CHAPTER 153 
Mesenteric Vascular Disease:
Acute Ischemia
MICHELLE C. MARTIN  /  MARK C. WYERS
A cute mesenteric ischemia (AMI) is a life-threatening con-
dition with a well-documented dismal prognosis as a result of
catastrophic abdominal events. Klass was the first surgeon to
focus on the restoration of arterial blood supply in an attempt
to salvage acutely ischemic bowel. He reported the first opera-
tive superior mesenteric artery (SMA) embolectomy for AMI
in 1951.1 The next 2 decades produced more such reports
and increasing success with SMA thromboembolectomy and
thromboendarterectomy2 for the treatment of acute SMA
thrombosis. Unfortunately, successful outcomes after the
treatment of acute thrombotic SMA occlusion remained
elusive, with mortality rates of 70% to 90%. Early and liberal
use of angiography was championed by Boley3,4 and Clark5,6
and their respective coauthors in the early 1970s. With an
aggressive approach, including the use of vasodilators, they
demonstrated a reduction in the AMI mortality rate to
approximately 50%. This mortality rate has not been repro-
duced or improved on, despite all the major advances that
have taken place in the subsequent 40 years. In fact, more
contemporary reviews still report mortality rates between
60% and 80%.7,8 Treatment of acute mesenteric arterial
occlusions has traditionally been surgical, with intensive
medical support, as well as some limited interventional
options for nonocclusive mesenteric ischemia (NOMI).
There are, however, increasing reports of endovascular or
hybrid endovascular-surgical treatments for all forms of AMI
that can be applied to the treatment of well-selected patients.
INCIDENCE AND RISK FACTORS
AMI is uncommon, accounting for less than 1 of every 1000
hospital admissions.9 Women are affected three times as fre-
quently as men are. Patients typically present in their 60s to
70s and often have a number of medical comorbidities. Clini-
cal risk factors may provide some clue as to the specific
pathophysiologic process. Patients with a history of atrial
fibrillation or flutter, recent myocardial infarction, congestive
heart failure, or peripheral arterial emboli are at risk for an
SMA embolus. In contrast, a careful history may reveal post-
prandial abdominal pain, weight loss, and food intolerance,
all of which clearly raise the suspicion of an acute SMA
thrombotic occlusion. A review of a national database
2398
identified that patients undergoing angioplasty and stenting
for AMI had higher rates of comorbidities than those under-
going open surgical repair, including hypertension, peripheral
vascular disease, coronary artery disease, atrial fibrillation or
flutter, and chronic renal failure.10 Finally, a patient with
NOMI is likely to be critically ill and to have suffered a sig-
nificant hemodynamic insult in the preceding hours to days.
Cardiac surgery and hemodialysis patients are classically at
highest risk for NOMI. The diagnostic algorithm should be
tailored on the basis of the suspected cause—arterial embo-
lization, arterial thrombosis, or nonocclusive ischemia.
PATHOPHYSIOLOGIC CLASSIFICATION
Arterial Embolism
Arterial embolism is the most common pathophysiologic
mechanism of AMI, accounting for 40% to 50% of cases.11
Most embolic events are thromboembolic and arise from a
cardiac source. The historical elements that place a patient
at risk for a thromboembolic event include atrial tachyar-
rhythmia, low ejection fraction (congestive heart failure,
cardiomyopathy), recent myocardial ischemia or infarction,
and ventricular aneurysm. Nearly one third of patients with
an SMA embolus have had an antecedent embolic event.
There is some speculation, however, that the overall
incidence of thromboembolism is declining secondary to
better guidelines for and compliance with anticoagulation
in patients with atrial fibrillation.12
Although significantly less common than a cardiac source,
additional proximal arterial sources of atheroembolic mate-
rial should also be considered. In these instances, a previous
history of cardiac valvular disease, endocarditis, proximal
aneurysm, or recent catheter-based angiography may be
noted.13
The SMA is the mesenteric vessel most commonly affected
by emboli because of its oblique origin from the visceral aortic
segment. Thromboemboli tend to lodge in the proximal
SMA because of their size, just beyond the first few jejunal
branches as the SMA tapers. A minority (15%) may lodge at
the SMA origin, but 50% lodge distal to the middle colic
artery,14 creating a classic pattern of ischemia that spares the

Figure 153-1  Intraoperative photograph of a patient with a superior
mesenteric artery embolus. Note the relative sparing of the proximal
jejunum and proximal transverse colon. (Courtesy R. M. Zwolak.)
first portion of the small intestine and the transverse colon
(Fig. 153-1). Atheroembolic emboli, in contrast, tend to be
smaller and therefore lodge in the more distal mesenteric
circulation. As a result, these emboli are likely to affect bowel
perfusion less often and in more localized areas.
Arterial Thrombosis
Acute arterial thrombosis superimposed on preexisting severe
atherosclerotic disease is the next most common cause of
AMI, accounting for 25% to 30% of cases.11,15 Many patients
with visceral atherosclerotic disease are asymptomatic before
a thrombotic event. Autopsy studies have shown that 6% to
10% of the population has a greater than 50% stenosis in at
least one mesenteric artery.19 Further, the incidence of asymp-
tomatic celiac artery or SMA stenosis greater than 50% in
patients undergoing arteriography for other peripheral vascu-
lar disease may be as high as 27%.16 Bowel infarction is more
insidious in onset because extensive collaterals are able to
maintain viability until there is final closure of a critically
stenotic vessel or collateral. Consideration must also be given
to how vascular collaterals, interrupted by previous abdomi-
nal surgery or bowel resection, may affect the region of bowel
involvement. Once established, however, the pattern of
infarction is more confluent, unlike that seen with embolic
causes. There is no sparing of the proximal jejunum or middle
colic distribution because the SMA origin is almost uniformly
occluded.17,18
Acute-on-chronic presentations are not uncommon.
Endean et al19 suggested that up to 20% of AMI patients have
a history of postprandial abdominal pain, food avoidance, or
weight loss. Even for patients with asymptomatic mesenteric
arterial lesions, the natural history of mesenteric occlusive
disease is progressive and potentially morbid. In one report,
86% of patients with more advanced three-vessel mesenteric
atherosclerosis experienced vague abdominal discomfort, had
frank mesenteric ischemia, or died during a 2.6-year mean
follow-up interval.20 Therefore, a history of symptoms of
chronic mesenteric ischemia should be elicited.
CHAPTER 153  Mesenteric Vascular Disease: Acute Ischemia 2399
In addition, complications of mesenteric revascularization
SECTION 25 MESENTERIC VASCULAR DISEASE
with angioplasty and stenting for chronic mesenteric isch-
emia can lead to AMI. Immediate endovascular failures
including distal embolization, vessel perforation, dissection,
stent migration, and thrombosis result in higher mortality
and morbidity and longer hospital length of stay compared
with stent patients without complications.21 The use of
antiplatelet therapy reduces the risk of distal embolization
or vessel thrombosis perioperatively. All patients who have
undergone revascularization for mesenteric ischemia require
long-term follow-up as both open and endovascular ap-
proaches can lead to the development of AMI secondary to
graft or stent thrombosis as a result of intimal hyperplasia,
in-stent stenosis, or stent fracture.
Spontaneous visceral artery dissection and acute exten-
sion of aortic dissection can also serve as mechanisms for
abrupt mesenteric vessel occlusion and thrombosis, as dis-
cussed later.
Nonocclusive Mesenteric Ischemia
Mesenteric vasospasm, usually in the distribution of the
SMA, is the sine qua non of NOMI. This form of AMI
accounts for approximately 20% of presentations and carries
the highest mortality rates because of its frequent association
with multisystem organ failure.22,23 Initial descriptions were
in postmortem observation of small intestinal gangrene in
patients who had shown no evidence of arterial or venous
occlusive disease.24 Several reports both remotely and recently
have described this diagnosis in patients with severe cardiac
failure, sometimes but not always with concomitant visceral
athererosclerosis.3,14,25-29 These observations formed the basis
for the hypothesis that cardiac failure, peripheral hypoxemia,
paradoxical splanchnic vasospasm, and reperfusion injury
may all contribute to the development of NOMI. Perhaps
resulting from excessive sympathetic activity during cardio-
genic shock or hypovolemia, the vasospasm represents a
homeostatic mechanism that attempts to maintain cardiac
and cerebral perfusion at the expense of visceral and periph-
eral organs. Vasopressin and angiotensin are the likely neu-
rohormonal mediators of this process.30,31 In the current era,
vasoactive medications such as epinephrine, norepinephrine,
and vasopressin have also been associated with the develop-
ment of NOMI.29-32 Once mesenteric vasospasm is initiated,
it may persist even after correction of the initiating event.
Although intestinal autoregulation may initially offset reduc-
tions in blood flow, the autoregulatory capacity is exceeded
after several hours.28
The exact mechanism of persistence of vasospasm is
unknown, but it plays an important role in the development
and maintenance of occlusive and nonocclusive mesenteric
ischemia as well as in reperfusion phenomena complicating
mesenteric revascularization.33 The degree of ischemia-
reperfusion injury appears to be related to the frequency as
well as the duration of ischemic episodes. Clark and Gewertz34
demonstrated that two 15-minute periods of low flow fol-
lowed by reperfusion resulted in more severe histologic injury
2400 SECTION 25  Mesenteric Vascular Disease
than a single 30-minute period of ischemia. NOMI results in
an analogous scenario, whereby hypoperfusion may be partial
and occasionally repetitive. Episodic reperfusion is thought
to prime the ischemic tissue with leukocytes that are attracted
to and produce reactive oxygen species.35 This concept is
supported by studies demonstrating attenuation of ischemia-
reperfusion injury by reperfusion with leukopenic blood or
blockade of endothelial cell surface receptors for leukocyte
adherence.36,37 Reports of NOMI after elective mesenteric
revascularization further support reperfusion injury in the
pathogenesis of NOMI.33
FINAL COMMON PATHWAY
OF BOWEL ISCHEMIA
The degree of reduction in blood flow that the bowel can
tolerate without permanent cellular damage is remarkable.
Only one fifth of the mesenteric capillaries are open at
any given time, and normal oxygen consumption can be
maintained with only 20% of maximal blood flow.38 Proposed
mechanisms that result in the preservation of splanchnic
tissue perfusion include direct arteriolar smooth muscle
relaxation and a metabolic response to adenosine and other
metabolites of mucosal ischemia.39 In addition, the intestinal
mucosa is able to extract increasing amounts of oxygen
during hypoperfusion40 to preserve mucosal integrity during
periods of metabolic insult. Prolonged ischemia, whatever
the pathophysiologic cause, leads to disruption of the intes-
tinal mucosal barrier, primarily through the actions of reac-
tive oxygen metabolites and polymorphonuclear neutrophils.8
The mucosal surfaces are affected first because the metabolic
demand of the mucosa is much higher than that of the
serosa. Clinically, this may be manifested with malabsorp-
tion and heme-positive diarrhea before the onset of other
symptoms.
DIAGNOSTIC EVALUATION
Delays in diagnosis and treatment remain the greatest chal-
lenge to reducing morbidity and mortality for all forms of
AMI.41 The pathologic causes of abdominal pain and tender-
ness in the elderly population fluctuate, and all too frequently,
AMI is not included in the initial differential diagnosis. Boley
demonstrated that in patients with SMA embolism, a condi-
tion that usually results in the most rapid clinical decline
because of the lack of established collateral circulation, sur-
vival decreases from approximately 50% to 30% when the
diagnosis is made more than 24 hours after the onset of symp-
toms.14 Two more recent reviews suggested that only one
third of AMI patients were correctly identified before surgical
exploration or death.42,43 Bowel necrosis is probably the best
indicator that there has been a delay in diagnosis and together
with advanced patient age has been linked to higher mortal-
ity rates.41 A high index of suspicion in the setting of a
compatible history and physical examination serves as a cor-
nerstone of prompt treatment. Once AMI is suspected, the
clinician should quickly move to appropriate testing to
confirm the diagnosis, keeping in mind that the best first test
may be an operation or arteriography.
Recently, there has been a paradigm shift in the diagnostic
algorithm for AMI. The older model, as championed by Boley
and associates,4,44 advocated early and aggressive use of diag-
nostic angiography. Today, computed tomographic angiogra-
phy (CTA) has supplanted diagnostic angiography when
occlusive AMI (but not necessarily NOMI) is suspected.
With nearly universal 24-hour access to high-resolution
CTA, the diagnosis of SMA embolus or thrombotic occlusion
can be confirmed, and the bowel can be evaluated concomi-
tantly to support or to refute the diagnosis.
Angiography still plays an important role in the diagnosis
and treatment of AMI, however. In fact, with an ever-
expanding list of endovascular treatments or adjuncts, its
therapeutic role is, in many ways, strengthened. Only its
timing and application may be somewhat changed. Gone are
the days when arteriography was performed and the patient
returned hours later, after the study had been read. Increas-
ingly, vascular surgeon–interventionalists are able to combine
the final steps of diagnosis and treatment on one table in the
operating room environment. This allows general and vascu-
lar surgeons to work together to provide definitive treatment.
In a well-designed treatment pathway, this coupling of angi-
ography and definitive surgical treatment can save precious
time in the treatment of these challenging patients.
Clinical Presentation
Many of the signs and symptoms of AMI are easily mistaken
for other, more common intra-abdominal pathologic pro-
cesses, such as pancreatitis, cholecystitis, appendicitis, diver-
ticulitis, and bowel obstruction. The classic description of
early symptoms is pain that is greater than expected on the
basis of physical examination findings. However, depending
on the exact cause of AMI and the timing of presentation,
this classic presentation may be absent in 20% to 25% of
cases.22 Until there is transmural involvement of the bowel,
there is relatively little peritoneal irritation and therefore
tenderness to palpation may be minimal. For patients who
present with SMA embolism, the onset is more abrupt,
without a prodrome, with rapid progression. On occasion, as
in Klass’ original description, there may be sudden and force-
ful bowel evacuation shortly after the onset of pain.1 An
intermediate rate of progression can be seen with SMA
thrombosis because many of these patients have developed
collaterals. Their subacute presentation may start weeks
before the final acute insult that prompts them to seek
medical attention. Patients may have abdominal pain, disten-
tion, diarrhea, acidosis, sepsis, or gastrointestinal bleeding,
singly or in combination. NOMI patients may have the most
insidious onset and a protracted clinical course. Furthermore,
they are least able to offer any history because they are already
critically ill, frequently in a hospital critical care setting. The
pain associated with NOMI can be variable in location as
well as in character.

Laboratory Evaluation
The most common laboratory abnormalities are hemocon-
centration, leukocytosis, high anion gap, and possibly lactic
acidosis in more advanced cases. High amylase, aspartate
aminotransferase, and lactate dehydrogenase can also be
observed. All these serum markers, however, are insensitive
and nonspecific for the diagnosis of mesenteric isch-
emia.45,46  D-dimer elevation after 2 hours has been cor-
related with the presence of AMI in a rat model.47 Similarly,
Acosta et  al42 showed elevated D-dimer levels in AMI
patients who presented within 24 hours of the onset of
symptoms, in contrast to patients with inflammatory condi-
tions or bowel obstruction. No patient with a D-dimer
concentration of 0.3  µg/mL (1.6  nmol/L) or less had acute
SMA occlusion, suggesting this as a possible exclusionary
test.42 In recent investigations, urinary fatty acid–binding
protein (FABP) levels hold promise as a diagnostic test
for AMI.48 First discovered in rodents, the human homo-
logue was found to be elevated in cases of documented
bowel infarction.49,50 Thuijls et  al48 demonstrated elevated
plasma and especially urinary levels of intestinal FABP,
liver FABP, and ileal bile acid–binding protein in patients
diagnosed with intestinal ischemia. Fifty consecutive patients
suspected of AMI had levels taken before diagnosis. In
all 22 patients with confirmed AMI, all three levels were
elevated. Furthermore, the urinary concentration of ileal
bile acid–binding protein was elevated specifically when
the ileum was involved, allowing localization. Overall, the
test was rapid and potentially useful for early diagnosis of
intestinal ischemia.
Diagnostic Imaging
Abdominal Plain Radiography
Abdominal plain radiographs are normal in up to 25% of
patients with AMI.51 However, ileus may be an early finding
consistent with mesenteric ischemia, and advanced cases of
intestinal ischemia may show evidence of bowel wall edema
(“thumbprinting”) or pneumatosis. Plain abdominal radiog-
raphy is most useful in excluding other causes of abdominal
pain, such as bowel obstruction or perforation.
Duplex Ultrasonography
Duplex ultrasonography accurately identifies high-grade
stenoses of the celiac artery and SMA. It is the noninvasive
diagnostic study of choice in patients with symptoms sug-
gesting chronic mesenteric ischemia but has little or no
role in the diagnosis of AMI for several important reasons.
It is highly technologist dependent, and many hospitals
do not have ready access to such specialized vascular labo-
ratory testing, especially during off-hours. The presence of
intestinal gas—which is the rule in any nonfasting patient,
let alone someone suspected of having AMI—can easily
obscure visualization of the mesenteric vessels. Any abdomi-
nal tenderness also compromises the study and adds to the
patient’s suffering.
CHAPTER 153  Mesenteric Vascular Disease: Acute Ischemia 2401
SECTION 25 MESENTERIC VASCULAR DISEASE
Computed Tomography
Several authors have described the use of ultrafast multide-
tector CTA (MDCTA) for the evaluation of both acute and
chronic mesenteric ischemia.52-55 The widespread availability
of the newest generation of computed tomography (CT)
scanners has evolved the diagnostic algorithm for AMI and
offers greater speed than angiography. CTA provides a signifi-
cant amount of information about the central arterial and
venous circulations. Accurate timing of contrast injection
and fine slices through the upper abdomen usually provide
excellent visualization of the celiac artery and SMA (Figs.
153-2 and 153-3). CT can also exclude other causes of
abdominal pain and assess bowel perfusion to some extent.
The timing of intravenous contrast administration is tailored
to the specific clinical question. The use of traditional oral
“positive” contrast agents detracts from image quality, and
most visceral CTA protocols recommend the use of a “nega-
tive” oral contrast agent such as water (500 to 750 mL) given
immediately before the scan. This prevents image artifact
from pooled areas of high opacification within the intestinal
tract and also enhances the ability to see bowel wall enhance-
ment (or the lack thereof) in the late arterial phase of the
arterial contrast bolus.51 Main branches of the celiac artery
and SMA are seen remarkably well by use of MDCTA because
of thinner collimation (0.5 to 1.5 mm) and overlapping data
acquisition. This reduces the amount of volume averaging
and creates higher quality three-dimensional volume sets for
reformatting and interpretation.
Initial interest in so-called biphasic CT was generated in
the evaluation of pancreatic and hepatic lesions; it includes
an arterial phase and a delayed phase, allowing time-based
visualization of the portal venous system. This method has
been applied more recently to detect the early findings of
AMI. That is, the same scan is used to detect arterial narrow-
ings or occlusions and to assess associated changes in bowel
wall thickness, pneumatosis, and mucosal or bowel wall
enhancement patterns that support the diagnosis of AMI and
can also diagnose mesenteric venous thrombosis (Fig. 153-4).
Kirkpatrick et al56 sought to improve on a previous retrospec-
tive report that used single-detector helical CT.57 Sixty-two
patients suspected of having AMI underwent biphasic
MDCTA and were evaluated prospectively. As in the previ-
ous study, no single CT finding was both sensitive and specific
(Table 153-1). Twenty-six patients, however, had AMI con-
firmed at surgical exploration or on pathologic examination,
and all these patients had been correctly identified by the
interpreting radiologist as having AMI. An additional four
scans interpreted as demonstrating AMI turned out to be false
positives, with the ultimate diagnosis of Crohn’s disease (2),
neutropenic enterocolitis (1), and infectious enterocolitis
(1). Thus, the initial interpretation had a sensitivity of 100%
and a specificity of 89% for the diagnosis of AMI. In the same
study, CTA visualization was judged to be satisfactory in all
cases up to second-order branches of both the celiac artery
and the SMA. Angiography was available in only three
patients but correlated well with the CTA findings. In a more
2402 SECTION 25  Mesenteric Vascular Disease

A B C

D E
Figure 153-2  A, Three-dimensional volume rendering of arterial phase MDCTA shows an abrupt mid–superior mesenteric artery (SMA) occlusion
consistent with embolus. B, Sagittal multiplanar reformat shows the same occlusion. C, SMA occlusion seen on an axial CTA slice (arrow).
D, Coronal multiplanar reformat reveals left kidney infarction. E, Transverse portal venous phase MDCTA depicts thrombus in the left ventricle
as the likely embolic source. (From Aschoff AJ, et al: Evaluation of acute mesenteric ischemia: accuracy of biphasic mesenteric multi-detector CT
angiography. Abdom Imaging 34:345-357, 2009.)

recent retrospective chart review using similar MDCTA pro-
tocols and even higher resolution CT, Aschoff et al58 were
able to duplicate Kirkpatrick’s findings in terms of overall
accuracy. Again, no one CT finding was perfectly sensitive
or specific for AMI, but using a combination of CT criteria
(pneumatosis, bowel edema, other solid-organ infarction) to
generate an overall impression, these authors were able to
achieve positive and negative predictive values of 100% and
96%, respectively.
Arteriography
Traditional catheter-based arteriography (Fig. 153-5) has
been supplanted by MDCTA as the definitive diagnostic
study for occlusive forms of AMI. Patients with strongly
suspected NOMI may still benefit from a more traditional
angiographic approach, as long as there is no immediate
need for exploration based on the physical examination.
Arteriography’s role in the therapy for all forms of AMI,
however, has been strengthened. It offers several comple-
mentary or stand-alone treatment options, depending on the
specific disease, including injection of intra-arterial vasodila-
tors,59 thrombolysis,60 and angioplasty with or without stent-
ing.61 These are discussed in more detail in the sections on
treatment of nonocclusive mesenteric ischemia and endo-
vascular treatment. As vascular surgeons become accom-
plished interventionalists and as intraoperative fluoroscopy
improves, the confirmatory diagnostic arteriogram can be
accomplished in the operating room, followed by immediate
revascularization and surgical exploration and thus limiting
a delay to treatment.
Magnetic Resonance Angiography
Magnetic resonance angiography (MRA) of the splanchnic
vessels is theoretically appealing because it is noninvasive,
avoids the risk of allergic reaction and nephrotoxicity associ-
ated with iodinated contrast agents, and may not be as opera-
tor dependent as duplex ultrasound. Magnetic resonance
imaging of the mesenteric vasculature can incorporate both
functional and anatomic evaluations, which hold promise for
the diagnosis of chronic mesenteric ischemia.62,63
 CHAPTER 153  Mesenteric Vascular Disease: Acute Ischemia 2403

SECTION 25 MESENTERIC VASCULAR DISEASE

A

Figure 153-3  CTA sagittal multiplanar reformat shows an acute B

thrombotic occlusion of the proximal superior mesenteric artery.
Bowel resection was performed 3 days before this image was obtained.
The concomitant celiac stenosis suggests an acute-on-chronic presen-
tation of acute mesenteric ischemia. (From Aschoff AJ, et al: Evaluation
of acute mesenteric ischemia: accuracy of biphasic mesenteric multi-
detector CT angiography. Abdom Imaging 34:345-357, 2009.)

C
Figure 153-4  A, CTA demonstrating hepatic venous air (circle).
B, The superior mesenteric artery is occluded (arrow). C, There is
extensive colonic pneumatosis and ascites (arrows). (From http://www.
learningradiology.com/notes/ginotes/mesentericischemiapage.htm.)

Table 153-1 Analysis of Computed Tomography Findings

Finding Patients with AMI (n = 26) Control Group (n = 36) Sensitivity (%) Specificity (%)

Pneumatosis intestinalis 11 0 42 100

SMA or combined celiac and IMA occlusion* 5 0 19 100
Arterial embolism 3 0 12 100
SMA or portal venous gas 3 0 12 100
Focal lack of bowel wall enhancement 11 1 42 97
Free intraperitoneal air 5 2 19 94
Superior mesenteric or portal venous thrombosis 4 2 15 94
Solid-organ infarction 4 2 15 94
Bowel obstruction 3 2 12 94
Bowel dilatation 17 6 65 83
Mucosal enhancement 12 7 46 81
Bowel wall thickening 22 10 85 72
Mesenteric stranding 23 14 88 61
Ascites 19 24 73 33

From Kirkpatrick ID, et al: Biphasic CT with mesenteric CT angiography in the evaluation of acute mesenteric ischemia: initial experience. Radiology 229:91-98, 2003.
AMI, Acute mesenteric ischemia; IMA, inferior mesenteric artery; SMA, superior mesenteric artery.
*Patients with both celiac and IMA occlusion also had evidence of distal disease in the SMA distribution.
2404 SECTION 25  Mesenteric Vascular Disease
Figure 153-5  Lateral aortogram of a patient with acute mesenteric
ischemia due to superior mesenteric artery thrombosis (small arrow).
Note the chronic occlusion of the celiac artery (large arrow).
The weakness of MRA is its relatively poor spatial resolu-
tion, which, even on the best systems, is limited to 1 mm3.
Gadolinium-enhanced MRA does not currently provide suf-
ficient resolution to evaluate distal braches or the inferior
mesenteric artery or to demonstrate distal emboli, nonoc-
clusive low-flow states, small-vessel occlusion, or vasculitis.64
This essentially limits evaluation of the mesenteric arteries
to the proximal celiac artery and SMA. In addition, the
secondary signs of AMI, such as indurated fat and bowel wall
thickening, which are routinely delineated by CT, are more
difficult to assess with MRA. In essence, these issues as well
as the lack of uniform and timely availability and difficulty
in obtaining interpretation make MRA a less reliable
modality.
Diagnostic Laparoscopy
Laparoscopy in the setting of AMI has limited ability to assess
bowel viability. Serosal color can be difficult to judge and can
be distorted significantly by a malfunctioning or improperly
calibrated camera. Furthermore, segmental ischemia can be
missed because of the difficulty in “running” the bowel along
its entire length and over all surfaces. To increase the
sensitivity of diagnostic laparoscopy, some authors have
successfully used fluorescein with a laparoscopic ultraviolet
light.65-67 Nevertheless, diagnostic laparoscopy for this indica-
tion has not been widely accepted68 because it may still miss
areas of nonviable bowel.
TREATMENT
Initial Resuscitation and Critical Care
Fluid resuscitation of a patient with AMI should begin imme-
diately with isotonic crystalloid solution and continue with
blood, if necessary. Electrolyte imbalances (hyperkalemia)
should be monitored and corrected. Invasive monitoring
(hourly urine output, continuous central pressure, and arte-
rial pressure monitoring) is advisable from the beginning to
ensure that all parameters are optimized before intravenous
contrast administration or operative exploration. Broad-
spectrum antibiotics should be given to guard against trans-
located bacteria and sepsis. If there are no contraindications,
intravenous heparin should also be administered to maintain
a partial thromboplastin time greater than twice normal.
The presentation of sepsis and organ dysfunction in these
patients is common, and for the most part, these disorders are
managed as they would be in other situations. Vasopressors,
however, may worsen ischemia in marginally viable bowel
and exacerbate visceral vasospasm. Before the initiation of
any vasopressor, volume resuscitation must be confirmed by
the presence of adequate right-sided heart filling pressures.
Because of the large and ongoing fluid sequestration in these
patients, 24-hour crystalloid requirements in excess of 15 L
are not uncommon. When necessary, better vasopressor
options include low- to mid-dose dopamine (3 to 8 µg/
kg/min) and epinephrine (0.05 to 0.10 µg/kg/min). Pure
α-adrenergic agents should be avoided if possible, even after
successful revascularization.8
Treatment of Nonocclusive Mesenteric Ischemia
NOMI accounts for more than 10% to 20% of cases of acute
mesenteric circulatory disorders and leads to extensive irre-
versible intestinal necrosis. The prognosis is poor, despite the
absence of organic obstruction in the principal arteries. The
primary treatment of NOMI is medical, with extensive criti-
cal care support and prompt arteriography. Operative explo-
ration is reserved for signs of peritonitis suggesting the
presence of gangrenous bowel that requires excision.
Interventional therapies can be initiated at the time of
the diagnostic arteriogram and are targeted at relieving vaso-
spasm by intra-arterial infusions of vasodilator medications
(Fig. 153-6). The angiographic appearance of NOMI can
be subtle, but Siegelman et  al69 described four reliable arte-
riographic criteria for the diagnosis of mesenteric vasospasm:
(1) narrowing of the origins of multiple branches of the
SMA, (2) alternate dilatation and narrowing of the intes-
tinal branches—the “string of sausages” sign (Fig. 153-7),
(3) spasm of the mesenteric arcades, and (4) impaired filling
of the intramural vessels. The most common intra-arterial

Figure 153-6  Arteriogram with selec-
tive superior mesenteric artery (SMA)
injections. A, Severe SMA vasospasm
with narrowing of all SMA branches.
Intramural vessels are not seen owing to
severe ischemia. B, There is significant
improvement after several hours of vaso-
dilator administration. (From Trompeter
M: Non-occlusive mesenteric ischemia:
etiology, diagnosis, and interventional A B
therapy. Eur Radiol 12:1179-1187, 2002.)
agent used in the majority of reports is the phosphodiesterase
inhibitor papaverine. There are multiple case reports of the
local infusion of vasodilators—either papaverine18,70,71 or
prostaglandin analogues72—leading to improvement.
Boley et al4 reported favorable mortality rates of 40% to
50% with the aggressive use of intra-arterial vasodilators and
suggested that the extent of bowel resection during laparot-
omy (whatever the cause of ischemia) could be significantly
reduced if vasodilatation were performed preoperatively.
Once the angiographic diagnosis of NOMI is made and
other causes of acute abdomen are excluded, intra-arterial
Figure 153-7  Selective superior mesenteric artery arteriogram in a
patient with nonocclusive mesenteric ischemia. Note the “string of
sausages” appearance of some of the ileocolic branches (arrow). (From
Clark RA, et al: Superior mesenteric angiography and blood flow mea-
surement following intra-arterial injection of prostaglandin E1. Radiology
134:327-333, 1980.)
CHAPTER 153  Mesenteric Vascular Disease: Acute Ischemia 2405
SECTION 25 MESENTERIC VASCULAR DISEASE
papaverine is initiated at a dose of 30 to 60 mg/h and often
continued for several days as long as the patient’s condition
remains stable or until there is improvement. Because papav-
erine is metabolized primarily in the liver, hypotension is
uncommon as long as the catheter remains in the SMA, but
careful monitoring of the blood pressure, heart rate, and
rhythm is appropriate. If a sudden decrease in blood pressure
is noted, the papaverine infusion should be substituted with
saline, and a plain abdominal radiograph should be obtained
to confirm the position of the catheter. Finally, heparin
sodium is chemically incompatible with papaverine and
should not be infused simultaneously through the same
catheter. In the case of resolved abdominal symptoms,
a second arteriogram is advisable before the cessation of
papaverine, unless the risk of contrast nephropathy precludes
it (see Fig. 153-6B).
Mitsuyoshi et al72 showed that eight of nine patients with
MDCTA evidence of NOMI (Fig. 153-8) treated promptly
with high-dose intravenous or intra-arterial prostaglandin E1
survived. Intravenous dosing was 0.01 to 0.03 µg/kg/min and
was continued for a mean of 4.8 days. In contrast, in the group
that was not imaged with MDCTA or treated with prosta-
glandin E1, 9 of 13 patients died. Although these results are
admirable, it is not clear whether they are ascribable to pros-
taglandin E1 treatment or to a heightened awareness of the
problem, earlier imaging with MDCTA, and prompt diagno-
sis and supportive treatment.
Surgical Treatment
Surgical exploration is required for all patients who have
evidence of any threatened bowel, regardless of the underly-
ing cause. The intraoperative appearance of the bowel can be
deceiving. Bowel that is nearing irreversible necrosis can be
deceptively normal in appearance; conversely, bowel that
appears severely ischemic may be viable after revasculariza-
tion. Thus, in all cases the surgeon should proceed with
revascularization before resecting any intestine unless faced
with an area of frank necrosis or perforation and peritoneal
2406 SECTION 25  Mesenteric Vascular Disease

Figure 153-8  CTA appearance of non-

occlusive mesenteric ischemia. A, Sag­
ittal volume-rendered image shows
diffuse narrowing of the main celiac and
superior mesenteric arteries. B, Coronal
oblique volume-rendered image of the
same patient shows pruning of the supe-
rior mesenteric artery branches (arrows).
Note the dilated, fluid-filled small intes-
tine and the superior mesenteric vein
(arrowheads). (From Horton KM, et al: Mul-
tidetector CT angiography in the diagnosis
A B of mesenteric ischemia. Radiol Clin North
Am 45:275-288, 2007.)

soilage. In this case, resection of the affected bowel without small lymphatics that are divided to gain exposure of the
reanastomosis and with containment of the spillage should SMA. The SMA lies to the left of the superior mesenteric
be achieved rapidly before revascularization. Only in a very vein and can be fragile. Exposure of the more proximal
few patients—those who are already in extremis and present segments is possible by judicious mobilization of the inferior
with massive bowel necrosis—can revascularization conscio- pancreatic border (exercise caution in dealing with the
nably be withheld. Preparation and draping of all patients pancreas), the nearby splenic vein, and its tributaries from
undergoing laparotomy for presumed AMI should include the pancreas.
both lower extremities at least to the knee to allow the
harvest of saphenous or femoral vein for bypass.
The abdomen is best explored through a vertical midline
incision (Fig. 153-9). There are two variations in the tech-
nique for exposing the SMA below the pancreas. Selection
between the two is based on the surgeon’s level of confidence
regarding the need for simple embolectomy or more complex Marginal artery
arterial repair with or without bypass. In the case of a con-
firmed embolus and a more normal-appearing SMA, the
artery can be approached anteriorly at the base of the trans-
verse mesocolon without formal mobilization of the fourth A
portion of the duodenum or ligament of Treitz. If the SMA Celiac artery
is diseased or thrombosis is the cause, a more lateral approach SMA
to the SMA above the fourth portion of the duodenum is (under
preferred to facilitate a retrograde bypass, if necessary. These pancreas)
Ascending
techniques are described in the sections that follow and are Duodenum branch of
depicted in Figures 153-9 and 153-10. left colic artery
IMA
Superior Mesenteric Artery Embolectomy
Anterior exposure of the SMA for straightforward embo-
lectomy is achieved by elevating the omentum and transverse Ureter Superior
colon; the small intestine is wrapped in moist laparotomy rectal artery
pads and retracted to the right. A horizontal incision is B
made in the peritoneum at the base of the transverse
Figure 153-9  A and B, Operative exposure of the infrapancreatic
mesocolon (see Fig. 153-9B, dotted line). Careful dissection superior mesenteric artery (SMA). IMA, Inferior mesenteric artery.
in the mesentery initially uncovers venous tributaries of (From Kazmers A: Operative management of acute mesenteric ischemia.
the superior mesenteric vein, autonomic nerve fibers, and Ann Vasc Surg 12:187-197, 1998.)
 CHAPTER 153  Mesenteric Vascular Disease: Acute Ischemia 2407

SECTION 25 MESENTERIC VASCULAR DISEASE

Celiac artery

Occlusion

SMA
Aorta

Ligament
of Treitz

Duodenum
A

C Graft

If D E
thrombus
Figure 153-10  A, Operative exposure
and preparation of the superior mesen-
teric artery (SMA) for bypass or patch. If embolus
B, Linear arteriotomy. C-E, Creation B
Patch
of a beveled, end-to-end anastomosis.
F, Patch closure of the SMA. (From
Kazmers A: Operative management of
acute mesenteric ischemia. Ann Vasc Surg
12:187-197, 1998.) F

A segment of the proximal SMA between the middle and
right colic branches is isolated. Near-circumferential dissec-
tion is frequently required to isolate and to control any of the
jejunal branches in this segment. After systemic hepariniza-
tion, the artery is opened transversely (Fig. 153-11) in a
segment of sufficient diameter to allow direct repair. For
diminutive vessels, a short longitudinal arteriotomy with
patch closure may be considered. The proximal SMA is
vented to allow any clot to be expelled without the use of an
embolectomy catheter if possible. When necessary, catheter
embolectomy is typically performed with a 3F or 4F balloon
catheter. With extraction of the embolus, torrential and pul-
satile inflow should be expected.
Distally, a smaller embolectomy catheter, typically 2F or
3F, is employed. Great care must be taken to avoid damage
or rupture of the fragile mesenteric arteries. Difficulty in
passing a catheter down multiple small branches adds to the
complexity of the distal embolectomy. An alternative or
adjunct to balloon embolectomy of the distal mesenteric
vessels is for the surgeon to place a hand on either side of
the mesentery and “milk” thrombotic material out of the
vessels. After all macroscopic clot is cleared, consideration
can also be given to the administration of a small, one-time
dose of a thrombolytic agent (recombinant tissue plasmino-
gen activator or urokinase) into the distal vessels. When all
thrombus is removed, the arteriotomy is closed primarily

SMA
Figure 153-11  Traditional transverse arteriotomy
for superior mesenteric artery (SMA) embolectomy.
(From Kazmers A: Operative management of acute
mesenteric ischemia. Ann Vasc Surg 12:187-197, 1998.)
2408 SECTION 25  Mesenteric Vascular Disease
with interrupted sutures or with vein patch, and flow is
re-established.
Superior Mesenteric Artery Bypass
As mentioned previously, when bypass is considered, the
lateral portion of the SMA is exposed rather than the more
limited exposure provided by a strictly anterior approach.
The peritoneum is opened lateral to the duodenum, down
over the aorta, and onto the left or right common iliac artery
(see Fig. 153-9B, dashed line). Several combinations of graft
orientation and conduit are available. The decision is influ-
enced largely by the suitability of potential inflow vessels for
a proximal anastomosis and by the presence or absence of
peritoneal soilage. In the emergent setting, a single bypass to
the SMA is all that is required. The preference for two-vessel
revascularization,73 which most surgeons espouse in the
performance of elective bypass for chronic symptoms, does
not apply.
Graft orientation is influenced mainly by the degree of
atherosclerosis and occlusive disease present in the inflow
vessels and by the overall lie of the graft. Given the choice,
most surgeons prefer a retrograde graft orientation, with its
origin from the right common iliac artery in a “lazy C” con-
figuration (Fig. 153-12A). This avoids any aortic clamping
and usually provides a good lie to prevent kinking. Second-
choice inflow sources for retrograde bypasses involve similar
lazy C grafts from the left iliac artery or distal infrarenal
aorta. With any of these configurations, the graft lie tends
to be improved by increasing the graft length slightly and
B dynamically and physiologically stressful aortic cross-clamp
Celiac
artery
Aorta
Vein
SMA graft
Graft
C Graft
A Common
Iliac
artery
Figure 153-12  Optimal orientation for retrograde superior mesen-
teric artery (SMA) bypass. A, Prosthetic. B, Vein. C, Proximal iliac graft
anastomosis. (From Kazmers A: Operative management of acute mesen-
teric ischemia. Ann Vasc Surg 12:187-197, 1998.)
Left renal
vein
SMA
Synthetic
bypass
Aorta
Duodenum
Figure 153-13  Short retrograde aorta–superior mesenteric artery
(SMA) bypass. (From Valentine RJ, et al: Anatomic exposures in vascular
surgery, ed 2, Philadelphia, 2003, Lippincott Williams & Wilkins.)
performing an end-to-end graft-to-SMA anastomosis, as pic-
tured in Figure 153-10C to E. Alternatively, a very short
retrograde bypass using a larger diameter graft (8 to 10  mm)
can be configured from the immediately infrarenal aorta (Fig.
153-13), but the potential for kinking with shorter grafts
can be more difficult to anticipate until all the retractors
are removed. When distal inflow sources are unclampable,
heavily diseased, or aneurysmal, an antegrade bypass can be
considered. Advantages of the antegrade bypass include the
fact that the supraceliac aorta is often relatively free of disease
and the straighter graft orientation is less prone to kinking.
Dissection of the supraceliac aorta is technically more
demanding, however; it requires more time and adds a hemo-
if a partial occluding clamp is not possible. In addition, for
most aortas, the application of a side-biting clamp with suf-
ficient room to create an anastomosis produces a functional
aortic occlusion.
Synthetic bypass grafts of 6- to 8-mm Dacron or externally
supported polytetrafluoroethylene are preferred because of
the better size match, ease of handling, availability, kink
resistance, and general perception that long-term patency is
better. The superior patency of prosthetic mesenteric bypasses,
however, is not well documented. Therefore, the choice of
conduit is heavily influenced by the degree of abdominal
contamination and the perceived risk of subsequent graft
infection. The actual rate of mesenteric graft infection is not
known with certainty, but when present, it is potentially
catastrophic and likely to involve virulent organisms. There-
fore, if good-quality vein is available, it is preferred in the
presence of significant peritoneal soilage. Great saphenous
vein and thigh femoral vein are the primary options. Modrall
et al74 reported that symptomatic recurrences were less
common in patients bypassed with femoral vein conduit com-
pared with great saphenous vein. In practice, however, the
additional time and expertise required to harvest a deep leg
vein is too much to consider in such critically ill patients.
Great caution must be used in fashioning a vein graft because

Greater omentum
Transverse
colon
Aorta
Graft
Common Iliac
A artery
B C
Figure 153-14  A-C, Technique for omental flap coverage of a retro-
grade superior mesenteric artery bypass. (From Kazmers A: Operative
management of acute mesenteric ischemia. Ann Vasc Surg 12:187-197,
1998.)
the smaller diameter and thin-walled nature of veins make
them more prone than synthetic grafts to kinking and exter-
nal compression. When prosthetic graft use is unavoidable,
Kazmers75 illustrated a useful technique to provide coverage
of a retrograde bypass by bringing an omental flap through
the transverse mesocolon (Fig. 153-14).
Assessment of Bowel Viability
After revascularization has been accomplished, the viability
of the bowel must be reassessed. If possible, 20 to 30 minutes
of reperfusion time should be permitted while retractors are
being repositioned before a decision is made about viability.75
The initial clinical evaluation of the bowel consists of assess-
ment for visible and palpable pulsations in the mesenteric
arcade, normal color and appearance of the bowel serosa,
peristalsis, and bleeding from cut surfaces. Each of these is
subjective and prone to inaccuracy; with the use of clinical
criteria alone, bowel viability can be successfully determined
with a sensitivity of only 82% and a specificity of 91%.76
Wright and Hobson77 reported that absence of pulsatile
signals on the antimesenteric border of the intestine as
detected with a continuous wave 9- to 10-MHz Doppler ultra-
sound probe implies a nonviable segment. The clinical prac-
ticality of this technique combined with surgical judgment
has been demonstrated in multiple studies.76,78,79 As a stand-
alone method of determining intestinal viability, however,
Doppler assessment has its limitations because it may
miss weak signals in small vasoconstricted vessels in other-
wise viable bowel.80 Other adjunctive methods of bowel
viability assessment have been proposed. Highly accurate
CHAPTER 153  Mesenteric Vascular Disease: Acute Ischemia 2409
quantification of perfusion is possible with use of fluorescein
SECTION 25 MESENTERIC VASCULAR DISEASE
and a perfusion fluorometer81 or a laser Doppler flowmeter,82
but special equipment requirements and technical consider-
ations make this less practical for routine clinical use.
Whitehill et al83 found that Doppler ultrasound evaluation,
photoplethysmography, and fluorescein injection may be too
sensitive in some cases for an accurate determination of
bowel viability, yielding false-positive results by detecting
levels of flow below that needed to sustain tissue viability.
Ultimately, accurate determination of intestinal viability
is the product of clinical judgment and timely re-evaluation.
The need to preserve as much bowel length as possible should
deter the surgeon from being overly aggressive in resecting
any questionably viable bowel. The option of deferring
extensive bowel resection and re-anastomosis underscores
the fundamental importance of a mandatory second-look
procedure.
Endovascular Treatment
Superior Mesenteric Artery Embolization
Acute arterial occlusion caused by thromboembolization
progresses to bowel necrosis faster than either NOMI or
mesenteric venous thrombosis. Restoration of flow must be
accomplished within a few hours to prevent bowel necrosis
and the incipient downward spiral that frequently results in
death. Based on this, one would suspect that thrombolysis
takes too long to achieve timely revascularization. Neverthe-
less, there are increasing numbers of successful, single-patient
case reports of percutaneous endovascular procedures using
mechanical and chemical thrombectomies.84-92 It is difficult
to determine the technical failure rate from such small case
reports, which by their nature focus on positive results.
If it is more broadly applied, one could easily surmise that
revascularization failure is more common with endovascular
lysis than with direct surgical embolectomy. Wang et al93
offered a retrospective report of seven patients with SMA
emboli who were treated with catheter-based thrombolysis,
which was successful in only four. Despite a shorter time to
diagnosis and initiation of treatment in the lysis group com-
pared with a similar cohort of nine surgically treated patients,
there was no survival difference. Even when technically suc-
cessful, percutaneous catheter thrombectomy and certainly
chemical thrombolysis can be very time-consuming com-
pared with a straightforward open embolectomy.
Schoots et al9 reviewed 20 case reports and 7 small series
published during a 47-year span for a total of 48 patients.
Interestingly, only 33% of patients demonstrated total or
near-total arteriographic occlusion of the SMA before treat-
ment. Technical resolution of thrombus was achieved in 43
patients, but 18 patients still required operative exploration
for bowel resection. Only one surgical embolectomy was per-
formed. Forty-three of the patients survived. This review does
not give any credence to the use of percutaneous thromboly-
sis as an efficacious or even safe mode of therapy for acute
SMA embolism. It only serves to magnify the enormous pub-
lication bias inherent in the literature on this topic.
2410 SECTION 25  Mesenteric Vascular Disease
Another shortcoming of a less invasive approach to SMA
embolism is the lack of a built-in assessment of bowel viabil-
ity. Surgical treatment incorporates open embolectomy with
a thorough assessment of intestinal viability. Patient mortal-
ity is closely associated with bowel necrosis, and when resec-
tion is necessary, it cannot be delayed. Therefore, a significant
weakness of a less invasive approach is that there is often no
direct evaluation of intestinal viability. To avoid abdominal
exploration, the patient’s overall clinical condition, labora-
tory markers, and occasionally laparoscopy are substituted.
These substitutes are unreliable, however, and diagnostic
laparoscopy for this indication has not been widely accepted
because it may miss areas of nonviable bowel.68
Superior Mesenteric Artery Thrombosis
Terminal thrombosis of an atherosclerotic SMA is perhaps
the most challenging AMI cohort to treat endovascularly.
Successful treatment requires revascularization, meaning that
some method must be used to quickly recanalize an elongated
occlusion that, unlike with embolic presentations, typically
occupies the origin and initial 3 to 6 cm of the SMA. As
described previously, operative bypass to the SMA is tradi-
tionally required. The operation can be complex, and recov-
ery is challenging in these very ill patients. Thus, a less
invasive option for SMA revascularization is theoretically
appealing.
Endovascular treatment of mesenteric ischemia has been
well described for subacute or chronic presentations, espe-
cially in patients at high operative risk or as a bridge to elec-
tive surgical bypass after the acute illness has resolved.94-97
However, it is not generally applied to patients with AMI
who require emergent revascularization with the potential
need for bowel resection. Although a percutaneous procedure
has the potential to restore blood flow more expeditiously
without the need to obstruct inflow and outflow, it does not
allow an assessment of bowel viability. Furthermore, endovas-
cular treatments necessitate advanced endovascular skills
and, even in the most experienced hands, can take substan-
tial time, which might actually delay revascularization. Nev-
ertheless, a few case reports of percutaneous interventional
treatment of AMI have been published.85,87,88,90,98 Widespread
experience is lacking, and this approach has shortcomings
similar to those discussed for the endovascular treatment of
SMA embolism. Indeed, our experience with percutaneous
stenting in acutely ischemic patients has been disappointing
in terms of both technical success and patient outcome.99
This experience led directly to a more efficacious hybrid
technique. In our practice, we now reserve percutaneous mes-
enteric stenting for patients with chronic or subacute presen-
tations who do not require a detailed assessment of bowel
viability.
Hybrid Procedure: Retrograde Open
Mesenteric Stenting
Wyers et al99 from Dartmouth reported a hybrid open-
interventional approach for the treatment of acute
atherosclerotic SMA thrombosis that involves an efficient,
less invasive mesenteric revascularization without compro-
mising important general surgical principles. In fact, the
general surgical principles of thorough abdominal explora-
tion, sepsis control, and low threshold for second-look opera-
tions must be honored to increase the chances of a favorable
outcome. Similar to a technique in an earlier case report by
Milner et al,100 the Dartmouth authors described retrograde
open mesenteric stenting (ROMS) of the SMA in six patients.
In this ROMS approach, the visceral peritoneum is incised
horizontally or longitudinally at the base of the transverse
mesocolon, the SMA is controlled, and a local thromboen-
darterectomy of the SMA is performed if necessary. Placing
a patch angioplasty then facilitates retrograde cannulation of
the SMA with a long, flexible sheath directed toward the
aorta (Fig. 153-15). Because of the superior pushability with
sheath access so close to the obstruction, technical success
was 100%, even in the five patients who had previous unsuc-
cessful attempts to cross the SMA from a percutaneous ante-
grade approach. Often, more than one balloon-expandable
stent is required to fully treat these SMA lesions, which are
typically 3 cm or longer (Fig. 153-16).
This was a small series with no statistically significant
results, but the ROMS outcomes were promising. The ROMS
group suffered only 17% in-hospital mortality, compared with
80% among five patients treated with conventional mesen-
teric bypass. Recurrent stenosis after ROMS, as with all forms
of mesenteric stenting,61,95 happens frequently and relatively
Transverse
colon
Aorta
Cutout
showing
stent in
SMA
origin
SMA
Pancreas
SMV
Figure 153-15  Retrograde open mesenteric stenting with a long 6F
sheath placed through the patched superior mesenteric artery (SMA).
The inset illustrates a stent deployed in the proximal SMA. SMV, Supe-
rior mesenteric vein.

Figure 153-16  Retrograde open mesenteric
stenting. A, Intraoperative arteriogram during
retrograde superior mesenteric artery (SMA)
injection. Note the proximity of the sheath’s point
of entry (black arrow) and the sheath’s tip (white Aorta
arrow) to the proximal SMA occlusion. There is no
reflux of contrast material into the aorta. B, Intra-
operative lateral fluoroscopic image of two stents
(underscored by a white line) deployed in the SMA
origin with the 0.018-inch wire still in place. Note
the lumbar vertebral bodies to the left. C, Com-
pletion retrograde arteriogram with free reflux of
contrast material into the aorta and no residual
angiographic stenosis. P, Approximate location of
SMA patch angioplasty. (From Wyers MC, et al: Ret-
rograde mesenteric stenting during laparotomy for
acute occlusive mesenteric ischemia. J Vasc Surg A C
45:269-275, 2007.)
early, so we recommend duplex surveillance for the first
month and every 3 months thereafter. Most patients with
recurrent stenosis can be re-treated with a percutaneous
approach as outpatients. Many of these patients remain poor
operative candidates and have limited life expectancies
because of comorbidities.101 In this situation, even repeated
SMA dilatations are a viable, safe option. For patients who
make a good recovery and are nutritionally sound, a more
durable operative bypass may be considered.94 ROMS during
emergent laparotomy for AMI is a promising technique and
an attractive alternative to emergent surgical bypass. This
method needs to be tested by others to determine its true
value in comparison to traditional methods.
OTHER CONSIDERATIONS
Visceral Dissection
Acute Aortic Dissection
Visceral malperfusion is a devastating complication of acute
Stanford type A and B dissection, as discussed in Chapter
138. Recent population-based studies have estimated that the
incidence of acute aortic dissection ranges from 2.9 to 4.7 per
100,000 person-years, with visceral involvement reported at
varying rates.102-105 Risk factors for aortic dissection include
older age, male gender, hypertension, and structural abnor-
malities of the aortic wall, without any known specific risks
for mesenteric involvement.106,107 The initial manifestations
of acute aortic dissection are complicated by malperfusion
syndromes in 25% to 40% of patients.108-110 The mechanism
of end-organ ischemia is a result of either a dynamic or static
obstruction. A dynamic obstruction occurs when the septum
prolapses into the vessel ostium during the cardiac cycle and
the compressed true lumen, although anatomically intact, is
unable to provide adequate perfusion. In static obstruction,
CHAPTER 153  Mesenteric Vascular Disease: Acute Ischemia 2411
SECTION 25 MESENTERIC VASCULAR DISEASE
Anterior
Anterior Aorta
SMA
SMA
Spine
B
Aorta SMA
P
the cleavage plane of the dissection extends into the branch
vessel, reducing true lumen flow, which may be further com-
promised by false lumen thrombosis. When a dissection
shears the aortic intimal-medial layer around the vessel
ostium and the branch vessel flow is provided by the false
lumen, there is rarely evidence of ongoing malperfusion.111
The goals of treatment of aortic dissection with malperfu-
sion syndrome primarily involve repairing the entry tear,
either surgically or with an endograft, thereby changing the
flow dynamics of the true and false lumen, resolving a dynamic
obstruction. When persistent malperfusion occurs, aortic fen-
estration equalizes peak systolic pressure between the two
lumina in the aorta, decompressing the false lumen. Unlike
dynamic obstruction, static obstruction is unlikely to resolve
with restoration of aortic true lumen flow alone and usually
requires revascularization by stenting or bypass.
See treatment of malperfusion syndrome in Chapter 138
for further detailed discussions.
Spontaneous Visceral Dissection
Spontaneous visceral dissection is a rare vascular pathologic
process. Patients usually present with acute abdominal pain,
but there are reports of intestinal angina with weight loss
from a chronic dissection causing lumen compromise.
However, with the increasing popularity of CT scan for inves-
tigating abdominal pain combined with technical advances
in MDCTA, spontaneous isolated celiac and SMA dissection
has been reported more frequently in recent years as an inci-
dental finding. Most commonly identified by CT, it can also
be diagnosed by duplex ultrasound, magnetic resonance
imaging, and catheter-based arteriography.112,113 Reported risk
factors include hypertension, male gender, atherosclerosis,
pregnancy, connective tissue disorders, fibromuscular dyspla-
sia, vasculitis, and trauma; however, a definitive pathologic
cause is rarely identified.114 Spontaneous dissections of the
2412 SECTION 25  Mesenteric Vascular Disease

A B

C D
Figure 153-17  Reconstructed CTA findings indicated for primary endovascular stenting. Severe compression of the true lumen (A) and a patent
superior mesenteric artery stent and complete obliteration of the false lumen (B) at 60-month follow-up CT. Large dissecting aneurysm (C, 20 mm
in diameter) and nearly complete disappearance of the aneurysm (D) at 36-month follow-up CT. (From Min SI, et al: Current strategy for the treat-
ment of symptomatic spontaneous isolated dissection of superior mesenteric artery. J Vasc Surg 54:461-466, 2011.)

SMA are associated with a broad spectrum of clinical pic-
tures, from asymptomatic incidental findings to acute cata-
strophic bowel ischemia or infarction and aneurysmal SMA
rupture. Treatment options range from conservative manage-
ment to anticoagulation, endovascular stenting, and open
surgical repair, although no consensus guidelines exist
for management.115 Studies have demonstrated successful
treatment with endovascular stents for symptomatic SMA
dissection.115,116
A literature search by Gobble et al116 found 106 articles
on spontaneous isolated celiac and SMA dissection, identify-
ing the average age at presentation to be 54 years old, with
prevalence four times greater in men. Approximately half of
the patients presented with aneurysmal degeneration of the
SMA. Expectant management (bowel rest, observation) was
successful in only 31 of 56 patients, of whom 21 were symp-
tomatic. Of the 25 who failed to respond to expectant man-
agement, surgical intervention was successful in 12, whereas
13 died. Anticoagulation was successful in 15 of 23 patients;
7 of the 8 failures were treated with successful surgery, and
1 patient died. Open surgical repair was 100% successful
in 22 patients, whereas endovascular stenting was successful
in 4 of the 5 patients in whom it was used as a primary treat-
ment (the 1 failure had recurrent dilatation of a false lumen
that was successfully treated with an additional stent at a later
date). Two rescue stents for failed expectant management
were both successful, as were five rescue stents for failed
anticoagulation. Overall, 11 of 12 stents were initially suc-
cessful, with successful later stenting of the one failure. Min
et al115 showed similar results with only 50% successful
expectant management without anticoagulation or antiplate-
let therapy (7 of 14), with two failures successfully rescued
with endovascular stenting, and 100% successful primary
endovascular stenting. Overall conclusions include poor out-
comes for expectant management alone and improved out-
comes for anticoagulation, even if rescue surgical intervention
was needed. Endovascular stenting is a viable option both as
a primary treatment and as a rescue therapy for nonsurgical
initial management (Fig. 153-17).116
Second-Look Surgery
Even after reperfusion and careful assessment, bowel viability
cannot be determined with certainty at the time of initial
exploration. The frequency of bowel resection is routinely
higher during second-look surgery (53%) compared with the
initial exploration and revascularization procedure (31%).41
The decision to perform this second-look surgery is made at
the time of initial operation. This plan is essentially inviolate,
regardless of the clinical status of the patient. Typically, at

the conclusion of the initial procedure, the surgeon leaves
transected ends of the intestine stapled shut without reanas-
tomosis. Likewise, the abdominal fascia can be left open if
bowel edema is significant, in anticipation of a return to the
operating room within the next 48 hours. Certainly, if the
patient’s clinical condition deteriorates at any point, reopera-
tion is immediate. This strategy allows the preservation of as
much bowel as possible, resecting only areas of bowel that are
clearly nonviable at each procedure. The patient is returned
to the operating room 12 to 48 hours later, and the abdomen
is re-explored. By this time, the viability of the bowel has
usually declared itself, but a third look is occasionally required.
This mandatory return protects the patient from ongoing
bowel necrosis before irreversible physiologic changes develop
and before perforation that would risk further sepsis, abscess,
or graft infection. Mesenteric blood flow is reassessed, and the
bowel anastomoses are performed if the condition of the
bowel is satisfactory.
Intraoperative Vasodilators
Splanchnic vasospasm may persist for variable periods,
causing continued bowel ischemia after a successful revascu-
larization.14,117 Low flow after ischemia can also result from
relative hypovolemia, myocardial depression, and sepsis. To
improve local vasospasm in the mesenteric arcades, papaver-
ine can be administered selectively in the SMA. Alterna-
tively, intravenous glucagon administration increases cardiac
output and flow to all layers of the small and large intestine
and liver while inhibiting gastrointestinal motility and secre-
tory function. This has been shown to improve survival in an
animal model118,119 but has not been tested extensively in
humans. Glucagon administration should be coupled with
additional volume resuscitation to avoid vasodilatation-
mediated hypotension.
Duplex Follow-Up
Duplex ultrasound seems to be the most reasonable, cost-
effective way to obtain objective data for clinical decision
making after various forms of mesenteric revascularization.
Robust reports of Doppler ultrasound follow-up after mesen-
teric bypass have been lacking, however. Liem et al120 char-
acterized duplex-derived flow velocities in mesenteric artery
bypass grafts for the first time. Postprandial scans were per-
formed in a longitudinal follow-up of 43 mesenteric grafts, for
a total of 167 duplex examinations. Midgraft flows were
higher in smaller diameter grafts (6 mm) and saphenous vein
grafts compared with larger diameter grafts (7 mm) but were
not affected by graft orientation or inflow source. Two grafts
failed during the follow-up interval, but unfortunately, no
CHAPTER 153  Mesenteric Vascular Disease: Acute Ischemia 2413
duplex scan characteristics were found to predict graft
SECTION 25 MESENTERIC VASCULAR DISEASE
thrombosis.
Restenosis is common and happens early after mesenteric
stenting,61,95 including ROMS patients. Therefore, frequent
duplex surveillance is required to judge the need for
re-intervention. Although the published data on Doppler
ultrasound of native (unstented) mesenteric arteries are very
good,121-123 the literature that focuses on stented mesenteric
vessels is meager and derived primarily from series of chronic
mesenteric ischemia.124-127 Absolute velocity thresholds that
indicate the need for prompt re-intervention have yet to be
identified. However, these studies suggest that standard
(unstented) velocity criteria overestimate the degree of ste-
nosis (see Chapter 152).
SELECTED KEY REFERENCES
Aschoff AJ, Stuber G, Becker BW, Hoffmann MH, Schmitz BL, Schelig H,
Jaeckle T: Evaluation of acute mesenteric ischemia: accuracy of biphasic
mesenteric multi-detector CT angiography. Abdom Imaging 34:345–357,
2009.
Good example of CTA technique.
Kassahun WT, Schulz T, Richter O, Hauss J: Unchanged high mortality rates
from acute occlusive intestinal ischemia: six year review. Langenbecks Arch
Surg 393:163–171, 2008.
Good review article.
Kazmers A: Operative management of acute mesenteric ischemia. Ann Vasc
Surg 12:187–197, 1998.
Excellent illustrations of operative technique.
Kirkpatrick ID, Kroeker MA, Greenberg HM: Biphasic CT with mesenteric
CT angiography in the evaluation of acute mesenteric ischemia: initial
experience. Radiology 229:91–98, 2003.
Establishes CTA as the best diagnostic imaging choice.
Kougias P, Lau D, El Sayed HF, Zhou W, Huynh TT, Lin PH: Determinants
of mortality and treatment outcome following surgical interventions for
acute mesenteric ischemia. J Vasc Surg 46:467–474, 2007.
Good look at factors that influence patient survival.
Min SI, Yoon KC, Min SK, Ahn SH, Jae HJ, Chung JW, Ha J, Kim SJ:
Current strategy for the treatment of symptomatic spontaneous isolated
dissection of superior mesenteric artery. J Vasc Surg 54:461–466, 2011.
Small series of SMA dissections with suggested treatment algorithm.
Oldenburg WA, Lau LL, Rodenberg TJ, Edmonds HJ, Burger CD: Acute
mesenteric ischemia: a clinical review. Arch Intern Med 164:1054–1062,
2004.
Good review article.
Park WM, Gloviczki P, Cherry KJ, Jr, Hallett JW, Jr, Bower TC, Panneton
JM, Schleck C, Ilstrup D, Harmsen WS, Noel AA: Contemporary man-
agement of acute mesenteric ischemia: factors associated with survival.
J Vasc Surg 35:445–452, 2002.
Good contemporary series and discussion.
Wyers MC, Powell RJ, Nolan BW, Cronenwett JL: Retrograde mesenteric
stenting during laparotomy for acute occlusive mesenteric ischemia. J Vasc
Surg 45:269–275, 2007.
Description of new technique for revascularization of the SMA.
The reference list can be found on the companion Expert Consult website
at www.expertconsult.com.

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