Springer Science+Business Media, Inc.
2005 Abdom Imaging (2006) 31:277292
Abdominal Published online: 10 November 2005
Imaging
UPDATE
Ischemia and infarction of the small bowel and
colon: spectrum of imaging findings
S. Romano,1 F. Lassandro,1 M. Scaglione,1 L. Romano,1 A. Rotondo,2 R. Grassi2
1
Department of Diagnostic Imaging, A.Cardarelli Hospital, Viale Cardarelli 9, 80131 Naples, Italy
2
Magrassi-Lanzara Department, Institute of Radiology, Second University of Naples, Piazza Miraglia 5, 80138 Naples, Italy
Mesenteric ischemia presents as an abdominal emer-
gency due to decreased intestinal blood ow secondary
to mesenteric arterial vascular hypoperfusion, occlu-
sion, or impaired venous drainage [1]. The small bowel
or colon may be involved. Distinction between intes-
tinal ischemia and infarction sometimes is not consid-
ered adequately in the interpretative process: the
ischemia may be a transient and a totally reversible
event, whereas infarction may be one of the possible
consequences that requires surgical or interventional
management. Despite continuing advances in imaging
and surgical techniques, early detection of intestinal
ischemia before infarction develops remains difficult
[2]. Early diagnosis is important to improve survival
rates [2, 3]; in most cases of late or missed diagnosis,
mortality rate from intestinal infarction is very high,
from 60% to 90% [46]. Prognosis of an ischemic
intestinal insult depends upon clinical factors, such as
its acuteness, duration and severity, the presence of
collateral vascular circulation, the response of the
mesenteric vascular branches and intestinal wall to the
injury [7], extent of intestinal involvement, and the
timeliness of diagnosis and intervention. From a phase
in which the intestinal vascular injury may be sus-
pected and the imaging findings of ischemia noted, the
severity of mural damage may proceed rapidly to
infarction with dire consequences. Differences in bowel
wall findings may be appreciable between small bowel
arterial and venous infarctions [810].
Radiologic descriptions of intestinal ischemia and
infarction reported in the literature are rich [1013] but
not pathognomonic. Currently, there is no report of a
direct correlation between bowel wall findings and a
confirmed diagnosis of ischemia or infarction. Most lit-
erature on this topic is characterized by nonhomoge-
Correspondence to: S. Romano; email: stefromano@libero.it
DOI: 10.1007/s00261-005-0376-7
neous material and methodology of study. Some
parameters regarding the timing of imaging in which
studies are performed, intravenous and/or oral contrast
medium administration, dynamics of the acute vascular
injury, and the different etiologies (superior or inferior
venous or arterial mesenteric vessels, occlusive or non-
occlusive event) are sometimes difficult to summarize in a
comparative classification. However, diagnostic imaging
may play a pivotal role in the detection of the degree and
severity of intestinal ischemia and assessment for evi-
dence of infarction.
In the following sections, imaging ndings (wall
thickness and enhancement, caliber of intestinal loops,
presence of air-uid levels, intestinal peristalsis, mesen-
teric arterial and venous vessel viabilities, mural and/or
portal/mesenteric pneumatosis) from different method of
study (abdominal plain lm, sonography [US], and
computed tomography [CT]) will be correlated to various
phases of intestinal changes from ischemia and infarction
due to mesenteric vessels hypoperfusion or occlusion
based on experience in our institutions.
Etiology of intestinal ischemia and
infarction
Injuries from intestinal ischemia may have an arterial or
venous origin, with involvement of the superior mesen-
teric artery (SMA) or vein (SMV), inferior mesenteric
artery (IMA) or vein (IMV) or from the reduced blood
ow associated with shunting of blood from the
splanchnic bed [14]. Extent and site of injury depends
upon anatomic conditions and the presence of collateral
vessels, which often differ across subjects.
Small Bowel, ascending and right transverse
colon
Occlusion of the SMA may be due to embolism or
thrombosis. Emboli may arise from the left atrium in
278 S. Romano et al.: Ischemia and infarction of the small bowel and colon
patients affected by chronic cardiac insufciency and
brillation; however, they may originate from septic
endocardial foci or from aortic atheromatic plaques.
Emboli may occlude the proximal portion or one of the
distal branches of the SMA. Occlusive thrombosis in-
volves more frequently the origin of the SMA, where wall
aortic atheroma apposition may cause partial obstruction
of the orice. In case of obstruction of the SMA at the
origin by an embolus, most of the small intestine and the
right colon are subject to ischemia. If an atheromatous
disease progressively occludes the lumen of the vessel, the
formation of collateral vascular circulation may cause a
gradual ischemic insufciency. Also to be considered is
the nonocclusive hypoperfusion injury due to a decreased
systemic arterial supply not related to the presence of
endoluminal vascular obstruction.
Although the clinical symptomatology may be vari-
able in case of a nonacute occlusive event, patients with
acute SMA occlusion are usually elderly and affected by
cardiovascular disease, presenting with sudden and se-
vere abdominal pain, diarrhea, and vomiting; intestinal
peristalsis tends to decrease, passing from initial spasm
to intestinal paralysis. Leucocytosis is usually high and
there is presence of occult blood in the feces. Patient
conditions may rapidly proceed to shock.
Alternatively, occlusion of the SMV may be due to
thrombosis originating at the origin or in one of the
distal branches or from portal thrombosis extending to
mesenteric vessels, causing impaired venous drainage of
the intestinal wall that leads to intramural hemorrhage.
Frequently observed in patients affected by cirrhosis
and/or portal hypertension, mesenteric vein thrombosis
may also be primary. Coagulation disorders such as
polycythemia and elevated platelet levels in patients after
splenectomy, systemic disease such as lupus elythema-
tosis, or the use of estrogen-progesterone therapy may be
related to a risk of developing of mesenteric thrombosis.
Clinical symptomatology and ndings are usually pro-
gressive but similar to those caused by SMA obstruction,
with abdominal pain, diarrhea, and evidence of occult
blood in the feces. Depending upon the intestinal extent
of the impaired venous drainage, bloody diarrhea, acute
anemia, and hypovolemia may be noted.
Left transverse, descending, sigmoid colon and
rectum
The occlusive syndrome of the IMA is uncommon and
generally due to thrombosis from atherosclerotic disease.
Formation of collateral vessels, from the colic branches
of the SMA and from the hemorrhoidal arteries, bran-
ches of the hypogastric arteries, are often not effective to
prevent an acute colorectal ischemia due to occlusion
of the IMA at the origin. In fact, ischemia of the left side
of the colon may also be a postoperative complication of
aortic aneurysm surgery that requires sacrice of the
IMA. Usually observed in the elderly, clinical symp-
tomatology includes left lower abdominal pain and
diarrhea; endoscopy may reveal edema and cyanosis of
the sigmoid-rectal mucosa. Leucocytosis is a common
nding of ischemic disease of the intestine that may
progress to peritonitis with paralytic ileus and shock.
Impaired venous drainage of the left side of the colon
derives from occlusion of the IMV. Thrombophlebitis
disease and thrombosis from systemic affections may be
the underlying cause.
Imaging methods
Abdominal plain lm remains in most institutions the
rst examination performed in the diagnosis of the acute
abdomen, even in the era of multidetector CT (MDCT)
technology; the assessment or progression of an intesti-
nal disease may be followed with this basic imaging
study.
US may be of interest in follow-up of patients with an
acute abdomen of indeterminate origin or to monitor a
pathologic condition that does not require immediate
surgery.
CT examinations using single or multidetector row
equipment is performed with intravenous contrast
enhancement; in case of acute abdomen from indetermi-
nate cause, a delay of 65 sec from the start of injection is
usually used; however, when the clinical suspicion is
intestinal infarction, a biphasic study (arterial and venous
phases) may be performed. Acquisition of 3-mm slice
thickness may show an optimal intestinal wall evaluation
in most cases. MDCT allows multiplanar reformatting
with thinner slices, often using specic software proto-
cols, that may be helpful to study the mesenteric vascular
pattern, especially for the terminal branches. In an
emergency, all examinations are performed without
endoluminal opacication by oral or rectal contrast
medium administration in our institutions.
Pathophysiology from ischemia to
infarctionimaging findings
correlations
Small bowel
Arterial etiology
Imaging ndings related to the pathophysiology of
intestinal vascular injury from arterial occlusion or
hypoperfusion may be divided into four stages.
First stage. The rst and immediate response of the
intestine to a vascular injury is spasm of the involved
loops. Abdominal radiograph at this phase shows a
gasless abdomen from spastic ileus (Fig. 1A). US and CT
examinations may or may not (in case of nonocclusive
hypoperfusion) show an occlusion of the SMA; the bo-
wel wall may show normal enhancement (Fig. 1B).
S. Romano et al.: Ischemia and infarction of the small bowel and colon
Fig. 1. First stage of small bowel ischemia. A Digital radi-
ography of patient with acute symptomatology shows gasless
abdomen. B Axial CT scan shows spasticity of the intestinal
loops that appear collapsed; mesenteric vessels are opacified
and the small bowel wall presents normal enhancement. The
patient was cardiopathic; the imaging findings were correlated
to a splanchnic hypoperfusion syndrome.
Second stage. In a more advanced phase, when the
arterial supply is occluded without reperfusion, the
intravascular blood volume decreases as blood ows out
through the patent venous system; the microvascular
wall becomes damaged because it derives oxygen through
direct diffusion from the blood [7]. Disruption of
microvascular integrity increases permeability, so that
minimal residual blood may extravasate through the
damaged vascular wall and cause hemorrhagic foci on
the thinned bowel wall [7]. At this phase enterocytes
cannot produce the normal amount of secretions; intes-
tinal microflora can proliferate, causing production of
gas. Abdominal plain film may show a mild gaseous
279
Fig. 2. Second stage of small bowel ischemia. Axial CT
scan in a patient with acute abdomen. Note the paper thin
small bowel wall (arrow) distended only by gas. Enhancement
of the mesenteric vessels is normal at the origin. The patient
moved to other institution where some hours later findings of
intestinal arterial injury were disclosed on CT examination.
Fig. 3. Second stage of persistent small bowel ischemia
with infarction. Axial CT scan in a patient with acute abdomen
shows the small bowel distended by gas, without enhance-
ment of the intestinal wall; mural and portal pneumatosis is
visible (arrow). Surgery confirmed the small bowel infarction.
dilatation of the loops with total loss of their tone; CT
may show all these findings, the typical paper thin
bowel wall, and decreased wall enhancement (Fig. 2); US
is not informative at this stage because of an increased
amount of gas in the intestinal loops. If the bowel
ischemia persists long enough without reperfusion, rather
than proceeding through a third stage, the entire bowel
280 S. Romano et al.: Ischemia and infarction of the small bowel and colon
Fig. 4. Second stage of persistent small bowel ischemia
with infarction. Axial CT scan. A Portal and gastric
pneumatosis in a patient with intestinal infarction. B Note the
absence of mural thickening of the bowel loops distended by
gas that presents considerable reduction of wall enhance-
ment. The terminal arterial mesenteric vessels appear nono-
pacified. Surgery confirmed the presence of small bowel
infarction.
wall may become necrotic and intramural air may dissect
into the necrotic mucosa and spread through the mes-
enteric veins and into portal veins [7] (Figs. 3, 4).
Third stage. If the underlying pathologic process is re-
moved, the reperfused intestine from transient arterial
insufciency may have a different pattern [7]. Depending
on degree of microvascular wall damage, blood plasma,
contrast medium, or red blood cells may extravasate
through the disrupted vascular wall and mucosa, causing
considerable bowel wall thickening and bloody fluid
filling of the bowel lumen [7] (Fig. 5A). Abdominal
radiography shows a mild dilatation of the loops, pre-
senting with a slight thickened wall, sparse and subtle
valvulae conniventes, and evidence of air-fluid levels. US
may show a fluid-filled lumen, bowel wall thickening,
evidence of some extraluminal fluid and decreased peri-
Fig. 5. Third stage of small bowel ischemia. A Axial CT scan
shows wall thickening of small bowel loops in the right
abdomen, with fluid in the lumen. Hyperdensity of the wall is
due to microvascular damage with extravasation of the con-
trast medium through the mucosa. There was lack of
enhancement of the terminal arterial vessels. B US shows
bowel wall thickening of a loop distended by fluid, with some
extraluminal fluid.
stalsis (Fig. 5B), and SMA occlusion at the origin. CT
may add information regarding occlusion of the SMA
and the degree of parietal enhancement of the small
bowel. The intestinal mucosa may remain viable if the
reperfusion is prompt enough (Fig. 6); otherwise, it be-
comes infarcted and necrotic [7] (Fig. 7).
Fourth stage. When diagnosis of infarction is late,
radiologic ndings are related to increased hydrostatic
pressure inside the intestinal loops that allows extrava-
sation of plasma, contrast medium, or blood cells into
S. Romano et al.: Ischemia and infarction of the small bowel and colon 281

Fig. 6. Third stage of small bowel ischemia with reperfusion. MDCT (A) coronal and (B) axial views of an SMA thrombosis
(arrow in A); (A, C) note the opacification of the vessel downstream to the occlusion. Some ileal segments appear thickened with
hypodensity of the submucosa (arrow in D) from reperfusion phenomena. Note the renal infarction in B.

the submucosa. Abdominal plain radiograph shows
markedly dilated loops with thickened wall and valvulae
conniventes, and diffuse evidence of air-uid levels
(Fig. 7A). US shows mainly the presence of extraluminal
fluid and the absence of peristalsis (Figs. 8, 9). CT
findings may or may not show occlusion of the SMA
(because persistent hypoperfusion due to luminal nar-
rowing without a real thromboembolism may appear
with the same findings), bowel wall enhancement is poor
in case of necrosis, and pneumatosis may be present
(Figs. 10, 11).
Venous etiology
Thrombosis of the SMV slows blood ow. The intestinal
vascular injury may be divided into four stages.
First stage. Impaired venous drainage disease may
present a less acute symptomatology than arterial
ischemia. Visualization of a true initial phase that also in
this case may be characterized on plain abdominal lm
by spastic reex ileus without bowel distention [15] is
difficult to identify. US may show homogeneous hypo-
echoic intestinal wall due to edema that is the earlier
change of the submucosa in intestinal infarction [16],
whereas CT may show a thrombus in the proximal or a
peripheral branch of the SMV or into the portal-mes-
enteric vein junction, with homogeneous thickened
intestinal tract involved (Figs. 12, 13).
Second stage. A subsequent hypotonic reex ileus on
plain lm may be masked by progressive intestinal
intramural and mesenteric edema. Intramural blood
volume increases as arterial blood keeps owing into the
bowel wall and the increased intravascular hydrostatic
pressure dilates the blood vessels, enlarging the fene-
strations between the vascular endothelial cells [7]. This
causes extravasation of plasma, contrast material, or red
282 S. Romano et al.: Ischemia and infarction of the small bowel and colon
blood cells into the bowel wall or lumen; tension in the
submucosal extravascular compartment or prolonged
stasis-induced thrombosis of the microvessels may cause
a stoppage to the arterial flow [7]. Imaging findings at
this stage are related to bowel wall thickness, intramural
hemorrhage, and submucosal edema. US may show a
thickened intestinal loop (Fig. 14) with hyperechoic
mucosal layers and hypoechogenicity of the layers due to
edema, and occlusion of the SMV at its origin. SMV
viability may be appreciated at CT examination, yet also
in this case the most important CT finding is related to
the appearance of the involved intestinal segment, with
the typical alternating different density layers (target
sign), a more evident hyperdense mucosa due to surface
hemorrhage and ulceration, and a hypodense edematous
submucosa (Fig. 15). This stage of impaired venous
drainage may be reversible because deeper layers of the
Fig. 7. Fourth stage of small bowel
ischemia with infarction. A Digital
radiograph shows an ischemic small
bowel loop in the left abdomen with a
thickened wall. B MDCT coronal view
shows endoluminal occlusion of the
proximal SMA (arrow). C Lack of
enhancement of the SMA distal
branches, with evidence of infarcted
loops, confirmed by surgery.
intestinal wall are preserved; but if the vascular injury
persists, there are three possibilities: healing, chronicity
of the affection, or progression to intestinal infarction.
Healing of the affected segment with restitution of ve-
nous flow (Fig. 16) may lead to circumferential granu-
lation tissue formation in response to the parietal layer
damage.
Third stage. Persistence of a venous thrombosis leads
to mesenteric vascular engorgement and edema with
formation of venous collateral vessels [16]. The imaging
findings may be commonly observed in patients affected
by chronic vascular disorders. Plain radiography may
show a masked intestinal endoluminal air or wall
thickening of some intestinal involved segment. US may
be used to evaluate the viability of the portal vein and
S. Romano et al.: Ischemia and infarction of the small bowel and colon
Fig. 8. Fourth stage of small bowel ischemia. Sonogram of
patient with intestinal infarction. Note the thickened valvulae
conniventes (arrowhead).
mesenteric proximal branches and the presence of
thickened bowel wall and peritoneal fluid. CT may re-
veal all these findings and mesenteric engorgement
(Fig. 17).
Fourth stage. Progression to intestinal infarction causes
an extensive submucosal hemorrage and edema. Al-
though this process seems to be slow, cyanosis may lead
to bowel wall loss of integrity, and intestinal bacteria
may invade the intestinal wall, causing necrosis and
peritonitis; serosanguineous or bloody uid and intia-
mural and mesenteric vein gas may be appreciated
Diagnostic ndings of infarcted loops due to impaired
venous drainage are marked wall thickness, diffuse mural
hypodensity with lack of wall enhancement, and intia-
mural and portal-mesenteric pneumatosis. Conventional
plain lm may show the thickened bowel wall and evi-
dence of parietal pneumatosis or pneumoperitoneum. US
may show a markedly thickened intestinal segment with
absence of peristalsis and presence of peritoneal inho-
mogeneous uid. CT ndings are related to evidence of
vascular occlusion, absence of wall enhancement of the
intestinal segment involved (Fig. 18), and presence of
peritoneal fluid and gas in vascular branches, bowel wall,
or peritoneum.
Colon
Vascular injury to large bowel comprises a wide spec-
trum of pathologic and clinical ndings, ranging from
an ischemic self-limiting and transient event to bowel
283
Fig. 9. Fourth stage of small bowel ischemia. Sonogram of
fixed, infarcted loops with marked parietal thickening.
infarction [1719]. Pathologic findings of ischemic
colitis are mural necrosis and ulceration, submucosal
edema and hemorrhage, and transmural infarction [17].
Ischemic colitis has been considered a form of nonoc-
clusive ischemic disease usually observed in the elderly
[17], without evidence of vascular obstruction of a
major vein or artery and no correlation between the
length and site of colonic involvement and the distri-
bution of the SMA, SMV, IMA, or IMV [17, 2022].
However, the Griffith and Sudeck points (the junction
between the distribution of the SMA and IMA near the
splenic flexure and the anastomotic plexus between the
IMA and the hypogastric supply, respectively) have
been described as most commonly affected by ischemic
colitis [17, 23]. Mucosal damage is usually a self-limited
disease, whereas necrosis of the muscle layer may load
to severe stricture, sepsis, or necrosis. Although no
previous correlation has been established between the
degree of wall thickening, the length of involvement,
and the presence or development of colonic infarction
except for pneumatosis coli [17], a grading scale for
vascular injury to the colon should be done by con-
sidering the same morphodynamic changes as for small
bowel from ischemia to infarction. The entire colon
may be affected, but the distribution may also be
patchy and related to the distribution of vascular
branches from superior or inferior mesenteric vessels.
Imaging findings to be considered include site and
length of the colonic affected segment, appearance and
degree of wall thickness, pericolic streakiness, presence
of submucosal edema, peritoneal fluid, pneumatosis
coli, mesenteric or portal gas and pneumoperitoneum
284 S. Romano et al.: Ischemia and infarction of the small bowel and colon

Fig. 10. Fourth stage of small bowel ischemia. A Abdominal

plain film shows dilatation of some intestinal segments with
presence of air-fluid levels and an intramural bubble-like pne-
umatosis of a loop in the mid-right region. B, C MDCT coronal view
shows an extended thrombosis of the SMA (arrowhead), with
evidence of an infarcted segment (arrow).

Fig. 11. Fourth stage of small bowel ischemia. Coronal sitive contrast medium from previous examinations performed
(A,B) and axial (C) MDCT views of a patient with intestinal in another institution. C Note the diffuse necrosis and intra-
infarction due to occlusion of SMA ileocolic branches mural pneumatosis.
(arrowhead in B). B There is some residual endoluminal po-

or pneumoretroperitoneum. Recognition of severity Colonoscopy is frequently used for the diagnosis of

factors at the early stage of ischemic colitis may im- ischemic colitis, but its value is limited because this
prove the prognosis of this disease [18, 19, 24, 25]. procedure may be dangerous in case of severe colitis
S. Romano et al.: Ischemia and infarction of the small bowel and colon
Fig. 12. First stage of small bowel impaired venous drain-
age. A, B MDCT coronal MIP reconstructions show the
endoluminal defect in the SMV (arrow in A, B), with relatively
thickened appearance of small bowel loops. B. The same
patient presented a SMA thrombosis (arrowhead).
[24]. Further, endoscopic biopsy often cannot reveal the
extension of ischemic injury into the colic wall because
the biopsied fragments are limited to the mucosa and
part of the submucosa [24]. Diagnostic imaging may
play an effective role in clinical assessment of acute
ischemia. Abdominal plain film in the acute setting
shows only an abnormal nonspecific gaseous distention
of the affected segment [15]. Barium examinations are
accurate with reported rates of 82% and 90% for single
and double contrast studies, respectively [2628]. Typ-
ical findings are represented by spasm, ulcerations,
transverse ridging, intramural barium, and strictures
[26, 28]. However, the most characteristic finding is
reported to be thumbprinting, which is seen in 75% of
cases [26, 28] and is caused by submucosal edema or
hemorrhage [26], so that the major role of this imaging
285
Fig. 13. First stage of small bowel impaired venous drain-
age. US (longitudinal scan) shows a homogeneous thickened
intestinal segment due to SMV thrombosis.
Fig. 14. Second stage of small bowel impaired venous
drainage. US (axial scan) shows an intestinal segment char-
acterized by hyperechoic mucosa with hypoechogenicity of
the other mural layers due to edema in a patient with SMV
thrombosis.
method may be limited to the subacute or chronic
phase.
US has recently been advocated as a useful diag-
nostic tool in predicting prognosis [29], whereas in an
experimental study some investigators observed that
the progressive disappearance of the stratification of
the bowel wall was related to the duration of the
splanchnic blood flow reduction and to the severity of
the ischemic injury [30, 31]. Recently, alterations in
pericolic fat added to changes in the colon wall and
absence or marked reduction in color Doppler mural
flow seem to be predictive factors of transmural
necrosis [24].
CT seems to be the comprehensive imaging method to
conrm a clinical suspicion, to suggest the diagnosis of
ischemia, and to detect any eventual complications [17].
A classification on different stages of vascular disease of
the large bowel may be considered.
286 S. Romano et al.: Ischemia and infarction of the small bowel and colon
Fig. 15. Second stage of small bowel impaired venous
drainage. A, B MDCT axial scans show some small bowel
loops characterized by wall thickness, intramural hemor-
rhage, and submucosal edema; there is no evidence of defi-
nite endoluminal thrombosis in the SMV at the origin, but
Arterial etiology
First stage. Acute ischemic damage may be focal or
diffuse; the characteristic pattern of injury consists of
hemorrhage into the lamina propria that is associated
with supercial epithelial necrosis [32, 33]. This may be
associated with an inflammatory pseudomembrane [32].
These early changes may progress to full-thickness
mucosal ulceration [32]. CT is the imaging methodol-
ogy that may be more informative at this stage with
regard to wall damage. If the left colon is affected,
hyperdensity of the mucosa from hemorrhagic phe-
nomena may give rise to a typical finding of the little
rose appearance on transverse axial CT scans
(Fig. 19). Mural thickening associated with extensive
submucosal edema and fluid in surrounding fat has
been described for ischemic colitis of the descending
colon in an acute phase [34]. Submucosal edema and a
shaggy contour, pericolic streakiness, and a small
there is an indeterminate opacification of some peripheral
branches. C, D Two days later there is progression of the
impaired venous drainage in the affected loops and an end-
oluminal defect of filling in the SMV.
amount of peritoneal or retroperitoneal fluid may be
observed in the absence of an evident occlusion of the
arterial mesenteric vessels (Fig. 20).
Second stage. Progression of ischemic damage with-
out reperfusion may cause a concentric and symmetric
mild intramural thickening and homogeneous attenu-
ation of the colonic wall with a sharply dened con-
tour, with or without minimal pericolic streakiness;
peritoneal uid is usually of moderate amount
(Fig. 21). If the ischemic segment is reperfused, sub-
mucosal edema may be strongly evident, with wall
thickening and heterogeneous enhancement, loss of
colonic haustra, and various degrees of pericolic
streakiness (Fig. 22).
Third stage. When colonic ischemia proceeds to
infarction, the typical imaging ndings are the lack of
wall enhancement and intramural pneumatosis (Fig. 23).
S. Romano et al.: Ischemia and infarction of the small bowel and colon
Fig. 16. Second stage of small bowel impaired venous
drainage and healing after therapy. A, B MDCT coronal views
show massive portomesenteric thrombosis, with sufferance
from impaired venous drainage of the small bowel (arrows).
MDCT examination 7 months later showed a complete resti-
tution with normal opacification of the portomesenteric ves-
sels and normal appearance of the intestine.
Venous etiology
First stage. This stage may demonstiale wall thickening
with hyperdensity of the mucosa from hemorrhage (Fig. 24).
Second stage. A more evident submucosal hypodensity
from edema of the colonic wall, shaggy contour and
pericolic streakiness may indicate progression of im-
paired venous drainage (Fig. 25).
287
Fig. 17. Third stage of small bowel impaired venous drain-
age. (A) MDCT axial scan shows SMV thrombosis (arrow)
with an intestinal segment in the pelvis characterized by dif-
fuse wall thickening with (B) submucosal edema and mes-
enteric engorgement.
Third stage. Progression of disease may lead to
homogeneous thickening of the intestinal colonic wall
with decreased enhancement (Fig. 26). Although mural
necrosis may be the last stage, most cases recover
with pharmacologic therapy without any intestinal
resection.
Considerations and conclusions
Mesenteric ischemia may result from occlusive or
nonocclusive mesenteric arterial ischemia, venous
thrombosis, vasculitis, or dissecting aneurysm [35]. A
spectrum of pathologic changes ranging from minimal
mucosal edema to rapid total intestinal dissolution
may occur [10]. Some investigators have graded the
pathologically proved longitudinal extent of the bowel
ischemia correlated with radiographic findings [10].
Evidence of spastic ileus with a gasless abdomen has
been reported in 24% of cases at the initial radio-
graphic examination [10, 36, 37]. Although bowel
288 S. Romano et al.: Ischemia and infarction of the small bowel and colon
dilatation has been used to predict irreversibility of the
ischemia [10], it can occur in the ileus from any other
cause [11, 38]. Moreover, all signs considered in eval-
b
Fig. 18. Fourth stage of small bowel impaired venous
drainage with infarction. MDCT findings. A Scout view show
evidence of suffering loops in the lower left abdominal quad-
rant. B, C. Axial scans show SMV thrombosis (arrow) and
evidence of markedly thickened small bowel loop, with de-
creased wall enhancement and slight hyperdensity of the
mucosa from hemorrhagic phenomena. Note some intramural
pneumatosis in the segment located in the pelvis. The patient
did not recover after medical therapy and required partial
intestinal resection.
Fig. 19. First stage of colon ischemia. MDCT axial scan in a
symptomatic patient. Note the parietal thrombosis of the IMA
at the origin (arrow), with the little rose appearance of the
descending colon.
uation of intestinal ischemia may present nonspecifici-
ty; wall thickening may be due to neoplasm, radiation
changes, of inflammatory bowel disease [38]; portal
venous gas may be of benign origin [39] and has been
seen with abscesses and ulcerative lesions of the gas-
trointestinal tract [11]. Specific film signs of colonic
infarction are less commonly reported; however, a ne-
gative plain film should not exclude ischemia of the
colon [10]. In the acute setting, ischemic colon may
present an unusual gaseous distension on plain film,
whereas in chronic phase there is a parietal thickening
with thumbprinting appearance. Predicting the revers-
ibility of the process in mesenteric ischemia is becom-
ing important because conservative treatment may be
the choice in relatively stable patients [10]. Distinction
between vascular arterial or venous occlusion etiology
in intestinal infarction has been not frequently con-
sidered. A study investigating whether different CT
appearances of small bowel ischemia might correlate
with resulting morbidity or mortality showed that it is
more serious in the case of arterial origin than of ve-
nous origin [7], whereas reperfusion is correlated to
have a higher survival rate [7]. The same study attested
S. Romano et al.: Ischemia and infarction of the small bowel and colon 289

Fig. 20. First stage of colon ischemia. MDCT axial scans in

a symptomatic patient. Note the wall thickening with submu-
cosal edema of the right and transverse (A) colon and the
little rose appearance of the descending colon (B). No
definite occlusion of the mesenteric vessels was found at this
CT examination.

that a thickened bowel wall (>3 mm in wall diameter

in area where the bowel was adequately distended [40])
seems to be a sign of bowel necrosis [7], whereas small
bowel dilatation may be due to ischemia-induced de-
creased motility, longer duration of ischemia, and in-
creased intraluminal gas [7]. In effect, because the
mucosa is the most vascularized part of the gut, it is
more vulnerable to ischemic attack: normal mucosal
enhancement under conditions of reperfused arterial
insufficiency or impaired venous drainage represents
returning or maintaining of blood supply, and the
bowel tends to be viable [7]. CT allows a correct but
often too late diagnosis of small bowel vascular injury Fig. 21. Second stage of colon ischemia. CT axial scans
[13, 36, 37] if it is performed as the unique imaging (A,B). Note the homogeneous symmetric thickening of the left
method when bowel necrosis is evident. Serial colon, the dirty appearance of the pericolic fat, and the per-
abdominal plain films and US should show some sistent evidence of some peritoneal fluid. C Double contrast
findings suggesting the diagnosis of intestinal ischemia barium enema confirmed the features of ischemic colitis (arrow).
[24], especially in case of hypoperfusion from the
mesenteric vessels or if a vascular occlusion is periph- Although rich in radiologic suggestive and specic
eral and may be not strongly evident at CT examina- ndings, a small bowel ischemic event from impaired
tion. venous drainage is less serious than arterial lack of blood
290 S. Romano et al.: Ischemia and infarction of the small bowel and colon

Fig. 22. Second stage of colon ischemia with reperfusion. A

Fig. 23. Third stage of colon ischemia with infarction. A, B
Axial CT scan shows marked thickening of the colonic wall,
Axial CT scans show absence of wall enhancement and
with heterogeneous enhancement and pericolic streakiness;
evidence of pneumatosis in the left colon wall (arrows) from
this appearance is related to reperfusion phenomena in
infarction.
ischemic arterial injury. B Fourteen hours later there is a
moderate reduction of the wall thickness of the right colon,
persistence of pericolic streakiness, and extension of the
ischemic appearance to the small bowel. No clear defect of
opacification of mesenteric vessels was found.

supply [7] because, thrombosis that involves the portal

vein or the more proximal portion of the SMV usually
does not result in bowel infarction; the rich venous col-
lateral circulation in the root of the mesentery and ret-
roperitoneum [14] may overlap the occlusion, although
infarction from segmentary branch occlusion is known
[14]. Moreover, patients who have chronic vascular dis-
ease such as hypercoagulable states or portal hyperten-
sion and use estrogen are successfully treated with
heparinic therapy. Although mesenteric venous throm-
bosis may produce a higher incidence of abnormal
findings on CT, because of an increased congestion and Fig. 24. First stage of colonic impaired venous drainage.
edema in the bowel wall and mesentery [8], other forms Same patient as in Fig. 15, axial CT scan. Note the hyper-
of acute mesenteric ischemia may present a different density of the colonic mucosa from impaired venous drainage.
S. Romano et al.: Ischemia and infarction of the small bowel and colon
Fig. 25. Second stage of colonic impaired venous drainage.
MDCT axial (A) and coronal reconstruction (B) images show
the homogeneous thickening of the right colon (A) in a patient
with massive portal thrombosis (arrow in B) after liver trans-
plantation.
pathologic pattern. Radiologic findings correlated with
clinical symptoms may allow the differentiation of the
ischemic phases and the indication regarding the imme-
diate therapy required.
References
1. Tendler DA (2003) Acute intestinal ischemia and infarction. Semin
Gastrointest Dis 14:6676
2. Jacobs JE, Birnbaum BA, Maglinte DDT (1999) Vascular disorders
of the small intestine. In: Herlinger H, Maglinte DDT, Birnbaum
291
Fig. 26. Late third stage of colonic impaired venous drain-
age with ulcerations. MDCT coronal (A) and axial (B) scans
show the presence of thrombus in the terminal right colonic
vein (arrow), with subsequent thickened appearance of the
ascending colon, with evidence of irregular mucosa surface
from ulcerations, that is better appreciated in the wide window
setting (B).
BA (eds). Clinical imaging of the small intestine, 2nd ed. New York:
Springer-Verlag, pp 439465
3. Goldberg MA, Mueller PR, Saini S, et al. (1991) Importance of
daily rounds by the radiologist after interventional procedures of
the abdomen and chest. Radiology 180:767770
4. Scholz FJ (1993) Ischemic bowel disease. Radiol Clin North Am
31:11971218
5. Sanchez-Fernandez P, Mier y Diaz J, Blanco-Benavides R (2000)
Acute mesenteric ischemia. Profile of an aggresive disease. Rev
Gastroenterol Mex 65:134140
6. Betzler M (1998) Surgical technical guidelines in intestinal ischemia.
Chirurg 69:17
7. Chou CK, Mak CW, Tzeng WS, Chang JM (2004) CT of small
bowel ischemia. Abdom Imaging 29:1822
292 S. Romano et al.: Ischemia and infarction of the small bowel and colon
8. Wolf EL, Sprayregen S, Bakal CW (1992) Radiology in intestinal
ischemia. Plain film, contrast and other imaging studies. Surg Clin
North Am 71:107124
9. Rosen A, Korobkin M, Silverman P, et al. (1984) Mesenteric vein
thrombosis: CT identification. AJR 143:8386
10. Yamada K, Saeki M, Yamaguchi T, et al. (1998) Acute mesenteric
ischemia CT and plain radiographic analysis of 26 cases. Clin
Imaging 22:3441
11. Alpern MB, Glazer GM, Francis IR (1988) Ischemic or infarcted
bowel: CT findings. Radiology 166:149152
12. Klein HM, Lensing R, Klosterhalfen B, et al. (1995) Diagnostic
imaging of mesenteric infarction. Radiology 197:7982
13. Federle MP, Chun G, Jeffrey RB, Rayor R (1984) Computed
Tomographic findings in bowel infarction. AJR 142:9195
14. Petras RE (2004) Ischemic bowel disease. In: Mills SE (ed).
Sternbergs diagnostic surgical pathology. Philadelphia: Lippincott
Williams & Wilkins, pp 15091511
15. Grassi R, Di Mizio R, Pinto A, et al. (2004) Serial plain abdominal
film findings in the assessment of acute abdomen: spastic ileus,
hypotonic ileus, mechanical ileus and paralytic ileus. Radiol Med
108:5670
16. Kim JY, Ha HK, Byun JY, et al. (1993) Intestinal infarction sec-
ondary to mesenteric venous thrombosis: CT-pathologic correla-
tion. JCAT 17:382385
17. Balthazar EJ, Yen BC, Gordon RB (1999) Ischemic colitis: CT
evaluation of 54 cases. Radiology 211:381388
18. Robert JH, Mentha G, Rohner A (1993) Ischaemic colitis: two
distinct patterns of severity. Gut 34:46
19. Marston A, Pheils MT, Thomas ML, Morson BC (1966) Ischaemic
colitis. Gut 7:115
20. Brandt LJ, Boley SJ (1993) Ischemic and vascular lesions of the
bowel. In: Sleisenger MH, Fordtran JS (eds). Gastrointestinal dis-
ease: pathophysiology, diagnosis, management. 5th ed. Philadelphia:
Saunders, pp 19401945
21. Eisenberg RL, Montgomery CK, Margulis AR (1979) Coltis in the
elderly: ischemic colitis mimicking ulcerative and granulomatous
colitis. AJR 133:11131118
22. Zimmermann BJ, Granger DN (1992) Reperfusion injury. Surg
Clin North Am 72:6583
23. Rogers AI, David S (1995) Intestinal blood flow and diseases of
vascular impairement. In: Haubrich WS, Schaffner F, Berck JE
(eds). Gastroenterology. 5th ed. Philadelphia: WB Saunders, pp
12121234
24. Ripolles T, Simo` L, Mart` nez-Perez MJ, et al. (2005) Sonographic
findings in ischemic colitis in 58 patients. AJR 184:777785
25. Longo WE, Ballantyne GH, Gusberg RJ (1992) Ischemic colitis:
patterns and prognosis. Dis Colon Rectum 35:726730
26. Szucs RA, Wolf EL, Gramm HF, et al. (2001) Miscellaneous
abnormalities of the colon. Colonic ischemia. In: Gore RM, Levine
MS (eds). Texbook of gastrointestinal radiology. Philadelphia: WB
Saunders, pp 11021106
27. Gore RM, Calenoff L, Rogers LF (1979) Roentgenographic man-
ifestations of ischemic colitis. JAMA 241:11711173
28. Greenberg HM, Goldberg HI, Axel L (1981) Colonic urticaria
pattern due to early ischemia. Gastrointest Radiol 6(2):145149
29. Danse EM, Van Beers BE, Jamart J, et al. (2000) Prognosis of
ischemic colitis: comparison of color doppler sonography with early
clinical and laboratory findings. AJR 175:11511154
30. Cheung AH, Jiranek GC, Haggitt RC, et al. (1992) Use of ultra-
sound to detect intestinal wall ischemia in piglets. Ultrasound Med
Biol 18:843849
31. Cheung AH, Wang KY, Jiranek GC, et al. (1992) Evaluation of a
20-MHz ultrasound transducer used in diagnosing porcine small
bowel ischemia. Invest Radiol 27:217223
32. Petras RE (2004) Acute ischemic colitis. In: Mills SE (ed). Stern-
bergs diagnostic surgical pathology. Philadelphia: Lippincott Wil-
liams & Wilkins, pp 1495
33. Whitehaed R (1972) The pathology of intestinal ischemia. Clin
Gastroenterol 1:613637
34. Gore RM, Miller FH, Pereles FS, et al. (2000) Helical CT in the
evaluation of the acute abdomen. AJR 174:901913
35. Ottinger LW, Austen WG (1967) A study of 136 patients with
mesenteric infarction. Surg Gynecol Obstet 124:251261
36. Lund EC, Han SY, Holley HC, et al. (1998) Intestinal ischemia:
comparison of plain radiographic and computed tomographic
findings. Radio graphics 8:10831108
37. James S, Balfe DM, Lee JKT, Picus D (1987) Small-bowel disease:
categorization by CT examination. AJR 145:863868
38. Smerud MJ, Johnson CD, Stephens DH (1990) Diagnosis of bowel
infarction: a comparison of plain films and CT scans in 23 cases.
AJR 154:99103
39. Meyers MA, Ghahremani GG, Clements JL, et al. (1977) Pne-
umatosis intestinalis. Gastrointest Radiol 2:91105
40. Taourel PG, Deneuville M, Pradel JA, et al. (1996) Acute mesen-
teric ischemia: diagnosis with contrast-enhanced CT. Radiology
199:632636
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.