ABC | Volume 114, Nº4, April 2020

Statement Luso-Brazilian Position Statement on Hypertensive Emergencies – 2020 Arq Bras Cardiol. 2020; 114(4)736-751 Figure 1 – Normal fundoscopy (A). Fundoscopy of an individual with malignant hypertension and papilledema (B). A B the end of the first day of treatment. Greater and faster decreases may lead to cerebral hypoperfusion and loss of vascular autoregulation mechanisms. 32,33 Due to the need for rapid BP control, intravenous medications are recommended, of which the most frequently used are sodium nitroprusside (arterial and venous vasodilator), nicardipine (dihydropyridine calcium-channel blocker with arteriolar vasodilation action), clevidipine (short-acting dihydropyridine calcium-channel blocker), labetalol (alpha- adrenergic and beta-adrenergic blocker), or fenoldopam (peripheral dopamine-1 receptor agonist). During pregnancy, magnesium sulfate, diazoxide, or hydralazine are recommended. Corticosteroids (dexamethasone), mannitol (may be used in the absence of renal disease), and anticonvulsants (in case of seizures) may also be used. 23,30 Within the first 24 to 48 hours, oral medications should be introduced to improve BP control (renin-angiotensin- aldosterone system blockers and calcium-channel blockers), with a gradual DBP reduction to values below 90 mmHg in the following 2 to 3 months. 1,2,5,22 6. Malignant or Accelerated Hypertension Malignant hypertension is characterized by hypertension at varying levels, but usually very high BP (stage 3), retinopathy with papilledema, and rapidly progressive TOD (kidneys and heart), with a fatal outcome in the absence of therapeutic intervention (Figure 1). Severe BP elevation in the presence of retinal hemorrhages and exudates but no papilledema on fundoscopy is known as accelerated hypertension (Figure 2). After demonstration that the clinical findings and prognosis of these two forms of hypertension are similar, 34 the terms “malignant” and “accelerated” became interchangeable, and the World Health Organization currently uses the term accelerated- malignant to define this complication. Characteristically, malignant hypertension presents with systemic vascular changes affecting particularly the kidneys (known as malignant nephrosclerosis) and involving basically two processes: (a) proliferative endarteritis affecting small and large arterioles with intimal thickening, fragmentation, and reduplication of the internal elastic lamina and smooth muscle proliferation; the progression of this lesion, which resembles an “onion skin,” may lead to occlusion of the vessel lumen with consequent reduction in renal blood flow; (b) necrotizing changes in arterioles, especially in the glomerular hilum, and vessel wall reconstruction with eosinophilic granular material that exhibits the characteristics of fibrin (fibrinoid necrosis), causing destruction of the normal morphology and deep lumen narrowing. These changes may occur in organs other than the kidneys and are primarily responsible for the fatal complications of the disease (Figure 3). 35 The prognosis of malignant hypertension is almost always fatal if not early recognized or properly treated; in the past, the associated mortality reached 80% within 2 years. 36 However, since the introduction of antihypertensive treatment, studies have shown that the survival of individuals with malignant hypertension has improved substantially. 37-39 In a publication including almost 500 patients in Birmingham (United Kingdom), the authors reported a significant improvement in 5-year survival from 32% before 1977 to 91% in patients diagnosed between 1997 and 2006. 38 Management of patients with malignant hypertension usually includes the use of four classes of drugs, and hypertensive complications may stabilize and, in some cases, even be reversed. 7. Stroke and Hypertensive Emergency Stroke may present as a HE. Individuals with chronic hypertension present a right shift in the autoregulation curve for CBF causing them to tolerate substantially higher BP values without developing encephalopathy. Patients with chronic hypertension who have their BP values aggressively and rapidly reduced may present symptoms of cerebral hypoperfusion, even when the values are within the autoregulation range, as observed in normotensive individuals. Finally, patients with severe hypertension may lose the ability of autoregulation, thus presenting an increased risk of cerebral ischemia with abrupt BP reductions. 16-18 742