1. Freeman, R. K.: Defining the role of amepartum monitoring, Contemp. Ob./Gyn. 13(3):65, 1979. 2. Beacham, E. 19., and Hernquist, W. C.: Abdominal pregnancy at Charity Hospital in New Orleans, AM J. OBSTET. GYNECOL. 84:1257. 1962.
6., and 2. Luqman, W., Smith, M., hikin, R,, ‘%$LmbS, Moore, W.: Maternal giycemia and birth .ti;eight, presented at Endocrinology 70, Seventh Bienniaf International Conference, Royal College of Physicians, London, July, 1979. (Abst. 77.)
ucose ~Q~eostas~e an uration To thr Editors: In a previous paper in your Joua~L,~ it was suggested that a normal glucose tolerance test performed before 24 weeks of gestation could not exclude gestational diabetes. We have analyzed data on 52 uneventful pregnancies at risk for diabetes terminating in physiologic labor and delivery at 40 + 2 weeks of the caiculated gestation. All subjects received a standardized glucose tolerance test after 24 weeks of gestation and had a fasting serum glucose (FBS) value of < 110 mg/lOO ml and a serum glucose value 2 hours following testing of < 140 mgi 100 ml. FBS had no correlation with gestational age at the time of testing (p > 0.2). The 2 hour postprandial value correlated with the FBS value (p < 0.05) but had a stronger correlation with gestational age at the time of testing (p < 0.005). This finding is being communicated. But further analyses of the data revealed that the 2 hour postprandial value/FBS value ratio also had a positive correlation with gestational age at the time of testing (p < 0.05) and a negative correlation with the gestational age at labor and delivery (11 < 0.005). These data are in agreement with the proposals of Tyson and Hock’ but further suggest that glucose homeostasis is dynamically related to gestational age even in the absence of diabetes. They also suggested that standardization of populations on the basis of a “normal” glucose tolerance test at undefined weeks of gestation may be questioned. If the magnitude of the fetoplacental unit is responsible for this phenomenon, it is possible that fetal maturation, fetal adiposity, and glycemic indices may have subtle interrelations.
w. Luqman,M.D. C. Suunders, M.D. w. Moore, M.D. M. Smith, Ph.D. R. Kulwin, B.A. ETldocrine-Metnbolisrn Service Department of Medicine and Depar-tmelct oj Obstetric5 wd Gpd0g
Madigan Army Medical Center Tacoma, Washington 98431 FE !. Tyson,
J. E., and
Hock,
R. A.: Gestation&
tional diabetes: An approach to therapy, GYNECOL.
125:1009,
1976.
and AM.
pregestaJ. OBSTET.
Flaksman and associates,” in their report on ia.zic prematurity and respiratory distress syndrome fail to mention the gender of their infants. other similar reports in the JoUaNA8.2’ 3 and elsewhere-‘-6 also do not designate gender. In our series of infants with “iatrogenic RIB,” we have noted an overwhelming male predominance. Brie hundred consecutive infants with RDS who -were admitted to our nursery in the latter part of 1977 were studied. Of these 100, 67 were male, which is consistent with the usual male predominance of RIDS.’ Iiowever, of the 28 infants deemed to have “iatrogenic RDS” 24 were male (x” = 6.16, p < 0.02. Table I).8
‘Fable I. Distribution or infants with iatrogenic and nonpreventable RDS by gender, as seen at the North Central Illinois Perinatal center, Peoria, Illinois, in late 1977
Male infant5 Female infants
24 4
Total Mean birth weight I SD
(grams) Vean gestaiionai age 2 SD (wk.)
28 2,355,3
35.3
43 29
67 33
72
100
k 687
1,724.Q
+ 650
i- 2.8
32.!
2: 3.6 __s_______l_
Wecenriyp Nielsen and associates” reported that at all stages of gestation male fetuses were associated with lower lecithinisphingomyelin (L/S) ratios than female fetuses, as well as lower amniotic fluid cortiso! levels. Their findings are consistent with the usual male predominance of RDS. and they also may explain the overwhelming male predominance in “‘iatrogenic RDS” which we have seen, for if a physician electively intervenes relatively late in pregnancy (as is attested to by the greater birth weights and gestational ages of infants with iatrogenic RDS,‘. 3-7 Table I) he is much more likely to encounter an immature male fetus rather than an immature female fetus. We wonder if Flaksman and colleagues have noted a similar overwhelming male predominance in iaK~Og&c
Volume 135 Number4
Correspondence
RDS, which would be consistent with the recently reported data on later maturation of L/S ratios in gestations with male fetuses. William Department of Pediatrics Peoria School of Medicine St. Francis Hospital-Medical 530 N.E. Glen Oak Avenue Peoria, Illinois 61637
F. Powers, M.D., M.P.H. Bonnie Patterson, M.D.
Center
REFERENCES
1. Flaksman, R. J., Vollman, J. H., and Benfield, D. G.: latrogenic prematurity due to elective termination of the uncomplicated pregnancy: A major perinatal health care problem. AM.J.OBSTET.GYNECOL. 132:885, 19’78. 2. Goldenberg, R. L.,, and Nelson, K.: latrogenic respiratory distress syndrome: An analysis of obstetric events preceding delivery of infants who develop respiratory distress syndrome, AM. J. OB,STET. GYNECOL. 123:617, 1975. 3. Hack, M., Fanaroff, A. A., Klaus, M.H., Mendelawitz, B. D., and Merkatz, I. R.: Neonatal respiratory distress following elective delivery. A preventable disease? AM. J. OBSTET. GYNECOL. 12!6:43, 1976. 4. Maisels, M. J., Rees, R., Marks, K., and Friedman, Z.: Elective delivery of the term fetus: An obstetrical hazard, J. A. M. A. 238:2036, 1977. 5. Cowett, R. M., and Oh, W.: Foam stability predictions of respiratory distress in infants delivered by repeat elective cesarean section, N. Engl. J. Med. 295: 1222, 1976. 6. Lewins, M. J., Whitfield, J. M., and Chance, G. W.: Neonatal respiratory distress 1978: The potential for prevention, Can. Med. Assoc. J. 120:1076, 1979. 7. Miller, H. C.: Respiratory distress syndrome of newborn infants. Ill. Stat&call evaluation of factors possibly affecting survival of premature infants, Pediatrics 31:573, 1963. 8. Powers, W. F.: Prevlentable neonatal respiratory distress syndrome (RDS) in North Central Illinois, I. M. J. In press. 9. Nielsen, H. C., Torday, J. S., Fencl, M., and Avery, M. E.: Sex differences in human fetal lung maturation, Pediatr. Res. 13:361, 19179.
We thank Drs. Patterson and Powers for their comments. Of the infants in our study who had hyaline membrane disease (26), 14 were female and 12 were male. Richard Care
Medical
Center
J. Flabman,
M.D.
Unit
of Akron
Contamination of iintrauterine pressure transducers To the Editor:
I was most interes;ted in the perceptive report Baker and colleagues “Water-borne contamination
pressure transducers,” AK J. OBSTET. 133:923, 1979), concerning the potential of the intrauterine pressu.re transducer, used in direct electronic fetal monitoring, as a source of nosocomial infection. Baker and colleagues concluded by stating that, “. ingenious engineering solutions to the problems of decontamination must be sought by the manufacturers who design this equipment.” It is most unfortunate that Baker and colleagues did not cite the paper of Roberts, A. M. and Steer, P. J.: Bacterial motility and intrauterine catheter-borne infection, Br. J. Obstet. Gynaecol. 84:336, 1977, in which the potential risks of bacterial infection secondary to intrauterine infections are most nicely described, analyzed, and discussed and the solutions to the problem are delineated as well. The British authors described multiple methods and techniques that may be used to reduce bacterial contamination from intrauterine catheters, including the use of “micropore bacterial ultrafilter,” “. . placing a loop in the catheter,” and care in being sure that catheter is not filled with amniotic fluid. It appears that the problem(s) described by Baker and colleagues have been publicized and published at least 2 years ago by Roberts and Steer who also proposed solutions to the problem(s) described, in contradistinction to Baker and colleagues. GYNECOL.
Syluain Fribourg, Southern Calijornia Permanente Medical 13652 Cantara Street Panorama City, California 91402
M.D., Group
F.A.C.0.G
REFERENCE
1. Roberts, trauterine Gynaecol.
A. M:, and Steer, catheter-borne 84:336, 1977.
P. J.: Bacterial infection,
motility Br. J.
and inObstet.
To the Editors:
T” 1 v the Editors:
Intensive
intrauterine
Reply to Dr. Fribourg
Reply to Drs. Powers and Patterson
Regional Neonatal Children’s Hospital 281 Locust Street Akron, Ohio 44308
551
of of
We thank Dr. Fribourg for his comments and for emphasizing an article dealing with the subject of contamination of monitoring equipment. We have reported that in routine obstetric use there is contamination of intrauterine pressure transducers with water-borne bacteria. The article by Roberts and Steer does not deal spe’cifically with intrauterine pressure transducers but with the intrauterine catheter in an in vitro situation. Roberts and Steer suggest “the dome or membrane may be contaminated by bacteria,” but there is no substantiation of this in their article. They point out that this pressure transducer cannot be autoclaved and they suggest that sterilization with a bactericidal fluid be performed. However, the manufacturers of this pressure transducer suggest this in their methods of care omfthese transducers but leave it as an option rather than making it a necessary part of
6., and 2. Luqman, W., Smith, M., hikin, R,, ‘%$LmbS, Moore, W.: Maternal giycemia and birth .ti;eight, presented at Endocrinology 70, Seventh Bienniaf International Conference, Royal College of Physicians, London, July, 1979. (Abst. 77.)
ucose ~Q~eostas~e an uration To thr Editors: In a previous paper in your Joua~L,~ it was suggested that a normal glucose tolerance test performed before 24 weeks of gestation could not exclude gestational diabetes. We have analyzed data on 52 uneventful pregnancies at risk for diabetes terminating in physiologic labor and delivery at 40 + 2 weeks of the caiculated gestation. All subjects received a standardized glucose tolerance test after 24 weeks of gestation and had a fasting serum glucose (FBS) value of < 110 mg/lOO ml and a serum glucose value 2 hours following testing of < 140 mgi 100 ml. FBS had no correlation with gestational age at the time of testing (p > 0.2). The 2 hour postprandial value correlated with the FBS value (p < 0.05) but had a stronger correlation with gestational age at the time of testing (p < 0.005). This finding is being communicated. But further analyses of the data revealed that the 2 hour postprandial value/FBS value ratio also had a positive correlation with gestational age at the time of testing (p < 0.05) and a negative correlation with the gestational age at labor and delivery (11 < 0.005). These data are in agreement with the proposals of Tyson and Hock’ but further suggest that glucose homeostasis is dynamically related to gestational age even in the absence of diabetes. They also suggested that standardization of populations on the basis of a “normal” glucose tolerance test at undefined weeks of gestation may be questioned. If the magnitude of the fetoplacental unit is responsible for this phenomenon, it is possible that fetal maturation, fetal adiposity, and glycemic indices may have subtle interrelations.
w. Luqman,M.D. C. Suunders, M.D. w. Moore, M.D. M. Smith, Ph.D. R. Kulwin, B.A. ETldocrine-Metnbolisrn Service Department of Medicine and Depar-tmelct oj Obstetric5 wd Gpd0g
Madigan Army Medical Center Tacoma, Washington 98431 FE !. Tyson,
J. E., and
Hock,
R. A.: Gestation&
tional diabetes: An approach to therapy, GYNECOL.
125:1009,
1976.
and AM.
pregestaJ. OBSTET.
Flaksman and associates,” in their report on ia.zic prematurity and respiratory distress syndrome fail to mention the gender of their infants. other similar reports in the JoUaNA8.2’ 3 and elsewhere-‘-6 also do not designate gender. In our series of infants with “iatrogenic RIB,” we have noted an overwhelming male predominance. Brie hundred consecutive infants with RDS who -were admitted to our nursery in the latter part of 1977 were studied. Of these 100, 67 were male, which is consistent with the usual male predominance of RIDS.’ Iiowever, of the 28 infants deemed to have “iatrogenic RDS” 24 were male (x” = 6.16, p < 0.02. Table I).8
‘Fable I. Distribution or infants with iatrogenic and nonpreventable RDS by gender, as seen at the North Central Illinois Perinatal center, Peoria, Illinois, in late 1977
Male infant5 Female infants
24 4
Total Mean birth weight I SD
(grams) Vean gestaiionai age 2 SD (wk.)
28 2,355,3
35.3
43 29
67 33
72
100
k 687
1,724.Q
+ 650
i- 2.8
32.!
2: 3.6 __s_______l_
Wecenriyp Nielsen and associates” reported that at all stages of gestation male fetuses were associated with lower lecithinisphingomyelin (L/S) ratios than female fetuses, as well as lower amniotic fluid cortiso! levels. Their findings are consistent with the usual male predominance of RDS. and they also may explain the overwhelming male predominance in “‘iatrogenic RDS” which we have seen, for if a physician electively intervenes relatively late in pregnancy (as is attested to by the greater birth weights and gestational ages of infants with iatrogenic RDS,‘. 3-7 Table I) he is much more likely to encounter an immature male fetus rather than an immature female fetus. We wonder if Flaksman and colleagues have noted a similar overwhelming male predominance in iaK~Og&c
Volume 135 Number4
Correspondence
RDS, which would be consistent with the recently reported data on later maturation of L/S ratios in gestations with male fetuses. William Department of Pediatrics Peoria School of Medicine St. Francis Hospital-Medical 530 N.E. Glen Oak Avenue Peoria, Illinois 61637
F. Powers, M.D., M.P.H. Bonnie Patterson, M.D.
Center
REFERENCES
1. Flaksman, R. J., Vollman, J. H., and Benfield, D. G.: latrogenic prematurity due to elective termination of the uncomplicated pregnancy: A major perinatal health care problem. AM.J.OBSTET.GYNECOL. 132:885, 19’78. 2. Goldenberg, R. L.,, and Nelson, K.: latrogenic respiratory distress syndrome: An analysis of obstetric events preceding delivery of infants who develop respiratory distress syndrome, AM. J. OB,STET. GYNECOL. 123:617, 1975. 3. Hack, M., Fanaroff, A. A., Klaus, M.H., Mendelawitz, B. D., and Merkatz, I. R.: Neonatal respiratory distress following elective delivery. A preventable disease? AM. J. OBSTET. GYNECOL. 12!6:43, 1976. 4. Maisels, M. J., Rees, R., Marks, K., and Friedman, Z.: Elective delivery of the term fetus: An obstetrical hazard, J. A. M. A. 238:2036, 1977. 5. Cowett, R. M., and Oh, W.: Foam stability predictions of respiratory distress in infants delivered by repeat elective cesarean section, N. Engl. J. Med. 295: 1222, 1976. 6. Lewins, M. J., Whitfield, J. M., and Chance, G. W.: Neonatal respiratory distress 1978: The potential for prevention, Can. Med. Assoc. J. 120:1076, 1979. 7. Miller, H. C.: Respiratory distress syndrome of newborn infants. Ill. Stat&call evaluation of factors possibly affecting survival of premature infants, Pediatrics 31:573, 1963. 8. Powers, W. F.: Prevlentable neonatal respiratory distress syndrome (RDS) in North Central Illinois, I. M. J. In press. 9. Nielsen, H. C., Torday, J. S., Fencl, M., and Avery, M. E.: Sex differences in human fetal lung maturation, Pediatr. Res. 13:361, 19179.
We thank Drs. Patterson and Powers for their comments. Of the infants in our study who had hyaline membrane disease (26), 14 were female and 12 were male. Richard Care
Medical
Center
J. Flabman,
M.D.
Unit
of Akron
Contamination of iintrauterine pressure transducers To the Editor:
I was most interes;ted in the perceptive report Baker and colleagues “Water-borne contamination
pressure transducers,” AK J. OBSTET. 133:923, 1979), concerning the potential of the intrauterine pressu.re transducer, used in direct electronic fetal monitoring, as a source of nosocomial infection. Baker and colleagues concluded by stating that, “. ingenious engineering solutions to the problems of decontamination must be sought by the manufacturers who design this equipment.” It is most unfortunate that Baker and colleagues did not cite the paper of Roberts, A. M. and Steer, P. J.: Bacterial motility and intrauterine catheter-borne infection, Br. J. Obstet. Gynaecol. 84:336, 1977, in which the potential risks of bacterial infection secondary to intrauterine infections are most nicely described, analyzed, and discussed and the solutions to the problem are delineated as well. The British authors described multiple methods and techniques that may be used to reduce bacterial contamination from intrauterine catheters, including the use of “micropore bacterial ultrafilter,” “. . placing a loop in the catheter,” and care in being sure that catheter is not filled with amniotic fluid. It appears that the problem(s) described by Baker and colleagues have been publicized and published at least 2 years ago by Roberts and Steer who also proposed solutions to the problem(s) described, in contradistinction to Baker and colleagues. GYNECOL.
Syluain Fribourg, Southern Calijornia Permanente Medical 13652 Cantara Street Panorama City, California 91402
M.D., Group
F.A.C.0.G
REFERENCE
1. Roberts, trauterine Gynaecol.
A. M:, and Steer, catheter-borne 84:336, 1977.
P. J.: Bacterial infection,
motility Br. J.
and inObstet.
To the Editors:
T” 1 v the Editors:
Intensive
intrauterine
Reply to Dr. Fribourg
Reply to Drs. Powers and Patterson
Regional Neonatal Children’s Hospital 281 Locust Street Akron, Ohio 44308
551
of of
We thank Dr. Fribourg for his comments and for emphasizing an article dealing with the subject of contamination of monitoring equipment. We have reported that in routine obstetric use there is contamination of intrauterine pressure transducers with water-borne bacteria. The article by Roberts and Steer does not deal spe’cifically with intrauterine pressure transducers but with the intrauterine catheter in an in vitro situation. Roberts and Steer suggest “the dome or membrane may be contaminated by bacteria,” but there is no substantiation of this in their article. They point out that this pressure transducer cannot be autoclaved and they suggest that sterilization with a bactericidal fluid be performed. However, the manufacturers of this pressure transducer suggest this in their methods of care omfthese transducers but leave it as an option rather than making it a necessary part of
