OBSTETRICS
Changes in fetal heart rate-uterine contraction patterns associated with eclampsia RICHARD KEE
H.
S. KOH,
PAUL, M.B.,
M.D., B.S.,
STEVEN
G. BERNSTEIN,
Los Angeles,
California
F.A.C.O.G. M.R.C.O.G.,
F.R.C.S.(C.)
M.D.
Eclamptic seizures have been associated with fetal bradycardia and rapid onset or progression of labor. The fetal heart rate (FHR)-uterine contraction patterns during 14 seizures in 10 eclamptic patients were studied. Some seizures occurred in patients in whom magnesium sulfate levels were in the therapeutic range. The FHR response during an eclamptic episode was generally prolonged bradycardia. Uterine activity was noted to increase during seizure activity and preceded the fall in FHR. As seizure actlvlty subsided, uterine hyperactivity diminished and the FHR rose, frequently demonstrating compensatory tachycerdia. The clinical implications and possible pathophysiologic mechanisms of the FHR-uterine contraction observations are discussed. (AM. J. OBSTET. GYNECOL. 130: 165,
1978.)
Materiel and methods
has been associated with fetal bradycardia and rapid onset or progression of labor.’ Spontaneous uterine contractility is known to be greater following eclampsia than in normal labor.2 Few objective data regarding fetal heart rate (FHR)-uterine contraction (UC) patterns in the eclamptic patient exist.” This report describes the FHR-UC findings encountered during seizures and discusses their clinical significance and the possible pathophysiologic mechanisms. ECLAMPTIC
SEIZURE
During the years 1970 through 1976, at Women’s Hospital, Los Angeles County-University of Southern California Medical Center, FHR-UC data were available during 14 seizure episodes in 10 eclamptic patients. Seven had a single seizure; two had two seizures, and one had three seizures. All FHR-UC data were obtained by direct methods with the use of a fetal electrode and an open-ended intrauterine pressure catheter.
Results Fetal bradycardia was often, but not always, observed shortly after the onset of the convulsion with gradual recovery occurring as the seizure subsided. The interval from seizure onset to FHR fall occurred within five minutes. Six patients demonstrated fetal bradycardia (less than 120 beats per minute) and the duration varied from one half minute to nine minutes. Transitory fetal tachycardia frequently occurred following the period of fetal stress imposed during the seizure
From the Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynecology, Los Angeles County-University of Southern California Medical Center. Received for publication Revised August
May
16, 1977.
4, 1977.
Accepted Aug-ust 15, 1977. Reprint 5K-22,
requests: Dr. Richard H. Paul, Women’s Hospital 1240 N. Mhion Rd., Los Angeles, Califonzia
90033.
165
166
January 15, 1978 Am. J. Obstet. Gynecol.
Paul, Koh, and Bernstein
Fig. 1. The monitor recording during an unobserved and unmedicated convulsion is shown. The fetal response to this stress is demonstrated by “bradycardia” and compensatory tachycardia with decreased FHR variability.
episode. Additional factors suggesting fetal stress were the loss of beat-to-beat variability and transitory late decelerations during the recovery phase. Uterine hyperactivity, as evidenced by an increased uterine tone and UC frequency, coincided with the eclamptic seizures. The duration of increased uterine activity varied from two and a half to 14 minutes. Adequate FHR and/or UC data during 12 seizures revealed a seizure duration from 30 to 80 seconds with a usual duration of approximately one minute. In eight seizure episodes with good-quality UC recordings, it was noted that the onset of the convulsion coincided with an apparent uterine contraction. The most commonly encountered FHR-UC pattern during a convulsive episode is shown in Fig. 1. The duration of the seizure was approximately 50 to 60 seconds, as judged by the loss of FHR data due to patient movement during the seizure and the broad deflections on the UC recording. Fetal bradycardia of approximately five minutes’ duration was noted two and a half minutes after the onset of the convulsion. Uterine activity increased concomitant with the seizure and gradually decreased 10 to 12 minutes later. There were no maternal or perinatal deaths, and all 10 mothers were discharged in apparently good condition with their newborn infants. Two illustrative cases are briefly described here.
Case reports Case 1. B. T. (S76-4396), a 20-year-old primigravid woman with no prenatal care, was admitted at term in early labor with ruptured membranes and complaining of a mild headache. She weighed 285 pounds and was 5 feet, 6 inches tall. She had hypertension (150/90 mm. Hg) and proteinuria (3+). The fundal height was 40 cm. and the fetal heart rate was 140 beats per minute (b.p.m.). Vaginal examination confirmed rupture of the membranes with clear fluid. The cervix was completely effaced and 2 cm. dilated. The presenting part was the vertex at the zero station. There was no evidence of hyperreflexia or edema. Oxytocin augmentation and internal fetal monitoring began soon after admission. Magnesium sulfate, 3 Gm., was given intravenously as a loading dose, followed by a constant infusion of 1 Gm. per hour. Eight hours later, vaginal examination revealed no progress and the decision was made to deliver by cesarean section. Just prior to operation, the patient developed an eclamptic seizure (Fig. 2, upper panel). Magnesium sulfate, 4 Gm., was given intravenously and the infusion rate was increased to 1.5 Cm. per hour. The serum magnesium sulfate level obtained during the seizure was 3.3 mEq. per liter. The patient was stabilized over the next two hours with the magnesium sulfate infusion rate of 2 Cm. per hour. As shown in Fig. 2, middle panel, magnesium sulfate, 1 Gm. intravenously, was
Volume Number
FHR-UC changes with eclampsia
130 2
167
Fig. 2. Three convulsive episodes in the patient described in Case 1 are shown. The serum magnesium sulfate level prior to the third seizure (lower panel) was 4.5 m.Eq per liter. given just prior to transfer to the operating room. A second seizure occurred during the transfer and the characteristic FHR changes were noted. The intrauterine pressure catheter became dislodged during the seizure. An additional 4 Gm. of magnesium sulfate was given intravenously. Twenty minutes later, a third seizure (Fig. 2, lower panel) occurred while the patient was being prepared on the operating table. The serum magnesium sulfate level at this time was 4.5 mEq. per liter. Diazepam was administered intravenously to abate the attack. Cesarean section with the use of general anesthesia was performed after a two-hour period of stabilization. A male infant weighing 3,200 grams was delivered with an Apgar score of 7 at one minute and 8 at five minutes. The venous cord blood pH was 7.25. Case 2. S. R. (S76-5238), a 17-year-old primigravid woman, was admitted at term in labor with severe preeclampsia. She had hypertension (180/ 115 mm. Hg), moderate pretibial edema, hyperreflexia, and 3+ pro-
teinuria. The fundal height was 35 cm. and the fetal heart rate was 150 b.p.m. Vaginal examination revealed the cervix to be completely effaced and 5 cm. dilated. The presentation was the vertex at the zero station. Amniotomy yielded clear liquor and internal monitoring was begun. The patient was given magnesium sulfate, 3 Gm. intravenously and 10 Cm. intramuscularly. Diastolic blood pressure stabilized between 70 and 100 mm. Hg. A second dose of magnesium sulfate, 5 Gm. intramuscularly, was repeated four hours later. Vaginal examination revealed no progress had occurred despite adequate uterine contractions. Approximately 30 minutes following the magnesium sulfate injection, while being prepared for cesarean section, the patient had an eclamptic seizure, as shown in the upper pane1 of Fig. 3. The serum magnesium sulfate level at this time was 4.9 mEq. per liter. The patient received diazepam to control the seizure, and magnesium sulfate, 3 Gm.. was given intravenously.
166
Paul, Koh, and Bernstein
Fig. 3. FHR-UC tracings from three varying FHR responses to an eclamptic contraction in each case.
January 15, 1978 Am. J. Obstet. Gynecol.
different episode.
Cesarean section was performed following stabilization over the next one and a half hours. A male infant weighing 3,940 grams was delivered with an Apgar score of 7 at one minute and 8 at five minutes.
Comment The fetal outcome in this study was generally good, despite the presence of severe maternal disease and episodes of presumed hypoxic insult. Although most seizures provoked marked fetal bradycardia with subsequent evidence of compensatory FHR changes, this was not always present, as shown in the middle and lower panels of Fig. 3. Minimal FHR changes occurred in the two patients in the two lower panels. This minimal fetal response no doubt depends on fetal tolerance and the severity of the stress, which are impossible to quantitate. Although seizure activity was usually associated with an apparent uterine contraction, it is not possible to
patients (upper panel, Case 2) demonstrates the The onset of seizure activity coincides with a uterine
state categorically that the uterine contraction provokes the seizure. However, it appears plausible that the increase in maternal blood pressure which usually accompanies a UC and/or the maternal pain might be the triggering factors which precipitate a convulsion. The mechanisms responsible for the uterine hyperactivity associated directly with eclamptic seizure are not clearly understood but may involve uterine hypoxia resulting from decreased uterine blood flow. Brontanek and associats4 found that uterine blood flow was reduced both before and during contractions and suggested that a decrease in blood flow may actually stimulate uterine contractions. They may also involve release of vasoactive agents with oxytocic actions such as norepinephrine in the mother.5 The transitory fetal distress associated with the eclamptic seizure is probably related to the impairment of uteroplacental blood flow caused by intense vasospasm and uterine hyperactivity. The momentary
Volume
130
Number
2
maternal respiratory arrest throughout the seizure further aggravates the fetal hypoxia. The use of magnesium sulfate in the treatment of eclampsia stemmed from its success in allaying the convulsions of tetanus. Monitoring the serum levels of magnesium sulfate is ideal for optimum management. The drug level attained varies with the body weight of
FHR-UC
changes
with eclampsia
169
the patient and with renal function. This ;vas no doubt a factor involved in Case 1. However. judged from our experience, eclamptic convulsions and tht-ir recurrrnte can occur despite therapeutic levels of magnesium sulfate (3.5 to 7.0 m.Eq per liter).6 1ndividu;il response to a given drug varies, and adjunctive ant icon\ulsants must be utilized when magnesium sulfate, has f’ailed.
REFERENCES
1. Pritchard, J. A., and MacDonald, P. C.: William’s Obstetrics, ed. 15, New York. 1976, Appleton-Century-Crofts, p. 570. 2. Talledo, 0. E.. and Zuspan, F. P.: Spontaneous uterine contrartility in eciampsia, Clin. Obstet. Gynecol. 9: 910, 1966. 3. Boehm, F. H., and Growdon, J. H., Jr.: The pffect of eclamptic convulsions on the fetal heart rate, AM. J. OBSTET. GYNECOL. 120: 85 1, 1974.
4. Brontanek, V., Hendricks, C. H., and Yoshida, ‘f.: Changes in uterine blood flow during uterine contractions, AM. J. OBSTET. GYNECOL. 103: 1108, 1969. 5. Zuspan, F. P.: Adrenal gland and sympathetic nervous system response in eclampsia, AM. J. ORsrET. GYNECOL. 114: 304, 1972. 6. Chesley, L. C., and Tepper, I.: Plasma levels of magnesium attained in magnesium sulfate therapy for pre-eclampsia and eclampsia, Surg. Clin. North ,4m. April, 1957, p. 353.
Changes in fetal heart rate-uterine contraction patterns associated with eclampsia RICHARD KEE
H.
S. KOH,
PAUL, M.B.,
M.D., B.S.,
STEVEN
G. BERNSTEIN,
Los Angeles,
California
F.A.C.O.G. M.R.C.O.G.,
F.R.C.S.(C.)
M.D.
Eclamptic seizures have been associated with fetal bradycardia and rapid onset or progression of labor. The fetal heart rate (FHR)-uterine contraction patterns during 14 seizures in 10 eclamptic patients were studied. Some seizures occurred in patients in whom magnesium sulfate levels were in the therapeutic range. The FHR response during an eclamptic episode was generally prolonged bradycardia. Uterine activity was noted to increase during seizure activity and preceded the fall in FHR. As seizure actlvlty subsided, uterine hyperactivity diminished and the FHR rose, frequently demonstrating compensatory tachycerdia. The clinical implications and possible pathophysiologic mechanisms of the FHR-uterine contraction observations are discussed. (AM. J. OBSTET. GYNECOL. 130: 165,
1978.)
Materiel and methods
has been associated with fetal bradycardia and rapid onset or progression of labor.’ Spontaneous uterine contractility is known to be greater following eclampsia than in normal labor.2 Few objective data regarding fetal heart rate (FHR)-uterine contraction (UC) patterns in the eclamptic patient exist.” This report describes the FHR-UC findings encountered during seizures and discusses their clinical significance and the possible pathophysiologic mechanisms. ECLAMPTIC
SEIZURE
During the years 1970 through 1976, at Women’s Hospital, Los Angeles County-University of Southern California Medical Center, FHR-UC data were available during 14 seizure episodes in 10 eclamptic patients. Seven had a single seizure; two had two seizures, and one had three seizures. All FHR-UC data were obtained by direct methods with the use of a fetal electrode and an open-ended intrauterine pressure catheter.
Results Fetal bradycardia was often, but not always, observed shortly after the onset of the convulsion with gradual recovery occurring as the seizure subsided. The interval from seizure onset to FHR fall occurred within five minutes. Six patients demonstrated fetal bradycardia (less than 120 beats per minute) and the duration varied from one half minute to nine minutes. Transitory fetal tachycardia frequently occurred following the period of fetal stress imposed during the seizure
From the Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynecology, Los Angeles County-University of Southern California Medical Center. Received for publication Revised August
May
16, 1977.
4, 1977.
Accepted Aug-ust 15, 1977. Reprint 5K-22,
requests: Dr. Richard H. Paul, Women’s Hospital 1240 N. Mhion Rd., Los Angeles, Califonzia
90033.
165
166
January 15, 1978 Am. J. Obstet. Gynecol.
Paul, Koh, and Bernstein
Fig. 1. The monitor recording during an unobserved and unmedicated convulsion is shown. The fetal response to this stress is demonstrated by “bradycardia” and compensatory tachycardia with decreased FHR variability.
episode. Additional factors suggesting fetal stress were the loss of beat-to-beat variability and transitory late decelerations during the recovery phase. Uterine hyperactivity, as evidenced by an increased uterine tone and UC frequency, coincided with the eclamptic seizures. The duration of increased uterine activity varied from two and a half to 14 minutes. Adequate FHR and/or UC data during 12 seizures revealed a seizure duration from 30 to 80 seconds with a usual duration of approximately one minute. In eight seizure episodes with good-quality UC recordings, it was noted that the onset of the convulsion coincided with an apparent uterine contraction. The most commonly encountered FHR-UC pattern during a convulsive episode is shown in Fig. 1. The duration of the seizure was approximately 50 to 60 seconds, as judged by the loss of FHR data due to patient movement during the seizure and the broad deflections on the UC recording. Fetal bradycardia of approximately five minutes’ duration was noted two and a half minutes after the onset of the convulsion. Uterine activity increased concomitant with the seizure and gradually decreased 10 to 12 minutes later. There were no maternal or perinatal deaths, and all 10 mothers were discharged in apparently good condition with their newborn infants. Two illustrative cases are briefly described here.
Case reports Case 1. B. T. (S76-4396), a 20-year-old primigravid woman with no prenatal care, was admitted at term in early labor with ruptured membranes and complaining of a mild headache. She weighed 285 pounds and was 5 feet, 6 inches tall. She had hypertension (150/90 mm. Hg) and proteinuria (3+). The fundal height was 40 cm. and the fetal heart rate was 140 beats per minute (b.p.m.). Vaginal examination confirmed rupture of the membranes with clear fluid. The cervix was completely effaced and 2 cm. dilated. The presenting part was the vertex at the zero station. There was no evidence of hyperreflexia or edema. Oxytocin augmentation and internal fetal monitoring began soon after admission. Magnesium sulfate, 3 Gm., was given intravenously as a loading dose, followed by a constant infusion of 1 Gm. per hour. Eight hours later, vaginal examination revealed no progress and the decision was made to deliver by cesarean section. Just prior to operation, the patient developed an eclamptic seizure (Fig. 2, upper panel). Magnesium sulfate, 4 Gm., was given intravenously and the infusion rate was increased to 1.5 Cm. per hour. The serum magnesium sulfate level obtained during the seizure was 3.3 mEq. per liter. The patient was stabilized over the next two hours with the magnesium sulfate infusion rate of 2 Cm. per hour. As shown in Fig. 2, middle panel, magnesium sulfate, 1 Gm. intravenously, was
Volume Number
FHR-UC changes with eclampsia
130 2
167
Fig. 2. Three convulsive episodes in the patient described in Case 1 are shown. The serum magnesium sulfate level prior to the third seizure (lower panel) was 4.5 m.Eq per liter. given just prior to transfer to the operating room. A second seizure occurred during the transfer and the characteristic FHR changes were noted. The intrauterine pressure catheter became dislodged during the seizure. An additional 4 Gm. of magnesium sulfate was given intravenously. Twenty minutes later, a third seizure (Fig. 2, lower panel) occurred while the patient was being prepared on the operating table. The serum magnesium sulfate level at this time was 4.5 mEq. per liter. Diazepam was administered intravenously to abate the attack. Cesarean section with the use of general anesthesia was performed after a two-hour period of stabilization. A male infant weighing 3,200 grams was delivered with an Apgar score of 7 at one minute and 8 at five minutes. The venous cord blood pH was 7.25. Case 2. S. R. (S76-5238), a 17-year-old primigravid woman, was admitted at term in labor with severe preeclampsia. She had hypertension (180/ 115 mm. Hg), moderate pretibial edema, hyperreflexia, and 3+ pro-
teinuria. The fundal height was 35 cm. and the fetal heart rate was 150 b.p.m. Vaginal examination revealed the cervix to be completely effaced and 5 cm. dilated. The presentation was the vertex at the zero station. Amniotomy yielded clear liquor and internal monitoring was begun. The patient was given magnesium sulfate, 3 Gm. intravenously and 10 Cm. intramuscularly. Diastolic blood pressure stabilized between 70 and 100 mm. Hg. A second dose of magnesium sulfate, 5 Gm. intramuscularly, was repeated four hours later. Vaginal examination revealed no progress had occurred despite adequate uterine contractions. Approximately 30 minutes following the magnesium sulfate injection, while being prepared for cesarean section, the patient had an eclamptic seizure, as shown in the upper pane1 of Fig. 3. The serum magnesium sulfate level at this time was 4.9 mEq. per liter. The patient received diazepam to control the seizure, and magnesium sulfate, 3 Gm.. was given intravenously.
166
Paul, Koh, and Bernstein
Fig. 3. FHR-UC tracings from three varying FHR responses to an eclamptic contraction in each case.
January 15, 1978 Am. J. Obstet. Gynecol.
different episode.
Cesarean section was performed following stabilization over the next one and a half hours. A male infant weighing 3,940 grams was delivered with an Apgar score of 7 at one minute and 8 at five minutes.
Comment The fetal outcome in this study was generally good, despite the presence of severe maternal disease and episodes of presumed hypoxic insult. Although most seizures provoked marked fetal bradycardia with subsequent evidence of compensatory FHR changes, this was not always present, as shown in the middle and lower panels of Fig. 3. Minimal FHR changes occurred in the two patients in the two lower panels. This minimal fetal response no doubt depends on fetal tolerance and the severity of the stress, which are impossible to quantitate. Although seizure activity was usually associated with an apparent uterine contraction, it is not possible to
patients (upper panel, Case 2) demonstrates the The onset of seizure activity coincides with a uterine
state categorically that the uterine contraction provokes the seizure. However, it appears plausible that the increase in maternal blood pressure which usually accompanies a UC and/or the maternal pain might be the triggering factors which precipitate a convulsion. The mechanisms responsible for the uterine hyperactivity associated directly with eclamptic seizure are not clearly understood but may involve uterine hypoxia resulting from decreased uterine blood flow. Brontanek and associats4 found that uterine blood flow was reduced both before and during contractions and suggested that a decrease in blood flow may actually stimulate uterine contractions. They may also involve release of vasoactive agents with oxytocic actions such as norepinephrine in the mother.5 The transitory fetal distress associated with the eclamptic seizure is probably related to the impairment of uteroplacental blood flow caused by intense vasospasm and uterine hyperactivity. The momentary
Volume
130
Number
2
maternal respiratory arrest throughout the seizure further aggravates the fetal hypoxia. The use of magnesium sulfate in the treatment of eclampsia stemmed from its success in allaying the convulsions of tetanus. Monitoring the serum levels of magnesium sulfate is ideal for optimum management. The drug level attained varies with the body weight of
FHR-UC
changes
with eclampsia
169
the patient and with renal function. This ;vas no doubt a factor involved in Case 1. However. judged from our experience, eclamptic convulsions and tht-ir recurrrnte can occur despite therapeutic levels of magnesium sulfate (3.5 to 7.0 m.Eq per liter).6 1ndividu;il response to a given drug varies, and adjunctive ant icon\ulsants must be utilized when magnesium sulfate, has f’ailed.
REFERENCES
1. Pritchard, J. A., and MacDonald, P. C.: William’s Obstetrics, ed. 15, New York. 1976, Appleton-Century-Crofts, p. 570. 2. Talledo, 0. E.. and Zuspan, F. P.: Spontaneous uterine contrartility in eciampsia, Clin. Obstet. Gynecol. 9: 910, 1966. 3. Boehm, F. H., and Growdon, J. H., Jr.: The pffect of eclamptic convulsions on the fetal heart rate, AM. J. OBSTET. GYNECOL. 120: 85 1, 1974.
4. Brontanek, V., Hendricks, C. H., and Yoshida, ‘f.: Changes in uterine blood flow during uterine contractions, AM. J. OBSTET. GYNECOL. 103: 1108, 1969. 5. Zuspan, F. P.: Adrenal gland and sympathetic nervous system response in eclampsia, AM. J. ORsrET. GYNECOL. 114: 304, 1972. 6. Chesley, L. C., and Tepper, I.: Plasma levels of magnesium attained in magnesium sulfate therapy for pre-eclampsia and eclampsia, Surg. Clin. North ,4m. April, 1957, p. 353.
