How do I manage the patient with malignant hypertension?

Malignant hypertension was originally defined as hypertension in association with grade IV retinopathy (papilloedema), although it is now clear that hypertension associated with grade III retinopathy (retinal haemorrhages without papilloedema) shares the same poor prognosis. The identification of malignant hypertension should prompt an urgent and active search for secondary causes of hypertension, particularly renal disease (acute renal failure must be excluded), renovascular disease and phaeochromocytoma.

Management is based on the published experience from case series rather than randomised controlled trials. In the absence of hypertensive heart failure, aortic dissection or fits and confusion (hypertensive encephalopathy), bed rest and oral antihypertensive treatment are the mainstays of management, the aim being to reduce the diastolic blood pressure gradually to 100mmHg in the first few hours of presentation. Too rapid reduction in BP may precipitate “watershed” cerebral infarction. Oral therapy with adrenoceptor blockers (e.g. atenolol 50–100mg) ± a thiazide diuretic (e.g. bendrofluazide 2.5mg) will lower the blood pressure smoothly in most patients. There is less experience with newer antihypertensive agents. Nifedipine given via the sublingual route may produce a rapid and unpredictable reduction in BP and should be avoided. Similarly, angiotensin-converting enzyme inhibitors should also be avoided because of the risk of first dose hypotension. Older drugs such as hydralazine (25–50mg 8 hourly), or methyldopa (10–20mg 8 hourly) have been used successfully and are an alternative in individuals in whom adrenoceptor blockers are contraindicated.

Hypertensive encephalopathy (headache, fits, confusion, nausea and vomiting) demands intensive care, intra-arterial BP monitoring and a more urgent, but nevertheless controlled, blood pressure reduction with parenteral antihypertensive therapy. Labetalol (initial dose 15mg/hr) or sodium nitroprusside (initial dose 10 micrograms/min) are effective and readily titratable agents. The aim is to titrate the dose upwards to produce a controlled reduction in diastolic blood pressure to 100mmHg over 1–2 hours. For hypertensive encephalopathy in the context of pre-eclampsia, intravenous magnesium sulphate is a specific therapy. The presence of focal neurological signs should prompt a CT head scan to exclude haemorrhagic stroke or subarachnoid haemorrhage, in which case nimodipine should be started.