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Preeclampsia can not be accurately defined until its cause is known.It is descr
ibed as a syndrome comprising of hypertension, oedema and proteinuria occurring
after 20 weeks gestation. Hypertension-140/90 mm of Hg or more on at least two
occasions four hours or more apart after the 20th week of pregnancy in a woman k
nown to be normotensive and in whom blood pressure has returned to normal by the
sixth postpartum week. Proteinuria is defined as the excretion of 0.3 g protei
n or more within 24 Hr or a measurement of 1+ or more using
Classification This is classified as mild or severe forms as the latter is ass
ociated with increased maternal and fetal morbidity. Severe form is said to
occur if 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
at least 6 hrs apart 2. Proteinuria > 5g in 24 hour > 3 + un dipstick 3. Oligur
ia < 400 mm in 24 h 4. Cerebral signs – headache, blurred vision or altered cons
ciousness 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 endotheli
al cells, it looses its functions and in addition also produces proagulants, vas
oconstrictions and mitogens. The increased pressor sensitivity of the maternal v
essels 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 endothehos
is Renal failure (ATN, Cortical necrosis) Cardiovascular - ↓ Plasma Volume, ↓
CVP, AP ↑ & SVR Contractility usually unchanged. Brain HT encephatopathy, is
chaemia and infarction, vasospasm, Haemorrhage Oedema Eclampsia Liver Altered LF
T, Periportal hepatic necrosis, Subcapsulaar haemorrhage, FDP, HELLP. Lungs Leak
ing Capillaries pulmonary Oedema ARDS Coagulation consumption) Thrombocytopeni
a Platelet Production (↑ Platelet activation and ↑ Less often Erythrocyte destru
ction
Prediction and Prevention No ideal predictive tests that fulfils all described
criteria.Two most important predictive factors: 1. Nulliparity Preeclampsia in
5.8% primigravida, 0.4% Secundagravida. 2. Family History Considerable evidence
support significant genetic contribution Aetiology & pathophysiology are still
not understood fully and this has hindered development of effective premature m
easures. . 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
haemorrhage is a major cause of maternal deaths (60%) Significant risk of CVA oc
curs when MAP > 140mmHg (180/120). The aim of treatment is to prevent intracer
ebral haemorrhage while not affecting uteroplacental blood flow and maternal ren
al functions.
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