few days to many years; the median interval is about 3 years.179 Most patients have an initial episode of

GI bleeding (i.e., herald bleed) that is followed in hours, days, or weeks by catastrophic hemorrhage.

Patients may also complain of back or abdominal pain and less commonly have fever or signs of sepsis

from infection of the graft.

The diagnosis of an aortoenteric fistula must be considered in any patient with an aortic prosthesis or

an abdominal aortic aneurysm who presents with GI hemorrhage. Endoscopy should be urgently

performed following resuscitation to disclose evidence of an aortoenteric fistula or another cause of

bleeding (e.g., peptic ulcer disease with stigmata of recent hemorrhage). If endoscopy fails to

demonstrate an aortoenteric fistula or another convincing source of bleeding and the patient is not

massively bleeding, computed tomography may be helpful in detecting perigraft infection or other

evidence of an aortoenteric fistula. In patients who are actively bleeding, exploratory laparotomy with

exposure of the proximal graft should be undertaken. Identification of an aortoenteric fistula or erosion

requires resection of the graft with extra-anatomical bypass and repair of the duodenal wall, or aortic

reconstruction using a variety of techniques such as aortic reconstruction with popliteal vein or human

allografts.180 The operative management of aortoduodenal fistulas is considered in greater detail in

Chapter 96.

Meckel Diverticulum

Bleeding from a Meckel diverticulum is a common cause of lower GI hemorrhage in children but is rare

in older adults. Meckel diverticula are present in approximately 2% of the population. The lifetime risk

of a complication from a Meckel diverticulum is about 4%.181 About 25% of patients with symptomatic

Meckel diverticula present with hemorrhage.182 In a series of 17 patients who bled from Meckel

diverticula, 11 experienced frank hemorrhage while 6 had chronic occult blood loss. The incidence of GI

hemorrhage is greatest in the first decade of life and steadily decreases from that point. In one series,

no patient older than 40 years of age, and only one patient older than 31 years, bled from a Meckel

diverticulum,182 although it has been reported in the very elderly.183 The pathogenesis of this bleeding

involves the occurrence of ectopic gastric mucosa with peptic ulceration of adjacent bowel wall.

Although these lesions may be demonstrated by enteroclysis, abdominal scintigraphy following the

intravenous injection of 99technetium-pertechnetate demonstrates the ectopic gastric mucosa within the

diverticulum, suggesting the correct diagnosis. Treatment consists of resecting the diverticulum with

adjacent bowel. Diverticulectomy alone will be associated with persistence of the ulcer and the

possibility of recurrent hemorrhage.

Small Intestinal Diverticulum

Diverticular disease of the small intestine is another uncommon cause of either UGI hemorrhage

(duodenal) or LGI hemorrhage (jejunoileal diverticula).184 The pathogenesis is similar to that of colonic

diverticula with erosion of a vasa recta through the diverticular wall and the acute onset of massive

hemorrhage. Depending on the location of the diverticulum, patients may present with either

hematemesis, melena, or hematochezia. Hemorrhage from this source can be a vexing diagnostic

problem because jejunoileal lesions are beyond the reach of the gastroscope and bleeding from duodenal

diverticula may be difficult to discern. Mesenteric angiography or intraoperative enteroscopy may

localize the site of hemorrhage in actively bleeding patients. Segmental resection of the involved

intestine is the treatment of choice.

Hemorrhage Following Endoscopic Procedures

Significant hemorrhage can occur following endoscopic biopsy, sphincterotomy, and other traumatic

procedures. Fortunately these complications are uncommon. Colonoscopy may rarely cause clinically

significant bleeding (0.1% to 0.2%).185 Biopsy of lesions increase the risk up to 10-fold. Usually this is

minor and self-limited and may occur up to 12 days after the procedure.186 The bleeding site can be

confirmed by tagged red cell scanning, arteriography, or colonoscopy. Arteriography and colonoscopy

can be used therapeutically as described previously. Endoscopically placed bands such as those used for

esophageal varices, have also been reported to be successful in arresting hemorrhage.98 Surgical

treatment is rarely required.

Hemorrhage following endoscopic biliary sphincterotomy occurs in approximately 2% of patients.187

Mild immediate bleeding is common and is usually self-limited. Late hemorrhage usually occurs within

48 hours of the procedure but can occur many days after sphincterotomy.188 More severe hemorrhage

can usually be controlled by epinephrine injection,188 making the need for operative treatment

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uncommon.

References

1. Peura DA, Lanza FL, Gostout CJ, et al. The American College of Gastroenterology Bleeding

Registry: preliminary findings. Am J Gastroenterol 1997;92:924–928.

2. Raju GS, Gerson L, Das A, et al. American Gastroenterological Association (AGA) Institute technical

review on obscure gastrointestinal bleeding. Gastroenterology 2007;133:1697–1717.

3. Laine L, Yang H, Chang SC, et al. Trends for incidence of hospitalization and death due to GI

complications in the United States from 2001 to 2009. Am J Gastroenterol 2012;107:1190–1195.

4. Vreeburg EM, Snel P, de Bruijne JW, et al. Acute upper gastrointestinal bleeding in the Amsterdam

area: incidence, diagnosis, and clinical outcome. Am J Gastroenterol 1997;92:236–243.

5. Lingenfelser T, Ell C. Lower intestinal bleeding. Best Pract Res Clin Gastroenterol 2001;15:135–153.

6. Cappell MS, Friedel D. Initial management of acute upper gastrointestinal bleeding: from initial

evaluation up to gastrointestinal endoscopy. Med Clin North Am 2008;92:491–509, xi.

7. Richter JM, Christensen MR, Kaplan LM, et al. Effectiveness of current technology in the diagnosis

and management of lower gastrointestinal hemorrhage. Gastrointest Endosc 1995;41:93–98.

8. Bramley PN, Masson JW, McKnight G, et al. The role of an open-access bleeding unit in the

management of colonic haemorrhage. A 2-year prospective study. Scand J Gastroenterol

1996;31:764–769.

9. Longstreth GF. Epidemiology and outcome of patients hospitalized with acute lower gastrointestinal

hemorrhage: a population-based study. Am J Gastroenterol 1997;92:419–424.

10. Kok KY, Kum CK, Goh PM. Colonoscopic evaluation of severe hematochezia in an Oriental

population. Endoscopy 1998;30:675–680.

11. Kaplan RC, Heckbert SR, Koepsell TD, et al. Risk factors for hospitalized gastrointestinal bleeding

among older persons. Cardiovascular Health Study Investigators. J Am Geriatr Soc 2001;49:126–

133.

12. Fiaccadori E, Maggiore U, Clima B, et al. Incidence, risk factors, and prognosis of gastrointestinal

hemorrhage complicating acute renal failure. Kidney Int 2001;59:1510–1519.

13. Cheng HC, Chuang SA, Kao YH, et al. Increased risk of rebleeding of peptic ulcer bleeding in

patients with comorbid illness receiving omeprazole infusion. Hepato Gastroenterol 2003;50:2270–

2273.

14. van Leerdam ME, Vreeburg EM, Rauws EA, et al. Acute upper GI bleeding: did anything change?

Time trend analysis of incidence and outcome of acute upper GI bleeding between 1993/1994 and

2000. Am J Gastroenterol 2003;98:1494–1499.

15. Mellemkjaer L, Blot WJ, Sorensen HT, et al. Upper gastrointestinal bleeding among users of

NSAIDs: a population-based cohort study in Denmark. Br J Clin Pharmacol 2002;53:173–181.

16. Verhamme K, Mosis G, Dieleman J, et al. Spironolactone and risk of upper gastrointestinal events:

population based case-control study. BMJ 2006; 333:330.

17. Dalton SO, Johansen C, Mellemkjaer L, et al. Use of selective serotonin reuptake inhibitors and risk

of upper gastrointestinal tract bleeding: a population-based cohort study. Arch Intern Med

2003;163:59–64.

18. Masclee GM, Valkhoff VE, Coloma PM, et al. Risk of upper gastrointestinal bleeding from different

drug combinations. Gastroenterology 2014;147:784–792.e9.

19. Garcia Rodriguez LA, Lin KJ, Hernandez-Diaz S, et al. Risk of upper gastrointestinal bleeding with

low-dose acetylsalicylic acid alone and in combination with clopidogrel and other medications.

Circulation 2011;123:1108–1115.

20. Daniel WA, Egan S. The quantity of blood required to produce a tarry stool. JAMA 1939;113:2232.

21. Schiff L, Stevens RJ, Shapiro N, et al. Observations on the oral administration of citrated blood in

man. II. The effect on the stools. Am J Med Sci 1942;203:409–412.

22. Hilsman JH. The color of blood-containing feces following the instillation of citrated blood at

various levels of the small intestine. Gastroenterology 1999;15:131–134.

23. Barnert J, Messmann H. Management of lower gastrointestinal tract bleeding. Best Pract Res Clin

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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

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more than 70% of patients, and a second treatment increases the rate of control from 90% to 95%.

Continued or recurrent hemorrhage after endoscopic treatment often requires emergency portal

decompression either with transjugular intrahepatic portosystemic shunting (TIPS) or rarely

surgery.144–146 Following an initial episode of variceal hemorrhage several options are available for the

prevention of further hemorrhage. These options, as well as the operative management of bleeding

esophageal varices are discussed in detail in Chapter 59.

Mallory–Weiss Tears

The Mallory–Weiss syndrome is acute UGI hemorrhage that occurs after retching or vomiting. Mallory

and Weiss described the laceration of the gastric cardia and postulated that violent emesis against an

unrelaxed cardia was the mechanism of injury. They were able to produce similar mucosal tears in

cadavers by forcing gastric contents against an occluded gastroesophageal junction.147 The typical

patient is an alcoholic who begins to retch and vomit after an alcohol binge although this syndrome may

also be found in nonalcoholics with bouts of emesis. Initially the vomitus consists of gastric contents

without blood and subsequently the patient develops hematemesis and/or melena. Overall, these lesions

account for about 5% to 10% of patients with UGI bleeding.120,136,148

The initial management of these patients is similar to that of patients bleeding from other sources of

UGI hemorrhage and includes volume resuscitation, gastric lavage, and decompression. Most patients

with Mallory–Weiss tears stop bleeding spontaneously, either before treatment or after these early

measures. Once bleeding has stopped, rebleeding is rare.

In patients who continue to bleed despite these maneuvers, nonoperative and operative therapeutic

options are available. Nonoperative management, consisting of endoscopic electrocoagulation, banding

or injection therapy, has been successfully applied to these lesions.149 In cases not amenable to

endoscopic therapy, operative management consists of oversewing the laceration through an anterior

longitudinal gastrotomy in the middle third of the stomach.

LOWER GI HEMORRHAGE

Although the passage of maroon or bright red blood per rectum may occur in the presence of a massive

UGI hemorrhage, this finding most commonly indicates a source distal to the ligament of Treitz. The

absence of blood in bilious nasogastric lavage further supports a distal location of hemorrhage.

Although numerous potential causes of LGI hemorrhage are possible (Table 65-2), colonic diverticulosis

and colitis are by far the most common. Small bowel sources and other colonic pathology such as colon

cancer are relatively unusual causes of acute GI hemorrhage.

Diagnostic Approach

The most important question to answer when presented with a patient with LGI hemorrhage is not,

“What is bleeding?” but rather, “Where is the bleeding?” The common causes of colonic hemorrhage are

mucosal in nature, not palpable, and not visible from the serosal surface of the bowel. Therefore, it is

imperative that the surgeon makes every effort to localize the source of bleeding preoperatively since it

is usually impossible to locate intraoperatively. If the surgeon waits to attempt localization until it is

clear that surgical treatment will be required it may be too late. Colonoscopy, tagged RBC scanning

and/or angiography should be obtained as early as possible after presentation.

After determination that the bleeding is likely from an LGI source, it is important to first exclude

anorectal causes of hemorrhage, such as hemorrhoidal bleeding. At this point, colonoscopy is usually

performed as it can rule out anorectal causes of bleeding, but also help determine non-anorectal causes

of hemorrhage. In the authors’ experience, despite studies showing high value, colonoscopy in an

actively bleeding patient with an unprepped colon is seldom therapeutic. However, it can be of

significant diagnostic benefit. It is usually fairly easy to determine when bleeding is from a neoplasm,

and noting the location helps guide the surgeon in decision making. Conversely in AVMs and

diverticular bleeding, locating the actual source of bleeding is often unsuccessful due to the presence of

blood and stool. However, noting the extent of blood in the colon can be helpful to guide future surgical

decision making. For example, if blood is only noted in the sigmoid colon and rectum, this suggests

bleeding is from a distal source and a sigmoid colectomy may suffice if bleeding persists. Alternatively

if blood is noted throughout the entire colon, the location of the bleed is unclear and a total colectomy

may be necessary. The terminal ileum should be intubated as well. While a small amount of blood can

1694

reflux into the terminal ileum, if an extensive amount of blood is noted then a small bowel source

should be considered and the surgeon should be hesitant about performing a total colectomy if bleeding

persists.

Alternatively, a tagged RBC scan can be obtained as soon as practical, or in occasional cases of

massive hemorrhage, conventional angiography or MDCT. If the tagged RBC scan localizes a bleeding

site, the patient is then sent for angiography to attempt to embolize the bleeding vessel. If the tagged

RBC scan does not demonstrate bleeding, then it is probable that bleeding has stopped. One may then

proceed to colonoscopy after adequate mechanical bowel preparation.

If the bleeding is rapid enough to warrant emergency surgery, bleeding can usually be demonstrated

by tagged RBC scan, MDCT, or angiography. It should be the very rare patient who will need to

proceed to surgery for LGI hemorrhage with failed preoperative localization. In these cases a careful

search for small bowel bleeding sources, possibly including intraoperative small bowel endoscopy,

should be performed.

Colonic Diverticulosis

9 In Western society, the prevalence of colonic diverticula increases with age such that about 60% of

people in their seventh decade of life are affected and the incidence increases roughly 1% per year.

Only about 20% of patients with diverticulosis have symptoms attributable to these lesions and less than

5% experience hemorrhage.150 Hemorrhage from diverticular disease is most often massive, associated

with hematochezia, and accompanied by varying degrees of hemorrhagic shock. Classically, patients

present with a sudden occurrence of mild lower abdominal discomfort, rectal urgency, and the

subsequent passage of a large bloody stool. Because the colon can contain large volumes of blood,

neither the volume nor the frequency of bloody stools is a reliable guide to the rate of hemorrhage.

Despite the massive nature of hemorrhage, most patients with diverticular disease stop bleeding

spontaneously. Most series report bleeding ceases spontaneously in 80% of cases, although up to 25% to

50% can rebleed. Of those who rebled, less than one-fourth required surgery.151

Bleeding associated with diverticular disease comes from a perforated vasa recta located at the neck

or apex of a diverticulum. The vasa recta penetrates the colonic wall from the serosa to the submucosa

through obliquely oriented connective tissue septa. Protrusion of colonic mucosa through this

connective tissue plane causes apposition of the diverticulum and the vasa recta (Fig. 65-4). Ulceration

of the mucosa within the neck of the diverticulum and disruption of the arterial wall produces

hemorrhage into the lumen of the bowel. Although diverticular disease is more prevalent in the left

colon, right-sided lesions account for half or more episodes of bleeding.151,152 Risk factors for rebleeding

are hypertension, NSAID use, coagulopathy, renal failure, ischemic heart disease, and cluster type

diverticula.153,154

Figure 65-4. Colonoscopic view of a colonic diverticulum. A vasum rectum is seen entering the diverticulum and forming one of

the walls.

The massive nature of the bleeding caused by colonic diverticula limits the diagnostic usefulness of

1695

colonoscopy. Rarely is a bleeding vessel seen within a diverticulum and the presence of blood or clot

within a diverticulum is of no diagnostic benefit. Selective mesenteric arteriography may demonstrate

the luminal extravasation of contrast; however, in one study of patients bleeding from diverticulosis,

angiographic localization was effective in less than 20% of patients.155 Failure to visualize a bleeding

point is usually due to cessation of active bleeding at the time of angiography.

Given the relatively low risk of recurrent hemorrhage, patients who stop bleeding should be treated

expectantly. About 10% of patients bleeding from colonic diverticula continue to bleed and ultimately

require operative intervention. Embolization of bleeding vessels in the colon has been reported to be

safe and effective in the majority of patients; however there is a definite risk of ischemic

complications.156,157 The rapid nature of the hemorrhage and the difficulty in defining the site of

bleeding through the endoscope can limit endoscopic attempts at control of diverticular hemorrhage,

especially in patients with large volume rapid bleeding.

If the site of bleeding can be localized, patients who continue to bleed from diverticular disease

should undergo resection of the colon segment that contains the site of bleeding. Even after successful

localization of a bleeding source, the least operation that can usually be contemplated is a

hemicolectomy or wide segmental colectomy. Segmental colon resection has been associated with

rebleeding rates of only 0% to 15% and mortality rates of 0% to 13%. Tagged RBC scanning, while

sensitive, cannot always pinpoint a bleeding site with great accuracy. Although angiography usually

gives more precise localization, correlation between the vascular pattern and the anatomic location is

sufficiently imprecise to warrant at least a segmental resection. Finally, measurement with colonoscopy

is notoriously misleading with even experienced endoscopists making mistakes about the precise site of

a lesion. If the location is unable to be localized and the blood appears confined to the colon, a total

abdominal colectomy should be performed as most studies show rebleeding rates of 0%, and “blind”

segmental colectomy has been shown to have a rebleeding rate of up to 75%.65 However, the surgeon

and patient should be aware of a failure rate even after total abdominal colectomy as the small bowel

could potentially be the source. There are few worse sights for the surgeon than blood coming from an

ileostomy after a blind total abdominal colectomy for bleeding.

Although a total colectomy, often with end ileostomy, for nonlocalized ongoing colonic hemorrhage

may occasionally be necessary, it should be performed only after exhaustive attempts to localize the site

of bleeding. Total colectomy is associated with greater perioperative morbidity rates than segmental

resection and postoperative volume losses from ileostomies or diarrhea may present a significant

problem to elderly patients.

Colonic Angiodysplasia

Sometimes called vascular ectasias or arteriovenous malformations, these lesions are believed to arise

from the age-related degeneration of previously normal intestinal submucosal veins and overlying

mucosal capillaries. Angiodysplasia is located most frequently in the cecum and ascending colon,

although it may be found more distally in 20% to 30% of cases. Multiple lesions may be present in as

many as 40% to 75% of all cases.158 Microscopically, angiodysplasia consists of dilated, thin-walled

vessels that appear to be ectatic veins and venules localized within the submucosa. A dilated submucosal

vein is often found and occasionally an enlarged artery. Angiodysplasia is generally thought to be an

acquired lesion associated with aging, but the exact etiology is unknown.

The prevalence of colonic angiodysplasia in the general population appears to be less than 1%.159

These lesions may present with hematochezia, melena, occult blood loss, or iron-deficiency anemia.

Bleeding lesions are most commonly found in the right colon. As compared to diverticular bleeding,

episodes of hemorrhage from vascular ectasias are usually less severe, and are somewhat more likely to

recur. After the initial episode of hemorrhage, the majority of patients will stop bleeding

spontaneously.160

Vascular ectasias may be diagnosed by either colonoscopy or by selective mesenteric angiography.

Colonoscopy has been reported to have a sensitivity of 80% in demonstrating vascular ectasias.161

However, colonoscopic diagnosis of these lesions in actively bleeding patients may be confounded by

the presence of other incidental lesions including traumatic and suction artifacts produced during the

examination. In addition, after significant bleeding and hypovolemia, the shunting of blood flow away

from the intestinal mucosa may obscure these lesions in inadequately resuscitated patients. When

vascular ectasias are located, colonoscopy can be used effectively to treat vascular ectasias either by

coagulation or possibly injection of sclerosants.162,163

Selective mesenteric angiography may also demonstrate these lesions and compliment colonoscopy,

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Although studies in the 1960s and 1970s demonstrated acute erosions of the gastric mucosa in as many

as 60% to 100% of critically ill patients, the incidence has markedly decreased over the past four

decades. Factors postulated to have been important in this phenomenon include (1) the widespread use

of prophylactic gastric alkalinization; (2) improvements in the ability to detect and treat sepsis; (3)

improvements in the ability to monitor and correct hemodynamic instability; and (4) the ability to

provide adequate nutritional support of critically ill patients.

In general, stress gastritis is characterized by the appearance of multiple superficial gastric ulcerations

within 12 to 14 hours of an acute injury. These lesions, initially localized to the fundus and body of the

stomach, later involve the entire gastric surface. Patients at greatest risk include those with sepsis,

major burns, severe trauma, and critically ill patients with a coagulopathy and respiratory

insufficiency.130 In this setting, the disease appears to represent the gastric component of the multiorgan

failure syndrome.

The pathogenesis of this disease is discussed in detail in Chapter 45. The primary defect is in the

protective processes that maintain the integrity of the gastric mucosal barrier. Although some gastric

acid secretion is required for the development of stress gastritis, it is clear that the hypersecretion of

acid is not the cause of mucosal injury. Altered gastric mucosal blood flow and impaired clearance of

hydrogen ions from the mucosa appear to be of particular importance; therefore, the best method of

prevention of stress gastritis is to prevent gastric ischemia and acid injury. Stress gastritis should be

differentiated from the deep, often solitary ulcerations occurring in patients with severe central nervous

system lesions (Cushing ulcers).

Generally hemorrhage is the only symptom that patients with stress gastritis experience. Overt

bleeding is often heralded by the appearance of flecks of blood in the gastric aspirate. The superficial

nature of the lesions makes perforation unlikely.

Prophylactic therapy is directed toward preventing hemorrhage, primarily by neutralizing gastric

acid, augmenting mucosal defenses, and removing or preventing physiologic stress. The gastric pH

should be maintained between 3.5 and 4.5.131 Antacids, H2

-receptor antagonists, PPIs, and sucralfate

have all been used to prevent stress gastritis. Alkalinization of the gastric contents is associated with

oral and fecal flora colonization of the stomach and has raised concerns about an increased risk of

nosocomial pneumonia. This concern prompted the use of sucralfate as a preferred prophylactic agent

for some time instead of antacids or cimetidine.132 However, a prospective, randomized trial of 1,200

critically ill patients receiving either ranitidine or sucralfate for stress ulcer prophylaxis found that those

patients receiving ranitidine had a lower bleeding rate (1.7%) than the sucralfate group (3.8%) but

there was no difference in mortality or incidence of ventilator-assisted pneumonia.133 Since that time,

studies have shown PPIs to be a safe and effective method of stress prophylaxis, but the number of

studies with high-quality data is still lacking.

The success of these prophylactic measures has led to a dearth of recent experience in managing

patients bleeding from stress gastritis. Based on early reports, attention to blood replacement,

intravascular volume restoration, and correction of coagulation defects are associated with the cessation

of hemorrhage in nearly 80% of cases and as such are the principal means of initial treatment. A variety

of nonoperative techniques have been employed with variable success in arresting hemorrhage from

stress gastritis including endoscopic and embolization techniques and the selective catheterization of the

left gastric artery with continuous infusion of vasopressin.134

Based on these same early experiences, very few patients bleeding from erosive gastritis require

operative intervention to arrest hemorrhage. A variety of surgical treatment options have been reported

including vagotomy and pyloroplasty with oversewing of bleeding sites, vagotomy and

hemigastrectomy, total gastrectomy, and gastric devascularization. The dilemma facing the surgeon is

that these critically ill patients poorly tolerate extensive procedures, yet lesser operations often fail to

control hemorrhage. Regardless of the operation performed, mortality risk depends on the underlying

illness, particularly in the presence of multiple organ failure. Mortality rates between 30% and 60% are

commonly quoted, with as many as one-fourth of the deaths resulting from continued hemorrhage.

Rebleeding rates ranging from 25% to 61% have been reported. The combination of vagotomy,

hemigastrectomy, and oversewing of bleeding points has been touted as more successful in these

patients; however, rebleeding rates of 11% to 44% and operative mortality rates ranging from 33% to

63% have been associated with this procedure.135 More extensive operations, such as near total

gastrectomy or total gastrectomy are associated with significant mortality although they successfully

stop hemorrhage.

Gastroesophageal Varices

1692

Cirrhosis is a leading cause of death in the United States and variceal hemorrhage is a common mode of

death for these patients. About 30% of people with cirrhosis develop gastroesophageal varices; of these

individuals, about 30% bleed as a result of the varices, usually within 1 to 2 years of diagnosis.

Gastroesophageal varices are a significant cause of UGI hemorrhage, accounting for about 20% of such

cases. Patients with bleeding gastroesophageal varices tend to have much higher rebleeding rates,

transfusion requirements, lengths of hospitalization, and risk of death than do patients bleeding from

nonvariceal causes.120,136

Although the basic tenets of resuscitation for massive variceal hemorrhage are similar to those for any

cause of massive bleeding, intravenous volume resuscitation should be particularly judicious. The

hyperaldosteronemic state of cirrhosis promotes sodium and water retention with aggravation of ascites

and peripheral edema. Accurate blood replacement is imperative since overtransfusion may worsen

portal hypertension and exacerbate hemorrhage. Invasive cardiac monitoring with Swan–Ganz

catheterization may be particularly useful for guiding volume replacement. Coagulation deficits should

be aggressively corrected by administering fresh frozen plasma. Thrombocytopenia, secondary to

hypersplenism or dilution, should be treated promptly with pooled platelet transfusions. Sedatives are

best avoided or used sparingly because cirrhosis impairs the liver’s ability to metabolize many of these

drugs. Adequate prophylaxis for delirium tremens should be administered to alcoholics.

As with other sources of UGI hemorrhage, early endoscopy is imperative for successful diagnosis and

therapy.137 The identification of varices alone is not adequate to incriminate them as the source of the

hemorrhage since up to half of patients with cirrhosis bleed from a source other than varices.

Furthermore, endoscopy may identify factors associated with a heightened risk of variceal hemorrhage

such as the size and number of varices and the presence of red, blue, or other colored spots on the varix.

The presence of gastric and duodenal varices and portal hypertensive changes in the gastric mucosa

(portal gastropathy) will influence therapeutic decisions and prognosis.

Although vasopressin has commonly been used in the management of variceal hemorrhage, its use has

been limited due to the potent vasoconstrictive properties causing cardiac and peripheral ischemia,

arrhythmias, hypertension, and bowel ischemia. More recent reports suggest the superiority of

somatostatin or its synthetic analog, octreotide. It is thought that octreotide causes splanchnic arteriolar

vasoconstriction and reduces variceal and azygous vein flow with limited direct effects on portal

pressure.138 Meta-analyses have shown that the infusion of somatostatin is more effective and safer than

vasopressin in the pharmacologic control of variceal hemorrhage.139,140 Other studies have shown that

somatostatin or octreotide can improve the results of sclerotherapy or endoscopic variceal

ligation.141,142 Although neither somatostatin nor vasopressin plus nitroglycerin definitively treat the

bleeding esophageal varices, these modalities may provide initial control of hemorrhage, reducing

transfusion requirements and providing time for resuscitation before definitive treatment.

Another temporizing method used for massively bleeding patients is balloon tamponade using a

Sengstaken–Blakemore tube or a Minnesota tube. These devices consist of a gastric tube with

esophageal and gastric balloons. In the case of a Minnesota tube, a proximal esophageal lumen allows

for the aspiration of swallowed secretions. Inflation of the gastric (and if required esophageal) balloons

tamponade the bleeding varices, controlling hemorrhage in more than 80% of cases. Hemorrhage recurs

in 25% to 50% of patients upon deflation of the balloons, thus limiting this technique to a temporizing

role.143 The greatest value of these tubes is for arresting massive hemorrhage that has been

unresponsive to other measures, allowing time for resuscitation and angiographic definition of the

portal system before definitive treatment.

When used inappropriately, these tubes can be associated with significant morbidity and mortality.

Complications occur in 4% to 9% of patients with the most frequent being aspiration pneumonitis.

Measures to prevent pulmonary complications include endotracheal intubation before tube insertion and

the placement of an esophageal tube to remove swallowed salivary secretions. Other significant

complications include esophageal rupture or necrosis and airway occlusion during the attempted

removal of an incompletely deflated gastric balloon. Because of the availability of endoscopy, these

tubes are rarely used today.

8 Endoscopic sclerotherapy, endoscopic clipping or endoscopic variceal ligation (banding) have

become the most widely used modalities for the initial definitive control of bleeding esophageal varices.

Several studies have confirmed that these techniques arrest acute variceal hemorrhage in 90% to 95% of

patients. In general, a patient bleeding from esophageal varices should undergo urgent pharmacologic

therapy and banding of the varices at the time of the first emergency endoscopy. Sclerotherapy can be

used if ligation is technically difficult.137 A single endoscopic treatment controls variceal bleeding in

1693

 

from early PPI use. An 80-mg intravenous bolus of omeprazole or pantoprazole followed by an infusion

at 8 mg/hr produces the most reliable acid suppression.110 All patients should be tested for Helicobacter

pylori (H. pylori) infection and treated if found. Treatment of the infection significantly reduces the

recurrence of hemorrhage when compared to no treatment or chronic antisecretory treatment alone.111

Interestingly H. pylori infection may be less common in patients with bleeding ulcers than in those with

nonbleeding ulcers.112

Endoscopic Treatment

The endoscopic appearance of a bleeding ulcer has important prognostic and therefore therapeutic

implications, as alluded to in Tables 65-6 and 65-7. A modification of the system employed by Forrest et

al.113 is shown in Table 65-8. In this system, category I findings are indicative of active bleeding while

category II findings provide evidence of recent hemorrhage. In general, only actively bleeding ulcers

(i.e., Forrest category I lesions) are treated endoscopically.

Table 65-8 Forrest Classification of Endoscopic Appearance of Bleeding Ulcers

A variety of endoscopic techniques are available to arrest hemorrhage from bleeding ulcers. The

precise method of treatment is less important than the correct selection of patients and the experience

of the endoscopist. Examples of methods typically include mechanical, thermal, or injection.

Mechanical ligation of bleeding vessels can be achieved with endoscopic ligation (banding),

endoscopic clipping, or endoloop ligation.114–116 Of these three methods, endoscopic clipping is the

method most commonly employed for bleeding ulcers.

Heater probes and monopolar and bipolar electrocoagulation probes can also effectively control UGI

hemorrhage. Monopolar probes apply high-frequency electrical current to the tissue, resulting in

localized heating to 100°C and sealing of the bleeding vessel by coagulation necrosis of the surrounding

tissue and vessel wall. Multipolar electrocoagulation (bicap) probes consist of three equally spaced pairs

of bipolar microelectrodes. This orientation of electrodes allows coagulation of tissue from tangential

approaches and eliminates some of the disadvantages of the monopolar probe, such as the unpredictable

depth of thermal injury, adherence of tissue, and clot dislodgement. Direct thermal coagulation of a

bleeding point can also be produced by applying a heater probe, consisting of an aluminum tip coated

with Teflon. The tip is rapidly heated to 250°C by an inner coil. The tip can be irrigated with a water jet

to prevent accumulation of debris and clot. Heat conducted from the probe produces tissue coagulation

to a depth of 1 to 5 mm.

Injection of epinephrine to induce vasoconstriction has been used successfully to control acutely

bleeding ulcers, particularly as an adjunct to electrocautery or mechanical hemostasis with clips. A

meta-analysis of 15 studies concluded that injection alone was inferior to either clips alone, or clips plus

injection.117 This study showed no difference between clips and thermocoagulation.

Although not commonly employed, the injection of sclerosants has been well described as a method of

treating esophageal varices and has been used for controlling nonvariceal bleeding. Sodium morrhuate

and ethanolamine oleate are most commonly used to treat esophageal varices, whereas ethanol and

polidocanol are most commonly used for nonvariceal sites. These agents act by thrombosing bleeding

vessels and causing necrosis and subsequent fibrosis of surrounding tissue. Clinical experience with

sclerosants has been similar to that obtained with electrocoagulation. In one large multicenter study of

332 actively bleeding patients or patients with stigmata of recent hemorrhage who underwent injection

of 98% alcohol around the lesions, less than 1% continued to bleed, 6% rebled, and only 3% required

emergency operative intervention.118

A meta-analysis of 25 randomized trials of endoscopic therapy for bleeding ulcers concluded that

endoscopic treatment methods have a beneficial effect on survival by reducing the rate of recurrent

hemorrhage. This analysis suggested that endoscopic therapy results in a relative reduction of 69% in

1690

recurrent bleeding, 62% in emergent surgery, and 30% in mortality rate, with the greatest benefit seen

in actively bleeding ulcers and ulcers with nonbleeding visible vessels.119 The effectiveness of early

aggressive endoscopic diagnosis and treatment is further supported by a report of 562 patients bleeding

from a variety of causes of whom only 2.5% required emergency operations to control hemorrhage.120

Several other more recent studies have confirmed the critical role of endoscopy and control of UGI

hemorrhage.43,121,122 For most patients with evidence of persistent bleeding, a second attempt at

endoscopic hemostasis should be attempted because this can provide up to 75% of patients with durable

hemostasis. Exceptions may include patients with ulcers greater than 2 cm in diameter and those who

have hypotension associated with a rebleeding episode, since such patients may be at an increased risk

for failure of repeat endoscopic hemostasis.104,121,123

Operative Treatment

The successful use of endoscopic therapies has relegated operative procedures to a rescue role for those

cases in which endoscopy is unsuccessful in arresting hemorrhage. Numerous studies have attempted to

identify those patients at greatest risk of continued or recurrent bleeding. Of the many factors

examined, those associated with the highest risk of rebleeding included patients in hypovolemic shock

during the initial endoscopy, ulcers greater than 2 cm in diameter, and endoscopic stigmata of recent or

ongoing hemorrhage (Forrest type I and II lesions).123 Many studies have demonstrated the ability of

endoscopy to identify those patients at greatest risk of rebleeding. In one review, the presence of active

bleeding was associated with a 90% to 100% chance of continued or recurrent hemorrhage. A

nonbleeding visible vessel had a 40% to 50% chance, adherent clot 20% to 30%, oozing without visible

vessel 10%, flat spot 5% to 10%, and clean-based ulcer 1% to 2%.124 Even in those patients who rebleed

following initial endoscopic therapy, two-thirds may be successfully retreated endoscopically thus

avoiding operative intervention.90 Factors that must be considered in decisions regarding the timing of

operative intervention include the magnitude of the initial (or recurrent) hemorrhage, the physiologic

ability of the patient to withstand continued or recurrent hemorrhage, and the likelihood of recurrent or

continued hemorrhage. It is generally accepted that elderly patients and those with significant

concurrent medical problems should undergo operative intervention earlier during the course of the

hemorrhage since these individuals will poorly tolerate continued bleeding, recurrent hypotension, and

repeated transfusions.

The type of operation depends on the pathology encountered. For bleeding gastric ulcers, the

operation of choice depends on the patient’s condition and location of the ulcer. For favorably located

ulcers, excision of the ulcer with closure of the gastrotomy will suffice. If the ulcer is unfavorably

located, for example, near the gastroesophageal junction, simple oversewing of the vessel through the

base of the ulcer may adequately control bleeding.125 If a gastric ulcer is left in situ, follow-up

endoscopy is necessary 4 to 8 weeks later to either confirm healing or obtain tissue to rule out

malignancy. Extensive gastric resections such as antrectomy, subtotal or total gastrectomy are generally

not performed in these unstable patients.

For patients bleeding from duodenal ulcers, the type of surgery performed has changed since the

development of PPIs and treatment of H. pylori. Formerly, truncal vagotomy, pyloroplasty, and

oversewing of the bleeding vessel were the most widely used operation. However, the trend is now

more toward direct ligation of the bleeding vessel through the duodenotomy.126 When performed,

ligation should incorporate the gastroduodenal artery proximal and distal to the ulcer as well as the

transverse pancreatic artery. Despite the above noted trend, a recent study has shown vagotomy and

drainage may be superior to simple oversewing of the vessel.127

Angiographic Embolization

Of late, much has been written about the use of transcatheter embolization for peptic ulcer disease. In

general, angiographic embolization is used after failure of endoscopic treatment in patients who cannot

or will not undergo surgery. One large review (including nonulcer UGI indications) showed a high

technical success rate (i.e., localization of bleeding and deployment of the embolic agent) but a clinical

success rate of only 51%.128 Other reviews have shown higher success rates ranging from 69% to 100%

technical success rate and 63% to 97% clinical success rate.129 Significant ischemic complications can

occur however. While this technique has utility in select patients, it should not be considered as a firstline treatment option for bleeding peptic ulcers, but may have a role as a safe alternative to surgery for

ulcers refractory to endoscopic treatment.

Stress Gastritis

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COMMON CAUSES OF GI HEMORRHAGE AND TREATMENT

Upper GI Hemorrhage

Peptic Ulcer Disease

Peptic ulcer disease is the most common cause of acute UGI hemorrhage, accounting for nearly 40% of

cases in most series although this proportion may be decreasing.89 About 15% to 20% of patients with

peptic ulcer disease experience bleeding during the course of their disease and as many as 20% of these

patients will have bleeding as the initial manifestation. Hemorrhage is the principal cause of death from

peptic ulcer disease and has replaced intractable pain as the most frequent indication for surgery.

Complications of peptic ulcer disease occur more commonly in older patients who often have coexisting

medical problems, which profoundly influence their risk of morbidity and mortality.

Duodenal ulcers occur slightly more frequently than gastric ulcers. Penetration of the ulcer through

the posterior wall of the duodenal bulb is associated with erosion into the gastroduodenal artery or one

of its branches, resulting in brisk hemorrhage. Patients may present with hematemesis of bright red

blood and clots or with melena alone. Between 80% and 90% of patients stop bleeding spontaneously

during the initial stages of therapy with volume resuscitation.

In general, patients with gastric ulcers tend to be older and have coexisting medical problems that

increase morbidity and mortality compared with duodenal ulcers. Bleeding may occur from any site in

the stomach, although ulcers occurring at the incisura are most common. At this site, involvement of the

branches of the left gastric artery may result in brisk, if not torrential, hemorrhage. The clinical

presentation of patients bleeding from gastric ulcers is similar to that of duodenal ulcers, with

hematemesis, melena, and hematochezia.

6 An important risk factor for the development of GI hemorrhage and gastroduodenal ulcer formation

is the use of NSAIDs. NSAID use has been associated with a continuum of mucosal injury ranging from

small acute mucosal hemorrhages to large chronic ulcers. It has been estimated that 10% to 15% of

regular NSAID users have chronic gastric ulcers.90 Symptoms correlate poorly with the degree of

mucosal injury since as many as 20% of ulcers penetrating the muscularis are asymptomatic.91 Case

control and cohort studies have suggested that NSAIDs are associated with a relative risk of GI

hemorrhage and ulceration ranging from about 2 to 9.1.92 Ketorolac, in particular, has been associated

with a high risk of GI bleeding (relative risk approaches 25).93 The risk of NSAID-associated

complications is highest in patients with a history of UGI bleeding, the elderly, those patients taking

oral anticoagulants,94 or corticosteroids. Patients with a prior history of peptic ulcer disease also appear

to be at increased risk of NSAID-associated GI hemorrhage and tend to have a significantly worse

outcome when compared to individuals not using NSAIDs.95

The tremendous frequency with which NSAIDs are used by the elderly underscores the magnitude of

this problem. Individuals with a history of NSAID-induced hemorrhage may benefit from the

prostaglandin E1 analog, misoprostol, which has been shown to prevent NSAID-induced gastric erosions

and ulcers.96 Histamine (H2

)-receptor blockers (ranitidine and cimetidine) are effective in preventing

NSAID-induced duodenal ulcers, but appear to have little effect on the occurrence of gastric lesions.91,97

Proton pump inhibitors (PPIs) have also been shown to be protective in patients on NSAIDs, with

greater efficacy than H2 blockers.98 NSAIDs are also associated with lower GI bleeding, including lesions

not generally considered related to NSAID-induced ulcers such as diverticulosis.99,100 Selective COX-2

inhibitors have been marketed as being safer than nonselective NSAIDs, although some of these have

been withdrawn from the U.S. market for other safety concerns. It appears that these selective

inhibitors cause fewer UGI problems overall than traditional NSAIDs, the main benefit being fewer

uncomplicated ulcers. Various studies have shown no decrease in complicated events, including

clinically significant bleeding episodes.101,102 However, in a Cochrane systematic review of the GI safety

of COX-2 inhibitors, COX-2 inhibitors produced significantly fewer gastroduodenal ulcers (relative risk,

0.26; 95% CI = 0.23–0.30) and ulcer complications (relative risk, 0.39; 95% CI = 0.31–0.50), as well

as fewer withdrawals caused by GI symptoms when compared to nonselective NSAIDs.103

Medical Treatment

7 Once bleeding from the UGI tract is confirmed, treatment with a PPI should be initiated. Acute use of

a PPI has been shown in several studies to decrease rebleeding.43,104–107 Although the Scottish

Intercollegiate Guidelines Network (SIGN) recommended withholding PPI therapy until after

endoscopy,108,109 in our opinion the balance of evidence would suggest no harm and perhaps a benefit

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Wireless Capsule Endoscopy

Imaging of the small intestine is also possible with wireless capsule endoscopy (CE) which consists of a

battery, light source, imaging-capturing system, and transmitter. This capsule endoscope is 11 × 30 mm

and is moved solely by peristalsis. This system captures and sends usually two images per second

(newer versions can send more frames per second) for about 8 hours to an ultra–high-frequency band

radiotelemetry unit worn by the patient. In 85% of cases, the capsule reaches the cecum within this time

frame.62 The location of the capsule is suggested by the strength of the signal. Several studies have

shown high diagnostic yields using this technique and found it to be at least equivalent to and in some

studies superior to double balloon enteroscopy in patients with obscure GI bleeding.63 It has also been

shown to have a higher diagnostic yield with comparable outcomes when compared to angiography.64

The main risk of CE is capsule retention. One difficulty with CE is the very large amount of data to be

reviewed. For an 8-hour study, 50,000 to 60,000 images are generated, which takes approximately 40

to 60 minutes to review.

Selective Visceral Arteriography

Selective visceral arteriography is primarily useful in patients with UGI or LGI bleeding in whom

endoscopy cannot be performed or has been unsuccessful in determining the site of ongoing, rapid

hemorrhage. Successful angiographic identification of the source of bleeding occurs in 27% to 86% of

instances and depends primarily upon the presence of active arterial bleeding at the time of the study

(Fig. 65-2).55,65 The extravasation of contrast may be detected if the patient is bleeding at rates greater

than 0.5 to 1 mL/ min66; this correlates clinically with the requirement for continuous volume infusion

to maintain hemodynamic stability. Pennoyer et al.,67 however, were unable to identify any clinical

parameters (including tachycardia, numbers of transfusions, or orthostatic hypotension) that could

increase the diagnostic yield of selective angiography, including scintigraphy demonstrating ongoing

bleeding. However, a study by Hammond et al.68 found an early (within 2 minutes) positive

scintigraphy has a 60% positive predictive value for a positive angiogram. Additionally, it has been

shown that a positive scintigram increases the likelihood of a positive angiogram from 22% to 53%.69

Several groups have used heparin, vasodilators, or thrombolytics to improve the diagnostic yield of

arteriography in patients with nondiagnostic studies.70,71 Mernagh et al.72 found that the administration

of heparin intravenously for 24 hours increased the diagnostic yield of visceral angiography from 33%

(6 of 18) to 67% (12 of 18). Others have found that the intra-arterial infusion of a vasodilator, heparin,

and/or urokinase (a thrombolytic) failed to identify the source of bleeding in 5 of 7 patients.73 It should

be noted that these provocative techniques are not commonly employed.

Figure 65-2. Selective celiac arteriography with injection into the common hepatic artery in a patient bleeding from a duodenal

diverticulum. Extravasation of contrast from a branch of the gastroduodenal artery can be seen (arrow).

One major advantage of visceral arteriography is its therapeutic potential. Transcatheter embolization

of bleeding vessels was first reported in the early 1970s.74,75 Modern instruments allow superselective

catheterization of terminal vessels allowing satisfactory embolization with less risk for ischemic

complications. Further discussion of therapeutic use can be found below.

Abdominal Scintigraphy

1687

Abdominal scintigraphy with 99mtechnetium (Tc)-labeled RBCs lacks the spatial resolution and

diagnostic precision of angiography and endoscopy; however, it is of most value in detecting

intermittently bleeding lesions, those with very low rates of hemorrhage such as vascular

malformations, and in evaluation of LGI bleeding due to the lower sensitivity of endoscopy within the

LGI tract as compared to the UGI tract. Abdominal scintigraphy utilizing 99mTc-RBCs has been shown to

be the most sensitive examination due to its ability to detect bleeding rates as low as 0.04 to 0.1

mL/min.76,77 In a review of seven retrospective studies with nearly 400 patients, the median diagnostic

accuracy of scintigraphy was 82% (range, 52% to 95%). However, in this review, 99mTc-RBCs was

incorrect in 5% to 48% of instances (median 18%).65 Suzman et al.78 summarized 20 retrospective

studies containing 804 positive studies and reported a false-positive rate of 19%. The large variation in

these studies results from differences in scan timing, technical skills, and expertise. Additionally, precise

localization of the site of bleeding may be complicated by the rapid distribution of isotope throughout

the intestine by peristalsis or by accumulation in the right colon.79 More recent techniques of cine

scintigraphy may improve the diagnostic accuracy (Fig. 65-3).80 One area where radionuclide scanning

has a clear role is in the diagnosis of Meckel diverticulum. 99Tc-pertechnate is secreted by ectopic

gastric mucosa in Meckel diverticula.81 This study should be considered early in the evaluation of young

individuals with LGI bleeding.

Figure 65-3. Cine-99Tc erythrocyte scintigraphy showing extravasation of isotope in the right colon. Only a small portion of the

image set is shown. Arrows point to accumulation of isotope in right colon. Bleeding was due to delayed hemorrhage following

endoscopic polypectomy.

CT Scanning

CT scanning has been used to detect GI bleeding using a variety of specialized techniques.82–84

Multidetector-row helical computed tomography (MDCT) is establishing itself as a rapid, noninvasive,

and accurate diagnostic method in acute GIB. In arterial phase MDCT, active GI bleeding is defined as

active contrast extravasation with a focal area of high attenuation within the bowel lumen.85 Yoon et

al.86 presented the first prospective study evaluating the accuracy of MDCT and found an overall

sensitivity of 90.9% for the detection of acute GI bleeding and specificity of 99%. Additional studies

have supported its use.87,88 Limitation of MDCTs are radiation dose, contrast allergies, contrast

nephropathy, and it being a purely diagnostic rather than therapeutic modality. However, it is fast,

accurate, widely available, reproducible, noninvasive, and a positive study can subsequently guide

interventionalists to directly perform time-saving super-selective angiograms of the bleeding site.85 In

the future this may continue to become a more available and useful technique.

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Prognostic systems for UGI hemorrhage have been more widely adopted than those for LGI

hemorrhage. One widely used system is the Rockall score for assessing the risk of death and rebleeding

in patients with UGI hemorrhage (Table 65-4). Using this model, Rockall et al. found that rebleeding

occurred in less than 5% of patients and mortality was virtually zero (0% to 0.2%) in patients with

scores of 0 to 2. In contrast, a fourth to nearly one-half of patients with a Rockall score of 5 to 8+

rebled; the mortality rate for these patients was 11% to 41%. In this study, rebleeding significantly

affected the likelihood of death, particularly for patients with intermediate scores of 3 or 4 and 5 to 7 in

which there was a three- to fivefold increase in mortality rates.26

The Rockall classification has been widely accepted as accurate and importantly has been externally

validated.27–30 However, the full classification scheme requires endoscopic assessment. An alternative

scoring system – the Glasgow–Blatchford bleeding score (GBS) – is based on clear and readily available

clinical and laboratory indices without the need for endoscopy Table 65-5. It was designed to predict

need for clinical intervention due to UGI hemorrhage. This scoring system has been subjected to multiinstitutional trials and found to be at least as effective as and possibly more accurate than the Rockall

system.31,32 These authors suggested that patients with a score of 0 can be safely managed as

outpatients.

Conversely, patients with LGI bleeding typically present with less hemodynamic instability. Factors

that is indicative of a severe lower GIB thus necessitating more urgent intervention include:

Heart rate >100/min

Initial systolic blood pressure 115 mm Hg or less

History of syncope

Nontender abdominal examination

Bleeding per rectum during the first 4 hours of evaluation

History of aspirin use

Charlson Comorbidity Index score of more than 2.33

INITIAL EVALUATION AND RESUSCITATION

Upon presentation, two large-bore intravenous lines should be placed in peripheral veins and

intravascular volume resuscitation begun with an isotonic saline solution. Most patients stop bleeding

spontaneously, and crystalloid volume resuscitation is all that is required. Blood is drawn for type and

crossmatch, complete blood count with platelet count, electrolyte measurement, liver function tests, and

coagulation profiles. It is important to emphasize that on presentation, the hematocrit or hemoglobin

level may not accurately reflect the magnitude of acute blood loss. Estimates of the severity of

hemorrhage must be based on clinical parameters.

The massively bleeding patient should receive packed red blood cells (RBCs) to restore intravascular

volume and oxygen-carrying capacity. The decision to transfuse blood or blood products depends on the

1682

individual needs of the patient and the cause of the bleeding. The risks of the blood products (i.e.,

infection and allergic reactions) must be weighed against the risks of withholding transfusion (i.e.,

anemia, decreased oxygen-carrying capacity, coagulopathy). In general, blood products are used early in

the management of patients with limited cardiac and pulmonary reserve (who are unable to withstand

or compensate for an acute reduction in their systemic oxygen delivery) and those with lesions that are

at particular high risk for continued or recurrent hemorrhage (e.g., gastroesophageal varices).

Careful hemodynamic monitoring of these potentially critically ill patients is vital to successful

management. There are no clear recommendations, but it seems reasonable for those patients who are

actively bleeding and those who have recently sustained significant hemorrhage to be admitted to an

intensive care unit for close monitoring of hemodynamic parameters and evidence of continued or

recurring hemorrhage. The presence of significant underlying illnesses, such as cardiac, renal, hepatic,

or pulmonary insufficiency, may necessitate noninvasive monitoring or invasive cardiac monitoring

with central venous and arterial catheters. The information gained from these devices allows cardiac

performance to be optimized during intravascular volume replacement. The placement of a urinary

catheter and frequent monitoring of heart rate, blood pressure, urine output, and mental status are the

minimum necessary to monitor patients who have suffered GI hemorrhage. The importance of prompt,

adequate resuscitation and diligent observation cannot be overemphasized as the cornerstone for

managing these potentially mortally ill patients.

Table 65-5 Glasgow–Blatchford Bleeding Score (GBS)

DIAGNOSTIC APPROACH

5 After the restoration of circulating blood volume, the next step is to identify the source of bleeding so

that definitive therapy may be instituted. If the patient presents with hematemesis, localization of the

bleeding to the esophagus, stomach, or duodenum is relatively straightforward and

esophagogastroduodenoscopy (EGD) should be performed promptly to identify the source of bleeding.

When blood or coffee-ground guaiac-positive material is present in the gastric aspirate, EGD will likely

define the site of bleeding. Bright red blood per rectum strongly suggests a lower GI source of bleeding

unless the patient is hemodynamically unstable in which case the hemorrhage may originate from a

source proximal to the ligament of Treitz. A general algorithm for evaluating patients with acute UGI

and LGI hemorrhage is presented in Algorithm 65-1.

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Algorithm 65-1. Diagnostic steps in the evaluation of gastrointestinal hemorrhage.

Table 65-6 Predictors of Persistent or Recurrent Bleeding in Patients with

Nonvariceal UGI Hemorrhage

Gastric Aspiration

Recent studies have called into question the routine placement of nasogastric tubes (NGTs) in all

1684

patients with suspected GI bleeding. In patients with hematemesis, gastric aspiration is not necessary to

obtain a diagnosis of a UGI bleed. However, it can provide useful information regarding the rate of

hemorrhage. Knowing the degree to which a patient is bleeding may help guide clinical decision

making, such as the need to initiate octreotide, transfuse blood emergently, urgently perform an EGD,

or determine whether or not ICU monitoring is necessary.34

In the absence of hematemesis, aspiration of gastric fluid after the placement of a NGT may be used

to distinguish between a UGI and LGI source of bleeding. Two studies with more than 700 patients

found that the presence of blood in the gastric aspirate was a good indicator of a UGI source; however,

its absence was unreliable in predicting the presence or absence of a UGI source.35,36 In one study of

220 patients with UGI sources of bleeding, the sensitivity, specificity, and accuracy of the nasogastric

aspirate was 42% (95% confidence interval [CI] = 32, 51%), 91% (95% CI = 83, 95%), and 66% (95%

CI = 59, 72%), respectively.36 While a clear aspirate does not rule out a UGI source of bleeding,

aspiration of blood confirms it. Additionally, placing an NGT may help remove blood from the gastric

lumen to improve visualization once the EGD is performed. However, NGT placement can be associated

with pain, aspiration, and pneumothorax.37 Additionally, other less invasive methods may indicate a

UGI source (black stool, BUN/creatinine ratio >30, and age younger than 50 years). Due to these

factors, NGT placement prior to EGD should not be routine but instead individualized to each patient.

Endoscopy

Esophagogastroduodenoscopy

EGD will identify the site of bleeding in about 95% of cases of UGI bleeding and is the initial diagnostic

study for patients suspected of bleeding from the esophagus, stomach, or duodenum.38 The sensitivity of

the procedure is significantly enhanced when performed within the first 24 hours of presentation.4 A

systematic review of the literature found that early endoscopy (i.e., performed within 24 hours of

admission) was associated with a decreased transfusion requirement and decreased length of stay.39 A

prospective, randomized trial found that early endoscopy allowed the triaging of 46% of patients to

outpatient care without any adverse effects.40 Previous consensus guidelines and several cohort studies

have related various endoscopic stigmata of recent or active hemorrhage to a heightened risk of

rebleeding or continued bleeding.41–44 Laine and Peterson41 analyzed data from 37 prospective trials in

which patients with bleeding ulcers did not receive endoscopic therapy; they found that the rate of

further bleeding was less than 5% for those patients with a clean ulcer base and increased to 10% for

patients with a flat spot, 22% for those with an adherent clot, 43% for those with a nonbleeding visible

vessel, and 55% for those with active bleeding. Endoscopic features predictive of persistent or recurrent

bleeding and mortality are shown in Tables 65-6, 65-7, and 65-8. In addition to these ulcer-specific

factors, endoscopy allows identification of lesions with a high risk of continued hemorrhage and

mortality (i.e., gastroesophageal varices), and those with a low risk (e.g., Mallory–Weiss tears). The

efficacy of endoscopy-based modalities to control UGI hemorrhage is discussed in subsequent sections.

Colonoscopy

Although the efficacy of colonoscopy in determining the cause of occult GI bleeding is undisputed,

historically its role in the evaluation of patients with acute LGI bleeding was less well agreed upon.

Recently however, newer studies have established it as the procedure of choice for patients with

suspected LGI bleeding despite its limitations.45–48 Colonic lavage with a polyethylene glycol solution

can be used to clear the lumen of clot and stool providing adequate visualization of the mucosa,49 but

others have reported good visualization of the mucosa even in the absence of mechanical bowel

preparation.50

Studies have shown a diagnosis is made in 74% to 100% of patients with an LGI bleed undergoing

colonoscopy, and a pool analysis of six recent studies found a composite yield of 91% for

colonoscopy.47,48,51,52 A meta-analysis examined the role of colonoscopy as the primary diagnostic

modality for patients with acute lower GI bleeding and found that 69% (range 48% to 90%) of urgent

colonoscopies identified a source or a presumptive source of bleeding.53 Even in the setting of

unprepped bowel, urgent colonoscopy has been shown to identify bleeding colon and distal ileal lesions

in 82 of 85 patients (97%).50 Stigmata of recent hemorrhage for LGI bleeding are similar to those of

UGI lesions and include an actively bleeding site, a nonbleeding visible vessel, and an adherent clot;

these findings have been associated with continued hemorrhage and therefore the need for urgent

colectomy.7,54 Jensen et al.45 reported that 25% to 50% of patients with any of these three factors

continued to bleed or rebled and ultimately required urgent colectomy. Others have found colonoscopy

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to be less accurate in the diagnosis of LGI bleeding, for example, Al Qahtani et al.55 reported a series of

136 patients in which colonoscopy identified only 45% of the sources of bleeding.

Enteroscopy

For those patients who present with hematochezia in whom the initial EGD and colonoscopy is

nondiagnostic, repeating these studies before evaluating the small intestine is warranted given the very

small frequency in which the bleeding originates from the small intestine (1%). Repeating the EGD and

colonoscopy when the patient is better resuscitated will often detect lesions such as ulcers or vascular

ectasias that were obscured by blood at the initial endoscopy or the vasoconstriction of the GI mucosa

that accompanies hemorrhagic shock.

Endoscopy of the small bowel with an enteroscope or a pediatric colonoscope will allow inspection of

the proximal 60 cm of the jejunum56 and the use of a long videoenteroscope may allow visualization of

100 to 150 cm of intestine beyond the ligament of Treitz.57 Jensen et al.58 in an experience with more

than 200 patients with obscure sources of GI bleeding reported success in identifying the etiology in

79% of instances using enteroscopy. In their experience, vascular ectasias and postbulbar ulcers were

the most common causes of obscure GI bleeding.

Table 65-7 Predictors of Mortality in Patients with Nonvariceal UGI Hemorrhage

Intraoperative enteroscopy using a combination of push enteroscopes per os and per rectum or via

enterotomy can allow examination of the entire small bowel. While the endoscopist manipulates the

scope, the surgeon manually advances the bowel over the endoscope. After the bowel is telescoped onto

the endoscope it is slowly withdrawn while the endoscopist examines the mucosal lumen and the

surgeon watches the transilluminated bowel wall. While this technique can be effective, it is limited by

its invasive nature.59

Double Balloon Enteroscopy

This technique utilizes a long enteroscope and a long overtube. Both the overtube and the enteroscope

have balloons at the end. When the balloon of the enteroscope is inflated it “grabs” the mucosal surface

and allows advancement of the overtube whose balloon is deflated. The overtube balloon is then

inflated while the enteroscope balloon is deflated. The enteroscope is then advanced while the inflated

overtube balloon grips the mucosa. Using these alternate inflation–deflation cycles, long distance

advancement of the enteroscope has been achieved.2 In one U.S. multicenter study, the average distance

achieved was 360 cm with a diagnosis made in 43% of cases.60 In some cases lesions may be seen that

are missed by other techniques.61

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and include proctalgia and/or pain at the injection site, local bruising and inflammatory reaction.

Efficacy data are sparse but one large randomized controlled trial demonstrated improvement in

continence for half the patients treated with SOLESTA.56 The FDA-approved SNS for treatment of fecal

incontinence in 2011. It is a two-stage procedure, in which there is a trial period, involving

percutaneous implantation of an electrode into S3. If there is a >50% improvement in symptoms, the

patient proceeds to the second stage which involves placement of a permanent stimulator. Between 50%

and 92% success rates have been reported with an improvement of ≥50% reduction in the number of

incontinent episodes per week compared to baseline. Perfect continence has been achieved in 40% of

subjects.57–68 Since SNS was approved, it has largely replaced overlapping sphincteroplasty as the first

line treatment. Finally, colostomy is a last resort in patients in whom all other treatment modalities

have failed.

SUMMARY

The colon, rectum, anus all help coordinate very complicated functions. Understanding their physiology

is important in the management of their associated pathology.

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37. Saunders MD, Cappell MS. Endoscopic management of acute colonic pseudo-obstruction. Endoscopy

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38. Vanek VW, Al-Salti M. Acute pseudo-obstruction of the colon (Ogilvie’s syndrome). An analysis of

400 cases. Dis Colon Rectum 1986;29:203–210.

39. Johnson CD, Rice RP, Kelvin FM, et al. The radiologic evaluation of gross cecal distension:

emphasis on cecal ileus. AJR Am J Roentgenol 1985;145:1211–1217.

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of the literature (October 1948 to March 1980) and report of four additional cases. Dis Colon

Rectum 1982;25:157–166.

41. Ponec RJ, Saunders MD, Kimmey MB. Neostigmine for the treatment of acute colonic pseudoobstruction. N Engl J Med 1999;341:137–141.

42. Trevisani GT, Hyman NH, Church JM. Neostigmine: safe and effective treatment for acute colonic

pseudo-obstruction. Dis Colon Rectum 2000; 43:599–603.

43. Saunders MD, Kimmey MB. Systematic review: acute colonic pseudo-obstruction. Aliment Pharmacol

Ther 2005;22:917–925.

44. Rockwood TH, Church JM, Fleshman JW, et al. Patient and surgeon ranking of the severity of

symptoms associated with fecal incontinence: the fecal incontinence severity index. Dis Colon

Rectum 1999;42:1525–1532.

45. Jorge JM, Wexner SD. Etiology and management of fecal incontinence. Dis Colon Rectum

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1993;36:77–97.

46. Byrne CM, Solomon MJ, Young JM, et al. Biofeedback for fecal incontinence: short-term outcomes

of 513 consecutive patients and predictors of successful treatment. Dis Colon Rectum 2007;50:417–

427.

47. Keck JO, Staniunas RJ, Coller JA, et al. Biofeedback training is useful in fecal incontinence but

disappointing in constipation. Dis Colon Rectum 1994;37:1271–1276.

48. Bartlett L, Sloots K, Nowak M, et al. Biofeedback for fecal incontinence: a randomized study

comparing exercise regimens. Dis Colon Rectum 2011;54:846–856.

49. Schwandner T, Konig IR, Heimerl T, et al. Triple target treatment (3T) is more effective than

biofeedback alone for anal incontinence: the 3T-AI study. Dis Colon Rectum 2010;53:1007–1016.

50. Barisic GI, Krivokapic ZV, Markovic VA, et al. Outcome of overlapping anal sphincter repair after 3

months and after a mean of 80 months. Int J Colorectal Dis 2006;21:52–56.

51. Demirbas S, Atay V, Sucullu I, et al. Overlapping repair in patients with anal sphincter injury. Med

Princ Pract 2008;17:56–60.

52. Evans C, Davis K, Kumar D. Overlapping anal sphincter repair and anterior levatorplasty: effect of

patient’s age and duration of follow-up. Int J Colorectal Dis 2006;21:795–801.

53. Fleshman JW, Peters WR, Shemesh EI, et al. Anal sphincter reconstruction: anterior overlapping

muscle repair. Dis Colon Rectum 1991;34:739–743.

54. Jesudason SR, Mathai V, Gladwin G, et al. Functional outcome of overlapping sphincter repair for

anal incontinence. Trop Gastroenterol 1999;20:189–190.

55. Lamblin G, Bouvier P, Damon H, et al. Long-term outcome after overlapping anterior anal sphincter

repair for fecal incontinence. Int J Colorectal Dis 2014;29(11):1377–1383.

56. Graf W, Mellgren A, Matzel KE, et al. Efficacy of dextranomer in stabilised hyaluronic acid for

treatment of faecal incontinence: a randomised, sham-controlled trial. Lancet 2011;377:997–1003.

57. Altomare DF, Ratto C, Ganio E, et al. Long-term outcome of sacral nerve stimulation for fecal

incontinence. Dis Colon Rectum 2009;52:11–17.

58. Boyle DJ, Murphy J, Gooneratne ML, et al. Efficacy of sacral nerve stimulation for the treatment of

fecal incontinence. Dis Colon Rectum 2011;54:1271–1278.

59. Damon H, Barth X, Roman S, et al. Sacral nerve stimulation for fecal incontinence improves

symptoms, quality of life and patients’ satisfaction: results of a monocentric series of 119 patients.

Int J Colorectal Dis 2013;28:227–233.

60. Devroede G, Giese C, Wexner SD, et al. Quality of life is markedly improved in patients with fecal

incontinence after sacral nerve stimulation. Female Pelvic Med Reconstr Surg 2012;18:103–112.

61. George AT, Kalmar K, Panarese A, et al. Long-term outcomes of sacral nerve stimulation for fecal

incontinence. Dis Colon Rectum 2012;55:302–306.

62. Lim JT, Hastie IA, Hiscock RJ, et al. Sacral nerve stimulation for fecal incontinence: long-term

outcomes. Dis Colon Rectum 2011;54:969–674.

63. Maeda Y, Lundby L, Buntzen S, et al. Outcome of sacral nerve stimulation for fecal incontinence at

5 years. Ann Surg 2014;259:1126–1131.

64. Mellgren A, Wexner SD, Coller JA, et al. Long-term efficacy and safety of sacral nerve stimulation

for fecal incontinence. Dis Colon Rectum 2011; 54:1065–1075.

65. Michelsen HB, Thompson-Fawcett M, Lundby L, et al. Six years of experience with sacral nerve

stimulation for fecal incontinence. Dis Colon Rectum 2010; 53:414–421.

66. Takano S, Boutros M, Wexner SD. Sacral nerve stimulation for fecal incontinence. Dis Colon Rectum

2013;56:384.

67. Wexner SD, Coller JA, Devroede G, et al. Sacral nerve stimulation for fecal incontinence: results of

a 120-patient prospective multicenter study. Ann Surg 2010;251:441–449.

68. Wexner SD, Hull T, Edden Y, et al. Infection rates in a large investigational trial of sacral nerve

stimulation for fecal incontinence. J Gastrointest Surg 2010; 14:1081–1089.

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Chapter 65

Acute Gastrointestinal Hemorrhage

Jason S. Mizell and Richard H. Turnage

Key Points

1 Upper gastrointestinal (UGI) hemorrhage accounts for about 80% of cases of acute GI blood loss.

2 The most common cause of acute UGI hemorrhage is peptic ulcer disease and the most common

cause of acute lower gastrointestinal (LGI) hemorrhage is diverticulosis.

3 Upper GI bleeding typically presents with hematemesis (the vomiting of blood) or melena (the

passage of black, tarry stool), whereas lower GI bleeding typically causes hematochezia (the passage

of fresh blood from the rectum).

4 Most patients (about 80%) suffering from GI hemorrhage will stop bleeding spontaneously. Those

who do not stop or those who rebleed are at particularly high risk to suffer an in-hospital

complication, require operative control of their hemorrhage, or die.

5 Esophagogastroduodenoscopy (EDG) is the initial diagnostic study of choice for patients suspected of

bleeding from the esophagus, stomach or duodenum and colonoscopy is the procedure of choice for

evaluating patients with a suspected lower GI hemorrhage.

6 Nonsteroidal anti-inflammatory drugs are an important risk factor for the development of GI

hemorrhage in general and gastroduodenal ulcer formation in particular.

7 Treatment of patients bleeding from gastroduodenal ulcer is intravenous proton pump inhibitor and

endoscopic thermocoagulation or mechanical ligation or clipping of the bleeding vessel.

8 In general, a patient bleeding from esophageal varices should undergo urgent pharmacologic therapy

with intravenous octreotide and endoscopic banding of the bleeding varices.

9 Lower GI hemorrhage due to diverticulosis is generally managed nonoperatively due to a low risk of

persistent or recurrent bleeding.

1 Acute gastrointestinal (GI) hemorrhage is categorized as upper or lower depending upon the location

of the bleeding relative to the ligament of Treitz. Upper GI (UGI) hemorrhage (i.e., bleeding from the

esophagus, stomach, or duodenum) accounts for about 80% of cases of acute GI blood loss, with most of

the remainder coming from the colon. The small intestine is the site of hemorrhage in about 1% to 5%

of cases.1,2 Although it may be decreasing,3 the incidence of UGI bleeding is estimated to be about 37 to

150 episodes per 100,000 individuals depending upon the population sampled,4 whereas the incidence

of lower GI (LGI) bleeding is about 20 cases per 100,000 individuals.5 Overall, GI hemorrhage accounts

for roughly 300,000 hospitalizations and 30,000 deaths annually in the United States.6

2 The differential diagnosis of overt UGI and LGI hemorrhage and the relative frequency of the most

common causes of GI bleeding are shown in Tables 65-1 and 65-2 and Figure 65-1A,B, respectively.

Although the incidence varies by age, overall the most common causes of acute UGI hemorrhage are

peptic ulcer disease (31% to 58%), gastritis and mucosal erosions (9% to 30%), and gastroesophageal

varices (3% to 23%)1,4 whereas diverticulosis (24% to 47%), all forms of colitis (6% to 26%), neoplasms

(9% to 17%), and angiodysplasia (2% to 12%) account for most instances of lower GI

hemorrhage.1,5,7–10

PATIENT CHARACTERISTICS

Patients who suffer significant GI hemorrhage are more commonly older (average age approximately 60

to 70 years)1,4) and male compared with individuals without GI bleeding. Furthermore, these

individuals are more likely to use alcohol, tobacco, aspirin, nonsteroidal anti-inflammatory drugs

(NSAIDs), and anticoagulants.1,11 Predictors of risk for acute GI bleeding are shown in Table 65-3.

Coexisting chronic illnesses are common in patients suffering either a UGI or LGI hemorrhage.

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Various studies have suggested a correlation between GI bleeding and correlates of poor health such as

the use of multiple medications, reduced levels of physical activity, and inability to complete basic selfcare tasks.11 Cardiovascular,11 hepatic, and renal disease12 are particular risk factors for acute GI

bleeding. The presence of these chronic illnesses, as well as chronic obstructive pulmonary disease and

cirrhosis, also greatly increase the risk of rebleeding after endoscopic control.13 Tobacco is also

associated with higher rates of significant GI hemorrhage. A prospective cohort study of 5,888 men and

women found that the multivariate-adjusted hazard ratio for subjects who smoked more than half a pack

per day was 2.14 (95% CI = 1.22, 3.75) for UGI bleeding.11

Certain medications increase the risk of GI hemorrhage. Many studies have related the use of NSAIDs

and aspirin to significant GI bleeding. The risk is particularly elevated for UGI bleeding but NSAIDs

increase the risk of LGI hemorrhage as well. In Vreeburg’s review of 951 patients with UGI hemorrhage,

41% used NSAIDs or aspirin. Van Leerdam reported that more than half of the patients bleeding from

ulcers were actively taking NSAIDs or ASA.14 Mellemkjaer et al.15 found that the observed to expected

ratio of UGI hemorrhage in a cohort of 156,138 users of NSAIDs was 4.1 (95% CI = 3.8, 4.5). Other

medications known to increase the risk of GI hemorrhage include corticosteroids, spironolactone,16 and

the selective serotonin reuptake inhibitors (SSRIs).17,18

The use of anticoagulants is also an important risk factor for acute GI bleeding. Coumadin is a

particularly common cause. Kaplan found the age- and sex-adjusted hazard ratio for GI bleeding in

patients taking oral anticoagulants was 2.59 (95% CI = 1.71, 3.93).11 Vreeburg et al.4 reported that

17% of their patients with UGI hemorrhage were taking coumadin and the international normal ratio

(INR) was greater than 4 in more than half of these patients. Because coumadin metabolism can be

affected by so many interfering substances, inadvertent coumadin toxicity is a common problem, often

presenting with GI hemorrhage. Antiplatelet agents such as clopidogrel and ticlopidine are also

associated with an increased risk of GI hemorrhage.19

Table 65-1 Differential Diagnosis of Acute Upper Gastrointestinal Hemorrhage by

Anatomic Site

CLINICAL PRESENTATION

3 The presentation of GI bleeding can range from mild asymptomatic bleeding to overt GI bleeding.

UGI bleeding typically presents with hematemesis (the vomiting of blood) or melena, whereas LGI

bleeding typically presents with hematochezia. Melena is a black, tarry stool resulting from the

degradation of blood by enteric bacteria. It may occur with the loss of as little as 50 to 200 mL of

blood.20,21 Bleeding from the small intestine or right colon may also appear black if it has remained in

the GI tract for more than 12 to 14 hours.22 Hematochezia is the passage of bright red blood, marooncolored blood, or blood clots from the rectum. However, massive UGI hemorrhage can cause

1679

hematochezia in as many as 11% of patients, but this is typically associated with hemodynamic

instability.23 Patients with acute GI bleeding may present with the hemodynamic consequences of

hemorrhage including light-headedness, dizziness, orthostatic syncope or near syncope, shortness of

breath, or palpitations from tachycardia.

Table 65-2 Differential Diagnosis of Acute Lower Gastrointestinal Hemorrhage by

Anatomic Site

Figure 65-1. A: The relative frequency of the most common causes of upper gastrointestinal hemorrhage in the United States.

These data represent the percentage of patients with each of these causes of UGI hemorrhage for 482 patients in a survey of the

members of the American College of Gastroenterology published by Peura et al.1 in 1997. These data are very similar to that

reported by Vreeburg in a multi-institutional study of 951 patients sustaining a UGI hemorrhage in the hospitals in and

surrounding Amsterdam.4 B: The relative frequency of the most common causes of lower gastrointestinal hemorrhage. These data,

reported by Lingenfelser and Ell5 are the percentage of patients with each of these causes of lower GI hemorrhage in 912 patients

collected in five studies from Europe, the Orient, and the United States

1,7–10

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The medical history and physical examination provide important clues of the etiology of the patient’s

hemorrhage and the potential risk to the patient’s life. The occurrence of melena after several days of

worsening epigastric or upper abdominal pain suggests peptic ulcer disease; whereas hematemesis or

melena following vomiting or retching strongly suggests a Mallory–Weiss tear. Massive, painless UGI

hemorrhage in a patient with cirrhosis suggests bleeding from gastroesophageal varices, although other

etiologies including peptic ulcer disease or a Mallory–Weiss tear must also be considered. The medical

history should elicit the presence of risk factors for GI hemorrhage alluded to in the previous

paragraphs and in Table 65-3 .

A systematic physical examination will document the magnitude of bleeding and the patient’s ability

to compensate. Massive hemorrhage is associated with signs and symptoms of hypovolemic shock,

including cool, clammy, mottled skin, tachycardia, tachypnea, flat jugular veins, oliguria, and perhaps

hypotension. These responses may be altered by advanced age, concomitant medical problems, and

particular medications. Physical examination should also document evidence of cirrhosis and portal

hypertension (i.e., ascites, spider angiomas, hepatosplenomegaly, palmar erythema, and large

hemorrhoidal veins). A rectal examination may demonstrate bright red blood or melena. The clinical

scenario alone will usually not localize the location of the bleeding, so other diagnostic studies are often

required to identify the cause and site of bleeding.

PROGNOSTIC FACTORS

4 Most patients (approximately 80%) suffering from GI hemorrhage will stop bleeding spontaneously.

Those who do not stop or those who rebleed are at particularly high risk to suffer an in-hospital

complication, require operative control of their hemorrhage, or die. Several classification systems have

been developed to separate patients with low risk of complications from those with a high risk of

complications due to acute UGI and LGI hemorrhage. These systems have also been used to stratify

those patients who may be safely managed as an outpatient from those requiring in-hospital care.24 The

BLEED classification system addresses both UGI and LGI hemorrhage and consists of the following

parameters: ongoing bleeding, low systolic blood pressure, elevated prothrombin time, erratic mental

status, and unstable comorbid disease. Patients with at least one BLEED criterion are more likely to

suffer in-hospital complications from UGI bleeding (31% vs. 4%) or LGI bleeding (38% vs. 12%) than

are patients with no criteria.25

Table 65-3 Characteristics of Individuals at an Increased Risk of Developing

Acute Gastrointestinal Bleeding

Table 65-4 Rockall Risk Scoring System and Rates of Rebleeding and Mortality

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