Surgical Management of PUD complications may 2024.pptx

Describes surgical procidures to decrease gastric acid secration and it's complications

1. Management of complications of PUD Presenter: Aschalew (GSRIII) Moderator; Dr Basit (Assistant professor of surgery)

2. Outline of presentation Anatomy of stomach and doudneum Physiology of stomach and doudneum Pathophysiology of PUD Common complications of PUD Management of complications of PUD Summary references

3. Anatomy of stomach and doudneum

4. Cont. In 50% of patients, there are more than two vagal nerves at the esophageal hiatus criminal nerve of Grassi Supply to pylorus 4

5. Histology

6. Function The stomach stores food and facilitates digestion through a variety of secretory and motor functions Secretory functions Production of mucus, bicarbonate, acid, pepsin, intrinsic factor, and a variety of GI hormones Motor functions Food storage (receptive relaxation and accommodation) Grinding and mixing Controlled emptying of ingested food A periodic interprandial “housekeeping” 6

7. Acid secretion (3 phases) 7

8. Motor function of stomach Feeding phase Receptive relaxation and accommodation Segmental gastric motility Interprandial phase Four phases 8

9. Gastric Mucosal Barrier A variety of factors are important in maintaining an intact gastric mucosal layer When these defenses break down, ulceration occurs Components Mucous barrier Bicarbonate secretion Epithelial barrier Hydrophobic phospholipids (Cell membranes) Tight junctions Restitution A process of replacing sloughed or denuded SECs by migration of adjacent cells Microcirculation (reactive hyperemia) Providing nutrients and oxygen for the cellular functions involved in cytoprotection Buffering and rapidly removing “Back-diffused” hydrogen Afferent sensory neurons Protective reflexes 9

10. Pathophysiology of PUD Peptic ulcers are focal defects in the gastric or duodenal mucosa -may be acute or chronic - gastric ulcer patients are 10 years older than duodenal ulcer patients. - Gastric ulcer has a higher mortality - Duodenal ulcer , M:F -2:1 -gastric ulcer ,M:F-1:1 10

11. Etiology H.pylori infection NSAIDS Smoking Stress Physiological Trauma Burns Psychological Zollinger -Ellison syndrome ( gastrinoma ) Antral G-cell hyperfunction and/or hyperplasi a 11 90% of the causes in USA

12. pathophysiology 12

13. H pylori Inhibitory effect on antral D cells Production of toxins ( Vacuolating cytotoxin ( vacA ) and Cytotoxin -associated gene A ( cagA )) Producing local inflammation Gastric metaplasia Decreasing bicarbonate production ( doudenum ) 13

14. Cont. Up to 90% of patients with duodenal ulcers, and 70 to 90% of patients with gastric ulcers, have H. pylori infection. Curing H. pylori infection dramatically alters the natural history of PUD Eradication therapy decrease the recurrent ulcer rate from over 75% to 20% in patients only taking PPI. 14

15. NSAIDS Risk of peptic ulcer in chronic NSAID users is about 25% (15% gastric and 10% duodenal) Complications of PUD (specifically hemorrhage and perforation) are much more common in patients taking NSAIDs >50% of patients had hx of use. Most of them asymptomatic until they develop these life-threatening complications. Smokers are about twice as likely to develop PUD as non-smokers. 15

16. Types of gastric ulcers 16

17. Clinical Manifestations Abdominal pain Complaint of over 90% of patients with PUD The pain is typically non-radiating, burning in quality, and located in the epigastrium Pain of duodenal ulcer Usually experienced 2 to 3 hours after a meal and at night Two thirds of patients with duodenal ulcers will complain of pain that awakens them from sleep Pain of gastric ulcer More commonly occurs with eating and is less likely to awaken the patient at night 17

18. Investigation complete blood count, liver chemistries, serum creatinine, serum amylase, and calcium H.pylori test Urea breath Endoscopy Serology Culture Radiography 18

19. Medical Treatment Patients with PUD should stop smoking and avoid alcohol and NSAIDs (including aspirin). If initial H. pylori testing is negative, the ulcer patient may be treated with H 2 -receptor blockers or PPIs If ulcer symptoms persist, an empiric trial of anti-H. pylori therapy is reasonable (false-negative H. pylori tests are common) If H. pylori infection is documented, it should be treated with one of several acceptable regimens In a symptomatic patient with persistent H. pylori infection following treatment, another regimen could be tried. e.g., quadruple therapy 19

20. Treatment Regimens for H. pylori Infections 20

21. Long term PPI tx Generally, antisecretory therapy can be stopped after 3 months long-term maintenance therapy for peptic ulcer should be considered in: All patients admitted to hospital with an ulcer complication All high-risk patients on NSAIDs or aspirin (the elderly or debilitated) All patients with a history of recurrent ulcer or bleeding Patients on anti coagulants. 21

22. Complications of PUD Bleeding Perforation Gastric outlet obstruction Interactablity/non healing ulcers.

23. Surgical Treatment Gastric cancer must always be considered in gastric ulcer Fundamentally, the vast majority of peptic ulcers are adequately treated by a variant of one of the 3 basic operations: Highly selective vagotomy Vagotomy and drainage Vagotomy antrectomy Distal gastrectomy (for type I gastric ulcers) 23

24. Definitive mx of ulcers

25. Cont. Today, most emergency operation involve simple patch of a perforated ulcer oversewing of a bleeding ulcer But even in the current era, vagotomy may improve outcomes in emergency ulcer surgery 25

26. Highly Selective Vagotomy /Parietal cell vagotomy /Proximal gastric vagotomy mortality risk <0.5%) The operation severs the vagal nerve supply to the proximal two thirds of the stomch It preserves the vagal innervation to the antrum and pylorus, and the remaining abdominal viscera 26

27. Cont. Gastric emptying of solids is typically normal in patients after parietal cell vagotomy Liquid emptying may be normal or increased due to decreased compliance associated with loss of receptive relaxation and accommodation GI side effects are rare Can be done laparascopically HSV has not performed particularly well as a treatment for type II (gastric and duodenal) and III 27

28. Vagotomy and Drainage Main procedures under this are: Truncal vagotomy and pyloroplasty Truncal vagotomy and gastrojejunostomy Unlike HSV, V+D is widely accepted as a successful operation for complicated PUD 28

29. Cont. 29 2 to 3 cm

30. Vagotomy and Antrectomy Removes about 35% of the distal stomach The extremely low ulcer recurrence rate The applicability of the operation to many patients with complicated PUD higher operative mortality rate when compared with HSV or V+D 30

31. Distal Gastrectomy Distal gastrectomy without vagotomy Truncal vagotomy is added for type II and III gastric ulcers, or if the patient is believed to be at increased risk for recurrent ulcer Subtotal gastrectomy (75% distal gastrectomy) without vagotomy is rarely used to treat PUD today 31

32. Gastric resection for PUD Antrectomy with or without Vagotomy An antrectomy for duodenal or pyloric channel ulcer removes about 35% of the distal stomach. Reconstruction- Billroth I/II or Roux-en-Y GJ

33. ssss

34. Magnitude of the problem

35. Common complications of PUD UGIB - peptic ulcers account half of UGIB. - Most peptic ulcer–related deaths in U.S. - hx ; typically present with melena : heamatemesis : abdominal pain is uncommon. : shock may be present with only clue being previous hx of PUD. -NG aspiration is necessary to confirm UGIB - early endoscopy ,to confirm cause and plan heamostatic therapy.

36. Bleeding ulcer ¾ of the patients will stop bleeding with acid suppression and kept NPO. ¼ will continue to bleed or will rebleed . -such patients , fairly well delineated based on clinical factors -presence of shock,hematemesis -transfusion requirement more than 4 units /24hrs -active bleeding or exposed vessel on endoscopy. -risk stratification needed to predict rebleed and death. - blatchford and rockall score

37. Bleeding ulcer Endoscopic mx - Injection with epinephrine -Electrocautery -clipping *10-15% endoscopic mx may fail… Persistent bleeding or rebleeding Surgical consultation and early operation -bleeding from high risk lesions -age more than 60 -ulcer greater than 2 cm -transfusion more than 6 unit/24hrs -concurrent indication( perfo,obs ).

38. Surgical mx of bleeding ulcer Surgical options -pyloromyotomy with over sewing of ulcer. -V and A -Avoid resection in patients with shock .

39. Bleeding ulcer

40. Intractable Ulcer Rare indication for ulcer operation today Intractable PUD should raise red flags for the surgeon endoscopically proven ulcer greater than 5 mm that does not heal after 12 weeks of treatment with a PPI. 40

41. Intractable Ulcer For duodenal ulcer -HSV with or without GJ. -for gastric ulcer -wedge resection with HSV. -distal gastrectomy to include ulcer. *its unnecessary to add vagotomy in type 1 or 4 ulcers. - Type 4 gastric ulcers may be difficult to resect with distal gastrectomy.

42. GOO least frequent complication of PUD- 3-5% Most cases are associated with duodenal or pyloric channel ulceration. Clinical features; - -early satiety, bloating - indigestion, anorexia, nausea, vomiting , - epigastric pain, and weight loss P/E- succussion splash -visible peristalsis at epigastric area -malnutrition and signs of dehydration. -DX-UGI endoscopy, UGI contrast studies, CT scan -basic labs=CBC, OFT, electrolytes 42

43. GOO Mx - Initial measures -I V fluid replacement(NS), -correct electrolytes, -NG tube, Nutritional support. -Surgery- V+A(standard procedure), - V+D or HSV + GJ HSV + GJ-minimally invasive can be done laparascopically Do Biopsy for pyloric/gastric ulcer

44. Mx of perforations Hx and P/E- Risk factors for PUD * sudden severe, diffuse abdominal pain, vomiting CLF -has 3 phases…chemical peritonitis, Lucid phase, bacterial peritonitis P/E- signs of dehydration,Hemodynamic instability, Peritoneal signs DX-Labs- CBC, OFT, electrolytes,amylase, erect c- Xray

45. Mx of PPU Initial management: insertion of a NG tube, IV fluid replacement, catheterize, IV PPI, broad spectrum antibiotics and analgesia Surgical options: Simple patch Patch and HSV Patch and V+D Wedge excision and V+D Distal gastrectomy conservative option?

46. Treatment Non-operative management Criteria Age <70 years Improvement in symptoms within 12-24 hr No hemodynamic instability No sign of peritonitis No evidence of free extravasations of contrast on upper GI contrast studies Management Nasogastric decompression Fluid resuscitation with replacement of fluid and electrolytes Proton pump inhibitors Broad-spectrum antibiotics Serial abdominal examinations, preferably by the same examiner Subsequent follow-up endoscopy (to monitor ulcer healing) Treatment of H. pylori 46

47. Algorithm for PPU

48. Types of omental patch Johan Mikulicz Radecki (1880) 1st surgeon who closed a perforated peptic ulcer (PPU) by simple closure Cellan – Jones (1929) suggested a pedicle omentoplasty without primary closing of the defect “A rapid method of treatment in perforated duodenal ulcers” BMJ 15th June 1929 In 1937 Roscoe Graham published his results with a free omental graft Surg Gynecol Obstet 1937:235–238

49. Patch failure Partial gastrectomy with BI or BII conversion of the perforation in to pyloroplasty Omental plugging closure of the perforation using a serosal patch. 52

50. Contraindications for definitive mx Generally, contraindications relate to the patient's clinical status and include: Pre-operative shock Severe generalized peritonitis Intra-abdominal abscess Delay in the diagnosis and operative treatment (usually more than 24 hours) Severe concurrent medical illness precluding a safe extension of operating time

51. Gastric ulcer perforations

52. Gastric ulcer perforations Gastric resection was the procedure of choice for gastric ulcers . omental patch closure, primary closure, and ulcer excision are being considered.

53. Giant duodenal ulcer >2cm ulcers Less related to H.pylori infection. NSAID use plays more prominent role. Biopsy should be taken to R/O malignancy(19%).

54. Surgical mgt of Giant PUD perforations surgical techniques free omental plug Doudnostomy tube (as controlled fistula) jejunal serosal patch Triple tube ostomy Bancroft closure

55. Post operative complications Problems around the anastomoses Obstruction Leaks Oesophagitis Bleeding Alkaline reflux gastritis and vomiting Problems due to vagus nerve transection and decreased stomach function Diarrhea Gastric atony Gastric outlet obstruction Gallstones Dumping Vitamin b12 deficiency and iron deficiency anemia Malnurtrition

56. Post vagotomy and gastrectomy complication Dumping syndrome. - Rx- dietary modification and somatostatin analogue ( octreotide ) - surgery= small percentage / rarely- *simple takedown of GJ *jejunal interposition *conversion to Roux-en-y GJ

57. Reference Schwartz’s Principles of Surgery 11E Greenfield's Surgery Scientific Principles & Practice, 5 th E. Lippincott Maingot's Abdominal Operations 13ed Master Techniques in Surgery Gastric Surgery (2013) Sabiston text book of surgery 21st e Uptodate 2021

58. thank you.