Anastomotic-Transverse Colon Fistula Following Gastrectomy: A Case Report of Delayed Diagnosis 14 Years After Surgery

Introduction

A gastric-transverse colon fistula represents an abnormal connection between the gastric remnant and transverse colon, typically secondary to peptic ulcers, malignancies, iatrogenic injury, or inflammatory conditions. Delayed fistula formation following gastrectomy is clinically uncommon [1]. Most cases present within the first few years postoperatively, and the manifestation of a gastrocolic fistula more than a decade after surgery is exceedingly rare, with only sporadic cases reported. This profound delay, coupled with the nonspecific nature of its classic triad of symptoms (refractory diarrhea, malnutrition, and weight loss), frequently leads to misdiagnosis and prolonged patient symptomology. This report describes the case of a 60-year-old man with a gastrocolic fistula from the gastrectomy anastomosis to the transverse colon 14 years following partial gastrectomy.

Case Report

A 60-year-old male patient presented with recurrent watery diarrhea that had persisted for 6 years and significantly worsened during the preceding 6 months. Notably, the diarrhea first began approximately 8 years after his initial subtotal gastrectomy with Billroth I anastomosis, establishing a clear timeline of a 14-year symptom-free interval after surgery followed by 6 years of progressive symptoms. Characteristic features included postprandial and nocturnal occurrence (2–10 episodes/day), undigested food particles in stool, refractoriness to antidiarrheal agents (montmorillonite/probiotics), and 4-kg weight loss during recent exacerbation. Surgical history included subtotal gastrectomy with Roux-en-Y reconstruction for gastric perforation 14 years prior (operative details unavailable). Surveillance endoscopy documented residual gastritis and unexplained colonic anatomical changes despite no recorded colonic surgery. On admission, physical examination revealed tachycardia (106 beats/min), moderate nutrition status, surgical scar on the abdomen, no tenderness or masses, and normal bowel sounds. Notable laboratory abnormalities included hypoalbuminemia (albumin, 28.3 g/L), hypokalemia (potassium, 3.36 mmol/L) and carbohydrate antigen 19-9 elevation (144 U/mL). Stool studies suggested microbial dysbiosis (4+ GP cocci/bacilli), and the occult blood was positive. To confirm the diagnosis, upper gastrointestinal tract contrast-enhanced imaging was performed, but no clear fistula was observed (Figure 1). Gastroscopy and colonoscopy suggested a possible gastric-transverse colon fistula: gastroscopy revealed 2 anastomotic sites, with 1 leading to the jejunum and 1 leading to the colon (Figure 2); colonoscopy showed gastric mucus pool containing fecal matter, with anastomotic tissue clamps traceable (Figure 3). The initial report of the abdominopelvic contrast-enhanced computed tomography (CT) scan described only postoperative gastric changes and nonspecific intestinal wall thickening. However, upon targeted retrospective review by a senior gastrointestinal radiologist after the endoscopic diagnosis was established, the CT images were found to reveal distorted anatomy with inflammatory stranding and tissue plane disruption between the gastric remnant and the transverse colon. Although the fistula tract itself was not visualized as a distinct air-filled or contrast-filled channel, the presence of a secondary opening, significantly smaller than the surgical anastomosis, was inferred from these inflammatory changes (Figure 4).

The patient had undergone gastric surgery, followed by persistent postprandial watery diarrhea containing undigested food. Direct endoscopic detection revealed an abnormal channel between the stomach and colon, with 2 anastomotic sites, fecal matter in the mucus pool, and traceable tissue clamps. CT demonstrated abnormal thickening between the stomach and colon. The diagnosis was considered to be a gastric-transverse colon fistula (secondary to partial gastrectomy). In combination with the laboratory test results, the patient’s negative stool pathogen culture and Clostridium difficile toxin test ruled out infectious diarrhea. Endoscopy showed no typical ulcerative lesions, and tests for autoantibodies were negative. This ruled out inflammatory bowel disease. The patient had no history of pancreatic disease, with normal serum lipase, amylase, and blood glucose levels, and no imaging evidence of pancreatic atrophy or pancreatic duct calcification. This ruled out pancreatic insufficiency. Imaging and multiple endoscopic biopsies did not suggest malignant lesions. Tumors were temporarily ruled out. The elevated carbohydrate antigen 19-9 levels were likely due to the local inflammatory response at the fistula site.

The patient was placed on a fasting regimen and received total parenteral nutrition and human albumin supplementation to optimize nutritional status. During the fasting period, the patient continued to have loose stools, which indicated the persistence of the fistula. A consultation with the gastrointestinal surgery department was sought, and the patient was considered a candidate for surgery. The key to the surgery was to sever the abnormal passage and restore the normal physiological pathway. The patient underwent laparoscopic surgery under general anesthesia, consisting of resection of the gastrocolic fistula and affected gastric and colonic tissue, intestinal adhesion lysis, and gastric-jejunal Roux-en-Y anastomosis (Figure 5). The postoperative wound healed well. Sutures were removed 20 days postoperatively. After resuming diet, the patient had no abdominal pain, distension, or reflux, and diarrhea was completely resolved. At last follow-up, bowel movements occurred every 2 to 3 days, with formed, yellow, soft stools, and no melena or hematochezia.

This case exemplifies an exceptionally delayed presentation of a gastrocolic fistula 14 years following the index surgery. Its protracted diagnostic path across multiple institutions underscores the critical importance of considering anatomical complications even in the remote postoperative period, challenging the common clinical assumption that such issues arise early.

Discussion

This case offers several important insights for clinicians. First, it demonstrates that gastrocolic fistula can present as an extremely late complication, even following Billroth I anastomosis. Second, it underscores the decisive role of combined endoscopic examination in diagnosis when imaging findings are inconclusive. Third, it illustrates the efficacy of a multidisciplinary integrated treatment model centered on surgical resection.

Gastric-colonic fistula represents a rare long-term complication following major gastrectomy. The literature indicates its highest incidence occurs after Billroth II anastomosis, with a reported prevalence of approximately 1% to 7% [2]. Common causative factors include recurrence of malignant lesions, infiltration or ulceration, surgical adhesions, and local chronic inflammation. Furthermore, incomplete gastrectomy, inadequate vagotomy, residual G cells, or gastrinomas leading to hyperacidity, combined with surgery-related gastrointestinal wall compression and adhesions, may induce compressive ulcers and ultimately perforation [3,4]. Patients typically present with chronic diarrhea, vomiting, and malnutrition, characterized by fecal vomiting and undigested food in stools. Diagnosis primarily relies on endoscopy and gastrointestinal radiography, with CT and MRI serving as supplementary tools. Following adequate nutritional support, surgical resection of the affected gastrocolonic segment with restoration of gastrointestinal continuity (commonly via Roux-en-Y anastomosis) constitutes the primary therapeutic approach [3,4].

In the present case, a gastrocolic fistula developed 14 years following a major gastrectomy, representing a delayed complication. Compared with similar cases reported in the literature, this case presents certain distinctive features and insights regarding the surgical approach, time to onset, and diagnostic process. In published case reports [3,5–8], gastric-colonic fistula, although rare as a long-term complication following gastric surgery, exhibits certain commonalities. The overwhelming majority of reported cases involved Billroth II anastomosis as the primary procedure, closely linked to the pathological basis of common postoperative complications, such as bile reflux and anastomotic ulcers, associated with this technique. Notably, this case occurred following a Billroth I anastomosis. In contrast, reports of gastrocolic fistulae following Billroth I anastomosis are exceedingly rare. This procedure restores a more physiologically appropriate continuity of the digestive tract, theoretically reducing the risk of bile reflux into the gastric stump significantly. Therefore, the etiology in this case is more likely attributable to either a minute leak at the anastomotic margin or local ischemia, which may have led to the formation of a concealed abscess that ultimately perforated into the adjacent colon, or to chronic residual gastritis/anastomotic inflammation causing local tissue erosion and perforation [9]. Additionally, the patient’s previous colonoscopy report mentioned “postoperative changes in the colon”, but the patient denied a history of surgery, strongly suggesting unrecognized iatrogenic colonic injury or early postoperative formation of a concealed fistula during the initial surgery.

In terms of onset timing, the interval between colonic fistula surgery and symptom manifestation varies considerably, ranging from 1.5 to 30 years [3,5–8]. In the present case, the patient presented symptoms 8 years after surgery and received a definitive diagnosis in the fourteenth year, representing a 6-year disease course. This underscores the insidious nature of onset and diagnostic delay. Clinically, nearly all cases present with diarrhea and weight loss as core symptoms, with some patients additionally experiencing fecal vomiting or abdominal pain [3,5–8]. Our patient exhibited diarrhea and weight loss without vomiting. This nonspecific symptom spectrum is the primary reason for frequent misdiagnosis as functional bowel disorder or malabsorption syndrome.

In our case, the diagnostic process for the patient proved equally challenging. The patient’s persistent diarrhea was primarily due to the fistula, which causes ingested food to bypass most of the small intestine and enter the colon directly. Undigested food components create a hyperosmotic environment in the colon, stimulating increased colonic secretion and resulting in watery stools [10]. Additionally, factors such as excessive fermentation of undigested carbohydrates by colonic bacteria (leading to gas and acid production), intestinal microbiota dysbiosis [11], and the direct entry of undigested food into the colon, bypassing the proximal small intestine, can contribute to the diarrhea. The Roux-en-Y anatomy makes significant bile acid [12] contribution to the diarrhea less likely. Apart from atypical symptoms, imaging findings were subtle, which further delayed the patient’s diagnosis. The patient underwent multiple abdominal CT scans, gastrointestinal contrast studies, and endoscopies, none of which revealed evidence of a fistula, suggesting conventional imaging modalities may have a high false-negative rate for small fistula lesions. In this case, despite the fistula eventually being deemed sizable enough to permit endoscopic passage, its CT appearance was masked by postoperative anatomical distortion and inflammatory changes, underscoring that the functional size of a fistula does not always correlate with its radiographic conspicuity.

Therapeutically, surgical excision of the fistula with gastrointestinal reconstruction is the established definitive treatment, with Roux-en-Y anastomosis currently the preferred re-connection technique [5–8]. The successful management of this case adhered to this principle: laparoscopic excision of the fistula followed by Roux-en-Y gastrojejunostomy yielded favorable outcomes, validating the reliability of this surgical approach. Adequate preoperative preparation is crucial [13]; in this case, fasting, parenteral nutrition, and albumin infusion significantly improved nutritional status, laying the foundation for surgical success. For smaller fistulas, under strict indication criteria, endoscopic closure of the fistula opening, fistula tract obliteration, and drainage may facilitate healing [14].

The successful outcome in this complex case was predicated on a multidisciplinary collaboration involving gastroenterology, gastrointestinal surgery, and radiology teams. This model of care – integrating diagnostic endoscopy, specialized radiological re-evaluation, nutritional support, and definitive surgery – provides a replicable framework for managing similar complex, delayed-presentation fistulas.

Conclusions

For patients with persistent postprandial diarrhea with undigested food following gastrectomy, even years postoperatively, gastrocolic fistula should be highly suspected. Future research should focus on establishing clearer guidelines for the endoscopic surveillance of high-risk patients with long-standing gastrointestinal reconstructions and evaluating the long-term outcomes of different surgical repair techniques in this specific patient population.