2 Incidence Upper GI bleed 100/100,000 Above the ligament of Treitz Lower GI Bleed 20/100,000Below the ligament of TreitzBoth are more common in males and elderly.
3 Causes of Upper GI Bleed 1) Peptic ulcer disease - most commoncauseA) duodenal ulcers 29%will rebleed in 10% of cases within24-48hB) gastric ulcers 16%more likely to rebleedC) stomal ulcers <5%
4 Causes of Upper GI Bleed 2) Erosive gastritis, esophagitis, duodenitissome causes are ETOH, ASA, NSAID’s3) Esophageal and gastric varicescauses by portal hypertension4) Mallory-Weiss syndrome – longitudinalmucosal tear in the cardioesophagealregioncaused by repeated retching
5 Causes of Upper GI Bleed 5) stress ulcers6) arteriovenous malformation7) malignancy8) aortoenteric fistula
6 Causes of Lower GI Bleeding 1) Hemorrhoids - most common cause2) Diverticulosis – common, painless,and can be massiveCaused from an erosion into apenetrating artery from thediverticulum.3) Arteriovenous malformations – commonand seen in people with hypertension andaortic stenosis
7 Causes of Lower GI Bleeding 4) CA/polyps5) inflammatory bowel disease6) infectious gastroenteritis7) 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, 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.
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 bleedsCoagulation studiesLiver function studiesType and cross-match
11 Diagnosis Diagnostic ECG Abdominal series - not beneficial unless specific indicationsAngiography - can be diagnostic and therapeutic but requires a brisk bleed at .5-2ml/minBleeding scans - can only be diagnostic but are more sensitive then angiography and require a bleeding rate of only .1ml/minColonoscopy - 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 varicesBalloon tamponadeSurgeryMust get early consultation with gastroenterologist and general surgeon for significant GI bleeds.
15 Epidemiology10% 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.
16 PathophysiologyProstaglandins 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 CausesH. 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 CausesNSAID’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.
20 CausesBile saltsEmotional stressType O bloodProlonged use of corticosteriodsCaffeinated beveragesNote diet and alcohol are not predisposing factors to the development of peptic ulcers.
21 Clinical FeaturesEpigastric 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 DiagnosisDefinite 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, histologicstudy, or culture can be done.2) noninvasivea) serologic studies which can not be done as afollow up for cure due to antibodies beingpositive for several years after eradication ofinfection.b) urea breath test can be used to confirm cure.c) stool antigens test can also be used to confirmcure.
24 Treatment Stop any offending agents such as NSAID’s. 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 begiven with renal failure patients due toaccumulation which can cause osteoporosis andencephalopathy.e) magnesium causes diarrhea.
26 Treatment H2- Antagonists – inhibit gastric acid secretion a) equally as effective as antacids with bettercompliance due to decreased frequency ofdoses.b) cimetidine inhibits cytochrome p450 systemgreater than other H2-antagonists whichwill cause an increase in drugs such aswarfarin, phenytoin, diazepam, TCA’s, propranolol,etc.c) renal excretion and therefore must adjust doses inpatients with renal disease.
27 Treatment Proton Pump Inhibitors - inhibit gastric acid secretion 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 drugmetabolism.d) pantoprazole has been shown to decreasebleeding from peptic ulcers.
28 TreatmentSulcralfate – locally binds to the base of the ulcer and therefore protects it from acida) Also has been shown to absorb bile acids,inhibit pepsin activity, and increaseprostaglandin production.b) Needs an acidic environment to worktherefore not beneficial to give antacidsc) Causes constipation, dry mouth and inhibitsthe absorption of many medications.
29 TreatmentMisoprostol – prostaglandin E1 analogue which acts as natural prostaglandin in the bodya) Only indicated for prevention of NSAID-induced gastric ulcers in high risk patients.b) contraindicated in pregnant women andwomen in childbearing age because itcauses spontaneous abortion.c) can cause diarrhea and crampy abdominalpain.
30 TreatmentBismuth 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 forthe treatment of H. pylori.
31 TreatmentIf 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 PUDGI 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 % 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) DiverticulosisB) CancerC) HemorrhoidsD) AV malformations
36 Questions2) Colonoscopy is diagnostic and therapeutic and is more accurate than bleeding scans and angiography for GI bleeds.T/F3) Only 40% of patients who are infected with H. pylori will develop ulcers.
37 Questions4) Treatment of ulcers which are positive for H. pylori need?A) only a longer coarse of PPIB) addition of antibioticsC) need an inpatient coarse oftreatmentD) can be treated the same as ulcersthat are negative for H. pylori