Jurnal Manajemen Eklampsia Di Egypt

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CLINICAL ARTICLE

Management of eclampsia at Assiut University Hospital, Egypt

Diaa E.M. Abd El Aal , Ahmed Y. Shahin

Department of Obstetrics and Gynecology, Women's Health Center, Assiut University, Assiut, Egypt

a b s t r a c ta r t i c l e i n f o

Article history:

Received 1 April 2011

Received in revised form 11 October 2011

Accepted 23 November 2011

Keywords:

Eclampsia

Intensive care unit

Magnesium sulfate

Nifedipine

Objective:To evaluate the protocol used for management of eclampsia at Assiut University Hospital, Assiut,

Egypt. Methods: In a prospective cross-sectional study, data were collected from 1998 women treated for

eclampsia at Assiut University Hospital between January 1990 and January 2010, including 1594 cases of

prepartum eclampsia, 75 of intrapartum eclampsia, 16 of intercurrent eclampsia, and 313 of postpartum

eclampsia. The treatment regimen included use of nifedipine as an antihypertensive, magnesium sulfate as

an anticonvulsant, rapid interruption of pregnancy, and admission to the ICU. Data were evaluated for control

of blood pressure, prevention and control of convulsions, and maternal and perinatal outcomes. Results:

Magnesium sulfate was effective in controlling convulsions in 98.1% of women. Nifedipine initiated a smooth

decline in blood pressure (P>0.0001). There were 79 maternal deaths (3.95%). Maternal morbidity occurred

in 439 (22%) women. Twenty-seven percent of women delivered vaginally (most of these women were

admitted postpartum). Perinatal mortality occurred in 7.9% of cases. Conclusion:A combination of nifedipine

as an antihypertensive drug, magnesium sulfate as an anticonvulsant, rapid interruption of pregnancy, and

managing the patients in the ICU resulted in a marked improvement in the outcome for both mother and

fetus at Assiut University Hospital.

2011 International Federation of Gynecology and Obstetrics. Published by Elsevier Ireland Ltd. All rights reserved.

1. Introduction

In low-resource countries, annually 150 maternal deaths per

100000 births are related to hypertensive disorders of pregnancy, as

compared with 4 maternal deaths per 100000 births in high-income

countries [1]. Hypertensive disorders of pregnancy signicantly

increase fetal and neonatal morbidity and mortality[1].

Administration of calcium ion channel blockers such as nifedipine

is an ideal approach to the treatment of patients with hypertensive

disorders of pregnancy. The resulting vasodilator effect of nifedipine

is pronounced in vessels with high vasoconstrictor tone without

diminishing cardiac output. Nifedipine is effective in postpartum con-

trol of blood pressure among women with eclampsia[2].

Both the American Congress of Obstetricians and Gynecologists

[3,4]and the Royal College of Obstetricians and Gynecologists[5]rec-

ommend the use of magnesium sulfate for treatment of eclampsia,

and good results have been obtained with its use [6]. Management

of affected patients in the intensive care unit (ICU) is strongly recom-

mended by all centers.

The aim of the present study was to evaluate the current protocol

used for management of women with eclampsia in a women's health

hospital in Egypt in terms of control of blood pressure, preventionand control of convulsions, and maternal and perinatal outcomes.

2. Materials and methods

In a prospective cross-sectional study conducted at the Women's

Health Hospital, Assiut University, Egypt, data were reviewed from

all women with eclampsia who were admitted to the Department of

Obstetrics and Gynecology between January 1, 1990, and January 1,

2010. The study was approved by the Institutional Review Board

and Ethics Committee.

The study exclusion criteria were all non-eclamptic causes ofts,

including hysterical causes and epilepsy. On admission, each patient

underwent electroencephalography (EEG) after rst-aid measures,

including inserting an intravenous line and clearing the respiratory

airway, were carried out. A careful history of tting was obtained

from the relatives and attendants who usually came in with the pa-

tient. Any suspicious EEG changes suggestive of epilepsy were taken

as exclusion criteria.

A complete and thorough medical history, including personal,

menstrual, obstetric, past history of previous convulsions, antipsy-

chotic drugs, and family history of hypertension and convulsions

was taken from the patient, and a clinical and obstetric examination

was conducted. Urine analysis (particularly for proteinuria), complete

blood analysis, and renal and hepatic function tests were carried out.

The previous protocol for management of eclampsia before

1990 comprised the following points. Control of convulsions was

International Journal of Gynecology and Obstetrics 116 (2012) 232236

Corresponding author at: Department of Obstetrics and Gynecology, Women's

Health Center, Assiut University, Assiut, Egypt. Tel.: +20 105212137; fax: + 20

2088333327.

E-mail address:[email protected](D.E.M. Abd El Aal).

0020-7292/$ see front matter 2011 International Federation of Gynecology and Obstetrics. Published by Elsevier Ireland Ltd. All rights reserved.

doi:10.1016/j.ijgo.2011.10.018

Contents lists available at SciVerse ScienceDirect

International Journal of Gynecology and Obstetrics

j o u r n a l h o m e p a g e : w w w . e l s e v i e r . c o m / l o c a t e / i j g o
http://dx.doi.org/10.1016/j.ijgo.2011.10.018http://dx.doi.org/10.1016/j.ijgo.2011.10.018http://dx.doi.org/10.1016/j.ijgo.2011.10.018mailto:[email protected]://dx.doi.org/10.1016/j.ijgo.2011.10.018http://www.sciencedirect.com/science/journal/00207292http://www.sciencedirect.com/science/journal/00207292http://dx.doi.org/10.1016/j.ijgo.2011.10.018mailto:[email protected]://dx.doi.org/10.1016/j.ijgo.2011.10.018


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conducted by an intravenous bolus dose of 1020 mg of valium over a

period of 25 minutes, followed by a continuous intravenous infusion

of 2030 mg of valium in 500 mL of 5% dextrose into a large vein at a

rate not exceeding 2.5 mg/minute until the patient was drowsy (usu-

ally a total dose of 1030 mg), and then by continuous intravenous

infusion of valium at a rate of 2.510 mg/hour to maintain drowsiness

for 24 hours after either delivery or the last t. Control of blood pres-

sure was attempted with no preferred anti-hypertensive agent. Inter-

ruption of pregnancy was achieved by induction of labor or bycesarean delivery according to the obstetric indication. Patients

were managed in a semi-dark room with limited facilities because

of the unavailability of ICU at that time.

Allstudied women were treated by thecurrent protocol as follows.

Control of convulsions was started by a loading dose of magnesium

sulfate (46 g intravenously), given over 10 minutes in 100 mL of 5%

dextrose, followed by 12 g/hour of magnesium sulfate (1 g/hour if

the patient weighed b55 kg; 2 g/hour if the patient weighed

>55 kg), given by continuous intravenous drip. Patient monitoring

included the presence of hypoactive knee jerk: if it became absent,

the intravenous drip was discontinued. The respiratory rate was

observed: rates above 12 cycles/minute ensured the absence of respi-

ratory depression. An indwelling urinary catheter was inserted: the

lowest acceptable urinary output was 25 mL per hour or 600 mL per

24 hours. An intravenous line was established to maintain a continu-

ous route for the administration of drugs and to maintain uid bal-

ance. If excess magnesium was suspected, respiration was supported

and the specic antidote (calcium gluconate or calcium chloride)

was administered (10 mL of a 10% solution by intravenous injection

very slowly in not less than 10 minutes). Monitoring of magnesium

sulfate toxicity continued when nifedipine treatment was started.

Control of blood pressure was achieved with antihypertensive

drugs when the diastolic blood pressure was more than 110 mm Hg.

Nifedipine was used primarily, and other drugs (angiotensin-convert-

ing enzyme inhibitors or sodium nitroprusside drip) were also ad-

ministered if nifedipine treatment alone failed. The pregnancy was

terminated immediately after the patient became hemodynamically

stable (i.e. convulsions and blood pressure were under control), ei-

ther by cesarean or by vaginal delivery if labor was imminent (maxi-mally within 2 hours).

Immediately after delivery, the patient was transferred to ICU and

underwent meticulous observation, including heart rate and blood

pressure monitoring (every 15 min), and temperature and respirato-

ry rate measurement (every 4 hours). Two venous cannulae were

inserted. A urinary catheter was inserted to measure urine volume

in 24 hours, and creatinine clearance and uid balance (intake and

output). Arterial cannulation in a radial artery was performed (Allen

test) to permit peripheral blood gas analysis and to detect collateral

ulnar circulation. Samples were taken for analysis of blood gases (pe-

ripheral arterial CO2 [PaCO2] and peripheral arterial O2[PaO2]), and

liver and kidney function (1 mL of arterial blood in a sterilized hepa-

rinized syringe, and 10 mL of venous blood in 2 sterile glass tubes, re-

spectively). A control sample was taken immediately postpartum andbefore any treatment was received (except for the loading dose of

magnesium sulfate). The other 3 samples were taken 30 minutes,

24 hours, and 48 hours after delivery. Internal jugular vein cannula-

tion was done for all patients. Fluid intake was balanced according

to central venous pressure (68 cm H2O). Respiration was mechani-

cally assisted if needed.

Data are expressed as number (percentage) or meanSD. Blood

pressure values before and after nifedipine were compared via 2-

tailed Studentttest. APvalue of 0.05 was taken as signicant.

3. Results

Data from 1998 women were included in the study: 1594 (79.8%)

women had prepartum eclampsia (took place before true labor

pains), 75 (3.8%) had intrapartum eclampsia (eclamptic ts after the

onset of true labor pains), 16 (0.8%) had intercurrent eclampsia

(eclampticts had no relation to labor pains), and 313 (15.7%) had

postpartum eclampsia (ts after delivery).

There were no signicant differences in age or parity among the

groups of patients with different types of eclampsia, but pregnancy

duration (weeks) was signicantly longer among women with post-

partum eclampsia (Table 1). A recurrence of convulsions while re-

ceiving magnesium sulfate treatment occurred in only 39 (1.95%) ofwomen. The highest rate of recurrence was 35.9% (14 cases) in the

postpartum group as compared with 61.5% (24 cases) in the prepar-

tum group, 2.7% (1 case) in the intrapartum group, and 0% (no

cases) in the intercurrent group.

A sublingual dose of 1020 mg of nifedipine initiated a smooth

and predictable decline in blood pressure (systolic and diastolic)

within 5 minutes, and produced a peak effect between 30 and 60 mi-

nutes. After nifedipine administration, blood pressure decreased to

approximately 16% of the pretreatment values. Good blood pressure

control was achieved in 93.5% of the patients. In all groups, there

was a signicant reduction in systolic and diastolic blood pressure

after nifedipine administration (Pb0.0001) (Table 2).

The dose needed to control blood pressure varied among the dif-

ferent groups of patients, with marked individual variations in re-

sponse to treatment. There was no correlation between the

nifedipine dose required per day and either the pre- or post-

treatment blood pressure.

There were 79 maternal deaths, representing a case fatality rate of

3.95%. The highest rate occurred in the postpartum group (25 cases)

(Table 3). With regard to maternal morbidity, 439 (22%) women

had severe morbidity. The postpartum group had the highest rate of

morbidity (31.3%), whereas the intercurrent group had the lowest

rate (12.5%).

The most common morbidities were a marked deterioration in

kidney function without reaching acute renal failure (78 women), a

marked deterioration in liver function (49 women), a signicant de-

terioration in arterial blood gases and acidbase parameters (87

women), postpartum hemorrhage (44 women), thrombocytopenia

(38 women), recurrence of ts while receiving treatment (25women), coagulation disorders (29 women), HELLP (hemolytic ane-

mia, elevated liver enzymes, low platelet count) syndrome (20

women), acute renal failure that required dialysis (15 women), and

visual disturbances (8 women, 2 of whom had temporary loss of vi-

sion) (Table 3). Women with intrapartum eclampsia had the highest

increase in serum bilirubin, liver enzymes (Table 4), and blood urea;

those in the prepartum group had the highest increase in serum cre-

atinine; and those in the postpartum group had the highest increase

in uric acid. The intrapartum group showed the highest reduction in

creatinine clearance (Table 5).

Arterial blood gases and acidbase balance were affected in all 4

patient groups. Thus, statistical analysis was done for all patients

with eclampsia. pH showed a signicant increase after 24 and

Table 1

Clinical characteristics of women with different types of eclampsia.

Item Prepartum

eclampsia

(n=1594)

Intrapartum

eclampsia

(n=75)

Intercurrent

eclampsia

(n=16)

Postpartum

eclampsia

(n=313)

Age, y

Mean SD 25.1 6.4 25.5 6.8 23.5 6.0 25.0 6.3

Range 1645 1845 1835 1745

Parity

Mean SD 1.7 2.3 2.0 2.5 1.0 2.2 1.6 2.3

Range 09 08 06 09

Duration of pregnancy, wk

Mean SD 37.1 2.8 37.8 2.6 36.6 3.4 3 9 2.2 a

Range 3640 3540 3539 3641

a

Signicant atPb

0.05.

233D.E.M. Abd El Aal, A.Y. Shahin / International Journal of Gynecology and Obstetrics 116 (2012) 232236


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48 hours (Pb0.01 andPb0.001). PaCO2(mm Hg) decreased markedly

after 30 minutes and reached its lowest level after 48 hours (Pb0.05,

Pb0.01). PaO2 (mm Hg) was reduced markedly after 30 minutes

(Pb0.05) and continued to decrease signicantly (Pb0.05). Base ex-

cess increased after 30 minutes (not signicant), but had decreased

signicantly after 48 hours (Pb0.05). Bicarbonate concentration

showed a signicant increase after 30 minutes (Pb0.05). Oxygen sat-

uration remained nearly the same (Table 6).

There was a high incidence of cesarean delivery (73%) among the

patient cohort: the incidence was highest in the prepartum group

(89.6%), and lowest in the postpartum group (2.9%) (Table 7). The in-

cidence of perinatal mortality was 7.9%: the incidence was highest in

the intrapartum group (12.1%) and lowest in the intercurrent group

(7.4%). The overall incidence of low Apgar score at 1 minute (need-

ing resuscitation) was 48.2%: the incidence was highest among

women with prepartum eclampsia (50.2%) and lowest among

women with intercurrent eclampsia (26.6%). At 5 minutes, the inci-

dence of low Apgar score had dropped markedly to 7.4%. Most of

the neonates with low Apgar score at 5 minutes had intracranial

hemorrhage and marked respiratory distress syndrome owing to

prematurity (Table 8).

4. Discussion

The present study showed that magnesium sulfate controlled con-

vulsions in 98.1% of women and prevented recurrence in almost the

same percentage. It has been reported that eclamptic convulsions

rarely, if ever, develop after the administration of standard regimens

of magnesium sulfate [6]. By contrast, Pritchard [3]and Sibai et al.

[4] reported that 10 of 83 women (12%), in whom eclampsia was

treated before delivery, experienced convulsions shortly after injec-

tion of the loading dose; however, most women remained free of sei-

zures after an additional 2 g of intravenous magnesium sulfate.

Similar results were obtained by Smith and McEwan[7],and Rozen-

berg[8]. Magnesium sulfate, rather than phenytoin, reduces the risk

ratio of seizure recurrence and maternal death, and improves fetaloutcomes among eclamptic women[9]. Abd El Aal et al.[10]reported

that magnesium sulfate was effective in controlling convulsions in

98% of women, and that only 2% of women showed recurrence. Ola-

dokun et al. [11] reported repeated convulsion in 15% of patients

receiving anticonvulsants. The reason behind this wide variation in

results is unclear; it might be attributed to differences in ethnicity,

and to better outcomes due to ICU management in the present study.

In Australia, Lee et al.[12]reported that no single antihyperten-

sive drug was superior to other agents, and that nifedipine and labe-

talol had equal efcacy. In the present study, although good blood

pressure control was achieved in 93.5% of patients by the use of ni-

fedipine alone, variable doses of nifedipine were needed to control

blood pressure, starting with a 1020 mg single oral dose and a

total dose ranging from 40 to 60 mg/day. There was wide variability

and marked individual variations in nifedipine dose according to the

response to treatment. In addition, there was no correlationbetween

the dose of nifedipine required per day and the pre- or post-

treatment blood pressure. The presentndings are consistent with

those of Barton et al. [2], who suggested a total dose of 60 mg/day

in divided doses (10 mg/4 hours). Similarly, Fenakel et al. [13]sug-

gested an initial dose of 1030 mg of nifedipine sublingually, and

achieved good blood pressure control in 95.8% of patients by oral ad-

ministration of 80120 mg/day nifedipine. Other studies also indi-

cate that oral nifedipine signicantly reduces both systolic anddiastolic blood pressure[10,14,15].

Luan [16]reported that early termination of pregnancy leads to

good outcome. No deaths occurred among 106 cases of eclampsia

after early termination of pregnancy by either vaginal or cesarean de-

livery. In the present study the maternal mortality rate was 4.1%,

which is nearly 50% lower than previous results at our institute[10].

Other studies have reported mortality rates ranging from as low as

2.9% [17], 3.3% (a population of eclamptic patients who were mori-

bund at admission)[18], 9.5%[19], and 13%[3] to as high as 23.3%.

Onuh and Aisien [20] reported a case fatality rate of 10.7% (11

Table 2

Changes in blood pressure after use of nifedipine among the different groups of

patients.

Group Systolic blood pressure,

mm Hg

Diastolic blood pressure,

mm Hg

Before After Before After

Prepartum eclampsia

(n=1594)

163.222.2 140.214.2 a 113.814.9 969.8a

Intrapartum eclampsia

(n=75)

168.520.2 139.112.3 a 114.213.7 95.2 9.5a

Intercurrent eclampsia

(n=16)

157.220.4 142.711.9 a 117.310.1 954.7a

Postpartum eclampsia

(n=313)

165.121.4 140.515.9 a 113.114.2 96.5 9.8a

a Signicant atPb0.0001.

Table 3

Maternal outcome among the different groups of patients.a

Maternal outcome Prepartum

eclampsia

(n=1594)

Intrapartum

eclampsia

(n=75)

Intercurrent

eclampsia

(n=16)

Postpartum

eclampsia

(n=313)

Survived 1543 (96.9) 71 (94.7) 16 (100.0) 289 (92.3)

Died 51 (3.1) 4 (5.3) 0 (0.0) 24 (7.7)

Morbidity 324 (20.3) 15 (20.0) 2 (12.5) 98 (31.3)

a

Values are given as number (percentage).

Table 4

Liver function tests among the different groups of patients.a

Prepartum

eclampsia

(n=1594)

Intrapartum

eclampsia

(n=75)

Intercurrent

eclampsia

(n=16)

Postpartum

eclampsia

(n=313)

Bilirubin, mg/mL

b1 513 (32.2) 46 (61.3) 9 (56.3) 229 (73.2)

12 972 (61.0) 20 (26.7) 6 (37.5) 68 (21.7)

>2 109 (6.8) 9 (12.0) 1 (6.2) 16 (5.1)

SGOT, U/mL20 821 (51.5) 34 (45.3) 9 (56.3) 162 (51.8)

>20 773 (48.5) 41 (54.7) 7 (43.7) 151 (48.2)

SGPT, U/mL

16 834(52.3) 29 (38.7) 9 (56.3) 176 (56.2)

>16 760 (47.7) 46 (61.3) 7 (43.7) 137 (43.8)

Abbreviations: SGOT, serum glutamic oxaloacetic transaminase; SGPT: serum glutamic

pyruvic transaminase.a Values are given as number (percentage).

Table 5

Kidney function tests among the different groups of patients.a

Prepartum

eclampsia

(n=1594)

Intrapartum

eclampsia

(n=75)

Intercurrent

eclampsia

(n=16)

Postpartum

eclampsia

(n=313)

Blood urea, mg/dL

b25 972 (61.0) 19 (25.4) 7 (43.8) 176 (56.2)

>25 622 (39.0) 56 (74.6) 9 (56.2) 137 (43.8)

Serum creatinine, mg/dL

1.4 954 (59.8) 24 (32.0) 7 (43.8) 170 (54.3)

>1.4 640 (41.2) 51 (68.0) 9 (56.2) 139 (45.7)

Serum uric acid, mg/dL

6 1083 (67.9) 30 (40.0) 6 (37.5) 187 (59.7)

>6 511 (32.1) 45 (60.0) 10 (62.5) 126 (40.3)

Creatinine clearance, mL/min

100 1076 (67.5) 35 (46.7) 7 (43.8) 193 (60.7)

>100 518 (32.5) 40 (53.3) 9 (56.2) 120 (39.3)

a


234 D.E.M. Abd El Aal, A.Y. Shahin / International Journal of Gynecology and Obstetrics 116 (2012) 232236


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maternal deaths among 103 women with eclampsia), and a maternal

mortality ratio of 22.97%. Munro[21]reported that 23% of study pa-

tients required ventilation, and 35% had at least 1 major complication.

The latest Saving Mothers Report (20052007) indicates that 55.3% of

maternal deaths caused by hypertensive disorders of pregnancy were

due to eclampsia. This compares to a value of 17.8% in the present

study: the postpartum group had the highest ratio (26.4%), and theprepartum group had the lowest ratio (16.1%).

In the present study, there was marked signicant decrease in

PaO2after 30 minutes. The main cause of a decrease in peripheral ar-

terial oxygen tension may be an increase in oxygen consumption and

utilization by tissues over time to overcome the period of tissue hyp-

oxia that follows low cardiac output. Young and Weinstein [22]

recorded shallow slow breathing in 79% of patients with eclampsia

who received 2 g of magnesium sulfate by rapid intravenous infusion,

which may explain the high PaCO2 noted in their study. In the present

study, magnesium sulfate was given by infusion, which may explain

the absence of similar respiratory effects in the patients.

Templeton and Kelman[23]found that, although patients with

eclampsia had a slightly lower mean PO2 value as compared with

normal pregnant women, the differences were insignicant and

most patients with eclampsia had a PaO2 value within the normal

range. They also found a signicant increase in the (Aa) PO2differ-

ence, and an increase in physiological shunt, which indicates the

presence of a degree of pulmonary ventilation/perfusion imbalance.

Belfort and Kirshon[24]found a decrease in arterial O2and CO2ten-

sion in women with severe hypertensive disorders of pregnancy.

Their results are compatible with the results of the present study,

which found a decrease in O2and CO2tension. Belfort and Kirshon

[24] suggested that critical tissue hypoxia among patients with

eclampsia may explain the association of multiorgan dysfunction

with severe end-stage disease. In the present study, the pH increased

signicantly, possibly due to respiratory alkalosis. Belfort and Kir-

shon[24]also reported the same changes in PaCO2, pH, and arterial

blood base balance.

Kelton et al. [25] reported profound and progressive thrombocyto-penia, which was particularly associated with compromised liver and

renal function. Although these serious changes may occur occasional-

ly with minimal hypertension, thrombocytopenia was not correlated

with severity of hypertension in the present study.

The incidence of cesarean delivery was 76.7% among all groups in

the present study as compared with values of 50.12% to 60% in previ-

ous reports[16,19].At Assiut University Hospital, cesarean delivery is

preferred for eclamptic patients. It is preferred for patients who are

sure of their dates, and those whose cervix is not dilated enough to

deliver within 4 hours to avoid maternal deterioration. It is also pre-

ferred for those who, owing to a lack of health education, are usually

admitted with no previous prenatal care and with unsure dates in

order to protect a potentially preterm birth or a fetus with intrauter-

ine growth restriction from going through vaginal delivery.

The perinatal mortality was 7.5% in the present study; only 1 neo-

natal death was reported during treatment for eclampsia, which rep-

resents an improvement of 5% over previous results obtained at our

institution before implementing the current protocol [10]. Thesend-

ings are low in comparison to other studies: with the exception of

Taner et al. [19], who recorded a high perinatal mortality of 59.1%,

reported values vary from 1 among 14 cases [21], to 6.4% [12] or

193 per 1000[17]. Mortality was mostly related to either abruptio

placentae or extreme prematurity[3]. All of these results are compa-

rable to the presentndings. The higher rates of cesarean delivery in

the present study might be justied by saving many preterm infantsfrom the sequelae of vaginal delivery. Also, most of the women pre-

sented with no labor pain and had ts before attending.

In conclusion, the combination of nifedipine as an antihyperten-

sive drug, magnesium sulfate as an anticonvulsant, rapid termination

of pregnancy, and ICU management resulted in a marked improve-

ment in maternal and fetal outcomes of eclampsia. Future studies

similar to the Lampet trial, which is still in the recruitment phase,

and comparisons of labetalol and magnesium sulfate for seizure pre-

vention in eclampsia are needed.

Conict of interest

The authors have no conicts of interest.

References

[1] World Health Organization. The hypertensive disorders of pregnancy. WHO Tech-nical Report Series, 758. Geneva: World Health Organization; 1987.

[2] Barton JR, Hiett AK, Conover WB. The use of nifedipine during the postpartum pe-riod in patients with severe preeclampsia. Am J Obstet Gynecol 1990;162(3):78892.

[3] Pritchard JA. The use of magnesium ion in the management of eclampogenic tox-emias. Surg Gynecol Obstet 1955;100(2):13140.

[4] Sibai BM, Lipshitz J, Anderson GD, Dilts Jr PV. Reassessment of intravenous MgSO4therapy in preeclampsia-eclampsia. Obstet Gynecol 1981;57(2):199202.

[5] Royal College of Obstetricians and Gynecologists. The Management of SeverePre-eclampsia/Eclampsia. Guideline No. 10(A)http://www.rcog.org.uk/les/rcog-corp/GTG10a230611.pdfPublished 2006.

[6] Zuspan FP. Problems encountered in the treatment of pregnancy-induced hyper-tension. A point of view. Am J Obstet Gynecol 1978;131(6):5917.

[7] Smith GC, McEwan HP. Use of magnesium sulphate in Scottish obstetric units. Br J

Obstet Gynaecol 1997;104(1):115

6.

Table 6

Changes in arterial blood gases and acidbase status among all patients.a

Time at sample taking b

T T +30 min T +24 h T+ 48 h

pH 7.34 0.01 7.37 0.30 7.41 0.01 c 7.410.01 d

PaCO2, mm Hg 33.700.61 31.600.56c 31.100.46 d 30.300.49 d

PaO2, mm Hg 116.206.30 106.904.70e 98.103.50 c 96.302.10 c

Base E 1.81 2.04 1.85 1.32 0.56 1.50 1.751.44 e

Bicarbonate 18.900.34 20.301.40e 21.201.16 17.800.28

O2saturation 97.470.33 97.540.25 97.580.27 97.650.35

a Values are given as meanSD.b T indicates immediately postpartum and before any treatment (except loading

dose of magnesium sulfate).c Signicant atPb0.01.d Signicant atPb0.001.e Signicant atPb0.05.

Table 7

Mode of delivery among the different groups of patients.a

Mode of delivery Prepartum

eclampsia

(n=1594)

Intrapartum

eclampsia

(n=75)

Intercurrent

eclampsia

(n=16)

Postpartum

eclampsia

(n=313)

Vagi nal delivery 109 (6.8) 35 (46.7) 6 (37.5) 295 (94.2)

Ce sare an de liver y 1485 (93.2) 40 ( 53.3) 10 (62.5) 18 ( 5.8)

a


Table 8

Fetal outcome among the different groups of patients.a

Fetal outcome Prepartum

eclampsia

(n=1594)

Intrapartum

eclampsia

(n=75)

Intercurrent

eclampsia

(n=16)

Postpartum

eclampsia

(n=313)

Survived 1496 (93.5) 66 (88) 15 (93.8) 289 (92.3)

Died 98 (6.5) 9 (12) 1 (6.2) 24 (7.7)

Apgar score at 1 minute

03 184 (12.4) 4 (6.1) 1 (6.6) NA

37 492 (32.8) 11 (16.7) 3 (20) NA710 820 (54.8) 51 (77.2) 11 (73.4) NA

Apgar score at 5 minutes

03 3 (0.2) 0 (0) 0 (0) NA

37 106 (7.1) 2 (3) 0 (0) NA

71 1359 (90.8) 64 (97) 15 (100) NA

Abbreviation: NA, not applicable.a Values are given as number (percentage).

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