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Gastrointestinal Bleeding 2012. Pathophysiology of GI Bleeding Mucosal lesions – Acid-peptic disease, drug-induced (NSAIDs), Infectious (H. pylori), inflammatory.

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Presentation on theme: "Gastrointestinal Bleeding 2012. Pathophysiology of GI Bleeding Mucosal lesions – Acid-peptic disease, drug-induced (NSAIDs), Infectious (H. pylori), inflammatory."— Presentation transcript:

1 Gastrointestinal Bleeding 2012

2 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

3 Sources of GI Bleeding Upper GI Tract Proximal to the Ligament of Treitz 70% of GI Bleeds Lower GI Tract Distal to the Ligament of Treitz 30% of GI Bleeds

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6 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.

7 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%

8 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

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

10 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

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

12 History – HPI 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

13 Physical Exam Including: HR, BP, tilt test, RR, O 2 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

14 Work Up Labs CBC Serial HgB Platelets BMP BUN, Cr Type and Crossmatch Coagulation studies Stool WBCs to eval for infectious etiol Imaging studies?

15 Localization of Bleeding History NG Tube EGD Colonoscopy Tagged RBC Scan Angiography

16 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 cc of blood in the upper GI tract. – Stool turns black after 8 hours of sitting within the gut. 50% present with hematemesis NGT with positive blood on aspirate 11% of brisk bleeds have hematochezia Melena (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 use H. pylori infection Increased age Upper 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 Lesion AV Malformation-angiodysplasia

19 Duodenal Ulcer

20 Varices

21 Esophagitis

22 GI Malignancy Esophageal Tumor

23 GI Malignancy Gastric Carcinoma

24 Angiodysplasia

25 Lower GI Bleed 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 ( % of the time)

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% Barnet J and H Messmann H. Nat Rev Gastroenterol Hepatol 6, (2009).

27 Diverticulosis

28 Diverticulitis-NOT A CAUSE OF GI BLEEDING

29 Colonic Polyps

30 Malignancy Colon Carcinoma

31 Hemmorrhoids

32 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.

33 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

34 Basic Admission Orders 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

35 Basic Admission Orders (Cont.) IVF: ?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

36 Obscure GI Bleed Present: Fe Defic anemia Etiology: – Younger than 40 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:

37 Obscure GI Bleed Work Up – EGD, Colonoscopy both neg – Repeat – CE, PE or DE, – angiography

38 PillCam SB Latest Generation PillCam SB –11 mm x 26 mm –1 camera –2 frames per second –Std optics / 1 lens –Standard lighting control –Standard angle of view (AOV) 140° –Depth of field 0-30 mm PillCam SB 2 –11 mm x 26 mm –1 camera –2 frames per second –New optics / 3 lenses –Advanced Automatic Light Control –Extra wide angle of view (AOV) 156° –Depth of field 0-30 mm

39 Image Spectrum: PillCam Capsule Endoscopy Bleeding Celiac DiseaseTumors Suspected Crohn’s

40 References Harrison’s Principles of Internal Medicine 14 th 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, (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:

41 THE END

42 Peptic Ulcer Disease

43 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.

44 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.

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 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.

47 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.

48 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.

49 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.

50 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.

51 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.

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 be given with renal failure patients due to accumulation which can cause osteoporosis and encephalopathy. e) magnesium causes diarrhea.

54 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.

55 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.

56 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.

57 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.

58 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.

59 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.

60 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.

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) Diverticulosis B) Cancer C) Hemorrhoids D) AV malformations

64 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

65 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

66 Answers 1) C 2) T 3) F 4) B


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