4. Preeclampsia is a multisystem disorder of characterized by
development of hypertension to the extent of 140/90 mm Hg,
and proteinuria after the 20th week in a previously
normotensive woman.
Eclampsia
Refers to the occurrence of grand mal seizure in a pregnant
woman with preeclampsia, and is one of the most serious
complications of the disease.
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5. The exact cause of preeclampsia remains unknown, but there is a
constant concern with identifying risk factors like:-
Nulliparity
Multifetal gestations
Maternal age extremities
Preeclampsia in a previous pregnancy
Chronic hypertension
DM
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6. The clinical classification of preeclampsia is arbitrary and is
principally classified as mild and severe based on the level of
blood pressure and proteinuria for management purpose.
A. Mild is sustained rise of blood pressure of more than 140/90
mm Hg but less than 160 mm Hg systolic or 110 mm Hg
diastolic without significant proteinuria.
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7. A. Severe is when blood pressure rises to ≥ 160
mmHg SBP∕110 mmHg DPB and proteinuria
≥ +3 on dipstick or 3 gm/24 hr.
But recent updates stated that, all preeclamptic
women should be treated as sever preeclampsia
as worsening of mild preeclampsia have a great
extent and conservative management is
associated with serious maternal complications
(von Dadelszen et al., 2007)
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9. facial edema
Pulmonary edema due to capillary leak and low oncotic
pressure.
Abdominal examination may reveal evidences of chronic
placental insufficiency, such as scanty liquor or growth
retardation of the fetus.
Severe headache
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10. PATHOPHYSIOLOGY OF
PREECLAMPSIA
In normal pregnancy
Invasion of the endovascular trophoblasts into the walls of the spiral
arterioles of the uteroplacental bed.
In the first trimester it invades up to decidual segments
In the second trimester it invades upto the myometrial segments
spiral arterioles become distended
This physiological change transforms the spiral arterioles into a low
resistance, low pressure, high flow system
Increased PGI2
Increased nitric oxide(NO)
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11. In Preeclampsia
There is failure of the second wave of endovascular trophoblast
migration and here is reduction of blood supply to the fetoplacental unit
There is an imbalance in different components of prostaglandins
prostaglandin (PGI2) decreased
increased synthesis of thromboxane (TXA2)
increased vascular sensitivity to the pressor agent angiotensin-II
Angiotensinase activity is depressed, following elimination proteinuria
Nitric oxide (NO) is decreased then, contributes to the development of
hypertension.
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12. Increased endothelial cells dysfunction lead to
vasoconstriction
Activated leukocytes cause endothelial injury due to
inflammatory mediators cytokines imbalance
Increased reactive oxygen species
Decreased nitric oxide lead to endothelial cell damage
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16. Brodie, H., & Malinow, A. (1999). Anesthetic management of
preeclampsia/eclampsia. International journal of obstetric anesthesia, 8(2), 110-
124.
Gul, A., Cebeci, A., Aslan, H., Polat, I., Ozdemir, A., & Ceylan, Y. (2005).
Perinatal outcomes in severe preeclampsia-eclampsia with and without HELLP
syndrome. Gynecologic and obstetric investigation, 59(2), 113-118.
Sanjay, G., & Girija, W. (2014). Preeclampsia–eclampsia. The Journal of
Obstetrics and Gynecology of India, 64(1), 4-13.
Sibai, B. M. (1990). Magnesium sulfate is the ideal anticonvulsant
inpreeclampsia-eclampsia. American journal of obstetrics and gynecology,
162(5), 1141-1145.
Sibai, B. M. (2005). Diagnosis, prevention, and management of eclampsia.
Obstetrics & Gynecology, 105(2), 402-410.
von Dadelszen, P., Menzies, J., Gilgoff, S., Xie, F., Douglas, M. J., Sawchuck,
D., & Magee, L. A. (2007). Evidence-based management for preeclampsia.
Front Biosci, 12(5), 2876-2889.
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