Benign gastrocolic fistula

Educational disclaimer. This article is intended for clinician education and historical context. It is not a substitute for current society guidelines or individualised clinical judgement. Patients with suspected gastrocolic fistula should be evaluated by a multidisciplinary team experienced in gastroenterology, advanced endoscopy, hepato-pancreato-biliary or upper gastrointestinal surgery, and nutrition support.

Introduction

A gastrocolic fistula (GCF) is an abnormal communication between the stomach and the colon — most often the transverse colon. It is uncommon today. Gastric or colonic adenocarcinoma is now the most common cause, with benign causes dominated by NSAID-, aspirin-, or corticosteroid-related peptic ulcer disease; less common benign aetiologies include Crohn’s disease, diverticulitis, post-bariatric gastrogastric fistulas and adjacent fistulas, tuberculosis (in endemic settings), and post-operative or post-radiation injury (Sumitomo et al. 2025; Hossain et al. 2024; Liu et al. 2020; Pearce et al. 2023). Benign GCF has become rarer since the introduction of proton pump inhibitors (PPIs) in 1989 and the development of effective Helicobacter pylori eradication regimens; only ~100 cases of benign GCF were reported by the late 1980s, and only a small number of case reports appear each subsequent decade (Sumitomo et al. 2025).

A historical case of benign GCF managed by open en bloc resection is presented first, followed by a modern-equivalent management note and a discussion of the current diagnostic and therapeutic algorithm.

Historical case report

A 72-year-old man (CR) was diagnosed radiologically with peptic ulcer disease five years before admission. He had intermittent burning epigastric pain worsened by hunger and relieved by food. One year prior to presentation he began occasional vomiting of clear fluid and, at times, undigested food. He passed melaena on one occasion. He felt weak and had lost 50 lb over six months despite a good appetite. He smoked 10 cigarettes per day for more than 50 years and had previously undergone inguinal herniorrhaphy and laparotomy for blunt abdominal trauma. On examination he was emaciated, pale, and dehydrated, hypothermic (T 95 °F), with a regular pulse of 60/min and blood pressure 100/60 mmHg. The abdomen was scaphoid with a midline infraumbilical scar and a left inguinal herniorrhaphy scar; no abdominal masses were palpable.

Preliminary investigations were:

Test Result Unit Test Result Unit
Hb 11.2 g/dL WBC 10.2×10⁹/L
Na 135 mmol/L K 4.1 mmol/L
Cl 88 mmol/L HCO3⁻ 32 mmol/L
Urea 11 mmol/L Creat 100 μmol/L
Glucose 4.7 mmol/L Total protein 48 g/L
Albumin 26 g/L Globulin 22 g/L

Gastroscopy showed a 5 cm posterior antral ulcer with “mucosal islands in the ulcer base” and a narrowed pylorus, and biopsies were taken. Barium meal (Fig 1) showed a large gastric pouch arising from the posterior surface of the stomach, interpreted as either a giant gastric ulcer or a gastric diverticulum; a gastrocolic fistula was not considered. Endoscopic biopsy results, barium enema, gastric acid analysis, and serum gastrin were not available preoperatively. The patient was assessed as having a gastric ulcer with gastric outlet obstruction, transfused blood and plasma, and given prophylactic antibiotics and heparin. A central venous line was placed for parenteral nutrition, a urethral catheter was sited, and exploratory laparotomy was performed through an upper midline incision. A large indurated area of the posterior gastric wall at the incisura was adherent to the transverse colon and pancreas; the duodenum was not scarred and the pylorus was not narrowed. The intraoperative assessment was non-metastatic resectable gastric carcinoma. During partial gastrectomy, a 7 cm posterior gastric ulcer and a fistula between stomach and transverse colon were identified. The operation comprised partial gastrectomy, transverse colectomy, Billroth II reconstruction, and colostomy with mucous fistula. Histology of the endoscopic biopsies and resected specimens showed only chronic inflammation; no malignancy was detected. Parenteral nutrition was begun on postoperative day 1; the colostomy was functional on day 4 and the patient took fluids orally by day 5, when parenteral nutrition was stopped. Recovery was uneventful. He gained 19 lb at home over three months. Colostomy closure was performed five months after the index operation; two months later the colostomy site had healed and the patient reported only occasional dumping.

Modern equivalent: A patient presenting today with weight loss, hypoalbuminaemia, a 5–7 cm posterior antral ulcer, and intraoperative findings of induration adherent to the transverse colon would be investigated and treated quite differently from the historical pathway above. Workup would include CT with oral contrast (the modern first-line imaging test, often demonstrating the fistula directly), upper endoscopy and colonoscopy with multiple biopsies (mandatory because malignancy is the most common cause), and H. pylori testing (Radiopaedia 2022; Maastricht VI 2022; ACG 2024). Gastric acid analysis is essentially obsolete; serum gastrin is reserved for suspected Zollinger-Ellison syndrome and requires PPIs to be held appropriately before testing (Cingam et al. 2021). Preoperative optimisation follows the SNAP framework (Sepsis control, Nutrition, Anatomical definition, Procedure), with enteral nutrition preferred over parenteral when feasible and supplemented by parenteral nutrition only if necessary (Tarasconi et al. 2022; Polk et al. 2020; Sumitomo et al. 2025). High-dose PPI therapy is started; NSAIDs/aspirin/corticosteroids are stopped if feasible; H. pylori is eradicated if present. Octreotide and somatostatin can be added in selected high-output cases, with somatostatin specifically improving spontaneous closure rate (Stevens et al. 2019). Surgical management remains en bloc resection (partial gastrectomy + segmental transverse colectomy with primary anastomoses or staged stoma diversion) when malignancy cannot be excluded; laparoscopic en bloc resection is feasible in selected benign cases (Pearce et al. 2023). Routine truncal vagotomy is no longer added; long-term PPI therapy and H. pylori eradication address the recurrence risk (StatPearls Truncal Vagotomy 2022).

Discussion

1. Pathology of gastrocolic fistulae

A gastrocolic fistula is an abnormal communication between the stomach and the colon, almost always the transverse colon (which lies in direct anatomical apposition to the greater curvature). Like other internal fistulae, it may be direct (mucosa-to-mucosa) or indirect (through an intermediate abscess cavity), and it may be spontaneous (a complication of an underlying disease) or traumatic (post-operative, post-radiation, or after penetrating injury).

The causes of spontaneous GCF, re-ordered by current frequency, are:

  • Gastric or colonic adenocarcinoma — the most common cause in modern series (Sumitomo et al. 2025; Hossain et al. 2024).
  • NSAID-, aspirin-, or corticosteroid-related benign peptic ulcer disease, with or without underlying H. pylori infection — the most common benign cause; the typical patient is middle-aged or older, often with chronic anti-inflammatory drug use (Hossain et al. 2024).
  • Crohn’s disease — gastrocolic and gastro-jejunal fistulas are rare but recognised complications (Liu et al. 2020).
  • Diverticulitis and other inflammatory conditions of the transverse colon.
  • Post-bariatric fistulas — gastrogastric and adjacent fistulas after Roux-en-Y gastric bypass (Pearce et al. 2023).
  • Tuberculosis — relevant in endemic regions.
  • Post-radiation or post-operative injury.

In benign disease, the ulcer that produces a GCF typically penetrates posteriorly from the greater curvature or posterior antral wall into the superior aspect of the transverse colon. CR’s case is consistent with this mechanism.

2. Clinical presentation

The classical triad of diarrhoea, weight loss, and faeculent vomiting/eructation is a useful teaching point but is present in only a minority of contemporary cases; many patients present with non-specific complaints such as epigastric pain, fatigue, foul-smelling belching, and progressive weight loss (Hossain et al. 2024; Sumitomo et al. 2025). Physical signs include anemia, dehydration, electrolyte derangement, hypoalbuminaemia, and vitamin deficiencies. A palpable abdominal mass is present in a small minority.

The undernutrition and occasionally profound diarrhoea reflect retrograde flow of faecal material from colon to stomach with bacterial overgrowth of the small intestine, deconjugation of bile salts (with mucosal injury and a cathartic effect on the colon), and disordered digestion and absorption.

3. Investigations and diagnosis

The diagnostic workflow has shifted decisively from the historical barium-based approach to a CT- and endoscopy-based one:

  • CT with oral contrast is the first-line imaging test, often demonstrating the fistulous tract directly as well as the underlying ulcer or mass and any associated abscess or stricture. It also helps stage suspected malignancy (Radiopaedia 2022).
  • Upper endoscopy with biopsy of the gastric ulcer and colonoscopy with biopsy of the colonic side are mandatory for tissue diagnosis. The fistulous orifice is often missed at endoscopy, so a normal endoscopy does not exclude GCF (Liu et al. 2020; Hossain et al. 2024).
  • Barium enema and barium meal are no longer first-line but remain useful adjuncts when CT is equivocal. Oral contrast-enhanced ultrasound has been reported as sensitive in Crohn’s-related GCF in expert hands (Liu et al. 2020).
  • H. pylori testing (stool antigen, urea breath test, or biopsy-based testing including molecular assays where available) is mandatory in any patient with a gastric ulcer. H. pylori gastritis is an ICD-11 disease entity, and all patients found to be infected should be treated (Malfertheiner et al., Maastricht VI 2022; Chey et al., ACG 2024).
  • Serum gastrin is reserved for suspected Zollinger-Ellison syndrome. Fasting gastrin > 1000 pg/mL together with gastric pH < 2 is considered diagnostic; PPIs must be discontinued (with H2-blocker bridging) before measurement (Cingam et al. 2021). Gastric acid analysis is essentially obsolete.
  • Endoscopy is indicated for new dyspepsia in any patient ≥ 60 years, or for any patient with alarm features (weight loss, anemia, dysphagia, melaena, persistent vomiting), as per the ACG/CAG 2017 dyspepsia guideline (Moayyedi et al. 2017).

4. Management — the SNAP / SOWATS framework

Modern management of gastrointestinal fistulas, including GCF, follows the SNAP framework — Sepsis control, Nutrition, Anatomy, Procedure — extended in some centres to SOWATS (Sepsis control, Optimizing nutrition, Anatomy, Timing of surgery, Surgical procedure) (Tarasconi et al. 2022; Polk et al. 2020):

  • Sepsis control. Identify and drain abscess collections (percutaneous or operative); start broad-spectrum antibiotics covering Gram-negative enteric organisms and anaerobes, and de-escalate based on cultures.
  • Nutrition. Enteral nutrition is preferred over parenteral whenever feasible — typically via a nasojejunal tube placed beyond the fistula. Parenteral nutrition is used as a supplement or when enteral nutrition fails. Nutritional optimisation (NRS-2002 / SGA assessment; protein 1.5–2.0 g/kg/day; correction of micronutrient deficiencies; serum prealbumin/albumin trending; control of glycaemia) is essential before any elective definitive surgery (Polk et al. 2020; Sumitomo et al. 2025).
  • Anatomy. Define the fistula completely with CT, contrast studies, and endoscopy — including proximal and distal bowel, abscess cavities, and any associated stricture or mass.
  • Procedure. Plan staged closure once sepsis is controlled and nutrition optimised, typically 6–12 weeks after the index decompression where conservative management has not achieved closure.

Pharmacological adjuncts. All patients receive high-dose PPI therapy (e.g., IV pantoprazole or oral equivalent) to reduce gastric acid flow across the fistula. NSAIDs, aspirin, and corticosteroids should be stopped if feasible. H. pylori should be tested for and eradicated if positive — bismuth quadruple therapy (PPI + bismuth + tetracycline + metronidazole or tinidazole) is the recommended first-line regimen in regions of high clarithromycin resistance, with eradication rates of 85–90% (Chey et al. 2024; Malfertheiner et al. 2022). Somatostatin and octreotide can be added in selected patients with high-output fistulas: a Cochrane review showed that somatostatin specifically improves the spontaneous-closure rate, while octreotide reduces the time to closure (Stevens et al. 2019).

Spontaneous closure has been reported in up to ~37% of selected non-operative benign-GCF series with appropriate medical management, and overall recovery rates may approach 93% under combined conservative-then-surgical management (Sumitomo et al. 2025).

5. Endoscopic closure options

Selected small, benign GCFs are now amenable to endoscopic closure, especially when malignancy has been excluded and sepsis is controlled. Reported techniques include (Polese et al. 2020; Hossain et al. 2024):

  • Over-the-scope clips (OTSC, e.g., Ovesco) — pooled success rates of ~70–80% in fistulas < 1 cm; multiple clips can be deployed for larger defects, sometimes combined with endoscopic suturing or fibrin glue.
  • Covered self-expanding metal stents (SEMS) — useful for larger leaks/fistulas; stent fixation devices such as stentfix OTSC are increasingly used to prevent migration.
  • Endoscopic suturing.
  • Fibrin sealant — typically as an adjunct to clips or stents.
  • Septal-occluder devices and dual-scope ("rendezvous") techniques — reported in selected cases of refractory benign GCF.

Endoscopic closure should be undertaken in centres with the relevant expertise and is generally reserved for benign fistulas without malignancy or refractory sepsis.

6. Surgical management

When malignancy cannot be excluded, when conservative and endoscopic management fail, or when sepsis demands source control, surgical management is required:

  • En bloc resection (partial gastrectomy + segmental transverse colectomy, with reconstruction as Billroth II / Roux-en-Y gastrojejunostomy and primary colocolostomy, or with staged stoma diversion in unstable patients) remains the gold standard when malignancy is present or cannot be excluded. Approximately 70% of patients with benign GCF in the historical literature were treated by en bloc resection; modern operative mortality is ~5.5%, down from ~16% historically (Sumitomo et al. 2025).
  • Limited operations — fistula excision with closure of both defects, partial gastrectomy with colonic-defect closure, or partial colectomy with gastric-defect closure — are associated with higher rates of recurrence and mortality in benign disease and are reserved for highly selected patients.
  • Laparoscopic en bloc resection is feasible in selected benign cases at experienced centres, with favourable peri-operative outcomes reported (Pearce et al. 2023).
  • Staged operations with initial proximal diversion (colostomy or ileostomy ± mucous fistula) are appropriate in the presence of peritonitis, sepsis, or hostile anatomy; definitive resection is performed 6–12 weeks later once nutrition and physiology are optimised (Tarasconi et al. 2022).
  • Routine truncal vagotomy is no longer recommended. Long-term PPI therapy combined with H. pylori eradication and the removal of ulcerogenic drugs has superseded vagotomy as the strategy to prevent recurrent or marginal ulceration. Truncal vagotomy is reserved for highly selected patients with complicated, medically refractory PUD (StatPearls Truncal Vagotomy 2022).

7. Postoperative care and follow-up

Postoperative care includes continuation of PPI therapy, H. pylori eradication if positive, NSAID/aspirin avoidance where possible, repeat endoscopy at 8–12 weeks to confirm ulcer healing (mandatory in any biopsy-proven gastric ulcer to exclude missed malignancy), and nutritional follow-up. Patients with a Billroth II or Roux-en-Y reconstruction should be counselled about dumping syndrome, bile reflux, and vitamin B12 / iron deficiency, and offered appropriate surveillance.

Conclusion

Benign gastrocolic fistula is now uncommon. The modern diagnostic and therapeutic algorithm is:

  1. Image with CT with oral contrast; perform upper endoscopy and colonoscopy with biopsies; test for H. pylori; consider gastrin only if Zollinger-Ellison syndrome is suspected.
  2. Manage by the SNAP/SOWATS framework: source-control sepsis; optimise nutrition (enteral preferred over parenteral); define anatomy; plan staged procedure.
  3. Start high-dose PPI; stop NSAIDs/aspirin/corticosteroids; eradicate H. pylori if positive. Consider somatostatin/octreotide as adjuncts in high-output fistulas.
  4. For small, benign fistulas in selected patients, consider endoscopic closure (OTSC, covered SEMS, fibrin sealant, septal-occluder devices, dual-scope techniques).
  5. Reserve en bloc surgical resection — open or laparoscopic — for malignancy or when conservative and endoscopic management fail. Avoid routine vagotomy.
  6. Continue long-term PPI therapy, H. pylori eradication when indicated, NSAID avoidance, and structured endoscopic and nutritional follow-up.

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