particularly in patients who are massively bleeding or in whom colonoscopy was unrevealing or

incomplete. Characteristic angiographic findings include a densely opacified and slowly emptying,

dilated, tortuous vein (found in 90% of patients), a vascular tuft (seen in 66% to 75% of patients), and

an early-filling vein (usually a segmental vein in the cecum or right colon, although at times, it may be

the ileocolic vein).

The natural history of these lesions was revealed by the clinical course of 101 patients with colonic

vascular ectasias.161 Of the 15 asymptomatic individuals without a history of bleeding, none bled during

a period of follow-up to 68 months (mean, 23 months). For 31 patients with overt bleeding or anemia

who were treated only with blood transfusion, the rebleeding rates at 1 and 3 years were 26% and 46%,

respectively. This study suggests that the risk of bleeding for incidentally discovered lesions is minimal

and empiric therapy is not warranted. However, the risk of recurrent hemorrhage for most symptomatic

patients is substantial and may increase with time.

Medical treatment of vascular ectasias has been used although there is currently no proven effective

medical therapy. Hormone treatment using high-dose estrogens and progesterone has been used since

the 1950s but convincing proof of efficacy is lacking. Indeed, most evidence would suggest no

antibleeding effect of hormonal treatment.164 More recently the antiangiogenic drug thalidomide,

hormones, and octreotide have been suggested as treatment options but data are lacking.165–167

Endoscopic therapy has, however, proved to be more effective. Nonrandomized investigations with

vascular ectasias managed with monopolar electrocoagulation, endoscopic injection sclerotherapy,

contact probes, and lasers have been published with good results. All methods appear to be effective for

treating bleeding vascular ectasias and all are associated with procedure-related morbidity rates of 2%

to 10%. Perforation has been reported in all of these experiences with rates of 2% to 3%.

Patients bleeding from vascular ectasias in whom endoscopic hemostatic methods are unsuccessful or

unavailable can be treated with resection of the colon following preoperative localization of the

bleeding site. For the usual patient bleeding from a vascular ectasia in the cecum or ascending colon, a

right colectomy with ileotransverse colostomy is the treatment of choice. The value of preoperative

localization of the bleeding site cannot be overstated, and every effort should be made to determine the

site of hemorrhage prior to laparotomy.

Ischemic Colitis

Ischemic colitis is a common cause of LGI hemorrhage especially in the elderly. Bleeding is a common

presenting manifestation of ischemic colitis occurring in approximately one-half to three-fourths of

patients but is usually not massive.168,169 Although ischemic colitis may occur with occlusion of a major

artery (such as ligation of the inferior mesenteric artery during abdominal aortic aneurysm repair), in

most cases it results from impaired local microvascular perfusion of the colonic wall. It occurs most

commonly in the elderly who often have significant medical comorbidities. Renal failure requiring

hemodialysis, hypertension, cardiovascular disease, vasoactive medications, and a variety of other risk

factors have been associated with the disease.170 In many cases a specific initiating event cannot be

identified. Any segment of the colon may be involved. Profound ischemia may lead to full-thickness

necrosis, peritonitis, and perforation. Lesser degrees of ischemia may result in vague mild to moderate

abdominal pain (helping differentiate it from diverticulosis), diarrhea, and mild to moderate bleeding.

Life-threatening hemorrhage is uncommon.

Ischemic colitis can be diagnosed with colonoscopy in which case the mucosa may vary from

edematous to hemorrhagic and necrotic. Rarely is angiography helpful in these cases as it rarely

demonstrates major vessel occlusion.169 Most patients will recover uneventfully with supportive care

alone. When operative management is required it is often necessitated by peritonitis or other signs of

full-thickness necrosis. In these critically ill patients the mortality rate is relatively high due to the

critical nature of these patients’ pre-existing comorbid conditions.

UNUSUAL CAUSES OF ACUTE GASTROINTESTINAL HEMORRHAGE

As outlined in Tables 65-1 and 65-2, a wide variety of other pathologic processes may present with

acute GI hemorrhage. Although these lesions generally comprise a relatively small percentage of the

total number of cases of overt GI hemorrhage, they can present vexing problems to the clinician faced

with a bleeding patient in whom the usual etiologies have been excluded. There are a number of case

reports in the literature of extremely rare causes of GI bleeding that will not be discussed here. The

1697

following lesions occur commonly enough that clinicians are likely to encounter them in their practice.

Dieulafoy Vascular Malformation

Dieulafoy vascular malformation is an unusual cause of recurrent hematemesis, in which bleeding

originates from an unusually large (1- to 3-mm diameter) artery running through the gastric submucosa

for variable distances. Erosion of the gastric mucosa overlying the vessel results in necrosis of the

arterial wall and brisk hemorrhage. The size of the mucosal defect is usually small (2 to 5 mm) and

without evidence of chronic inflammation. These lesions may rarely occur in other anatomic locations of

these lesions such as the colon.171–173

Painless hematemesis and melena are typical. Recurrent bleeding with spontaneous cessation is also

common. In a collective review of 101 cases, the mean age of the patients was 52 years, and the lesion

occurred twice as frequently in men as women. There was no significant association with alcohol abuse

or antecedent symptoms.174

The diagnosis is most frequently made endoscopically by demonstrating arterial bleeding from a

pinpoint mucosal defect. Occasionally, a small arterial vessel may be seen protruding from the gastric

mucosa. Characteristically, the lesions are located within 6 cm of the esophagogastric junction along the

lesser curvature although they may occur in other sites as well.

Most patients can be managed endoscopically by injection of epinephrine, sclerotherapy, banding,

clipping or coagulation.175,176 A subset of patients will require retreatment or surgical excision for

control of hemorrhage. After cessation of hemorrhage few patients rebleed from these lesions even

when treated only be endoscopic methods.177

Gastric Antral Vascular Ectasia

Sometimes abbreviated as GAVE syndrome, this entity is also known as “Watermelon Stomach” because

of its characteristic endoscopic appearance. Longitudinal erosions are seen in the antrum radiating from

the pylorus. It usually causes chronic blood loss and not acute hemorrhage. The etiology is not known

but there is a prominent association with connective tissue disorders. It can usually be treated by

endoscopic argon coagulation but occasionally antrectomy is necessary.178

Angiodysplasia of the Stomach and Small Intestine

Angiodysplastic lesions may occur throughout the GI tract. Similar to colonic lesions, they appear as

minute, flat, or slightly raised red lesions with round or stellate shapes. The margins are

characteristically sharp with a pale mucosal halo surrounding the lesion. The lesions are frequently

multiple and are found most commonly in the stomach and duodenum, although esophageal and small

intestinal involvement has also been described.

In general, these lesions may be diagnosed by endoscopy, although their minute size and sessile

nature may complicate their detection. The lesions may also be readily mistaken for submucosal

hemorrhage associated with acute gastritis or trauma artifact from an NGT or the endoscope. The

lesions may also be demonstrated arteriographically since they have many of the features described for

colonic vascular ectasia.

Endoscopic injections of sclerosants, electrocoagulation, and laser photocoagulation have all been

used to treat gastroduodenal angiodysplasia with good results. The multiplicity of lesions often

necessitates several courses of therapy to eliminate recurring hemorrhage. Surgical resection of the

gastric or intestinal wall containing the lesion as well as oversewing of the bleeding lesion have been

reported to successfully control hemorrhage.

Aortoenteric Fistula

Although communication between the aorta and the intestine may occur as a result of aneurysmal

disease or infectious aortitis (primary aortoenteric fistula), most of those encountered currently are due to

the erosion of an aortic vascular prosthesis through the wall of the distal duodenum (secondary

aortoenteric fistula). The incidence of aortoenteric fistula following aortic reconstructive surgery is about

1% with most of these fistulas arising from the proximal graft anastomosis. Secondary aortoenteric

fistulas are believed to develop after prolonged contact of a prosthetic graft with a fixed segment of

intestine. Ultimately erosion of the graft through the bowel wall results in a low-grade infection around

the graft; involvement of the infection with the suture line leads to dehiscence of the anastomosis and

massive hemorrhage.

The interval between aortic reconstructive surgery and the onset of GI hemorrhage may range from a

1698