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Maternal hypothermia: An unusual complication of magnesium sulfate therapy
Maternal hypothermia: An unusual complication of magnesium sulfate therapy John F. Rodis, M.D., Anthony M. Vintzileos, M.D., Winston A. Campbell, M.D., Jeffrey L. Deaton, M.D., and David J. Nocbimson, M.D. Farmington, Connecticut Reported is a case of maternal hypothermia associated with magnesium sulfate therapy for treatment of preterm labor. Hypothermia was accompanied by fetal and maternal bradycardia. After discontinuation of magnesium sulfate infusion, maternal temperature, pulse, and fetal heart rate gradually returned to normal. No adverse effects were noted on either maternal or fetal outcome. (AM J OBSTET GYNECOL
1987;156:435-6.)
Key words: Hypothermia, magnesium sulfate
Magnesium sulfate is commonly used in the treatment of preeclampsia and preterm labor. Known maternal side effects are respiratory depression, electrocardiogram abnormalities (increased P-R interval, prolonged QRS interval, increased T wave), depression of deep tendon reflexes, and cardiac arrest. 1 To the best of our knowledge this is the first case report of maternal hypothermia secondary to magnesium sulfate therapy. Case report B. H., a 30-year-old woman, gravida 7, para 2-1-3-3, was transferred to the University of Connecticut Health Center at 305/1 weeks' gestation because of preterm labor. Past obstetric history was significant for a preterm vaginal breech delivery, two spontaneous vaginal deliveries at term, a molar pregnancy, and two elective firsttrimester abortions. Physical examination revealed an oral temperature of 99.8° F, pulse 80 bpm, respirations 20/min, and blood pressure 130170 mm Hg. Careful speculum examination revealed the cervix to be closed and uneffaced with no vaginal bleeding noted. Ultrasound revealed a single viable fetus in a vertex presentation with a complete placenta previa. Amniotic fluid volume appeared adequate. Estimated fetal weight was 1825 gm. Fetal biophysical profile was reassuring. An external fetal monitor revealed uterine contractions every 8 to IO minutes and a baseline fetal heart rate of 140 to 150 bpm. The patient received Celestone, 12 mg intramuscularly, to promote fetal pulmonary maturity and a 4 gm
intravenous loading dose of magnesium sulfate. A maintenance infusion of magnesium sulfate was initiated at a rate of 2 gm/hr. Persistent contractions necessitated an increase in the infusion to 3 gm/hr, which eliminated all uterine activity. After 2 hours at the new infusion rate the serum magnesium level was 5.2 mg/di. Maternal vital signs were oral temperature of 97° F, pulse 94 bpm, and blood pressure 120/80 mm Hg. Twelve hours after admission the fetal heart rate was noted to be 110 bpm. The maternal vital signs were rectal temperature 95.8° F, pulse 64 bpm, blood pressure 90/50 mm Hg, and respirations 18/min. The patient complained of lethargy and diplopia. In spite of a serum magnesium level of only 6.6 mg/di, the magnesium sulfate infusion was discontinued. During the next 6 hours the patient's visual and cerebral abnormalities cleared. Maternal temperature slowly increased, and 6 hours after cessation of magnesium sulfate therapy vital signs were temperature 98° F, pulse 80 bpm, and blood pressure 120/60 mm Hg. No uterine contractions or bleeding was noted and baseline fetal heart rate returned to 130 to 140 bpm with normal variability. Forty-eight hours after admission the patient had an episode of heavy vaginal bleeding, uterine contractions, and fetal tachycardia. A primary cesarean section was performed. A 1790 gm female infant was delivered with Apgar scores of 3 and 8 at 1 and 5 minutes, respectively. Arterial and venous cord pH values were 7.28 and 7.35, respectively. Placental cultures taken were later reported positive for Listeria monocytogenes.
From the Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynecology, The University of Connecticut Health Center. Received for publication July 15, 1986; revised August 22, 1986; accepted August 27, 1986. Reprint requesfs:johnRodis, M.D., Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynecology, The University of Connecticut Health Center, Farmington, CT 06032.
Comment In humans, body temperature is maintained within a narrow range despite extremes in environmental conditions and physical activity. The control of body temperature is ~ function of cerebral centers located in the hypothalamus. Oral temperatures <96° F are rarely encountered.2 Rectal temperatures are usually 0.5° to 435
436 Rodis et al.
1.0° F higher than oral values. When there is a strong stimulus for heat production, muscle activity may increase to the point of shivering or even to a generalized rigor. Instillation of cool intravenous fluids could have caused the observed hypothermia, but this is an unlikely cause in this patient. The fact that the temperature gradually returned to normal after discontinuation of magnesium sulfate, even though the total infusion rate remained constant, implicated the drug rather than the fluids as the source of hypothermia. Hypothermia may also occur in patients with myxedema or infection. Since the patient was clinically euthyroid before and after the episode of hypothermia and had no history of thyroid disease, these are unlikely causes. Despite the recovery of Listeria monocytogenes from the placenta, the prompt resolution of hypothermia after cessation of magnesium sulfate therapy would support that magnesium sulfate rather than infection was the cause of the significant decrease in body temperature in this patient. In conclusion, it appears that maternal hypothermia
February 1987 Am J Obstet Gynecol
may be a complication of intravenous magnesium sulfate administration. One could hypothesize that magnesium sulfate might act centrally at the hypothalamic level or peripherally at the motor end plate to suppress inuscle activity, hence causing decreased heat production that results in hypothermia. It is possible that milder degrees of hypothemia occur more commonly in patients receiving magnesium sulfate. However, this may not be brought to the attention of the physician, especially in the setting of severe preeclampsia or premature labor, when the attendant would be most concerned with other vital signs. The effect of magnesium sulfate on maternal temperature regulation appears to be reversible and does hot seem to be associated with significant maternal or neonatal morbidity. REFERENCES I. Wacker WEC, Pavis AF. Magnesium metabolism. N Engl J Med I 968;278:65. 2. Petersdorf RG. Disturbances of heat regulation. In: Petersdorf RG, Adams RD, Braunwald E, et al. eds. Harrison's principles of internal medicine. 10th ed. New York: McGraw-Hill, 1983:50-7.
1987;156:435-6.)
Key words: Hypothermia, magnesium sulfate
Magnesium sulfate is commonly used in the treatment of preeclampsia and preterm labor. Known maternal side effects are respiratory depression, electrocardiogram abnormalities (increased P-R interval, prolonged QRS interval, increased T wave), depression of deep tendon reflexes, and cardiac arrest. 1 To the best of our knowledge this is the first case report of maternal hypothermia secondary to magnesium sulfate therapy. Case report B. H., a 30-year-old woman, gravida 7, para 2-1-3-3, was transferred to the University of Connecticut Health Center at 305/1 weeks' gestation because of preterm labor. Past obstetric history was significant for a preterm vaginal breech delivery, two spontaneous vaginal deliveries at term, a molar pregnancy, and two elective firsttrimester abortions. Physical examination revealed an oral temperature of 99.8° F, pulse 80 bpm, respirations 20/min, and blood pressure 130170 mm Hg. Careful speculum examination revealed the cervix to be closed and uneffaced with no vaginal bleeding noted. Ultrasound revealed a single viable fetus in a vertex presentation with a complete placenta previa. Amniotic fluid volume appeared adequate. Estimated fetal weight was 1825 gm. Fetal biophysical profile was reassuring. An external fetal monitor revealed uterine contractions every 8 to IO minutes and a baseline fetal heart rate of 140 to 150 bpm. The patient received Celestone, 12 mg intramuscularly, to promote fetal pulmonary maturity and a 4 gm
intravenous loading dose of magnesium sulfate. A maintenance infusion of magnesium sulfate was initiated at a rate of 2 gm/hr. Persistent contractions necessitated an increase in the infusion to 3 gm/hr, which eliminated all uterine activity. After 2 hours at the new infusion rate the serum magnesium level was 5.2 mg/di. Maternal vital signs were oral temperature of 97° F, pulse 94 bpm, and blood pressure 120/80 mm Hg. Twelve hours after admission the fetal heart rate was noted to be 110 bpm. The maternal vital signs were rectal temperature 95.8° F, pulse 64 bpm, blood pressure 90/50 mm Hg, and respirations 18/min. The patient complained of lethargy and diplopia. In spite of a serum magnesium level of only 6.6 mg/di, the magnesium sulfate infusion was discontinued. During the next 6 hours the patient's visual and cerebral abnormalities cleared. Maternal temperature slowly increased, and 6 hours after cessation of magnesium sulfate therapy vital signs were temperature 98° F, pulse 80 bpm, and blood pressure 120/60 mm Hg. No uterine contractions or bleeding was noted and baseline fetal heart rate returned to 130 to 140 bpm with normal variability. Forty-eight hours after admission the patient had an episode of heavy vaginal bleeding, uterine contractions, and fetal tachycardia. A primary cesarean section was performed. A 1790 gm female infant was delivered with Apgar scores of 3 and 8 at 1 and 5 minutes, respectively. Arterial and venous cord pH values were 7.28 and 7.35, respectively. Placental cultures taken were later reported positive for Listeria monocytogenes.
From the Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynecology, The University of Connecticut Health Center. Received for publication July 15, 1986; revised August 22, 1986; accepted August 27, 1986. Reprint requesfs:johnRodis, M.D., Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynecology, The University of Connecticut Health Center, Farmington, CT 06032.
Comment In humans, body temperature is maintained within a narrow range despite extremes in environmental conditions and physical activity. The control of body temperature is ~ function of cerebral centers located in the hypothalamus. Oral temperatures <96° F are rarely encountered.2 Rectal temperatures are usually 0.5° to 435
436 Rodis et al.
1.0° F higher than oral values. When there is a strong stimulus for heat production, muscle activity may increase to the point of shivering or even to a generalized rigor. Instillation of cool intravenous fluids could have caused the observed hypothermia, but this is an unlikely cause in this patient. The fact that the temperature gradually returned to normal after discontinuation of magnesium sulfate, even though the total infusion rate remained constant, implicated the drug rather than the fluids as the source of hypothermia. Hypothermia may also occur in patients with myxedema or infection. Since the patient was clinically euthyroid before and after the episode of hypothermia and had no history of thyroid disease, these are unlikely causes. Despite the recovery of Listeria monocytogenes from the placenta, the prompt resolution of hypothermia after cessation of magnesium sulfate therapy would support that magnesium sulfate rather than infection was the cause of the significant decrease in body temperature in this patient. In conclusion, it appears that maternal hypothermia
February 1987 Am J Obstet Gynecol
may be a complication of intravenous magnesium sulfate administration. One could hypothesize that magnesium sulfate might act centrally at the hypothalamic level or peripherally at the motor end plate to suppress inuscle activity, hence causing decreased heat production that results in hypothermia. It is possible that milder degrees of hypothemia occur more commonly in patients receiving magnesium sulfate. However, this may not be brought to the attention of the physician, especially in the setting of severe preeclampsia or premature labor, when the attendant would be most concerned with other vital signs. The effect of magnesium sulfate on maternal temperature regulation appears to be reversible and does hot seem to be associated with significant maternal or neonatal morbidity. REFERENCES I. Wacker WEC, Pavis AF. Magnesium metabolism. N Engl J Med I 968;278:65. 2. Petersdorf RG. Disturbances of heat regulation. In: Petersdorf RG, Adams RD, Braunwald E, et al. eds. Harrison's principles of internal medicine. 10th ed. New York: McGraw-Hill, 1983:50-7.