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Intrauterine fetal reanimation in acute intrapartum fetal distress
27
Human Development, 29 (1992) 21-33 Elsevier Scientific Publishers Ireland Ltd.
Early
EHD 01247
Intrauterine fetal reanimation in acute intrapartum fetal distress R. Caldeyro-Barcia Faculty
of Medicine,
University
of Uruguay,
Casilla
de correo
16120,
Distrito
6, Montevideo
(Uruguay)
Summary Uterine contractions during labour may produce acute intrapartum fetal distress. Intrauterine fetal reanimation is possible by reducing the strength of uterine contractions. Betamimetic therapy appears successful for this. Key words: fetal distress; reanimation;
betamimetic drugs
Introduction During human labor uterine contractions may produce acute intrapartum fetal distress (AIFD) by three different mechanisms: (1) Occluding the intramyometrial aspect of the maternal vessels supplying blood to the intervillous space (IVS); this mechanism is inevitable if contractions are strong. (2) Occluding the maternal aorta and the right common iliac artery by compression against the lumbar spine and the pelvic brim; this mechanism only occurs if the mother is supine. (3) Occluding the umbilical vessels which supply fetal blood to the chorionic villi; this mechanism is facilitated by the presence of loops of the cord around the fetal neck or trunk and by the lack or scarcity of amniotic fluid. It usually occurs after rupture of membranes. These three mechanisms may act in isolation or combined. Their effect is enhanced by aggravating factors such as placental insufficiency, arterial hypotension of the mother, etc. AIFD is diagnosed by the presence of type II dips (‘late deceleration’) in the fetal heart rate tracing and confirmed by disturbances in fetal homeostasis such as hypoxemia, hypercapnea, acidosis (fall in fetal pH, increase in base deficit). These distur-
to: R. Caldeyro-Barcia, Faculty of Medicine, University of Uruguay, Casilla de correo 16120, Distrito 6, Montevideo, Uruguay.
Correspondence
28 bances may damage fetal organs (causing sequelae in the surviving children) and eventually cause fetal or neonatal death. The most commonly used treatment for AIFD was to deliver the distressed fetus as soon as possible by cesarean section or forceps delivery and reanimate the depressed newborn infant. New approach to the management of AIFD In May 1969 the author of the present paper demonstrated that AIFD could be successfully managed with the fetus in utero, by reducing the strength of uterine contractions, giving an intravenous infusion to the mother of a betamimetic drug, such as orciprenaline, in doses of lo-20 pg/min for at least 40 min [ 11. This method reduced the intensity of the contractions, type II dips disappeared from the FHR tracing and fetal pH increased slowly reaching normal values in approximately 40-60 min. Fetal PCO~and base deficit diminished progressively reaching normality in a similar period of time. Figure 1 illustrates the first case reported. At 0430 h there was a severe AIFD. All uterine contractions produced type II dips in FHR tracing. The fetal pH (7.02) was abnormally low and the fetal PCO~ (60 mmHg) and the base deficit (15 mequiv./l) were abnormally high. This case of AIFD was caused by mechanism No. 1 combined with placental insufficiency. Five minutes after the onset of the i.v. infusion of orciprenaline the intensity of uterine contractions was reduced to 30% of the original value and type II dips disappeared. Periodic sampling of fetal blood obtained from the scalp by the method of Saling showed a progressive rise of fetal pH and a concomitant fall in base deficit and Pco~; all variables reached normal values 45 min after the onset of betamimetic infusion. A female infant weighing 3450 g, with an Apgar score of 8 at 5 min, was delivered by cesarean section. The values of pH, Pco2 and base deficit were normal in the umbilical vessels at birth and also in the newborn infant 60 min later. The placenta had extensive chorangiomatosis which caused placental insufficiency. This fact explains the appearance of AIFD when uterine contractions and all other factors studied were normal. The neurological development of the child was normal at discharge from the Hospital and at 1 month and 1 and 4 years of age. Figure 2 shows a case of AIFD caused by abnormally strong (70-80 mmHg) and frequent (5-10 min) uterine contractions. The mechanism involved in this case corresponds to No. 1. All contractions caused type II dips of large amplitude. Fetal pH fell from 7.05 to 7.00 (severe fetal acidosis from 1432 h to 1440 h). Base deficit increased from 12 to 15 mequiv./l in the same period. PCO~ increased from 51 to 60 mmHg. All these data indicate a severe AIFD aggravating as time elapses. Five minutes after the onset of orciprenaline infusion the intensity of uterine contractions was reduced to less than 30 mmHg. Type II dips disappeared and in fetal blood the pH rose reaching normal values (7.30) 40 min after the onset of the betamimetic infusion. A similar change occurred with PCO* and base deficit which diminished until reaching normal values in the same time interval. The difference between the fetus in Fig. 2 and that in Fig. 1 is the way of birth. In Fig. 2 cervical dilatation which was 7 cm at 1442 h, and progressed to full dilata-
29 FETAL LO-ITO2 -IS
mm
-
Bose
CAPILLARY
Hg -
Excess
mEq/liler
-
BLOOD
55-
so
- 8-
-7
‘45-42
-
43 -
-6 -s-5 - -5 -
5-u
HotJR
20 microgram/minute Fig. 1. Simultaneous recording of fetal heart rate and uterine contractions (amniotic pressure). Fetal capillary blood was sampled 7 times from the scalp. At 0430 h a severe AIFD was present as shown by the type II dips and fetal acidosis. (Modified from Caldeyro-Barcia et al. [I].)
FETAL II I I)? “lnl fig
51----60
Il.J*r t:\rrrr 111t: q i I i I c r
-12--15
CAPILLARY
BLOOD
50
-12
7.307.20-
45
--10
33-
42-u
-6 -
-5
-
..;
o-e-7.30
PII
7.10-
7.20 7.10 7.00
l /-T-I.-~~-
7.00-o-.---Ix!als/min
16 0
-160
FETAL HEART RATE
120
-120
HO
80
-8 0
AMNIOTIC PRESSURE
IIOI’H
t IJ:30
14!40
14:so
ORCIPRENALINE
I.V.
c-IS:10
15:oo INFUSION
20
15:20 b
microgramdmi~3te b
(:EHvICAL
tItt.ATATION
7
cm
8
Enl
9
‘“l
10
Enl
Fig. 2. Simultaneous recording of fetal heart rate and uterine contractions (amniotic pressure), as in Fig. 1. Severe AIFD was present between 1430 h and 1440 h. As in Fig. 1, the infusion of orciprenaline resulted in a successful intrauterine fetal reanimation.
30
tion at 1512 h. Spontaneous vaginal birth occurred at 1530 h. A male infant weighing 3375 g was born in vigorous condition, Apgar score 9 at 1 min and 10 at 5 min. The neurological development, checked as mentioned in the legend for Fig. 1, was normal. Figure 3 illustrates an AIFD caused by mechanisms No. 2 and No. 3 in addition to mechanism No. 1 which is always present. Uterine contractions had a normal intensity (50 mmHg) and frequency (4 contractions per 10 min). Each contraction caused a dip in FHR; these dips are simultaneous with the contractions. They have abrupt descending and ascending limbs and the bottom is flat (when the duration of the dip is longer than 30 s). These characteristics give a square shape to the dips and correspond to mechanism No. 3, i.e. to the total occlusion of the umbilical vessels by the uterine contractions. This diagnosis was supported (at birth) by the presence of two tight loops of the umbilical cord around the fetal neck and also because the membranes had been ruptured at 1105 h. The presence of mechanism No. 2, i.e. the occlusion by uterine contractions of the aorta and of the common iliac artery is shown in the tracing of blood pressure in the maternal right femoral artery. Each uterine contraction caused a fail in pressure and the disappearance of the pulsations corresponding to the heart beats of the
B..\SF: EXCESS mEq/liter p II -
-----7.9 -7.26 ORCIPRENALINE I.V. INFUSION 10 mierogramslminute
I *
Hour
I....I....I lt30 (:ERVICAI.
ll40
. . . . I....&,... ll50
DILATATION
160
l. . ..I.. ..I....I...*Llminutrr 1240 12*0 6 cm
8 cm
IO
cm
Fig. 3. Simultaneous recording of fetal heart rate and uterine contractions (amniotic pressure), as in Figs. 1 and 2. In addition, the recording of blood pressure in the maternal right femoral artery and of maternal heart rate are shown. At 1150 h a moderate AIFD was present caused by mechanisms No. 2 and ,No. 3. A successful intrauterine fetal reanimation was obtained with the infusion of orciprenaline. Forceps delivery at 1249 h of a female newborn weighing 3355 g. Apgar score 7 at 1 min and 9 at 5 min. The neurological development of the child was normal. After Caldeyro-Barcia et al. [2].
31
mother. The latter effect can be detected by feeling with the fingers the pulsation of the femoral artery. At 1150 h fetal pH had fallen to 7.26 (from a previous value of 7.30 at 1126 h), base deficit at 1150 h was 7.9 mequiv./l, a marked rise from the previous value of 5.0 mequiv./l found at 1126 h. The fall in fetal pH and the rise in fetal base deficit indicated the progressive development of an AIFD. Without any therapeutic action the fetus would have become progressively more acidotic. The long duration of the occlusion of the umbilical vessels (more than 60 s) was important in this case for the development of AIFD. The administration of an i.v. infusion of orciprenaline to the mother started at 1148 h at the rate of only 10 pg/min. At 1152 h the intensity of uterine contractions diminished to 20 mmHg, i.e. less than half of the pre-infusion value. These weak contractions did not occlude the umbilical vessels and the ‘umbilical dips’ disappeared completely from the FHR tracing. The weak uterine contractions were also unable to occlude the maternal aorta and the right common iliac artery and they did not produce any longer the transient falls in the blood pressure recorded in the right femoral artery of the mother. As the causes of AIFD had disappeared, fetal pH (which was 7.26 at 1150 h) increased to 7.30 at 1210 h. In the same period, fetal base deficit diminished from 7.9 to 5.0 mequiv.il. The fetal condition improved markedly. Since the dose of orciprenaline was small, there was little tachycardia, both in the fetus and the mother and there was no fall in maternal arterial pressure. Uterine contractions partially escape from the inhibition caused by orciprenaline and from 1205 h onwards, recover an intensity of 30 mmHg. These weak contractions are able to promote the progress of labor. Cervical dilatation, which was 6 cm at 1155 h, progressed to full dilatation at 1215 h. The fetal head, in station 0 at 1155 h, descended to station +2 at 1215 h. Table I illustrates the success or failure of intrauterine fetal reanimation in our series of 84 fetuses with AIFD treated with betamimetic infusion. In 68 cases fetal pH increased more than 0.10 pH units after 40 min of infusion and they were conTABLE I Success or failure of intrauterine fetal reanimation according to the main cause of AIFD in our series of 84 cases. Main cause of fetal distress
n
Increase in fetal pH after &mimetic More than 0.10
Uterine hypercontractitity Umbil. occlusion Occlusion of aorta Placental lesions Art. hypotension Combined causes
38 12 6 10 4 14
32 10 6 8 2 10
84
68 Success
Less than 0.05 5 1 0 1 1 3 11 Dubious
No change or fall I 1 0 1 1 1 5 Failure
32 TABLE II Neurological development of the children according to the results of intrauterine fetal reanimation in 84 cases of AIFD. Effect of @mimetic therapy
n
Success Dubious
(68) (11)
Failure
(5)
Neurological development 1 month
1 year
4 years
6i 5 6 4 1
3 65 4 7 3 2
2 66 1 10 1 4
Abnormal Normal Abnormal Normal Abnormal Normal
sidered successful reanimations. In 11 cases fetal pH increased less than 0.05 pH units and they were considered as dubious results. In 5 cases the fetal pH did not change and even fell during betamimetic infusion and they were considered failures. In the 11 dubious cases and the 5 failures, the fetuses were extracted promptly by cesarean section or forceps delivery. Table II illustrates the neurological development of the 84 children according to the success of betamimetic therapy. In all groups (success, dubious or failure) the proportion of abnormal exams is greater at 1 month than at 4 years of age. The group of successful reanimation shows the lowest incidence of abnormal neurological development at all the ages studied. The group of 5 failures shows, at all ages, the highest proportion of abnormal neurological development, i.e. the highest incidence of sequelae in the nervous system.
After successful intrauterine fetal reanimation was published in 1969 by our group [l], several authors have confirmed our results. Esteban-Altirriba [3] in Spain reported a large series with results similar to our own. Hutchon [4] in Scotland reported 4 cases of severe fetal bradycardia which were treated with ritodrine. Recovery of fetal heart rate occurred immediately. Pediatric follow up has not shown any neurological abnormality. Zalel et al. [5] successfully treated with ritodrine 40 patients with uterine hypercontractility dysfunction in Israel. Katz et al. [6] from the same group as Zalel, treated 51 cases of cord prolapse with ritodrine before performing the cesarean section. Goyert et al. [7] in the USA, successfully treated with ritodrine, cases of uterine hyperstimulation caused by administration of excessive dose of prostaglandin Ez. References 1 Caldeyro-Barcia, R., Magafla, J.M., Castillo, J.B. et al. (1969): In: Perinatal Factors Affecting Human Development, pp. 248-253. Scientific Publication No. 185, Pan American Health Organization, Washington D.C.
33 2 Caldeyro-Barcia, R., Mendez-Bauer, C., Pose, S.V. and Poseiro, J.J. (1973): In: Maternal and Child Health Practices, pp. 332-394. Editors: H.M. Wallace, E.M. Gold and E.F. Lis. Charles C. Thomas, Springtield. 3 Esteban Altirriba, J., Gamissans, O., Duran, P. et al. (1972): In: Perinatale Medizin, pp. 198-208. Editors: E. Saling and J.W. Dudenhausen. Georg Thieme Verlag, Stuttgart. 4 Hutchon, D.J.R. (1982): Br. J. Obst. Gynaecol., 89, 671-674. 5 Zalel, Y., Katz, Z., Blickstein, I. et al. (1990): Int. J. Gynecol. Obstet., 31, 237-241. 6 Katz, Z., Schwartz, Z., Lancet, M. et al. (1988): Obstet. Gynecol., 72, 278-281. 7 Goyert, G.L. and Mariona, F.G. (1987): Obstet. Gynecol., 70, 468-470.
Human Development, 29 (1992) 21-33 Elsevier Scientific Publishers Ireland Ltd.
Early
EHD 01247
Intrauterine fetal reanimation in acute intrapartum fetal distress R. Caldeyro-Barcia Faculty
of Medicine,
University
of Uruguay,
Casilla
de correo
16120,
Distrito
6, Montevideo
(Uruguay)
Summary Uterine contractions during labour may produce acute intrapartum fetal distress. Intrauterine fetal reanimation is possible by reducing the strength of uterine contractions. Betamimetic therapy appears successful for this. Key words: fetal distress; reanimation;
betamimetic drugs
Introduction During human labor uterine contractions may produce acute intrapartum fetal distress (AIFD) by three different mechanisms: (1) Occluding the intramyometrial aspect of the maternal vessels supplying blood to the intervillous space (IVS); this mechanism is inevitable if contractions are strong. (2) Occluding the maternal aorta and the right common iliac artery by compression against the lumbar spine and the pelvic brim; this mechanism only occurs if the mother is supine. (3) Occluding the umbilical vessels which supply fetal blood to the chorionic villi; this mechanism is facilitated by the presence of loops of the cord around the fetal neck or trunk and by the lack or scarcity of amniotic fluid. It usually occurs after rupture of membranes. These three mechanisms may act in isolation or combined. Their effect is enhanced by aggravating factors such as placental insufficiency, arterial hypotension of the mother, etc. AIFD is diagnosed by the presence of type II dips (‘late deceleration’) in the fetal heart rate tracing and confirmed by disturbances in fetal homeostasis such as hypoxemia, hypercapnea, acidosis (fall in fetal pH, increase in base deficit). These distur-
to: R. Caldeyro-Barcia, Faculty of Medicine, University of Uruguay, Casilla de correo 16120, Distrito 6, Montevideo, Uruguay.
Correspondence
28 bances may damage fetal organs (causing sequelae in the surviving children) and eventually cause fetal or neonatal death. The most commonly used treatment for AIFD was to deliver the distressed fetus as soon as possible by cesarean section or forceps delivery and reanimate the depressed newborn infant. New approach to the management of AIFD In May 1969 the author of the present paper demonstrated that AIFD could be successfully managed with the fetus in utero, by reducing the strength of uterine contractions, giving an intravenous infusion to the mother of a betamimetic drug, such as orciprenaline, in doses of lo-20 pg/min for at least 40 min [ 11. This method reduced the intensity of the contractions, type II dips disappeared from the FHR tracing and fetal pH increased slowly reaching normal values in approximately 40-60 min. Fetal PCO~and base deficit diminished progressively reaching normality in a similar period of time. Figure 1 illustrates the first case reported. At 0430 h there was a severe AIFD. All uterine contractions produced type II dips in FHR tracing. The fetal pH (7.02) was abnormally low and the fetal PCO~ (60 mmHg) and the base deficit (15 mequiv./l) were abnormally high. This case of AIFD was caused by mechanism No. 1 combined with placental insufficiency. Five minutes after the onset of the i.v. infusion of orciprenaline the intensity of uterine contractions was reduced to 30% of the original value and type II dips disappeared. Periodic sampling of fetal blood obtained from the scalp by the method of Saling showed a progressive rise of fetal pH and a concomitant fall in base deficit and Pco~; all variables reached normal values 45 min after the onset of betamimetic infusion. A female infant weighing 3450 g, with an Apgar score of 8 at 5 min, was delivered by cesarean section. The values of pH, Pco2 and base deficit were normal in the umbilical vessels at birth and also in the newborn infant 60 min later. The placenta had extensive chorangiomatosis which caused placental insufficiency. This fact explains the appearance of AIFD when uterine contractions and all other factors studied were normal. The neurological development of the child was normal at discharge from the Hospital and at 1 month and 1 and 4 years of age. Figure 2 shows a case of AIFD caused by abnormally strong (70-80 mmHg) and frequent (5-10 min) uterine contractions. The mechanism involved in this case corresponds to No. 1. All contractions caused type II dips of large amplitude. Fetal pH fell from 7.05 to 7.00 (severe fetal acidosis from 1432 h to 1440 h). Base deficit increased from 12 to 15 mequiv./l in the same period. PCO~ increased from 51 to 60 mmHg. All these data indicate a severe AIFD aggravating as time elapses. Five minutes after the onset of orciprenaline infusion the intensity of uterine contractions was reduced to less than 30 mmHg. Type II dips disappeared and in fetal blood the pH rose reaching normal values (7.30) 40 min after the onset of the betamimetic infusion. A similar change occurred with PCO* and base deficit which diminished until reaching normal values in the same time interval. The difference between the fetus in Fig. 2 and that in Fig. 1 is the way of birth. In Fig. 2 cervical dilatation which was 7 cm at 1442 h, and progressed to full dilata-
29 FETAL LO-ITO2 -IS
mm
-
Bose
CAPILLARY
Hg -
Excess
mEq/liler
-
BLOOD
55-
so
- 8-
-7
‘45-42
-
43 -
-6 -s-5 - -5 -
5-u
HotJR
20 microgram/minute Fig. 1. Simultaneous recording of fetal heart rate and uterine contractions (amniotic pressure). Fetal capillary blood was sampled 7 times from the scalp. At 0430 h a severe AIFD was present as shown by the type II dips and fetal acidosis. (Modified from Caldeyro-Barcia et al. [I].)
FETAL II I I)? “lnl fig
51----60
Il.J*r t:\rrrr 111t: q i I i I c r
-12--15
CAPILLARY
BLOOD
50
-12
7.307.20-
45
--10
33-
42-u
-6 -
-5
-
..;
o-e-7.30
PII
7.10-
7.20 7.10 7.00
l /-T-I.-~~-
7.00-o-.---Ix!als/min
16 0
-160
FETAL HEART RATE
120
-120
HO
80
-8 0
AMNIOTIC PRESSURE
IIOI’H
t IJ:30
14!40
14:so
ORCIPRENALINE
I.V.
c-IS:10
15:oo INFUSION
20
15:20 b
microgramdmi~3te b
(:EHvICAL
tItt.ATATION
7
cm
8
Enl
9
‘“l
10
Enl
Fig. 2. Simultaneous recording of fetal heart rate and uterine contractions (amniotic pressure), as in Fig. 1. Severe AIFD was present between 1430 h and 1440 h. As in Fig. 1, the infusion of orciprenaline resulted in a successful intrauterine fetal reanimation.
30
tion at 1512 h. Spontaneous vaginal birth occurred at 1530 h. A male infant weighing 3375 g was born in vigorous condition, Apgar score 9 at 1 min and 10 at 5 min. The neurological development, checked as mentioned in the legend for Fig. 1, was normal. Figure 3 illustrates an AIFD caused by mechanisms No. 2 and No. 3 in addition to mechanism No. 1 which is always present. Uterine contractions had a normal intensity (50 mmHg) and frequency (4 contractions per 10 min). Each contraction caused a dip in FHR; these dips are simultaneous with the contractions. They have abrupt descending and ascending limbs and the bottom is flat (when the duration of the dip is longer than 30 s). These characteristics give a square shape to the dips and correspond to mechanism No. 3, i.e. to the total occlusion of the umbilical vessels by the uterine contractions. This diagnosis was supported (at birth) by the presence of two tight loops of the umbilical cord around the fetal neck and also because the membranes had been ruptured at 1105 h. The presence of mechanism No. 2, i.e. the occlusion by uterine contractions of the aorta and of the common iliac artery is shown in the tracing of blood pressure in the maternal right femoral artery. Each uterine contraction caused a fail in pressure and the disappearance of the pulsations corresponding to the heart beats of the
B..\SF: EXCESS mEq/liter p II -
-----7.9 -7.26 ORCIPRENALINE I.V. INFUSION 10 mierogramslminute
I *
Hour
I....I....I lt30 (:ERVICAI.
ll40
. . . . I....&,... ll50
DILATATION
160
l. . ..I.. ..I....I...*Llminutrr 1240 12*0 6 cm
8 cm
IO
cm
Fig. 3. Simultaneous recording of fetal heart rate and uterine contractions (amniotic pressure), as in Figs. 1 and 2. In addition, the recording of blood pressure in the maternal right femoral artery and of maternal heart rate are shown. At 1150 h a moderate AIFD was present caused by mechanisms No. 2 and ,No. 3. A successful intrauterine fetal reanimation was obtained with the infusion of orciprenaline. Forceps delivery at 1249 h of a female newborn weighing 3355 g. Apgar score 7 at 1 min and 9 at 5 min. The neurological development of the child was normal. After Caldeyro-Barcia et al. [2].
31
mother. The latter effect can be detected by feeling with the fingers the pulsation of the femoral artery. At 1150 h fetal pH had fallen to 7.26 (from a previous value of 7.30 at 1126 h), base deficit at 1150 h was 7.9 mequiv./l, a marked rise from the previous value of 5.0 mequiv./l found at 1126 h. The fall in fetal pH and the rise in fetal base deficit indicated the progressive development of an AIFD. Without any therapeutic action the fetus would have become progressively more acidotic. The long duration of the occlusion of the umbilical vessels (more than 60 s) was important in this case for the development of AIFD. The administration of an i.v. infusion of orciprenaline to the mother started at 1148 h at the rate of only 10 pg/min. At 1152 h the intensity of uterine contractions diminished to 20 mmHg, i.e. less than half of the pre-infusion value. These weak contractions did not occlude the umbilical vessels and the ‘umbilical dips’ disappeared completely from the FHR tracing. The weak uterine contractions were also unable to occlude the maternal aorta and the right common iliac artery and they did not produce any longer the transient falls in the blood pressure recorded in the right femoral artery of the mother. As the causes of AIFD had disappeared, fetal pH (which was 7.26 at 1150 h) increased to 7.30 at 1210 h. In the same period, fetal base deficit diminished from 7.9 to 5.0 mequiv.il. The fetal condition improved markedly. Since the dose of orciprenaline was small, there was little tachycardia, both in the fetus and the mother and there was no fall in maternal arterial pressure. Uterine contractions partially escape from the inhibition caused by orciprenaline and from 1205 h onwards, recover an intensity of 30 mmHg. These weak contractions are able to promote the progress of labor. Cervical dilatation, which was 6 cm at 1155 h, progressed to full dilatation at 1215 h. The fetal head, in station 0 at 1155 h, descended to station +2 at 1215 h. Table I illustrates the success or failure of intrauterine fetal reanimation in our series of 84 fetuses with AIFD treated with betamimetic infusion. In 68 cases fetal pH increased more than 0.10 pH units after 40 min of infusion and they were conTABLE I Success or failure of intrauterine fetal reanimation according to the main cause of AIFD in our series of 84 cases. Main cause of fetal distress
n
Increase in fetal pH after &mimetic More than 0.10
Uterine hypercontractitity Umbil. occlusion Occlusion of aorta Placental lesions Art. hypotension Combined causes
38 12 6 10 4 14
32 10 6 8 2 10
84
68 Success
Less than 0.05 5 1 0 1 1 3 11 Dubious
No change or fall I 1 0 1 1 1 5 Failure
32 TABLE II Neurological development of the children according to the results of intrauterine fetal reanimation in 84 cases of AIFD. Effect of @mimetic therapy
n
Success Dubious
(68) (11)
Failure
(5)
Neurological development 1 month
1 year
4 years
6i 5 6 4 1
3 65 4 7 3 2
2 66 1 10 1 4
Abnormal Normal Abnormal Normal Abnormal Normal
sidered successful reanimations. In 11 cases fetal pH increased less than 0.05 pH units and they were considered as dubious results. In 5 cases the fetal pH did not change and even fell during betamimetic infusion and they were considered failures. In the 11 dubious cases and the 5 failures, the fetuses were extracted promptly by cesarean section or forceps delivery. Table II illustrates the neurological development of the 84 children according to the success of betamimetic therapy. In all groups (success, dubious or failure) the proportion of abnormal exams is greater at 1 month than at 4 years of age. The group of successful reanimation shows the lowest incidence of abnormal neurological development at all the ages studied. The group of 5 failures shows, at all ages, the highest proportion of abnormal neurological development, i.e. the highest incidence of sequelae in the nervous system.
After successful intrauterine fetal reanimation was published in 1969 by our group [l], several authors have confirmed our results. Esteban-Altirriba [3] in Spain reported a large series with results similar to our own. Hutchon [4] in Scotland reported 4 cases of severe fetal bradycardia which were treated with ritodrine. Recovery of fetal heart rate occurred immediately. Pediatric follow up has not shown any neurological abnormality. Zalel et al. [5] successfully treated with ritodrine 40 patients with uterine hypercontractility dysfunction in Israel. Katz et al. [6] from the same group as Zalel, treated 51 cases of cord prolapse with ritodrine before performing the cesarean section. Goyert et al. [7] in the USA, successfully treated with ritodrine, cases of uterine hyperstimulation caused by administration of excessive dose of prostaglandin Ez. References 1 Caldeyro-Barcia, R., Magafla, J.M., Castillo, J.B. et al. (1969): In: Perinatal Factors Affecting Human Development, pp. 248-253. Scientific Publication No. 185, Pan American Health Organization, Washington D.C.
33 2 Caldeyro-Barcia, R., Mendez-Bauer, C., Pose, S.V. and Poseiro, J.J. (1973): In: Maternal and Child Health Practices, pp. 332-394. Editors: H.M. Wallace, E.M. Gold and E.F. Lis. Charles C. Thomas, Springtield. 3 Esteban Altirriba, J., Gamissans, O., Duran, P. et al. (1972): In: Perinatale Medizin, pp. 198-208. Editors: E. Saling and J.W. Dudenhausen. Georg Thieme Verlag, Stuttgart. 4 Hutchon, D.J.R. (1982): Br. J. Obst. Gynaecol., 89, 671-674. 5 Zalel, Y., Katz, Z., Blickstein, I. et al. (1990): Int. J. Gynecol. Obstet., 31, 237-241. 6 Katz, Z., Schwartz, Z., Lancet, M. et al. (1988): Obstet. Gynecol., 72, 278-281. 7 Goyert, G.L. and Mariona, F.G. (1987): Obstet. Gynecol., 70, 468-470.