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Preeclampsia and Eclampsia
Preeclampsia and Eclampsia
Preeclampsia can not be accurately defined until its cause is known.It is describ
ed as a syndrome comprising of hypertension, oedema and proteinuria occurring af
ter 20 weeks gestation. Hypertension-140/90 mm of Hg or more on at least two occa
sions four hours or more apart after the 20th week of pregnancy in a woman known
to be normotensive and in whom blood pressure has returned to normal by the six
th postpartum week. Proteinuria is defined as the excretion of 0.3 g protein or m
ore within 24 Hr or a measurement of 1+ or more using
Classification This is classified as mild or severe forms as the latter is assoc
iated with increased maternal and fetal morbidity. Severe form is said to occur i
f one or more of the conditions in this table is
Definition of severe pre-eclampsia
1. Arterial pressure > 160mmHg systolic or > 110mmHg diastolic on two occasions a
t least 6 hrs apart 2. Proteinuria > 5g in 24 hour > 3 + un dipstick 3. Oliguria
< 400 mm in 24 h 4. Cerebral signs – headache, blurred vision or altered consciou
sness 5. Pulmonary oedema or cyanosis 6. Epigastric or right upper quadrant pain
7. Impaired liver function 8. Hepatic rupture 9. Thrombocytopenia
Hypertensive Disorders During Pregnancy: Indications of Severity Abnormality Dia
stolic blood pressure Proteinuria Headache Visual disturbances Upper abdominal p
ain Oliguria Convulsion Serum creatinine Thrombocytopenia Liver enzyme elevation
Fetal growth restriction Pulmonary edema Mild < 100 mg Hg Trace to 1 + Absent A
bsent Absent Absent Absent Normal Absent Minimal Absent Absent Severe 110mmHg or
higher Persistent 2 + or more Present Present Present Present Present (eclampsi
a) Elevated Present Marked Obvious Present
Material Vascular Disease
Faculty Placentation Genetic Immunologic or Inflammatory Factors Reduced Uteropl
acental Perfusion
Excessive Trophoblast
Vasoactive Agents: Prostaglandins Nitric Oxide Endothelins Endothelial Activatio
n Capillary Leak Vasospasm Edema Proteinuria Hemoconcentration Hyper tension Oli
guria Liver Ischemia Thrombo cytopenia Activation of Coagulation
Noxious Agents: Cytokines Lipid Peroxidases
Seizures
Abruption
Pathophysiology The summary is that as a result of the damage of the endothelial
cells, it looses its functions and in addition also produces proagulants, vasoc
onstrictions and mitogens. The increased pressor sensitivity of the maternal ves
sels leads to profound vasospasm and reduced organ perfusion which are
arious Changes etus IUGR Preterm delivery Abruptio placental
aternal idneys - Proteinuria, ↓ GFR, ↑ Plasma Creatinine - Glomerular endothehosis R
enal failure (ATN, Cortical necrosis) Cardiovascular - ↓ Plasma Volume, ↓ CVP, AP ↑ &
SVR Contractility usually unchanged. Brain HT encephatopathy, ischaemia and infa
rction, vasospasm, Haemorrhage Oedema Eclampsia Liver Altered LFT, Periportal he
patic necrosis, Subcapsulaar haemorrhage, FDP, HELLP. Lungs Leaking Capillaries
pulmonary Oedema ARDS Coagulation consumption) Thrombocytopenia Platelet Product
ion (↑ Platelet activation and ↑ Less often Erythrocyte destruction
Prediction and Prevention No ideal predictive tests that fulfils all described cr
iteria.Two most important predictive factors: 1. Nulliparity Preeclampsia in 5.8%
primigravida, 0.4% Secundagravida. 2. Family History Considerable evidence suppo
rt significant genetic contribution Aetiology & pathophysiology are still not und
erstood fully and this has hindered development of effective premature measures.
. Anti-platelet therapy Low dose Aspirin . Calcium Supplementation
TREATMENT
Delivery is the cure for Preeclampsia. The prime objective is to prevent convuls
ion. The management ideally should be multidisciplinary. It is based on the seve
rity of the disease and also influenced by gestational age.
Management should include 1. Treatment of hypertension The risk of cerebral haem
orrhage is a major cause of maternal deaths (60%) Significant risk of CVA occurs
when MAP > 140mmHg (180/120). The aim of treatment is to prevent intracerebral
haemorrhage while not affecting uteroplacental blood flow and maternal renal fun
ctions.
Prolonged treatment of HT is advisable when the fetus is immature in an attempt
to delay delivery. However, this can only be undertaken provided the mother is n
ot placed at risk and that strict monitoring of both the mother and the fetus is
carried out at frequent regular intervals, hospitalization and bed rest may be
all that is required in some patients.
Antihypertensive therapies