Hypertensive emergencies

1. How does a “hypertensive emergency” differ from “hypertensive urgency”?

A “hypertensive emergency” is a clinical situation in which severely elevated blood pressure is associated with acute, progressive target-organ damage that needs to be treated immediately with a safe and controlled reduction of blood pressure. “Hypertensive urgencies” (if they truly exist; see Question 15 below) are characterized by elevated blood pressures in a patient who has no acute, progressive target-organ damage; these are typically treated with oral antihypertensive medications and close follow-up thereafter. Typical scenarios that are hypertensive emergencies include the following:

• Hypertensive encephalopathy: typically a diagnosis of exclusion (see later)

• Acute left ventricular failure and/or pulmonary edema (see later)

• Subarachnoid or intracerebral hemorrhage

• Acute aortic dissection: Target blood pressure is <120/70 mm Hg, within 20 minutes (see later).

• Acute myocardial infarction or acute coronary syndrome

• Adrenergic crisis: for example, pheochromocytoma, phencyclidine, or cocaine overdose (see later)

• Glomerulonephritis or acute kidney injury

• Epistaxis, gross hematuria, or threatened suture lines after vascular surgery

• Eclampsia (some authorities would include preeclampsia here, but most obstetricians hasten to deliver the baby and lower blood pressure BEFORE a seizure occurs)

The absolute level of blood pressure does not distinguish between emergencies and urgencies. Patients who were previously normotensive can develop a hypertensive emergency with a blood pressure that is only 30 to 50 mm Hg higher than their usual and customary blood pressure (e.g., 160/100 in a woman with preeclampsia). Conversely, some patients with chronic hypertension remain asymptomatic and might qualify as only hypertensive urgencies, even with a blood pressure of 250/150 mm Hg. Seldom, if ever, does such a high blood pressure require hospitalization if there is no acute target-organ damage.

2. What is “malignant hypertension,” and how does it differ from “accelerated hypertension”?

Malignant hypertension is the term historically given when severely elevated blood pressure was accompanied by retinal hemorrhages, exudates, and originally papilledema. The term arose in the 1920s when no effective treatment was available, and the prognosis of patients with this condition was similar to cancer. Now that treatment is available and effective, the term is used predominantly by hospital-based coders. In the last millennium, “accelerated hypertension” was severely elevated blood pressure without papilledema; this term is now only rarely used outside its historical context.

3. What are the epidemiologic characteristics of patients who present with a hypertensive emergency?

Most such patients have a history of stage 2 hypertension that has not been adequately treated. The most common cause of this is nonadherence to prescribed medication. In the last millennium, patients presenting with “malignant hypertension” typically had very high blood pressures (before treatment) and were often cigarette smokers. Secondary hypertension, especially renovascular hypertension, was often found in patients with Keith-Wagener-Barker Grade III (hemorrhages/exudates) or IV (frank papilledema) retinopathy; chronic kidney disease was also very common in such patients in the 1970s.

4. What is the pathophysiology of “malignant hypertension”?

A rapid and sustained rise in blood pressure causes endothelial dysfunction and then frank arteritis, leading to platelet and fibrin deposition within the vessel and eventually fibrinoid necrosis. The juxtaglomerular apparatus of the kidney releases renin when it senses relative ischemia, which increases circulating angiotensin II levels and causes severe vasoconstriction. The kidney responds to the elevated blood pressure with natriuresis, causing relative volume depletion and further activating the renin-angiotensin-aldosterone system. These events typically reinforce each other and lead to the “vicious cycle” of increasing blood pressure and worsening vascular function.

5. What were the typical pathologic findings in “malignant hypertension?”

The patient’s blood vessels undergo myointimal proliferation (and medial thickening, leading to the “onion-skin” appearance) and fibrinoid necrosis. If the process is chronic, vascular smooth muscle hypertrophy occurs and collagen deposits in the small vessels and arterioles.