final goo and its management and complications .pptx

Goo

1. Applied anatomy of stomach Peptic ulcer disease, Hypertrophic pyloric stenosis and GOO Dr Purnendu Paul GENERAL SURGERY JIMSH

2. Definition Gastric outlet obstruction (GOO, also known as pyloric obstruction) is not a single entity; it is the clinical and pathophysiological consequence of any disease process that produces a mechanical impediment to gastric emptying.

3. Anatomy: SAC- LIKE ORGAN LOCATED MOSTLY IN THE LEFT UPPER PART OF THEABDO/LIEN It is located beneath the diaphragm and is attached superiorly to the esophagus and distally to the duodenum. The stomach is divided into 4 portions: Cardia, B ody , Antrum and Pylorus. HAS 2 SURFACES (ANTERIOR & POSTERIOR), 2 CURVATURES (GREATER & LESSER), & 4 REGIONS (CARDIA, FUNDUS, PYLORUS & ANTR UM ) The gastric wall is made up of 4 layers: mucosa, Submucosa, Muscularis Propria, and Serosa inflammation, scarring, or infiltration of the antrum and pylorus are associated with the development of gastric outlet obstruction.

4. Relations ANTERIOR RELATIONS - DIAPHRAGM, ANTERIOR ABDOMINAL WALL, LEFT COSTAL MARGIN, b THE LEFT LOBE OF THE LIVER POSTERIOR RELATIONS – L E S S E R S A C , P A N C R E A S , L E F T S U P R A R E N A L G L A N D, L E F T K I D N E Y, SPLEEN, S P L E N I C A R T E R Y & T H E T R A N V E R S E COLON SUPERIOR RELATIONS - LEFT DOM E OF THE DIAPHRAGM

5. Stomach Anatomical Relation

6. Blood Su pply FROM THE COELIAC Trunk - LEFT GASTRIC, SPLENIC ( SHORT GASTRIC & LEFT GASTROEPIPLOIC), HEPATIC Artery (GASTRODUODENAL[SUPERIOR PANCREATICODUODENAL & RIGHT EPIPLOIC],CYSTIC, & RIGHT GASTRIC)

7. The veins draining the stDmach are generally parallel to arteries. The left gastric (coronary vein) and right gastric veins usually drain into the Portal vein, though occasionally the coronary vein drains into the Splenic vein. The right gastroepiploic vein drains into the Superior mesenteric vein near the inferior border of the pancreatic neck, and the left gastroepiploic vein drains into the Splenic vein. , .

8. NERVE SUPPLY VAGUS (ANTERIOR & POSTERIOR) The vagus constitutes the motor and secr e tory nerve supply for the stomach. The extrinsic sympathetic nerve supply to the stomach originates at spinal levels T5 through T10 and travels in the splanchnic nerves to the cel i ac ganglion. Postganglionic sympathetic nerves then travel from the celiac ganglion to the stomach along the blood vessels.

9. Background •CIinicaI entities that can result in GOO generally are categorized into 2 well- defined groups of causes Benign Malignant. •This classification facilitates discussion of management and treatment.

10. Etiology Major Benign causes of Gastric outlet obstruction (GOO) are: PUD Gastric Polyps 3 . I ngestion Of caustics 4 . Pyloric Stenosis . 5. congenital duodenal webs 6. Gall stone obstruction (Bouveret syndrome) y. Pancreatic pseudocysts 8. Bezoars

11. Malignant ca u ses: Pancreatic cancer is the m o st common malignancy causing GOO. Outlet obstruction may occur in 10- 20 % of patients with pancreatic carcinoma. Other tumors that may obstruct the gastric outlet include D uod en al cancel Ampul l ary cancer. Cholangiocarcinomas. Gastric cancer. Metastases to the gastric outlet also may be caused by other primary tumors. ,

12. Within the pediatric population, pyloric stenosis constitutes the most important cause of GOO. Pyloric stenosis occurs in 1 per 750 births. It is more common in boys than in girls and also is more common in first- born children. Pyloric sten o sis is the result of gradual hypertrophy of the circular smooth muscle of the pylorus. ’

13. Py l or ic St e nos is

14. Pathophysiology Intrinsic or extrinsic obstruction of the pyloric c hannel or duodenum is the usual pathophysiology of gastric outlet obstruction; as previously noted, the mechanism of obstruction depends upon the underlying etiology. Patients present with intermittent symptoms ” that progress until obstruction is complete. •. Vomiting is ihe cardinal symptom. ’ Initially, patients may demonstrate better tolerance to liquids than solid food.

15. ° In a later stage, patients may develop significant weight loss due to poor caloric intake. Malnutrition is a late sign, but it may be very profound in patients with concomi tant malignancy. In the acute or chronic phase of obstruction, continuous vomiting may lead to dehydration and electrolyte abnormalities. ° When obstruction persists, patients may develop significant and progressive gastric dilatation. The stomach eventually loses its contractility. Undigested food accumulates and may represent a constant , risk for aspiration pneumonia .

16. PUD man i fests in approxîmately 5% of all patients with GOO. Ulcers within the pyloric channel and fi r s t po rtion of the duodenum usually are resp o nsible f o r out l et obstruction . Obstruction can occur in an acute setting secondary to acUt£' inflammation and edema or, more commonly, in a chronic setting secondary to scarring and fibrosis. Helicobacter pylori has been implicated as a frequent associated finding in patients with GOO, but its exact incidence has not been defined precisely.

17. Clinical features Gastric out)et obstruction from a Peptic ulcer or Incomplete obstruction typically present with symptoms of the following: 1. retention, including early satiety, bloating or eplgastr i c fullness, indigestion, anorexia, nausea, vomiting, epigastric pain, and weight loss. 2 . More than 60% of patients with PUD com plain of abdominal pain which is typically n o n- radiating, burning in quality, and located in the epigastrium. Two- thirds of patients with duodenal ulcers will complain of pain that awakens them from sleep.

18. The pain of gastric ulcer more c o mmon Iy occurs with eating and is less likely to awaken the patient at night. 3 Nausea nnd vomiting are the cardinal symptoms. 4- Vomiting — Non- b i lious , and it characteristically contains und i gested food particles 5 . Loss of pe ri odicity . 6. Early stages of Obstruction: vomiting is intermittent and usually occurs within 1 hour of a mea l . 7 Very often it is possibl e to recognize foodstuff taken several days previously. 8 . Patient loses weight, appears unwell and dehydrated

19. 9 . Frequently malnourished a nd dehydrated and h a ve a metabolic insufficiency 10 . Weight loss , most significant with malignant disease

20. Metabolic effects Prolonged vomiting causes loss of hydrochloric acid & produces an increase of bicarbonate in the plasma to compensate for the lost chIoride------- hypokaIem ic hypoch loremic metabolic al kalos is . Alkalosis shi ft s the intracellular potassium to the extrace l Iufar compartment, and the serum potassium is increased fa ctitiously . With continued vomiting, the renal excretion of potassium increases in o r der to preserve sodium. Dehydration and electrolyte abnormalities- - Increase in BUN and creatinine are late features of dehydration.

21. The adrenocortical response to hypovolemia intensifies the exchange of potassium for sodium at the distal tubule, with subsequent aggravation of the hypokalemia.

22. Paradoxically acidic urine Initially, the urine has a low chloride and high bicarbonate content, reflecting the primary metabolic abnormality. This bicarbonate is excreted along with sodium and so, with t ime , the patient becomes progressively hyponatraemic and more profoundly dehydrated. Because of the ‹dehydration, a phase of sodium retention follows and potassium and hydrogen are excreted in preference. T his r esults in the urine becoming paradoxically acidic. Alkalosis leads to a lowering of the circulating ionized calcium and tetany can occur.

23. Electrolyte changes in pyloric stenosis 1. Hyponatremia z. Hypokalemla 3 . Hypomagnesemia 4 . Hypo c hloraemia 5. Metabolic alkaiosis 6. Paradoxical aciduria

24. Physical examination Chronic dehydrated and Malnourished patient On Examination : 1. Distended abdomen and a succession splash may be audible on shaking the patient's abdomen. Positive succussion splash is d o ne with 4 hours empty stomach, by placing a stethoscope over the epigastric region and shaking the patient adequately.

25. 2. A dilated stomach may be appreciated as a tympan i c mass in the epigastric area and/or left upper quadrant 3. Visible gastric peristalsis (VGP) may be elicited by asking the patient to drink a cup of water. 4. Auscultopercussion test shows dilated stomach.

26. Investigations CBC for Anemia Electrolyte Studies for metabolic Disorder L ive r function tests may be helpful, particu l arly when a malignant et i oIogy is suspected. A test for H py l ori is helpful when the diagnosis of PUD is suspected ' 5. Plain abdominal radiographs, contrast upper GI Studies (G as trografin o r barium), and CT scans with oral contrast are helpful. 6. ECG for Hypokalemia ,

27. 7. Barium meal study: Absence of duodenal cap. Dilated stomach where greater curvature is bolow tho jevel of fliac crest. Mottled stomach Bar i um does not pass tnto duodenum.

28. Film Findings:

29. Contrast study demonstrating an enlarged stomach. The point of obstruction is visualis ed at the pyloric- duodenal junction (string sign).

30. Diagnostic Procedures Upper GI endoscopy can help visualize the gastric outlet and may provide a tissue diagnosis when the obstruction is intraluminal. The Sodium Chloride load test is a traditional clinical non- imaging study that may be helpful. , • The traditional sodium chloride load test is performed by infusing 750 ml of sodium chloride solution into the stomach via a nasogastric tube (NGT). A diagnosis of gastric outlet obstruction (GOO) i s made if more than 4 ml remain in the stomach after 30 minutes. ’”

31. Nuclear gastric emptying studies meas u re the passage of orally administered radionuclide over time. U nfortunately , both the nuclea r test and the saline l o ad test may produce abnormal results in functional states. The specific cause may be identified as an ulcer mass or I nt rinsic tumo r. In the presence of PUD, perform Endoscopic biopsy to rule out the presence of malignancy. In the case of peripancreatic malignancy, CT scan-guided biopsy may be helpful in establishing a preoperative , diagnosis. •'

32. Conservative Management 1. Correcting the metabolic and electrolyte abnormality by IV flu i ds. 2. Rehydrated wi th intravenous Isoton i c saline with potassium supplementation or double strength sa l i ne, calcium, potassium, magnesium. . Replacing the sodium chloride and wate r allows the kidney to correct the acid- base abnormality g. F ollowing rehydration it may become obvious that the patient is also anemic. 5. Blood tran s fu s ion to be given if there is anamia.

33. 6.Place a NGT to decompress the stomach. Occasionally, a large tube is required because the undigested food bloc k s tubes with small diamet ers . When acute PUD has been identified as a primary cause of gastric outlet obstruction (GOO), focus treatment on the reduction of acid production. H2 blockers and PPIs are the mainstay of treatment. Treat H py lo ri infection, when identified, according to current recommendations. 9.Although most patients improve temporarily with treatment, scarring and fibrosis may worsen over time. ,

34. 10. STOMACH WASH. The stomach should be emptied using a w ide- bore gastric tube . Pass an orogastric tube and lavage the stomach unti l clear reflux c omes out. TPN support. Pneumatic balloen dilatation of a chronic, benign stricture can be performed via endoscopy. Patients who are candidates for balloon dilatation are likely to present wi t h recurrent GOO.

35. Endoscopic Balloon Dilation: If the GOO is irreversible, or is caused by fibrotic scarring, rather than edema and spasm, it requi res a definitive treatment. Before the advent of endoscopic balloon dilation (EBD), surgery was the only treatment for these patients. Recent data suggest that EBD is an effective alternative to surgery in a majority of patients with ulcer- related and caustic induced GOO. Patients with a possibility of malignancy would not be candidates , f o r EBD. I n inflammatory conditions like Crohn's disease or infection like tuberculosis caus i ng GOO, specific treatment f o r the antecedent disease is mandatory and may obviate the need for surgery or EBD. ”

36. Indications f o r Surgery Gastric outlet obstruction due t o benign ul c er disease maybe treated medically i f results of i mag i ng studies or endoscopy determ i ne - acute Inflammation and edema are the principle cause s. If medical therapy fails, then surgical therapy Typically, If resolution or Improvement is not seen within 48 - 7 2 hours, surgical interve nti on i s necessary

37. Surgical Management More than 75% of patients presenting with GOO eventually require surgical intervention. Operative management should offer relief of obstruction and correction of the a ci d problem. The most common surgical procedures performed for GOO related to PUD are Vagotomy and antrectomy, Vagotomy and pyloroplasty, Tru ncal vagotomy and gastrojeju nostomy, Pyloroplasty Laparoscopic variants of the aforementioned procedures. Vagotomy and antrectomy with Billroth II reconstruction (gastrojejunostomy) seem to offer the best results. Vagotomy and pyloroplasty and pyloroplasty alone, although used with some success, can be technically difficult to perform due to scarring at the gastric outlet.

38. Management of malignant disease The management of GOO secondary to malignancy is controversial. Of patients with periampullary cancer, 30- 50% present with nausea and vomiting at the time of diagnosis. Most of these tumors are unresectable (approximately ' 4O % of gastric cancers and 80- 90 % o f periampullary „ cancers.) When tumors are found to be unresectable, 13- 20 % of patients eventually develop GOO before they succumb to their disease.

39. Gastrojejunostomy remains the surgical treatment of choice for GOO secondary to malignancy. " Feeding jejunostomy should again be considered to combat malnutrition and slow recovery of gastric emptying.

40. Peptic ulcers are defined as erosions in the gastric or duodenal mucosa that extend through the muscularis mucosae. Benign Gastric Ulcer Duodenal Ulcer PEPTIC ULCER DISEASE

41. Pathogenesis Protective (or defensive) factors mucosal bicarbonate secretion, mucus production, blood flow, growth factors, cell renewal, endogenous prostaglandins

42. Damaging (or aggressive) factors hydrochloric acid secretion, pepsins, ethanol ingestion, smoking, duodenal reflux of bile, ischemia, hypoxia, H. pylori infection . NSAIDs.

43. 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.

44. 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 Breath tests or faecal antigen tests

45. 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.

46. 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.

47. ACID HYPERSECRETORY STATES AND ULCER DISEASE Zollinger -Ellison (ZE) syndrome – gastrinoma Anastomotic or Marginal Ulceration

48. 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

49. Duodenal Ulcer 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.

50. 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

51. 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.

52. 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

53. 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

54. 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

55. Bleeding Duodenal Ulcer The most commonly used system for classifying the endoscopic appearance of bleeding ulcers is the Forrest classification

56. 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 .

57. Surgical procedures for peptic ulcers Truncal Vagotomy

58. Selective Vagotomy

59. Parietal Cell Vagotomy

60. 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

61. INTRODUCTION A condition characterised by hypertrophy of the two circular muscle layers of the pylorus. Resulting in constriction and obstruction of gastric outlet. Described by Hirschprung in 1888

62. EPIDEMIO L O G Y AND ETIO L O G Y INCIDENCE - 1.5 to 4 per 1000 live births EPIDEMIOLOGY - Male : female ratio = 4:1 Increased risk in first born boys ETIOLOGY IDIOPATHIC GENETIC-11q14-22 and Xq23 Rarely autosomal dominant FAMILIAL ETHNIC ORIGIN (more in whites): more commonly seen in Caucasians ENVIRONMENTAL   Erythromycin or azithromycin exposure Transpyloric feeding of premature babies

63. ETIOLOGY (contd.) EME R GIN G N E W TH E ORIES GI hormones like gastrin, substance P (could produce chronic pylorospasm and stenosis) , Epidermal growth factor, deficiency of NO (can induce muscle spasm preventing smooth muscle relaxation in stomach).  Muscle layer deficient in quantity of nerve terminals markers for nerve supporting cells peptide containing nerve fibres  This abnormal innervation of muscular layer leads to failure of relaxation of pyloric muscle, increased synthesis of growth factors

64. CLINICAL PRESENTATION ONSET at 2 to 8 weeks of age (commonly at around one month of age) SYMPTOMS  Projectile ,forcible,     frequent episodes of non- bilious coffee ground vomiting 30 to 60 minutes after feeding. Weight loss Persistent hunger Lethargy Constipation or hunger diarrhoea

65. CLINICAL PRESENTATION(contd) SIGNS Palpable,olive shaped, mobile, smooth, firm mass (1.5 to 2 cm) with all borders well made out, moves with respiration, with impaired resonance on percussion to right of epigastric area.(95% cases)

66. CLINICAL PRESENTATION(contd) SIGNS (contd.) Visible gastric peristalsis from left upper quadrant to epigastrium (golf ball waves) Signs of dehydration Jaundice (2%) (due to decreased hepatic glucuronosyl transferase associated with starvation)

67. DIAGNOSIS ABDOMEN X RAY (erect posture) upper abdominal gas bubble in the stomach.  ABDOMINAL ULTRASONOGRAPHY ( Gold standard at present) Doughnut sign or cervical pyloric sign pyloric muscle thickeness >4 mm   pyloric length >16mm in presence of functional gastric outlet obstruction

68. DIAGNOSIS (contd.) BARIUM MEAL/ Fluoroscopy Peristaltic waves ( caterpillar sign ) Delayed gastric emptying Elongated and narrow pyloric canal- String sign / Railroad track sign The pylorus indents the contrast-filled antrum ( shoulder sign ) or base of the duodenal bulb ( mushroom sign)

69. The barium may outline crowded mucosal folds as parallel lines - DOUBLE TRACT SIGN Bulge in the distal antrum with streak of barium pointing towards pyloric canal- BEAK SIGN Double tract sign Beak sign

70. DIAGNOSIS ( contd.) BIOCHEMICAL CHANGES Dehydration Malnutrition Hypochloraemic hypokalaemic metabolic alkalosis Paradoxical aciduria Hyperbilirubinemia ARTERIAL BLOOD GAS ANALYSIS Low serum levels of potassium and chloride Increased blood pH and high blood bicarbonate level

71. MANAGEM E NT Medical but not a surgical emergency RESUSCITATION MEDICAL TREATMENT – Atropine methyl nitrate orally is tried to relax the pylorus muscle.

72. PRE OPERATIVE PREPARATION Resuscitation with IV rehydration. Correct hypovolaemia with 10 ml/kg 0.9 % saline. Correct hypochloraemic alkalosis and hypokalaemia (over 24-48 hrs): 0.45% NaCl in 5% dextrose with added KCl at a rate of 120-150 mL/kg/24hr. Nasogastric tube drainage to prevent aspiration of vomited secretions.

73. Surgery should take place when : Dehydration corrected Normal serum Na and K Chloride ion >90mmol/l Bicarbonate ion < 28 mmol/l

74. Surgery FREDET-RAMSTEDT’s PYLOROMYOTOMY >>> conventional open procedure LAPARASCOPIC PYLOROMYOTOMY > DOUBLE –Y PYLOROMYOTOMY>

75. PYLOROMYOTOMY FR E D E T-RAMST E D T ’s PYLOROMYOTOMY Division of pyloric muscle fibres without opening of bowel lumen. Done via right upper quadrant incision or laparoscopically. Caution not to open mucosa and avoid the prepyloric vein of Mayo.

76. LAPARASCOPIC PYLOR O MYOTOMY Effective alternative Time to achieve full enteral feeding is significantly shorter ( 18.5hrs) in those treated laparoscopically vs those having open pyloromyotomy(23.9 hrs) Better cosmesis

77. A, Laparoscopic pyloromyotomy is started using a retractable blade. B, A spreader with grooves on the outer surface is used to complete the pyloromyotomy. Intact mucosal bulging along with independent muscular wall motion is confirmed.

78. DOUBLE –Y PYLOROMYOTOMY Has also been safely and effectively performed .

79. The double-Y pyloromyotomy (Alayet's pyloromyotomy) seems to be a good technique for the surgical management of IHPS. It offered a better functional outcome in terms of postoperative vomiting during the first postoperative week and weight gain during the first 10 days in our initial series while having a safety profile similar to Ramstedt's pyloromyotomy.

80. POST OPERATIVE CARE Patient started on feedings of glucose and water or an electrolyte infant formula ( eg - pedialyte) 4-6 hrs after surgery. Gradual increase in oral fluids till feeds are accepted without emesis. Full feedings reached after 24 hrs from surgery. Antibiotic prophylaxis not required. Postoperative monitoring for 12 hrs required in patients with Hypoglycemia Hypothermia Respiratory depression and apnoea(due to CSF alkalosis and intraoperative hyperventilation)

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