- Represents a clinical and pathophysiological consequence of any disease process which produces mechanical impediment to gastric emptying
- Obstruction is at the level of pylorus
Etiology
| Benign causes | Malignant causes |
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Pathogenesis
- Intrinsic or extrinsic obstruction of pyloric channel/duodenum
- Depends on underlying etiology
- Obstruction of stomach → hypertrophy of stomach → dilation → gastritis and depressed acid secretion
Metabolic effects
- Prolonged vomiting causes loss of HCl and K+
- Leads to elevated bicarbonate levels as bicarbonate cannot be excreted without Cl–
- Results in hypokalemic hypochloremic metabolic alkalosis
- Aldosterone stimulates kidneys to preserve Na+ + H2O – K+ and H+ is excreted in the urine
- Causes paradoxical aciduria
- Alkalosis also leads to hypocalcemia – can cause tetany
Clinical features
- Nausea and vomiting – cardinal signs
- Vomiting – nonbilious, contains undigested food particles
- Weight loss – most common with malignancy
- Visible gastric peristalsis – seen by asking patient to drink water
Investigations
- Succussion splash – empty stomach for 4 hours, place stethoscope over epigastric region and shake patient
- Splashing sound indicates presence of gas and fluid
- FBC – anaemia
- Serum electrolytes – hypochloremia, hypokalemia, hyponatremia, metabolic alkalosis
- Urinalysis – aciduria
- XR abdomen – large gastric shadow and large amount of gastric fluid
- Gastric aspiration – if >400ml of juice obtained, presume a diagnosis of GOO
- Oesophagogastro-duodenoscopy and biopsy
- Barium meal – dilated stomach, hour glass/tea cup deformity
Treatment
- Correct electrolyte imbalance – IV fluids, acid-base correction
- Blood transfusion for anaemia
- Stomach wash to clean contents
Surgery
- Endoscopic balloon dilation
- Truncal vagotomy
- Pyloroplasty – if cause is pyloric stenosis
- Billroth I – gastroduodenostomy
- Billroth II – gastrojejunostomy