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Intrauterine fetal tachypnea
356
Communications
in brief
October Am. J. Obstet.
Megalocystis has been associated with pulmonary hypoplasia secondary either to extrinsic pressure on the fetal thorax or to the oligohydramnios itself. The compression of the abdomen and thorax was so severe in this case that it was felt to be incompatible with life. Decompression of the bladder apparently was lifesaving, and the presence of the fistulous tract allowed enough continued drainage for the fetus to reach 37 weeks’ gestation without repeat intervention. A recent article described the use of an indwelling suprapubic catheter that was placed into the fetus, which would minimize the need for repeat intervention.’ The inability to determine the L/S ratio is an interesting finding in that it did not reflect the pulmonary status of the baby. There is a strong possibility that the maternal bladder may have been inadvertently tapped. No amniotic fluid was present during labor or delivery to confirm these results. Although vaginal delivery has been advised with the prune-belly syndrome, abdominal dystocia was encountered in this case, where the abdominal girth was proportionately much larger than the fetal head. Most of the reported cases of prune-belly syndrome secondary to megalocystis have had poor outcomes, although some infants have done well after correction of the genitourinary anomalies.’ This baby is presently doing well at 6 months of age. In addition to the lack of abdominal musculature, he has an elevated bilirubin level secondary to biliary atresia and also has a suprapubic cystotomy. Present plans are to readmit him at 1 year of age to correct the genitourinary anomalies. How aggressively one should manage a case such as this is difficult to determine. Our experience demonstrates the feasibility of intrauterine intervention in the second trimester with continuation of the pregnancy until term. REFERENCES
1. Golbus, M. S., Harrison, M. R., Filly, R. A., et al.: In utero treatment of urinary tract obstruction, AM. J. OBSTET. GYNECOL.
142:383,
1982.
2. Eagle, J. F., and Barrett, G. S.: Congenital deficiency of abdominal musculature with associated genito-urinary abnormalities: A syndrome, Pediatrics 6:721, 1950.
Intrauterine fetal tachypnea ROBERTO ROMERO, M.D. FRANK A. CHERVENAK, M.D. RICHARD L. BERKOWITZ, M.D. JOHN C. HOBBINS, M.D. Department of Obstetrics and Gynecology, Yale University School of Medicine, New Haven, Connecticut Reprint requests: Roberto Romero, M.D., Yale University School of Medicine, Department of Obstetrics and Gynecology, 333 Cedar St., P. 0. Box 3333, New Haven, Connecticut 06510. 000%9378/82/190356+02$00.20/O
0
1982 The C.V.Mosby
Co
1, 1982 Gynecol.
RECENT DEVELOPMENTS in real-time gray-scale ultrasonography have made possible the observation and study of fetal breathing movements. Research has been directed toward fetal breathing movements as an indicator of fetal well-being. The normal rate of fetal breathing has been defined by Manning and associates’ to be 12 to 60 breaths per minute. Much attention has been directed toward decreased fetal breathing movement as a predictor of fetal compromise. However, observations of abnormally increased fetal breathing movements have been limited to two previously reported cases.‘, 2 Two further cases of intrauterine fetal tachypnea are presented and clinical implications are discussed. Case I. A 20-year-old, gravida 2, para I-O-O- 1, Class A diabetic woman was admitted at 36 weeks of gestation after a nonreactive nonstress test and an equivocal contraction stress test.
Past obstetric history revealed a spontaneous vaginal delivery after a term gestation during which the patient was diagnosed as having gestational diabetes. Past medical and surgical history was not remarkable. Family history revealed the patient’s grandmother to have diabetes. During this pregnancy results of a 3-hour glucose tolerance test performed at 27 weeks of gestation were normal. Plasma glucose values were as follows: fasting, 96 mg/dl; 1 hour, 144 mgidl; 2 hours, 90 mg/dl; and 3 hours, 119 mg/dl. Because of glycosuria in a random urine sample and the previous history of gestational diabetes, a repeat 3-hour glucose tolerance test was performed at 35 weeks; plasma glucose values were as follows: fasting, 100 mg/dl; 1 hour, 226 mg/dl; 2 hours, 250 mg/dl; and 3 hours, 199 mg/dl. A test for hemoglobin A,C performed at this time showed a value of 9.0% (normal value, 4% to 8%). The patient was placed on a 2,200 calorie American Diabetic Association diet. A nonstress test was nonreactive and a contraction stress test was equivocal. Because of the gestational diabetes at 36 weeks of gestation and an equivocal contraction stress test, an amniocentesis for determination of the lecithin/sphingomyelin (L/S) ratio was performed. The following day the L/S ratio was 5.0, a repeat
contraction stress test was positive, and the decision was made to induce labor. Four hours after the beginning of the induction, there was difficulty in obtaining an adequate fetal heart rate tracing with the external monitor. With Doppler ultrasound, the nursing staff detected unusual frequency changes in the fetal heart rate. A real-time linear array transducer was applied, and intermittent episodes of fetal breathing movements at a rate of 80 to 90 per minute were detected. Breathing movements were shallow. The fetal heart rate was 140 bpm. The plasma glucose level at this time was 160 mg/dl. Artificial rupture of the membranes was performed. An internal fetal heart rate tracing revealed moderate cord patterns and occasional late decelerations. A scalp pH was 7.26. Subsequently, the late decelerations recurred, and a scalp sample pH was 7.13. An emergency cesarean section was performed. A female infant, with Apgar scores of 5 and 7, was delivered: the umbilical cord pH was 7.20. The respiratory rate of the neonate was 50 bpm. The results of a Dextrostix test dropped to 25 mgidl, but the infant responded rapidly to oral feeding. Ca~r 2. A 29-year old, gravida 3, para l-0-1-1, Class B diabetic woman was transferred to Yale-New Haven Hospital at
Volume
144
Communications
Number 3
34 weeks of gestation because of polyhydramnios, falling plasma estriol values, and decreasing insulin requirements. The patient was diagnosed as diabetic during her first pregnancy at the time of a routine glucose screen. After delivery, she was placed on a diet and required 30 units of NPH insulin daily for adequate control. During this pregnancy plasma glucose levels were in the range of 200 to 300 mgidl, and she required 170 U of NPH insulin and 70 U of regular insulin in the morning and 90 LJ of NPH insulin and 70 U of regular insulin in the afternoon. Despite these high doses of insulin, control of diabetes was considered to he poor. Three days prior to admission the patient had been admitted to another hospital for the treatment of maxillary sinusitis with parenteral antibiotics. A precipitate drop of insulin requirements was observed to the extent that no insulin was required to maintain a plasma glucose level of 120 mg/dl. Serial unconjugated free estriol levels showed an 80% drop compared with previous values. Four days after admission, a real-time examination revealed a singleton fetus in a breech presentation with an increased amount of amniotic fluid. Fetal breathing frequency was 100 to 120 per minute and very vigorous. Episodes of fetal apnea were also observed. The fetal heart rate was 130 bpm. An attempt was made to perform a contraction stress test. but this was technically impossible because of the continuous fetal movement. External fetal heart rate monitoring was uninterpretable. Because of the precipitate fall in insulin requirements, the fall in estriol values, the inability to monitor the patient adequately, the presence of polyhydramnios, and an unexplained fetal tachypnea, the decision was made to perform a repeat cesarean section. A 2,500 gm female infant, with Apgar scores of 9 and 9, was delivered. Physical examination of the newborn infant including respiratory rate was within normal limits. The cord pH was 7.23. A Dextrostix test showed a value of 45 mg/dl, but values became normal after oral feeding. Intrauterine fetal tachypnea is a rare event, prior to this report only two cases have been reported the English literature. Manning and associates’ had
in brief
357
deteriorating fetal status. In the other case it was discovered during an attempt to investigate an unexplained sound detected during external fetal monitoring. All reported cases of intrauterine fetal tachypnea have occurred in diabetic mothers. In the two cases presented in this report, there was objective evidence of chronic hyperglycemia and poor metabolic control. This finding suggests that either hyperglycemia or another metabolic derangement associated with diabetes may have a role in the production of intrauterine fetal tachypnea. Although intrauterine fetal tachypnea falls outside the accepted limits of normal for the fetal breathing rate, it remains to be determined whether these findings have biologic and clinical significance as an indicator of fetal compromise. In Boddy and Dawes’2 case of intrauterine fetal tachypnea, fetal death occurred 48 hours after the observation. In the current report one patient underwent cesarean section because of documented fetal acidosis. In the other patient, a combination of falling estriol levels, a precipitate drop in insulin requirements, and an inability to monitor the patient adequately prompted delivery of the infant, who had an umbilical cord pH of 7.23. Fetal distress was not observed in only one of the reported cases of intrauterine fetal tachypnea. More observations are necessary to determine if intrauterine fetal tachypnea is an indicator of fetal compromise per se or merely associated with poor metabolic control of diabetes mellitus. Since
submission
of this
manuscript,
Duff and associates 1982) have reported an antepartum death in a fetus with intrauterine fetal tachypnea born to a nondiabetic mother. This case supports the view that intrauterine tachypnea is a sign of fetal compromise and that it may occur without maternal carbohydrate intolerance.
(AM. J. OBSTET. GYNECOL. 142:1054,
and in
observed only one case after they recorded 3,000 hours of fetal breathing in 1,200 patients. In one of our patients the observation was made as part of the evaluation of
REFERENCES 1. Manning, F. A., Heaman, M., Boyce, D., et al.: Intrauterine fetal tachypnea, Obstet. Gynecol. 5&X:398, 1981. 2. Boddy, K., and Dawes, G. S.; Fetal breathing, Br. Med. Bull. 31:1, 1975.
Communications
in brief
October Am. J. Obstet.
Megalocystis has been associated with pulmonary hypoplasia secondary either to extrinsic pressure on the fetal thorax or to the oligohydramnios itself. The compression of the abdomen and thorax was so severe in this case that it was felt to be incompatible with life. Decompression of the bladder apparently was lifesaving, and the presence of the fistulous tract allowed enough continued drainage for the fetus to reach 37 weeks’ gestation without repeat intervention. A recent article described the use of an indwelling suprapubic catheter that was placed into the fetus, which would minimize the need for repeat intervention.’ The inability to determine the L/S ratio is an interesting finding in that it did not reflect the pulmonary status of the baby. There is a strong possibility that the maternal bladder may have been inadvertently tapped. No amniotic fluid was present during labor or delivery to confirm these results. Although vaginal delivery has been advised with the prune-belly syndrome, abdominal dystocia was encountered in this case, where the abdominal girth was proportionately much larger than the fetal head. Most of the reported cases of prune-belly syndrome secondary to megalocystis have had poor outcomes, although some infants have done well after correction of the genitourinary anomalies.’ This baby is presently doing well at 6 months of age. In addition to the lack of abdominal musculature, he has an elevated bilirubin level secondary to biliary atresia and also has a suprapubic cystotomy. Present plans are to readmit him at 1 year of age to correct the genitourinary anomalies. How aggressively one should manage a case such as this is difficult to determine. Our experience demonstrates the feasibility of intrauterine intervention in the second trimester with continuation of the pregnancy until term. REFERENCES
1. Golbus, M. S., Harrison, M. R., Filly, R. A., et al.: In utero treatment of urinary tract obstruction, AM. J. OBSTET. GYNECOL.
142:383,
1982.
2. Eagle, J. F., and Barrett, G. S.: Congenital deficiency of abdominal musculature with associated genito-urinary abnormalities: A syndrome, Pediatrics 6:721, 1950.
Intrauterine fetal tachypnea ROBERTO ROMERO, M.D. FRANK A. CHERVENAK, M.D. RICHARD L. BERKOWITZ, M.D. JOHN C. HOBBINS, M.D. Department of Obstetrics and Gynecology, Yale University School of Medicine, New Haven, Connecticut Reprint requests: Roberto Romero, M.D., Yale University School of Medicine, Department of Obstetrics and Gynecology, 333 Cedar St., P. 0. Box 3333, New Haven, Connecticut 06510. 000%9378/82/190356+02$00.20/O
0
1982 The C.V.Mosby
Co
1, 1982 Gynecol.
RECENT DEVELOPMENTS in real-time gray-scale ultrasonography have made possible the observation and study of fetal breathing movements. Research has been directed toward fetal breathing movements as an indicator of fetal well-being. The normal rate of fetal breathing has been defined by Manning and associates’ to be 12 to 60 breaths per minute. Much attention has been directed toward decreased fetal breathing movement as a predictor of fetal compromise. However, observations of abnormally increased fetal breathing movements have been limited to two previously reported cases.‘, 2 Two further cases of intrauterine fetal tachypnea are presented and clinical implications are discussed. Case I. A 20-year-old, gravida 2, para I-O-O- 1, Class A diabetic woman was admitted at 36 weeks of gestation after a nonreactive nonstress test and an equivocal contraction stress test.
Past obstetric history revealed a spontaneous vaginal delivery after a term gestation during which the patient was diagnosed as having gestational diabetes. Past medical and surgical history was not remarkable. Family history revealed the patient’s grandmother to have diabetes. During this pregnancy results of a 3-hour glucose tolerance test performed at 27 weeks of gestation were normal. Plasma glucose values were as follows: fasting, 96 mg/dl; 1 hour, 144 mgidl; 2 hours, 90 mg/dl; and 3 hours, 119 mg/dl. Because of glycosuria in a random urine sample and the previous history of gestational diabetes, a repeat 3-hour glucose tolerance test was performed at 35 weeks; plasma glucose values were as follows: fasting, 100 mg/dl; 1 hour, 226 mg/dl; 2 hours, 250 mg/dl; and 3 hours, 199 mg/dl. A test for hemoglobin A,C performed at this time showed a value of 9.0% (normal value, 4% to 8%). The patient was placed on a 2,200 calorie American Diabetic Association diet. A nonstress test was nonreactive and a contraction stress test was equivocal. Because of the gestational diabetes at 36 weeks of gestation and an equivocal contraction stress test, an amniocentesis for determination of the lecithin/sphingomyelin (L/S) ratio was performed. The following day the L/S ratio was 5.0, a repeat
contraction stress test was positive, and the decision was made to induce labor. Four hours after the beginning of the induction, there was difficulty in obtaining an adequate fetal heart rate tracing with the external monitor. With Doppler ultrasound, the nursing staff detected unusual frequency changes in the fetal heart rate. A real-time linear array transducer was applied, and intermittent episodes of fetal breathing movements at a rate of 80 to 90 per minute were detected. Breathing movements were shallow. The fetal heart rate was 140 bpm. The plasma glucose level at this time was 160 mg/dl. Artificial rupture of the membranes was performed. An internal fetal heart rate tracing revealed moderate cord patterns and occasional late decelerations. A scalp pH was 7.26. Subsequently, the late decelerations recurred, and a scalp sample pH was 7.13. An emergency cesarean section was performed. A female infant, with Apgar scores of 5 and 7, was delivered: the umbilical cord pH was 7.20. The respiratory rate of the neonate was 50 bpm. The results of a Dextrostix test dropped to 25 mgidl, but the infant responded rapidly to oral feeding. Ca~r 2. A 29-year old, gravida 3, para l-0-1-1, Class B diabetic woman was transferred to Yale-New Haven Hospital at
Volume
144
Communications
Number 3
34 weeks of gestation because of polyhydramnios, falling plasma estriol values, and decreasing insulin requirements. The patient was diagnosed as diabetic during her first pregnancy at the time of a routine glucose screen. After delivery, she was placed on a diet and required 30 units of NPH insulin daily for adequate control. During this pregnancy plasma glucose levels were in the range of 200 to 300 mgidl, and she required 170 U of NPH insulin and 70 U of regular insulin in the morning and 90 LJ of NPH insulin and 70 U of regular insulin in the afternoon. Despite these high doses of insulin, control of diabetes was considered to he poor. Three days prior to admission the patient had been admitted to another hospital for the treatment of maxillary sinusitis with parenteral antibiotics. A precipitate drop of insulin requirements was observed to the extent that no insulin was required to maintain a plasma glucose level of 120 mg/dl. Serial unconjugated free estriol levels showed an 80% drop compared with previous values. Four days after admission, a real-time examination revealed a singleton fetus in a breech presentation with an increased amount of amniotic fluid. Fetal breathing frequency was 100 to 120 per minute and very vigorous. Episodes of fetal apnea were also observed. The fetal heart rate was 130 bpm. An attempt was made to perform a contraction stress test. but this was technically impossible because of the continuous fetal movement. External fetal heart rate monitoring was uninterpretable. Because of the precipitate fall in insulin requirements, the fall in estriol values, the inability to monitor the patient adequately, the presence of polyhydramnios, and an unexplained fetal tachypnea, the decision was made to perform a repeat cesarean section. A 2,500 gm female infant, with Apgar scores of 9 and 9, was delivered. Physical examination of the newborn infant including respiratory rate was within normal limits. The cord pH was 7.23. A Dextrostix test showed a value of 45 mg/dl, but values became normal after oral feeding. Intrauterine fetal tachypnea is a rare event, prior to this report only two cases have been reported the English literature. Manning and associates’ had
in brief
357
deteriorating fetal status. In the other case it was discovered during an attempt to investigate an unexplained sound detected during external fetal monitoring. All reported cases of intrauterine fetal tachypnea have occurred in diabetic mothers. In the two cases presented in this report, there was objective evidence of chronic hyperglycemia and poor metabolic control. This finding suggests that either hyperglycemia or another metabolic derangement associated with diabetes may have a role in the production of intrauterine fetal tachypnea. Although intrauterine fetal tachypnea falls outside the accepted limits of normal for the fetal breathing rate, it remains to be determined whether these findings have biologic and clinical significance as an indicator of fetal compromise. In Boddy and Dawes’2 case of intrauterine fetal tachypnea, fetal death occurred 48 hours after the observation. In the current report one patient underwent cesarean section because of documented fetal acidosis. In the other patient, a combination of falling estriol levels, a precipitate drop in insulin requirements, and an inability to monitor the patient adequately prompted delivery of the infant, who had an umbilical cord pH of 7.23. Fetal distress was not observed in only one of the reported cases of intrauterine fetal tachypnea. More observations are necessary to determine if intrauterine fetal tachypnea is an indicator of fetal compromise per se or merely associated with poor metabolic control of diabetes mellitus. Since
submission
of this
manuscript,
Duff and associates 1982) have reported an antepartum death in a fetus with intrauterine fetal tachypnea born to a nondiabetic mother. This case supports the view that intrauterine tachypnea is a sign of fetal compromise and that it may occur without maternal carbohydrate intolerance.
(AM. J. OBSTET. GYNECOL. 142:1054,
and in
observed only one case after they recorded 3,000 hours of fetal breathing in 1,200 patients. In one of our patients the observation was made as part of the evaluation of
REFERENCES 1. Manning, F. A., Heaman, M., Boyce, D., et al.: Intrauterine fetal tachypnea, Obstet. Gynecol. 5&X:398, 1981. 2. Boddy, K., and Dawes, G. S.; Fetal breathing, Br. Med. Bull. 31:1, 1975.