Accelerated hypertension

Definitions and terminology. Accelerated hypertension is a severe elevation of blood pressure (usually diastolic > 120–130 mmHg) with grade III retinopathy — flame haemorrhages, cotton-wool spots and hard exudates. Malignant hypertension is the same picture with grade IV retinopathy, that is, papilloedema. The modern classification is more useful:

Pathophysiology. A rapid rise in blood pressure overwhelms vascular autoregulation, causing endothelial injury, loss of vasomotor tone and increased permeability. The histological hallmarks are fibrinoid necrosis of arterioles and proliferative (onion-skin) endarteritis. This triggers a self-perpetuating cycle: ischaemia → renin– angiotensin activation → further vasoconstriction and pressure natriuresis → volume depletion → more renin release. In the brain, breakthrough of cerebral autoregulation produces vasogenic cerebral oedema (hypertensive encephalopathy, PRES); in small vessels it causes microangiopathic haemolytic anaemia with thrombocytopenia.

Causes. Essential hypertension that is untreated or where treatment has been abruptly stopped (the commonest scenario, and abrupt clonidine or beta-blocker withdrawal is a classic trigger). Secondary causes are disproportionately represented: renal parenchymal disease, renovascular disease (bilateral renal artery stenosis, fibromuscular dysplasia), primary aldosteronism, phaeochromocytoma, Cushing's syndrome, coarctation, systemic sclerosis renal crisis, and eclampsia. Drugs and toxins: cocaine, amphetamines, sympathomimetics and decongestants, ciclosporin and tacrolimus, erythropoietin, NSAIDs, corticosteroids, VEGF inhibitors and tyrosine kinase inhibitors, MAOI–tyramine interaction, and steroid or liquorice excess.

Clinical features by target organ. Eye — blurred vision, visual loss; grade III/IV retinopathy on fundoscopy. Brain — hypertensive encephalopathy with headache, nausea, vomiting, visual disturbance, confusion, seizures and coma; also intracerebral haemorrhage, subarachnoid haemorrhage and ischaemic stroke. Heart — acute pulmonary oedema, acute coronary syndrome, aortic dissection. Kidney — acute kidney injury with haematuria, proteinuria and red cell casts. Blood — microangiopathic haemolytic anaemia with schistocytes and thrombocytopenia. In older patients, presentation may be non-specific — delirium, falls or unexplained deterioration — so fundoscopy and urinalysis must be performed in every severely hypertensive older patient.

Investigations. Fundoscopy is mandatory and is the single most important bedside investigation. Also: urinalysis and urine microscopy for haematuria, proteinuria and casts; urea, electrolytes and creatinine; full blood count with a blood film for schistocytes; LDH, haptoglobin and reticulocyte count; ECG and troponin; chest radiograph; and echocardiography. Imaging as indicated: CT or MRI brain for neurological features (PRES shows posterior white-matter oedema), CT aortogram for suspected dissection. Investigate for secondary causes once stabilised — renal ultrasound with Doppler, plasma aldosterone-to-renin ratio, plasma or urinary metanephrines, and a full drug and substance history.

Management. Hypertensive urgency: treat with oral agents (amlodipine, an ACE inhibitor, a beta-blocker) and reduce the pressure gradually over 24–48 hours, with close outpatient follow-up. Never use sublingual short-acting nifedipine — the uncontrolled fall in pressure precipitates stroke and myocardial infarction, a particular danger in the older patient with impaired cerebral autoregulation. Hypertensive emergency: admit to a monitored bed with intra-arterial pressure monitoring and use titratable intravenous agents. The general rule is to reduce the mean arterial pressure by no more than 20–25% in the first hour, then to about 160/100 mmHg over the next 2–6 hours, and to normal over 24–48 hours. Important exceptions: in aortic dissection, reduce systolic pressure to < 120 mmHg and heart rate < 60/min within 20 minutes using a beta-blocker (esmolol or labetalol) FIRST, then a vasodilator; in acute ischaemic stroke, do not lower unless > 220/120 mmHg (or thrombolysis is planned, when the target is < 185/110 mmHg). Drug choice by context: labetalol or nicardipine for encephalopathy and stroke; glyceryl trinitrate for acute pulmonary oedema or ACS; esmolol plus a vasodilator for dissection; phentolamine for phaeochromocytoma; labetalol or hydralazine with magnesium for eclampsia. Avoid diuretics unless there is pulmonary oedema, since these patients are often volume-depleted from pressure natriuresis.

The 2024 ESC hypertension guideline and the 2025 AHA/ACC guideline both reinforce a shift away from treating a number toward treating the presence of acute target-organ damage. Specific practice points: for hypertensive urgency without organ damage there is no benefit and potential harm from rapid parenteral lowering — oral therapy with follow-up within days is preferred, and routine admission is discouraged; the 2025 AHA/ACC guideline provides drug- and condition-specific intravenous protocols (labetalol, nicardipine, clevidipine, esmolol, enalaprilat, fenoldopam) rather than a single generic target; and both guidelines advise against short-acting oral or sublingual agents in any setting. The 2025 guideline also adds a Class IIb recommendation for renal denervation in patients whose hypertension remains uncontrolled despite optimal therapy or who cannot tolerate medication.