![if !IE]> <![endif]>
Describe the pathophysiology of preeclampsia.
The hallmark of preeclampsia is vasospasm that occurs secondary to increased circulating levels of renin, aldos-terone, angiotensin, and catecholamines. Aldosterone also causes sodium and water retention, which leads to general-ized edema. Since almost every organ system is affected in the parturient with preeclampsia, it is best to take a systematic approach when discussing the changes seen in preeclampsia.
Central Nervous System Cerebral edema and cerebral vasospasm lead to the central nervous system effects of preeclampsia. Intracranial pressure increases in some cases but cerebral blood flow and oxygen consumption remain normal. Clinical findings related to the above changes include headache, hyperreflexia, blurred vision, vertigo, blindness, seizures, and coma. Cerebral hemorrhage is the leading cause of death in the preeclamptic patient.
Pulmonary Intubation may be exceedingly difficult secondary to laryngeal and upper airway edema. Increased secretions and airway congestion predispose the mother to upper airway infections. Pulmonary capillary leak into the interstitium accounts for intrapulmonary shunting and a deteriorating alveolar to arterial (A-a) oxygen gradient.
Cardiovascular Generalized vasoconstriction produces hypertension, impaired tissue perfusion, and cellular hypoxia. Translocated fluid from the vascular compart-ment to the interstitium leads to generalized edema, hypo-volemia, and hemoconcentration. An inverse relationship exists between the intravascular volume and the degree of hypertension. Hemoconcentration leads to increased blood viscosity, which further exacerbates tissue hypoxia. Although the hematocrit is typically elevated, a relative anemia usually exists and blood loss is poorly tolerated. Vasospasm leads to an increase in systemic vascular resistance (SVR), which increases cardiac work. The already hyperdynamic cardiovascular system becomes stressed further and cardiac output rises. Over time, left ventricular hypertrophy occurs leading to left ventricular dysfunction. Cotton and colleagues (1985) have shown that central venous pressure does not necessarily correlate with pulmonary capillary wedge pressure and left ventricular end diastolic volume in preeclampsia. Consequently, pulmonary artery catheters may be necessary in some preeclamptic patients.
Renal Renal blood flow is reduced leading to a decrease in the glomerular filtration rate and creatinine clearance. Almost all renal function tests are impaired. An increasing uric acid level correlates with the severity of disease. Damaged glomeruli allow for renal loss of proteins.
Hepatic Vasospasm leads to hepatic periportal hemor-rhages and hepatocellular damage. Swelling of the liver capsule from subcapsular hematomas may produce abdominal pain. Hepatic rupture has been reported in severe cases. Elevated liver enzymes occur with deteriorating hepatic function.
Hematologic Coagulation abnormalities also occur. The most common finding is thrombocytopenia that can occur with or without other coagulopathies. A syndrome of h emolysis, elevated liver function tests and low platelet count (acronym HELLP) has been described. There is also frequently a qualitative platelet abnormality even without a quantitative problem. The prothrombin time, thrombin time and partial thromboplastin time can also be elevated. Fibrinogen levels can decrease and frank DIC can occur.
Uteroplacental Intervillous blood flow is decreased 2- to 3-fold and is a major contributing factor of fetal morbidity and mortality. The incidence of premature labor is high due to placental hypoperfusion. Because of decreased uteroplacental blood flow, the placenta is often small and shows signs of premature aging. The uterus is also hyper-active and markedly sensitive to oxytocin. The parturient with preeclampsia is at an increased risk for placental abruption.
Copyright © 2018-2023 BrainKart.com; All Rights Reserved. Developed by Therithal info, Chennai.