Eclampsia pathophysiology: Difference between revisions
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Revision as of 12:35, 7 August 2021
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Eclampsia Microchapters |
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Diagnosis |
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Treatment |
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Case Studies |
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Eclampsia pathophysiology On the Web |
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American Roentgen Ray Society Images of Eclampsia pathophysiology |
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Risk calculators and risk factors for Eclampsia pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
While multiple theories have been proposed to explain preeclampsia and eclampsia, it occurs only in the presence of a placenta and is resolved by its removal.[1] E. W. Page suggested that placental hypoperfusion is a key feature of the process. It is accompanied by increased sensitivity of the maternal vasculature to pressure agents leading to vasospasm and hypoperfusion of multiple organs. Further, an activation of the coagulation cascade leads to microthombi formation and aggravates the perfusion problem. Loss of plasma from the vascular tree with the resulting edema additionally compromises the situation. These events lead to signs and symptoms of toxemia including hypertension, renal, pulmonary, and hepatic dysfunction, and - in eclampsia specifically - cerebral dysfunction.[1] Preclinical markers of the disease process are signs of increased platelet and endothelial activation.[1]
Pathophysiology
Placental hypoperfusion is linked to abnormal modeling of the fetal-maternal interface that may be immunologically mediated[1] The invasion of the trophoblast appears to be incomplete.[2] Adrenomedullin, a potent vasodilator, is produced in diminished quantities by the placenta in preeclampsia (and thus eclampsia).[3] Other vasoactive agents are at play including prostacyclin, thromboxane A2, nitric oxide, and endothelins leading to vasoconstriction.[4] Many studies have suggested the importance of a woman's immunological tolerance to her baby's father, whose genes are present in the young fetus and its placenta and which may pose a challenge to her immune system.[5]
Eclampsia is seen as form of a hypertensive encephalopathy in the context of those pathological events that lead to preeclampsia. It is thought that cerebral vascular resistance is reduced, leading to increased blood flow to the brain. In addition to abnormal function of the endothelium, this leads to cerebral edema.[6] Typically an eclamptic seizure will not lead to lasting brain damage; however, intracranial hemorrhage may occur.[7]
Histopathology
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References
- ↑ 1.0 1.1 1.2 1.3 JM Roberts, DW Cooper. "Series, Pre-eclampsia trio. Pathogenesis and genetics of pre-eclampsia". The Lancet 2001; 357:53-56.
- ↑ Zhou Y, Fisher SJ, Janatpour M, Gembacev O, Dejana E, Wheelock M; et al. "Human cytotrophoblasts adopt a vascular phenotype as they differentiate: a strategy for successful endovascular invasion?". J Clin Invest 1997;99:2139-51.
- ↑ Hongshi L., Dakour J, Kauman S, Guilbert LJ, Winkler-Lowen B, Morrish DW. "Adrenomedullin is decreased in preeclampsia because of failed response to epidermal growth factor and impaired syncytialization". Hypertension 2003, vol. 42, no5, pp. 895-900.
- ↑ ACOG. "Diagnosis and Management of Preeclampsia and Eclampsia". ACOG Practice Bulletin # 33, 2002,.
- ↑ "Sex Primes Women for Sperm". BBC News. 2002-02-06. Text " http://news.bbc.co.uk/2/hi/health/1803978.stm" ignored (help); Check date values in:
|date=(help);|access-date=requires|url=(help) - ↑ Cipolla MJ (2007). "Cerebrovascular function in pregnancy and eclampsia". Hypertension. 50 (1): 14–24. doi:10.1161/HYPERTENSIONAHA.106.079442. PMID 17548723. Unknown parameter
|month=ignored (help) - ↑ Richards A, Graham D, Bullock R. "Clinicopathological study of neurological complications due to hypertensive disorders of pregnancy". J Neurol Neurosurg Psychiatry 1988;51:416-21.