atyp eclm

Pioneer Medical Journal Vol. 3, No. 5, JANUARY - JUNE, 2013

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ATYPICAL ECLAMPSIA: CASE REPORT

AGWU F.E., NDUKA E.C, AND NWACHUKWU K.C.

Department Of Obstetrics and Gynaecology,

Federal Medical Centre, Umuahia.

Correspondence to: NDUKA E.C.

Email: [email protected]

ABSTRACT:

Occurrence of Eclampsia before 20 weeks gestation, after 48 hours postpartum or in absence of

typical signs of hypertension and /or proteinuria is termed Atypical Eclampsia. We report a case

of a 27 year old booked para2+0

nurse with 2 living children who developed Eclampsia on the 6th

postpartum day without preceding pre-eclampsia. Problems of atypical Eclampsia lie in its

unpredictable onset. A high index of suspicion and close follow-up will help in the early

detection of this condition. This is crucial especiallyin developing countries where Eclampsia is

a major cause of maternal mortality and facilities for timely diagnosis and management of these

cases are inadequate.

Key Words: Atypical Eclampsia, Management, Umuahia.

INTRODUCTION:

Eclampsia is defined as the development of convulsions and/or unexplained coma during

pregnancy or postpartum in patients with signs and symptoms of preeclampsia after 20 weeks

prepartum and before 48 hours postpartum1.

Occurrence of Eclampsia before 20 weeks, after 48 hours postpartum or in absence of typical

signs of hypertension and/or proteinuria is known as Atypical Eclampsia2.Eclampsia, as well as

Atypical Eclampsia, is an important cause of maternal mortality and morbidity3,4

. Correct and

timely diagnosis and management of these cases is challenging for obstetricians.

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We report a case of Atypical Eclampsia occurring on 6th

postpartum day without prior history of

preeclampsia.

CASE REPORT:

Mrs. U.O., a 27 year old Nurse, a booked para2+0

with 2 living children, who had elective lower

segment caesarean section at 39 weeks gestation on account of breech presentation with previous

caesarean section, with an outcome of a live female neonate with good Apgar scores and birth

weight of 3.6kg.

She had emergency lower segment caesarean section due to cephalopelvic disproportion in

labour in her previous pregnancy two year before. Her family history was unremarkable.

During this index pregnancy, her antenatal period was uneventful and she remained

normotensive. Her post-operative course was uneventful and she was discharged home on the 5th

postoperative day.

On the 6th

post operative day, however, she developed severe occipital and frontal headaches. On

the next day, she was managed in a peripheral hospital for a generalized tonic-clonic seizure and

had eight episodes of similar seizures, treated with 10mg of intravenous diazepam before being

transferred to our emergency department.

On admission in our facility, her Glasgow Coma Scale (GCS) score was 6, blood pressure

180/110 mmHg, pulse 120 beats/minute, respiratory rate 24 breaths/minute, and temperature

37oC. Her neck was supple and non-tender, and her pupils were equal and reactive to light.

Cardiovascular, respiratory, and abdominal examination findings revealed no abnormalities. The

ophthalmologic examination and laboratory results (full blood count serum electrolyte, urea,

creatinine, uric acid and calcium; liver function test; random blood sugar; coagulation profile;

cerebro-spinal fluid examination) were normal except urinalysis that revealed proteinuria of 1+

Consultant Obstetrician and the anesthesiology team were immediately alerted and invited.

Immediate resuscitation measures were commenced, ensuring airway patency, breathing and

circulatory maintenance and monitoring of urinary output via an indwelling urethral catheter

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connected to a uribag. MgSO4seizure prophylaxiswas commenced using Pritchard’s regimen.

Broad spectrum antibiotics and anti-malarial treatments were started. She had two further

episodes of similar seizures while being resuscitated necessitating intubation by

anaesthesiologists who were already on ground. She was immediately transferred to Intensive

Care Unit. (ICU) on mechanical ventilation. While on admission, neurology team and

cardiology team opinions were sought. Neurological examination findings were normal; though

Computed Tomography Scan (CT), Magnetic Resonance Imagining (MRI) and Electro

Encephalogram (EEG) requested were not done because of financial constraint. Cardiologists

excluded any cardiac cause. Patient was transferred to the ward from the ICU after 24 hours

when her condition was adjudged stable. Her condition remained stable for the next one week

and she was discharged home with a blood pressure of 100/60 mmHg, and a follow-up

appointment in clinic given. At follow-up visit, here blood pressure was 110/70 mmHg,

urinalysis was negative for protein and glucose and her wound had healed well. She was

referred to the family planning clinic for contraceptive counseling and told to book early in a

tertiary hospital in her future pregnancy.

DISCUSSION:

Pre-eclampsia is a multisystem disorder. It usually warns about occurrence of Eclampsia

beforehand. However, hypertension is only one of the signs and is not always present in

preeclamptic patents developing Eclampsia2. It is difficult to predict which organ system will

predominantly be involved.

Eclampsia, a rare but serious complication of pre-eclampsia, becomes more problematic when it

develops without prior preeclamptic signs and symptoms5. Our patient remained free of signs

and symptoms throughout antenatal period and post-operative period until the 6th

post-operative

day when she developed neurological symptom (headache). Our diagnosis of Eclampsia was

based on the clinical presentation, biochemical findings and the exclusion of other underlying

disorders.

Our differential diagnostic considerations included cerebral vein thrombosis, subarachnoid

haemorrhage from an aneurysm, hypertensive encephalopathy,previously undiagnosed brain

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tumours. These differentials were ruled out on cardiac and neurological evaluation in our

patient. CT Scan, MRI and EEG requested to rule out these differentials were not done because

of financial constraints. Infectious disorders were unlikely because of the clinical course and

negative findings on cerebrospinal fluid study. Biochemical investigations ruled out metabolic

causes like hypoglycaemia and hypocalcaemia.

By definition, our patient had atypical Eclampsia since she developed seizure on the 6th

post

operative/post-partum day without prior signs of pre-eclampsia (hypertension and proteinuria).

She only complained of headache a day before seizure manifestation, and this highlights the fact

that such prodromal symptom in post-partum women even in the absence of preceding

proteinuria and hypertension should cast suspicion on impending Eclampsia. Adie et.al. reported

162 cases of Eclampsia in a period of two years of which 8% (13) had features of atypical

eclampsia with normal blood pressure and without preeclampsia prodromi. In their study, post-

partum convulsions had occurred in 31% of patients5.In another study, Katz et.al.reported 53

cases of Eclampsia in the absence of pre-eclamptic signs. In their patients, seizures were the

main manifestation of disease in 60% of cases6, as observed in our patient. The most common

cause of convulsions in association with hypertension or proteinuria during pregnancy or

immediate post-partum is Eclampsia. However, late post-partum eclampsia is defined as

Eclampsia that occurs more than 48 hours, but less than four weeks, after delivery7. All

Eclamptic patientsin developing countries are at higher risk of maternal death3,4

, mainly

because of poor utilization of maternity services and lack of intensive care facilities and man

power needed to manage the maternal complications from eclampsia5 This however, was not

the case in our patient who had supervised pregnancy and delivery, and benefited from expert

management and intensive care facilities when atypical eclampsia developed. Low incidence of

eclampsia in developed countries is probably related to seizure prophylaxis in patients with

classic presentation of severe preeclampsia.

Current management schemes designed to prevent eclampsia are based on early detection of

preeclampsia and subsequent use of preventive therapy in such women. This management

schemes assume that the clinical course in the development of eclampsia is characterized by a

gradual process that begins with progressive weight gain followed by hypertension and

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proteinuria, which is followed by the onset of premonitory symptoms, and ends with the onset of

generalized convulsions or coma8.

Most women who develop eclampsia do have prior history of pre-eclampsia. However, as

shown in the patient reported on as well as in other studies9,the onset of convulsions does not

necessarily follow the presumed progression from pre-eclampsia to eclampsia.

CONCLUSION

Eclampsia may be an unusual presenting scenario in atypical cases before detection of overt

hypertension or proteinuria. Even minor clues in diagnosis, such as a marginally elevated blood

pressure or trace proteinuria, may be critical for appropriate and timely management.

Obstetricians should be aware of atypical presentations, maintain a high level of suspicion, and

be ready to take immediate live-saving steps.

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REFERENCES:

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Obstet. Gynecol. 2009:200:481.

2. Imdad A, Sheikh L., Malik A. - Atypical eclampsia J. of Pakistan Med. Association

2009:59:489-90.

3. Ezem B.U., Okeudo C. - Maternal Mortality in Imo State University Teaching

Hospital, Orlu: A 5 year Review, Ebonyi Med. J 2011:10:2:117-122.

4. Audu B.M., Takai U.I., Bukar M. - Trends in maternal mortality at University of

Maiduguri Teaching Hospital, Maiduguri, Nigeria – A five year review. Nig Med. J.

2010; 51(4):147-151.

5. Adie V., Moodley J. - Atypical eclampsia J. Obstet. Gynaecol 2005; 25:352.

6. Nirromaneshe S., Mirzale F. - Atypical post-partum eclampsia: status epilepticus

without preeclampticprodromi. Women Birth 2008:21:171-3.

7. Albayrak M, Ozdemir L., Demiraran Y., Dikici S. - Atypical preeclampsia and

eclampsia: report of four cases and review of the literature. J. Turkish –German

Gynecol. Assoc. 2010;11:115-7.

8. Sibai B.M. - Diagnosis, prevention and management of eclampsia. Obstet. Gynecol.

2005;105:402-10.

9. Mattar F, Sibai B.M. - Eclampsia VIII Risk factors for maternal morbidity. Am J.

Obstet Gynecol. 2000; 182:307-12.

atyp eclm

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