Delayed diagnosis of foley catheter-associated intraperitoneal bladder rupture in an older patient

Bladder rupture is an uncommon but potentially life-threatening condition, with an estimated incidence of 0.002% of hospital admissions.^[1,2] Because the presenting features are often nonspecific, diagnosis might be delayed or missed, increasing the risk of peritonitis, sepsis, and death.^[1] Older patients with multiple comorbidities may be particularly susceptible to bladder injury even in the absence of significant trauma.^[3] Because its management differs substantially, bladder rupture can be classified as intraperitoneal or extraperitoneal. Intraperitoneal rupture requires surgical repair, whereas extraperitoneal rupture can often be managed conservatively with catheter drainage.^[4] We report a case of intraperitoneal bladder rupture following urethral catheterization in an older patient with multiple comorbidities, including neurogenic bladder and cystitis, which was initially overlooked and ultimately required surgical repair.

An 81-year-old woman presented to the emergency department (ED) with diffuse abdominal discomfort. She reported passing loose stools earlier that day but denied recent flatus or defecation. On examination, the abdomen was soft and nondistended, with diffuse tenderness but no rebound tenderness. She had no indwelling catheter on arrival and routinely underwent clean intermittent catheterization at home. A Foley catheter was inserted in the ED. It drained 850 mL of residual urine, followed by 400 mL of reddish and cloudy urine.

Her history included a neurogenic bladder, recurrent urinary tract infection, dementia, and an ascending aortic thrombus for which she was receiving apixaban. Laboratory findings revealed worsening renal function, with blood urea nitrogen (BUN) and creatinine (Cr) levels of 31.9 mg/dL and 1.70 mg/dL (reference 8-20 mg/dL and 0.5-0.9 mg/dL, respectively), corresponding to an estimated glomerular filtration rate (eGFR) of approximately 28 mL/(min·1.73 m²). These values increased from 13.3 mg/dL and 0.42 mg/dL, respectively, two weeks earlier. C-reactive protein concentration was 3.09 mg/dL (reference <0.5 mg/dL), and urinalysis showed >100 white blood cells and red blood cells per high-power field (reference <5 cells/high-power field for both), which is consistent with cystitis.

Because the patient’s acute diffuse abdominal pain and abdominal tenderness raised concerns about a surgical abdomen, noncontrast abdominopelvic computed tomography (CT) was performed on hospital day (HD) 1. Intravenous contrast was withheld because of acute kidney injury. It showed bilateral hydronephrosis, diffuse bladder wall thickening, and mild peritoneal changes. The scan was initially reviewed by the attending emergency physician, and the patient was admitted. Although a retrospective review revealed findings suggestive of bladder rupture (Figure 1), these findings were not recognized initially. On HD 4, the radiologist issued an addendum to the formal radiological report describing Foley balloon migration into the intraperitoneal space, associated free air, and worsening peritoneal thickening, raising suspicion of bladder rupture with peritonitis.

Figure 1. Axial (A) and coronal (B) noncontrast abdominopelvic CT images obtained on hospital day 1. The white arrow indicates the balloon of the Foley catheter, which migrated through the posterior bladder wall into the intraperitoneal cavity above the bladder dome. Although these findings were present on the initial CT, they were not recognized during the initial interpretation. CT: computed tomography.

Renal function subsequently improved, with BUN and Cr levels of 14.3 mg/dL and 0.53 mg/dL, respectively, corresponding to an eGFR of 89 mL/(min·1.73 m²). Contrast-enhanced CT was therefore performed and clearly demonstrated intraperitoneal bladder rupture (Figure 2A, B). This finding was confirmed by cystography on HD 5 (Figure 3). Preoperative preparation was initiated immediately after diagnostic confirmation, and bladder repair was performed on HD 6. Through a low midline incision, a 1-cm posterior bladder wall defect was identified and repaired in two layers. Water-tight bladder closure was confirmed intraoperatively by saline instillation, with no leakage observed. Postoperatively, urethral catheter drainage was maintained. At the patient’s request, the catheter was maintained instead of resuming clean intermittent catheterization, and she was discharged with the catheter in place on HD 14. The postoperative course was uneventful.

Figure 2. Axial (A) and coronal (B) contrast-enhanced abdominopelvic CT images obtained on hospital day 4. The white arrow indicates the balloon of the Foley catheter, which migrated beyond the bladder dome into the intraperitoneal cavity. Intraperitoneal free air and worsening peritoneal thickening are also visible, which is consistent with intraperitoneal bladder rupture. CT: computed tomography.

Figure 3. Intraperitoneal bladder rupture on cystography. Cystography demonstrating contrast extravasation from the perforated bladder into the intraperitoneal cavity, which is consistent with intraperitoneal bladder rupture (white arrows).

The key lesson from this case is that misinterpretation of early noncontrast CT findings in a high-risk older patient can delay the diagnosis of bladder rupture and expose the patient to life-threatening peritonitis.

In our patient, several factors contributed to the delayed diagnosis. Chronic bladder wall vulnerability associated with neurogenic bladder and recurrent cystitis, together with apixaban therapy, led to hematuria being initially attributed to anticoagulation rather than injury.^[5,6] In addition, abdominal discomfort and pyuria mimicked acute cystitis, further obscuring the diagnosis. Several factors may also have contributed to bladder rupture. Acute cystitis superimposed on a chronic neurogenic bladder may have rendered the bladder wall more vulnerable to perforation during urethral catheterization. Previous reports have also suggested that catheter-related factors, including catheter caliber and insertion technique, may contribute to bladder perforation, particularly in patients with a vulnerable bladder wall. ^[1,7]

CT signs of bladder rupture are divided into direct findings, including bladder wall discontinuity and contrast extravasation, and indirect findings, such as free air, ascites, and hydronephrosis.^[8] In our patient, the initial noncontrast CT lacked the characteristic direct findings of bladder rupture and showed only subtle abnormalities, including bilateral hydronephrosis, mild peritoneal changes, and balloon malposition, making the diagnosis difficult during the initial interpretation. CT cystography remains the gold standard for diagnosing bladder rupture, with an overall sensitivity and specificity of approximately 95% and 100%, respectively, although the sensitivity for predicting intraperitoneal rupture is lower, at approximately 78%.^[9] When intravenous contrast cannot be used because of impaired renal function, noncontrast CT may be the only feasible imaging modality. This case highlights the importance of maintaining a high index of suspicion and carefully reviewing subtle findings on noncontrast CT when contrast-enhanced imaging is not feasible.^[10]

In accordance with the European Association of Urology (EAU) guidelines on urological trauma, surgical repair is the standard treatment for iatrogenic intraperitoneal bladder rupture.^[4] Conservative management may be considered only in selected patients without peritonitis or ileus. In our patient, delayed diagnosis resulted in peritonitis, making surgery the only appropriate treatment. Although delayed diagnosis and treatment are associated with increased morbidity and mortality, ^[7] our patient achieved a favorable outcome following prompt surgical repair once the diagnosis was established, despite being older, having multiple comorbidities, and having a diagnostic delay.

In conclusion, intraperitoneal bladder rupture after Foley catheterization is rare. Particular caution is warranted during urethral catheterization in patients with acute cystitis, particularly those with underlying neurogenic bladder. Persistent symptoms or unexplained imaging findings after catheterization require timely re-evaluation to avoid delayed diagnosis and life-threatening complications.

Funding: None.

Ethical approval: This study was approved by the Institutional Review Board of Chungbuk National University Hospital (IRB No. 2025-07-032).

Conflicts of interest: Nothing declared.

Contributors: All the authors contributed significantly to the writing and revision of this manuscript and approved the final version.