Cardiovascular emergencies

Aortic dissection

Overview and approach

Aortic dissection is an acute aortic syndrome caused by separation of wall layers; proximal involvement may need emergency surgery.

  • A tear in the inner layer of the aorta lets blood split the inner and middle layers. If blood goes through the outer wall it is often fatal.
  • Relatively uncommon; usually men in their 60s and 70s (about 2:1 male)2. Symptoms mimic other conditions, so diagnosis is often delayed, but early detection and treatment greatly improve survival.
  • Acute aortic syndromes include dissection (up to 80%), intramural haematoma and penetrating aortic ulcer, which sit on a continuum1,2.
  • How it starts: usually a transverse intimal tear, most often on the right lateral wall of the ascending aorta within about 10 cm of the valve, where shear stress is highest; the next most common site is the descending aorta just beyond the ligamentum arteriosum2,3. Less often, a vasa vasorum bleed forms a medial haematoma that then breaks through the intima2,4.
  • How it spreads: pulsatile flow drives blood along the elastic laminae, usually between the middle and outer thirds of the media, creating a false lumen. It mostly extends distally but can track back towards the aortic root2,3. Heavy atherosclerosis or medial scarring tends to stop it2,3.
  • A second, distal tear can let blood re-enter the true lumen ("double-barrelled aorta"). This can prevent fatal rupture, and the false channel may later line with endothelium as a chronic dissection3.
  • Where: ascending aorta about 65%, descending thoracic 20%, arch 10%, abdominal 5%4.
  • Stanford: Type A involves the ascending aorta, wherever the tear started (about two-thirds; more dangerous; mortality rises about 1-2% per hour in the first 48 hours). Type B spares the ascending aorta1,4. Location, not injury type, drives treatment1.
  • DeBakey: I = ascending and descending; II = ascending only; III = descending only. I and II are managed as Stanford A, which is why Stanford is used in practice2,3.
  • Timing: acute if symptoms began less than 2 weeks ago; chronic after that4.
  • Variants: intramural haematoma (bleeding into the wall with no intimal flap, mostly descending, can progress to dissection or rupture) and penetrating atherosclerotic ulcer (plaque erodes into the media, mid to distal descending aorta, in widespread atherosclerosis)2.
  • Why the wall fails: anything that weakens the media. In hypertension, the vasa vasorum thicken and the outer media becomes ischaemic, losing smooth muscle and organised matrix3. Cystic medial degeneration is the most common histological finding, but it is also seen in people who never dissect, and inflammation is typically absent3.
Assessment and clinical features

Abrupt severe chest/back pain, pulse/BP difference, neurological signs, aortic regurgitation and malperfusion; features may be incomplete.

  • Sudden severe chest or upper back pain, tearing or ripping, often with sweating, spreading to the neck or down the back; sudden severe abdominal pain; loss of consciousness; shortness of breath; stroke-like symptoms (vision change, speech difficulty, one-sided weakness); weak pulse in one arm or thigh; leg pain; difficulty walking2.
  • Pain site follows the dissection: anterior chest, neck or jaw suggests ascending aorta; interscapular back or abdomen suggests descending. The pain often moves as the dissection propagates1,2,4.
  • Ascending dissection may cause MI, aortic regurgitation (diastolic murmur), pericardial effusion or shock1.
  • Every feature maps to a mechanism2,4:
    • Rupture through the adventitia: tamponade, haemomediastinum, haemothorax (usually left).
    • Branch occlusion by the false lumen: carotid (stroke), coronary (MI, more often the right ostium, so inferior), spinal arteries (paraplegia), renal (AKI, haematuria, refractory hypertension), mesenteric (bowel ischaemia), subclavian or iliac (limb ischaemia, pulse deficit).
    • Aortic root distortion: aortic regurgitation.
    • Compression of nearby structures: Horner's syndrome (superior cervical ganglion), SVC syndrome, hoarseness, dysphagia, airway compromise.
  • Aortic regurgitation complicates more than half of proximal dissections, from root widening or a haematoma disrupting the annulus. Look for bounding pulses, wide pulse pressure, an early diastolic murmur along the right sternal border and heart failure2.
  • Blood pressure is often high: underlying hypertension, the sympathetic response to pain, or renal artery involvement driving renin release4. Hypotension suggests tamponade, rupture or severe aortic regurgitation2.
  • Painless presentations: cardiac ischaemia, syncope (9%), heart failure (7%), stroke (6%)1.
  • Chest pain plus neurology, or symptoms above and below the diaphragm, is dissection until proven otherwise1.
  • Useful signs: focal neurology, diastolic murmur, pulse deficit (up to 30%, can be fleeting); arm BP difference above 20 mmHg is significant1.
  • Risk factors: uncontrolled hypertension (present in about 70%), atherosclerosis, aortic aneurysm, bicuspid aortic valve, coarctation, Turner, Marfan, Ehlers-Danlos, Loeys-Dietz, giant cell arteritis or Takayasu arteritis, male sex, age 60+, cocaine, pregnancy (third trimester and peripartum), high-intensity weightlifting1,2,3. Also iatrogenic or traumatic (catheters, valve or aortic surgery)1,3.
  • Two typical patients: an older man with long-standing hypertension, or a younger adult with a connective tissue disorder such as Marfan syndrome3.
Differentials and investigations

Urgent senior assessment and definitive imaging selected by stability; ECG/troponin cannot safely exclude dissection.

  • Differentials: ACS, stroke, PE, pericarditis, aneurysm rupture, and other causes of acute chest or abdominal pain.
  • ECG is often normal (about 30% in Type A) and may show ischaemia; a dissection reaching a coronary ostium can cause a true STEMI, usually inferior1,2.
  • Chest X-ray is insensitive (sensitivity 65%, specificity 86%)1. Look for a widened superior mediastinum and a left pleural effusion. The effusion is often a reactive serosanguinous one and does not mean rupture unless there is hypotension and a falling haemoglobin2.
  • CT angiography is the gold standard (sensitivity above 95%); it shows the flap, the extent and branch involvement1,2.
  • Echo: transthoracic echo is quick but misses many (sensitivity 60-85%; better for the proximal ascending aorta). TOE is very accurate for the ascending and descending aorta (around 98% sensitivity) but has a blind spot at the arch, and is operator dependent. Both show aortic regurgitation and pericardial effusion1,2.
  • MRI is accurate but slow, so it suits stable patients and follow-up1,2. The best test depends on stability and local expertise2,4.
  • Bloods: FBC, UEC, LFT, troponin and cross-match1.
  • D-dimer: ADD-RS of 0 with D-dimer below 500 ng/mL ruled out dissection with a miss rate of about 1 in 1000 in a meta-analysis. Apply only to a low-risk population1.
Management and follow-up

Immediate cardiothoracic/vascular involvement, monitored analgesia and specialist-led haemodynamic control; treatment depends on anatomy and complications.

  • All dissections are surgical emergencies: discuss with cardiothoracic/vascular early1.
  • The aim is to stop the false lumen extending by lowering shear stress: both the pressure and the force and rate of each LV contraction (dP/dt)2,4.
  • Lower shear force: SBP below 120 mmHg and heart rate 60-80, with an arterial line, in ICU. If arm pressures differ, use the higher one. Labetalol or another beta-blocker (e.g. esmolol) is usually first; a calcium channel blocker is an alternative if beta-blockers are contraindicated; give vasodilators like GTN only after beta-blockade1,2.
  • Why rate control first: a vasodilator on its own causes reflex tachycardia and a stronger contraction, which raises shear stress and can extend the dissection2.
  • If the patient is hypotensive, think tamponade, rupture or acute aortic regurgitation rather than pushing rate control2.
  • Type A is managed surgically (mortality about 20% at 14 days with surgery versus about 50% without)1. Surgery removes the intimal flap, closes off the false lumen and places an interposition graft, with a composite valve-graft if the aortic valve is disrupted2.
  • Perioperative complications include MI, paraplegia, renal failure, tamponade, bleeding and sepsis2.
  • Uncomplicated Type B is managed medically. Complicated Type B (about 25%: progression, malperfusion, uncontrolled hypertension, ongoing pain or impending rupture) may need endovascular stenting1,2.
  • Long term: lifelong BP and heart-rate control (beta-blocker plus other antihypertensives), and serial CT or MRI to watch for extension or aneurysm, especially after Type B dissection or intramural haematoma2. Marfan syndrome carries a high risk of later complications2.
  • Prevention: control BP (home monitoring), stop smoking, maintain healthy weight with a low-salt diet and exercise, wear a seatbelt, and tell your doctor about family history, connective tissue disorder or bicuspid valve. If you have an aneurysm, ask how often monitoring and surgery are needed. People with genetic risk may need medicines even if BP is normal.
Red flags and clinical pearls

Dissection can mimic ACS or stroke. Avoid reflex antithrombotic/thrombolytic treatment when the history raises concern for dissection.

  • Complications: death from severe bleeding, organ damage (kidney failure, bowel ischaemia), stroke, aortic regurgitation, and rupture into the pericardium (tamponade).
  • The most common cause of death is rupture into the pericardium, pleura or peritoneum3.
  • Think of dissection in syncope or malperfusion syndromes1.
  • An inferior STEMI with chest pain radiating to the back, a new early diastolic murmur or unequal arm pressures: think dissection before giving antiplatelets or thrombolysis1,2.
  • Rapid recognition matters because mortality climbs hourly in Type A1.
  • Viva point: dissection is less likely in a heavily atherosclerotic aorta, because medial scarring stops the haematoma spreading3.
References
  1. Acute Aortic Syndrome, Emergency Medical Education (resus.com.au)
  2. Creager MA, Loscalzo J. Diseases of the aorta. In: Longo DL, et al., editors. Harrison's Principles of Internal Medicine. 18th ed. New York: McGraw-Hill; 2012. Chapter 248.
  3. Mitchell RN. Blood vessels. In: Kumar V, Abbas AK, Aster JC, editors. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Philadelphia: Elsevier; 2015. Chapter 11.
  4. Lilly LS, editor. Pathophysiology of Heart Disease. 5th ed. Philadelphia: Lippincott Williams & Wilkins; 2011. Chapter 15, Diseases of the peripheral vasculature.

Last updated from Sen’s notes on 21 October 2026.