PRE - ECLAMPSIA & ECLAMPSIA
PRESENTED BY : FAISAL BALOCH (FBNA)
SOURCE:
• OBSTETRIC & GYNE BY TEN TEACHERS
PRE ECLAMPSIA -
Pre-eclampsia is defined as hypertension measuring at least 140/90 mmHg recorded on a
minimum of two separate occasions, at least 4 hours apart, along with the presence of at
least 300 mg of protein in a 24-hour urine collection. It arises de novo after the 20th week
of gestation in a woman who was previously normotensive and resolves completely by the
sixth postpartum week.
RISK FACTORS FOR PRE-ECLAMPSIA:
• First pregnancy
• Multiparous woman with a previous history of pre-eclampsia
• Pre-eclampsia in any previous pregnancy
• Interval of 10 years or more since the last childbirth
• Age 40 years or older
• Body mass index (BMI) of 35 or higher
• Family history of pre-eclampsia (in mother or sister)
• Booking diastolic blood pressure of 80 mmHg or more
• Booking proteinuria (defined as ≥1+ on more than one occasion or quantified at ≥0.3 g/24
hours)
• Multiple pregnancy
• Certain pre-existing medical conditions, including:
o Pre-existing hypertension
o Pre-existing renal disease
o Pre-existing diabetes
o Presence of antiphospholipid antibodies
PATHOPHYSIOLOGY :
Pre-eclampsia only occurs in pregnancy, but has been described in pregnancies lacking a
fetus (molar pregnancies) and in the absence of a uterus (abdominal pregnancies),
suggesting that it is the presence of trophoblast tissue that provides the stimulus for the
disorder.
Development of pre-eclampsia is a two-stage process, which originates in early pregnancy
1. First stage – abnormal placentation
• In the first stage, trophoblast invasion
is patchy and the spiral arteries retain
their muscular walls.
• This is thought to prevent the
development of a high-flow, low-
impedance uteroplacental circulation
and leads to uteroplacental ischaemia
• The reason why trophoblasts invade
less effectively in these pregnancies
is not known but may reflect an
abnormal adaptation of the maternal
immune system.
2. Second stage – maternal response
• In the second stage, uteroplacental
ischaemia results in oxidative and
inflammatory stress, with the
involvement of secondary mediators
leading to endothelial dysfunction, vasospasm and activation of the coagulation system.
• Pre-eclampsia is a truly multisystem disorder, affecting multiple organ systems, often concurrently.
SYSTEM MANIFESTATIONS
1. Cardiovascular system
Normal pregnancy is characterized by marked peripheral vasodilatation resulting in a
fall in total peripheral resistance. Pre-eclampsia is characterized by marked peripheral
vasoconstriction, resulting in hypertension. The intravascular high pressure and loss of
endothelial cell integrity results in greater vascular permeability and contributes to the
formation of generalized oedema.
2. Renal system
In the kidney, a highly characteristic lesion called glomeruloendotheliosis is seen. This
is relatively specific for pre-eclampsia (it is not seen with other hypertensive disorders)
and is associated with impaired glomerular filtration and selective loss of intermediate
weight proteins, such as albumin and transferrin, leading to proteinuria. This in turn
causes a reduction in plasma oncotic pressure and exacerbates the development of
oedema.
3. Haematological system
In the event of endothelial damage, platelets adhere to the damaged area. Furthermore,
diffuse vascular damage is associated with the laying down of fibrin. Pre-eclampsia is
association with increased fibrin deposition and a reduction in the platelet count may
accompany.
4. The liver
In the liver, subendothelial fibrin deposition is associated with elevation of liver
enzymes. This can be associated with haemolysis and a low platelet count due to
platelet consumption (and subsequent widespread activation of the coagulation
system). The presence of these finding is called HELLP syndrome (haemolysis,
elevation of liver enzymes and low platelets). HELLP syndrome is a particularly severe
form of pre-eclampsia, occurring in just 2–4 % of women with the disease. It is
associated with a high fetal loss rate (of up to 60 %).
HELLP Syndrome : acronym for haemolysis, elevation of liver enzymes, low platelets.
Women with HELLP syndrome typically present with epigastric pain, nausea, and
vomiting. Hypertension may be mild or even absent.HELLP syndrome is associated with
a range of serious complications including acute renal failure, placental abruption, and
stillbirth.The management of HELLP syndrome involves stabilizing the mother, correcting
any coagulation deficits, and assessing the fetus for delivery.
5. Neurological system
The development of convulsions in a woman with pre-eclampsia is defined as
eclampsia. Vasospasm and cerebral oedema have both been implicated in the
pathogenesis of eclampsia. Retinal haemorrhages, exudates and papilloedema are
characteristic of hypertensive encephalopathy and are rare in pre-eclampsia,
suggesting that hypertension alone is not responsible for the cerebral pathology.
CLINICAL PRESENTATION OF PRE-ECLAMPSIA
• The classic symptoms of pre-eclampsia include frontal headache, visual disturbance, and
epigastric pain. However, the majority of women with pre-eclampsia are asymptomatic or
only complain of general vague ‘flu-like’ symptoms.
• Clinical examination should include a complete obstetric and neurological examination.
Hypertension is usually the first sign, but may occasionally be absent or transient until the
late stages of the disease.
• Dependent oedema of the feet is very common in healthy pregnant women. However,
rapidly progressive oedema of the face and hands may suggest pre-eclampsia.
Epigastric tenderness is a concerning sign and indicates liver involvement.
• Neurological examination may reveal hyperreflexia and clonus in severe cases. Urine
testing for protein should be considered a routine part of the clinical examination .
MANAGEMENT AND TREATMENT OF PRE-ECLAMPSIA
The goal of management is to minimize maternal risk while allowing continued fetal growth
when possible. In severe cases, this may not be feasible, and early delivery may become
necessary.
Principles of Management
• Early recognition of the often symptomless syndrome
• Awareness of the serious nature of severe pre-eclampsia
• Strict adherence to established clinical guidelines for:
o Hospital admission
o Monitoring and investigations
o Use of antihypertensive and anticonvulsant therapy
• Timely delivery to prevent maternal or fetal complications
• Postnatal follow-up and counselling regarding future pregnancies
A diagnosis of pre-eclampsia usually warrants hospital admission.
Women with mild hypertension, minimal proteinuria, and normal labs may be managed as
outpatients, with frequent follow-up for maternal and fetal assessment.
Women with moderate to severe hypertension, significant proteinuria, or abnormal
hematological or biochemical parameters require inpatient management.
Maternal Investigations
To monitor for maternal complications, the following tests should be conducted:
• Full blood count
• If platelets are normal, clotting studies are generally not necessary
• Serum renal profile
• Serum liver profile
• Repeat proteinuria quantification
Fetal Monitoring
To assess fetal well-being, the following are used:
• Ultrasound for fetal size, amniotic fluid volume, and maternal and fetal Doppler studies
• Cardiotocography (CTG) to evaluate fetal heart rate patterns:
o Loss of baseline variability or decelerations may indicate fetal hypoxia
o Should be used in conjunction with ultrasound
Antihypertensive Treatment
The most common cause of maternal death in pre-eclampsia is cerebral bleeding due to
uncontrolled systolic blood pressure. Therefore, antihypertensive therapy aims to lower
maternal blood pressure, prevent stroke, and maintain adequate uteroplacental perfusion to
avoid compromising the fetus.
Commonly used antihypertensives:
1. Methyldopa 3. Nifedipine
Centrally acting agent with a long Calcium channel blocker with rapid
safety record. Only available orally. onset
Takes 24+ hours to work Given orally
Can cause sedation and depression. May cause headache, which can
2. Labetalol mimic disease progression
Both alpha- and beta-blocker 4. Hydralazine
Preferred first-line drug (per NICE Used in severe cases
guidelines) Given as intravenous infusion
Can be given orally or intravenously Dose can be titrated rapidly based
Good safety profile on blood pressure response
Often used along with IV labetalol
SCREENING AND PREVENTION OF PRE-ECLAMPSIA
Purpose of Screening
The goal of screening is to accurately predict which women are at risk of developing pre-
eclampsia. This allows:
• Targeted increased antenatal surveillance for high-risk women
• Safe community-based antenatal care for low-risk women
• Development and implementation of preventive interventions
Role of Doppler Ultrasound
• Uterine artery Doppler waveform analysis has been investigated as a predictive tool.
• This method may be helpful in women already identified as high-risk based on medical or obstetric
history.
• However, it is not effective for screening low-risk women.
Preventive Interventions
1. Low-dose aspirin (75 mg daily)
o Modestly reduces the risk of pre-eclampsia
o Recommended for high-risk women
2. Calcium supplementation
o May reduce risk, but only effective in women with low dietary calcium intake
ECLAMPSIA
Eclampsia is a life-threatening condition requiring immediate intervention. Eclampsia
is defined as the occurrence of tonic–clonic convulsions or coma in a woman with pre-
eclampsia, in the absence of any other identifiable neurological cause. It is a severe
complication of pre-eclampsia and is associated with significant maternal morbidity and
mortality.
The estimated incidence of eclampsia is 27.5 cases per 100,000 pregnancies, with a case
fatality rate of 3.1%. The most serious maternal complications include cerebrovascular
events, particularly cerebral haemorrhage, which is the leading cause of death in women
with eclampsia and HELLP syndrome (haemolysis, elevated liver enzymes, and low
platelets).
Clinical Manifestations of Eclampsia
• Generalized tonic–clonic seizures
• Loss of consciousness or coma
• Severe headache
• Visual disturbances (e.g., blurred vision, photophobia)
• Epigastric or right upper quadrant pain
• Nausea and vomiting
• Facial (especially periorbital) and hand oedema
• Hyperreflexia and clonus
• Agitation or confusion
• Papilloedema
• Decreased urine output (oliguria)
• Elevated blood pressure (may be mild, moderate, or severe)
Risk Factors for Eclampsia
• Uncontrolled hypertension
• Primigravidity (first pregnancy)
• Obesity
• Age below 20 years
• Black ethnicity
• Diabetes
• Fewer than two prenatal care visits
WARNING SIGNS OF IMPENDING ECLAMPSIA
• Epigastric pain and right upper quadrant tenderness
• Severe headache
• Agitation and confusion
• Hyper-reflexia and clonus
• Facial (especially periorbital) oedema
• Poor urine output
• Papilloedema
• Uncontrolled hypertension
PREVENTION OF ECLAMPSIA
All women with pre-eclampsia are at risk of developing eclampsia, regardless of the
perceived severity of their condition. Magnesium sulphate should be given with a low
threshold in women who are unstable or have severe pre-eclampsia. Preventive strategies
include:
• Close monitoring of blood pressure and neurological signs
• Prophylactic administration of magnesium sulphate in high-risk patients
TREATMENT OF ECLAMPSIA
1. Emergency Management
• Call for senior help and emergency alert team
• Follow standard ABC (Airway, Breathing, Circulation) approach
• Ensure airway patency, administer oxygen, and secure IV access
2. Magnesium Sulphate Therapy
Magnesium sulphate is the drug of choice for both treatment and prevention of
convulsions in eclampsia.
Dosage:
• Loading dose: 4 grams IV given slowly over 5–10 minutes
• Maintenance dose: 1 gram/hour as continuous IV infusion, usually for 24 hours after the last seizure
3. Monitoring:
Magnesium sulphate has a narrow therapeutic window. Signs of overdose include loss
of deep tendon reflexes, respiratory depression, and cardiac arrest.
4. Antidote:
If toxicity occurs, the antidote is 10 ml of 10% calcium gluconate given slowly via IV.
