Teaching Case

A 64-year-old woman presented to the emergency department complaining of sudden and severe upper-back and chest tearing pain, shortness of breath, diaphoresis and refractory dull abdominal pain. An EKG and complete blood count (CBD) were ordered showing no abnormalities.

A contrast-enhanced triphasic aortic CT-scan was performed depicting a complex Type B triple-barreled aortic dissection (note the position of the intimomedial flap immediately after the origin of the left subclavian trunk) (Fig. 1a, arrowhead) with multiple penetrating ulcers (Figure 1a, arrow). Many high-flow re-entry tears were also demonstrated (Fig. 1b, arrowhead). The classic ‘Mercedes-Benz’ sign was also identified (Fig. 2a) at the descending thoracic and abdominal aorta revealing two false lumen and a central partially collapsed true lumen with intimal calcification (Fig. 2a, arrowhead). The main visceral trunks (celiac trunk, SMA and left renal artery) emerge from one of the false lumens (Fig. 3) without hypoperfusion signs due to the great and multiple re-entry tears (Fig. 1c, arrowhead). An emergent endovascular reparation was performed (Fig. 4) with 2 superimposed endoprosthesis and posterior angioplasty (Fig. 4). A week after a contrast-enhanced CT revealed type IA and IB endoleaks (Fig. 5).

Aortic dissection is the most common and severe manifestation of the acute aortic syndrome, which also comprise penetrating ulcer, ruptured aneurysm and intramural haematoma. The prognosis of the type A aortic dissection is poor compared to the type B, reaching a mortality rate of 1%/hour with 50% of the patients expected to be dead by the third day and around the 80% by the third week. In comparison to type A aortic dissection, death rates are lower but still significant being at least a 10% the first month [1]. Most aortic dissections are seen in elderly hypertensive patients being a small minority secondary to connective tissue disorders such as Marfan’s and Ehlers-Danlos syndromes. Other conditions like bicuspid aortic valve, aortic coarctation, pregnancy, Turner’s syndrome or fluoroquinolones are considered predisposing factors. [2] About 30% of patients presenting a type B aortic dissection have a complicated dissection associating malperfusion syndromes, uncontrollable pain or dissection worsening (increase in the extension, progression to a triple-barreled dissection, penetrating ulcers, etc). [2] Tri-phasic CT scan is the first diagnostic test of choice as it is not only able to confirm and classify the type of dissection but also to check for distal complications such as hypoperfusion, extension of the false lumen, intramural haematoma and penetrating ulcers with a reported sensitivity and specificity of nearly 100%. [3] Identifying the true lumen could be sometimes challenging specially in such complex dissections. When there is no clear continuation of one lumen with normal aorta, the following features are useful: True lumen: · Smaller cross-sectional area (higher velocity flow); · Surrounded by calcifications (if present); · Usually contains the origin of coeliac trunk, SMA and right renal artery. False lumen: · Larger cross sectional area (slower, more turbulent flow); · ‘Beak sign’ – On the axial plane acute angles at the edge of the lumen should be seen; · Usually contains the origin of the LEFT renal artery. Although the management of type B aortic dissections has been classically conservative (antihypertensive pharmacotherapy), complicated type B dissections, as in our patient, are considered high-risk and require surgical or endovascular repair. [1]

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