GI Bleeding Flashcards
Approximately 50% of admissions
for GI bleeding are for
upper GI (UGI) bleeding (from the esophagus, stomach, and duodenum), 40% are for lower GI (LGI) bleeding (from the colon and anorectum), and 10% are for obscure bleeding (from the small intestine)
Severe GI bleeding
hematemesis, melena, hematochezia, or positive nasogastric lavage) accompanied by shock or orthostatic hypotension,
a decrease in the hematocrit value by at least 6% (or a decrease in the hemoglobin level of at least 2 g/dL), or transfusion of at least 2 units of packed red blood cells.
Hematemesis is defined as vomiting of blood, which is indicative of bleeding from the esophagus, stomach, or duodenum.
Hematemesis includes vomiting
of bright red blood, which suggests recent or ongoing bleeding, and dark material (coffee-ground emesis), which suggests
bleeding that stopped some time ago
Melena
can signify bleeding that originates from a UGI, small bowel,
or proximal colonic source and generally occurs when
50 to 100 mL or more of blood is delivered into the GI tract (usually the upper tract), with passage of characteristic stool occurring several hours after the bleeding event
refers to
bright red blood per rectum and suggests active UGI or small bowel bleeding or distal colonic or anorectal bleeding
Hematochezia
refers to subacute bleeding that is not clinically
visible.
Occult
GI bleeding
is bleeding from a site that is not
apparent after routine endoscopic evaluation with esophagogastroduodenoscopy (upper endoscopy) and colonoscopy,
and possibly small bowel radiography
Obscure GI bleeding
for the vascular space to equilibrate with extravascular fluid, and hemodilution results from intravenous administration of saline.
it takes over 24 to 72 hours
A
mean corpuscular volume (MCV) lower than 80 fL suggests
chronic GI blood loss and iron deficiency, which can be confirmed by the finding of low blood iron, high total iron-binding capacity (TIBC), and low ferritin levels
suggests chronic liver disease
or folate or vitamin B12 deficiency.
A high MCV (>100 fL)
An elevated white blood
cell count may occur in more than half of patients with UGI
bleeding and has been associated with greater severity of
bleeding.6
A low platelet count can contribute to the severity
of bleeding and suggests chronic liver disease or a hematologic disorder
Maroon-colored stool can be seen with an
actively bleeding UGI source or a small intestinal or proximal
colonic source
Patients should be transfused with
packed red blood cells, platelets, and fresh frozen plasma as
necessary to keep the hemoglobin level greater than
7 gm/dL,
platelet count higher than 50,000/mm3
, and prothrombin time
less than 15 seconds, respectively.
7 g/dL or when the hemoglobin level was less than
9 g/dL.14 The former (“restrictive”) transfusion strategy was
associated with a higher survival rate and lower rebleeding
rate in patients with bleeding due to
peptic ulcer or ChildPugh class A or B cirrhosis but the opposite results in those with Child-Pugh class C cirrhosis
infusion of a PPI in a high dose
before endoscopy accelerates the resolution of endoscopic
stigmata of bleeding in ulcers (see later) and reduces the need
for endoscopic therapy but
does not result in improvement in
the transfusion requirement, rebleeding rate, need for surgery,
or death rate
Patients with a strong suspicion of portal
hypertension and variceal bleeding should be started empirically on intravenous octreotide (bolus followed by infusion which can reduce the risk of
rebleeding to a rate similar to that following endoscopic therapy
Patients who are hemodynamically stable without evidence of ongoing
bleeding can undergo urgent endoscopy (within 12 hours),
often in the GI endoscopy unit rather than the ICU.
sary
Middleof-the-night endoscopy should be avoided, except for the most
severely bleeding or high-risk patients, because well-trained
endoscopy nurses, optimal endoscopic equipment, and surgical backup may not be available at night. In the rare patient
with massive bleeding and refractory hypotension, endoscopy
can be performed in the operating room, with the immediate
availability of surgical management
severe UGI bleeding, gastric lavage with a large (34 French) orogastric tube should be performed to evacuate blood and clots from the stomach to prevent aspiration and allow adequate endoscopic visualization
Using iced saline lavage to prevent
or decrease UGI bleeding is of no value and may impair coagulation and cause hypothermia.
Gastric lavage with lukewarm
tap water is as safe as lavage with sterile saline and much less
expensive.
placed on the tip of the endoscope can help to visualize bleeding sites behind mucosal
folds, deploy endoscopic clips by modifying the angle of
endoscopic approach, avoid mucosal “white-out” at corners,
and remove blood clots
A clear plastic cap
Patients should receive 6 to 8 L of polyethylene glycol purge
orally or via a nasogastric tube over
4 to 6 hours until the rectal
effluent is clear of stool, blood, and clots
Metoclopramide, 10 mg,
may be given intravenously before the purge and repeated every 4 to 6 hours to facilitate gastric emptying and reduce nausea
. In patients with severe or ongoing active hematochezia, urgent colonoscopy should be performed within 12 hours,
but only after thorough cleansing of the colon.
Patients with
mild or moderate self-limited hematochezia should undergo
colonoscopy within 24 hours of admission after a colonic
purge
Capsule endoscopy has the advantage of directly
visualizing the small intestine to identify potential sources or
active bleeding. Disadvantages are that the procedure
takes 8
hours to complete
Injection therapy is most commonly performed with a
sclerotherapy needle and submucosal injection of epinephrine, diluted to a concentration of
1 : 10,000 or 1 :20,000, into or
around the bleeding site or stigma of hemorrhage
Injection therapy can also be performed
with a sclerosant, such as ethanolamine or alcohol, but
these agents are associated with increased tissue damage and
other risks.
Angiography generally is diagnostic of
extravasation into the intestinal lumen only when the arterial bleeding rate is at least
0.5 mL/min.
The sensitivity of mesenteric angiography is 30% to 50% (with higher sensitivity rates for active GI bleeding than for recurrent acute or chronic occult bleeding), and the specificity is 100%
Radionuclide imaging has been reported to detect
bleeding at a rate of
0.04 mL/min
bleeding (bleeding scans) are technetium
sulfur colloid and technetium pertechnetate–labeled autologous red blood cells
The rate of true-positive scans is higher for active bleeding with hemodynamic instability than for less severe bleeding.
The most common reason for a false-positive result is rapid transit of luminal blood, such that labeled blood is detected in the colon even though it originated from a more proximal site
in the GI tract.
Technetium pertechnetate scintigraphy can identify ectopic
gastric mucosa in a
Meckel’s diverticulum. This diagnosis
should be considered in a pediatric or young adult patient
with unexplained GI bleeding
Of the potential causes of severe UGI bleeding, peptic ulcer is
the most common, accounting for approximately
40%
mortality rate of 5% to 10%
for severe UGI bleeding has not changed since
riceal bleeding.
Bleeding is self-limited in
80% of patients with UGI hemorrhage, even without specific therapy.
Of the remaining 20% who continue to bleed or rebleed, the mortality rate is 30% to 40%.
peptic ulcer, most commonly gastric or duodenal
ulcer, accounted for
50% of UGI bleeds
The
mortality rate associated with peptic ulcer bleeding is 5% to 10%
Factors Predictive of a Poor Prognosis afterHemorrhage from Peptic Ulcer
Age > 60 years
Bleeding onset in hospital
Comorbid medical illness
Shock or orthostatic hypotension
Fresh blood in nasogastric tube
Coagulopathy
Multiple transfusions required
Higher lesser curve gastric ulcer (adjacent to left gastric artery)
Posterior duodenal bulb ulcer (adjacent to gastroduodenal
artery)
Endoscopic finding of arterial bleeding or visible vessel
The prevalence of Hp infection is over
80% of the population in many developing countries and 20% to 50% in industrialized countries.
Hp gastritis most commonly involves the
antrum and predisposes patients to duodenal ulcers,
whereas
gastric body–predominant gastritis is associated with gastric
ulcers.
Gastric ulcers are about 4 times as
common as duodenal ulcers in patients who take NSAIDs.
Patients at high risk
of rebleeding without treatment are those with a
active arterial bleeding (90%), an NBVV (50%), or an adherent clot (33%)
endoscopic hemostasis alone decreases
the rebleeding rate to approximately 15% to 30% The adjunctive intravenous administration of a high-dose PPI
(e.g., pantoprazole, 80-mg bolus and 8 mg/hr for 72 hours) decreases this rate even further
An endoscopically identified NBVV that has a translucent (pearl or whitish) color has a higher risk of rebleeding than a
darkly colored pigmented protuberance (clot), because the translucent stigma likely represents the arterial wall
Patients with major stigmata of ulcer hemorrhage (spurting, NBVV, or adherent clot) benefit most from
endoscopic hemostasis, whereas those with a flat spot or clean
ulcer base do not.
Patients with oozing bleeding and no other
stigma (e.g., a clot or NBVV) may benefit from endoscopic
hemostasis but not from a high-dose PPI infusion
The risk of rebleeding from a peptic ulcer decreases significantly
72 hours after the initial episode of bleeding.
untreated NBVVs have found that these lesions resolve over 4 days and adherent
clots tend to resolve over 2 days.
The most commonly used treatment for ulcer bleeding
worldwide is
epinephrine injection therapy; it is widely available, easy to perform, safe, and inexpensive. Therapy with epinephrine alone seems to be more effective when used inhigh doses (13 to 20 mL) than in low doses (5 to 10 mL)
application of hemoclips was
shown to be superior to that for
epinephrine injection alone
but comparable to that for thermocoagulation
is generally defined as a blood clot over an ulcer that is resistant to several minutes of vigorous target jet water irrigation
An adherent clot
Randomized controlled studies have shown that
endoscopic treatment of an adherent clot can decrease the
rebleeding rate to less than 5%
Patients with clean-based ulcers at endoscopy after target irrigation have a rebleeding rate of
less than 5%
inject 0.5- to 1-mL aliquots of epinephrine (1 :20,000) via a sclerotherapy needle
into 4 quadrants of the ulcer within 1 to 2 mm of the bleeding site
After epinephrine injection, the thermal probe is placed directly on the bleeding site to tamponade the site and stop the bleeding, and coagulation is applied with long (10- second
Intravenous H2 receptor antagonists can raise the intragastric pH acutely, but tolerance to these agents develops rapidly
and the pH usually returns to 3 to 5 within 24 hours.
Several
studies have shown that in normal subjects, intravenous
administration of a PPI can consistently keep gastric pH
higher than 4 (and often 6) over a 72-hour infusion.
intravenous H2 receptor antagonists for the prevention of
recurrent ulcer bleeding have shown no definite benefit
no difference between high-dose intravenous continuous infusion of a PPI (80 mg bolus followed by 8 mg/hr for 3
days) and
non–high-dose intermittent or oral administration
(for 3 days)
Whether oral administration is as effective as
intravenous administration of a PPI is unclear, although
studies have shown that high-dose oral administration (e.g., omeprazole, 40 mg twice daily) reduces rebleeding to rates that would be expected from endoscopic hemostasis
In fact, the increase in intragastric pH with high-dose oral PPI administration is almost identical (although delayed by 1 hour) to that with intravenous PPI administration.1
decreases the risk of rebleeding from peptic ulcers when compared with placebo or an H2 receptor blocker.
octreotide
The proposed
mechanisms of action include a reduction in splanchnic and
gastroduodenal mucosal blood flow, a decrease in GI motility,
inhibition of gastric acid secretion, inhibition of pepsin secretion, and gastric mucosal cytoprotective effects
Somatostatin or octreotide can be considered in
patients with severe ongoing bleeding who are not responsive
to endoscopic therapy, an intravenous PPI, or both, and are
not surgical candidates, although their effectiveness in these
patients is uncertain
routine second-look
endoscopy is not recommended for most patients with peptic
ulcer bleeding,
except in those in whom the initial endoscopic examination was suboptimal because excessive blood
obscured the view, technical problems with hemostasis
occurred, clinically significant bleeding recurred, or less effective endoscopic techniques such as epinephrine injection alone
The risk of rebleeding from peptic ulcers that started bleeding
in the outpatient setting and required endoscopic hemostasis
is greatest in the first
72 hours after diagnosis and treatment.
Factors that predicted failure of endoscopic retreatment included an
ulcer size of at least 2 cm and hypotension
on initial presentation
recurrent bleeding despite 2 sessions of endoscopic hemostasis should be considered for
angiographic
embolization or surgical therapy
For patients with severe atherosclerotic cardiovascular
disease who require aspirin, however, a dose of 81 mg/day
should be started within
7 days.
High-Risk Endoscopic Stigmata
Patients who have undergone endoscopic hemostasis for
active arterial bleeding, an NBVV, or an adherent clot should
be observed in the hospital for
72 hours while they receive
high-dose intravenous infusions of a PPI
Intermediate-Risk Stigmata
Patients with oozing from an ulcer and no other stigmata (e.g.,
spurting, NBVV, clot), severe comorbidity, or shock on presentation should undergo endoscopic hemostasis. Initiation of an
oral PPI and observation in the hospital for
24 to 48 hours after
endoscopic hemostasis are recommended. Such patients do
not benefit from high-dose intravenous PPIs after successful
endoscopic hemostasis
Low-Risk Endoscopic Stigmata
Patients with a clean-based ulcer or flat spot in the ulcer base
can generally resume a
normal diet immediately, begin an oral
PPI once daily, and be discharged from the emergency department or hospital when stable
All patients with peptic ulcer bleeding should be tested for Hp
infection and,
if the result is positive, should receive antibiotic
therapy in standard fashion
bleeding can lead to a false-negative rapid urease test
Antibiotic therapy
does not have to be started immediately and can be initiated
on an outpatient basis when the patient has resumed a normal
diet.
Patients who are Hp positive and who will need longterm PPI treatment because of the concomitant use of aspirin
or other NSAIDs do not necessarily need to be treated for
Hp infection; recurrent ulceration will be prevented by the
PPI.
Patients who require
an antiplatelet medication such as clopidogrel and have a
history of ulcer bleeding will have less chance of recurrent
bleeding
if they take aspirin (81 mg) and a PPI daily compared
with clopidogrel alone.1
Because selective COX-2 inhibitors result in rebleeding rates similar to those associated with
NSAID and PPI co-therapy,
their use may not be worth the
increased cardiovascular risk
Repeat upper endoscopy should be considered in patients
with a gastric ulcer after
6 to 10 weeks of acid suppressive
therapy to confirm healing of the ulcer and absence of malignancy
Upper endoscopy is essential for diagnosing
severe erosive esophagitis, but endoscopic therapy generally
has no role unless a focal ulcer with a stigma of recent hemorrhage is found. These patients should be treated with a daily
PPI for
8 to 12 weeks and undergo repeat endoscopy to exclude
underlying Barrett’s esophagus
stressrelated mucosal injury (SRMI, or stress ulcers), characterized
by diffuse bleeding from erosions and superficial ulcers.
The 2 main risk
factors are
severe coagulopathy and mechanical ventilation
for longer than 48 hours
prophylactic treatment with oral omeprazole or
intravenous cimetidine results in similar bleeding rates, but
that omeprazole is more effective than cimetidine in maintaining the luminal gastric pH above 4
A potential harmful
effect of gastric acid suppression to prevent stress ulcers is
proliferation of bacteria in the stomach secondary to the
increased gastric pH, and the associated risk of aspiration and
ventilator-associated pneumonia.
SRMI is diffuse, endoscopic therapy is generally not feasible.
is a large (1- to 3-mm) submucosal artery
that protrudes through the mucosa, is not associated with a
peptic ulcer, and can cause massive bleeding.
A Dieulafoy’s lesion
It usually is
located in the gastric fundus, within 6 cm of the gastroesophageal junction, although lesions in the duodenum, small intestine, and colon have been reported
Mallory-Weiss tears are mucosal or submucosal lacerations
that occur at the
gastroesophageal junction and usually extend
distally into a hiatal hernia
Endoscopy usually reveals a single tear that begins at the gastroesophageal junction and extends several millimeters distally into a hiatal hernia sac
Patients generally present with hematemesis or coffee-ground emesis and typically with nonbloody vomiting followed by hematemesis, although some patients do not recall vomiting. The tear is thought to result from increased intra-abdominal pressure, possibly in combination with a shearing effect caused by negative intrathoracic pressure above the diaphragm, which is often related to vomiting in patients with a history of alcohol abuse
Mucosal
(superficial) Mallory-Weiss tears can start healing within
hours and can heal completely within
48 hours
The rebleeding
rate among patients hospitalized for a Mallory-Weiss tear is
approximately
10%; risk factors for rebleeding include shock
at presentation and active bleeding at endoscopy.1
are linear erosions or ulcerations in the
proximal stomach at the end of a large hiatal hernia,
Cameron’s lesions
diaphragmatic pinch (Fig. 20-14).183 Cameron’s lesions are thought to be caused by mechanical trauma and local ischemia as the hernia moves against the diaphragm and only secondarily by acid and pepsin
is characterized by rows or stripes of
ectatic mucosal blood vessels that emanate from the pylorus
and extend proximally into the antrum The cause
is uncertain, and the lesion may represent a response to
mucosal trauma from contraction waves in the antrum
Gastric antral vascular ectasia (GAVE), also described as
“watermelon stomach,” associated with cirrhosis and scleroderma patients with GAVE who do not have
portal hypertension demonstrate linear arrays of angiomas (classic GAVE), whereas those with portal hypertension have more diffuse antral angiomas.
iron deficiency anemia or melena, with a mildly decreased hematocrit value suggestive of a slow UGI bleed. GAVE is most commonly reported in older women and also seems to be more common in patients with end-stage renal disease
4 to 8 weeks apart are needed to achieve eradication of the lesions and a reduction in bleeding from the antral ectasias
and occasionally classic GAVE are sometimes mistaken for gastritis by an unsuspecting endoscopist.
diffuse type of antral
angiomas
argon plasma coagulation has been shown to be equally (80%) effective in cirrhotic and noncirrhotic patients with GAVE
(TIPS) in patients with portal hypertension and cirrhosis
does not decrease bleeding from GAVE or diffuse antral angiomas.
is caused by increased
portal venous pressure and severe mucosal hyperemia that results in ectatic blood vessels in the proximal gastric body
and cardia and oozing of blood.
Portal hypertensive gastropathy (PHG)
mosaic or snakeskin pattern and are not associated
with bleeding.
is a rare form of UGI bleeding that
occurs most commonly in patients with acute pancreatitis,
chronic pancreatitis, pancreatic pseudocyst, or pancreatic
cancer or after ERCP with pancreatic duct manipulation. It
can also result from rupture of a splenic artery aneurysm into
the pancreatic duct
Hemosuccus pancreaticus
Bleeding from an aortoenteric fistula is usually acute and massive, with a high mortality rate.
A primary aortoenteric fistula is a communication between the native abdominal aorta (usually an atherosclerotic abdominal aortic aneurysm)
and, most commonly, the
third portion of the duodenum
self-limited herald bleed occurs hours to months
before a more severe exsanguinating bleed
history
of an abdominal aortic aneurysm or by palpation of a pulsatile abdominal mass.
Secondary aortoenteric fistulas usually occur between the
small intestine and an
infected abdominal aortic surgical
graft. The fistula typically occurs between the third portion of
the duodenum and the proximal end of the graft but may
occur elsewhere in the GI tract. The fistula usually forms between 3 and 5 years after graft placement.
urgent CT with intravenous contrast or MR angiography first
second
most common cause of severe UGI bleeding (after PUD)
Esophageal
variceal bleeding related to portal hypertension is the
acute mortality rate with each bleed is approximately 30%,
and the long-term survival rate is less than 40% after 1 year
with medical management alone.
Bleeding from gastric
varices caused by splenic vein thrombosis is treated by
splenectomy
cause
selective splanchnic vasoconstriction and lower portal pressure without causing the cardiac complications seen with
vasopressin
Somatostatin and its long-acting analog, octreotide,
The dose of octreotide for acute variceal hemorrhage is a
50-µg bolus followed by a continuous infusion of 50 µg/hr for
up to 5 days.
prolonged prothrombin time that does not
correct with fresh frozen plasma may benefit from infusion of
human recombinant factor VIIa.
Up to 20% of cirrhotic patients who are hospitalized with
GI bleeding have a bacterial infection at the time of admission
to the hospital,
and infection develops during the hospitalization in up to 50%
administration of an antibiotic to cirrhotic patients
with variceal bleeding is associated with a decrease in the
rates of mortality and bacterial infections
oral norfloxacin (400 mg twice daily), intravenous ciprofloxacin (400 mg every 12 hours), and intravenous levofloxacin (500 mg every 24 hours), and intravenous ceftriaxone, 1 g every 24 hours, administered for 7 days.
Balloon tamponade of varices is seldom used now to control
gastroesophageal variceal bleeding
Sengstaken-Blakemore tube has gastric and esophageal balloons, with a single aspirating port in the stomach.
The Minnesota tube also has gastric and esophageal balloons and has aspiration ports in the esophagus and stomach.
The LintonNachlas tube has a single large gastric balloon and aspiration ports in the stomach and esophagus
endoscopic
band ligation is as effective as sclerotherapy in achieving
initial hemostasis and reducing the rate of rebleeding from
esophageal varices.
Acute hemostasis generally can be
achieved in 80% to 85% of cases, with a rebleeding rate of 25%
to 30%.
lace 2 bands on each esophageal
variceal column, one distally near the gastroesophageal junction and another 4 to 6 cm proximally
is an interventional radiologic procedure in which an
expandable metal stent is placed via percutaneous insertion
between the hepatic and portal veins, thereby creating an
intrahepatic portosystemic shunt.
(TIPS)
TIPS is effective for shortterm control of bleeding gastroesophageal varices, especially
those that fail endoscopic therapy
TIPS are a rate of shunt occlusion of up to 80% (less with
polytetrafluoroethylene-coated stents) within 1 year and
development of new or worsening hepatic encephalopathy in
approximately 20% of patients
LGIB
Most patients are older than
70 years of age. Patients usually present with painless hematochezia and a decrease in the hematocrit value but without
orthostasis.
If orthostasis is associated with hematochezia, a
briskly bleeding UGI source should be excluded (see earlier);
severe painless hematochezia results from a foregut source in
approximately 15% of patients
is generally the most common cause
of acute LGI bleeding and occurs in approximately 30% of
cases.
Diverticulosis
Colonic polyps or cancer, colitis, and anorectal disorders each account for approximately 20% of cases
*Severe lower GI bleeding is defined as
continued bleeding within the first 24 hr of hospitalization (transfusion of 2 or more units of packed red blood cells and/or hematocrit
value drop of 20% or more) and/or recurrent bleeding after 24 hr of stability (need for additional transfusions, further hematocrit value decrease of 20% or more, or
readmission to the hospital for lower GI bleed within 1 wk of discharge).
Predictive factors include tachycardia, hypotension, syncope, a nontender abdomen, rectal bleeding on presentation, aspirin use, and more than 2 comorbid illnesses
Urgent colonoscopy following a rapid bowel purge has been
shown to be safe, provide important diagnostic information,
and allow therapeutic intervention.
Patients usually ingest 6 to 8 L of polyethylene glycol solution orally or via a nasogastric tube over 4 to 6 hours until the rectal effluent is clear of stool, blood, and clots. Metoclopramide, 10 mg, may be
given intravenously before the purge and repeated every 3 to 4 hours to facilitate gastric emptying and reduce nausea
Urgent colonoscopy for LGI bleeding generally is performed
6 to 36 hours after the patient is admitted to the
hospital
diverticular bleeding, the timing of endoscopy (0 to 12 hours,
12 to 24 hours, or more than 24 hours after admission) is not
significantly associated with the finding of active bleeding or
other stigmata that would prompt colonoscopic hemostasis.
no difference between urgent
(≤12 hours after presentation) and elective (36 to 60 hours after
presentation) colonoscopy in terms of further bleeding, blood
transfusions, hospital days, or hospital charges
Histopathologically, diverticula in the colon are actually
pseudodiverticula because they do not contain all layers of the colonic wall.
Diverticula form when colonic tissue is pushed
out by intraluminal pressure at points of entry of the small arteries (vasa recta), where they penetrate the circular muscle layer of the colonic wall
Although most diverticula are in the left
colon,
several series have suggested that diverticula in the
right colon are more likely to bleed
Two thirds of definitive diverticular bleeds (with stigmata of hemorrhage)
emanate from the region of the splenic flexure of the colon or proximally
is diagnosed when colonoscopy reveals diverticulosis without
stigmata, and no other significant lesions are seen in the colon
and by anoscopy, terminal ileum examination, and push
enteroscopy.
Presumptive diverticular hemorrhage
is used when
another lesion is identified as the cause of hematochezia, and
colonic diverticulosis is evident
incidental diverticulosis
Patients with diverticular bleeding typically are older,
have been taking aspirin or other NSAIDs, and present with painless hematochezia
In at least 75% of patients with
diverticular bleeding, the bleeding stops spontaneously, these patients require transfusion of fewer than 4 units of packed red blood cells
The term colitis refers to any form of inflammation of the colon.
Severe LGI bleeding may be caused by ischemic colitis, inflammatory bowel disease, or possibly infectious colitis
Ischemic colitis can present as painless or painful hematochezia with mild left-sided abdominal discomfort
The painless subtype usually results from mucosal
hypoxia and is thought to be caused by hypoperfusion of the intramural vessels of the intestinal wall, rather than by largevessel occlusion, which is often painful and clinically more severe with worse outcomes
Risk factors associated with ischemic colitis have been
reported to include
older age, shock, cardiovascular surgery,
heart failure, chronic obstructive pulmonary disease, ileostomy, colon cancer, abdominal surgery, irritable bowel syndrome, constipation, laxative use, oral contraceptive use, and use of an H2 receptor antagonist.
The superior mesenteric
artery supplies blood to the right colon (cecum, ascending
colon, hepatic flexure, proximal transverse colon, and
midtransverse colon),
whereas the inferior mesenteric artery
supplies blood to the left colon (distal transverse colon, splenic flexure, descending colon, sigmoid colon, and rectum).
The colon has an abundant blood supply, but the watershed area
between the superior and inferior mesenteric arteries has the fewest collateral vessels and is at most risk for ischemia
colon normally receives 10% to 35% of cardiac output, and ischemia can occur if blood flow decreases by more than 50%.
ischemia is usually made by colonoscopy,
but in severe cases of large-vessel ischemia there may be
“thumbprinting” noted on plain film radiographs or colonic wall thickening on CT
large-vessel mesenteric ischemia usually have
worse outcomes, including higher rates of rebleeding, perforation, surgery, and death
Bleeding occurs after approximately 1% of colonoscopic polypectomies.
It is most common 5 to 7 days after polypectomy
but can occur from 1 to 14 days after the procedure;
risk factors for postpolypectomy bleeding include a large polyp
size (>2 cm), thick stalk, sessile type, location in the right
colon, use of warfarin or heparin, and use of aspirin or another
NSAID
Chronic
radiation effects occur 6 to 18 months after completion of
treatment and manifest as bright red blood with bowel movements. Bowel injury resulting from chronic radiation is related
to vascular damage, with subsequent mucosal ischemia, thickening, and ulceration.
Much of this damage is thought to
result from chronic hypoxic ischemia and oxidative stress.
is characterized by bright red blood
per rectum that can coat the outside of the stool, drip into
the toilet bowl, be seen on tissue after wiping, and often
appear as a large amount of fresh blood in the toilet
Hemorrhoidal bleeding
mild, intermittent, and self-limited
painless severe hematochezia from a solitary or multiple rectal ulcers located 3 to 10 cm
above the dentate line
Rectal Ulcers
mean age of 71 years
hospitalized for other medical problems from 3 to 14 days (average 7.5 days) prior to the onset of bleeding
is commonly defined as GI bleeding of
uncertain cause after a non-diagnostic upper endoscopy, colonoscopy, and barium small bowel follow-through
Obscure GI bleeding
In patients younger than age 40, bleeding is more likely
to be due to a tumor, Meckel’s diverticulum, or Crohn’s
disease. Angioectasias or an NSAID-induced ulcer are common
causes in those 40 years of age and older.
refers to visible acute GI bleeding (e.g.,
melena, maroon stool, hematochezia) in patients with a nondiagnostic upper endoscopy, colonoscopy, and small bowel
series.
Obscure
overt GI bleeding
refers to a positive fecal occult
blood test result, usually in association with unexplained iron
deficiency anemia.
Obscure occult GI bleeding
In patients with obscure GI bleeding, the following possibilities exist:
(1) the lesion was within reach of a standard
endoscope and colonoscope but not recognized as the bleeding site (e.g., Cameron’s lesions, angioectasias, internal hemorrhoids);
(2) the lesion was within reach of the endoscope and
colonoscope but was difficult to visualize (e.g., a blood clot obscured visualization of the lesion; varices became inapparent in a hypovolemic patient; a lesion was hidden behind a mucosal fold) or present intermittently (e.g., Dieulafoy’s lesion, angioectasias); or
(3) the lesion was in the small intestine beyond the reach of standard endoscopes (e.g., neoplasm,
angioectasias, diverticulum).
also referred to as angiodysplasia, is the formation of aberrant blood vessels found
throughout the GI tract that develop with advancing age.
Angioectasia,
is the lesion that results from dilatation of the
terminal aspect of a blood vessel. Any of the vascular lesions
may cause overt or obscure GI bleeding in adults, particularly
in older adults and those who take antiplatelet and anticoagulant drugs
Telangiectasia
Aortic stenosis has been associated with GI bleeding from
angioectasia
(Heyde’s syndrome).
Overt or obscure GI bleeding occurs in approximately
20% of patients with a left ventricular assist device (LVAD),
especially elderly patients, with angioectasia as one of the
most frequent causes of bleeding
also known as Osler-Weber-Rendu disease, is a hereditary
condition characterized by diffuse telangiectasias and large
AVMs
Hereditary Hemorrhagic Telangiectasia
HHT,
The most striking clinical feature is telangiectasias on the lips, oral mucosa, and fingertips
The diagnosis of HHT is based on 4 criteria
(1) spontaneous and recurrent epistaxis, (2) multiple mucocutaneous telangiectasias, (3) visceral AVMs (GI, pulmonary, brain, liver),
and (4) a first-degree relative with HHT
is a congenital blind intestinal pouch
that results from incomplete obliteration of the vitelline duct during gestation
A Meckel’s diverticulum
Characteristic features of
Meckel’s diverticula have been described by the “rule of 2s”: They occur in 2% of the population, are found within 2 feet of the ileocecal valve, are 2 inches long, result in a complication in 2% of cases, have 2 types of ectopic tissue (gastric and pancreatic) within the diverticulum, present clinically most commonly at age 2 (with intestinal obstruction), and have a male-to-female ratio of more than 2 :1
The most common complications of Meckel’s diverticula are bleeding, obstruction, and diverticulitis, which can occur in children or adult
The diagnostic test for a
Meckel’s diverticulum is a
99mTc-pertechnetate scan (Meckel’s
scan), because technetium pertechnetate has an affinity for gastric mucosa
The accuracy of the Meckel’s
scan can be improved with administration of an H2 receptor antagonist for 24 to 48 hours before the test.
Tumors of the small intestine comprise only 5% to 7% of all
GI tract neoplasms but are the
most common cause of obscure
GI bleeding in patients younger than age 50
The most
common small intestine neoplasms are adenomas (usually
duodenal), adenocarcinomas (Fig. 20-23), carcinoid tumors
(usually ileal), GISTs, lymphomas, hamartomatosis polyps
(Peutz-Jeghers syndrome), and juvenile polyps (
is the most common site of small intestinal
diverticula.
The duodenum
Push enteroscopy can be performed with a colonoscope (160 to 180 cm in length) or dedicated push enteroscope (220 to 250 cm in length).
For patients with unexplained overt GI bleeding and negative
upper endoscopy and colonoscopy results, capsule endoscopy
is generally recommended as the next step. If capsule endoscopy reveals a lesion in the proximal jejunum, push enteroscopy can be performed
Normal fecal blood loss is
0.5 to 1.5 mL/day
If the FOBT or FIT was
obtained for colon cancer screening in a patient 50 years of age
or older, the patient should
undergo colonoscopy and possibly
upper endoscopy
Upper endoscopy should also be considered in a patient with a positive FOBT result who does not
have iron deficiency anemia.
patients with a positive FIT result (which
detects only human hemoglobin from the LGI tract)
and
normal colonoscopy result requires upper endoscopy is uncertain (and unlikely)
If a FOBT was performed for iron deficiency anemia, the patient should be evaluated with upper
endoscopy and colonoscopy. If the results of both examinations are negative, the small bowel should be imaged as
described earlier with capsule endoscopy, possibly followed
by deep enteroscopy if a lesion is detected on capsule
endoscopy
Iron deficiency anemia is common, with a frequency of
2% to 5% in adult men and postmenopausal women
A transferrin saturation index (serum iron divided by TIBC) lower than
15% is a sensitive indicator of iron deficiency
anemia
In iron deficiency anemia, the serum iron concentration is decreased and the level of transferrin (TIBC) is increased.
A serum ferritin level
lower than 15 ng/mL has a
sensitivity of 59% and specificity of 99% for iron deficiency, whereas a cutoff ferritin level of 41 ng/mL has a sensitivity and specificity of 98%.
Iron deficiency anemia has also been associated
with Hp infection.
is the site of iron absorption in the small
intestine.
The duodenum
Roux-en-Y gastric bypass
surgery are at high risk of iron malabsorption because of bypass of the duodenum, where most iron is absorbed.
Patients with unexplained iron deficiency anemia should undergo upper endoscopy and colonoscopy to rule out a GI tract lesion that may cause chronic blood loss.
Celiac disease commonly manifests as iron deficiency
anemia, primarily because of iron malabsorption resulting from blunted duodenal villi.
