There are a few different ways that meconium aspiration develops respiratory and other issues in fetuses and infants, such that the fetus or baby develops this clinical Syndrome. The following are all different types of respiratory difficulties caused by the inhalation/presence in the lungs while the fetus was still in the womb, or during or after the baby’s delivery.
Meconium is a viscous and thick substance, and the thicker it is, the more likely the fetus or baby can develop more severe complications.
One of the ways that a fetus or baby can develop respiratory complications from inhaling meconium is when the meconium blocks the fetus’ airways. Meconium can block the airways completely or partially.
Such airway blockage can result in “ball valve obstruction” or atelectasis. These are terms used when airways allow air to come into the lungs but not to exit, causing the build-up of excess air, possible hyper-expansion, or, in the case of atelectasis, the collapse of the lung(s). Any build up can create pressure in the airways, and such pressure can rupture alveoli, cause pulmonary air leakages, or allow air into the soft tissues, which can cause interstitial emphysema. Extreme ball valve obstruction or atelectasis can create even more severe problems such as tension pneumothorax (excess buildup of air between the lungs and chest cavity), which can cause circulatory issues and even potentially cardiac arrest. Other serious problems of any airway obstruction include persistent pulmonary hypertension (which increases the workload on the heart) and pneumomediastinum (the problematic presence of air in the organs in the chest cavity other than the lungs).
Non-specific Cytokine Release
MAS can also be triggered when a baby’s aspiration of meconium results in the release of various cytokines. Cytokines are particular substances secreted by immune cells and act as the “mediators” or “communicators” between different types of cells that, among other things, manage the body’s immune system response. Aspiration of meconium can trigger the release of cytokines because the body recognizes meconium as a threat. The cytokine release is such that the fetus or baby can develop a systemic inflammatory response, which in turn induces the clinical syndrome.
Inactivation of Surfactant
Another way that MAS can occur after the entry of meconium into a baby or fetus’s lungs is when the meconium prevents surfactants in baby’s respiratory system from activating. Pulmonary surfactants are certain chemicals and substances that line the surface of the lung, and which help ensure proper lung function by increasing the lung’s ability to stretch and expand, preventing lung collapse (atelectasis, see above), and fixing collapsed airways. When these surfactants are not activated (because of, for example, the presence of meconium), lung functioning can be impaired which can create various respiratory difficulties.
Meconium aspiration syndrome can also develop because meconium in the fetus’ lungs triggers chemical pneumonitis. Further, the cytokines released when the baby’s body detects meconium can also trigger chemical pneumonitis. Chemical pneumonitis is defined as inflammation as a result of inhaling certain chemicals or chemical fumes, and certain components of meconium can create this effect. Chemical pneumonitis can cause and exacerbate breathing difficulties, the severity of which depends on the amounts and types of chemicals inhaled.
Persistent Pulmonary Hypertension
As noted above in airway blockages, as a result of the stress in the uterus that either (or both) caused the meconium aspiration and/or was caused by the meconium aspiration, some babies with meconium in their lungs develop persistent pulmonary hypertension. This persistent pulmonary hypertension can make it even more difficult for the body to get sufficient oxygen flowing in the bloodstream.