Peptic ulcer disease PRESENTED BY Fadi Haddad INTRODUCTION

Peptic ulcer disease PRESENTED BY : Fadi Haddad.

INTRODUCTION : • The stomach: • Anatomy: • The stomach starts at the end of the LES, and ends at the pyloric sphincter • ➢ The main anatomical parts of the stomach are: the cardia, fundus, body, antrum, and pylorus. ➢ The left border of the stomach is called the greater curvature, and it’s attached to the greater omentum. The right border of the stomach in called the lesser curvature and it’s attached to the lesser omentum.

Blood supply: All parts of the stomach are supplied by the branches of the celiac trunk. • The celiac trunk gives 3 major arteries; left gastric, splenic and common hepatic. • left gastric artery lesser curvature • The splenic artery left gastroepiploic artery greater curvature • terminal branches of the splenic artery short gastric arteries fundus of the stomach • common hepatic artery gives two arteries before becoming the hepatic artery proper 1. right gastric artery (to the lesser curvature) 2. gastroduodenal artery descends posteromedial to the second part of the duodenum and terminates as right gastroepiploic artery greater curvature and the superior pancreaticoduodenal arteries.

➢ Venous drainage of the stomach : • Right and left gastric veins →Directly to the portal vein. • Left gastroepiploic vein → splenic vein. • Right gastroepiploic vein→ SMV. Innervation : ➢ Anterior gastric wall → left vagus nerve. ➢ Posterio gastric wall→ right vagus nerve. ➢ Gastroduodenal pain is sensed via sympathetic afferents from T 5 to T 10

• Physiology: • The major secretory cells of the stomach: 1. Parietal cells gastric acid 2. chief cells pepsinogen 3. Goblet cells mucus cell 4. G-Cells gastrin 5. D cells somatostatin. gastric acid secretion : gastrin, Acetylcholine and histamine. gastric acid secretion : Somatostatin and prostaglandins decrease

Peptic ulcer disease : • Peptic ulcer disease represents a spectrum of diseases characterized by ulceration of the stomach or proximal duodenum due to imbalance between acid secretion & mucosal defense mechanisms. • Epidemiology: It’s a very common disease But the incidence is decreasing due to discovery and eradication of H. pylori, better medical treatment, improvement in the quality of life, and more precautions in the use of NSAIDs and aspirin.

Classification: • Duodenal: at the antral-pyloric junction (more common). • Gastric ulcers: usually fall within one of five categories (Modified Johnson Classification). • 1. Type 1. Lesser curvature 60% to 70%, associated with low mucosal protection. • 2. Type 2. Lesser curvature and duodenal 15%, associated with high acid secretion. • 3. Type 3. Prepyloric 20%, associated with high acid secretion. • 4. Type 4. Proximal stomach/cardia, associated with low mucosal protection. • 5. Type 5. Anywhere in stomach, medication induced.

ETIOLOGY : 1. Helicobacter pylori (the most common cause) is associated with 90% to 95% of duodenal ulcers and 70% to 90% of gastric ulcers. Infection produces chronic antral gastritis, increased acid and gastrin secretion, and decreased mucosal resistance to acid. If eradicated, it has A very low reoccurrence rate. 2. NSAIDs (2 nd most common cause) use confers an eightfold increase in risk of duodenal ulcers and a 40 -fold increase in risk of gastric ulcers due to suppression of prostaglandin production. Dose-dependent relationship, ulcers do not recur when NSAID discontinued. 3. Acid hypersecretion Associated with duodenal ulcers. EX: Zollinger Ellison syndrome 4. Smoking

• loss of the protective mucous barrier ( mucus and HCO 3−) and/or excessive secretion of H+ and pepsin. ➢ Protective factors are mucus, HCO 3−, prostaglandins (that increases mucous production) , mucosal blood flow, and growth factors. ➢ Damaging factors are H+, pepsin, Helicobacter pylori (H. pylori), nonsteroidal anti-inflammatory drugs (NSAIDs), stress, smoking, and alcohol.

CLINICAL PRESENTATIONS : Signs and Symptoms: ➢ Usually asymptomatic. ➢ If symptomatic: it presents with burning/Gnawing intermittent epigastric discomfort that either relieved by food (duodenal ulcer) or exacerbated by food (gastric ulcer). ➢ It may present also with nausea, vomiting, Wight loss, upper GI bleeding or the complications. ➢ ALARM Symptoms may indicate malignancy. Complications: ➢ Bleeding. ➢ Perforation. ➢ Obstruction

DIAGNOSIS : • History • Investigations: • Esophagogastroduodenoscopy (EGD) to confirm the diagnoses, once the diagnosis is confirmed, we have to look for the cause: • 1. H. Pylori infection • tests: ➢ Non-invasive: Serological antibody tests, Urea breath test, Fecal antigen test. ➢ Invasive: Biopsy (gold standard) → to rule out malignancy, Culture + Urase test. 2. Fasting serum Gastrin levels to rule out ZES in at least three times occasions ➢ If there’s no history of NSAIDs, with -ve h. pylori test. ➢ If a patient is experiencing recurrent ulcers despite medica treatment. ➢ If a patient has multiple ulcers or ulcers in unusual sites. 3. Endoscopic biopsy of gastric ulcers is mandatory to exclude malignancy if symptoms or signs (weight loss, anemia, obstructions), or appearance of ulcer (associated mass, folds around ulcer) are present. Multiple biopsies are necessary to

Treatment : • Medical: • ➢ H. pylori eradication: Triple therapy (1 PPI omepraz + 2 antibiotics clarithromycin and metronidazole or amoxicillin) , for 10 -14 days. • ➢ NSAIDs -associated PUD → Stop the drug, then initiate anti-secretory Treatment (PPI or H 2 antagonists). • ➢ Smoking cessation. • ➢ Follow up with endoscopy: After 12 weeks re-endoscopy is used to see wither the ulcers have healed. If not, malignancy is suspected and further biopsies are taken.

• Surgical: ➢ Rarely done nowadays, unless PUD is complicated. • ➢ Indications For surgery: • 1. Non-healing ulcers. • 2. Perforated Ulcers. • 3. Bleeding Ulcers. • 4. Gastric outlet obstruction. • 5. Malignant Ulcers

• Principles of Surgical treatment: • 1. In treating PUD, we are trying to reduce Gastric acid secretion by cutting the Parasympathetic stimulation (vagus nerve) through surgical vagotomy. Nowadays, the role of surgical vagotomy has decreased as we discovered a way to perform pharmacological vagotomy (PPI or H 2 blockers). • 2. In Vagotomy, the higher level you cut the vagus nerve, the more you paralyze the stomach (especially the antrum) and delay gastric emptying. • So in Truncal Vagotomy, it’s mandatory to perform a drainage procedure; pyloroplasty, antrectomy, or gastrojejunostomy

• Surgical options for PUD: • 1. Highly selective Vagotomy : transection of the vagal fibers to the body of. ( fibers that supplying parietal cells are ligated ) • • Advantages: We don’t remove any part of the stomach, We don’t interfere with the process of emptying (no need for drainage procedure) • • Disadvantages: high recurrence rate (15%) after 10 years

• 2. Selective Vagotomy: here We cut the nerve supply to the whole stomach, except the hepatobiliary and celiac branches. 3. Truncal vagotomy: The vagus nerve is cut, It’s mandatory here to perform a drainage procedure a) Truncal vagotomy with pyloroplasty b) Truncal Vagotomy with antrectomy, and anastomosis: transection of the vagus nerve trunk, then the distal 40% of the stomach is removed anastomosed with the duodenum (Billroth I anastomosis) or Jejunum (Billroth II anastomosis)

Complicated Peptic ulcer disease : • • • 1. Bleeding PUD It’s the leading cause of death due to PUD. ➢ Mortality rate is 5 -10% ➢ The most common cause of UGI bleeding. The most common site of bleeding duodenal ulcer is the posterior wall, typically eroding the gastroduodenal artery. Signs and symptoms: 1 - Fresh or coffee-ground hematemesis. 2 - Melena 3 - If the bleeding is chronic, the patient may have signs and symptoms of anemia

• • Treatment : Aggressive resuscitation & correction of any coagulopathy. ➢ Spontaneous cessation is seen in 70% of cases. Then we do endoscopy: ➢ We may need electrocautery or epinephrine. ➢ Findings indicates high risk of bleeding: • Large sized ulcer. • Visible vessels on a non-bleeding ulcer. • Visible clots. Surgical intervention indications : repeated episodes of bleeding, continued hemodynamic instability, ongoing transfusion requirement of more than 4 to 6 units of packed red blood cells over 24 hours, and more than one unsuccessful endoscopic intervention.

2. Perforated PUD: Most commonly seen in the anterior duodenal wall. History: 1. Sudden onset of severe abdominal pain (less dramatic in elderly/ hospitalized and immunocompromised) 2. Peritonism (Fever/tachycardia and guarding). investigations: 1. CBC→ leukocytosis 2. 2. Abdominal/chest X-ray →free subdiaphragmatic air.

Treatment : • Stabilize the patient: • Aggressive fluid resuscitation, analgesia, broad spectrum antibiotics , PPI. • ( NPO / NGT /FOLEY CATHER) • Then we send the patient to the operation room, to do: • 1. Graham patch. ( piece of omentum incorporated into the suture closure of perforation ) • 2. Graham patch + HSV • 3. Graham patch + truncal vagotomy + pyloroplasty.

3. Gastric outlet obstruction: • It occurs due to: • 1. Healing of a circumferential ulcer & fibrosis by scar tissue. • 2. Edema & spasm • 3. Antral tumors. 1. presentation: ➢ Recurrent vomiting of poorly digested food. ➢ Dehydration. ➢ Hypochloremic hypokalemic metabolic alkalosis. 2. Physical examination: ➢ Dilated full stomach. ➢ Visible peristaltic waves. ➢ +ve succession splash. 3. NG tube will expel a muddy fluid in large quantities

TREATMENT : • Stabilize the patient → insert NG tube, start IV hydration, Electrolytes correction and anti-secretory medications. • When the patient is stable → Do endoscopy : EGD is necessary for evaluating the nature of the obstruction and for ruling out malignant etiology, and endoscopic hydrostatic balloon dilation can be performed at the same time. • Indications for surgical therapy include: persistent obstruction after 7 days of nonoperative management and recurrent obstruction. Antrectomy to include the ulcer and truncal vagotomy is the ideal operation for most patients.

4. Non-healing PUD: • • • ➢ Rule out Cancer. ➢ Look for persistent H. pylori. ➢ Non-compliant patient. ➢ Use of NSAIDs. ➢ Motility disorder. ➢ ZES.