GASTRIC OUTLET OBSTRUCTION

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GASTRIC OUTLET OBSTRUCTION

  1. 1. GASTRIC OUTLET OBSTRUCTION PROF.MINOCHA
  2. 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. 3. CausesTwo 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. 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. 5. Frequency• The incidence less than 5% in pts. with PUD-- leading benign cause• Peripancreatic malignancy, the most common malignant etiology--- 15-20%.
  6. 6. EtiologyMajor benign causes of gastric outletobstruction (GOO) are--- PUD gastric polyps ingestion of caustics pyloric stenosis congenital duodenal webs gallstone obstruction (Bouveret syndrome) pancreatic pseudocysts and bezoars
  7. 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. 8. Etiology(Contd)Pediatric age group--- Pyloric stenosisPyloric stenosis occurs in 1 per 750 births Boys˃ Girls More common in first-born childrenPyloric stenosis ---- gradual hypertrophy of the circular smooth muscle of the pylorus
  9. 9. Etiology(Contd)• Pancreatic cancer is the most common malignancy causing GOO• Outlet obstruction may occur in 10-20%Other tumors include--- Ampullary cancer Duodenal cancer Cholangiocarcinomas Gastric cancer Metastases to the gastric outlet by other primary tumors
  10. 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. 11. Clinical features• Nausea and vomiting are the cardinal symptoms• Vomiting -- Nonbilious, 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. 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, epig astric pain, and weight loss Frequently malnourished and dehydrated and have a metabolic insufficiency Weight loss , most significant with malignant diseaseAbdominal pain is not frequent and usually relates to the underlying cause, eg, PUD, pancreatic cancer
  13. 13. Physical examinationChronic dehydration and MalnutritionOn examination :Distended stomach and a succussion splashmay be audible on shaking the patient’sabdomenA dilated stomach may be appreciated as atympanitic mass in the epigastric area and/orleft upper quadrant
  14. 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. 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. 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. 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. 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. 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 necessaryThe choice of surgical procedure depends upon the patients particular circumstances
  20. 20. • In cases of malignant obstruction, weigh the extent of surgical intervention for the relief of GOO against the malignancys type and extent, as well as the patients 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 patients realistic prognosis and personal wishes
  21. 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

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