Abstract
Massive chronic urinary retention, particularly with volumes exceeding 10 l, is an exceptional manifestation of bladder outlet obstruction (BOO) and may remain undetected until complications arise. We present the case of a 55-year-old who developed progressive abdominal distension with minimal lower urinary symptoms. Ultrasonography demonstrated a markedly enlarged bladder with a volume exceeding 10 l and bilateral hydroureteronephrosis. Following emergency referral, urethral catheterization drained 9.8 l and was followed by significant post-obstructive diuresis requiring monitoring and intravenous fluid replacement. Despite extensive radiological changes, renal impairment was relatively mild. Further evaluation identified a 28 ml prostate, and transurethral resection of the prostate (TURP) histology confirmed benign prostatic hyperplasia (BPH). This case highlights the remarkable compensatory capacity of the urinary tract in chronic obstruction and reinforces the importance of early recognition, close monitoring, and definitive management of BOO. Long-term bladder function remains under assessment because of suspected detrusor underactivity.
Introduction
Chronic urinary retention (CUR) is characterized by painless, progressive urinary retention with persistently elevated post-void residual volumes. Patients often adapt to gradual bladder distension and may present with abdominal symptoms rather than lower urinary tract complaints [1]. BPH remains the commonest cause of BOO, and delayed diagnosis may cause hydronephrosis, renal impairment, and irreversible detrusor dysfunction [2]. Giant CUR with bladder volume exceeding 5 l is exceptionally rare, and reports describing bladder volumes exceeding 8–10 l are scarce [3]. We report an exceptional case of giant CUR with a bladder volume exceeding 10 l, bilateral hydroureteronephrosis and cortical thinning, successfully managed with definitive surgical treatment (e.g. Table 1). Such cases present significant challenges regarding safe decompression, management of post-obstructive diuresis (POD), and predicting recovery of bladder function [4].
Timeline summarizing the patient's presentation, diagnostic investigations and treatment.
| 2024 | Previous renal function normal (creatinine 101 μmol/l) |
|---|---|
| Pre-January 2026 | Longstanding poor urinary stream with worsening urinary frequency and post-micturition dribbling over the preceding year. Progressive abdominal distension and bloating prompted GP assessment. |
| 6 January 2026 | Ultrasound showing >10 l, catheterization, CT, and admission |
| 9 January 2026 | Discharge from hospital |
| 29 January 2026 | Flexible cystoscopy |
| 25 March 2026 | Transrectal ultrasound for prostate sizing (29 ml) |
| 3 June 2026 | TURP |
Case report
A 55-year-old man was referred to the emergency department following an outpatient ultrasound requested by his general practitioner for progressive abdominal bloating. His medical history included hypertension, hypercholesterolaemia and childhood circumcision. He described longstanding poor urinary stream with worsening frequency and post-micturition dribbling during the preceding year but denied acute urinary retention, haematuria or urinary tract infection. Ultrasound performed in January 2026 demonstrated bilateral hydronephrosis, right renal cortical thinning and a severely distended urinary bladder with an estimated volume of 10 233 ml. Following urgent referral to Urology, a 16-Fr two-way urethral catheter was inserted and immediately drained 3 l of urine before temporary clamping.
Immediate computed tomography (CT) of the urinary tract confirmed bilateral hydroureteronephrosis with a markedly distended bladder containing ~5.6 l (Figs 1 and 2). Initial blood investigations demonstrated a serum urea of 5.8 mmol/l, creatinine of 139 μmol/l and estimated glomerular filtration rate (eGFR) of 49 ml/min/1.73 m2. Previous renal function (2024) had shown a creatinine of 101 μmol/l, indicating deterioration consistent with chronic obstructive uropathy. Other biochemical parameters were unremarkable.
Axial CT of the patient after 3 l of urine drained via catheterization in the emergency department.
Coronal CT of the patient after 3 l of urine drained via catheterization in the emergency department.
Patient was admitted; the catheter was fully unclamped, and urinary output/fluid status was monitored closely. A further 6.8 l of urine drained over 15-minutes, resulting in a total initial drainage of ~9.8 l. Subsequently, he developed POD with urine output averaging 300–400 ml/hour, necessitating continued fluid balance monitoring and replacement. Repeat blood tests the following day demonstrated stable renal function, and digital rectal examination revealed a smooth, benign-feeling prostate. Following stabilization of fluid balance, the patient was discharged on 9 January 2026 with the catheter and booked for outpatient investigations.
Flexible cystoscopy performed on 29 January 2026 demonstrated multiple diffuse haemorrhagic spots throughout the bladder mucosa, consistent with chronic overdistension (Fig. 3). Serum prostate-specific antigen measured 0.6 μg/l. Transrectal ultrasound in March 2026 demonstrated a prostate volume of only 28 ml. Following multidisciplinary discussion and counselling regarding treatment options, the patient underwent TURP in June 2026 with histology demonstrating prostatic tissue with features of BPH. The patient continues under follow-up to assess recovery of bladder function. Owing to prolonged bladder overdistension, persistent detrusor underactivity remains a concern, and intermittent self-catheterization will be considered should adequate spontaneous bladder emptying not recover.
Flexible cystoscopy demonstrating diffuse haemorrhagic bladder mucosal changes following chronic overdistension.
Discussion
CUR is defined by a post-void residual volume exceeding 300 ml, with most patients retaining ~1 l of urine [1, 5]. Giant CUR is exceptionally uncommon, with published reports generally describing retained volumes of 4–6 l, mostly secondary to neurogenic bladder [3, 6]. Extreme bladder distension exceeding 8 L has only rarely been described in the literature (Table 2) [3]. Previously reported cases have predominantly involved neurogenic bladder secondary to diabetic autonomic neuropathy or chronic bladder outlet obstruction (BOO) [7, 8]. Presentations have ranged from incidental asymptomatic retention to significant mass-effect complications, including inferior vena cava compression [8]. The present case is particularly notable for the patients young age and the development of marked bilateral hydroureteronephrosis, right renal cortical thinning, and renal impairment despite a relatively modest prostate volume.
Comparison of the present case with previously published cases of giant urinary bladder with reported volumes exceeding 8 l. The table summarizes patient demographics, estimated bladder volume, clinical presentation, relevant comorbidities or underlying aetiology, and distinctive clinical features [7–10].
| Study | Age | Bladder volume | Clinical presentation | Underlying comorbidity/aetiology | Unique features |
|---|---|---|---|---|---|
| Yücel et al., 2016 | 66 M | 10.5 l | 3-day history of abdominal distention. | Diabetes mellitus; subsequently considered to have diabetic autonomic neuropathy causing neurogenic bladder | No previous neurological or urological disorder. |
| Sharma et al., 2018 | 80 M | 11 l | 10-year history of painless progressive abdominal distension and four-month history of bilateral lower-limb oedema | Diabetes mellitus and previous spinal cord injury; urodynamics demonstrated an underactive, low-compliance neurogenic bladder. | Severe compression of the IVC and common iliac veins caused bilateral lower-limb oedema; mild bilateral hydroureteronephrosis |
| Nur Bazlaah et al., 2020 | 69 M | 10.1 l | 2-month history of abdominal distension and two-day history of left scrotal swelling. | CUR secondary to prostatomegaly. | Unusual presentation with unilateral scrotal swelling, which resolved after catheterization |
| Akintelure et al., 2025 | 63 M | 15 L | Asymptomatic—incidental finding on CT upon investigation of iron deficiency anaemia. | Suspected BPH | Remarkably preserved renal function despite ~15 l of retention and absence of significant lower urinary tract symptoms. |
| Present case | 55 M | 10 l | Progressive abdominal bloating and tense abdomen; longstanding poor urinary stream, increasing frequency and post-micturition dribbling | Longstanding voiding dysfunction; relatively small prostate (28 ml on subsequent sizing) | Marked bilateral hydroureteronephrosis with right renal cortical thinning and extreme retention occurred despite only modest prostatic enlargement. |
Massive CUR develops insidiously as gradual bladder distension allows progressive increases in bladder compliance, enabling patients to remain relatively asymptomatic despite urine accumulation [1, 4, 11]. Prolonged overdistension, however, results in irreversible detrusor injury characterized by smooth muscle degeneration, collagen deposition, and impaired contractility [5, 11]. Consequently, progressive abdominal distension may become the predominant presenting feature, while lower urinary tract symptoms remain minimal, delaying diagnosis and increasing the risk of upper urinary tract damage [1]. Despite marked bilateral hydroureteronephrosis and right renal cortical thinning, our patient demonstrated only modest renal impairment, illustrating that preserved serum creatinine does not exclude advanced obstructive uropathy [4]. Cross-sectional imaging should therefore be considered in those with unexplained abdominal enlargement or longstanding lower urinary tract symptoms [3].
Initial management consists of prompt bladder decompression followed by definitive treatment of the underlying obstruction [1]. Although gradual bladder decompression was traditionally recommended because of concerns regarding haematuria and POD, contemporary evidence supports immediate complete drainage in most patients provided close clinical monitoring is maintained [4, 11]. Our patient developed significant POD, producing 300–400 ml of urine/hour, requiring careful fluid and electrolyte replacement. Physiological POD represents the normal renal excretion of retained water and solutes after relief of obstruction and typically resolves once homeostasis is restored [4]. In contrast, pathological POD persists beyond restoration of euvolaemia and may result in dehydration, electrolyte disturbance, hypovolaemic shock and, if untreated, death [4, 5]. Meticulous monitoring of urine output, fluid balance, electrolyte levels, body weight and haemodynamic status is therefore essential [4].
An additional feature of this case was the relatively small prostate volume of 28 ml despite severe BOO requiring TURP. Histopathology confirmed BPH, highlighting the poor correlation between prostate size and the degree of obstruction [6]. Clinical management should therefore be guided by symptoms, objective evidence of obstruction and its functional consequences rather than prostate volume alone [1, 6].
Conclusion
Giant urinary bladder resulting from CUR is an exceptionally uncommon manifestation of BOO, with only a handful of published cases [3]. The estimated volume of ~10 l in our patient places this case among the largest to date. This case demonstrates that profound CUR can progress silently, with abdominal distension becoming the dominant feature. Management requires cautious bladder decompression, surveillance for POD, and counselling regarding persistent detrusor dysfunction requiring life-long catheter dependence [6]. In addition, this report highlights that BOO may occur despite a relatively small prostate volume and underscores the important role of community ultrasonography in facilitating prompt management [1, 5, 6].
Conflicts of interest
None declared.
Funding
None declared.
Patient consent
Written informed consent for publication of this case report and images was obtained.
