Stomach

High-yield ABSITE review organized by disease process. Anatomy first, then GERD, hiatal hernia, PUD, volvulus, adenocarcinoma, GIST, neuroendocrine tumors, MALToma, and post-gastrectomy syndromes.

Anatomy

• Vascular supply — five arteries:
  • Left gastric (celiac → lesser curve). Most important cephalad. Often has an aberrant / accessory / replaced left hepatic artery — palpate before dividing.
  • Right gastric (proper hepatic → lesser curve).
  • Left gastroepiploic (splenic → greater curve).
  • Right gastroepiploic (gastroduodenal → greater curve).
  • Short gastrics (splenic → fundus).
  • All five can be sacrificed and the stomach survives on any single remaining vessel — this is why gastric conduits work.
• Venous drainage parallels arteries → portal system. Left gastric vein (coronary vein) is a key porto-systemic collateral (varices).
• Vagal anatomy: anterior (left) vagus gives off the hepatic branch; posterior (right) vagus gives off the celiac branch. The criminal nerve of Grassi is the most posterior branch of the right vagus, arising above the GE junction — commonly missed in truncal vagotomy → recurrent ulcer.
• Cells and secretions:
  • Parietal cells (fundus/body) — HCl, intrinsic factor.
  • Chief cells (fundus/body) — pepsinogen.
  • G cells (antrum) — gastrin.
  • D cells (antrum) — somatostatin (inhibits gastrin).
  • Enterochromaffin-like (ECL) cells — histamine.
  • Mucous cells — mucin, bicarbonate.
• Siewert–Stein classification — for esophago-gastric junction (EGJ) tumors:
  • Type I: distal esophagus, 1–5 cm above the anatomic EGJ. Treat like esophageal cancer (esophagectomy).
  • Type II: cardia, within 1 cm above and 2 cm below EGJ. Extended total gastrectomy with distal esophagectomy.
  • Type III: subcardial stomach, 2–5 cm below EGJ. Total or subtotal gastrectomy.

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GERD

• Alarm symptoms — dysphagia, odynophagia, weight loss, anemia, GI bleeding. Any one of these → upper endoscopy to rule out malignancy.
• Medical management:
  • Lifestyle — weight loss, HOB elevation, avoid trigger foods.
  • PPI trial — 8-week course. If no improvement → EGD.
• Indications for surgical evaluation:
  • Failed medical management, patient preference to avoid lifelong PPI, extra-esophageal manifestations (asthma, hoarseness, chronic cough, chest pain, aspiration).
• Bile reflux clue — atypical symptoms plus prior GI surgery → work up with impedance probe; management is Roux-en-Y conversion.
• Preop workup:
  • Barium swallow (anatomy, motility, hiatal hernia).
  • Upper endoscopy (esophagitis, Barrett’s, mass).
  • Ambulatory pH testing — DeMeester score > 14.72 = reflux.
  • Esophageal manometry — must rule out dysmotility (achalasia, scleroderma) before a full 360° wrap.
• DeMeester components: % total time pH < 4, % upright < 4, % supine < 4, number of reflux episodes, number ≥ 5 min, longest episode.
• Surgical goals:
  • Restore normal anatomic position of stomach + GE junction.
  • Recreate anti-reflux valve.
  • Fully reduce any hiatal hernia (requires mediastinal dissection).
  • Close crural defect.
  • Complete fundic mobilization.
  • 2 cm “floppy” fundoplication over a 54 F bougie.
• Fundoplication variants:
  • Nissen — 360° full wrap. Best reflux control, more postop dysphagia.
  • Toupet — posterior 270°.
  • Dor — anterior 180–200°.
  • Thal — anterior 270°.
  • Belsey Mark IV — anterior 270°, trans-thoracic.
  • Lind — posterior 300°.
  • Hill repair — gastropexy to arcuate ligament.
• Partial wraps — less postop dysphagia, may have less durable reflux control. Evidence supports either. Use partial wrap when manometry shows any dysmotility.
• Intra-op capnothorax — high end-tidal CO₂, ventilation difficulty during mediastinal dissection. Differential: capnothorax, hypoventilation, CO₂ embolus, malignant hyperthermia.
  • Management: enlarge the pleural tear to avoid tension → place a red rubber catheter with one end in the pleural tear, other end in the abdomen (equalizes pressures) → at end of case, bring one end out and place to water seal while anesthesia does a Valsalva. Needle decompression is a backup — prep the lower chest.
• Post-op 2 cm pneumothorax on CXR: observe, self-resolves.
• Post-op care: scheduled anti-emetics (avoid retching), soft diet for 2 weeks, avoid meat / raw veg / bread / carbonated drinks for 4–6 weeks.
• Post-op dysphagia: common early. Severe or persisting > 6 weeks → esophagram (concern for slipped wrap or recurrent hernia) → dilation if no anatomic issue.

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Hiatal Hernia

• Types:
  • I — sliding (> 90%). GE junction migrates into the chest. Do NOT repair unless GERD indication.
  • II — pure paraesophageal. Fundus herniates alongside a fixed GEJ. Repair.
  • III — mixed (sliding + paraesophageal). Repair.
  • IV — another organ in the chest (colon most common). Repair.
• Diagnosis: often incidental on CXR; confirm with barium swallow, CT chest, EGD.
• Indications for repair:
  • All symptomatic type II–IV.
  • Especially those with obstructive symptoms or volvulization.
  • Asymptomatic PEH → routine elective repair if good surgical candidate.
  • Watchful waiting for asymptomatic minimally symptomatic patient who is a poor surgical candidate.
  • Hiatal hernia found at time of sleeve gastrectomy → repair concurrently.
• Operative principles:
  • Laparoscopic preferred; open or trans-thoracic acceptable.
  • Excise the sac — key step, reduces early recurrence.
  • Mesh reinforcement in defects > 5–8 cm — decreases short-term recurrence, long-term safety debated. NCCN / SAGES: reasonable for large defects, not mandatory.
  • Permanent suture to reapproximate crura.
  • Fundoplication at time of repair (see GERD principles above).
  • Collis gastroplasty — esophageal lengthening if inadequate intra-abdominal esophagus (< 2.5 cm).
  • Gastropexy or gastrostomy — alternative to Collis for select patients.

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Peptic Ulcer Disease

• H. pylori: present in ~75% of gastric ulcers, ~95% of duodenal ulcers.
• Triple therapy: PPI + clarithromycin + amoxicillin (or metronidazole). 14 days.
• Gastric ulcer types (modified Johnson):
  • Type I — lesser curve, incisura. Low acid, mucosal defect. MC. Treat with distal gastrectomy (includes ulcer + antrum).
  • Type II — gastric ulcer + duodenal ulcer. High acid. Vagotomy + antrectomy.
  • Type III — prepyloric. High acid. Vagotomy + antrectomy.
  • Type IV — high on lesser curve near GEJ. Low acid. Csendes or subtotal gastrectomy with Roux-en-Y.
  • Type V — anywhere, NSAID-induced. Stop NSAIDs, PPI.
• Underlying malignancy present in ~5% of gastric ulcers — always biopsy the ulcer edge and antrum (H. pylori test).

Bleeding ulcer

• Initial: resuscitate, NG tube, PPI drip, urgent EGD.
• Endoscopic control 90% effective. Techniques: clips, thermal, injection of vasoactive / sclerosing agent.
• Rebleed risk by finding:
  • Actively bleeding pulsatile vessel — up to 80%.
  • Visible vessel — ~50%.
  • Adherent clot — 15–25%.
  • Clean base — < 5%.
• Rebleed after 1st EGD: repeat EGD (or angiography). Identify and treat etiology (NSAIDs, tobacco, H. pylori, PPI).
• Surgical indications: uncontrollable bleeding with endoscopy or persistent hemodynamic instability.
  • Gastric ulcer: midline laparotomy → anterior gastrotomy → oversew, biopsy, close.
  • Duodenal ulcer: longitudinal anterior duodenotomy → three-point suture ligation (above, below, and U-stitch under the ulcer to control GDA and its branches — the pancreaticoduodenal artery). Ligate GDA above duodenum if bleeding continues. Close duodenotomy transversely.

Perforated ulcer

• Fluid resuscitation, NG decompression, PPI, empiric antibiotics (ampicillin, ceftriaxone, metronidazole, fluconazole).
• Graham patch — omental tongue tacked over the perforation with 3–4 sutures. Open or laparoscopic. Approximate the perforation edges if the tissue permits.
• Small amount of free air + stable patient → possible contained perforation → non-operative trial (rare on exams).
• Refractory ulcer (recurrent despite PPI + H. pylori eradication) → add an acid-reducing procedure:
  • Truncal vagotomy + pyloroplasty.
  • Highly selective (parietal cell) vagotomy — preserves pyloric innervation, no drainage procedure.
  • Vagotomy + antrectomy — highest recurrence prevention but most morbid (Billroth reconstruction). Reserved for stable patients with anatomic indications (large antral ulcer, pyloric scarring).
• Marginal ulcer after RYGB or gastric bypass — treated same as duodenal ulcer perforation (omental patch + medical optimization).

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Gastric Volvulus

• Often associated with paraesophageal hernia; high morbidity / mortality.
• Three types:
  • Organoaxial (most common) — rotation along long axis (GEJ to pylorus).
  • Mesoaxial — rotation along short axis (bisecting lesser/greater curvature).
  • Combined.
• Borchardt’s triad: severe epigastric pain, retching without vomiting, inability to pass an NG tube.
• Treatment: emergent surgery — reduction, hernia repair, gastropexy ± partial gastrectomy if devitalized. In frail patients, endoscopic decompression with double PEG-tube fixation is an option.

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Gastric Adenocarcinoma

• Risk factors: H. pylori, tobacco, heavy ETOH, high salt, nitrates, atrophic gastritis, pernicious anemia, prior gastric surgery.
• Lauren classification:
  • Intestinal type — glandular, better prognosis, associated with H. pylori / dietary risk.
  • Diffuse type — signet-ring cells, “linitis plastica” (leather-bottle stomach), worse prognosis, often hereditary.
• Hereditary syndromes:
  • Hereditary diffuse gastric cancer (HDGC) — autosomal dominant, CDH1 (E-cadherin) germline mutation. Prophylactic total gastrectomy age 18–40. Women also at increased breast cancer risk (like BRCA).
  • Lynch syndrome (mismatch repair).
  • Juvenile polyposis (SMAD4).
  • Peutz–Jeghers (STK11).
  • FAP (APC gene, 5q21).
• Staging: CBC, CMP, CT chest/abdomen/pelvis, EUS ± FNA, PET/CT, upper endoscopy with biopsy.
  • Staging laparoscopy with peritoneal washings per NCCN for clinical > T1b tumors being considered for surgery or chemoRT (skip if known metastatic disease going to palliative therapy).
• T stage:
  • T1a — lamina propria / muscularis mucosa.
  • T1b — submucosa.
  • T2 — muscularis propria.
  • T3 — subserosa.
  • T4 — through serosa or adjacent structures.
• N stage: N1 = 1–2 nodes, N2 = 3–6, N3 ≥ 7. M1 = distant.
• Unresectable: peritoneal disease, distant mets, root of mesentery involvement, para-aortic nodal disease (biopsied), encasement of major vessels (excluding splenic).
• Neoadjuvant: cT2 or higher, or any N+ (parallel to esophageal / rectal).
• Surgical principles:
  • ≥ 4 cm margins, lymph node harvest ≥ 15.
  • Subtotal gastrectomy for distal (Siewert III / antral) lesions.
  • Total gastrectomy with esophagojejunostomy for proximal (Siewert II) lesions; may need distal esophagectomy for margins.
  • Tumors crossing the GEJ = treat as esophageal cancer.
  • No prophylactic splenectomy — only if spleen or hilum grossly involved.
  • T4 tumors → en bloc resection of involved structures.
• Lymphadenectomy:
  • D1 — perigastric nodes (stations 1–6).
  • D2 — adds nodes along left gastric, common hepatic, celiac, splenic (stations 7–11).
  • Standard in Asia is D2; Western trials failed to show survival benefit and D2 had higher morbidity → NCCN recommends R0 with ≥ D1 or modified D2.
• R-status: R0 = negative micro margin; R1 = negative gross, positive micro; R2 = positive gross.
• Adjuvant chemo (5-FU based) for T3, T4, or node-positive disease post R0.

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GIST (Gastrointestinal Stromal Tumor)

• Origin: interstitial cells of Cajal (pacemaker cells).
• Most common site: stomach (60–70%), then small bowel (~25%), then colon/rectum/esophagus.
• Genetics:
  • KIT (CD117) gain-of-function mutation — ~75%.
  • PDGFRA mutation — ~10%. D842V substitution is imatinib-resistant → use avapritinib.
  • Wild-type / SDH-deficient — ~15% (includes Carney triad, NF1-associated).
• IHC: CD117 positive (specific), DOG1 positive, CD34 often positive. Negative for smooth muscle actin, desmin, S-100 (rules out leiomyoma / schwannoma).
• Presentation: incidental on imaging, GI bleed, obstruction (large tumors), or vague abdominal pain. Rarely lymph-node positive.
• Miettinen–Lasota risk stratification — based on size (≤ 2, 2–5, 5–10, > 10 cm), mitotic count (≤ 5 vs > 5 per 50 HPF), and location (gastric better than non-gastric):
  • Gastric < 2 cm + mitoses ≤ 5 → essentially benign.
  • Gastric 5–10 cm + mitoses ≤ 5 → intermediate.
  • Any > 10 cm, or mitoses > 10, or any non-gastric with unfavorable features → high risk.
• Surgery:
  • Wedge (partial) gastrectomy with R0 negative margins. Micro margin adequate — no defined cm requirement like adenocarcinoma. See the wedge gastrectomy case prep for technique.
  • Do NOT do a lymphadenectomy — GISTs almost never spread to nodes.
  • Do NOT rupture the tumor — intraop rupture automatically makes it high-risk and mandates adjuvant imatinib.
• Neoadjuvant imatinib — consider for large (> 5 cm), poorly positioned, or unresectable GIST to shrink for organ preservation (e.g., distal GEJ mass).
• Adjuvant imatinib — indicated for intermediate / high-risk disease for ≥ 3 years.
• Metastatic disease — imatinib first-line, sunitinib second-line, regorafenib third-line, ripretinib fourth-line.
• Surveillance: CT abdomen/pelvis with contrast every 3–6 months for 5 years, then annually.

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Neuroendocrine Tumors of the Stomach

Gastric carcinoid (Type I / II / III)

• Type I (~70–80%) — associated with chronic atrophic gastritis and hypergastrinemia (achlorhydria → G-cell hyperplasia → ECL hyperplasia → carcinoid).
  • Multiple small (< 1 cm), well-differentiated, excellent prognosis.
  • Treatment thresholds:
    • < 1 cm and ≤ 5 lesions: endoscopic surveillance ± endoscopic resection.
    • 1–2 cm or > 5 lesions: endoscopic vs surgical resection; consider antrectomy to remove gastrin drive.
    • > 2 cm or invasion / positive nodes: formal partial gastrectomy with regional LND.
• Type II (~5%) — associated with MEN1 + Zollinger–Ellison syndrome. Gastrin-driven from a duodenal or pancreatic gastrinoma.
  • Treatment: address the gastrinoma first; then follow the same size-based algorithm as Type I.
• Type III (~15–25%) — sporadic, no hypergastrinemia. Solitary, larger, aggressive, high metastatic potential (~50%).
  • Formal (subtotal or total) gastrectomy with lymphadenectomy regardless of size.
• Type IV (poorly differentiated neuroendocrine carcinoma) — treated as small-cell / large-cell carcinoma with platinum-based chemotherapy.
• Staging workup: chromogranin A, 5-HIAA (rarely functional for gastric), Ga-68 DOTATATE PET/CT, EGD with EUS, biopsy for grading (Ki-67, mitotic count).

Zollinger–Ellison Syndrome (gastrinoma)

• Clinical: multiple refractory ulcers, ulcers in unusual locations (jejunum), diarrhea, PPI-refractory reflux.
• Diagnosis:
  • Fasting gastrin > 1000 pg/mL with gastric pH < 2 = essentially diagnostic.
  • Intermediate gastrin (150–1000) → secretin stimulation test: paradoxical rise in gastrin > 200 = positive.
  • Hold PPI ≥ 7 days before gastrin measurement (false-positive elevation).
• Location: ~60% duodenal, ~30% pancreatic (head), remainder ectopic. In Passaro’s / gastrinoma triangle — bounded by cystic duct / CBD superiorly, junction of pancreatic neck-body medially, junction of D2/D3 inferiorly.
• Association: MEN1 (~25% of gastrinomas). Screen for parathyroid and pituitary.
• Localization: Ga-68 DOTATATE PET/CT (best), EUS, CT, MRCP, intra-op ultrasound.
• Treatment:
  • Medical control: high-dose PPI.
  • Surgical resection for localized disease: enucleation of small duodenal or pancreatic head tumors; formal resection for larger or malignant.
  • MEN1 patients: parathyroidectomy first if hypercalcemia (reduces gastrin secretion).
  • Metastatic disease: PPI + somatostatin analogs (octreotide / lanreotide), DOTATATE peptide receptor radionuclide therapy, everolimus/sunitinib.

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MALToma (Gastric MALT Lymphoma)

• Low-grade B-cell lymphoma of mucosa-associated lymphoid tissue.
• Strongly associated with H. pylori.
• Biopsy shows expansion of the marginal zone with sheets of neoplastic small lymphoid cells.
• Treatment: triple therapy for H. pylori → regression in ~80% of early-stage disease.
• Non-regressing or advanced: radiation, rituximab-based chemotherapy.
• Surgery is not first line — reserved for complications (bleeding, perforation, obstruction) or high-grade transformation to DLBCL.

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Post-Gastrectomy Syndromes

• Retained antrum syndrome — antral tissue left in the duodenal stump after gastric resection. G cells bathed in alkaline fluid → continuous gastrin release → recurrent ulceration in the gastric remnant.
  • Check gastrin level to rule out gastrinoma.
  • Treatment: PPI; definitive is vagotomy + resection of retained antrum.
• Dumping syndrome:
  • Early (20–30 min post-meal): tachycardia, diaphoresis, dizziness, flushing, cramping. Due to abrupt hyperosmolar load into small bowel.
  • Late (1–4 hr post-meal): hypoglycemic symptoms. Rapid carbohydrate load → insulin surge → rebound hypoglycemia.
  • Treatment: small frequent meals, avoid sugary drinks. Refractory → octreotide.
• Alkaline reflux gastritis — after Billroth I / II reconstruction. Diagnose with impedance studies. Medical management: prokinetics, bile-acid binding resins. Surgical: conversion to Roux-en-Y with ≥ 50 cm Roux limb to prevent recurrent bile reflux.
• Afferent limb syndrome — Billroth II complication. Obstruction of the afferent limb → increased pressure → obstructive jaundice, cholangitis, pancreatitis; can cause duodenal stump blow-out; bacterial overgrowth → deconjugation of bile acids → steatorrhea, malnutrition, B12 deficiency, megaloblastic anemia.
  • B2 patient with SBO symptoms + bilious emesis + megaloblastic anemia → afferent limb syndrome.
  • Treatment: conversion to RY or Billroth I. Antibiotics can control overgrowth temporarily but relapses are common. Do NOT decompress with an NG — go to OR (like an internal-hernia bypass patient).
• Braun enterostomy — side-to-side anastomosis between afferent and efferent limbs of a Billroth II; diverts bile away from the gastric remnant, mitigates afferent-limb and alkaline reflux issues.
• Marginal ulcer — at the gastrojejunal anastomosis (RYGB, Billroth II). Treated medically first; perforation managed like a duodenal ulcer perforation (Graham patch).

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Rapid-Fire Questions

• Q: Types of hiatal hernia? A: I = sliding (most common), II = pure paraesophageal, III = mixed, IV = another organ (usually colon).

• Q: Siewert I, II, III? A: I = 1–5 cm above EGJ (esophageal cancer), II = within 1 cm above / 2 cm below (extended total gastrectomy), III = 2–5 cm below (subtotal/total gastrectomy).

• Q: Gastric ulcer types and acid states? A: I = lesser curve, low acid; II = gastric + duodenal, high acid; III = prepyloric, high acid; IV = high lesser curve, low acid; V = NSAID-related.

• Q: Most missed vagal branch in truncal vagotomy? A: Criminal nerve of Grassi — most posterior branch of the right (posterior) vagus above the GEJ.

• Q: DeMeester score cutoff for reflux? A: > 14.72.

• Q: Which fundoplication for a patient with dysmotility? A: Partial wrap (Toupet or Dor) — 360° Nissen risks severe dysphagia.

• Q: Rebleed risk from a clean-based ulcer? A: < 5%. Adherent clot 15–25%, visible vessel 50%, actively bleeding vessel up to 80%.

• Q: Approach to a duodenal ulcer bleeder in the OR? A: Longitudinal anterior duodenotomy → three-point suture ligation controlling the GDA and pancreaticoduodenal branches → close transversely.

• Q: How much margin do you need for gastric adenocarcinoma? A: ≥ 4 cm, with lymph node harvest ≥ 15.

• Q: Prophylactic gastrectomy — who and when? A: CDH1 (hereditary diffuse gastric cancer) carriers, ages 18–40.

• Q: GIST margin required? A: R0 (negative microscopic margin); no defined cm margin. No lymphadenectomy.

• Q: Adjuvant imatinib duration for high-risk GIST? A: ≥ 3 years.

• Q: Ki-67 or mitotic count that flips a GIST to high risk? A: Mitoses > 10 per 50 HPF, or any size > 10 cm, or non-gastric with unfavorable features, or intraop rupture.

• Q: Which GIST mutation is imatinib-resistant? A: PDGFRA D842V. Use avapritinib.

• Q: Three types of gastric carcinoid? A: Type I — atrophic gastritis + hypergastrinemia (MC, best prognosis). Type II — MEN1 + ZES. Type III — sporadic, aggressive, formal gastrectomy + LND.

• Q: ZES workup? A: Fasting gastrin > 1000 with pH < 2 = diagnostic. Intermediate values → secretin stimulation (paradoxical rise > 200). Hold PPI ≥ 7 days first.

• Q: Gastrinoma triangle borders? A: Cystic duct / CBD superiorly, junction of pancreatic neck-body medially, junction of D2/D3 inferiorly (Passaro’s triangle).

• Q: Gastric mass biopsy shows expansion of marginal zone with sheets of small lymphoid cells — diagnosis? A: MALToma — treat with H. pylori triple therapy first.

• Q: Bilroth II patient with intermittent pain + megaloblastic anemia + bilious emesis relieving symptoms? A: Afferent limb syndrome.

• Q: Post-op capnothorax during PEH repair — first move? A: Enlarge the tear (avoid tension), place red rubber catheter through it, at end of case pull one end out and put to water seal during Valsalva.

• Q: Post-Nissen patient can’t swallow secretions — problem and management? A: Wrap too tight — return to OR.

• Q: Post-op day 2 PEH repair, CXR shows 2 cm pneumothorax — what do you do? A: Nothing. Will self-resolve.

• Q: Zollinger–Ellison — most common inherited syndrome association? A: MEN1 (parathyroid, pituitary, pancreas). Screen for hypercalcemia.

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Quick Reference Table — Gastric Malignancies

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Quick-Reference Cards

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Related Case Preps

• Wedge Gastrectomy (robotic) — for GIST, Type I / II carcinoid < 2 cm, small benign masses.
• Distal Gastrectomy + Reconstruction — for distal adenocarcinoma (Siewert III / antral).
• Hiatal / Paraesophageal Hernia — for PEH repair with fundoplication.
• Graham Patch — for perforated duodenal ulcer.
• Gastrojejunostomy — for gastric outlet obstruction.

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