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    ppt ppt Presentation Transcript

    • Preoperative Case Presentation & Sharing of Information on Vomiting Jeffy G. Guerra, MD Level III Surgery Resident OMMC-Surgery 053006
    • General Data:
      • C.P., 68F
      • SAB, Mla
    • Chief Complaint:
      • Vomiting
    • History of Present Illness:
      • 8 years PTA epigastric pain, on/off, moderate, slightly relieved by antacid consult : ulcer
      • 1 year PTA Persistence of Ssx, consult
      • Rx: Cimetidine
      • lost to follow-up
      • 8 months PTA episodes of regurgitation,
      • gastrointestinal reflux
      • 1 month PTA (+) black tarry stool
      • no consult
      • 25 days PTA epigastric pain vomiting unrelieved by antacid,
      • admitted: IV started, H2 block and BT, 2 units,
      • apparently d/c well
      • 2 days PTA vomiting, 3x, nonprojectile, postprandial, partially digested food
      • 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
    • 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
      • Past Medical History: NSAID use
      • Family History: no history of cancer in the family
      • Personal Social History: non-smoker
      • non-alcoholic beverage drinker
      • Physical Examination:
          • Conscious, coherent, ambulatory, NICRD
          • BP:110/70 CR:75 RR:21 T:37 ºC
          • 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
    • Salient Features:
      • 68F
      • Known case of PUD
      • Epigastric pain,
      • Gastrointestinal reflux, regurgitation
      • Vomiting
      • Slight tenderness Epigastric area
      • DRE: E/N
    • VOMITING Systemic Mechanical Neurologic Infectious UGIT LGIT Stomach Small Bowel Esophagus Duodenum Colon Sphincter Fnxn Mechanical Obstruction
      • Mechanical Obstruction
      • Stricture
      • Mass
    • Clinical Diagnosis: Surgical 30% Gastric Outlet obstruction 2 to gastric mass Medical/Surgical 70% Gastric outlet obstruction 2 stenosis 2 PUD Treatment Certainty Diagnosis
    • Do I need a para-clinical diagnostic procedure?
      • Yes.
      • To increase the certainty of my primary diagnosis.
      • To determine my treatment plan
    • Para-clinical Diagnostic Procedure / 5k perforation Sn rate: 95% SP rate: 98% Endoscopy with Biopsy / 3k radiation Sn rate: 88% SP rate: 85% CT scan / 2k radiation Sn rate: 80-85% SP rate: 82% UGIS Availability Cost Risk Benefit
    • Endoscopy Result: Gastric Outlet Obstruction; pyloric channel, secondary to healed pyloric ulcer, 98% obstructing No Biopsy done
    • Pre-Treatment Diagnosis: Surgical Surgical Treatment 95% Gastric outlet obstruction 2 stenosis 2 healed PUD 5% Gastric Outlet obstruction 2 to stenosis 2 malignancy Certainty Diagnosis
    • Goals of Treatment:
          • Resolution of the obstruction
          • Maintenance of bowel continuity
          • No recurrence
          • No complications
    • TREATMENT OPTIONS *Csendes A. et al. RCT on three techniques for GOO treatment. *Millat B. Surgical treatment of complicated Duodenal ulcer: RCT x 15k MR: 1% RR: 50% /// / Endoscopic baloon dilatation / 3k MR: 1% RR: 1% /// /// Vagotomy + gastrojejunostomy* / 3k MR: 5% RR: 2% /// /// Vagotomy + Antrectomy / 3k MR:1% RR: 10% /// /// Vagotomy + Jaboulay gastroduodenostomy Bowel continuity Local recurrence Resolution of obstruction AVAILABILITY COST RISK BENEFIT
    • 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
    • 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
    • Mobilization of left lateral segment of the liver
    • Division of triangular ligament
    • Exposure of esophagogastric junction
    • Exposure of anterior vagus nerve
    • 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
    • Drainage via Gastrojejunostomy
    • Anastomotic site
    • Posterior serosal suture
    • Gastric incision
    • Posterior mucosal suture
    • Anterior mucosal suture
    • Completion of anastomotic defect
    • Post-op Care
      • Postoperative care:
        • Intravenous fluids
        • nasogastric decompression
        • Analgesics
        • hemodynamics
      • The nasogastric tube is removed upon return of gastrointestinal transit, and feeding is slowly begun.
    • Outcome:
          • Resolution of obstruction
          • Live patient
          • No complications
          • Satisfied patient
          • No medico-legal suit
    • Sharing of information
      • 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
    • Epidemiology O A Blood group Higher Lower Socio-economic M : V = 3 : 1 M : V = 1.5 : 1 Sex 20 – 45 40 – 60 Age Duodenal ulcer Gastric ulcer  
    • 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.
      • 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.
    • Pathogenesis
      • Still debated
      • Traditionally duodenal ulcers are seen as a problem with acid hypersecretion and gastric ulcers as a mucosal resistance problem
      • Gastric acid. Central in pathogenesis – no benign ulceration occurs without gastric acid
      • Gastric stases. Delayed emptying of normal amounts of acid with increased exposure
      • 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
      • 4)    Mucosal resistance
      • 5)    Genetic predisposition
    • Clinical Picture
      • 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
      • 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.
      • 1)    Epigastric pain – Brought on by meals often within 30 minutes
      • 2)    Nausea and vomiting
      • 3)    Weight loss
      • 4)    Epigastric tenderness
    • Complications
      • 1)    Bleeding
      • 2)    Perforation
      • 3)    Gastric outlet obstruction
      • 4)    Penetration
    • 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.
    • Surgical principle for definitive ulcer surgery
    • 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).
    • Gastric outlet obstruction
      • Cycles of inflammation and repair may cause obstruction at the gastroduodenal junction as a result of edema, muscular spasm and fibroses.
      • 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.
      • 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
      • 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
    • 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.
      • 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
    • 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.
      • 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.
      • 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.
    • Complications of PUD surgery
    • 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
    • Complications of gastrectomy
      • Early complications
        • bleeding
        • anastomotic leakage
        • obstruction
        • hepatobiliary-pancreatic complications (pancreatitis, bile duct injury)
      • Late complications are classified as follows :
        • 1)    Ulcer recurrence
          • a) Recurrent ulcer (anastomotic,stomal,marginal)
          • b) gastrojejenocolic fistula
      • 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
      • 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.
        • 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.
      • 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
    • References:
      • 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
      • Edwards LW, Herrington JL Jr. Vagotomy and gastroenterostomy—vagotomy and conservative gastrectomy. Ann Surg, 1953; 137: 873– 83.
      • 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.
      • Fischer AB. Twenty-five years after Billroth II gastrectomy for duodenal ulcer. World J Surg, 1984; 8: 293–302.
      • Kuwada, S et al. Long-term outcome of endoscopic dilation of nonmalignant pyloric stenosis. Gastrointestinal Endoscopy 1995; 41(1) 15-17.
      • 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] .
      • 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.
    • Questions
      • Gastric Outlet Obstruction secondary to healed pyloric ulcer may present with which of the following?
      • vomiting
      • hyponatremia
      • hypochloremia
      • epigastric pain
      • All of the above
      • 2. What is the most common complication of peptic ulcer disease?
      • bleeding
      • perforation
      • intractability
      • obstruction
      • 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.
      • 4. Which of the following choices is/are late complication/s of vagotomy?
      • postvagotomy diarrhea ,
      • reflux esophagitis and
      • Gallstones
      • Delayed gastric emptying
      • Which of the following is/are not early complication of gastric surgery ?
      • Bleeding
      • anastomotic leakage
      • hepatobiliary-pancreatic complications (pancreatitis, bile duct injury)
      • gastrojejenocolic fistula
    • Thank you!