Communications
! 8 ,‘\
-__”
--IS
Fig. 2. Chromosomal
lf)
analysis
---_
I__
of fetal peripheral
tinued to show the theta lutein cysts. At 6 weeks postpartum the patirllt \vas normotensiw, with normal pelvic findings. kidne) function test results. and intravenous pyelogram. (:hl-omowme anal!,& of the fetal blood and fetal tissue j-e\ealetl a ti9,S?nortnalities. ‘I‘hre include the follorl:ing: small for gestational age, dysplasticcranial bones, small eyes with col~~l~on~;~s. facial cl&s. cutaneous s$act~l~ of hands aid feet. sinwati ~rc‘ases. cardiac defects. meningorr~~~elocele. or spina bifida, ornphalocele, and nlaldevelopmcnt of genitalia in nlales. X.he placenta char:~ctcristicall! dm~c~nst~-ate5 hydatidiform degeneration. which \\a4 prcsc’nt in .X to 55!1 of specimens. ‘Ili~ reversal ~rssocialion is evt‘i~ stronger, that is, the pr-C*Seilcc ot li~tlatitliform degeneration 1riea115 triploitl\ i.7’; of the tinlc. Due to the molar condition of the plac.cnta tlirrr. is a higll risk of clcveloping pregnan(‘yinducctl Ii\ pcrtcnsion ear1~ in gestation. Bcischer. Fortllllc’ , and I~itqeral” reported two patients with sewre prc-t*cl;nnpsia iti association \\ ith triploid! s~11cl1x~n1e at I Ci ant1 I i weeks’ gestation. Our patient inanil~stcd \t‘\UC prc-cclatnp~ia .it 1X weeks’ gestation. a t’ettls and placenta colraisrcnt \vith triploicly syndrome and bil,itcral tl1cc.a lutcin cysts. In \ iew of’s kno\\.n association of ll)diltidifi)rlll nlolc \\.ith early OIlset of‘ prcglmiq-intluccd tit pcl-tension. arid tlieca lutein cysts. we feel that t tic :tssoc.iatic~n of’placental hydatidiform degeneration, prc-cc hi11 psi;\, and 1tieca lutein cysts may be a conmori. hilt [cttwcc,gni/ed part of the triploidy s~ntlrontc.
..__
blood
]$
banding
111
~7-.-..--22
19”-----20
with Giemsa
in brief
of chromosomes
We wish to express thanks Cytopathology Laboratory Health, Bethesda, Maryland, chromosome analvses.
consis-
to Dr. Elizabeth kv. Chu and the of’ the National Institutes of for their help in preparing the
REFERENCES I. LS’ertelecki. \2’., et al: The clinical syndrome of triploidy, Obstet. Gynecol. 47:69. 1976. 2. Beischer, N. A., Fortune, D. W., and Fitzgeral, M. G.: Hydatidiform mole and coexistent foetus, both with triplid? chromosome constitution, Br. Med. J. 3:476. !967.
False negative oxytocin challenge test: Report of three cases
OXYTOCIN CHALLENGE ‘1‘~s.r (OC-I‘), which reflects unteroplacental respiratory function. is considered useful in the evaluation of‘ fetal well-being. Hence obstetricians employ it in the manageg-elnent of high-risk prcgnanc)-. The concept that a negative OCT ensures fetal survival for seven days is well accepted.‘, ’ However, a review of the literature reveals 20 instances* in
~I‘HF.
Reprint requests: Dr. David Gal, The Brookdale Hospital Medical Center, Department of Obstetrics and Gynecology, Linden Blvd. at Brookdale Plaza. Brooklyn. New York I 12 12. *Ref@rences will be supplied on request. OOO’L-9378/79/OlOt
11+03$00.30/0
0
19i9
TIw
c;. v.
i%shy
CO.
112
Communications
in brief
which fetal death occurred negative OCT, a c‘ircurnstance “false negative OCT.” ‘l‘hree negative OCT’s are presented
within seven days of ;t which mm be termed additional dases of false IWIT.
In Case I, 0. P., an I X-year-old primigr-avid wom;m, wa5 first seen in our pr-enatal clinic at 20 weeks’ gestarirm. AI 30 weeks’ gestation she developed mild pre-eclampsia and \tas admitted to the hospital. The plasma estl-iol level was 4.2 trg. per milliliter and the OCX‘ was negative (Fig. 1 ,,4). .I‘reatment consisted only of bed rest. .Two days afrer the negative ~~~~~1‘.
he noted violen letal movements I~~llowul 1~~ absent trtal atliviT\. The f&l heartbeat cwrld not be hear-d. The ncsT morning rhe patienr spontaneously entered labor and was delivered of a 2.900 Lgrx~~ t’emale stillbor-rr infant. The amniotic fluid contained thick meconium. Postmortem examination of the, l&ra. cot-d. and placenta did not contribute to our knowledge of’ the causr of death.
Communications
thirty-fifth week of gestation. The plasma estriol level irlc-I-eased gradually from 5.1 to 13.1 ng. per milliliter at :3X ~ccks and fcntt- OCT’s were negative. At 39 weeks, six days following the last negative OCT (Fig. 1, R) the patient complaincd of’lack of fetal activity for 48 hours. The diagnosis of fetal death was corrfirmcd by sonography and labor was induced the following morning. The patient was delivered of a Y,S50 gram. maccratcd. meconium-covered fetus. The placenta \howetl mat-ked calcifications and fihrinoid degettcrarion. No pros% abnormalities bcere found in the fetus or cctird. Autops) wax not permitted. In (:asc 9. U’. A., a 26.year-old woman. gravida 2. para 1. had an uneventful pregnancy until the thirty-second week of gestation. at s\,hich time she was discovered to have Class A diabctcs. I’la\rna rstriol levels were determined weekly after the thit-tyfifth week. The level increased gradually throllgh the fijrtieth \\eek. I-lowct\cr, at 11 weeks the plasma estriol \alue dropped fi-om a previous level of 10 to 5.5 ng. pet milliliter. OCT’\ \\ere also performed at weekly intervals beginning at the thirtv-sixth week of gestation and were negatiw, including that pe&rmed at 41 weeks (Fig. 1, C). Foul da>s after the last OC’l‘ the patient reported absent fetal movements for a period of 1,‘) hours. The fetal heartbeat was not audible. .l’he patient \vas delivered of a nonmacerated
in brief
stillhorn infant Z-1 hours later. after ox)tocitl induction ot labor. No ahnormalities of cord or fetus Mere found. The placenta showed marked calcifications and tibrinoid degeneration.
The
three
cases reported
occurred
among
would appear that this small incidence of talse negatisit\- should not be permitted to negate the continued LW of this \~aluahle test irt tbc mattagement of high-risk
pregnanq REFERENCES
1. Freeman. R. K.: The use of the oxytocin challenge test folantepartum clinical evaluation of uteroplacental respiratot-% function, A%. J, OHSI P I GI.~%LX.. 121: 481, 1975. 2. Schifrin, B. S.. Lapidus, iQ.. Doctor, G. S., et al.: Contraction stress test for antepartum f’etal evaluation. Obstet. Gynecol. 45: 459. 1975.
Information for authors Most of the provisions of the Copyright Act of 1976 became effective on January 1. 1978. Therefore, all manuscripts must be accompanied by the following written statement, signed by one author: “The undersigned author transfers all copyright ownership of‘ the manuscript (title of article) to The C. V. Mosby Company in the event the work is published. The undersigned author warr-ants that the article is original, is not under consideration by another journal, and has not been previously published. I sign for and accept responsibility fijr releasing this material on behalf of any and all co-authors.”
will be consulted,
when possible.
1,732
! 8 ,‘\
-__”
--IS
Fig. 2. Chromosomal
lf)
analysis
---_
I__
of fetal peripheral
tinued to show the theta lutein cysts. At 6 weeks postpartum the patirllt \vas normotensiw, with normal pelvic findings. kidne) function test results. and intravenous pyelogram. (:hl-omowme anal!,& of the fetal blood and fetal tissue j-e\ealetl a ti9,S?nortnalities. ‘I‘hre include the follorl:ing: small for gestational age, dysplasticcranial bones, small eyes with col~~l~on~;~s. facial cl&s. cutaneous s$act~l~ of hands aid feet. sinwati ~rc‘ases. cardiac defects. meningorr~~~elocele. or spina bifida, ornphalocele, and nlaldevelopmcnt of genitalia in nlales. X.he placenta char:~ctcristicall! dm~c~nst~-ate5 hydatidiform degeneration. which \\a4 prcsc’nt in .X to 55!1 of specimens. ‘Ili~ reversal ~rssocialion is evt‘i~ stronger, that is, the pr-C*Seilcc ot li~tlatitliform degeneration 1riea115 triploitl\ i.7’; of the tinlc. Due to the molar condition of the plac.cnta tlirrr. is a higll risk of clcveloping pregnan(‘yinducctl Ii\ pcrtcnsion ear1~ in gestation. Bcischer. Fortllllc’ , and I~itqeral” reported two patients with sewre prc-t*cl;nnpsia iti association \\ ith triploid! s~11cl1x~n1e at I Ci ant1 I i weeks’ gestation. Our patient inanil~stcd \t‘\UC prc-cclatnp~ia .it 1X weeks’ gestation. a t’ettls and placenta colraisrcnt \vith triploicly syndrome and bil,itcral tl1cc.a lutcin cysts. In \ iew of’s kno\\.n association of ll)diltidifi)rlll nlolc \\.ith early OIlset of‘ prcglmiq-intluccd tit pcl-tension. arid tlieca lutein cysts. we feel that t tic :tssoc.iatic~n of’placental hydatidiform degeneration, prc-cc hi11 psi;\, and 1tieca lutein cysts may be a conmori. hilt [cttwcc,gni/ed part of the triploidy s~ntlrontc.
..__
blood
]$
banding
111
~7-.-..--22
19”-----20
with Giemsa
in brief
of chromosomes
We wish to express thanks Cytopathology Laboratory Health, Bethesda, Maryland, chromosome analvses.
consis-
to Dr. Elizabeth kv. Chu and the of’ the National Institutes of for their help in preparing the
REFERENCES I. LS’ertelecki. \2’., et al: The clinical syndrome of triploidy, Obstet. Gynecol. 47:69. 1976. 2. Beischer, N. A., Fortune, D. W., and Fitzgeral, M. G.: Hydatidiform mole and coexistent foetus, both with triplid? chromosome constitution, Br. Med. J. 3:476. !967.
False negative oxytocin challenge test: Report of three cases
OXYTOCIN CHALLENGE ‘1‘~s.r (OC-I‘), which reflects unteroplacental respiratory function. is considered useful in the evaluation of‘ fetal well-being. Hence obstetricians employ it in the manageg-elnent of high-risk prcgnanc)-. The concept that a negative OCT ensures fetal survival for seven days is well accepted.‘, ’ However, a review of the literature reveals 20 instances* in
~I‘HF.
Reprint requests: Dr. David Gal, The Brookdale Hospital Medical Center, Department of Obstetrics and Gynecology, Linden Blvd. at Brookdale Plaza. Brooklyn. New York I 12 12. *Ref@rences will be supplied on request. OOO’L-9378/79/OlOt
11+03$00.30/0
0
19i9
TIw
c;. v.
i%shy
CO.
112
Communications
in brief
which fetal death occurred negative OCT, a c‘ircurnstance “false negative OCT.” ‘l‘hree negative OCT’s are presented
within seven days of ;t which mm be termed additional dases of false IWIT.
In Case I, 0. P., an I X-year-old primigr-avid wom;m, wa5 first seen in our pr-enatal clinic at 20 weeks’ gestarirm. AI 30 weeks’ gestation she developed mild pre-eclampsia and \tas admitted to the hospital. The plasma estl-iol level was 4.2 trg. per milliliter and the OCX‘ was negative (Fig. 1 ,,4). .I‘reatment consisted only of bed rest. .Two days afrer the negative ~~~~~1‘.
he noted violen letal movements I~~llowul 1~~ absent trtal atliviT\. The f&l heartbeat cwrld not be hear-d. The ncsT morning rhe patienr spontaneously entered labor and was delivered of a 2.900 Lgrx~~ t’emale stillbor-rr infant. The amniotic fluid contained thick meconium. Postmortem examination of the, l&ra. cot-d. and placenta did not contribute to our knowledge of’ the causr of death.
Communications
thirty-fifth week of gestation. The plasma estriol level irlc-I-eased gradually from 5.1 to 13.1 ng. per milliliter at :3X ~ccks and fcntt- OCT’s were negative. At 39 weeks, six days following the last negative OCT (Fig. 1, R) the patient complaincd of’lack of fetal activity for 48 hours. The diagnosis of fetal death was corrfirmcd by sonography and labor was induced the following morning. The patient was delivered of a Y,S50 gram. maccratcd. meconium-covered fetus. The placenta \howetl mat-ked calcifications and fihrinoid degettcrarion. No pros% abnormalities bcere found in the fetus or cctird. Autops) wax not permitted. In (:asc 9. U’. A., a 26.year-old woman. gravida 2. para 1. had an uneventful pregnancy until the thirty-second week of gestation. at s\,hich time she was discovered to have Class A diabctcs. I’la\rna rstriol levels were determined weekly after the thit-tyfifth week. The level increased gradually throllgh the fijrtieth \\eek. I-lowct\cr, at 11 weeks the plasma estriol \alue dropped fi-om a previous level of 10 to 5.5 ng. pet milliliter. OCT’\ \\ere also performed at weekly intervals beginning at the thirtv-sixth week of gestation and were negatiw, including that pe&rmed at 41 weeks (Fig. 1, C). Foul da>s after the last OC’l‘ the patient reported absent fetal movements for a period of 1,‘) hours. The fetal heartbeat was not audible. .l’he patient \vas delivered of a nonmacerated
in brief
stillhorn infant Z-1 hours later. after ox)tocitl induction ot labor. No ahnormalities of cord or fetus Mere found. The placenta showed marked calcifications and tibrinoid degeneration.
The
three
cases reported
occurred
among
would appear that this small incidence of talse negatisit\- should not be permitted to negate the continued LW of this \~aluahle test irt tbc mattagement of high-risk
pregnanq REFERENCES
1. Freeman. R. K.: The use of the oxytocin challenge test folantepartum clinical evaluation of uteroplacental respiratot-% function, A%. J, OHSI P I GI.~%LX.. 121: 481, 1975. 2. Schifrin, B. S.. Lapidus, iQ.. Doctor, G. S., et al.: Contraction stress test for antepartum f’etal evaluation. Obstet. Gynecol. 45: 459. 1975.
Information for authors Most of the provisions of the Copyright Act of 1976 became effective on January 1. 1978. Therefore, all manuscripts must be accompanied by the following written statement, signed by one author: “The undersigned author transfers all copyright ownership of‘ the manuscript (title of article) to The C. V. Mosby Company in the event the work is published. The undersigned author warr-ants that the article is original, is not under consideration by another journal, and has not been previously published. I sign for and accept responsibility fijr releasing this material on behalf of any and all co-authors.”
will be consulted,
when possible.
1,732
