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GI Ischemia
Three clinicopathologic patterns of ischemic injury:
Transient injury (hypotension, hypoperfusion):
the damage is usually confined to the mucosa and is
Acute ischemia (sudden thromboembolic occlusion of
the mesenteric arteriesis):
often fulminant - transmural necrosis may develop.
Chronic (recurrent) ischemia: mural fibrosis and


Clinical Features

Most cases in patients over age 50, with known cardiovascular

Rare cases involving younger patients:
Coagulation disorders
Long distance runners



Combined involvement of small and large

intestine is not infrequent.

A review of
over 1000
cases of




Symptoms may range from:

transient bloody diarrhea/abdominal pain

a full-blown surgical emergency due to an

infarcted bowel.
The reaction of the colon to ischaemia three phases:
(1) acute: haemorrhage and necrosis;
(2) reparative: granulation tissue
formation and fibrosis;
(3) residual pathology: ischaemic
stricture and chronic complications.

Pathologic Features
Gross examination:

sharp demarcation from

the adjacent unaffected bowel.
- patches of pale
- mucosal granularity
and erythema;
- areas of petechial
- superficial

With time: a more darkly and diffusely

congested and oedematous mucosa with a
cobblestone-type appearance.

Acute ischaemic necrosis of the colon: the mucosa is deeply

congested and coarsely
cobblestoned due to submucosal oedema and haemorrhage.

More involved cases of

- geographic areas of ulceration;
- pseudomembranes;
- marked submucosal edema.

Mucosal necrosis leads

to greenish grey
ulceration, which is
typically superficial.

When infarction of the colon involves only part

of the thickness of the wall, mucosal necrosis
may give rise to a shaggy white or grey membrane,
loosely adherent to the luminal surface.

Transmural necrosis may cause initial pallor,

followed by a black or a more congested and
haemorrhagic red/purple discoloration.
Perforation inflammatory peritoneal reaction may
then ensue.

With the formation of a stricture and the

disappearance of any acute changes, the
macroscopic picture may resemble a Crohns disease

- Submucosal edema can be prominent enough
to appear masslike;
- Most common location is splenic flexure
watershed zone. All other regions of
colorectum can be involved.
- Healed ischemic lesions may form strictures
that mimic CD.
Endoscopic appearance of
ischemic colitis showing
mucosal erythema, edema,
ulcerations, and
pseudomembrane formation.

Acute ischemic lesions of the colon:
- Mucosa with necrosis of the superficial portion
- Remaining crypts with atrophic or withered appearance cytologic atypia
In more severe cases only a shadowy outline of the normal histology remains, with socalled ghost outlines of crypts

- Paucity or complete absence of acute inflammatory cells

Fibrin thrombi within mucosal and submucosal capillaries are often found and are non-specific .

- Cryptitis and crypt abscesses can be present (usually not prominent)

- Hemorrhage into the lamina propria
- Hyalinization of the lamina propria (can be highlighted by trichrome stain)
- Sloughed necrotic mucosa may produce a microscopic appearance of a
With greater severity and duration of ischaemia: necrosis of the muscularis propria and
often of the subserosa with associated perforation and peritoneal inflammation.

Ischemic colitis: superficial mucosal erosion with withered atrophic

crypts. The lamina propria has a hyalinized appearance as well as
hemorrhage, a finding that is usually associated with ischemic colitis.

Trichrome-stained section shows blue staining of lamina propria in

hyalinized areas ,
allowing distinction of ischemia from CD colitis

A. Ischemic colitis: a hyalinized, smudgy-appearing lamina propria

with markedly regenerative crypt epithelium. Note that there is
very little inflammation yet the surface is sloughing.
B. Atrophic or withering crypts with nuclear atypia. Although this
atypia is regenerative, it can easily be misinterpreted as
dysplasia, if viewed out of context. The hyalinized lamina propria

Acute colonic ischaemia, showing dissolution of the

upper parts of the crypts. There is haemorrhage, oedema and a
mild acute inflammatory infiltrate.

The effects of acute ischaemia are followed by

subacute and chronic inflammation, with the
formation of granulation tissue and a mixed
population of acute and chronic inflammatory cells.
Capillary proliferation, macrophage activity and
fibroblast production complete the picture until the
mucosal epithelium begins to regenerate.
The presence of iron-positive granules in histiocytes
reflects previous haemorrhage in the submucosa
and mucosa, and can be useful in differentiating
ischaemia from inflammatory bowel disease.
Epithelial cell regeneration is visible at the margin of
the mucosal ulcers.

The chronic phase of ischemia

may be difficult to diagnose because
the only histologic findings may be:
- submucosal fibrosis;
- stricture formation.

Differential diagnosis
Enteric Bacterial Infectious

Enterohemorrhagic Escherichia coli

Clostridium difficile (pseudomembranous colitis)
Clostridium perfringens
Clostridium septicum (neutropenic enterocolitis)

Acute and chronic radiation colitis

Collagenous colitis
Colonic amyloidosis
Inflammatory bowel disease

C. difficile
Certain phases of C. difficileinduced
pseudomembranous colitis can mimic ischemic
- Early lesions: the presence of a volcanic (eruptive)
inflammatory exudate;
- late (type II or III) lesions: characterized by
mucosal necrosis and the presence of a
necroinflammatory pseudomembrane that can
mimic ischemic colitis.

CD: Diffuse mucosal erythema with plaques

of yellow exudate.

E. coli Enterohemorrhagic
Toxin-mediated infectionnumerous fibrin thrombi
ischemic-appearing lesion with pseudomembranes
Especially in the right colon
Acute hemorrhagic (infectious) colitis may mimic
- Relative preservation of mucosal integrity and
without withering (attenuated) crypts;
- Intramucosal hemorrhage;
- Capillary fibrin thrombi (especially in the early
stages of infection, before significant infiltration of
neutrophils has occurred).

C. perfringens

Toxins produced by C. perfringens coagulative necrosis of the

mucosa that mimics acute ischemia (enteritis necroticans)

Coagulative necrosis;
Scant or negligible neutrophilic exudate;
Surface colonization by clostridial organisms;
Intestinal pneumatosis.

Clinically, the rapid development of toxemia and multiorgan failure

helps distinguish this condition from ischemic colitis.

Granular surface of small bowel

mucosa with flecks of yellow exudate.

Dense colonization of surface by

gram-positive bacilli (Brown-Hopps

C. septicum
Neutropenic enterocolitispatients who are
neutropenic, commonly because of chemotherapy.
Toxins produced by C. septicum coagulative necrosis
of the mucosa and submucosa, mimicking ischemia.

Mucosa with:
Coagulative necrosis;
Marked edema;
The absence of an acute inflammatory reaction.

Collagenous colitis

Collagenous colitis:
Detachment of the surface epithelium
A thickened and irregular subepithelial collagen band (can mimic
ischemia-related hyalinosis)

In contrast to ischemia, collagenous colitis is characterized by:

A dense mononuclear infiltrate in the lamina propria;
Increased intraepithelial lymphocytes;
Positive IHC staining for type III collagen.

Clinically: nonbloody, watery diarrhea and overwhelmingly female.

A trichrome stain can often help distinguish true fibrosis in cases of

collagenous colitis (positive) from hyalinosis related to ischemic
colitis (negative).

Colonic amyloidosis
Amyloid deposition in the lamina propria can
mimic ischemia-related hyalinosis.
A Congo red, Sirius red, or crystal violet stain: to
highlight the presence of amyloid.
- NO crypt or surface epithelial injury.
- vascular involvement by amyloidosis
superimposed ischemic colitis as a result of the
underlying vascular pathologic process.

Prognosis and Therapy

The prognosis depends on:
-etiology of the
- the severity of the

1/3 of cases are mild and transient

(simple supportive care), whereas
1520% may require surgery
mortality rate of up to 60%.

Treatment is entirely dependent on

- Acuteness;
- Severity of the

In more severe cases:

- Decompression of a distended colon;
- Empiric broad-spectrum antibiotics

Surgical pathology of the GI tract, liver, biliary tract
and pancreas, Robert D. Odze, John R. Goldblum,
second edition, Saunders Elsevier
Surgical pathology of the GI tract, liver, biliary tract
and pancreas, Robert D. Odze, John R. Goldblum,
thirth edition, Saunders Elsevier
Morson and Dawsons Gastrointestinal Pathology,
Neil Sheperd, Bryan Warren, Geraint Williams, Joel
Greenson, Gregory Lauwers and Marco Novelli, fifth
edition, 2013