Hypertensive emergency (HTE) is defined as an acute and severe elevation in blood pressure (BP) resulting in new and ongoing evidence of target organ damage / dysfunction (TOD). While no absolute BP threshold exists for this condition, in most cases, systolic BP (SBP) exceeds 180 mm Hg and diastolic BP (DBP) exceeds 120 mm Hg. The rate in rise of BP and the absolute change from an individual's chronic baseline BP may be more important than the actual BP reading.

The causes of TOD can vary and are often multifactorial. Acute elevations in BP, whether discrete or relative to a patient's baseline, can overwhelm the body's autoregulatory mechanisms, leading to increased vascular permeability, tissue edema, and ultimately, in conditions such as hypertensive encephalopathy or acute cardiogenic pulmonary edema. Hypertension-induced direct shear forces may lead to vascular endothelial damage, which can inappropriately activate the clotting cascade and platelet aggregation, causing microvascular thromboses and tissue hypoperfusion (thrombotic microangiopathy).

HTE most commonly affects the heart, brain, kidneys, retinas, and blood vessels. In developed countries, the most common clinical presentations include acute congestive heart failure / pulmonary edema, ischemic stroke, and acute coronary syndrome. Less common presentations include hemorrhagic stroke and aortic dissection.

Symptoms related to HTE are variable and dependent on the target organ(s) impacted. These may include chest pain, dyspnea, visual disturbances, altered mental status, focal neurologic deficits, seizures, and decreased urine output. It should be noted that the presence of headache or lightheadedness alone does not imply that an HTE exists.

HTE can occur in any individual regardless of age, sex, race / ethnicity, or socioeconomic status. While chronic hypertension is common and affects approximately 30% of the adult population, only 1%-2% of those individuals will at some point develop a true HTE. Risk factors for HTE overlap those for chronic hypertension and include male sex, age over 75 years, African ancestry, smoking, alcohol use disorder, and lower socioeconomic status. Noncompliance and withdrawal from antihypertensive medications (most notably clonidine) may also precipitate HTE.

Other special populations are at increased risk for HTE. Pediatric causes may include acute glomerulonephritis, congenital renal disease, congenital adrenal hyperplasia, bronchopulmonary dysplasia, and coarctation of the aorta. Pregnant patients may develop severe preeclampsia or eclampsia. Secondary causes of severe hypertension may also precipitate HTE and include the use of NSAIDs or immunosuppressive medications (eg, tacrolimus, cyclosporin, steroids), endocrinopathies (ie, Cushing syndrome, hyperthyroidism, pheochromocytoma), chronic kidney disease, renal artery stenosis, untreated obstructive sleep apnea, sympathomimetic drug use, and withdrawal states (ie, alcohol withdrawal, benzodiazepine withdrawal).

The abundance of ambiguous terminology in the medical literature, including "malignant hypertension," "hypertensive crisis," and "hypertensive urgency," can lead to confusion and overly aggressive, unsafe management. Some experts advocate for discontinuing the use of many of these terms altogether.