Aortic dissection

Contents

Overview

Aortic dissection occurs when a tear in the intimal layer allows blood to enter and propagate through the media, creating a false lumen. It is a life-threatening emergency with an untreated mortality in type A dissection of approximately 1–2% per hour in the first 48 hours. Early diagnosis and appropriate management — surgical for type A, medical for uncomplicated type B — are critical.

Classification

The Stanford classification is the most clinically useful:

Type A: Involves the ascending aorta, regardless of the site of the primary tear. Requires emergency surgical repair.

Type B: Confined to the descending aorta, distal to the left subclavian artery. Managed medically unless complicated.

The DeBakey classification is older and less commonly used:

  • Type I: ascending and descending
  • Type II: ascending only
  • Type III: descending only (equivalent to Stanford B)

Acute dissection: within 14 days of onset. Chronic: beyond 14 days. Acute type A carries the highest immediate mortality.

Pathophysiology

A primary intimal tear allows high-pressure aortic blood to enter the media, propagating an intramural haematoma along the plane of the media. The dissection can extend proximally (towards the heart) or distally. The false lumen may compress the true lumen, reducing perfusion to any vessel arising from the affected segment.

Predisposing factors include:

  • Hypertension (the most common risk factor, present in 70–80%)
  • Connective tissue disorders: Marfan syndrome (FBN1 mutation → fibrillin-1 deficiency → cystic medial necrosis), Ehlers-Danlos syndrome (EDS type IV)
  • Bicuspid aortic valve (associated with aortopathy)
  • Turner syndrome
  • Inflammatory aortitis (Takayasu, giant cell arteritis)
  • Iatrogenic (cardiac catheterisation, cardiac surgery, IABP)
  • Cocaine use (acute hypertensive surge)

The classic anatomical substrate is cystic medial necrosis — degeneration of elastic fibres and smooth muscle in the media, reducing aortic wall tensile strength.

Clinical Features

The hallmark presentation is sudden-onset severe chest or back pain, often described as tearing or ripping and maximal at onset. Pain may radiate to the jaw, neck, arms, or abdomen depending on dissection extent.

Key clinical features to elicit:

  • Pain character and radiation: anterior chest pain suggests type A; interscapular pain suggests descending aorta involvement
  • Pulse deficits: unequal arm blood pressures (>20 mmHg difference), absent peripheral pulses — from involvement of subclavian, iliac, or femoral arteries
  • Aortic regurgitation murmur: from involvement of the aortic root (type A)
  • Neurological deficits: from carotid or intercostal artery involvement (stroke, spinal cord ischaemia — paraplegia)
  • Haemodynamic instability: cardiac tamponade (type A dissection extending into the pericardium), severe AR, or haemothorax

The presentation is notoriously variable. Syncope at onset suggests tamponade or carotid involvement. A minority of patients present with painless dissection, particularly those with neurological features.

Investigations

CT aortogram is the investigation of choice in haemodynamically stable patients. CT with IV contrast, with ECG-gating if available, identifies the extent of dissection, the entry tear, false lumen, and involvement of branch vessels. Sensitivity exceeds 95%.

CXR: Widened mediastinum (>8 cm) in 60–90% of cases, but a normal CXR does not exclude dissection.

ECG: Usually normal or shows non-specific changes. ST elevation may occur if the dissection involves a coronary ostium (right more than left). ST changes and dissection must be distinguished before thrombolysis or PCI.

Echocardiography: TOE (transoesophageal echocardiography) has sensitivity approaching 98% for type A and is performed intraoperatively. TTE is useful for assessing the aortic root, pericardial effusion, and AR in the emergency setting. TTE has lower sensitivity than CT for dissection.

Bloods: FBC, coagulation, crossmatch (urgent), renal function, troponin (exclude MI; troponin also rises in dissection with coronary involvement), lactate (mesenteric ischaemia). D-dimer is elevated in dissection but is not specific.

MRI: Gold standard for chronic dissection imaging; not practical in the acute setting.

Management

Immediate

All patients require:

  • Adequate IV access (two large-bore cannulae)
  • Continuous monitoring: invasive arterial line in both arms if blood pressure differential is suspected
  • Analgesia: IV morphine or fentanyl for pain control (pain drives hypertension and tachycardia)
  • Blood pressure control: target systolic 100–120 mmHg, HR <60–70 bpm to reduce aortic wall stress

IV labetalol (combined alpha and beta blocker) is the agent of choice — reduces both heart rate and blood pressure simultaneously. IV esmolol (short-acting beta blocker) provides titratable rate control in the perioperative setting.

IV nitroprusside (vasodilator) may be added if BP target is not achieved with beta blockade alone. Never give a vasodilator without adequate beta blockade first — reflex tachycardia increases aortic wall stress.

Type A Dissection

Emergency surgical repair is the standard of care. The entry tear is resected, the false lumen obliterated, and the aorta reconstructed. The aortic root and valve may need replacement depending on degree of involvement.

Transfer to a cardiac surgical centre should not be delayed for further investigations once the diagnosis is established. In-transit haemodynamic support continues with beta blockade and analgesia. Cardiac tamponade from haemopericardium may require pericardiocentesis as a temporising measure if the patient is arresting — surgical repair remains the definitive treatment.

Type B Dissection

Uncomplicated type B dissection (no malperfusion, haemodynamic stability, pain controlled) is managed medically:

  • Strict BP and HR control as above
  • Surveillance CT at 48–72 hours, before discharge, and 1, 3, 6, and 12 months

Complicated type B dissection (defined by end-organ malperfusion, refractory pain, haemodynamic instability, or rapid aortic expansion) requires intervention:

  • Thoracic endovascular aortic repair (TEVAR): deployment of an endovascular stent graft to cover the primary tear, promoting false lumen thrombosis. Now the preferred intervention for complicated type B, with lower morbidity than open surgery.
  • Open surgery: reserved for failed TEVAR or anatomy unsuitable for endovascular repair.

Complications

  • Cardiac tamponade: type A dissection extending into the pericardium; may be the presenting feature
  • Acute aortic regurgitation: aortic root dilatation or leaflet prolapse; severe AR causes acute pulmonary oedema
  • Myocardial infarction: right coronary artery ostium involvement (type A)
  • Stroke: carotid artery involvement
  • Spinal cord ischaemia: intercostal and lumbar artery involvement → paraplegia; more common in type B and post-TEVAR
  • Mesenteric and renal ischaemia: true lumen compression
  • Limb ischaemia: iliac or femoral artery involvement

Viva Questions

How do you differentiate aortic dissection from STEMI in a patient presenting with chest pain?

The distinction is critical because thrombolysis given for a misdiagnosed dissection is potentially fatal. Features favouring dissection include sudden maximal-at-onset tearing or ripping pain, interscapular radiation, unequal blood pressures between arms (>20 mmHg), new aortic regurgitation murmur, pulse deficits, and neurological symptoms. The ECG in dissection is usually normal or shows non-specific changes, whereas STEMI shows regional ST elevation. A widened mediastinum on CXR raises suspicion for dissection. However, dissection can involve the right coronary ostium and produce inferior ST elevation — in any patient with anterior chest pain and ST changes, a brief risk assessment for dissection (examining pulse symmetry, BP in both arms, and CXR appearance) before PCI or thrombolysis is important. If dissection cannot be excluded, CT aortogram must precede any fibrinolytic therapy. When there is genuine diagnostic uncertainty, a senior cardiothoracic surgeon and interventional cardiologist should be involved simultaneously.

What is the acute management of a haemodynamically stable patient with type A aortic dissection?

The immediate priority is haemodynamic stabilisation before urgent transfer for surgical repair. Blood pressure should be reduced to a systolic of 100–120 mmHg and the heart rate to below 60–70 bpm to reduce aortic wall stress and minimise propagation of the dissection. IV labetalol is the preferred agent — its combined alpha and beta blockade reduces both heart rate and blood pressure simultaneously. If blood pressure remains above target despite beta blockade, IV nitroprusside can be added, but never before adequate rate control is established. Adequate analgesia with IV opioids is essential — pain drives sympathetic activation, worsening hypertension and tachycardia. Two large-bore IV cannulae, invasive arterial monitoring (right radial or femoral, depending on involvement of subclavian vessels), and blood products crossmatched. Urgent transfer to a cardiac surgical centre should not wait for further imaging once CT has confirmed the diagnosis. Any delay in transfer directly increases mortality.

What are the indications for intervention in type B aortic dissection?

Uncomplicated type B dissection — haemodynamically stable, pain controlled, and no evidence of end-organ malperfusion — is managed medically with blood pressure control and close surveillance. Intervention is required for complicated type B dissection, which is defined by: end-organ malperfusion (bowel ischaemia, renal failure, limb ischaemia, spinal cord ischaemia), refractory hypertension or pain despite optimal medical therapy, haemodynamic instability, haemothorax from aortic rupture, or rapid expansion of the aortic diameter on serial imaging. Thoracic endovascular aortic repair (TEVAR) is now the first-line intervention for complicated type B, covering the primary entry tear with a stent graft to redirect flow into the true lumen and promote false lumen thrombosis. TEVAR carries lower perioperative morbidity than open surgery for descending aortic disease, though spinal cord ischaemia remains a significant complication risk from intercostal artery coverage.