Ventilatory support and intubation are carried out as needed (Wyckof, 2015). Because some aspects of meconium aspiration syndrome are caused by surfactant deficiency, replacement therapy is beneficial (N atarajan, 20 16a). Also, inhaled corticosteroids may ameliorate the severity (Garg, 2016). Extracorporeal membrane oxygenation-ECMO-therapy is reserved for neonates who remain poorly oxygenated despite maximal ventilatory assistance (Hirakawa, 2017). In their review of randomized trials, EI Shahed and colleagues (2014) found that surfactant replacement may reduce the need for ECMO but did not lower the mortality rate. he proportion that requires ECMO treatment varies. In a report by Singh and coworkers (2009),r1.4 percent of7518 term newborns with the syndrome required such treatment, and these had a 5-percent mortality rate. Ramachandrappa and associates (2011) reported a higher mortality rate in late-preterm neonates with meconium aspiration compared with afected term newborns. Finally, pulmonary lavage with surfactant is being evaluated (Choi, 2012).
Few events evoke more apprehension in parents and obstetricians than the specter of "brain injury," which immediately
Diseases and Injuries of the Term Newborn 621 prompts concerns for disabling cerebral palsy and intellectual disability. Although most brain disorders or injuries are less profound, history has helped to perpetuate the more dismal outlook. In his irst edition of this textbook, Williams (1903) limited discussions of brain injury to those sustained from birth trauma. When later editions introduced the concept that asphyxia neonatorum was another cause of cerebral palsy, this too was linked to traumatic birth. Even as brain damage caused by traumatic delivery became uncommon during the ensuing decades, the belief-albeit erroneous-was that intrapartum events caused most neurological disability. his was a major reason for the escalating cesarean delivery rate beginning in the 1970s. Unfortunately, because in most cases the genesis of cerebral palsy occurs long before labor, this did little to mitigate risks for cerebral palsy (O'Callaghan, 2013).
These realizations stimulated scientiic investigations to determine the etiopathogenesis of fetal brain disorders, including those leading to cerebral palsy. Seminal observations include those of Nelson and Ellenberg (1984, 1985, 1986a), discussed subsequently. hese investigators are appropriately credited with proving that these neurological disorders are due to complex multifactorial processes caused by a combination of genetic, physiological, environmental, and obstetrical factors. Importantly, these studies showed that few neurological disorders were associated with peripartum events. Continuing international interest was garnered to codiy the potential role of intrapartum events. In 2000, a task force of the American College ofObstetricians and Gynecologists was appointed to study the �icissitudes of neonatal encephalopathy and cerebral palsy. he multispecialty coalition reviewed contemporaneous data and provided criteria to deine various neonatal brain disorders. heir indings were promulgated by the American Academy of Pediatrics and American College of Obstetricians and Gynecologists (2003).
Ten years later, a second task force of these organizations updated the indings (American College of Obstetricians and Gynecologists, 2014c). he 2014 Task Force findings are more circumspect in contrast to the earlier ones. Speciically, more limitations are cited in identiying cause(s) of peripartum hypoxic-ischemic encephalopathy (HIE) compared with other etiologies of neonatal encephalopathy. he 2014 Task Force recommends multidimensional assessment of each afected infant.