Key Words
Thoracoabdominal aortic aneurysm - Paraplegia - Spinal cord
Introduction
The repair of thoracoabdominal aortic aneurysms (TAAs) remains a formidable challenge
for most cardiovascular surgeons. One of the main goals in the management of patients
with an extensive thoracic aortic aneurysm is end organ protection, both viscera and
spinal cord. Early postoperative morbidity and mortality remains high when permanent
spinal cord injury (SCI) occurs. The incidence of paraplegia increases when the segmental
arteries (SAs) that are sacrificed start from the lower thorax and extend into the
abdomen and when the number sacrificed is between 8 to 12[1]. However, when the distal aorta is approached in two or more stages the incidence
of spinal cord injury decreases significantly[2]. Experimental and clinical data suggests that staged SA sacrifice leads to a less
dramatic drop in collateral network perfusion pressure (CNPP) during the second stage,
an increase in arterial diameter and density of the intraspinous and paraspinous vessels,
and a greater margin of safety to prevent SCI.
The patient’s cardiopulmonary status and anatomical features of the TAA may not afford
a staged repair due to significant thrombus burden, calcification, and uniform dilatation
throughout the aneurysm. In certain circumstances, however, the configuration of the
TAA allows for partial resection or reconstruction that prepares for further proximal
or distal aortic replacement. This staged approach may provide less of a physiological
insult and lower risk of paraplegia in these patients. Our previous clinical experience
suggests that completion or segmental resection of extensive TAAs months to years
after the first aortic replacement results in excellent neurologic outcomes[2]. We present an intentional staged approach in two consecutive cases of extensive
TAAs with favorable anatomical configuration.
Case Presentation
Patient 1
A 78-year-old female with a history of hypertension presented with back pain and was
discovered on computerized tomography (CT) scan to have an aortic arch and Type II
thoracoabdominal aortic aneurysm (TAA) ([Figure 1A]). The maximum diameter of the TAA was 8.6 cm and the aortic arch measured 5.3 cm.
In light of the aortic arch aneurysm and extensive distal aortic aneurysmal disease,
an aortic arch replacement with elephant trunk was performed. Her postoperative course
was uneventful. Due to the high risk (10%) of spinal cord ischemia in Type II TAA
repairs, we decided to approach her aneurysm in a staged manner. The distal portion
of the descending thoracic aorta narrowed to 3.5 cm for a length of 2.5 centimeters
before it expanded to a diameter above 6 centimeters in the abdominal aorta segment.
We decided to resect the aorta from the narrowed portion to the aortic bifurcation
(Type III TAA repair) ([Figure 1B]). She underwent the extensive aortic resection with hypothermic circulatory arrest
(18°C), sequential ligation of SAs (T10-L5), spinal fluid drainage, and visceral reimplantation
with a multi-branched graft ([Figure 1B]). Somatosensory and motor evoked potentials were performed intra-operatively. Her
postoperative course was uneventful. She returned 2 months later for a thoracic endovascular
aortic repair (TEVAR) to cover the descending thoracic aortic portion adjoining the
elephant trunk to the proximal end of the graft ([Figure 1C]). The TEVAR was performed under general anesthesia with spinal cord fluid drainage
and topical cooling to a bladder temperature of 33°C. The patient had no clinical
evidence of spinal cord injury after each intervention.
Figure 1. Panel A. Patient 1 pre-operative scan, revealing a distal aortic arch aneurysm and Type II
TAA. Panel B. Postoperative CT scan after first stage, showing aortic arch replacement with elephant
trunk and Type IV repair (highlighted in red). Panel C. CT scan after second stage with TEVAR.
Patient 2
A 67-year-old male with a history of hypertension, hyperlipidemia, and Type B aortic
dissection presented with periodic episodes of back pain, early satiety, and a 60
pound weight loss. His CT scan revealed a TAA that spanned from the distal aortic
arch to the level of the renal arteries ([Figure 2A]). The diameter of the segment of aorta at the level of diaphragm was 7 cm, which
was displacing and narrowing the esophagogastric junction, resulting in the patient
only being able to tolerate a pureed diet. The patient was discharged home for 7 days
while his clopidogrel was discontinued and prepared for an elective aortic arch replacement
with an elephant trunk. He was readmitted with aspiration pneumonia the day prior
to the scheduled operation. A gastrostomy tube was placed for nutritional support.
Due to his prolonged pre-operative management, weight loss, and further rapid expansion
of his TAA (9 cm), we decided to change our approach to an open TAA repair and TEVAR
of the distal aortic arch and proximal descending thoracic aorta. The CT scan indicated
a narrowing of the TAA at the level of the middle of the descending thoracic aorta
([Figure 2A]). He underwent a TAA repair from the mid-descending thoracic aorta to below the
renal arteries with full cardiopulmonary support (22°C), spinal fluid drainage, somatosensory
evoked potential (SSEP) and motor-evoked potential (MEP) monitoring, sequential SA
ligation (T8-L3), and patch technique to reimplant the visceral vessels ([Figure 2B]). Six weeks later, he underwent a carotid-subclavian artery bypass and a TEVAR from
the left carotid artery to the aortic graft ([Figure 2C]). The patient had no clinical evidence of spinal cord injury.
Figure 2. Panel A. Patient 2 with Type III TAA and (Panel B) CT scan following open repair from mid-descending thoracic aorta to below renal
arteries (highlighted in red). Panel C. TEVAR repair of distal aortic arch to mid-descending thoracic aorta.
Discussion
Paraplegia is a one of the most dreadful complications after TAA repair, carrying
a cumulative in-hospital and 1-year mortality of nearly 80%. Over the last two decades,
several adjuncts such as hypothermia, permissive hypertension, and cerebral spinal
fluid drainage have been consistently used in clinical practice to prevent SCI. Several
centers feel strongly that re-implantation of one or a series of intercostal arteries
onto the aortic graft has a positive impact on preventing spinal cord ischemia. Conversely,
other surgeons have shown similar neurologic outcomes without implantation of intercostal
arteries[1]. We do not feel intercostal artery implantation should be considered unless there
neurologic monitoring indicates ischemia, which does not ameliorate with increasing
the blood pressure and spinal fluid drainage. The occlusion of greater than 8 SAs
and crossing beyond the diaphragm in one setting increases the incidence of SCI. In
both cases, the number of SAs involved would have exceeded 12 and with the aneurysms
spanning into the abdominal segment, the predicted risk of SCI could have been as
high as 12.5%[1]. On the contrary, the staging of the TAA repair only required eight SAs to be sacrificed
during the open procedure lowering the risk of SCI[1].
Staged repair of thoracoabdominal aortic aneurysms lowers the incidence of paraplegia
in experimental animals. The reduction in the CNPP is significantly lower if the sacrifice
of SAs is performed in two settings. Our experimental data indicates that the CNPP
drops to 80% of the baseline aortic pressure and requires over 120 hours to return
to baseline if all SAs are sacrificed at one setting. These findings were consistent
if the SAs were ligated in open repair setting or covered utilizing an endovascular
technique. However, when a staged repair was undertaken, the incidence of clinically
evident SCI and histopathological evidence of neuronal injury was decreased significantly[3]. The restoration of the CNPP at 120 hours after SA ligation suggests that the second
stage should not performed until after the seventh postoperative days. Interestingly,
the order in which the thoracoabdominal aorta was managed; either thoracic first and
abdominal aorta to follow or vice versa, the incidence of SCI was similar. In both
cases, we performed the abdominal aortic portion first; however, this decision was
based purely on their particular anatomy. Despite the lower incidence of SCI we continue
to utilize spinal fluid drainage since in the experimental model there was evidence
of neuronal damage despite normal motor function.
In conclusion, we present two cases of complex TAA who were approached in a two-stage
manner with good clinical outcomes. This approach should be considered when anatomical
characteristics are favorable and an extensive aortic replacement is needed. Since
this approach requires a lag time between interventions, the risk of waiting needs
to be weighed against the risk of rupture of the remaining, untreated aortic aneurysm.
Our limited clinical experience with this approach has resulted in acceptable outcomes
and an enthusiasm to apply this approach to similar patients.
