Abstract: 
Objective: The aim of this study was to assess if we are managing cases of eclampsia properly by testing our local protocol and to identify any specific preventable factors which may have led to the development of eclampsia in patients managed at the New Women's Hospital over a period of 3 years from 1.1.1993 to 31.12.1995 -Hamad Medical Corporation, Doha, Qatar. 

Methods: This study was performed retrospectively. The total number of deliveries were 30,873 of which 11 of them developed eclampsia. 

Results: Age of patients ranged between 18-45(mean 27years), parity ranged between 0-4(meanl), gestational age at the time of eclampsia ranged between 29- 41weeks(mean36weeks), maximum blood pressure BP (systolic BP. ranged between 120-200mmHg- meanI60mmHg),and( diastolicBP 80- 130mmHg(meanl02mmHg), the number of fits ranged between 1-3. A local protocol was followed using diazepam, or diazepam-hydralazine. Forty-five percent of the of patients had coma following the eclamptic fit, but just 18% of the cases had post echzmpsia complications including HELLP syndrome- (haemolysis,elevated liver enzymes,low platelets count) and acute renal failure (ARF). 

There was no maternal mortality. Forty five percent of the patients had symptoms of impending eclampsia, while the others were asymptomatic and were admitted due to other reasons. Just 27% of the patients were admitted with pre-eclampsia.
 
Conclusion: Despite the low incidence of maternal morbidity and nil mortality of eclamptic women in our department during the period of the study, modification of our Obstetric care by having a high index of suspicion even with apparently low risk patients with normal or slightly elevated BP is the key to management and prevention of this fatal condition, since, many eclamptic convulsions are not preceded by warning signs of impending eclampsia. In addition to the use of short term postpartum anticonvulsant therapy which may be beneficial in cases of raised intrapartum blood pressure since they are at risk of postpartum eclampsia . 

Key words: eclampsia, convulsions, BP (Blood pressure)   

Introduction: 

Eclampsia is the occurrence of one or more convulsions during pregnancy, labour or puerperium in association with the syndrome of pre-eclampsia, a multisystem disorder that is usually associated with raised blood pressure & proteinuria. It is relatively uncommon in developed countries where it complicates about one in every 2,OOOdeliveries. Eclampsia can be 20 times more common in developing countries, which have maternal mortality rates 100-200 times higher than Europe & North America, where 10% of maternal deaths are due to eclampsia. 

Eclampsia accounts for more than 50,000 maternal deaths worldwide each year (1,2) 
The incidence ranges from 0.2% -0..5 % of all deliveries. The perinatal mortality rate is between 10-28%. Maternal mortality vary according to the level of care provided, which needs a high facility that can offer high risk obstetrical care in a tertiary care centre(3). 

The first study that evaluated eclampsia at our unit was prepared in 1988. It showed that 2 cases of eclampsia occurred before 1979 and both of them died unfortunately. So this study was conducted to evaluate our local protocol in the management of eclampsia after that first study was reviewed. 

Materials and Methods: 

From January 1,1993 to December 31,1995, 11 cases of eclampsia were managed at the New Women Hospital, -Hamad Medical Corporation .It is the only maternity hospital in Qatar, with approximately 10,000 deliveries annually. The management of eclampsia at this hospital is directed towards: stopping convulsions, controlling blood pressure, stabilizing the mother and delivering the fetus regardless of the duration of pregnancy. The anticonvulsant diazepam was used in a similar way to that of Lean and co-workers and Crowther (3) and the Eclampsia Trial Collaborative Group(l). Severe hypertension was treated by intravenous hydralazine. 

Eclampsia was diagnosed by the occurrence of convulsions during pregnancy, labour, and 7 days postpartum, with or without hypertension (a systolic "BP of ?:140mmHg and a diastolic BP of ;?90 mmHg), with or without protienuria (+ l or more in a random urine sample or > O.3gmIL in a 24 hours urine collection) ,after excluding all other causes of convulsions. 

In the studied group, no patient had another cause of convulsions. Records of patients with a discharge diagnosis of eclampsia were reviewed. The retrospective review included prenatal records, emergency room visits, gravidity, parity, personal and family history of hypertension, future hypertension or pre-eclampsia, number of prenatal care visits, diagnosis leading to the admission ,gestational age at the onset of convulsions, total number of fits and its recurrence after treatment, maternal and perinatal outcome and complications of eclampsia. Mode of delivery and its indication, baby's weight, Apgar Score and duration of stay in hospital were also recorded. 

The Protocol for Management of Eclampsia in the New Women's Hospital: 

The patient is managed in the labor room or in the intensive care area where there is one to one nursing. The patient is turned on her side, oral trauma is avoided by padded tongue blade, a plastic airway is inserted and oxygen is given with suctioning of the nasal and oral passages. A wide bore intravenous line or central venous pressure (CVP) line is secured. 

Convulsions are terminated by the use of diazepam at a loading dose of IOmg intravenously over 2 minutes, repeated if convulsions recurred. This is followed by an intravenous infusion of 40mg diazepam in 500ml of normal saline as a drip to keep the patient sedated up to 24hours after delivery or the last convulsion, in instances of postpartum eclampsia. The rate of infusion is titrated against the level of consciousness, keeping the patient sedated. A foley catheter was inserted and volume recorded hourly on an Input- Output chart. Intravenous hydralazine was used in cases of severe hypertension i.e BP>1601110mmHg,aiming to keep diastolic BP between 90andlOOmmHg. 

The investigations requested included a complete blood count (including haemoglobin, haematocrit, white blood cells and platelets), kidney function Tests (including blood urea and serum creatinine). 

Liver function test (including total bilirubin, serum alkaline phosphatase and transaminases), uric acid, coagulation profile (including prothrombin time, partial thromboplastin time, fibrin degradation products and fibrinogen level), random blood sugar, urinanalysis and urine culture and sensitivity. Decision for delivery was taken irrespective of fetal maturity once the patient was stabilized. Induction of Labor was accomplished by oxytocin and amniotomy in cases of favorable cervices, but if the cervix was unfavorable or the fetal weight was less than l200gms, Caesarean section was considered. 

Results: 

Over a three years period, 30,873 deliveries took place at the new women's hospital from  (1.1.1993/31.12.1995). Eleven women developed eclampsia during this period. 

Maternal age ranged between 18-45 years (mean 27 years), 1. parity ranged between 0-4 (mean 1), gestational age ranged j between 29-4lweeks (mean 36weeks).The mean systolic BP , recorded at time of convulsions or immediately thereafter was l60mmHg (range l20-200mmHg) while the mean diastolic ; blood pressure was 102mmHg (range 80-l30mmHg). Four patients had a systolic BP < 140mmHg & a diastolic BP < 90 : mmHg at the time of first fit.
 
Eight patients had recurrent convulsions. All of them had! already received intravenous diazepam & were on diazepam drip. None of our patients received magnesium sulphate. 

The number of fits ranged between 1-3. Three had only 1 fit, 5 had 2 fits & 3 had 3 fits. 4 of  the fits were antepartum, 2 intrapartum & 5 postpartum. 

Five patients had premonitory symptoms of eclampsia (45%), the most common of which was headache. The other 6 patients (55%) were asymptomatic. Five out of the eleven patients (45%) had C-sections for eclampsia with unfavourable cervix, severe pre-eclampsia with unfavourable cervix & for fetal distress. Five patients had spontaneous vaginal deliveries, the eleventh delivery was induced by prostaglandin E 2-3mg vaginal tablet. Two of the spontaneous deliveries were expedited by the use of ventouse due to intrapartum eclampsia during the second stage of labour. 

Tables number 1& 2.
Two patients had no prenatal care visits, one of them had a convulsion at home & the other one was admitted with labour pain & developed intrapartum eclampsia, the other 9 patients had between 1-16 prenatal care visits. The diagnosis on admission ranged between eclampsia developed at home, severe pre-eclampsia, labour pain, acute asthmatic attack precipitated by upper respiratory tract infection, IUGR -fetal intrauterine growth restriction & urinary tract infection. No patient received anti-convulsant treatment prior to the development of convulsions, even those who were diagnosed to have moderate to severe pre-eclampsia. In all of these eclamptic patients the anticonvulsant used was intravenous diazepam followed by diazepam 
drip (protocol). The antihypertensive drug used was intravenous hydralazine used for 7 patients & methyl dopa for 1 patient, no antihypertensive was given to the other 3patients because their blood pressure did not exceed 140\90 mmHg. The perinatal mortality rate was 25%; as there were 2 early neonatal deaths and one still born baby. 

There were 12births including one set of twin & ten singletons. The birth weight ranged between 745gms & s 3290gms. Two patients had maternal morbidity in the form of HELLP syndrome (haemolysis, elevated liver enzymes & low I platelets count), the other had in addition to HELLP syndrome, I acute renal failure which did not require dialysis. Family history t of hypertension was found in 3 patients, one patient developed i pregnancy induced hypertension.

All patients were investigated for complete blood count, serum urea & creatinine. 

Urine for protien (including randum protien & 24 hours urine protien) was checked in only 8 patients, one of them had no protienuria, while the others had a range between (2.4-2.5gml24 hours) urine protien (mean 2.5). Liver function test was checked in 9 patients, uric acid for only 2 patients & coagulation profile for 6 patients. The total stay in the hospital ranged between 3& 4 days.

Discussion: 

Eclampsia is a universal syndrome recorded in most parts of the world. The efforts to diminish its mortality are productive in developed countries (4,5). 

The incidence of eclampsia in this study was 0.3per 1000 deliveries which is less than that obtained from other developing countries (0.5-10 per l000deliveries)(1,6,7) but matches reports from developed countries (0.05 -0.5)(1,3,4). The focus of secondary prevention of eclampsia should not be simply to prevent convulsions only, but also to prevent the dangerous underlying multisystemic disturbances. 

Possible preventable factors were investigated, so that pitfalls in the management should be changed & at risk patients can be picked up & treated promptly. We found in this study that our practice may be too restrictive in identification of at risk patients, because of the low index of suspicion for the atypical presentation that we had in a relatively high number of patients (4 out of 11) i. e 36% with only slightly elevated BP without any symptoms of impending eclampsia, these findings were similar to those obtained by Sibai (5) & Douglas et al(4) . 

Changes of clinical significance may occur weeks before clinically detectable hypertension, which may be missed during routine prenatal visit (8). Monitoring renal & liver function tests & platelets count can give early warning of impending decompensation (4). It was disappointing that some important biochemical tests were not done even after the onset of convulsions in this group of eclamptic patients. The same problem was encountered in the United Kingdom in the eighties (9). Sibai et al (8), reported that failure to prevent eclamptic convulsions were physician error, patient failure & abrupt or late onset of eclampsia. No anticonvulsant therapy was given to our patients having severe pre-eclampsia (physician error). 

The extent of endothelial damage is the most acceptable factor in the pathogenesis of eclampsia, so that eclampsia can precede pre-eclampsia which makes prevention more difficult. In uncomplicated pregnancies, the recommended number of optimal prenatal care visit is 12. (7,10). This results in prompt identification &management of pre-eclampsia through bed rest & initiation of therapy (10). In the mentioned cases, only 3 patients had 9 prenatal visits or more, so the opportunity for intervention in such patients is limited. Campbell & Templeton (11) investigated the possible leading factors to eclampsia in 66 patients. They concluded that appropriate prenatal care will not prevent most cases of severe pre- eclampsia \ eclampsia & 47%of the patients developed convulsions following admission to the hospital. Sibai (5), noted the same findings. We had a much higher percentage of convulsions under medical supervision than Campbell, Templeton & Sibai. 

Low dose aspirin had been tried to prevent pre- eclampsia&eclampsia in many studies, the largest of which was .the Collaborative Low Dose Aspirin Study in Pregnancy (CLASP)(12), by comparing the effect of 6Omglday of aspirin to placebo in both nulliparous women & women with poor Obstetric histories. They concluded that low dose aspirin can be justified in women liable for early onset pre-eclampsia severe enough to result in very pre-term delivery.

Eight patients had recurrent convulsions while receiving diazepam treatment. The Collaborative Eclampsia Trial Group (1), demonstrated that significantly fewer recurrences of fits occurred with magnesium sulphate than with diazepam, 
magnesium sulphate is the drug of choice for routine anticonvulsant management of women with eclampsia in many countries all over the world nowadays,(13,14). 

A clinical trial of magnesium sulphate versus diazepam i worth considering at our department. A well-established protocol of magnesium sulphate therapy should be used. A study 0 eclampsia in Qatar performed in 1988(15), which showed that 2cases of eclampsia were recorded before 1979 & both of them died due to cerebrovascular accidents. 

Fortunately no maternal deaths were encountered in our study. Modifications of our obstetric care, by making a high index of suspicion of pre-eclampsia & eclampsia even in low risk women, together with the use of short-term Postpartum anticonvulsant therapy may be of benefit in cases of raise intrapartum BP as they are at risk of postpartum eclampsia.

References: 

1. Duley L. which anticonvulsant for women with eclampsia? Evidence from the collaborative eclampsia trial. Lancet 1995; 345: 1455-1463. 

2. Agudelo A, gueta A. C. Epidemiology of eclampsia in colombia. 1nt J Gynecol Obstet 1998; 61:1-8. 

3. Cowther C. Magnesium sulphate versus diazepam in the management of eclampsia: a randamized controlled trial. Br J Obstet Gynecol 1990; 97: 110-117. 

4. Douglas K.A, Redman C. W:G. Eclampsia in the United Kingdom. Br Med J 1994; 309: 1395-1400. 

5. Sibia B.M. Eclampsia ffi Maternal perinatal outcome in 254 consecutive cases. Am J Obstet Gyncol 1990; 163: 1049-1055 

6. Cincotta R, Ross A. A review of eclampsia in Melbourne. Aust N Z J Obstet Gynecol1996; 36:264-267. 

7. Thomas P, Golding J Peters 1:J. Delayed antenatal care: does it affect pregnancy outcome? Soc Sci Med 1991; 32: 715-723. 

8. Sibia B.M. Abdella 1:N; Spinnato J.A, et al. The incidence of non preventable eclampsia, Erclampsia ~ 1986: 154: 581- 586. 

9. Department of health, Welsh Office, Scotish Home and Health Department, Department of Health and social Services Northern Ireland. Report on confidential enquiries into maternal deaths in the United Kingdom 1985-1987. London:HMSO, 1991. 

10. Abi-said D, Annegers J.p, Cantrell D.C,et al. Case control study of the risk factors for eclampsia. Am J epidemiol 1995; 142: 437-441. 

11. Campbell D.M, Tempelton. A.A. is eclampsia preventable? In: Bonnar J, MacGillivary I, Symonds E.M., eds.  Pregnancy hypertension. Baltimore: University Park Press 1980. 

12. ClAP A randomized trial of low-dose aspirin for the prevention and treatment of pre-eclampsia among 9364 pregnant women. Lancet 1994; 343; 619-629. 

13. Chein P.F.~ Khan K.S, Arnott N. Magnesium sulphate in the treatment of eclampsia and pre-eclampsia: an overview of the evidence from randomised trials. Br J Obster Ghnecol1996; 103: 1085-1091. 

14. Usta I.M, Sibia B.M. Emergent management of puerpera 1 eclampsia. ObstetGyneacol ClinNorthAm 1995; 22: 315- 335. Manoj M, El Nayal Z, Ahmed A.H. Eclampsia: dark room care or bright lighyts of intensive care.l.

15. Obsestet Gynecol 1989; 10 (Supp.I): 13-15. 

Pages (6): [ < 1 2 3 4 5 6 > ]