Abstract

PRE-ECLAMPSIA, PATHOPHYSIOLOGY AND MANAGEMENT

*Dr. Hawraa Saadi Ismael Albuslman and Dr. Israa Abdulameer Kadhim

ABSTRACT

Pathophysiological Foundations Some evidence supports the hypothesis of maternal immune system involvement in the disease. In case there are problems of immunological adaptation to the trophoblast, there will be problems in trophoblast perfusion, with consequent hypoxia. These primary alterations would trigger a series of local hypoxia phenomena, and reoxygenation could amplify the local effects, such as the formation of oxygen-reactive species, activation of the maternal inflammatory system, and acceleration of cellular apoptosis processes that would limit the establishment of normal placentation and imbalance between pro-angiogenic factors, such as the vascular endothelial growth factor (VEGF) and the placental growth factor (PlGF), and soluble antiangiogenic factors such as the soluble fms-like tyrosine kinase-1 (sFLT-1), with predominance of the latter, resulting in generalized activation of the maternal inflammatory system, universal endothelial dysfunction, and limited placental vascularization. Universal arteriolar spasm due to endothelial activation results in an insidious and progressive process, culminating in multiple organ insufficiency. Preeclampsia should be interpreted as a chronic disease with potential for progressive multiple organ failure. This evolutionary character must be taken into account, as well as its unpredictability and clinical instability in decisions. Endothelial activation basically determines: vasoconstriction and consequent increase in peripheral resistance; changes in capillary permeability, which are responsible for edema; and activation of the coagulation system. The kidneys suffer from anatomo pathological patterns (glomerular endotheliosis and focal sclerosis), with consequent proteinuria and impairment of the glomerular filtration. In the liver, ischemia occurs with varying intensity, leading to dysfunction with elevated levels of transaminases. Focal or confluent edema and/or hemorrhage distend the capsule, and may result in hepatic rupture with massive bleeding. Vasospasm hinders the uteroplacental blood flow with varying intensity, depending on the moment of the process and on the existence of a chronic pre-existing injury. Regarding coagulation, there is activation and consumption of platelets with progressive consumption and disseminated coagulation. The brain can be affected by ischemia aggravated by diffuse edema, resulting in seizure (eclampsia) or stroke. Patients presenting severe conditions, particularly eclampsia, should receive differentiated care, given the progressive functional limitation of multiple organs.

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