Gastric outlet obstruction

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

Outlet obstruction causes progressive retention, early satiety, postprandial fullness and non-bilious vomiting, often of food eaten many hours earlier. Bilious vomiting suggests the block lies beyond the ampulla or that anatomy is altered. On examination there may be dehydration, visible peristalsis, upper abdominal distension and a succussion splash, but these findings are neither sensitive nor specific. Prolonged poor intake creates sarcopenia, micronutrient deficiency and refeeding risk.

Aetiology has shifted from ulcer scarring toward malignancy in many contemporary adult services. Intrinsic lesions include antral cancer, pyloric ulcer and duodenal tumour; extrinsic causes include pancreatic cancer, inflammatory pancreatic mass and nodal compression. Acute ulcer oedema may be reversible, whereas dense fibrosis is not. Gastroparesis remains a mimic, but that diagnosis requires a patent outlet and objective delayed emptying rather than assumption from a food-filled stomach.

Initial treatment separates resuscitation from definitive relief. Replace sodium chloride, potassium, magnesium and renal losses according to serial results, decompress when distension or aspiration warrants it, and provide thiamine and controlled nutrition for depleted patients. CT precedes or complements endoscopy, which supplies histology. The MDT then weighs endoscopic balloon dilatation, enteral stenting, gastrojejunostomy or tumour-directed treatment by cause, durability required, operative risk and expected survival.

Key points

Gastric outlet obstruction is a mechanical block at the antrum, pylorus or proximal duodenum; retained food and delayed emptying alone do not define its cause.
Gastric, duodenal and pancreatic malignancy must be considered in an adult with new obstruction, especially with weight loss, anaemia, jaundice, a mass or progressive course.
Benign causes include peptic-ulcer scarring, inflammatory oedema, Crohn's disease, pancreatitis or pseudocyst, bezoar and postoperative or anastomotic stenosis.
Repeated vomiting depletes hydrochloric acid and volume, producing hypochloraemic, hypokalaemic metabolic alkalosis with paradoxical aciduria when depletion becomes severe.
Contrast CT defines level, mural disease, extrinsic compression and metastases; upper-GI endoscopy after initial decompression directly inspects and biopsies the narrowing.
A nasogastric tube can relieve distension and reduce aspiration risk but does not diagnose or definitively treat a tumour or fibrotic stricture.
Benign peptic narrowing may improve as oedema settles with PPI and H. pylori treatment, while fixed stenosis can require graded balloon dilatation or surgery.
Malignant obstruction is managed through an MDT using systemic or oncological treatment, duodenal stenting, surgical bypass or other expert techniques according to prognosis and goals.

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

Malignant obstruction

Gastric, duodenal and pancreatic cancers can narrow the distal stomach or proximal duodenum, often with progressive weight loss or jaundice.

Peptic scarring and inflammation

Chronic peptic-ulcer fibrosis or acute inflammatory oedema around the pylorus can impede emptying, particularly with H. pylori or NSAID exposure.

Postoperative and other structural causes

Anastomotic stricture, Crohn disease, pancreatitis, pseudocyst, bezoar and altered upper-GI anatomy can create a mechanical block.

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

1
Mechanical retention
Luminal narrowing prevents gastric contents entering the duodenum, causing progressive distension, early satiation and late vomiting of recognisable food.
2
Hydrogen and chloride loss
Repeated vomiting removes gastric acid and volume, producing hypochloraemic metabolic alkalosis, hypokalaemia and compensatory renal sodium retention.
3
Nutritional and aspiration decline
Continued retention reduces oral intake and allows regurgitated material to enter the airway, causing weight loss, dehydration and pneumonia.

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

Retained meal vomiting

Progressive postprandial fullness followed by large-volume non-bilious vomiting of stale food is characteristic. Ask whether liquids still pass and quantify urine output and weight loss.

Aspiration threatRed flag

Coughing, hypoxaemia, altered consciousness or copious supine vomiting signals airway danger. Sit upright, use suction and seek anaesthetic support before sedation or transfer.

Contraction alkalosisRed flag

Weakness, cramps, arrhythmia and reduced consciousness can accompany severe chloride, potassium and volume depletion. An apparently high bicarbonate should prompt urgent correction and ECG review.

Malignant pattern

Short progressive history, disproportionate weight loss, iron-deficiency anaemia, palpable epigastric node or mass, jaundice or new symptoms in later life should accelerate CT, biopsy and cancer MDT review.

Peptic scar pattern

Long ulcer history, prior H. pylori or NSAID exposure and a short concentric pyloric narrowing may suggest benign disease, but adult obstruction still requires adequate malignancy exclusion.

Perforation or ischaemiaRed flag

Sudden severe pain, guarding, fever, lactate rise or free air suggests a complication beyond simple retention and needs emergency surgical management.

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
U&E, magnesium and blood gasFirst step
Why
Quantify vomiting-related depletion and guide safe fluid replacement.
Interpretation and limitations
Low chloride and potassium with raised bicarbonate support contraction alkalosis. Renal impairment and lactate indicate physiological consequence; correct potassium only with appropriate renal and ECG monitoring.
02
FBC, LFT and nutritional profile
Why
Find anaemia, biliary involvement and consequences of prolonged poor intake.
Interpretation and limitations
Iron-deficiency anaemia raises malignant or ulcer bleeding concern. Cholestasis can indicate pancreatic or nodal compression; phosphate depletion and weight loss inform refeeding precautions.
03
Contrast CT abdomen and pelvis
Why
Define the transition, primary lesion, extrinsic disease and complications.
Interpretation and limitations
Review antral and duodenal wall, pancreas, nodes, liver and peritoneum. A distended stomach without a visible cause may still need endoscopic evaluation; a metastatic pattern changes the intervention goal.
04
Upper-GI endoscopy with biopsy
Why
Directly inspect, sample and sometimes traverse or treat the obstruction.
Interpretation and limitations
Decompress and plan aspiration protection first when large retained volume is likely. Multiple adequate biopsies are required from suspicious tissue; a negative superficial sample may need repeat or EUS-guided acquisition.
05
Water-soluble contrast study
Why
Answer selected anatomical or functional questions when endoscopy and CT leave uncertainty.
Interpretation and limitations
It can demonstrate transit and stricture length in altered anatomy but adds no histology. Aspiration risk and the possibility of perforation determine whether and how it is used.
06
Histology and cancer staging
Why
Distinguish benign ulcer scarring from gastric, duodenal or pancreatobiliary malignancy.
Interpretation and limitations
The route follows the lesion: mucosal biopsy for luminal tumour, EUS or radiological biopsy for selected extrinsic masses, and full staging only after tissue and MDT review where feasible.

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

Gastroparesis

Delayed emptying with no endoscopic or imaging transition point supports a motor disorder only after medicines and metabolic causes are reviewed.

Proximal small-bowel obstruction

A transition beyond the duodenum, dilated small bowel and prior abdominal surgery favour adhesional or other intestinal obstruction.

Rumination or functional vomiting

Effortless early postprandial return without retained stomach, biochemical depletion or structural narrowing suggests a behavioural or gut-brain disorder.

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

01DecompressStabilise retained stomachFirst stepPersistent vomiting, distension or imaging confirms a functionally important gastric outlet blockage.

1Keep nil by mouth, elevate the head, assess aspiration and insert venous access; use nasogastric decompression when indicated with position and output documented.
2Replace isotonic fluid, chloride, potassium and magnesium according to serial laboratory, ECG, urine output and renal findings rather than a fixed generic bag sequence.
3Give thiamine and plan controlled nutrition in major depletion, while arranging CT and an endoscopy strategy that accounts for the food-filled stomach and sedation risk.

02DiagnoseFind and sample the transitionInitial physiology is sufficiently controlled for anatomical investigation and tissue acquisition.

1Use contrast CT to map intrinsic and extrinsic disease, complications and metastases, then communicate the exact transition and likely cause to the endoscopy team.
2Perform high-quality upper-GI endoscopy with adequate aspiration precautions and multiple targeted biopsies, avoiding forceful traversal or premature dilatation of an uncharacterised malignant-looking stricture.
3EscalationEscalate non-diagnostic tissue through repeat endoscopy, EUS or radiological biopsy and route confirmed cancer to the appropriate oesophago-gastric or pancreatobiliary MDT.

03RelieveChoose durable palliation or cureThe cause, stage, expected course and patient's treatment priorities have been clarified.

1For inflammatory peptic narrowing, treat ulcer and H. pylori first where safe; use graded balloon dilatation for selected benign fixed stenosis and plan surgery when recurrence or anatomy makes endoscopy unsuitable.
2For malignancy, compare stenting, surgical bypass, tumour resection and systemic or radiotherapy response by speed, durability, performance status, expected survival and local expertise.
3After restoring transit, advance nutrition with refeeding safeguards, monitor recurrent vomiting and stent or anastomotic complications, and maintain cause-specific oncological or ulcer follow-up.

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

Reduces acid-driven oedema and promotes healing when peptic ulcer contributes to pyloric or duodenal narrowing.

Proton-pump inhibitor for peptic inflammatory obstruction

Use a named full-dose formulary PPI through an available route while active ulcer inflammation is treated, then define duration from endoscopic healing, H. pylori status and whether fixed scarring remains.

PPI cannot relieve malignant or dense fibrotic obstruction. Review interactions and long-term indication, and plan H. pylori testing around PPI washout when the acute situation permits.

There is no therapeutic role for driving gastric contraction against an unrelieved fixed blockage.

Prokinetic treatment

Do not prescribe while a mechanical gastric outlet obstruction is present; reconsider only after anatomy is patent and a separate motility disorder is objectively supported.

Metoclopramide and domperidone are contraindicated when stimulation may harm in obstruction, bleeding or perforation. Vomiting relief must come from decompression and cause-directed treatment rather than unsafe motility stimulation.

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

Volume and kidney injury

Persistent vomiting causes severe extracellular depletion, orthostatic hypotension and acute kidney injury despite apparently little diarrhoeal loss.

Electrolyte and rhythm disturbance

Potassium, chloride and hydrogen loss causes alkalosis, weakness and arrhythmia, requiring correction before sedation or intervention.

Aspiration and malnutrition

A distended food-filled stomach increases aspiration risk during sleep or procedures, while prolonged obstruction causes sarcopenia and micronutrient deficiency.

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

Chart nasogastric or vomit volume, oral intake, abdominal distension, aspiration signs, urine output and daily weight during initial correction.
Trend sodium, chloride, potassium, bicarbonate, magnesium, phosphate, creatinine and ECG findings until depletion and alkalosis are stably corrected.
Monitor for refeeding syndrome as nutrition resumes after prolonged restriction, using the NICE CG32 risk and laboratory framework.
Track biopsy adequacy, pathology, staging and MDT decision, with repeat tissue acquisition when a malignant-looking lesion has a non-diagnostic superficial sample.
After balloon dilatation or stenting, review perforation, bleeding, migration, tumour ingrowth, recurrent vomiting and the durability of oral intake.
For benign peptic disease, confirm H. pylori cure, ulcer healing and NSAID modification so oedema or scarring does not recur.

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

Urine may be acidic

Severe volume and potassium depletion can make the kidney retain sodium in exchange for hydrogen, producing paradoxical aciduria despite systemic alkalosis.

Food needs a cause

Retained gastric contents occur in both gastroparesis and obstruction; a transition, biopsy and patent-outlet assessment decide which mechanism is present.

Decompression buys safety

Removing retained volume can reduce vomiting and aspiration and improve endoscopic visualisation, but it does not alter the underlying stricture biology.

Negative biopsy may miss

Infiltrative gastric cancer or extrinsic pancreatic disease can leave superficial mucosa non-diagnostic, requiring a different depth or route of tissue acquisition.

Durability changes choice

A stent may restore intake quickly while bypass can last longer; expected survival, operative fitness and future treatment shape the better option.

11Common pitfallsFrequent interpretation and management errors.

01
Calling a food-filled stomach gastroparesis without excluding a fixed pyloric or duodenal lesion.
02
Giving metoclopramide or domperidone before mechanical obstruction is relieved.
03
Correcting potassium without concurrent chloride, volume, renal and ECG assessment.
04
Performing sedated endoscopy without anticipating a large retained gastric volume and aspiration risk.
05
Accepting one superficial negative biopsy from an irregular malignant-looking narrowing as definitive reassurance.
06
Restoring full calories immediately after prolonged starvation without assessing refeeding risk.