Cerebral palsy and intrapartum fetal acidemia

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Letters

July 1990 Am J Obstet Gynecol

The cause of the increase in the incidence of ectopic pregnancy is multifactorial. A discussion of the hypothetical explanations for the difference between the observed increase in the rate of ectopic pregnancy between Hungary and Finland is beyond the scope of this short communication.

our study legal abortions did not show any strong association with the increase of the rate of ectopic pregnancy. The comparison of figures from Hungary and Finland again gives indirect support to this observation.

I thank Andras Klinger, PhD, Central Statistical Office, Budapest, for his valuable help. Akos A. Jakobovits, MD

Department of Obstetrics and Gynecology, University of Turku, Kunamyllynkatu 4-8, SF 20520 Turku, Finland

Department of Obstetrics and Gynecology, Toldy Ferenc Hospital, TOrteli ut 1-3, H-2701 Cegted, Hungary

Juha I. Miikinen, MD, and Risto V. Erkkola, MD Pekka J. Laippala, PhD

Department of Public Health , University of Tampere, Tampere, Finland

REFERENCES 1. Thornburn J, Friberg B, Schubert W, Wassen A-C, Lindblom B. Background factors and management of ectopic pregnancy in Sweden. Acta Obstet Gynecol Scand 1987; 66:597-602. 2. Flett GMM, Urquhart DR, Fraser C, Terry PB, Fleming JC. Ectopic pregnancy in Aberdeen 1950-1985. Br J Obstet Gynaecol 1988;95:740-6. 3. Frau LM, McKay HT. Hughes JM, Cates W Jr. Epidemiologic aspects of pregnancy. In: Langer A, Iffy L, eds. Extrauterine pregnancy. Littleton. Massachusetts: PSG Publishing, 1986: 179-93.

Reply To the Editors: We thank Dr. Jakobovits for the interest concerning our article . In his letter Dr. Jakobovits has shown a negligible increase in the rate of ectopic pregnancy in Hungary, which is in opposition to the great increase of ectopic pregnancy in many countries in western Europe and in the United States. He did not endeavor to hypothesize the reasons for this difference, and we do agree that this may turn out to be somewhat difficult. However, at least two obvious differences between Hungary and Finland should be pointed out. First, although the exact figures for Hungary are not available to us, the use of an intrauterine contraceptive device has probably been much more limited in Hungary than in Finland, especially in the 1970s and early 1980s. This could be considered as an additional, yet indirect evidence for the role of the intrauterine contraceptive device in the increase in the rate of ectopic pregnancy. Second, the effect of improved diagnosis also needs consideration. In Finland this may explain some of the increase in the rate of ectopic pregnancy, but to be able to compare Hungary and Finland in this regard, we must know the workup used in Hungary for the diagnosis of ectopic pregnancy in the years of the study, e.g., how widespread the use of highly sensitive pregnancy tests, ultrasonography, and laparoscopy has been. Incidentally, an interesting observation on the relation between legal abortion and ectopic pregnancy may be made when one is looking at the statistics from Hungary and Finland. The rates of legal abortion in Hungary have been more than fivefold those in Finland. In

Cerebral palsy and intrapartum fetal acidemia To the Editors: I believe that the data of Dennis et al. do not warrant the author's conclusions (Dennis J, Johnson A, Nutch L, Yudkin P, Johnson P. Acid-base status at birth and neurodevelopmental outcome at four and one-half years. AMJ OBSTET GYNECOL 1989;161:21320). Just as Baird's documentation of the interacting social factors that influence health and child-bearing failed to be accepted in America, I to speak of "impairment codes" does not have current American obstetric clinical or medical-legal implications. The present issue on this side of the Atlantic is cerebral palsy and its possible relationship to intrapartum fetal acidemia. The authors started with a data base of 1210 cases at term, which should have produced at the most only two cases of cerebral palsy. If only 10% to 20% of cases of cerebral palsy are due to intrapartum fetal distress, I believe the authors whould have to have had access to at least 5000 cases to have one case of cerebral palsy caused by obstetric events. Furthermore, no information is given about genetic factors, which may have a significant role in developmental "impairment." While the authors spoke of "physiologic acidosis," no mention was made of lactic acid in their discussion. Hendricks 2 noted that fetal difficulty occurred more frequently when maternal lactic acid values failed to increase near term. The literature on lactic acid as a fetal substrate is extensive.' Presumably, its production by the placenta has fetal benefits, although it may at the same time contribute to the apparent acidemia of the fetus" Nevertheless, such a metabolic acidemia would not be "physiologic" in that it is highly variable. Years ago, Kaiser and J5 showed that altering maternal pH likewise altered fetal pH. In any population of newborns, to attempt to discuss the significance of fetal acidosis in the absence of maternal pH determinations is in my opinion futile . I continue to believe that the possible role of fetal acidemia will be delineated only when routine maternal and umbilical pH values are obtained on thousands of deliveries. Then, when cases of cerebral palsy occur,

Letters

Volume 163 Number 1, Part I

we can accurately determine the significance (if any) of "fetal acidosis." Robert C. Goodlin, MD Department of Health and Hospitals, City and County of Denver, 777 Bannock St., Denver, CO 80204-4507

REFERENCES 1. Editorial. Lancet 1989;2:657-8. 2. Hendricks CH. Studies on lactic metabolism in pregnancy and labor. AM] OBSTET GYNECOL 1957;73:492-508. 3. Battaglia FC, Hay WHo Energy and substrate requirements for fetal and placental growth and metabolism. In: Beard RW, Nathanielsz PW. Fetal physiology and medicine. London: Butterworths, 1984. 4. Suidan ]S, Wasserman ]F, Young BK. Placental contribution to lactate production by the human fetoplacental unit. Am] Perinatol 1984; 1:306-9. 5. Goodlin RC, Kaiser I. The impact of acidosis on the human fetus. Am] Med Sci 1957;233:662-71.

Reply To the Editors: We find it difficult to relate the comments in the first part of Dr. Goodlin's letter to our own particular study. Our study was designed to find out whether acid-base status at birth in term infants would be predictive of neurodevelopmental outcome at age 4 to 5 years. The outcome we were concerned with was not primarily cerebral palsy; rather it was the relatively large proportion of children (10% to 20%) with disability caused by subtle neurodevelopmental impairment. As Dr. Goodlin correctly points out, cerebral palsy is a relatively rare condition. Had we wished to study the possible association of acid-base status at birth and cerebral palsy, we would not have chosen a cohort design. We used as outcome measures a wide range of standardized developmental tests. Dr. Goodlin suggests that results of such tests carry no clinical or medicolegal validity. On the contrary, such tests are widely used in clinical practice on both sides of the Atlantic, and our experience in the United Kingdom is that tests of this type are certainly recognized in courts of law as valid measures of neurodevelopmental status in children. We showed no association whatever between poor performance on these tests and our measure of acid-base status. The "impairment codes" that Dr. Goodlin has singled out were derived from these standardized tests and merely represent one of many attempts to ensure that we were not missing any associations in our data. We believe the conclusions we have drawn are entirely valid within the context of our study and are well supported by our data. Dr. Goodlin, as expected, raises several pertinent issues on the question of fetal acidosis. In particular, he poses the question as to whether maternal acidosis in labor could have made a significant contribution to the fetal acidosis at birth. If so, this "apparent" fetal acidemia could not be considered physiologic. This is extremely unlikely because of several issues. In our study

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we were considering severe levels of fetal acidosis: a first level that produced a pH <7.12 and a second level with a pH <7.04 (mean pH for this group was 6.97). At these fetal levels the maternal contribution would be small. l In the original study from which our cohort was drawn, simultaneous umbilical arterial and venous measurements were made. 2 The base excess was always greater and the pH lower in the umbilical artery than in the umbilical vein. Hence we assumed the acidosis to be mainly emanating from the fetus. A further study of these paired samples demonstrated that maternal intrapartum factors as opposed to fetoplacental factors made a comparatively small contribution to fetal arterial acidosis. 3 Hence we do not agree with Dr. Goodlin's suggestion that in the absence of measures of maternal acid-base status our umbilical arterial measures are "futile." As to the question of the "physiologic" nature of the response, it is the production of lactic acid by the fetoplacental unit as an energy-supplying response to anaerobiosis-the very process referred to by Dr. Goodlin-that we term "physiologic." The issue of acidosis and its relation to asphyxial injury needs urgent resolution. We believe our study is entirely valid in suggesting that a one-off measure of umbilical arterial pH and base deficit is not a good measure of fetal asphyxia, a view increasingly shared by others. 4-6 J. Dennis, DM, A. Johnson, MD, L. Mutch, MD, P. Yudkin, MA, and P. Johnson, MB, ChB Nuffield Department of Obstetrics and Gynaecology, Level 3 Maternity Department, John Radcliffe Hospital, Headington, Oxford, England OX3 9DU

REFERENCES 1. Hendricks CH. Studies on lactic metabolism in pregnancy and labor. AM] OBSTET GYNECOL 1957;73:492-508. 2. Sykes GA, Johnson P, Ashworth F, et al. Do Apgar scores indicate asphyxia? Lancet 1982; 1 :494-6. 3. Yudkin PL, Johnson P, Redman CWG. Obstetric factors associated with cord blood gas values at birth. Eur] Obstet Gynecol Reprod Bioi 1987;24:167-76. 4. Thorp ]A, Sampson ]E, Parisi VM, Creasy RK. Routine umbilical cord blood gas determinations? AM] OBSTET GyNECOL 1989;161:600-5. 5. Gilstrap LC, Leveno K], Burris j, Williams ML, Little BB. Diagnosis of birth asphyxia on the basis of fetal pH, Apgar score, and newborn cerebral dysfunction. AM ] OBSTET GYNECOL 1989; 161 :825-30. 6. Dijxhoorn M], Visser GHA, Huisjes H], Fidler V, Touwen BCL. The relation between umbilical pH values and neonatal neurological morbidity in full term appropriate-fordates infants. Early Hum Dev 1985; 11 :33-42.

Spontaneous resolution of a nuchal fetal cystic hygroma diagnosed early in the second trimester of pregnancy To the Editors: We read with interest the article by Bronshtein et al. (Bronshtein M, Rottem S, Yaffe N, Blu-