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.
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