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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3900_Библиотеки_им_академика_М_И_Перельмана
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Abstract Intestinal infarction following abdominal aortic aneurysm (AAA)
repair is lethal. Prevention is the key to combating this complication. It has
been shown that heightened vigilance to avert, detect, and intervene early on
intestinal ischemia in the setting of AAA repair can decrease the incidence and
mortality of this frequently lethal disease.
Keywords Mesenteric ischemia , Intestinal ischemia incidence , Mesenteric
arterial anatomy.
Definition
The term intestinal ischemia refers to a spectrum of disease. The common
endoscopic grading system includes: grade I ischemia, which affects the
mucosa and may lead to sloughing, grade II ischemia, which penetrates the
muscularis layer, and grade III or transmural ischemia, which includes gross
bowel infarction.
Incidence
Fortunately, intestinal ischemia is not a common problem following elective
(i.e., nonruptured) open AAA repair. The literature sites an incidence of 1–2%
in this setting. If subclinical ischemia evident only on endoscopy is included,
the rate increases to 4.5%, as demonstrated in a study by Bast et al. in which
100 patients underwent routine colonoscopy following open AAA repair.
1
Those patients who undergo open repair of ruptured AAAs are at highest
risk for intestinal ischemia, with a variable incidence of 3–30%. When Bast
et al. assessed this subset of patients, 17.6% were found to demonstrate some
degree of ischemia on routine postoperative colonoscopy.
1
Data on intestinal ischemia following elective endovascular AAA repair
have only begun to emerge, but initial studies report rates of clinically evident
Chapter 23
Mesenteric Ischemia Following
Abdominal Aortic Aneurysm Repair
Kerianne H. Quanstrum and Gilbert R. Upchurch, Jr.
G. Upchurch and E. Criado (eds.) Aortic Aneurysms, Contemporary Cardiology
DOI: 10.1007/978-1-60327-204-9_23, © Humana Press, a part of
Springer Science + Business Media, LLC 2009
325
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326 K.H. Quanstrum and G.R. Upchurch Jr
colon ischemia similar to those seen with open repair, ranging from 1.3% to
2.9%.
2–
4
In one study that examined both small and large bowel ischemia fol-
lowing elective endovascular AAA repair, incidence of small bowel ischemia
was somewhat higher than that seen in open repair, 0.8% compared to 0.2–
0.6%, and was attributed to microembolization of aneurysm plaque.
2
As is the case with open ruptured repair, endovascular repair of ruptured
AAA results in higher rates of intestinal ischemia compared to the elective
setting. In a study by Champagne et al. in which patients with ruptured AAA
underwent routine postoperative endoscopy following endovascular repair,
23% showed evidence of ischemia, including 8% who required operation.
5
Further, this study corroborated the hypothesis that atheroembolization is a
major contributor to intestinal ischemia in endovascular ruptured AAA repair,
as pathology specimens from all three of the patients requiring operation
revealed atheroemboli underlying the areas of necrotic bowel.
Mesenteric Arterial Anatomy
Prior to discussing the causes of intestinal ischemia following AAA repair,
a review of mesenteric arterial anatomy is in order. The mesenteric arterial
system involves extensive collateralization (Fig. 1 ), such that chronic intestinal
ischemia rarely occurs unless at least two of the three main mesenteric arteries are
compromised. The celiac and the superior mesenteric artery (SMA) exchange
collaterals via the pancreaticoduodenal arteries (Fig. 2 ). The SMA and the
inferior mesenteric artery (IMA) collateralize via the marginal artery of
Drummond, which joins the left branch of the SMA’s middle colic artery to the
ascending branch of the IMA’s left colic artery (Figs. 3 and 4 ). In addition, the
meandering mesenteric artery, also known as the central anastomotic artery,
provides a route of direct anastomosis between the trunks of the SMA and
IMA (Figs. 5 and 6 ). The IMA also collateralizes with the iliac system via the
capillary network in the rectal wall, through which the IMA’s superior hemor-
rhoidal artery exchanges with the middle and inferior hemorrhoidal branches
of the internal iliac, or hypogastric, arteries (Figs. 1 , 3 , and 4 ). Finally, the
internal iliac arteries themselves receive collaterals from the external iliac,
lumbar, and femoral arteries.
Etiology
The causes of intestinal ischemia in the setting of AAA repair are several,
and can be divided into anatomic, embolic and mechanical, and physiological
entities (Table 1 ).
Anatomic
Given the collateral flow within the mesenteric arterial system, ligation or
exclusion of the IMA, as often performed during AAA repair, should not, on
its own, compromise intestinal blood flow in the setting of otherwise nondis-
eased vessels. A patient with an AAA, however – a disease whose risk factors
include increased age, smoking, coronary artery disease, high cholesterol, etc.
– often has coexistent atherosclerotic disease. In the setting of atherosclerosis
of all three main mesenteric vessels, for example, ligation of the IMA – or
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Chapter 23 Mesenteric Ischemia Following Abdominal Aortic Aneurysm Repair 327
exclusion of the IMA, as necessarily occurs during endovascular AAA repair
– could be the critical event that precipitates overt bowel ischemia. In the set-
ting of celiac stenosis, in which SMA is the main source of blood flow to the
stomach and duodenum via the pancreaticoduodenal collaterals, ligation or
exclusion of the IMA, leaving the SMA as the primary source of blood supply
to the entire gastrointestinal tract, could similarly prove disastrous. In the set-
ting of SMA stenosis, on the other hand, the role of the internal iliac arteries
as collateral flow to the left colon gains importance if IMA is ligated. As it is
not infrequent, particularly during endovascular repair of AAA, that one, and
occasionally both, of the internal iliac arteries must be sacrificed, the patient
may be at risk for bowel ischemia if conscious steps are not taken to maintain
flow to the left colon. Finally, in the setting of atherosclerosis of the IMA,
the left colon will be receiving most of its blood supply from other sources,
including collaterals from the SMA or internal iliac arteries. Ligation, then, at
Fig. 1 Mesenteric collateral vessels. Reproduced with permission from Mulholland et al.
22(Fig. 94.4A)
Median arcuate ligament
of diaphragm
Inferior phrenic
artery
Superior
mesenteric
artery
Celiac axis
Splenic artery
Gastroduodenal and
pancreaticoduodenal
collaterals
Mesenteric
collaterals
Sigmoidal arteries
Middle hemorrhoidal artery
Inferior hemorrhoidal artery
Inferior mesenteric
artery
Superior hemorrhoidal
artery
Hypogastric artery
(internal iliac artery)
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328 K.H. Quanstrum and G.R. Upchurch Jr
the root of the IMA should not affect that supply to any great extent, provided
that the collateral sources are left intact.
Embolic and Mechanical
Embolization of atherosclerotic plaque or thrombos during aortic clamping in
open AAA repair, or during intraluminal stent manipulation in endovascular
repair, is another factor likely to be at work in the event of intestinal ischemia.
As mentioned earlier, based on histological review of the pathology specimens
of patients who underwent operation for necrotic bowel, this mechanism is
strongly suggested to be a contributor to bowel ischemia in the setting of
endovascular AAA repair. Undue compression of mesenteric vessels by retrac-
tors during open AAA repair has also been hypothesized to contribute to bowel
ischemia. Finally, in the setting of AAA rupture, when intestinal ischemia is
most common, it is thought that the resulting retroperitoneal hematoma com-
presses the mesenteric vessels to compromise flow.
Physiologic
Particularly in the setting of atherosclerotic disease affecting the mesenteric
arteries, physiological factors alone, including intra- or perioperative hypotension,
Superior
mesenteric artery
Jejunal arterial branches
IIeal arterial branches
IIeocolic artery
Right colic artery
Middle colic artery
Anterosuperior
pancreaticoduodenal
artery
Posterosuperior
pancreaticoduodenal
artery
Gastroduodenal artery
Celiac trunk
Fig. 2 Distribution of the celiac artery and superior mesenteric artery (SMA). Reproduced with permission from
Mulholland et al.
22(Fig. 94.1)
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Middle colic
Marginal artery
of Drummond
Left colic
Superior
hemorrhoidal
Middle hemorrhoidal
Inferior hemorrhoidal
Uterine
Obturator
Internal iliac
Internal pudendal
Inferior vesical
Fig. 4 Marginal artery of Drummond. Reproduced with permission from Mulholland et al.
22(Fig. 95.3)
Fig. 3 Distribution of the superior mesenteric artery (SMA) and inferior mesenteric artery (IMA). Reproduced
with permission from Mulholland et al.
22(Fig. 94.2)
Marginal artery of
Drummond
Superior mesenteric artery
Inferior mesenteric artery
Marginal artery
Sigmoid artery
Middle colic artery
Right colic artery
Marginal artery
IIeocolic artery
Superior hemorrhoidal artery
Middle sacral artery
Hypogastric artery
Middle hemorrhoidal artery
Inferior hemorrhoidal artery
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330 K.H. Quanstrum and G.R. Upchurch Jr
Fig. 5 Selective inferior mesenteric artery (IMA) angiography
demonstrates the marginal artery of Drummond (single arrow,
image right) and the larger meandering mesenteric artery,
or central anastomotic artery (paired arrows, image left).
Reproduced with permission from Mulholland et al.
22(Fig. 94.3)
Fig. 6 Angiography demonstrates an enlarged
inferior mesenteric artery ( IMA ) ( black arrow ) and
meandering mesenteric artery ( white arrow ) in the
setting of celiac and superior mesenteric artery
( SMA ) occlusion. Reproduced with permission
from Mulholland et al.
22
(Fig. 94.16B)
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Chapter 23 Mesenteric Ischemia Following Abdominal Aortic Aneurysm Repair 331
hypovolemia, or use of pressors, might be sufficient to precipitate intestinal
ischemia. Piotrowski et al. published findings suggesting that preoperative
shock was the most important risk factor for colon ischemia following open
repair of ruptured AAA, while large intraoperative blood loss was also pre-
dictive.
6
In contrast, a study by Meissner et al. found no correlation between
intestinal ischemia following ruptured AAA repair and either perioperative
shock or volume administration, but documented that low perioperative
cardiac output and use of alpha -adrenergic pressors were predictive.
7
While
reports in the literature are conflicting as to which physiological mechanism is
most predictive of bowel ischemia, it is intuitive that each can contribute.
Diagnosis and Management
Diagnosis
For purposes of intraoperative detection of inadequate intestinal perfusion dur-
ing AAA repair, several methods have been proposed. Other than in cases of
gross ischemia or infarction, visual inspection of the bowel is generally inad-
equate to recognize malperfusion. Management of the IMA appears critical.
Relatively simple adjuncts to determine the safety of IMA ligation versus the
need for implantation into the aortic graft include Doppler ultrasound of the
relevant mesenteric vessels,
8
endoluminal pulse oximetry of the bowel wall,
9
or
laser Doppler monitoring of serosal blood flow
10,
11
following IMA occlusion.
Each of these methods has demonstrated good sensitivity in small, nonrand-
omized studies, but none has been universally adopted. Intravenous fluorescein
injection followed by Wood’s lamp examination of the bowel wall,
12
intraperi-
toneal xenon injection followed by gastrointestinal -activity monitoring,
13
and
measurement of intraluminal pH
14
are other methods that have been proposed.
None of these methods is universally accessible due to the need for specialized
equipment, however, and none has been rigorously validated in the literature.
The classic presenting sign of intestinal ischemia following AAA repair is
bloody diarrhea. Classic symptoms such as abdominal pain out of proportion
to physical examination may be masked by the use of epidural anesthesia
or intravenous narcotics; while fever, leukocytosis, lactic acidosis, or gen-
eral sepsis are less specific signs whose significance may be confounded by
the physiological changes associated with the operation itself. Regardless,
Table 1 Causes of mesenteric ischemia during AAA repair.
Anatomic Embolic and Mechanical Physiologic
Preexisting atherosclerosis
of one or more mesenteric
vessels
Embolization of atherosclerotic plaque:
during aortic clamping in open repair or
during intraluminal stent manipulation in
endovascular repair
Hypotension, hypovolemia, low cardiac
output, use of pressors, e.g., leading
to poor visceral perfusion
Compression of mesenteric vessels by
retractors during open repair
Compression of mesenteric vessels by
retroperitoneal hematoma in the setting of
AAA rupture
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332 K.H. Quanstrum and G.R. Upchurch Jr
postoperative diarrhea, whether bloody or not, is uncommon following AAA
repair, when ileus would be the more expected scenario, and thus should
lead to consideration of sigmoidoscopy. Similarly, any suspicion of intestinal
ischemia on the part of the surgeon, whether because of clinical presentation
or the mere presence of risk factors for the event, should prompt endoscopic
examination. Liberal use of endoscopy has been suggested to avoid the cata-
strophic event of intestinal infarction. In the setting of ruptured AAA repair,
in fact, when intestinal ischemia is most frequent, several authors have pro-
moted routine postoperative endoscopy in the first 24–48 h. following surgery.
Vascular surgeons at Case Medical Center instituted routine colonoscopy
following open ruptured AAA repair, with resultant improved mortality rates
for ischemic colitis that they attributed to earlier diagnosis and treatment.
15
In
a second study, these authors instituted the same mandate for endovascular
repair of ruptured AAA.
5
While an effect on mortality was not documented
due to the lack of a comparison group, it is notable that among the patients in
the study found to have any degree of intestinal ischemia, not a single death
occurred during 30-day follow-up. The effects on outcome of routine endos-
copy after ruptured AAA repair await more rigorous examination to determine
whether this strategy should become common practice. Of note, flexible sig-
moidoscopy, as opposed to full colonoscopy, is usually sufficient to diagnose
intestinal ischemia, as the rectosigmoid colon is involved in 95% of cases in
which intestinal ischemia occurs.
16
Management
Management of intestinal ischemia varies with endoscopic findings (Table 2 ).
Mucosal ischemia alone (i.e., grade I), associated with a near-zero mortality
rate, generally warrants only supportive management, including optimization
of fluid status, bowel rest, empirical antibiotics, serial abdominal examina-
tions, and repeat endoscopy to confirm resolution or evaluate for progression
that may warrant more aggressive management. With more advanced ischemia
that penetrates the muscularis propria (grade II), recovery also commonly
occurs with conservative management alone. In this case, however, patients are
at risk of developing strictures as the bowel wall heals, and thus they should
undergo contrast enema once the acute phase of ischemia has resolved. Finally,
transmural involvement of the bowel (grade III) requires urgent laparotomy.
Even in the setting of prompt operation, mortality can run as high as 90%,
generally due to sepsis and multisystem organ failure.
Table 2 Management of intestinal ischemia.
Grade I Grade II Grade III
Supportive: Optimization of fluid status,
bowel rest, empirical antibiotics, serial
abdominal examinations, consideration
of followup endoscopy
Supportive management, including
lower threshold for follow-up endos-
copy; contrast enema to evaluate for
intestinal strictures after the acute
phase of ischemia has resolved
Urgent exploratory laparotomy
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Chapter 23 Mesenteric Ischemia Following Abdominal Aortic Aneurysm Repair 333
Recommendations
Preoperative Planning
Preoperative assessment of the patency and dominance of the celiac, SMA,
IMA, and internal iliac arteries is essential prior to AAA repair. First and
foremost, a complete history and physical examination should be obtained
to detect any history of symptoms suggesting mesenteric ischemia, such as
postprandial pain, unintentional weight loss, or food fear. In most cases, CT
angiography is adequate to assess the characteristics and measurements of the
aortic aneurysm and its relationship to visceral and renal arteries, as well as the
patency of the visceral vessels themselves. Compromise of any one or combi-
nation of the mesenteric arteries may require a more creative operative plan,
varying from IMA implantation into the aortic graft, to internal iliac artery
bypass, to a more complex reconstruction involving the celiac or SMA.
Treatment of the IMA
A study from Massachusetts General Hospital sited ligation of a patent IMA
as the most common factor found to be present, at a rate of 75%, in patients
who developed colon ischemia following open abdominal aortic surgery.
17
Implantation of the IMA into the aortic graft, therefore, has been heralded
to prevent, or at least to lessen the risk of, intestinal ischemia. The efficacy
of this practice has not strictly been borne out in the literature, however.
Senekowitsch et al. performed a study in which patients were prospectively,
randomly assigned to undergo IMA ligation or implantation.
18
There was no
statistically significant difference in rates of ischemic colitis as diagnosed by
routine postoperative colonoscopy and biopsy sampling. There was a nonsta-
tistically significant trend favoring IMA implantation, however, with relative
risk for ischemic colitis as low as 0.55, p = 0.203. Of note, in the final analysis,
the study was found to be underpowered. Further, nonrandom implantation
of the IMA, as dictated by surgeon judgment, is likely to have a clinically
significant effect on the risk of developing ischemic colitis for a given patient.
To answer this question definitively would require taking patients in whom it
was judged by the surgeon that IMA implantation would be beneficial, and
randomizing those patients to undergo implantation versus ligation. Of course,
such a study would be unethical and impossible. We recommend, therefore,
implantation of the IMA in those patients in whom it is judged to be feasible
and beneficial. In some cases, the benefit – indeed, the necessity – will be
obvious, such as in the patient with SMA stenosis and a large IMA supplying
the majority of their intestinal blood flow (Fig. 6 ). For purposes of assessing
benefit in more subtle cases, measurement of IMA stump pressure has been
proposed, with a pressure of at least 40 mmHg thought to be sufficient to allow
for safe ligation.
19
In practice, however, simple visual inspection of IMA back-
flow is usually employed. When the IMA must be ligated without implanta-
tion, we recommend the standard practice of ligating at the wall of the aorta in
order to avoid interruption of any proximal collateral vessels.
Treatment of the Internal Iliac Arteries
It has been promulgated that maintaining patency of one or both internal iliac
arteries lessens the risk of bowel compromise. Maintaining perfusion to one
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334 K.H. Quanstrum and G.R. Upchurch Jr
internal iliac artery, in fact, is often considered the standard of care in open
AAA repair. Two case series, however, have demonstrated that unilateral
or bilateral internal iliac artery interruption can be performed during either
endovascular or open AAA repair without inducing buttock necrosis or colon
ischemia requiring operation.
20,
21
This can be performed provided that (1) the
internal iliac arteries are interrupted as proximally as possible, ideally at their
origin, in order to maintain distal collateral flow from the external iliac and
femoral arteries; (2) distal embolization is avoided; and (3) ligation, when
bilateral, is performed in a staged fashion. Unfortunately, neither of these case
series involved a control group. The surgical tenet remains, therefore, that
perfusion to one internal iliac artery should be maintained wherever possible.
If ligation of both internal iliacs is necessary, this may be done without undue
increase in rates of intestinal ischemia provided that the three mentioned
criteria are met.
Conclusion
Intestinal infarction following AAA repair is lethal, but largely preventable in
the elective setting. Vigilance on the part of the surgeon is essential. Attention
to the possibility of intestinal ischemia, and due diligence in preoperative
planning, procedural execution, and postoperative monitoring so as to avert its
development or allow for timely intervention, respectively, can decrease the
incidence and mortality of this otherwise deadly complication.
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