Answers are grounded in this paper and cite their sources.
Perinatal hypoxic-ischemic cerebral injury is an extremely important medicolegal problem for the practicing clinician.1 Brain injury that occurs during the perinatal period is one of the most commonly recognized causes of severe, long-term neurologic deficit in infants and children often termed cerebral palsy (CP).2 Despite marked improvements during the past several decades in perinatal practice aimed at improving care, the incidence of CP attributed to intrapartum asphyxia has remained essentially unchanged.3-6 This unanticipated observation appears to be attributable to several factors: 1. There is increasing evidence that in most cases the brain injury associated with CP is not related to perinatal events; 2. The improved survival of very low birth weight infants who are at great risk for developing hemorrhagic ischemic cerebral injury; 3. The limitations of current markers of perinatal stress used to identify those infants during labor at greatest risk for developing hypoxic-ischemic cerebral injury secondary to intrapartum asphyxia; and 4. The lack of specific postnatal interventions to treat infants who develop hypoxic-ischemic encephalopathy (HIE).3-17 These observations raise two critical issues. First, can those cases of CP, attributed to intrapartum asphyxia, be identified and possibly prevented, and second, what are the legal issues raised by such injury? To attempt to answer these two questions, I will review the current understanding of the major neuropathologic subtypes associated with perinatal hypoxic-ischemic cerebral injury, the postulated mechanism(s) and timing of such injury, strategies for identification of high-risk infants, and potential preventative strategies. CP may be defined as a nonprogressive motor disorder of early onset that affects approximately 2 to 3 per 1000 school-aged children.3-5 The origin of the brain injury resulting in CP may occur during the antepartum, peripartum, or postnatal period. However, the overwhelming evidence suggests that in approximately 70% to 80% of cases, CP is antepartum in origin. …
No takes yet. Share an insight, caveat, or question.
Jeffrey M. Perlman (1997) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: