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300 F.G. Opelka, J.B. Gathright, Jr., and D.E. Beck
History and physical examination fall short of an adequate
classification system to ultimately predict patient needs or
clinical outcome. A patient may portray a worrisome history
of massive hemorrhage and still resolve spontaneously with
simple, supportive measures. Other patients may sequester
blood in large volume and seem to have stopped bleeding.
While under observation their scenario promptly changes
with ongoing, massive hemorrhage. They require prompt
therapy. Still other patients may bleed aggressively, stop for a
few days, and then repeat their massive exsanguinations. In
addition, diagnostic studies often are invasive procedures with
limited sensitivities and specificities.
More and more, physicians witness special patient groups
with massive lower gastrointestinal hemorrhage. Current disease managements call for concurrent care with anticoagulants
or antiplatelet agents for underlying cardiovascular conditions.
Current treatment regimens incorporate long-term anticoagulants and antiplatelet agents. Hemorrhage in these patients
proves more life-threatening. Landefeld and Goldman
5
noted a
22% long-term risk of bleeding on anticoagulant therapy with
warfarin. Gastrointestinal hemorrhage is one of five independent risk factors. Current increased patient exposure to
antiplatelet therapy associated with treatment of cardiovascular conditions may increase the comorbid challenges in
patients with lower gastrointestinal massive hemorrhage.
Etiologies
Common causes for lower gastrointestinal hemorrhage
include colonic diverticula, angiodysplasia, ischemic colitis,
and inflammatory bowel disease. Hemorrhage also stems
from intestinal tumors or malignancies. Unusual causes
include nonsteroidal antiinflammatory drug (NSAID)-related
nonspecific colitis, Meckel’s diverticulum, and anorectal diseases. The reported mortality with varying etiologies is summarized in Table 20-1.
Diverticular Disease
Diverticulosis is a common malady in Western civilization.
Approximately 50% of the population by age 60 years has
evidence of diverituclosis.
sion diverticula or pseudodiverticula that are actually outpouchings of the mucosa and submucosa through defects in
the muscular layer of the bowel at sites of penetration of the
10
Most diverticula represent pul-
vasa recta. It is theorized that slow intestinal transit and
increased intraluminal pressure within the segmentation
process promote the development of the diverticula.
The precise mechanism of diverticular hemorrhage is
unknown. In the late 1800s, Kebs outlined the vascular
anatomy of the vasa recta and the mucosal blood supply.
11
Further, Drummond,
in 1916, displayed the relationship
between the vasa recta and the neck of the diverticulum. In
1976, Meyers et al.
12
defined the bleeding sites as the ruptured
vasa recta in the diverticulum. He noted structural changes
located eccentrically in the vasa recta at the site of rupture,
intimal thickening with thinning of the media, the absence of
any acute or chronic inflammation, and stated that these vascular changes were typically the result of focal injury. It is
generally accepted that thinning of the media in the vasa recta
predisposes to intraluminal rupture: focal injury may occur
from trauma related to a fecalith.
It is unclear how frequently diverticula are the true cause of
hemorrhage. The incidence spans a range of 15% to 48%.
Oftentimes, authors attribute the condition to diverticula after
the hemorrhage has ceased despite a lack of proof of actual
cause, a presumptive diagnosis. Diagnostic evaluations, such
as colonoscopy, do not identify a precise source for the hemorrhage without the presence of witnessed bleeding or an
adherent clot. Oftentimes, for lack of a more precise etiology,
diverticula are present and, therefore, become the primary
culprit. Despite being considered a major source for colonic
hemorrhage, bleeding from diverticula is a relatively rare
event affecting only 4%–17% of patients with diverticulosis.
In most cases, bleeding ceases spontaneously, but in
10%–20% of cases, the bleeding continues unabated in the
absence of intervention.
14
Once bleeding has occurred, the
natural history and risk of rebleeding are poorly understood.
15
Finne
comments that the risk of rebleeding after an episode
of bleeding is approximately 25% but increases to 50%
among patients who have had two or more prior episodes of
diverticular bleeding. Right sided colonic diverticula occur
less frequently than left sided or sigmoid diverticula but are
thought to be responsible for a disproportionate incidence of
diverticular bleeding. This finding is not well established,
however, and there is often difficulty distinguishing between
bleeding from an arteriovenous malformation or angiodysplasias and bleeding from diverticulosis. The overall high
prevalence of diverticulosis in the population at risk for lower
gastrointestinal hemorrhage makes the exact diagnosis of
many bleeding episodes equivocal.
13
TABLE 20-1. Mortality of lower gastrointestinal bleeding by etiology
Investigator Diverticulosis (%) Angiodysplasia (%) Cancer/polyp (%) Colitis/ulcer (%) Anorectal (%) Other (%) Mortality (%)
Jensen and Machicado,
Longstreth,
Bramley et al.,
Richter et al.,
Rossini et al.,
Jensen and Machicado,91988 20 37 14 11 5 5 NA
2
1997 41 3 9 16 5 14 3.6
7
8
3
1997 23 40 15 12 5 4 NA
6
1996 24 7 10 21 9 4 5.1
1995 48 12 11 6 3 6 2
1989 15 4 30 22 0 11 NA
20. Lower Gastrointestinal Hemorrhage 301
Operative management of diverticular bleeding is indicated
when bleeding continues unabated and is not amenable to
angiographic or endoscopic therapy. It also should be considered in patients with recurrent bleeding localized to the same
colonic segment. In a stable healthy patient, the operation
consists of a segmental bowel resection (usually a right colectomy or sigmoid colectomy) followed by a primary anastomosis. One additional note about diverticular hemorrhage
focuses on recurrence for patients who stopped bleeding and
required no operative intervention. In Longstreth’s San Diego
2
study,
the author noted that 9% of patients returned within 1
year with another episode. At 2 years, there was little change,
10%; 19% at 3 years; and 25% at 4 years.
Angiodysplasia
Angiodysplasia was described by Margolis et al.16in 1960
when they noted the radiographic features during an
intraoperative angiogram performed for colonic bleeding.
Angiodysplasias are thin-walled arteriovenous communications located within the submucosa and mucosa of the intestine. Angiodysplasias may be congenital or, more typically,
acquired. They could be isolated or multiple. In the acquired
form, distortions of the postcapillary venules may arise as a
degenerative lesion associated with increases in intraluminal
pressure. The intraluminal pressure occurs from loss of the
precapillary sphincter and a resultant increased pressure
transmitted through the capillary bed into the venules. As
these vessels respond to the arterial flow, it results in thickening and ectasia. The vessels eventually entangle as tufts
within the submucosa and erode into the mucosa proper.
No one is quite certain precisely why angiodysplasias
occur. Current hypotheses suggest a loss of vascular integrity
related to loss of transforming growth factor (TGF) β signaling cascade or from a deficiency in mucosal type IV collagen.
McAllister et al.
duction alters TGF β and, thus, the integrity of the vascular
endothelial cells. Roskell et al.
type IV collagen in pathologic specimens of angiodysplasia.
Angiodysplasias are uncommon before age 60, increase
with age, and are associated with aortic stenosis (Heyde’s
syndrome), chronic renal failure, and von Willebrand’s disease. Osler-Weber-Rendu (hereditary hemorrhagic telangiectasias) is a hereditary condition with telangiectasias of the
lung, nervous system, skin, and intestine. These patients present with multiple lesions. In 1995, Christopher Gostout
torialized in questioning the association of angiodysplasias
with aortic stenosis.
When angiodysplasias are noted during angiography or
colonoscopy, unless a hemorrhagic blush is seen during the
angiogram or colonoscopy, it is difficult to accurately accuse
this malady as the source of hemorrhage.
angiodysplasia was the diagnosis chosen when no bleeding
source could be identified and the abnormal vessels were
present. In addition, many drew an association between the
17
suggest that a genetic error in endoglin pro-
18
noted the loss of mucosal
20
In the past,
19
edi-
angiodysplasias and aortic stenosis. The association between
the ecstatic vascular tufts and aortic stenosis was dispelled by
21
Imperiale and Ransohoff
in the late 1980s. However, the
association persisted in anecdotes until Bhutani and col-
20
leagues
reviewed 37 patients and found no greater incidence
of aortic valvular disease than the control group.
Angiography remains the gold standard for the diagnosis of
angiodysplasia. After injection of contrast, a series of images
are collected in three phases. In the arterial phase, the radiographic findings of angiodysplasia demonstrate early venous
filling which normally occurs in later phases. During the next
phase, capillary phase, small, tortuous tufts are seen entangled and filled with contrast. Finally, the late phase study
demonstrates a persistent of this arteriovenous tuft and a persistent of a slow, emptying vein.
22
When angiography identifies a bleeding angiodysplasia, treatment with embolization
therapy or directed infusion of vasopressin will decrease or
stop the bleeding.
Colonoscopy has increased as a screening agent for
colorectal cancers as well as during the investigation for colorectal bleeding. Expectantly, more angiodysplasias are seen
during endoscopy than in the past. In contrast to the angiographic findings described by Boley et al., Bhutani et al.
highlighted the colonoscopic criteria in describing these
lesions. The mucosal surface contains a cherry red lesion that
is typically flat. The lesions are greater than 2 mm in size and
have a “fern-like” appearance. A central feeding vessel is not
always visible. It is important to identify these lesions during
scope insertion. Occasionally, the inexperienced endoscopists
may attribute colonoscopic suction trauma to an angiodysplastic area. By searching for the vascular muscular lesions
during scope insertion, the endoscopist will avoid misnaming
scope mucosal trauma as angiodysplasia. Initial experience in
identifying these lesions related to a few angiographic studies.
The early evidence suggested the lesions were predominantly
right sides. Since colonoscopy has become more available,
both left and right sided lesions are thought to occur.
Other Causes of Lower Gastrointestinal
Hemorrhage
Multiple other etiologies cause lower gastrointestinal bleeding and most are not associated with a massive hemorrhage or
acute symptomatic anemia. Colonic ischemia, inflammatory
bowel disease, and colonic malignancies occur frequently.
Each presents in a different manner. Typically, ischemic colitis presents with the abrupt onset of abdominal pain, followed
by colic and a mucoid, bloody diarrhea. Inflammatory bowel
disease, Crohn’s, and ulcerative colitis present with a change
in stool patterns. Patients develop diarrhea followed by hematochezia or melena. Localized transmural involvement or
colic could add pain-related symptoms. Colorectal carcinomas are associated with exophytic, ulcerative lesions that may
bleed insidiously. Only rarely does the malignant process
proceed to acute, symptomatic hemorrhage.
20
302 F.G. Opelka, J.B. Gathright, Jr., and D.E. Beck
More unusual causes of hemorrhage involve small intestinal tumors, known also as gastrointestinal stromal tumors
(GIST). These lesions enlarge and surpass their blood supply.
In that event, the ischemia in the tumor will ulcerate and may
cause a localized hemorrhage. Meckel’s diverticulum represent another atypical cause of bleeding. These lesions occur
in the distal ileum. Ectopic gastric mucosa leads to localized
acidic contents and resultant ulcerations of the contralateral
intestinal wall. Finally, NSAID-associated intestinal hemorrhage occurs most frequently in the terminal ileum and
cecum. Long-acting NSAIDS cause a localized mucosal
injury. These remnants from the agents have been noted at the
site of perforating ulcers. It seems that the terminal ileum and
cecum may serve as a reservoir and harbor these agents long
enough to establish the mucosal defects. Diaphragm-like
strictures are pathognomonic for NSAID injuries and may
result from a healing ridge related to repeated injuries from
the agents.
Occult Hemorrhage
Obscure or occult gastrointestinal bleeding is a condition that
frustrates the patient and the physicians. The hemorrhage is
often massive and intermittent. The traditional tests of nuclear
scintigraphy, colonoscopy, and angiography provide no solution. It occurs infrequently. One study noted occult bleeding in
no more than 5% of all patients admitted with lower gastrointestinal massive hemorrhage. Frequent recurrences create
chronic anemic states in patients and require occasional admissions for transfusions. These patients may harbor angiodysplasias in the small intestine or right colon. Patients in this
situation may benefit from small bowel contrast radiography or
capsule endoscopy.
cecal magnification may reveal small angiodysplasias.
If the occult hemorrhage recurs and investigations fail to
reveal the source, a variety of provocative diagnostic angiographic studies have been described. Most studies prefer to
incite bleeding using either heparin or thrombolytics. Once
the site of bleeding is identified, it may be difficult to control
without an operation. In these instances, the surgeon should
prepare and hold an operating room. Once the location is
identified, a superselective catheter is left in the distal artery.
During the conduct of surgery, the surgeon can palpate the
catheter within the vessel and direct the surgical resection.
23–26
Additionally, elective angiography with
Initial Assessment, Resuscitation,
and Stabilization
Massive lower gastrointestinal hemorrhage requires prompt
clinical attention. Patients who present with symptoms secondary to the bleeding have urgent resuscitation needs. These
symptoms further define the significance of the hemorrhage.
Patients may demonstrate pallor, fatigue, angina, tachypnea,
cardiac palpitations, postural hypotension, and syncope.
Prompt attention requires placement of vascular access
with large bore intravenous fluids. Further hemodynamic
monitoring requires cardiac rhythm monitoring and placement of a urinary catheter. A nasogastric tube placed will
screen for the presence of upper gastric sources for bleeding.
Kovacs and Jensen
hemorrhage presentations involved an upper gastrointestinal
source. The nasogastric tube is effective in detecting prepyloric hemorrhage. The nasogastric decompression need not
be continued after an appropriate period of observation to
exclude upper intestinal sources.
The treatment goals for resuscitation are to restore volume
and, replete red blood cell deficiencies and their impact on
oxygen delivery. In addition, all coagulopathies require reversal. Patients require laboratory profiles that include a
complete blood count, serum electrolytes, a coagulation profile, and a type and crossmatch for packed red blood cells.
The initial specific diagnostic evaluation begins with a digital anorectal examination and anoscopy. A rigid proctosigmoidoscopy will allow the examiner to evacuate the rectum of
blood and clots. A complete mucosal assessment serves to
exclude internal hemorrhoids, anorectal solitary ulcers, neoplasms, and colitis. If nothing is found and subsequent surgery becomes necessary, the evaluation of the rectum and
anorectal function greatly aids in surgical decisions. A normal
anorectal examination allows the surgeon to consider a primary rectal anastomosis as a treatment possibility. In the
event that the physician discovers a source for bleeding during the examination, oftentimes therapy can immediately control the hemorrhage.
Once the resuscitation demonstrates a stable patient, the
next phase of the diagnostic evaluation ensues. What is the
first test to evaluate the cause of bleeding? Currently, three
tests are considered for the initial evaluation. These tests
include colonoscopy, nuclear scintigraphy, and angiography.
Colonoscopy and angiography offer therapeutic intervention
whereas nuclear scanning is purely diagnostic. Decisions as
to which test to use depend on the clinical judgment, local
expertise, severity of the event, and the current activity of the
hemorrhage.
It may be helpful to subdivide patients into three general
clinical categories based on the history, physical, and the initial laboratory data. Is the hemorrhagic event 1) minor and
self-limited, 2) major and self-limited, or 3) major and ongoing? Major ongoing hemorrhage requires prompt intervention
with angiography or surgery. Minor, self-limited may undergo
a colonic lavage and colonoscopy within 24 hours. Major,
self-limited may be more difficult to define. Within the spectrum of these three clinical groups, the major, self-limited
hemorrhage patients create the current controversy. These
patients need a diagnostic test to determine if they require
prompt therapy or observation. Should these patients undergo
nuclear imaging or colonoscopy?
Radionuclide imaging (Figure 20-1) detects the slowest
bleeding rates. It is able to detect rates of 0.1–0.5 mL/min.
27
noted 17.9% of lower gastrointestinal
20. Lower Gastrointestinal Hemorrhage 303
and allow for reimaging within 24 hours. Nuclear scintigraphy
has variable results, suggesting that scan timing, technical
skills, and experience may increase accuracy. Current reports
suggest accuracies ranging from 24% to 91%.
29
Ng et al.30recommend nuclear imaging for the patients with
a major, self-limited hemorrhage. Their data suggest that the
timing of the blush predicts the success of angiography. In
other words, if the nuclear scan demonstrates an immediately
positive blush (within the first 2 minutes of scanning), it is
highly predictive of a positive angiogram (60%). The data of
Ng et al. seemed predictive for surgery in 24% of patients if
the first blush was positive. Just as important, if the initial
images in the Ng et al. study did not demonstrate a blush, the
study is highly predictive of a negative angiogram (93%) and
the need for surgery decreased to 7%. Thus, if the nuclear scan
is negative, it provides objective evidence that the patient is not
actively bleeding and may be evaluated by colonoscopy.
Colonoscopy
Many authors believe that colonoscopy has clearly demon-
FIGURE 20-1. Selected images from a 99mTc-labeled RBC gastrointestinal bleeding study in a patient with known diureticulosis.
Images acquired at 1 minute (A) and 14 minutes (B). Abnormal
increased isotopic activity developed in the proximal transverse
colon, which progressed antegrade to the descending colon.
Thus, it is a technique that is more sensitive than angiography.
Unfortunately, the nuclear scanning cannot reliably localize the
site of hemorrhage. The specificity (precise origin) using
radionuclide scans of small bowel versus large intestine bleeding does not reliably compare with angiography.
28
Two general
techniques are used for nuclear imaging, technetium sulfur colloid scans and 99mTc pertechnetate-tagged red blood cells
(RBCs). Sulfur colloid scans have a short half-life and detect
very low rates of hemorrhage (0.1 mL/min). It is effective to
detect brisk hemorrhage but cannot detect sporadic bleeding.
The more frequently preferred agent for lower gastrointestinal
hemorrhage radionuclide scanning is the pertechnetate-tagged
RBC scans. The tagged RBC scans may cover a period of hours
strated the highest efficacy and should be the first study in
patients with major bleeding that appears self-limited.
general, this may be true if efficacy of the study includes a
broad array of the common etiologies for properly defined
massive hemorrhage. Controversy abounds with colonoscopy
as the preferred first study if the etiologies for hemorrhage are
unlikely sources for major hemorrhage. Whether colonoscopy
should be undertaken emergently depends on the general ability to maintain a stable patient. If the hemodynamic profile
continues to drift toward hypotension and the massive hemorrhage continues unabated during the resuscitation process, the
rate of hemorrhage may require more prompt attention.
Patients with extremely brisk hemorrhage require a prompt
angiogram. Colonoscopy in such patients proves difficult to
prep with lavage and the acute exsanguinations may limit
intraluminal visualization to deploy all the therapeutic options
except for only the most experienced endoscopists.
If the patient appears stable with self-limited hemorrhage,
colonoscopy is the preferred diagnostic study. Jensen et al.
have long been proponents of “emergency colonoscopy.” This
group and others have demonstrated high cecal intubation
rates (95%) and a diagnostic accuracy of 72% and 86%. On a
cautious note, the Jensen diagnostic studies demonstrated
atypical etiologies for massive hemorrhage including
ischemic colitis, inflammatory bowel disease, and cancer. The
rate of bleeding in these conditions may be more amenable to
urgent colonoscopy (within 24 hours) rather than emergent
colonoscopy in patients diverticular or angiodysplastic, hemorrhagic rates.
Should the patient undergo a colonic lavage before
colonoscopy? Longstreth
2
reported that 80.8% of patients had
colonoscopy after electrolyte-polyethylene glycol solution
purge, usually within 24 hours of admission. His report
reflects the more typical approach to patients. Once the
31
In
3,4,9
304 F.G. Opelka, J.B. Gathright, Jr., and D.E. Beck
patient undergoes observation and stabilization, the need for
acute intervention seems avoided. Then the endoscopist may
plan for a more controlled, stable, urgent colonoscopy with a
lavage which occurs within the first 24 hours. The Longstreth
Kaiser Permanente study demonstrated a broad scope of etiologies (see Table 20-2).
The major benefit of colonoscopy depends on the ability to
provide a definitive localization of ongoing active bleeding
and the potential for therapy. Many landmarks for colonoscopy
may be obscured during hemorrhage. Because of the inability
to appreciate all intraluminal landmarks and locate the segment that is bleeding, once the endoscopist highlights a bleeding source, the region of the intestine requires a tattoo to mark
the site with India ink. In such patients, if the hemorrhage continues and fails medical management, the tattoo greatly assists
the surgeon in localizing the hemorrhage.
The endoscopist has many therapeutic options to control
the bleeding. Kovacs and Jensen
27
have described several
therapeutic tools to control bleeding in upper and lower
gastrointestinal hemorrhage. Therapeutic armamentarium for
the colon includes thermal agents such as heater probes, bipolar coagulation, and laser therapy. Injection therapy primarily
uses topical and intramucosal epinephrine. Mechanical therapy includes endoscopically applied clips (Figure 20-2).
27
FIGURE 20-2. Clip applied to bleeding diverticular vessel.
Angiography
Angiography is diagnostic and therapeutic in the treatment of
intestinal hemorrhage. The clinical judgment for choosing
angiography involves three different types of hemorrhage. First,
acute, major hemorrhage with ongoing bleeding requires emergency angiography. Second, patients with an early blush during
nuclear scintigraphy may benefit from therapeutic angiography.
Finally, angiograms may define a potential source for hemorrhage in occult and recurrent gastrointestinal hemorrhage. To
appreciate an angiographic blush of contrast, the study requires
a hemorrhage rate of at least 1 mL/min.
angiography vary greatly. Patient selection will increase yields
and avoid overuse of angiograms. Generally, reports demonstrate yields that range from 40% to 78%.
ABLE 20-2. Final diagnosis in patients hospitalized for acute lower
T
gastrointestinal hemorrhage
Colonic diverticulosis 91 (41.6)
Colorectal malignancy 20 (9.1)
Ischemic colitis 19 (8.7)
Acute colitis, unknown cause 11 (5.0)
Hemorrhoids 10 (4.6)
Postpolypectomy hemorrhage 9 (4.1)
Colonic angiodysplasia 6 (2.7)
Crohn’s disease 5 (2.3)
Other 22 (10.1)
Unknown 26 (11.9)
Total 219 (100)
31
32
Positive yields with
33–36
n (%)
Angiography provides highly accurate localization of the
site of bleeding (Figure 20-3) and the angiographic blush may
suggest a specific etiology, but it lacks the accuracy of
colonoscopy. Highly accurate localization provides for
focused therapy. Hemorrhagic site may receive highly selective, intraarterial vasopressin infusion. The potent arterial
contraction may reduce or halt the hemorrhage. Infusion rates
of vasopressin are at concentrations of 0.2 U/min and may
progress to 0.4 U/min. The systemic effects and cardiac
impact of vasopressin may limit maximizing the dosage.
Vasopressin controls bleeding in as many as 91% of patients.
Bleeding may recur in as many as 50% of patients once the
vasopressin is tapered.
Angiographic technology also allows for arterial embolization to control hemorrhage. Superselective mesenteric
angiography with current microcatheters allows for embolization of the vasa recta of the intestine, vessels as small as
1 mm. In the past, arterial embolization of larger vessels
risked intestinal ischemia or infarction. The risk of intestinal
infarctions of larger selective vessels may exceed 20%. Arteriography also has complication rates related to angiography,
separate from the therapy delivered at the site of bleeding.
These include arterial thrombosis, distant arterial emboli, and
renal toxicity from the angiographic dye.
Embolization therapy provides immediate arrest of the
bleeding. Embolization uses a combination of agents to control bleeding including Gelfoam pledgets, coils, and
37
polyvinyl alcohol particles. In 2001, Funaki et al.
reported
experience with microcoil embolization in 27 patients.
They succeeded in 93% and had reasonable long-term
20. Lower Gastrointestinal Hemorrhage 305
units during the resuscitation and the hemorrhage remains
ongoing, surgical intervention becomes eminent.
The surgeon tailors the approach to the patient and depends
on the diagnostic information gathered before the operation.
All patients require an open laparotomy with a thorough
examination of the entire intestine. The first objective in surgery focuses on the location of the intraluminal blood with
the hope of segmentally isolating the possible sources of
bleeding. If the colon visually appears filled with blood and
the small intestine remains spared, the surgeon must still
examine the entire abdomen and then focus on colonic
sources of bleeding. If the small bowel contains blood, then
the operative team has a larger area of concern and close
inspection.
Once the surgeon completes the initial visual inspection, a
complete exploration ensues. The exploration begins in the
stomach, duodenum, and considers possible missed upper gastrointestinal sources. Next, the small intestine must undergo
examination from the ligament of Treitz to the ileocecal valve.
Palpation of the intestine may demonstrate such etiologies as
a Meckel’s diverticulum, ileitis, colitis, or a GIST.
Upon completion of the exploration phase, if no source
appears obvious, the surgeon may consider intestinal
enteroscopy. The enteroscope or colonoscope will expose the
luminal surface and transilluminate the intestinal wall for
occult lesions. Transillumination may identify vascular
anomalies, small ulcers or tumors. Endoscopic access to the
FIGURE 20-3. Angiogram demonstrating extravasation (hemorrhage)
in cecum.
intestine may require upper enteroscope, a transgastric
approach, a transcolonic approach, or insertion through the
anus. Once a hemorrhage site is identified, the surgeon can
perform an appropriate segmental resection. Intraoperative
results—81%. Most of his patients had diverticular hemorrhages. His recurrent bleed patients had angiodysplasias. In a
similar experience, Peck et al.
38
reported rebleeding in three
of four patients with cecal angiodysplasias. The data suggest
that angiodysplasias have multiple feeding vessels and may
contribute to the recurrence.
endoscopy is a technically difficult endeavor. A team
approach with two surgeons or the availability of an experienced endoscopist is important to identify the elusive lesions
causing the hemorrhage.
If the source of bleeding cannot be found, and it appears to
arise from the colon, the surgeon should perform a subtotal or
total colectomy. Stable patients will tolerate a primary ileosig-
Operative Therapy
Surgical therapy for massive lower intestinal bleeding is rare,
often definitive, and associated with significant mortality.
Most sources of bleeding spontaneously resolve or are controlled with the current therapeutic interventions. Few
patients currently require surgical treatment. If the patient is
hemodynamically unresponsive to the initial resuscitation,
then radiographic, radionuclide, and endoscopic evaluations
are usurped by the need for urgent surgery. Other patients may
have the site of hemorrhage localized, yet the available therapeutic interventions fail to control the bleeding. Patient mortality increases with their transfusion requirements,
suggesting the severity of the hemorrhage. Bender noted a
reduced mortality (7%) for patients requiring less than 10
units of blood. The mortality increased to 27% for patients in
excess of 10 units.
39
Therefore, once a patient reaches 6–7
moid or ileorectal anastomosis in this circumstance. Unstable
patients require an end ileostomy with closure of the rectal
stump or a mucous fistula. Once stable, the patient may return
for ileostomy closure. The rectum and sigmoid colon require
reexamination endoscopically to assure no bleeding persists.
Before the endoscopy, a simple saline “washout” with a
transanal catheter or via the rigid proctosigmoidoscope may
provide for safe passage and careful examination of the
remaining mucosa.
The key concerns with operative management are, first, a
delay in the decision to operate until the hemorrhage reaches
a critical point beyond 10 units of blood. This seems to contribute to the high mortality rate. Second, mortality rates for
patients requiring urgent surgery consistently reach a range
hovering between 10% and 35%.
40
Few authors note mortalities less than 10% or greater than 40%. Third, notable recurrence rates of 10% are attributable to the limits of isolating the
306 F.G. Opelka, J.B. Gathright, Jr., and D.E. Beck
precise cause of the bleeding. The rates of recurrence increase
if a surgeon elects to perform a limited right or left colectomy
without precise localization of the hemorrhage. Limited
segmental colectomies continue to have high mortality rates
and excessive persistent bleed rates of 20%.
41
A total colectomy offers the same mortality with a lower chance of recurrent or persistent hemorrhage.
New Frontiers
Horton and Fishman42commented about the advanced imaging
within computerized tomography. Current thinly sliced, fast
image acquisition combined with three-dimensional software
packages has revolutionized the imaging of the vascular tree.
Abdominal, and specifically intestinal vascular imaging now
details smaller than “named” vessels. Current use focuses on
chronic conditions such as mesenteric ischemia and inflammatory bowel disease. Case reports and animal modeling note it is
a feasible study for gastrointestinal hemorrhage. New scanners
promise even more with 16 0.5-mm slices acquired in 0.4 seconds. Image acquisition synchronized with intravascular contrast may outline a site of contrast extravasation or blush. The
detail available may define intestinal hemangiomas, arteriovenous malformations, and angiodysplasias. The sensitivity and
specificity of computed tomographic angiography in patients
with gastrointestinal hemorrhage are unknown and require further comparison studies to current diagnostic studies.
Anderson
43
noted magnetic resonance angiogram creates
images using the bright signal from blood. The three-dimensional images are reconstructed using computerized imaging to
project a two-dimensional image that mimics a conventional
angiogram. Further improvement develops from contrastenhanced magnetic resonance angiography (CEMRA). With
current techniques, the resultant images are not as specific or as
refined as an angiogram. The technique may detect the extravasation of blood pooling in various segments of the intestine. In
addition to localizing the side, the study may distinguish small
intestine versus large intestine. These studies may prove an
enhancement when compared with nuclear scintigraphy.
Wireless capsular endoscopy is an ideal diagnostic adjunct
for patients with occult hemorrhage.
24,25
The first generation
of capsules are 11 × 30 mm. The capsules are easily swallowed and tolerated. The current system captures two images
per second and transmits the images to a recording apparatus
secured to a belt the patient wears. Transmitted images are
later reviewed by the endoscopist.
Lewis and Swain
44
reported the results from the first clinical trial. They noted a source of occult hemorrhage in 7 of 11
patients. The sites noted included angiodysplasia, ileal ulcers,
and a tumor. Rossini et al.
45
corroborated their work in noting
success in 7 of 10 patients.
The evaluation and management of lower gastrointestinal
hemorrhage remains a challenge for surgeons. An algorithm
summarizing the management is provided in Figure 20-4.
FIGURE 20-4. Algorithm for the management of lower gastrointestinal hemorrhage.
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21
Endometriosis
Michael J. Snyder and Steven J. Stryker
Endometriosis is a disease characterized by the presence of
endometrial glands and stroma outside the uterine cavity. It is
one of the most common conditions requiring surgery for
women during their reproductive years. Endometriosis,
although not fatal, may be associated with disabling pain and
intractable infertility. The degree of symptoms varies widely and
does not always correspond to the extent of pathology encountered at surgery. Small lesions may cause severe pain and infertility whereas larger lesions may be asymptomatic and found
only incidentally during surgery for other diagnoses. Diagnosis
is typically made or confirmed at laparoscopy or during laparotomy. Colon and rectal surgeons often become involved in the
management of patients with intestinal endometriosis. This
involvement may occur as a result of a combined procedure with
a gynecologist or in management of an endometrioma masquerading as a neoplastic or inflammatory lesion. Treatment for
endometriosis is usually multimodal and may include an operation in those patients with infertility, pelvic pain, obstruction, or
a poor response to hormonal suppression. Although advances in
diagnostic tests and therapy have been made, endometriosis
remains a frustrating and incompletely understood disease for
both patients and physicians.
Epidemiology
The true prevalence of endometriosis is unknown. There is no
noninvasive screening test for endometriosis, and its diagnosis depends on the visual or pathologic identification of
implants during laparoscopy or laparotomy. Various authors
have estimated that up to 15% of all women of reproductive
age and one-third of infertile women have endometriosis.
study by Houston et al.
endometriosis. After reviewing the medical records for
Caucasian women in Rochester, Minnesota, during the 1970s,
they estimated that 6.2% of premenopausal women have
endometriosis.
Although endometriosis is primarily a disease of the repro-
ductive years, the widespread use of exogenous estrogens and
3
is the only population-based study of
1,2
increasing obesity in our society have made it more prevalent
in postmenopausal women. Conversely, there is a decrease in
the incidence of the disease when women use oral contraceptives or experience multiple pregnancies.
coupled with the fact that the incidence of endometriosis
increases over time after a woman’s last childbirth, suggest
that uninterrupted menstrual cycles predispose susceptible
individuals to the development of endometrial implants.
There is no racial predilection for endometriosis other than in
Japanese women, who have double the incidence of the
disease compared with Caucasian women.
4
These observations,
6
Etiology
The precise etiology that completely explains the cause and
pathogenesis of endometriosis is unknown. The two most
popular theories as to etiology are coelomic metaplasia and
the implantation of viable endometrial cells from retrograde
menstruation through the fallopian tubes. Coelomic metaplasia, postulated by Meyers, suggests that under the correct hormonal milieu, the coelomic epithelium will undergo
metaplastic changes and transform into endometrial tissue.
He bases his theory on studies demonstrating that the peritoneum and uterine endometrium both originate from embryonic coelomic epithelium. Although this theory offers a good
explanation for endometriosis in men and nonmenstruating
women, it does not adequately address the anatomic distribution and clinical pattern of endometriosis. The vast majority
of endometriosis occurs in the pelvis, but the peritoneum at
risk with this theory is evenly distributed throughout the
abdominal cavity. In addition, metaplasia should worsen with
A
age and endometriosis clearly does not.
Retrograde menstruation, first proposed by Sampson
1921, remains the most plausible explanation for the distribution of endometrial implants. This theory postulates that
endometriosis arises from retrograde menstruation through the
fallopian tubes and into the peritoneal cavity. Viable endometrial tissue has been demonstrated in menstrual effluent, and
5
7
8
in
308
21. Endometriosis 309
endometriosis has been induced both in primates, with artifi-
9
cially produced retrograde menstruation,
and in women volunteers who permitted injection of menstrual tissue into their
peritoneum.
10
This theory, however, is probably only part of
the answer.
Whereas retrograde menstruation is very common, occurring in virtually all women, endometriosis affects only a small
minority. Clearly, other factors must be involved to permit the
implantation and growth of endometrial tissue. Several studies
indicate a possible genetic aspect to endometriosis. Simpson
11
et al.
demonstrated that the disease seems to occur more frequently within families. He found a 7% relative risk for blood
relatives of affected individuals as opposed to a 1% relative
risk for nonblood controls. Additionally, the clinical manifestations of the disease were more severe among the related
group. It seems that the inheritance pattern is polygenic or a
combination of genetic and environmental factors. This conclusion is consistent with the clinical associations with delayed
childbearing and uninterrupted cyclic menstruation.
Dmowski et al.
12
have theorized that the genetic factor may
involve the immune system. They demonstrated depressed cellular immunity in monkeys with spontaneous endometriosis.
Other investigators have confirmed alterations in both cellular
and humoral immunity in women with endometriosis.
13,14
The
most striking change observed in cellular immunity is the high
concentration of activated macrophages and decreased functional capacity of natural killer cells. The most significant
abnormality in humoral immunity is the presence of autoantibodies against different cellular components. These changes
have been observed in both the peritoneal cavity and the systemic circulation, suggesting that endometriosis may be a
systemic disease. It is still unclear whether these changes represent manifestations of the disease or a subsequent reaction to
it. This research, however, suggests that mild subclinical
immunosuppression may subsequently lead to endometriosis
many years later.
Clinical Manifestations
The most common sites where endometriosis occurs are summarized in Table 21-1. The most frequent of these are in the
pelvis. Potential sites of implantation in the abdomen include
the appendix, small bowel, and diaphragm. Rarely, implantation may occur in the inguinal canal (in patients with hernias),
surgical incisions, the vulva, vagina, cervix, or systemically in
the lungs, bronchi, or kidneys.
TABLE 21-1. Sites and incidence of endometriosis
Common Less common Rare
Ovaries 60%–75% Appendix 2% Diaphragm
Uterosacral ligaments 30%–65% Ureter 1%–2% Inguinal canal
Cul-de-sac 20%–30% Terminal ileum 1% Liver
Uterus 4%–20% Bladder <1% Spleen
Rectosigmoid colon 3%–10% Abdominal scars < 1% Kidney
Because the majority of women have disease confined to the
pelvis, the most common presenting complaints relate to menstrual irregularities, pelvic pain, and infertility. Many women
with endometriosis may be completely asymptomatic and the
natural history of the disease in these patients has never been
well defined. In studies with placebo arms, a few interesting
observations have been made. A trial involving infertile women
with otherwise asymptomatic endometriosis revealed that
laparoscopic scoring of the severity of the disease increased
over the length of the study in almost 50% of the placebo
15
group.
Another study compared pain scores in women receiving placebo versus gonadotropin-releasing hormone (GnRH)
analogs.
16
The cumulative dysmenorrhea rate and severity of
pain were significantly lower in the treatment group suggesting
a progressive course of the disease when untreated. Other studies on infertile women revealed that mild endometriosis can
spontaneously resolve and that medical therapy may only suppress the disease until hormonal stimulation resumes.
17
Ovarian hormones to varying degrees influence all
endometrial tissue, and many of the clinical manifestations of
endometriosis reflect the changing concentration of these hormones during a typical menstrual cycle. Under the influence
of pituitary-stimulating hormones, the ovary begins to secrete
estrogen at the beginning of the menstrual cycle. This stimulates endometrial mitosis with cellular proliferation in concert
with neovascularization. At the midpoint of the cycle, progesterone production by the corpus luteum begins and promotes
secretory changes in the endometrium in anticipation of
implantation. The loss of progesterone at the end of the menstrual cycle from involution of the corpus luteum destabilizes
the endometrium and induces menstruation.
Pelvic Pain and Dysmenorrhea
Pain is the most common symptom of endometriosis, affecting up to 80% of patients subsequently diagnosed with the
disease. Endometriosis has been discovered in 30%–50% of
women undergoing laparoscopy for pelvic pain.
associated with endometriosis presents as dysmenorrhea, dyspareunia, or chronic noncyclic pelvic pain. There are women,
however, with extensive endometriosis and little or no pain.
Total lesion volume does seem to correlate directly to the
degree of pain.
19
Symptoms are related to the depth of penetration of the lesion, the type of lesion, and its location.
Implants involving the uterosacral ligaments and rectovaginal
septum are most frequently implicated. The pain is typically
most intense just before menstruation and lasts for the duration of menstruation. The pain is often associated with back
pain, dyschezia, and levator muscle spasm, and is more severe
with advanced stages of endometriosis.
Dysmenorrhea occurs in most women with endometriosis.
The association is not well understood, and some have
hypothesized that high uterine pressures cause dysmenorrhea
with retrograde menstruation, a consequence of these
increased pressures.
20
Other investigators, however, have
18
Pelvic pain
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