Clinical Review

Management of obstetric hypertensive emergencies

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A strategy based on the triad of diagnosis, stabilization, and delivery can minimize risk of catastrophic end-organ damage.


 

References

Life-threatening obstetric hypertensive emergencies cannot be entirely prevented, but the risk of serious complications can be minimized.

The spectrum of hypertensive disease that can complicate pregnancy is broad—ranging from so-called “white coat” hypertension to gestational hypertension, chronic hypertension, chronic hypertension with superimposed preeclampsia, to preeclampsia.

Particularly challenging, however, is hypertension in pregnancy that becomes severe enough to qualify as a hypertensive crisis, bringing on immediate risk to both fetus and mother.

Risk may evolve over days—or hours—and may present as worsening blood pressure culminating in hypertensive crisis. Fetal morbidity and mortality, including placental abruption and acute fetal distress, are often directly linked to the maternal risks of hypertensive encephalopathy and cerebrovascular accident.

Placental abruption and fetal distress are common with severe hypertension even without encephalopathy and cerebrovascular accident. Abruption is unpredictable and potentially catastrophic, even with intense monitoring.

Aggressive BP control, while fundamental, needs to be balanced against the risks to both mother and fetus of overcorrection and undercorrection.

Defining a crisis

What truly defines hypertensive obstetric emergency is a matter of some debate.

Persistent blood pressures above 200 mm Hg systolic and/or 115 mm Hg diastolic qualify, but some have advocated 160/110 mm Hg as the threshold for emergent treatment of blood pressure. Others suggest that the rate of change in blood pressure is what precipitates the crisis, as opposed to the absolute blood pressure readings.

Why BP control is critical

The true pathophysiology of hypertensive crisis in pregnancy is obscure, but undoubtedly shares characteristics seen in the nonpregnant adult. Diagnosing a hypertensive emergency in the nonpregnant adult, in contrast to diagnosis of an obstetric hypertensive emergency, relies more on clinical manifestations of hypertension than on absolute blood pressure level.1

Pathophysiology

In the nonpregnant adult, 2 independent processes are thought to be necessary for the full-blown encephalopathic picture: dilation of the cerebral vasculature and fibrinoid necrosis. In the initial phases of severe hypertension, the cerebral vessels constrict to maintain cerebral perfusion pressure in the face of increased systemic arterial pressure. Once the limits of autoregulation are exceeded, reflex cerebral dilatation and resultant overperfusion lead to microvascular damage, exudation, microthrombus formation, and increased intracranial pressure, which in turn result in the encephalopathic picture.

In pregnancy, a prominent feature seems to be loss of cerebrovascular autoregulation, resulting in hypertensive encephalopathy once the upper limits of cerebral perfusion pressures are exceeded.2 Rapid control of blood pressure is needed even more because of the risks of placental abruption and stroke (See). Stroke is of special concern in the setting of thrombocytopenia or HELLP (hemolysis, elevated liver enzymes, and low platelet count) syndrome. Cerebral edema may be more closely associated with endothelial cell injury than with blood pressure,3 although control of blood pressure may help minimize the endothelial cell injury.

Minimizing organ damage

First, restore normal BP

The most important clinical objective for treatment of acute hypertensive crisis in the nonpregnant adult is to minimize end organ damage, especially to the brain4; in obstetric cases, the major morbidity and mortality result from cardiac and renal, as well as cerebrovascular damage. Fetal morbidity and mortality, although not inconsequential, is often directly linked to the maternal condition, and therefore management is based on the triad of diagnosis, stabilization, and delivery.

The physiological dysfunctions described above are best tended to by aggressively controlling blood pressure. With restoration of acceptable blood pressures, generally in the range of 140 to 150 mm Hg systolic and 90 to 100 mm Hg diastolic, cardiac dysfunction begins to reverse, renal function tends to improve, and the restoration of cerebral autoregulatory capability lessens (but does not eliminate) the likelihood of stroke.

Rule out other causes

The foremost goal of therapy for malignant hypertension is to restore normal blood pressure, which depends on correct diagnosis so that appropriate pharmacotherapy may be initiated. For example, clinical situations that could cause malignant hypertension include such disparate entities as acute aortic dissection, acute left ventricular failure, pheochromocytoma, monoamine oxidase inhibitor–food (tyramine) interactions, eclampsia, and acute cocaine intoxication, to name but a few.

Frequently, chronic hypertension or severe preeclampsia defines the underlying “cause” of the severe hypertension, but consideration of other diagnoses, such as uncontrolled hyperthyroidism or pheochromocytoma, should not be overlooked. For example, in pheochromocytoma blood pressures tend to be paroxysmal with wide fluctuations. In hyperthyroidism, clinical signs or symptoms would be expected to accompany the clinical picture, such as the presence of proptosis, exophthalmos, lid lag, tremor, elevated temperature, and a wide pulse pressure, to name but a few.

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