AHMADU BELLO UNIVERSITY ZARIA

COURSE CODE: NURS 513

COURSE TITLE: COMMUNITY HEALTH SEMINAR

Seminar Presentation

On

ECLAMPSIA as a leading cause of maternal mortality in Nigeria

By

GROUP (7)
HADIZA ADAMU AUDU U18DLNS20510 (GROUP LEADER)
MADAFOR ADA U18DLNS20413
NWOSU ELIZABETH U18DLNS20251
CHUKWAMA KELICHA U18DLNS20506
HASSANA YUSUF U18DLNS20274
ADEWUYI OLUYINKA

E-TUTOR: AISHA SALIHU

DECEMBER, 2021
Overview

This study was aimed at finding out Eclampsia a leading cause of maternal mortality in

Nigeria. Ten percent of all pregnancies are complicated by hypertension. Eclampsia and

preeclampsia account for about half of these cases worldwide, and these conditions have been

recognized and described for years despite the general lack of understanding of the disease.

In the fifth century, Hippocrates noted that headaches, convulsions, and drowsiness were

ominous signs associated with pregnancy. In 1619, Varandaeus coined the term eclampsia in

a treatise on gynecology.

INTRODUCTION

Hypertensive disorders of pregnancy are a heterogeneous group of conditions that include

chronic hypertension, gestational hypertension, preeclampsia, and preeclampsia superimposed

on chronic hypertension. Hypertension in pregnancy is defined as a systolic BP of 140 mm Hg

and a diastolic BP of 90 mm Hg on two separate measurements at least 4–6 hours apart.

Diagnose women who develop hypertension after 20 weeks' gestation and who do not have

proteinuria or other criteria for preeclampsia with gestational hypertension. Preeclampsia is a

multiorgan disease process characterized by hypertension and proteinuria or one of the

following features, which are diagnostic when they develop in the setting of new-onset

hypertension after 20 weeks' gestation.

Eclampsia is preeclampsia complicated by generalized tonic-clonic convulsions. The

progression of preeclampsia to eclampsia is sudden and without prediction. The onset of

eclamptic convulsions can be antepartum (38% to 53%), intrapartum (18% to 36%), or

postpartum (11% to 44%). Eclampsia affects about 1 in every 200 women with preeclampsia.

You can develop eclampsia even if you don’t have a history of seizures.
Definition: Eclampsia can be defined as a seizure activity or coma in a woman with signs and

symptoms of preeclampsia or PIH, after the exclusion of other cerebral or neuropathological

conditions. Nonetheless, eclampsia in the absence of hypertension with proteinuria has been

demonstrated to occur in 38% of cases reported in the United Kingdom. Similarly, hypertension

was absent in 16% of cases reviewed in the United States.

Eclampsia is a severe complication of preeclampsia. It’s a rare but serious condition where

high blood pressure results in seizures during pregnancy. Seizures are periods of disturbed

brain activity that can cause episodes of staring, decreased alertness, and convulsions (violent

shaking). Eclamptic convulsions are more common from late pregnancy up to 48 hrs

postpartum (E. Okpere 2003). Rare cases of eclampsia have been reported prior to 20 weeks'

gestation or as late as 23 days postpartum (S R Fugate, 2005), but other causes of convulsions

should be sought when they occur after 5 days postpartum (Okpere).

Definition of other terms:

Preeclampsia is the occurrence of systolic BP>140 mmHg/diastolic BP>90mmHg recorded

on 2 separate occasions at least 4-6 hours apart and in the presence of at least 300mg protein

in a 24-hr urine collection, arising de novo after the 20th week of gestation in a previously

normotensive woman & resolving completely within the puerperium. It may occur before the

20th week in molar pregnancies. Preeclampsia can be classified as mild or severe.

Severe preeclampsia is also known as fulminating preeclampsia or imminent eclampsia. It is

the transitional condition characterized by progressive worsening of signs and symptoms. It is

diagnosed in the presence of (1) a systolic BP>160 mm Hg/diastolic BP> 110 mm Hg on 2

occasions at least 6 hours apart in a woman on bed rest and (2) the presence of significant
proteinuria. Marked proteinuria is defined as 5 g or more of protein in a 24-hour urine

collection.

TYPES/TIME OF ONSET OF ECLAMPSIA

The onset of eclamptic convulsions can be:

1. Antepartum (before the onset of labour) – almost all cases (91%) develop at or

beyond 28 weeks. The remaining cases occur between 21 and 27 weeks of gestation.

Eclampsia occurring before the 20th week of gestation is usually associated with

molar or hydropic degeneration of the placenta, with or without a coexistent fetus.

2. Intrapartum (occuring in labour), or

3. Postpartum (after delivery) – usually within the first 48 hourrs, A rear entity is Late

postpartum eclampsia (develop beyond 48 hours but < 4 weeks postpartum) – here do

an extensive neurological evaluation include neurologic exam, brain imaging, lumbar

puncture, and blood tests, as needed to rule out the presence of other cerebral

pathology.

TYPE INCIDENCE PROGNOSIS

Antepartum Eclampsia 25%
Intrapartum Eclampsia 50%
Postpartum Eclampsia 25% Very poor

SIGN AND SYMPTOMS

Because preeclampsia can lead to eclampsia, it may have symptoms of both conditions.

However, some of the symptoms may be due to other conditions, such as kidney disease or

diabetes.

The following are common symptoms of preeclampsia:

 Elevated blood pressure

 swelling in your face or hands

  headaches

 excessive weight gain

 nausea and vomiting

 vision problems, including episodes with loss of vision or blurry vision

 difficulty urinating

 abdominal pain, especially in the right upper abdomen

Patients with eclampsia can have the same symptoms as those noted above, or may even

present with no symptoms prior to the onset of eclampsia.

The following are common symptoms of eclampsia:

 Seizures

 Loss of consciousness

 Agitation

PATHOPHYSIOLOGY OF ECLAMPSIA.

Eclampsia is a disease which appears only during pregnancy, characterized by hypertension,

proteinuria and oedema. It is widely widespread, and in the underdeveloped countries, is the

leading cause of maternal mortality; its pathogenesis is thought to be associated to a hypoxic

placenta, which is responsible for the maternal vascular dysfunction. It occurs more

commonly in first pregnancies and primarily affects maternal, renal, cerebral, hepatic and

clotting functions while elevating blood pressure and the delivery of the placenta is the only

way to control this pathology.

The placenta and fetal membranes presumably play a role in the development of preeclampsia

because of the prompt resolution of the disease following delivery. A common pathway

thought to be associated with the development of preeclampsia is uteroplacental ischaemia.

Uteroplacental ischaemia predisposes to the production and release of biochemical mediators

that enter the maternal circulation, causing widespread endothelial dysfunction and

generalized arteriolar constriction and vasospasm, as well as cellular & end-organ

dysfunction.

The occurrence of these events in the brain leads to cerebral oedema, cerebral vasospasm &

cerebral hypoxia. This results in cerebral ischaemia & haemorrhage leading to seizures+/-

coma. Eclampsia is a multisystemic disorder that affects the CN, haematological, hepatic,

renal, and pulmonary & CV systems. There are also changes in the eye.

CNS

a. Fibrinoid necrosis

b. Thrombosis

c. Microinfarcts

d. Petechial haemorrhage

e. Cerebral oedema

Haematological

a. Haemoconcentration

b. Thrombocytopaenia

c. DIC

d. Microangiopathic haemolysis

Hepatic

a. Sinusoidal fibrin deposition

b. Periportal haemorrhage

c. Portal capillary thrombi

d. Centrilobular necrosis
 e. Subcapsular haematoma

f. Hepatocellular necrosis

These will result in increased serum levels of ALAT, ASAT & LDH

Renal

a. Glomeruloendotheliosis

b. Increased lipid vacuoles in cytoplasm

c. Swollen mesangial cells

d. Deposition of Ig, complements, fibrin & fibrin degradation products

These will result in decreased GFR, decreased renal plasma flow, & decreased uric acid

plasma.

Pulmonary

a. Non-cardiogenic pulm oedema with superimposed cardiogenic pulm oedema

b. Aspiration pneumonitis

c. ARDS

CVS

a. Generalized vasospasm

b. Increased peripheral vascular resistance

c. Increased LV stroke work index

d. Decreased CVP

e. Decreased pulm wedge pressure

Eye Changes

a. Retinal vasospasm

b. Retinal oedema
 c. Serous retinal detachment

RISK FACTORS OF ECLAMPSIA

The following are considered risk factors for eclampsia:

 Primigravidity and Nulliparity

 Family and personal history of preeclampsia and eclampsia

 Poor outcome of previous pregnancy, including intrauterine growth restriction, abruptio

placentae, or fetal death

 Multifetal gestation, molar pregnancy,fetal hydrops, Teen preg.

 Advance maternal age (>35 years)

 Lower socioeconomic status and

 Medical conditions like Obesity, Chronic hypertension, Renal disease, Thrombophilias-

antiphospholipid antibody syndrome, Protein C and Protein S defieiencies, Antithrombin

deficiency, Vascular and connective tissue disorders, Gestationl diabetes and Systemic

lupus erythematosus.

CAUSES

The exact cause of the seizures is unknown, although several processes have been implicated in

their development cerebral vasoconstriction, cerebral hypoxia & cerebral oedema have been

implicated; these lead to cerebral ischaemia & hence fits areas of cerebral vasospasm may be

severe enough to cause focal ischemia, which may in turn lead to seizures.

Pathologic alterations in cerebral blood flow and tissue oedema induced by vasospasm may

result in headaches, visual disturbances, and hypertensive encephalopathy, resulting in a seizure.

Genetic, immunologic, endocrinologic, nutritional, and even infectious agents have been

proposed as the cause for preeclampsia/eclampsia. Despite extensive research, no definitive

cause has been identified.

CAUSE OF ECLAMPTIC SEIZURES

Eclampsia manifests as one seizure or more, with each seizure generally lasting 60-75 seconds.

There are four stages during an Eclamptic convulsion

 Premonitory stage: the eyes protrude and rolled up with twitches of the face and hands.

Foaming at the mouth may occur. This is followed by

 Tonic stage: with generalized tonic contraction of the whole body muscles with

opisthotonus ± cyanosis.

 Clonic stage: A convulsion occurs with alternating contraction and relaxation of the

body muscles. It starts in the jaw, moves to the muscles of the face and eyelids, and then

spreads throughout the body.

 Coma: coma or period of unconsciousness, lasting for a variable period, follows. After

the coma phase, the patient may regain some consciousness, and she may become

combative and very agitated.

Severity of Eclampsia

Eclampsia is considered severe if one or more of the following is present (Eden’s criteria):

1. Coma of 6 or more hours.

2. Temperature 39oC or more.

3. Pulse over 120/min.

4. Systolic blood pressure over 200 mmHg.

5. Respiratory rate over 40/min.

6. More than 10 convulsions.

DIAGNOSIS OF ECLAMPSIA

The diagnosis of eclampsia is secure in the presence of hypertension, proteinuria, and

convulsions.
However, women in whom eclampsia develops exhibit a wide spectrum of signs, ranging from

severe hypertension, severe proteinuria, and to absent or minimal HT and no proteinuria.

Hypertension is considered the hallmark for the diagnosis of eclampsia. The hypertension can be

severe or mild, but in 16% of the cases, hypertension may be absent.

However the diagnosis of eclampsia is usually associated with proteinuria (at least 1 on dipstick)

and several clinical symptoms (headaches, blurred vision, photophobia, epigastric pain) that

occurs before or after the convulsions are potentially helpful in establishing the diagnosis.

Abnormal weight gain (with or without clinical edema) in excess of 1 kg per week during the

third trimester might be the first sign before the onset of eclampsia.

DIFFERENTIAL DIAGNOSIS OF ECLAMPSIA

 Cerebrovascular accidents – Hemorrhage, embolism or thrombosis and Hypoxic ischemic

encephalopathy

 Seizure disorder

 Meningitis.

 Cerebral malaria

 Metabolic diseases – Hypoglycemia, hyperglyceamia, hyponatremia

 Head injuries

 Hypertensive encephalopathy

 Drugs overdose and withdrawal syndromes

 Tetanus and Strychnine poisoning.

 Previously undiagnosed brain tumors

INVESTIGATIONS OF ECLAMPSIA
No single laboratory test or set of laboratory determinations is predictive of maternal or neonatal

outcome in women with eclampsia BUT some investigations can be useful in planning

management.

1. Urinalysis – Proteinuria is typically one of the presenting symptoms in patients with

eclampsia and is very useful in making diagnosis especially in the atypical cases

2. A full blood cell (FBC) count may reveal the following:

 Anemia due to microangiopathic hemolysis or hemoconcentration due to third

spacing

 Thrombocytopenia (< 100,000) due to hemolysis and low platelet count

associated with HELLP syndrome (seen in 20-25% of patients with eclampsia)

 Elevated lactate dehydrogenase (LDH) levels (threshold of 180–600 U/L)

 With thrombocytopenia do Clotting profile to rule out DIC

3. E/U/Cr – The serum creatinine level is elevated in eclampsia because of a decreased

intravascular volume and a reduced glomerular filtration rate (GFR) or renal failure.

Electrolytes derengemment (hyponatremia) may be the cause of convulsion.

4. Liver enzymes (ASAT, ALAT) may show elevated levels due to hepatocellular injury

and HELLP syndrome

5. Random blood sugar rule out hypoglycemia as cause of seizure or result of seizure, and

rule out hyperglycemia as cause of mental status changes.

6. Imaging studies (CT scan and MRI) may be indicated after initial stabilization,

especially if there is doubt about the diagnosis or possible injuries secondary to seizure

activity.
 7. Electroencephalography and CSF Studies are rarely useful in management; however,

they may be indicated if epilepsy or meningitis is considered in the diagnosis.

8. Transabdominal Ultrasonography is used to estimate gestational age. This may also be

used to rule out abruption placentae, which can complicate eclampsia.

MANAGEMENT OF ECLAMPSIA

The goal of management is to prevent mortality and limit maternal and fetal morbidity until

delivery which is the only definitive treatment of Eclampsia.

Because the primary manifestations of eclampsia associated morbidity and mortality result from

seizure-induced aspiration, pulmonary edema, recurrent seizure activity, or neurologic sequelae;

the principle of managements is thus:

1. Control of convulsions using magnesium sulfate

2. Control BP by given antihypertensive medication to lower blood pressure whenever it is

considered dangerously high

3. Maintenance of fluid and electrolyte balance and

4. Delivery of the fetus to achieve a "cure."

 The initiation of management is to institute a supportive care

 Do not leave the woman alone but call for help, including appropriate personnel

such as the anaesthetist and senior obstetrician

MEDICAL MANAGEMENT OF ECLAMPSIA

1. CONTROL OF CONVULSION/ PREVENTION OF RECURRENT CONVULSIONS

Magnesium sulfate is the drug of choice to treat and prevent subsequent convulsions in

women with eclampsia and has been shown to be associated clinically significant

reduction of reoccurrence of convulsions and maternal death compare to other

anticonvulsants like Diazepam, Phenytoin, and Paraldehyde and Lytic coctail.

It is usually given intramuscular (IM) called the Pritchart’s regimen or as an intravenous

(IV) protocol; the Zuspan regimen. In both regimen loading and maintenance doses are

given

Loading dose: same in both regimen

• IV MgSO4 4g diluted to 20mls (8mls MgSO4 + 12mls of sterile water/Normal

saline) given slowly over 5-10 min. Plus IM MgSO4 10g (5g each buttock)

Maintenance dose:

• For the IM regimen = IM MgSO4 5g 4hourly in alternate buttocks for 24 hours

after delivery or 24 hours after last fit (whichever come last). You may add 2mls

of 1% Xylocaine to the IM MgSO 4 to reduce the pain especially in patient that are

conscious).

• For the IV regimen = 1g/hr continuous IV infusion using 10g MgSo4 in 1000mls

of normal saline.

Loading dose is given irrespective of urinary output

Maintenance Dose: Should only be given if

• Urinary output > 25ml/hr (>100ml in the last 4 hrs)

• RR ≥ 12 /min

• Patellar reflex (Knee Jerk) present

If seizure occurs in first 20 min after loading dose: the convulsion is usually short, and no

additional treatment is indicated.

If seizure occurs longer than 20min after the loading dose: give an additional 2g MgSO4

IV bolus slowly over 5 minutes.

2. CONTROL OF BLOOD PRESSURE

The primary goal of therapy is to prevent life-threatening clinical conditions such as

hypertensive encephalopathy, CVA, acute left ventricular failure and acute aortic

dissection give antihypertensive whenever the BP ≥ 160/110 mmHg.

a. Hydralazine 10 mg intravenous (IV) push (slowly over 5-10 minutes) repeated

every 30-minute intervals as indicated aiming at achieving DBP between 100-90

mmHg

b. However, if there is no success by 40 mg IV alternative agent (Labetalol) should

be employed or the patient can be given nifedifine

Labetalol is initiated at a 20 mg IV bolus. If the effect is suboptimal, 40 mg should

be administered after 10 minutes and then 80 mg every 10 minutes for 2 additional

doses (up to 220 mg). As with all beta-blockers, its use is contraindicated in

asthmatics.

Nifidifine is given as a 10-mg initial oral dose to be repeated in 30 minutes if

necessary. Nifedipine given sublingually is no longer recommended.

Diuretics are used only in the setting of pulmonary edema.

 • Care must be taken not to decrease the BP too drastically; an excessive

decrease can cause inadequate uteroplacental perfusion and fetal distress.

• In the rare instances of hypertensive crisis, either sodium nitroprusside (initial

rate 0.25 mcg/kg/min to a maximum dose of 5 mcg/kg/min) or nitroglycerine

(initial IV infusion rate of 5 mcg/min, titrated to affect every 3 to 5 minutes to

a maximum dose of 100 mcg/min) is administered – avoid nitroglycerine in

patients with hypertensive encephalopathy.

3. MAINTENANCE OF FLUID AND ELECTROLYTES BALANCE:

This is critical because excessive admistration of fluid can lead to pulmonary edema and

when fluid replacement is not adequate renal failure can occur.

• Monitor urinary output hourly

• There is no evidence of the benefit of fluid expansion and a fluid restriction

regimen is associated with good maternal outcome; fluids should be limited to

80-100 ml/hour or 1 ml/kg/hour or previous hour urinary output + 30mls.

• The regime of fluid restriction should be maintained until there is a postpartum

dieresis

• If there is associated maternal haemorrhage, fluid restriction is inappropriate.

4. DELIVERY

 Every attempt should be made to stabilize the mother and resuscitate the fetus in utero

before proceeding to an emergent, potentially compromising delivery. The decision of

whether to proceed with caesarean section or vaginal delivery should be individualized

based on obstetrical factors predicting vaginal delivery success and anticipated interval

to delivery (gestational age, fetal condition, presence of labour, and cervical Bishop

score) but vaginal delivery is preferable from a maternal standpoint. And in the absence
 of fetal malpresentation or fetal distress, oxytocin or prostaglandins may be initiated to

induce labour if the patient is not in labour.

 Caesarean delivery is considered in patients with an unfavorable cervix and/or a

gestational age of 30 weeks or less, as induction under these circumstances may result in

a prolonged intrapartum course associated with a high rate of intrapartum complications

But generally the patient should be delivered by the safest and shortest possible means –

should be delivered within 12 hours of admission.

 For vaginal delivery, Continuous electronic fetal monitoring should be initiated following

maternal stabilization. Transient fetal bradycardia lasting at least 3 to 5 minutes is a

common finding after an eclamptic seizure and does not necessitate immediate delivery

adequate maternal pain relief for labour and delivery is vital and may be provided with

either systemic opioids or epidural anesthesia. The second stage should be shorten and

AMTL should be done.

NURSING MANAGEMENT OF ECLAMPSIA

Aims

 To keep the mother alive during the fit

 To prevent more fits

 To control hypertension

 To correct fluid & electrolyte imbalance

 To deliver the baby

Resuscitation & Nursing Care

 Remove:
 • Tight fitting clothes

• Dentures

• Ornaments & jewellery

 The bed should be secured

 The patient’s limbs should also be secured

 The patient is nursed on her left lateral side

 Airway should be kept patent:

• Mouth gag

• Oropharyngeal airway

• Suctioning

 Breathing:

• RR should be maintained btw 12 & 20 c/m

• Oxygen, if available

 IV line should be secured for sample collection, fluid & drug administration

 Urinary catheter should be inserted

 Vital signs should be closely monitored

 Foetal monitoring, if foetus is still alive

 The presence of knee jerk reflex should be determined

 Urinary output should be monitored every hour.

Monitoring

 Pulses for Arrythmias

 Resp. rate for respiratory depression: should be ≥ 12 /min

 Deep Tendon Reflex (Knee Jerk): must be present

  Hourly urine output >25mls/hr

 Close monitoring of the BP & urinary output

 Careful monitoring of the antihypertensives & gradual tailing off as the BP normalize

COMPLICATIONS OF ECLAMPSIA

 Maternal complications

 Foetal complications

Maternal complications

– Respiratory insufficiency with hypoxia

– Cardiac failure

– Renal failure

– CNS complications

– Musculoskeletal injuries

– Obstetric complication

– Liver and coagulation disorders

– Maternal mortality

Foetal complications

– Acute foetal distress

– Birth asphyxia

– Prematurity

– Perinatal mortality
 NURSING CARE PLAN OF ECLAMPSIA

S/N
NURSING NURSING NURSING SCIENTIFIC
EVAUATION
DIAGNOSIS/PROBLEM OBJECTIVES INTERVENTION/ACTION PRINCIPLES/RATIONALE

1 Altered tissue Patient will 1. Monitor vital sign, 1 & 2. Indicate if there is Patient blood
perfusion(cerebral, demonstrate palpate peripheral pulse adequate systemic pressure was below
peripheral and renal adequate and note capillary refill. perfusion. fluid/blood 140/90mmhg,urinary
etiology related to perfusion as Assess urinary output. needs and developing output of above
impaired to decrease evidenced by 2. Weigh patient daily and complication 30ml/hour. fetal
uteroplacental perfusion stable vital evaluate changes in 3. to avoid uterine pressure heart between 120-
*impaired glomerular signs, mentation. on the vena cava and 160mmhg,there was
perfusion palpable 3. Place patient on left prevent supine hypotension absence of seize and
pulse, alert recumbent position. syndrome. increases decrease in presence
and oriented 4. Monitor maternal venous return and of edema.
absence of wellbeing periodically. circulatory volume,
seizure. 5. Ensure safety by putting enhance placenta and renal
the side rails. perfusion.
6.monitor patient for tonic- 4.monitor blood pressure 4
clonic convulsions hourly to detect for
7. Insert Foley’s catheter increase which is a warning
as indicated by the of worsening condition,
physician. then 1 hourly if condition is
8.Administer magnesium worsening.
sulfate as ordered by 5.To avoid fall and injury.
physician and monitor 6.To institute appropriate
signs of toxicity measures.
9. Administer fluid as 7.urine output should be in
prescribed. congruence with fluid
intake
Magnesium sulfate is given
to control the blood
pressure with pregnancy
induced hypertension
8. Replacement of fluid.
Maintains circulating
volume and tissue
perfusion.
2 Ineffective breathing Patient will 1. put patient in a dorsal 1. it prevent he tongue Patient breathing
pattern related to breath 18-20 position with the head from falling backward and was 20 times per
decrease cardiac output times/minute pointed to one side ensure free flow of saliva minute within 24
within 24 2. suction any secretion 2. it removes any hours of nursing
hours of from the mouth obstruction intervention.
nursing 3. resuscitate by 3. it removes any
intervention cardiopulmonary obstruction/secretion from
resuscitation if necessary air way
4. administer oxygen PRN 4. it simulate heart beat and
respiration.
3 Fluid volume deficit Patient fluid 1. give prescribed I.V 1. it restore fluid loss back Patient fluid was
related to disease will be infusion into the blood vessel maintained within 15
condition maintain 2. monitor the rate of 2. it helps to prevent to 30 minute of
within 15 to infusion circulatory overloads nursing intervention.
30 minute of 3. maintain intake and 3. it helps to monitor the
nursing output. function of the kidney.
intervention
4 Risk for injury related Patient will 1. observe patient 1. constant observation Patients do not
to episode of convulsion not injure constantly prevent patient from injure herself and
herself and 2. Keep away all injuring herself others throughout
 others within dangerous articles or 2. Removal of all the period of
the period of instrument from the dangerous articles hospitalization.
hospitalization patient. minimizes the risk of
3. Keep patient on bed injury.
with rails most of the time. 3. railing of bed prevent
patient from falling off bed.
5 Self-care deficit related Patient 1. give daily bed bath 1. It helps to keep patient Patient personal
to unconsciousness personal 2. Change patient position clean. hygiene was
hygiene will 2 hourly 2. it stimulates circulation maintained
be maintained 3. monitor vital signs ¼ 3. it helps to monitor the throughout his
throughout his hourly patient progress admission.
admission
period

ECLAMPSIA AS A LEADING CAUSE OF MATERNAL MORTALITY.

Maternal mortality is defined as the death of any woman while pregnant or within 42 completed

days of termination of pregnancy, irrespective of the duration or site of pregnancy, from any

cause related to or aggravated by pregnancy, but not from accidental or incidental causes.

Pregnancy, although considered a physiological state, carries risk of serious maternal morbidity

and at times of death. Eclampsia is a very serious complication of pregnancy responsible for high

maternal and perinatal mortality. Eclampsia is an acute and life-threatening complication of

pregnancy characterized by the appearance of tonic clonic seizures (convulsions), usually in a

woman who has developed pre-eclampsia. Eclampsia includes convulsions and coma that happen

during pregnancy but are not due to pre-existing or organic brain disorder. Eclampsia related

complications include CVA (cerebro vascular accident), pulmonary oedema, renal failure,

HELLP (haemolysis, elevated liver enzyme, and low platelet count) syndrome, DIC

(Disseminated Intravascular Coagulation) and hepatic failure.

Maternal mortality is an index to judge the health care by a country to the women population. It

also reflects the educational and socio-economic state of a country as well as public health

consciousness. Between 1990 and 2010, maternal mortality worldwide dropped by almost 50%

but is still unacceptably high. Almost all maternal deaths (99%) occur in developing countries.

Nigeria is among those countries, which has a very high maternal mortality ratio. The high
number of maternal deaths in some areas reflects inequities in access to health services, and

highlights the gap between the rich and the poor. Despite the several global and regional

interventions and initiatives from governments and other concerned agencies, maternal mortality

continues to be very high in Sub-Saharan Africa and India, with eclampsia as a major cause. In

developed countries with effective antenatal screening programmes, advanced diagnostic and

therapeutic intervention and extensive research, the disease has become a rare complication of

pregnancy. Unfortunately, such changes have not occurred in developing countries and

eclampsia continues to be a very serious problem.

Two major causes of maternal death in Nigeria are haemorrhage and eclampsia. This is

also the major cause of maternal mortality in eastern part of India. The present study was

undertaken to determine the incidence of maternal mortality associated with eclampsia and to

assess how socio-demographic and clinical characteristics of the women influence the deaths.

This study was also done to assess the mode of death in eclampsia in rural area of Nigeria.

In practical life, it has a severe impact on the family, community and eventually, the

nation. The young surviving children left motherless are unable to cope with daily living and are

at an increased risk of death. Reduction of maternal mortality is the objective of MDGs,

especially in low income countries, where one in 16 women die of pregnancy related

complications.

Hypertensive disorders of pregnancy are a major cause of maternal and fetal morbidity

and mortality all over the world. Eclampsia is a well-recognized complication of hypertensive

disorders of pregnancy. In the developed countries like UK, eclampsia is rare, but in developing

countries, the prevalence has been estimated to be up to 20 times higher. Of the estimated

600,000 women worldwide who die each year of pregnancy related complications, more than

50,000 die of preeclampsia or eclampsia, and 99% of these deaths occur in developing countries.
 In the present study, there were 256 maternal deaths out of 52413 deliveries, giving a

MMR of 518.48 per 1,00,000 live births. This MMR is much higher than the national averages

which is 212 per 1,00,000 live births. Malda Medical College and Hospital, being a teaching

institution and a tertiary care centre, receives complicated cases from rural areas. Admissions of

moribund cases referred from peripheral hospitals have inflated this mortality ratio, like in other

teaching institutions of Nigeria. Similar studies from tertiary care institution by Pal et al (12),

Purandare et al (13) and Verma et al (14) also reported MMR between 213 to 879 per 1,00,000

live births.

Majority of patients in the present study belong to low socio-economic group and were

illiterate. Most of them were from rural areas, had no antenatal visit and presented late with

complication of eclampsia. It favours the observation that education, good antenatal care, early

referral to intensive care units for standard care can reduce its incidence and complications. Due

to lack of awareness, people do not seek medical advice at an early stage. As the majority of

masses belong to low socio-economic group, they do not report to hospitals even in late stages. It

is, therefore, reasonable to assume that quite a large number of patients die at home without

getting to hospital. This is also comparable to other Indian studies.

Age and parity distribution of eclamptic mother shows that age below 24 years was

commonly affected. This is comparable with another Nigeria study. In the study, eclampsia

related deaths were mainly seen in younger age group and in primi gravidas. This is because of

early marriage and early pregnancy. In rural Nigeria, due to social customs, teenage pregnancy is

a very common practice. Low socio-economic status and illiteracy are also important causes of

early marriage and child birth.

The majority of deaths in our study were in the late third trimester (ante partum).

Maximum deaths occurred within 12 hours of admission and in unbooked cases. This is mainly
due to late referral, poor antenatal checkup and transfer of moribund patients just before death to

the tertiary hospital. A study done by Berhan et al also supports the findings.

Previously, obstetric haemorrhage was the major cause of maternal mortality in Nigeria at

primary, secondary and tertiary care setups. However, recently, paradigm shift has been observed

in tertiary health care setup like medical colleges. In our study, it was observed that eclampsia

contributes to 43.57% of all maternal deaths, whereas eclampsia causes 12% of all global

maternal deaths. A study from Northern Nigeria by Sarkar et al also supports the claim.

While reviewing the mode of deaths in eclampsia, it was observed that pulmonary oedema is the

commonest cause of death in eclampsia. Incidence of pulmonary oedema is higher in eclampsia

due to leaky pulmonary capillaries. In our setup, due to lack of intensive care monitoring, poorly

monitored fluid therapy due to lack of central venous pressure monitoring and pulmonary

capillary wedge pressure monitoring leads to increased risk of pulmonary oedema. Lack of

ventilatory support is another cause of increased incidence of maternal mortality in pulmonary

oedema. In UK, commonest cause of death in eclampsia is CVA.

There were 5,191 women who delivered at the University of Maiduguri Teaching

hospital from 2011-2019 out of which 294 were diagnosed with eclampsia. The age of the

women ranges from 13-40 with a mean age of 21.39± 5.12. Majority of the patients were

resident at high density areas 86.7%, 89.4% were married and 60.3% had no formal education.

The age range of 20-29(48.3%) had the highest prevalence (Sangari et al. 2020).

Eclampsia contributes significantly to maternal mortality in Nigeria. Efforts should be

made by all concerned to improve facilities and social infrastructures that will directly or

otherwise minimize.
CONCLUSION

Despite all the recent research efforts, there are no reliable tests or signs to predict the

development of eclampsia in women with preeclampsia and patients with eclampsia are at risk

for maternal and perinatal morbidity and mortality. However, with appropriate management the

risks to both mother and fetus can be minimized.

Eclampsia no doubt contributes significantly to maternal mortality in Nigeria, more so in

Northern geopolitical zone. Effort should be made by all concern to improve facilities and social

infrastructures that will directly or otherwise minimize the occurrence of eclampsia. Skilled and

prompt attendant of patient in emergency situations will help to curtail mortalities from

preventable morbidities.

RECOMMENDATIONS

Eclampsia is no doubt the major cause of maternal morbidity and mortality in developing

countries including Nigeria, particularly in Maiduguri, Borno State in the North-east of Nigeria.

To address eclampsia in the North east part of Nigeria:

1. Proper care and attention are to be giving toward alleviation of eclampsia to women age

20-29, women that are primigravidae and women in third trimester of pregnancy.

2. Attention should be giving to women with low socio-economic status.

3. Women should be encouraged and educated on the importance of antenatal care.

4. Those that managed pregnancy and deliveries should take special cognizance of higher

rate of eclampsia during the raining season (May-September).

5. All tertiary health institutions are to be sensitized and equip with equipment and

personnel toward the management of eclampsia.

6. Facilities for management of eclampsia should be improved at all level of health care

institutions.
7. Physiotherapy should be included into the ante natal care program of pregnant women in

University of Maiduguri Teaching Hospital.

8. Further studies should be carried out to explore the effect of exercise on preeclampsia.
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