ACCELERATED HYPERTENSION

• Hypertensive emergencies are acute, life-threatening
• usually with marked increases in blood pressure (BP), generally systolic ≥180 and diastolic ≥120 mmHg

• There are 2 major clinical syndromes induced by severe hypertension

Accelerated (malignant) hypertension

• Marked hypertension with grade III/IV retinopathy
• There may be renal involvement (malignant nephrosclerosis)
• The presence of papilloedema does not affect prognosis or treatment

Hyponatraemic hypertensive syndrome (HHS)

• If this condition is suspected, refer to the renal team urgently
• Severe hypertension related to renal ischemia
• most commonly due to severe atherosclerotic renovascular disorder
• Excessive stimulation of renin-angiotensin-aldosterone system
• heavy polyuria, renal electrolyte loss and proteinuria

Main presenting symptoms

• Neurological manifestations of hyponatraemia and/or hypertensive encephalopathy
• may be disproportionate to degree of hyponatraemia and/or hypertension

Symptoms and signs

• Complete history
• particular attention to pre-existing hypertension and target-organ damage

Hypertensive encephalopathy

• Symptoms and signs of cerebral oedema
• insidious onset of headache, nausea, and vomiting
• followed by non-localising neurological symptoms e.g. restlessness, confusion
• if hypertension not treated, seizures and coma

Intracerebral or subarachnoid bleeding, lacunar infarcts

• Focal and non-local neurological symptoms and signs

Left ventricular (LV) failure

• Dyspnoea

Fundi

• Retinal haemorrhages and exudates
• representing both ischemic damage and leakage of blood and plasma
• Papilloedema

Renal

• Haematuria (usually non-visible) and proteinuria suggests acute kidney injury due to malignant nephrosclerosis
• In HHS, heavy polyuria and signs of dehydration

BP

• Sustained hypertension ≥180/120 mmHg requires treatment
• BP ≥180/120 mmHg and grade III/IV retinopathy requires urgent assessment

Immediate investigations

• Fundoscopy
• FBC, U&E
• Urinalysis
• haematuria
• proteinuria
• renal electrolyte loss
• ECG +/- echocardiogram
• CXR
• Ultrasound scan of the renal tract
• If neurological symptoms present, MRI scan to check for;
• ischemic stroke or haemorrhage (not usually treated with aggressive BP reduction)
• oedema of parieto-occipital regions white matter (reversible posterior leukoencephalopathy syndrome)

• Safe decrease of BP
• sustained high BP alters cerebral autoregulation
• In HHS, correct hyponatraemic dehydration. See hyponatraemia
• Treat underlying hypertensive disease
• If any doubt about the need for treatment, seek advice from renal medicine SpR/consultant

Safe decrease in BP

• Aim to reduce blood pressure by no more than 25% in first 24–48 hr
• sudden reduction of BP will reduce cerebral perfusion and can be dangerous
• Initial aim of treatment is to steadily lower diastolic BP to approximately 100–105 mmHg within 6-12 hrs, or 25% of presenting value whichever is higher, with 2 exceptions:
• patient has aortic dissection – see Aortic dissection guideline, reduce systolic BP to <100 mmHg and maintain
• patient has pulmonary oedema, reduce BP until clinical improvement occurs but not <90/60 mmHg

Oral agents

• Slower onset of action and inability to control degree of BP reduction limits use in hypertensive crises
• use when no rapid access to parenteral medication
• if no hypertensive encephalopathy and/or grade III/IV retinopathy, may be tried as first line therapy

First line

The following may be used:

• Labetalol 50–800 mg twice daily (in 3–4 divided doses in high doses)
• maximum 2.4 g daily
• Nifedipine SR 10–40 mg 12-hrly
• Amlodipine 5–10 mg daily
• Doxazosin 1–16 mg daily
• Hydralazine 25–50 mg twice daily
• Do NOT use liquid/sublingual nifedipine or captopril
• excessive and uncontrolled hypotensive response causing ischemia (MI, angina or stroke)

Parenteral therapy

Acute pulmonary oedema or acute coronary syndrome

• Prefer glyceryl trinitrate. See Glyceryl trinitrate guideline
• if patient has pulmonary oedema, reduce BP until clinical improvement occurs but not <90/60 mmHg

Hyperadrenergic states

• e.g. pheochromocytoma, cocaine overdose and methamphetamine overdose
• Do not use beta blockers or labetalol (beta-blocking effects) in the acute setting
• blockade of vasodilatory peripheral beta-adrenergic receptors with unopposed alpha-adrenergic receptor stimulation can lead to a further elevation in blood pressure
• Sodium nitroprusside may be used. See Sodium nitroprusside guideline

Further choice

• If no evidence of pulmonary oedema, or other contraindications (e.g. bronchospasm, heart block, hyperadrenergic states), prefer labetalol
• particularly when there is associated aortic dissection
• see Labetalol guideline
• In most other hypertensive emergencies, use sodium nitroprusside
• see Sodium nitroprusside guideline

If improving

• In patients treated with parenteral agents, start oral treatment before parenteral agent withdrawn
• Continue maintenance oral treatment. See NICE Hypertension guidelines
• Aim to reduce BP gradually over 7–10 days to a target of:
• patients <80 yr: 140/90 mmHg
• patients >80 yr: 150/90 mmHg

Assessment

• Assess kidneys in more detail e.g. CT/MR of renal arteries, urine PCR
• Carefully assess all patients for secondary causes of hypertension

If not improving

• Seek advice from renal team

• During parenteral therapy, measure BP every 15 min
• Once maintenance therapy has started, measure BP 4-hrly
• Monitor urine output and serum U&E daily

• Address other risk factors for cardiovascular disease (smoking, cholesterol, obesity) and advise
• Discharge home when BP ≤160/90 mmHg and condition stable
• Refer to hypertension clinic for follow-up as outpatient
• Following discharge, provide close follow-up care and advise weekly BP and U&E monitoring by GP