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Peptic ulcer disease

Peptic ulcer disease

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Peptic ulcer disease

  1. 1. PEPTIC ULCER DISEASE Dr. Lala Robin. MS Gen. Surgery. Senior Resident CMC
  2. 2. Definition  Peptic ulcers are defined as erosions in the gastric or duodenal mucosa that extend through the muscularis mucosae.  Benign Gastric Ulcer  Duodenal Ulcer
  3. 3. Pathogenesis Protective (or defensive) factors  mucosal bicarbonate secretion,  mucus production,  blood flow,  growth factors,  cell renewal,  endogenous prostaglandins
  4. 4. Damaging (or aggressive) factors  hydrochloric acid secretion,  pepsins,  ethanol ingestion, smoking,  duodenal reflux of bile,  ischemia, hypoxia,  H. pylori infection.  NSAIDs.
  5. 5. Helicobacter pylori Infection  H. pylori is a spiral or helical gram-negative rod with four to six flagella that resides in gastric-type epithelium within or beneath the mucous layer. This location protects the bacteria from acid and antibiotics. Its shape and flagella aid its movement through the mucous layer, and it produces enzymes that help it adapt to this hostile environment.  Most notably, H. pylori is a potent producer of urease, which is capable of splitting urea into ammonia and bicarbonate, creating an alkaline microenvironment in the setting of an acidic gastric milieu.  H. pylori organisms are microaerophilic and can live only in gastric epithelium.
  6. 6. mechanisms responsible for H. pylori– induced GI injury  Production of toxic products that cause local tissue injury - Infection with H. pylori leads to the disruption of the gastric mucous barrier by the enzymes produced by the organism.  Induction of a local mucosal immune response.  Increased gastrin levels with a resultant increase in acid secretion.  Gastric metaplasia occurring in the duodenum  protective response to decreased duodenal pH  allows H. pylori to colonize these areas of the duodenum  Some strains of H. pylori produce cytotoxins, notably the Cag A and Vac A products, and the production of cytotoxins seems to be associated with the ability of the organism to cause gastritis, peptic ulceration and cancer.
  7. 7.  The causative role of H. pylori infection in the pathogenesis of gastritis and PUD was first elucidated by Marshall and Warren in Australia in 1984.  To prove this connection, Marshall himself ingested inocula of H. pylori after first confirming that he had normal gross and microscopic gastric mucosa. Within days, he developed abdominal pain, nausea, and halitosis as well as histologically confirmed presence of gastric H. pylori infection.  Warren and Marshall, received the Nobel Prize for Medicine and Physiology in 2005.  H. pylori is now classed by the World Health Organisation as a class 1 carcinogen
  8. 8. RUT kit  done in antral biopsy • 13 C and 14 C breath tests and the CLO test • Giemsa or the Warthin– Starry stains, and culture
  9. 9. H. Pylori Eradication  PPI + Clarithromycin + Amoxicillin  PPI + Clarithromycin + Metronidazole  Duration – 14 days.  PPI to be continued.  Ulcer healing to be checked after 8-12 weeks with endoscopy. Then PPI can be stopped.  The profound hypochlorhydria produced by proton pump inhibitors combined with antibiotics is also effective in eradicating the organism.
  10. 10. NONSTEROIDAL ANTIINFLAMMATORY DRUGS AND ULCER DISEASE  NSAIDs increase the risk of peptic ulcers.  NSAIDs are the most commonly identified risk factor for peptic ulcer bleeding, especially in older adults; the risk is drug specific and dose dependent.  NSAIDs decrease the mucosal defense by suppression of prostaglandin synthesis in gastric and duodenal mucosa  Acid suppression is the mainstay in the therapy of NSAID-associated ulcer disease.
  11. 11. LOW-DOSE ASPIRIN AND ULCER DISEASE  Even at very low doses (75 mg daily), aspirin decreases gastric mucosal prostaglandin levels and can cause significant gastric lesions.  PPI given with low-dose aspirin, can significantly decrease the risk of developing peptic ulceration
  12. 12. ACID HYPERSECRETORY STATES AND ULCER DISEASE  Zollinger-Ellison (ZE) syndrome – gastrinoma  Anastomotic or Marginal Ulceration
  13. 13. SEVERE SYSTEMIC DISEASE (STRESS ULCER)  A breakdown of the gastroduodenal mucosal barrier, often a result of severe physiologic stress and splanchnic hypoperfusion, combined with gastric acid may lead to ulceration and bleeding.  It can develop within hours in critically ill patients, typically starting in the fundus and spreading distally.  Head Injury  Cushing ulcer  Extensive burns  Curling ulcer
  14. 14. Duodenal ulceration
  15. 15. Incidence  Incidence has come down drastically due to wide spread use of gastric antisecretory agents and H. pylori eradication therapy  peak incidence is now in a much older age group than previously  more common in men
  16. 16. Pathology  Most occur in the first part of the duodenum  A chronic ulcer penetrates the mucosa and into the muscle coat, leading to fibrosis  pyloric stenosis  kissing ulcers - a posterior and an anterior duodenal ulcer  Anteriorly placed ulcers tend to perforate  posterior duodenal ulcers tend to bleed, sometimes by eroding into the gastroduodenal artery.
  17. 17. Histopathology  destruction of the muscular coat is observed  base of the ulcer is covered with granulation tissue,  the arteries in this region showing the typical changes of endarteritis obliterans
  18. 18. Clinical Manifestations  midepigastric abdominal pain  relieved by food intake  When the pain becomes constant, this suggests that there is deeper penetration of the ulcer.  Referral of pain to the back is usually a sign of penetration into the pancreas.  Diffuse peritoneal irritation is usually a sign of free perforation
  19. 19. Diagnosis  Routine laboratory studies include complete blood count; liver chemistries; and serum creatinine, serum amylase, and calcium levels.  A serum gastrin level should also be obtained in patients with ulcers that are refractory to medical therapy or require surgery.  An upright chest radiograph is usually performed when ruling out perforation.
  20. 20. Upper gastrointestinal radiography  demonstration of barium within the ulcer crater, which is usually round or oval and may or may not be surrounded by edema  with double-contrast studies, 80% to 90% of ulcer craters can be detected
  21. 21. Flexible upper endoscopy  most reliable method for diagnosing gastric and duodenal ulcers.  visual diagnosis  endoscopy provides the ability to sample tissue to evaluate for malignancy and H. pylori infection Duodenal Ulcer Benign Healing Gastric Ulcer
  22. 22. Helicobacter pylori testing  The gold standard for diagnosis of H. pylori is mucosal biopsy performed during upper endoscopy  evaluation of biopsy samples with either a urease assay or histologic examination  Culturing of gastric mucosa obtained at endoscopy  can also be performed to diagnose H. pylori. The sensitivity is approximately 80%, and specificity is 100%
  23. 23. H. Pylori – Non-invasive testing  Serology  used to test for the presence of IgG antibodies to H. pylori  Antibody titers can remain high for 1 year or longer; consequently, this test cannot be used to assess eradication after therapy  Urea breath test  The carbon-labeled urea breath test is based on the ability of H. pylori to hydrolyze urea as a result of its production of urease  Stool antigen  H. pylori bacteria are present in the stool of infected patients
  24. 24. Treatment  Medical management  Antiulcer drugs fall into three broad categories— 1. drugs targeted against H. pylori, 2. drugs that reduce acid levels by decreasing secretion or chemical neutralization, and 3. drugs that increase the mucosal protective barrier.
  25. 25. Surgical Treatment Recommendations for Complications Related to Peptic Duodenal Ulcer Disease  Intractable: Parietal cell vagotomy ± antrectomy  Bleeding: Oversewing of bleeding vessel with treatment of H. pylori  Perforation: Patch closure with treatment of H. pylori  Obstruction: Rule out malignancy and gastrojejunostomy with treatment of H. pylori
  26. 26. Bleeding Duodenal Ulcer  Upper GI bleeding  Most nonvariceal bleeding (70%) is attributable to peptic ulcers  The initial approach to an upper GI bleed is similar to the approach to a trauma patient. Large-bore intravenous access, rapid restoration of intravascular volume with fluid and blood products as the clinical situation dictates, and close monitoring for signs of rebleeding all are essential to effective management of these patients.  NG tube placement  all patients with a potentially substantial acute upper GI bleed should undergo endoscopy within 24 hours
  27. 27. Bleeding Duodenal Ulcer • The most commonly used system for classifying the endoscopic appearance of bleeding ulcers is the Forrest classification
  28. 28. Bleeding Duodenal Ulcer  All patients undergoing endoscopic examination should be tested for H. pylori status.  For high-risk patients requiring intervention, the best initial approach is endoscopic control, which results in primary hemostasis in approximately 90% of patients. The most common method of control is injection of a vasoconstrictor at the site of bleeding.  Thermocoagulation, clipping  All high-risk patients should be placed in a monitored setting, preferably an intensive care unit, until all bleeding has stopped for 24 hours.  all highrisk patients should be placed on a PPI administered intravenously, with an initial bolus followed by continuous infusion or intermittent dosing for up to 72 hours.  catheter-directed angiography and endovascular embolization
  29. 29. Bleeding Duodenal Ulcer - Surgery  upper midline laparotomy  anterior wall of the duodenal bulb is opened longitudinally, and the incision can be carried across the pylorus.  The gastroduodenal artery is oversewn, with a three-point U stitch technique, which effectively ligates the main vessel (superior and inferior stitches) and prevents back-bleeding from any smaller branches (medial stitch), such as the transverse pancreatic artery  duodenotomy is closed transversely to avoid narrowing
  30. 30. Duodenal Ulcer Perforation  sudden-onset, severe epigastric pain  free air visible on the chest radiograph  diffuse peritonitis  first portion of the duodenum
  31. 31. Duodenal Ulcer Perforation - management  Resuscitation  NG tube placement  Laparotomy  The most important component of the operation is a thorough peritoneal toilet to remove all of the fluid and food debris.  place an omental patch over the perforation  For very large perforations (>3 cm) - jejunal serosa (Thal patch), pyloric exclusion procedure
  32. 32. Gastric outlet obstruction  Acute inflammation of the duodenum  functional gastric outlet obstruction  delayed gastric emptying, anorexia, nausea, and vomiting  patients may become dehydrated and develop a hypochloremic hypokalemic metabolic alkalosis secondary to the loss of gastric juice rich in hydrogen and chloride  Chronic inflammation of the duodenum fibrosis and stenosis of the duodenal lumen  painless vomiting of large volumes of gastric contents, with metabolic abnormalities  Endoscopic dilation and H. pylori eradication are the mainstays of therapy  Patients with refractory obstruction are best managed with primary antrectomy and reconstruction along with vagotomy.
  33. 33. Intractable peptic ulcer disease  failure of an ulcer to heal after an initial trial of 8 to 12 weeks of therapy or if patients relapse after therapy has been discontinued.  rule out gastrinoma  truncal vagotomy, selective vagotomy, or highly selective vagotomy, with or without an antrectomy.
  34. 34. Surgical procedures for peptic ulcers Truncal Vagotomy
  35. 35. Selective Vagotomy
  36. 36. Parietal Cell Vagotomy
  37. 37. Gastric Ulcers  Gastric ulcers can occur at any location in the stomach, although they usually manifest on the lesser curvature, near the incisura.  Modified Johnson Classification
  38. 38.  H. pylori and NSAIDs are the important aetiological factors.  Gastric ulceration is also associated with smoking  Chronic gastric ulcers are much more common on the lesser curve (especially at the incisura angularis)  Large chronic ulcers may erode posteriorly into the pancreas and, on other occasions, into major vessels such as the splenic artery. Less commonly, they may erode into other organs such as the transverse colon
  39. 39. Malignancy in gastric ulcers  any gastric ulcer should be regarded as being malignant, no matter how classical the features of a benign gastric ulcer. Multiple biopsies should always be taken
  40. 40. Thank you

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