COMPROMISED BABY
CAUSATION

  1.  

    Author Freeman JM; Nelson KB
    Institution Department of Neurology, Johns Hopkins Medical Institution, Baltimore, Maryland.
    Title Intrapartum asphyxia and cerebral palsy.
    Source Pediatrics 1988 Aug; 82 (2): p240-9
    ISSN 0031-4005
    Abstract Signs of presumed hypoxia/asphyxia of the fetus are not uncommon and can be detected during labor, in the delivery room, and during the early neonatal period. Virtually no single sign or symptom has sufficient correlation to enable prediction of later cerebral palsy with a reasonable degree of medical certainty. To attribute cerebral palsy to prior asphyxia with reasonable certainty, there must be evidence that a substantial hypoxic injury occurred and that a sequence of events ensued which would prove the clinical impact of that hypoxic insult. Few cases of cerebral palsy meet these criteria.

  2. Author Adamson SJ; Alessandri LM; Badawi N; Burton PR; Pemberton PJ; Stanley F
    Institution Department of Neonatology, Princess Margaret Hospital for Children, Subiacco, Western Australia.
    Title Predictors of neonatal encephalopathy in full-term infants [see comments]
    Source BMJ 1995 Sep 2; 311 (7005): p598-602
    ISSN 0959-8138
    Abstract OBJECTIVE--Preliminary investigation of the contribution of adverse antepartum and intrapartum factors to neonatal encephalopathy in singleton neonates born full term. DESIGN--Matched case-control study based on incidence density sampling of controls. SETTING--Two major teaching hospitals (one paediatric and one obstetric) and three peripheral maternity hospitals in Perth, Western Australia (population 1.2 million). SUBJECTS--89 cases, all the full term singleton neonates born during an eight month period in 1992 who fulfilled one or more of six criteria during the first week of life (seizures, abnormal conscious state, persistent hypertonia or hypotonia, and feeding or respiratory difficulties of central origin). One full term control infant without neonatal encephalopathy was matched to each case by sex, hospital of delivery, time of day and day of the week of birth, and maternal health insurance status. MAIN OUTCOME MEASURES--Odds ratio estimates of relative risk of neonatal encephalopathy associated with antepartum and intrapartum factors. RESULTS--Estimated incidence of moderate or severe encephalopathy in first week of life was 3.75 per 1000 full term live births. Thirteen cases and no controls had evidence suggestive of important intrapartum hypoxia, and in only five of these cases was the neurological condition at birth attributed to events during the intrapartum period. Univariate conditional logistic regression analysis identified significant differences between cases and controls for maternal vaginal bleeding in pregnancy, maternal thyroxine treatment, congenital abnormalities, induction of labour, interval from membrane rupture to delivery, maternal pyrexia in labour, augmentation of labour, abnormal intrapartum cardiotocograms, and meconium in labour. Family history of convulsions also approached significance. CONCLUSIONS--Our preliminary results suggest that intrapartum hypoxia, according to currently used criteria, was not the cause of neonatal encephalopathy in most cases in this population. Our findings suggest that many aetiologies of neonatal encephalopathy originate in the antepartum period.

  3. Author Blair E; Stanley FJ
    Institution National Health and Medical Research Council Research Unit in Epidemiology and Preventive Medicine, Queen Elizabeth II Medical Centre, Nedlands, Western Australia.
    Title Intrapartum asphyxia: a rare cause of cerebral palsy [published erratum appears in J Pediatr 1988 Aug; 113(2):420] [see comments]
    Source J Pediatr 1988 Apr; 112 (4): p515-9
    ISSN 0022-3476
    Abstract Data on all children with spastic cerebral palsy (N = 183) and on a matched group of control children (N = 549) born in Western Australia between 1975 and 1980 were compared to investigate the relationship between birth asphyxia and spastic cerebral palsy. Information on perinatal events for both the children with cerebral palsy and the control subjects was collected by means of epidemiologic methods to reduce bias. An association between clinically observed perinatal signs of birth asphyxia and spastic cerebral palsy was found (relative risk 2.84; 95% confidence interval 1.85 to 4.37). The population-attributable risk proportion was 14.1%. The likelihood of birth asphyxia's causing perinatal brain damage was assessed by two independent observers using defined criteria. It was estimated that in only about 8% (15/183) of all the children with spastic cerebral palsy was intrapartum asphyxia the possible cause of their brain damage. The contribution of intrapartum events and obstetric mismanagement to overall cerebral palsy rates is probably less than was previously thought.

    Author Paneth N
    Institution Program in Epidemiology, College of Human Medicine, Michigan State University, East Lansing.
    Title The causes of cerebral palsy. Recent evidence.
    Source Clin Invest Med 1993 Apr; 16 (2): p95-102
    ISSN 0147-958X
    Abstract Cerebral palsy (CP), unlike many other neurodevelopmental disorders, is associated with abnormalities of pregnancy and birth, particularly 'birth asphyxia' and low birthweight. Associations, however, need not be causal, and some prenatally damaged infants manifest clinical signs suggestive of birth asphyxia in the perinatal period. The lack of a clinically reliable indicator of impaired fetal-placental gas exchange limits our confidence that birth asphyxia plays a true causal role in cerebral palsy. Premature delivery is the single most important antecedent of cerebral palsy, and the increase in survival of very small infants resulting from newborn intensive care may augment this contribution in the future. Cranial ultrasound imaging can describe patterns of neonatal brain damage in the low birthweight infant that are highly predictive of later cerebral palsy. Future research on the causes of cerebral palsy may benefit from improvements in the neurological assessment of the fetus prior to labor and from a clearer understanding of the role of endocrine factors, particularly thyroid disorders, in neurologic development.

  4. Author Anslow P
    Institution Department of Neuroradiology, The Radcliffe Infirmary NHS Trust, Oxford, UK.
    Title Birth asphyxia.
    Source Eur J Radiol 1998 Jan; 26 (2): p148-53
    ISSN 0720-048X
    Abstract The term birth asphyxia covers a number of clinical and physiological definitions. Birth asphyxia is a relatively common clinical event. In the majority of cases the outcome in terms of brain damage and future development of the child is excellent. However, a small number of children go on to develop patterns of brain damage which are then associated with disability. The article seeks to provide a basic understanding of the various mechanisms involved in producing injury.

  5. Author Schneider H
    Institution Universitats-Frauenklinik, Bern, Switzerland.
    Title -Neonatal asphyxia as the cause of brain damage in children?-.
    Vernacular Title [Geburtsasphyxie als Ursache kindlicher Hirnschaden?]
    Source Arch Gynecol Obstet 1995; 256 Suppl:S32-42
    ISSN 0932-0067
    Abstract The prevalence of cerebral palsy (CP) has increased over the last 15 years in most countries. This is explained by an improved survival of very low birth weight prematures. In term infants birth asphyxia is of minor significance as a cause for CP. In only 10% of all CP cases following delivery at term, birth asphyxia must be discussed as a possible cause. In premature deliveries events during the perinatal period are of greater significance for the later development of a CP. Only severe forms of oxygen deficit, leading to tissue damage in the brain and other organs with clinical symptoms during the first days of life, are of significance for the long term prognosis. Even in the presence of severe birth asphyxia the causal relationship with a psychomotor handicap is not proven, since brain damage may have developed during pregnancy before the onset of labour and may be the cause of birth asphyxia. Brain damage and birth asphyxia may be the result of a common pathology of pregnancy.

  6. Author Yudkin PL; Johnson A; Clover LM; Murphy KW
    Institution Nuffield Department of Obstetrics and Gynaecology, John Radcliffe Hospital, Oxford, UK.
    Title Assessing the contribution of birth asphyxia to cerebral palsy in term singletons.
    Source Paediatr Perinat Epidemiol 1995 Apr; 9 (2): p156-70
    ISSN 0269-5022
    Abstract In a geographically-based study, we investigated the risk of cerebral palsy following intrapartum asphyxia at term, and the contribution of intrapartum asphyxia at term to the overall rate of cerebral palsy. We used stringent criteria for identifying intrapartum asphyxia, while recognising that the initial hypoxial insult might have occurred in the antenatal period. In the first part of the investigation, a cohort of 160 term, singleton infants, with a low ( or = 3) 1-minute Apgar score, was followed to the age of 5 years. Six infants in the cohort had presumed intrapartum asphyxia, of whom two died in the neonatal period, three had spastic quadriparesis, profound developmental delay and visual impairment, and one was unimpaired. The frequency of cerebral palsy associated with birth asphyxia was estimated as one in 3700 full-term livebirths. To assess the impact of birth asphyxia on the overall rate of cerebral palsy, all cases of cerebral palsy born in the study period were identified. Of the 30 cases, the three identified in the follow-up study were the only ones whose impairment could be attributed to birth asphyxia in a full-term birth. Birth asphyxia at term therefore was associated with 10% [95% confidence interval (CI) 2.1, 26.5] of all cases of cerebral palsy and with 20% (95% CI 4.3, 48.1) of the 15 cases of cerebral palsy in children born at term.

    Author Breart G; Rumeau-Rouquette C
    Institution Inserm unite 149, Paris, France.
    Title [Cerebral palsy and perinatal asphyxia in full term newborn infants]
    Vernacular Title [Infirmite motrice cerebrale et asphyxie perinatale chez l'enfant ne a terme.]
    Source Arch Pediatr 1996 Jan; 3 (1): p70-4
    ISSN 0929-693X
    Abstract Actual data on the frequency of cerebral palsy (CP) and "infirmite motrice cerebrale" (IMC), and their relationship with perinatal asphyxia and perinatal managements, are presented. In France, the frequency of IMC at 9 years of age, approximates 1 per thousand, for the 1972, 1976, 1981 generations. Three surveys, two English and one Australian, show an association between perinatal asphyxia and CP. However computation of percent attributable risk indicates that asphyxia can explain only one case of CP out of six among term neonates. These surveys show also that 10% of CP only could be prevented by improving perinatal managements. This, in addition to other factors such as the increase in survival of very preterm babies, explains the absence of a significant reduction of CP frequency despite improvements in the perinatal care.

  7. Author Nelson KB; Ellenberg JH
    Title Antecedents of cerebral palsy. Multivariate analysis of risk.
    Source N Engl J Med 1986 Jul 10; 315 (2): p81-6
    ISSN 0028-4793
    Abstract We examined prenatal and perinatal factors predicting cerebral palsy, using multivariate analysis to investigate which factors were most important and the proportion of cases for which they accounted. Maternal mental retardation, birth weight below 2001 g, and fetal malformation were among the leading predictors. Breech presentation was also a predictor, but breech delivery was not. A third of the children with cerebral palsy who had breech presentations had a major noncerebral malformation. Among 189 children with cerebral palsy, 40 (21 percent) had at least one of three clinical markers suggestive of asphyxia; only 17 of these 40 children (9 percent of all cases) lacked major congenital malformation or other intrinsic defects that might have contributed to an unfavorable outcome. When all the principal risk factors present by the time labor began were considered, the 5 percent of the population at highest estimated risk was seen to have contributed 34 percent of the cases. When all the risk factors present during the period beginning before pregnancy and extending through the nursery stay were included, the 5 percent at highest risk was seen to have contributed 37 percent of the cases. Thus, the inclusion of information about the events of birth and the neonatal period accounted for a proportion of cerebral palsy only slightly higher than that accounted for when consideration was limited to characteristics identified before labor began.

    Author Blair E; Stanley FJ
    Institution National Health and Medical Research Council Research Unit in Epidemiology and Preventive Medicine, Queen Elizabeth II Medical Centre, Nedlands, Western Australia.
    Title Intrapartum asphyxia: a rare cause of cerebral palsy [published erratum appears in J Pediatr 1988 Aug; 113(2):420] [see comments]
    Source J Pediatr 1988 Apr; 112 (4): p515-9
    ISSN 0022-3476
    Abstract Data on all children with spastic cerebral palsy (N = 183) and on a matched group of control children (N = 549) born in Western Australia between 1975 and 1980 were compared to investigate the relationship between birth asphyxia and spastic cerebral palsy. Information on perinatal events for both the children with cerebral palsy and the control subjects was collected by means of epidemiologic methods to reduce bias. An association between clinically observed perinatal signs of birth asphyxia and spastic cerebral palsy was found (relative risk 2.84; 95% confidence interval 1.85 to 4.37). The population-attributable risk proportion was 14.1%. The likelihood of birth asphyxia's causing perinatal brain damage was assessed by two independent observers using defined criteria. It was estimated that in only about 8% (15/183) of all the children with spastic cerebral palsy was intrapartum asphyxia the possible cause of their brain damage. The contribution of intrapartum events and obstetric mismanagement to overall cerebral palsy rates is probably less than was previously thought.

  8. Author Bohr L; Greisen G
    Institution Neonatalklinikken GN, H:S Rigshospitalet, Juliane Marie Centret.
    Title [Prognosis after perinatal asphyxia in full-term infants. A literature review]
    Vernacular Title [Prognosen for mature nyfodte med perinatal asfyksi. En litteraturgennemgang.]
    Source Ugeskr Laeger 1998 May 4; 160 (19): p2845-50
    ISSN 0041-5782
    Abstract Reviewing the literature published during the last 30 years we found comparable systematic studies of outcome for 1042 term infants born alive after likely intrapartum hypoxia-ischaemia. Fifty-two percent had no sequelae, 8% had developmental delay without associated handicaps, 4% had a single handicap, 11% were multihandicapped and 14% were dead as a consequence of the intrapartum hypoxia-ischaemia. The frequency of single handicaps exceeded the frequency found among the controls and in population studies. The frequency of children with developmental delay did not differ from that found among the controls. Outcome is closely related to the severity of hypoxic-ischaemic encephalopathy in the newborn.

    Author Nelson KB; Grether JK
    Institution Neuroepidemiology Branch, National Institute of Neurological Disorders and Stroke, Bethesda, Maryland, USA.
    Title Potentially asphyxiating conditions and spastic cerebral palsy in infants of normal birth weight.
    Source Am J Obstet Gynecol 1998 Aug; 179 (2): p507-13
    ISSN 0002-9378
    Abstract OBJECTIVE: Our purpose was to examine the association of cerebral palsy with conditions that can interrupt oxygen supply to the fetus as a primary pathogenetic event. STUDY DESIGN: A population-based case-control study was performed in four California counties, 1983 through 1985, comparing birth records of 46 children with disabling spastic cerebral palsy without recognized prenatal brain lesions and 378 randomly selected control children weighing or = 2500 g at birth and surviving to age 3 years. RESULTS: Eight of 46 children with otherwise unexplained spastic cerebral palsy, all eight with quadriplegic cerebral palsy, and 15 of 378 controls had births complicated by tight nuchal cord (odds ratio for quadriplegia 18, 95% confidence interval 6.2 to 48). Other potentially asphyxiating conditions were uncommon and none was associated with spastic diplegia or hemiplegia. Level of care, oxytocin for augmentation of labor, and surgical delivery did not alter the association of potentially asphyxiating conditions with spastic quadriplegia. Intrapartum indicators of fetal stress, including meconium in amniotic fluid and fetal monitoring abnormalities, were common and did not distinguish children with quadriplegia who had potentially asphyxiating conditions from controls with such conditions. CONCLUSION: Potentially asphyxiating conditions, chiefly tight nuchal cord, were associated with an appreciable proportion of unexplained spastic quadriplegia but not with diplegia or hemiplegia. Intrapartum abnormalities were common both in children with cerebral palsy and controls and did not distinguish between them.

  9. Author Paneth N; Fox HE
    Title The relationship of Apgar score to neurologic handicap: a survey of clinicians.
    Source Obstet Gynecol 1983 May; 61 (5): p547-50
    ISSN 0386-9792

  10. Author Depp R
    Institution Department of Obstetrics and Gynecology, Jefferson Medical College, Philadelphia, PA 19107, USA.
    Title Perinatal asphyxia: assessing its causal role and timing.
    Source Semin Pediatr Neurol 1995 Mar; 2 (1): p3-36
    ISSN 1071-9091
    Abstract Perinatal asphyxia, whether prenatal, intrapartum, or neonatal is thought to be a significant contributor to newborn morbidity and mortality as well as long-term neurological deficits. Development of an intrapartum tool/test that can reliably identify and discriminate between varying degrees of fetal acidemia and suggest whether it is respiratory or metabolic in nature would be highly desirable. This article critically reviews the available experience with the currently available monitoring techniques and the significance of abnormalities of fetal and intrapartum measurements with respect to the predictive value of the observations available to the clinician.


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