Post on 14-Apr-2018
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Gastrointestinal Bleeding
Jarrett Lefberg
South Pointe Hospital
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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
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Causes of Upper GI Bleed
2) Erosive gastritis, esophagitis, duodenitis
some causes are ETOH, ASA, NSAIDs
3) Esophageal and gastric varices
causes by portal hypertension
4) Mallory-Weiss syndrome longitudinal
mucosal tear in the cardioesophageal
region
caused by repeated retching
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Causes of Upper GI Bleed
5) stress ulcers
6) arteriovenous malformation
7) malignancy8) aortoenteric fistula
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Causes of Lower GI Bleeding
1) Hemorrhoids - most common cause
2) Diverticulosis common, painless,
and can be massive
Caused from an erosion into apenetrating artery from the
diverticulum.
3)Arteriovenous malformations commonand seen in people with hypertension and
aortic stenosis
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Causes of Lower GI Bleeding
4) CA/polyps
5) inflammatory bowel disease
6) infectious gastroenteritis7) Meckel diverticulum
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Diagnosis
Questions to ask in history
Any hematemesis, coffee-ground emesis, melena, orhematochezia.
Any weight loss or changes in bowel habits.
Any vomiting and retching.
Any history aortic graft.
Any history of ASA, NSAIDs, steroids.
Any ETOH abuse.
Any history of iron or bismuth which can simulatemelena and beets which can simulate hematochezia.Note stool guaiac testing will be negative.
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Diagnosis
Physical examVital 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 thatcan mimic upper GI bleeds.
Proper abdominal exam and rectal exam.
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Diagnosis
Lab CBC Electrolytes
Glucose BUN/CreatineBUN will be elevated in upper GI
bleeds Coagulation studies
Liver function studies Type and cross-match
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Diagnosis
Diagnostic ECG
Abdominal series - not beneficial unless specificindications
Angiography - can be diagnostic and therapeutic butrequires a brisk bleed at .5-2ml/min
Bleeding scans - can only be diagnostic but are moresensitive then angiography and require a bleeding rate
of only .1ml/min Colonoscopy - is diagnostic and therapeutic and more
accurate than bleeding scans and angiography
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Treatment
Large-bore intravenous lines with fluidreplacement.
Class I + II hemorrhage replace with crystalloid.
Class III + IV hemorrhage replace withcrystalloid and blood.
NG tube should be placed and can determineupper GI from lower GI but not 100%. Also NG
tubes will not worsen varice bleeds. Foley catheter for hypotension patients to
monitor output.
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Treatment
Proton-pump inhibitor
Endoscopy
Somatostatin, octretide for varices Balloon tamponade
Surgery
Must get early consultation withgastroenterologist and general surgeon forsignificant GI bleeds.
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Peptic Ulcer Disease
Jarrett Lefberg
South Pointe Hospital
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Epidemiology
10% US population >17 years of age havepeptic ulcer disease at some time.
White Americans have a 10% prevalenceof H. pylori by age 35 and 80% by age 75.
Black Americans have a 45% prevalenceof H. pylori by age 25.
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Pathophysiology
Prostaglandins produce mucous and bicarbonateions which protect the tissue in the stomach bybeing destroyed with hydrochloric acid andpepsin.
Dyspepsia is the imbalance between theprotective 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.
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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.
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Causes
H. pylori - a spiral, urease producing flagellatedbacterium which lives between the mucus geland mucosa. Its production of urease,cytotoxins, proteases and other compoundsdisturb the gel and increase tissue exposure toacid and pepsin.
H. pylori is seen in 95% of patients withduodenal ulcers and 80% of gastric ulcers.
Note only 10-20% of patients who areinfected with H. pylori will develop ulcers.
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Causes
NSAIDs - inhibit prostaglandins which in turnincreases tissue exposure to acid and pepsin.
Zollinger-Ellison syndrome - is a gastrinsecreting tumor which creates such a high acidlevel it over rides the protective gel.
Cigarette smoking - inhibits bicarbonate ionproduction and increases gastric emptying.
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Causes
Bile salts
Emotional stress
Type O blood
Prolonged use of corticosteriods
Caffeinated beverages
Note diet and alcohol are notpredisposing factors to thedevelopment of peptic ulcers.
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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. Paincan be relieved by food.
Physical exam of uncomplicated PUD, there maybe a finding ofepigastric tenderness.
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Diagnosis
Definite diagnosis can only be made byvisualization with an upper GI orendoscopy.
Endoscopy has the advantage of beingable to take a biopsy which is definitelyneeded for gastric ulcers to rule out
malignancy.
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Diagnosis
Several ways to determine H. pylori infection 1) invasive
a) during endoscopy a rapid urease test, histologicstudy, or culture can be done.
2) noninvasivea) serologic studies which can not be done as a
follow up for cure due to antibodies beingpositive 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.
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Treatment
Stop any offending agents such asNSAIDs.
Bland diets with frequent feedingshas not been shown to be effective.
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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.
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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, TCAs, propranolol,
etc.
c) renal excretion and therefore must adjust doses in
patients with renal disease.
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Treatment
Proton Pump Inhibitors - inhibit gastric acidsecretion
a) heal ulcers faster then H2-antagonists andantacids.
b) omeprazole has also been shown to affectthe cytochrome p450 system.
c) lansoprazole does not affect other drug
metabolism.d) pantoprazole has been shown to decreasebleeding from peptic ulcers.
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Treatment
Sulcralfate locally binds to the base of theulcer and therefore protects it from acid
a) Also has been shown to absorb bile acids,
inhibit pepsin activity, and increaseprostaglandin 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.
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Treatment
Misoprostol prostaglandin E1 analogue whichacts 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.
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Treatment
Bismuth compounds decrease pepsinactivity, increase mucus secretion, form abarrier protection on ulcers, augment
prostaglandin synthesis, slow hydrogenion diffusion across mucosal barrier, andH. pylori bactericidal effect.
a) Used in triple drug combinations forthe treatment of H. pylori.
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Treatment
If H. pylori positive then must be givenantibiotics to prevent recurrence of ulcer.
Usually done with triple or quadrupletreatment regimens.
Some antibiotics in regimens aremetronidazole, tetracycline, amoxicillin,
clarithromycin.
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Complications of PUD
GI bleeding is the most commoncomplication of PUD and the mostcommon cause of upper GI bleeding.
Please see previous lecture on
management of GI Bleeding.
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Complications of PUD
Perforation
Initially a chemical peritonitis develops which thenprogresses to a bacterial peritonitis.
Anterior perforation - patients will have sudden
abdominal pain with guarding and rebound. 60-70% willdemonstrate free air of x-rays.
Posterior perforation - patients will develop back painwith no free air on x-ray and may mimic pancreatitis butlipase will be normal or only slightly elevated.
No free air on x-rays cannot rule our perforation.
IV fluids, electrolyte corrections, NG tube, broadspectrum antibiotics and surgery.
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Complications of PUD
Gastric outlet obstruction
Scaring from healed ulcers or edema from active ulcerwith 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.
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Questions
The most common cause of a lower GIbleed is?
A) Diverticulosis
B) Cancer
C) Hemorrhoids
D) AV malformations
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Questions
2) Colonoscopy is diagnostic andtherapeutic and is more accurate thanbleeding scans and angiography for GI
bleeds.
T/F
3) Only 40% of patients who are infected
with H. pylori will develop ulcers.
T/F
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Questions
4) Treatment of ulcers which are positivefor H. pylori need?
A) only a longer coarse of PPI
B) addition of antibioticsC) need an inpatient coarse of
treatment
D) can be treated the same as ulcersthat are negative for H. pylori
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Answers
1) C
2) T
3) F 4) B