Presentation is loading. Please wait.

Presentation is loading. Please wait.

UGI Bleeding.

Similar presentations


Presentation on theme: "UGI Bleeding."— Presentation transcript:

1 UGI Bleeding

2 Epidemiology of Upper GI Bleeding
Bleeding from a source above the ligament of Treitz 1 case/1,000 adults/year 50% of cases are peptic ulcer disease (25% rebleed) 40-80% of cases of bleeding cease spontaneously 10% mortality rate Epidemiology of Upper GI Bleeding Upper gastrointestinal (GI) bleeding occurs with a prevalence of approximately 100 cases per 100,000 adults per year. Peptic ulcer disease accounts for 50-60% of all cases of upper GI haemorrhage.1,2 In the United States there are approximately 150,000 hospital admissions per year for bleeding ulcers.3 Bleeding ceases spontaneously in about 80% of patients, however, despite advances in therapy and a decreased incidence of ulcer disease there has been no decrease in morbidity and mortality (6-7%) for the past 30 years.1,3-6 This may be due to the fact that patients presenting with upper GI bleeding are an increasingly higher risk group6 or that newer endoscopic haemostatic technologies are not yet being widely practised.7 Endoscopic therapy has improved patient outcomes,8 nevertheless, the search has continued for less invasive medical modalities. References: 1. Silverstein FE, et al. The national ASGE survey on upper gastrointestinal bleeding: II Clinical prognostic factors. Gastrointest Endosc 1981;27:80-93. 2. Longstreth GF. Epidemiology of hospitalization for acute upper gastrointestinal hemorrhage: a population-based study. Am J Gastroenterol 1995;90: 3. Kurata J, Corboy ED. Current peptic ulcer time trends: an epidemiological profile. J Clin Gastroenterol 1988;10: 4. Gustavsson S, et al. Trends in peptic ulcer surgery: a population-based study in Rochester, Minnesota Gastroenterology 1988;94: 5. NIH Consensus Conference. Therapeutic endoscopy and bleeding ulcers. JAMA 1989;262: 6. Allen R, Dykes P. A study of the factors influencing mortality rates from gastrointestinal hemorrhage. Q J Med 1976:45: 7. Chung CS. Surgery and gastrointestinal bleeding. Gastrointest Endosc Clin N Am 1997;7(4): 8. Laine L, Peterson WL. Bleeding peptic ulcer. N Engl J Med 1994;331(11):

3 Prognostic Factors Hemodynamic instability
Hematochezia from upper GI source Increasing number of units transfused Age > 60 years Concurrent illness (cardiac, respiratory, renal, neoplastic, CNS) Onset while hospitalized for other reason Coagulopathy Risk or Prognostic Factors: Clinical Clinical predictors of increased risk from GI bleeding include haemodynamic instability, fresh red blood in the emesis, haematochezia, and increasing number of units transfused. Melena can occur with as little as 50 to 100 mL of blood infused into the upper GI tract1, however, haematochezia from an upper GI bleeding source implies a blood loss of greater than 1000 mL,2 and is usually associated with shock.3,4,5 In addition, it is recognised that patients over the age of 60 or with other concurrent illness,4,5 and patients with coagulopathy or with onset of GI bleeding while already hospitalized for another reason3,6 are at increased risk of mortality after an acute episode of bleeding. Bleeding pattern can also predict the need for urgent endoscopy, which was recommended in patients with coffee ground vomiting with melena or with haematemesis with or without melena.7 References: 1. Daniel WA Jr, Egan S. The quantity of blood required to produce a tarry stool. JAMA 1939;113:2232. 2. Schiff L, et al. Observations on the oral administration of citrated blood in man. II. The effect on the stools. Am J Med Sci 1942;203: 3. NIH Consensus Conference. Therapeutic endoscopy and bleeding ulcers. JAMA 1989;262: 4. Schiller KFR, et al. Haematemesis and melena with special reference to factors influencing the outcome. BMJ 1970;2:7-14. 5. Branicki RJ, et al. Bleeding peptic ulcer: a prospective evaluation of risk factors for rebleeding and mortality. World J Surg 1990;14: 6. Peterson WL. Clinical risk factors. Gastrointest Endosc 1990;36:S14-5. 7. Wara P, Stodkilde H. Bleeding pattern before admission as guideline for emergency endoscopy. Scand J Gastroenterol 1985;20:72-8.

4 Etiology of UGI Bleeding
Non GI Hemopytsis, nose bleed Esophageal Esophagitis, ulcer, varices, malignancy, MW tear Gastric Gastritis, ulcer, varices, malignancy, AVM Duodenal Duodenitis, ulcer, varices, malignacy (rare), AVM, aortoenteric fistula

5 Etiology Incidence PUD 50% Esophagitis 15% Gastritis 10% Varices 10%
Duodenitis 5% MW tear 3% (much more common in young) Esophageal ulcer 3% Carcinoma 3%

6

7 Presentation Melena or hematochezia 70% (charting, iron pepto)
Hematemesis or coffee ground emesis 30% (charting, testing) Syncope 14%, presyncope 40% Heartburn 40%, epigastric pain 20% Dysphagia 10% Wt. loss 12%

8 Important History Evidence of complications CP/SOB/presyncope
Appearance, frequency and amount of vomit/BM (elderly unreliable) Duration of symptoms Use of NSAID/ASA/corticosteroids Previous history of GI bleeding Co-morbidities = cardiac, respiratory, neoplastic, CNS

9 Physical Exam ABC’s Vitals Orthostatic bp (scoping)
Rectal exam (what does –ve OB really mean)

10 Initial Management ABC’s Npo Head down, raise legs 2 IV’s CBC
Urea/Cr (? upper vs lower bleeding, ? reliable) G&T LFTs Coagulation status ECG/cardiac enzymes NG?

11 Prognostic Factors: Endoscopic
Endoscopic factors have been identified that can predict the risk of a poor outcome. Ulcers of greater than 1 cm in size have been associated with an increased risk of rebleeding and increased mortality.1 Laine and Peterson (1994) estimated the prevalence and outcomes of bleeding ulcers according to the endoscopic appearance of the ulcer, based on a review of over 30 studies.2 This review reported a 5% (range 0-10%) risk in patients with a clean ulcer base. The risk increased progressively when the endoscopic findings include a flat spot (10%), adherent clot (22%), non bleeding visible vessel (43%), or active bleeding (55%).2 It has been proposed that patients with a clean ulcer base can be discharged within 24 hours, while patients with other endoscopic stigmata warrant hospitalization for at least three days since most episodes of rebleeding occur within that time period.3 References: 1. Branicki RJ, et al. Bleeding peptic ulcer: a prospective evaluation of risk factors for rebleeding and mortality. World J Surg 1990;14: 2. Laine L, Peterson WL. Bleeding peptic ulcer. N Engl J Med 1994;331(11): 3. Lin H-W, et al. Clinical courses and predictors for rebleeding in patients with peptic ulcers and non-bleeding visible vessels: a prospective study. Gut 1994;35: Laine, Peterson, N Engl J Med 1994.

12

13 Clot on Vessel - Gastric Ulcer

14 Overview of Management
Initial management Endoscopic therapy Surgical therapy Pharmacologic therapy Overview of Management Initial management of acute GI bleeding is aimed at stabilizing the patient. Once clinically stable, treatment may include endoscopic therapy, surgical therapy and/or pharmacologic therapy. This presentation will focus primarily on the use of pharmacologic agents for acid suppression, with a brief overview of other treatment options. In particular, this presentation will provide a review of non-variceal acute GI bleeding, with a special reference to the role of proton pump inhibitors in this clinical setting.

15 Endoscopic Therapy Perform early (ideally within 24 h)
Indications for haemostatic therapy: (1) +/-Adherent clot, (2) Nonbleeding visible vessel, (3) Active bleeding (oozing, spurting) (Laine, Peterson. 1994) Heater probe, bipolar electrocoagulation or injection therapy Decreases in rebleeding, surgery and mortality (Cook, et al. 1992, Sacks, et al. 1990) Endoscopic Therapy Following initial stabilization the patient should undergo diagnostic endoscopy as soon as possible. The presence of endoscopic stigmata indicating a high risk of bleeding (nonbleeding visible vessel or active bleeding) would be considered an indication for endoscopic therapy.1 Either heater probe or bipolar electrocoagulation appear to be the preferred thermal methods, injection therapy with epinephrine, ethanol, normal saline, or various sclerosants is an equivalent alternative, while laser therapy is less portable and expensive.1 Preliminary results suggest combination therapy with injection and electrocoagulation may be promising to prevent rebleeding, especially in patients with selected endoscopic stigmata.2,3 Most individual clinical trials have shown a decreased rate of rebleeding, but not a significant decrease in mortality after endoscopic therapy. However, two meta-analyses have demonstrated a significant decrease in mortality after endoscopic therapy.4,5 References: 1. Laine L, Peterson WL. Bleeding peptic ulcer. N Engl J Med 1994;331(11): 2. Chung SS, et al. Randomised comparison between adrenaline injection alone and adrenaline injection plus heat probe treatment for actively bleeding ulcers. BMJ 1997;314: 3. Tekant Y, et al. Combination therapy using adrenaline and heater probe to reduce rebleeding in patients with peptic ulcer haemorrhage: a prospective randomized trial. Br J Surg 1995;82(2):223-6. 4. Cook DJ, et al. Endoscopic therapy for acute nonvariceal upper gastrointestinal hemorrhage: a meta-analysis. Gastroenterology 1992;102(1): 5. Sacks HS, et al. Endoscopic hemostasis: an effective therapy for bleeding peptic ulcers. JAMA 1990;264:494-9.

16 Surgical Therapy Endoscopic management failure
Other extenuating circumstances Patient survival improved by optimal timing Individualized by clinical context, endoscopic and surgical expertise Surgical Therapy Surgery should be considered when endoscopic management fails or if there exist other extenuating circumstances (i.e., inability to transfuse, perforation, etc.). It must be recognized, that patient survival may be improved by optimal timing of surgery. In a study of 71 patients, a 4% mortality rate was reported in patients subjected to early surgery (based on history of prior bleeding or endoscopic stigmata indicating a high risk of rebleeding), as compared to a 10% mortality rate in patients in whom surgery was delayed (surgery only for persistent or recurrent bleeding).1 All patients who died were greater than 60 years of age. However, this study did not assess the impact of early endoscopic therapy or optimal medical management and may not be applicable to current practice. Therefore, the timing for surgery should be individualized based on the clinical context, and the available endoscopic and surgical expertise. References: 1. Morris DL, et al. Optimal timing of operation for bleeding peptic ulcer: prospective randomized trial. Br Med J 1984;288:

17 Surgical Therapy Outcomes in 92 patients with rebleeding after endoscopic therapy: endoscopic retreatment vs. surgery. Surgical Therapy In a recent trial, Lau, and colleagues compared endoscopic treatment with surgery in patients with recurrent bleeding after initial endoscopic control of bleeding ulcers.1 Consecutive patients that experienced rebleeding after initial endoscopic therapy were randomized to undergo immediate endoscopic retreatment (n=48) or to undergo surgery (n=44). Of the 48 patients assigned to endoscopic retreatment 35 (73%) had long-term control on bleeding and salvage surgery was necessary in 13 patients (27%). No significant differences in 30-day mortality were seen in the endoscopic group compared to the surgery group (10% vs. 18%, P=0.37). However, there were significantly fewer complications in the endoscopic retreatment group (15% vs. 36%, P=0.03). Of the 7 patients with complications in the endoscopic retreatment group, 6 were seen in patients who underwent salvage surgery. Hypotension at randomization and an ulcer size of >2 cm were independent predictors of the failure of endoscopic retreatment. The authors concluded that in patients with peptic ulcers and rebleeding after initial endoscopic therapy, endoscopic retreatment reduces the need for surgery without increasing the risk of death and with a lower rate of complications. References: 1. Lau JYW, Sung JJY, Lam Y-H, et al. Endoscopic retreatment caompared with surgery in patients with recurrent bleeding after initial endoscopic control of bleeding ulcers. New Engl J Med 1999;340:751-6. Lau, et al. NEJM N/A=not applicable

18 Pharmacologic Therapy
Splanchnic blood pressure modifiers vasopressin, somatostatin, octreotide Anti-fibrinolytic agents tranexamic acid Acid suppressing agents H2-receptor antagonists (H2RAs), proton pump inhibitors (PPIs) Pharmacologic Therapy Clinical trials have assessed the use of agents that modify splanchnic blood pressure, including vasopressin, somatostatin or its analogue octreotide; anti-fibrinolytic agents such as tranexamic acid; and acid suppressing agents such as H2-receptor antagonists (H2RAs) and proton pump inhibitors (PPIs). Despite the large number of clinical trials this area remains controversial, and appears to be an area where clinical practice patterns vary and are not always based on existing evidence from the literature.

19 Somatostatin/Octreotide
Effects: Lowers splanchnic blood pressure Decreases gastric acid secretion Increases duodenal bicarbonate secretion Meta-analysis: (Imperiale, Birgisson, 1997) 14 trials (n=1,829); SOM (12 trials), OCT (2 trials) 0.53 risk of rebleeding vs. H2RAs RR=0.73 among investigator-blinded trials Studies did not control for confounders, i.e., endoscopic therapy Somatostatin/Octreotide Vasopressin, a drug that lowers splanchnic blood pressure and induces vasoconstriction, has been extensively studied in the treatment of upper GI haemorrhage. Because of lower toxicity recent interest has focused on somatostatin and a somatostatin analogue (octreotide), which not only lower splanchnic blood pressure but also decrease gastric acid secretion and increase duodenal bicarbonate secretion.1,2 In 1997, Imperiale and Birgisson published a meta-analysis comparing the efficacy of these agents to that of H2-receptor antagonists (H2RAs).3 Of 14 trials involving 1,829 patients with acute non-variceal upper GI bleeding, 12 evaluated somatostatin and 2 octreotide. The relative risk (RR) of rebleeding in patients treated with somatostatin or octreotide was 0.53 (95% CI, 0.43, 0.63) compared to those treated with H2RAs. The effect was more modest if only the 7 investigator-blinded trials were included, (RR 0.73). No statistically significant differences in need for surgery were seen. The effectiveness of somatostatin was limited to peptic ulcer. This meta-analysis reported significant heterogeneity among the trials. Inclusion criteria varied and allowed for a spectrum of bleeding severity. The proportion of patients with active bleeding ranged from 13 to 100%, and as such the rate of continued bleeding ranged from 15 to 90%. The largest trial, in which 534 patients were evaluable for efficacy, found that somatostatin therapy did not differ from placebo. In addition, since data from the studies was only available at a summary level, adjustment for many determinants of outcomes, such as endoscopic treatment, were not possible. References: 1. Bloom SR, et al. Inhibition of gastrin and gastric-acid secretion by growth-hormone release-inhibiting hormone. Lancet 1974;2: 2. Johansson C, Aly A. Stimulation of gastric mucus output by somatostatin in man. Eur J Clin Invest 1982;12:37-9. 3. Imperiale TF, Birgisson S. Somatostatin or octreotide compared with H2 antagonists and placebo in the management of acute nonvariceal upper gastrointestinal hemorrhage: a meta-analysis. Ann Intern Med 1997;127(12):

20 Acid Suppressing Agents
H2-receptor antagonists (H2RAs) Cimetidine, ranitidine, famotidine, nizatidine Proton pump inhibitors (PPIs) Pantoprazole, omeprazole (oral, IV) Esomeprazole (Nexium) (oral) Lansoprazole (oral) Acid Suppressing Agents In vitro data have indicated that acid plays an important role in impairing haemostasis and causing clot digestion.1,2 H2RAs have been widely used for the treatment of acute upper GI bleeding. A number of these agents are available in IV form including cimetidine, ranitidine, and famotidine and an increase in intragastric pH has been demonstrated with these agents. PPIs are capable of producing profound acid suppression in the stomach. The recent availability of PPIs in intravenous (IV) formulations has generated renewed interest in the pharmacological management of acute upper GI bleeding with acid suppressive therapy. The role of IV H2RAs and PPIs in the management of acute upper GI bleeding will be the focus of the ensuing discussion. References: 1. Patchett SE, et al. Clot lysis by gastric juice: an in vitro study. Gut 1989;30(12): 2. Green FW, et al. Effect of acid and pepsin on blood coagulation and platelet aggregation. Gastroenterology 1978;74:38-43.

21 Role of Acid in Hemostasis
Impairs clot formation Impairs platelet aggregation & causes disaggregation Accelerates clot lysis Predominantly acid-stimulated pepsin May impair integrity of mucus/bicarbonate barrier Role of Acid in Haemostasis Poor haemostasis in the upper GI tract has been related to a number of factors, one of which is the negative effect acid in the gut has on blood coagulation and platelet aggregation. Reduction in pH is associated with prolonged clot formation times. The prothrombin time, which measures the activity of the tissue thromboplastin-induced (extrinsic) clotting system, and the activated partial thromboplastin time, which measures the activity of the contact-induced (intrinsic) clotting system, are both prolonged by 50% at pH 6.5 relative to pH 7.4.1 Intraluminal gastric juice not only impairs clot formation but also accelerates clot lysis. Acid in the gastric juice appears to play a major role in impairing clot formation, via its role in inhibiting platelet aggregation, while acid-stimulated pepsin in the gastric contents plays a major role in accelerating clot lysis. Acid is a pivotal common denominator affecting both the formation and dissolution of clots in the gastric lumen, and may contribute to mucus degradation. Therefore, theoretically, maintenance of a high intragastric pH during management of upper GI bleeding is warranted. References: 1. Green FW, et al. Effect of acid and pepsin on blood coagulation and platelet aggregation. Gastroenterology 1978;74:38-43.

22

23 Effect of PPI on Gastric pH
Increase intragastric pH pH>6.0 for 84->99% of day Continuous infusion (CI) superior to intermittent bolus administration Clinical improvements in rebleeding and/or surgery with: Bolus 80 mg + CI 8 mg/h Effect of PPI on Gastric pH Studies have shown that PPIs can maintain intragastric pH above 6.0 for up to 84% to more than 90% of the day, when administered by continuous infusion (CI).1,2 Time above pH 6.0 is somewhat lower when PPIs are administered by intermittent bolus injections. Most recently, Lin, et al reported a pH >6.0 over 84% of the time in 50 patients treated with omeprazole 40 mg bolus plus CI 6.7 mg/h,1 while Labenz, et al. reported a pH >6.0 for over 99% of the final 12 hours of a 24 hour dosing period in patients administered omeprazole 80 mg bolus plus CI 8 mg/h.2 Results of these and other studies suggest that a rapid and sustained increase in intragastric pH above 6.0 is best achieved by administration of a PPI by continuous infusion after an initial bolus dose. This has been shown to be superior to administration by bolus injection, infusion of lower doses, and infusion with a lower loading dose.3 Clinical improvements in rebleeding and need for surgery have been seen with a regimen of 80 mg by bolus followed by 8 mg/h by CI. References: 1. Lin H-J, et al. A prospective randomized comparative trial showing that omeprazole prevents rebleeding in patients with bleeding peptic ulcer after successful endoscopic therapy. Arch Intern Med 1998;158:54-8. 2. Labenz J, et al. Efficacy of primed infusions with high dose ranitidine and omeprazole to maintain high intragastric pH in patient with peptic ulcer bleeding: a prospective randomised controlled study. Gut 1997;40:36-41. 3. Brunner G, et al. Optimizing the intragastric pH as a supportive therapy in upper GI bleeding. Yale J Biol Med 1996;69:

24 Role of PPI For UGI Bleeding: Summary of Clinical Trials
10 RCTs PPI (n=1,150); controls (n= 1,142) Minimal benefit with intermittent bolus Clinical benefits with bolus plus continuous infusion (CI) Decreased need for surgery and/or rebleeding Dose: Bolus 80 mg + CI 8 mg/h x 3 d Role of PPI For Upper GI Bleeding: Summary of Clinical Trials PPI therapy appears to be effective in decreasing requirements for surgery and transfusion in patients with acute GI bleeding. The10 randomized controlled trials reviewed included 1150 patients treated with PPI therapy and 1142 in the control groups. With the exception of a significant decrease in need for surgery reported in one study and a lower rate of continued bleeding in another study, no significant improvements in rebleeding, surgery or mortality were demonstrated in studies of IV PPI therapy administered by bolus injections. However, when the PPI was administered by bolus plus continuous infusion, PPI therapy was associated with significant benefits on re-bleeding and/or the need for surgery in 3 of 4 studies. The most effective regimen appeared to be a loading dose of 80 mg followed by continuous infusion of 8 mg/h. When administered intravenously, continuous infusion of high dose PPI appears to provide the profound acid suppression needed to promote haemostasis and provide some beneficial clinical effects. More confirmation is required on orally administered PPIs. Based on an overall review of available data, the patient subgroups likely to benefit the most from acute IV PPI therapy are those with non-actively bleeding, high risk lesions. In addition to their possible effects on haemostasis, PPIs may accelerate healing and shorten the time required for a high risk ulcer stigma to become a low risk lesion.

25 Role of PPI For Upper GI Bleeding: Summary
H2RAs Unlikely to provide necessary pH increases Tolerance a problem Minimal benefit in clinical trials PPIs can provide profound acid suppression pH>6.0 over 24-hours Suggested benefits on rebleeding and/or need for surgery Mortality benefits not yet demonstrated Role of PPI For Upper GI Bleeding: Summary Acid clearly plays an important role in impairing haemostasis in the gut at the level of the gastric mucosa. Therefore, theoretically, suppression of acid such that the GI environment approaches a neutral pH should have important beneficial effects on the control of bleeding in the upper GI tract. Controlled clinical trials of H2RA therapy have not demonstrated significant improvements in clinical outcomes. Furthermore, intragastric pH studies have demonstrated that these agents are unlikely to provide adequate acid suppression and tolerance to their effects develops rapidly. Continuous infusion of PPIs provides profound acid suppression as measured by 24-hour intragastric pH levels and as a result may provide an environment for effective coagulation. Clinical trials suggest beneficial effects with PPIs on rebleeding and need for surgery when used in high doses and administered as a bolus loading dose followed by continuous infusion. Benefits on mortality rates have yet to be demonstrated, however, neither the individual studies nor an aggregate analysis would provide adequate patient numbers to demonstrate statistical differences in mortality due to its infrequent occurrence.

26 Role of PPI For Upper GI Bleeding: Summary
Reasonable to consider initiating as soon as possible following presentation to hospital Administer as bolus + continuous infusion (CI) IV bolus 80 mg + CI 8 mg/h x 3 d Continue therapy, probably with an oral PPI Likely most beneficial for patients with high risk, non-actively bleeding lesions Further trials needed to determine optimal patient group for acute IV PPI therapy Role of PPI For Upper GI Bleeding: Summary Theoretically, acid suppression should be undertaken immediately upon presentation to hospital in order to rapidly achieve an optimal pH for early haemostasis. Although, the issue of time to onset of treatment was not specifically addressed, most trials initiated acid suppressive therapy immediately after endoscopy, which was generally performed within 12 hours of admission. It is unclear whether more rapid initiation of therapy, both endoscopic and medical, would offer additional benefits. An effective regimen appears to be a loading dose of 80 mg administered by bolus injection followed by 8 mg/h by continuous infusion for at least 3 days. Therapy should probably be continued with an oral PPI to ensure healing of the ulcer. Treatment may accelerate healing of non-actively bleeding, high risk lesions. The subgroup at very high risk, i.e. those patients with spurting, or oozing bleeding, is less likely to benefit. We conclude that IV PPI therapy is a promising adjunct to endoscopic haemostatic therapy, however, further studies are needed to determine the patient population who might benefit the most from acute treatment.

27

28 Peptic Ulcer Disease Causes: Infectious: H.P., Herpes, CMV
Drugs: NSAIDS, corticosteroids Neoplastic ICU Stress Types: DU = pain between meals GU = pain with meals, epigastric

29 Risk Factors for Ulcers and Bleeding
The major factors that have been identified as causes of gastric or duodenal ulceration include Helicobacter pylori, and the use of non steroidal anti-inflammatory drugs (NSAIDs). H. pylori is implicated in approximately 70-90% of patients with nonbleeding duodenal ulcer, but several studies have suggested that its occurrence is lower in patients with bleeding duodenal ulcers.1,2 NSAIDs have been shown to increase both the risk of ulceration and of ulcer bleeding,3,4 with a greater role in the formation of gastric ulcers. Ulceration is more frequent in the first month of treatment and appears to be dose-dependent.3,4 Doses of ASA as low as 75 mg/day have been associated with an increased risk of bleeding.5 Current evidence suggests that corticosteroids alone have little impact on the risk of ulceration or bleeding, but when taken in combination with NSAIDs they may double the risk of ulcer complications,4 and increase the risk of bleeding ten-fold.6,7 Oral anti-coagulants taken alone have been associated with a relative risk of bleeding of 3.3. In combination with NSAIDs the relative risk increased to References: 1. Hosking SW, et al. Randomized controlled trial of short term treatment to eradicate Helicobacter pylori in patients with duodenal ulcer. BMJ 1992;305:502. 2. Hosking SW, et al. Differing prevalence of Helicobacter in bleeding and nonbleeding ulcers [abstract]. Gastroenterology 1992;102:A Sommerville K, et al. Non-steroidal anti-inflammatory drugs and bleeding peptic ulcer. Lancet 1986;I:462-4. 4. Gabriel SE, et al. Risk of serious gastrointestinal complications related to use of non-steroidal anti-inflammatory drugs: a meta-analysis. Ann Intern Med 1991;115: 5. Swedish Aspirin Low-Dose Trial (SALT) of 75 mg aspirin as secondary prophylaxis after cerebrovascular ischaemic events. The SALT Collaborative Group. Lancet 1991;338: 6. Piper JM, et al. Corticosteroid use and peptic ulcer disease: role of nonsteroidal anti-inflammatory drugs. Ann Intern Med 1991;114: 7. Shorr RI, et al. Concurrent use of nonsteroidal anti-inflammatory drugs and oral anticoagulants places elderly persons at high risk for hemorrhagic peptic ulcer disease. Arch Intern Med 1993;153(14):

30 Peptic Ulcer Disease – Helicobacter Pylori
Most common chronic bacterial infection in man 15% of infected go on to PUD Dx via C13/C14 breath testing, histology, serology, urease testing (5-15% false negative) false negative if ABO or acid suppression within the last week (except serology) Serology $30 (not for eradication) Breath Testing 13C non-radioactive urea metabolized to CO2 exhaled and quantified

31 Peptic Ulcer Disease – When to Test for H.P.
GU = test for H.P. as other causes of GU are common, especially NSAID induced ulcers, maliganancy (repeat endoscopy) DU = if not on NSAID may treat empirically for H.P.

32 Helicobacter Pylori Eradication
Proven to decrease ulcer recurrence/bleeding Tx if any history of upper GI bleeding and H.P. positive Treatment Options: PCA= PPI + Clarithomycin 500mg bid + Amoxil 1g bid for 7 days PCM = PPI + Clarithoromycin 500mg bid + Metronidazole 500 mg bid X 7 days (resistance)

33 H.P. Eradication Antibiotics are very effective
Test for eradication only in complicated ulcer disease eg. bleeding, pyloric outlet obstruction, recurrent ulceration or persistent symptoms Most cost effective method = breath testing 1/12 after antibiotics are complete 7/7 after stopping acid suppression

34 NSAID And Upper GI Ulceration
2-4% annual risk of PUD related complication on NSAID (bleeding, outlet obstruction, symptomatic ulcer) Lowest possible dose of NSAID/ASA (2-4X risk even if <325 mg ASA daily) Prophylaxis if: Previous PUD or GI bleed NSAID + corticosteroids >65 (75 in Ontario guidelines) serious comorbidity

35 NSAIDS & UGI Bleeding Classic NSAID inhibit COX-1 and COX-2
Inhibition of COX 1 results in decreased gastric PG and hence poor protective barrier in the GI tract COX-2 expressed predominantly in actively inflammed tissues, therefore less damage to normal GI tract COX-2 ulcer risk approx to that of classic NSAID + PPI

36 COX-2 Inhibitors & UGI Ulceration
1149 pt. with R.A. endoscopy pre and post 12 weeks therapy for GI ulceration Compared celecoxib (2x max. dose) vs. naproxen (max. dose) vs. placebo No difference ulceration between placebo and celecoxib vs. p<0.001 difference between celecoxib and naproxen Near identical study with Vioxx (rofecoxib)

37 NSAIDS and UGI Bleeding Prophylaxis
Options: Misoprostol 200mg qid + standard NSAID Side effects diarrhea, cramps $38/month, 4% S/E PPI + standard NSAID More effective than Misoprostol $53/month (Pantoprazole) Cox –2 inhibitor ($40-75/month) ? Add PPI PPI twice as expensive as misoprotol with just drug cost, but cost of admits and assessment for bleeding make comprable (no studies I’m aware of) I say qid hassle of misoprostol and side effect plus more relapse so cost about similar I suggest PPI (Hawkey NEJM 1998) COX 2 ? As about as good as PPI and NSAID but no direct comaprison, slightly more expensive

38 NSAIDS, H.P. And UGIB Prophylaxis
In high risk patients (previous PUD or ongoing dyspepsia), test and treat for H.P. prior to NSAID initiation decreases risk UGI to that of PPI or celebrex How to test Time consideration of breath testing Most bleeds in first month Previous studies show no benefit for primary prophylaxis with H.P. eradication if already on an NSAID

39 A may well have b, who can very quickly become c

40

41 Esophageal Variceal Bleeding
BE SUPICIOUS, if patient is cirrhotic/heavy drinker think varices first 30-50% mortality without early intervention Causes of death are classically aspiration, sepsis, renal failure or encephalopathy Treatment options: Medical - endoscopic Tamponade - TIPS - Surgical Think varices first call me next. Still pud number one cause of GI bleed in patients wiht

42 Esophageal Variceal Bleeding
Medical = octreotide (72 hours) or somatostatin forget vasopressin Endoscopic = ligation (banding), sclerotherapy

43

44 Esophageal Varices Tamponade = Blakemore tube                                                                         

45 Esophageal Varices TIPS = transjugular intrahepatic portosystemic shunts or Surgical Shunts = desperate measures

46 TIPS

47 TIPS

48 TIPS

49


Download ppt "UGI Bleeding."

Similar presentations


Ads by Google