GASTRIC OUTLET OBSTRUCTION

1. GASTRIC OUTLET OBSTRUCTION PROF.MINOCHA

2. Definition Gastric outlet obstruction ( GOO , pyloric obstruction ) is not a single entity---- Clinical and pathophysiological consequence of any disease process that produces a mechanical impediment to gastric emptying

3. Causes Two well-defined groups of causes— Benign & Malignant In the past--  peptic ulcer disease   more prevalent, benign causes most common Now-- only 37% have benign disease and the remaining have obstruction secondary to malignancy

4. Diagnostic and treatment dilemma Exclude functional nonmechanical causes of obstruction, such as diabetic gastroparesis Once mechanical--- differentiate between benign and malignant ( definitive Tt varies) Diagnosis and treatment Urgent, because delay further compromise pts. nutritional status Delay also further compromise edematous tissue and complicate surgical intervention

5. Frequency The incidence less than 5% in pts. with   PUD -- leading benign cause Peripancreatic malignancy , the most common malignant etiology--- 15-20%.

6. Etiology Major benign causes of gastric outlet obstruction (GOO) are--- PUD gastric polyps ingestion of caustics   pyloric stenosis congenital duodenal webs gallstone obstruction ( Bouveret syndrome ) pancreatic pseudocysts and bezoars

7. Etiology( Contd ) PUD --- 5% of all patients with GOO Ulcers within the pyloric channel & D-1 responsible for outlet obstruction Obstruction -- Acute -- secondary to acute inflammation and edema , Chronic-- secondary to scarring and fibrosis   Helicobacter pylori  

8. Etiology( Contd ) Pediatric age group---  P yloric stenosis     Pyloric stenosis  occurs in 1 per 750 births Boys˃ Girls More common in first-born children   Pyloric stenosis  ---- gradual hypertrophy of the circular smooth muscle of the pylorus  

9. Etiology( Contd ) Pancreatic cancer  is the most common malignancy causing GOO Outlet obstruction may occur in 10-20% Other tumors include ---   A mpullary cancer Duodenal cancer   C holangiocarcinomas   G astric cancer Metastases to the gastric outlet by other primary tumors

10. Pathophysiology Intrinsic or extrinsic obstruction of the pyloric channel or duodenum Intermittent symptoms that progress until obstruction is complete . Vomiting is the cardinal symptom. Initially, better tolerance to liquids than solid food In a later stage, significant weight loss due to poor caloric intake . Malnutrition is a late sign, -- very profound in patients with concomitant malignancy Continuous vomiting may lead to dehydration and electrolyte abnormalities When obstruction persists, may develop significant and progressive gastric dilatation The stomach eventually loses its contractility. Undigested food accumulates ------------- constant risk for aspiration pneumonia

11. Clinical features Nausea and vomiting are the cardinal symptoms Vomiting -- N onbilious , and it characteristically contains undigested food particles Early stages --- vomiting intermittent and usually occurs within 1 hour of a meal Very often it is possible to recognise foodstuff taken several days previously Pt. loses weight, appears unwell & dehydrated

12. Clinical features( Contd ) GOO from a  duodenal ulcer  or incomplete obstruction typically present with symptoms of----------- Gastric retention, including early satiety, bloating or epigastric fullness, indigestion, anorexia, nausea, vomiting, epigastric pain, and weight loss Frequently malnourished and dehydrated and have a metabolic insufficiency Weight loss , most significant with malignant disease Abdominal pain is not frequent and usually relates to the underlying cause, eg , PUD, pancreatic cancer

13. Physical examination Chronic dehydration and Malnutrition On examination : Distended stomach and a succussion splash may be audible on shaking the patient’s abdomen A dilated stomach may be appreciated as a tympanitic mass in the epigastric area and/or left upper quadrant

14. Metabolic effects Dehydration and electrolyte abnormalities-- Increase in BUN and creatinine are late features of dehydration 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 The adrenocortical response to hypovolemia intensifies the exchange of potassium for sodium at the distal tubule, with subsequent aggravation of the hypokalemia

15. 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 ionised calcium, and tetany can occur.

16. Management Involves Correcting the metabolic abnormality & Dealing with the mechanical problem Rehydrated with i /v isotonic saline with potassium supplementation. Replacing the sodium chloride and water allows the kidney to correct the acid–base abnormality Following rehydration it may become obvious that the patient is also anaemic , the haemoglobin being spuriously high on presentation

17. Management( contd ) The stomach should be emptied using a Wide-bore gastric tube . Pass an orogastric tube and lavage the stomach until it is completely emptied Then endoscopy and contrast radiology Biopsy of the area around the pylorus is essential to exclude malignancy The patient should also have an anti- secretory agent , initially given intravenously to ensure absorption

18. Management( contd ) Early cases -- settle with conservative treatment, ( Oedema around the ulcer diminishes as the ulcer is healed) Severe cases treated surgically, usually with a gastroenterostomy rather than a pyloroplasty Endoscopic treatment with balloon dilatation -- useful in early cases (Dilating the duodenal stenosis may result in perforation, and the dilatation may have to be performed several times and may not be successful in the long term)

19. Indications(Surgery) GOO due to benign ulcer disease may be 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 Typically, if resolution or improvement is not seen within 48-72 hours, surgical intervention is necessary The choice of surgical procedure depends upon the patient's particular circumstances

20. In cases of malignant obstruction, weigh the extent of surgical intervention for the relief of GOO against the malignancy's type and extent, as well as the patient's anticipated long-term prognosis As a guiding principle, undertake major tumor resections in the absence of metastatic disease(in fit pts) In patients with largely metastatic disease, determine the degree of surgical intervention for palliation in light of the patient's realistic prognosis and personal wishes

21. 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