Surgery

Current practice dictates that the proximal dissection should be repaired early to
prevent extention and rupture, and to operate on distal dissection extending
proximally using cardiopulmonary bypass. Of patients with type A dissections,
the IRAD database revealed lower 30-day mortality in surgically treated patients
than those treated medically (see clinical outcomes in aortic dissection).
The goal of surgery is to prevent progession of the dissection and to relieve
obstruction in peripheral branches: thus, the intimal tear is excised and the
origin of the false lumen excluded by proximal and distal suturing of the edges of
the aorta. A prosthetic Dacron graft may be needed to approximate the ends of
the aorta. Surgery requieres a period of deep hypothermic circulation arrest.
Where the aortic valve is involved, the false channel is decompressed by the
surgary described above, but may still required replacement or repair. Where the
aorta iss very friable, the whole ascending aorta and valve may be replaced
using a composite graft containing a prossthesis with resuturing of the coronary
arteries to the conduit. Preservation of the native aortic valve, which avoids the
complications associated with a prosthetic valve, usually requires approximation
of the two layer of dissected aortic wall and resuspention of the commissures
with pladgeted sutures. However, prosthetic valve replacement is frequently
advisable in the setting of pre-existent valve disease or in Marfans syndrome to
reduce the likelihood of re-operation.
Surgical fenestration has been used as a means of decompressing an occlusive
false lumen in the descending aorta in patient with viceral or limb ischaemia.
Fenestration may be performed alongside ascending aortic surgary and
additional abdominal aortic grafting. It should ideally be perfermed whitin 48
hours of presentation to prevent thrombotic occlusion of the false lumen. In one
series, surgical fenestration in decending aortic dissection was associated with
mortality rates of 77 and 53 per cent at 3 and 5 years,respectively. Fenestration
can also be done percutaneously and is usually done in the pararenal or
infrarenal area (see below).
Percutaneous interventional treatment
In type B dissection, the persistense of a false lumen has an adverse effect of
clinical outcome (higher rates of re-operation and mortality) where an active
communication persists between true and false lumina, compared to where there
is thrombosis of the false lumen. The deployment of ballon-expendable or selfexpanding endoluminal stents may be performed to re-establish flow into branch
vassel in compromised by pressure from the false lumen over the origin of the
vessel, a fenestration procedure may be undertaken to decompress the false
lumen. Similarly, endoluminal exclution with a stant graft prosthesis (consisting
of circumferential nitinol stent springs arranged as a tube and covered with a
Dacron or polyytetrafluoroethylene [PTFE] graft exterior) placed over the false
lumen entry site will decompress the false lumen, causing the flap to oppose the
aortic wall and relieve branch vessel compromise. The adventage of
endooluminal exclusion in acute disssection is that it combines closure of the
false lumen and prevent subsequent dilatation with relief to branch vessel
obstruction.
Stent grafts are sized by measurement from pre-procedure imaging. They require
a proximal neck of ideally 20 mm of normal aorta above the false lumen origin to
ensure secure deployment against the aortic wall. The potential for ischaemia

through occlusion of the left subclavian artery may be predicted by preliminary

occlusive ballon inflation for 20 minutes at its origin to assess the integrity of the
collateral circulation, perhaps using a partially covered graft if necessary. The
position of the undeployed graft may be obtained using aortography,
intravascular ultrasound or TOE. The distal neck may be normal supracoeliac
aorta or biluminal descending thoracic aorta. In the absence of a distal neck, the
shortest graft that effectively covers the entry site is used.
These techniqques are being increasingly used in type B dissections, parrticularly
when complications ensue. Short-term results from stenting may appear
encouraging, with overall major events seen in 11 per cent, including in-hospital
mortality of 5 per cent,stroke rate of 2 per cent, paraplegia in 1 per cent. Further,
2 per cent of cases were complicated by transformation to type A dissection. The
investigation of STEnt grafts in patients with type B aortic dissection (INSTEAD)
trial compared the use of covered stents with medical therapy alone for
uncomplicated type B dissection. Short-term results at 12 mouths indicated
equivalent mortality in patients with uncomplicated acute type B dissection who
were treated with conventional medical therapy alone or with endovascular
stenting. Registry data relating to 180 patients treated with the endovascular
Talent thoracic stent graft for acute or chronic aortic dissection are also avaible.
Intermediate term (mean 22 months) follow-up yielded survivval rates of 91 per
cent and 82 per cent at 24 and 36 months, respectively. Emergency status (vs
evective cases) was an independent predictor of major adverse events. Analysis
of the IRAD database suggests that endovascular treatment seems to provide inhospital complications occurred in 20 per cent of patients treated with an
endovascular technique and 40 per cent of patients who underwent open surgery
than after endovascular treatment with a three-fold increase in risk for open
surgical repair.
Thus, there are many uncertainties relating to use stent-graft techniques in
aortic dissection. A key question to be answered by furture studies is whether
there is any role for stenting without conventional surgery for type A dissection.
As described above, the fenestration technique may be employed using an
endovascular approach(usually as a bridge to definitive endoluminal repair)
using a needle to pass a quide wire through the intimal flap, then balloon
dilatation of the puncture site. Several fenestrations can be performed in order to
equalize pressures in the true and false lumina, and stenting of branches may be
performed to optimize flow. In cases where ebdoluminal repair or fenetration a
considered, digital subtraction angiography, or magnetic resonance angiography,
is an essential prelude to allow assessment of the access arteries (usually the
iliacs), measurement of the aorta to permit selection of the correct device length
and diameter confirmation of branch vessel involvement and biluminal
manometry prior to fenestration.
Penetrating
Haematoma

Atherosclerotic

Ulceration

And

Intramural

Aortic

These entities are radiological distinct from classicial dissection, with no intimal
flap evident. In penetrating atherosclerotic ulcers (PAU), a visible crater extends
into the aortic wall and is associated with haematoma within the media of the
aortic wall. An intramural haematoma (IMH) is present where significant
thickening or enhancement of the aortic wall is seen in the absence of a flap or
dissection. The clinical features of these two variants may differ from dissection.
Patients with PAU/IMH are older than patients with both type A and B dissections,

and thus are commonest between the seventh and ninth decades. Patients with
PAU/IMH are almost always hypertensive (94 per cent). PAU and IMH are most
common in the descending aorta (94 per cent and 71 per cent, respectively). PAU
and IMH tent to occur in more dilated aortas and have an association with
abdominal aortic aneurysms. The presentation with anterior or posterior chest
pain is similar to, and may be indistinguishable from, that of classical dissection.
In one review of over 200 cases presenting as aortic dissection, one-eighth of
cases were reclassified to either PAU and IMH. However, PAU/IMH generally do
not cause arterial vessel compromise, and tend to be focal without propagation.
Penetrating atherosclerotic ulceration
Penetrating ulcers occur within severely atherosclerotic, frequently calcified
descending thoracic or abdominal aortae, in contrast to classial dissection, which
is more often associated with hypertension. Ulcers are generally focal lesion
appearing as an irregular outpouching of the aortic wall. Ulceration may precede
both IMH or dissection; dissection following PAU is usually shorter, and contained
by neighbouring fibrosis and calcification, with a thicker flap. When compared to
dissection and IMH, PAU is most commonly associated with aortic rupture.
Optimal treatment of PAAU is yet to be established. Medical treatment has been
shown to be effective in most patients, additionally, several registries have
shown favourable outcomes with open surgary and endovascular repair in
selected patients. A large series of patients presenting with PAU identified
rupture at presentation as the main indicator of medical failure. Therefore these
patients are more likely to benefit from early intervention. Patients who are
asymptomatic or found to have PAU as an incidental finding rarely require
intervention but should be followed up for any progressive increase in size of the
ulcer.
Intramural aortic haematoma
IMH occurs when blood accumulated in the vessel media in the absence of a flap.
Formation of an IMH may follow rupture of the vasa vasorum, or from extention
of a PAU (which is identified in 20 per cent of IMH). Extention of IMH towards the
intima may lead to a tear and subsequent dissection. It is thought likely that the
radical level in the wall a which an IMH occurs determines whether an acute
dissection or haematoma develops. It may be that if blood collects to the
adventitia, there is less likelihood of intimal rupture. This would also explain a
higher