Surgery chapters
Stomach and duodenum: peptic ulcer complications, gastric outlet obstruction and gastric cancer
Surgical anatomy of the stomach, H. pylori and peptic ulcer, the three big complications of peptic ulcer (perforation, bleeding and gastric outlet obstruction), operations on the stomach and their after-effects, and gastric cancer, GIST and lymphoma.
- Perforated peptic ulcer (usually the anterior duodenal wall) gives sudden severe pain and board-like rigidity; gas under the diaphragm on erect chest X-ray, CT if unsure; treat with resuscitation, omental patch repair and H. pylori eradication.
- Bleeding comes mostly from a posterior duodenal ulcer eroding the gastroduodenal artery; endoscopic therapy first, then embolisation or surgery. Benign gastric outlet obstruction causes hypochloraemic hypokalaemic metabolic alkalosis with paradoxical aciduria; correct with normal saline plus potassium.
- Gastric cancer is mostly adenocarcinoma (intestinal or diffuse); diagnose by endoscopy and biopsy, stage with CT and laparoscopy, cure needs gastrectomy with D2 lymphadenectomy plus perioperative chemotherapy.
On this page
Overview
Peptic ulcer disease is now mostly treated with PPIs and H. pylori eradication, so elective ulcer surgery has almost disappeared. Surgeons still meet its complications: perforation, bleeding and gastric outlet obstruction. Gastric cancer remains common worldwide and is usually found late.
Surgical anatomy in brief
| Artery | Course |
|---|---|
| Left gastric (coeliac trunk) | Upper lesser curve |
| Right gastric (hepatic artery) | Lower lesser curve |
| Right gastroepiploic (gastroduodenal) | Lower greater curve |
| Left gastroepiploic (splenic) | Upper greater curve |
| Short gastrics (splenic) | Fundus |
| Gastroduodenal | Behind the first part of the duodenum |
- Parietal cells (body and fundus): acid and intrinsic factor. Chief cells: pepsinogen. G cells (antrum): gastrin.
- Vagus nerves: anterior (left) and posterior (right); they drive acid secretion and antral emptying.
Peptic ulcer disease
Causes: H. pylori (most duodenal ulcers and many gastric ulcers), NSAIDs and aspirin (often together with H. pylori), smoking, Zollinger-Ellison syndrome (gastrinoma: multiple, distal or recurrent ulcers), stress ulcers in critical illness.
| Feature | Duodenal ulcer | Gastric ulcer |
|---|---|---|
| Acid | Normal or high | Normal or low |
| Pain | Hunger pain, relieved by food, night pain | Pain brought on by food |
| Cancer risk | Almost never malignant | Must be biopsied (cancer can look like a benign ulcer); repeat endoscopy to confirm healing |
Diagnosis: endoscopy (with biopsy of every gastric ulcer) and H. pylori testing (urea breath test, stool antigen, biopsy urease test).
Treatment: PPI plus H. pylori eradication (for example PPI plus clarithromycin plus amoxicillin or metronidazole); stop NSAIDs. Local resistance patterns differ, so follow current national guidance.
Perforated peptic ulcer
- Commonest site: anterior wall of the first part of the duodenum. Anterior gastric ulcers also perforate; posterior gastric ulcers may leak into the lesser sac with few signs.
- Now mostly elderly patients on NSAIDs.
Clinical features:
- Sudden, severe epigastric pain that spreads over the whole abdomen; may be felt in the shoulder tip.
- The patient lies still; board-like rigidity; the abdomen does not move with breathing; loss of liver dullness.
- Early phase of chemical peritonitis, then a quieter interval, then bacterial peritonitis after some hours.
- Fluid tracking down the right paracolic gutter can mimic appendicitis.
Investigations:
- Erect chest X-ray: gas under the diaphragm in just over half of cases; its absence does not exclude perforation.
- CT abdomen: more accurate; shows extraluminal gas and fluid.
- Serum amylase: can rise mildly, but not to pancreatitis levels; always check to avoid operating on pancreatitis.
Management:
- Resuscitate: IV fluids, nasogastric tube, urinary catheter, analgesia, IV PPI, broad-spectrum antibiotics.
- Laparoscopic or open repair: peritoneal lavage, then close the hole and cover it with a pedicled omental patch (Graham patch), or use the patch alone.
- Biopsy a gastric perforation; a large gastric ulcer or cancer may need gastrectomy.
- After recovery: H. pylori eradication and stop NSAIDs. Definitive acid-reducing operations are no longer needed.
- Conservative (Taylor) treatment: only for selected patients with a sealed leak (water-soluble contrast shows no leak) and mild signs, under close watch.
No gas under the diaphragm does not rule out perforation. If the story fits, get a CT.
Bleeding peptic ulcer
- Commonest cause of upper GI bleeding; often elderly patients on NSAIDs or anticoagulants.
- The worst bleeds come from a posterior duodenal ulcer eroding the gastroduodenal artery, or a lesser curve gastric ulcer eroding the left gastric artery.
Risk scores: Glasgow-Blatchford (before endoscopy; who needs intervention) and Rockall (rebleeding and death). Endoscopic stigmata are graded by the Forrest classification: active spurting and a visible vessel carry the highest rebleeding risk.
Management:
- Resuscitate (two large cannulae, blood, correct coagulopathy).
- Endoscopy within 24 hours (immediately if unstable): dual therapy such as adrenaline injection plus clips or a heater probe.
- IV PPI after endoscopic haemostasis to reduce rebleeding.
- Rebleeding or failed endoscopy: repeat endoscopy, angiographic embolisation, or surgery.
Indications for surgery: continued bleeding despite endoscopy, significant rebleeding, massive transfusion (more than about 6 units), when embolisation is unavailable or fails. Elderly patients tolerate rebleeding poorly and should go to theatre earlier.
Operation for a bleeding duodenal ulcer: mobilise the duodenum, open the pylorus and duodenum longitudinally, under-run the gastroduodenal artery with sutures above, below and medially (the transverse pancreatic branch), then close as a pyloroplasty.
Gastric outlet obstruction
Causes: in adults today the commonest cause is gastric (antral) cancer; next is scarring from chronic duodenal or pyloric channel ulcer ("pyloric stenosis", usually duodenal not pyloric). Others: pancreatic cancer invading the duodenum, adult hypertrophic pyloric stenosis, gastric bezoar.
Treat every adult outlet obstruction as malignant until biopsy proves otherwise.
Clinical features:
- Projectile, non-bilious vomiting of large volumes of stale food eaten a day or more before.
- Weight loss, dehydration; visible gastric peristalsis from left to right; succussion splash more than about 4 hours after a meal.
Metabolic effects (benign obstruction)
- Loss of HCl in vomit causes hypochloraemic metabolic alkalosis.
- Early, the kidney excretes bicarbonate with sodium and some potassium, so the urine is alkaline.
- As dehydration worsens, aldosterone makes the kidney hold sodium and swap it for K+ and H+: hypokalaemia develops and the urine becomes acidic despite systemic alkalosis (paradoxical aciduria).
- Alkalosis lowers ionised calcium, so tetany may occur.
The picture is milder in cancer because the stomach makes less acid.
Weight 60 kg; serum chloride 80 mmol/L; target 100 mmol/L
Chloride deficit = 0.2 × 60 × (100 − 80) = 240 mmol (0.2 L/kg is the extracellular space)
This is given as 0.9% saline (154 mmol/L Cl) with potassium; about 240 / 154 ≈ 1.6 L, on top of maintenance and losses.
Management:
- IV 0.9% saline with potassium chloride; this lets the kidney correct the alkalosis. Monitor urine output.
- Empty the stomach with a wide-bore nasogastric or orogastric tube; lavage if needed.
- IV PPI.
- Endoscopy with biopsy once the stomach is empty; contrast study or CT.
- Benign: early cases may settle with PPI; endoscopic balloon dilatation; gastrojejunostomy (or pyloroplasty) if this fails.
- Malignant: gastrectomy if resectable; otherwise duodenal stent or palliative gastrojejunostomy.
Benign pyloric stenosis = hypochloraemic, hypokalaemic metabolic alkalosis with paradoxical aciduria; the fluid of choice is 0.9% sodium chloride with added potassium.
Operations on the stomach and their after-effects
| Operation | What it is |
|---|---|
| Billroth I | Distal gastrectomy with gastroduodenal anastomosis |
| Billroth II (Polya) | Distal gastrectomy, duodenal stump closed, gastrojejunal anastomosis |
| Roux-en-Y | Gastric remnant joined to a Roux limb of jejunum; prevents bile reflux; now preferred |
| Truncal vagotomy + drainage | Cuts both vagal trunks; needs pyloroplasty or gastrojejunostomy because the pylorus stops opening |
| Highly selective vagotomy | Denervates only the acid-secreting body; keeps antral nerves (nerves of Latarjet "crow's foot"), so no drainage needed |
Post-gastrectomy syndromes
| Problem | Mechanism and treatment |
|---|---|
| Early dumping (almost at once after eating) | Hyperosmolar food rushes into the jejunum, drawing fluid in; vasomotor symptoms (sweating, palpitations, faintness, flushing) with abdominal fullness and diarrhoea; small dry meals, avoid sugary fluids, lie down after meals; octreotide; revision to Roux-en-Y if severe |
| Late dumping (in the second hour after a meal) | Rapid sugar absorption causes a surge of insulin, then reactive hypoglycaemia; eat less carbohydrate, take sugar when symptoms start |
| Bile (alkaline) reflux gastritis and vomiting | Bile enters the remnant; Roux-en-Y diversion |
| Afferent loop syndrome | After Billroth II; obstructed afferent limb fills with bile and then empties suddenly, causing projectile bilious vomiting that relieves pain |
| Post-vagotomy diarrhoea | Intermittent; loperamide, codeine |
| Nutritional | Iron deficiency, B12 deficiency (lifelong injections after total gastrectomy), osteoporosis, weight loss |
| Gastric stump cancer | Risk rises after 10 or more years, especially after drainage operations |
Gastric cancer
Risk factors
- H. pylori (chronic atrophic gastritis, then intestinal metaplasia, dysplasia and cancer: the Correa sequence); H. pylori mainly causes distal cancers.
- Diet high in salt, smoked and pickled food, nitrosamines; low fruit and vegetables.
- Smoking; pernicious anaemia and atrophic gastritis; adenomatous gastric polyps; previous gastric surgery (stump).
- Blood group A; hereditary diffuse gastric cancer (CDH1, E-cadherin); Lynch syndrome.
- Proximal (cardia) cancers relate to obesity and reflux, not H. pylori.
Pathology
- Almost all are adenocarcinoma.
- Lauren classification:
- Intestinal type: gland-forming, arises on intestinal metaplasia, older men, polypoid or ulcerating, better prognosis.
- Diffuse type: poorly cohesive signet ring cells spreading through the wall; younger patients; worse prognosis. Extensive diffuse spread gives a rigid, thick "leather bottle" stomach (linitis plastica).
- Early gastric cancer: limited to the mucosa and submucosa regardless of nodes; about 90% survive 5 years after resection. Japanese screening finds many at this stage.
- Advanced cancer: invades the muscularis propria; Borrmann types I to IV (IV = diffusely infiltrating).
Spread and classic signs
| Route | Sign |
|---|---|
| Lymphatic | Virchow node in the left supraclavicular fossa (Troisier sign); Irish node (left axillary) |
| Transperitoneal | Ascites, Krukenberg tumours (ovaries), Blumer shelf (rectovesical or rectouterine pouch on rectal examination), Sister Mary Joseph nodule (umbilicus) |
| Blood | Liver first, then lung and bone |
| Direct | Pancreas, transverse colon, spleen, liver |
Clinical features
- Early disease: vague dyspepsia, indistinguishable from benign disease. Alarm features in anyone over about 55 or with new dyspepsia: weight loss, anaemia, dysphagia, persistent vomiting, a mass, GI bleeding.
- Advanced: epigastric mass, cachexia, outlet obstruction (antral tumours), dysphagia (cardia tumours), the signs of spread above, acanthosis nigricans, migratory thrombophlebitis.
PPIs can heal a malignant ulcer and mask symptoms. Do endoscopy with biopsy before long-term acid suppression in patients with alarm features.
Investigations and staging
- Upper GI endoscopy with multiple biopsies: the diagnostic test.
- CT chest, abdomen and pelvis: liver and lung metastases, nodes.
- Endoscopic ultrasound: depth of invasion for early tumours.
- Staging laparoscopy with peritoneal washings: finds peritoneal deposits missed by CT; done before any attempt at cure.
- PET-CT in selected cases. Tumour markers (CEA, CA 19-9) are not diagnostic.
Treatment
- Early cancer (mucosal): endoscopic mucosal resection or submucosal dissection.
- Resectable cancer: perioperative chemotherapy (for example FLOT) plus surgery.
- Distal (antral) tumours: subtotal (distal) gastrectomy with Roux-en-Y or Billroth II reconstruction.
- Proximal and body tumours, and diffuse type: total gastrectomy with Roux-en-Y oesophagojejunostomy.
- Aim for clear margins (about 5 cm from the tumour edge for gastric cancer) and a D2 lymphadenectomy (perigastric N1 nodes plus nodes along the left gastric, common hepatic, coeliac and splenic arteries), keeping the spleen and pancreas when possible.
- Palliation: chemotherapy (HER2-targeted therapy if positive), stent or gastrojejunostomy for obstruction, radiotherapy or embolisation for bleeding.
Gastric cancer is adenocarcinoma; H. pylori is a class 1 carcinogen for it. Diagnosis is by endoscopy and biopsy; staging laparoscopy detects peritoneal spread.
Other gastric tumours
| Tumour | Key facts |
|---|---|
| GIST (gastrointestinal stromal tumour) | Mesenchymal, from the interstitial cells of Cajal; commonest site stomach; c-kit (CD117) and DOG1 positive; mucosa often intact (submucosal mass), may ulcerate and bleed; size above 5 cm and high mitotic count predict malignancy; spreads to liver and peritoneum, rarely lymph nodes; treat by wedge or local resection without lymphadenectomy; imatinib for advanced, unresectable or high-risk tumours |
| Gastric lymphoma (MALT) | Commonest site of extranodal lymphoma; low-grade MALT lymphoma is linked to H. pylori and may regress after eradication; higher grades need chemotherapy |
| Neuroendocrine (carcinoid) tumours | Associated with atrophic gastritis and high gastrin |
"GIST gets imatinib, MALT gets H. pylori eradication, adenocarcinoma gets D2."
Other conditions worth knowing
- Gastric volvulus: usually with a paraoesophageal hernia; Borchardt triad: severe epigastric pain, retching without vomiting, inability to pass a nasogastric tube.
- Acute gastric dilatation: after surgery or trauma; decompress with a nasogastric tube.
- Dieulafoy lesion: a large submucosal artery in the upper stomach that bleeds massively through a tiny defect.
- Superior mesenteric artery syndrome: third part of the duodenum compressed between the aorta and SMA after rapid weight loss.
Expect: the commonest site of perforation (anterior first part of duodenum), gas under the diaphragm on erect chest X-ray and the value of CT, omental (Graham) patch and H. pylori eradication; posterior duodenal ulcer eroding the gastroduodenal artery and indications for surgery in bleeding; gastric outlet obstruction with hypochloraemic hypokalaemic alkalosis, paradoxical aciduria, succussion splash and saline with potassium; Billroth I and II; early vs late dumping; gastric cancer risk factors (H. pylori, diet, pernicious anaemia), Lauren types and linitis plastica, Virchow node, Krukenberg tumour, Sister Mary Joseph nodule, staging laparoscopy and D2 gastrectomy; GIST and imatinib; MALT lymphoma and H. pylori.
Quick revision
- Perforation: anterior duodenum; sudden pain, rigidity; erect CXR, CT; omental patch; eradicate H. pylori.
- Bleeding: posterior DU, gastroduodenal artery; endoscopic dual therapy, IV PPI; embolisation or surgery for failure.
- Outlet obstruction: cancer commonest now; projectile non-bilious vomiting, succussion splash; HCl loss → hypochloraemic hypokalaemic alkalosis, paradoxical aciduria; saline plus KCl; biopsy.
- Early dumping = osmotic, vasomotor, straight after meals; late dumping = reactive hypoglycaemia in the second hour.
- Gastric cancer: adenocarcinoma; intestinal vs diffuse (signet ring, linitis plastica); Virchow, Krukenberg, Blumer, Sister Joseph.
- Staging: endoscopy, CT, staging laparoscopy. Surgery: subtotal or total gastrectomy with D2 plus perioperative chemotherapy.
- GIST: c-kit, imatinib, no lymphadenectomy. MALT lymphoma: eradicate H. pylori.
Written by The House Job from standard references (Bailey & Love).
FAQ
Why is 0.9% saline with potassium the fluid of choice in pyloric stenosis?
The patient has lost hydrochloric acid and is short of chloride, sodium, potassium and water; replacing these allows the kidney to excrete bicarbonate and correct the alkalosis.
What is paradoxical aciduria?
In prolonged vomiting the kidney conserves sodium by exchanging it for hydrogen and potassium ions, so the urine becomes acidic even though the blood is alkaline.
Can a perforated ulcer be present with a normal chest X-ray?
Yes; gas under the diaphragm is seen in only about half of cases, so CT is used when clinical suspicion remains.
What is linitis plastica?
A diffuse-type gastric adenocarcinoma that infiltrates the whole wall, making the stomach small, thick and rigid like a leather bottle; it carries a poor prognosis.
How is a gastric GIST treated?
By complete local or wedge resection with clear margins, without formal lymph node clearance; imatinib is used for advanced, unresectable or high-risk tumours.