Pathophysiological changes in Pre-eclampsia
1-Cardiovascular changes:
➧ Hypertension in pre-eclampsia is due to marked vasoconstriction because both cardiac output and arterial compliance are reduced.
➧ There is a reversal of the normal circadian rhythm, with the highest blood pressure now at night, and a loss of the normal pregnancy-associated refractoriness to pressor agents; the sensitivity to infused angiotensin II increases weeks before the overt disease.
➧ Increases in insulin resistance and sympathetic nervous system tone also occur and have been implicated in the vasoconstriction characteristic of pre-eclampsia.
➧ The heart may reveal endocardial necrosis similar to that caused by hypoperfusion in hypovolemic shock.
2-Renal changes:
➧ Renal hemodynamics increase markedly in normal gestation, and renal plasma flow (RPF) and GFR decrease in pre-eclampsia (~25%); thus, values may be still above or at those of a non-pregnant state.
➧ The proteinuria of pre-eclampsia is associated with a pathognomonic renal lesion known as glomerular endotheliosis, in which the endothelial cells of the glomerulus swell and endothelial fenestrations are lost.
➧ Podocyturia has been recently associated with pre-eclampsia during clinical disease.
➧ The decrement in RPF is attributable to vasoconstriction, whereas the fall in GFR relates both to the decrement of RPF and the development of glomerular endotheliosis. In rare cases, acute renal failure may develop.
3-Cerebral changes:
➧ There is increased cerebral blood flow in pre-eclamptic women. Cerebral edema and intracerebral parenchymal hemorrhage are common autopsy findings in women who died from eclampsia. However, cerebral edema in eclampsia does not correlate with the severity of hypertension, suggesting that edema is secondary to endothelial dysfunction rather than a direct result of blood pressure elevation.
➧ Findings from head computed tomography (CT) scans and magnetic resonance imaging (MRI) are similar to those seen in hypertensive encephalopathy, with vasogenic cerebral edema and infarctions in the subcortical white matter and adjacent gray matter, predominantly in the parietal and occipital lobes. This syndrome is known as a posterior reversible leuko-encephalopathy syndrome (PRES).
4-Hepatic changes:
➧ Pre-eclampsia also affects the liver. Manifestations include elevated aspartate aminotransferase and lactic dehydrogenase levels, the increments are usually small, except when the HELLP syndrome supervenes.
➧ The gross hepatic changes in pre-eclampsia are petechiae ranging from occasional to confluent areas of infarction, as well as subcapsular hematomas, some having ruptured and caused death.
➧ The characteristic microscopic lesion is periportal, manifesting as hemorrhage into the hepatic cellular columns and at times concurrent infarction.
5-Coagulation changes:
➧ Pre-eclampsia is associated with activation of the coagulation system, with thrombocytopenia (usually mild) as the most commonly detected abnormality.
➧ There is increased platelet activation and size, plus decrements in their lifespan.
➧ The hypercoagulability of a normal pregnancy is accentuated (e.g. reduced antithrombin III, protein S, and protein C) even when platelet counts appear normal.
➧ Occasionally, the coagulopathy can be severe, as in the HELLP syndrome.
6-Eye changes:
➧ The severity of retinal changes depends upon the degree of hypertension. Retinal changes are likely to occur when SBP is above 150 mmHg and DBP is more than 100 mmHg.
➧ Visual disturbances occur including scotoma, diplopia, diminished vision, and photopsia.
➧ The three most common visual complications are hypertensive retinopathy, exudative retinal detachment, and cortical blindness.
➧ Possible explanations for these complications include coexisting or preexisting systemic vascular disease, changes in the hormonal milieu, endothelial damage, abnormal autoregulation, hypoperfusion ischemia, or hyperperfusion edema.
7-Metabolic changes:
➧ These include dyslipidemia with elevated triglycerides, free fatty acids, and low-density lipoprotein (LDL) cholesterol, and reduced high-density lipoprotein (HDL) cholesterol, with an increased prevalence of low dense LDL.
➧ Insulin resistance and uric acid, other components of the metabolic syndrome, are also increased in pre-eclampsia.
8-Utero-Placental changes:
➧ Shallow and abnormal placentation is a hallmark of pre-eclampsia, highlighted by a failure of the normal trophoblastic invasion of the spiral arteries, these vessels fail to remodel and dilate.
➧ This aberration underlies theories that restriction of placental blood flow leads to a relatively hypoxic uteroplacental environment, with subsequent events mediated through hypoxemia-induced genes resulting in the release of factors (e.g. antiangiogenic proteins) that enter the mother’s circulation and initiate the maternal syndrome.
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