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Dehydration-induced oligohydramnios
Volume 163 Number 3
5.
6. 7.
8. 9. 10. 11.
12. 13.
South: a decade of experience. Abstract 211. Sixth Congress, International Society for the study of Hypertension in Pregnancy. Montreal, May 25, 1988. Pritchard ]A, Cunningham FG, Pritchard SA. The Parkland Memorial Hospital protocol for treatment of eclampsia: evaluation of 245 cases. AM] OBSTET GVNECOL 1984; 148:951. Sibai BM, McCubbin ]H, Anderson GD, Lipshitz], Dilts PV. Eclampsia. 1. Observations from 67 recent cases. Obstet GynecoI1981;58:609. Sibai BM, Spinnato ]A, Watson DL, Lewis ]A, Anderson GD. Effect of magnesium sulfate on electroencephalographic findings in pre-eclampsia and eclampsia. Obstet Gynecol 1984;64:261. Delgado-Escueta AV, Bajorek ]G. Status epilepticus: mechanisms of brain damage and rational management. Epilepsia 1982;23(Suppl 1):S29-41. Department of Health. Report on confidential enquiries into maternal deaths in England and Wales 1982-84. London: Her Majesty's Stationery Office, 1989;34: 10-19. Kaunitz AM, Hughes ]M, Grimes DA, et al. Causes of maternal mortality in the United States. Obstet Gynecol 1985;65:605-12. Richards A, Graham D, Bullock R. Clinicopathological study of neurological complications due to hypertensive disorders of pregnancy. ] Neurol Neurosurg Psychiatry 1988;51:416. Berkowitz RD, ed. The management of hypertensive crises during pregnancy. In: Critical care of the obstetric patient. New York: Churchill Livingstone, 1983:299-334. Donaldson]O. Neurology of pregnancy. 2nd ed. London: WB Saunders, 1989:269-310.
Digoxin-like immunoreactive factor and respiratory distress syndrome To the Editors: Digoxin-like immunoreactive factor, as measured with a commercial digoxin antibody assay (Stratus I, Dade, Miami), begins to appear in measurable amounts (> 1.9 ng/ dl) in serum of normal pregnant women at approximately the thirty-fifth week of pregnancy.' Newborn respiratory distress syndrome also becomes infrequent at this gestational age. I found that when the maternal serum digoxin-like immunoreactive factor level is <1.9 ng/dl, the newborn will likely have respiratory distress syndrome. As shown in Table I, 18 patients who had amniocentesis at 32 to 39 weeks for determination of fetal lung maturity (lecithin/spingomyelin) had simultaneous maternal serum digoxin (digoxin-like immunoreactive factor) determinations by our clinical laboratory. A positive relationship was found (X·, p < 0.02). Eleven patients were delivered by cesarean section between 29 and 31 weeks' gestation because of severe hypertension; all had received steroids, anticonvulsants, and antihypertensive agents. Only four mothers had serum levels of digoxin >0.2 ng/dl immediately before delivery and none of their infants had more than mild respiratory distress syndrome as diagnosed by our neonatologists. By contrast, the other seven patients with no detectable maternal serum digoxin-like immunoreactive factor (digoxin) were all delivered of infants with severe respiratory distress syndrome. These cases support the concept but do not prove a causal relationship between maternal levels of digoxin-
Letters
1091
Table I. Eighteen cases with serum endoxin and amniotic fluid lecithin/ sphingomyelin determinations (receiving no drug therapy)
Maternal serum endoxin (digoxin) value
>0.19 mg/dl <0.20 mg/dl
Amniotic fluid lecithin / sphingomyelin ratio
>1.8
7
o
<1.9
2
9
like immunoreactive factor and fetal lung development. Both the elevated digoxin-like immunoreactive factor and minimal respiratory distress syndrome could reflect responses to fetal stress in preterm deliveries.' In pregnant sheep, Liggins and Forester· found that fetal adrenal cortisol production modulated both the onset of labor and fetal lung development. It has been proposed that digoxin-like immunoreactive factor is a steroid, has an adrenal origin, and plays the same role in humans as does cortisol in fetal sheep.' Digoxin-like immunoreactive factor is in part bound to serum proteins, serum levels are depressed by drugs (steroids, antihypertensives, and tocolytic agents) and there is a need for a more specific test of pregnancyrelated digoxin-like immunoreactive factor.' Despite these problems, studies should continue of digoxin-like immunoreactive factor in pregnancy complications. Robert C. Goodlin, MD City and County of Denver, Department of Health and Hospitals, 777 Bannock St., Denver, CO 80204-4507
REFERENCES 1. Goodlin RC, Makowski EL. Fetal endoxin and complications of pregnancy. West] Med 1988;148:590-2. 2. Liggins GC, Forester CS. Control of parturition in man. Bioi Reprod 1977;16:39-69.
Dehydration-induced oligohydramnios To the Editors: I read with interest the case report by Sherer et al. (Sherer DM, CullenJBH, Thompson HO, Woods JR J r. Transient oligohydramnios in a severely hypovolemic gravid woman at 35 weeks' gestation, with fluid reaccumulating immediately after intravenous maternal hydration. AM J OBSTET GYNECOL 1990; 162:770-1) in which severe nausea, vomiting, and diarrhea were associated with transient oligohydramnios. The authors attributed the oligohydramnios to maternal hypovolemia. However, the reactive nonstress test suggested that uterine blood flow was supplying adequate oxygenation to the fetal-placental unit. I propose that maternal plasma hyperosmolality, rather than hypovolemia, resulted in the development of oligohydramnios. Although plasma osmolality was not measured at presentation, the plasma sodium level was elevated for pregnancy' and maternal urine sample demonstrated a potent antidiuretic response. Because
1092
Letters
fetal plasma osmolality parallels maternal plasma osmolality (via transplacental flow), it is likely that a fetal antidiuretic response also was elicited. We have demonstrated that maternal dehydration (plasma osmolality increase of 10 mOsm) resulted in marked reductions in ovine amniotic fluid volume! probably as a result of vasopressin-mediated reductions in fetal urine3 and lung fluid production.' These findings, together with the case report, illustrate the importance of maintaining adequate hydration during exercise, thermal exposure, or gastrointestinal losses in pregnancy. Michael C. Ross, MD Department of Obstetrics and Gynecology, University of CaliforniaLos Angeles, 1000 West Carson St., Torrance, CA 90509
REFERENCES 1. Davison JM, Gilmore EA, Durr J, Robertson GL, Lindheimer MD. Altered osmotic thresholds for vasopressin secretion and thirst in human pregnancy. Am J Physiol 1984;246:Fl05-9. 2. Schreyer P, Sherman DJ, Ervin MG, Day L, Ross MG. Maternal dehydration: impact on ovine amniotic fluid volume and composition. J Devel Physiol [In press]. 3. Robillard JE, Weitzman RE. Developmental aspects of the fetal renal response to exogenous vasopressin. Am J Physiol 1980;238:F407-14. 4. Ross MG, Ervin G, Leake RD, Fu P, Fisher DA. Fetal lung liquid regulation by neuropeptides. AMJ OBSTET GVNECOL 1984;150:421-5.
Reply To the Editors: We appreciate Dr. Ross' comments concerning our case report and the opportunity to reply. Unfortunately we did not test maternal plasma and urine osmolality; however, plasma sodium, which was high for pregnancy, and low maternal urine specific gravity suggest an antidiuretic response that was appropriate for the severe maternal hypovolemic condition. We agree that maternal hyperosmolality could possibly be the underlying mechanism resulting in oligohydramnios. However, it would be difficult to differentiate between the independent effects of maternal hypovolemia and maternal hyperosmolality (and possible subsequent fetal hyperosmolality) in this case. Fetal antidiuretic hormone secretion is indeed a possible response to maternal hyperosmolality and may explain the oligohydramnios via a decrease in fetal urine output as suggested above. A reactive nons tress test, although reassuring, does not in itself imply uterine blood flow supplying adequate oxygenation to the fetal-placental unit. I. 2 A contraction stress test might have exposed a partially compromised fetal-placental unit as a result of compromised uterine blood flow. 3 Because of prematurity, oligohydramnios, and the possibility of causing iatrogenic umbilical cord compression, we elected not to perform this test. Retrospectively, because of the reaccumulation of the amniotic fluid volume with correc-
September 1990 Am J Obstet Gynecol
tion of the maternal hypovolemia, further testing for fetal well-being was not necessary. David M. Sherer, MD,Jacquelyn B. H. Cullen, MD, Howard O. Thompson, MD, and James R. Woods,Jr., MD Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynecology, Strong Memorial Hospital, Box 668, The University of Rochester School of Medicine and Dentistry, 601 Elmwood Ave., Rochester, NY 14642.
REFERENCES 1. Rochard F, Schifrin BS, Goupil F, Legrand H, Sureau C. Nonstressed fetal heart rate monitoring in the antepartum period. AM J OBSTET GVNECOL 1976;126:699-706. 2. Gennser G, Persson P. Biophysical assessment of placental function. Clin Obstet Gynecol 1986;13:521-52. 3. Freeman R, Anderson G, Dorchester W. A prospective multi-institutional study of antepartum fetal heart rate monitoring. II. Contraction stress test for primary surveillance. AM J OBSTET GVNECOLI982; 143:778-81.
A comment on thumbtacks for hemorrhage control
To the Editors: I read with interest the report by Patsner and Orr (Patsner B, Orr JW Jr. Intractable venous sacral hemorrhage: use of stainless steel thumbtacks to obtain hemostasis). Over the past 91/2 years we have had occasion to use the thumbtack maneuver outlined in this article on two occasions. Both patients were undergoing extensive cytoreductive surgery. In both instances the venous bleeding could not be controlled by packing, clips, bone wax, or ligature. A steel thumbtack was used in each case and worked almost immediately. These are the only two instances in which we were in need of this "trick," so it is difficult to assess its efficacy. Two caveats apply: First, not all thumbtacks are steel, and care must be taken not to use a metal that might corrode; second, when subsequent x-ray films are ordered for these patients, a panic-stricken call from the radiologist who is apt to be worried about the thumb-
Fig. 1. Radiograph showing placement of thumbtack (PA).
5.
6. 7.
8. 9. 10. 11.
12. 13.
South: a decade of experience. Abstract 211. Sixth Congress, International Society for the study of Hypertension in Pregnancy. Montreal, May 25, 1988. Pritchard ]A, Cunningham FG, Pritchard SA. The Parkland Memorial Hospital protocol for treatment of eclampsia: evaluation of 245 cases. AM] OBSTET GVNECOL 1984; 148:951. Sibai BM, McCubbin ]H, Anderson GD, Lipshitz], Dilts PV. Eclampsia. 1. Observations from 67 recent cases. Obstet GynecoI1981;58:609. Sibai BM, Spinnato ]A, Watson DL, Lewis ]A, Anderson GD. Effect of magnesium sulfate on electroencephalographic findings in pre-eclampsia and eclampsia. Obstet Gynecol 1984;64:261. Delgado-Escueta AV, Bajorek ]G. Status epilepticus: mechanisms of brain damage and rational management. Epilepsia 1982;23(Suppl 1):S29-41. Department of Health. Report on confidential enquiries into maternal deaths in England and Wales 1982-84. London: Her Majesty's Stationery Office, 1989;34: 10-19. Kaunitz AM, Hughes ]M, Grimes DA, et al. Causes of maternal mortality in the United States. Obstet Gynecol 1985;65:605-12. Richards A, Graham D, Bullock R. Clinicopathological study of neurological complications due to hypertensive disorders of pregnancy. ] Neurol Neurosurg Psychiatry 1988;51:416. Berkowitz RD, ed. The management of hypertensive crises during pregnancy. In: Critical care of the obstetric patient. New York: Churchill Livingstone, 1983:299-334. Donaldson]O. Neurology of pregnancy. 2nd ed. London: WB Saunders, 1989:269-310.
Digoxin-like immunoreactive factor and respiratory distress syndrome To the Editors: Digoxin-like immunoreactive factor, as measured with a commercial digoxin antibody assay (Stratus I, Dade, Miami), begins to appear in measurable amounts (> 1.9 ng/ dl) in serum of normal pregnant women at approximately the thirty-fifth week of pregnancy.' Newborn respiratory distress syndrome also becomes infrequent at this gestational age. I found that when the maternal serum digoxin-like immunoreactive factor level is <1.9 ng/dl, the newborn will likely have respiratory distress syndrome. As shown in Table I, 18 patients who had amniocentesis at 32 to 39 weeks for determination of fetal lung maturity (lecithin/spingomyelin) had simultaneous maternal serum digoxin (digoxin-like immunoreactive factor) determinations by our clinical laboratory. A positive relationship was found (X·, p < 0.02). Eleven patients were delivered by cesarean section between 29 and 31 weeks' gestation because of severe hypertension; all had received steroids, anticonvulsants, and antihypertensive agents. Only four mothers had serum levels of digoxin >0.2 ng/dl immediately before delivery and none of their infants had more than mild respiratory distress syndrome as diagnosed by our neonatologists. By contrast, the other seven patients with no detectable maternal serum digoxin-like immunoreactive factor (digoxin) were all delivered of infants with severe respiratory distress syndrome. These cases support the concept but do not prove a causal relationship between maternal levels of digoxin-
Letters
1091
Table I. Eighteen cases with serum endoxin and amniotic fluid lecithin/ sphingomyelin determinations (receiving no drug therapy)
Maternal serum endoxin (digoxin) value
>0.19 mg/dl <0.20 mg/dl
Amniotic fluid lecithin / sphingomyelin ratio
>1.8
7
o
<1.9
2
9
like immunoreactive factor and fetal lung development. Both the elevated digoxin-like immunoreactive factor and minimal respiratory distress syndrome could reflect responses to fetal stress in preterm deliveries.' In pregnant sheep, Liggins and Forester· found that fetal adrenal cortisol production modulated both the onset of labor and fetal lung development. It has been proposed that digoxin-like immunoreactive factor is a steroid, has an adrenal origin, and plays the same role in humans as does cortisol in fetal sheep.' Digoxin-like immunoreactive factor is in part bound to serum proteins, serum levels are depressed by drugs (steroids, antihypertensives, and tocolytic agents) and there is a need for a more specific test of pregnancyrelated digoxin-like immunoreactive factor.' Despite these problems, studies should continue of digoxin-like immunoreactive factor in pregnancy complications. Robert C. Goodlin, MD City and County of Denver, Department of Health and Hospitals, 777 Bannock St., Denver, CO 80204-4507
REFERENCES 1. Goodlin RC, Makowski EL. Fetal endoxin and complications of pregnancy. West] Med 1988;148:590-2. 2. Liggins GC, Forester CS. Control of parturition in man. Bioi Reprod 1977;16:39-69.
Dehydration-induced oligohydramnios To the Editors: I read with interest the case report by Sherer et al. (Sherer DM, CullenJBH, Thompson HO, Woods JR J r. Transient oligohydramnios in a severely hypovolemic gravid woman at 35 weeks' gestation, with fluid reaccumulating immediately after intravenous maternal hydration. AM J OBSTET GYNECOL 1990; 162:770-1) in which severe nausea, vomiting, and diarrhea were associated with transient oligohydramnios. The authors attributed the oligohydramnios to maternal hypovolemia. However, the reactive nonstress test suggested that uterine blood flow was supplying adequate oxygenation to the fetal-placental unit. I propose that maternal plasma hyperosmolality, rather than hypovolemia, resulted in the development of oligohydramnios. Although plasma osmolality was not measured at presentation, the plasma sodium level was elevated for pregnancy' and maternal urine sample demonstrated a potent antidiuretic response. Because
1092
Letters
fetal plasma osmolality parallels maternal plasma osmolality (via transplacental flow), it is likely that a fetal antidiuretic response also was elicited. We have demonstrated that maternal dehydration (plasma osmolality increase of 10 mOsm) resulted in marked reductions in ovine amniotic fluid volume! probably as a result of vasopressin-mediated reductions in fetal urine3 and lung fluid production.' These findings, together with the case report, illustrate the importance of maintaining adequate hydration during exercise, thermal exposure, or gastrointestinal losses in pregnancy. Michael C. Ross, MD Department of Obstetrics and Gynecology, University of CaliforniaLos Angeles, 1000 West Carson St., Torrance, CA 90509
REFERENCES 1. Davison JM, Gilmore EA, Durr J, Robertson GL, Lindheimer MD. Altered osmotic thresholds for vasopressin secretion and thirst in human pregnancy. Am J Physiol 1984;246:Fl05-9. 2. Schreyer P, Sherman DJ, Ervin MG, Day L, Ross MG. Maternal dehydration: impact on ovine amniotic fluid volume and composition. J Devel Physiol [In press]. 3. Robillard JE, Weitzman RE. Developmental aspects of the fetal renal response to exogenous vasopressin. Am J Physiol 1980;238:F407-14. 4. Ross MG, Ervin G, Leake RD, Fu P, Fisher DA. Fetal lung liquid regulation by neuropeptides. AMJ OBSTET GVNECOL 1984;150:421-5.
Reply To the Editors: We appreciate Dr. Ross' comments concerning our case report and the opportunity to reply. Unfortunately we did not test maternal plasma and urine osmolality; however, plasma sodium, which was high for pregnancy, and low maternal urine specific gravity suggest an antidiuretic response that was appropriate for the severe maternal hypovolemic condition. We agree that maternal hyperosmolality could possibly be the underlying mechanism resulting in oligohydramnios. However, it would be difficult to differentiate between the independent effects of maternal hypovolemia and maternal hyperosmolality (and possible subsequent fetal hyperosmolality) in this case. Fetal antidiuretic hormone secretion is indeed a possible response to maternal hyperosmolality and may explain the oligohydramnios via a decrease in fetal urine output as suggested above. A reactive nons tress test, although reassuring, does not in itself imply uterine blood flow supplying adequate oxygenation to the fetal-placental unit. I. 2 A contraction stress test might have exposed a partially compromised fetal-placental unit as a result of compromised uterine blood flow. 3 Because of prematurity, oligohydramnios, and the possibility of causing iatrogenic umbilical cord compression, we elected not to perform this test. Retrospectively, because of the reaccumulation of the amniotic fluid volume with correc-
September 1990 Am J Obstet Gynecol
tion of the maternal hypovolemia, further testing for fetal well-being was not necessary. David M. Sherer, MD,Jacquelyn B. H. Cullen, MD, Howard O. Thompson, MD, and James R. Woods,Jr., MD Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynecology, Strong Memorial Hospital, Box 668, The University of Rochester School of Medicine and Dentistry, 601 Elmwood Ave., Rochester, NY 14642.
REFERENCES 1. Rochard F, Schifrin BS, Goupil F, Legrand H, Sureau C. Nonstressed fetal heart rate monitoring in the antepartum period. AM J OBSTET GVNECOL 1976;126:699-706. 2. Gennser G, Persson P. Biophysical assessment of placental function. Clin Obstet Gynecol 1986;13:521-52. 3. Freeman R, Anderson G, Dorchester W. A prospective multi-institutional study of antepartum fetal heart rate monitoring. II. Contraction stress test for primary surveillance. AM J OBSTET GVNECOLI982; 143:778-81.
A comment on thumbtacks for hemorrhage control
To the Editors: I read with interest the report by Patsner and Orr (Patsner B, Orr JW Jr. Intractable venous sacral hemorrhage: use of stainless steel thumbtacks to obtain hemostasis). Over the past 91/2 years we have had occasion to use the thumbtack maneuver outlined in this article on two occasions. Both patients were undergoing extensive cytoreductive surgery. In both instances the venous bleeding could not be controlled by packing, clips, bone wax, or ligature. A steel thumbtack was used in each case and worked almost immediately. These are the only two instances in which we were in need of this "trick," so it is difficult to assess its efficacy. Two caveats apply: First, not all thumbtacks are steel, and care must be taken not to use a metal that might corrode; second, when subsequent x-ray films are ordered for these patients, a panic-stricken call from the radiologist who is apt to be worried about the thumb-
Fig. 1. Radiograph showing placement of thumbtack (PA).