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• W2022647576 abstract "Intrapartum hypoxia leading to neonatal hypoxic-ischemic encephalopathy (HIE) is the leading cause of cerebral palsy targeted in malpractice law suits, because it is believed that the health care providers may avert the neurologic damage by intervention for fetal heart rate patterns that are believed to indicate hypoxia. Unfortunately, because of the high costs involved with later care of such damaged children, it is common for plaintiffs' attorneys to be willing to pursue actions against physicians and hospitals even when causation criteria are not fully met. The possibility of large judgments awarded by juries often leads to the settlement of such cases by physicians and hospitals. This study helps to further clarify the basis for the American College of Obstetricians and Gynecologists-American Academy of Pediatrics, (ACOG-AAP) criteria necessary to attribute later cerebral palsy to hypoxia proximate to birth of term infants.See related article, page 587 See related article, page 587 The authors should be congratulated on an extensive review of factors associated with HIE and the contribution of HIE to later death and neurologic damage. Clearly, over the years, there has been decreasing attribution of HIE to later cerebral palsy and, although at one time the majority of neurologic and developmental abnormalities in children were attributed to hypoxia preceding birth,1Little W.J. On the influence of abnormal parturition, difficult labors, premature birth and asphyxia neonatorum on the mental and physical condition of the child, especially in relation to deformities.Trans Obstet Soc London. 1862; 3: 293Google Scholar, 2Quilligan E.J. Paul R.H. Fetal monitoring: is it worth it.Obstet Gynecol. 1975; 45: 96-100PubMed Google Scholar the authors' findings of 14.5% infants with later cerebral palsy attributable to hypoxia-ischemia during labor at term would appear to be a reasonable estimate. A proportion of cases of cerebral palsy have evidence of hypoxia preceding labor, and it may be difficult to apportion cause when hypoxia was also present intrapartum.3Freeman R.K. Intrapartum fetal monitoring—a disappointing story.N Engl J Med. 1990; 322: 624-626Crossref PubMed Scopus (101) Google Scholar It should be pointed out that the majority of cases of cerebral palsy are found in children born prematurely, and the myriad factors involved in neurologic damage in this group are even more diverse than with term infants. When evaluating cerebral palsy, one finds that there may be more than 1 causative factor. The criteria promulgated by ACOG and AAP4American College of Obstetricians and Gynecologists and American Academy of PediatricsNeonatal encephalopathy and cerebral palsy: defining the pathogenesis and pathophysiology. ACOG, Washington, DC2003Google Scholar to attribute intrapartum hypoxia as a cause of neonatal encephalopathy and later cerebral palsy include: (1) an umbilical arterial pH of ≤ 7.0, (2) early onset of moderate-to-severe neonatal encephalopathy, (3) a diagnosis of cerebral palsy with quadriparesis of the spastic or dyskinetic type, and (4) the absence of other possible causes. These 4 required criteria have been questioned as being too restrictive. Perhaps one reason for this is that other factors, either alone or in combination with hypoxia, may be involved. In 1955, Eastman and DeLeon5Eastman N.J. DeLeon M. The etiology of cerebral palsy.Am J Obstet Gynecol. 1955; 69: 950-961Abstract Full Text PDF PubMed Google Scholar reviewed the obstetric records of 96 cases of cerebral palsy delivered at the Johns Hopkins Hospital and compared them with 11,195 records from infants born at the same hospital between 1945 and 1949. He noted that the incidence of intrapartum fever was 7 times more likely to be observed in mothers of children who later were diagnosed with cerebral palsy. He also noted that prolonged neonatal fever for greater than 3 days was 300 times more likely in birth records of children with cerebral palsy than in the controls. Eastman opined that fever during labor may be a finding associated with difficult or prolonged labors and may not actually signal infection as a cause of later cerebral palsy. Recent attention has focused on maternal fever caused by chorioamnionitis and the fetal inflammatory response syndrome (FIRS), which is believed to be a cause of ischemic brain damage mediated by proinflammatory cytokines. There is evidence that hypoxia and FIRS may be additive, and perhaps cases of cerebral palsy that do not meet the umbilical arterial pH ≤ 7.0 threshold may result from a combination of hypoxia and FIRS. In fact, there may be a final common pathway involving proinflammatory cytokines as the damaging agents in both situations.6Hermansen M.C. Hermansen M.G. Perinatal infections and cerebral palsy.Clin Perinatol. 2006; 33: 315-333Abstract Full Text Full Text PDF PubMed Scopus (57) Google Scholar It would be of interest to see what proportion of cerebral palsy cases not meeting the ACOG-AAP criteria for damaging intrapartum hypoxia-ischemia had intrapartum maternal fever and/or prolonged neonatal fever. It is obvious that an understanding of causative intrapartum factors leading to later cerebral palsy is complex. When litigation is involved, we would be better served if we had specialized courts in which judges were more knowledgeable and better able to exclude evidence based on junk science from jury deliberations. If medical expert witnesses were retained by the court rather than the adversarial lawyers in such law suits, they could be of better assistance to the court in understanding the actual evidence for or against intrapartum causation of later cerebral palsy. Certainly, substandard care can lead to intrapartum hypoxia resulting in later cerebral palsy, and it appears that often the substandard care is attributable to system failures frequently caused by poor communication between providers. Recently, there have been numerous initiatives aimed at “crew resource management” similar to safety programs used in the airlines. One large hospital system has used protocols aimed at uniform approaches to such things as oxytocin usage, operative vaginal delivery, shoulder dystocia, the use of magnesium sulfate, and combined certification of physicians and nurses through a web-based interactive fetal monitoring course. They have shown dramatic decreases in malpractice claims paid, decrease in cesarean section rates, and overall fewer adverse outcomes.7Clark S.J. Belfort M.A. Byrum S.L. et al.Improved outcomes, fewer cesarean deliveries, and reduced litigation: results of a new paradigm in patient safety.Am J Obstet Gynecol. 2008; 199: 105.e1-105.e7Abstract Full Text Full Text PDF PubMed Scopus (137) Google Scholar Thus, although tort reform, as described previously, would help to focus litigation related to causation, the newer initiatives focused on communication and better outcomes are making inroads on liability caused by substandard practice. A systematic review of the role of intrapartum hypoxia-ischemia in the causation of neonatal encephalopathyAmerican Journal of Obstetrics & GynecologyVol. 199Issue 6PreviewThe object of this review was to determine the incidence, morbidity, and mortality of an umbilical arterial pH < 7.0; the incidence of hypoxic-ischemic encephalopathy; and the proportion of cerebral palsy associated with intrapartum hypoxia-ischemia in nonanomalous term infants. A systematic review of the English language literature on the association between intrapartum hypoxia-ischemia and neonatal encephalopathy was conducted by using Pubmed and Embase. For nonanomalous term infants, the incidence of an umbilical arterial pH < 7.0 at birth is 3.7 of 1000, of which 51 of 297 (17.2%) survived with neonatal neurologic morbidity, 45 of 276 (16.3%) had seizures, and 24 of 407 (5.9%) died during the neonatal period. Full-Text PDF" @default.
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• W2022647576 title "Medical and legal implications for necessary requirements to diagnose damaging hypoxic-ischemic encephalopathy leading to later cerebral palsy" @default.
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