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Vascular Causes

Angiodysplasias. Angiodysplasias (a 13.1) are cited as the source of lower gastrointestinal bleeding in up to 30% of patients, though a rate of 3-12% is probably more realistic (64).

The majority of angiodysplasias (62%) are located in the right hemicolon, often occurring several at a time. The vast majority of affected individuals do not bleed (22, 42) and therapy is not always indicated for every angiodysplasia detected by colonoscopy. In addition, an angiody-splasia detected during urgent colonoscopy is not automatically the source of bleeding. The angiodysplasia must either be clearly actively bleeding (0 13.1a, b) or have stigmata such as adherent clots or submucosal bleeding.

The risk of rebleeding after an initial, untreated bleeding episode is high and increases over the years. In a study by Richter et al. (42) the risk of rebleeding increased from 26 % in the first year to 46% after three years. Prognosis is especially poor for an-giodysplasias related to hereditary hemorrhagic telangiectasia (Osler-Rendu-Weber disease). After endoscopic therapy of these vascular malformations, rebleeding occurs almost as a rule (46). The reason is perhaps that the entire lower gastrointestinal tract is usually affected.

It is not clear why angiodysplasias bleed. However, histo-logical analyses reveal mucosal thinning underneath the an-giodysplasia and occasional ulcerations (4). Nonsteroidal anti-inflammatory drugs and acetylsalicylic acid can play a role in pathogenesis.

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Fig. 13.14 Bleeding in ulcerating radiation proctitis. The 65-year-old patient had undergone radiation therapy for prostate cancer. Histology was compatible with radiation damage; there was no evidence of infiltration of the prostate carcinoma in the rectum.

Fig. 13.16 Bleeding per rectum caused by previous radiation therapy for prostate cancer. Reddened mucosa and neovascularization. An ulcer resulting from radiation-induced inflammation (covered with fibrinous exudate) can also be seen.

Fig. 13.15 Bleeding angiodysplasias in the rectum of a 75-year-old female patient. The angiodysplasia was caused by radiation therapy of an endometrial carcinoma.

Fig. 13.16 Bleeding per rectum caused by previous radiation therapy for prostate cancer. Reddened mucosa and neovascularization. An ulcer resulting from radiation-induced inflammation (covered with fibrinous exudate) can also be seen.

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Endoscopic therapy

► It is important to avoid use of opiates (10, 19) and cold-water lavage of the mucosa (9) during colonoscopy as they reduce blood flow in the mucosa, decreasing diagnostic yield in angiodysplasia.

► Endoscopic therapy employs various methods of thermocoagulation. Successful use of heater probes, monopolar and bipolar probes, Nd:YAG laser, and argon plasma coagulation (APC) has been reported.

► Three things should be noted with regard to practical application of thermocoagulation: First, as little power as necessary should be used, especially in the cecum and ascending colon and each application should be brief in order to limit depth of coagulation and avoid perforation. Laser coagulation in these regions is not without risks (46). Second, larger vascular malformations should be coagulated around their periphery and the supplying vessel should be obliterated if possible. Not until after this has been done can the center of the angiodysplasia be treated. Contact thermocoagulation procedures involve a risk of bleeding as adherent tissue can be torn on withdrawal of the probe from the coagulated area. Non-contact procedures, such as APC, have a distinct advantage in this regard.

Radiation proctitis. Radiation proctitis due to radiation therapy of small tumors in the pelvis (Figs. 13.14, 13.26-13.28) can also lead to blood loss, but bleeding generally does not present a problem. A more serious problem is neovasculariza-tion resulting from tissue ischemia in radiation-induced en-darteritis obliterans (Figs. 13.15-13.17). This can lead to considerable morbidity from recurrent blood loss. Following radiation therapy of prostate cancer, 13% of patients report more or less pronounced rectal blood loss over a period of 4-41 months (55). Another publication has reported a lower rate of 4%; Crook et al. (18) reported that 5% of patients who underwent radiation therapy complained of daily blood loss and 9% of weekly bleeding. Resulting anemia can become problematic.

Chronic radiation injury usually presents endoscopi-cally with multiple telangiectasias (Fig. 13.17) often extending into the anal canal. The mucosa is pale, lacking vessels, and vulnerable. In severe cases, there can also be ulcerations (Figs. 13.14, 13.16, 13.26) and massive hemorrhage.

Endoscopic therapy

► As with other angiodysplasias endoscopic thermocoagulation has proved effective. A study of 18 men and four women demonstrated that, among contact procedures, bipolar probes and heater probes were equally successful (29). After four sessions, the frequency of heavy rectal bleeding decreased from 75% to 33% among those treated with a bipolar probe and from 67 % to 11 % among those treated with a heater probe. No complications were observed.

► There are a number of reports on laser use for these indications. Lasers included KTP lasers (53), argon lasers (54), and Nd:YAG lasers (28, 56). Laser therapy is also successful in significantly reducing the number of bleeding episodes and transfusions. The frequency of complications reported in these studies was between 0-9 %. In order to avoid perforation, energy delivery should be as low as possible (Nd:YAG laser e.g., < 30 W) and the length of the pulse as short as possible (e.g., one second).

► A recent and promising therapy option is (noncontact) argon plasma coagulation. Its success in radiation-induced vascular malformation in the rectum has been

Fig. 13.17 Neovascularization in rectum.

View of rectum (retroflexed instrument) with a view of the upper margin of the anus and the instrument shaft. Marked neovascu-larization can be seen, partly affecting the anal region. This is also a delayed effect of radiation for prostate carcinoma. Bleeding ceased after thermocoagulation of the an-giodysplasias using APC.

Fig. 13.17 Neovascularization in rectum.

View of rectum (retroflexed instrument) with a view of the upper margin of the anus and the instrument shaft. Marked neovascu-larization can be seen, partly affecting the anal region. This is also a delayed effect of radiation for prostate carcinoma. Bleeding ceased after thermocoagulation of the an-giodysplasias using APC.

Portal Hypertension Nursing

Fig. 13.19 Rectal varices in a 31-year-old man with portal hypertension associated with liver cirrhosis resulting from sclerosing cholangitis.

Fig. 13.18 Spurting hemorrhage from a rectal varix. The 35-year-old patient had portal hypertension as a result of alcoholic liver cirrhosis.

Fig. 13.19 Rectal varices in a 31-year-old man with portal hypertension associated with liver cirrhosis resulting from sclerosing cholangitis.

repeatedly reported (16, 21, 47-49). The setting used for coagulation varied in these reports. Reported rates of argon gas flow were 0.6-3 L/min and electrical power ranged from 40-70 W. It should be noted that only the endoscopist who reported complications (rectal strictures) had used the highest power setting (70 W) (47). Thus, it is apparently advisable to keep energy delivery as low as possible. Gas flow should also be kept low because of the rigidity of the rectal wall in patients with radiation damage, which lowers compliance (flexibility). Success rates for APC are good. In most cases reduced rectal bleeding and increased hemoglobin levels are reported, though complete relief of symptoms can only be achieved among a minority of patients. Endo-scopic therapy must be repeated due to new formation of telangiectasias.

Colon varices. Bleeding from colon varices (Figs. 13.18,13.19) in patients with portal hypertension is not uncommon.

In the vast majority of cases, varices are limited to the rectum, where they present as tortuous gray-blue lesions running perpendicular to the folds. If only briefly glimpsed, they can be confused with solid polypoid structures, especially in situations involving acute bleeding, obscuring visualization. The risk of bleeding is 8-9%.

Endoscopic therapy

► Endoscopic therapy options include (based on treatment of varices in the upper gastrointestinal tract) sclerother-apy, band ligation, and intravariceal injection of acrylic glue.

Ectasia Colon
Fig. 13.20 Vascular ectasia in ascending colon in a patient with Turner syndrome. The patient was suffering from extreme lower gastrointestinal hemorrhage.

► In principle, choice of therapy depends on the actual situation and one's own experience. Based on our own experience with rubber band ligation, this method is not advisable.

Vascular ectasia. Vascular ectasia in the colon without portal hypertension (also called phlebectasia) is uncommon. It is described in conjunction with cavernous hemangiomas in Turner's syndrome (Fig. 13.20). In our own clinical files, such a case led to severe lower gastrointestinal rebleeding. The vascular ectasias were primarily in the cecum, ascending colon, and transverse colon.

Endoscopic therapy

► Despite reports on endoscopic therapy of cavernous hemangiomas (1,25), the safety of endoscopic intervention remains unclear. A further endoscopic therapy option is injection of sclerosing agents, similar to procedures for skin hemangiomas (59).

► The therapy of choice for larger cavernous hemangiomas thus remains surgical intervention.

- |T] 13.2 Bleeding from a Dieulafoy ulcer in the intestine -

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