Aortic Dissection

A 60-year-old man with a history of long-standing hypertension presents with sudden onset severe chest pain described as tearing and ripping, radiating to the back between the scapulae. The pain reached maximum intensity at onset. He appears diaphoretic and anxious. Blood pressure is 180/100 mmHg in the right arm and 150/90 mmHg in the left arm. On examination, there is pulse asymmetry between the upper limbs. A chest X-ray shows widened mediastinum. Diagnosis?

Diagnosis is Aortic dissection.

1. Definition

Aortic dissection is a life-threatening condition characterized by a tear in the intimal layer of the aorta, allowing blood to enter between the intima and media, forming a false lumen that propagates proximally or distally, leading to compromised blood flow to vital organs.

2. Classification

2.1 Stanford Classification

  1. Type A – involves ascending aorta (proximal)
  2. Type B – involves descending aorta distal to left subclavian artery

2.2 DeBakey Classification

  1. Type I – ascending + arch + descending aorta
  2. Type II – ascending aorta only
  3. Type III – descending aorta only
    • IIIa – above diaphragm
    • IIIb – below diaphragm

3. Etiology / Risk Factors

  1. Hypertension (most common, ~70–75%)
  2. Sudden increase in blood pressure (e.g. cocaine, heavy lifting, stimulants)
  3. Connective tissue disorders
    • Marfan syndrome
    • Ehlers–Danlos syndrome
  4. Congenital conditions
    • Bicuspid aortic valve
    • Coarctation of aorta
  5. Preexisting aortic aneurysm
  6. Atherosclerosis
  7. Pregnancy (especially third trimester)
  8. Iatrogenic (cardiac surgery, catheterization)
  9. Family history

4. Pathophysiology

  1. Intimal tear → blood enters media → false lumen formation
  2. Dissection propagates anterograde (distal) or retrograde (proximal)
  3. Proximal (Type A) leads to:
    • Acute aortic regurgitation
    • Cardiac tamponade
    • Aortic rupture
  4. Distal (Type B) leads to:
    • Branch vessel occlusion → organ ischemia
  5. False lumen expansion compresses true lumen → malperfusion

5. Clinical Features

5.1 Core Features

  1. Chest pain – sudden onset, severe, tearing / ripping
  2. Pain reaches maximum intensity immediately
  3. Pain location:
    • Anterior chest → Type A
    • Back / interscapular → Type B
  4. Pain may migrate with progression

5.2 Associated Features

  1. Diaphoresis, nausea, vomiting
  2. Hypertension (common)
  3. Hypotension → suggests rupture or tamponade (poor prognosis)
  4. Pulse deficit / BP difference >20 mmHg between arms
  5. Neurological deficits (~20%)
  6. Syncope
  7. New early diastolic murmur → acute aortic regurgitation
  8. Dyspnea or hemoptysis (rupture)

6. Complications

  1. Aortic rupture (most fatal)
  2. Cardiac tamponade
  3. Acute aortic regurgitation
  4. Myocardial infarction (coronary involvement)
  5. Stroke (carotid involvement)
  6. Renal failure (renal artery involvement)
  7. Mesenteric ischemia
  8. Limb ischemia
  9. Multiorgan failure and death

7. Diagnosis

7.1 Initial Evaluation

  1. ECG – may show ischemia; can be normal
  2. Chest X-ray – widened mediastinum, pleural effusion
    • May be normal in up to 20%

7.2 Laboratory

  1. D-dimer elevated (sensitive, not specific)
  2. Troponin elevated if coronary involvement
  3. CBC → leukocytosis or anemia
  4. Renal function tests → renal ischemia
  5. Lactate elevated → tissue hypoperfusion

7.3 Definitive Imaging

  1. CT angiography (CTA) – first-line in stable patients
  2. Transesophageal echocardiography (TEE) – unstable patients
  3. MRI – highly accurate (used in stable or follow-up cases)
  4. Transthoracic echocardiography (TTE) – limited but useful for complications
  5. Aortography – rarely used now

8. Treatment

8.1 Initial Stabilization

  1. ICU monitoring (arterial line, IV access)
  2. Pain control → IV morphine
  3. Heart rate control → IV β-blockers (first-line)
    • Esmolol, labetalol
    • Target HR ≈ 60 bpm
  4. Blood pressure target: 100–120 mmHg systolic (maintain end-organ perfusion)
  5. Add vasodilator (nitroprusside or nicardipine) only after β-blocker

8.2 Type A Dissection

  1. Surgical emergency
  2. Requires urgent surgical repair
  3. Includes:
    • Excision of intimal tear
    • Aortic graft replacement
    • ± Aortic valve repair/replacement
  4. Untreated mortality ~50% within 48 hours

8.3 Type B Dissection

  1. Medical management (uncomplicated)
  2. Indications for intervention:
    • Malperfusion syndromes
    • Aortic rupture / impending rupture
    • Persistent pain or expansion
  3. Endovascular repair (TEVAR) preferred in complicated cases

9. Key Clinical Insight

Sudden severe “tearing” chest pain + radiation to back + pulse/BP asymmetry + widened mediastinum = aortic dissection → initiate emergent imaging (CTA) and immediate BP/HR control (IV β-blocker) → urgent surgical management for type A (ascending) dissections

10. Exam Level Pearls

  1. Tearing chest pain radiating to back = classic
  2. Pain maximal at onset
  3. Type A = surgery, Type B = medical management
  4. β-blocker FIRST, then vasodilator
  5. BP difference >20 mmHg = key diagnostic clue
  6. CTA = first-line imaging; TEE = unstable patients
  7. Hypotension = rupture/tamponade (poor prognosis)
  8. Most common risk factor is hypertension
  9. Always exclude before thrombolysis for MI
By Prabin Duwadee at

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