Gastric outlet obstruction

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Obstruction can arise within the antrum, pylorus or proximal duodenum or from external compression. Peptic scarring and active oedema remain benign causes, while distal gastric cancer and pancreatic malignancy are major acquired causes in adults. Less common mechanisms include Crohn disease, bezoar, pancreatitis-related collections and postoperative anastomotic narrowing. The history establishes time course but cannot assign benignity.

Physiological repair precedes definitive testing. Vomiting removes gastric hydrochloric acid and generates metabolic alkalosis; accompanying chloride, circulating-volume and potassium depletion impairs renal bicarbonate excretion and maintains it. Aldosterone-mediated potassium and hydrogen loss can reinforce the disturbance. Nasogastric decompression reduces vomiting and aspiration and improves endoscopic visualisation. Restore chloride-rich fluid and potassium with observations, urine output, renal function, blood gas and electrolyte reassessment. The replacement volume and rate depend on losses and cardiac/renal reserve, not a universal bag count.

Treatment follows cause and intent. Endoscopic biopsy must be adequate because superficial benign tissue can miss an infiltrative tumour. A fit patient with resectable gastric cancer enters specialist MDT staging, perioperative chemotherapy and planned oncological resection when appropriate, rather than automatic palliation because vomiting occurred. In incurable malignant obstruction, a stent often restores intake quickly while gastrojejunostomy may be more durable in a fitter person with longer prognosis. Nutrition and symptom response require review after either intervention.

Key points

Gastric outlet obstruction causes early satiety, postprandial fullness and large-volume non-bilious vomiting of stale food because the block lies before bile enters the duodenum.
Repeated hydrogen and chloride loss produces hypochloraemic metabolic alkalosis; volume contraction activates aldosterone and promotes renal potassium and hydrogen loss.
Initial management is nil by mouth, nasogastric decompression, aspiration protection and measured chloride, potassium and volume correction before sedation or definitive intervention.
CT defines wall thickening, extrinsic pancreatic or nodal compression and metastatic disease; endoscopy directly inspects the channel and obtains multiple biopsies.
Benign peptic stenosis may improve as oedema settles with H pylori eradication and PPI, but fixed fibrosis often needs endoscopic balloon dilation or surgery.
For gastric-cancer outflow obstruction that is not curable, NICE offers an uncovered self-expanding metal stent or palliative surgery according to fitness, prognosis and disease extent.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Peptic pyloroduodenal disease

Active ulcer inflammation causes reversible oedema, while repeated healing deposits fixed fibrosis that narrows the pylorus or proximal duodenum.

Malignant narrowing

Distal gastric adenocarcinoma grows through the outlet wall, while pancreatic or nodal tumour can compress the duodenum from outside.

Postoperative or inflammatory stricture

Anastomotic scarring, Crohn inflammation, pancreatitis-related collections or caustic injury can narrow the gastric exit through distinct structural mechanisms.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Gastric retention
Failure of outflow accumulates food, secretions and swallowed air, stretching the stomach and causing early satiety, visible peristalsis and vomiting.
2
Chloride depletion alkalosis
Loss of gastric hydrochloric acid raises bicarbonate while extracellular-volume contraction and aldosterone perpetuate renal hydrogen and potassium excretion.
3
Nutritional failure
Reduced intake and recurrent vomiting deplete energy, protein and micronutrients, producing sarcopenia and refeeding risk once patency returns.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Stale-food vomiting

Large-volume non-bilious vomit containing food eaten many hours earlier strongly suggests retained gastric contents.

Visible gastric peristalsis

A distended stomach may generate left-to-right waves and a succussion splash several hours after intake.

Contraction alkalosis

Low chloride and potassium with raised bicarbonate reflects prolonged gastric acid loss and renal volume-conserving responses.

Malignant trajectoryRed flag

Progressive early satiety, weight loss, anaemia or a mass suggests infiltrative or extrinsic cancer until excluded.

Aspiration complicationRed flag

Cough, hypoxaemia, fever or new infiltrates after vomiting indicates respiratory contamination and may require airway support.

Red flags requiring action

Progressive vomiting, weight loss, iron-deficiency anaemia or a palpable epigastric mass requires urgent investigation for gastric, pancreatic or duodenal malignancy.
Fever, guarding, lactate rise, haematemesis or respiratory deterioration suggests aspiration, perforation, ischaemia or bleeding rather than uncomplicated retention.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Renal profile, magnesium and blood gasFirst step
Why
Quantify dehydration, alkalosis and potassium or chloride depletion.
Interpretation and limitations
Correct deficits with ECG and renal monitoring; severe alkalosis increases arrhythmia and ventilatory risk before sedation.
02
Nasogastric aspirate and output chart
Why
Decompress the stomach and measure continuing losses.
Interpretation and limitations
Large stale output supports retention; blood raises mucosal injury or tumour and persistent volume guides replacement.
03
Contrast CT abdomen
Why
Locate narrowing and identify wall, pancreatic, nodal or metastatic disease.
Interpretation and limitations
Distension ending at the pylorus localises obstruction, but tissue is needed to distinguish inflammation from infiltrative cancer.
04
Upper-GI endoscopy with biopsy
Why
Inspect the outlet, obtain tissue and assess traversability for treatment.
Interpretation and limitations
Decompress first when possible; sample a malignant-looking lesion adequately and repeat if clinical-radiological concern persists despite superficial negative tissue.
05
Nutrition and refeeding assessment
Why
Identify sarcopenia, micronutrient depletion and risk during renewed feeding.
Interpretation and limitations
Plan route around obstruction and monitor phosphate, potassium, magnesium and fluid shifts in a severely depleted patient.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Gastroparesis

Autonomic or medicine-related impaired motility causes retention without a fixed transition point, requiring structural exclusion before physiological testing.

Small-bowel obstruction

A more distal block often causes bilious vomiting, diffuse small-bowel dilation and different transition anatomy on CT.

Functional vomiting

Disordered gut-brain interaction can cause recurrent vomiting, but objective retention, alkalosis, weight loss or a transition point demands structural assessment.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01Malignant obstructionRestore physiology before choosing durabilityFirst stepA 74-year-old has three weeks of stale-food vomiting, 7 kg weight loss, chloride 78 mmol/L, potassium 2.8 mmol/L and CT thickening at the gastric antrum. He weighs 65 kg, has pH 7.51 and bicarbonate 35 mmol/L, creatinine 90 micromol/L, adequate urine output and no heart failure or potassium-raising medicines.

1Keep nil by mouth and decompress 2.3 litres of retained gastric fluid. After senior volume assessment and ECG, prescribe a ready-mixed one-litre bag of sodium chloride 0.9% with potassium chloride 40 mmol by controlled peripheral IV infusion over eight hours: 125 mL/hour and 5 mmol potassium/hour. This individually chosen first replacement is within NHS SPS adult NBM guidance of 20–40 mmol/L, peripheral concentration no greater than 40 mmol/L and usual rate no greater than 10 mmol/hour. Record intake, gastric losses, urine output, pressure, pulse, lungs and the infusion site; check potassium, sodium, chloride, magnesium and creatinine after the first bag before prescribing further replacement.
2After the first infusion potassium is 3.2 mmol/L without creatinine rise or pulmonary congestion; magnesium is normal. Further chloride/potassium replacement is adjusted to ongoing losses and repeat results. By the next day, potassium is 3.6, chloride 96, pH 7.43 and pulse 86/min, with adequate urine output and effective decompression. Endoscopy can now proceed with a documented sedation/aspiration plan: the non-traversable antral mass is sampled with at least eight targeted biopsies, confirming gastric adenocarcinoma.
3Staging shows unresectable peritoneal disease; the MDT weighs rapid uncovered metal stenting against palliative bypass and selects stenting because frailty and prognosis make major surgery disproportionate.
4Verify the observed result: contrast and soft diet pass after stent expansion, vomiting stops, potassium remains normal and dietetic follow-up is arranged before discharge.

02Benign peptic stenosisTreat oedema before declaring fibrosisEndoscopy finds a short pyloric narrowing around an active H pylori-positive benign ulcer and biopsies show no malignancy.

1Decompress and correct electrolyte abnormalities before therapeutic endoscopy.
2Eradicate H pylori, stop NSAIDs and give ulcer-healing acid suppression.
3Reassess passage after inflammation settles and use graded endoscopic balloon dilation if fixed narrowing persists.
4Verify oral tolerance and repeat gastric-ulcer endoscopy and biopsies before accepting a benign outcome.

03Diagnostic discordanceChallenge a superficial benign biopsyCT shows irregular antropyloric thickening and weight loss, but first forceps biopsies report reactive mucosa.

1Review endoscopic images, biopsy number and whether tissue reached the abnormal area.
2Repeat expert sampling or obtain deeper tissue while maintaining decompression and nutrition.
3Discuss the imaging-pathology discrepancy at the oesophago-gastric MDT rather than labelling it peptic scarring.
4DefinitiveDocument the final diagnosis and definitive relief plan before removing decompression.

Key medicines and prescribing safety2 treatments · regimens, roles and cautions

Reduces acid-related oedema and supports ulcer healing after the mechanical obstruction has been decompressed and its cause investigated.

Omeprazole for a benign peptic-ulcer component

Once decompression has restored a reliable oral route, give omeprazole 20 mg orally once daily for a gastric-ulcer component; the current SmPC expects healing within 4 weeks and permits a further 4 weeks when healing is incomplete. A poorly responsive ulcer may use 40 mg once daily under specialist review while persistent obstruction and malignancy are reinvestigated. Use the morning dose as an intact capsule with water once oral absorption is reliable; do not chew or crush the enteric-coated contents.

Do not rely on PPI response to label an adult outlet obstruction benign. Exclude and biopsy gastric cancer and correct electrolyte and volume deficits before procedures. In hepatic impairment the SmPC states 10–20 mg daily may be sufficient, so avoid automatic escalation to 40 mg. Review the nelfinavir contraindication, clopidogrel and CYP2C19 interactions, acute interstitial nephritis and prolonged-treatment magnesium or B12 risk. No dose adjustment is required solely for renal impairment.

Replaces potassium, chloride and extracellular fluid lost during prolonged vomiting while decompression and diagnosis address the obstruction.

Premixed potassium chloride 0.3% in sodium chloride 0.9% for vomiting-related depletion

For the monitored 65 kg adult in the worked case, the initial prescription is one litre containing 40 mmol potassium over eight hours by controlled peripheral IV infusion. NHS SPS supports 20–40 mmol/L initially when a moderately hypokalaemic adult cannot use the enteral route; do not exceed 40 mmol/L peripherally or the usual 10 mmol/hour rate. Choose every subsequent dose from repeat potassium and continuing losses, not a prewritten series of bags. Never inject concentrated potassium directly; use a commercially prepared diluted bag.

Before and during infusion assess urine flow, fluid balance, potassium, sodium, chloride, magnesium, renal function and acid-base status; obtain ECG monitoring according to clinical risk, concentration and rate. The selected Baxter product is contraindicated in hyperkalaemia, hyperchloraemia, hypernatraemia, severe renal insufficiency with oliguria/anuria, uncompensated heart failure, Addison disease or product hypersensitivity. Lesser renal impairment requires lower individually reassessed doses. Review potassium-sparing diuretics, ACE inhibitors, ARBs and other potassium-raising medicines. Stop or reduce infusion for rising potassium or fluid overload and escalate new arrhythmia. Its total potassium ceiling is 2–3 mmol/kg/24 hours, not a replacement target.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Aspiration pneumonia

Large retained volumes reflux into the oesophagus and airway, causing hypoxaemia, chemical pneumonitis and later bacterial infection.

Acute kidney injury

Prolonged salt and water loss reduces renal perfusion, while alkalosis and potassium depletion increase arrhythmia and neuromuscular risk.

Severe malnutrition

Inability to pass adequate nutrition leads to rapid weight loss, immune impairment, poor wound healing and intolerance of cancer treatment.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Measure nasogastric losses, fluid input, urine output and daily weight during correction.
Repeat chloride, potassium, bicarbonate, magnesium and creatinine until stable before intervention.
Track aspiration signs and oxygen requirement throughout decompression and feeding trials.
After stent or bypass, document vomiting frequency, diet texture, weight and device or anastomotic complications.
Close the loop on biopsy, cancer stage and gastric-ulcer healing rather than treating restored intake as diagnosis.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Bile localises the block

Vomiting is usually non-bilious when obstruction lies proximal to the duodenal entry of the bile duct.

Potassium loss is partly renal

Volume contraction and aldosterone drive urinary potassium loss even though gastric fluid itself contains less potassium than chloride.

Stent and bypass trade time

A stent offers rapid low-burden relief, while surgical bypass may provide longer patency in a sufficiently fit patient.

Decompression improves diagnosis

Removing retained food lowers aspiration risk and permits better visualisation of the pylorus and gastric mucosa.

11Common pitfallsFrequent interpretation and management errors.

01
Sedating for endoscopy before decompressing a stomach full of retained food.
02
Correcting potassium without addressing chloride and volume depletion that sustains renal loss.
03
Accepting one superficial biopsy despite malignant imaging and weight loss.
04
Choosing a palliative stent before staging a potentially curable gastric cancer.

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