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.

References

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25. Mann C, Pouzeratte Y, Boccara G, et al. Comparison of intravenous or epidural patient-controlled

analgesia in the elderly after major abdominal surgery. Anesthesiology 2000;92:433–441.

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major abdominal surgery and postoperative ileus. Ann Surg 2004;240:728–734; discussion 34–35.

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28. Ljungqvist O. ERAS-enhanced recovery after surgery: moving evidence-based perioperative care to

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colorectal surgery in elderly patients. Colorectal Dis 2014;16(12):947–956.

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33. Greco M, Capretti G, Beretta L, et al. Enhanced recovery program in colorectal surgery: a metaanalysis of randomized controlled trials. World J Surg 2014; 38:1531–1541.

34. Walker EA, Roy-Byrne PP, Katon WJ. Irritable bowel syndrome and psychiatric illness. Am J

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35. Munakata J, Naliboff B, Harraf F, et al. Repetitive sigmoid stimulation induces rectal hyperalgesia

in patients with irritable bowel syndrome. Gastroenterology 1997;112:55–63.

36. Ogilvie H. Large-intestine colic due to sympathetic deprivation. Br Med J 1948;2:671.

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

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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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