
Growth
of abdominal aortic aneurysm after endoluminal repair
(Portuguese
PDF version)
Ricardo
Aun,1 Glauco Fernandes Saes,2 Adriano Tachibana,2
Alex Lederman,2 Hilton Waksman,2 Fernando Tavares Saliture
Neto,2 Otávio Ninomiya2
1.Director
of the Centro Paulista de Cirurgia Vascular, São Paulo, SP,
Brazil.
2.Physician, Centro Paulista de Cirurgia Vascular, São
Paulo, SP, Brazil.
Correspondence:
Centro Paulista de Cirurgia Vascular
Av. Albert Einstein, 627, 11° andar, Sala 1109
CEP: CEP 05651-901 - São Paulo, SP, Brazil
Phone: +55 (11) 3742.1365/3742.5117/3747.3109
Fax: +55 (11) 3747.3507
E-mail: aun@einstein.br
or aun@uol.com.br
ABSTRACT
The
authors report a post-operative aneurysmal sac growth with no endoleaks
presence. Low pressure inside the aneurismal sac was observed. Possible
causes for dilation and treatment are discussed. The original endoprosthesis
was maintained with surgical sac reduction.
Key-words:
abdominal aortic aneurysm, bleeding, surgery.
J
Vasc Br 2004;3(4):387-91
While endoluminal
stent-graft repair of abdominal or thoracic aortic aneurysms appears
effective in the short-term, it is a relatively new procedure and the
long-term success of the grafts is still uncertain; only very few cases
have reached a survival rate of more than four or five years. Endoleaks
and growth of the aneurysm diameter are two of the most serious and
frequent complications of endoluminal grafts. It must be noticed that
the aneurysm growth may occur even when no leak is detected by usual
imaging, especially computed tomography scans, ultrasound, magnetic
resonance and arteriography.
The expansion
of the aneurysmal sac after an endovascular repair may be delayed, even
if it presented initial regression in the short-term. Two methods can
be used to monitor pressure inside the aneurysmal sac, one is the direct
intraoperative approach by translumbar puncture, the other is the selective
cannulation of the branches of the inferior mesenteric artery. Other
methods under development consist of sensors implanted with the stent
graft. All these methods and theories are still not enough to explain
the cases developed with aneurysmal growth. In the case we report here,
there was no association between increased aneurismal volume and increased
aneurysm sac pressure, for example.
CASE
REPORT
An 80-year-old
patient with a 7,6 cm diameter aneurysm in the infrarenal abdominal
aorta underwent endoluminal repair with a bifurcated Excluder® endoprosthesis.
During computed tomography scan monitoring performed at every 6 months,
an aneurysm growth was detected with no evidence of endoleaks. After
3 years, the aneurysm diameter reached 11 cm but remained asymptomatic
up to three months ago, when the patient reported continuous and moderate
pain in the gastric mesentery and left flank. Another tomography scan
was required and revealed that the diameter had na increase to 12.5
cm. On physical examination, the patient presented with a visible abdominal
distension (Figure 1); there was a palpable non-pulsatile mass without
murmur or thrill in the vascular paths, and strong pulses were felt
in all segments. Arterial pressure was 130 x 190 mmHg, heart rate 78
bpm and respiratory frequency 14 ipm.
Figure
1 - Evident abdominal expansion due to a non-pulsatile and non-painful
mass on palpation

Computed
tomography scans requested are shown in Figures 2 and 3.
Figure
2 - Computed tomography scan of the abdomen showing an enlarged
aortic aneurysm after treatment with the Excluder® endoprosthesis,
which remained patent, and the interior of the aneurysmal sac with thrombosis.
October 11th, 2001. Anteroposterior diameter 8 cm.

Figure
3 -Computed tomography scan of the abdomen with evident volume increase
and no evident endoleak. Note the density difference between image A
and the rest of the aneurysmal sac B. May 6th, 2004.

The patient
was submitted to an open surgery for endoluminal stent-graft withdrawal
and aneurysm repair. The aneurysmal sac was approached retroperitoneally
with an oblique incision on the left. When opened, it revealed no pulsatile
wall motion and was deformable on palpation. There was no need for aortic
clamping because the aortic neck had already been dissected.
The aneurysmal
sac pressure, measured with a Jelco® 16 puncutre needle, revealed
to be 15 mmHg below the patient's mean blood pressure (97 mmHg at the
moment of puncture).
Figure
4 - Exposure of the aneurysm by left extraperitoneal approach and
aneurysmal sac puncture.

We proceeded
with the aneurysmal sac opening and emptying, no bleeding and a large
amount of serosanguinous fluid were detected (Figure 4), but there was
no sign of infection. The stent-graft was fully covered by thrombi and
jelly-like material (Figure 5).
Figure
5 - Intraoperative aspect of the aneurysmal sac showing the graft
completely covered by thrombi and jelly-like material.

The edges
of the aneurysm were overlapped and closed with an interrupted mattress
suture, as shown in Figure 6.
Figure
6 - Final aspect and closure of the aortic native wall with intermittent
mattress suture.

The biochemical,
cytological and bacterioscopic test results revealed a transudate fluid
whose components are presented in Table 1.
Table
1 - Biochemical and cytologic elements of the aneurysmal sac internal
fluid
 |
| Test
|
Dosage |
 |
| Amylase
|
39
mg/dl |
| Glucose
|
119
mg/dl |
| Creatinine
|
1.1
mg/dl |
| Urea
|
46
mg/dl |
| Protein
|
8.4
mg/dl |
| Cholesterol
|
585
mg/dl |
| Triglycerides
|
332
mg/dl |
| Erythrocytes
|
1,030,000
cel/mm³ |
| Leukocytes
|
5,400
cel/mm³ |
| Neutrophils
|
cel/mm³ |
| Eosinophils
|
cel/mm³ |
| Lymphocytes
|
cel/mm³ |
 |
No bacterial
increase was detected after 72 incubation hours. In the third postoperative
period the patient was discharged from hospital asymptomatic. Currently,
he is on the 60th postoperative day with no complaints and
totally recovered from the aneurysm. Imaging monitoring shows the prosthesis
attached to the wall
DISCUSSION
The case
we report here brings into light some important concepts of the endovascular
abdominal aortic aneurysm repair, which start to appear as the technique
becomes more widely known.
The first
one is that the abdominal aortic aneurysm may have a continued growth
after repair, even if no endoleak is detected.
Second,
the aneurysmal sac may have a delayed growth after endovascular repair,
even if it had an initial regression after surgery, and third, the repressurization
of the aneurysmal sac may contribute to its growth, however this can
happen with low internal pressures as well.
Because
of these potential problems, it is mandatory that all patients who have
undergone abdominal aortic aneurysm repair be monitored with an ultrasound,
angiotomography and arteriography scans to detect endoleaks in the postoperative
period. After leaks are excluded, the aneurysmal sac pressure measurement
can be measured with direct approach by translumbar puncture or selective
cannulation of the branches of the inferior mesenteric artery, besides
the intraoperative direct puncture of the aneurysmal sac.
White et
al.1 reported three cases of successful
endovascular aortic aneurysm repair that developed aneurysmal sac growth
in the 18th postoperative month. An increase in the internal
pressure of the aneurysmal sac was detected. Another report, by Lin
et al.,2 described an increase in the aneurysmal
sac size found in the late follow-up of three patients who had presented
initial regression in the aneurysm diameter after endovascular repair.
The mechanism
responsible for increasing the aneurysmal sac pressure after endovascular
repair is still unclear. Some theoretical studies discuss possible causes,
like:
a) direct
transmission of the stent-graft lumen pressure to the sac;1,3,4
b) low flow leak paths;2
c) proteolytic degradation of the clot, which makes the aneurysmal sac
wall thinner;
d) pressure transmitted through the graft wall associated with the porous
graft coverage would lead to the production of fluid and serous transudate
fluid.5
The aneurysmal
sac enlargement can be divided into five categories1,6,7
based on causative factors (see Table 2).
Table
2 - An overview of the main theories that try to explain the aneurysmal
sac expansion in the absence of endoleaks
 |
| Factors
|
Causes |
 |
I
- Pressure transmitted to the aneurysmal sac by the external limits
of the graft
|
-
thrombus-proximally placed
-
thrombus layer between the prosthesis and the wall
-
low flow leak path, intermittent or sealed by thrombu
|
II
- Pressure transmitted through the graft wall
|
-
graft porous material
-
transudate fluids
-
the graft wall is pulsatile
|
| III
- Pressure transmitted by collaterals |
- thrombi
in the inferior or lumbar mesentery artery
|
IV
- Pressure resultant from an accumulation of aneurysmal sac fluid
|
-
fibrinolysis of thrombus/hygroma
-
graft infection
-
enzymathic activity
|
| V
- Aneurysmal sac enlargement without increased pressure |
-
weakening of the aneurysmal wall by enzymathic activity
-
genetic modulation
-
growth factors
-
infection
|
 |
Based
on Dubenec et al.6.
There is
little information about which would be the best therapeutic approach
to the aneurysmal sac enlargement. Some alternatives are:
a) conservative
treatment monitored with imaging examinations; b) conservative treatment
with measurement of the internal pressure of the aneurysmal sac; c)
conventional surgical approach; and d) secondary endovascular treatment.
In the
case reported, after the internal pressure of the aneurysm and the site
of the stent-graft were detected, we opted for reducing the aneurysmal
sac volume by remodeling it, with no graft replacement. We believe that
increased enzymathic proteolytic activities inside the aneurysmal sac
may damage its wall and thereby promote the aneurysmal growth. This
hypothesis, however, needs further confirmation studies, as we did not
performed specific examinations yet.
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2. Lin PH, Bush RT, Katzman JB, et al. Delayed aortic
aneurysm enlargement due to endotension after endovascular abdominal
aortic aneurysm repair. J Vasc Surg 2003:38:840-2.
3.
Meier GH, Parker FM, Godziachvili V, Demasi RI, Parem FN, Gayle RG.
Endotension after endovascular aneurysm repair: the Ancure experience.
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4.
Parodi JC, Berguer R, Ferreira LM, La Mura R, Schermerhorn ML. Intra-aneurysmal
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5.
Williams GM. The management of massive ultrafiltration distending the
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Dubenec SR, White GH, Pasenau J, Tzilalis V, Choy E, Erdelez L. Endotension:
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White GH. What are the causes of endotension? J Endovasc Ther 2001;8:454-6.
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