Meconium Aspiration Syndrome - Causes, Symptoms, Pathophysiology, Diagnosis, and Treatment

Introduction

The first newborn's feces, or stool, is called meconium. Meconium aspiration syndrome happens when a newborn breathes amniotic fluid and meconium into the lungs shortly after birth. A significant cause of severe illness and infant death, meconium aspiration syndrome affects five to ten percent of newborns. It often happens when the fetus is under stress during birth, mainly if the baby is delivered past the due date.

What Are the Symptoms of Meconium Aspiration Syndrome (MAS)?

In most cases, newborns who have passed meconium into the amniotic fluid during labor and delivery do not breathe it into their lungs. Therefore, they will not have any signs or issues. However, babies that do inhale this fluid may have the following symptoms:

• The baby has cyanosis or bluish skin.

• Struggling to breathe (noisy breathing, grunting, using extra muscles to breathe, breathing rapidly).

• Not breathing (lack of respiratory effort or apnea).

• Amniotic fluid streaking or staining that is dark, greenish, or clearly shows meconium's presence.

• The infant's limpness at birth (abnormally low muscle tone).

What Are the Causes of Meconium Aspiration Syndrome?

Meconium is the first feces a newborn baby passes shortly after delivery before the infant begins to eat and absorb milk or formula. The infant may occasionally pass meconium while still in the uterus. This may occur when a baby is under stress due to a reduction in blood and oxygen flow. This frequently results from issues with the placenta or umbilical cord. The baby may breathe in the meconium once it has been passed into the amniotic fluid surrounding them. This could occur:

• While the fetus is still within.

• During labor.

• Instantly following birth.

• Right after birth, the meconium can obstruct the baby's airways. Swelling (inflammation) in the newborn baby's lungs after birth may result in breathing issues.

Risk elements that could stress the unborn child include:

• If the pregnancy lasts well past the due date, the placenta will "age."

• Decreased oxygen supply to the baby inside the uterus.

• The mother's diabetes during pregnancy (gestational diabetes).

• Labor that is difficult or lengthy.

• Pregnancy-related high blood pressure in the mother.

• A placental infection that affects the unborn child.

What Is the Pathophysiology of Meconium Aspiration Syndrome?

The pathophysiology of meconium aspiration syndrome is

• By the 10th week of life, the fetal intestines start to produce meconium, which comprises gastrointestinal, hepatic, and pancreatic secretions, cellular debris, swallowed amniotic fluid, lanugo, vernix caseosa, and blood. The amount of meconium gradually increases until it reaches 200 grams at birth. In utero, the passage is rare until term due to weak peristalsis, good anal sphincter tone, low amounts of motilin, and a cap of viscous meconium in the rectum, among other factors. Acidosis and hypoxia in pregnancy trigger a vagal response, which increases peristalsis and relaxes the anal sphincter, allowing meconium to pass. Therefore, the parasympathetic nervous system must be in good working order for meconium to pass, making it a maturational event and uncommon before term. Although the passage of meconium may be a physiological occurrence linked to growing gastrointestinal maturity and rising motilin levels, it can also result from acute and chronic acidosis and hypoxemia, with post-term and depressed fetuses being more likely to aspirate meconium.

• Factors Influencing Meconium Aspiration Syndrome - MAS's clinical characteristics correlate with meconium viscosity, with thick meconium being more closely tied to problems. This heavy meconium can clog the airways, causing atelectasis and ventilation-perfusion mismatch, or it can partially block the airways, causing ball valve air trapping. These obstructive characteristics result in the classic radiological image of areas of atelectasis and consolidation mixed with hyperexpanded zones and air leaks. By suppressing oxidative burst and phagocytosis, meconium harms neutrophil activity and causes an inflammatory response when it enters the airways. Others have discovered that meconium causes lung damage by triggering alveolar macrophages, which in turn causes these cells to produce more superoxide anions. Infants that aspirated meconium had higher levels of inflammatory cytokines in their bronchoalveolar lavage (BAL), which suggests that meconium can trigger the generation of inflammatory cytokines in utero. The presence of bile salts has been linked to surfactant displacement, type 2 pneumocyte damage, and subsequent surfactant deficit.

• Consequences of Meconium Aspiration Syndrome - These pathways culminate in pulmonary vasoconstriction, causing hypoxemia, acidosis, and hypercapnia. After that, pulmonary hypertension develops, aggravating hypoxemia and acidosis and starting a vicious cycle. In severe cases, the meconium from the airways absorbs and is expelled in urine, giving the liquid a turbid green color. Both in-utero gasping and postpartum aspiration with the baby's first breaths can result in meconium aspiration. It can be challenging to determine which mechanism was to blame in a given case. Infants that experience a more severe clinical course are more likely to aspirate while still in the womb, be depressed at birth, and experience respiratory distress at a young age.

How Is Meconium Aspiration Syndrome Diagnosed?

The different diagnostic methods for meconium aspiration syndrome are

• The fetal monitor may detect a sluggish heart rate before delivery.

• Meconium can be found in the amniotic fluid at birth. The most reliable test to look for potential meconium aspiration is using a laryngoscope to examine for meconium staining on the vocal cords.

• Abnormal breath sounds can be heard through a stethoscope, particularly coarse, crackly noises.

• A blood gas study reveals low blood acidity, low oxygen levels, and high carbon dioxide levels.

• The lungs may seem streaky or spotty on a chest X-ray.

How Is Meconium Aspiration Syndrome Managed?

The various management options are

Obstetrical Management:

• Fetal Monitoring: All labor and delivery attendants place a high premium on evaluating the status of the fetus. The high indication false positive rate complicates this judgment, though. Researchers have examined the connections between Apgar scores, umbilical cord pH, meconium-stained amniotic fluid (MSAF), and cardiotocograph (CTG) abnormalities. While detecting fetal danger, CTG has been found to have a high false-positive rate. 50 % of the newborns with MAS were correctly predicted by thick meconium, late decelerations, tachycardia on CTG, cord pH 7.16, Apgar scores six at 1 and 5 minutes, and meconium in the trachea. The absence of these symptoms correctly predicted 97 % of healthy infants. CTG abnormalities and MSAF have a better predictive value for fetal well-being than danger because they are not significantly connected with Apgar scores or cord pH. However, additional measurements such as the fetal ECG, head compression force analysis, CPK-BB, and the difference in maternal and fetal temperatures may enhance our capacity for prediction.

• Amino Infusion - Initial studies suggested that amnioinfusion would lessen the frequency and severity of later MAS by decreasing the MSAF. Later research, however, revealed that there was no statistically significant decline in unfavorable fetal outcomes due to this surgery. Additionally, this method earned a bad reputation because of its heightened correlation with infection, surgical or instrument deliveries, and anomalies in the fetal heart rate. The current agreement is that there is no evidence to support the use of amnioinfusion for MSAF in clinical settings with typical perinatal surveillance. However, it lowers the prevalence of MAS when there is little prenatal surveillance, and MSAF problems are common.

Neonatal Management

• Airway Clearing: Aspiration risk may not be decreased by intrapartum suctioning of the oropharynx and nasopharynx. Therefore, normal intrapartum upper airway suctioning is no longer recommended for babies born into a meconium-filled environment. In addition, the former recommendation for subsequent tracheal toileting has been contested because only depressed neonates are at risk for MAS. As a result, this potentially dangerous surgery should not be performed on a healthy, active infant. Unfortunately, there are no means to identify these neonates at risk after birth, although it is anticipated that many children with meconium stains may acquire MAS. The distinguishing characteristics of fetal depression are hypotonia, absence or depressed breathing, and heart rates under 100 beats per minute. It is recommended to reintubate and do suction under oxygen cover if meconium is recovered and there is no bradycardia. Positive pressure breathing should be started in cases of bradycardia, and airway toileting should be addressed afterward. It is recommended to perform a gastric lavage after the baby has stabilized since small amounts of meconium may still be present in the stomach and be aspirated later. The elimination of stubborn secretions in the stabilized infant may be helped by saline lavage and physical chest therapy carried out with the necessary precautions.

• Ventilatory Support - Ventilatory support is necessary for one-third of newborns with MAS. In this condition, air leaks are a significant issue; hence high oxygen concentrations are initially required. If air trapping is not a significant issue, continuous positive airway pressure (CPAP) or bubble CPAP may be helpful. If CPAP is insufficient, mechanical ventilation has been recommended to keep blood gases within normal ranges by employing low inspiratory pressures, short inspiratory and lengthy expiratory durations, and rapid rates. While enhancing oxygenation, increasing positive end-expiratory pressure (PEEP) may aggravate air trapping and increase the risk of pneumothorax. Low PEEP, therefore, seems to be a better choice. This method prevents air leaks while reducing pulmonary hypertension, a significant issue in MAS. Neuromuscular blockade and sedation support mechanical ventilation.

• High-Frequency Ventilation (HFV) - HFV provides effective gas exchange at low tidal volumes for treating MAS. Infants with MAS were treated more frequently with HFV. It was also demonstrated that newborns receiving HFV required longer periods of respiratory assistance and had a greater mortality rate than infants receiving other types of ventilation. There was increased morbidity and death because HFV was used more as a rescue drug for infants most at risk of major negative outcomes.

• Liquid Ventilation - In lamb models of MAS, liquid ventilation with perfluorocarbons has been observed to improve survival, gas exchange, and hemodynamic stability. It is widely expected for credible scientific proof of human trials.

• Surfactant Therapy - Surfactant insufficiency in MAS is not a deficient state but rather a result of the changed function. Surfactant is displaced off the alveolar surface by meconium, which prevents it from lowering surface tension. Type 2 pneumocytes are directly cytotoxic when it is present in large amounts.

• Bronchoalveolar Lavage - According to recent findings, surfactant performs better as a lavage solution than saline. It has been suggested that using a surfactant or dextran mixture can help the surfactant's ability to remove meconium. According to some research, partial liquid ventilation after perfluorocarbon lavage is more effective than surfactant lavage alone.

• Inhaled Nitric Acid (INO) - Inhaled nitric oxide (INO) is the most successful treatment for the PPHN that frequently goes along with MAS. INO should be taken at 20 parts per million (PPM). To maximize INO delivery within the lungs, sufficient lung expansion is necessary for effective use. Therefore, when there is a severe parenchymal illness of the lungs, as in MAS, good ventilation is required to reap the full benefits of INO.

• Steroid Therapy - An inflammatory response to meconium in the airway is characterized by increased cell numbers and pro-inflammatory cytokines such as interleukin (IL-1B), IL-6, and tumor necrosis factor (TNF). Improved lung function has been reported to correlate with lower cytokine levels. It has been discovered that steroids administered via intravenous or inhaled methods reduce this inflammatory response and enhance lung function in infants with MAS.

• Extracorporeal Membrane Oxygenation (ECMO) - The effectiveness of ECMO in newborns with MAS has been thoroughly studied since the 1990s, and it effectively lowers neonatal mortality and severe impairment. According to another research, MAS patients experienced fewer problems than non-MAS patients receiving ECMO. These results encourage thinking about ECMO entrance requirements for MAS that are more flexible.

• Antibiotics - Meconium is almost usually sterile. However, numerous employees often give antibiotics to infants with MAS for the following reasons:

  1. Meconium causes chemical pneumonitis that mimics bacterial pneumonitis and has segmental atelectasis.
  2. An infection could trigger the passage of the meconium in utero.
  3. Meconium-induced in vitro acceleration of bacterial growth raises the possibility of superimposed bacterial infection in MAS.

• Supportive Care - These newborns are readily agitated, quickly turn hypoxemic, and become acidotic, so it is crucial to maintain an ideal temperature environment and slight handling. Blood volume and systemic blood pressure should be closely monitored. To keep the right-to-left shunt through the patent ductus arteriosus from occurring, it is essential to use systemic vasopressors, transfusion therapy, and volume expansion to keep systemic blood pressure higher than pulmonary blood pressure.

• Newer Therapies - PPHN (persistent pulmonary hypertension of the newborn), a frequent complication of MAS, has been treated with NO as a pulmonary vascular relaxing agent. Studies indicate that even though mortality rates did not change noticeably, prolonged oxygenation improvement with nitric oxide and greater oxygenation at start-up with ECMO may have significant therapeutic advantages. Using particular nitric oxide lung expansion techniques may lessen the need for invasive ECMO. Before being utilized frequently in this situation, novel pharmaceutical therapies like Pentoxifylline, which has an anti-inflammatory function that prevents meconium-induced polymorph degranulation, CC10, and Tezosentan, are awaiting trials with sufficient power.

Conclusion:

Most of the time, the prognosis is excellent, and there are no adverse side effects. Breathing issues could emerge in more severe situations, although they usually go away in two to four days. On the other hand, fast breathing could last for days. A baby who needs a breathing machine may see a more cautious outcome with severe aspiration. Brain damage could result from complications from meconium aspiration or a lack of oxygen in the uterus. Rarely aspirating meconium results in irreversible lung damage.