الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
One in every 7 pregnancies has MSAF and, of these cases, approximately 5% develop MAS. Meconium directly alters the amniotic fluid, reducing antibacterial activity and subsequently increasing the risk of the perinatal bacterial infection. However, the most severe complication of meconium passage in utero is the perinatal aspiration of stained amniotic fluid (before, during, or immediately after birth) i.e., MAS.
Meconium aspiration may occur if the fetus is in distress, leading to a gasping breathing pattern. This aspiration induces hypoxia via four major pulmonary effects: airway obstruction, surfactant dysfunction, chemical pneumonitis, and PHN. In the industrialized world, approximately 10% of newborns who are born through MSAF develop MAS.
Of note, normal meconium is assumed to be sterile and consists of self-structures only. However, as meconium is stored inside the intestines, and is partly unexposed to the immune system when it becomes aspirated the innate immune system recognizes as a foreign and dangerous substance. The immune system, which is present at birth, responds within minutes with a low specificity and no memory in order to try to eliminate microbes.
This assumed chemical pneumonitis caused by meconium was first documented in 1978 when leukocyte infiltration was demonstrated in rabbit lungs after meconium aspiration. As a result, this altered internal response pattern of the defense systems in such animal models was taken into consideration on the pathophysiology in clinical MAS. Furthermore, apoptosis, cellular infiltration, increased airway responsiveness or increased cytokine concentrations in bronchoalveolar lavage of animal lungs instilled with meconium have later been demonstrated in numerous studies.
Although most infants with MAS have complete recovery of pulmonary function, this disease still has significant morbidity and mortality. Survivors may still have a slightly higher incidence rate of respiratory infections in the first year of life because the lungs are still in recovery. Severely affected infants have an increased risk of developing reactive airway disease (RAD) in the first 6 months of life. Some cases may develop chronic lung disease from intense pulmonary interventions.
Meconium aspiration syndrome is the most common cause of PHN, and when present, PHN can contribute directly and significantly to the morbidity and mortality of MAS. Unfortunately, the degree of PHN is not related to the degree of aspiration evident on chest roentgenograms. Therefore, even vigorous initially well infants with MSAF who have normal chest X-rays are susceptible to develop progressive hypoxic respiratory failure either immediately or few hours after delivery. This can be secondary to even minimal meconium aspiration with its consequences of inflammation and PHN.
Although the echocardiography is the gold standard for PHN diagnosis, new studies found that serum BNP is a useful biomarker in predicting and evaluating the course of PHN of the newborn and the effectiveness of its treatment. However, echocardiography is still the only presently feasible bedside clinical investigation used to confirm PHN diagnosis and to monitor disease progression