Acute urinary retention is a known complication of inguinal hernia repair. However, the development of severe agitation and delirium as a result of acute urinary retention following inguinal hernia repair is less commonly reported. Here, we present the case of a 40-year-old male with no relevant medical history who underwent open mesh hernia repair for an uncomplicated left-sided indirect inguinal hernia. Postoperatively, the patient became hypertensive, delirious, and violent. He was found to have urinary retention on a bladder scan. Urgent intervention with catheterization and bladder decompression resulted in the prompt resolution of the patient\'s symptoms. The patient regained his senses and did not remember the events that led to it. This case highlights the importance of recognizing and managing acute urinary retention to prevent the development of severe agitation and delirium following spinal anesthesia. Further research and awareness are necessary to better understand the underlying neurovisceral mechanisms and optimize preventive strategies.

BACKGROUND: Autonomic dysreflexia (AD) can be a life-threatening condition in patients with spinal cord injury. It is important to prevent bladder overdistension in these patients as it may trigger AD. Sensation-dependent bladder emptying (SDBE), as a method of bladder management, improves the quality of life and allows physiologic voiding. In this study, we report disruption of the SDBE habit after bladder overdistension leading to AD with chest pain.
METHODS: A 47-year-old male with a diagnosis of C4 American Spinal Cord Injury Association impairment scale A had been emptying his bladder using the clean intermittent catheterization method with an itchy sensation in the nose as a sensory indication for a full bladder for 23 years, and the usual urine volume was about 300-400 mL. At the time of this study, the patient had delayed catheterization for approximately five hours. He developed severe abdominal pain and headache and had to visit the emergency room for bladder overdistension (800 mL) and a high systolic blood pressure (205 mmHg). After control of AD, a hypersensitive bladder was observed despite using anticholinergic agents. The sensation indicating bladder fullness changed from nose itching to pain in the abdomen and precordial area. Moreover, the volume of the painful bladder filling sensation became highly variable and was noted when the bladder urine volume exceeded only 100 mL. The patient refused intermittent clean catheterization. Finally, a cystostomy was performed, which relieved the symptoms.
CONCLUSIONS: Patients using physiologic feedback, such as SDBE, for bladder management are recommended to avoid bladder overdistension.

Polyuria can lead to progressive chronic bladder overdistension. The impact of polyuria on the bladder has been extensively studied in settings of either diabetes or sucrose diuresis in animals. The goal of this study was to investigate the outcomes of polyuria in a hypertension setting.
Male Dahl/SS rats, a hypertension model, received a high-salt or normal diet for 6 weeks. Twenty-four-hour water intake, micturition patterns, and blood pressures were recorded biweekly. Conscious cystometry was carried out at the end of this period. Bladders were collected to measure contractile force and for histological analysis. Paired t-tests were used to compare changes between Week 0 and Week 6 within each group. Unpaired t-tests were used for comparisons between groups for all parameters at Week 6.
Six weeks of high-salt diet significantly increased water intake and total urine. Blood pressures and volume of urine per micturition was higher in rats on high-salt diet. Bladder overdistension in the high-salt diet group was confirmed by cystometry, shown by a significantly higher bladder capacity, and compliance. No difference in detrusor contractility was observed between both groups. Collagen content was significantly higher in the lamina propria of the high-salt group compared to the normal group, while the opposite was observed in the muscularis.
Polyuria, in a hypertension context, leads to changes in bladder morphology and function. These findings help clarify the deleterious clinical impact of polyuria on voiding function, highlighting the variable consequences of bladder overdistension according to the underlying pathology.