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Gastrointestinal Bleeding

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Lower GI Bleed 20/100,000. Below the ligament of Treitz ... get early consultation with gastroenterologist and general surgeon for significant GI bleeds. ... – PowerPoint PPT presentation

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Title: Gastrointestinal Bleeding


1
Gastrointestinal Bleeding
  • Jarrett Lefberg
  • South Pointe Hospital

2
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.

3
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 lt5

4
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

5
Causes of Upper GI Bleed
  • 5) stress ulcers
  • 6) arteriovenous malformation
  • 7) malignancy
  • 8) aortoenteric fistula

6
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

7
Causes of Lower GI Bleeding
  • 4) CA/polyps
  • 5) inflammatory bowel disease
  • 6) infectious gastroenteritis
  • 7) Meckel diverticulum

8
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, NSAIDs, 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.

9
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.

10
Diagnosis
  • Lab
  • CBC
  • Electrolytes
  • Glucose
  • BUN/Creatine BUN will be elevated in upper GI
    bleeds
  • Coagulation studies
  • Liver function studies
  • Type and cross-match

11
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

12
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.

13
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.

14
Peptic Ulcer Disease
  • Jarrett Lefberg
  • South Pointe Hospital

15
Epidemiology
  • 10 US population gt17 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.

16
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.

17
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.

18
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.

19
Causes
  • NSAIDs - 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.

20
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.

21
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.

22
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.

23
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.

24
Treatment
  • Stop any offending agents such as NSAIDs.
  • Bland diets with frequent feedings has not been
    shown to be effective.

25
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.

26
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.

27
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.

28
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.

29
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.

30
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.

31
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.

32
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.

33
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.

34
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.

35
Questions
  • The most common cause of a lower GI bleed is?
  • A) Diverticulosis
  • B) Cancer
  • C) Hemorrhoids
  • D) AV malformations

36
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

37
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

38
Answers
  • 1) C
  • 2) T
  • 3) F
  • 4) B
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