Hypertensive emergencies

Accelerated hypertension is a hypertensive emergency. There is a recent increase in blood pressure to very high levels (≥180 mm Hg systolic and ≥120 mm Hg diastolic) resulting in target organ damage - usually seen as neurological (eg, encephalopathy), cardiovascular or renal damage. The term malignant hypertension used to be reserved for cases where papilloedema was present but the two terms are now often used interchangeably¹.

Where there is no evidence of target organ damage, the condition is a hypertensive 'urgency' rather than 'emergency' and treatment may be more gradual.

Finding accelerated hypertension and target organ damage in a patient demands urgent admission for assessment and treatment to lower blood pressure within hours in order to minimise further end-organ damage and reduce the risk of life-threatening events such as myocardial infarction, encephalopathy and intracerebral haemorrhage or subarachnoid haemorrhage. The National Institute for Health and Care Excellence (NICE) recommends same day referral for accelerated hypertension¹.:

• With papilloedema and/or retinal haemorrhages; or

• With life-threatening symptoms such as new-onset confusion, chest pain, signs of heart failure, or acute kidney injury; or

• In patients suspected of having a phaeochromocytoma (labile or postural hypotension, headache, palpitations, pallor, abdominal pain or sweating).

Epidemiology

There is a projected incidence of 1 to 2 cases per million per year, so this is not a common condition. However, a recent study of the number of visits to emergency departments with associated conditions or complications (eg, eclampsia, cerebral infarction and acute pulmonary oedema) doubled from 2006 to 2013².

Aetiology

Accelerated or malignant hypertension may be associated with any cause of secondary hypertension³.

• Unilateral renovascular hypertension - eg, renal artery stenosis.

• Renin-secreting neoplasms.

• Trauma to the kidneys.

• Renal vasculitis - eg, scleroderma, polyarteritis and systemic lupus erythematosus.

• Phaeochromocytoma.

• Cocaine abuse.

• Drugs such as monoamine-oxidase inhibitors, combined oral contraceptives or the withdrawal of alcohol, alpha-stimulants such as clonidine, or beta-blockers.

• Sodium-volume overload and low renin levels - eg, acute glomerulonephritis, primary aldosteronism.

• Pre-eclampsia/eclampsia.

• Hyperthyroidism or hypothyroidism.

Presentation

This may be asymptomatic or may present with any of the many symptoms and/or signs of end-organ damage:

• Headache.

• Fits.

• Nausea and vomiting.

• Visual disturbance.

• Chest pain.

• Neurological deficit - eg, cerebrovascular event (CVE).

• Bleeding due to disseminated intravascular coagulopathy (DIC).

• Microangiopathic haemolytic anaemia.

Assessment³

The assessment and investigation of any patient thought to have accelerated hypertension should be undertaken urgently and by doctors with expertise in this field. This should include:

• Full history - including:
  

  • Past medical history.

  • Full systems review.

  • Drug history including recreational drugs and over-the-counter herbal remedies.

• Full examination - including:
  

  • Blood pressure measurements: lying, standing and in both arms (looking for coarctation or aortic dissection).

  • Fundoscopy - retinopathy: eg, grade III (flame haemorrhages, dot and blot haemorrhages, hard and soft exudates) to grade IV (papilloedema).

  • Cardiovascular examination: lying and standing blood pressure; look for signs of cardiac failure or pulmonary oedema, carotid or renal bruits, left ventricular heave, cardiac murmurs, third or fourth heart sounds.

  • Neurological examination.

• Blood tests:
  

  • FBC ± clotting screen.

  • U&Es, creatinine.

  • Liver and TFTs.

  • Blood sugar measurement.

  • ± Cardiac enzymes and fasting blood lipids.

• ± Ambulatory blood pressure monitoring.

• Urine dip testing for protein and blood.

• CXR: cardiac size, cardiac failure, etc.

• ECG: left ventricular hypertrophy or left atrial enlargement.

Subsequent investigations may include:

• CT/MRI scan of the head or kidneys.

• Plasma renin activity.

• Plasma aldosterone level.

• 24-hour urine for vanillylmandelic acid (VMA) and metanephrine levels.

• Auto-antibody levels - eg, antinuclear factor.

Management¹⁴

General measures

The aim is to reduce the blood pressure over 24-48 hours. Patients usually have altered blood pressure autoregulation and if the blood pressure is reduced too fast, there may be organ hypoperfusion.

• Initially, try to reduce the mean arterial pressure by approximately 25% over the first 24-48 hours.

• An arterial line is helpful for continuous blood pressure monitoring.

• There may be severe sodium and volume depletion; volume expansion with isotonic sodium chloride solution may be required.

Drugs

Initially, an intravenous (IV) route is usually used. Nitroprusside is often used as an IV drug but labetolol or nicardipine are alternatives which can be switched to oral formulations once blood pressure control is achieved. There is, however, some evidence that labetalol may produce a greater reduction in peripheral blood pressure in the immediate treatment of malignant hypertension⁵.

Phentolamine is the drug of choice for a phaeochromocytoma crisis. Also available parenterally are diltiazem, verapamil and enalapril. Hydralazine is reserved for use in pregnant patients.

Prognosis⁵

Without treatment, accelerated hypertension may result in death within a year in over 90% of patients, as a result of end-organ damage - eg, myocardial infarction, CVE or renal failure. The prognosis has improved dramatically over the period of a few decades and with optimal treatment the five-year survival rate is >90%.