodic umbilical cord pressure. A number of researchers are of the opinion about the effect of intestinal overdistension on the passage of meconium.
With asphyxia, the following cascade of reactions is triggered: as a result of spasm of the mesenteric vessels, intestinal motility increases, which in turn leads to relaxation of the anal sphincter and further release of meconium. At the same time, the entanglement of the umbilical cord around the neck leads to activation of the vagus and increased passage of meconium in the absence of asphyxia.
Risk factors for SAM include: extragenital pathology and complications of the gestational period, which lead to fetoplacental insufficiency, post-term pregnancy for more than 40 weeks, delayed birth, labor anomalies, prolonged labor in women with chronic fetal hypoxia, large fetus, irrational use of uterotonic drugs.
The main initiating link in the pathogenesis of SAM is the intrauterine penetration of meconium fluid into the respiratory tract below the glottis. In utero, the fetal airways are filled with fluid, which participates in the formation of amniotic fluid. In this case, the fetus produces respiratory movements with a closed glottis, which prevents the amniotic fluid from entering the lungs. Due to the opening of the sphincter mechanism, pulmonary fluid is swallowed.
Intrauterine breathing of the fetus has a number of features: firstly, the absence of surface tension, secondly, the absence of gas exchange in the lungs, thirdly, due to the horizontal position of the ribs in the fetus, the chest is constantly in a state of inspiration, and the high position of the diaphragm limits excursion movements of the chest.
A change in the nature of the fetal respiratory activity is one of the early markers indicating a violation of the fetal condition. Acute hypoxia is accompanied by a decrease in the depth of inspiration and the occurrence of shortness of breath.
An increase in intrauterine pressure due to increased labor provokes a diving reflex in the fetus, as when a person is immersed under water, due to the redistribution of blood flow and a slowdown in heart contractions, manifested by type 1 decelerations. In this case, the reflex activity of the central nervous system is suppressed, resulting in type 2 decelerations.
As a result of severe chronic antenatal hypoxia, the onset of labor leads to an increase in intrauterine pressure, which, together with negative pressure in the pleural cavity with an open glottis, creates conditions for the penetration of meconium water into the fetal respiratory tract.
One of the consequences of meconium aspiration syndrome is early mechanical obstruction of the airways, which after 48 hours forms chemical pneumonitis. A more serious complication is complete blockage of the airways, which contributes to the formation of subsegmental atelectasis. This leads to a decrease in ventilation-perfusion ratios, resulting in a decrease in the diffusion capacity of the lungs with increasing resistance of the pulmonary tract. The result of increased breathing and uneven ventilation are ruptures of the alveoli, which will additionally provoke air leakage from the lungs.
Prevention of SAM is careful monitoring of women at risk, especially in the third semester, which includes a functional assessment of the condition of the fetus, including assessment of the reactivity of the cardiovascular system, motor activity, frequency and type of DD and assessment of muscle tone.
Sources:
- Yeh TF Meconium Aspiration Syndrome: The Core Concept of Pathophysiology during Resuscitation //Neonatal Medicine. – 2021. – T. 24. – No. 2. – pp. 53-61.
- Chettri S., Bhat BV, Adhisivam B. Current concepts in the management of meconium aspiration syndrome //The Indian Journal of Pediatrics. – 2021. – T. 83. – No. 10. – pp. 1125-1130.
- Lee JH et al. Meconium aspiration syndrome: a role for fetal systemic inflammation //American journal of obstetrics and gynecology. – 2021. – T. 214. – No. 3. – P. 366. e1-366. e9.
- Oliveira CPL et al. Meconium aspiration syndrome: risk factors and predictors of severity //The Journal of Maternal-Fetal & Neonatal Medicine. – 2021. – T. 32. – No. 9. – pp. 1492-1498.
- Lindenskov PHH et al. Meconium aspiration syndrome: possible pathophysiological mechanisms and future potential therapies //Neonatology. – 2015. – T. 107. – No. 3. – pp. 225-230.
Aspiration syndrome. Aspiration of amniotic fluid. Meconium aspiration syndrome. Aspiration of milk.
Aspiration of amniotic fluid
During the prenatal period, amniotic fluid is present in the fetal respiratory tract before the tracheal bifurcation. When the fetal respiratory center is excited, aspiration occurs (the contents of the respiratory tract penetrate all the way to the alveolar ducts), which can lead to the shutdown of individual segments of the lungs and contribute to the development of hyaline membrane disease, pulmonary edema, and an infectious process. Clinically, the child exhibits signs of SDD: many moist rales of various sizes are heard over the lungs against the background of weakened breathing. X-rays of the lungs reveal focal shadows.
Treatment.
Timely sanitation of the respiratory tract. If pneumonia develops, use antibacterial therapy.
Meconium aspiration syndrome
Meconium aspiration syndrome occurs in 1-2% of newborns, more often in post-term infants, those born at term in a state of hypoxia, and in children with intrauterine growth retardation. Asphyxia and other forms of intrauterine stress can cause increased intestinal motility and the passage of meconium into the amniotic fluid. When viscous meconium enters the respiratory tract, it causes the development of SDR, obstruction and a pronounced inflammatory reaction with the development of severe respiratory failure. In case of meconium aspiration syndrome, areas of large, irregularly shaped shadows alternating with areas of increased transparency are identified by x-ray. The lungs appear emphysematous, the dome of the diaphragm is flattened.
Treatment. If the meconium is thick, in the form of clumps, the nose and oropharynx should be cleared of it before the chest exits the birth canal. Immediately after birth, as with aspiration of amniotic fluid, endotracheal intubation is performed and the contents from the trachea are sucked out until it is completely cleared. Removing swallowed meconium from the stomach prevents re-aspiration. All children are given oxygen therapy, sometimes up to long-term mechanical ventilation (in severe cases). Antibiotic therapy is indicated for meconium aspiration syndrome.
Milk aspiration
Aspiration of milk is associated with incoordination of swallowing movements, most often caused by the immaturity of the neuromuscular system. Premature babies are susceptible to this aspiration, since their stomach capacity is small and the evacuation of its contents is slow. Milk aspiration may develop within a few weeks of birth. In case of repeated aspirations, choking or coughing during feeding, it is necessary to exclude anatomical defects (tracheoesophageal fistula, esophageal atresia, etc.). The entry of milk into the lungs causes attacks of apnea and cyanosis. Possible airway obstruction.
Treatment.
After aspiration, it is necessary to suck out the contents from the nasal cavity and oropharynx and trachea as quickly as possible. In the future, to prevent aspiration, the baby should be fed in the right lateral position. When inflammatory changes develop, broad-spectrum antibiotics are prescribed. Source: Children's diseases. Baranov A.A. // 2002.
What is meconium aspiration?
The frequency of meconium staining of amniotic fluid ranges from 8 to 20% of the total number of births. In 50% of these children, meconium is found in the trachea and bronchi, but only 1/3 of newborns develop meconium aspiration syndrome.
Etiology
Hypoxia and other forms of intrauterine fetal stress cause increased intestinal motility, relaxation of the external anal sphincter, and passage of meconium.
The first respiratory movements of the fetus are detected already at the 11th week of the gestational period. Periods of breathing rarely last more than 10 minutes and alternate with apnea lasting up to 1-2 hours. Hypoxia leads to the appearance of premature deep “sighs”, during which meconium amniotic fluid enters the respiratory tract. The movement of meconium into the small airways occurs quickly, within an hour after birth.
The pathogenesis of respiratory disorders in aspiration syndrome is primarily associated with impaired airway patency and a mechanical obstacle to filling the lungs with air. In this case, complete or partial obstruction with the development of the valve mechanism may occur in any part of the respiratory tract. With complete obstruction of the airways, air cannot penetrate into the underlying sections, resulting in the collapse of areas of the lung with the formation of subsegmental atelectasis. The valve mechanism of obstruction is that when you inhale, air, flowing around an obstacle, enters the distal parts of the respiratory tract, and when you exhale, the obstacle completely blocks the lumen of the bronchus and does not allow air to escape, since the lumen of small airways increases with inhalation and decreases with exhalation.
The retention and accumulation of air below the site of obstruction leads to overstretching of the alveoli, the formation of “air traps” and emphysema. As a result, lung compliance decreases, ventilation-perfusion ratios deteriorate, and intrapulmonary shunting and airway resistance increase. Against the background of increased breathing and uneven ventilation, rupture of the alveoli may occur, leading to air leakage from the lungs.
In addition to mechanical obstruction, the presence of meconium, containing bile salts and active proteolytic enzymes, causes chemical inflammation of the bronchial and alveolar epithelium. This creates the preconditions for the development of bacterial flora and the progression of tracheobronchitis and pneumonia.
Uneven ventilation, disruption of ventilation-perfusion relationships and associated pneumonitis lead to the development of hypoxemia, hypercapnia and acidosis.
When hypoxia and acidosis occur, pronounced spasm of the pulmonary vessels develops, which leads to the development of secondary pulmonary hypertension. The pressure in the pulmonary artery can reach the systemic level and even exceed it. Fetal communications do not close, but on the contrary, the shunting of blood through the ductus arteriosus and the oval window increases. The blood shunt from right to left can reach 70 - 80%.
Pulmonary hypertension, in turn, has a negative effect on the function of the right and then the left ventricles of the heart. An acute increase in right ventricular afterload is accompanied by a decrease in ejection fraction, which leads to a decrease in left ventricular preload and cardiac output.
According to various obstetric hospitals, the presence of meconium in amniotic fluid is recorded in 2–10% of cases, but massive meconium aspiration syndrome (MAC) is 5–10 times less common.
What is the danger of meconium aspiration in newborns?
Aspirated meconium causes an inflammatory reaction in the trachea, bronchi, and pulmonary parenchyma due to the lipids it contains, proteolytic enzymes and its increased osmolarity. Obstruction of the deep airways, “air traps,” and atelectasis also occur due to bronchial obstruction and inactivation of surfactant, which leads to collapse of the alveoli during exhalation. In addition to chemical inflammation and atelectasis, edema, perifocal emphysema with the development of pulmonary hypertension, pneumothorax and other types of “air leak” occur in the lungs.
The results of recent studies have revealed a high level of immunoreactive endothelin-1 in the blood of newborns with meconium aspiration, which has a pronounced vasoconstrictor effect, which contributes to the development of pulmonary hypertension and pulmonary vascular hyperreactivity. The mortality rate for severe forms of meconium aspiration until recently was 50%. Currently, due to the improvement of methods of primary resuscitation and the use, if necessary, of high-chopper ventilation, mortality has significantly decreased.
If the meconium is thick, in the form of clumps, you should clear it from the newborn’s nose and oropharynx before the chest exits the birth canal. Immediately after birth, as with aspiration of amniotic fluid, endotracheal intubation is performed and the contents from the trachea are sucked out until it is completely cleared. Removing swallowed meconium from the stomach prevents re-aspiration. All children are given oxygen therapy, sometimes up to long-term artificial ventilation (in severe cases). Meconium aspiration in newborns is treated with antibiotic therapy.
