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Page 4 of 9 Lou et al. Vessel Plus 2022;6:38 https://dx.doi.org/10.20517/2574-1209.2021.108

Spinal cord malperfusion
Spinal cord malperfusion is due to extension of the dissection with compromised flow to intercostal or
lumbar arteries, including the artery of Adamkiewicz. In ATAAD, this is most often due to a dynamic
mechanism for which central aortic repair to restore true lumen flow with or without lumbar drain
[6]
insertion is generally sufficient to resolve . In patients with descending or thoracoabdominal aortic
dissection involvement, the main treatment is TEVAR with endovascular fenestration and/or stenting if
there is false lumen thrombosis and occlusion of intercostal arteries.

Cerebral malperfusion
Cerebral malperfusion complicating ATAAD is a clinical challenge that has not been extensively
investigated in the literature. The available studies demonstrate that cerebral malperfusion and stroke are
predictive of increased in-hospital mortality . In an IRAD study of 2402 patients undergoing surgical
[10]
[11]
repair of ATAAD, 15.1% presented with cerebral malperfusion and neurologic deficits . Compared to
patients with normal cerebral perfusion, patients with cerebral malperfusion had an increased incidence of
postoperative cerebrovascular accident (17.5% vs. 7.2%; P < 0.001), acute kidney injury (28.3% vs. 18.1%;
P < 0.001), and in-hospital mortality (25.7% vs. 12.0%; P < 0.001).

There have been some reports of using an endovascular approach with carotid artery stenting and/or
external shunting (femoral artery to common carotid artery) with improvements in neurological status
prior to delayed open central aortic repair. However, the general consensus is that immediate central aortic
repair should be performed to restore cerebral perfusion. Central cannulation is preferred, and in some
cases, it may be preferable to directly cannulate the carotid artery either with a cut-down technique or a
graft sewn end-to-end to eliminate the false lumen flow and ensure true lumen cerebral perfusion.

The ongoing areas of debate in the management of ATAAD complicated by cerebral malperfusion are the
appropriateness of central aortic repair and the timing of this repair. In another IRAD analysis by
[12]
Di Eusanio et al. of 1873 patients presenting with ATAAD, including 87 (4.7%) with stroke and 54 (2.9%)
with coma, patients who were selected to undergo surgical management demonstrated enhanced survival
and often times reversal of neurological deficits. All patients presenting with coma and 76.2% of those with
stroke died with isolated medical management. For those patients undergoing surgical repair, mortality was
27.0% for patients presenting with stroke and 44.0% for those with coma (P < 0.001). Surgery was found to
be protective against mortality in ATAAD patients presenting with cerebral malperfusion (OR = 0.058,
P < 0.001). Moreover, postoperative stroke and coma resolved in 84.3% and 78.8% of cases, respectively.
Thus, the authors concluded that “in patients selected to undergo surgery demonstrated improved late
survival and frequent reversal of neurologic deficits….intervention should always be considered”.

Although somewhat contentious, the IRAD data suggest that there is evidence to support a role for surgical
intervention in comatose ATAAD patients. In these patients, the timing of intervention becomes
particularly critical with the earlier the intervention being associated with improved outcomes.
Tsukube et al. analyzed their results of 181 patients with ATAAD, 27 of whom presented with coma
[13]
(GCS < 11), who were managed with central aortic repair at index hospitalization. Of this group, 21 patients
were immediately operated upon within 5 h of presentation and the remainder were treated medically, three
of whom eventually underwent repair. Hospital mortality was 14% in the immediate group and 67% in the
delayed group, and full recovery of consciousness was seen in 86% of the immediate group and 17% in the
delayed group. While the available data are scant, they do indicate that the presence of brain malperfusion
or cerebral dysfunction is not a contraindication to surgical intervention, and an individualized approach
must be considered for optimal patient outcomes.