Perinatal asphyxia is caused by lack of oxygen delivery (hypoxia) to end organs due to an hypoxemic or ischemic insult occurring in temporal proximity to labor (peripartum) or delivery (intrapartum). Hypoxic–ischemic encephalopathy is the clinical manifestation of hypoxic injury to the brain and is usually graded as mild, moderate, or severe. The search for useful biomarkers to precisely predict the severity of lesions in perinatal asphyxia and hypoxic–ischemic encephalopathy (HIE) is a field of increasing interest. As pathophysiology is not fully comprehended, the gold standard for treatment remains an active area of research. Hypothermia has proven to be an effective neuroprotective strategy and has been implemented in clinical routine. Current studies are exploring various add-on therapies, including erythropoietin, xenon, topiramate, melatonin, and stem cells. This review aims to perform an updated integration of the pathophysiological processes after perinatal asphyxia in humans and animal models to allow us to answer some questions and provide an interim update on progress in this field.

Objective: To evaluate natural history of fetuses congenital diaphragmatic hernia (CDH) prenatally diagnosed in countries where termination of pregnancy is not legally allowed and to predict neonatal survival according to lung area and liver herniation. Methods:Prospective study including antenatally diagnosed CDH cases managed expectantly during pregnancy in six tertiary Latin American centres. The contribution of the observed/expected lung-to-head ratio (O/E-LHR) and liver herniation in predicting neonatal survival was assessed.Results: From the total population of 380 CDH cases, 144 isolated fetuses were selected showing an overall survival rate of 31.9% (46/144). Survivors showed significantly higher O/E-LHR (56.5% vs 34.9%; P < .001), lower proportion of liver herniation (34.8% vs 80.6%, P < .001), and higher gestational age at birth (37.8 vs 36.2 weeks, P < 0.01) than nonsurvivors. Fetuses with an O/E-LHR less than 35%

This study on fetuses with isolated left-sided congenital diaphragmatic hernia (CDH) and severe pulmonary hypoplasia provides evidence that fetal endoscopic tracheal occlusion may be of benefit in improving neonatal survival in settings with neonatal intensive care limitations, such as unavailability and/or inexperience in the use of extracorporeal membrane oxygenation therapy, and thus a high neonatal mortality rate. What are the clinical implications of this work? The outcomes reported in this study may be of interest to centers in which termination of pregnancy is illegal and neonatal management is considered suboptimal, as they demonstrate that fetal intervention in experienced fetal surgery centers represents an improvement in neonatal survival for fetuses with isolated severe left-sided CDH.

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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.