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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