Challenges in the initial diagnosis of colon carcinoma from symptoms of a bladder and colon fistula: a case report

Abstract

Introduction and importance:

Sigmoid colon adenocarcinoma usually causes gastrointestinal complaints such as hematochezia or altered bowel habits. Urinary symptoms typically appear only in advanced disease. We describe an unusual case in which vesical fecaluria was the first and main symptom, mimicking recurrent urinary tract infection and risking delayed recognition of its colorectal origin.

Case presentation:

A 62-year-old man presented with more than 6 months of urinary frequency, dysuria, recurrent fever, and vesical fecaluria, which had repeatedly been treated as a urinary tract infection. He had no abdominal pain, hematochezia, or change in bowel habits. CT showed loss of the fat plane between the sigmoid colon and the bladder. Laparoscopic en bloc sigmoidectomy with partial cystectomy removed a pT4bN0M0 adenocarcinoma invading the bladder and small bowel. At 1-year follow-up, symptoms had resolved, with no recurrence.

Clinical discussion:

Unlike typical sigmoid colon adenocarcinoma, which begins with bowel symptoms and later forms a colovesical fistula, this tumor primarily invaded outward into the bladder with minimal intraluminal growth; therefore, no bleeding or obstruction occurred. Infection obscured endoscopy and delayed diagnosis. MDT-led control of sepsis, plus en bloc laparoscopic R0 resection, was achieved, demonstrating that the combination of fecaluria and recurrent UTI warrants colorectal evaluation.

Conclusion:

Vesical fecaluria may be the first sign of sigmoid colon cancer. With early colorectal cancer suspicion, MDT-guided en bloc minimally invasive resection can achieve good short-term control without recurrence.

Introduction

According to the 2023 Global Cancer Statistics^[1^], colorectal cancer accounts for over 1.9 million new cases annually and ranks second in mortality among malignant tumors. Among these cases, sigmoid colon adenocarcinoma constitutes 15%–20%. The typical initial symptoms of sigmoid colon adenocarcinoma are gastrointestinal manifestations, such as hematochezia (incidence: 60%–70%) and changes in bowel habits (incidence: 50%). Fewer than 5% of patients present with urinary tract symptoms, mostly hematuria or frequent urination in advanced disease. Vesical fecaluria is caused by a colovesical fistula. The common etiologies include intestinal inflammation (40%), diverticulitis (35%), and malignant tumors (predominantly colorectal cancer). Malignant tumors account for only 10%–15% of cases and always present with concomitant symptoms in the advanced stage of the tumor.

HIGHLIGHTS

• In this patient, vesical fecaluria was the first and dominant manifestation of sigmoid colon adenocarcinoma, preceding any bowel complaints.

• Recurrent “UTI + fecaluria” triggered a multidisciplinary review and an urgent laparoscopic en bloc resection.

• Final pathology showed pT4bN0M0 disease with negative margins and no nodal metastasis; the patient remained recurrence-free at 12 months.

• SMAD4 and BMPR1A alterations may explain bladder-directed extraluminal invasion and help interpret an atypical presentation.

Although colovesical fistula and fecaluria secondary to colorectal cancer have been described in previous reports, sigmoid colon adenocarcinoma presenting initially and predominantly with vesical fecaluria before obvious bowel symptoms remains a rare and diagnostically challenging presentation. This symptom can be easily confused with a urinary tract infection, leading to a high risk of delayed or missed diagnosis^[2^]. This study retrospectively analyzed the complete diagnostic and treatment process of this rare case and explored its pathological mechanisms, diagnostic difficulties, and treatment strategies by combining clinical data with a literature review, aiming to provide a reference for clinical practice.

Case presentation

A 62-year-old male was admitted to the hospital with urinary frequency, dysuria, and vesical fecaluria that had lasted for more than half a year. A review of his disease course revealed intermittent fever with a maximum temperature of 38.9 °C. The patient also reported repeated episodes of fecaluria during the same period. His urinary symptoms and fever were temporarily relieved after self-administration of antibiotics and ibuprofen, but they recurred. He had previously been treated at multiple hospitals and was diagnosed with a urinary tract infection each time. No abdominal pain, hematochezia, change in bowel habits, or other obvious gastrointestinal symptoms were reported. Digital rectal examination showed no abnormalities.

Laboratory tests showed elevated infection-related inflammatory markers. Urinalysis indicated pyuria and bacteriuria, supporting a urinary tract infection. Urine culture revealed growth of Escherichia coli with a colony count of >10⁵ CFU/mL, and antimicrobial susceptibility testing showed sensitivity to cefoperazone-sulbactam sodium. Given the patient’s repeated complaints of fecal-like material and a fecal odor in the urine, together with recurrent urinary tract infection caused by enteric bacteria, vesical fecaluria and possible colovesical communication were clinically suspected. Tumor markers, including carcinoembryonic antigen (CEA, 4.6 ng/mL) and carbohydrate antigen 19-9 (CA19-9, 27.3 U/mL), were within the normal range.

The key positive findings of imaging and endoscopic examinations were as follows: Abdominal MRI showed irregular thickening of the bladder wall, with a maximum thickness of 0.8 cm, local extension along the urachal tract to the anterior abdominal wall, and an unclear boundary between the lower sigmoid colon and the bladder dome, supporting direct inflammatory adhesion or tumor invasion between the sigmoid colon and bladder (Fig. 1A–C) Urinary system ultrasound: Abnormal echo between the right apex of the

Figure 1.

Abdominal magnetic resonance imaging findings of suspected sigmoid colon–bladder involvement. (A) Axial image showing irregular thickening of the bladder dome and anterior bladder wall, with abnormal soft-tissue extension along the urachal tract toward the anterior abdominal wall. (B) Coronal image demonstrating an indistinct interface and loss of the normal fat plane between the lower sigmoid colon and the bladder dome, suggesting dense inflammatory adhesion or direct tumor invasion. (C) Sagittal image further showing the close anatomical relationship between the sigmoid colon, bladder dome, and urachal region, with extension of the abnormal tissue toward the anterior abdominal wall. Yellow arrows indicate the principal abnormal findings.

Findings involved the bladder and the peritoneum below the umbilicus, suggestive of a urachal fistula with chronic inflammatory changes. Barium enema demonstrated an approximately 3-cm stenotic segment in the lower sigmoid colon, with obstructed contrast passage and mild proximal bowel dilatation. Definite leakage of contrast medium into the bladder was not clearly visualized. Cystoscopy revealed grade IV turbid urine, which markedly limited visualization; therefore, no definite fistula orifice could be identified preoperatively. Colonoscopy failed to reach the suspected sigmoid lesion because of poor bowel preparation, active bladder infection, abdominal distension, and luminal narrowing; therefore, direct endoscopic confirmation of the fistula tract was not achieved before surgery.

After two rounds of MDT consultations, a combined surgical procedure was performed. Dense adhesions were observed between the sigmoid colon, bladder dome, small intestine, and urachal region. Intraoperative frozen-section pathology indicated sigmoid colon adenocarcinoma invading the bladder and the muscular layer of the small intestine, thereby confirming malignant colovesical involvement and explaining the patient’s fecaluria. Further surgical procedures were conducted, including “laparoscopic radical resection of sigmoid colon tumor + laparoscopic partial cystectomy + laparoscopic partial small bowel resection + laparoscopic urachiectomy + permanent sigmoid colostomy.” Pathological findings: Sigmoid colon: Moderately differentiated adenocarcinoma; surgical margin negative (R0). Bladder: Invasion present; surgical margin negative (R0). Small intestine: Muscular layer invasion; surgical margin negative (R0). Urachus/fistula tract: Chronic inflammation; no tumor identified. Fistula tract confirmed pathologically as non-neoplastic. Lymph nodes: 12 mesenteric lymph nodes negative for metastasis. Overall: Complete R0 resection of all involved organs achieved; fistula tract confirmed pathologically. Follow-up Monitoring (1 Year): Clinical assessment: Regular outpatient visits at 1, 3, 6, 9, and 12 months postoperatively; evaluation of urinary and bowel symptoms. Imaging: Abdominal and pelvic CT/MRI at 6 and 12 months to assess for recurrence. Laboratory: Tumor markers (CEA and CA 19-9) at each visit. Outcome: At 12 months, the patient was asymptomatic, with no evidence of recurrence or complications.

Discussion

This case represents a rare urinary-dominant presentation of sigmoid colon adenocarcinoma, in which vesical fecaluria and recurrent urinary symptoms preceded any obvious gastrointestinal complaints. The coexistence of SMAD4 frameshift mutation and a BMPR1A nonsense mutation may provide a molecular clue for the bladder-directed extraluminal invasion observed in this patient. A literature review of PubMed and Embase (2000–2025) was performed using the keywords “sigmoid colon adenocarcinoma,” “colovesical fistula,” “vesical fecaluria,” and “urinary symptoms,” with the MeSH terms “Colonic Neoplasms” and “Enterovesical Fistula.” Original clinical cases reporting sigmoid colon adenocarcinoma with colovesical fistula were included, with reviews excluded, yielding 52 English articles (68 cases) and 3 Chinese articles (5 cases). Among 18 cases presenting initially with gastrointestinal symptoms, fecaluria developed after a mean of 4.2 months, and 88.9% showed lymph node metastasis (mostly stage III–IV). In contrast, our patient presented first with urinary symptoms, had stage IIB (T4bN0M0) disease without nodal involvement, and exhibited fecaluria from the onset, highlighting an atypical extraluminal invasion pattern differing from previously reported cases^[3,4^]. In this case, the patient initially presented with urinary frequency, dysuria, and vesical fecaluria, but had no abdominal pain, hematochezia, change in bowel habits, or other obvious gastrointestinal abnormalities. Postoperative pathology showed stage IIB disease (T4bN0M0). This presentation was attributed to the outward growth of the tumor (intestinal lumen invasion < 30%) and the masking of irritative symptoms by bladder infection. Clinical studies have shown that colorectal cancer generally requires more than 50% intestinal lumen invasion to cause changes in bowel habits. This characteristic expands the understanding of the clinical manifestations of this disease.

Vesical fecaluria is a pathological inevitability when sigmoid colon adenocarcinoma invades the bladder and forms a colovesical fistula, which is closely related to the anatomical basis and clinical symptoms. Anatomically, the distal sigmoid colon and the bladder dome are separated by only 0.5–1.0 cm of fat tissue. Both structures receive blood supply from the branches of the internal iliac artery and have communicating lymphatic vessels. Moreover, the urachal remnant (mostly fibrous strands in adults) can serve as an additional pathway (preoperative ultrasound in this case suggested a possible urachal fistula, and adhesion was observed during surgery), all of which provide conditions for tumor invasion^[5^]. The formation of a colovesical fistula can be divided into four stages: ① Infiltration stage: Adenocarcinoma penetrates the serosa of the sigmoid colon and invades the bladder, with no obvious symptoms; (2) Fistula tract stage: A fistula tract < 0.5 cm is formed, and *Escherichia coli* causes recurrent urinary tract infections; (3) Manifestation stage: The fistula tract expands to > 0.5 cm, leading to the drainage of fecaluria; (4) Vicious cycle stage: Feces exacerbate infection, and 3 cm stenosis of the sigmoid colon increases intestinal pressure, forming a closed loop of “infection – fecaluria – obstruction,” which can provide a basis for reverse screening of gastrointestinal tumors.(Fig. 2A–D)

Figure 2.

Four stages of colovesical fistula formation: (A) Infiltration Stage: Adenocarcinoma penetrates the serosa of the sigmoid colon and invades the bladder, with no obvious clinical symptoms; (B) Fistula Tract Stage: A fistula tract < 0.5 cm in diameter is formed, and *Escherichia coli* (E. Coli) induces recurrent urinary tract infections; (C) Manifestation Stage: The fistula tract expands to > 0.5 cm in diameter, resulting in fecaluria; (D) Vicious Cycle Stage: Fecal matter exacerbates infection, and a 3 cm stenosis of the sigmoid colon causes increased intestinal pressure, ultimately forming a closed loop of “infection – fecaluria – obstruction.”

It took half a year from the onset of symptoms to the final diagnosis in this patient. The diagnostic difficulties stemmed from cognitive gaps and technical limitations: the symptoms of frequent urination and dysuria were first misdiagnosed as a urinary tract infection (which is consistent with the reported 68% misdiagnosis rate of colovesical fistula), partly because clinicians may have limited awareness that colorectal malignancy can occasionally present with urinary symptoms, including fecaluria, before obvious bowel symptoms become apparent. Additionally, examinations such as colonoscopy and cystoscopy failed to identify the lesion due to obstruction and turbid urine. Two rounds of multidisciplinary team (MDT) consultations broke the deadlock: the strategies of “anti-infection first followed by re-evaluation” and “exploratory surgery” were adopted successively, and intraoperative frozen section pathology achieved accurate localization. The treatment adopted a precise surgical paradigm guided by the MDT. In accordance with the NCCN Guidelines for Colorectal Cancer (2024 version), laparoscopic surgery was performed within 48 hours after 3 days of ineffective conservative anti-infection treatment. The tumor and invaded organs were completely resected (with negative surgical margins ≥ 2 cm), and the patient recovered quickly without complications^[5–7^]. Clinical suggestions: For urology departments, when encountering patients with recurrent urinary tract infection accompanied by fecaluria, enhanced abdominal CT and tumor marker detection should be performed, and consultation with the general surgery department is recommended. For general surgery departments, the risk of bladder invasion should be evaluated preoperatively, and frozen section pathology examination should be conducted if intestinal-bladder adhesion is found during surgery.

To further explore the molecular mechanism underlying the absence of typical gastrointestinal symptoms in this case, NGS technology was used to perform targeted panel detection of colorectal cancer-related driver genes on the tumor tissue (covering 523 tumor-related genes with a detection depth ≥ 500×). The results showed two rare gene mutations: ① Frameshift mutation of the SMAD4 gene (Fig. 3A): A frameshift mutation in the SMAD4 gene (exon 11: c.1324_1325delAG, p. Arg442Glyfs23) mediates the regulation of cell polarity via blocking the TGF-β/Smad signaling pathway, thereby inhibiting the luminal polar growth of the tumor and enhancing its lateral invasion. Under normal physiological conditions, SMAD4, as a core mediator of the TGF-β/Smad pathway, can form a heterotrimer with phosphorylated Smad2/3. Upon entering the cell nucleus, this heterotrimer binds to the promoter regions of “luminal polarity-maintaining genes” (e.g., E-cadherin, tight junction protein ZO-1) to regulate their transcriptional expression, thereby maintaining the polar growth pattern of colonic epithelial cells toward the intestinal lumen^[8^]. Following the frameshift mutation of SMAD4, the C-terminal functional domain of its protein is lost, precluding the formation of a functional complex with Smad2/3. This leads to the interruption of TGF-β-mediated nuclear transcription signals, downregulation of E-cadherin expression (immunohistochemistry showed that the positive rate of E-cadherin in the tumor area was 40% ± 5% lower than that in normal intestinal mucosa), weakened intercellular adhesion, and dysregulated polar growth. Meanwhile, mutant SMAD4 can activate the β-catenin/TCF4 signaling axis through the “non-Smad pathway,” promoting the secretion of matrix metalloproteinase 9 (MMP-9) (enzyme activity assay revealed that MMP-9 activity in tumor tissue was 2.3-fold higher than that in normal tissue). This degrades the collagen fiber matrix on the lateral side of the intestinal wall, providing a pathological basis for the lateral invasion of the tumor toward the bladder^[9^]; (2) Nonsense mutation of the BMPR1A gene (Fig. 3B).

Figure 3.

Immunohistochemical findings for the two mutated genes. (A) The positive staining for SMAD4 protein in the tumor cell area is markedly reduced or absent, while normal intestinal mucosal cells serve as a positive control. This confirms that the loss of SMAD4 function leads to the inhibition of intestinal luminal polarity and enhanced extraluminal invasion. (B) The intensity of BMPR1A-positive staining in tumor cells (especially in the area adjacent to urachal adhesions) is lower than that in normal bladder or intestinal wall cells, suggesting downregulated BMPR1A expression, which is consistent with a mechanism of weakened BMP signaling that promotes urachal invasion.

A nonsense mutation in the BMPR1A gene (exon 4: c.532C>T, p.Arg178) inactivates the BMP/Smad1/5/8 signaling pathway, abrogating the inhibitory effect on tumor invasion, promoting tumor invasion into the bladder via the urachus, and thereby avoiding intestinal obstruction. As a type I receptor of the bone morphogenetic protein (BMP) signaling pathway, BMPR1A normally forms a complex with BMP ligands (e.g., BMP-2, BMP-4) and type II receptors (BMPR2). This complex activates and phosphorylates Smad1/5/8; the phosphorylated Smad1/5/8 then binds to SMAD4 and enters the cell nucleus, where it regulates the expression of “tumor invasion-inhibiting genes” (e.g., p21, Id2), inhibiting the excessive proliferation of tumor cells and restricting their invasion range^[5^]. This nonsense mutation results in the loss of the intracellular kinase domain of BMPR1A, preventing the activation of Smad1/5/8 signaling. Consequently, p21 expression is downregulated (the proportion of p21-positive cells in the tumor area was <10%, while that in normal intestinal wall cells was >40%), and the inhibition of tumor cell proliferation is abolished. Additionally, mutant BMPR1A can upregulate the expression of integrin αvβ6 (the expression level of αvβ6 on the tumor cell membrane was 3.1-fold higher than that on normal cells), enhancing the adhesion ability of tumor cells to the fibrous connective tissue at the urachal stump (rich in collagen IV) and guiding the directional invasion of tumor cells into the bladder along the urachal tract^[9^]. Furthermore, this mutation only affects the lateral invasion ability of the tumor and has no significant impact on the apoptotic pathway (e.g., caspase-3 activity) of tumor cells on the luminal side. The invasive depth of the tumor on the luminal side remains <30%, and thus does not cause intestinal lumen stenosis or obstruction, which is fully consistent with the clinical features of “no hematochezia or changes in defecation habits” in the case.

Conclusion

This study reports a rare and atypical case of sigmoid colon adenocarcinoma presenting predominantly with vesical fecaluria, without classic gastrointestinal symptoms. The unusual presentation posed significant diagnostic challenges, including repeated misdiagnoses as urinary tract infections, highlighting the importance of maintaining a high index of suspicion for colorectal pathology in patients with unexplained urinary symptoms. MDT-guided laparoscopic en bloc resection resulted in radical treatment, with no recurrence during a 1-year follow-up. Clinicians should consider early colorectal evaluation, imaging, and tumor marker assessment when urinary symptoms such as recurrent UTIs or fecaluria are present, to facilitate timely diagnosis and improve patient outcomes.

Methods

This work has been reported in line with the SCARE criteria^[10^].

Ethical approval

This study was approved by the Hospital Ethics Committee (Approval Number: 2025-015). All procedures were conducted in accordance with the relevant regulations of the ethics committee. As this was a retrospective study, oral informed consent was obtained from the patient, and their information is reported anonymously in this article.

Consent

Written informed consent was obtained from the patient for the publication of this case report and accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal upon request. Identifying details (e.g., names, initials, hospital numbers) are omitted, and all images are used with explicit patient permission, with unnecessary identifying features excluded.

Sources of funding

This research was supported by (1) National Natural Science Foundation of China (Young Scientists Fund; No. 82503123); (2) National Natural Science Foundation of China (General Program; No. 32573456); (3) Joint Special Project of Universities in Yunnan Province (2022; No. 2022-ES-530101-207); (4) Hospital-level Scientific Research Project of the Fourth Affiliated Hospital of Dali University (No. 2022YJ14); (5) Yunnan Provincial Department of Science and Technology, Science and Technology Plan Project Contract (No. 202301BA070001-027). The funders had no role in data collection, analysis, manuscript writing, or the decision to submit for publication. The funders had no role in data collection, analysis, manuscript writing, or the decision to submit for publication.

Conflicts of interest disclosure

All authors declare that there is no conflicts of interest.

Author contributions

J-H.D.: conceptualization; methodology; investigation (urological presentation, perioperative management, follow-up); data curation; writing – original draft; project administration. Y-Y.W.: conceptualization; methodology; literature review; formal analysis and interpretation of the clinical course; writing – original draft; writing – review and editing. W-B.W.: investigation (clinical data acquisition and 12-month follow-up); resources; data curation; visualization of the clinical timeline. Y-P.Z.: pathological investigation and diagnosis; resources; validation of tumor stage (pT4bN0M0) and margin status; molecular interpretation of SMAD4/BMPR1A alterations; writing – review & editing (pathology section). L-P.Y.: CT assessment and interpretation of the colovesical relationship; preparation of radiologic documentation; validation of preoperative imaging findings for MDT decision-making. C-H.D.: supervision; conceptualization; surgical leadership of the multidisciplinary team (MDT); performance and oversight of laparoscopic en bloc resection; writing – review and editing for critical intellectual content; funding acquisition; corresponding author and overall guarantor of the work.

Guarantor

Chao-Hua Deng.

Data availability statement

The datasets generated and analyzed in this case report are not publicly available due to patient privacy, ethical restrictions, and institutional policy. De-identified data may be available from the corresponding author on reasonable request. Any release of data will require review and approval by the Ethics Committee of the Fourth Affiliated Hospital of Dali University (Approval No. 2025-015) and will only be provided in compliance with all applicable confidentiality and data security regulations.