Pre-Eclampsia

Eclampsia
 Preeclampsia clinically defined by
hypertension and proteinuria, with or
without pathologic edema. (>300g)

 Eclampsia is considered a complication of

severe preeclampsia, is commonly
defined as new onset of grand mal seizure
activity and/or unexplained coma during
pregnancy or postpartum in a woman
with signs or symptoms of preeclampsia. It
typically occurs during or after the 20th
week of gestation or in the postpartum
period.
 Severe preeclampsia is defined as the presence of
1 of the following symptoms or signs in the presence
of preeclampsia:

 SBPof 160 mm Hg or higher or DBP of 110 mm Hg or

higher on 2 occasions at least 6 hours apart

 Proteinuria
of more than 5 g in a 24-hour collection
or more than 3+ on 2 random urine samples
collected at least 4 hours apart

 Pulmonary edema or cyanosis

 Oliguria (< 400 mL in 24 h)

 Persistent headaches

 Epigastric pain and/or impaired liver

function

 Thrombocytopenia

 Oligohydramnios, decreased fetal

growth, or placental abruption
HELLP syndrome

 Haemolysis - ↑ bilirubin

 Elevated liver enzymes

 Low Platelet

Presentation of severe pre-eclampsia

 CAUSES
 Unknown

 Several theories – none proven

 Inadequate trophoblastic invasion of uterine wall by

placenta a dominant theory
Immunological response

Inadequate maternal antibody response to

the fetal allograft results in vascular
damage from the circulating immune
complexes
Circulating toxins
Release of vasoconstrictive substances in the blood

Endothelial Damage
Primary endothelial damage results in decrease
prostacyclin (vasodilator) and an increase in
thromboxane (vasoconstrictor)
Pathophysiology

CVS – Vasospasm → hypertension

Renal – Glomerulo-endotheliosis → proteinuria, oliguria

CNS – oedema, haemorrhage → convulsion

Predisposing Factors
 Nulliparity
 Family history of pre-eclampsia/eclampsia
 Multiple pregnancy
 Diabetes mellitus
 Hydatidiform mole
 Hydrops fetalis
 Extremes of age
 Lower socio-economic
history
A history should be able to assist in making
a diagnosis of Pre-Eclampsia
Findings
Patients with severe preeclampsia display
end-organ effects and may complain of the
following:
 Headache
 Visual disturbances - Blurred, scintillating
scotomata
 Altered mental status
 Although hypertension is an important
characteristic of preeclampsia, because
the underlying pathophysiology of
preeclampsia is a diffuse endothelial cell
disorder influencing multiple organs,
hypertension does not necessarily need to
precede other preeclamptic symptoms or
laboratory abnormalities.
Presenting symptoms other than
hypertension may include, as previously
mentioned, edema, visual disturbances,
headache, and epigastric or right upper
quadrant tenderness.
 Blindness - May be cortical or retinal
 Dyspnea
 Edema
 Epigastric
or right upper quadrant
abdominal pain
 Weakness or malaise - May be evidence
of hemolytic anemia
investigation
 Allwomen who present with new-onset
hypertension should have the following
laboratory tests:
 Complete blood cell (CBC) count, PT and
PTT, GXM
 Urea and electrolytes (LDH)
 Serum alanine aminotransferase (ALT) and
aspartate aminotransferase (AST) levels
 Serum creatinine
 Uric acid
 CTG
 Ultrasound to determine fetal biometry,
weight, presentation, biophysical profile,
placental location
 24hr urine collection to determine
objectively the creatinine clearance and
proteinuria
Maternal complications
 Seizuresand stroke
 DIC and its complications
 Increased likelihood of caesarean section
 Renal failure
 Hepatic failure or rupture
 Death
FOETAL complications
 Growth restriction
 Oligohydramnios
 Placental infarction
 Placental abruption
 Prematurity and its consequences
 Perinatal death
Management PE
 The optimal management of a woman
with preeclampsia depends on
gestational age and disease severity.
 Mild pre-eclampsia:
-Alpha methyl dopa 250-500mg every 8-
12hr
-Slow release Nifedipine 10mg every 12hr
-bed rest
-DVT prophylaxis
-vitals and fetal heart every 4hrs
 Normal diet as low salt diet may worsen
intravascular depletion
 A course of dexamethasone may be give
if GA< 34/40
 The mother may be treated on an
outpatient basis(if optimal) and would be
instructed to do kick chart monitoring and
return if any signs of severe PE, decrease
in movements, abdominal pain, PV
bleeding or spontaneous labour
 Management of severe
pre-eclampsia
 Blood pressure must be initially lowered to
150-155 systolic and 100-105 diastolic via
hydrazine stat 10mg IM and BP rechecked
in 30 min or IV titration at 1mg/min until
diastolic is 100mmHg
 Labetolol IV 20-40mg with a max of 320
mg daily until diastolic is 100mmHg.
 Magnesium Sulphate 10 grams IM with 5
grams IM every 4-6 hr alternate locations
or IV 4 grams by slow infusion with 1-2
grams per hour IV.
 IM Magnesium Sulphate is mixed with 1ml
of 2% lidocaine to decrease pain
 Before administering follow up doses it
must be ensured that the patient has a
respiratory rate of at least 18 breaths per
minute, peripheral reflexes intact and
urinary output of 1ml/kg/min (signs of
magnesium sulphate toxicity)
 Insert a urinary catheter
 Because delivery is the only cure for
preeclampsia, clinicians must try to
minimize maternal risk while maximizing
fetal maturity.
 Todeliver the fetus by the safest and most
expiditious means taking maturity and risk
to fetus into consideration along with
maternal risks.
Eclampsia
Active seizures should be treate
d with intravenous magnesium s
ulfate as a first-line agent.
A loading dose of 4 g should be given by
an infusion pump over 5-10 minutes,
followed by an infusion of 1 g/h
maintained for 24 hours after the last
seizure. Recurrent seizures should be
treated with an additional bolus of 2 g or
an increase in the infusion rate to 1.5 g or
2 g per hour.
Magnesium Sulphate
Toxicity
Magnesium Sulphate has a narrow
therapeutic index. The therapeutic serum
concentration is 4-7 mg/dl.
Signs of Magnesium toxicity include:
 ECG Changes
 Loss of Patellar reflex
 Slurred Speech
 Muscle Paralysis
 Cardic Arrest
Antidote
1 gram Calcium Gluconate ( 10 ml of a
10% solution given over 10 minutes
 Additionally patient should be kept NPO
until after resuscitation and investigations as
emergency delivery may be needed.
 Urgent delivery if:
- maternal blood pressure is uncontrollable
-evidence of thrombocytopenia or
coagulopathy
-significant renal impairment
-fetal distress or lack of fetal growth over 10-
14 days.
-Eclampsia
 If
seizures persist after administering
Magnesium Sulphate twice then give
Diazepam 10mg IV, if still persistent then
Phenytoin slow IV infusion.
 CT brain is indicated for eclampsia to rule
out brain lesions
References
 Labour
Ward Protocol UHWI by Dr Leslie
Samuels MBBS, DM, FACOG

 “Obstetrics by Ten Teachers” 20th edition