1. GASTRIC OUTLETOBSTRUCTION

2. STOMACH SAC-LIKE ORGAN LOCATED MOSTLY IN THE LEFTUPPER PART OF THE ABDOMEN HAS 2 SURFACES (ANTERIOR & POSTERIOR), 2CURVATURES (GREATER & LESSER), & 4 REGIONS(CARDIA, FUNDUS, PYLORUS,& ANTRUM The gastric wall is made up of 4 layers: mucosa,submucosa, muscularis propria, and serosa 3. STOMACH The mucosa forms thick longitudinally oriented foldsor rugae which flatten with distention. The muscularis propria is a combination of 3 musclelayers: inner oblique, middle circular and outerlongitudinal 4. STOMACH 5. STOMACH 6. STOMACH It functions primarily as a reservoir to store large quantitiesof recently ingested food Its volume ranges from about 30ml in a neonate to 1.5 to 2Lin adulthood. The gastroesophageal junction generally lies to the left ofthe 10th thoracic vertebral body, 1-2cm below thediaphragmatic hiatus. The gastroduodenal junction lies at L1 and generally to theright of the midline, but may be lower 7. STOMACH ANTERIOR RELATIONS DIAPHRAGM, ANTERIORABDOMINAL WALL, LEFT COSTAL MARGIN, & THELEFT LOBE OF THE LIVER POSTERIOR RELATIONS LESSER SAC, PANCREAS,LEFT SUPRARENAL GLAND, LEFT KIDNEY, SPLEEN,SPLENIC ARTERY, & THE TRANVERSE COLON SUPERIOR RELATIONS LEFT DOME OF THEDIAPHRAGM 8. POSTERIOR RELATIONS 9. STOMACH BLOOD SUPPLY: FROM THE COELIAC AXIS LEFT GASTRIC, SPLENIC (SHORT GASTRIC & LEFT GASTROEPIPLOIC), HEPATIC (GASTRODUODENAL[SUPERIOR PANCREATICODUODENAL & RIGHT EPIPLOIC], CYSTIC, & RIGHT GASTRIC) 10. STOMACH 11. STOMACH NERVE SUPPLY: VAGUS (ANTR & POSTR) The vagus constitutes the motor and secretory nerve supply for the stomach. When divided, in the operation of vagotomy, the neurogenic (reflex) gastric acid secretion is abolished but the stomach is, at the same time, rendered atonic so that it empties only with difficulty 12. STOMACH ; because of this, total vagotomy must always beaccompanied by some sort of drainage procedure, either apyloroplasty (to enlarge the pyloric exit and render thepyloric sphincter incompetent) or by a gastrojejunostomy(to drain the stomach into the proximal small intestine).Drainage can be avoided if the nerve of Latarjet ispreserved, thus maintaining the innervation and functionof the pyloric antrum (highly selective vagotomy). 13. STOMACH The sympathetic innervation is derived from preganglionic fibers arising predominantly from T6 to T8 spinal nerves. 14. STOMACH LYMPHATIC DRAINAGE: DIV INTO 3 AREAS, HOWEVER ALL DRAIN EVENTUALLY TO THE PARAAORTIC NODES 15. STOMACH 16. BARIUM MEAL TRACING 17. DUODENUMDUODENUM 25cm LONG, C-SHAPED CURVE AROUND THE HEAD OF THE PANCREAS,DIVIDED INTO 4 PARTS 1ST PART 5cm LONG, ASCENDS FROM THE GASTRODUODENAL JUNCTION,OVERLAPPED BY THE LIVER & GALL BLADDER IMMEDIATELY POSTR ARE THE PORTAL VEIN, COMMON BILE DUCT &GASTRODUODENAL ARTERY SEPARATING IT FROM THE INFERIOR VENACAVA 2nd PART 7.5CM LONG, DESCENDS IN A CURVE AROUND THE HEAD OFPANCREAS, CROSSED BY THE TRANSVERSE COLON & LIES ON THERIGHT KIDNEY AND URETER 18. DUODENUM 3rd PART 10cm LONG, RUNS TRANSVERSELY TO THE LEFTCROSSING THE INFERIOR VENA CAVA, AORTA & L3VERT 4th PART ASCENDS UPWARDS & TO THE LEFT TO END AT THEDUODENOJEJUNAL JUNCTION BLOOD SUPPLY THE SUPERIOR & INFERIORPANCREATICODUODENAL ARTERIES 19. DUODENUM The luminal surface of the duodenum is lined withmucosa, forming circular folds known as the plicaecirculares or valvulae conniventes The duodenal bulb has smooth, featureless mucosa The duodenal wall is composed of outer longitudinal andinner circular muscle layers The first few centimeters of the duodenum areintraperitoneal, whereas the remainder is retroperitoneal 20. PATHOLOGY OF GASTRIC OUTLETOBSTRUCTION FOLLOWINGCHRONIC PEPTIC ULCER DISEASE 21. OUTLINE Introduction/Definition Epidemiology Etiology Pathology/Pathophysiology Complications 22. INTRODUCTION Gastric outlet obstruction is not a single entity. GOO is the clinical and pathophysiologicalconsequence of any symptom complex that produce amechanical impediment to gastric emptying. It usually follows chronic PUD 23. Introduction contd GOO is a common and early complication of DU in Africa and India 24. Epidemiology Incidence of GOO has been reported to be less than5% in patients with PUD Though is the leading benign cause GOO Peri-pancreatic malignancy is the leading malignantcause FMC Owerri (jan 2011 oct 2012) 7 cases of GOO 3 PUD, all male 4 gastric ca 25. Etiology The factors predisposing to chronicity of PUD may include:- persistent imbalance between theaggressive and defensive factors- non eradication of H. pylori infection- non compliance to anti PUDmedication etc. 26. Etiology contd However, GOO usually occur at the pyloro-duodenalarea. It is caused by:- cicatrization- edema- pyloro-duodenal spasm 27. Pathogenesis/ pathophysiology Obstruction of the stomachhypertrophy of the stomachDilatationGastritis &depressed acid secretion 28. Complications /Effects Malnourishment weight loss Iron deficiency anaemia Vomiting of gastric content resulting in:- dehydration- shock- electrolyte imbalance( Na, Cl, K)- metabolic alkalosis-paradoxic aciduria- acute kidney injury 29. HISTORY AGE:20-45 years with peak 30-35 years Known or suspected case of chronic pud Epigastric and Lt hypochondrial pain :-relieved by alkali, milk +/- food.-gnawing/biting-periodic (spontanous healing)-association with food and time of day-radiates to the back (?pancrease penetration-Generalised (perforation) 30. Anorexia,nausea. Easy satiety Vomiting: -characteristic unpleasant -copious -projectile -Non bilous -Food taken several days ago. 31. Feeling of unwell Appetite is maintained but fear of pain often prevent patient from eating Weight loss. Abdominal swelling 32. Examination Chronically ill looking Wasted Dehydrated may be pale shock 33. Epigastric/Rt hypochondrial tenderness Distended abdomen Visible gastric peristalsis Succussion splash 34. investigations1) Stabilise patient FBC (anaemia) SEUCR (hypochloraemia, hypokalaemia,hyponatraemia,elevated Hco3) BLOOD GASES(metabolic alkalosis) URINALYSIS (paradoxical aciduria) 35. investigation2)To confirm diagnosis Plain x-ray of abdomen:shows large gastric shadow and a large amount of gastric fluid. Gastric aspiration:a wide bore stomach tube is placed early in the morning and the stomach is aspirated of resting juice.if >400ml of juice is obtained a presumptive diagnosis of GOO can be made. 36. investigation Esophagogastroduodenoscopy + biopsy(histology and bacterioloical investigation).Aim is to viualise the stomach mucosa and any ulcer. Barium meal: -markely dilated stomach with a lot of residue -presence of an ulcer crater -trifoil deformity of the duodenal cap. 37. .-Hour glass deformity-Tea cup deformity-Abrupt obstruction to barium 38. 3)Pre- op preparation FBC SEUCR Urinalysis RVS 39. 4)Detection of H.pylori Non invasive:serologycarbon labelled urea breath test Invasive: Rapid urease test,histology and culture. 40. OUTLINEINTRODUCTION;PRINCIPLES OF TREATMENT; -Objectives(Goals) of mgt. -Factors influencing choice of rx. -Patient selection.GENERAL MEASURES;SPECIFIC/DEFINITIVE MEASURES; 41. OutlineCOMLICATIONS(& their mgt);FOLLOW UP;PROGNOSIS;CHALLENGES;CONCLUSION. 42. INTRODUCTION.PUD,largely medically condition.Becomes a surgical pathology when complicated e.g8-20% of patients developing complications only require surgery.It largely describes a surgically amenable pathology. 43. Introdefinitions.PUD:Break in acid secreting GIT mucosa; exposed to acid and pepsin secretn; more than 5mm in diameter;heals by granulation tissue formation.Erosion: Break in GI mucosa;not penetrating musclaris mucosa;7days, marked weight loss 53. GeneralX)Antsecretory therapy:IV PPI e.g 40mg of Omeprazole stat then 20mg 12hrlyNB:Should be discontinued 72hrs before surgery(return of g acidity) 54. SPECIFIC/DEFINITIVE MEASURESNONOPERATIVE MEASURES:i)Warm Saline Lavage+H.PyloriEradication(usu for acuteedematous active ulcer)Recurrencehigh in chronic active edematousulcers.ii)Endoscopic Balloon dilation.Maybe useful in elderly frail patientsunfit for surgery.Repeat necessary. 55. SPECIFIC/DEFINITIVE MEASURE.OPERATIVE MEASURES:Operative Principle:i-Surgically achieving physiologiccontrol of acid production;ii-Ensuring normal gutcontinuity(Resection andReconstruction);iii-Minimizing Postgastrectomy&Postvagotomy sequalae. 56. ..contdGuiding Principlescontdiv-Postvagotomy Completenessassessment(Intraop/Postop).v-Antibiotics Prophylaxisvii-DVT Prophylaxisviii-Anaesthesia (G.A)x-Postop Analgesia and Fluid mgt. 57. SPECIFIC MEASURES1)Antral Oedema with Failure OfLavage or Recurrence:a)Parietal Cell Vagotomy+ GJ+H.PyloriEradication.(It maintains antral innervation,prevents ductal motility problems andlesser sequalae).Nb:Criminal nerve of Grassi must beidentified and severed. 58. Specifics..b)Truncal/Selective Vagotomy+ BillrothI/II+ Kocherisation + HPEradication(GJ done should be retrocolic vertical isoperistaltic Nonloop Notension; Mayos GJ)TV/SV+Antrectomy+ GJ/GD+ Kocherisation+ HPEradication 59. Specifics..2)Obstructing TypesII&III ulcers(Involved in stenosis/cicatrisation.i)Distal Gastrectomy+Truncalvagotomy+ GJ(Mayos)+HPE3)Hourglass stomach:i)Billroth I/II+TruncalVagotomy+HPE. 60. Completeness Test(Postvagotomy)Intraop TestsI)Burge Test-Manometer passed via esophagogastric balloon and pylorus is stimulted.Any change in pressure indicates incomplete vagotomy.II)Grassi Test-Glass electrode inserted through an gastrostomy to measure P.H and MAO.A p.H 1.2-2 surrounded by area of 5.5-7,indicate actual area of incomplet. 61. Postop Testi)Pentagastrin test -Peak acidoutput reduction of >/50% isindicative of completeness.ii)Insulin (Hollanders )test. Largelyprognostic.Done 1week postvagotomy.If positve in a short time,recurrence risk is high. 62. COMPLICATIONS IMMEDIATE:i)Primary haemorrhage ii)Injury tocontiguous stricturesiii)Anaesthetic complications EARLY:i)Early Postgastrectomy/Postvagotomysyndromes. 63. Postgastrectomy Synd(Relatedto Resection)i)Early dumping -Results fromdisruption of the pyloric sphinctermechanism>Hyperosmolar chymetransit>rapid shift of fluid>luminaldistension>autonomic responses.Occurs 20-30mins after ingestionof meal. Characterized by both GIand cardiovascular symptoms. 64. Cardiovascular symptoms- flushing, diaphoresis, palpitations,dizziness, fainting,blurring of vision.GI- nausea, vomiting,explosive diarrhea, cramping abd.pain.Mgt-Patient informed preop-Spontaneous relief.-Dietary(less sugar),freq. small meals(Most will resolve). 65. -Long acting somatostatin analogue(octreotide) is highly effecttive for bothGI and CV symptoms in longstandingcases.Its expensive. - quickly absbd>Hyperglycemia> large amt of insulin release>OVERSHOOT > Profound hypoglycemia. Adrenaline release-diaphoresis, tremor ,giddiness ,confusionMgt-Small meals,less CH2O.-Antiperistaltic loop. 67. ComplicationscontdPostgastrectomy Synd(Related toReconstruction):iii)Affarent loop synd :May occurwithin few days of op or years after.Usuwhen>30-40cm.Xterised by a).RUQabd.pain radiating to interscapulararea.b)Projectile bilious vomiting notcontaining food and relievessymptoms. 68. Mgt(a surgical emergency). -A high index of suspicion. -Convert BillrothII to I. -Enteroenterostomy (e.g Braun,easier) below the stoma.-Creation of a Roux-en-Y 69. iv)Efferent loop synd: Quite rare. >50% occur within 1st mth postop. Usu from herniation of limb behind anastomosis (R-L fashion).Mgt-Reduce retroanastomosis hernia -Close retroanastomosis space. 70. v)Duodenal Blow out: Usu occurs4-5th day postop.Life threatening.Mgt-Control fistula and sepsis-Enteroenterostomy later. 71. Vi)Postvagotomy diarrhoea:Occurs in >30% of px.Part of Dumping synd. Usu disappears after 3-4 mths.Mgt-self limiting-Cholestyramine(4g tds)-1year,Jejunal Interposition. 72. Vii)Postvagotomy Gastroparesis: Occurs in both TV&SV, not in PCV. Paresis allows liquid(loss of receptive relaxation) not solid(dependent on antral pump mech)Mgt-Prokinetics [Metochlopramide(cholinergic enhancing) and Erythromycin(motilin receptor binding)].Usu suffices. 73. LATEviii) Metabolic Disturbance:-Fe def. anemia(more common)(Microcytic anemia)-B12 def anemia(def in Intrinsic facotor)(macrocytic anemia)(I.M cyanocobalimine 4 mthly)-Hypocalcemia(osteoporosis,osteomalacia)Calcium 1-2g/day.VitD 500-5000U/day. 74. ix)Alkaline Reflux Gastritis: severe epig pain+bilious vomiting+wgt loss. Usu ffng Billroth II.Diagnosis largely clinical but HIDA scan shows bile reflux into stomach/esoph endoscopy show beefy red ,friable mucosa.Mgt-BillrothII to a Roux-en-Y GJ. 75. X)Blind Loop synd.:Bacterialovergrowth in static loop causing bindB12 and deconjugate bile acid withresultant Megaloblastic anemia. Xi)Retained Antrum synd:Fromretained terminal antrum in the duodstump,continually bathed in alkalinesecretion>increased gastrinrelease>increased acid secretion>recurrent ulcer. 76. FOLLOW UP. Events in the follow up periodi-H.Pylori Eradicationii-H.pylori screening(to documenteradication)-serology-CLUB test(4weeks after)iii-BAO output monitoringiv-Yearly upper GI endoscopy+biopsy.v-Nutritional supplementation.vi-Life stylemodification(alcohol,smoking) 77. PROGNOSIS Factors affecting Prognosis:i)Age/Physiologic reserve-H.pyloriinfection load increases by about1%/year(more in elderly and theypresent more severecomplication.Less physiologic resrveto tolerate homeostatic changes fromGOO.ii)Duration of illness:Longer the poorerearly presentation is better outcome. 78. Prognosis..iii)Co-morbidities.Iv)Previous surgeryV)Previously documented failed medical therapy(HPE)Overall prognosis is good with improved surgical and medical therapy. 79. CHALLENGES i)Poor patient knowledgebase/compliance to medical therapy. ii)Substandard medications for HPE iii)Poor status of health facility(screening test,endoscopy) Iv)Financial constraints HPE(PPI) V)Poor life style/socioeconomic status 80. CONCLUSION:Though PUDx is largely medically managed with the place of the surgeon gradually being relegated to the background following improved medical therapy.However, considering our third world and its attendant constraints,the surgeons place can not be overemphasized. 81. THANK YOU