Practice Easily Missed?

Acute aortic dissection

BMJ 2011; 343 doi: (Published 29 July 2011) Cite this as: BMJ 2011;343:d4487
  1. Aaron M Ranasinghe, Walport clinical lecturer 1, lecturer2,
  2. Daniel Strong, clinical fellow3,
  3. Barry Boland, consultant in emergency medicine4,
  4. Robert S Bonser, consultant cardiac surgeon1, honorary professor2
  1. 1Department of Cardiac Surgery, Queen Elizabeth Hospital, University Hospitals Birmingham NHS Foundation Trust, Birmingham B15 2TH, UK
  2. 2School of Clinical and Experimental Medicine, University of Birmingham, Birmingham B15 2TT
  3. 3New Cross Hospital, Royal Wolverhampton Hospitals NHS Trust, Wolverhampton WV10 0QP, UK
  4. 4Emergency Department, Queen Elizabeth Hospital, University Hospitals Birmingham NHS Foundation Trust, Birmingham B15 2TH
  1. Correspondence to: R S Bonser robert.bonser{at}
  • Accepted 20 June 2011

Acute aortic dissection is caused by an aortic intimal tear with propagation of a false channel in the media. Depending on the site and extent of the tear, it may cause chest, back, or abdominal pain, or collapse caused by rupture or malperfusion (transient or persistent ischaemia of any organ as a result of arterial branch obstruction). It is anatomically categorised according to involvement of the ascending aorta (type A, DeBakey type I/II) (fig 1); the categorisation dictates management.

Fig 1 The two most common classifications of aortic dissection. The Stanford classification divides dissections into type A (involving the ascending aorta) and type B (no ascending involvement). The DeBakey classification subdivides Stanford type A into ascending and descending (type I) and ascending alone (type II). DeBakey type III is equivalent to Stanford type B. Stanford type A (DeBakey types I and II) dissection requires surgery, whereas most Stanford type B dissection is treated medically. DeBakey type I dissection has the greatest propensity for malperfusion. Neither classification reports the site of the intimal tear, and some dissections may propagate in a retrograde way. Adapted and reproduced with permission from Nienaber and Eagle1

Case scenario

A 64 year old hypertensive man presented to an emergency department with sudden onset, severe, sharp chest pain. Right arm blood pressure was 100/70 mm Hg and an electrocardiogram showed inferior ST segment depression. Troponin T was raised (0.2 ng/mL). Acute coronary syndrome was provisionally diagnosed, anti-platelet therapy administered, and coronary angiography planned. On later questioning, he described a left arm weakness that had resolved. Further examination noted left arm hypertension (155/90 mm Hg), a right carotid bruit, and diastolic murmur. Computed tomography showed a type A acute aortic dissection (see fig 2) for an example from another case) involving the right coronary ostium and brachiocephalic …

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