Hypertensive Emergency
Severe hypertension (usually SBP >180 and/or DBP >120 mmHg) with acute end-organ damage requiring immediate but controlled BP reduction.
Key Facts
Definition: severe hypertension with evidence of acute end-organ damage (brain, heart, kidneys, eyes, aorta) Differs from hypertensive urgency: urgency = severe BP WITHOUT end-organ damage Target: reduce MAP by no more than 25% in first hour, then to 160/100 mmHg over 2-6 hours First-line IV agents: labetalol, sodium nitroprusside, GTN infusion, nicardipine Malignant hypertension: severe hypertension with grade III/IV retinopathy (haemorrhages, papilloedema) Avoid rapid BP reduction: risk of watershed cerebral infarction, coronary or renal hypoperfusion Common presentations: hypertensive encephalopathy, aortic dissection, acute pulmonary oedema, eclampsia Mortality: untreated malignant hypertension has ~90% 1-year mortality
Overview
Key Facts
A hypertensive emergency is severe hypertension (typically SBP >180 mmHg and/or DBP >120 mmHg) accompanied by evidence of acute, ongoing end-organ damage. This requires immediate but controlled blood pressure reduction, typically in an ICU/HDU setting.
Epidemiology
- Affects ~1-2% of hypertensive patients
- More common in men, Black African/Caribbean ethnicity, and those with poor medication adherence
- UK incidence: approximately 1-5 per 100,000 per year
- Declining incidence due to improved hypertension management
Aetiology
- Most commonly occurs in patients with poorly controlled essential hypertension
- Non-adherence to antihypertensive medications is the commonest precipitant
- Secondary causes: renal artery stenosis, phaeochromocytoma, pre-eclampsia/eclampsia
- Drug-related: cocaine, amphetamines, MAOi interactions, abrupt clonidine withdrawal
Pathophysiology
- Severe BP elevation overwhelms vascular autoregulation
- Endothelial damage leads to fibrinoid necrosis of arterioles
- Activation of RAAS and release of vasoconstrictors creates a vicious cycle
- Microvascular thrombosis and ischaemia cause end-organ damage
- Cerebral autoregulation failure leads to hypertensive encephalopathy
Clinical Presentation
Hypertensive Encephalopathy
- Severe headache, visual disturbance, confusion, nausea/vomiting
- Seizures, altered consciousness
- Papilloedema on fundoscopy
Acute Aortic Dissection
- Sudden tearing chest/back pain radiating between scapulae
- BP differential between arms >20 mmHg
- Aortic regurgitation murmur
Acute Left Ventricular Failure
- Acute dyspnoea, orthopnoea, pink frothy sputum
- Bilateral crepitations, third heart sound
Acute Coronary Syndrome
- Chest pain, ST changes, troponin rise
Acute Kidney Injury
- Oliguria, rising creatinine, haematuria
Pre-eclampsia/Eclampsia
- Hypertension >140/90 mmHg after 20 weeks gestation with proteinuria
- Seizures in eclampsia
Red Flags
- Papilloedema or retinal haemorrhages
- Altered consciousness or focal neurology
- Chest pain with aortic dissection features
- Acute pulmonary oedema
- Seizures
- Oliguria with rising creatinine
Differential Diagnosis
| Diagnosis | Key Features | Investigation |
|---|---|---|
| Hypertensive urgency | Severe BP without end-organ damage | Clinical assessment, ABPM |
| Ischaemic stroke | Focal neurology, sudden onset | CT head |
| Haemorrhagic stroke | Sudden headache, focal neurology, reduced GCS | CT head |
| Phaeochromocytoma crisis | Paroxysmal headache, sweating, palpitations, pallor | 24h urinary metanephrines |
| Cocaine/amphetamine toxicity | Drug history, agitation, mydriasis | Urine toxicology |
| Pre-eclampsia/eclampsia | Pregnancy, proteinuria, oedema | Urine PCR, bloods |
| Aortic dissection | Tearing chest/back pain, BP differential | CT aortogram |
| Raised intracranial pressure | Headache, vomiting, papilloedema, focal signs | CT head |
Diagnosis / Investigation
Bedside
- Blood pressure: both arms (>20 mmHg difference suggests aortic dissection)
- ECG: LVH, ischaemia, arrhythmia
- Urinalysis: haematuria, proteinuria
- Fundoscopy: retinal haemorrhages, exudates, papilloedema
- Pregnancy test: if appropriate
Bloods
- FBC: microangiopathic haemolytic anaemia (schistocytes on film)
- U&Es: AKI assessment
- LDH, haptoglobin: haemolysis screen
- Troponin: myocardial injury
- Coagulation screen: DIC
- Blood film: schistocytes (MAHA)
Imaging
- CT head: stroke, intracranial haemorrhage, posterior reversible encephalopathy syndrome (PRES)
- CT aortogram: aortic dissection
- Chest X-ray: pulmonary oedema, mediastinal widening
- Echocardiography: LV function, aortic dissection flap
Special Tests
- MRI brain: PRES (posterior white matter oedema on T2/FLAIR)
- Urine toxicology: cocaine, amphetamines
Management
Non-pharmacological
- Admit to ICU/HDU for continuous arterial BP monitoring
- Establish IV access
- Bed rest with head elevation
Pharmacological
General principles:
- Reduce MAP by ≤25% in first hour
- Aim for 160/100 mmHg over next 2-6 hours
- Gradual further reduction to normal over 24-48 hours
IV agents (situation-dependent):
- Labetalol IV: 20mg bolus, then 1-2mg/min infusion (first-line for most emergencies)
- Sodium nitroprusside: 0.25-10 mcg/kg/min (potent, requires arterial line monitoring; risk of cyanide toxicity)
- GTN infusion: 1-10mg/hour (preferred in ACS and acute pulmonary oedema)
- Nicardipine IV: 5-15mg/hour (alternative to labetalol)
- Hydralazine IV: 5-10mg bolus (preferred in eclampsia alongside magnesium sulphate)
- Esmolol IV: ultra-short-acting beta-blocker for aortic dissection
Specific scenarios:
- Aortic dissection: target SBP <120 mmHg and HR <60 bpm; IV labetalol or esmolol + GTN
- Eclampsia: IV magnesium sulphate 4g loading dose + labetalol/hydralazine
- Phaeochromocytoma crisis: IV phentolamine 2-5mg boluses
Surgical/Interventional
- Emergency surgery for aortic dissection (Type A)
- Delivery for eclampsia if appropriate
Referral Criteria
- All hypertensive emergencies require immediate hospital admission
- ICU/HDU admission for IV antihypertensive therapy
- Urgent specialist input: cardiology, neurology, renal, obstetrics as appropriate
Prognosis
- Untreated malignant hypertension: ~90% 1-year mortality
- With appropriate treatment: 5-year survival >70%
- Hypertensive encephalopathy: usually reversible with prompt treatment (PRES)
- Aortic dissection: Type A mortality ~1-2% per hour if untreated; surgical mortality ~15-25%
- Eclampsia: maternal mortality ~1% in UK
- Long-term: patients remain at high risk and require aggressive BP management and secondary cause investigation
Other Relevant Information
Hypertensive Retinopathy Classification
| Grade | Features | Significance |
|---|---|---|
| I | Arteriolar narrowing | Mild hypertension |
| II | AV nipping | Moderate hypertension |
| III | Haemorrhages, cotton wool spots | Accelerated hypertension |
| IV | Papilloedema | Malignant hypertension |
Key Differences: Emergency vs Urgency
| Feature | Hypertensive Emergency | Hypertensive Urgency |
|---|---|---|
| End-organ damage | Present | Absent |
| Setting | ICU/HDU | Outpatient/ward |
| Treatment route | IV | Oral |
| BP reduction speed | Hours | Days |
| Risk if untreated | Immediate | Weeks-months |