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Aortic Dissection

Clinical Subject Page

Aortic Dissection

ICD-10

I71.00

Specialty

Cardiology

Onset

Acute

Reviewed

June 2026

On This Page

Overview

Aortic dissection is a life-threatening condition in which an intimal tear allows blood to split the layers of the aortic wall, creating a false lumen that can impair organ perfusion or rupture.

Etiology & Risk Factors

    • Etiology

      • Chronic hypertension (most common)
      • Connective tissue disorders (Marfan, Ehlers-Danlos)
      • Bicuspid aortic valve
      • Aortic aneurysm
      • Atherosclerosis
      • Iatrogenic injury (catheterization, surgery)
      • Blunt chest trauma
      • Pregnancy (rare)

      Risk Factors

      • Male sex
      • Age >60 years
      • Long-standing hypertension
      • Smoking
      • Family history of aortic disease
      • Cocaine or stimulant use
      • Known thoracic aortic aneurysm

Pathophysiology

        • An aortic dissection occurs when a tear develops in the aortic intima, allowing blood to enter the wall of the aorta and separate its layers.

          Mechanism

          • A transverse tear in the intima (entry tear) occurs.
          • Blood enters the media of the aortic wall.
          • Blood dissects between the intima and media, creating a false lumen alongside the normal true lumen.
          • The hematoma spreads (propagates) along the length of the aorta.

          Consequences

          • Rising pressure in the aortic wall may cause aortic rupture.
          • The false lumen can compress or occlude branch arteries, causing ischemia of organs supplied by:
            • Coronary arteries → myocardial ischemia/infarction
            • Carotid arteries → stroke
            • Renal arteries → acute kidney injury
            • Mesenteric arteries → bowel ischemia
            • Lower limb arteries → limb ischemia
          • Sometimes a second intimal tear (re-entry tear) forms, allowing blood to flow back into the true lumen.

          Simple Flow

          Intimal tear → Blood enters the media → False lumen forms → Dissection spreads → Compression of branch vessels + risk of aortic rupture → Organ ischemia and life-threatening hemorrhage

Clinical Presentation

  1. Symptoms

    • Sudden severe tearing chest pain
    • Back or interscapular pain
    • Abdominal pain
    • Syncope
    • Dyspnea
    • Neurological deficits

    Signs

    • Blood pressure difference between arms
    • Pulse deficit
    • New early diastolic murmur (aortic regurgitation)
    • Hypotension or shock
    • Focal neurological deficits

History Taking

  • Key Questions

    • Sudden onset of pain?
    • Chest, back, or abdominal pain?
    • Pain migration?
    • Syncope?
    • Weakness or stroke symptoms?
    • History of hypertension?
    • Connective tissue disorder?
    • Cocaine use?
    • Previous aneurysm or aortic surgery?

    Red Flags

    • Sudden tearing pain
    • Hypotension
    • Neurological deficit
    • Pulse asymmetry
    • Signs of cardiac tamponade

Act Immediately

Aortic Dissection · Immediate Management

AORTIC DISSECTION = SURGICAL EMERGENCY — ACT IMMEDIATELY Tear in the aortic intima allows blood into the media, creating a false lumen that can propagate, rupture, or occlude branch vessels. Untreated Type A dissection has a mortality of ~1–2% per hour in the first 24–48 hours — suspicion must trigger immediate action, not deliberation.
Immediate Management Algorithm
1
Suspect & Stabilise
Sudden severe tearing/ripping chest or back pain, often migrating. High-flow O2, 2x large-bore IV access, continuous monitoring, analgesia (IV opioids).
0–10 minutes
2
Confirm Diagnosis
CT aortogram with contrast = investigation of choice (fast, widely available). TEE if unstable/can't transport. Check BP in BOTH arms — discrepancy >20 mmHg is suggestive.
<30 minutes
3
Heart Rate Control FIRST
IV Beta-blocker (esmolol or labetalol) — target HR <60 bpm. Must precede vasodilators to prevent reflex tachycardia worsening aortic shear stress.
Immediately after diagnosis
4
BP Control
Add IV vasodilator (nitroprusside or nicardipine) once HR controlled. Target SBP 100–120 mmHg within 20 minutes. Maintain adequate end-organ perfusion.
Within 20 minutes
5
Definitive Management
Type A — emergency cardiothoracic surgery. Type B (uncomplicated) — medical management; TEVAR/surgery if complicated (malperfusion, rupture, refractory pain/HTN).
Urgent referral
Stanford Type A
InvolvesAscending aorta (± arch, ± descending). DeBakey I/II.
RiskCardiac tamponade, acute aortic regurgitation, coronary occlusion (MI), stroke.
ManagementEmergency surgery — mortality without surgery ~1–2%/hour in first 48h.
VS
Stanford Type B
InvolvesDescending aorta only, distal to left subclavian artery. DeBakey III.
RiskRenal/mesenteric/limb malperfusion, rupture (less common than Type A).
ManagementMedical management first-line if uncomplicated; TEVAR/surgery if complicated.
Drug Dose / Target Role / Notes
Esmolol 500 mcg/kg load, then 50–200 mcg/kg/min infusion Ultra-short-acting cardioselective beta-blocker; first-line for rapid, titratable HR control.
Labetalol 20 mg IV bolus, then infusion 1–2 mg/min Combined alpha/beta blockade — controls both HR and BP; useful alternative/adjunct to esmolol.
Sodium Nitroprusside 0.3–0.5 mcg/kg/min, titrate to SBP 100–120 Potent arterial/venous vasodilator. Only after adequate beta-blockade to avoid reflex tachycardia.
Nicardipine 5 mg/hr, titrate up to 15 mg/hr Alternative vasodilator to nitroprusside; avoids cyanide toxicity risk, easier to titrate.
IV Opioid Analgesia Morphine/Fentanyl titrated Pain itself raises catecholamines/HR/BP — adequate analgesia supports haemodynamic control.
Clinical Features to Trigger Suspicion
Pain — sudden, severe, "tearing/ripping," maximal at onset, may migrate as dissection extends
BP discrepancy — >20 mmHg difference between arms; pulse deficit
New aortic regurgitation murmur — suggests proximal (Type A) involvement
Neurological deficits — carotid involvement; syncope (tamponade)
Risk factors — hypertension, connective tissue disease (Marfan, Ehlers-Danlos), bicuspid aortic valve, cocaine use, prior cardiac surgery, pregnancy
CXR — widened mediastinum (insensitive; normal CXR does not exclude diagnosis)
Key Pitfalls
Never give vasodilator before beta-blocker — unopposed vasodilation causes reflex tachycardia and worsens shear stress
Avoid thrombolysis — if dissection misdiagnosed as ACS/STEMI, thrombolytics are catastrophic
Don't delay imaging for normal CXR/ECG — both can be normal in true dissection
Watch for tamponade — muffled heart sounds, raised JVP, hypotension (Beck's triad) in Type A
Time-critical referral — involve cardiothoracic surgery early for any suspected Type A, even before imaging completes if unstable

Investigations

  • Laboratory
    CBC
    Renal function
    Troponin
    D-dimer (may support exclusion in low-risk patients)
    ECG
    Often normal or nonspecific
    May show ischemic changes
  • Imaging
    CT angiography (first-line in stable patients)
    Transesophageal echocardiography (unstable patients)
    MRI angiography (stable patients)
  • Chest X-ray
    Widened mediastinum
    Pleural effusion

Diagnosis

  • Clinical suspicion
  • CT angiography (preferred)
  • TEE or MRI when appropriate
  • Classification using Stanford (A/B) or DeBakey systems
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Management

      • Initial Medical Therapy

        • ICU admission
        • IV β-blocker (Esmolol or Labetalol)
        • Target HR <60 bpm
        • IV vasodilator (Nicardipine/Nitroprusside) after β-blockade
        • Adequate pain control (IV opioids)

        Definitive Treatment

        • Stanford Type A: Emergency surgical repair
        • Stanford Type B: Medical management unless complications develop; TEVAR for complicated cases

Complications

      • Aortic rupture
      • Cardiac tamponade
      • Acute aortic regurgitation
      • Myocardial infarction
      • Stroke
      • Acute kidney injury
      • Mesenteric ischemia
      • Limb ischemia
      • Death

Prognosis

  • Untreated Stanford type A dissection has a very high mortality.
  • Early diagnosis and prompt treatment significantly improve survival.
  • Long-term follow-up with strict blood pressure control is essential.

Key Points / Clinical Pearls

  • Hypertension is the most common risk factor.
  • CT angiography is the diagnostic test of choice in stable patients.
  • Lower heart rate before lowering blood pressure.
  • Stanford Type A = Surgery; Type B = Usually medical management.
  • Sudden tearing chest or back pain is the classic presentation.