{'fraction_non_alphanumeric': 0.015435501653803748, 'fraction_numerical': 0.0, 'mean_word_length': 5.648351648351649, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 1, 'zh_pornsignals.json': 0}}
Meconium aspiration syndrome in mammals.

Abstract
 Meconium aspiration syndrome (MAS) is a common obstetric and paediatric problem and is one of the most common causes of neonatal respiratory distress. The pathophysiology of MAS is complex. The underlying mechanism of MAS is fetal hypoxia which causes redistribution of fetal blood, increased intestinal peristalsis and relaxation of the anal sphincter in utero, leading to the passage of meconium into the amniotic fluid. If hypoxia is severe and persistent, the fetus gasps for air, but instead aspirate amniotic fluid contaminated with meconium. Aspiration of meconium produces multiple physiological and structural changes in the neonatal lung which relates partially to the amount of aspirated meconium. The structural and functional sequels of MAS include airways obstruction, atelectasis, chemical pneumonitis, hypoxemia, acidosis, pulmonary hypertension and occasionally death. MAS survivors can develop airway hyperreactivity and nervous sequelae. The morbidity and mortality of human MAS have declined the last decades because of new therapies but remains a major paediatric problem. Although the prevalence and significance of MAS in veterinary medicine have been poorly investigated, there is ample evidence that intrapartum hypoxia in animals also causes meconium expulsion, amniotic staining and aspiration. The lungs of affected animals showed airway obstruction, focal atelectasis and alveolitis. Meconium staining of the skin and aspiration are indicators of fetal or perinatal hypoxia and postnatal respiratory distress in domestic animals. Experimental models have been developed to study the pathogenesis of MAS in laboratory animals. This review focuses on the current concepts of the pathophysiology of MAS in human and veterinary medicine.