Transcript Gastrointestinal Bleeding - Kardz Medicine | Better Information

Gastrointestinal Bleeding
2012
Pathophysiology of GI Bleeding
• Mucosal lesions
– Acid-peptic disease, drug-induced (NSAIDs),
Infectious (H. pylori), inflammatory bowel dz
• Portal hypertension
– Esophageal varices, hypertensive gastropathy
• Coagulopathy - Hemophilia, hepatic
coagulopathy, CHF w/hepatic congestion
• Vascular lesions - hemangiomas
Sources of GI Bleeding
• Upper GI Tract
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Proximal to the Ligament of Treitz
70% of GI Bleeds
• Lower GI Tract
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Distal to the Ligament of Treitz
30% of GI Bleeds
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
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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
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CA/polyps
inflammatory bowel disease
infectious gastroenteritis
Meckel diverticulum
History
– HPI
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Hematemesis (coffee grounds vs. bright red)
Hematochezia
Melena - dark, tarry stool
Pain symptoms
– PMHx
• ulcer disease, joints, skin
– Social Hx
• EtOH
– Medications
• NSAIDs, steroids, ASA, Plavix, Coumadin, Lovenox, Heparin, Iron
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Physical Exam Including:
HR, BP, tilt test, RR, O2 saturation
General appearance, Mental status
Neck veins, oral mucosa
Skin temperature and color
Abdominal exam
Rectal
Stigma of Cirrhosis
NG Tube findings (upper vs. lower g.i. source)
Urine output
Work Up
• Labs
• CBC
• Serial HgB
• Platelets
• BMP
• BUN, Cr
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Type and Crossmatch
Coagulation studies
Stool WBCs to eval for infectious etiol
Imaging studies?
Localization of Bleeding
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History
NG Tube
EGD
Colonoscopy
Tagged RBC Scan
Angiography
Upper GI Bleed
• 50% present with hematemesis
• NGT with positive blood on aspirate
• 11% of brisk bleeds have hematochezia
• Melena (black tarry stools)—this develops with approximately
150-200cc of blood in the upper GI tract.
– Stool turns black after 8 hours of sitting within the gut.
Upper GI Bleed
• Risk Factors
• NSAID use
• H. pylori infection
• Increased age
• Upper GI Bleeding accounts for approximately
350,000 hospitalizations per year.
Upper GI Bleed
• Etiology of Upper Bleeds
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Duodenal Ulcer-30%
Gastric Ulcer-20%
Varices-10%
Gastritis and duodenitis-5-10%
Esophagitis-5%
Mallory Weiss Tear-3%
GI Malignancy-1%
Dieulafoy Lesion
AV Malformation-angiodysplasia
Duodenal Ulcer
Varices
Esophagitis
GI Malignancy
• Esophageal Tumor
GI Malignancy
• Gastric Carcinoma
Angiodysplasia
Lower GI Bleed
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Acute LGIB: <3d
Chronic LGIB: > several days
Hematochezia
Blood in Toilet
Clear NGT aspirate
Normal Renal Function
Usually Hemodynamically stable
– <200ml : no effect on HR**
– >800ml: SBP drops by 10mmHg, Hr increases by 10
– >1500ml: possible shock
OR
– 10% Hct: tachycardia*
– 20% Hct: orthostatic hypotension
– 30% Hct: shock
Stops spontaneously (80 - 85% of the time)
Lower GI Bleed
• Etiology of hematochezia
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Diverticular-17-40%
Angiodysplasia-9-21%
Colitis (ischemic, infectious, chronic IBD, radiation injury)-2-30%
Neoplasia, post-polypectomy-2-26%
Anorectal Disease (including rectal varices)-4-10%
Upper GI Bleed-0-11%
Small Bowel Bleed-2-9%
Barnet J and H Messmann H. Nat Rev Gastroenterol Hepatol 6, 637-646 (2009).
Diverticulosis
Diverticulitis-NOT A CAUSE OF GI
BLEEDING
Colonic Polyps
Malignancy
• Colon Carcinoma
Hemmorrhoids
Management of GI Bleed
• Oxygen
• IV Access-central line or two large bore
peripheral IV sites
• Isotonic saline for volume resuscitation
• Start transfusing blood products if the patient remains unstable despite
fluid boluses.
• Airway Protection
• Altered Mental Status and increased risk of aspiration with massive upper
GI bleed.
Management of GI Bleed
• ICU admit indications
• Significant bleeding (>2u pRBC) with hemodynamic instability
• Transfusion
• Brisk Bleed, transfusing should be based on hemodynamic status, not lab
value of Hgb.
• Cardiopulmonary symptoms-cardiac ischemia or shortness of breath,
decreased pulse ox
• 1 unit PRBC increases Hgb by 1mg/dL and increase Hct by 3%
• FFP for INR greater than 1.5
• Platelets for platelet count less than 50K
Basic Admission Orders
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Admit to ICU/intermediate care/telemetry s/o …
Dx: Upper/Lower G.I. Bleed
Condition:
VS:
Allergies:
Activity: Bedrest
Nursing: Is/Os, ? Foley
Diet: NPO
Basic Admission Orders (Cont.)
• IVF: NSS @ ?cc/h
• Medications: I.V. Protonix, convert
medications to i.v., hold anti-hypertensives
• Labs: serial H/H, type and cross, coags, Chem
7, LFTs
• Consults: GI, +/- Surgery
Obscure GI Bleed
• Present: Fe Defic anemia
• Etiology:
– Younger than 40
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Tumors
Meckel’s diverticulum
Dieulafoy’s lesion
Crohn’s Disease
Celiac Disease
– Greater than 40
• Angioectasia
• NSAID enteropathy
• Celiac
Gerson LB. Clin Gastroenterol & Hepatol 2009;7:828-833.
Obscure GI Bleed
• Work Up
– EGD, Colonoscopy both neg
– Repeat
– CE, PE or DE,
– angiography
PillCam SB Latest
Generation
PillCam SB
PillCam SB 2
– 11 mm x 26 mm
– 11 mm x 26 mm
– 1 camera
– 1 camera
– 2 frames per second
– 2 frames per second
– Std optics / 1 lens
– New optics / 3 lenses
– Standard lighting control
– Advanced Automatic Light Control
– Standard angle of view (AOV)
140°
– Extra wide angle of view (AOV)
156°
– Depth of field 0-30 mm
– Depth of field 0-30 mm
Image Spectrum:
PillCam Capsule Endoscopy
Bleeding
Suspected Crohn’s
Tumors
Celiac Disease
References
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Harrison’s Principles of Internal Medicine 14th edition
Gastrointestinal Atlas.com endoscopy photos
Pocket Medicine, 3rd edition
Barnet J and H Messmann H. Diagnosis and management of lower gastrointestinal bleeding. Nat Rev Gastroenterol Hepatol
6, 637-646 (2009).
Gerson LB. Recurrent Gastrointestinal Bleeding After Negative Upper Endoscopy and Colonoscopy. Clin Gastroenterol &
Hepatol 2009;7:828-833.
Melmed GY and Simon KL. Capsule Endoscopy: Practical Applications. Clin Gastrolenterol & Hepatology 2005;3:411-422.
AGA Institute. AGA Institute Medical Position Statement on Obscure Gastrointestinal Bleeding. Gastroenterology
2007;133:1694-1696.
THE END
Peptic Ulcer Disease
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
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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
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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
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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
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1) C
2) T
3) F
4) B