Chapter17: INTESTINES: Ischemic Bowel Disease

Question 1

The majority of the GI tract is supplied by the what arteries?

Answer 1

• celiac,
• superior mesenteric, and
• inferior mesenteric arteries

Question 2

What happens as the GIT arterial blood supply As they approach the intestinal wall?

Answer 2

the superior and inferior mesenteric arteries ramify into the mesenteric arcades.

Question 3

What makes it possible for the small intestine and colon to tolerate slowly progressive loss of the blood supply
from one artery?

Answer 3

• *Interconnections between arcades**, as well as
• *collateral supplies from the proximal celiac and distal pudendal and iliac circulations.**

In contrast, acute compromise of any major vessel can lead to infarction of
several meters of intestine.

Question 4

The damage in the any major vessel in the intestinal blood supply can result to what?

Answer 4

• Damage can range from mucosal infarction, extending no deeper than the muscularis mucosa;
• to mural infarction of mucosa and submucosa;
• to transmural infarction involving all three wall layers.

Question 5

While mucosal or mural infarctions are often secondary what?

Answer 5

to acute or chronic hypoperfusion

Question 6

Transmural infarction is generally caused by what?

Answer 6

acute vascular obstruction.

Question 7

Important causes of acute arterial obstruction includewhat?

Answer 7

• severe atherosclerosis (which is often prominent at the origin of mesenteric vessels),
• aortic aneurysm,
• hypercoagulable states,
• oral contraceptive use, and
• embolization of cardiac vegetations or
• aortic atheromas.

Question 8

What are the other cause that can result to intestinal hypoperfusion?

Answer 8

• cardiac failure, shock , dehydration, or vasoconstrictive drugs.
• Systemic vasculitides, such as polyarteritis nodosum, Henoch-Schönlein purpura, or Wegener granulomatosis, may also damage intestinal arteries.
• Mesenteric venous thrombosis, which can also lead to ischemic disease, is uncommon but can result from inherited or acquired hypercoagulable states, invasive neoplasms, cirrhosis, trauma, or abdominal masses that compress the portal drainage.

Question 9

Intestinal responses to ischemia occur in two phases.

Answer 9

1. The initial hypoxic injury occurs at the onset of vascular compromise. While some damage occurs during this phase, the epithelial cells lining the intestine are relatively resistant to transient hypoxia.
2. The second phase, reperfusion injury, is initiated by restoration of the blood supply and it is at this time that the greatest damage occurs. In severe cases this may trigger multiorgan failure. While the underlying mechanisms of reperfusion injury are incompletely understood, they involve free radical production, neutrophil infiltration, and release of inflammatory mediators, such as complement proteins and TNF ( Chapter 1 ). Activation of intracellular signaling molecules and transcription factors, including hypoxia-inducible factor 1 (HIF-1) and NF-κB, also contribute to intestinal ischemia-reperfusion injury.

Question 10

The severity of vascular compromise, the time frame during which it develops, and the vessels
affected are the major variables in ischemic bowel disease.

Two aspects of intestinal vascular
anatomy also contribute to the distribution of ischemic damage.

Answer 10

1. Intestinal segments at the end of their respective arterial supplies are particularly susceptible to ischemia.
2. Intestinal capillaries run alongside the glands, from crypt to surface, before making a
   hairpin turn at the surface to empty into the post-capillary venules

Question 11

Intestinal segments at the end of their respective arterial supplies are particularly susceptible to ischemia. These watershed zones include what?

Answer 11

• the splenic flexure,
  
  • where the superior and inferior mesenteric arterial circulations terminate, and,
• to a lesser extent, the sigmoid colon and rectum
  
  • where inferior mesenteric, pudendal, and iliac arterial circulations end.

Generalized hypotension or hypoxemia can therefore cause localized injury, and ischemic disease should be considered in the differential diagnosis of focal
colitis of the splenic flexure or rectosigmoid colon.

Question 12

Intestinal capillaries run alongside the glands, from crypt to surface, before making a hairpin turn at the surface to empty into the post-capillary venules.

This allows
oxygenated blood to supply cryptsbut _leaves the surface epithelium vulnerable to
ischemic injury._

What is the significance of this anatomy?

Answer 12

This anatomy protects the crypts, which contain the epithelial stem cells
that are necessary to repopulate the surface.

Thus, surface epithelial atrophy, or even
necrosis and sloughing, with normal or hyperproliferative crypts is a morphologic
signature of ischemic intestinal disease.

Question 13

What is the morphologic signature of ischemic intestinal disease?

Answer 13

Intestinal capillaries run alongside the glands, from crypt to surface, before making a hairpin turn at the surface to empty into the post-capillary venules.

This _allows
oxygenated blood to supply crypts_but leaves the surface epithelium vulnerable to ischemic injury.

This anatomy protects the crypts, which contain the epithelial stem cells that are necessary to repopulate the surface.

Thus, surface epithelial atrophy, or even
necrosis and sloughing, with normal or hyperproliferative crypts is amorphologic
signature of ischemic intestinal disease.

Question 14

Despite the increased susceptibility of watershed zones,what may involve any level of the gut from stomach to anus?

Answer 14

mucosal and mural infarction

The lesions may be continuous but are more often segmental and patchy ( Fig. 17-24A ).

The mucosa is hemorrhagic and may be ulcerated and dark red or purple as a result of luminal hemorrhage (
Fig. 17-24B ).

The bowel wall is also thickened by edema that may involve the mucosa or extend into the submucosa and muscularis propria.

When severe, there is extensive mucosal
and submucosal hemorrhage and necrosis, but serosal hemorrhage and serositis are
generally absent

Question 15

When can substantial portions of the bowel are generally involved?

Answer 15

in transmural infarction due to acute arterial obstruction.

For reasons described above, the splenic flexure is the site at greatest risk.

The demarcation between normal and ischemic bowel is sharply defined and the infarcted bowel is initially intensely congested and dusky to purple-red.

Later, blood-tinged mucus or frank blood accumulates in the lumen and the wall becomes edematous, thickened, and rubbery.

There is coagulative necrosis of the muscularis propria within 1 to 4 days, and perforation may occur.

Serositis, with purulent exudates and fibrin deposition, may be prominent.

Question 16

In transmurahl infarction, why is the splenic flexure at greatest risk?

Answer 16

watershed zones include the splenic flexure, where the superior and inferior mesenteric arterial circulations terminate

. For reasons described above, the splenic flexure is the site at greatest risk.

Question 17

What happens in mesenteric venous thrombosis?

Answer 17

arterial blood continues to flow for a time, resulting in a less abrupt transition from affected to normal bowel.

However, propagation of the thrombus may
lead to secondary involvement of the splanchnic bed. The ultimate result is similar to that
produced by acute arterial obstructionbecauseimpaired venous drainage eventually
prevents oxygenated arterial blood from entering the capillaries

Question 18

Microscopic examination of ischemic intestine it demonstrates what?

Answer 18

demonstrates atrophy or sloughing of
surface epithelium ( Fig. 17-24C ).

In contrast, crypts may be hyperproliferative.
Inflammatory infiltrates are initially absent in acute ischemia, but neutrophils are recruited within hours of reperfusion.

Chronic ischemia is accompanied by fibrous scarring of the lamina propria ( Fig. 17-24D ) and, uncommonly, stricture formation.

In acute phases of ischemic damage bacterial superinfection and enterotoxin release may induce pseudomembrane formation that can resemble Clostridium difficile–associated pseudomembranous colitis (discussed later).

Question 19

In acute phases of ischemic damage bacterial superinfection and enterotoxin release may induce what?

Answer 19

pseudomembrane formation that can resemble Clostridium difficile–associated pseudomembranous colitis (discussed later).

Question 20

Answer 20

FIGURE 17-24 Ischemia.

• A, Jejunal resection with dusky serosa.
• B, Mucosa is stained with blood after hemorrhage.
• C, Characteristic attenuated villous epithelium in this case of acute jejunal ischemia.
• D, Chronic colonic ischemia with atrophic surface epithelium and fibrotic lamina propria

Question 21

Ischemic bowel disease tends to occur in what?

Answer 21

.

older individuals with coexisting cardiac or vascular
disease

.

Question 22

Acute transmural infarction typically presents with what?

Answer 22

• sudden, severe abdominal pain and tenderness,
• sometimes accompanied by nausea, vomiting, bloody diarrhea, or grossly melanotic stool.
• Patients may progress to shock and vascular collapse within hours as a result of blood loss.
• Peristaltic sounds diminish or disappear, and muscular spasm creates board-like rigidity of the abdominal wall.

Question 23

Why does in Acute transmural infarction the diagnosis of intestinal necrosis may be delayed or missed, with disastrous consequences?

Answer 23

Because these physical signs overlap with those of other abdominal emergencies, including:

• acute appendicitis,
• perforated ulcer,
• and acute cholecystitis,

the diagnosis of intestinal necrosis may be delayed or missed, with disastrous consequences.

As the mucosal barrier breaks down, bacteria enter the circulation and sepsis can develop;
mortality may exceed 50%.

The overall progression of ischemic enteritis depends on the underlying cause and severity of injury

Question 24

The overall progression of ischemic enteritis depends on the underlying cause and severity of injury.

Answer 24

• Mucosal and mural infarctions
• Chronic ischemia
• CMV infection
• Radiation enterocolitis
• Necrotizing enterocolitis (NEC)

Question 25

Describe Mucosal and mural infarctions

Answer 25

• by themselves may not be fatal.
• However, these may progress to more extensive infarction if the vascular supply is not restored by correction of the insult or, in chronic disease, by development of adequate collateral supplies.

Question 26

Why does the diagnosis of nonocclusive ischemic enteritis and colitis can be particularly difficult?

Answer 26

because there may be a confusing array of nonspecific abdominal symptoms, including
intermittent bloody diarrhea and intestinal pseudo-obstruction.

Question 27

Chronic ischemia may masquerade as what?

Answer 27

inflammatory bowel disease, with episodes of
bloody diarrhea interspersed with periods of healing.

Question 28

CMV infection causes ischemic GI disease due what?

Answer 28

to the viral tropism for and infection of endothelial cells.

CMV infection, which can be a complication of immunosuppressive therapy, is discussed further in Chapter 8

Question 29

CMV infection, which can be a complication of what?

Answer 29

immunosuppressive therapy,

Question 30

When does Radiation enterocolitis occurs?

Answer 30

when the GI tract is irradiated.

In addition to epithelial
damage, radiation-induced vascular injury may be significant and produce changes that
are similar to ischemic disease.

In addition to clinical history, the presence of bizarre
“radiation fibroblasts”within the stroma may provide animportant clue to the etiology.
Acute radiation enteritis manifests as anorexia, abdominal cramps, and a malabsorptive
diarrhea, while chronic radiation enteritis or colitis is often more indolent and may
present as an inflammatory colitis

Question 31

What is an important clue to the etiology to Radiation enterocolitis?

Answer 31

In addition to clinical history, the presence of bizarre
“radiation fibroblasts” within the stroma may provide an important clue to the etiology.

Question 32

What is the manifestation of Acute radiation enteritis?

Answer 32

manifests as anorexia, abdominal cramps, and a malabsorptive
diarrhea,

Question 33

What is the manifestation of chronic radiation enteritis or colitis

Answer 33

is often more indolent and may
present as an inflammatory colitis

Question 34

What is Necrotizing enterocolitis (NEC) ?

Answer 34

is an acute disorder of the small and large intestines that can result in transmural necrosis.

It is the most common acquired GI emergency of
neonates, particularly those who are premature or of low birth weight, and occurs most
often at the time of oral feeding.

NEC is discussed in more detail in Chapter 10 , but is
noted here because ischemic injury is generally considered to contribute to the
pathogenesis