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Colonic Arteriovenous Shunt
Fig. 13.7 Visible vessel on the base of a diverticulum.
Sigmoid Colon Srs Visible

Fig. 13.8 Visible vessel.

a Visible vessel, protruding near the edge of a small diverticulum. b Closed with a hemoclip (Olympus).

Fig. 13.8 Visible vessel.

a Visible vessel, protruding near the edge of a small diverticulum. b Closed with a hemoclip (Olympus).

Fig. 13.9 Adherent clot on a diverticular orifice. An open diverticular orifice is visible next to this
Paciente Con Cancer Estomago
Fig. 13.10 Clot, inside a diverticulum, but not adherent. Unlike an adherent clot (Fig. 13.9), it can be easily washed off.

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Adherent Clot

Fig. 13.11 Blood clot on a diverticulum.

a Adherent clot on a diverticulum, not removable with irrigation.

b, c Needle injection of epinephrine

(1:10 000) into the wall of the diverticular orifice.

d The orifice is swollen afterward and the mucosa is whitish in color from the vaso-constrictive effect of the epinephrine. The clot was subsequently removed by irrigation.

Fig. 13.11 Blood clot on a diverticulum.

a Adherent clot on a diverticulum, not removable with irrigation.

b, c Needle injection of epinephrine

(1:10 000) into the wall of the diverticular orifice.

d The orifice is swollen afterward and the mucosa is whitish in color from the vaso-constrictive effect of the epinephrine. The clot was subsequently removed by irrigation.

Table 13.2 Localization of bleeding sites in emergency colonoscopy (n = 282 patients) (based on reference 36)

Bleeding site

Frequency in %

Rectum

15.1

Sigmoid colon

15.1

Descending colon

19.7

Transverse colon

12.7

Ascending colon

15.1

Cecum

2.6

Terminal ileum

1.7

right hemicolon (Tab. 13.2) and, second, insertion up to the terminal ileum can help determine whether blood is flowing from above, a clear indication of a more proximal bleeding site. Ohyama et al. (36) report that even under conditions of urgent colonoscopy, the cecum was inspected in 56% of patients and that terminal ileum insertion was achieved in 27 % of patients.

For diagnosing hemorrhoidal bleeding or locating a bleeding site in the anorectal region, it is important to inspect the anal transitional zone with a retroflexed instrument. Proctoscopy (anoscopy) can also be performed, if necessary.

Diagnostic yield for urgent colonoscopy in acute lower gastrointestinal bleeding is reported in the literature at 48-90% (3,38,63). Two recent publications report diagnostic yields of 89-97 % (13,36), which perhaps is a reflection of more consistent use of urgent colonoscopy.

The frequency of colonic bleeding source reported varies from one publication to the next. One reason could be that studies often fail to differentiate between probable and definite sources of bleeding. In addition, the definition of acute lower gastrointestinal bleeding is far from uniform. Moreover, differences in patients' overall health statuses also certainly play a role (Tab. 13.3). Table 13.4 provides an overview of the frequencies of bleeding sources cited in the literature. Age can provide a clue to the cause of acute lower gastrointestinal bleeding: younger patients tend to bleed from hemorrhoids, vascular malformation, and rectal ulcers, while older patients tend to bleed from diverticula, vascular malformation, and neoplasias.

In the diagnostic report, the examiner should make clear whether diagnosis of the bleeding source is definite or probable. Only if there are clear indications of active or prior bleeding (Tab. 13.5) should the finding be reported as a bleeding source. Therapy is only indicated when the bleeding source can be clearly identified. Reported figures for endoscopic interventions range between 3 % and 62 %. Success rates of endoscopic therapy in urgent colonoscopy are currently around 70 %. The rate of complications is low for colonoscopy in acute lower gastrointestinal bleeding (1.3%) (overview in 63).

Table 13.3 Comparison of results of emergency colonoscopy in acute lower gastrointestinal bleeding among patients in intensive care units with a control group (recently hospitalized inpatient patients) (40)

■ Differential Diagnosis of Acute Lower Gastrointestinal Bleeding

Diverticula

Diverticula are the reported source of gastrointestinal bleeding in 17-40% of patients (Tab. 13.4). An estimated 3-5% patients with colonic diverticula experience bleeding once in their lifetime. However, the correlation may not always be causal since diverticula are often cited as the bleeding source in the colon for lack of evidence of another source.

Table 13.3 Comparison of results of emergency colonoscopy in acute lower gastrointestinal bleeding among patients in intensive care units with a control group (recently hospitalized inpatient patients) (40)

Diagnosis

Noninten-

Intensive-

sive-care

care unit

unit patients

patients

(n = 77)

(n = 12)

Diverticula

38 %

17%

Ischemic colitis

13%

50%

Angiodysplasia

6%

8%

Postpolypectomy rebleeding

6%

-

Rectal ulcer

5%

8%

NSAID colitis

5%

8%

Carcinoma

4%

-

Misc.

22 %

1%

Table 13.4 Overview of the distribution of sources of hematochezia reported in the literature (compiled based on reference 61)

Source of hematochezia

Frequency (%%)

Diverticula

17-40

Arteriovenous malformation

2-30

Colitis (ischemic, infectious, chronic inflammatory bowel disease, radiation colitis)

9-21

Neoplasias, postpolypectomy bleeding

11-14

Anorectal sources (incl. hemorrhoids, rectal varices)

4-10

Upper gastrointestinal tract bleeding (incl. ulcers, varices)

0-11

Small bowel (incl. Crohn disease, arteriovenous malformation, Meckel diverticula, tumors)

2-9

A recent study identified colon diverticula as the bleeding source in 22 % of patients with acute lower gastrointestinal bleeding, whether based on active bleeding (Figs. 13.2,13.3), or based on stigmata such as visible vessels (Figs. 13.5-13.8) or adherent clots (Figs. 13.9-13.11) (30). This study also showed that findings on stigmata identified as related to an increased risk for rebleeding peptic ulcers could also be applied to diverticular bleeding. Among patients in the group in which bleeding source was actively treated with endoscopic therapy (Figs. 13.2-13.5, 13.813.11), there was no rebleeding, compared with 53 % of those who did not undergo endoscopic intervention. Epinephrine injection and bipolar coagulation were used.

Table 13.5 Diagnostic criteria for urgent colonoscopy

Definite criteria for a bleeding source in the large intestine in urgent colonoscopy

► Active bleeding from a lesion

► Nonbleeding visible vessel

► Adherent clot

Stigmata of bleeding in the colon or in a particular colon segment

► Fresh blood in a colon segment

► Ulceration on a diverticulum with fresh blood in surrounding area

► No sign of fresh blood in the terminal ileum

These excellent results are contradicted, however, by another current study (8) in which a retrospective analysis of diverticular bleeding was conducted. Using the same endoscopic intervention measures, this study found earlier rebleeding in 38 % of patients and late rebleeding in 23 %. At first glance, the results of these two studies appear contradictory. Yet, a closer look reveals that Jensen et al. (30) consistently advise their patients to discontinue use of nonsteroidal anti-inflammatory drugs and acetylsalicylic acid and to follow a high-fiber diet. It is therefore entirely possible that these additional factors help explain differing results and that nonendoscopic factors also play an important role in treatment outcome.

Endoscopic therapy methods. There is no consensus on which therapeutic measure offers the most optimal treatment for diverticular bleeding. Systematic comparative studies are lack-

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Fig. 13.12 Oval erosion (arrow) with fibrinous exudate on the edge of a diverticulum, protruding into the diverticulum neck.

Fig. 13.13 Small, round, erosion with fibrinous exudate on the base ("dome") of a diver-ticulum.

■ w ing and publications on the principles of endoscopic therapy tend to have a casuistic character. Studies have reported on the success of injection therapy (Figs. 13.2,13.11) using epinephrine and fibrin glue, as well as thermocoagulation by means of laser, heater probes, and bipolar coagulation. An interesting report has also been written on mechanical hemostasis of diverticular bleeding using hemoclips (27) (Figs. 13.4,13.5,13.8).

Endoscopic therapy

► As a rule, the methods used for achieving endoscopic he-mostasis must be adapted individually. The size of diverticula and exact localization of bleeding relative to the diverticulum opening are important factors. It is also important to remember that the diverticulum wall is very thin and that thermocoagulation thus is associated with an increased risk of perforation.

► If the diverticulum itself is the source of bleeding, epinephrine solution (1:10000) can be injected into the sub-mucosa of the four quadrants of the diverticulum neck. In addition to the vasoconstrictive effect of epinephrine, compression of the supplying vessel also assists in achieving hemostasis. Alternatively, if the vessel or bleeding source is localized in a wider diverticulum, epinephrine injection can be made directly into the mucosa of the tip of the diverticulum, which occasionally elevates the bleeding source, enabling better visualization of the source.

Adherent clots should be injected with epinephrine solution (Fig. 13.11) and carefully removed, in order to evaluate the underlying lesion better. This can be done either with a powerful blast of water or carefully with a snare. If bleeding is localized at the edge of the diverticulum, thermocoagulation may also be used. Laser is less suitable since the depth of coagulation is difficult to calculate. When using a bipolar coagulation probe, it is important that power be kept as low as possible (10-15 W) and that each application be brief (one second). A balance should be achieved in terms of applying pressure with the probe: on the one hand, the greater the pressure, the better the vessel is sealed, while on the other hand, greater pressure also increases coagulation depth and thus perforation risk (32)

In the midst of the discussion on optimal endoscopic treatment of diverticular bleeding, one should keep in mind that spontaneous cessation of bleeding occurs in over two-thirds of diverticular bleeding cases and that rebleeding occurs frequently in the course of disease. In one study (34) the risk of rebleeding was 9% in the first year, 10% in the second year, 19% in the third year, and 25% in the fourth year.

Pathogenesis of diverticular bleeding. Diverticular bleeding characteristically occurs when a vessel ruptures either near the tip of the diverticulum or in the diverticulum neck on the side opposite the mesentery. The blood vessels near the diverticulum are located very close to the surface, separated only by a thin layer of mucosa from the lumen. Foutch (23) made an important observation when he noted the presence of ulcerations near bleeding diverticula. The pathogenesis of these ulcers or erosions (Figs. 13.12, 13.13), which may erode surface vessels, remains unclear. It has often been suggested that they are caused by mechanical lesions from coproliths or digestive material, though there is lacking evidence to support this explanation. Another possibility is chemically induced ulcerating lesions. As early as 1990, Wilson et al. (58) reported that use of nonsteroidal anti-inflammatory drugs could promote myriad complications related to diverticular disease of the colon. Foutch's observations (23) point in the same direction.

In the western hemisphere, diverticula appear mostly in the left hemicolon, especially in the sigmoid colon (up to 90%). Yet, for unexplained reasons, it is diverticula in the right hemicolon that have a greater bleeding tendency. One hypothesis suggests that mucosal lesions induced by use of nonsteroidal anti-inflammatory drugs occur more frequently in the right hemicolon (41).

|T| 13.1 Angiodysplasia bleeding

|T| 13.1 Angiodysplasia bleeding

Bleeding, starshaped angiodysplasias in ascending colon. Note the clearly dilated veins resulting from the arteriovenous shunt.

b Bleeding angiodysplasia, located in the cecum opposite the Bauhin valve.

c Extensive angiodysplasia in ascending colon. In addition to numerous angiodysplasias in the ascending colon, the 68-year-old patient had similar, smaller, arteriovenous malformations in the small intestine.

Bleeding, starshaped angiodysplasias in ascending colon. Note the clearly dilated veins resulting from the arteriovenous shunt.

b Bleeding angiodysplasia, located in the cecum opposite the Bauhin valve.

c Extensive angiodysplasia in ascending colon. In addition to numerous angiodysplasias in the ascending colon, the 68-year-old patient had similar, smaller, arteriovenous malformations in the small intestine.

d e f d-f Angiodysplasia in ascending colon (d). Coagulation with APC (Erbe) (e). Afterward, angiodysplasia was no longer detected, and coagulated mucosa is in its place (f).

d e f d-f Angiodysplasia in ascending colon (d). Coagulation with APC (Erbe) (e). Afterward, angiodysplasia was no longer detected, and coagulated mucosa is in its place (f).

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