ACS Guide to Lower GI Bleeding Diagnosis and Treatment

© 2006 WebMD, Inc. All rights reserved. ACS Surgery: Principles and Practice
5 GASTROINTESTINAL TRACT AND ABDOMEN 6 LOWER GASTROINTESTINAL BLEEDING — 1

6 LOWER GASTROINTESTINAL
BLEEDING
Michael J. Rosen, M.D., and Jeffrey L. Ponsky, M.D., F.A.C.S.

Approach to Lower GI Bleeding
Lower gastrointestinal bleeding is defined as abnormal hemor- the nature and duration of the bleeding, including stool color and
rhage into the lumen of the bowel from a source distal to the liga- frequency. The patient should also be asked about any associated
ment of Treitz. In the majority of cases, lower GI bleeding derives symptoms of potential significance (e.g., abdominal pain, changes
from the colon; however, the small bowel is identified as the source in bowel habits, fever, urgency, tenesmus, or weight loss), as well
of bleeding in as many as one third of cases,1,2 and the upper GI as about relevant past medical events (e.g., previous GI bleeding
tract is identified as the source in as many as 11% of patients pre- episodes, injuries, surgical procedures, peptic ulcer disease,
senting with bright-red blood per rectum.3 inflammatory bowel disease [IBD], and abdominal or pelvic irra-
Lower GI bleeding is more common in men than in women. diation). Any complicating comorbid conditions (e.g., heart or
The incidence rises steeply with advancing age, exhibiting a liver disease and clotting disorders) should be investigated. A com-
greater than 200-fold increase from the third decade of life to the prehensive review of medications—in particular, nonsteroidal
ninth. This increase is largely attributable to the various colonic anti-inflammatory drugs (NSAIDs) and anticoagulants—is
disorders commonly associated with aging (e.g., diverticulosis and mandatory.12
angiodysplasia).4-6 The exact incidence of lower GI bleeding is not The physical examination should include determination of pos-
known, because there is no standardized technique for localizing tural vital signs so that intravascular volume status can be accu-
it. Several investigators, however, estimate the incidence to be in rately estimated. A drop in the orthostatic blood pressure greater
the range of 20 to 27 cases per 100,000 adults.4,7 A 1997 survey than 10 mm Hg or an increase in the pulse rate greater than 10
of GI bleeding from the American College of Gastroenterology beats/min indicates that more than 800 ml of blood (> 15% of the
found that lower GI hemorrhage accounted for 24% of all GI total circulating blood volume) has been lost. Marked tachycardia
bleeding events.8 Another study published the same year found and tachypnea in association with hypotension and depressed
that 0.7% of 17,941 discharges from a Veterans Affairs hospital mental status indicates that more than 1,500 ml of blood (> 30%
were for patients who had had lower GI bleeding.9 of the total circulating blood volume) has been lost. A complete
The basic components of management are (1) initial hemody- abdominal examination, including digital rectal examination and
namic stabilization, (2) localization of the bleeding site, and (3) anoscopy, should be performed.
site-specific therapeutic intervention. There are many conditions Laboratory evaluation should include a complete blood count,
that can cause lower GI hemorrhage [see Discussion, Etiology of measurement of serum electrolyte concentrations, a coagulation
Lower GI Bleeding, below]; accordingly, successful localization profile (prothrombin time and partial thromboplastin time) [see
depends on timely and appropriate use of a variety of diagnostic 1:4 Bleeding and Transfusion], and typing and crossmatching.
tests. Despite the abundance of diagnostic modalities available, A nasogastric tube should be placed for gastric lavage. If lavage
attempts to localize the source of the hemorrhage fail in as many yields positive results (i.e., the aspirate contains gross blood or so-
as 8% to 12% of patients.10,11 Once the bleeding site is localized, called coffee grounds), esophagogastroduodenoscopy (EGD) is
the appropriate therapeutic intervention must be carried out as indicated [see 5:18 Gastrointestinal Endoscopy]. An aspirate that
expeditiously as possible. contains copious amounts of bile is strongly suggestive of a lower
Lower GI bleeding can be acute and life-threatening, chronic, GI source of bleeding, and the workup proceeds accordingly [see
or even occult. In what follows, we focus on severe, life-threaten- Investigative Studies, below]. The choice is less clear-cut with a
ing hematochezia, reviewing the wide array of possible causes of clear aspirate. In the absence of bile, such an aspirate cannot rule
lower GI bleeding and outlining the diagnostic and therapeutic out a duodenal source for the bleeding. Accordingly, there is
modalities available for treating this difficult clinical problem. some degree of latitude for clinical judgment: depending on the
overall clinical picture, the surgeon may choose either to perform
EGD to rule out a duodenal bleeding source or to proceed with
Initial Evaluation and colonoscopy on the assumption that the source of the bleeding is
Resuscitation in the lower GI tract.
Initial evaluation of a pa- Resuscitative efforts should begin immediately, with the aim of
tient with lower GI bleeding maintaining the patient in a euvolemic state. Two large-bore
should include a focused his- peripheral intravenous catheters should be inserted and isotonic
tory and physical examination, I.V. fluid administered. A Foley catheter should be placed to facil-
to be carried out simultane- itate monitoring of intravascular volume status. Whether and in
ously with resuscitation. Of what form to administer blood products is determined on an indi-
particular importance in tak- vidual basis, with appropriate weight given to the presence or
ing the history is to ascertain absence of comorbid conditions, the rate of blood loss, and the


Patient presents with acute lower GI bleeding

Resuscitate as necessary.
Simultaneously, take history (nature and duration of bleeding,
associated symptoms, past medical history, complicating
comorbid conditions, medications) and perform physical
exam (postural vital signs, complete abdominal exam). Order
laboratory tests (CBC, serum electrolytes, coagulation profile,
and typing and crossmatching).
Place NG tube for gastric lavage.

NG aspirate contains gross blood NG aspirate is clear

Perform esophagogastroduodenoscopy (EGD). Duodenal source cannot be ruled out.
Use clinical judgment: depending on clinical picture,
either (1) look for upper GI source (e.g., with EGD)
(see left) or (2) proceed with colonoscopy (see right).

Colon is adequately visualized on
Colonoscopy identifies bleeding source
colonoscopy, but no bleeding source
is apparent

Examine ileum; if no active bleeding is
noted, perform EGD.
Lesion is amenable to endoscopic
therapy

Treat endoscopically (e.g., with
fulguration, vasoconstrictors, or clips).
Surgical therapy is indicated

Endoscopic Endoscopic
therapy succeeds therapy fails

Bleeding site was localized preoperatively

Perform segmental resection.

Bleeding site was not localized preoperatively
Treat surgically. General criteria:
Attempt to localize bleeding site intraoperatively > 4 units of blood/24 hr needed for
(e.g., with EGD, colonoscopy, enteroscopy). hemodynamic stability; bleeding
continues for 72 hr; rebleeding
occurs within 1 wk.

Bleeding site cannot be localized Bleeding site is localized
intraoperatively intraoperatively

Perform subtotal colectomy. Perform segmental resection.


Approach to Lower GI Bleeding

NG aspirate contains copious bile

Perform colonoscopy.

Bleeding volume is such that colonoscopy
is not feasible or, if attempted, is ineffective

Perform selective mesenteric arteriography,
guided (if feasible and desired) by
radiolabeled RBC scanning.
Consider helical CT scanning.

Lesion is amenable to angiographic therapy

Treat with vasopressin infusion (initially,
0.4 U/min, then 0.2 U/min). (Transcatheter
embolization is an alternative.)

Vasopressin fails Vasopressin succeeds


degree of hemodynamic stability. Severe hemodynamic instability ed. Depending on the indication and on the technique employed,
may necessitate monitoring in the intensive care unit. the diagnostic yield from push enteroscopy has ranged from 13%
to 78%.19 Typically, yields are highest (40% to 60%) in patients
with significant GI hemorrhage.
Investigative Studies
RADIOLABELED RED BLOOD CELL SCANNING
A number of diagnostic
techniques are available for de- Radionuclide scanning is highly sensitive for lower GI hemorrhage:
termining the source of lower it is capable of detecting bleeding at rates as slow as 0.1 to 0.4
GI hemorrhage, the most use- ml/min.20 Two imaging tracers, both labeled with technetium-99m
ful of which are colonoscopy (99mTc), are currently available for radionuclide scanning in this
[see 5:18 Gastrointestinal Endos- setting: 99mTc-labeled sulfur colloid (99mTc-SC) and 99mTc-labeled
copy], radionuclide scanning, red blood cells (RBCs). 99mTc-SC requires no preparation time
computed tomography, and and can be injected immediately into the patient; however, its rapid
angiography (in the form of absorption into the liver and the spleen can often hinder accurate
selective mesenteric arteriography). The goal of these tests is to localization of overlying bleeding sites.9 At our institution, we pre-
locate the site of bleeding accurately so that definitive therapy can fer to use 99mTc-labeled RBCs. This agent requires some prepara-
be properly directed. Which diagnostic test is chosen for a specific tion time, but it has a much longer half-life than 99mTc-SC does, it
patient depends on several factors, including the hemodynamic sta- is not taken up by the liver and spleen, and it can be detected on
bility of the patient, the bleeding rate, the comorbid conditions pres- images as long as 24 to 48 hours after injection [see Figure 1].21,22
ent, and the local expertise available at the physician’s hospital. One study directly compared these two techniques and found
99mTc-labeled RBC scanning to have an accuracy of 93%, com-
COLONOSCOPY
pared with an accuracy of only 12% for 99mTc-SC scanning.23
Several large series that evaluated the diagnostic utility of colo- The high sensitivity of 99mTc-labeled RBC scanning—80% to
noscopy in patients with lower GI bleeding found this modality to 98%—is well attested, but there is considerable disagreement in
be moderately to highly accurate, with overall diagnostic yields rang- the literature with regard to its specificity in identifying the
ing from 53% to 97% [see Table 1].3,13-17 Those studies that report- anatomic site of bleeding.24-27 For example, on one hand, a 1996
ed morbidity found colonoscopy to be safe as well, with an aver- study found radiolabeled RBC scanning to be 97% accurate for
age complication rate of 0.5%. Colonoscopy has both a higher localizing bleeding in 37 patients undergoing surgical resection27;
diagnostic yield and a lower complication rate than arteriography on the other hand, a 1990 study reported a 42% rate of incorrect
in this setting and thus would appear to be a more attractive initial resection when surgical therapy was based solely on this modali-
test in most circumstances.3,18 An argument has been made—one ty.26 In 2005, one group retrospectively reviewed 127 bleeding
with which we agree—that colonoscopy should be considered the scans in an effort to identify factors that might predict a positive
procedure of choice for structural evaluation of lower GI bleeding scan.28 The investigators found that tagged RBC scans were 48%
and that arteriography should be reserved for patients with mas- accurate in localizing bleeding sites later confirmed by
sive, ongoing bleeding in whom endoscopy is not feasible or endoscopy, surgery, or pathologic evaluation. Multivariate analy-
colonoscopy fails to reveal the source of the hemorrhage.12 sis demonstrated that both the number of units of blood trans-
The merits of colonic purging have been extensively debated in fused in the 24 hours preceding the scan and the lowest record-
the literature.3,11,14 Although no firm conclusion has been reached, ed hematocrit differed significantly between patients with positive
we feel that adequate colonic purging can improve both the diag- scans and those with negative scans. However, the clinical signif-
nostic yield and the safety of colonoscopy. Given the absence of icance of a positive scan was unclear in this study, in that the rate
any definitive data suggesting that colonic purging either reacti- of endoscopy was not significantly different between patients who
vates or increases bleeding,12 it is our practice to administer an oral had positive scans and those who did not.
purge after the patient has been adequately resuscitated. To date, no prospective, randomized trials have compared
If the entire colon has been adequately visualized and no source radionuclide scanning with colonoscopy as the initial diagnostic
for the bleeding has been identified, the ileum should be intu- procedure for patients with lower GI hemorrhage. In our view,
bated; fresh blood in this region suggests a possible small bowel
source. If no active bleeding is observed in the ileum, upper GI
endoscopy should be performed to rule out an upper GI bleed- Table 1 Diagnostic Accuracy of Colonoscopy in
ing site. Localizing Source of Lower GI Hemorrhage
When colonoscopy and routine upper GI endoscopy fail to
locate a bleeding source, push enteroscopy may be helpful. This
Study No. of Patients Diagnostic Yield (%)
procedure can be carried out in several ways. It can be performed
purely endoscopically with a pediatric colonoscope.This approach Richter13 78 70 (90%)
generally requires a high level of skill on the part of the endos-
copist, in that the lack of retroperitoneal attachments of the small Jensen3 80 68 (85%)
intestine makes endoscopic navigation extremely challenging. In Rossini14 409 311 (76%)
most cases, only the proximal 150 cm of the small intestine can be
evaluated in this way. Alternatively, push enteroscopy can be per- Goenka15 166 141 (85%)
formed in the operating room at the time of exploratory laparoto- Ohyama16 345 307 (89%)
my. The surgeon can manually “milk” the small bowel over the
scope to evaluate its distal portion. In addition, an enterotomy can Chaudhry17 85 82 (97%)
be made, and the scope can be passed in both a retrograde and an Total 1,163 979 (84%)
antegrade fashion so that the entire small intestine can be evaluat-


CT evaluation of GI bleeding has several noteworthy advan-
tages: the scanners typically are readily available, mobilization of
special teams or units is not required, the scans can be completed
rapidly in the emergency department, and bowel preparation is
unnecessary. In one experimental study, CT scanners were able to
detect arterial bleeding at rates as low as 0.07 ml/min, which sug-
gests that CT scanning is more sensitive than angiography for this
purpose.30 In addition, CT scans are noninvasive and carry little
morbidity. Unfortunately, like radionuclide scanning, CT has no
therapeutic capability.
A 2003 study of 19 patients with GI hemorrhage compared
triphasic helical CT evaluation with colonoscopy and surgery for
localization of bleeding sites.30 In this series, five patients had small
bowel bleeding sites, and 14 had colonic sites. Helical CT scanning
correctly identified four of the five small bowel lesions and 11 of the
14 colonic lesions.These findings, though preliminary, suggest that
CT is a potentially valuable evaluation method in certain cases of
GI bleeding. Perhaps CT scanning can eventually replace radionu-
clide scanning, which is often inaccurate. One potential drawback
to the use of CT in this setting is the excessive dye load if angiog-
raphy is employed as well.
Figure 1 99mTC-labeled RBC scan demonstrates collection of
tracer at hepatic flexure. ANGIOGRAPHY

Selective Mesenteric
however, given that radionuclide scanning (unlike colonoscopy Arteriography
and angiography) has no therapeutic intervention capabilities, its
Selective mesenteric arteri-
best use is in patients with non–life-threatening lower GI bleeding
ography is somewhat less sen-
as a prelude and a guide to mesenteric angiography after active
sitive than radionuclide scan-
hemorrhage has been confirmed.
ning for lower GI hemorrhage:
COMPUTED TOMOGRAPHY bleeding must be occurring
at a rate of at least 1.0 to 1.5
With the ongoing improvements in high-speed abdominal
ml/min to be detectable with
CT scanning, there has been growing interest in the evaluation
this test.31 The procedure in-
of GI bleeding with CT.29 Helical CT scanners can provide
volves percutaneous placement of a transfemoral arterial catheter
direct or indirect evidence of the source of GI bleeding. Typical
for evaluation of the superior mesenteric, inferior mesenteric, and
findings that can facilitate localization of bleeding sites include
celiac arteries. A positive test result is defined as extravasation of
spontaneous hyperdensity of the peribowel fat, contrast enhance-
contrast into the lumen of the bowel [see Figure 2]. Once the bleed-
ment of the bowel wall, vascular extravasation of the contrast
ing vessel has been localized angiographically, the area must be
medium, thickening of the bowel wall, polyps, tumors, and vas-
marked so that it can be successfully identified intraoperatively;
cular dilatation.
this is commonly accomplished by infusing methylene blue into
the bleeding artery [see Figure 3].32,33
In several large series [see Table 2], the overall diagnostic yield of
arteriography ranged from 27% to 67%.27,34-38 The complication
rate for arteriography performed for lower GI bleeding ranges
from 2% to 4%.2,38 Reported complications include contrast aller-
gy, renal failure, bleeding from arterial puncture, and embolism
from a dislodged thrombus.12
Unlike radionuclide scanning, arteriography provides several
therapeutic options, including vasopressin infusion and emboliza-
tion of bleeding vessels. Nonetheless, given that arteriography has
a lower diagnostic yield and a higher complication rate than
colonoscopy does, it is reasonable to attempt colonoscopy first in
patients with lower GI hemorrhage and to reserve angiography for
patients in whom the volume of bleeding is such that colonoscopy
would be neither safe nor accurate.
Provocative Angiography for Continued Obscure Bleeding
In a minority of patients, obscure bleeding persists despite neg-
ative findings from endoscopy, mesenteric arteriography, and radio-
labeled RBC scanning.This obscure bleeding presents a consider-
Figure 2 Angiographic study documents extravasation of contrast able diagnostic challenge, which some investigators have proposed
into small bowel. addressing by means of so-called provocative angiography.39,40


hematochezia and diverticulosis in a prospective series of 121 pa-
tients.47 In this series, none of the patients treated endoscopically
with epinephrine injections, bipolar coagulation, or both required
surgery and none experienced recurrent bleeding episodes. A
2001 study from another group, however, reported high rates of
recurrent bleeding episodes in both the early and the late post-
treatment periods.48 In the absence of prospective, randomized tri-
als, it is difficult to draw definitive conclusions about the utility of
endoscopic therapy in treating diverticular hemorrhage.
Angiodysplasias resulting in GI hemorrhage typically are amen-
able to endoscopic treatment. That these lesions are frequently
found in the right colon makes perforation a concern; this compli-
cation is reported in approximately 2% of patients.49 Good success
rates have been reported with both injection and thermal meth-
ods.50 In one series, endoscopic fulguration was successful in 87%
of patients, and no rebleeding episodes occurred over a 1- to 7-
year follow-up period.50 Bleeding from multiple telangiectatic
lesions in the distal colon resulting from radiation injury can be
treated with thermal contact probes, lasers, or noncontact devices
Figure 3 Intraoperative examination of the bowel is aided by such as the argon plasma coagulator.51
injection of methylene blue dye, which facilitates localization of the
Postpolypectomy hemorrhage can often be successfully treated
bleeding site and thereby helps direct surgical resection.
by endoscopic means. Methods used include simple resnaring of
the stalk while pressure is maintained52; electrocauterization, with
or without epinephrine injection; endoscopic band ligation; and
placement of metallic clips. For patients whose bleeding is attrib-
Provocative angiography involves the use of short-acting anticoag- utable to benign anorectal causes, endoscopic therapy may include
ulant agents (unfractionated heparin, vasodilators, thrombolytics, epinephrine injection, sclerosant injection, or band ligation of
or combinations thereof) in association with angiography. Once internal hemorrhoids.53
the bleeding point has been localized, methylene blue is injected
and the patient is immediately brought to the OR for surgical ANGIOGRAPHIC THERAPY
treatment.To date, unfortunately, little has been published on this Diagnostic use of angiog-
technique, but it does appear to be a promising approach to this raphy in patients with lower
difficult problem. GI bleeding can often be fol-
lowed by angiographic thera-
py.The two main angiograph-
Management
ic treatment options are intra-
Although, in the majority of cases, lower GI bleeding stops arterial injection of vaso-
spontaneously, in a significant number of cases, hemorrhage con- pressin and transcatheter
tinues and necessitates therapeutic intervention. Treatment op- embolization.
tions include endoscopic therapy, angiographic therapy, and sur- Vasopressin acts to control bleeding by causing arteriolar vaso-
gical resection. constriction and bowel wall contraction.9 Once the bleeding site
has been localized angiographically, the catheter is positioned in
ENDOSCOPIC THERAPY

When colonoscopy identi-
fies a bleeding source, endo-
scopic treatment may be an Table 2 Diagnostic Accuracy of Mesenteric
option [see 5:18 Gastrointestinal
Angiography in Localizing Source of
Endoscopy]. Endoscopic mo-
dalities used to treat lower GI Lower GI Hemorrhage
bleeding include use of ther-
mal contact probes,41,42 laser Study No. of Patients No. of Positive
Angiograms (%)
photocoagulation,43 electrocau-
terization,44 injection of vaso- Pennoyer34 131 37 (28%)
constrictors, application of metallic clips,45 and injection scle-
rotherapy.46 The choice of a specific modality often depends on the Ng27 49 22 (45%)
nature of the offending lesion and on the expertise and resources Rantis35 30 8 (27%)
available locally. A 1995 survey of members of the American
College of Gastroenterology found that endoscopic therapy was Leitman36 68 27 (40%)
used in 27% of patients presenting with lower GI bleeding.8 Casarella37 69 46 (67%)
Diverticular hemorrhage can be difficult to treat endoscopical-
ly because of the high bleeding rate and the location of the bleed- Colacchio38 98 40 (41%)
ing point within the diverticulum. In 2000, one group of investi- Total 445 180 (40%)
gators reported their experience with endoscopic therapy for severe


the main trunk of the vessel. Infusion of vasopressin is initiated at zation therapy should be the first choice for angiographic treat-
a rate of 0.2 U/min and can be increased to a rate of 0.4 U/min. ment of lower GI bleeding.65,66
Within 20 to 30 minutes, another angiogram is performed to
SURGICAL THERAPY
determine whether the bleeding has ceased. If the bleeding is
under control, the catheter is left in place and vasopressin is con- Although there are no ab-
tinuously infused for 6 to 12 hours. If the bleeding continues to be solute criteria for surgical
controlled, infusion is continued for an additional 6 to 12 hours at treatment of lower GI bleed-
50% of the previous rate. Finally, vasopressin infusion is replaced ing, there are several factors—
by continuous saline infusion, and if bleeding does not recur, the including hemodynamic sta-
catheter is removed.54,55 tus, associated comorbidities,
The vasoconstrictive action of vasopressin can have deleterious transfusion requirements, and
systemic side effects, including myocardial ischemia, peripheral persistent bleeding—that are
ischemia, hypertension, dysrhythmias, mesenteric thrombosis, instrumental in making an
intestinal infarction, and death.9,36 Occasionally, simultaneous I.V. appropriate and timely deci-
administration of nitroglycerin is necessary to counteract these sion whether to operate. In general, patients who require more than
systemic effects. The reported success rate of vasopressin in con- 4 units of blood in a 24-hour period to remain hemodynamically
trolling lower GI bleeding ranges from 60% to 100%, and the inci- stable, whose bleeding has not stopped after 72 hours, or who expe-
dence of major complications ranges from 10% to 20%.56-58 rience rebleeding within 1 week after an initial episode should
Rebleeding rates as high as 50% have been reported.57,58 undergo surgery.9
An alternative for patients with coronary vascular disease, If the patient’s hemodynamic status permits, surgical treatment
severe peripheral vascular disease, or other comorbidities that should be undertaken after accurate localization of the bleeding
prevent safe administration of vasopressin is transcatheter embo- site.When possible, directed segmental resection is the procedure
lization. In this technique, a catheter is superselectively placed of choice: it is associated with rebleeding rates ranging from 0% to
into the identified bleeding vessel and an embolizing agent (e.g., 14% and mortality rates ranging from 0% to 13%.10,36,67 Blind
a gelatin sponge, a microcoil, polyvinyl alcohol particles, or a bal- segmental colectomy should never be performed: it is associated
loon) is injected. Several small series found this technique to be with rebleeding rates as high as 75% and mortality rates as high as
90% to 100% successful at stopping bleeding.59-63 Equally im- 50%.68 If hemodynamic compromise and ongoing hemorrhage
pressive was the finding that the rebleeding rates in these series make it necessary to perform surgical exploration before the bleed-
were 0%. The complication rates of this procedure are generally ing site can be localized, every effort should be made to identify
reasonable as well; however, intestinal infarction has been the source of bleeding intraoperatively before embarking on resec-
reported.36,64 tion. Intraoperative options for bleeding-site localization include
The use of small microcatheters and the ability to superselec- colonoscopy (to allow for this option, patients should always be
tively embolize individual vessels have reduced the potential for placed in the lithotomy position), EGD, and transoral passage of
ischemic perforation. It is possible that as more experience is a pediatric colonoscope for enteroscopy with simultaneous
gained with these techniques, superselective embolization may intraperitoneal assistance for small bowel manipulation.9 If the
replace catheter-directed vasoconstrictive therapy, thus obviating bleeding site still cannot be accurately localized, subtotal colecto-
the potential deleterious systemic effects of vasopressin adminis- my is the procedure of choice. This procedure is associated with
tration. Some researchers have suggested that with the exception mortality rates ranging from 5% to 33%,69,70 which underscores
of cases of diffuse bleeding lesions or cases whose demands exceed the importance of accurate preoperative localization of bleeding
the technical limitations of superselective catheterization, emboli- before surgical intervention.

Discussion

Etiology of Lower GI Bleeding cularis to supply the mucosa9; as the diverticulum expands, these
As noted, lower GI bleeding has a wide array of possible causes vessels are displaced. A 1976 anatomic study of colonic specimens
[see Table 3].9,71 Of these, diverticular disease is the most common, from patients with diverticular bleeding used angiography to
accounting for 30% to 40% of all cases.72 Arteriovenous malfor- demonstrate that in all cases, the vasa recta overlying the divertic-
mations (AVMs), though extensively described in the literature, ulum ruptured into the lumen of the diverticulum, not into the
are considerably less common causes, accounting for 1% to 4% of peritoneum [see Figure 4].76
cases.73,74 Other significant causative conditions are IBD, benign It has been estimated that approximately 17% of patients with
and malignant neoplasms, ischemia, infectious colitis, anorectal colonic diverticulosis experience bleeding, which may range from
disease, coagulopathy, use of NSAIDs, radiation proctitis, AIDS, minor to severe and life-threatening.77 As many as 80% to 85% of
and small bowel disorders. diverticular hemorrhages stop spontaneously.78 In one series,
surgery was unlikely to be necessary if fewer than 4 units of packed
DIVERTICULAR DISEASE RBCs were transfused in a 24-hour period, whereas 60% of
The reported prevalence of colonic diverticulosis in Western patients receiving more than 4 units of packed RBCs in a 24-hour
societies is 37% to 45%.75 The vast majority of colonic diverticula period required surgical intervention.5 The risk of a second bleed-
are actually false diverticula (pseudodiverticula) that contain only ing episode is approximately 25%.3 Semielective surgical therapy
serosa and mucosa [see 5:12 Diverticulitis]. They occur at weak is usually offered after a second diverticular bleeding episode
points in the colonic wall where the vasa recta penetrate the mus- because once a second such episode has occurred, the risk that a


Table 3 Common Causes of Lower GI cytomegalovirus) can result in severe lower GI bleeding, but this
Hemorrhage is a relatively rare occurrence.
Increasing use of radiation therapy to treat pelvic malignancies
Cause of Bleeding Frequency
has led to a corresponding increase in the incidence of chronic
radiation proctitis.87 Radiation therapy damages bowel mucosa,
Diverticulosis 17%–40% resulting in the formation of vascular telangiectases that are prone
to bleeding.88 From 1% to 5% of cases of acute lower GI bleeding
Arteriovenous malformation 2%–30%
from radiation-induced proctocolitis are severe enough to necessi-
Colitis 9%–21% tate hospitalization.4,14 In a survey of patients with prostate cancer
who underwent pelvic irradiation, 5% of the patients reported
Neoplasia (including postpolypectomy bleeding) 7%–33%
hematochezia daily.89 Initial therapy for clinically significant hema-
Benign anorectal disease 4%–10% tochezia related to radiation proctitis should include some form of
endoscopic treatment (e.g., argon-beam coagulation). Surgery
Upper GI source 0%–11%
should be reserved for unstoppable hemorrhage or other major
Small bowel source 2%–9% complications, such as fistulas and strictures.87
NEOPLASIA
third will follow exceeds 50%.79 In a series of 83 conservatively
Significant GI bleeding from colorectal neoplasia [see 5:15
managed cases of diverticular disease, the predicted yearly recur-
Adenocarcinoma of the Colon and Rectum] accounts for 7% to 33%
rence rates were 9% at 1 year, 10% at 2 years, 19% at 3 years, and
of cases of severe lower GI hemorrhage.3,11,14,36,90 Such bleeding is
25% at 4 years.4
believed to result from erosions on the luminal surface.91 One
COLITIS report identified ulcerated cancers as the cause in 21% of cases of
hematochezia.14 Adenomatous polyps are implicated in 5% to
The broad term colitis includes IBD, infectious colitis, radiation
11% of cases of acute lower GI bleeding.7,8,14,92,93 Lower GI hem-
colitis, and idiopathic ulcers. IBD, in turn, includes Crohn disease
orrhage, either immediate or delayed, is the most common report-
[see 5:11 Crohn Disease] and ulcerative colitis [see 5:13 Fulminant
ed complication after endoscopic polypectomy, occurring in 0.2%
Ulcerative Colitis]. Patients with IBD usually present with bloody
diarrhea that is not life-threatening; however, 6% to 10% of to 6% of cases.3,4,94,95 Immediate postpolypectomy bleeding is
patients with ulcerative colitis have lower GI bleeding severe believed to result from incomplete coagulation of the stalk before
enough to necessitate emergency surgical resection,80,81 and 0.6% transection.52 Delayed bleeding has been reported as long as 15
to 1.3% of patients with Crohn disease have acute life-threatening days after polypectomy and is thought to be secondary to slough-
lower GI bleeding.80,82 In one review, 50% of patients with intesti- ing of the coagulum; it is less common than immediate bleeding,
nal hemorrhage from IBD experienced spontaneous cessation of occurring in only 0.3% of cases.14,52
bleeding.80 Approximately 35% of patients whose bleeding stops COAGULOPATHY
without intervention will have another bleeding episode. Because
of this high recurrence rate, semielective surgery is recommended Lower GI bleeding can be a presenting symptom both for pa-
after the first episode of severe GI bleeding secondary to IBD. tients with iatrogenic coagulopathy from heparin or warfarin ther-
Colitis caused by various infectious agents (e.g., Salmonella apy and for patients with a hematologic coagulopathy from throm-
typhi,83,84 Escherichia coli O157:H7,85 Clostridium difficile,86 and bocytopenia [see 1:4 Bleeding and Transfusion]. It is unclear, howev-
er, whether severe coagulopathy leads to spontaneous hemorrhage
or whether it predisposes to bleeding from an existing lesion.96,97 In
an early series of leukemic patients with thrombocytopenia and severe
GI hemorrhage, 50% of bleeding patients had platelet counts lower
than 20,000/mm3 without any identifiable mucosal lesions; fur-
thermore, when the platelet count rose above 20,000/mm3, the
incidence of bleeding decreased to 0.8%.96 The investigator con-
cluded that severe thrombocytopenia led to spontaneous GI hem-
orrhage. Other investigators subsequently challenged this conclu-
sion, arguing that spontaneous bleeding from coagulopathy is in
fact rare.98 In one report, the distribution of pathologic lesions in
patients with GI bleeding who were taking heparin or warfarin was
essentially equivalent to that in the general population.98 Regardless
of what the precise relation between coagulopathy and GI hemor-
rhage may be, a thorough investigation for an anatomic lesion is
imperative in the workup of patients with lower GI bleeding even
in the face of coagulopathy or thrombocytopenia.
BENIGN ANORECTAL DISEASE

Hemorrhoids, ulcer/fissure disease, and fistula in ano [see 5:17
Benign Rectal,Anal, and Perineal Problems] must not be overlooked
as causes of GI hemorrhage: in one review comprising almost
Figure 4 Shown is the appearance of a bleeding diverticulum on 18,000 cases of lower GI bleeding, 11% were attributable to ano-
colonoscopy. rectal pathology. It is crucial to remember that identification of


lishes the diagnosis.111 During endoscopy, angiodysplasias appear
as red, flat lesions about 2 to 10 mm in diameter, sometimes
accompanied by a feeding vessel [see Figure 5].6,41,44,72
Typically, the bleeding caused by colonic AVMs is chronic, slow,
and intermittent.9 Although these lesions can cause severe lower
GI hemorrhage, they are a relatively uncommon cause: in most
large series, they account for only about 2% of cases of acute
bleeding.74,104 The bleeding stops spontaneously in 85% to 90% of
cases,10 but it recurs in 25% to 85%.112 Accordingly, definitive sur-
gical or colonoscopic treatment should be rendered once the
lesion has been identified.
COLONIC ISCHEMIA

Acute lower GI bleeding can also be a presenting symptom of
colonic ischemia. In several large series, colonic ischemia account-
ed for 3% to 9% of cases of acute lower GI hemorrhage.4,7,8,14,92
Other vascular diseases reported as potential causes are poly-
arteritis nodosa, Wegener granulomatosis, and rheumatoid vas-
culitis.113,114 The resultant vasculitis can cause ulceration, necrosis,
and ultimately hemorrhage.115
Figure 5 Shown is the appearance of an arteriovenous malforma-
SMALL INTESTINAL SOURCES
tion on colonoscopy.
Small intestinal sources account for 0.7% to 9% of cases of acute
lower GI bleeding.3,4,116-118 About 70% to 80% of cases of small
bowel hemorrhage are attributable to AVMs; other, less common
a benign anorectal lesion does not eliminate the possibility of a causes are jejunoileal diverticula, Meckel’s diverticulum,119 neopla-
more proximal cause of hemorrhage. In general, patients with hem- sia, regional enteritis, and aortoenteric fistulas [see Figure 6].90,120,121
orrhoids identified on physical examination should still undergo
thorough endoscopic evaluation of the colon to rule out other
pathologic conditions.
Portal hypertension [see 5:10 Portal Hypertension], congestive
heart failure, and splenic vein thrombosis can cause colonic or
anorectal varices, which can result in massive lower GI hemor-
rhage.99 The reported incidence of anorectal varices in patients
with portal hypertension ranges from 78% to 89%.100,101 If local
measures fail to control hemorrhage, some form of portosystemic
shunting is indicated.
COLONIC ARTERIOVENOUS MALFORMATIONS

The term arteriovenous malformation includes vascular
ectasias, angiomas, and angiodysplasias. AVMs are ectatic blood
vessels seen in the mucosa and submucosa of the GI tract. They
are degenerative lesions of the GI tract, occurring more frequent-
ly with advancing age.9 In autopsy series, the reported incidence
of colonic AVMs is 1% to 2%.102 In patients older than 50 years,
the incidence of colonic AVMs is estimated to range from 2% to
30%.103-106 In healthy asymptomatic adults, the prevalence is esti-
mated to be approximately 0.8%.107
Colonic AVMs are believed to derive from chronic colonic wall
muscle contraction, which leads to chronic partial obstruction of
the submucosal veins, causing the vessels to become dilated and
tortuous. This process eventually renders the precapillary sphinc-
ters incompetent, resulting in direct arterial-venous communica-
tion.108,109 Colonic AVMs are most commonly found in the
cecum.10 They have been associated with several systemic diseases,
including atherosclerotic cardiovascular disease, aortic stenosis,
chronic renal disease, collagen vascular disease, von Willebrand
disease, chronic obstructive pulmonary disease, and cirrhosis of
the liver; to date, however, no definite causal relationship to any of
these conditions has been established.6,21,44,110
The diagnosis of a colonic AVM is made at the time of angiog-
raphy or colonoscopy. During angiography, visualization of ectat- Figure 6 Shown are intraoperative specimens of small bowel
ic, slow-emptying veins, vascular tufts, or early-filling veins estab- tumors causing lower GI hemorrhage.


Accurate localization of a bleeding site in the small intestine can be patients hospitalized for lower GI bleeding, benign anorectal dis-
highly challenging: the length and the free intraperitoneal position ease was the cause.123 Other significant causes of lower GI hem-
of the small bowel make endoscopic examination difficult, and the orrhage in this population are colonic histoplasmosis, Kaposi sar-
nature of the overlying loops makes angiographic localization coma of the colon, and bacterial colitis.123,124
imprecise. For these reasons, the small intestine is usually left for
NSAID USE
last in the attempt to localize the source of lower GI bleeding and
is examined only after sources in the colon, the upper GI tract, and The association between NSAID use and upper GI hemor-
the anorectum have been ruled out.9 rhage is well known.125 Current data suggest that NSAIDs have a
toxic effect on colonic mucosa as well.126 An epidemiologic study
AIDS
estimated the incidence of NSAID-associated large bowel bleed-
The etiology of lower GI bleeding in patients with AIDS differs ing to be 7/100,000.127 A retrospective review found that patients
from that in the general population.91 In AIDS patients, lower GI who had experienced lower GI bleeding were twice as likely to
bleeding is caused predominantly by conditions related to the have taken NSAIDs as those who had not.128 NSAIDs have also
underlying HIV infection. Cytomegalovirus colitis is the most been linked to diverticular hemorrhage: in one study, 92% of
common cause of such bleeding in this population, occurring in patients with diverticular bleeding were taking NSAIDs.107 The
39% of cases.122 AIDS patients with hemorrhoids or anal fissures exact mechanism of NSAID-induced colonic injury is unknown;
often experience significant bleeding as a result of HIV-induced nevertheless, heightened clinical awareness of this potential cause
thrombocytopenia.122 A 1998 study reported that in 23% of AIDS of lower GI bleeding is warranted.91

References

1. Briley CA Jr, Jackson DC, Johnsrude IS, et al: Acute 15. Goenka MK, Kochhar R, Mehta SK: Spectrum of trointestinal hemorrhage. Dis Colon Rectum 40:471,
gastrointestinal hemorrhage of small-bowel origin. lower gastrointestinal hemorrhage: an endoscopic study 1997
Radiology 136:317, 1980 of 166 patients. Indian J Gastroenterol 12:129, 1993 28. Olds GD, Cooper GS, Chak A, et al: The yield of
2. Koval G, Benner KG, Rosch J, et al: Aggressive an- 16. Ohyama T, Sakurai Y, Ito M, et al: Analysis of urgent bleeding scans in acute lower gastrointestinal hem-
giographic diagnosis in acute lower gastrointestinal colonoscopy for lower gastrointestinal tract bleed- orrhage. J Clin Gastroenterol 39:273, 2005
hemorrhage. Dig Dis Sci 32:248, 1987 ing. Digestion 61:189, 2000 29. Yamaguchi T,Yoshikawa K: Enhanced CT for initial
3. Jensen DM, Machicado GA: Diagnosis and treat- 17. Chaudhry V, Hyser MJ, Gracias VH, et al: Colo- localization of active lower gastrointestinal bleeding.
ment of severe hematochezia: the role of urgent noscopy: the initial test for acute lower gastrointesti- Abdom Imaging 28:634, 2003
colonoscopy after purge. Gastroenterology 95:1569, nal bleeding. Am Surg 64:723, 1998 30. Ernst O, Bulois P, Saint-Drenant S, et al: Helical
1988 CT in acute lower gastrointestinal bleeding. Eur
18. Cohn SM, Moller BA, Zieg PM, et al: Angiography
4. Longstreth GF: Epidemiology and outcome of for preoperative evaluation in patients with lower Radiol 13:114, 2003
patients hospitalized with acute lower gastrointesti- gastrointestinal bleeding: are the benefits worth the 31. Baum S, Athanasoulis CA, Waltman AC: Angio-
nal hemorrhage: a population-based study. Am J Gas- risks? Arch Surg 133:50, 1998 graphic diagnosis and control of large-bowel bleed-
troenterol 92:419, 1997 ing. Dis Colon Rectum 17:447, 1974
19. Lin S, Branch MS, Shetzline M: The importance of
5. McGuire HH Jr: Bleeding colonic diverticula: a indication in the diagnostic value of push enter- 32. Athanasoulis CA, Moncure AC, Greenfield AJ, et al:
reappraisal of natural history and management. Ann oscopy. Endoscopy 35:315, 2003 Intraoperative localization of small bowel bleeding
Surg 220:653, 1994 sites with combined use of angiographic methods
20. Alavi A, Dann RW, Baum S, et al: Scintigraphic
6. Foutch PG: Angiodysplasia of the gastrointestinal detection of acute gastrointestinal bleeding. Radiol- and methylene blue injection. Surgery 87:77, 1980
tract. Am J Gastroenterol 88:807, 1993 ogy 124:753, 1977 33. Schrodt JF, Bradford WR: Presurgical angiographic
7. Bramley PN, Masson JW, McKnight G, et al: The 21. Gupta N, Longo WE, Vernava AM 3rd: Angiodys- localization of small bowel bleeding site with meth-
role of an open-access bleeding unit in the manage- plasia of the lower gastrointestinal tract: an entity readi- ylene blue injection. J Ky Med Assoc 94:192, 1996
ment of colonic haemorrhage: a 2-year prospective ly diagnosed by colonoscopy and primarily managed 34. Pennoyer WP, Vignati PV, Cohen JL: Management
study. Scand J Gastroenterol 31:764, 1996 nonoperatively. Dis Colon Rectum 38:979, 1995 of angiogram positive lower gastrointestinal hemor-
8. Peura DA, Lanza FL, Gostout CJ, et al: The Amer- 22. McKusick KA, Froelich J, Callahan RJ, et al: rhage: long term follow-up of non-operative treat-
ican College of Gastroenterology. Bleeding Registry: 99mTc red blood cells for detection of gastrointesti- ments. Int J Colorectal Dis 11:279, 1996
preliminary findings. Am J Gastroenterol 92:924, nal bleeding: experience with 80 patients. AJR Am J 35. Rantis PC Jr, Harford FJ, Wagner RH, et al: Tech-
1997 Roentgenol 137:1113, 1981 netium-labelled red blood cell scintigraphy: is it use-
9. Vernava AM 3rd, Moore BA, Longo WE, et al: 23. Bunker SR, Lull RJ, Hattner RS, et al: The ideal ful in acute lower gastrointestinal bleeding? Int J
Lower gastrointestinal bleeding. Dis Colon Rectum radiotracer in gastrointestinal bleeding detection. Colorectal Dis 10:210, 1995
40:846, 1997 AJR Am J Roentgenol 138:982, 1982 36. Leitman IM, Paull DE, Shires GT 3rd: Evaluation
10. Boley SJ, DiBiase A, Brandt LJ, et al: Lower intesti- 24. Kester RR,Welch JP, Sziklas JP:The 99mTc-labeled and management of massive lower gastrointestinal
nal bleeding in the elderly. Am J Surg 137:57, 1979 RBC scan: a diagnostic method for lower gastroin- hemorrhage. Ann Surg 209:175, 1989
11. Caos A, Benner KG, Manier J, et al: Colonoscopy testinal bleeding. Dis Colon Rectum 27:47, 1984 37. Casarella WJ, Galloway SJ,Taxin RN, et al: “Lower”
after Golytely preparation in acute rectal bleeding. J 25. Suzman MS, Talmor M, Jennis R, et al: Accurate gastrointestinal tract hemorrhage: new concepts
Clin Gastroenterol 8:46, 1986 localization and surgical management of active low- based on arteriography. Am J Roentgenol Radium
12. Zuccaro G Jr: Management of the adult patient with er gastrointestinal hemorrhage with technetium- Ther Nucl Med 121:357, 1974
acute lower gastrointestinal bleeding. American labeled erythrocyte scintigraphy. Ann Surg 224:29, 38. Colacchio TA, Forde KA, Patsos TJ, et al: Impact of
College of Gastroenterology Practice Parameters 1996 modern diagnostic methods on the management of
Committee. Am J Gastroenterol 93:1202, 1998 26. Hunter JM, Pezim ME: Limited value of tech- active rectal bleeding: ten year experience. Am J
13. Richter JM, Christensen MR, Kaplan LM, et al: netium 99m-labeled red cell scintigraphy in local- Surg 143:607, 1982
Effectiveness of current technology in the diagnosis ization of lower gastrointestinal bleeding. Am J Surg 39. Bloomfeld RS, Smith TP, Schneider AM, et al:
and management of lower gastrointestinal hemor- 159:504, 1990 Provocative angiography in patients with gastroin-
rhage. Gastrointest Endosc 41:93, 1995 27. Ng DA, Opelka FG, Beck DE, et al: Predictive value testinal hemorrhage of obscure origin. Am J
14. Rossini FP, Ferrari A, Spandre M, et al: Emergency of technetium Tc 99m-labeled red blood cell scintig- Gastroenterol 95:2807, 2000
colonoscopy. World J Surg 13:190, 1989 raphy for positive angiogram in massive lower gas- 40. Shetzline MA, Suhocki P, Dash R, et al: Provocative


angiography in obscure gastrointestinal bleeding. ment pathway. Curr Surg 60:344, 2003 85. Cohen MB, Giannella RA: Hemorrhagic colitis
South Med J 93:1205, 2000 64. Gomes AS, Lois JF, McCoy RD: Angiographic associated with Escherichia coli O157:H7. Adv
41. Krevsky B: Detection and treatment of angiodyspla- treatment of gastrointestinal hemorrhage: compar- Intern Med 37:173, 1992
sia. Gastrointest Endosc Clin N Am 7:509, 1997 ison of vasopressin infusion and embolization. AJR 86. Gould PC, Khawaja FI, Rosenthal WS: Antibio-
42. Foutch PG: Colonic angiodysplasia. Gastroenter- Am J Roentgenol 146:1031, 1986 tic-associated hemorrhagic colitis. Am J Gastro-
ologist 5:148, 1997 65. Funaki B: Microcatheter embolization of lower enterol 77:491, 1982

43. Rutgeerts P, Van Gompel F, Geboes K, et al: Long gastrointestinal hemorrhage: an old idea whose 87. Tagkalidis PP, Tjandra JJ: Chronic radiation
term results of treatment of vascular malformations time has come. Cardiovasc Intervent Radiol proctitis. ANZ J Surg 71:230, 2001
of the gastrointestinal tract by neodymium Yag laser 27:591, 2004 88. den Hartog Jager FC, van Haastert M, Batterman JJ,
photocoagulation. Gut 26:586, 1985 66. Darcy M: Treatment of lower gastrointestinal et al: The endoscopic spectrum of late radiation
bleeding: vasopressin infusion versus emboliza- damage of the rectosigmoid colon. Endoscopy
44. Rogers BH: Endoscopic diagnosis and therapy of
tion. J Vasc Interv Radiol 14:535, 2003 17:214, 1985
mucosal vascular abnormalities of the gastrointesti-
nal tract occurring in elderly patients and associated 67. Wright HK, Pelliccia O, Higgins EF Jr, et al: 89. Crook J, Esche B, Futter N: Effect of pelvic
with cardiac, vascular, and pulmonary disease. Controlled, semielective, segmental resection for radiotherapy for prostate cancer on bowel, blad-
Gastrointest Endosc 26:134, 1980 massive colonic hemorrhage. Am J Surg 139:535, der, and sexual function: the patient’s perspec-
1980 tive. Urology 47:387, 1996
45. Binmoeller KF, Thonke F, Soehendra N: Endo-
scopic hemoclip treatment for gastrointestinal 68. Eaton AC: Emergency surgery for acute colonic 90. Ellis DJ, Reinus JF: Lower intestinal hemorrhage.
bleeding. Endoscopy 25:167, 1993 haemorrhage—a retrospective study. Br J Surg Crit Care Clin 11:369, 1995
46. Jaspersen D, Korner T, Schorr W, et al: Diagnosis 68:109, 1981 91. Zuckerman GR, Prakash C: Acute lower intesti-
and treatment control of bleeding intestinal angio- 69. McGuire HH Jr, Haynes BW Jr: Massive hemor- nal bleeding. Part II: etiology, therapy, and out-
dysplasias with an endoscopic Doppler device. rhage for diverticulosis of the colon: guidelines comes. Gastrointest Endosc 49:228, 1999
Bildgebung 62:14, 1995 for therapy based on bleeding patterns observed 92. Wagner HE, Stain SC, Gilg M, et al: Systematic
in fifty cases. Ann Surg 75:847, 1972 assessment of massive bleeding of the lower part
47. Jensen DM, Machicado GA, Jutabha R, et al:
Urgent colonoscopy for the diagnosis and treatment 70. Setya V, Singer JA, Minken SL: Subtotal colecto- of the gastrointestinal tract. Surg Gynecol Obstet
of severe diverticular hemorrhage. N Engl J Med my as a last resort for unrelenting, unlocalized, 175:445, 1992
342:78, 2000 lower gastrointestinal hemorrhage: experience 93. Makela JT, Kiviniemi H, Laitinen S, et al:
with 12 cases. Am Surg 58:295, 1992 Diagnosis and treatment of acute lower gastroin-
48. Bloomfeld RS, Rockey DC, Shetzline MA: Endo-
scopic therapy of acute diverticular hemorrhage. Am 71. Jensen DM, Machicado GA: Colonoscopy for testinal bleeding. Scand J Gastroenterol 28:1062,
J Gastroenterol 96:2367, 2001 diagnosis and treatment of severe lower gastroin- 1993
testinal bleeding: routine outcomes and cost 94. Geenen JE, Schmitt MG Jr, Wu WC, et al: Major
49. Naveau S, Aubert A, Poynard T, et al: Long-term
analysis. Gastrointest Endosc Clin N Am 7:477, complications of coloscopy: bleeding and perfo-
results of treatment of vascular malformations of the
1997 ration. Am J Dig Dis 20:231, 1975
gastrointestinal tract by neodymium YAG laser pho-
tocoagulation. Dig Dis Sci 35:821, 1990 72. Foutch PG, Rex DX, Lieberman DA: Prevalence 95. Macrae FA, Tan KG, Williams CB: Towards safer
and natural history of colonic angiodysplasia colonoscopy: a report on the complications of
50. Santos JC Jr, Aprilli F, Guimaraes AS, et al: Angio-
among healthy asymptomatic people. Am J 5000 diagnostic or therapeutic colonoscopies.
dysplasia of the colon: endoscopic diagnosis and treat-
Gastroenterol 90:564, 1995 Gut 24:376, 1983
ment. Br J Surg 75:256, 1998
73. Heer M, Ammann R, Buhler H: Clinical signifi- 96. Gaydos LA, Freireich EJ, Mantel N: The quanti-
51. Eisen GM, Dominitz JA, Faigel DO, et al: An anno-
cance of colonic angiodysplasias. Schweiz Med tative relation between platelet count and hemor-
tated algorithmic approach to upper gastrointestinal
Wochenschr 114:1416, 1984 rhage in patients with acute leukemia. N Engl J
bleeding. Gastrointest Endosc 53:853, 2001
74. Sebastian JJ, Lucia F, Botella MT, et al: Diffuse Med 266:905, 1962
52. Habr-Gama A, Waye JD: Complications and haz-
gastrointestinal angiodysplasia associated with 97. Wilkinson JF, Nour-Eldin F, Israels MC, et al:
ards of gastrointestinal endoscopy. World J Surg
cryptogenic hepatic cirrhosis and coagulopathy Haemophilia syndromes: a survey of 267 pa-
13:193, 1989
simulating von Willebrand disease. Rev Esp tients. Lancet 2:947, 1961
53. Trowers EA, Ganga U, Rizk R, et al: Endoscopic Enferm Dig 88:631, 1996
hemorrhoidal ligation: preliminary clinical experi- 98. Mittal R, Spero JA, Lewis JH, et al: Patterns of
75. Hughes LE: Postmortem survey of diverticular gastrointestinal hemorrhage in hemophilia.
ence. Gastrointest Endosc 48:49, 1998
disease of the colon: I. Diverticulosis and diverti- Gastroenterology 88:515, 1985
54. Athanasoulis CA, Baum S, Rosch J, et al: Mesen- culitis. Gut 10:336, 1969
teric arterial infusions of vasopressin for hemorrhage 99. Cappell MS, Price JB: Characterization of the
76. Meyers MA, Alonso DR, Gray GF, et al: syndrome of small and large intestinal variceal
from colonic diverticulosis. Am J Surg 129:212,
Pathogenesis of bleeding colonic diverticulosis. bleeding. Dig Dis Sci 32:422, 1987
1975
Gastroenterology 71:577, 1976
55. Rahn NH 3rd,Tishler JM, Han SY, et al: Diagnostic 100. Chawla Y, Dilawari JB: Anorectal varices—their
77. Rushford AJ: The significance of bleeding as a frequency in cirrhotic and non-cirrhotic portal
and interventional angiography in acute gastroin-
symptom in diverticulitis. Proc R Soc Med 49:577, hypertension. Gut 32:309, 1991
testinal hemorrhage. Radiology 143:361, 1982
1956
56. Levinson SL, Powell DW, Callahan WT, et al: A cur- 101. Goenka MK, Kochhar R, Nagi B, et al: Recto-
78. Bokhari M, Vernava AM, Ure T, et al: Diver- sigmoid varices and other mucosal changes in
rent approach to rectal bleeding. J Clin Gastro-
ticular hemorrhage in the elderly—is it well toler- patients with portal hypertension. Am J Gastro-
enterol 3:9, 1981
ated? Dis Colon Rectum 39:191, 1996 enterol 86:1185, 1991
57. Clark RA, Colley DP, Eggers FM: Acute arterial
79. Luk GD, Bynum TE, Hendrix TR: Gastric aspi- 102. Baer JW, Ryan S: Analysis of cecal vasculature in
gastrointestinal hemorrhage: efficacy of transcathe-
ration in localization of gastrointestinal hemor- the search for vascular malformations. AJR Am J
ter control. AJR Am J Roentgenol 136:1185, 1981
rhage. JAMA 241:576, 1979 Roentgenol 126:394, 1976
58. Browder W, Cerise EJ, Litwin MS: Impact of emer- 80. Robert JR, Sachar DB, Greenstein AJ: Severe 103. Danesh BJ, Spiliadis C, Williams CB, et al:
gency angiography in massive lower gastrointestinal gastrointestinal hemorrhage in Crohn’s disease. Angiodysplasia—an uncommon cause of colonic
bleeding. Ann Surg 204:530, 1986 Ann Surg 213:207, 1991 bleeding: colonoscopic evaluation of 1,050 pa-
59. Matolo NM, Link DP: Selective embolization for 81. Binder SC, Miller HH, Deterling RA Jr: Emer- tients with rectal bleeding and anaemia. Int J
control of gastrointestinal hemorrhage. Am J Surg gency and urgent operations for ulcerative colitis: Colorectal Dis 2:218, 1987
138:840, 1979 the procedure of choice. Arch Surg 110:284, 104. Heer M, Sulser H, Hany A: Angiodysplasia of the
60. Encarnacion CE, Kadir S, Beam SA, et al: 1975 colon: an expression of occlusive vascular dis-
Gastrointestinal bleeding: treatment with gastroin- 82. Cirocco WC, Reilly JC, Rusin LC: Life-threaten- ease. Hepatogastroenterology 34:127, 1987
testinal arterial embolization. Radiology 183:505, ing hemorrhage and exsanguination from Crohn’s 105. Richter JM, Hedberg SE, Athanasoulis CA, et al:
1992 disease: report of four cases. Dis Colon Rectum Angiodysplasia: clinical presentation and colono-
61. Bookstein JJ, Chlosta EM, Foley D, et al: Trans- 38:85, 1995 scopic diagnosis. Dig Dis Sci 29:481, 1984
catheter hemostasis of gastrointestinal bleeding using 83. Reyes E, Hernandez J, Gonzalez A: Typhoid co- 106. Zuckerman G, Benitez J: A prospective study of
modified autogenous clot. Radiology 113:277, 1974 litis with massive lower gastrointestinal bleeding: bidirectional endoscopy (colonoscopy and upper
62. Peck DJ, McLoughlin RF, Hughson MN, et al: an unexpected behavior of Salmonella typhi. Dis endoscopy) in the evaluation of patients with occult
Percutaneous embolotherapy of lower gastrointes- Colon Rectum 29:511, 1986 gastrointestinal bleeding. Am J Gastroenterol 87:
tinal hemorrhage. J Vasc Interv Radiol 9:747, 1998 84. Maguire TM, Wensel RH, Malcolm N, et al: 62, 1992
63. Gady JS, Reynolds H, Blum A: Selective arterial Massive gastrointestinal hemorrhage cecal ulcers 107. Foutch PG: Diverticular bleeding: are non-
embolization for control of lower gastrointestinal and Salmonella colitis. J Clin Gastroenterol steroidal anti-inflammatory drugs risk factors for
bleeding: recommendations for a clinical manage- 7:249, 1985 hemorrhage and can colonoscopy predict out-


come for patients? Am J Gastroenterol 90:1779, athlete. Am J Gastroenterol 88:1157, 1993 orrhage in patients with AIDS. AIDS Patient
1995 115. Sokol RJ, Farrell MK, McAdams AJ: An unusual Care STDS 13:343, 1999
108. Boley SJ, Sammartano R, Adams A, et al: On the presentation of Wegener’s granulomatosis mimic- 123. Chalasani N, Wilcox CM: Etiology and outcome
nature and etiology of vascular ectasias of the king inflammatory bowel disease. Gastroentero- of lower gastrointestinal bleeding in patients with
colon: degenerative lesions of aging. Gastroenter- logy 87:426, 1984 AIDS. Am J Gastroenterol 93:175, 1998
ology 72:650, 1977
116. Klinvimol T, Ho YH, Parry BR, et al: Small bowel 124. Becherer PR, Sokol-Anderson M, Joist JH, et al:
109. Mitsudo SM, Boley SJ, Brandt LJ, et al: Vascular causes of per rectum haemorrhage. Ann Acad Gastrointestinal histoplasmosis presenting as hema-
ectasias of the right colon in the elderly: a distinct Med Singapore 23:866, 1994 tochezia in human immunodeficiency virus–
pathologic entity. Hum Pathol 10:585, 1979
117. Gilmore PR: Angiodysplasia of the upper gas- infected hemophilic patients. Am J Hematol
110. Imperiale TF, Ransohoff DF: Aortic stenosis, idio- trointestinal tract. J Clin Gastroenterol 10:386, 47:229, 1994
pathic gastrointestinal bleeding, and angiodysplasia: 1988
is there an association? A methodologic critique of 125. Allison MC, Howatson AG, Torrance CJ, et al:
the literature. Gastroenterology 95:1670, 1988 118. Netterville RE, Hardy JD, Martin RS Jr: Small Gastrointestinal damage associated with the use
bowel hemorrhage. Ann Surg 167:949, 1968 of nonsteroidal antiinflammatory drugs. N Engl J
111. Boley SJ, Sprayregen S, Sammartano RJ, et al: Med 327:749, 1992
The pathophysiologic basis for the angiographic 119. Lu CL, Chen CY, Chiu ST, et al: Adult intussus-
signs of vascular ectasias of the colon. Radiology cepted Meckel’s diverticulum presenting mainly 126. Davies NM: Toxicity of nonsteroidal anti-inflam-
125:615, 1977 lower gastrointestinal bleeding. J Gastroenterol matory drugs in the large intestine. Dis Colon
Hepatol 16:478, 2001 Rectum 38:1311, 1995
112. Helmrich GA, Stallworth JR, Brown JJ: Angio-
dysplasia: characterization, diagnosis, and 120. Longo WE, Vernava AM 3rd: Clinical implica- 127. Langman MJ, Morgan L, Worrall A: Use of anti-
advances in treatment. South Med J 83:1450, tions of jejunoileal diverticular disease. Dis inflammatory drugs by patients admitted with
1990 Colon Rectum 35:381, 1992 small or large bowel perforations and haemorrhage.
113. Burt RW, Berenson MM, Samuelson CO, et al: 121. Buchman TG, Bulkley GB: Current management Br Med J (Clin Res Ed) 290:347, 1985
Rheumatoid vasculitis of the colon presenting as of patients with lower gastrointestinal bleeding. 128. Holt S, Rigoglioso V, Sidhu M, et al: Nonsteroidal
pancolitis. Dig Dis Sci 28:183, 1983 Surg Clin North Am 67:651, 1987 antiinflammatory drugs and lower gastrointestinal
114. Moses FM: Gastrointestinal bleeding and the 122. Chalasani N, Wilcox CM: Gastrointestinal hem- bleeding. Dig Dis Sci 38:1619, 1993

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