This document summarizes preeclampsia, including its classification, etiology, epidemiology, risk factors, symptoms, complications, prevention, and conclusion. Preeclampsia is a pregnancy complication characterized by hypertension and proteinuria. It remains a leading cause of maternal and infant mortality. The pathophysiology involves poor placentation leading to placental ischemia and release of factors causing maternal endothelial dysfunction. Risk factors include previous preeclampsia, age under 18 or over 40, family history, chronic hypertension, diabetes, and obesity. Symptoms may include edema, headaches and nausea. Complications can include eclampsia, HELLP syndrome, stroke and death. Prevention focuses on delivery, and treatment involves blood pressure management

1. Department of Pathophysiology
Medical Faculty P. J. Šafarik University Košice
Preeclampsia
Nasim Badarna
GM- 3
2015/2016

2. outlines
• Introduction
• Classification
• Etiology
• Epidemiology
• Risk factors
• Symptoms
• Complication
• Prevention
• Conclusion

3. Introduction
• Preeclampsia, first described >100 years ago, is a
common pregnancy disorder known as one of the
leading causes of maternal and infant mortality.
• Preeclampsia is a dangerous complication that
usually occurs in the third trimester of pregnancy
and worsens over time, characterized by
hypertension, proteinuria, and other systemic
disturbances.

4. • hypertension (onset > 20 weeks) + proteinuria
OR
• hypertension (onset > 20 weeks) + multisystemic
signs:
- CNS
- pulmonary edema
- renal dysfunction
- liver impairment
- thrombocytopenia
* Proteinuria is not required for diagnosis

5. Hypertension
• Elevation of BP ≥140 mmHg systolic and/or ≥90 mmHg
diastolic, on two occasions at least 6 hours apart.
•  Hypertension:
•
SBP > 140 or DBP > 90
•  Severe hypertension:
•
SBP > 160 or DBP > 110
• BP > 4 hours apart

6. Proteinuria
means the presence of an excess
of serum proteins in the urine.
• presence of 0.3 g or greater in a 24-hour urine
specimen (abnormally high).
• Can be secondary to hypertension; proteinuria in
someone with high blood pressure is also a first
sign of declining kidney function.

7. Classification of hypertension in
pregnancy
• Chronic Hypertension
“Preexisting Hypertension”
• - present prior to pregnancy/present prior to 20 weeks
• Gestational Hypertension
Develops in late pregnancy, after 20 weeks gestation.
Mild hypertension without proteinuria or other signs
of preeclampsia(absence of severe features).
Resolves by 12 weeks postpartum
• Preeclampsia
» Mild Preeclampsia; absence of severe features
» Severe Preeclampsia; Severe features
• Preeclampsia superimposed on Chronic Hypertension

9. Severe Preeclampsia
• Severe features:
– Symptoms of central nervous system dysfunction = Blurred
vision, scotomata, altered mental status, severe headache
– Symptoms of liver distention = epigastric pain
– Nausea, vomiting
– Hepatocellular injury = Serum transaminase concentration at
least twice normal
– Systolic blood pressure ≥160 mm Hg or diastolic ≥110 mm
Hg  Severe Hypertention
– Thrombocytopenia = <100,000 platelets per cubic milimeter
– Proteinuria = 5 or more grams in 24 hours
– Oliguria = <500 mL in 24 hours
– Severe fetal growth restriction
– Pulmonary edema or cyanosis
– Cerebrovascular accident

10. Pathophysiology
• the pathophysiology of preeclampsia remains largely unknown.
However there is strong evidence that a major cause is an abnormal
placenta with the involvement of the trophoblast cells found in this
tissue.
• one subset of trophoblast, syncytiotrophoblast, which forms the
epithelial layer of the villi, is in direct contact with maternal blood.
• The clinical syndrome arises from secondary systemic circulatory
disturbances due to generalized maternal endothelial dysfunction.
• There are two broad categories, maternal and placental.

11. Placental Preeclampsia
• Placental preeclampsia appears to progress in two stages:
1. Arises from poor development of the early placenta and its maternal
blood supply, called poor placentation. This results in poor uterine
and placental perfusion, yielding the
2. second stage , a state of hypoxia and increased oxidative stress and
the release of anti-angiogenic proteins along with inflammatory
mediators into the maternal plasma.
A major consequence is generalized Endothelial dysfunction.

12. poor placentation
• By 20th week of pregnancy, the placenta requires increasing
access to the maternal blood supply. This is created by
extensive remodeling of maternal spiral arteries, which are the
end arteries of the uteroplacental circulation. Remodeling
depends on one of the subtypes of the trophoblasts.
trophoblast invasion
is inhibited, the
arteries are poorly
remodeled, and the
capacity of the
circulation is too
small. This is called
poor placentation.
Fig. 1
poor placentation; hypoxia as
a result.

13. Placental Factors That Might
Cause the
Maternal Syndrome
• A hypoxic placenta releases factors into the circulation
that cause the clinical features of this condition.
• These clinical features appear to arise from a
generalized inflammatory response, which the causes
are not fully understood, But it is believed that the
hypoxic placenta suffers oxidative stress, Such stress is
probably the cause of the increased release of
trophoblast debris into circulation.
• This debris is proinflammatory

14. Placental Factors That Might Cause the
Maternal Syndrome
• Several candidate released factors have been
suggested; the strongest is the soluble receptor for
vascular endothelial growth factor (VEGF)–1, also
known as sFlt1 (soluble fms-like tyrosine kinase 1). It
binds vascular endothelial growth factors and
deprives the systemic endothelium of essential
survival factors.
• It is therefore anti-angiogenic causes hypertension
and proteinuria, the typical features of preeclampsia.
****higher sFlt1 concentrations in the blood

15. Immunological Considerations
• In preeclampsia, The abnormal implantation may stem
from the maternal immune system's response to the
placenta, due to lack of established immunological
tolerance in pregnancy.

16. Epidemiology
• Common:
affecting around 5% ~ 10% of pregnancies
• Mortality:
12-13% of maternal mortality
It has the potential to kill mother or baby

17. Pregnancy-Related Mortality United
States (1998-2005)
Fig 2
being among the leading causes of maternal death.
Preeclampsia (12.3%)
Other medical conditions (13.2%)
Embolism (18%)
PE (10%)
AFE (8%)
Cardiomyopathy (11.5%)
CVA (6%)
Anesthesia (1%) Unknown (2.1%)
Hemorrhage (12.5%)
Obstet Gynecol 2010
Cardiovascular disease (12.4%)
Infection (11 %)

18. Risk Factors
• Preeclampsia in a previous pregnancy
• Age >40 years or <18 years
• Family history of pregnancy-induced hypertension
• Chronic hypertension
• Chronic renal disease
• Antiphospholipid antibody syndrome or inherited
thrombophilia
• Vascular or connective tissue disease
• Diabetes mellitus (pregestational and gestational)
• Multifetal gestation
• High body mass index
• Male partner whose previous partner had preeclampsia
• Hydrops fetalis
• Nulliparity

19. Symptoms
• Symptoms can
include edema (swelling)
, nausea, and headaches
during pregnancy.
• Other symptoms were
described with Severe
preeclampsia

20. complications
• Eclampsia; if preeclampsia left untreated, it may result
in seizures .
• HELLP syndrome is defined as hemolysis, elevated liver
enzymes (liver dysfunction), and thrombocytopenia
– This condition may occur in 10–20% of patients with
severe preeclampsia and eclampsia.
• the development of hemorrhagic or ischemic stroke,
acute kidney injury, and acute respiratory distress
syndrome (ARDS).
• the fetus may suffer nutritional and respiratory
insufficiency, asphyxia, or death.

21. Prevention
• Preeclampsia cannot be prevented because the
pathogenesis of preeclampsia is not yet completely
understood.
• Definitive Treatment = Delivery
It is one of the most common reasons for induced
pre-term delivery.
• antihypertensive therapy for prevention of stroke.
– Choice of drug therapy:
• Acute – IV labetalol, IV hydralazine..
• Long-term – Oral methyldopa or labetalol

22. Conclusion
The term ‘‘preeclampsia’’ describes a syndrome
(a cluster of clinical features) not a disease. The
condition is varied in its presentation, features,
and outcomes.
• Further studies are being held for a better
understanding of the etiology of preeclampsia.
This helps us as doctors to find a better
treatment for affected pregnant women.

23. • Thank you for your attension

24. References
•
• From the Preeclampsia Project, University of California, San Francisco Supported by National Institutes of Health Grant No. HD 24180.
Received for publication January 3, 1989; revised April 19, 1989; accepted May 16, 1989. Reprint requests: James M. Roberts, MD,
Department of Obstetrics, Gynecology and Reproductive Sciences, University of California, San Francisco, HSE-1462, San Francisco,
CA 94143-0550.
• 6/1/IJ998
• Nuffield Department of Obstetrics and Gynaecology, University of Oxford, John Radcliffe Hospital, Oxford OX3 9DU, UK.
• *To whom correspondence should be addressed.
• E-mail: christopher.redman@obs-gyn.ox.ac.uk
• Hypertension in Pregnancy: Report of the American College of Obstetricans and Gynecologists’ Task Force on Hypertension in
Pregnancy. ACOG, 2013. District I ACOG Medical Student Education Module 2011
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• https://en.wikipedia.org/wiki/hypertension
• 5. SCIENCE www.sciencemag.org - W O M E N ’ S H E A L T H
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B. Gulbis, G. J. Burton, Placenta 24 (suppl. A) S86 (2003). S. E. Hiby et al., J. Exp. Med. 200, 957 (2004). P. Parham, Nat. Rev.
Immunol. 5, 201 (2005). A. Moffett-King, Nat. Rev. Immunol. 2, 656 (2002). H. Haller et al., J. Reprod. Immunol. 23, 41 (1993). S. A.
Karumanchi, Y. Bdolah, Endocrinology 145, 483 (2004). S. E. Maynard et al., J. Clin. Investig. 111, 649 (2003). N. M. Page et al.,
Nature 405, 797 (2000).
• . C. W. Redman, I. L. Sargent, Placenta 24 (suppl. A), S21 (2003). B. Huppertz et al., Placenta 24, 181 (2003) M. T. Raijmakers, R.
Dechend, L. Poston, Hypertension 44, 374 (2004). N. Sattar, I. A. Greer, BMJ 325, 157 (2002). M. van Dijk et al., Nat. Genet. 37, 514
(2005). D. Haig, in Evolution in Health and Disease, S. C. Stearns, Ed. (Oxford Univ. Press, Oxford, 1999), pp. 77–90.
• Redman CW, Sargent IL (2005). "Latest Advances in Understanding Preeclampsia". Science 308 (5728): 1592–
1594. doi:10.1126/science.1111726.PMID 15947178.

25. • 13
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• ^ Jump up to:a b c Longo, Dan L. (Dan Louis) (2012). Harrison's principles of internal medicine. New York: McGraw-Hill. pp. 55–61. ISBN 978-0-07-
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• Emile R. Mohler (2006). Advanced Therapy in Hypertension and Vascular Disease. PMPH-USA. pp. 407–408. ISBN 9781550093186.
• Jump up^ Jun Wu, Cizao Ren, Ralph J. Delfino, Judith Chung, Michelle Wilhelm, & Beate Ritz (2009). "Association Between Local Traffic-Generated
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• Jump up^ Bramham, K; Parnell, B; Nelson-Piercy, C; Seed, PT; Poston, L; Chappell, LC (Apr 15, 2014). "Chronic hypertension and pregnancy
outcomes: systematic review and meta-analysis.". BMJ (Clinical research ed.) 348: g2301. doi:10.1136/bmj.g2301.PMC 3988319. PMID 24735917.
• ^ Jump up to:a b c d e f g h i j k l m n Mustafa, Reem; Ahmed, Sana; Gupta, Anu; Venuto, Rocco C. (2012). "A Comprehensive Review of Hypertension in
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• Fig.1
Epidemiology of preeclampsia and eclampsia in the
• United States, 1979-1986
• Audrey F. Saftlas, PhD, David R. Olson, PhD, Adele L. Franks, MD, Rani K. Atrash, MD, and Robert Pokras, MS Atlanta, Georgia
• http://www.sciencedirect.com.sci-hub.io/science/article/pii/000293789091176D
• Fig. 2
• Hypertension in Pregnancy: Report of the American College of Obstetricans and Gynecologists’ Task Force on Hypertension in Pregnancy. ACOG,
2013.
• District I ACOG Medical Student Education Module 2011
• taken from Obstet Gynecol 2010
•
• Fig. 3
• SCIENCE www.sciencemag.org - W O M E N ’ S H E A L T H
•
• Hypertension in Pregnancy: Report of the American College of Obstetricans and Gynecologists’ Task Force on Hypertension in Pregnancy. ACOG,
2013.
• District I ACOG Medical Student Education Module 2011