Gastrointestinal Bleeding
Jarrett Lefberg
South Pointe Hospital
Incidence
Upper GI bleed 100/100,000
Above the ligament of Treitz
 Lower GI Bleed 20/100,000
Below the ligament of Treitz
 Both are more common in males and
elderly.

Causes of Upper GI Bleed

1) Peptic ulcer disease - most common
cause
A) duodenal ulcers 29%
will rebleed in 10% of cases within
24-48h
B) gastric ulcers 16%
more likely to rebleed
C) stomal ulcers <5%
Causes of Upper GI Bleed
2) Erosive gastritis, esophagitis, duodenitis
some causes are ETOH, ASA, NSAID’s
 3) Esophageal and gastric varices
causes by portal hypertension
 4) Mallory-Weiss syndrome – longitudinal
mucosal tear in the cardioesophageal
region
caused by repeated retching

Causes of Upper GI Bleed
 5)
stress ulcers
 6) arteriovenous malformation
 7) malignancy
 8) aortoenteric fistula
Causes of Lower GI Bleeding
1) Hemorrhoids - most common cause
 2) Diverticulosis – common, painless,
and can be massive
Caused from an erosion into a
penetrating artery from the
diverticulum.
 3) Arteriovenous malformations – common
and seen in people with hypertension and
aortic stenosis

Causes of Lower GI Bleeding
 4)
CA/polyps
 5) inflammatory bowel disease
 6) infectious gastroenteritis
 7) Meckel diverticulum
Diagnosis








Questions to ask in history
Any hematemesis, coffee-ground emesis, melena, or
hematochezia.
Any weight loss or changes in bowel habits.
Any vomiting and retching.
Any history aortic graft.
Any history of ASA, NSAID’s, steroids.
Any ETOH abuse.
Any history of iron or bismuth which can simulate
melena and beets which can simulate hematochezia.
Note stool guaiac testing will be negative.
Diagnosis
Physical exam






Vital signs may show hypotension and
tachycardia.
Cool, clammy skin then in shock.
Spider angiomata, palmer erythema, jaundice,
and gynecomastia seen in liver disease.
Petechiae and purpura seen in coagulopathy.
Careful ENT exam to rule out causes that
can mimic upper GI bleeds.
Proper abdominal exam and rectal exam.
Diagnosis
Lab
CBC
Electrolytes
Glucose
BUN/Creatine –BUN will be elevated in upper GI
bleeds
 Coagulation studies
 Liver function studies
 Type and cross-match




Diagnosis
Diagnostic
ECG
 Abdominal series - not beneficial unless specific
indications
 Angiography - can be diagnostic and therapeutic but
requires a brisk bleed at .5-2ml/min
 Bleeding scans - can only be diagnostic but are more
sensitive then angiography and require a bleeding rate of
only .1ml/min
 Colonoscopy - is diagnostic and therapeutic and more
accurate than bleeding scans and angiography

Treatment





Large-bore intravenous lines with fluid
replacement.
Class I + II hemorrhage replace with crystalloid.
Class III + IV hemorrhage replace with
crystalloid and blood.
NG tube should be placed and can determine
upper GI from lower GI but not 100%. Also NG
tubes will not worsen varice bleeds.
Foley catheter for hypotension patients to
monitor output.
Treatment
Proton-pump inhibitor
 Endoscopy
 Somatostatin, octretide for varices
 Balloon tamponade
 Surgery
 Must get early consultation with
gastroenterologist and general surgeon for
significant GI bleeds.

Peptic Ulcer Disease
Jarrett Lefberg
South Pointe Hospital
Epidemiology
10% US population >17 years of age have
peptic ulcer disease at some time.
 White Americans have a 10% prevalence
of H. pylori by age 35 and 80% by age 75.
 Black Americans have a 45% prevalence
of H. pylori by age 25.

Pathophysiology
Prostaglandins produce mucous and bicarbonate
ions which protect the tissue in the stomach by
being destroyed with hydrochloric acid and
pepsin.
 Dyspepsia is the imbalance between the
protective mucosa and acid/pepsin.
 Peptic ulcer which is a defect beyond muscularis
mucosa will develop if there is an imbalance.
 Note -stress ulcers do not extent through
the muscularis mucosa.

Pathophysiology
 Two
types of peptic ulcers
1) Duodenal ulcers which occur
in the first portion of the duodenum.
2) Gastric ulcers which usually
occur in the lesser curvature of the
stomach.
Causes
H. pylori - a spiral, urease producing flagellated
bacterium which lives between the mucus gel
and mucosa. Its production of urease,
cytotoxins, proteases and other compounds
disturb the gel and increase tissue exposure to
acid and pepsin.
 H. pylori is seen in 95% of patients with
duodenal ulcers and 80% of gastric ulcers.
 Note only 10-20% of patients who are
infected with H. pylori will develop ulcers.

Causes

NSAID’s - inhibit prostaglandins which in turn
increases tissue exposure to acid and pepsin.

Zollinger-Ellison syndrome - is a gastrin
secreting tumor which creates such a high acid
level it over rides the protective gel.

Cigarette smoking - inhibits bicarbonate ion
production and increases gastric emptying.
Causes
Bile salts
 Emotional stress
 Type O blood
 Prolonged use of corticosteriods
 Caffeinated beverages

 Note
diet and alcohol are not
predisposing factors to the
development of peptic ulcers.
Clinical Features
Epigastric pain - (gnawing, aching or burning)
is the main complaint.
 Gastric ulcers usually develop pain shortly after
eating.
 Duodenal ulcers usually develop pain 2-3 hours
after eating and awaken patients at night. Pain
can be relieved by food.
 Physical exam of uncomplicated PUD, there may
be a finding of epigastric tenderness.

Diagnosis
Definite diagnosis can only be made by
visualization with an upper GI or
endoscopy.
 Endoscopy has the advantage of being
able to take a biopsy which is definitely
needed for gastric ulcers to rule out
malignancy.

Diagnosis



Several ways to determine H. pylori infection
1) invasive
a) during endoscopy a rapid urease test, histologic
study, or culture can be done.
2) noninvasive
a) serologic studies which can not be done as a
follow up for cure due to antibodies being
positive for several years after eradication of
infection.
b) urea breath test can be used to confirm cure.
c) stool antigens test can also be used to confirm
cure.
Treatment
 Stop
any offending agents such as
NSAID’s.
 Bland
diets with frequent feedings
has not been shown to be effective.
Treatment

Antacids – neutralize gastric acids.
a) good for acute pain relief and healing ulcers.
b) poor compliance due frequency of doses.
c) inhibit absorption of some drugs such as warfarin,
digoxin, some anticonvulsants and antibiotics.
d) aluminum causes constipation and should not be
given with renal failure patients due to
accumulation which can cause osteoporosis and
encephalopathy.
e) magnesium causes diarrhea.
Treatment

H2- Antagonists – inhibit gastric acid secretion
a) equally as effective as antacids with better
compliance due to decreased frequency of
doses.
b) cimetidine inhibits cytochrome p450 system
greater than other H2-antagonists which
will cause an increase in drugs such as
warfarin, phenytoin, diazepam, TCA’s, propranolol,
etc.
c) renal excretion and therefore must adjust doses in
patients with renal disease.
Treatment

Proton Pump Inhibitors - inhibit gastric acid
secretion
a) heal ulcers faster then H2-antagonists and
antacids.
b) omeprazole has also been shown to affect
the cytochrome p450 system.
c) lansoprazole does not affect other drug
metabolism.
d) pantoprazole has been shown to decrease
bleeding from peptic ulcers.
Treatment

Sulcralfate – locally binds to the base of the
ulcer and therefore protects it from acid
a) Also has been shown to absorb bile acids,
inhibit pepsin activity, and increase
prostaglandin production.
b) Needs an acidic environment to work
therefore not beneficial to give antacids
c) Causes constipation, dry mouth and inhibits
the absorption of many medications.
Treatment

Misoprostol – prostaglandin E1 analogue which
acts as natural prostaglandin in the body
a) Only indicated for prevention of NSAID
-induced gastric ulcers in high risk patients.
b) contraindicated in pregnant women and
women in childbearing age because it
causes spontaneous abortion.
c) can cause diarrhea and crampy abdominal
pain.
Treatment

Bismuth compounds – decrease pepsin
activity, increase mucus secretion, form a
barrier protection on ulcers, augment
prostaglandin synthesis, slow hydrogen
ion diffusion across mucosal barrier, and
H. pylori bactericidal effect.
a) Used in triple drug combinations for
the treatment of H. pylori.
Treatment
If H. pylori positive then must be given
antibiotics to prevent recurrence of ulcer.
 Usually done with triple or quadruple
treatment regimens.
 Some antibiotics in regimens are
metronidazole, tetracycline, amoxicillin,
clarithromycin.

Complications of PUD

GI bleeding is the most common
complication of PUD and the most
common cause of upper GI bleeding.
 Please
see previous lecture on
management of GI Bleeding.
Complications of PUD





Perforation
Initially a chemical peritonitis develops which then
progresses to a bacterial peritonitis.
Anterior perforation - patients will have sudden
abdominal pain with guarding and rebound. 60-70% will
demonstrate free air of x-rays.
Posterior perforation - patients will develop back pain
with no free air on x-ray and may mimic pancreatitis but
lipase will be normal or only slightly elevated.
No free air on x-rays cannot rule our perforation.
IV fluids, electrolyte corrections, NG tube, broad
spectrum antibiotics and surgery.
Complications of PUD
Gastric outlet obstruction
 Scaring from healed ulcers or edema from active ulcer
with development of obstruction.
 Obstruction will cause gastric dilation, vomiting,
dehydration, metabolic alkalosis.
 Patients will develop upper abdominal pain with
vomiting, early satiety, weight loss, succussion splash.
 Abdominal x-ray will show dilated stomach shadow with
large air-fluid level.
 IV fluids, electrolyte corrections, NG tube, and surgery if
needed.
Questions

The most common cause of a lower GI
bleed is?
A) Diverticulosis
B) Cancer
C) Hemorrhoids
D) AV malformations
Questions
2) Colonoscopy is diagnostic and
therapeutic and is more accurate than
bleeding scans and angiography for GI
bleeds.
T/F
 3) Only 40% of patients who are infected
with H. pylori will develop ulcers.
T/F

Questions

4) Treatment of ulcers which are positive
for H. pylori need?
A) only a longer coarse of PPI
B) addition of antibiotics
C) need an inpatient coarse of
treatment
D) can be treated the same as ulcers
that are negative for H. pylori
Answers
1)
 2)
 3)
 4)

C
T
F
B