This document provides an overview of preeclampsia and eclampsia. It begins with an introduction and outlines risk factors and classifications. It then describes clinical features such as hypertension and proteinuria. The pathophysiology section explains how abnormal placentation leads to reduced blood flow and imbalance of prostaglandins. Complications are also discussed, including renal failure, pulmonary edema, and intrauterine growth restriction. The document provides information on diagnosis and management of preeclampsia and eclampsia.

1. HARAMAYA UNIVERSITY
COLLEGE OF HEALTH AND MEDICAL SCIENCES
SCHOOL OF GRADUATE STUDIES
Feb, 2021
Harar, Ethiopia
2/11/2021
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2. SET BY:
ID. NO.
1. Sintayehu worku…… Sgs070/13
2. Shefena G/yesus…. .. Sgs069/13 2/11/2021
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3.  Introduction
 Risk factors
 Classification
 Clinical features
 Pathophysiology
 complications
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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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8. HTN
Proteinuria
Oliguria (<300 ml/24 hr.)
HELLP syndrome
Cerebral and visual disturbances
Persistent severe epigastric pain
Retinal hemorrhages
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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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15. Acute renal failure
Pulmonary edema
Abruptio placenta
DIC
IUGR
Preterm delivery
Still birth
Mortality
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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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