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MS WordPerinatologist Corner - C.E.U/C.M.E. Modules
Hypertension in Pregnancy
Sponsored by The Indian Health Service Clinical Support Center
Part 1: Mild Pre-Eclampsia
4. Read the material on mild pre-eclampsia
Women who enter pregnancy with high blood pressure are obviously different from those who later develop the preeclampsia syndrome. Nevertheless, their underlying disease may complicate their pregnancy, and up to one in three of them will develop superimposed preeclampsia. Likewise, a third of them may have a small for gestational age infant, and they are at increased risk for preterm birth, placental abruption, and perinatal death. If significant renal disease is part of their picture (creatinine >1.4 mg/dL), these risks will all be exaggerated.
Preeclampsia-eclampsia: classification
This entity will be discussed first, as it is the more common and most serious clinical problem. An understanding of its pathophysiology is very useful in order to understand its differentiation from the other classifications, as well as its appropriate management.
Preeclampsia may be defined as mild or severe. Mild preeclampsia is defined as above: systolic >140 and diastolic >90, accompanied by >1+ proteinuria. The majority of patients will only have mild disease, but an important, and largely unpredictable, subset will progress to the severe syndrome, thus mandating constant vigilance once the diagnosis is established. Severe preeclampsia is a life-threatening disease and requires delivery, regardless of gestational age (more on this later) in order to be reversed. Severe preeclampsia is defined by one of the following criteria:
- Blood pressure>160 mm Hg systolic or >110 mm Hg diastolic
- Proteinuria of >5.0 g on a 24-hour collection (3-4+ on dipstick)
- Oliguria of <500 mL/24 hours and/or serum creatinine >1.2 mg/dL
- Thrombocytopenia (<100,000 mm3) with elevated hepatic enzyme activities and/or evidence of microangiopathic hemolytic anemia ("HELLP" syndrome), usually accompanied by epigastric pain
- Cerebral or visual symptoms (headache, scotomata), seizures (eclampsia)
- Pulmonary edema
- Fetal growth restriction
You will notice that various end organs are targeted here: the vasculature itself, the kidney, the liver, the central nervous system, the cardiopulmonary system, the uteroplacental unit.
The art of medicine
A major goal in the management of mild preeclampsia is the recognition and prevention of severe preeclampsia. A better understanding of the physiology will make that recognition easier.
Pathophysiology and etiology
The etiology of preeclampsia is still unknown, although many interesting hypotheses have been advanced. The pathophysiology of the disease however, has been fairly well elucidated. The final common pathway in the development of severe preeclampsia is currently thought to be generalized vascular endothelial dysfunction. This results in arterial vasospasm (clinically manifest as hypertension, oliguria, etc.), increased capillary permeability (clinically manifest as proteinuria, cerebral edema, pulmonary edema, etc.), and actual endothelial lesions with platelet activation (clinically manifest as HELLP syndrome, abruptio placentae, etc.). The net effect is downstream hypoperfusion with resultant hypoxic-ischemic damage to one or more target organs.
Hypertension is really not the most significant abnormality of this entity; under-perfusion is what accounts for its most serious sequelae. This concept is very important in implementing appropriate management.
The inciting event is theorized to occur soon after conception and is the result of defective placentation with poor vascularization of the trophoblast. This may be the result of immune maladaptation between the maternal host and the fetal partial allograft, genetic predisposition, and vascular mediated factors.
Effect of parity
Preeclampsia primarily affects two subpopulations of women: young nulliparas and older multigravidas. There is evidence to suggest "primipaternity" rather than "primiparity" is the problem, as women who conceive soon after initiating sexual activity, and those later in life who acquire a new partner, seem to be the most susceptible, presumably as a result of not acquiring tolerance to new male antigens.
Vascular and genetic
Vascular factors may also play a key role in maternal susceptibility as women with chronic hypertension, diabetes, underlying renal disease, vasculitis (e.g., lupus), have a several-fold increased incidence of the disease compared to well women. Certain families also seem to have a genetic tendency to preeclampsia. This is well seen in certain Navajo kindreds where there exists a strong family history of the disease in multiple maternal female relatives.
Whatever the predisposing factor, the trophoblast presumably fails to establish normal remodeling of the spiral arteries at the maternal interface, and responds to the relative ischemia by the production of cytokines that eventually damage the maternal vascular endothelium and result in the clinical syndrome we know as severe preeclampsia.
