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1352
GASTROINTESTINAL IMAGING
CT Findings of Acute Small-Bowel
Entities
Mark D. Sugi, MD
Christine O. Menias, MD
Meghan G. Lubner, MD
Sanjeev Bhalla, MD
Vincent M. Mellnick, MD
Matt H. Kwon, MD
Douglas S. Katz, MD
Abbreviations: ACE = angiotensin-converting
enzyme, GVHD = graft-versus-host disease,
HSP = Henoch-Schönlein purpura, SMA = su-
perior mesenteric artery, SLE = systemic lupus
erythematosus
RadioGraphics 2018; 38:1352–1369
https://doi.org/10.1148/rg.2018170148
Content Codes:
From the Department of Radiology, Mayo
Clinic, 13400 E Shea Blvd, Scottsdale, AZ 85259
(M.D.S., C.O.M.); Department of Radiology,
University of Wisconsin Hospital, Madison, Wis
(M.G.L.); Division of Diagnostic Radiology,
Mallinckrodt Institute of Radiology, Washington
University School of Medicine, St. Louis, Mo
(S.B., V.M.M.); Stony Brook University School
of Medicine, Stony Brook, NY (M.H.K.); and
Department of Radiology, NYU Winthrop Hos-
pital, Mineola, NY (D.S.K.). Recipient of a Cer-
tificate of Merit award for an education exhibit at
the 2016 RSNA Annual Meeting. Received May
26, 2017; revision requested September 28 and
received December 11; accepted December 14.
For this journal-based SA-CME activity, the au-
thor M.G.L. has provided disclosures (see end of
article); all other authors, the editor, and the re-
viewers have disclosed no relevant relationships.
Address correspondence to M.D.S. (e-mail:
sugi.mark@mayo.edu).
©
RSNA, 2018
SA-CME LEARNING OBJECTIVES
After completing this journal-based SA-CME
activity, participants will be able to:
■■Identify common CT features of dif-
fuse and regional small-bowel disorders.
■■Differentiatebetween vascular and
nonvascular causes of acute small-bowel
disorders on the basis of CT findings.
■■Provide an appropriate imaging pro-
tocol for patients with suspected acute
intestinal disease, using clinical history
and laboratory data.
See rsna.org/learning-center-rg.
Although a broad spectrum of entities can induce acute pathologic
changes in the small bowel, there are relatively few imaging features
that are characteristic of a specific diagnosis on the basis of CT
findings. Specific clinical information, including time course and
onset of disease, patient risk factors, and any recent pharmacologic
or radiation therapy, is often instrumental in refining the differential
diagnosis. A wide spectrum of disorders is reviewed in this article;
however, given the breadth of disorders associated with the small
bowel, neoplastic and infectious conditions affecting the small bow-
el that can manifest acutely are not specifically discussed. Vascular
diseases that can affect the small bowel regionally or diffusely, in-
cluding thromboembolic and hypoperfusion phenomena, as well as
a spectrum of vasculitides, are reviewed. Iatrogenic causes of small
bowel disorders are discussed, including angiotensin-converting
enzyme inhibitor–induced angioedema, and chemotherapy- and
radiation therapy–associated patterns of disease. Autoimmune and
hereditary conditions that can affect the small bowel, including
systemic lupus erythematosus and genetic C1 esterase inhibitor de-
ficiency, respectively, are reviewed.
©
RSNA, 2018 • radiographics.rsna.org
Introduction
The small bowel is associated with a group of acute disorders that
are distinct from those that affect the colon, in part because of its
unique vascular supply and physiologic functions, which differ from
those of the colon. Nonlocalized acute abdominal pain is often the
first clinical presentation of disease, which leads to an initial imaging
examination, usually performed with intravenous contrast-material–
enhanced CT in the emergency department setting.
Diffuse or regional acute disorders of the small bowel often
manifest with nonspecific findings at CT, most commonly mural
stratification and circumferential bowel wall thickening. On intra-
venous contrast-enhanced CT images of the abdomen and pelvis,
the “target” or “double halo” sign (Fig 1) represents mural strati-
fication caused by hyperenhancement of both the inner mucosa
and the outer muscularis propria/serosa, with a middle layer of
low-attenuating submucosal edema (1). However, in the absence of
intravenous contrast enhancement, stratified hyperenhancement is
not depicted, and the only indications of underlying disease may be
bowel wall thickening (with or without associated edema), perien-
teric inflammatory change, and/or ascites. Because the physiologic
mechanisms underlying acute small-bowel disorders vary widely,
attention to secondary extraintestinal imaging findings and avail-
able clinical and laboratory data is helpful for suggesting a more
specific diagnosis.
RG  •  Volume 38  Number 5 Sugi et al  1353
TEACHING POINTS
■■ On intravenous contrast-enhanced CT images of the abdo-
men and pelvis, the “target” or “double halo” sign represents
mural stratification caused by hyperenhancement of both the
inner mucosa and the outer muscularis propria/serosa, with a
middle layer of low-attenuating submucosal edema.
■■ Dilated loops of small bowel (>3 cm in diameter) with pa-
per-thin walls should raise strong suspicion for acute vascular
compromise owing to thromboembolic disease.
■■ Mechanical obstruction of two points along a short segment
of small bowel in a single location can lead to a twisted C-
or U-shaped configuration, the typical appearance seen in
closed-loop small-bowel obstruction at CT.
■■ Vasculitis should be considered under certain circumstances,
namely in young patients, when the affected segments of
small bowel are atypical in distribution (eg, in the duodenum
or a patchy distribution across multiple vascular territories)
and when there is associated systemic involvement by a simi-
lar process.
■■ CT findings of ACE inhibitor–induced angioedema include cir-
cumferential wall thickening (most commonly involving the
jejunum), mural stratification, straightening of bowel loops,
interloop or mesenteric edema, and ascites.
Multidetector CT Protocols
The use of oral contrast material in conjunc-
tion with multidetector CT for the evaluation of
small-bowel disorders has evolved with improving
detector and CT technology, changing practice
needs, and practical clinical considerations. Positive
oral contrast material, typically barium-based or
water-soluble iodinated solutions, was previously
routinely used for maintaining high diagnostic ac-
curacy of CT for small-bowel and related disor-
ders, particularly for differentiating between bowel
loops and fluid collections (2).
Multidetector CT provides improved spatial
and contrast resolution and more efficient scan-
ning, with fewer or no artifacts. Multidetector CT
enterography with multiplanar reconstructions
has been shown to be highly useful for diagnosing
a number of clinical conditions, including acute
mesenteric ischemia, small-bowel obstruction, and
inflammatory bowel disease (3).
Multiple recent studies and reviews assessing
the diagnostic accuracy of abdominal and pelvic
multidetector CT, without the administration of
oral contrast material, have been performed, partic-
ularly in the emergency setting. Resultant recom-
mendations against the routine use of oral contrast
material (eg, in patients with suspected small-
bowel ischemia) have been made by the American
College of Radiology (4).While it has been sug-
gested that underdistention of the small bowel may
pose a greater challenge for image interpretation in
some situations, it is also recognized that oral con-
trast material has the potential to obscure subtle
but abnormal findings in the small-bowel wall (5).
In acute hemorrhage, for example, intralumi-
nal extravasation of intravenous contrast material
may be obscured by oral contrast material, and
subtle bowel wall thickening may also be more
difficult to interpret if oral contrast material is
within the lumen. In acute mesenteric ischemia,
high-attentuation oral contrast material may
make it more difficult to appreciate differential
enhancement of the bowel wall, potentially mask-
ing hypoenhancement and ischemia.
From a radiation-dose standpoint, oral
contrast material may lead to slightly increased
patient doses, largely owing to the use of au-
tomated exposure control. This mechanism
modulates the tube current according to patient
size and the density of internal structures, as
determined by a scout image. Thus, the addi-
tion of positive oral contrast material may lead
to higher levels of radiation exposure compared
with those of a similar scan of the same patient
obtained without the administration of oral con-
trast material (6).
In addition to dose considerations, matters of
patient tolerance and preference (eg, unpleasant
taste and resulting distention) and the increased
time delay to imaging, diagnosis, and treatment are
important considerations in the emergency setting.
Collectively, the potential disadvantages of the ad-
ministration of oral contrast material and the recent
evidence documenting no decrease in the diagnos-
tic accuracy of multidetector CT in the absence of
oral contrast material suggest that its routine use
in the emergency setting is not warranted. Under
certain circumstances, particularly in patients with a
body mass index of 25 or less, oral contrast material
may still have a limited role (7).
Multidetector CT protocols can be imple-
mented to enhance diagnostic accuracy for
small-bowel disease. The primary branch point
in the protocol selection algorithm is determined
by clinical suspicion for a vascular or nonvascular
cause. If a vascular cause is suspected (eg, acute
mesenteric ischemia, arterial or venous thrombo-
sis, or gastrointestinal hemorrhage), a CT angiog-
raphy or three-phase CT protocol (nonenhanced,
arterial, and delayed phases) can be performed
(3). The multi-phasic examination optimizes the
probability of visualizing a wide range of pertinent
findings related to vascular disease, including dif-
ferential enhancement characteristics of the bowel
wall, arterial or venous blush within the intestinal
lumen, and vascular filling defects.
If there is clinical suspicion for a nonvascular
cause, routine intravenous contrast-enhanced
CT of the abdomen and pelvis with multiplanar
reconstructions (coronal and sagittal images, in
addition to routine axial images) may be per-
formed. This protocol allows for the sensitive
1354 September-October 2018 radiographics.rsna.org

Figure 1.  Target or double halo sign. (a, b) Coronal (a) and axial (b) intravenous contrast-enhanced CT im-
ages in a 59-year-old woman with end-stage renal disease and small vessel ischemia show enhancement of the
inner mucosa and outer muscularis propria/serosa (arrows), with a middle layer of low-attenuating submucosal
edema. Note the reactive ascites and interloop edema owing to ischemic change of the jejunum. (c) Illustration
shows an axial view of the inner mucosa and outer muscularis propria/serosa, with an inset labeling a double
halo or target sign. (Reprinted, with permission, from Mayo Foundation for Medical Education and Research.)

diagnostic evaluation of small-bowel obstruction,

angioedema, and iatrogenic causes of small-bowel
disease, including chemotherapy- or radiation
therapy–induced enteritis, as well as inflamma-
tory bowel disease, hemorrhage, and mechanical
perforation.
At our institutions and elsewhere (8), exami-
nations are performed with a 64–detector row
or greater CT scanner, with portal venous phase
images of the abdomen and pelvis acquired ap-
proximately 70–90 seconds after the initiation of
the intravenous bolus injection.
For patients with clinical suspicion for new or a
known history of inflammatory bowel disease, CT
enterography may be performed to acquire a base-
line examination or to assess progression of dis-
ease. In addition to the routine administration of
intravenous contrast material, neutral oral contrast
material (eg, contrast material with an attenua-
tion value of 10–30 HU, which is slightly denser
than water [9]) may be administered to provide
adequate distention of the small bowel, without
obscuring key findings related to enhancement.
Commonly used oral contrast materials, which
have been shown to be superior to water owing
to diminished absorption and thus more optimal
distention, include polyethylene glycol and solu-
tions containing low-attenuation barium con-
trast material. Reduced motion artifacts can be
achieved by inhibiting peristalsis with glucagon
(0.1 mg administered intravenously), and patients
are requested to fast for several hours before the
examination. Detailed protocols for CT enterog-
raphy have been previously described (9).
Vascular Causes of
Small-Bowel Disorders
Acute Mesenteric Ischemia
A basic understanding of mesenteric vascular
anatomy is helpful when approaching sus-
pected acute ischemia of the small bowel. The
dominant vascular supply to most of the small
bowel arises from the superior mesenteric artery
(SMA) thorough the jejunal and ileal mesen-
teric arcades. The duodenum is unique in that it
receives its blood supply from both the superior
and inferior pancreaticoduodenal arteries, which
are branches of the gastroduodenal and superior
mesenteric arteries, respectively (10).
The causes of acute mesenteric ischemia can
be divided into occlusive or nonocclusive disease
and further classified as arterial or venous. Imag-
ing findings vary according to both pathophysiol-
ogy (eg, acute embolism versus acute changes
related to progressive nonocclusive disease) and
time course of the disease, as acute restriction of
RG  •  Volume 38  Number 5 Sugi et al  1355
Figure 2.  Acute mesenteric ischemia due to SMA thrombosis in a 62-year-old man who presented with severe abdominal pain.
Axial intravenous contrast-enhanced CT images show a thrombus (arrow in a) at the SMA origin, with absence of enhancement
and several dilated paper-thin loops of jejunum with high-attenuation layering intraluminal fluid (arrowheads in b) corresponding
to hemorrhagic infarction, which was confirmed at surgery.
blood flow will manifest with findings different
from those seen in stages of reperfusion (11).
Arterial thromboembolism accounts for an
estimated two-thirds of cases of acute intestinal
ischemia, with only 5%–10% of cases attributed
to a venous cause (12). A small remainder is at-
tributed to nonocclusive disease, although this
process may be more commonly seen in practice,
given that the aforementioned estimates are based
on the older surgical literature, published during a
time when imaging with CT was less prevalent.
Acute Arterial Embolism.—Arterial occlusive
disease can be further categorized as embolism or
thrombosis (Fig 2), with embolism being far more
prevalent than thrombosis, accounting for nearly
half of all cases of acute mesenteric ischemia (11).
Imaging features of acute arterial embolism reflect
markedly diminished or complete occlusion of the
blood supply. Mucosal and serosal enhancement
may be completely absent, as blood flow ceases
to reach the small bowel. Progressive ischemia
with transmural infarction and associated loss of
muscle tone may manifest as diffusely thin-walled
loops of bowel at CT.
Dilated loops of small bowel (>3 cm in diam-
eter) with paper-thin walls (Fig 3) should raise
strong suspicion for acute vascular compromise
owing to thromboembolic disease (10). Dysfunc-
tional peristalsis ensues, which may lead to air-fluid
levels or blood-fluid levels (in cases of infarction
and/or hemorrhage) on CT images. When the
downstream sequelae of arterial embolism are seen,
the radiologist should search for causative vascular
findings, paying particular attention to the SMA.
Approximately half of embolic occlusions of
the SMA occur just distal to the origin of the
middle colic artery, with a smaller percentage
(15%) occurring at the origin of the SMA (11). Pa-
tients with thromboembolic occlusion of the SMA
often have an antecedent embolic event related to
underlying cardiac disease, which can lead to the
development of mural thrombus (12). The astute
radiologist may find additional clues in the lower
chest, such as a dilated left ventricle with intracar-
diac thrombus, even at CT of the abdomen and
pelvis, if the acquisition volume is large enough.
Acute Venous Thrombosis.—Acute thrombosis
of the superior mesenteric vein (Fig 4) is an un-
usual cause of bowel ischemia, given the exten-
sive collateralization between the mesenteric and
systemic venous systems, but it may occur in
certain conditions associated with hypercoagu-
lability. Restriction of venous outflow from com-
plicated small-bowel obstruction, such as with a
closed-loop obstruction, may lead to ischemia,
hemorrhage, and/or infarction (12).
On CT images, mucosal enhancement may be
normal or increased in the setting of inflamma-
tion, unless the patient has concomitant arterial
disease. Wall thickening due to edema or hemor-
rhage with a target sign may be depicted, along
with engorgement of the venous mesentery (10).
Increased hydrostatic pressure and edema cause
prominent thickening of the bowel wall (13),
which may lead to subsequent transmural necro-
sis and superinfection as the mucosal barrier is
broken down. However, this finding is more com-
mon with arterial-based disease (12,14).
Secondary findings of mesenteric venous en-
gorgement, and particularly mesenteric edema,
are more characteristic of venous than arterial
disease (Fig 5). CT manifestations of venous
1356 September-October 2018 radiographics.rsna.org

Figure 3.  Acute mesenteric ischemia with small-bowel

infarction in a 72-year-old woman who presented with dif-
fuse abdominal pain and hypotension. (a, b) Coronal (a)
and axial (b) intravenous contrast-enhanced CT images
show multiple dilated poorly-enhancing paper-thin loops of
bowel, with extensive pneumatosis (white arrow in a) and
portal venous gas (black arrow in a). Note the gas within
a jejunal mesenteric venous branch (arrowheads in b).
(c) Photograph obtained during laparotomy shows exten-
sive small-bowel necrosis (*).

thrombosis may also be depicted and are often

more pronounced in cases of closed-loop small-
bowel obstruction, in which venous engorge-
ment occurs secondarily to focal mechanical
obstruction of venous outflow.

Imaging of Acute Mesenteric Ischemia.—CT

angiography with arterial and venous phases is the
ideal noninvasive imaging modality for patients
with suspected acute mesenteric ischemia. In addi-
tion to its estimated 90% sensitivity for mesenteric
ischemia, CT angiography is also useful in identi-
fying alternative diagnoses and changes of chronic
ischemia, stenosis, and the presence of collateral
pathways (13). Positive oral contrast material
should be avoided in this situation. CT angiogra-
phy may be performed with no oral contrast mate-
rial or with negative or neutral contrast material
(eg, water) to delineate wall enhancement.
Other Disease Considerations.—Nonocclusive
mesenteric ischemia comprises a spectrum of dis-
eases related to low flow or vasospasm, which can
develop in cardiac disease, hypovolemia, or sepsis
(12). In this setting, there is considerable overlap
with the CT findings of hypoperfusion complex
described in the next section.
A final entity to consider is ischemic compromise
in closed-loop small-bowel obstruction. Mechani-
cal obstruction of two points along a short segment
of small bowel in a single location can lead to a
twisted C- or U-shaped configuration (Fig 6), the
typical appearance seen in closed-loop small-bowel
obstruction at CT (15). This usually occurs owing
to adhesions but can also be seen in association
with external or internal hernias, with or without
concurrent adhesions.
When longer segments of bowel are involved,
or if the bowel is out of the plane of the image,
the appearance may be closer to that of “balloons
on a string” (16). The closed loop of small bowel
quickly becomes strangulated as the vascular supply
is abruptly cut off, resulting in a “beak sign” of the
mesenteric vessels as they taper to a single point
(15). Multiple bowel loops radiating to a central
point at CT, when associated with vascular and
mesenteric congestion, should raise strong suspi-
cion for a closed-loop obstruction (9,16).
Hypoperfusion Complex
The small bowel normally receives approximately
20% of resting cardiac output (12), but this fraction
can sharply decrease in the setting of constriction
of the splanchnic circulation or in blunt trauma.
RG  •  Volume 38  Number 5 Sugi et al  1357

Figure 4.  Acute mesenteric venous ischemia in a 43-year-old woman with positive test results for lupus anticoagulant
who presented with acute abdominal pain. Axial (a) and coronal (b) intravenous contrast-enhanced CT images show
an occlusive thrombus within the superior mesenteric vein (white arrow) and its jejunal branches, with several loops of
thick-walled jejunum (arrowheads) that show marked mural edema and a target appearance of the bowel, which is poorly
enhancing. Note the mesenteric edema and fluid (black arrow in b), common features of mesenteric venous ischemia.

Figure 5.  Acute mesenteric venous ischemia in a 53-year-old man with a history of cirrhosis who presented with in-
creasing abdominal distention and abdominal pain. Coronal (a) and axial (b) oral and intravenous contrast-enhanced
CT images show an occlusive thrombus in the superior mesenteric vein (arrow in a), which is associated with diffuse
circumferential small-bowel wall thickening, mesenteric edema (arrowheads), and fluid.

Acutely diminished perfusion volume can lead to
the development of the so-called hypoperfusion com-
plex at CT, also referred to as “shock bowel” (17).
Hypovolemia leads to decreased arterial inflow and
venous outflow, with resultant ischemic change.
A wide spectrum of clinical entities can
provoke nontraumatic hypoperfusion, including
cardiac arrest, sepsis, and diabetic ketoacido-
sis. Indirect traumatic injuries to the head and
spinal cord may also produce similar findings.
Findings of hypoperfusion at CT often mani-
fest early and prominently in the small bowel
as compared with the manifestations seen in
other visceral organs and may include luminal
distention, intense mucosal hyperenhance-
ment (greater than that of the adjacent psoas
muscle on contrast-enhanced CT images), and
mural stratification (18). While the hypoperfu-
sion complex can develop in any segment of the
gastrointestinal tract, it most commonly involves
the jejunum (Fig 7), with findings of marked
mucosal enhancement, bowel wall thicken-
ing, and intraluminal fluid seen on intravenous
contrast-enhanced CT images (8).
Extraintestinal manifestations of hypoperfusion
at CT include a collapsed or slitlike inferior vena
cava, a small aorta, “shock pancreas” (ie, peripan-
creatic fluid and/or fat stranding with heteroge-
neous parenchymal enhancement), and relative
hypoenhancement of the spleen and liver. Addi-
tional features include ascites and hyperenhancing
adrenal glands and kidneys (17). These additional
CT findings help differentiate hypoperfusion
complex–related small-bowel injury from bowel
ischemia related to mesenteric venous occlusion.
In cases of hypovolemic shock secondary to
blunt abdominal trauma, follow-up CT after ad-
equate resuscitation and recovery from the acute
1358 September-October 2018 radiographics.rsna.org

Figure 6.  Surgically confirmed closed-loop small-bowel obstruction in two patients. (a) Axial intravenous contrast-
enhanced CT image in a 51-year-old woman, who underwent low anterior resection for rectal cancer 2 months earlier,
shows a radial configuration of thickened jejunal loops and their mesenteric vessels, converging to a central point
of obstruction. Note the mural stratification and target appearance of the ischemic segments (arrows), with associ-
ated mesenteric edema, fluid, and vascular engorgement. (b) Coronal intravenous contrast-enhanced CT image in
a 43-year-old woman with recurrent small-bowel obstructions, which required prior exploratory laparotomy, shows
a U-shaped segment of ileum (dashed crescent) obstructed at two points, producing the closed-loop configuration.

Figure 7.  Hypoperfusion complex in a 30-year-old

man who presented after a motor vehicle collision.
Axial intravenous contrast-enhanced CT image shows
several thickened loops of jejunum with marked mu-
cosal hyperenhancement (white arrows). Note the
relatively collapsed inferior vena cava (arrowhead),
small-caliber aorta (black arrow), and regional edema,
which are features of the hypoperfusion complex.

traumatic incident may show complete resolution

of the initial small-bowel findings at CT (19).
This indicates reversibility of the initial insult, as
there are stages of hypovolemic shock, progress-
ing from compensated to uncompensated and
uncompensated to irreversible (20).
Acute disruption of the autoregulatory
mechanisms of vascular circulation results in
adrenergic responses that attenuate splanchnic
perfusion, which may initially be maintained
in the compensated state by apposing mecha-
nisms aimed at maintaining cardiac output and
sufficient blood pressure. When compensatory
measures are overcome by ongoing hemorrhage
or other causes of hypoperfusion, the uncom-
pensated state results in early ischemic changes,
which can rapidly become irreversible without
resuscitation (20).
Small-Bowel Vasculitides
Vasculitis comprises a spectrum of diseases char-
acterized by inflammation and necrosis of blood
vessels. The vasculitis may be the predominant
feature of the disorder or a less prominent fea-
ture, with substantial overlap among conditions
(21). Attempts to subcategorize the vasculitides
have been made by defining the dominant caliber
of the vessel involved as large, medium, or small,
although there is substantial overlap, often with
indistinguishable clinical presentations (22).
Refining the differential diagnosis requires
consideration of clinical data, imaging features,
and findings at histologic analysis. Patients with
vasculitis involving the small bowel typically
present with acute or subacute hematochezia,
secondary to changes of mesenteric ischemia.
Vasculitis should be considered under certain
circumstances, namely in young patients, when
the affected segments of small bowel are atypical
in distribution (eg, in the duodenum, or a patchy
distribution across multiple vascular territories)
and when there is associated systemic involve-
ment by a similar process (23).
The predominant caliber of the vessel involved
correlates with the findings in the small bowel.
In large-vessel vasculitis such as giant cell (ie,
temporal) arteritis, the clinical presentation may
be indistinguishable from that of thromboem-
RG  •  Volume 38  Number 5 Sugi et al  1359
Figure 8.  Lupus vasculitis in a 43-year-old woman with a his-
tory of SLE who presented with severe abdominal pain. Axial
oral and intravenous contrast-enhanced CT image shows di-
lated loops of small bowel with diffuse symmetric wall thick-
ening and mucosal hyperenhancement. Note the corkscrew
appearance of the terminal vessels (arrows), a feature of small-
vessel ischemic disease related to the underlying vasculitis.
bolic occlusive disease, with mesenteric ischemia
being the primary manifestation. Medium-vessel
vasculitides, such as polyarteritis nodosa (PAN),
may manifest similarly with symptoms related
to ischemia from underlying vascular luminal ir-
regularity, hemorrhage, or occlusion. PAN is also
associated with aneurysm formation, and thus
patients may present with acute abdominal pain
secondary to aneurysm rupture (24).
Distinguishing thromboembolic phenomena
from PAN is important, as the treatment regi-
mens differ substantially, with the potential for
either condition to be fatal as a result of progres-
sive gastrointestinal complications. In contrast,
appropriate treatment of PAN with cyclophos-
phamide and corticosteroids may result in a 90%
rate of remission or cure (25). As with other vas-
culitides, there is a spectrum of disorders related
to the stage and extent of disease, and thus subtle
changes of luminal irregularity or ectasia are
often early findings that may precede complete
occlusion or aneurysm formation.
Vasculitides affecting small-caliber vessels
include microscopic polyangiitis, systemic lupus
erythematosus (SLE) (26), and Henoch-Schönlein
purpura (HSP) (22). SLE should be suspected
in young female patients of childbearing age with
associated clinical signs and symptoms including
malar rash, oral ulcers, Raynaud phenomenon, and
synovitis, as well as the presence of autoantibodies
(27). Small-vessel vasculitis results in inflammatory
change at the level of the arterioles, venules, and
capillaries, often manifesting with multifocal muco-
sal and submucosal hemorrhage, with intervening
segments of normal bowel (23,28).
The terminal mesenteric vessels may develop
a “corkscrew” appearance, which in the setting
of vasculitis is suggestive of small-vessel isch-
emic disease (Fig 8). Genitourinary findings
may precede changes to the bowel and include
hydronephrosis owing to vesicoureteral reflux
or fibrotic change at the bladder trigone. The
presence of both gastrointestinal and genitouri-
nary features may further suggest an underlying
vasculitis, as both systems are often affected in
SLE and in HSP (23).
HSP, the most common vasculitis in children
but one that also affects adults, typically mani-
fests in the 1st decade of life (ages 3–10 years)
and is characterized by a tetrad of findings: ab-
dominal pain, arthralgia, purpura, and hematuria
(29). Importantly, a minority of patients may
have gastrointestinal symptoms before experienc-
ing symptoms related to the joints, skin, and kid-
neys. The gastrointestinal manifestations of HSP
are related to hemorrhage and intramural edema
and as with other vasculitides may include
segmental involvement of the small bowel, with
areas of intervening normal bowel (Fig 9) (23).
Use of multiphase multidetector CT that
includes a nonenhanced phase, which may be
prompted by worsening anemia or the search
for the cause of gastrointestinal hemorrhage, has
specific value in this setting for the evaluation
of high-attenuation change in the bowel wall. In
the absence of other signs of HSP, the findings
of bowel wall thickening secondary to intra-
mural hemorrhage with edema may mimic a
number of other entities, potentially prompting
unnecessary surgical intervention (23).
Other small-vessel vasculitides, including
granulomatosis with polyangiitis (GPA; previ-
ously called Wegener granulomatosis) and eo-
sinophilic GPA (previously called Churg-Strauss
syndrome), predominantly affect the respiratory
system and kidneys. However, they can involve
any part of the gastrointestinal tract, with protean
manifestations ranging from mild inflammation
to ulceration and perforation (23). Circumferen-
tial bowel wall thickening and regional mesen-
teric vascular engorgement are common over-
lapping features at CT, and further diagnostic
workup may require skin biopsy or other histo-
pathologic analysis (23).
Angioedema of the Small Bowel
Medication-induced angioedema of the small
bowel is a relatively uncommon and somewhat
underdiagnosed condition associated with medi-
cations that inhibit the renin-angiotensin system.
These most commonly include the angiotensin-
converting enzyme (ACE) inhibitors (30), par-
ticularly lisinopril and enalapril, and to a lesser
1360 September-October 2018 radiographics.rsna.org
extent the angiotensin II receptor blockers (31).
The incidence of ACE inhibitor–induced angio-
edema is estimated at approximately 0.3% of
patients receiving this common class of medica-
tions (32), with contributing risk factors includ-
ing African descent, a history of drug rash or
seasonal allergies, and age greater than 65 years.
Other reports note that adult women who are
overweight are at particular risk for this disorder,
which can occur days to years after these medica-
tions are initially administered (33).
While the exact physiologic mechanism of
drug-induced angioedema is unknown, previ-
ous studies have demonstrated elevated levels
of circulating bradykinin during acute episodes,
with subsequent normalization of these levels
following drug withdrawal (34). Bradykinin, an
inflammatory mediator that increases vascular
permeability and acts as a potent vasodilator, is
normally degraded by ACE.
The importance of clinical history is under-
lined by the potentially alarming CT findings
that can be mistaken for ischemia and other
conditions that might warrant surgical consulta-
tion. In a series of 20 patients with features of
small-bowel angioedema ultimately attributed to
ACE inhibitor use, symptoms resolved within 4
days of hospitalization. However, several pa-
tients who were initially misdiagnosed with isch-
emia underwent exploratory laparotomy (26).
CT findings of ACE inhibitor–induced angio-
edema include circumferential wall thickening
(most commonly involving the jejunum), mural
stratification, straightening of bowel loops, inter-
loop or mesenteric edema, and ascites (Fig 10)
(26,35). The laboratory findings are helpful, as
there is usually a normal serum lactate level and
a normal or only mildly elevated white blood
cell count.
Removing the inciting agent (the ACE inhibi-
tor) usually leads to complete resolution of the
angioedema. Certain patients may experience
repetitive episodes if the medication is not
recognized as the inciting agent or if the cause
is hereditary, while others may develop other
sites of angioedema in the body, including in
the head and neck. Keeping this relationship in
mind is important for the radiologist, who may
have the opportunity to be the first to suggest
the diagnosis.
Hereditary forms of recurrent angioedema
are associated with genetic C1 esterase inhibi-
tor deficiency and may affect the small bowel
and other parts of the body. Similar to that seen
in patients with ACE inhibitor–induced angio-
edema, elevated levels of bradykinin have been
demonstrated during acute episodes of angio-
edema in patients with the hereditary form (36).
Figure 9.  HSP vasculitis in a 42-year-old man
who presented with bloody stools. Axial intrave-
nous contrast-enhanced CT image shows multi-
ple jejunal loops with the target sign (arrows) and
mesenteric vascular engorgement and ascites.
Immunologic Causes
of Small-Bowel Disorders
Graft-versus-Host Disease
Graft-versus-host disease (GVHD) affecting the
gastrointestinal tract after bone marrow trans-
plant was described in 1981 in a small case series
(37). Since then, both the understanding of the
pathophysiology of GVHD and the development
of new immunosuppressant agents have advanced
substantially. GVHD was initially divided into
acute and chronic forms, with 100 days being
arbitrarily assigned as the temporal threshold
following allogeneic hematopoietic stem cell
transplant for distinguishing acute versus chronic
disease. The 2005 National Institutes of Health
consensus guidelines refined the diagnostic crite-
ria for these two entities, particularly for unifor-
mity in clinical trials, with chronic GVHD being
defined as distinct from acute GVHD by the
presence of at least one diagnostic clinical sign or
histologic feature (38).
GVHD can affect the entire length of the
gastrointestinal tract, from the esophagus to the
rectum. A number of findings may precede the
gastrointestinal manifestations, including hepa-
tosplenomegaly, gallbladder wall thickening, and
most notably, a diffuse pruritic maculopapu-
lar rash (39). The most common CT features,
other than small-bowel wall thickening, include
engorgement of the vasa recta, mesenteric fat
stranding, and circumferential thickening of the
colon (39,40).
Although commonly diffuse, these findings
may alternately have a regional preponderance,
similar to the changes of radiation therapy–in-
duced enteritis or vasculitis-associated small-
bowel disease. Segments of thickened bowel
with associated surrounding inflammatory
RG  •  Volume 38  Number 5 Sugi et al  1361

Figure 10.  ACE inhibitor–induced angioedema in two pa-

tients. (a) Coronal intravenous contrast-enhanced CT image
in a 39-year-old woman with diffuse abdominal pain who
had recently started an increased dose of lisinopril shows sev-
eral loops of edematous small bowel, with long-segment je-
junal mural stratification (arrows). (b) Axial oral and intrave-
nous contrast-enhanced CT image in a 47-year-old woman
being treated with an ACE inhibitor shows stratification of
the small bowel (arrowheads), prompting exploratory lapa-
rotomy, the results of which were negative. (c) Axial CT im-
age of the same patient as in b obtained 1 month later and
after the discontinuation of the ACE inhibitor shows com-
plete resolution of the inflammatory changes (*).

Figure 11.  GVHD in a 29-year-old woman with

a history of acute myeloid leukemia who pre-
sented with recurrent small-bowel obstruction 2
years after undergoing allogeneic stem cell trans-
plant. Fluoroscopic image from a small-bowel
follow-through examination shows several sepa-
rated featureless loops of small bowel (arrows),
with the classic “toothpaste” or “ribbonlike”
appearance, representing the chronic stricturing
changes of GVHD.

bowel, with decreased mucosal thickness and a

change and normal segments of intervening
upstream or downstream small bowel are com-
monly seen (Fig 11).
Earlier reports of CT findings in GVHD fo-
cused on diminished enhancement of the small
fluid-filled lumen (41), although these features
may be more representative of the later stages of
disease. More recent studies have further dem-
onstrated that the small bowel will frequently
show mucosal hyperenhancement in GVHD
at CT (Fig 12), although this finding may be
obscured by positive oral contrast material, if
administered (40).
The chronicity and temporal course of find-
ings in GVHD are the subjects of much scrutiny
and have been analyzed by a National Insti-
tutes of Health working group (38). In acute
1362 September-October 2018 radiographics.rsna.org

Figure 12.  GVHD in a 21-year-old woman with a history of myeloid sarcoma who presented with neutropenic fever
73 days after undergoing allogeneic stem cell transplantation. Axial (a) and coronal (b) intravenous contrast-enhanced
CT images show diffuse bowel wall edema with a target appearance (arrows), resulting in diffuse luminal narrowing.
The results of an endoscopic biopsy confirmed steroid-refractory GVHD.

Figure 13.  Chronic enteropathy in a 59-year-old woman who underwent chemotherapy and radiation therapy for
cervical cancer 10 years earlier and presented to the emergency department with vomiting and abdominal pain.
Axial (a) and coronal (b) intravenous contrast-enhanced CT images show multiple thick-walled pelvic ileal loops
(arrows in a) showing the target sign, with associated luminal narrowing (arrowheads in b) and relative distal small-
bowel obstruction owing to radiation strictures.

disease, GVHD often manifests at intravenous Iatrogenic Causes of Small-Bowel

contrast-enhanced CT with fluid-filled loops of
avidly enhancing small bowel (target sign), with
distinct separation of bowel loops (39).
In contrast to other causes of acute enteritis
discussed here, GVHD more often involves the
small bowel diffusely and may involve the colon
(39). In chronic disease, bowel wall thickening can
be conspicuously absent at imaging, while dilated
fluid-filled loops of featureless small bowel have
been described (41). This chronic appearance is
referred to as a “toothpaste” or ribbonlike ap-
pearance on small-bowel barium follow-through
images, as the jejunum loses its characteristic fold
pattern and both the jejunum and ileum appear
homogeneously featureless (37).
Disorders: Radiation Therapy– and
Chemotherapy-induced Enteritis
Radiation therapy is widely used in the treat-
ment of multiple gastrointestinal, urologic,
and gynecologic malignancies. Although radia-
tion targeting continues to improve with newer
targeted techniques, the sensitivity of the small
bowel renders it susceptible to both acute and
chronic changes when it is present within a ra-
diation port (42,43). Gastrointestinal symptoms
related to acute radiation enteropathy typically
peak in the 4th week of treatment and have been
shown to have a substantial negative impact on
the patient’s quality of life (44). In contrast,
chronic enteropathy (Fig 13) may develop as
RG  •  Volume 38  Number 5 Sugi et al  1363
Figure 14.  Acute perforated radiation enteritis in
a 62-year-old woman who presented with an acute
surgical abdomen after undergoing radiation therapy
for cervical carcinoma. Axial oral and intravenous
contrast-enhanced CT image shows several thickened
fluid-filled loops of ileum, pelvic ascites, and pockets of
mottled gas (arrowheads), findings indicative of small-
bowel perforation. A long segment of perforated ileum
was resected at laparotomy.
Figure 15.  Chronic radiation enteritis in a 66-year-old
woman with a history of cervical carcinoma and previ-
ous chemotherapy and radiation therapy who presented
with recurrent small-bowel obstruction. Fluoroscopic
image from a small-bowel follow-through examination
shows several thickened loops of ileum (arrowheads) in
the pelvis, with a “stacked coin” appearance and lumi-
nal narrowing (arrows) representing strictures, related
to chronic radiation enteropathy.
early as 18 months after therapy and has been
reported to develop as late as 30 years after
radiation therapy (30).
The pathophysiology underlying the small-
bowel symptoms involves cell death of the most
radiosensitive mucosal cells, which have higher
rates of mitotic turnover. Acute changes can
mimic intestinal ischemia, as the epithelial cells
lining arterioles are often involved, resulting in an
obliterative endarteritis (45).
Changes of small vessel ischemia due to radia-
tion therapy–induced obliterative endarteritis
manifest at CT as mucosal hyperenhancement
and circumferential bowel wall thickening, with
progression to ulceration and perforation in more
severe cases (45,46). There is typically segmental
involvement of loops exposed within the radiation
port(s), and correlating the patient’s prior radia-
tion therapy history with these findings can provide
a clue to the correct diagnosis. In cases of larger
abdominal radiation ports, the terminal ileum is
often the first to show manifestations of radiation
damage, in part because of its relatively fixed posi-
tion relative to the rest of the small bowel (45).
In the acute setting, CT findings of acute
radiation enteritis may include mucosal hyperen-
hancement, wall thickening, and ulcer formation
(45). Localized inflammatory changes including
interloop edema, regional free fluid, and pneuma-
tosis may also be seen (Fig 14). Chronic find-
ings include submucosal thickening, stricturing,
fistula formation, and luminal narrowing (Fig
15) secondary to chronic intimal inflammation.
The diagnosis of acute radiation enteritis primar-
ily remains one of exclusion and depends largely
on clinical history and the time course. However,
recognition is helpful as these changes may be
reversible, resolving with time following comple-
tion of therapy.
In contrast to radiation therapy–induced
enteritis, which tends to affect the small bowel
within or near the radiation port, chemotherapy-
induced enteritis is generally more uniform and
diffuse. Molecularly targeted therapies have a set
of mechanisms of action that differ from those of
traditional cytotoxic agents, which act to limit cells
that are rapidly proliferating (47). Many of these
newer agents—the “mabs” and the “nibs” (eg,
bevacizumab, rituximab, and imatinib)—target
specific growth factor receptors and commonly
induce enteritis (Fig 16).
The abdominal and pelvic CT features are
similar to those seen with other causes of inflam-
matory enteritis (Fig 17), including mucosal
and serosal hyperemia with submucosal edema
(47,48). Pneumatosis intestinalis with subserosal
and/or submucosal gas can be seen with tradi-
tional cytotoxic agents and targeted therapies. As
discussed previously, this finding is not necessar-
ily indicative of ischemia or transmural infarc-
tion, and thus correlation with the clinical setting
1364 September-October 2018 radiographics.rsna.org

Figure 16.  Sunitinib-related enteritis

in a 58-year-old man with metastatic
renal cell carcinoma who presented
with abdominal pain and diarrhea.
Coronal oral and intravenous contrast-
enhanced CT image shows long seg-
ments of thickened small bowel (ar-
rows) with mural stratification, charac-
terized by marked hyperenhancement
of the mucosa and muscularis propria.

Figure 17.  Bevacizumab-related enteritis in a 58-year-old man with metastatic rectal carcinoma who presented with
abdominal pain and diarrhea. (a) Coronal intravenous contrast-enhanced CT image shows a long segment of small-
bowel wall thickening with mural stratification (arrowheads). (b) Axial intravenous contrast-enhanced CT image shows
mesenteric venous engorgement (arrowheads) and regional mesenteric edema (arrows).

is important to avoid unnecessary intervention.
Furthermore, the specific type of cancer being
treated is important to identify, as the pathologic
manifestations within the small bowel may differ
accordingly. For example, intratumoral hemor-
rhage has been observed to be relatively common
following imatinib treatment of bulky gastrointes-
tinal stromal tumors, which can also extend into
the small-bowel lumen or even into the peritoneal
cavity (47).
trauma to the small bowel or transmural pen-
etration from an ingested foreign body may also
cause acute perforation (Fig 18). Blunt trauma
secondary to a fall from an elevated height or a
motor vehicle collision can also result in acute
perforation (Fig 19), with concomitant mes-
enteric vascular injury. Clinical history plays a
particularly important role in determining the
appropriate imaging examination for evaluating a
possible perforated viscus.

Acute Small-Bowel Perforation Crohn Disease

Acute perforation of the small bowel can oc-
cur secondary to a wide variety of mechanisms,
including ischemic, infectious, autoimmune,
diverticular, surgical/iatrogenic, and malignant
diseases. Alternatively, blunt or penetrating
Crohn disease is an inflammatory bowel disease
characterized by transmural inflammation and
“skip” areas of normal intervening bowel (49).
A progressive sequence of disease manifesta-
tions is well recognized, beginning with active
RG  •  Volume 38  Number 5 Sugi et al  1365

Figure 18.  Surgically-confirmed foreign body perforation in two patients. (a) Axial nonen-
hanced CT image in a 16-year-old girl who ingested a small bone shows a linear density in a
loop of small bowel in the mid-left abdomen (arrow), extending through the bowel wall, with
perforation that was later confirmed at surgery. (b) Axial intravenous contrast-enhanced CT
image in a 78-year-old woman with right-sided abdominal pain shows a thin bone (arrow)
causing focal small-bowel perforation, with associated mural edema, mesenteric fat stranding,
and ascites.

Figure 19.  Surgically-proven traumatic jejunal perforation in two patients who each presented after a motor vehicle
collision. (a) Axial intravenous contrast-enhanced CT image in a 24-year-old man shows diffuse long-segment jejunal
mural hyperenhancement with associated mesenteric edema, triangular fluid within the leaves of the mesentery (ar-
rows), and hemoperitoneum. (b) Axial intravenous contrast-enhanced CT image in a 27-year-old man shows focal per-
foration in a jejunal segment with mural hyperenhancement (arrowheads) and active mesenteric arterial extravasation
(arrow), corresponding to mesenteric injury at the level of the ligament of Treitz.

inflammation and progressing eventually to
stricturing and penetrating disease (50). In
practice, patients presenting with acute symp-
toms will generally undergo CT, with routine
intravenous contrast material administration
protocols, whereas outpatient workup will often
include either CT or MR enterography for
better characterization of the disease. Features
of active inflammatory bowel disease are well
characterized at CT enterography (Fig 20) and
include mucosal and mural hyperenhancement,
bowel wall thickening, engorgement of the vasa
recta (the “comb sign”), and perienteric fat
stranding (49,51).
The terminal ileum is most often affected first,
although segments of small bowel upstream may
also be affected, with or less commonly without
terminal ileum involvement (51). Secondary find-
ings reflective of transmural disease in both acute
and chronic disease include stricture with up-
stream dilatation (Fig 21) and abscess and fistula
formation (Fig 22). Knowledge of the normal
small-bowel fold patterns is useful for identifying
more proximal small-bowel disease.
As a general rule, the ileum is defined by
its smoother wall with fewer folds (valvulae
conniventes) in comparison with those of the
jejunum, which has more folds that are closer
together. Recognizing this pattern can also be
useful in identifying conditions that primar-
ily affect the fold pattern such as scleroderma,
which causes a stacked coin appearance, with
1366 September-October 2018 radiographics.rsna.org

Figure 20.  Active Crohn disease enteritis in a 53-year-old

man. Axial intravenous contrast-enhanced CT image shows
segmental wall thickening with mucosal hyperenhance-
ment of the distal ileum (arrow) and dilatation of the bowel
upstream to the inflamed ileal segment (*).

Figure 21.  Active inflammation superimposed on stricturing Crohn disease with low-grade obstruction in two pa-
tients. (a) Coronal intravenous contrast-enhanced CT image in a 56-year-old woman shows marked wall thickening
and mucosal hyperenhancement of the neoterminal ileum, with the classic comb sign representing mesenteric en-
gorgement (arrowheads). Note the marked luminal narrowing (*) and upstream dilatation, corresponding to active
stricturing Crohn disease. (b) Coronal oral and intravenous contrast-enhanced CT image in a 39-year-old woman
shows marked mural thickening and hyperenhancement, with a dilated loop of ileum upstream to the inflammatory
stricture (arrow).

close approximation of folds at barium evalua-
tion of the small bowel, and celiac sprue, which
is characterized by reversal of the normal jejunal
and ileal fold patterns.
Of note, the presence of submucosal fat deposi-
tion in the small bowel is often seen with chronic
inflammatory conditions but can be a normal
finding in as many as 21% of patients without
inflammatory bowel disease (52), most commonly
involving the ileum in overweight individuals.
Hemorrhage in the Small Bowel
Acute regional or diffuse spontaneous hemor-
rhage in the small bowel is relatively rare but has
been described in patients undergoing anticoag-
ulation therapy or with bleeding diatheses. The
most common location of acute small-bowel
bleeding is in the jejunum (69%). However,
hemorrhage can be diffuse or even multifo-
cal, uncommonly causing hematoma formation
across multiple segments of small bowel (53).
On CT images, hemorrhage may manifest as
circumferential thickening of the bowel wall of
varying length and is often most evident on CT
images obtained without intravenous contrast
material. A potential secondary consequence
is bowel obstruction owing to mass effect (53),
although most of these patients are managed
conservatively.
Three-phase multidetector CT is an ad-
ditional tool that can be used to detect gas-
trointestinal bleeding at sites inaccessible with
RG  •  Volume 38  Number 5 Sugi et al  1367

Figure 22.  Crohn disease with fistula formation in

a 68-year-old man. Coronal intravenous contrast-
enhanced CT image shows a stellate-appearing
complex enteroenteric/enterocolic fistula (*) with an
inflammatory soft-tissue mass tethering several seg-
ments of adjacent colon and small bowel to a central
point. Note the target appearance of the involved
small bowel and the associated mesenteric edema.

conventional endoscopy. It is particularly useful Acknowledgment.— We gratefully acknowledge Michael King

for detecting hemorrhage related to small-bowel
angiodysplasia (54).
Identifying Key Features for
Differential Diagnosis
A pattern-based approach to the abnormal small
bowel at CT has been previously described by
Macari et al (9). This strategy implements a
step-by-step algorithm for developing a dif-
ferential diagnosis based on five key features of
the small bowel, in conjunction with associated
CT abnormalities. These features are (a) the
enhancement characteristics of the bowel wall,
(b) the length of bowel involved, (c) the degree
of wall thickening, (d) proximal versus distal in-
volvement, and (e) the layer of the small-bowel
wall that is primarily affected. Clinical history
and laboratory data play an important adjunc-
tive role in further refining the diagnosis and
in determining an appropriate protocol for the
examination. Key findings in the small bowel,
associated CT features, and clinical and labora-
tory data for the entities discussed are summa-
rized in the Table.
Conclusion
The small bowel is subject to a wide spectrum of
disorders that can manifest with changes at CT
that are different than those seen in the colon.
There is substantial overlap of the imaging features
seen in acute disease, which is often initially evalu-
ated at CT, with circumferential wall thickening
and mural stratification being the most common
findings. An understanding of the pathophysiology
of the diseases that affect the small bowel can help
to invoke a search for secondary imaging features,
which can be used in conjunction with available
clinical information to develop a useful differential
diagnosis.
and the Mayo Clinic illustrators for creating Figure 1c.
Disclosures of Conflicts of Interest.—M.G.L. Activities related
to the present article: disclosed no relevant relationships. Activi-
ties not related to the present article: grants from Ethicon and
Philips. Other activities: disclosed no relevant relationships.
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Clinical and CT Features of Acute Small-Bowel Diseases

Diagnosis Primary CT Features Key Associated Imaging Features Clinical History and Laboratory Features
Acute mesenteric Focal or segmental absent or diminished wall enhancement; high Portomesenteric venous gas Hereditary and acquired hypercoagulabil-
ischemia attenuation in the bowel wall at nonenhanced CT; pneumatosis ity
intestinalis
Arterial embolism Thinning of the bowel wall (eg, paper-thin wall); bowel wall edema, Arterial emboli distal to middle colic artery; SMA Cardiac disease (eg, atrial fibrillation)
more common following reperfusion in primary ischemia occlusion; solid organ infarctions
Venous throm- Bowel wall edema or hemorrhage; diffuse upstream dilatation in cases Mesenteric venous engorgement and fat strand- Malignancy, hypercoagulable states
bosis of strangulating obstruction ing; venous thrombosis (eg, superior mesenteric
vein); ascites, sometimes with high attenuation
Hypoperfusion Intense mucosal enhancement; submucosal edema; luminal distention Slitlike inferior vena cava; small-caliber abdominal Profound hypotension; cardiac arrest;
1368 September-October 2018

complex with fluid; diffuse distribution aorta; hypoenhancing small spleen; shock pan- sepsis; diabetic ketoacidosis; severe
creas and liver; hyperenhancing adrenal glands head injury
Vasculitides Segmental small-bowel involvement, not confined to a singular Microaneurysms or focal stenoses in visceral arte- Mesenteric ischemia in a young patient;
vascular territory, demonstrating target sign, and changes of acute rial branches; mesenteric vascular engorgement; skin rash and arthralgia; positive anti-
mesenteric ischemia as listed above; areas of hemorrhage/hema- genitourinary involvement nuclear antibodies
toma
Angioedema Target sign with straightening of the involved segment; luminal disten- Prominent mesenteric vessels; ascites; rapid resolu- C1 esterase inhibitor deficiency; ACE-
tion with fluid tion with conservative therapy inhibitor therapy, particularly lisinopril;
benign abdominal examination; cutane-
ous and respiratory involvement
GVHD Diffuse wall thickening, with associated luminal narrowing; bowel Engorgement of vasa recta; mesenteric fat strand- Allogeneic bone marrow transplant (typi-
dilatation, proximal to thickened segments; target sign ing; thickening of distal esophagus or ascending cally within 100 days)
colon; ascites
Radiation ther- Segmental involvement of small bowel within the radiation port; Extraintestinal involvement of colon and solid Radiation therapy (>45 Gy); acute enter-
apy–induced fibrotic stricturing with ulceration; fistulas (eg, enterovesical fistula) organs in a nonanatomic distribution (radiation opathy peaks at 4 weeks of treatment
enteritis port)
Chemotherapy- Disruption of mucosal integrity, leading to pneumatosis intestinalis; Arterial thrombosis; portomesenteric venous gas Administration of cytotoxic (eg, 5-fluoro-
induced commonly involves the distal ileum; bowel perforation reported and pneumoperitoneum, in severe cases uracil) and biologic (eg, “-mabs” and
enteritis with the administration of bevacizumab “-nibs”) drugs
Mechanical per- Intraluminal foreign body, with focal perienteric fat stranding; extralu- Beam-hardening artifact, related to metallic objects Ingestion of a foreign body
foration minal gas with localized perforation
Crohn disease Mural hyperenhancement, asymmetrically involving mesenteric Fibrofatty proliferation; engorgement of the vasa Bimodal age distribution (20–50 y); family
border; focal wall thickening; strictures with upstream dilatation; recta (comb sign); mesenteric venous thrombo- history; oral ulcers
enteroenteric fistulas; perforation sis; adenopathy
Hemorrhage Intramural hyperattenuation, typically jejunal and most evident at Layering hemoperitoneum Over-anticoagulation therapy (eg, with
nonenhanced CT; circumferential wall thickening, with luminal warfarin); elevated international nor-
narrowing; small-bowel obstruction in a minority of patients malized ratio greater than 4
radiographics.rsna.org
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