Peptic ulcer disease

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peptic ulcer , h pylori , beeding peptic ulcer management


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Management of Peptic Ulcer Disease:

Management of Peptic Ulcer Disease Ayaskanta Singh

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A peptic ulcer is a defect in the gastric or duodenal wall that extends through the muscularis mucosa (the lowermost limit of the mucosa) into the deeper layers of the wall ( submucosa or the muscularis propria ). Sleisenger & Fordtran’s gastrointestinal and liver disease. , 9th ed . Philadelphia (Pa): Saunders; 2009

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Erosions are breaks in the surface epithelium that do not have perceptible depth. The term peptic ulcer disease is used broadly to include ulcerations and erosions in the stomach and duodenum . This is because pepsin, which is proteolytic in acidic solution, plays a major role in causing the mucosal breaks regardless of the cause of the inciting agent .


Diagnosis Patient history Confirmed by endoscopy Biopsy Gastric ulcer to determine if malignant Definitively diagnose H. pylori infection Contrast radiography / Barium Meal Limited utility in modern day practise


C/F Presentation: – Recurrent, episodic epigastric pain 1-3 hours after meals or at night – May have vague symptoms of nausea, pressure, fullness, hunger sensation – May be relieved with food or antacids, but pain returns within 30-60 minutes – Many patients, particularly the elderly, may be asymptomatic .

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GU Postprandial pain Vomiting Haematemesis > Melena Afraid to eat Lives on milk and fish Loses weight DU Hunger pain No vomiting Melena > Haematemesis Good appetite Eats almost anything No weight loss

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Complications Bleeding: anaemia, melaena , haematemesis Obstruction: vomiting, dysphagia , weight loss Perforation: pain, peritonitis Carcinoma in chronic gastric ulcer

Diagnostic approach to dyspepsia :

Diagnostic approach to dyspepsia

Treatment of peptic ulcer :

Treatment of peptic ulcer Lifestyle and dietary modification Drugs Operation Lifestyle & Dietary Modification Less stress Regular diet Avoid NSAID Quit smoking

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Medical therapy Treat the underlying cause Duodenal ulcers – Treatment success related to degree of acid suppression (pH > 3) – >90% will heal with 4 weeks of standard PPI therapy – There is no need to biopsy duodenal ulcers or perform followup EGDs

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Gastric ulcers – Treatment success related to duration of acid suppression – Healing requires 8-12 weeks of PPI therapy and may require “double dose” BID PPI – Most gastric ulcers should be biopsied to rule out malignancy (from base and edges) – Need for followup EGD after 8-12 weeks to assess for ulcer healing should be individualized, especially if biopsies were not obtained .

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ACh PGE 2 Histamine Gastrin Adenyl cyclase _ + ATP cAMP Protein Kinase (Activated) Ca ++ + Ca ++ Proton pump K K + H + Gastric acid Parietal cell Lumen of stomach Antacid Omeprazole Ranitidine H 2 M 3 Misoprostol _ _ _ + PGE receptor + + Gastrin receptor + + +

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Antacids Weak bases that neutralise acid Also inhibit formation of pepsin (As pepsinogen converted to pepsin at acidic pH ) Present day antacids : Aluminium Hydroxide Magnesium Hydroxide Not prescribed . OTC drug for symptomatic relief of dyspepsia Duration of action : 30 min when taken in empty stomach 2 hrs when taken after a meal Side effects : Al 3+ antacids – constipation (As they relax gastric smooth muscle & delay gastric emptying) Mg 2+ antacids – Osmotic diarrhoea . In renal failure Al 3+ antacid – Aluminium toxicity And Encephalopathy

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Histamine H 2 Receptor Antagonist Reversible competitive inhibitors of H 2 receptor Highly selective, No action on H 1 or H 3 receptors Very effective in inhibiting nocturnal acid secretion ( as it depends largely on Histamine ) Modest impact on meal stimulated acid secretion (As it depends on gastrin , acetyl choline and histamine ) Extremely safe drugs Cimetidine causes gynecomastia , galactorrhea (as it is antiandrogenic & increases prolactin level) Cimetidine inhibits CYP450 & increases conc. of Warfarin , Theophylline , Phenytoin , Ethanol.

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Proton Pump Inhibitors Most effective drugs in antiulcer therapy . Five PPIs are used as antisecretory agents— omeprazole , esomeprazole (S optical isomer of omeprazole ), lansoprazole , pantoprazole , and rabeprazole Prodrugs requiring activation in acid environment . Weakly basic drugs & so accumulate in canaliculi of parietal cell . Half life – 1.5 hrs . Activated in canaliculi & binds covalently to extracellular domain of H + K + ATPase . Acid secretion resumes only after synthesis of new molecules. Since it requires acid for activation - given 1/2 hr before meals

Potential S/E of PPIs :

Potential S/E of PPIs Extremely safe drugs

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Mucosal Protective Agents Sucralfate Misoprostol Colloidal Bismuth compounds

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Sucralfate Salt of sucrose complexed to sulfated aluminium hydroxide In acidic pH polymerises to viscous gel that adheres to ulcer crater Taken on empty stomach 1 hr. before meals Concurrent antacids, H 2 antagonist avoided ( as it needs acid for activation ) PGE 1 analogue Modest acid inhibition Stimulate mucus & bicarbonate secretion Enhance mucosal blood flow Approved for prevention of NSAID induced ulcer Diarrhea & cramping abd . pain – 20 % Not so popular as P.P.I are more effective & better tolerated Misoprosto l

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Eradication of H.pylori Nobel prize Medicine – 2005 Barry J Marshall J. Robin Warren Discovery of H.pylori & its role in ulcer

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Resistance of Clarithromycin 7.8%, Amoxicillin 0%, Metronidazole 39.2% Clarithromycin-based therapy still the first choice with eradication rate of 92.6% Gu Q,, Xia HH Digestion 2006

Management of bleeding peptic ulcer:

Management of bleeding peptic ulcer

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Initial assessment and risk stratification Hemodynamic status should be assessed immediately upon presentation and resuscitative measures begun as needed (Strong recommendation). Blood transfusions should target hemoglobin ≥ 7 g / dl, with higher hemoglobins targeted in patients with clinical evidence of intravascular volume depletion . Risk assessment should be performed to stratify patients into higher and lower risk categories and may assist in initial decisions such as timing of endoscopy, time of discharge, and level of care (Conditional recommendation).

Glasgow-Blatchford Score :

Glasgow-Blatchford Score scores of 6 or more were associated with a > 50% risk of needing an intervention

Rockall scoring system for risk of re-bleeding and death after admission to hospital for acute GI Bleeding:

Rockall scoring system for risk of re-bleeding and death after admission to hospital for acute GI Bleeding Following endoscopic therapy: Did not predict rebleeding -accurately identify patients at risk. ->6 score –managed in high dependency unit

Timing of upper GI endoscopy:

Timing of upper GI endoscopy Only be undertaken once appropriate resuscitation has been achieved to minimize cardiorespiratory complication of the procedure. Barkun A et al, Ann Internal Med 2003. Endoscopy within 24 hr is appropriate. No evidence to support emergency endoscopy for all comers. Majority (75%–80%) of patients bleeding stops spontaneously Severe life threatening, bleeding failure to respond to resuscitation measures –urgent endoscopy (within 12 h).

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NATURE REVIEWS Gastroenterology & Hepatology , Aug,09 In a recent UK audit of 208 hospitals (6750 patients), after hours endoscopy failed to be associated with reduced mortality, Gut 2010

Modified Forrest and Finlayson's classification :

Modified Forrest and Finlayson's classification Type I : Active bleeding: Ia : Spurting hemorrhage Ib : Oozing hemorrhage Type II : Stigmata of recent hemorrhage: IIa : Nonbleeding visible vessel IIb : Adherent clot IIc : Flat pigmentation Type III : Clean-base ulcers RB-5%,Mortality-2% RB-43%,Mortality-11% RB-55%,Mortality-11% RB-22%,Mortality-7% RB-10%,Mortality-3%

Therapy :

Therapy Non surgical therapy Drug therapy Endoscopic therapy Transcatheter arterial embolisation Surgical therapy

Pre-endoscopic medical therapy:

Pre-endoscopic medical therapy Pre-endoscopic intravenous PPI ( 80 mg bolus followed by 8 mg / h infusion) recommended . If endoscopy will be delayed or cannot be performed, intravenous PPI is recommended to reduce further bleeding . Nasogastric or orogastric lavage is not required in patients with UGIB for diagnosis, prognosis, visualization, or therapeutic effect . ACG Recommendations

Pre endoscopic PPI therapy with endotherapy:

Pre endoscopic PPI therapy with endotherapy No significant differences in mortality (6.1 vs. 5.5 % , rebleeding (13.9 vs. 16.6%), or surgery (9.9 vs. 10.2%, . Reduced stigmata of hemorrhage (active bleeding, non-bleeding visible vessel, and adherent clot) (37.2 vs. 46.5%) Endotherapy (8.6 vs. 11.7 %). I.V. PPI 80 mg bolus+8mg/h x 3d. Controls Endotherapy ( n=2223) Cochrane Database Syst Rev 2010


No trial shows benefit in reducing rebleeding rate or mortality using H2-RA. -not recommended Tranexamic acid as a standard therapy of peptic ulcer bleeding needs further randomized trials . Poor evidence of efficacy Questionable safety Gludd et al, Cochrane Data Base Syst Review 2012

Endoscopic therapy :

Endoscopic therapy Modality Types Thermal Argon laser Nd:YAG laser Electrocoagulation Heater probe Argon plasma coagulation Injection Hemospray Epinephrine Sclerosants Alcohol Thrombin Fibrin glue Mechanical Hemoclips Band ligation Endoloop Suture

Endoscopic management in forrest group:

Endoscopic management in forrest group Forrest I* Forrest IIa Forrest IIb Forrest IIc Forrest III 55 43 22 10 5 0 20 40 60 80 100 Patients with re-bleeding (%) *Patients did not receive endoscopic therapy 55 43 Endo therapy IV PPI bolus + infusion No endotherapy Oral PPI ? endotherapy IV PPI bolus + infusion Laine L & Peterson WL. 1994

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Adherent Clot : Endo Rx vs Conservative Prospective Trial Meta analysis by Kahi et al, 2005 confirmed these

Injection therapy:

Injection therapy The most convenient and least expensive method. The most commonly used solution is diluted adrenaline (1 in 10000) injected submucosally around the bleeding site in aliquots of 1–2 mL to a total volume of 5–10 ml. Haemostasis is postulated to occur due to a combined effect of vasoconstriction tamponade of the bleeding vessel Other agents used are normal saline, 3% saline, distilled water and 50% glucose in water. All these solutions have an effect similar to that of 1 in 10 000 epinephrine

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Sclerosants : absolute ethanol, polidocanol , ethanolamine, and sodium tetradecyl sulfate cause tissue desiccation or destruction. 0.1–0.2 mL /injection, total volume < 2 mL ) No convincing data to suggest that the combination of a sclerosant with epinephrine has a better outcome than epinephrine alone. Two thrombogenic compounds, fibrinogen and thrombin are used Needs repeated endoscopy with multiple injections and is of limited utility in practice. Thrombin alone has also been investigated, but has not been widely adopted.

Thermal coagulation:

Thermal coagulation Contact: Electrocoagulation Heater Probe Non-contact: APC Laser Monopolar Biopolar


Hemoclips Pre-loaded Rotatable Reopenable Triclip (Cook) Resolution (Boston) Quickclip 2 (Olympus)

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The major difficulty with hemoclip placement occurs when ulcers are difficult to reach (posterior duodenal bulb,post wall of stomach, high in lesser curvature) tangential application is required Fibrous base of a chronic ulcer Triclip : initial hemostasis in 81.5% Rebleeding within 24 hrs 14.5% Clip dislodged in 11% in second look endoscopy. Chan et al 2004 Hemoclips is superior to triclip for high risk ulcers.

Hemospray in Peptic Ulcer Bleed:

Hemospray in Peptic Ulcer Bleed N= 20 Hemostasis = 19(95%) Sung et al, Endoscopy’ 2011

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* Number of trials Thermal + Epi vs. Epi alone (2*) Clips + Epi vs. Epi alone (3*) Thermal + Epi vs. Thermal alone (4*) Rebleeding Odds Ratio (95% CI) 0.27 0.38 0.79 Favors dual therapy Favors monotherapy Which is the best modality? 0.2 0.5 1 2 5 Clips+ Epi vs. Clips alone (2*) 1.30 Not Injection alone Thermal alone or clips alone as good as combination with Epi ? Calvet Gastroenterology 2004, Marmo Am J Gastro 2007, Sung Gut 2007, Laine CGH 2008, Barkun GIE 2009

Medical therapy after endoscopy:

Medical therapy after endoscopy After successful endoscopic hemostasis , iv PPI therapy with 80 mg bolus followed by 8 mg / h continuous infusion for 72 h should be given to patients who have an ulcer with active bleeding, a non-bleeding visible vessel, or an adherent clot ( Strong recommendation , high-quality evidence) . Patients with ulcers that have flat pigmented spots or clean bases can receive oral PPI once-daily.( Strong recommendation, moderate-quality evidence ) .

Adjuvant PPI with endotherapy:

Adjuvant PPI with endotherapy ↓ re-bleed (5.9% vs 10.3%) ↓ re endotherapy (6.4% vs 11.6%) ↓ blood transfusion ↓ hospital stay trend to ↓ surgery & mortality I.V. ESOMEPRAZOLE 80 mg bolus+8mg/h x 3d. PLACEBO Endotherapy (n=767) Sung et al, Ann Intern Med, 2009

Repeat endoscopic therapy:

Repeat endoscopic therapy Not routinely required. Clinical evidence of bleeding, endoscopic hemostatic therapy should be applied . If further bleeding occurs after a second endoscopic therapeutic session, surgery or interventional radiology with transcathetherarterial embolization is generally employed (Conditional recommendation, low-quality evidence).


Surgery A common indication for emergency surgery is failure of endoscopic therapy. The usual scenarios are as follows: (1) spurting hemorrhage could not be stopped by endoscopic means; (2) the bleeding point could not be seen because of heavy active bleeding; and (3) recurrent bleeding appeared after initial endoscopic control Larger ulcers located at the high lesser curvature and posterior duodenal bulb.

Long term management :

Long term management The American Journal of GASTROENTEROLOGY 2012 Patients with SRH hospitalized for 3 days assuming no rebleeding may be fed clear liquids soon after endoscopy Patients with clean-based ulcers may receive a regular diet and be discharged after endoscopy assuming they are hemodynamically stable ,no medical problem, Hb stable

Management of Peptic Perforation:

Management of Peptic Perforation Initial resuscitation after ulcer perforation with restoration of fluids, electrolytes, and, if needed, blood. A nasogastric tube and a urinary catheter should be in place. Pain should be relieved with opiates . IV broad spectrum antibiotics administered , even though gastric juice contains few organisms .

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Surgery is the usual approach to an ulcer perforation. surgeon has to treat peritoneal contamination, the perforation, and the ulcer. Duodenal or juxtapyloric ulcer perforation Simple closure with the use of an omental patch . Whether to perform definitive ulcer surgery at the time of ulcer perforation ?? There is now evidence that H. pylori eradication and PPI use reduces relapse of ulceration after patch repair. Ref

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Perforated gastric ulcers Patients with are older, have significant co morbid illnesses, more chance of malignancy -- prognosis less favourable. Choice of surgery ??? No prospective controlled trials comparing simple closure and definitive treatment of a perforated gastric ulcer . Surgery depends upon the type and location of gastric ulcer. an angular notch ulcer along the lesser curvature -- antrectomy followed by a Billroth type I Gastroduodenostomy . Small prepyloric ulcers – simple closure

Management of Gastric outlet obstruction:

Management of Gastric outlet obstruction Medical Management Around half of patients improve during the period of nasogastric suctioning, volume resuscitation, rehydration ,and acid suppression. Improvement is noticeable in patients with active ulceration and acute edema . Surgery is deferred until after an adequate trial of conservative management .

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Endoscopic Management Endoscopic balloon dilation – successful . Gradual dilation over two or three sessions. The largest diameter of stenosis at which symptoms occur is unclear. dilation to 15 mm recommended , which is often associated with relief of symptoms. Thus can be managed with medical and endoscopic means in approximately 70% of cases, and only 30% may require bypass surgery .

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Surgical Management A variety of operations truncal vagotomy together with either a drainage procedure (either gastrojejunostomy or pyloroplasty ) . obstructing prepyloric gastric ulcer, an antrectomy followed by a Billroth type I gastroduodenostomy is the procedure of choice.


REFRACTORY ULCERS Most peptic ulcers heal within eight weeks of initiation of antisecretory therapy. Refractory ulcers - minority of patients whose ulcers persist despite conventional treatment . The following questions should be addressed . Non compliance ? Is there H. pylori infection? If antibiotic therapy already has been prescribed, the patient should be tested to confirm that the infection has indeed been eradicated. Drug resistance ? Is the patient still taking an NSAID? Does the patient smoke cigarettes?

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Has the duration of ulcer treatment been adequate? A large ulceration ( >2 cm) may require longer duration(12 weeks of therapy). Is there evidence of a hypersecretory condition? gastrinoma (ZES) or multiple endocrine neoplasia type 1 or hyperparathyroidism . Is the ulcer penetrating the pancreas, liver, or other organ ? Is the ulcer indeed peptic? Primary or metastatic neoplasms , infections (e.g., cytomegalovirus,Tuberculosis ), cocaine use, eosinophilic gastroenteritis, and Crohn’s disease .

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