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Pearls, Pitfalls, and Conditions that
Mimic Mesenteric Ischemia at CT
Laura A. Fitzpatrick, MD
Michael D. Rivers-Bowerman, MD,
  MSc, FRCPC
Seng Thipphavong, MD, FRCPC
Sharon E. Clarke, MD, PhD, FRCPC
Judy A. Rowe, MD, FRCPC
Andreu F. Costa, MD, MSc, FRCPC
Abbreviations: AMI = acute mesenteric
ischemia, IMA = inferior mesenteric artery,
NOMI = nonocclusive mesenteric ischemia,
SMA = superior mesenteric artery
RadioGraphics 2020; 40:545–561
https://doi.org/10.1148/rg.2020190122
Content Codes:
From the Department of Diagnostic Radiology,
Queen Elizabeth II Health Sciences Centre and
Dalhousie University, Victoria General Build-
ing, 1276 S Park St, 3rd Floor, Halifax, NS,
Canada B3H 2Y9 (L.A.F., M.D.R.B., S.E.C.,
J.A.R., A.F.C.); and Joint Department of
Medical Imaging, University Health Network,
Mount Sinai Hospital, Women’s College Hos-
pital, and University of Toronto, Toronto, On-
tario, Canada (S.T.). Presented as an education
exhibit at the 2018 RSNA Annual Meeting. Re-
ceived April 19, 2019; revision requested June
18 and received June 24; accepted July 11. For
this journal-based SA-CME activity, the au-
thor S.E.C. has provided disclosures; all other
authors, the editor, and the reviewers have dis-
closed no relevant relationships. Address cor-
respondence to A.F.C. (e-mail: andreufcosta@
gmail.com).
©
RSNA, 2020
SA-CME LEARNING OBJECTIVES
After completing this journal-based SA-CME
activity, participants will be able to:
„ Apply a systematic inside-out approach
to evaluating CT examinations of pa-
tients suspected of having AMI.
Describe the clinical manifestations
„
and key imaging findings for each sub-
type of AMI.
Discuss the conditions that mimic AMI
„ a challenge, and a high index of clinical and radiologic suspicion is
and potential pitfalls in the imaging diag-
nosis of AMI.
See rsna.org/learning-center-rg.
545
VASCULAR/INTERVENTIONAL RADIOLOGY
Acute mesenteric ischemia (AMI) is a life-threatening condition
with a high mortality rate. The diagnosis of AMI is challenging
because patient symptoms and laboratory test results are often
nonspecific. A high degree of clinical and radiologic suspicion is
required for accurate and timely diagnosis. CT angiography of the
abdomen and pelvis is the first-line imaging test for suspected AMI
and should be expedited. A systematic “inside-out” approach to
interpreting CT angiographic images, beginning with the bowel
lumen and proceeding outward to the bowel wall, mesentery, vas-
culature, and extraintestinal viscera, provides radiologists with a
practical framework to improve detection and synthesis of imaging
findings. The subtypes of AMI are arterial and venoocclusive dis-
ease, nonocclusive ischemia, and strangulating bowel obstruction;
each may demonstrate specific imaging findings. Chronic mesen-
teric ischemia is more insidious at onset and almost always second-
ary to atherosclerosis. Potential pitfalls in the diagnosis of AMI
include mistaking pneumatosis as a sign that is specific for AMI
and not an imaging finding, misinterpretation of adynamic ileus as
a benign finding, and pseudopneumatosis. Several enterocolitides
can mimic AMI at CT angiography, such as inflammatory bowel
disease, infections, angioedema, and radiation-induced enterocoli-
tis. Awareness of pitfalls, conditions that mimic AMI, and potential
distinguishing clinical and imaging features can assist radiologists in
making an early and accurate diagnosis of AMI.
©
RSNA, 2020 • radiographics.rsna.org
Introduction
Acute mesenteric ischemia (AMI) is a life-threatening condition
caused by decreased blood flow to the bowel. AMI accounts for less
than one in 1000 hospital admissions but has a high mortality rate
of 30%–90% in the acute setting (1,2). A recent decrease in popula-
tion-based and in-hospital mortality rates from AMI has been shown
and is likely the result of earlier recognition of disease and improved
treatment (3). Early diagnosis and intervention are key to reduc-
ing mortality in AMI. Because patient symptoms, laboratory tests,
and imaging findings are often nonspecific, diagnosing AMI can be
essential (4). One study (5) found that on-call radiologists were sig-
nificantly more likely to diagnose AMI correctly if it was mentioned
on the CT examination requisition.
Mesenteric ischemia can be acute (95% of cases) or chronic
(5% of cases) (1). The subtypes of AMI are arterial occlusion (both
embolic and thrombotic), venous occlusion, nonocclusive mesen-
teric ischemia (NOMI), and strangulating obstruction (Fig 1) (6).
Chronic mesenteric ischemia is typically associated with diffuse
atherosclerotic disease (1).
546  March-April 2020 radiographics.rsna.org
TEACHING POINTS
„ A systematic anatomically based approach to interpreting CT
angiography in patients suspected of having mesenteric isch-
emia can ensure a comprehensive evaluation and improved
detection of imaging findings, which can be subtle.
„ A potential imaging pitfall is to dismiss bowel dilatation as a
nonspecific ileus in patients with AMI. An adynamic ileus does
not always have benign causes and should raise suspicion for
AMA, in the appropriate setting. The large bowel may lose
its function to absorb water and form stool and be filled with
fluid.
„ One of the most important and specific imaging features of
occlusive AMI is that the involved segments of bowel corre-
spond to a vascular distribution. An abrupt interface between
normal and affected bowel may be seen. On occasion, the
distribution of disease rather than the bowel lumen and mural
changes lead to the diagnosis of AMI.
„ It is important to evaluate the extraintestinal viscera for evi-
dence of hypoperfusion. Infarcts of the spleen, liver, and kid-
neys are associated with NOMI, and elements of the CT hypo-
perfusion complex may be seen, such as a small-caliber aorta,
a collapsed inferior vena cava, and hyperenhancement of the
adrenal glands and kidneys.
„ In patients with adhesive small bowel obstruction, strangula-
tion should be considered if two of the following three find-
ings are present: reduced bowel wall enhancement, diffuse
mesenteric haziness, and a closed-loop mechanism. If these
three findings are absent, strangulation can be excluded.
Multidetector CT angiography of the abdo-
men and pelvis is the preferred test for diagnosis of
AMI (1). CT angiography is fast and accurate and
provides excellent assessment of the bowel, mes-
enteric vasculature, and other ancillary features
of AMI. The goal of this article is to review the
clinical manifestations, anatomy, CT angiographic
techniques, and imaging findings of AMI. We pres-
ent a systematic inside-out approach to evaluating
CT angiography of patients suspected of having
AMI. Conditions that mimic AMI and diagnostic
pitfalls are discussed, with emphasis on potential
distinguishing features.
Clinical Features
AMI typically occurs in elderly and hospitalized
patients with comorbid conditions. The mean age
of patients who receive a diagnosis of occlusive
AMI is 70 years (7). AMI in younger patients is
typically embolic or secondary to predisposing
conditions such as vasculitis, collagen vascular dis-
ease, hypercoagulability, or vasoactive medications
(4). Patients present with pain that is more severe
than that expected on the basis of the physical
examination. Other nonspecific symptoms include
nausea, vomiting, and diarrhea. Laboratory tests
are neither sensitive nor specific for AMI. Abnor-
mal laboratory test results that are associated with
AMI include leukocytosis, hemoconcentration,
metabolic acidosis, and elevated levels of lactate,
D-dimer, amylase, and liver enzymes (1). An in-
creased lactate level is not specific for and is often
a late marker of AMI (4).
Patients with chronic mesenteric ischemia
present with different symptoms, such as post-
prandial dull abdominal cramps that last for 1–2
hours (8). The pain arises from insufficient blood
supply to meet the increased demands of diges-
tion (9). Patients may present with an aversion
to food, early satiety, unintentional weight loss,
nausea, vomiting, and diarrhea (9,10).
Mesenteric Vascular Anatomy
The gastrointestinal tract is perfused by the celiac
axis, the superior mesenteric artery (SMA), and
the inferior mesenteric artery (IMA), which arise
from the abdominal aorta at approximately T12–
L1, L1–2, and L3–4, respectively (10,11). Con-
ventional anatomy is as follows (although variant
anatomy is common): The celiac axis supplies the
stomach, proximal duodenum, liver, pancreas, and
spleen (Fig 2a). Major branches of the celiac axis
are the left gastric, splenic, and common hepatic
arteries, the last of which divides into the proper
hepatic and gastroduodenal arteries. The gastro-
duodenal arteries give rise to the superior pancre-
aticoduodenal and right gastroepiploic arteries.
The SMA supplies the distal duodenum,
mesenteric small bowel, and right colon (Fig 2a).
Major branches of the SMA include the inferior
pancreaticoduodenal, jejunal, ileal, ileocolic, and
right and middle colic arteries. The IMA supplies
the distal transverse colon, the splenic flexure, the
descending colon, the sigmoid colon, and the up-
per rectum (Fig 2b). Major branches of the IMA
include the left colic artery, sigmoid branches
and terminal branch, and superior rectal ar-
tery. The middle to lower rectum is supplied by
branches of the anterior divisions of the internal
iliac arteries.
Vascular pathways between the mesenteric
arteries provide essential blood flow in patients
with vascular stenosis or occlusion (Fig 2b).
Celiac axis to SMA vascular pathways include
the pancreaticoduodenal arteries and the arc of
Buhler (11,12). The SMA to IMA vascular path-
ways include the marginal artery of Drummond,
which is an anastomosis between the terminal
branches of the SMA and the IMA along the
inner margin of the colon, and the arc of Riolan,
which is an anastomosis between the middle and
left colic arteries (12). Additional vascular path-
ways to the mesenteric arteries may also develop
from the lumbar, internal iliac, and phrenic arter-
ies in the setting of celiac axis, SMA, and/or IMA
stenosis or occlusion (4).
The superior mesenteric vein and inferior
mesenteric vein drain mesenteric venous blood
RG  •  Volume 40  Number 2 Fitzpatrick et al  547
into the portal venous system (Fig 2c). The
jejunal, ileal, right, and middle colic veins drain
into the superior mesenteric vein, which fol-
lows the course of the SMA (4,11). The superior
rectal, sigmoid, and left colic veins drain into the
inferior mesenteric vein, which drains into the
superior mesenteric vein or splenic vein (11).
CT Imaging Technique
According to the American College of Radiology
Appropriateness Criteria (1), multiplanar bipha-
sic CT angiography of the abdomen and pelvis is
the first-line imaging examination for suspected
AMI and chronic mesenteric ischemia. CT
angiography is readily available and fast, demon-
strates good interreader agreement, and is highly
accurate, with pooled sensitivity and specificity of
93.3% and 95.9%, respectively (13). CT angiog-
raphy is also the preferred modality in patients
with renal impairment, because the need for early
diagnosis outweighs any potential risk of contrast
material–induced nephropathy (1).
CT angiography should be performed with
thin sections (eg, 0.625 mm for a 64-section
scanner), multiplanar reformation, and three-
dimensional rendering (1). Imaging during both
the arterial and portal venous phases should be
performed to optimize assessment of the vascula-
ture and bowel enhancement. Although a non-
enhanced sequence can be performed to assess
for mural hemorrhage, atherosclerotic calcifica-
tions, and baseline bowel attenuation, results of
several studies (14,15) have suggested that this
is not required for diagnosis. A liberal dose of
intravenous iodinated contrast material optimizes
visualization of the mesenteric vasculature, bowel
wall, and solid viscera. At our institution, we use
a weight-based dose of 1.5 mL/kg of iohexol (350
mg of iodine per milliliter), with a rapid injection
rate of 4–5 mL/sec, followed by a saline solution
flush. Use of positive oral contrast material is not
recommended, because this obscures bowel wall
Figure 1.  Classification of mesen-
teric ischemia.
enhancement. To expedite the study, we do not
use negative or neutral oral contrast material,
although it can be used to distend the bowel (1).
Inside-Out Approach to CT
Image Interpretation
A systematic anatomically based approach to
interpreting CT angiography in patients sus-
pected of having mesenteric ischemia can ensure
a comprehensive evaluation and improved detec-
tion of imaging findings, which can be subtle. We
propose an inside-out approach, which involves
sequential assessment of the bowel lumen and
working outward to assess the bowel wall, mesen-
tery and peritoneal cavity, vasculature, and other
abdominopelvic viscera (Table 1). In the follow-
ing sections, we discuss the imaging findings of
mesenteric ischemia according to this framework.
Bowel Lumen
An adynamic ileus, in which the bowel is dilated
and often filled with fluid, is reported to be the
earliest finding of AMI and may represent aperi-
stalsis from ischemia or loss of contractility with
infarction (4). A potential imaging pitfall is to
dismiss bowel dilatation as a nonspecific ileus in
patients with AMI. An adynamic ileus does not
always have benign causes and should raise suspi-
cion for AMA, in the appropriate setting (Fig 3).
The large bowel may lose its function to absorb
water and form stool and be filled with fluid.
Bowel Wall
Circumferential edematous bowel wall thickening
is the most common finding in AMI (sensitivity,
85%–88%), but this finding is not specific (16).
Wall thickening is most pronounced in venous
ischemia, with a striated pattern corresponding
to the “target” or “halo” sign (Fig 4) (4), al-
though this finding is also seen with strangulating
obstruction, NOMI, and arterial occlusion with
reperfusion (6). The thickened bowel wall may be
548  March-April 2020 radiographics.rsna.org

hypoattenuating from edema or hyperattenuat-

ing from hemorrhage. The bowel wall can also
be thin, particularly in patients with arterial AMI
(Fig 3) (4).
Bowel wall enhancement can be increased,
decreased, or absent in patients with AMI (4).
Loss of mural enhancement is a specific finding
that indicates the loss of arterial perfusion and
impending infarction (Fig 3) (17). Mural hy-
poenhancement can be subtle; comparison with
other bowel loops may assist detection. Mural
hyperenhancement usually implies bowel viability
and is often seen with impaired venous drainage,
NOMI (eg, shock bowel), or acute arterial occlu-
sion with reperfusion (4).
Although pneumatosis intestinalis is associated
with multiple benign causes, in the appropriate
setting, pneumatosis should be considered suspi-
cious for ischemia. Pneumatosis does not neces-
sarily indicate necrosis, according to one study
(18) in which 47% of patients with AMI and
pneumatosis had viable bowel during surgery.
In the right clinical scenario, infarction is more
likely when pneumatosis is accompanied by por-
tomesenteric venous gas (Fig 3) (19).
One of the most important and specific imag-
ing features of occlusive AMI is that the involved
segments of bowel correspond to a vascular
distribution. An abrupt interface between nor-
mal and affected bowel may be seen (Fig 4). On
occasion, the distribution of disease rather than
the bowel lumen and mural changes lead to the
diagnosis of AMI.

Mesentery
Mesenteric findings in AMI are often nonspecific,
such as fat stranding adjacent to the ischemic
bowel segment and mesenteric fluid. The pres-
ence of fluid in a patient with bowel obstruction
raises the possibility of ischemia (20). Pneumo-
peritoneum and fluid collections may develop
after mural necrosis and perforation (4).

Mesenteric and Systemic Vasculature

The splanchnic arteries should be evaluated for
any thromboembolic occlusion and atheroscle-
rotic narrowing at the ostia, and the veins should
be assessed for thrombosis, thrombophlebitis,
or other causes of impaired venous return, such
as malignancy (4). The caliber of the mesenteric
vasculature, aorta, and inferior vena cava may be
small (Fig 3).

Solid Abdominal Viscera
Evaluation of the solid abdominal viscera can
provide additional clues to the diagnosis of AMI,
particularly in a patient with embolic arterial dis-
ease and NOMI. Peripheral wedge-shaped areas
Figure 2.  Illustrations show the anatomy of the celiac trunk and
SMA (a), the IMA and major mesenteric collateral arteries (b),
and the mesenteric venous drainage (c). IMV = inferior mesenteric
vein, SMV = superior mesenteric vein.
RG  •  Volume 40  Number 2 Fitzpatrick et al  549

(Fig 3). Hyperenhancement of the adrenal glands

Table 1: Anatomically Based “Inside-Out”
Approach to Systematic Identification of Fea-
and kidneys is seen with the CT hypoperfusion
tures of AMI at CT Angiography complex (21).
Bowel lumen
Subtypes of Mesenteric Ischemia
  Adynamic ileus
  Inability of large bowel to reabsorb water Arterial Occlusive AMI
Bowel wall Arterial occlusive disease is the most common
  Wall thickness cause of AMI, accounting for 60%–85% of cases
   Thick, especially in venous ischemia (4). The main causes are embolic (40%–50%)
   Thin, especially in arterial ischemia and and thrombotic (20%–30%) disease; less com-
NOMI mon causes include arterial dissection and
  Wall attenuation vasculitis (5%). Arterial emboli originate from
   Hypoattenuating if edematous the heart or aorta and typically lodge in the SMA
   Hyperattenuating if hemorrhagic distal to the origin of the middle colic artery
  Wall enhancement (1). They appear as a central filling defect in the
   Striated pattern with a target or halo sign arterial lumen (Fig 5). Emboli may also lodge
   Absent or hypoenhancing in other visceral arteries such as the spleen and
  Hyperenhancement kidneys. Because of the sudden nature and lack
  Pneumatosis intestinalis
of collateral vessels, patients usually present with
severe pain that is worse than that with arterial
Mesenteric vasculature
thrombosis (17).
 Arterial
Mesenteric arterial thrombosis typically occurs
  Embolic occlusion near the ostium on a background of atherosclero-
   Thrombotic occlusion sis, resulting in a long segment of affected bowel.
   Predisposing atherosclerotic disease with or Because of this, thrombosis has the worst prog-
without collateral arteries (chronic mesen- nosis of the AMI subtypes (Figs 3, 6) (4,17). Any
teric ischemia) new, intense, or persistent abdominal pain in a
   Vasospasm (NOMI)
patient with vasculopathy should raise suspicion
 Venous for AMI, and CT angiography should be per-
   Thrombosis or extrinsic narrowing formed to evaluate for arterial occlusion and new
   Engorged tributaries with or without collateral bowel findings. Unlike embolic AMI, collateral
veins vessels are often present owing to long-standing
   Synchronous portal and splenic vein throm- atherosclerotic disease.
bosis Bowel findings with arterial occlusive disease
   Portomesenteric venous gas are variable, but typically the bowel wall is thin,
  Aorta and inferior vena cava: diminutive without mural edema or hemorrhage, and bowel
  (NOMI) wall enhancement is decreased (6). The excep-
Mesentery
tion is in cases of arterial reperfusion, where the
  Fat stranding bowel wall is thick and shows a target pattern of
 Fluid enhancement. Bowel findings correspond to the
Peritoneal cavity distribution of the occluded artery (Fig 6) (17).
  Free air
  Free fluid Venoocclusive AMI
Solid viscera Venoocclusive disease accounts for approximately
  Infarcts (NOMI and embolic arterial phenom- 5%–15% of cases of AMI and generally occurs
enon) in younger patients (22). Common risk factors
  Hypoenhancement (NOMI) include hypercoagulability due to systemic or
  Hyperenhancing adrenal glands and kidneys inflammatory conditions, portal hypertension,
(NOMI, CT hypoperfusion complex) and recent surgery (1). Venous ischemia can also
occur because of extrinsic compression from tu-
mor encasement (Fig 4), which results in chronic
venous congestion and a more insidious onset of
of hypoenhancement that correspond to infarcts symptoms (7).
may develop in the liver, spleen, and kidneys. Mesenteric venous thrombi appear as luminal
The solid viscera may also demonstrate diffusely filling defects with a thin peripherally enhancing
decreased or delayed enhancement, which is rim corresponding to the venous wall. Tribu-
suggestive of multiorgan ischemia and failure taries to the occluded vein are engorged, and
550  March-April 2020 radiographics.rsna.org

Figure 3.  Thrombotic AMI that was missed at CT in a 62-year-old woman who had presented in the emer-
gency department five times in a 6-week period for abdominal pain, nausea, vomiting, weight loss, and
anorexia. (a) Coronal intravenous contrast material–enhanced CT image shows a diffusely distended stomach
and small bowel, with mural thinning and subtle areas of mural hyperenhancement (white arrowhead) rela-
tive to areas of hypoenhancement (black arrowheads). A new thrombotic occlusion of the SMA (arrow) is vis-
ible, with small distal branches (*). The study was misinterpreted as showing no evidence of ischemic enteritis.
(b) Follow-up coronal CT image acquired 2 days later shows persistent SMA thrombosis (arrow) with small
peripheral branches (*), worsening hypoenhancement of the small bowel wall (arrowheads), and persistent
bowel distention. However, the study was reported as showing no new findings of bowel ischemia. (c, d) Axial
contrast-enhanced CT images acquired 2 days later during the arterial (c) and portal venous (d) phases show
diffuse hypoenhancement and thickening of the bowel wall (arrows in c) and poor enhancement of the liver
and spleen. New intrahepatic portal venous gas is present (arrow in d). The patient died 1 day later.

Figure 4. Metastatic
neuroendocrine tumor
causing mesenteric ve-
nous obstruction and
ischemia in a 37-year-
old woman. Axial (a)
and coronal (b) CT im-
ages acquired with both
intravenous and positive
oral contrast material
show a spiculated mass
in the mesenteric root
(white arrow in b) and
hypoenhancing liver le-
sions corresponding to a metastatic small bowel neuroendocrine tumor. Edematous wall thickening of the mesenteric small bowel
and right colon (white arrowheads in a and b), vascular engorgement, mesenteric edema, and ascites are seen. The study was initially
interpreted as showing possible infectious enterocolitis. However, the duodenum and left colon are spared (black arrows in a and b),
and there is a sharp transition between normal and edematous bowel at the hepatic flexure (black arrowhead in a). These findings
correspond to distribution of the superior mesenteric vein, which is compressed by the mass, resulting in ischemia. The patient died
6 months later.
RG  •  Volume 40  Number 2 Fitzpatrick et al  551
synchronous splenic and portal vein thrombosis
may be present (Fig 7) (23). The bowel wall
is markedly thickened, with a target or halo
pattern of enhancement. Mesenteric stranding
and fluid are often prominent in patients with
venous ischemia (7,17).
Nonocclusive Mesenteric Ischemia
NOMI accounts for 15%–30% of cases of AMI
(24,25). The pathogenesis is incompletely under-
stood but is thought to be related to a homeostatic
mechanism that maintains cardiac and cerebral
blood flow at the expense of the splanchnic and
peripheral circulation (26). NOMI should be con-
sidered in the differential diagnosis for hospitalized
or critically ill patients with predisposing risk fac-
tors, because imaging findings may be subtle, and
the distribution of affected bowel may be discon-
tinuous or involve multiple vascular territories (Fig
8). Risk factors include any condition that results
in systemic hypoperfusion, including heart failure
and cardiogenic shock, long-term hemodialysis
and hypovolemia, septic shock, trauma or hemor-
rhagic shock, aortic insufficiency, and recent heart
surgery (27,28). Mesenteric vasospasm also can be
caused by vasoactive and cardiotonic drugs such
as digitalis, phenylephrine, amphetamines, vaso-
pressin, and cocaine (29).
CT angiography can show narrowing of the
mesenteric arteries to the first-order branches,
Figure 5.  SMA embolus causing AMI in a
92-year-old man with a history of Roux-en-Y
anastomosis for gastric cancer and atrial fibril-
lation who presented with acute postprandial
abdominal pain and watery bowel movements.
The patient was not taking anticoagulation med-
ications because of a history of falls. Axial (a),
coronal (b), and sagittal (c) CT images show a
long segment of distal small bowel, the cecum,
and the ascending colon with mural hyperen-
hancement, mild edematous wall thickening,
and adjacent stranding (black arrow). A central
filling defect in the SMA corresponds to an em-
bolism (white arrow in a and b). Note the sharp
demarcation with the transverse colon, which is
normal and typically spared in embolic ischemia
(arrowheads in c). The patient’s condition wors-
ened, with gastrointestinal bleeding and stroke.
He subsequently died in the hospital.
particularly with multiplanar reconstructions
and maximum intensity projection images
(17,30). Reduced caliber of the SMA (Fig 9)
has been reported (31) and validated with re-
spect to age- and sex-matched control subjects
(32,33), and when compared with prior CT ex-
aminations in the same individual (30). The af-
fected bowel may correspond to watershed areas
between vascular territories, such as the splenic
flexure and sigmoid colon. It is important to
evaluate the extraintestinal viscera for evidence
of hypoperfusion. Infarcts of the spleen, liver,
and kidneys are associated with NOMI (30),
and elements of the CT hypoperfusion complex
may be seen, such as a small-caliber aorta, a
collapsed inferior vena cava, and hyperenhance-
ment of the adrenal glands and kidneys (Figs 9,
10) The mainstay of treatment of NOMI is to
correct the underlying cause to improve mesen-
teric perfusion before bowel necrosis occurs.
Strangulating Bowel Obstruction
A strangulating bowel obstruction is defined as
ischemia or infarction of an obstructed loop, and
it occurs in approximately 10% of small bowel
obstructions (34). Strangulation is most com-
monly seen with a closed-loop obstruction, where
a segment of bowel is obstructed proximally and
distally at a single point. Timely surgical interven-
tion is critical owing to a very high mortality rate
552  March-April 2020 radiographics.rsna.org

Figure 6.  Thrombotic arterial disease

causing AMI in a 67-year-old woman who
had been feeling unwell for several weeks.
The patient was undergoing outpatient
placement of a vascular catheter for dialysis
and developed decreased consciousness
and hypotension. Axial (a), coronal (b),
and sagittal (c) CT images show severe
atherosclerotic disease with chronic
thrombosis of the abdominal aorta distal
to the SMA, and thrombotic narrowing at
the ostia of the celiac axis and SMAs (ar-
rows in c). The vasa recta are small (white
arrowheads), and mesenteric fluid is pres-
ent. The abdomen is distended from dif-
fusely distended bowels that show thin
hyperenhancing walls (black arrows in a
and b). The patient died later the same
week.

of 20%–40% (35). Although studies have been
performed to develop predictive risk models to
assess for strangulation in the setting of small
bowel obstruction, these have not been validated
for clinical use (20,36).
In one meta-analysis (34), researchers evalu-
ated five specific CT findings for their associa-
tion with strangulating bowel obstruction in 768
patients, 205 of whom had proven strangulation.
The authors found that reduced bowel wall
enhancement was the most specific finding (95%
[95% confidence interval: 75, 99]). Mesenteric
fluid was the most sensitive finding (89% [95%
confidence interval: 75, 96]); the absence of fluid
strongly suggests that there is no strangulation
(34). Findings of bowel wall thickening, mesen-
teric venous congestion, and free peritoneal fluid
were not accurate for prediction of strangulation.
In patients with adhesive small bowel obstruc-
tion, strangulation should be considered if two of
the following three findings are present: reduced
bowel wall enhancement, diffuse mesenteric hazi-
ness, and a closed-loop mechanism (Figs 11–13).
If these three findings are absent, strangulation
can be excluded (20).
Chronic Mesenteric Ischemia
Chronic mesenteric ischemia, also termed “intes-
tinal angina,” results from chronic stenosis or oc-
clusion of one or more of the celiac axis, SMA, or
IMA (3). Chronic mesenteric ischemia is almost
always secondary to atherosclerosis; less common
causes include fibromuscular dysplasia, vasculiti-
des such as Buerger disease and Takayasu arte-
ritis, and postsurgical intimal hyperplasia (8,9).
Patients usually present during the sixth decade
of life, and a majority of them are former or cur-
rent smokers (4). Approximately 50% of patients
have a history of peripheral vascular disease or
coronary artery disease (3).
CT angiographic findings of chronic mes-
enteric ischemia include stenotic or occlusive
mesenteric arterial plaques and prominent
collateral vessels. CT angiography is essential
to preprocedural treatment planning and allows
accurate grading of mesenteric arterial stenoses
RG  •  Volume 40  Number 2 Fitzpatrick et al  553

Figure 7.  Superior mesenteric vein thrombus causing AMI in a 49-year-old man with
ulcerative colitis who presented with diffuse abdominal pain, nausea, and nonbloody
diarrhea. Axial (a), coronal (b), and sagittal (c) intravenous contrast-enhanced CT im-
ages show an occlusive thrombus in the superior mesenteric vein (arrow in c) that
extends into the extrahepatic portal vein (arrow in b). An elongated segment of the
ileum with circumferential edematous wall thickening and mild perienteric stranding
(arrowheads) is visible.

Figure 8.  NOMI in a 61-year-old woman with chronic alcoholic liver disease who presented with reduced in-
take of food, nausea, vomiting, and weakness and was admitted to the hospital with functional decline. Axial CT
images of the upper (a) and mid (b) abdomen show diffuse dilatation of the stomach and small bowel, with thin
hyperenhancing walls (white arrowheads) and mesenteric edema. Air can be seen in the peripheral intrahepatic
portal veins (black arrowheads in a). Note the paucity of atherosclerotic disease in the aorta and the SMA origin
(arrow). The patient died within hours of the examination.
554  March-April 2020 radiographics.rsna.org

Figure 9.  NOMI in a 61-year-old woman 3 weeks after undergoing a double lung transplant
for interstitial lung disease, which was complicated by fever, leukocytosis, and hypotension.
Axial (a) and coronal (b) intravenous contrast-enhanced CT images show a diffusely dilated
small bowel, extensive pneumatosis (white arrows), a paper-thin wall, and mesenteric fluid.
Note the small caliber of the SMA (black arrow) and hypoenhancing kidneys (arrowheads in
a). The patient died soon thereafter.

and assessment of prior stent or surgical graft

patency (8).

Conditions that Mimic

Mesenteric Ischemia
A variety of disease processes can mimic AMI
and show similar bowel and mesentery imaging
findings at CT. In this section, we briefly de-
scribe common entities and highlight potentially
distinguishing features. A summary is provided in
Table 2.

Benign Pneumatosis
Pneumatosis intestinalis is not a diagnosis but
is an imaging sign that is associated with both
benign and life-threatening conditions (37).
Pneumatosis can arise from increased intralu-
minal pressure (eg, trauma, chronic cough, or
vomiting), increased mucosal permeability (eg,
ischemia, inflammation, or drugs), a defective
immune barrier (eg, immunosuppression), or
iatrogenic causes (eg, endoscopy or tube place-
ment) (38). Chronic conditions associated with
pneumatosis include autoimmune diseases and
those related to organ transplant (38).
Pneumatosis appears as linear, circumfer-
ential, or cystlike foci of gas in the bowel wall
(Fig 9) (39). The presence of bowel dilatation,
altered mural enhancement, portal venous gas,
and mesenteric edema suggests AMI as the
underlying cause, and the diagnosis can be sup-
ported further by the patient’s clinical condition
(40). The circular or cystlike form of pneumato-
sis is usually benign; patients are often asymp-
tomatic, and the results of physical examina-
Figure 10.  Shock bowel (NOMI) in a 55-year-old
man. Axial intravenous contrast-enhanced CT image
shows mural thickening and hyperenhancement of the
small bowel and ascending colon (white arrowheads).
Mesenteric edema is visible, and the inferior vena cava
is collapsed (black arrowhead).
tion are rarely abnormal (37). Patients who are
suspected of having benign pneumatosis may be
treated by addressing the presumptive cause and
by monitoring closely (40).
Imaging features that mimic pneumatosis
include pneumatosis cystoides intestinalis and
pseudopneumatosis. Pneumatosis cystoides intes-
tinalis is an idiopathic condition that is character-
ized by gas-filled bubblelike cysts in the bowel
submucosa and subserosa that typically affect
the colon (41). Proposed mechanisms include
inflammation, dysmotility, immune dysfunction,
and predisposing factors such as surgery, che-
motherapy, and pulmonary illness (41). Pseudo-
pneumatosis appears on images as small bubbles
RG  •  Volume 40  Number 2 Fitzpatrick et al  555

Figure 11.  Strangulating small bowel obstruction in a 79-year-old man who presented with epigastric and
right upper quadrant pain. US (not shown) examination was negative for cholecystitis but showed dilated loops
of bowel. (a) Coronal CT image shows a dilated segment of small bowel (arrowheads) with mild wall thickening,
hyperenhancement, mesenteric stranding, and fluid. (b) Photograph acquired at laparotomy shows that the
small bowel was ischemic and obstructed by an omental band but returned to normal on release of the band.
No bowel resection was required.

Figure 12.  Strangulating small bowel obstruction in a 65-year-old man with abdominal pain and
cramping, diaphoresis, and nausea. Axial positive oral contrast-enhanced (a) and coronal intravenous
contrast-enhanced (b) CT images show dilated loops of the left-sided small bowel and a “balloons-on-
a-string” configuration that corresponds to a closed-loop obstruction (transition zone not shown). Note
how a segment of obstructed small bowel shows mural hypoenhancement (black arrowheads), whereas
another segment shows relative hyperenhancement (white arrowhead). Mesenteric edema (*) and asci-
tes (arrow) are also present. At laparotomy, the obstructed bowel was necrotic.

of gas that are trapped between the bowel wall
and fluid in the lumen that mimic pneumato-
sis. Pseudopneumatosis typically appears in the
cecum and ascending colon and may be dis-
tinguished from pneumatosis by a lack of gas
bubbles that are antidependent to the air-fluid
level (Fig 14) (38).
Inflammatory Bowel Disease
Inflammatory bowel disease includes Crohn
disease and ulcerative colitis. Active inflammation
from Crohn disease manifests as segmental mural
hyperenhancement and wall thickening (Fig 15)
(42). Unlike AMI, the lumen is typically narrowed
at sites of active disease and the distribution is
characteristically discontinuous (ie, skip lesions).
This pattern typically is only seen with nonocclu-
sive, multiembolic, and vasculitic causes of AMI.
Mural inflammation in Crohn disease is asymmet-
ric, with more severe disease along the mesenteric
border, which leads to pseudosacculation of the
antimesenteric border (42). Mural ulceration,
fistulas, and abscesses are common in Crohn
disease, but not in AMI. Changes in the mesentery
such as fibrofatty proliferation, hypervascularity
(ie, the comb sign), and reactive lymphadenopa-
thy also should raise suspicion for Crohn disease
(43) rather than AMI. Chronic changes of Crohn
556  March-April 2020 radiographics.rsna.org

Figure 13.  Strangulating small bowel obstruc-

tion in a 59-year-old man with a history of a kid-
ney transplant who presented with abdominal
pain, distention, and vomiting. Coronal (a) and
sagittal (b) CT images acquired with intravenous
contrast material show diffusely distended loops
of small bowel. A closed-loop obstruction is pres-
ent in the right abdomen, with a singular transi-
tion zone (arrow) and a “balloons-on-a-string”
appearance. The obstructed bowel is ill-defined
and hypoenhancing, resulting in a “faceless” ap-
pearance (black arrowheads), with small bowel
feces and mesenteric edema (*). At laparotomy
and final pathologic evaluation, the obstructed
bowel was necrotic. A normally enhancing loop
of bowel is noted in the right lower quadrant for
comparison (white arrowhead in a).

Table 2: Clinical and Imaging Features of Enterocolitides that May Mimic AMI at CT

Enterocolitide Distinguishing Clinical History Distinguishing CT Features

Inflammatory bowel Previous flares Discontinuous segments of bowel (skip
disease (Crohn disease Insidious onset of abdominal pain lesions) in Crohn disease; continuous in
and ulcerative colitis) Frequent bowel movements ulcerative colitis, starting in distal rectum
Younger patient age Asymmetric wall thickening in Crohn disease,
more severe along mesenteric border
Luminal narrowing at sites of active disease
Paucity of atherosclerotic disease
Infectious enterocolitis Usually indolent onset of symptoms Can involve both small and large bowel
  (days to weeks) Marked bowel wall thickening
May be associated with recent travel, Pancolonic involvement with “accordion”
ingestion of contaminated food, or sign, which is classic for Clostridium difficile
antibiotic use colitis
Neutropenic enterocolitis Chemotherapy or immunosuppression Predilection for cecum and distal ileum
Angioedema History of hereditary angioedema or Segmental involvement of the jejunum and
acquired angioedema with triggers duodenum
Prominent target sign
Rapidly resolves at serial imaging (1–2 d)
Radiation enteritis Ongoing or prior radiation to the Uniform bowel wall thickening and hyperen-
abdomen or pelvis hancement in the radiation field
Gastrointestinal symptoms associated Predilection for terminal ileum and rectum
with radiation treatments Adjacent organ and soft-tissue involvement
(eg, cystitis)
Chronic—fibrosis, stricture, and bowel angu-
lation
Graft-versus-host disease History of allogenic hematopoietic cell Discontinuous segmental involvement of the
transplant in the previous approxi- bowel
mately 3 months Upstream bowel dilatation
Biliary findings (gallbladder distention, thick-
ening, and hyperenhancement)
Portal hypertension History of cirrhosis or chronic liver Edematous thickening of the small and large
disease bowel, most commonly the right colon
History of chronic or acute gastroin- Extraintestinal findings of portal hyperten-
testinal bleeding sion: cirrhosis, collateral vessels; spleno-
megaly, ascites

disease include mural fat deposition and fibroste- Ulcerative colitis is an inflammatory disease of
notic disease, which can result in upstream bowel the large bowel mucosa, beginning in the rectum
distention and obstruction (43). and progressing proximally in a continuous fash-
RG  •  Volume 40  Number 2 Fitzpatrick et al  557

Figure 14.  Pseudopneumatosis in a 48-year-old woman

who underwent a diverting loop ileostomy for an unrelated
reason. Axial positive oral and intravenous contrast–enhanced
CT image shows distention of the jejunum corresponding to
an adynamic ileus. Small bubbles of gas are trapped between
intraluminal fluid and the jejunal wall (white arrowheads).
However, there is a notable absence of gas bubbles that are
antidependent to the air-fluid level in the bowel lumen (black
arrowheads). The finding was mistaken for pneumatosis and,
because of a rigid abdomen and worsening condition, the pa-
tient underwent laparotomy, and the bowel was found to be
normal.

ion. Inflammation in the terminal ileum, which is
termed backwash ileitis, is seen in 20% of patients
with pancolitis (44). When the inflammation is
isolated to the left colon or anorectum, ulcerative
colitis can mimic AMI.
Infectious Enterocolitides
Gastrointestinal infections of the small and large
bowel can be caused by bacteria, viruses, and
parasites. In general, patients with infectious
enterocolitis have a more indolent onset of symp-
toms (ie, days to weeks), with nausea, vomiting,
diarrhea, and hematochezia. A history of recent
travel abroad, ingestion of potentially contami-
nated foods, or use of antibiotics may suggest
the diagnosis. Unlike AMI, colonic infections
typically result in pancolitis, such as that seen
in patients with C. difficile infection. However,
certain bacterial infections (eg, Campylobacter,
Salmonella) have a predilection for the right
colon, while parasitic schistosomiasis typically
affects the left colon (45). CT features include
bowel wall thickening with stratified or homo-
geneous hyperenhancement of the bowel wall,
adjacent mesenteric stranding, and in rare cases,
pneumatosis. C. difficile colitis classically appears
on images as a markedly thickened edematous
bowel wall with folds that are oriented in a paral-
lel fashion (ie, the accordion sign) (45).
Neutropenic Enterocolitis (Typhlitis)
The key feature that allows neutropenic entero-
colitis to be distinguished from AMI is the pa-
tient’s clinical history. Neutropenic colitis occurs
in patients undergoing chemotherapy for leuke-
mia, lymphoma, or another malignancy and in
patients with immunosuppression after an organ
transplant. The reported incidence of neutrope-
nic colitis in these patients is 5.3%–5.6% (46).
The combination of neutropenia and cytotoxic
drugs is thought to decrease the body’s defense
mechanisms against gastrointestinal tract micro-
organisms, which results in bacterial infection,
inflammation, and in some cases, necrosis (47).
Neutropenic enterocolitis should be suspected
in any patient with neutropenia who presents
with fever and abdominal pain (47). Neutrope-
nic enterocolitis has a predilection for the cecum
and distal ileum and shows right lower quadrant
inflammation and fluid at CT (48). Pneumatosis
intestinalis and perforation can occur.
Angioedema
Small bowel angioedema results from an in-
crease in vascular permeability and can be
hereditary or acquired. Hereditary angioedema
is an autosomal-dominant disorder in which pa-
tients have a deficiency or dysfunction of serum
C1 inhibitor and experience intermittent attacks
of edema involving the face, extremities, and
gastrointestinal tract (49). Triggers of acquired
angioedema include angiotensin-converting
enzyme inhibitors, iodinated contrast material,
aspirin, and insect bites (50). The hallmark of
enteric angioedema at CT is a striking target
sign, with marked circumferential edema in the
submucosal layer, and hyperenhancement of the
mucosa and serosa (Fig 16). The jejunum and
duodenum are the most common gastrointes-
tinal sites affected (49), and this distribution is
uncommon in AMI. Mesenteric vascular con-
gestion and fluid, ascites, and bowel dilatation
may be present (49,51). Unlike AMI and other
enterocolitides, angioedema can resolve rapidly
over 1–2 days at serial imaging.
Radiation Enteritis
Despite advances in radiation therapy tech-
niques, radiation-induced enteritis is a common
adverse effect that is experienced by 1.4%–15%
of patients who receive at least 45–55 Gy of
abdominal or pelvic radiation (52,53). The small
bowel is the most radiation-sensitive organ of the
gastrointestinal tract (54), with the fixed terminal
558  March-April 2020 radiographics.rsna.org

Figure 15.  Small bowel Crohn disease in a

28-year-old man with distal Crohn ileitis compli-
cated by penetrating fistulous disease. Axial (a)
and sagittal (b) intravenous contrast-enhanced
CT images show segmental mural hyperen-
hancement and thickening that correspond to
active inflammation. There is a stellate fistulous
complex involving the inflamed ileum and rec-
tosigmoid junction (arrowheads in a) leading to
an abscess (arrow in a). An intramural microab-
scess secondary to mucosal ulceration is present
(white arrow in b). Note the adjacent segment
of spared ileum (arrowhead in b) and paucity of
atherosclerotic disease (black arrow in b) in this
young patient.

ileum being the most commonly affected segment

(53,55). Although the rectum is the least radia-
tion-sensitive part of the gastrointestinal tract, it
is frequently involved owing to its fixed position
and proximity to irradiated pelvic organs (54).
In the acute phase, days to weeks after exposure,
radiation causes inflammation and injury to the
bowel mucosa and microvasculature. Patients
present with nausea, vomiting, pain, and diarrhea
(54,56). At CT, uniform edematous bowel wall
thickening, hyperenhancement, and fat strand-
ing are seen (Fig 17) (55). Unlike AMI, radiation
enteritis affects adjacent pelvic structures such as
the bladder (ie, cystitis), marrow (eg, conversion
to fatty marrow and insufficiency fractures), and
soft tissues (eg, stranding and edema). Chronic
radiation enteropathy occurs months to years
after exposure and results from progressive oblit-
erative endarteritis, which leads to ischemia and
fibrosis (54,56). Patients present with obstruc-
tion, malabsorption, or bleeding. At CT, ulcers,
fistulas, strictures, and angulated fixed bowels
may be seen (54,56,57).

Graft-versus-Host Disease
An allogenic hematopoietic cell transplant in-
volves the donation of human hematopoietic cells
to a patient with cancer (usually for a hemato-
logic malignancy) who underwent chemotherapy
and/or radiation therapy for myeloablation.
Graft-versus-host disease occurs because of histo-
compatibility differences between the graft and
the host, typically within 100 days of allogenic
hematopoietic cell transplant, with a reported
incidence of 15%–50% (58). Patients present
with diarrhea, abdominal pain, nausea, vomiting,
and fever.
CT findings of graft-versus-host disease mimic
those of AMI and include wall thickening of the
small and/or large bowel, mural hyperenhance-
ment, engorgement of the vasa recta, mesenteric
stranding, and ascites (Fig 18) (58–60). Unlike
Figure 16.  Angioedema in a 65-year-old woman with
a history of two episodes of small bowel angioedema
that rapidly resolved after therapy. Coronal intravenous
contrast–enhanced CT image shows marked circumfer-
ential edematous wall thickening involving a long seg-
ment of ileum (arrowheads), with mesenteric hyperemia
and edema. A small volume of ascites (arrow) also can
be seen. Laboratory test results showed C1 deficiency.
in AMI, if bowel dilatation is present, it appears
proximal to the affected segments (58), and the
distribution is discontinuous in approximately
one-half of cases (60). Another potential dis-
tinguishing feature relates to the biliary find-
ings seen in graft-versus-host disease, including
gallbladder distention, thickening, and hyperen-
hancement (58,59).
RG  •  Volume 40  Number 2 Fitzpatrick et al  559

Figure 17.  Radiation enteritis in a 68-year-old woman with rectal adenocarcinoma who was treated
with neoadjuvant chemotherapy and radiation therapy and presented with nausea, vomiting, diarrhea,
and volume depletion over several weeks. Coronal arterial phase (a) and sagittal portal venous phase (b)
intravenous contrast–enhanced CT images show circumferential edematous wall thickening and mural
hyperenhancement of the rectosigmoid and mesenteric small bowel (arrowheads), with mesenteric hy-
peremia and mesenteric fluid.

scribed with the use of endoscopy and include er-

ythema, edema, dilated capillaries, angioectasias,
and varices (61,62). These conditions can lead
to chronic or acute gastrointestinal tract bleed-
ing and are often confused for other diseases
that manifest similarly (62). At CT, increased
portal pressure may result in nonspecific bowel
wall thickening of the affected segment, without
changes in the luminal diameter or wall enhance-
ment. One study (63) found that approximately
35% of patients with cirrhosis demonstrate
colonic wall thickening, of which two-thirds were
limited to the right colon. This was postulated
to result from increased hydrostatic pressure
and fewer collateral vessel pathways for the right
colon. Extraintestinal features of portal hyperten-
sion including cirrhosis, portosystemic varices, an
enlarged extrahepatic portal vein, splenomegaly,
and ascites may be helpful for diagnosis.

Figure 18.  Graft-versus-host disease in a 45-year-old

man who underwent allogenic hematopoietic cell trans-
plant for lymphoma. Coronal intravenous contrast–
enhanced CT image shows marked edematous wall
thickening of the small and large bowel (arrowheads),
with stratified mural enhancement corresponding to
the target sign, perienteric stranding, and mesenteric
hyperemia. Note the absence of atherosclerotic disease
in the SMA (arrow).
Portal Hypertension
Portal gastropathy, enteropathy, and colopathy
correspond to pathologic changes to the gastro-
intestinal tract secondary to portal hypertension.
These changes predominantly have been de-
Conclusion
Mesenteric ischemia can be a challenge to diag-
nose and requires a high degree of clinical and
radiologic suspicion. Early diagnosis and inter-
vention are critical to reduce patient morbidity
and mortality. CT angiography of the abdomen
and pelvis is the first-line imaging examination
for diagnosis. A systematic inside-out approach to
interpreting CT angiographic images for sus-
pected mesenteric ischemia provides a framework
for comprehensive evaluation and can improve
detection and synthesis of imaging findings.
Awareness of the imaging features, pitfalls, and
potential conditions that mimic ischemia can
help radiologists to improve diagnostic accuracy.
560  March-April 2020 radiographics.rsna.org
Acknowledgment.—The authors thank the artists of Designs
that Cell (www.designsthatcell.ca) for creating the anatomical
images in Figure 2.
Disclosures of Conflicts of Interest.—S.E.C. Activities related
to the present article: disclosed no relevant relationships. Activi-
ties not related to the present article: grants/grants pending from
GE Healthcare, patent pending for systems and methods for
generating cancer prediction maps from multiparametric MRI
with deep learning. Other activities: spouse has grant support
from GE Healthcare.
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