Hypertensive emergencies occur when a relatively rapid elevation of BP develops in a short period.
An increase in systemic vascular resistance by increasing vasoconstriction mechanisms through renin-angiotensin activation, pressure natriuresis, hypoperfusion, and ischemia are the most common culprits of end-organ damage
. The classic vascular feature is fibrinoid necrosis of the small vessels. In addition, red cell destruction is common as they pass through these obstructed vessels leading to microangiopathic hemolytic anemia. Another feature of a hypertensive emergency is the loss of autoregulation in the brain, which can present as hypertensive encephalopathy.