Causes of Massively Distended Bladder
A massively distended bladder results from either mechanical obstruction preventing urine outflow or neurogenic dysfunction causing detrusor underactivity, with the most common causes being benign prostatic hyperplasia in men, pelvic organ prolapse in women, neurologic disease, and acute prolonged bladder overdistension following anesthesia or surgery. 1, 2, 3
Mechanical/Obstructive Causes
In Men
- Benign prostatic hyperplasia is the predominant cause in elderly males, representing the most frequent etiology of acute urinary retention 3
- Urethral strictures and bladder neck obstruction 3
- Prostate cancer causing outlet obstruction 4
In Women
- Pelvic organ prolapse is the primary mechanical cause in women 1, 3
- Pelvic masses (fibroids, ovarian tumors) compressing the bladder outlet 1
- Post-surgical complications affecting bladder outlet 1
Both Sexes
- Massive fecal impaction (fecaloma) can cause catastrophic bladder distension by filling the pelvic cavity and compressing the bladder outlet, potentially leading to bladder rupture 5
- Bladder or urethral stones 4
- Pelvic tumors or malignancies 4, 1
Neurogenic/Functional Causes
Acute Neurogenic Dysfunction
- Acute prolonged bladder overdistension (ApBO) following regional anesthesia, where primary neurogenic detrusor dysfunction causes retention with decreased or absent bladder sensation—patients do not complain, leading to delayed recognition 2
- Prolonged childbirth causing temporary neurogenic dysfunction 2
- Extensive surgery with associated neurologic complications 2
Chronic Neurogenic Conditions
- Spinal cord injury or disease 3
- Multiple sclerosis and other demyelinating diseases 3
- Diabetic neuropathy affecting bladder innervation 3
Detrusor Underactivity
- Detrusor underactivity with dysfunctional voiding results in episodes of hesitancy, urge incontinence, or overflow incontinence, with children showing dampness rather than soaking and voiding only once or twice daily 4
- Impaired bladder sensation leading to storage of large urine volumes overnight without arousal to void 4
- Detrusor decompensation as the clinical endpoint of chronic high-pressure bladder conditions 4
Iatrogenic Causes
- Regional anesthesia is a leading iatrogenic cause, as it produces temporary neurogenic detrusor dysfunction 2
- Medications with anticholinergic effects (antihistamines, antipsychotics, antidepressants) 3
- Opioid analgesics causing urinary retention 3
Rare Metabolic Causes
- Nephrogenic diabetes insipidus can lead to massive bladder distension with reports of hydronephrosis in 34% of cases, with some patients developing thick-walled bladder and post-micturition residual volume requiring cystostomy drainage 4
- Detrusor underactivity (42.3%) and acontractile detrusor (15.4%) documented in patients with diabetes insipidus and hydroureteronephrosis 4
Clinical Recognition
Physical examination reveals an enlarged bladder palpable on abdominal examination in severe cases, with a dull percussion note confirming bladder distension. 1 However, the bladder is rarely palpable despite massive distension, making suprapubic percussion for dullness critical 3.
Ultrasound is highly sensitive (>90%) for detecting bladder distension and should be performed immediately when retention is suspected. 4, 1
Critical Pitfall
The most dangerous scenario is acute prolonged bladder overdistension where decreased or absent bladder sensation means patients do not complain of discomfort, leading to delayed recognition and management—this occurs most commonly after regional anesthesia, prolonged childbirth, or extensive surgery. 2 Prevention through systematic bladder monitoring in high-risk situations is paramount, as recovery depends on whether reversible or irreversible detrusor damage has occurred 2.
Immediate Management Priority
The first intervention is immediate bladder drainage via urethral or suprapubic catheterization to prevent irreversible detrusor damage. 2, 3 Post-obstructive diuresis and hematuria are possible complications requiring close monitoring 3.