Gastric Outlet Obstruction
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Direct answer
The succussion splash elicited by rocking the abdomen, with vomiting of large volumes of undigested food eaten hours earlier, defines gastric outlet obstruction. In Indian adults the commonest cause is malignancy — antral gastric carcinoma or lymphoma — while benign peptic stricture, once the textbook cause, now appears mainly in younger patients with untreated acid disease. The signature biochemistry is hypochloraemic, hypokalaemic metabolic alkalosis with paradoxical aciduria from loss of gastric hydrochloric acid. Correction with normal saline and potassium chloride precedes any operation, because anaesthetising an alkalaemic, hypokalaemic patient invites arrhythmia and apnoea; definitive treatment then follows the cause — dilatation for benign strictures, stenting or gastrojejunostomy for malignancy.
What you must remember
- Causes by era and geography: malignancy of the gastric antrum or pyloric channel dominates adult Indian practice; peptic ulcer stricture, caustic ingestion and gastroduodenal tuberculosis remain in the differential.
- Clinical signs: visible gastric peristalsis, a succussion splash more than four hours after the last meal, dehydration and a distended stomach; classically the patient vomits previous meals and feels relieved afterwards.
- The classic biochemistry: hypochloraemic, hypokalaemic metabolic alkalosis with paradoxical aciduria — the kidney excretes hydrogen ions to conserve sodium and potassium when chloride is depleted.
- Investigation: upper GI endoscopy with biopsy is the pivotal test; a saline load test or gastrograffin meal may demonstrate retention, and CT stages malignant disease.
- Resuscitation sequence: nasogastric decompression, normal saline with potassium chloride, monitoring of urine output, serum chloride above 100 mmol/L and bicarbonate trend toward normal — usually 48 to 72 hours before intervention.
- Benign peptic strictures: endoscopic balloon dilatation (often repeated) with acid suppression; truncal vagotomy with gastrojejunostomy if dilatation fails.
- Malignant obstruction: duodenal stenting for palliation in advanced disease, or surgical gastrojejunostomy (open or laparoscopic) when prognosis justifies it; lymphoma may respond to chemotherapy alone.
- Watch the stomach: prolonged stasis causes gastritis, candidal overgrowth and protein-losing enteropathy, all of which worsen operative risk.
Correcting the chemistry before surgery
Understand the physiology and the management writes itself. Vomiting discards hydrochloric acid, so chloride and hydrogen are lost together; the extracellular volume contracts, aldosterone rises, and the distal nephron reabsorbs sodium in exchange for whatever cations it can spare. Because chloride is exhausted, the excretable anion becomes bicarbonate, and hydrogen and potassium are wasted into urine — hence urine that is paradoxically acidic while the blood is alkalaemic. Volume depletion also drives renal bicarbonate generation, deepening the alkalosis. The treatment is therefore sodium chloride with potassium chloride in generous volume, not acid, and not diuretics; as chloride is repleted, the kidney can excrete bicarbonate and the alkalosis resolves. Correction is judged by rising serum chloride, falling bicarbonate, a normalising blood pH and a healthy urine output. Only after this — and gastric decompression to shrink the atonic stomach — should endoscopy or theatre proceed. The exam vignette of a patient who becomes apnoeic after induction exists precisely to test whether you learned this order.
The Indian practice picture
Two patterns dominate Indian wards. The first is the elderly man with weight loss, a palpable epigastric mass and an outflow obstruction that endoscopy shows to be an ulcerated antral growth; the examiners expect you to stage with CT, biopsy, correct the alkalosis, and then choose between a palliative stent and a gastrojejunostomy depending on fitness and stage — with lymphoma, for which chemotherapy is definitive, always excluded before committing to surgery. The second is the younger patient with a chronic prepyloric ulcer stricture, long histories of pain self-treated with over-the-counter acidsuppressants; here balloon dilatation with Helicobacter pylori eradication and proton pump inhibitor maintenance is the modern ladder, with vagotomy and drainage held in reserve. A third entity worth naming for Indian vivas is gastric tuberculosis, which can mimic antral carcinoma exactly, and corrosive strictures after acid ingestion, which distort the anatomy enough to demand creative bypass rather than dilatation.
Frequently asked questions
What is paradoxical aciduria in gastric outlet obstruction?
Acidic urine despite a metabolic alkalosis, occurring because severe chloride depletion forces the kidney to excrete hydrogen ions to conserve sodium under high aldosterone drive.
How is the alkalosis of gastric outlet obstruction corrected?
Intravenous normal saline with potassium chloride over 48-72 hours, guided by serum chloride, bicarbonate and urine output — repleting chloride allows renal bicarbonate excretion.
Which is the commonest cause of gastric outlet obstruction in Indian adults?
Malignant antral gastric carcinoma (with lymphoma second), reflecting the pattern seen in Indian gastroenterology and surgical series.
What role does endoscopic balloon dilatation have?
It is first-line for benign peptic outlet strictures, commonly needing repeat sessions with acid suppression, reserving surgery for refractory strictures.
When is a duodenal stent preferred to gastrojejunostomy?
In advanced unresectable malignancy with short expected survival or poor operative fitness, a self-expanding metal duodenal stent restores feeding with far less physiological insult.