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CT Imaging of Acute Bowel Ischemia and Infarction - Department of ...

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<strong>CT</strong> <strong>Imaging</strong> <strong>of</strong> <strong>Acute</strong> <strong>Bowel</strong><br />

<strong>Ischemia</strong> <strong>and</strong> <strong>Infarction</strong><br />

R<strong>and</strong>y Fanous<br />

University <strong>of</strong> Toronto<br />

PGY3 Radiology


Outline<br />

• Anatomy<br />

– Vascular supply <strong>of</strong> bowel<br />

• Pathology<br />

– Stages<br />

– Contributing factors<br />

– Etiologies<br />

• <strong>CT</strong><br />

– Technique<br />

– Findings<br />

• Cases


Anatomy<br />

Vascular Supply <strong>of</strong> <strong>Bowel</strong>: Arterial<br />

• 1. Celiac = distal esophagus to descending duodenum<br />

– GDA (first branch <strong>of</strong> CHA) = anastomotic connections b/w celiac axis <strong>and</strong> SMA<br />

• 2. SMA = transverse duodenum to splenic flexure<br />

– Marginal artery <strong>of</strong> Drummond/ arcade <strong>of</strong> Riolan = anastomotic connections b/w<br />

SMA <strong>and</strong> IMA<br />

• 3. IMA = splenic flexure to rectum<br />

– Anastomotic connections to lumbar arteries (<strong>of</strong>f abdominal aorta) <strong>and</strong> internal<br />

iliacs<br />

• Watershed areas:<br />

– Splenic flexure<br />

– Ileocecal junction<br />

– Rectosigmoid junction


Anatomy<br />

Vascular Supply <strong>of</strong> <strong>Bowel</strong>: Arterial<br />

• 1. Celiac = distal esophagus to descending duodenum<br />

– GDA (first branch <strong>of</strong> CHA) = anastomotic connections b/w celiac axis <strong>and</strong> SMA<br />

• 2. SMA = transverse duodenum to splenic flexure<br />

– Marginal artery <strong>of</strong> Drummond/ arcade <strong>of</strong> Riolan = anastomotic connections b/w<br />

SMA <strong>and</strong> IMA Distribution provides clues to etiology…<br />

• 3. IMA = splenic flexure to rectum<br />

(b) SMA = jejunum, ileum, ascending, transverse<br />

– Anastomotic connections to lumbar arteries (<strong>of</strong>f abdominal aorta) <strong>and</strong> internal<br />

(c) IMA = descending (rectum spared)<br />

iliacs<br />

• Watershed areas:<br />

– Splenic flexure<br />

– Ileocecal junction<br />

– Rectosigmoid junction<br />

A. Vascular territories<br />

(a) Celiac = duodenum<br />

B. Watershed territories


Anatomy<br />

Vascular Supply <strong>of</strong> <strong>Bowel</strong>: Venous<br />

• SMV <strong>and</strong> IMV parallel the corresponding arteries <strong>and</strong> their drainage<br />

• IMV drains into splenic vein; splenic vein <strong>and</strong> SMV form portal<br />

confluence<br />

• Extensive anastomotic connections b/w mesenteric veins <strong>and</strong><br />

systemic venous circulation<br />

<strong>Bowel</strong> is highly vascularized with extensive collaterals<br />

(small >> large)


Anatomy<br />

Vascular Supply <strong>of</strong> <strong>Bowel</strong>: Blood Flow<br />

• Percentage <strong>of</strong> cardiac output received by bowel…<br />

– (a) Normal circumstances = 20%<br />

– (b) Post-pr<strong>and</strong>ial (splanchnic auto-regulation) = 35%<br />

– (c) Sympathetic stress response = 10%<br />

• Proportion <strong>of</strong> arterial blood to bowel wall…<br />

– 2/3 = mucosa (i.e. susceptible to ischemia)<br />

– 1/3 = remainder <strong>of</strong> the mural layers<br />

Ex. Shock = high-risk group<br />

(i.e. low flow state + stress response)


Pathology<br />

<strong>Ischemia</strong> <strong>and</strong> <strong>Infarction</strong>: Stages<br />

• 1 = mucosal ischemia<br />

– aka ischemic enteritis/ colitis<br />

– Reversible mucosal erosions <strong>and</strong> ulcerations<br />

• 2 = submucosal/ muscularis ischemia<br />

– Partial mural necrosis with possible repair +/- residual fibrotic strictures<br />

• 3 = transmural ischemia<br />

– aka bowel infarction<br />

– Non-reversible transmural gangrenous necrosis


Pathology<br />

<strong>Ischemia</strong> <strong>and</strong> <strong>Infarction</strong>: Contributing Factors<br />

• 1 = mucosal ischemia<br />

– aka ischemic enteritis/ colitis<br />

– Reversible mucosal erosions <strong>and</strong> ulcerations<br />

Important to realize that acute bowel<br />

ischemia does NOT refer to a single<br />

– Partial mural necrosis entity, with but possible rather repair a spectrum +/- residual <strong>of</strong> disease! fibrotic strictures<br />

• 2 = submucosal/ muscularis ischemia<br />

• 3 = transmural ischemia<br />

– aka bowel infarction<br />

– Non-reversible transmural gangrenous necrosis<br />

• Post-ischemic inflammatory response<br />

– i.e. release <strong>of</strong> a myriad <strong>of</strong> cytokines<br />

– Contributes to necrosis <strong>and</strong> further compromises mucosal integrity<br />

• Super-infection (esp. colon)<br />

– Translocation <strong>of</strong> intra-luminal bacteria, leading to mural infection, bacteremia <strong>and</strong><br />

sepsis (high mortality)


Pathology<br />

Etiologies<br />

1. Occlusive (75%):<br />

Arterial (thromboembolism)<br />

2. Non-occlusive (25%):<br />

Venous (bowel obstruction)<br />

• Occlusive (75%)<br />

– Mesenteric arterial (90%)<br />

• Ex. Thromboembolism (atrial fibrillation, aortic), mesenteric thrombosis, dissection etc.<br />

– Mesenteric venous (10%)<br />

• Ex. Neoplasm, infection, hypercoagubility (polycythemia, sickle cell, antithrombin III, protein C/S, oral<br />

contraceptives) etc.<br />

• Non-occlusive (25%)<br />

– Mechanical (bowel obstruction)<br />

• (a) Strangulation <strong>of</strong> mesenteric veins<br />

• (b) Over-distension with subsequent compromise <strong>of</strong> the local mucosal microcirculation<br />

– Hypoperfusion/ Vasospasm<br />

• Ex. Shock (hemorrhagic, septic, cardiogenic), severe dehydration, IVDU, pheochromocytoma, familial<br />

dysautonomia etc.<br />

– Inflammatory<br />

• Ex. Pancreatitis, appendicitis, diverticulitis, peritonitis etc.<br />

– Vasculopathy<br />

• Ex. Vasculitis (i.e. young patients, unusual sites), diabetic vasculopathy, fibromuscular dysplasia etc.<br />

– Others<br />

• Ex. XRT, chemotherapy, immunosuppression, corrosive injury etc.


Pathology<br />

Etiologies: Occlusive<br />

IMA atherosclerosis


Pathology<br />

Etiologies: Occlusive<br />

SMA thromboembolism


Pathology<br />

Etiologies: Occlusive<br />

SMA Cholesterol embolus


Pathology<br />

Etiologies: Occlusive<br />

Aortic stent occlusion <strong>of</strong> IMA


Pathology<br />

Etiologies: Occlusive<br />

Polycythemia ruba vera


Pathology<br />

Etiologies: Non-occlusive<br />

Cardiogenic shock


Pathology<br />

Etiologies: Non-occlusive<br />

Lupus


<strong>CT</strong><br />

Technique: Ischemic <strong>Bowel</strong> Protocol<br />

3 Types <strong>of</strong> contrast<br />

(a) IV (150 cc via mechanical injector at a rate <strong>of</strong> 2-4 ml/sec)<br />

(b) Oral<br />

(c) Rectal<br />

NB: <strong>Bowel</strong> distension (i.e. assess bowel wall thickness)<br />

NB: Positive vs. negative contrast Positive contrast indicated in suspected bowel obstruction <strong>and</strong> advantageous for delineation <strong>of</strong><br />

inner mural layer in setting <strong>of</strong> hypoattenuating mucosa. Otherwise, negative contrast allows optimal delineation <strong>of</strong> mural layers.<br />

3 Phases<br />

(a) Unenhanced<br />

•Differentiating hyperattenuating bowel wall caused by hemorrhage from that caused by hyperperfusion<br />

•Background atherosclerotic disease<br />

•Hyperattenuating intravascular clot<br />

(b) Arterial (30 sec)<br />

•Arterial occlusion<br />

(c) Portovenous (90 sec)<br />

•Venous occlusion<br />

•Assessment <strong>of</strong> the remainder <strong>of</strong> the organs<br />

Triple contrast<br />

Triple phased<br />

Triple planar<br />

3 Planes<br />

(a) Axial<br />

(b) Coronal<br />

(c) Sagittal


<strong>CT</strong><br />

Findings: Spectrum<br />

• Wide range <strong>of</strong> <strong>CT</strong> findings, as expected given the…<br />

– range <strong>of</strong> clinical manifestations<br />

– range <strong>of</strong> severity<br />

– range <strong>of</strong> underlying etiologies<br />

– +/- intramural hemorrhage<br />

– +/- superinfection<br />

Example:<br />

Diffuse vs. Segmental<br />

<strong>Bowel</strong> wall thickening vs. thinning<br />

<strong>Bowel</strong> wall hypoattenuation vs. hyperattenuation<br />

Mucosal hyperenhancement vs. no hyperenhancement


<strong>CT</strong><br />

Findings: Approach<br />

• Distribution<br />

– Diffuse<br />

– Segmental<br />

1. Distribution<br />

2. <strong>Ischemia</strong> = wall thickening, fluid, air<br />

3. <strong>Infarction</strong> = dilatation, wall thinning, AFL<br />

4. Perforation<br />

• <strong>Ischemia</strong><br />

– <strong>Bowel</strong> wall thickening = hypo vs. hyperattenuating; differential wall enhancement<br />

– Fluid = fat str<strong>and</strong>ing, mesenteric edema, ascites<br />

– Air = pneumotosis, portomesenteric venous gas<br />

• <strong>Infarction</strong><br />

– Dilatation<br />

– <strong>Bowel</strong> wall thinning<br />

– Fluid-filled loops/ AFLs<br />

• Perforation<br />

– Pneumoperitoneum<br />

– Intralumenal contrast extravasation<br />

– Abscess<br />

– Peritonitis


<strong>CT</strong><br />

Findings: Distribution<br />

• i.e. may provide clues to etiology<br />

• (a) Diffuse<br />

• (b) Segmental<br />

– Vascular territories<br />

– Watershed areas


<strong>CT</strong><br />

Findings: <strong>Bowel</strong> Thickening<br />

• s/t mural edema, hemorrhage, superinfection<br />

• Most SN, least SP (for ischemia, NOT infarction)<br />

• Range <strong>of</strong> SN = 26-96%<br />

– (a) ischemic colitis = 94%<br />

– (b) mesenteric ischemia = 80%<br />

– (c) bowel infarction = 26-38%<br />

• Occlusive = non-occlusive<br />

• Venous >> Arterial<br />

• (a) Hypoattenuating vs. hyperattenuating<br />

– Hypoattenuation = edema<br />

– Hyperattenuation = hemorrhage<br />

• (b) Differential bowel wall enhancement<br />

– i.e. mucosal hyperenhancement<br />

– s/t hyperemia (i.e. reperfusion or superinfection)<br />

– SN 33% SP 71%<br />

– Produces target sign


<strong>CT</strong><br />

Findings: <strong>Bowel</strong> Thickening<br />

Edema<br />

Hemorrhage<br />

Bacterial superinfection<br />

Target sign


<strong>CT</strong><br />

Findings: Fluid<br />

• (a) Fat str<strong>and</strong>ing (mesenteric/ pericolonic)<br />

• (b) Mesenteric edema<br />

• (c) Ascites<br />

• NB: study <strong>of</strong> SN <strong>and</strong> SP in non-occlusive venous ischemia (i.e.<br />

venous congestion from bowel obstruction)<br />

– (a) Str<strong>and</strong>ing = SN 58%, SP 79%<br />

– (b) Edema = SN 88%, SP 90%<br />

– (c) Ascites = SN 75%, SP 94%<br />

– NB: 2+ = SP 94%


<strong>CT</strong><br />

Findings: Air<br />

• s/t dissection <strong>of</strong> intra-luminal air s/t loss <strong>of</strong> mucosal integrity<br />

• SP approach 100%<br />

• (a) Pneumotosis<br />

– Non-dependent locules<br />

– Dissecting wall<br />

• (b) Portomesenteric venous gas<br />

– Periphery <strong>of</strong> liver<br />

– Mesenteric vessels


<strong>CT</strong><br />

Findings: Air<br />

Pneumotosis<br />

Portal venous gas<br />

Mesenteric venous gas


<strong>CT</strong><br />

Findings: <strong>Infarction</strong><br />

• (a) <strong>Bowel</strong> dilatation<br />

• (b) <strong>Bowel</strong> wall thinning (i.e. paper thin)<br />

– s/t destruction <strong>of</strong> intramural nerves <strong>and</strong> muscles<br />

• (c) AFLs/ fluid-filled (i.e. gasless bowel)<br />

– Fluid exudation into the lumen<br />

• NB: SN <strong>of</strong> dilatation <strong>and</strong>/or AFL = 56-91% (vs. 40% in ischemia)


<strong>CT</strong><br />

Findings: Complications<br />

• Perforation<br />

– Pneumoperitoneum<br />

– Intralumenal contrast extravasation<br />

– Abscess<br />

– Peritonitis


Cases<br />

Case #1


Cases<br />

Case #1: Large bowel ischemia


Cases<br />

Case #2


Cases<br />

Case #2: Large bowel ischemia


Cases<br />

Case #3


Cases<br />

Case #3: Small bowel <strong>Ischemia</strong>


Cases<br />

Case #4


Cases<br />

Case #4: Small <strong>and</strong> large bowel infarction


Cases<br />

Case #5


Cases<br />

Case #5: Small bowel obstruction with ischemia <strong>and</strong> perforation


References<br />

• Wiesner W, et al. <strong>CT</strong> <strong>of</strong> acute bowel ischemia. Radiology 2003;<br />

226:635-650<br />

• Sung RE, et al. <strong>CT</strong> <strong>and</strong> MR imaging findings <strong>of</strong> bowel ischemia from<br />

various causes. Radiographics 200; 20:29-42


Cases<br />

1. 2678623 = large bowel ischemia<br />

1. 804200566 = large bowel ischemia<br />

2. 2319634 = small bowel ischemia<br />

3. 6270051 = small <strong>and</strong> large bowel infarction<br />

4. 3259333 = small bowel obstruction with ischemia <strong>and</strong> perforation<br />

5. 800131666 = ischemic small bowel post-laparotomy that is normal at surgery

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