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Paper title: MDCT in Ischemic colitis: how to define the etiology and acute,
subacute and chronic phase of damage in the emergency setting

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Authors:
Berritto Daniela1, Iacobellis Francesca2, Mazzei Maria Antonietta3, Volterrani
Luca3, Guglielmi Giuseppe4, Brunese Luca5, Grassi Roberto2

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Affiliations:
1 Department of Radiology, Private Hospital “Villa Dei Fiori” S.r.l. Accredited to

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NHS - Corso Italia, 157 – 80011 Acerra (NA) - Italy

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2 Department of Radiology, Second University of Naples – P.zza L. Miraglia –

80132, Napoli - Italy

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3 Department of Medical, Surgical and Neuro Sciences, Section of Radiological

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Sciences, University of Siena, Viale Bracci 10, 53100 Siena, Italy
4 IRCCS-Casa Sollievo della Sofferenza, San Giovanni Rotondo, Italy.
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5 Department of Medicine and Health Science, University of Molise, Campobasso,
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Italy
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Email addresses:
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Daniela Berritto: berritto.daniela@gmail.com

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Francesca Iacobellis: francesca.iacobellis@libero.it

Maria Antonietta Mazzei: mamazzei@gmail.com
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Luca Volterrani: volterrani@unisi.it

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Giuseppe Guglielmi: giuseppe.guglielmi@unifg.it

Luca Brunese: luca.brunese@unimol.it
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Roberto Grassi: roberto.grassi@unina2.it

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 FS
Abstract:
Colon Ischemia (CI) is the most common vascular disorder of gastrointestinal
tract with a reported incidence of 6.1-44 cases/100000 person-years with

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confirmatory histopathology.

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However, the true incidence of CI poses some difficulty, and even vigilant
clinicians with high-risk patients often miss the diagnosis since clinical

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presentation is nonspecific or could have mild transient nature. Detection of CI

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results crucial to plan the correct therapeutic approach and reduce the reported
mortality rate (4-12%).

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Diagnosis of CI is based on a combination of clinical suspicion, radiological,
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endoscopic, and histological findings. Some AA consider colonoscopy as
diagnostic test of choice, however a preparation is required and it is not without
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risk, above all in severely ill patients.
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There are two types of colonic insult: ischaemic and reperfusive. The first one
occurs above all during ischaemic/non-occlusive mesenteric ischemia; in this
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case the colonic wall appears thinned with dilated lumen and fluid in paracolic
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space appears. When reperfusion occurs the large bowel wall appears thickened
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and stratified, because of subepithelial edema and/or hemorrhage, with

consequent lumen caliber reduction. Shaggy contour of the involved intestine
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and misty mesentery are associated to the pericolic fluid.

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The pericolic fluid results a crucial finding for CI diagnosis: in fact, in case of
ischemic CI, dilated thinned colonic wall could be misdiagnosed as a
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physiological colonic distension caused by the presence of intestinal gas,

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whereas, in case of reperfused CI, the thickening of large bowel wall is an

unspecific condition, similar to malignant or inflammatory diseases. Moreover
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pericolic fluid may increase or decrease depending on the evolution of the

ischemic damage suggesting the decision of a medical or surgical treatment.
Radiologists should not forget the hypothesis of CI, being aware that MDCT
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could be sufficient to suggest the diagnosis of the IC, allowing for early
identification and grading definition, and in a short term follow-up,
discriminating patients who need urgent surgery from patients in which a
medical treatment and follow-up and can be proposed.
 Keywords
Ischemia, Colitis, Emergency, Multidetector Computed Tomography.

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Manuscript

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1
2 Paper title
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4 MDCT in Ischemic colitis: how to define the etiology and acute, subacute and chronic phase of
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6 damage in the emergency setting
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10 Abstract
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12 Colon Ischemia (CI) is the most common vascular disorder of gastrointestinal tract with a
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reported incidence of 6.1-44 cases/100000 person-years with confirmatory histopathology.

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15 However, the true incidence of CI poses some difficulty, and even vigilant clinicians with high-
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17 risk patients often miss the diagnosis since clinical presentation is nonspecific or could have
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19 mild transient nature. Detection of CI results crucial to plan the correct therapeutic approach
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21 and reduce the reported mortality rate (4-12%).
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23 Diagnosis of CI is based on a combination of clinical suspicion, radiological, endoscopic, and
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histological findings. Some AA consider colonoscopy as diagnostic test of choice, however a
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27 preparation is required and it is not without risk, above all in severely ill patients.
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There are two types of colonic insult: ischaemic and reperfusive. The first one occurs above all
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31 during ischaemic/non-occlusive mesenteric ischemia; in this case the colonic wall appears
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33 thinned with dilated lumen and fluid in paracolic space appears. When reperfusion occurs the
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35 large bowel wall appears thickened and stratified, because of subepithelial edema and/or
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37 hemorrhage, with consequent lumen caliber reduction. Shaggy contour of the involved
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39 intestine and misty mesentery are associated to the pericolic fluid.

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The pericolic fluid results a crucial finding for CI diagnosis: in fact, in case of ischemic CI,
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43 dilated thinned colonic wall could be misdiagnosed as a physiological colonic distension
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caused by the presence of intestinal gas, whereas, in case of reperfused CI, the thickening of
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large bowel wall is an unspecific condition, similar to malignant or inflammatory diseases.
48 Moreover pericolic fluid may increase or decrease depending on the evolution of the ischemic
49
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50 damage suggesting the decision of a medical or surgical treatment.

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52 Radiologists should not forget the hypothesis of CI, being aware that MDCT could be sufficient
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54 to suggest the diagnosis of the IC, allowing for early identification and grading definition, and
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56 in a short term follow-up, discriminating patients who need urgent surgery from patients in
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58 which a medical treatment and follow-up and can be proposed.
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 Introduction
1
2 Ischemic colitis (IC) is the most common vascular disorder of gastrointestinal (GI) tract [1, 2]
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4 and the second most frequent cause of lower gastrointestinal bleeding [3].
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6 IC is the consequence of an acute interruption or chronic decrease in the colonic blood supply
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8 [4], which results in ischemic necrosis of variable severity [5, 6].
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10 The incidence of IC is underestimated because it could be a misdiagnosed cause of acute
11

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12 abdomen otherwise it could have a mild transient nature so clinical presentation can be
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nonspecific and highly variable [7].

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15 Although up to 85% of cases of IC, conservatively managed, improves within 1 or 2 days and
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17 completely resolves within 1 or 2 weeks, close to one-fifth of patients develops peritonitis or
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19 clinically deteriorates requiring surgery. Surgery should be limited to the excision of
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21 irreversibly necrotized intestine, as it can lead to bacteremia and sepsis, colonic stricture,
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23 persistent abdominal pain and bloody diarrhea, and protein-loosing enteropathy [7].
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That being so, in order to plan the correct therapeutic approach of IC, firstly it is crucial to
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27 early detect this condition and second to discriminate patients needing urgent operative
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intervention from patients in which a follow-up can be proposed as an alternative to surgery
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31 [8].
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35 Etiologic factors in colonic ischemia
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37 IC is the consequence of an acute interruption or chronic decrease in the colonic blood supply
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39 [4], which may be either occlusive or non-occlusive in origin [3].

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Many medical conditions and medications can cause ischemia by reducing blood flow to the
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43 colon [6].
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The most common cause of IC is low flow state [9] and can be considered as a form of non-
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occlusive ischemic disease (NOMI). In a minor percentage of cases, IC can be due to occlusive
48 causes (37.5% in our series) as Inferior Mesenteric Artery (IMA) thrombosis, embolism or
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50 atherosclerosis [10].
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54 Vascular colonic anatomy

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56 Two major arteries supply most of the blood to the colon: the superior mesenteric artery
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58 (SMA) (which supplies the ascending and transverse colon) and the inferior mesenteric artery
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 (IMA) (which supplies the descending and sigmoid colon). The internal iliac arteries supply the
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2 rectum.
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4 The splenic flexure and sigmoid colon are regions where two circulations (SMA and IMA) meet
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6 each other (so-called watershed areas).
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8 The differences in the mode of division of the inferior mesenteric artery are numerous, but
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10 most are referable to a common pattern. The IMA arises from the abdominal aorta and
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12 proceeding towards the pelvis gives off its first branch, the left colic artery. The left colic artery
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ascends directly towards the splenic flexure, before reaching which it divides. The sigmoid

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15 arteries exhibit two principal modes of origin. There is great variability in the mode of division
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17 of the sigmoid arteries, but the exact topographical pattern of these vessels is of small surgical
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19 importance.
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21 The vessels of the large bowel differ from those of the small intestine in not forming so many
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23 arcades and in having, alongside the mesenteric border of the colon, a marginal artery from
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which the vasa recti arise. While the vasa recti do not mutually anastomose, the marginal
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27 artery, first described by von Haller (1786) and later by Drummond (1913), is composed of the
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terminal portions of the branches from the major vascular arcades and therefore forms an
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31 important anastomosis between them: it can keep the left colon viable when the inferior
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33 mesenteric artery is occluded or is ligated during recto-sigmoidectomy.
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35 The adequacy of the blood supply to the distal colon is dependent on the marginal artery. In
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37 the absence of arterial disease the entire colon and rectum may be vascularized from
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39 branches of the superior mesenteric artery through the medium of this marginal vessel [11].
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43 WATERSHED AREAS
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Watershed areas correspond to the splenic flexure, also known as Griffith’s point, and sigmoid
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colon, or Sudeck’s point. These regions result particularly vulnerable to ischemic insults being
48 located between two different vascular systems.
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50 At the splenic flexure, the link between SMA and IMa systems, the marginal artery of
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52 Drummond is occasionally tenuous and is absent in up to 5% of patients; a 1.2–2.8 cm2 area
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54 may be devoid of vasa recta.

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56 Sudeck’s point refers to the anastomosis between sygmoid arteries and superior
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58 hemorroidary artery orginating from IMA.
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 A third potential watershed area is the right colon, where the marginal vessel is poorly
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2 developed in up to 50% of people [12-14].
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6 Diagnostic imaging modalities
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8 Different imaging methods have been used to diagnose CI, including plain radiography of the
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10 abdomen, barium enema (BE), Computed Tomography (CT), ultrasonography (US), and
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12 Magnetic resonance imaging (MRI). All can suggest or support the diagnosis, but none have
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findings that are specific enough to make a definitive diagnosis, except when infarction has
15 occurred. [15]
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19 PLAIN RADIOGRAPHY
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21 Plain radiography may show suggestive signs of early disease such as “thumbprinting” (which
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23 appears as rounded densities along the sides of a gas-filled distended colon, caused by
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25 submucosal hemorrhage and edema), loss of haustration, and dilation of colonic loops; in one
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27 retrospective report, these findings were present in 21% of 41 patients with CI and no patient
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29 had the signs of advanced changes such as intramural gas (pneumatosis linearis), portal
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31 venous gas, and megacolon [16].
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35 BARIUM ENEMA
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37 BE has been reported with a sensitivity approaching 80%. [17]. Today, it has a limited role in
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39 diagnosis and has been replaced by CT and colonoscopy, largely because of the latter’s greater
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41 accuracy and ability to allow sampling of the mucosa for pathology.
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43 Moreover BE should not be performed in any patient with a suspicion of gangrene,
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perforation, or peritonitis.
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48 ULTRASOUND
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50 Although US is not the standard diagnostic tool for patients with suspected CI, it could result
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52 useful in suggest the pathology by revealing some related findings: symmetric bowel wall
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54 thickening (100%), segmental involvement of the colon (80%), preservation of colon wall
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56 stratification (66%), altered pericolic fat (28%), free fluid (19%), and pneumatosis (1.7%) [18].
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58 However, experience with US in the setting of CI is very limited and it is believed that this
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60 technique lacks specificity for bowel wall thickening and has a high false negative rate [19].
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 False-negative sonographic studies can be explained by several circumstances. In patients who
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2 have early ischemia, imaging findings can be normal. Ischemic colitis with wall thinning can be
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4 missed on sonography, although this circumstance is more frequent in acute mesenteric
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6 ischemia [19].
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10 COMPUTED TOMOGRAPHY
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12 CT examination with intravenous contrast media (iv c.m.) is actually considered the main
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technique for the noninvasive diagnosis of IC and also in cases of acute abdomen from

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15 different and various origins, as it is readily available in emergency department [20, 21], it can
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17 suggest IC when it is unsuspected, can diagnose complications and exclude other illnesses
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19 [22].
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21 In case of abdominal pain, there are not pathognomonic CT findings of IC [23].
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23 CI is usually nonocclusive in nature, but CT (or CT-Angiography, CTA) can be used to identify
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25 whether or not vascular occlusions are present. With emerging technology, contrast-enhanced
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27 CT can sometimes assess patency of the celiac, SMA, and IMA without devoted CTA.
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29 Unfortunately, the IMA cannot be considerate a specific finding of IC since it results occluded
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31 in almost 10% of asymptomatic patients over 60 years of age [24].
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33 Few data exist on the sensitivity and specificity of CT for assessing vascular occlusion in CI; a
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35 meta-analysis regarding sensitivity and specificity of CT in the diagnosis of mesenteric arterial
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37 embolism, mesenteric arterial thrombosis, and mesenteric venous thrombosis reported a
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39 sensitivity and specificity of 93.3% and 95.9%, respectively [25].
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43 MAGNETIC RESONANCE IMAGING
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As recently proposed [26-29] MRI may be a substitute for invasive procedures in diagnosing
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and grading IC allowing for the early identification of pathological findings and for definition of
48 the grade of ischemic lesions.
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50 This method has been formally studied in only a small number of patients with CI; findings are
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52 similar to those of CT and as with CT, such findings usually are not specific enough to make a
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54 definitive diagnosis.
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56 The advantage of the using MRI for clinical management of IC is the possibility to perform a
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58 short-term follow-up without the employment of ionizing radiation or intravenous contrast
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60 material.
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 In particular MRI can discriminate patients with urgent operative intervention from patients in
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2 which a follow-up can be proposed as an alternative to surgery.
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6 COLONOSCOPY
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8 Colonoscopy is often considered the diagnostic test of choice in establishing the diagnosis of
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10 IC being the test with the higher sensitivity for this patholgy. It is possible to demonstrate
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12 mucosal changes and perform biopsies on them at the same time.
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However, just after one colonoscopy the diagnosis of CI cannot be confirmed unless mucosal

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15 gangrene is observed or infarction or ghost cells are evident at histopathology; thus, these
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17 histopathologic findings are uncommon and of limited value for CI diagnosis [30].
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19 In case of severe CI, CT should be performed to evaluate the distribution of disease whereas
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21 focused colonoscopy should be realized to confirm the nature of the CT abnormality. The
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23 endoscopic examination should be extended just until the distal limit of damaged bowel.
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25 Colonoscopy should not be avoided in case of acute peritonitis or evidence of irreversible
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27 ischemic damage (i.e., gangrene and pneumatosis) and it could be performed without bowel
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29 preparation to prevent hypoperfusion caused by dehydrating cathartics; in addiction it is not
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31 available in all the emergency departments” [31].
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33 Focusing the attention both on the diagnosis and follow-up of IC, this article aims to describe
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35 the CT radiological findings, which are useful to recognize this entity in correlation with
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37 etiology (occlusive and non-occlusive forms), to distinguish its phase (acute, sub-acute and
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39 chronic) and the extension and to identify the presence of reperfusion characterizing its
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41 effectiveness.
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Radiological diagnosis
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CT IMAGING AND TECHNIQUE
48 CT in acute abdomen is useful to exclude serious medical conditions other than CI (e.g.,
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50 diverticulitis), can suggest the diagnosis of CI, reveal which areas of the colon are involved, as
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52 well as recognize its the phase and the presence of reperfusion.
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54 CT images should be obtained with a spiral technique in a cranio-caudal direction (from the
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56 base of the lungs to the pelvic brim) and with patient in supine position.
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 Oral and rectal administration of contrast material is not recommended (or useful) for
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2 accurate CT examination and assessment of acute large bowel ischaemia, as it does not add
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4 any additional information for the final diagnosis.
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6 Acquisition of both unenhanced and contrast-enhanced CT scans is always necessary,
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8 acquiring images in the late arterial phase (start delay 45-50 seconds) and in the portal venous
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10 phase (start delay 70-80 seconds) with an intravenous injection of 2 mL/kg of non-ionic
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12 contrast material followed by 40 mL of saline solution using a peristaltic semi-automated
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power injector (4 mL/s flow rate) with an 18-gauge needle in the antecubital vein.
15 Unenhanced CT is useful not only to identify reperfusive phenomena or intramural
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17 hemorrhage, appearing as high attenuation areas of the large bowel wall, but also to
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19 constitute a baseline Hounsfield (HU) value of the large bowel wall for the assesment of
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21 contrast enhancemet.
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23 After medical treatment unenhanced CT could be useful to monitor the effectiveness of
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25 reperfusion, evaluating the reduction or the increase of retroperitoneal fluid as well as the
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27 large bowel caliber, and to detect the onset of large bowel wall necrosis like the presence of
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29 intestinal pneumatosis [32]. On the other hand, thanks to contrast-enhanced CT it is possible
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31 to evaluate the degree of large bowel wall enhancement, which becomes absent in the case of
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33 necrosis, and the presence of ischemic signs on splanchnic organs. Contrast-enhanced scans
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35 should be realized with an intravenous injection of 2 ml/kg of nonionic contrast material
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37 followed by 40 ml of saline solution using an automated power injector (3–4 ml/s flow rate),
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39 with an 18-gauge needle in the antecubital vein and should be performed in the late arterial
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41 phase (start delay 45–50 s) and in the portal venous phase (start delay 70–80 s). It is always
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43 recommended to visualize the CT images both with a window set for soft tissue (width, W:
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300–350; level, L 40–50) to detect the changes of the large bowel wall, splancnic organs,
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mesentery and vessels, and with window setting for the lung parenchyma (W: 450–100; L:
48 100–0) to recognize the presence extraluminal gas [33].
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52 RADIOLOGICAL KEY POINTS
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54 In the diagnosis of IC radiologist should indicate:
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56 The type of damage, which could be:
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58 Ischaemic
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60 Reperfusive; and in this case it should be indicated whether the reperfusion is effective or not.
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 The location and extension of the damage
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2 The phase of damage, which could be:
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4 Acute
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6 Subacute
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8 Chronic
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12 The type of damage
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Arterial ischemic damage
15 The colon is particularly susceptible to ischemia, perhaps owing to its relatively low blood
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17 flow, its unique decrease in blood flow during periods of functional activity, and its sensitivity
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19 to autonomic stimulation. The degree to which colonic blood flow must diminish before
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21 ischemia results varies with the acuteness of the event, the degree of preexisting vascular
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23 collateralization, and the length of time the low flow state persists. As mentioned above, the
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25 interruption or decrease in the colonic blood supply may be either occlusive or non-occlusive
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27 in origin (NOMI). In occlusive forms CT may demonstrate a thrombus or embolus in the
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29 corresponding mesenteric vessel.
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31 When there is an interruption in the colonic blood supply without reperfusion the colonic wall
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33 remains thin or “paper-thin” and unenhanced, associated with dilation of the lumen [34].
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35 Thinning of the large bowel wall or “paper- thin wall” is caused by volume loss of tissue and
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37 vessels in the large bowel wall and by the loss of intestinal muscular tone due to the lack of
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39 blood flow. Pericolic fluid could be present and is located in paracolic recess [9, 35]. The i.v.
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41 contrast media allows the evaluation of the large wall enhancement: it results large bowel
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43 wall hypodensity on enhanced CT, related to the absence of effective reperfusion due to the
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large bowel wall ischemic injury. These findings are useful in diagnosing the IC before
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reperfusion, being the only sign beyond dilation only gas-filled and “paper-thin wall”.
48 However, the latter could be misdiagnosed due to the similarity with the physiological
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50 distension of the colon caused by the presence of intestinal gas. Vascular pneumatosis is due
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52 to large bowel infarction in case of advanced and irreversible damage as well as
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54 neumoperitoneum/pneumoretroperitoneum or mesenteric pneumatosis. In case of NOMI,
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56 beyond intestinal damage, there is also a reduction of contrast enhancement of abdominal
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58 parenchyma, most commonly in the liver, spleen, kidneys, and pancreas (Figure 1).
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60 Reperfusive damage
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 Ischemia, both occlusive or NOMI, may be followed by reperfusion injury and, for relatively
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2 brief periods of ischemia, this combined injury may produce more damage than just reduction
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4 of blood flow without reperfusion. In case of IMA occlusion the reperfusion is always present
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6 if SMA is still viable. In this case the blood supply to the left colon is restored from SMA, after
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8 a more or less long-lasting ischemic period, which is depending on the effectiveness of the
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10 anastomotic circles between IMA and SMA. The appearance of reperfusion differs from the
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12 non-reperfused large bowel. It appears thickening of large bowel wall, usually resulting from
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subepithelial edema and/or hemorrhage, with consequent lumen caliber reduction.
15 The unenhanced phase may detect any hemorrhagic phenomenon of the large bowel wall;
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17 mucosal hyperdensity from hemorrhagic phenomena may determine a typical feature: the
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19 “little rose” sign.
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21 In a thickened large bowel segment, a stratified enhancement pattern corresponding to the
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23 classic target sign is useful for excluding malignant conditions. This pattern is produced by
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25 enhancing mucosa with adjacent edematous submucosa. Shaggy contour of the involved
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27 intestine and misty mesentery is associated to the pericolic fluid, which may increase or
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29 decrease depending on the evolution of the ischemic damage (Figure 2).
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31 In chronic phase, pericolic fluid is absent; in the injured colonic wall, fibrotic reaction develops
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33 leading to continuous mild and irregular circumferential thickening with gaping lumen [36,
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35 37], as well as the target sign, due to acute mucosal hemorrhagic and edematous phenomena,
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37 is absent.
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41 Location and extension
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43 A segmental pattern is typical in case of occlusive IC, which can be explained by the vascular
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anatomy of the colon and rectum where watershed susceptible areas exist.
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Left colon is affected most often (32.6%) followed by the distal colon (24.6%), right colon
48 (25.2%) and entire colon (7.3%) [38].
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50 No colonic region is spared from involvement in case of NOMI [39].
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52 Previous studies [40] report that ischemic changes are continously and uniformly distributed
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54 along an entire vascular colonic territory, with a marked distinction between ischemic and
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56 non-ischemic tracts; this constitutes a differential diagnostic element with others pathologies
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58 having similar imaging features but different distributions, as Crohn or other inflammatory
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60 conditions [41].
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 1
2 c. Phase of damage
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4 Imaging allows determining the morpho-functional alterations associated with the IC and
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6 allows estimating the timing of ischemic damage.
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8 In Acute phase, the main differential findings between occlusive IC and non-occlusive IC
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10 (NOMI) are represented by the paper-thin large bowel wall with dilated lumen in case of
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12 NOMI vs large bowel wall thickening and related signs as target sign and lumen caliber
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reduction in case of IMA occlusion.
15 In Subacute phase it is important to evaluate the effectiveness of reperfusion: in this sense,
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17 the changes in the large bowel wall thickness and in the pericolic fluid amount are useful
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19 parameters to be monitored. In case of effective reperfusion large bowel wall thickening
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21 decrease with progressive gaping of lumen while pericolic fluid should decrease (Figures 2 and
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23 3).
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25 In Chronic phase, rather than to define the etiology, it is important to assess the effects of the
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27 ischemic injury, represented by the non-uniform fibrosis of the large bowel wall (Figure 4).
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29 The more difficult form of IC to be detected at imaging are NOMI before reperfusion since the
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31 only paper-thin wall can be misdiagnosed like normal colon; in this cases the given the
32
33 suspicion is induced by medical history particular attention should be paid to the presence of
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35 pericolic fluid as well as to ischemic phenomena of parenchymal organs [38].
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37 Also in subacute phase the thickened affected colonic wall could be misinterpreted as a
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39 normal tract with collapsed lumen insted of as pathlogical; whereas, in chronic forms, the
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41 irregular thickening of large bowel could be misdiagnosed if the patient’s clinical history is
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43 unknown.
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RADIOLOGICAL FINDINGS CLASSIFICATION
48 The radiological findings can be summarized in 5 main categories [28, 42, 43] being variously
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50 combined, as described above, in relation to the pathophysiology of the developing anoxic
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52 process and to the timing of the examination:
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54 a. Vessels findings
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56 - Vascular occlusion
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58 Resulting as defect or stop in the vessel lumen
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60 - Vascular pneumatosis
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 Presence of gas within the mesenteric venules and portal venous system
1
2 b. Peritoneal/Retroperitoneal cavity findings
3
4 - Free fluid
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6 Presence of fluid in the peritoneal and/or retroperitoneal cavity
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8 - Pneumoperitoneum/pneumoretroperitoneum
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10 Presence of gas within the peritoneal or retroperitoneal spaces
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12 c. Bowel wall findings:
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- Bowel wall diameter

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15 Bowel-loop dilatation, defined as a large-bowel diameter >8 cm
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17 - Wall thickness
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19 The wall thickness is considered normal when less than 3 mm, with distended bowel loops; in
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21 the absence of distension, the wall is considered pathological when its thickness is greater
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23 than approximately 1 cm.
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25 - Wall enhancement
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27 The wall enhancement is considered pathological in presence of a double-halo or target
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29 configuration (two or three concentric rings) or when absent
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31 - Wall pneumatosis
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33 It is defined as the presence of small air bubbles within the bowel wall
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35 d. Mesentery findings:
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37 - Pericolic streakiness
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39 Corresponds to shaggy contour of the involved intestine and misty mesentery
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41 - Mesenteric pneumatosis
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43 It is defined as the presence of small air bubbles within the mesenteric fat
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e. Parenchymal findings
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- Ischemic injuries
48 Signs of ischemic damage involving liver, kidneys, spleen, pancreas.
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50 At CT scan parenchymal infarctions could be depicted as a hypodense parenchymal area, at
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52 times triangular in shape, with sharp peripheral contours or as a rounded central or marginal
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54 area with irregular appearance and ill-defined shape. Moreover, CT could show intralesional
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56 gas not correlated to bacterial infection.
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58 In the hyperacute phase, CT may show areas of mottled increased attenuation, representing
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60 areas of hemorrhagic infarct. In the acute-subacute phase, infarcts tend to become focal and
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 progressively better demarcated. In the chronic phase, infarcts may disappear completely but,
1
2 more commonly, they reveal progressive volume loss caused by fibrotic contraction of the
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4 infarct [44, 45].
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7

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8 Conclusions
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10 There are two types of colonic insult: ischaemic and reperfusive. In case of ischaemic form the
11

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12 colonic wall appears thinned with dilated lumen and fluid in paracolic space appears. When
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reperfusion occurs the large bowel wall appears thickened and stratified, because of

O
14
15 subepithelial edema and/or hemorrhage, with consequent lumen caliber reduction.
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17 The pericolic fluid results a crucial finding for CI diagnosis: in fact, in case of ischemic CI,
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19 dilated thinned colonic wall could be misdiagnosed as a physiological colonic distension
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21 caused by the presence of intestinal gas, whereas, in case of reperfused CI, the thickening of
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23 large bowel wall is an unspecific condition, similar to malignant or inflammatory diseases.
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25 Moreover pericolic fluid may increase or decrease depending on the evolution of the ischemic
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27 damage suggesting the decision of a medical or surgical treatment.
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54 References
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19 Figure legends
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23 Figure 1. Arterial ischemic damage in a patient with heart failure and consequent non-
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25 occlusive mesenteric ischemia (NOMI) without reperfusion. Note the “paper-thin” and
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27 unenhanced large bowel wall (white arrows) associated with dilation of the lumen (stars) a).
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29 In b) splenic infarction is evident (arrowhead).
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33 Figure 2. Reperfusive damage after SMA occlusion in patient with IMA ligation for previous
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35 sigmoidectomy.
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37 On MDCT in acute phase it appears thickening of large bowel wall (arrow in a and b) with
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39 consequent lumen caliber reduction.
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43 Figure 3. Same patient of Figure 2.
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Two days after, thanks to blood supply restoration, CT shows a reduction of large bowel wall
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thickening and progressive gaping of lumen (arrow in a and b).
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50 Figure 4. Reperfusive damage from still available SMA in patient with IMA occlusion.
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52 In acute phase (day 1) a) it appears thickening of large bowel wall on MDCT with consequent
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54 lumen caliber reduction, and the typical feature of “little rose” sign (white arrow). Shaggy
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56 contour of the involved intestine and misty mesentery is associated to the pericolic fluid
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58 (arrowhead).
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 In subacute phase (day 3) b) thanks to an effective reperfusion large bowel wall thickening
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2 decrease (white arrow) with progressive gaping of lumen while pericolic fluid decreases
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4 (arrowhead). Patient underwent a new CT in chronic phase c) showing fibrotic reaction that
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6 leads to continuous mild and irregular circumferential thickening with gaping lumen (arrow).
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Figure 1 Click here to download Figure Figure 1.jpg

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