Gastric Outlet Obstruction (GOO)

Gastric Outlet Obstruction Explained By Dr MSI.
Content taken from Bailey n Love Surgery, Schwartz Surgery and Multiple articles.

1. Gastric Outlet Obstructio n BY: Dr. Muhammad Saad Iqbal PGT S1 DHQ Sahiwal

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 THE ABDOMEN • 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 , body , A ntrum and P ylorus . • 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, M uscularis P ropria, 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, & 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

5. Blood Supply FROM THE COELIAC Trunk – LEFT GASTRIC, SPLENIC (SHORT GASTRIC & LEFT GASTROEPIPLOIC), HEPATIC Artery (GASTRODUODENAL[SUPERIOR PANCREATICODUODENAL & RIGHT EPIPLOIC],CYSTIC, & RIGHT GASTRIC)

6. The veins draining the stomach 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 .

7. NERVE SUPPLY • VAGUS ( ANTERIOR & POSTERIOR) The vagus constitutes the motor and secretory 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 celiac ganglion . Postganglionic sympathetic nerves then travel from the celiac ganglion to the stomach along the blood vessels.

8. Background  Clinical entities that can result in GOO generally are categorized into 2 well-defined groups of causes Benign M alignant.  This classification facilitates discussion of management and treatment .

9. Etiology • Major Benign causes of Gastric outlet obstruction (GOO) are: 1. PUD 2. Gastric Polyps 3. Ingestion of caustics 4. Pyloric Stenosis 5. Congenital duodenal webs 6. Gall stone obstruction (Bouveret syndrome) 7. Pancreatic pseudocysts 8. Bezoars

10. Malignant causes: • Pancreatic cancer is the most 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 a) Duodenal cancer b) Ampullary cancer . c) C holangiocarcinomas. d) Gastric cancer . • Metastases to the gastric outlet also may be caused by other primary tumors.

11. 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 stenosis is the result of gradual hypertrophy of the circular smooth muscle of the pylorus.

12. Epidemiology • The incidence of gastric outlet obstruction (GOO) has been reported to be less than 5% in patients with PUD , which is the leading benign cause of the problem. • Five percent to 8% of ulcer-related complications result in an estimated 2000 operations per year in the United States. • The incidence of GOO in patients with peripancreatic malignancy, the most common malignant etiology, has been reported as 15-20%.

13.  When peptic ulcer disease ( PUD ) was more prevalent, benign causes were the most common; however, one review shows that only 37% of patients with GOO have benign disease and the remaining patients have obstruction secondary to malignancy.

14. Pathophysiology • Intrinsic or extrinsic obstruction of the pyloric channel 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 the 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 concomitant 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 manifests in approximately 5% of all patients with GOO. Ulcers within the pyloric channel and first portion of the duodenum usually are responsible for outlet obstruction Obstruction can occur in an acute setting secondary to acute 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 outlet obstruction from a Peptic ulcer or incomplete obstruction typically present with symptoms of the following : 1. retention , including early satiety, bloating or epigastric fullness , indigestion, anorexia, nausea, vomiting, epigastric pain , and weight loss. 2 . More than 90% of patients with PUD complain of abdominal pain which is typically non-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 commonly occurs with eating and is less likely to awaken the patient at night. 3. Nausea and vomiting are the cardinal symptoms. 4 . Vomiting – Non-bilious, and it characteristically contains undigested food particles 5. Loss of periodicity . 6. Early stages of Obstruction: vomiting is intermittent and usually occurs within 1 hour of a meal. 7. Very often it is possible to recognize foodstuff taken several days previously. 8. Patient loses weight, appears unwell and dehydrated

19. 9. Frequently malnourished and dehydrated and have 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 chloride------- hypokalemic hypochloremic metabolic alkalosis.  Alkalosis shifts the intracellular potassium to the extracellular compartment, and the serum potassium is increased factitiously. • With continued vomiting, the renal excretion of potassium increases in order to preserve sodium. Dehydration and electrolyte abnormalities-- Increase in BUN and creatinine are late features of dehydration.

21. 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 time, 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. This results in the urine becoming paradoxically acidic.  Alkalosis leads to a lowering of the circulating ionized calcium, and tetany can occur.

22. • Clinical features of Paradoxical aciduria 1. Irritability, confused status, dehydration 2. Often convulsions can occur. 3. Features of alkalosis like rapid breathing (Cheyne-stokes breathing and tetany) • Investigations 1. Serum electrolytes 2. Arterial blood gas analysis 3. Serum calcium level estimation • Treatment : Double strength normal saline with IV potassium under ECG monitoring. Plus IV magnesium.

23. Electrolyte changes in pyloric stenosis 1. Hyponatremia 2. Hypokalemia 3. Hypomagnesemia 4. Hypochloraemia 5. Metabolic alkalosis 6. Paradoxical aciduria

24. Physical examination • Chronic dehydrated and Malnourished patient On Examination : 1. Distended abdomen and a succussion splash may be audible on shaking the patient’s abdomen. Positive succussion splash is done 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 tympanic 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. ( This test is done by placing a stethoscope over epigastric region . Skin is scratched from left side downwards, at several points away from the epigastrium using finger and these points are joined. Normally the greater curvature of the stomach lies above the level of umbilicus, while in GOO it lies below the level of umbilicus .

26. Investigations CBC for Anemia Electrolyte Studies for metabolic Disorder Liver function tests may be helpful, particularly when a malignant etiology is suspected . 4. A test for H pylori is helpful when the diagnosis of PUD is suspected 5. Plain abdominal radiographs, contrast upper GI studies (Gastrografin or 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 below the level of iliac crest . Mottled stomach Barium does not pass into duodenum.

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

29. Diagnostic Procedures • Upper GI endoscopy can help visualize the gastric outlet and may provide a tissue diagnosis when the obstruction is intraluminal . • The S odium 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 cc of sodium chloride solution into the stomach via a nasogastric tube (NGT). A diagnosis of gastric outlet obstruction (GOO) is made if more than 400 cc remain in the stomach after 30 minutes.

30. Nuclear gastric emptying studies measure the passage of orally administered radionuclide over time . • Unfortunately, both the nuclear test and the saline load test may produce abnormal results in functional states . • The specific cause may be identified as an ulcer mass or intrinsic tumor. • In the presence of PUD, perform E ndoscopic 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. • Needle-guided biopsy also may be helpful in establishing the presence of metastatic disease . This knowledge may impact the magnitude of the procedure planned to alleviate the GOO.

31. Conservative Management 1 . Correcting the metabolic and electrolyte abnormality by IV fluids . 2. Rehydrated with intravenous isotonic saline with potassium supplementation or double strength saline , calcium, potassium, magnesium . 3. Replacing the sodium chloride and water allows the kidney to correct the acid–base abnormality 4. Following rehydration it may become obvious that the patient is also anemic . 5. Blood transfusion if given if there is anemia .

32. 6. Place a NGT to decompress the stomach. Occasionally , a large tube is required because the undigested food blocks tubes with small diameters . 7. 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 . 8 . Treat H pylori infection, when identified, according to current recommendations . 9 . Although most patients improve temporarily with treatment, scarring and fibrosis may worsen over time .

33. 10. STOMACH WASH : The stomach should be emptied using a Wide-bore gastric tube/ Eswald’s tube. Pass an orogastric tube and lavage the stomach until it is completely emptied . 11. TPN support . 12. Pneumatic balloon dilatation of a chronic, benign stricture can be performed via endoscopy . Patients who are candidates for balloon dilatation are likely to present with recurrent GOO .

34. Published series using this technique report success rates of over 76% after multiple dilatations, although the rate of failure and recurrent obstruction is higher in patients treated with balloon dilatation who have not also been treated for H pylori infection . Patients who are negative for H pylori do not respond favorably to balloon dilatation and should be considered for surgical treatment early in the process.

35. Endoscopic Balloon Dilation: • If the GOO is irreversible, or is caused by fibrotic scarring, rather than edema and spasm, it requires 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 for EBD. • In inflammatory conditions like Crohn’s disease or infection like tuberculosis causing GOO, specific treatment for the antecedent disease is mandatory and may obviate the need for surgery or EBD .

36. GUIDELINES FOR BALLOON DILATION Patient selection • Only localized stricture of the stomach should be chosen. • The site of gastric cicatrization is not important . • CT scan to assess antral wall thickness may be a good modality to identify the “ right patients ” and to exclude malignancy. • Endosonography may also emerge as a useful adjunct in this regard, especially in helping direct intralesional steroid injections.

37. When should dilation be started ? • Patients with peptic-GOO can be dilated any time after gastric decompression is done as most have chronic cicatrisation. • In those with active ulceration one can wait for response to proton pump inhibitors. As stated previously , it is best to wait for 8 weeks after caustic ingestion to allow for natural healing.

38. Panel showing barium study in a patient with peptic pyloric stenosis with trifoliate deformity of duodenal bulb (A), and endoscopic pictures at the beginning (B), after 2 dilations (C) and after 4 dilations (D).

39. Indications for Surgery • Gastric outlet obstruction due to benign ulcer disease maybe treated medically if results of imaging studies or endoscopy determine - acute inflammation and edema are the principle causes (as opposed to scarring and fibrosis, which may be fixed ) • If medical therapy fails, then surgical therapy • Typically, if resolution or improvement is not seen within 48-72 hours, surgical intervention is necessary

40. 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 acid problem. The most common surgical procedures performed for GOO related to PUD are • Vagotomy and antrectomy, • Vagotomy and pyloroplasty, • Truncal vagotomy and gastrojejunostomy, • 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.

41. Pyloroplasty Types: Heineke-Mikulicz pyloroplasty involves a longitudinal incision across the pylorus that is closed transversely; this is the most commonly performed pyloroplasty Jaboulay pyloroplasty involves a side-to-side gastroduodenostomy without pylorus incision Finney pyloroplasty also involves a side-to-side gastro- duodenostomy but with pylorus incision

42. Truncal Vagatomy with Pyloroplasy

43. • Placement of a jejunostomy tube at the time of surgery should be considered . • This provides temporary feeding access in already malnourished patients. Also, in chronically dilated partial obstructions, the stomach may be slow to recover a normal rate of emptying

44. Complications of Vagotomy • Intraoperative complications can occur with injury to adjacent structures. • Early post-operative complications: – Delayed gastric emptying – Dysphagia and lesser curve necrosis( lesser curve necrosis specific to HSV). • Late complications include postvagotomy diarrhea , reflux esophagitis, Gallstones.

45. 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

46. 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.

47. – 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) Osteomalacia

48. 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 40% of gastric cancers and 80-90 % of periampullary cancers.) • When tumors are found to be unresectable , 13- 20% of patients eventually develop GOO before they succumb to their disease.

49. • Gastrojejunostomy remains the surgical treatment of choice for GOO secondary to malignancy. • Although surgeons traditionally have preferred ante colic anastomosis to prevent further obstruction by advancing tumor growth, a publication evaluating the retro colic anastomosis in this setting challenges conventional wisdom . • Results demonstrate that a retro colic anastomosis may be associated with decreased incidences of delayed gastric emptying (6% vs 17 %) and late GOO (2% vs 9 %). Feeding jejunostomy should again be considered to combat malnutrition and slow recovery of gastric emptying.

50. Postoperative Management  Admit patients to a monitor unit after the procedure.  Pay special attention to fluid and electrolyte status.  Most surgeons agree that perioperative antibiotics are advisable but may be limited to use during the immediate perioperative period in the absence of intervening infection.  If a gastric reconstruction is performed, an NGT is recommended.  The length of time that the NGT should remain in place is controversial; however, it is important to remember that a previously dilated stomach, the performance of a vagotomy, and the presence of metastatic cancer may all contribute to decreased gastric motility.  An anatomically patent gastrojejunostomy may fail to empty for days. This syndrome of delayed gastric emptying is a well-known entity and requires surgical patience. Again, preoperative planning for feeding access becomes important during this immediate postoperative period.  Aggressive pulmonary toilet, prophylaxis for gastritis and deep venous thrombosis (DVT), and early ambulation are advisable.

51. Follow-up • Closely monitor patients after surgery and upon discharge. After relief of gastric outlet obstruction, patients may continue to experience gastric dysmotility and may require medication to stimulate gastric emptying and motility. • In patients with malignancy, the potential for progressive and recurrent disease always remains. These patients should be monitored by a surgeon or an oncologist. • Closely monitor patients whose treatment consisted of balloon dilatation because most of these patients require subsequent dilatations to achieve satisfactory results.

52. Summary: Gastric outlet obstruction is most commonly associated with longstanding peptic ulcer disease and gastric cancer. • The metabolic abnormality of hypochloraemic alkalosis is usually only seen with peptic ulcer disease and should be treated with isotonic saline with potassium supplementation . • Endoscopic biopsy is essential to determine whether the cause of the problem is malignancy • Endoscopic dilatation of the gastric outlet may be effective in the less severe cases of benign stenosis • Operation is normally required, with a drainage procedure being performed for benign disease and appropriate resectional surgery if malignant.