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ORIGINAL RESEARCH |
From the Department of Obstetrics and Gynecology, The University of Texas Medical Branch, Galveston, Texas; and The American College of Obstetricians and Gynecologists, Washington, DC.
Address reprint requests to: Gary D. V. Hankins, MD, The University of Texas Medical Branch, 301 University Boulevard, Galveston, TX 77555-0587; E-mail: ghankins{at}utmb.edu.
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ABSTRACT |
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METHODS: A questionnaire designed to test both knowledge and practice patterns was mailed to 413 members of the Collaborative Ambulatory Research Network of The American College of Obstetricians and Gynecologists (ACOG), as well as 600 randomly selected non-Network ACOG Fellows. The questionnaire was composed of 15 knowledge questions and three clinical scenarios containing seven knowledge questions. Six of the questions directly assessed knowledge of cerebral palsy.
RESULTS: Of those who returned the questionnaire, 351 practiced obstetrics and were included in the statistical analyses. For the majority of questions, "Don’t know" was the most frequent response. The next most frequent response for 8/13 questions was the correct answer. Performance was strongest as regarded actual clinical practice and relatively weak regarding the antecedents of neonatal encephalopathy and cerebral palsy. The physicians’ actual knowledge scores showed a significant correlation with their self-assessments of knowledge (r = .41, P < .001). The majority of physicians rated their training on this topic in medical school, residency, and through continuing medical education as marginal or inadequate.
CONCLUSION: The results of this survey identified large knowledge gaps in this area, suggesting a need to develop educational projects to address these deficits by both professional organizations and individual teachers.
Neonatal encephalopathy, as a clinical phenomena of compromised neurological function in the term or near-term infant, manifests during the first days after birth. Hypoxic ischemic encephalopathy is only a subset of the much broader category of neonatal encephalopathy. Though most forms of cerebral palsy do not result from intrapartum events, two forms that are associated with hypoxic ischemic encephalopathy are spastic quadriplegia and dyskinetic cerebral palsy.1,2 The incidence rate of hypoxic ischemic encephalopathy is reported to be about 1.9 per 1000 births, and that of neonatal encephalopathy is reported as 3.8 per 1000 term births.3
Long-term neurologic injuries in children extend into adult life, particularly those involving the cerebral palsies with or without seizure disorders and mental retardation. The causes in most cases can be ascribed to antenatal factors4–6; however, blame has often inappropriately been ascribed to preventable intrapartum causes.6 Unfortunately this misperception, regardless of whether innocent or contrived, has led to unwarranted and unjustified litigation, as well as the potential for misdirection of valuable resources that could be better utilized to define the true genesis and quantify the scope of these injuries.
A recent international consensus statement regarding acute intrapartum events and subsequent cerebral palsy was published,7 and a task force hosted by The American College of Obstetricians and Gynecologists (ACOG) met over the last 2 years to construct an update for physicians about the antecedents and timing of neonatal encephalopathy and the subsequent occurrence of cerebral palsy. As one aspect of that task force, a questionnaire was developed and sent to members of the College; that questionnaire serves as the focus of this report. The purposes of the questionnaire were to assess the knowledge level of the physicians and to serve as an educational device. The results of that survey are described herein.
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MATERIALS AND METHODS |
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The survey was primarily in the form of multiple-choice questions pertaining to physicians’ practices and knowledge about neonatal encephalopathy. No instructions were given as to whether the respondents should answer the questions based on current knowledge or whether they could research for the answers. Items included 15 stand-alone knowledge questions and three clinical scenarios containing seven knowledge questions. The correct answer was based on the work of the ACOG Task Force as determined by the Task Force members and consultants to the Task Force. Six of the questions directly assessed knowledge of cerebral palsy. All but two knowledge questions contained the answer choice "Don’t know." The questionnaire also contained items concerning demographic information, educational background, and clinical practice patterns related to neonatal encephalopathy.
Data were analyzed using a computer-based software package, SPSS 10.0 (SPSS Inc., Chicago, IL). Descriptive statistics were computed for each item in the questionnaire. For comparisons between groups, differences on categorical measures were assessed using 
2 analysis. To account for potential changes in education, data analyses controlled for year of residency in three groups: before 1980, 1981–1990, and 1990–present. A simple knowledge score, consisting of the total number of correct responses to the 22 knowledge questions involving neonatal encephalopathy, was tabulated. Pearson correlation and analysis of variance was used to assess the relationships between sex, age, year residency was completed, professional education, rating of self-knowledge, and knowledge score. All analyses were tested for significance using an 
of .05, and findings for all statistically significant differences regarding correct and incorrect answers are reported.
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RESULTS |
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contains demographic information for the two groups.
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and 3. Of the 14 items, "Don’t know" was the most frequent response by physicians for six of the items. When "Don’t know" responses are not taken into account, correct answers, based on published research, were the most frequent responses in eight of the knowledge questions (Table 2). In five of these items, however, still less than half of the physicians sampled indicated the correct response. Of the remaining eight knowledge questions, when "Don’t know" responses were excluded, an incorrect answer was still the most frequent response (Table 3).
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–7 along with physicians’ responses. In Clinical Scenario I, a significant gender difference in responses emerged. Male physicians (77.7%) were less likely than female physicians (87.3%) to get a Kleihauer-Betke smear (2 = 5.339, P = .02) in the situation outlined. For Clinical Scenario II, physicians in different practice locations (see Table 1
for practice locations) indicated that they would administer different tests. Those in rural practice locations were the least likely to administer the Rh immune globulin (2 = 14.05, P = .007) and were least likely to test for premature rupture of membranes (25 = 10.74, P = .03); those in suburban locations were most likely to perform Kleihauer-Betke smears (2 = 12.25, P = .016).
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and 3, and responses to Clinical Scenarios II and III in Tables 5, 6, and 7. The knowledge scores were normally distributed (mean = 9.5 ± 0.1; range = 2–17) and were significantly correlated with self-assessment of knowledge regarding neonatal encephalopathy (r = .41, P < .001). Rating of self-knowledge of neonatal encephalopathy was the most consistent factor in explaining variation in the knowledge score (F4 = 14.016, P < .001). There was no effect of gender, age, or year in which residency was completed.
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2 = 11.58, P = .003). The primary sources of information about advances in neonatal encephalopathy were professional journals (36%) and ACOG committee opinions (33.7%). |
DISCUSSION |
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Almost half of the respondents either did not know, or else grossly overestimated the percentage of cases of cerebral palsy that could be attributed to an intrapartum asphyxial insult. The Fellows also performed poorly on knowledge regarding the time of injury of monochorionic twins when one twin dies; this is understandable, as this particular clinical circumstance has been the subject of substantial debate over the last decade.
The survey indicates that performance in clinical practice was generally both strong and consistent. For instance, Fellows were fully cognizant that electronic fetal monitoring cannot pinpoint the time of injury of a fetus.12 They also recognize the utility and value of placental histopathology examination and umbilical cord arterial blood sampling for a 39-week fetus who is the product of a precipitous delivery, had a number of postmature features, and has low Apgar scores at 1, 5, and 10 minutes. In another clinical scenario involving a motor vehicle accident, the Fellows provided appropriate counseling regarding the risk of significant fetal injury in more than 94% of responses and appropriately provided Rh immune globulin in 92%. When confronted with a clinical scenario involving the evaluation of a fetal heart rate tracing that changes from normal and reactive to one containing persistent late decelerations, only 15.5% accurately counseled the woman that there was a 99% probability that the tracing was a false positive if used as an indicator for subsequent development of cerebral palsy (35.5% did not know and 5.3% grossly overestimated the risk at 10%).
To conclude, issues of neonatal encephalopathy pathogenesis and histopathology are not well understood by practicing obstetricians throughout the United States. This is clearly an area where the knowledge gap needs to be closed, as there certainly are implications that directly relate to the practice of obstetrics as well as to the counseling of our patients. The primary sources of information about advances in neonatal encephalopathy include professional journals and ACOG committee opinions. To this end, the upcoming task force publications by ACOG should go far to close the information gap. Additionally, this area would appear to be an important priority for research publication of peer-reviewed work, as well as for other venues of continuing medical education.
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Footnotes |
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Received April 4, 2002. Received in revised form May 7, 2002. Accepted July 12, 2002.
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REFERENCES |
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2. Stanley FJ, Blair E, Hockey A, Petterson B, Watson L. Spastic quadriplegia in Western Australia: A genetic epidemiological study. I. Case population and perinatal risk factors. Dev Med Child Neurol 1993;35:191–201.[Medline]
3. Badawi N, Kurinczuk JJ, Hall D, Field D, Pemberton PJ, Stanley FJ. Newborn encephalopathy in term infants: Three approaches to population-based investigation. Semin Neonatol 1997;2:181–8.
4. Nelson KB, Dambrosia JM, Ting TY, Grether JK. Uncertain value of electronic fetal monitoring in predicting cerebral palsy. N Eng J Med 1996;334:613–8.
5. Nelson KB, Grether JK. Potentially asphyxiating conditions and spastic cerebral palsy in infants of normal birth weight. Am J Obstet Gynecol 1998;179:507–13.[Medline]
6. Blair E, Stanley F. When can cerebral palsy be prevented? The generation of causal hypotheses by multivariate analysis of a case-control study. Paediatr Perinatal Epidemiol 1993;7:272–301.[Medline]
7. MacLennan A. A template for defining a causal relation between intrapartum events and cerebral palsy: International consensus statement. For the International Cerebral Palsy Task Force. BMJ 1999;319:1054–9.
8. Blair E, Stanley F. Intrapartum asphyxia: A rare cause of cerebral palsy. J Pediatr 1988;112:515–9.[Medline]
9. Badawi N, Kurinczuk JJ, Keogh JM, Alessandri LM, O’Sullivan F, Burton PR, et al. Antepartum risk factors for newborn encephalopathy: The Western Australian case-control study. BMJ 1998;317:1554–8.
10. Adamson SJ, Alessandri LM, Badawi N, Burton PR, Pemberton PJ, Stanley F. Predictors of neonatal encephalopathy in full term infants. BMJ 1995;311:598–602.
11. Campbell S, Vyas S, Nicolaides KH. Doppler investigation of the fetal circulation. J Perinat Med 1991;19:21–6.
12. Ahn MO, Korst LM, Phelan JP. Normal fetal heart rate pattern in the brain-damaged infant: A failure of intrapartum fetal monitoring? J Matern Fetal Investig 1998;8: 58–60.[Medline]
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