Aortic dissection occurs when blood enters the medial layer of the aortic wall through a tear or penetrating ulcer in the intima and tracks along the media, forming a second blood-filled channel within the wall. 

As the separation of the layers of the media propagates, at least two channels form: the original lumen, which remains lined by the intima and which is called the true lumen, and the newly formed channel within the layers of the media, which is called the false lumen. The dissecting membrane separates the true and false lumens. Additional tears in the dissecting membrane that allow communication between the two channels are called reentry sites. Although the separation of layers primarily progresses distally along the length of the aorta, it can also proceed in a proximal direction; this process often is referred to as proximal extension or retrograde dissection.1

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Illustration of longitudinal sections of the aortic wall and lumen. Blood flows freely downstream in normal aortic tissue. In classic aortic dissection, blood entering the media through a tear creates a false channel in the wall. Intramural hematomas arise when hemorrhage from the vasa vasorum causes blood to collect within the media; the intima is intact. Penetrating aortic ulcers are deep atherosclerotic lesions that burrow into the aortic wall and allow blood to enter the media. In each of these conditions, the outer aortic wall is severely weakened and prone to rupture.

The extensive disruption of the aortic wall has severe anatomic consequences.

First, the outer wall of the false lumen is extremely thin, inflamed, and fragile, which makes it prone to expansion or rupture in the face of ongoing hemodynamic stress.

Second, the expanding false lumen can compress the true lumen and cause malperfusion syndrome by interfering with blood flow in the aorta or any of its branch vessels, including the coronary, carotid, intercostal, visceral, renal, and iliac arteries.

Finally, when the separation of layers occurs within the aortic root, the aortic valve commissures can become unhinged, which results in acute valvular regurgitation.

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Illustration of the potential anatomic consequences of aortic dissection, with a mapped diagram of affected regions (inset). A. Ascending aortic rupture and cardiac tamponade. B. Disruption of coronary blood flow. C. Injury to the aortic valve causing regurgitation. D, E, and F. Compromised blood flow to branch vessels, causing ischemic complications. (Images from Creager MA, Dzau VS, Loscalzo J, eds. Vascular Medicine. Philadelphia: WB Saunders; 2006. Copyright © Saunders/Elsevier, 2006. 

In most cases the vessel wall is abnormal with the following findings

Dissection vs. Aneurysm

The relationship between dissection and aneurysmal disease requires clarification. Dissection and aneurysm are separate entities, although they often coexist and are mutual risk factors. In most cases, dissection occurs in patients without aneurysms. The subsequent progressive dilatation of the weakened outer aortic wall results in an aneurysm. On the other hand, in patients with degenerative aneurysms, the ongoing deterioration of the aortic wall can lead to a superimposed dissection. The overused term dissecting aneurysm should be reserved for this specific situation.


For management purposes, aortic dissections are classified according to their location and chronicity. Improvements in imaging have increasingly revealed variants of aortic dissection that probably represent different forms along the ­spectrum of this condition.


To guide treatment, dissections are categorized according to their anatomic location and extent. The two traditional classification schemes that remain in common use are the DeBakey and the Stanford classification systems (Fig. 22-19).121,122

Illustration of the classification schemes for aortic dissection based on which portions of the aorta are involved. Dissection can be confined to the ascending aorta (left) or descending aorta (middle), or it can involve the entire aorta (right). (Reproduced with permission from Creager MA, Dzau VS, Loscalzo J, eds. Vascular Medicine. Philadelphia: WB Saunders; 2006. Copyright © Saunders/Elsevier, 2006, Fig. 35-2).

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 In their current forms, both of these schemes describe the segments of aorta that are involved in the dissection, rather than the site of the initial intimal tear. The main drawback of the Stanford classification system is that it does not distinguish between patients with isolated ascending aortic dissection and patients with dissection involving the entire aorta. Both types of patients would be classified as having type A dissections, despite the fact that their treatment, follow-up, and prognosis are substantially different.



Risk Factors



  1. Blood pressure control with beta blockers as they reduce both blood pressure and also heart rate hence reduce extra pressure on the aortic wall

  2. Guideline-based medical management of aortic dissection1
    Class Evidence
    European Society of Cardiology (2001)
       Immediate treatment
            Pain relief (morphine sulphate) I C
            Reduction of systolic blood pressure using beta-blockers (i.v. propranolol, metoprolol, esmolol or labetalol) I C
            Additional vasodilator for severe hypertension (i.v. sodium nitroprusside to titrate BP to 100-120 mmHg) I C
            For obstructive pulmonary disease, blood pressure lowering with calcium channel blockers II C
    Japanese Circulation Society (2006, revised 2011)
       Immediate treatment
            Medical treatment for uncomplicated type B cases (patent/thrombosed false lumen, ulcer-like projection) I C
            Medical treatment for cases resistant to anti-hypertensive treatment IIa C
       Chronic treatment
            Medical treatment if aortic diameter less than 50 mm and absence of rapid dilatation I C
            Exercise (e.g., cycling, running) should be kept to a blood pressure of less than 180 mmHg IIa C
            Beta-blockers should mainly be used for blood pressure treatment IIb C
            Target for systolic blood pressure is 130-135 mmHg IIb C
    American (AHA/ACC) guidelines 2010
       Initial management of thoracic aortic dissection
            Intravenous beta-blockade should be initiated and titrated to a target heart rate of <60 bpm I C
            Non-dihydropyridine calcium channel blocking agents as an alternative for rate control I C
            If systolic BP remains >120 mmHg after adequate heart rate control, angiotensin-converting enzyme inhibitors and/or other vasodilators should be administered to further reduce BP that maintains adequate end-organ perfusion I C
  3. Immediate surgical repair (for type A dissection or complicated type B dissection)
  4. Patients are often hypertensive

    Depending on the extent of dissection and occlusion of branches, end organ ischaemia may also be present (seen in up to 27% of cases) 5, including:

    • abdominal organ ischaemia
    • limb ischaemia
    • ischaemic or embolic stroke
    • paraplegia: involvement of artery of Adamkiewicz

    In some cases of aortic rupture, the involvement of coronary arteries may result in collapse and death. Symptoms of cardiac tamponade (Beck's triad) may also be seen.

    Angiography still is required for endoluminal repair.

    Risks of angiography include general risks of angiography plus the risk of catheterising the false lumen and causing aortic rupture.


    Aortic dissectionis the most common catastrophic event involving the aorta. The majority of aortic dissections are seen in elderly hypertensive patients.

    In a very small minority, and underlying connective tissue disorder may be present.

    Other conditions / predisposing factors are





    Complications of all types of aortic dissection include:

    • dissection and occlusion of branch vessels
      • abdominal organ ischaemia
      • limb ischaemia
      • ischaemic stroke
      • paraplegia: involvement of artery of Adamkiewicz
    • distal thromboembolism
    • aneurysmal dilatation: this is an indication for endovascular or surgical intervention 6
    • aortic rupture

    type A dissection may also result in:

    Although the combination of blood pressure control and surgical intervention has significantly lowered in hospital mortality, it remains significant, at 10-35%. Over the 10 years following diagnosis another 15-30% of patients require surgery for life-threatening complications 5.


    Content 3

    Content 11


    Content 1

    The true lumen of an aortic dissection is often...

    — correct!


    An essential part of the assessment of aortic dissection is identifying the true lumen, as the placement of an endoluminal stent graft in the false lumen can have dire consequences.

    The false lumen is often larger in size due to higher false luminal pressures, and, will often be of a lower contrast density due to the time delay in contrast opacification and relative size to the true lumen.


    Which of the following statements are FALSE, Stanford type A aortic dissections...

    — correct!


    Type A affects the ascending aorta and arch accounting for ~60% of aortic dissections. They require surgical management and may result in:



    The most appropriate first-line modality for the diagnosis of aortic dissections is...

    — correct!


    CT, especially with arterial contrast enhancement (CTA) is the investigation of choice, able not only to diagnose and classify the dissection but also evaluate for distal complications. It has reported sensitivity and specificity of nearly 100%.

    Conventional digital subtraction angiography has historically been the gold standard investigation. CTA has now replaced it as the first line investigation, not only due to it being non-invasive but also on account of better delineation of the poorly opacifying false lumen, intramural haematoma and end-organ ischaemia.

    However, angiography still is required for endoluminal repair.

    Aortic dissection can also be diagnosed on MRA and transoesophageal echocardiography. The diagnosis can only be suggested on plain radiographs with displacement of wall calfication medially. 


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