Volume 151 Number I

surveys5 show that it is quite rare for fetuses to be born depressed when fetal heart rate variability is maintained, despite the presence of various periodic changes, including late decelerations. The physiologic basis for this observation has been extensively de­scribed.6

Brand states that in true uteroplacental insufficiency, the Po2 should drop before acidemia occurs. This is not necessarily true of the respiratory component of acidosis. In studies where uterine blood flow is Jelib­erately reduced we have seen an increase in Pco2 as well as a decrease in Po2 •

7

A further difficulty with Brand's proposed test con­cerns atropine dosage. In experimental sheep in order to reliably produce total fetal blockade one needs to administer 200 µg/kg intravenously to the fetus. Brand proposes 400 µg of atropine to the mother. Variations in rate and quantity absorbed may make fetal dosage quite unpredictable, thus casting doubt on the validity of a "negative" test.

The most serious objection to the test is that the du­ration of atropine's action can be such that its effect on heart rate may be prolonged. If so, this prevents the use of the fetal heart rate as a screen for asphyxia following the test. This would be an untenable situation given the fact that the patients in whom the test is to be used are already having "persistent late decelera­tions," and the cumulative effect of such intermittent stresses may result in serious asphyxia after the fetus has successfully "passed the test."

]. T. Parer, M.D., Ph.D. University of California, San Francisco Department of Obstetrics, Gynecology and

Reproductive Sciences and Cardiovascular Research Institute

Room HSE 1462 San Francisco, California 9414 3

REFERENCES

I. Goodlin RC, Haesslein HC. Fetal reacting bradycardia. AM J 0BSTET GYNECOL 1977; 129:854-6.

2. Parer JT. The effect of atropine on heart rate and oxygen consumption of the hypoxic fetus. AM J 0BSTET GYNECOL 1984; 148: 1118-22.

3. Parer JT. Handbook of fetal heart rate monitoring. Phil­adelphia: WB Saunders, 1983.

4. Harris JL, Krueger TR, Parer JT. Mechanisms of late de­celerations of the fetal heart rate during hypoxia. AM J 0BSTET GYNECOL 1982;144:491-6.

5. Krebs HB, Petres RE, Dunn LJ, Jordaan HVF, Segreti A. Intrapartum fetal heart rate monitoring. I. Classification and prognosis of fetal heart rate patterns. AM J 0BSTET GYNECOL 1979; 133:762-72.

6. Court DJ, Parer JT. Experimental studies of fetal asphyxia and fetal heart rate interpretation. In: Nathanielsz PW, Parer JT, eds. Research in perinatal medicine. Ithaca, New York: Perinatology Press, 1984 (in press).

7. Yaffe H, Parer JT, Llanos A, Block B. Fetal hemodynamic responses to graded reductions of uterine blood flow in sheep [Abstract]. In: Scientific Abstracts. Dallas: Society. for Gynecologic Investigation, twenty-ninth annual meetmg, March 24-27, 1982:113.

Correspondence 143

The "lytic cocktail" induces recurrence of fits in the treatment of eclampsia

To the Editors: We feel that the "lytic cocktail" must be banned in

the treatment of eclampsia. In an effort to control 30 patients with eclamptic seizures, the Obstetrics Clinic of the Paulista Medical School administered a combi­nation of chlorpromazine and promethazine ( l 00 to 400 mg of each drug per 24 hours) and an intravenous priming dose of pethidine ( lOOmg/24 hr), diluted in a 5% glucose solution. This mixture of drugs proved to be a "cocktail" that induced recurrence of seizures rather than stopping them (Table I).

We have divided the cases into four groups as a func­tion of the grade of severity. Group A (Fig. 1) consisted of 12 patients with low arterial blood pressure levels who continued to have seizures throughout labor until their babies were delivered. Group B (Fig. 2) involved three patients who remained convulsive after delivery. Group C (Fig. 3) consisted of 11 eclamptic patients who experienced seizures during labor and the first 20

i II

J ii 1~

250

311

1).150

100

50

0

•••1111J1.• •1111,-.....-. ..

Fig. 1. Findings in group A.

Group B 10%

Fig. 2. Findings in group B.

144 Correspondence

11J Gftq>C

38,1% •&11.-.. .. ,,.....,, ..... 16N10

2!iO ,,..._./___......_'~------

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Fig. 3. Findings in group C.

J f I 11).8)

• • ao.1•

• 50

0

GnlupD 13'Jft

January 1, 1985 Am J Obstet Gynecol

----· .,,,. ........ ...,, ..

Fig. 4. Findings in group D.

Table I. Recurrence of seizures following administration of "lytic cocktail" in 30 patients

Perinatal mortality

Stillbirth 0 to 2 More than 2 Fetal during Neonatal Maternal

No. seizures seizures growth Stillbirth labor mortality mortality Delivery

Group A I 0 IUGR 2 0 Normal 2 2 0 IUGR 0 Forceps 3 0 Normal 0 Cesarean 4 I Normal 0 Forceps 5 0 Prete rm 0 Breech 6 0 0 Forceps 7 I IUGR 0 Cesarean 8 4 IUGR 0 Cesarean 9 2 0 Normal

IO 2 IUGR 0 Cesarean I I 4 IUGR 0 Cesarean 12 Normal 0 Normal

Group B 13 2 IUGR 0 Normal 14 2 Normal 0 Cesarean 15 2 Pre term 0 Normal

Group C 16 13 IUGR 0 Normal 17 Normal 0 Normal 18 9 0 Normal 19 IUGR 0 Normal 20 4 Normal 0 Breech 21 4 Normal 0 Normal 22 6 Normal 0 Normal 23 4 0 Normal 24 14 Normal 0 Cesarean 25 29 Normal 0 Cesarean 26 29 Normal 1 Cesarean

Group D 27 2 IUGR 0 Forceps 28 29 0 Normal 29 39 0 Forceps 30 0 Normal 0 Normal

Occurrence of seizures: 0, 20%; 1, 16.7%; 2, 20%; 0-2, 56.6%; >2, 43.3%. Fetal growth, 58%; stillbirth, 22.5%; stillbirth during labor, 8.3%; neonatal mortality, 16.6%; maternal mortality, 3.3%; delivery, 45.1 %. IUGR, Intrauterine growth retardation.

hours puerperium while being treated with the "lytic cocktail." Seizures stopped when this therapy was aban­doned. The only case of maternal mortality occurred in the latter group. The patient suffered 29 seizures

and died 2 hours after a cesarean section as she was receiving a blood transfusion for operative shock and 250 mg of thiopentane in an attempt to stop the sei­zures. There were four patients in group D (Fig. 4)

Volume 151 Number I

whose seizures stopped after delivery. One patient in this group had 39 seizures. The rate of intravenous dripping was governed by patient response, and par­adoxically, in some cases the increasing of dripping resulted in an increase in the number of convulsions.

It seems likely that the combination of phenothia­zines and pethidine is a convulsant therapy in eclamp­sia. There was a reduction in systolic pressure (Figs. 1-4) without a relevant decrease in diastolic pressure in most of the eclamptic patients. These observations were made for a very elevated cardiac rate (pulse up to 160 bpm). These clinical data suggest that there is a de­crease in blood flow in the brain. These findings rein­force the hypothesis of Sheehan and Lynch' that con­vulsions result from a vasomotor disturbance.

Dib El-Kadre, M.D. Caetano Giordano, M.D.

Department of Obstetrics and Gynecology Paulista Medical School 720 Botucatu Sao Paulo 04023, Brazil

REFERENCE 1. Sheehan HL, Lynch JB. Pathology of toxemia of preg­

nancy. London: Churchill Livingstone, 1973.

Coincidence of congenital aplasia of the vagina with ear and facial anomalies

To the Editors: I read with interest the article by Winer-Muram et

al. (Winer-Muram HT, Muram D, Wilroy RS, Cupp C. The concurrence of facioauriculovertebral spectrum and the Rokitansky syndrome. AMJ 0BSTET GYNECOL

1984; 149:569.) The statement that "the concurrence of the facioauriculovertebral spectrum and the Rokitan­sky syndrome has not been previously described" is not correct. A similar case has been published before.'

Katholieke Universiteit Nijmegen lnstituut voor Obstetrie!Gynaecologie Geert Grooteplein zuid 14

Wim Willemsen

Postbus 9101-6500 HB Nijmegen, The Netherlands

REFERENCE 1. Willemsen WNP. Renal-skeletal-ear- and facial-anamolies

in combination with the Mayer-Rokitansky-Kiister (MRK) syndrome. Eur J Obstet Gynecol Reprod Biol 1982; 14: 121.

Reply to Willemsen To the Editors:

This letter is being written in reply to Dr. Willemsen's comments about the article, The concurrence of fa­cioauriculovertebral spectrum and the Rokitansky syn­drome. The cases are similar, and indeed Dr. Willem­sen's comments are entirely justified. Our patient was seen and written up in October, 1982, at which time we were unaware of Dr. Willemsen's article which had

Correspondence 145

not been published as yet. The similarity of these two cases supports the hypothesis that a spectrum of mes­enchymal defects indeed exists.

We would like to thank Dr. Willemsen for his comments.

Division of Gynecology The University of Tennessee Center for the Health Sciences 853 Jefferson Avenue Memphis, Tennessee 38163

David Muram, M.D.

Prognostic significance of adenofibromatous pattern in ovarian epithelial malignancies

To the Editors: I read with great interest the article of Malkasian et

al. "Prognostic significance of histologic classification and grading of epithelial malignancies of the ovary" (AM J 0BSTET GYNECOL 1984; 149: 27 4), and would like to make the following comment.

Apart from stage, grade, and cell type, which have been studied and discussed by the authors, there is another factor that has not been mentioned at all, i.e., the presence or absence of adenofibromatous or cyst­adenofibromatous pattern. This histologic variant, which is more common with the serous cell type than with the other cell types of ovarian epithelial malig­nancies, has been listed as a separate subdivision in the World Health Organization classification. 1 Most prob­ably, in cases with this histologic variant the malignant epithelium induces an increased stromal cellularity, and as a consequence of this, the tumor exhibits histologi­cally a prominent fibrous stroma. It should be empha­sized that the stroma does not show any degree of atyp­ism or mitotic activity, thus ruling out the possibility of Miillerian adenosarcoma. Unfortunately, the prognos­tic significance of the presence or absence of adenofi­bromatous or cystadenofibromatous pattern in ovarian epithelial malignancies is still not known and yet has to be determined.

Benjamin Piura, M.D., M.R.C.O.G. Department of Obstetrics and Gynecology "B" Soroka Medical Center P.O. Box 151 Beer-Sheva, Israel

REFERENCE

1. Serov SF, Scully RE, and Sobin RH: Histological typing of ovarian tumours. In: International Histologic Classification of Tumours, No. 9, Geneva: World Health Organization, 1973.

Reply to Piura To the Editors:

The presence of epithelial malignancies of the ovary in association with adenofibromas or buried within these lesions has been known for some time. The ac­tivity of these lesions appears to be associated with the