EndocrinologyTier 1Disease (DEADMAN)

Acute metabolic derangements - hypertensive crisis

Description

Severe BP elevation, generally >=180/120mmHg, split into two clinically distinct entities by the presence of acute target-organ damage:
- Hypertensive urgency - severe BP elevation, no acute end-organ damage - manage over hours-days, usually as an outpatient/short admission with oral therapy
- Hypertensive emergency - severe BP elevation with acute end-organ damage (encephalopathy, ACS, aortic dissection, pulmonary oedema, AKI, eclampsia, retinal haemorrhage) - requires immediate IV therapy in a monitored setting
The distinction, not the absolute number, is what changes management urgency

More common in patients with poorly controlled/undiagnosed chronic hypertension, medication non-adherence, or a secondary cause
Hypertensive emergencies are less common than urgencies but carry materially higher morbidity/mortality given active organ injury

Abrupt rise in systemic vascular resistance overwhelms autoregulation in target organs (brain, heart, kidney, retina, placenta) -> endothelial injury, fibrinoid necrosis of small vessels -> the organ-specific complications seen in emergencies
Secondary causes to actively consider, especially with abrupt/severe or refractory presentations: renal artery stenosis, phaeochromocytoma, primary hyperaldosteronism, renal parenchymal disease, medication/substance-related (sympathomimetics, cocaine, MAOI-tyramine interaction, abrupt clonidine/beta-blocker withdrawal), pre-eclampsia/eclampsia in pregnancy
Non-adherence to established antihypertensive therapy remains the commonest single precipitant in known hypertensive patients

Distinguish urgency from emergency - the central diagnostic task

Careful history/examination for target-organ symptoms: chest pain (ACS/dissection), dyspnoea (pulmonary oedema), headache/visual disturbance/confusion (hypertensive encephalopathy), reduced urine output (AKI), visual loss (retinopathy/papilloedema)
Fundoscopy - papilloedema/haemorrhages support hypertensive emergency
ECG, troponin, renal function, urinalysis (proteinuria/haematuria), and CXR as indicated by symptoms
CT/CTA if dissection or stroke suspected; urgent CT/MRI brain if encephalopathy or focal neurology

Consider a secondary cause when

Age <30 or >55 at first presentation, resistant to multiple agents, abrupt/severe onset, associated features (paroxysmal symptoms with phaeochromocytoma, hypokalaemia with hyperaldosteronism)
Screening (renin/aldosterone ratio, plasma metanephrines, renal imaging) appropriately deferred to after acute stabilisation unless a specific cause is strongly suspected and changes immediate management (e.g. phaeochromocytoma)

A. Hypertensive urgency

Oral antihypertensive therapy, gradual BP reduction over hours-days, not IV agents
Resume/intensify existing oral regimen if non-adherence is the cause; address any reversible precipitant
Rapid aggressive BP lowering is not indicated and can itself cause harm (hypoperfusion)

B. Hypertensive emergency - general targets

IV antihypertensive therapy in a monitored setting
Reduce BP by ~20-25% within the first hour, then toward ~160/100-110mmHg over the next 2-6 hours, then gradually toward normal over 24-48 hours - avoid rapid normalisation, which risks organ hypoperfusion (brain, kidney, heart) that has autoregulated to the elevated pressure
Agents: labetalol, nicardipine, clevidipine, sodium nitroprusside, GTN, esmolol - choice guided by the specific end-organ syndrome

C. Syndrome-specific exceptions to the general rule

Aortic dissection - more aggressive and rapid target (systolic ~100-120mmHg within minutes) with combined HR and BP control (beta-blocker first to reduce shear stress, e.g. esmolol/labetalol, before adding a vasodilator) - avoid vasodilator-only therapy, which can reflexively increase shear stress
Acute ischaemic stroke - generally permissive hypertension unless thrombolysis/thrombectomy candidate (specific lower thresholds apply) or BP is extremely high - aggressive lowering can worsen penumbral perfusion
Pre-eclampsia/eclampsia - labetalol, hydralazine, or nifedipine; magnesium sulfate for seizure prophylaxis/treatment - a distinct pathway, delivery is the definitive treatment
Phaeochromocytoma crisis - alpha-blockade (phentolamine) before any beta-blockade - beta-blockade first causes unopposed alpha-mediated vasoconstriction and can precipitate severe hypertensive crisis
Acute pulmonary oedema - GTN/nitroprusside plus diuretic, avoid beta-blockade acutely if decompensated

Chronic poorly controlled hypertension, medication non-adherence
Secondary hypertension causes - renal artery stenosis, phaeochromocytoma, primary hyperaldosteronism, renal parenchymal disease
Sympathomimetic/stimulant use, abrupt antihypertensive withdrawal (esp. clonidine, beta-blockers)
Pregnancy (pre-eclampsia/eclampsia)

Hypertensive urgency - generally good outcome with gradual oral BP control and addressing the precipitant
Untreated/inadequately treated hypertensive emergency - progresses to irreversible organ damage (stroke, MI, renal failure, aortic rupture)
Overly rapid correction is a recognised iatrogenic complication - can cause cerebral, cardiac, or renal hypoperfusion in tissue that has autoregulated to chronically elevated pressure
Long-term outcome depends on identifying and treating the underlying driver (adherence support, secondary cause work-up once stable) - the acute episode is a marker of inadequately controlled chronic hypertension, not an isolated event

6 more sections, plus exam facts

Premium unlocks every note across every specialty, and the full exam fact library behind it.