6 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.
7 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%
8 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
9 Causes of Upper GI Bleed 5) stress ulcers6) arteriovenous malformation7) malignancy8) aortoenteric fistula
10 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
11 Causes of Lower GI Bleeding 4) CA/polyps5) inflammatory bowel disease6) infectious gastroenteritis7) Meckel diverticulum
12 History HPI PMHx Social Hx Medications Hematemesis (coffee grounds vs. bright red)HematocheziaMelena - dark, tarry stoolPain symptomsPMHxulcer disease, joints, skinSocial HxEtOHMedicationsNSAIDs, steroids, ASA, Plavix, Coumadin, Lovenox, Heparin, Iron
13 Physical Exam Including: HR, BP, tilt test, RR, O2 saturationGeneral appearance, Mental statusNeck veins, oral mucosaSkin temperature and colorAbdominal examRectalStigma of CirrhosisNG Tube findings (upper vs. lower g.i. source)Urine outputNGT Positive: UGIBNGT Negative: bleeding stopped. Bleeding is beyong pylorus
14 Work Up Labs CBC BMP Type and Crossmatch Coagulation studies Serial HgBPlateletsBMPBUN, CrType and CrossmatchCoagulation studiesStool WBCs to eval for infectious etiolImaging studies?BUN/Cr > 30 indicates GI bleed, prob UGIB.
15 Localization of Bleeding HistoryNG TubeEGDColonoscopyTagged RBC ScanAngiography
16 Upper GI Bleed 50% present with hematemesis NGT with positive blood on aspirate11% of brisk bleeds have hematocheziaMelena (black tarry stools)—this develops with approximately cc of blood in the upper GI tract.Stool turns black after 8 hours of sitting within the gut.
17 Upper GI Bleed Risk Factors NSAID useH. pylori infectionIncreased ageUpper GI Bleeding accounts for approximately 350,000 hospitalizations per year.
18 Upper GI Bleed Etiology of Upper Bleeds Duodenal Ulcer-30% Gastric Ulcer-20%Varices-10%Gastritis and duodenitis-5-10%Esophagitis-5%Mallory Weiss Tear-3%GI Malignancy-1%Dieulafoy LesionAV Malformation-angiodysplasia
25 Lower GI Bleed Acute LGIB: <3d Chronic LGIB: > several days HematocheziaBlood in ToiletClear NGT aspirateNormal Renal FunctionUsually Hemodynamically stable<200ml : no effect on HR**>800ml: SBP drops by 10mmHg, Hr increases by 10>1500ml: possible shockOR10% Hct: tachycardia*20% Hct: orthostatic hypotension30% Hct: shockStops spontaneously ( % of the time)*Pocket Medicine, 3rd edition**Barnet J and H Messmann H. Nat Rev Gastroenterol Hepatol 6, (2009).
26 Lower GI Bleed Etiology of hematochezia 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%Mnemonic for: painful --> I = infectious, inflam, ischemicIschemic colitis - usually elderly, transient hypoperfusion of mesenteric arteries, resulting in pain from episodic low BP or vasospasm.Water shed area: splenic flexure AND rectosigmoid.Barnet J and H Messmann H. Nat Rev Gastroenterol Hepatol 6, (2009).
30 Malignancy Colon Carcinoma Left: bleed Right: Fe defic anemia Colonoscopy better at detecting L cancer
31 Hemmorrhoids Painless: internal Painful: external Hemorrhoids more common than anal fissures.
32 Management of GI Bleed Oxygen IV Access-central line or two large bore peripheral IV sitesIsotonic saline for volume resuscitationStart transfusing blood products if the patient remains unstable despite fluid boluses.Airway ProtectionAltered Mental Status and increased risk of aspiration with massive upper GI bleed.
33 Management of GI Bleed ICU admit indications Transfusion Significant bleeding (>2u pRBC) with hemodynamic instabilityTransfusionBrisk Bleed, transfusing should be based on hemodynamic status, not lab value of Hgb.Cardiopulmonary symptoms-cardiac ischemia or shortness of breath, decreased pulse ox1 unit PRBC increases Hgb by 1mg/dL and increase Hct by 3%FFP for INR greater than 1.5Platelets for platelet count less than 50K
35 Basic Admission Orders (Cont.) IVF: ?cc/hMedications: I.V. Protonix, convert medications to i.v., hold anti-hypertensivesLabs: serial H/H, type and cross, coags, Chem 7, LFTsConsults: GI, +/- Surgery80mg IVB, then 8mg/hr or 40mg BID
36 Obscure GI Bleed Present: Fe Defic anemia Etiology: Younger than 40 TumorsMeckel’s diverticulumDieulafoy’s lesionCrohn’s DiseaseCeliac DiseaseGreater than 40AngioectasiaNSAID enteropathyCeliacGerson LB. Clin Gastroenterol & Hepatol 2009;7:Gerson LB. Clin Gastroenterol & Hepatol 2009;7:
37 Obscure GI Bleed Work Up EGD, Colonoscopy both neg Repeat CE, PE or DE,angiographyPE = proximal jejunumDE = distal ileum
38 PillCam SB Latest Generation 11 mm x 26 mm1 camera2 frames per secondStd optics / 1 lensStandard lighting controlStandard angle of view (AOV) 140°Depth of field 0-30 mmPillCam SB 211 mm x 26 mm1 camera2 frames per secondNew optics / 3 lensesAdvanced Automatic Light ControlExtra wide angle of view (AOV) 156°Depth of field 0-30 mm38
40 References Harrison’s Principles of Internal Medicine 14th edition Gastrointestinal Atlas.com endoscopy photosPocket Medicine, 3rd editionBarnet J and H Messmann H. Diagnosis and management of lower gastrointestinal bleeding. Nat Rev Gastroenterol Hepatol 6, (2009).Gerson LB. Recurrent Gastrointestinal Bleeding After Negative Upper Endoscopy and Colonoscopy. Clin Gastroenterol & Hepatol 2009;7:Melmed GY and Simon KL. Capsule Endoscopy: Practical Applications. Clin Gastrolenterol & Hepatology 2005;3:AGA Institute. AGA Institute Medical Position Statement on Obscure Gastrointestinal Bleeding. Gastroenterology 2007;133:
43 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.
44 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.
45 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.
46 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.
47 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.
48 CausesBile saltsEmotional stressType O bloodProlonged use of corticosteriodsCaffeinated beveragesNote diet and alcohol are not predisposing factors to the development of peptic ulcers.
49 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.
50 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.
51 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.
52 Treatment Stop any offending agents such as NSAID’s. Bland diets with frequent feedings has not been shown to be effective.
53 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.
54 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.
55 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.
56 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.
57 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.
58 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.
59 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.
60 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.
61 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.
62 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.
63 Questions The most common cause of a lower GI bleed is? A) DiverticulosisB) CancerC) HemorrhoidsD) AV malformations
64 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.
65 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