Acute Aortic Syndrome

Meet the patient

A 58-year-old hypertensive builder grips his chest at 03:00, then his back between the shoulder blades. He tells the triage nurse the pain "switched on in a single second — like I was torn in half". Right-arm BP is 200/110; the left radial pulse is absent and left-arm BP is 162/92.^[2][1]

Two exam questions are now live and both will kill him if you answer them wrong: is this type A or type B? and is it safe to thrombolyse the ECG changes? Everything below exists to answer those two questions at consultant depth, because the diagnosis is routinely missed at the front door — in IRAD the median time from emergency-department arrival to diagnosis was 4.3 hours, and delay was concentrated in women, in patients without abrupt or any pain, and in those first seen at a non-tertiary hospital.^[16]

What acute aortic syndrome is — three lesions, one algorithm

One umbrella, three lesions, one opening move. All three share medial wall stress producing a tear or bleed inside the wall, and an identical first 15 minutes of resuscitation.^[1]

• Classic dissection — a tear of the intima (and inner media) lets pulsatile blood enter and propagate along the media, splitting the wall into a true and false lumen separated by an intimal flap.
• Intramural haematoma (IMH) — a haemorrhage within the media with no intimal flap, thought to arise from rupture of the vasa vasorum. It is the second commonest AAS lesion after dissection, sits in the descending aorta in 60 percent, the ascending in 30 percent and the arch in 10 percent, and behaves like dissection when it is ascending.^[13][3]
• Penetrating aortic ulcer (PAU) — an atherosclerotic plaque ulcerates through the internal elastic lamina into the media; typically descending, in older, heavily atherosclerotic, hypertensive patients.^[1]

Chronicity is a number rule, not a judgement. On the 2020 SVS/STS reporting standards carried by the 2022 ACC/AHA guideline: hyperacute is under 24 hours, acute is 1 to 14 days, subacute is 15 to 90 days, chronic is over 90 days. The acute window is the surgical clock — untreated ascending dissection kills at 1 to 2 percent per hour from symptom onset, and in IRAD the mortality of type A managed medically stayed at 57 percent across 17 years while surgical mortality fell from 25 to 18 percent.^[3][2]

The epidemiology is brutal and brief. In IRAD's 17-year registry (n=4428, type A 2952 vs type B 1476 — type A exactly twice as common), type A in-hospital mortality fell from 31 percent to 22 percent and type A surgical mortality from 25 to 18 percent, while type B in-hospital mortality did not improve (12 to 14 percent). Pooled IRAD type B mortality is 13 percent overall — 9.6 percent with medical therapy, 6.5 percent after endovascular repair and 32.1 percent after open repair, which is case-mix, not a reason to operate. Women are significantly older at presentation, present later, and after adjustment for age and hypertension die more often than men (OR 1.4); type A surgical mortality in women was 32 percent versus 22 percent.^[2][3][18]

Stanford — the line that decides the whole operation

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A = ascending = theatre; B = beyond the subclavian = medical. That single sentence is the Stanford system, and it is the operative decision the surgeon is asking you to have already made when you phone.^[1]

• Stanford type A — any dissection involving the ascending aorta, with or without arch or descending extension. Surgical emergency.
• Stanford type B — confined to the descending aorta, distal to the left subclavian artery, ascending spared. Medical impulse-control; TEVAR for the complicated.^[1]

DeBakey is the anatomic description that examiners pair with Stanford: type I originates in the ascending aorta and propagates into the arch and descending; type II is confined to the ascending; type III originates distal to the left subclavian and runs distally (IIIa supradiaphragmatic, IIIb below the diaphragm). The shorthand: DeBakey I and II equal Stanford A; DeBakey III equals Stanford B.^[1]

The one-line discriminator: if the ascending aorta is involved, it is type A and it goes to theatre — no matter how far distally the flap has run. Everything else is type B and starts on a beta-blocker.^[1]

IMH and PAU borrow the same line. Ascending IMH behaves like type A — many centres operate, especially with a pericardial effusion, an aorta over 50 mm, or an intimal tear on TEE. Descending IMH and PAU behave like type B — medical, with TEVAR for persistent pain, expansion, or rupture.^[1]

Penn classification layers preoperative malperfusion onto type A for operative risk, and its classes are Aa (no ischaemia), Ab (local ischaemia — branch malperfusion), Ac (generalised ischaemia — circulatory collapse) and Abc (both). There is no "Ad". In Penn's own 1,192-patient, 25-year series, 30-day mortality rose from 5 percent in class A to 35 percent in class B-C, with adjusted odds ratios of 2.43 (B), 3.39 (C) and 13.08 (B-C) against class A.^[19]

ADD-RS plus D-dimer is the emergency-department rule-out. The aortic-dissection detection risk score sums high-risk conditions, pain features and exam findings (0 to 3). In the prospective ADvISED study (n=1850, 13 percent had AAS), ADD-RS 0 with a D-dimer under 500 ng/mL left 1 AAS in 294 patients — a failure rate of 0.3 percent (NPV about 99.7 percent) at an efficiency of 15.9 percent; widening to ADD-RS ≤1 with a negative D-dimer kept the same 0.3 percent failure rate while ruling out half the cohort. D-dimer alone is a rule-out only: pooled sensitivity 98 percent but specificity just 42 percent, giving a post-test probability of 0.3 percent in an AHA-defined low-risk population.^[17][4]

Why the wall fails — Laplace, dP/dt and the three openings

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Two physical variables decide whether the wall holds: tensile stress and the rate of pressure rise. Wall tension follows Laplace — stress equals pressure times radius over wall thickness — so a dilated, hypertensive aorta is under the most stress. The rate of rise of pressure (dP/dt) in systole is the hammer that drives the flap forward, which is precisely why we blunt it with a beta-blocker before we touch the pressure.^[1]

There are three ways in, one way the wall is weak.^[1]

• An intimal tear — pulsatile blood enters the media and propagates longitudinally. The tear sits where shear is highest: the right lateral ascending aorta near the sinotubular junction, or the aortic isthmus just distal to the left subclavian (the fixed-mobile junction sheared in deceleration trauma). No identifiable tear points to IMH.
• Vasa vasorum rupture — a localised intramural haemorrhage with secondary inflammatory weakening; this is IMH.
• Plaque ulceration — an atherosclerotic plaque erodes through the internal elastic lamina into the media; this is PAU.^[1]

Wall weakness has three faces, and one name to drop in a viva. Cystic medial degeneration (Erdheim) — loss of smooth muscle, elastic-fibre fragmentation, basophilic ground substance — is the dominant lesion in Marfan, Loeys-Dietz and the ageing hypertensive aorta. Atherosclerotic medial extension drives PAU; inflammatory destruction (Takayasu, giant-cell, syphilitic aortitis) is the third.^[1]

Malperfusion is the same flap, pointing at different branches. The intimal flap can obstruct any vessel it reaches — the coronary ostium (classically the RCA, an inferior STEMI), arch vessels (stroke, arm ischaemia), coeliac, SMA and IMA (mesenteric ischaemia, often painless with a rising lactate, and the worst of all complications — mortality 63 percent, and 95 percent in the IRAD patients left untreated), renal arteries (acute kidney injury, refractory hypertension), iliac and femoral arteries (the cold leg — the 6 Ps), and intercostal and lumbar arteries (paraplegia). Retrograde extension into the root distorts the valve — an aortic regurgitation murmur was documented in 31.6 percent of the original IRAD series — or ruptures into the pericardium as tamponade.^[1][3][12]

True versus false lumen decides who ischaemias. As the false lumen pressurises, the flap bows into the true lumen (dynamic obstruction), or seats across an ostium (static obstruction). A widely patent, pressure-equalised false lumen can be silent; a thrombosed false lumen pressing on a pressurised true lumen can ischaemie a kidney even when the dissection looks small.^[1]

The pain that names itself — and the bedside signs that betray it

The pain is sudden, severe, tearing or sharp, maximal at the first second, and it moves. In IRAD 93 percent of type A and 94 percent of type B report severe or worst-ever pain (chest pain in 83 and 71 percent respectively), and the profile is the discriminator from myocardial ischaemia, which crescendos. Patients clock the moment it began — "like a switch was thrown". IRAD's original series found sudden severe sharp pain the single commonest complaint — sharp, not tearing; a migrating pain that tracks the dissection line is the single most suggestive feature.^[2][12]

Location follows anatomy. Anterior chest pain points to an ascending tear; interscapular or back pain to the descending; abdominal, hip or leg pain means the flap has run distally. Syncope occurred in 13 percent (96 of 728) of IRAD patients and is the most ominous single feature — those with syncope died in hospital more often (34 versus 23 percent) and had far more tamponade (28 versus 8 percent) and stroke (18 versus 4 percent) — so it demands a bedside echo, not a faint work-up.^[24]

Run the bedside checklist in 60 seconds, every time.^[1]

• BP differential — over 20 mmHg between the arms, or between arm and leg, is the classic clue. Document the HIGHER arm BP as the titration target — the dissection may have taken the lower one offline.
• Pulse deficit — an absent or diminished carotid, brachial, radial or femoral pulse is specific for branch involvement; chart pulses serially.
• New aortic regurgitation murmur — a soft diastolic decrescendo at the left sternal border; acute severe AR may be surprisingly quiet.
• Neurological deficit — stroke (often right-sided, carotid malperfusion), paraplegia (intercostal loss), Horner syndrome at the isthmus.
• Tamponade physiology — Beck's triad of hypotension, raised JVP and muffled heart sounds with chest or back pain.^[1]

The 6 Ps name a malperfused limb in one breath: Pain, Pallor, Pulselessness, Paraesthesia, Paralysis, Perishing-cold. A pulseless cold leg beside tearing chest pain is a type B dissecting into the iliac axis until proven otherwise — call vascular and prepare for TEVAR.^[1]

The dissection-MI trap — check before you lyse

The single most dangerous misdiagnosis in emergency medicine is lysing a type A dissection that has malperfused a coronary ostium. Coronary-ostial involvement, usually the RCA, produces an abnormal ECG and troponin — sometimes a frank inferior STEMI — and the reflex to thrombolyse, anticoagulate or load antiplatelets then haemorrhages the dissection into the pericardium, mediastinum or pleura.^[1][3]

The classic trap: everyone reaches for the tenecteplase when the ECG shows inferior STEMI; the patient actually has a type A dissection with RCA-ostial malperfusion. Two bedside moves before lysis in any atypical ACS — bilateral arm BPs and a portable CXR for a widened mediastinum — catch most of these. CT aortogram before lysis is the correct reflex when the story does not fit.^[3]

Name the other killers in the chest-pain differential and one discriminator each.^[1]

• Pulmonary embolism — pleuritic, hypoxic, right-heart strain on echo; dissection radiates to the back with a BP differential.
• Tension pneumothorax — unilateral hyper-resonance and tracheal deviation; decompression reverses it. A left haemothorax in dissection is serosanguineous, not air.
• Acute pericarditis — pleuritic, relieved sitting forward, diffuse concave ST elevation with PR depression; beware the dissection-induced effusion that mimics it.
• Boerhaave syndrome — vomiting then pain, subcutaneous emphysema; Mackler triad. Contrast swallow confirms.
• Ruptured or symptomatic aortic aneurysm — CT aortogram from neck to pelvis; the thoracic dissection and the AAA can coexist.
• Acute pancreatitis, renal colic, mesenteric ischaemia — dissection malperfusing the coeliac axis or a renal artery can present as any of these; a rising lactate and refractory hypertension are the tell.^[1]

Imaging — CT for the stable, TEE for the crashing

The imaging choice is dictated by haemodynamics, not by which scanner is nearest. A stable patient gets a CT aortogram; a crashing patient gets a bedside TEE in theatre; the young, pregnant or renally impaired patient gets MRI.^[1][3]

Adjunct bloods support but never replace imaging. Troponin is often mildly raised from coronary malperfusion or shock — a raised troponin must not delay the scan. Creatinine plans the contrast; lactate tracks mesenteric and limb malperfusion. Genetic testing (FBN1, TGFBR1/2, SMAD3, COL3A1, ACTA2) is for the under-40s and the syndromic.^[1]

Rate before pressure — the anti-impulse ladder

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The order is fixed: rate, then pressure, then pain — never the other way round. Dropping the pressure before the rate unleashes reflex tachycardia that raises dP/dt and drives the flap forward. Begin all three within 15 minutes of a credible suspicion, before imaging, and run them in parallel with the surgical referral.^[1][3]

• Heart rate first — the 2022 ACC/AHA guideline makes an intravenous beta-blocker the initial treatment of every AAS unless contraindicated, targeting 60 to 80 bpm with an SBP under 120 mmHg, and a non-dihydropyridine calcium-channel blocker (verapamil or diltiazem) the alternative when beta-blockade is contraindicated or not tolerated. Bedside teaching and StatPearls run a tighter pair — about 60 bpm and an SBP of 100 to 120 mmHg — and either is defensible in a viva provided you say "or the lowest pressure that preserves end-organ perfusion". Beta-blockade needs caution in acute aortic regurgitation, where the compensatory tachycardia is doing useful work, and in heart block or bradycardia. A 40-patient emergency-department series shows how hard the tighter target is: on esmolol, 82.5 percent reached 80 bpm or less within the first hour but only 27.5 percent reached 60 bpm or less.^[3][26][5]
• Blood pressure second — intravenous vasodilators are added after the beta-blocker (never before it, because of compensatory tachycardia) to reach an SBP under 120 mmHg or the lowest pressure preserving end-organ perfusion; watch for hypotension, defined operationally as systolic under 90 mmHg or MAP of 60 mmHg or less, which complicated 12.5 percent of esmolol-treated patients in the first three hours.^[3][6][5]
• Analgesia alongside — pain itself raises heart rate and blood pressure, and intravenous opiates are the agents of choice; intravenous NSAIDs such as ketorolac are less suitable because they can raise blood pressure and harm the kidney. Once the diagnosis is made, blood-pressure control, analgesia and urgent surgery or transfer with minimal delay are the emergency-department priorities.^[3][14]

The drug ladder, agent by agent.^[5][7]

• Intravenous esmolol — the first-line beta-blocker for rate control; ultra-short-acting and given as a titratable continuous infusion, so it can be withdrawn quickly if the pressure collapses or the diagnosis changes.^[5][15]
• Intravenous labetalol — an alternative continuous-infusion regimen for type B dissection; in a direct comparison, high-dose labetalol infusion produced numerically more hemodynamic instability than an esmolol-combination regimen (50 versus 32 percent, difference not statistically significant), all episodes being hypotension.^[7]
• A vasodilator added only after the beta-blocker — intravenous vasodilators are adjuncts to beta-blockade to reach the blood-pressure goal: sodium nitroprusside is the classical partner to esmolol, and clevidipine achieved similar blood-pressure control at significantly lower cost in a head-to-head chart review.^[6][15]
• Intravenous opioid analgesia — for pain, which itself drives tachycardia and hypertension.^[14]

Surgery for A, impulse-control for B

Type A is an open operation; type B is medical unless it is complicated. That fork is the whole definitive-management question, and it is settled on the CT within minutes of arrival.^[1]

The elective surgery thresholds are the other half of the question. On the 2022 ACC/AHA guideline, operate on an asymptomatic aortic root or ascending aorta at 5.5 cm in sporadic disease and in bicuspid aortic valve, at 5.0 cm in Marfan syndrome, non-syndromic heritable thoracic aortic disease or a family history of dissection, and — in Loeys-Dietz — at 4.5 cm for TGFBR1, TGFBR2 and SMAD3, dropping to 4.0 cm when high-risk features are present. Growth of 0.5 cm in a year, or 0.3 cm a year for two consecutive years, is itself an indication.^[3]

TEVAR numbers to quote in a viva. Thoracic endovascular repair closes the entry tear, depressurises the false lumen and restores true-lumen flow. In IRAD type B, in-hospital mortality was 6.5 percent after endovascular repair against 32.1 percent after open repair, and a meta-analysis of 18 studies (12,789 patients) found TEVAR roughly halved 30-day/in-hospital mortality versus open surgery (OR 0.54, 95% CI 0.43–0.68) and reduced long-term death versus medical therapy alone (OR 0.46) — but at the cost of more paraplegia or paraparesis than medical therapy, so the cord is the trade, not a freebie. Insert a cerebrospinal fluid drain for extensive descending coverage or previous infrarenal aneurysm repair.^[3][23]

Complications arrive on a clock — learn the timing.^[1]

Named traps and preventable deaths

Three named traps account for most of the preventable mortality in this disease. Each is a way a patient with a salvageable dissection dies from a missed diagnosis or the wrong sequence of treatment.^[14][6]

• The missed-diagnosis and lysis trap — acute aortic dissection is often misdiagnosed because of atypical presentations; clinicians miss it because it is not considered in the differential of chest, back and abdominal pain, and lysing what is actually a dissection is the catastrophic end of that miss. Consider dissection before thrombolysing atypical chest pain.^[14]
• The cocaine trap — cocaine-related dissection strikes predominantly young men (mean age about 41 years, 88.9 percent male) and in a 45-case analysis 75 percent were Stanford type A — the opposite of the benign-type-B assumption — with an in-hospital mortality of 21.4 percent and a further 11.9 percent dead before arrival.^[10]
• The vasodilator-before-rate trap — beta-blockers are first-line and vasodilators are added to them, not substituted for them; inverting the order removes the protection against reflex tachycardia and further propagation. Rate, then pressure.^[7][6]

Two more errors worth naming. Do not chase a falsely low BP with IV fluids in tamponade from dissection — resuscitate as for obstructive shock and go to theatre. And in cardiac arrest with known dissection, chest compressions are likely ineffective and may extend the tear; survival is anecdotal.^[1]

The situations that bend the algorithm

Connective-tissue disease dissects younger, smaller, and more aggressively. Marfan (FBN1) is the archetypal type A of the young; operate at a root of 5.0 cm, or at 4.5 cm with features raising dissection risk (family history of dissection, growth ≥0.3 cm/y, diffuse root and ascending dilation, marked vertebral tortuosity) — and roughly 20 percent of large Marfan series are operated below 5.0 cm. In Loeys-Dietz the threshold is variant-specific: 4.5 cm for TGFBR1, TGFBR2 and SMAD3 without high-risk features, 4.0 cm with them, and 5.0 cm for TGFB3. Vascular Ehlers-Danlos (COL3A1) makes every artery fragile and surgery treacherous.^[3]

Bicuspid aortic valve raises dissection risk about eight-fold. In the Olmsted County cohort (416 patients, 6,530 patient-years) dissection incidence was 3.1 per 10,000 patient-years — age-adjusted relative risk 8.4 (95% CI 2.1–33.5) against the general population, rising to 17.4 per 10,000 patient-years in those aged 50 or more and 44.9 in those with a baseline aneurysm; the 25-year rate of aortic surgery was 25 percent. Operate at 5.5 cm, or at 5.0 to 5.4 cm with an additional dissection risk factor (family history of dissection, growth ≥0.3 cm/y), and at 4.5 cm if the patient is already having valve surgery.^[20][3]

Pregnancy-related dissection is rare, aortopathic, and often the first sign of the aortopathy. In IRAD it was 0.3 percent of all dissections and 1 percent of dissections in women, but 19 percent (20 of 105) of dissections in women under 35; of 29 cases, 45 percent were type A and 55 percent type B, onset clustered in the third trimester and the postpartum period (mean 12.5 days; the cohort covers up to 12 weeks), 69 percent had an aortopathy or positive family history — Marfan in most — and in 47 percent the aortopathy was unrecognised until the dissection. Type A came with a dilated aorta (mean ascending 54.7 mm); type B usually did not (mean descending 32.5 mm). Run a multidisciplinary delivery decision: type A before 26 weeks goes to emergency aortic surgery accepting fetal risk, while after about 28 weeks Caesarean followed by aortic repair gives the best joint survival. Beta-blockade runs throughout pregnancy and postpartum; calcium-channel blockers are generally avoided in Marfan syndrome, and ACE inhibitors and ARBs are contraindicated. Risk is low with a root under 4.0 cm and much higher above 4.5 cm — 4.0 to 4.5 cm is a shared decision, not a green light.^[21][3]

Cocaine-related dissection strikes young men, and it is usually type A, not type B. In a 45-case analysis (11 institutional plus 34 published cases), patients were young (mean age 41.3 years) and overwhelmingly male (88.9 percent); 75 percent were Stanford type A, symptoms began within a median of one hour of last use, and in-hospital mortality was 21.4 percent with a further 11.9 percent dying before reaching hospital. Ask every young hypertensive dissection patient about stimulant use.^[10]

Trauma, iatrogenic injury and the elderly close the list. Deceleration shears the aortic isthmus — the commonest site of blunt thoracic aortic injury, because it is the transition from mobile arch to fixed descending aorta; the ascending aorta (8 to 27 percent), arch (8 to 18 percent) and distal descending aorta (11 to 21 percent) account for the rest. TEVAR is first-line in the stable patient. Catheter-induced dissection during angiography or TAVR may be sealed with a covered stent in the lab. The elderly present atypically — in IRAD, patients aged 70 or more had fewer typical symptoms and signs, more hypotension (46 versus 32 percent) and higher in-hospital mortality (43 versus 28 percent), with age ≥70 an independent predictor of death — yet surgery still benefits selected patients.^[3][25]

Prognosis, disposition and lifelong surveillance

Type A lives or dies on the speed of the operation. Untreated ascending dissection kills at 1 to 2 percent per hour, and IRAD's medically managed type A mortality stayed at 57 percent while surgical mortality fell to 18 percent; the highest mortality falls on those operated 8 to 12 hours after diagnosis. Operator and centre volume move the number as much as physiology does — 10 versus 26 percent for an aortic specialist against a non-specialist, and 14 versus 24 percent for high- against low-volume surgeons. Ten-year survival after type A repair is 60 to 65 percent. Prognosis worsens with tamponade, shock, stroke and malperfusion (Penn Ab, Ac and Abc).^[3][2][19]

Type B does well when it stays uncomplicated and badly when it malperfuses. Uncomplicated medically managed type B has a 30-day mortality of 10 percent, but 20 to 50 percent develop delayed aortic expansion within 4 years, and INSTEAD-XL showed prophylactic TEVAR improved 5-year aorta-specific survival and delayed disease progression. Complicated type B on medical therapy alone reaches 20 percent mortality by day 2 and 25 percent by day 30; endovascular repair in IRAD carried 6.5 percent in-hospital mortality against 32.1 percent for open repair.^[3][9]

Disposition follows the fork: type A to the cardiac surgical theatre (transfer on impulse-control if aortic surgery is not on site), uncomplicated type B to HDU or ICU, complicated type B to the TEVAR suite or hybrid theatre. Every survivor enters a lifelong surveillance programme.^[1]

• Imaging — guideline-directed surveillance after repair is a CT or MRI scan at 6 and 12 months, then annually thereafter; in a population-based audit only 14 percent of survivors received it throughout follow-up, while mortality reached 14 percent at 5 years and 29 percent at 10 years, with aortic reintervention in 9 and 17 percent respectively.^[11]
• Blood pressure and remodelling — aggressive medical therapy to achieve optimal heart rate and blood-pressure control remains the gold standard for uncomplicated type B, but a significant proportion develop late aorta-related complications such as aneurysmal degeneration — the reason control and surveillance are lifelong.^[9]
• Family screening — contemporary guidelines span diagnosis, genetic evaluation and family screening, medical therapy, endovascular and surgical treatment, and long-term surveillance.^[3]

Evidence and regional practice

Two guidelines and one registry frame the entire topic.^[1][3]

The 2022 ACC/AHA aortic-disease guideline (Isselbacher et al.) is the dominant North American reference, superseding its 2010 predecessor, and the 2014 ESC guideline (Erbel et al.) is the European counterpart — both converge on anti-impulse therapy before definitive management, immediate surgery for type A, beta-blockade in connective-tissue aortic ectasia, and first-degree-relative screening.^[1][3]

Exam pearls — the mantra and the memory hooks

The mantra for the whole topic: rate before pressure, surgery for A, impulse-control for B. If you remember nothing else, remember that one line and the three named traps, and you will pass the stem.^[1][3]

• AAS = dissection + IMH + PAU — one umbrella, three related pathologies; initial management focuses on control of blood pressure to reduce aortic wall stress.^[13]
• Stanford A = ascending = theatre; Stanford B = descending = medical unless complicated. Type B without ascending involvement is treated medically unless fatal complications develop, for which TEVAR is the guideline recommendation.^[8]
• Pain = sudden, severe, maximal at onset — 93 to 94 percent report severe or worst-ever pain, but classic signs are often absent: aortic regurgitation in only 31.6 percent and a pulse deficit in 15.1 percent in the original IRAD series, so a high index of suspicion is mandatory.^[2][12]
• Bedside and imaging: suspect, then scan the whole aorta — CT was the initial imaging modality in 61 percent of IRAD patients, and its use for type A rose from 46 to 73 percent over 17 registry years.^[12][2]
• Anti-impulse before imaging if suspicion is credible: an intravenous beta-blocker (esmolol) to 60 to 80 bpm first, then a vasodilator added to bring the SBP under 120 mmHg, with an intravenous opiate alongside.^[3][5]
• Type A options: urgent open repair — surgical management for type A rose from 79 to 90 percent over 17 IRAD years, with in-hospital mortality falling from 31 to 22 percent.^[2]
• Type B: medical therapy is the mainstay; TEVAR for the complicated — endovascular management of type B rose from 7 to 31 percent over the same period, with no significant mortality trend (12 to 14 percent).^[2][8]
• Surveillance: CT or MRI at 6 and 12 months, then annually. Adherence is poor in practice — only 14 percent of repaired type A survivors received guideline-directed imaging throughout follow-up — while late mortality and reintervention remain substantial.^[11]

Ward-round test