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  1. 1. Preoperative Case Presentation & Sharing of Information on Vomiting Jeffy G. Guerra, MD Level III Surgery Resident OMMC-Surgery 053006
  2. 2. General Data: C.P., 68F SAB, Mla
  3. 3. Chief Complaint: Vomiting
  4. 4. History of Present Illness: 8 years PTA epigastric pain, on/off, moderate, slightly relieved by antacid consult : ulcer
  5. 5. 1 year PTA Persistence of Ssx, consult Rx: Cimetidine lost to follow-up
  6. 6. 8 months PTA episodes of regurgitation, gastrointestinal reflux
  7. 7. 1 month PTA (+) black tarry stool no consult
  8. 8. 25 days PTA epigastric pain vomiting unrelieved by antacid, admitted: IV started, H2 block and BT, 2 units, apparently d/c well
  9. 9. 2 days PTA vomiting, 3x, nonprojectile, postprandial, partially digested food
  10. 10. Few hours PTA persistence, consult- admitted IM-ER Dx: UGIB 2 PUD R/O Gastric Malignancy CBC, PC, BT, CXR electrolytes done (+) Saline loading test BT, 2 u PRBC ordered
  11. 11. Course in the Ward: IM • NPO, NGT • Meds: – FeSO4 tab, TID – Ranitidine 50mg TIV, q12 • No Subjective complaints • PPE: E/N • Plan: EGD • Referred to Surgery
  12. 12. Past Medical History: NSAID use Family History: no history of cancer in the family Personal Social History: non-smoker non-alcoholic beverage drinker
  13. 13. Physical Examination: • Conscious, coherent, ambulatory, NICRD • BP:110/70 CR:75 RR:21 T:37ºC • Pale palpebral conjunctiva, anicteric sclerae • Supple neck, (-) cervical LAD • Symmetrical chest expansion, clear breath sounds • Adynamic precordium, normal rate & regular rhythm • Flat, NABS, soft, (+) slight Direct tenderness, epigastric area, no mass • DRE: (+) yellow feces on tactating finger
  14. 14. Salient Features: • 68F • Known case of PUD • Epigastric pain, • Gastrointestinal reflux, regurgitation • Vomiting • Slight tenderness Epigastric area • DRE: E/N
  15. 15. VOMITING Systemic Mechanical Neurologic Infectious UGIT LGIT Stomach Small BowelEsophagus Duodenum Colon Sphincter Fnxn Mechanical Obstruction Mechanical Obstruction A. Stricture B. Mass
  16. 16. Clinical Diagnosis: Diagnosis Certainty Treatment Gastric outlet obstruction 2 stenosis 2 PUD 70% Medical/Surgi cal Gastric Outlet obstruction 2 to gastric mass 30% Surgical
  17. 17. Do I need a para-clinical diagnostic procedure? Yes. • To increase the certainty of my primary diagnosis. • To determine my treatment plan
  18. 18. Para-clinical Diagnostic Procedure Benefit Risk Cost Availability UGIS Sn rate: 80-85% SP rate: 82% radiation 2k / Endoscopy with Biopsy Sn rate: 95% SP rate: 98% perforation 5k / CT scan Sn rate: 88% SP rate: 85% radiation 3k /
  19. 19. Endoscopy Result: Gastric Outlet Obstruction; pyloric channel, secondary to healed pyloric ulcer, 98% obstructing No Biopsy done
  20. 20. Pre-Treatment Diagnosis: Diagnosis Certainty Treatment Gastric outlet obstruction 2 stenosis 2 healed PUD 95% Surgical Gastric Outlet obstruction 2 to stenosis 2 malignancy 5% Surgical
  21. 21. Goals of Treatment: • Resolution of the obstruction • Maintenance of bowel continuity • No recurrence • No complications
  22. 22. TREATMENT OPTIONS BENEFIT RISK COST AVAILABI LITY Resolution of obstruction Bowel continuity Local recurrence Vagotomy + Antrectomy /// /// MR: 5% RR: 2% 3k / Vagotomy + Jaboulay gastroduod enostomy /// /// MR:1% RR: 10% 3k / Vagotomy + gastrojejun ostomy* /// /// MR: 1% RR: 1% 3k / Endoscopic baloon dilatation / /// MR: 1% RR: 50% 15k x *Csendes A. et al. RCT on three techniques for GOO treatment. *Millat B. Surgical treatment of complicated Duodenal ulcer: RCT
  23. 23. Pre-op preparation: what I will do • Informed consent secured • Psychosocial support provided • Optimized patient’s physical health – Correction of anemia/electrolytes – Nutritional build-up • Patient screened for any health condition • Operative materials secured
  24. 24. Intra-op Management: How I will do It (Vagotomy, Gastrojejunostomy) • Patient supine under GETA • Asepsis and antisepsis technique • Sterile drapes place • Long vertical incision from xyphoid to supraumbilical area
  25. 25. Mobilization of left lateral segment of the liver
  26. 26. Division of triangular ligament
  27. 27. Exposure of esophagogastric junction
  28. 28. Exposure of anterior vagus nerve
  29. 29. Isolation/ligation of nerve trunk, anterior, posterior and esophageal branches • Anterior vagal trunk is encircled with hook and dissected sharply from esophageal musculature • Nerve trunk is ligated proximally and distally
  30. 30. Drainage via Gastrojejunostomy
  31. 31. Anastomotic site
  32. 32. Posterior serosal suture
  33. 33. Gastric incision
  34. 34. Posterior mucosal suture
  35. 35. Anterior mucosal suture
  36. 36. Completion of anastomotic defect
  37. 37. Post-op Care
  38. 38. • Postoperative care: – Intravenous fluids – nasogastric decompression – Analgesics – hemodynamics • The nasogastric tube is removed upon return of gastrointestinal transit, and feeding is slowly begun.
  39. 39. Outcome: • Resolution of obstruction • Live patient • No complications • Satisfied patient • No medico-legal suit
  40. 40. Sharing of information
  41. 41. SURGERY FOR PEPTIC ULCER DISEASE(PUD) • Ulcer in the GIT is characterized by an interruption in the mucosa stretching through the muscularis mucosa into the submucosa or deeper • Location - in order of decreasing frequency – Duodenum – Stomach – Esophagus
  42. 42. Epidemiology   Gastric ulcer Duodenal ulcer Age 40 – 60 20 – 45 Sex M : V = 1.5 : 1 M : V = 3 : 1 Socio-economic Lower Higher Blood group A O
  43. 43. Classification of Gastric Ulcers(GU) ( Gaintree – Johnson ) • Type 1 = incisura on the lesser curvature. No increased acid secretion. Mucosal resistance problem. • Type 2 = Gastric and duodenal ulcer. Gastric ulcer secondary to gastric stases caused by duodenal ulcer. • Type 3 = Prepyloric ulcer within 2-3cm of the pylorus. Often acid hypersecretors. Association with blood group O. Treated like duodenal ulcer.
  44. 44. • Type 4(Csendes) = High on lesser curvature near gastro-esophageal junction. As Type 1. • Type 5 = Secondary to chronic use of non-steroidal anti-inflammatory drugs (NSAID). Can occur anywhere in the stomach.
  45. 45. Pathogenesis • Still debated • Traditionally duodenal ulcers are seen as a problem with acid hypersecretion and gastric ulcers as a mucosal resistance problem
  46. 46. Gastric acid. Central in pathogenesis – no benign ulceration occurs without gastric acid Gastric stases. Delayed emptying of normal amounts of acid with increased exposure
  47. 47. Enviromental factors are very important. a) Helicobacter pylori infection. 90% of patients with DU and 50% of patients with GU b) NSAID use. The mucus gel layer contains bicarbonate. This layer adheres to the gastric mucosa. It protects the mucosa against back diffusion of hydrogen ions. NSAID’s suppress mucus cell function. c) Smoking
  48. 48. 4) Mucosal resistance 5) Genetic predisposition
  49. 49. Clinical Picture
  50. 50. DUODENAL ULCER 1) Epigastric pain – Central or slightly to the right Burning or gnawing Can spread to the back Relieved by ingestion of food or anti-acid Pain occurs when patient is hungry
  51. 51. 2) Different degrees of nausea and vomiting 3) Weight gain ( Pain relieved by ingestion of food) 4) Epigastric tenderness just to the right of the midline, may be absent.
  52. 52. GASTRIC ULCER 1) Epigastric pain – Brought on by meals often within 30 minutes 2) Nausea and vomiting 3) Weight loss 4) Epigastric tenderness
  53. 53. Complications 1) Bleeding 2) Perforation 3) Gastric outlet obstruction 4) Penetration
  54. 54. Management • Surgery is indicated and for the following: 1) Non-healing ulcer ( 8 – 12 weeks for GU, DU can be managed conservatively for longer since the risk for malignancy is low) 2) Complications • a) Perforation b) Bleeding if massive, c) Gastric outlet obstruction that does not clear up on conservative management.
  55. 55. Surgical principle for definitive ulcer surgery
  56. 56. Definitive ulcer operations for GU • Type 1 GU partial gastrectomy. Vagotomy not done. • Type 2 and 3 GU treated as DU. HSV contra-indicated due to high ulcer recurrence with prepyloric ulcers. • Type 4 GU treated with partial gastrectomy and excision of a long tongue of lesser curvature including the ulcer(Pauchet procedure).
  57. 57. Gastric outlet obstruction • Cycles of inflammation and repair may cause obstruction at the gastroduodenal junction as a result of edema, muscular spasm and fibroses.
  58. 58. • Edema and spasm can resolve with medical treatment. • Obstruction is mainly caused by DU and prepiloric GU. • Malignant tumors is the other important cause of gastric outlet obstruction.
  59. 59. • normal pylorus is about 20 mm in diameter and can distend to 25 mm • gastric outlet obstruction occur when the diameter of the antroduodenal segment is below 10 mm • A saline load test can be utilized in the objective measurement of outlet obstruction or gastric atony and the assessment of response to therapy
  60. 60. • The major benign causes of GOO are PUD, gastric polyps, ingestion of caustics, pyloric stenosis, congenital duodenal webs, gallstone obstruction (Bouveret syndrome), pancreatic pseudocysts, and bezoars
  61. 61. Clinical picture • Longstanding history of PUD • Progressive worsening of ulcer pain and early satiety. • Vomiting after meals of partially digested food without bile ( food eaten earlier the day or the previous day). • Dehydration and severe weight loss.
  62. 62. • Visible peristalses of the dilated stomach (rarely). • Succussion splash audible with to and fro movement of abdomen. • Tetany in cases of advanced alkaloses. • Develop hyponatremic, hypokalemic, hypochloremic metabolic alkaloses
  63. 63. Management 1) Resussitation initially with 0.9% sodium chloride. Potassium supplementation only after good urine output is established. 2) Gastric lavage with thick stomach tube ( 32 F) to remove food residue. 3) Diagnostic tests after gastric lavage : Gastroscopy with biopsies with or without barium meal to rule out malignancy.
  64. 64. 4) IV H2-blockers or proton pump inhibitors. 5) A nasogastric tube is passed. The patient may drink water. The amount of oral intake and drainage is charted. This gives an impression whether the obstruction is resolving. 6) Balloon dilatation of pyloric channel is possible but seldom produces a final solution.
  65. 65. 7) Surgery is indicated if the obstruction does not resolve after one week of conservative treatment. Mostly a truncal vagotomy and antrectomy is done although truncal vagotomy with a drainage procedure is sometimes performed.
  66. 66. Complications of PUD surgery
  67. 67. Complications due to vagotomy • Intraoperative complications can occur with injury to adjacent structures. • Early post-operative complication – delayed gastric emptying – dysphagia and lesser curve necroses( lesser curve necroses specific to HSV). • Late complications include postvagotomy diarrhea, reflux esophagitis and gallstones
  68. 68. Complications of gastrectomy • Early complications – bleeding – anastomotic leakage – obstruction – hepatobiliary-pancreatic complications (pancreatitis, bile duct injury)
  69. 69. • Late complications are classified as follows : – 1) Ulcer recurrence a) Recurrent ulcer (anastomotic,stomal,marginal) b) gastrojejenocolic fistula
  70. 70. 2) Mechanical problems a) Chronic afferent loop obstruction after BII anastomoses – abdominal pain relieved by vomiting , vomit mainly bile without food. b) Chronic efferent loop obstruction c) Internal herniation, jejenogastric intussusception and late gastroduodenal obstruction
  71. 71. 3) Pathophysiologic problems a) Alkaline reflux gastritis – reflux of bile into stomach. Pain not relieved with vomiting. Vomitus contains food and bile. b) Dumping(I)Early dumping – symptoms within 20 minutes after meal. Gastro-intestinal : Abdominal cramps, satiety, nausea, vomiting and explosive diarrhea. Cardiovascular : sweating, dizziness, weakness,dyspnea, palpitations and flushing.
  72. 72. – Due to sudden release of high osmolality chyme into duodenum with fluid shifts and release of gastro-intestinal hormones. • (II) Late dumping – only vasomotor symptoms. Caused by enteroglucagon secretion which leads to increased and prolonged insulin secretion with resultant hypoglycaemia.
  73. 73. 4) Malabsorption and Nutritional problems a) Malabsorption of protein, carbohydrates and fat b) Early satiety c) Anemia : Fe, folate and B12 deficiency. B12 problems mostly after total or near total gastrectomy. d) Osteopmalacia
  74. 74. References: 1. Csendes A. Maluenda F. et al. Prospective randomized controlled trial comparing three surgical techniques for the treatment of gastric outlet obstruction secondary to duodenal ulcer. Am J Surg. 1993 Jul 166:45-49 2. Edwards LW, Herrington JL Jr. Vagotomy and gastroenterostomy—vagotomy and conservative gastrectomy. Ann Surg, 1953; 137: 873– 83. 3. Emas S, Fernstrom M. Prospective, randomized trial of selective vagotomy with pyloroplasty and selective proximal vagotomy with and without pyloroplasty in the treatment of duodenal, pyloric and prepyloric ulcers. Am J Surg, 1985; 149: 236–43. 4. Fischer AB. Twenty-five years after Billroth II gastrectomy for duodenal ulcer. World J Surg, 1984; 8: 293–302. 5. Kuwada, S et al. Long-term outcome of endoscopic dilation of nonmalignant pyloric stenosis. Gastrointestinal Endoscopy 1995; 41(1) 15-17. 6. Gibson JB, Behrman SW, Fabian TC: Gastric outlet obstruction resulting from peptic ulcer disease requiring surgical intervention is infrequently associated with Helicobacter pylori infection. J Am Coll Surg 2000 Jul; 191(1): 32-7[Medline].
  75. 75. 7.Millat B, Fingerhut A et al. surgical treatment of complicated duodenal ulcer. Controlled trial. World J Surg. 2000 Mar. 24(3) 299-306. 8. Siu WT, Tang CN, Law BK, et al: Vagotomy and gastrojejunostomy for benign gastric outlet obstruction. J Laparoendosc Adv Surg Tech A 2004 Oct; 14(5): 266- 9[Medline]. 9. Haglund UH, Jansson RL, Lindhagen JG, Lundell LR, Svartholm EG, Olbe LC.Primary Roux-Y gastrojejunostomy versus gastroduodenostomy after antrectomy and selective vagotomy.Am J Surg. 1992 Apr;163(4):457-8.
  76. 76. Questions 1. Gastric Outlet Obstruction secondary to healed pyloric ulcer may present with which of the following? a. vomiting b. hyponatremia c. hypochloremia d. epigastric pain e. All of the above
  77. 77. 2. What is the most common complication of peptic ulcer disease? a. bleeding b. perforation c. intractability d. obstruction
  78. 78. 3. The following statements is/are true regarding gastric outlet obstruction. 1. Cycles of inflammation and repair may cause obstruction at the gastroduodenal junction as a result of edema, muscular spasm and fibroses. 2. Edema and spasm can resolve with medical treatment. 3. Obstruction is mainly caused by DU and prepiloric GU. 4. Malignant tumors is the other important cause of gastric outlet obstruction.
  79. 79. 4. Which of the following choices is/are late complication/s of vagotomy? 1. postvagotomy diarrhea, 2. reflux esophagitis and 3. Gallstones 4. Delayed gastric emptying
  80. 80. 5. Which of the following is/are not early complication of gastric surgery ? 6. Bleeding 7. anastomotic leakage 8. hepatobiliary-pancreatic complications (pancreatitis, bile duct injury) 9. gastrojejenocolic fistula
  81. 81. Thank you!