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Surgical Management of PUD complications may 2024.pptx
- 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 hyperplasia 11 90% of the causes in USA
- 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 H2-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 -IV 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: I. Simple patch II. Patch and HSV III. Patch and V+D IV. Wedge excision and V+D V. 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
- 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
- 52. 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
- 53. 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
- 55. Gastric ulcer perforations • Gastric resection was the procedure of choice for gastric ulcers . • omental patch closure, primary closure, and ulcer excision are being considered.
- 56. 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%).
- 57. Surgical mgt of Giant PUD perforations • surgical techniques I. free omental plug II. Doudnostomy tube (as controlled fistula) III. jejunal serosal patch IV. Triple tube ostomy V. Bancroft closure
- 59. 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
- 60. 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
- 61. Reference 1) Schwartz’s Principles of Surgery 11E 2) Greenfield's Surgery Scientific Principles & Practice, 5th E. Lippincott 3) Maingot's Abdominal Operations 13ed 4) Master Techniques in Surgery Gastric Surgery (2013) 5) Sabiston text book of surgery 21st e 6) Uptodate 2021
- 62. thank you.
Editor's Notes
- Sympathetic innervation parallels the arterial supply of the stomach the two nerves rotate so that the left trunk becomes anterior and the right trunk posterior to the esophagus. Both trunks innervate the stomach along the lesser curvature
- The vagus nerve also supplies motor function to the circular muscle fibers of the antrum and pylorus, which is why a drainage procedure is important after truncal vagotomy
- extend into the submucosa or deeper ultimately are caused by an imbalance between the action of peptic acid and mucosal defenses
- Alcohol Commonly mentioned as a risk factor for PUD, but confirmatory data are lacking
- Hypersecretion as well Local elaboration of cytokines (particularly interleukin 8) by infected antral mucosa Recruitment of inflammatory cells and release of inflammatory mediators Production of immunoglobulins as decreases mucosal defenses
- Only about 15 to 20% of patients colonized with H. pylori will develop peptic ulcer disease over their lifetime other factors are involved in the etiology of PUD,
- Nsaid and smokin…mechanism….nsaid and gastric perf….paper
- 4 types of gastric ulcer are described (Johnson)…paper Type I gastric ulcer The most common type It is typically located near the angularis incisura on the lesser curvature, close to the border between the antrum and the body of the stomach Patients usually have normal or decreased acid secretion Type II gastric ulcer Associated with active or quiescent duodenal ulcer disease Associated with normal or increased gastric acid secretion Type III gastric ulcer It is prepyloric Associated with normal or increased gastric acid secretion Type IV gastric ulcer Occurs near the gastroesophageal junction Acid secretion is normal or below normal Type V gastric ulcers They are medication induced and may occur anywhere in the stomach
- Indications All patients over 45 with the above symptoms All patients, regardless of age, with alarm symptoms (Recurrent vomiting, Dysphagia, Bleeding, Weight loss, Anemia) In the young patient with dyspepsia and/or epigastric pain, it may be appropriate to initiate empiric therapy for PUD without confirmatory testing
- The indications for surgery in PUD (in order of decreasing frequency) are: Perforation Obstruction Bleeding Intractability or non-healing
- Before denying the stable low-risk patient a HSV or TV and drainage as an adjunct to simple patch or oversew, the surgeon should consider that many patients having emergency operation for peptic ulcer will not take long-term PPI, do not have Helicobacter, or will continue to smoke or take NSAIDs
- It has been described as a useful part of the operative treatment for bleeding duodenal and gastric ulcer, perforated duodenal and gastric ulcer
- Reasons for resection…..add reasons …for better continuty….bill one..two..roux…compare
- Subtle presentation….may be shock at presentation.
- Blatch ford…BP, BUN,HGB,PULSE ,MELENA,SYNCOPE…LIVER AND CARDIAC FAILURE…SCORE..0-23 ROCKALL….AGE,SHOCK ,COMORBIDITIES…..includes indoscopic dx and stigmata.
- Avoid resection in patients with shock…..add picture
- *do serum Gastrin level- R/O ZES
- *current- gold standard procedure for GOO 2ry PUD is V+A with BilrothII***…..ct features Passage of a standard adult endoscope across the stricture may not be possible if there is complete or near complete obstruction *Hospital mortality for patients with obstructing peptic ulcer is 2% to 3%. *Double-contrast upper GI series may be better than EGD at elucidating gastric diverticula, fistula, tortuosity, stricture location, *consider UGI endoscopy- weight loss, recurrent vomiting, dysphagia, Bleeding, anemia
- *current- gold standard procedure for GOO 2ry PUD is V+A with BilrothII***..paper Passage of a standard adult endoscope across the stricture may not be possible if there is complete or near complete obstruction *Hospital mortality for patients with obstructing peptic ulcer is 2% to 3%. *Double-contrast upper GI series may be better than EGD at elucidating gastric diverticula, fistula, tortuosity, stricture location, *consider UGI endoscopy- weight loss, recurrent vomiting, dysphagia, Bleeding, anemia
- Perforations complicate 2 to 10 % of peptic ulcers *chemical peritonitis with in 2hrs of onset-bathing of the peritoneal cavity with acidic fluid, which likely results in the release of the vasoactive mediators that underlie the physiologic response *second phase (usually 2 to 12 hours after onset), abdominal pain may lessen –dilution of acid by peritoneal secretion *If there is no free air on the plain film, computed tomography (CT) or ultrasound can be useful to detect small amounts of free air or fluid *Elderly/immunocompromised pts –signs of perforation may be equivocal *leakage of small GI content into Rt paracolic gutter may mimic appendicitis *Duodenal, antral, and gastric body ulcers account for 60, 20, and 20 % of perforations respectively *MR—10-20%, higher in gastric perforation Perforations complicate 2 to 10 % of peptic ulcers *chemical peritonitis with in 2hrs of onset-bathing of the peritoneal cavity with acidic fluid, which likely results in the release of the vasoactive mediators that underlie the physiologic response *second phase (usually 2 to 12 hours after onset), abdominal pain may lessen –dilution of acid by peritoneal secretion *If there is no free air on the plain film, computed tomography (CT) or ultrasound can be useful to detect small amounts of free air or fluid *Elderly/immunocompromised pts –signs of perforation may be equivocal *leakage of small GI content into Rt paracolic gutter may mimic appendicitis *Duodenal, antral, and gastric body ulcers account for 60, 20, and 20 % of perforations respectively *MR—10-20%, higher in gastric perforation
- Conservative Rx- perforation>24 hrs -stable pt -no peritonitis -radiologic evidence of sealed perforation Choice of Operation for Peptic Ulcer. PUD depends on a variety of factors, including the type of ulcer (duodenal, gastric, recurrent, or marginal), the indication for operation, and the condition of the patient. Other important considerations are intra-abdominal factors (duodenal scarring/inflammation, adhesions, or difficult exposure), the ulcer diathesis status of the patient, the surgeon’s experience and personal preference, whether H pylori infection is present, the need for NSAID therapy, previous treatment, and the likelihood of future compliance with treatment. HSV it has higher recurrent ulcer rate than the other procedures 10-20 It is not useful for type ii or type iii gastric ulcers or for complicated pud five types of gastric ulcer are described, although the original Johnson classification contained three types (Fig. 26-30). The most common, Johnson type I gastric ulcer, is typically located near the angularis incisura on the lesser curvature, close to the border between antral and corpus mucosa. Patients with type I gastric ulcer usually have normal or decreased acid secretion. Type II gastric ulcer is associated with active or quiescent duodenal ulcer disease, and type III gastric ulcer is prepyloric ulcer disease. Both type II and type III gastric ulcers are associated with normal or increased gastric acid secretion and surgically are treated similar to duodenal ulcer. Type IV gastric ulcers occur near the GE junction, and acid secretion is normal or below normal. Type V gastric ulcers are medication induced and may occur anywhere in the stomach. Patients with gastric ulcers may have weak mucosal defenses that permit an abnormal amount of injurious acid backdiffusion into the mucosa.
- A patch of omentum is brought without tension and positioned over the perforation, and the sutures are successively tied from the superior to the inferior aspect across the omental patch to anchor the omental graft in place. The applied tension to the sutures should be strong enough to stabilize the omentum in place but loose enough to preserve the omental blood supply.[3,4,5] Strangulation of the omental patch due to increased tension on the knots is associated with a failure of the repair and continued postoperative leakage. [3,4,5]There are many modifications to the same that has been described. In this article we add yet another technique to the armamentarium of surgeons to tackle duodenal perforation. Cellan-Jones (1929) The classic pedicled omental accepted as the gold standard treatment erroneously attributed to Graham (1937) Roscoe Graham (1937) use of a free graft of the omentum 3 sutures classically used with a piece of omentum graft laid over these sutures, which are then tied Karanjia technique: modified Cellan-Jones omental pedicle is secured to the tip of a NGT passed through the PDU. NGT withdrawn for 5-6 cms before the omentum is secured to healthy serosa “Omentoplasty” - on lay patch with pedicle Suture closure of ulcer – sutures not cut Segment of omentum secured on top of the closed perforation with same suture Concerns: Poor seal obtained when suture knots interposed between duodenal serosa and the omental patch The apposition of omentum is not as broad as with original described omental patch
- Serosal patch recognized as a quicker way of closing a failed patch…since patients may not tolerate…resection procedures
- Features of malignancy of the ulcer….and type of ulcer.
- Resection versus excision and patch…similar out come….risk of malignancy is not as preveously thought..
- Explain nissen and bancroft.
- Delayed gastric emptying: The stomach loses the vagally mediated receptive relaxation. This leads to an increased intragastric pressure causing an increase emptying of liquids. The pylorus does not relax effectively, and a decrease in solid food emptying is seen. This is the reason the majority of surgeons perform a concomitant drainage procedure at the time of TV. [14] Postvagotomy diarrhea: Results from unconjugated bile salts entering the colon thus leading to osmotic diarrhea. This complication is rarely seen with HSV but is the most common undesirable sequela of TV. It is first treated with codeine/loperamide along with cholestyramine.[15] If this fails, one can consider a reversed jejunal interposition graft.[16] Postvagotomy hypergastrinemia: The parietal cells are denervated causing a decrease in stomach acid output. This leads to G-cell hyperplasia and hypergastrinemia due to the loss of negative feedback mechanisms. Ulcer recurrence: TV has the lowest rate of ulcer recurrence compared to the other vagotomies. Recurrence is further prevented with the addition of an antrectomy. [7] Dumping syndrome: This typically is seen only when an antrectomy or drainage procedure is done concomitantly with a TV.
- Surgical mx of complications…