Gastric outlet obstruction

1. GASTRIC OUTLET OBSTRUCTION

2. RELEVANT ANATOMY

3. STOMACH SAC-LIKE ORGAN LOCATED MOSTLY IN THE LEFT UPPER PART OF THE ABDOMEN HAS 2 SURFACES (ANTERIOR & POSTERIOR), 2 CURVATURES (GREATER & LESSER), & 4 REGIONS (CARDIA, FUNDUS, PYLORUS,& ANTRUM The gastric wall is made up of 4 layers: mucosa, submucosa, muscularis propria, and serosa

4. STOMACH The mucosa forms thick longitudinally oriented folds or rugae which flatten with distention. The muscularis propria is a combination of 3 muscle layers: inner oblique, middle circular and outer longitudinal

5. STOMACH

6. STOMACH

7. STOMACH It functions primarily as a reservoir to store large quantities of recently ingested food Its volume ranges from about 30ml in a neonate to 1.5 to 2L in adulthood. The gastroesophageal junction generally lies to the left of the 10th thoracic vertebral body, 1-2cm below the diaphragmatic hiatus. The gastroduodenal junction lies at L1 and generally to the right of the midline, but may be lower

8. STOMACH ANTERIOR RELATIONS – DIAPHRAGM, ANTERIOR ABDOMINAL WALL, LEFT COSTAL MARGIN, & THE LEFT 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 THE DIAPHRAGM

9. POSTERIOR RELATIONS

10. STOMACH BLOOD SUPPLY: FROM THE COELIAC AXIS – LEFT GASTRIC, SPLENIC (SHORT GASTRIC & LEFT GASTROEPIPLOIC), HEPATIC (GASTRODUODENAL[SUPERIOR PANCREATICODUODENAL & RIGHT EPIPLOIC], CYSTIC, & RIGHT GASTRIC)

11. STOMACH

12. 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

13. STOMACH ; because of this, total vagotomy must always be accompanied by some sort of drainage procedure, either a pyloroplasty (to enlarge the pyloric exit and render the pyloric sphincter incompetent) or by a gastrojejunostomy (to drain the stomach into the proximal small intestine). Drainage can be avoided if the nerve of Latarjet is preserved, thus maintaining the innervation and function of the pyloric antrum (highly selective vagotomy).

14. STOMACH The sympathetic innervation is derived from preganglionic fibers arising predominantly from T6 to T8 spinal nerves.

15. STOMACH LYMPHATIC DRAINAGE: DIV INTO 3 AREAS, HOWEVER ALL DRAIN EVENTUALLY TO THE PARAAORTIC NODES

16. STOMACH

17. BARIUM MEAL TRACING

18. DUODENUM DUODENUM 25cm LONG, C-SHAPED CURVE AROUND THE HEAD OF THE PANCREAS, DIVIDED INTO 4 PARTS 1 ST 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 VENA CAVA 2 nd PART 7.5CM LONG, DESCENDS IN A CURVE AROUND THE HEAD OF PANCREAS, CROSSED BY THE TRANSVERSE COLON & LIES ON THE RIGHT KIDNEY AND URETER

19. DUODENUM 3 rd PART 10cm LONG, RUNS TRANSVERSELY TO THE LEFT CROSSING THE INFERIOR VENA CAVA, AORTA & L3 VERT 4 th PART ASCENDS UPWARDS & TO THE LEFT TO END AT THE DUODENOJEJUNAL JUNCTION BLOOD SUPPLY – THE SUPERIOR & INFERIOR PANCREATICODUODENAL ARTERIES

20. DUODENUM The luminal surface of the duodenum is lined with mucosa, forming circular folds known as the plicae circulares or valvulae conniventes The duodenal bulb has smooth, featureless mucosa The duodenal wall is composed of outer longitudinal and inner circular muscle layers The first few centimeters of the duodenum are intraperitoneal, whereas the remainder is retroperitoneal

21. PATHOLOGY OF GASTRIC OUTLET OBSTRUCTION FOLLOWING CHRONIC PEPTIC ULCER DISEASE

22. OUTLINE Introduction/Definition Epidemiology Etiology Pathology/Pathophysiology Complications

23. INTRODUCTION Gastric outlet obstruction is not a single entity. GOO is the clinical and pathophysiological consequence of any symptom complex that produce a mechanical impediment to gastric emptying. It usually follows chronic PUD

24. Introduction contd GOO is a common and early complication of DU in Africa and India

25. Epidemiology Incidence of GOO has been reported to be less than 5% in patients with PUD Though is the leading benign cause GOO Peri -pancreatic malignancy is the leading malignant cause FMC Owerri ( jan 2011 – oct 2012) 7 cases of GOO 3 – PUD, all male 4 – gastric ca

26. Etiology The factors predisposing to chronicity of PUD may include: - persistent imbalance between the aggressive and defensive factors - non eradication of H. pylori infection - non compliance to anti PUD medication etc.

27. Etiology contd However, GOO usually occur at the pyloro -duodenal area. It is caused by: - cicatrization - edema - pyloro -duodenal spasm

28. Pathogenesis/ pathophysiology Obstruction of the stomach hypertrophy of the stomach Dilatation Gastritis & depressed acid secretion

29. 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

30. CLINICAL FEATURES/INVESTIGATIONS

31. 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)

32. Anorexia,nausea . Easy satiety Vomiting: -characteristic unpleasant -copious -projectile -Non bilous -Food taken several days ago.

33. Feeling of unwell Appetite is maintained but fear of pain often prevent patient from eating Weight loss. Abdominal swelling

34. Examination Chronically ill looking Wasted Dehydrated may be pale shock

35. Epigastric / Rt hypochondrial tenderness Distended abdomen Visible gastric peristalsis Succussion splash

36. investigations 1) Stabilise patient FBC ( anaemia ) SEUCR ( hypochloraemia , hypokalaemia,hyponatraemia,elevated Hco3) BLOOD GASES(metabolic alkalosis) URINALYSIS (paradoxical aciduria )

37. investigation 2)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.

38. investigation Esophagogastroduodenoscopy + biopsy(histology and bacterioloical investigation). Aim is to viualise the stomach mucosa and any ulcer. B arium meal: - markely dilated stomach with a lot of residue -presence of an ulcer crater - trifoil deformity of the duodenal cap.

39. . - Hour glass deformity -Tea cup deformity -Abrupt obstruction to barium

40. 3)Pre- op preparation FBC SEUCR Urinalysis RVS

41. 4)Detection of H.pylori Non invasive: serology carbon labelled urea breath test Invasive: Rapid urease test,histology and culture.

42. GOO SECONDARY TO CHRONIC PEPTIC ULCER DISEASE - Treatment

43. OUTLINE INTRODUCTION; PRINCIPLES OF TREATMENT; -Objectives(Goals) of mgt. -Factors influencing choice of rx. -Patient selection. GENERAL MEASURES; SPECIFIC/DEFINITIVE MEASURES;

44. Outline… COMLICATIONS(& their mgt); FOLLOW UP; PROGNOSIS; CHALLENGES; CONCLUSION.

45. INTRODUCTION. PUD,largely medically condition. Becomes a surgical pathology when complicated e.g… 8-20% of patients developing complications only require surgery. It largely describes a surgically amenable pathology.

46. Intro…definitions. 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;<5mm in diameter;occuring in both acid secreting and non-acid secreting mucosa; heals rapidly by epithelial bridging.

47. Intro… Chronic PUDx is characterized by -Presence of chronic inflam cells -Reactive mucosal epithlial changes -Attempt at healing +-malignant changes.

48. Intro.. GOO 2* Chronic PUDx is a surgically amenable obstructive complication of PUDx.It includes pathologic entities such as: -Chronic PUDx with active edematous ulcer; -Chronic PUDx with antral cicatrisation; -Chronic PUDx with Pyloric stenosis; -Hour glass stomach; -Teapot stomach.

49. PRINCIPLES. Guiding Principles lies in the recognition of GOO as an emergency, as such, GOAL of treatment include: -1)Resuscitation/stabilization.; -2)Relieve obstruction; -3)Patient selection/categorization; -4)Offer definitive curative care; -5)Prevent recurrence/Follow up care.

50. Principles…Factors Factors Influencing Choice Of Tx : Patient-specific Factors i).Stability:Shock,Fluid and electrolyte imbalance. ii) Obesity:DVT prophylaxis, concomitant bariatric surgery iii) Age:Better outcome in younger age iv) Comorbidities:Dm,Htn .

51. Principles…..Factors cont’d Lesion-related Factors: i) Nature:e.g edema Lavage+H.pylori rx ii) Location:Duodenal /Pyloric antral/ Body/ Fundus / cardia . iii)Associated Deformity:Resections iv)Presence of malignant transformation:Resections Surgeon’s expertise/Materials and manpower available

52. ……Patient selection/category Acutely Obstructed/Chronically Obstructed group:Nonop Tx for acutely obstructed. Frail Elderly:Low life expectant group:Nonop e.g. balloon dilation. Stable/Unstable group:Limited surgical time,extent of resection e.t.c Low/High lying lesion/Deformity.

53. GENERAL MEASURES. Resuscitation: (Wide bore canular ) i).Antishock Therapy:IVF NS/Ringer’s @25ml/kg over 1 st 30mins then repeated and reassess ii).Urethral catheter:Input/output monitor@30-50ml/hr.( CVP@10-15cmH20 ) iii).NGT- Decompress,lavage and aspirate

54. General Measures…cont’d Iv)Correction of electrolyte Imbalance: K+ correction,ensuring urine output, ideally under ECG monitoring. V)Correction of anemia. Vi)Renal challenge after adequate fluid volume resuscitation. Vii)Renal dialysis(resuscitative) in uremia.

55. General measures.. Viii)Calorie-Maintaining with fluid @ 100ml/kg first 10kg,50ml/kg 2 nd 10kg, 25ml/kg subsequent kgs. Ensuring at least 100g of glucose is delivered(in 2liters of 5%Dw) Ix) TPN:With period of inanition >7days, marked weight loss

56. General… X)Antsecretory therapy:IV PPI e.g 40mg of Omeprazole stat then 20mg 12hrly NB:Should be discontinued 72hrs before surgery(return of g acidity)

57. SPECIFIC/DEFINITIVE MEASURES NONOPERATIVE MEASURES : i)Warm Saline Lavage+H.Pylori Eradication( usu for acute edematous active ulcer)Recurrence high in chronic active edematous ulcers. ii)Endoscopic Balloon dilation.May be useful in elderly frail patients unfit for surgery.Repeat necessary.

58. SPECIFIC/DEFINITIVE MEASURE. OPERATIVE MEASURES: Operative Principle : i-Surgically achieving physiologic control of acid production; ii-Ensuring normal gut continuity(Resection and Reconstruction); iii-Minimizing Postgastrectomy &Postvagotomy sequalae.

59. …..cont’d Guiding Principles…cont’d iv-Postvagotomy Completeness assessment(Intraop/Postop). v-Antibiotics Prophylaxis vii-DVT Prophylaxis viii-Anaesthesia (G.A) x-Postop Analgesia and Fluid mgt.

60. SPECIFIC MEASURES … 1)Antral Oedema with Failure Of Lavage or Recurrence: a)Parietal Cell Vagotomy+ GJ+H.Pylori Eradication. ( It maintains antral innervation, prevents ductal motility problems and lesser sequalae). Nb:Criminal nerve of Grassi must be identified and severed.

61. Specifics.. b) Truncal /Selective Vagotomy+ BillrothI/II+ Kocherisation + HPEradication ( GJ done should be retrocolic vertical isoperistaltic Nonloop Notension ; Mayo’s GJ ) TV/ SV+Antrectomy + GJ/GD+ Kocherisation+ HPEradication

62. Specifics.. 2)Obstructing TypesII&III ulcers (Involved in stenosis/ cicatrisation . i)Distal Gastrectomy+Truncal vagotomy+ GJ(Mayo’s)+HPE 3)Hourglass stomach: i) Billroth I/ II+Truncal Vagotomy+HPE.

63. Completeness Test(Postvagotomy) Intraop Tests I)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.

64. Postop Test i) Pentagastrin test -Peak acid output reduction of >/50% is indicative of completeness. ii) Insulin (Hollander’s )test. Largely prognostic.Done 1week post vagotomy.If positve in a short time, recurrence risk is high.

65. COMPLICATIONS I MMEDIATE : i)Primary haemorrhage ii)Injury to contiguous strictures iii) Anaesthetic complications EARLY: i)Early Postgastrectomy/Postvagotomy syndromes.

66. Postgastrectomy Synd(Related to Resection ) i)Early dumpin g - Result s from disruption of the pyloric sphincter mechanism> Hyperosmolar chyme transit>rapid shift of fluid>luminal distension>autonomic responses. Occurs 20-30mins after ingestion of meal. Characterized by both GI and cardiovascular symptoms.

67. 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).

68. -Long acting somatostatin analogue (octreotide) is highly effecttive for both GI and CV symptoms in longstanding cases.Its expensive. -<1% fail to respond to conservative tx : +Jejunal 20cm Isoperistaltic loop Interposition(dilates overtime,reservoir fxn) +Jejunal 10cm antiperistaltic loop interpositn(substitute pylorus,delaying emptying)

69. ii)Late Dumping -Result from rapid gastric emptying too but specifically for CH2O meal being delivered> quickly absbd>Hyperglycemia> large amt of insulin release>OVERSHOOT > Profound hypoglycemia. Adrenaline release-diaphoresis, tremor ,giddiness ,confusion Mgt-Small meals,less CH2O. -Antiperistaltic loop.

70. Complications…cont’d Postgastrectomy Synd(Related to Reconstruction): iii) Affarent loop synd :May occur within few days of op or years after.Usu when>30-40cm.Xterised by a).RUQ abd.pain radiating to interscapular area. b)Projectile bilious vomiting not containing food and relieves symptoms.

71. 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

72. iv)Efferent loop synd : Quite rare. >50% occur within 1 st mth postop. Usu from herniation of limb behind anastomosis (R-L fashion). Mgt-Reduce retroanastomosis hernia -Close retroanastomosis space.

73. v)Duodenal Blow out : Usu occurs 4-5 th day postop.Life threatening. Mgt-Control fistula and sepsis -Enteroenterostomy later.

74. Vi)Postvagotomy diarrhoea:Occurs in >30% of px.Part of Dumping synd. Usu disappears after 3-4 mths . Mgt-self limiting - Cholestyramine (4g tds ) -<1% lasting >1year,Jejunal Interposition.

75. 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.

76. LATE viii) 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.

77. 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.

78. X)Blind Loop synd .:Bacterial overgrowth in static loop causing bind B12 and deconjugate bile acid with resultant Megaloblastic anemia. Xi)Retained Antrum synd:From retained terminal antrum in the duod stump,continually bathed in alkaline secretion>increased gastrin release>increased acid secretion> recurrent ulcer.

79. FOLLOW UP. Events in the follow up period i-H.Pylori Eradication ii-H.pylori screening(to document eradication)-serology -CLUB test(4weeks after) iii-BAO output monitoring iv-Yearly upper GI endoscopy+biopsy. v-Nutritional supplementation. vi-Life style modification( alcohol,smoking )

80. PROGNOSIS Factors affecting Prognosis : i)Age/Physiologic reserve-H.pylori infection load increases by about 1%/year(more in elderly and they present more severe complication.Less physiologic resrve to tolerate homeostatic changes from GOO. ii)Duration of illness:Longer the poorer early presentation is better outcome.

81. Prognosis.. iii)Co-morbidities. Iv)Previous surgery V)Previously documented failed medical therapy(HPE) Overall prognosis is good with improved surgical and medical therapy.

82. CHALLENGES i)Poor patient knowledge base/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

83. 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 surgeon’s place can not be overemphasized.

84. THANK YOU