A Rare Case of Newly-Diagnosed Type 2 Diabetes Mellitus Presenting as a Neurogenic Bladder

Document Type

Conference Proceeding

Publication Date

10-22-2025

Publication Title

J Endocr Soc

Keywords

ceftriaxone, hemoglobin A1c, infusion fluid, insulin, adult, bladder, bladder capacity, bladder dysfunction, bladder emptying, bloating, case report, clinical article, complication, computer assisted tomography, conference abstract, diabetic patient, diagnosis, edema, emergency ward, Foley balloon catheter, Gilles de la Tourette syndrome, glucose blood level, glucosuria, glycemic control, human, hydronephrosis, hydroureter, hyperglycemia, hypotonic bladder, indwelling catheter, ketonuria, kidney failure, laboratory test, leukocyte count, male, medical history, micturition, neurogenic bladder, non insulin dependent diabetes mellitus, normal anion gap metabolic acidosis, overactive bladder, prostate hypertrophy, pyuria, risk factor, serum osmolality, soreness, subcutaneous tissue, surgery, swelling, tachycardia, urethra obstruction, urinalysis, urinary frequency, urine volume, urosepsis

Abstract

Introduction: Diabetic cystopathy is a rare urologic complication of poorly controlled diabetes that presents as a neurogenic bladder. While this condition is a welldocumented but rarely observed complication of diabetes, its progression to severe outcomes, such as hydroureteronephrosis and pelvic calyceal rupture, is rare, especially in the context of newly diagnosed diabetes. Case Presentation: A 60-year-old male with a past medical history of Tourette syndrome who had not sought medical care for 10 years presented to the emergency department with a 1-month history of progressively worsening urinary frequency, urgency, incontinence, and abdominal bloating. He was tachypneic and tachycardic with abdominal distention, tenderness, guarding, and a non-reducible mass at the umbilicus. Laboratory tests showed a white blood cell count of 14,500/UL, blood glucose level of 951 mg/dL, and hemoglobin A1C of 15.5%. Urinalysis showed glucosuria and mild pyuria without ketonuria. Normal anion gap metabolic acidosis and elevated serum osmolality (316 mOsm/kg) was also noted, confirming a hyperosmolar hyperglycemic state (HHS). Computed tomography of the abdomen and pelvis revealed a massively distended bladder, severe left hydroureteronephrosis, and pelvic calyceal rupture without prostatic hyperplasia. A Foley catheter was inserted for bladder decompression with a urine output of 1,100 mL. He received ceftriaxone for urosepsis and intravenous fluids and insulin for his HHS. He was transitioned to a subcutaneous insulin regimen and discharged on mixed insulin. Discussion: Diabetic cystopathy is defined as a triad of increased bladder capacity, decreased bladder sensation, and poor bladder emptying. In its early compensated stage it manifests as an overactive bladder with diminished capacity and progresses to a decompensated stage with an atonic bladder resulting in voiding difficulties and upper urinary tract dysfunction such as hydronephrosis and renal failure. Although subclinical changes can occur within 5 to 10 years of diagnosis, symptoms become prevalent usually after 10 to 20 years. Risk factors include poor glycemic control, long duration of diabetes mellitus, and coexisting microvascular complications. Treatment involves glycemic control, indwelling catheter placement, cholinergics to decrease detrusor overstretch, and transurethral surgery for refractory cases. This case highlights the importance of recognizing bladder dysfunction as a potential manifestation of diabetes. This dysfunction can develop early in the disease process highlighting the necessity for early screening and management in diabetic patients. Studies should focus on early screening and standardized diagnostic criteria for bladder dysfunction at the time of diabetes diagnosis to facilitate timely intervention and prevent irreversible complications such as pelvic calyceal rupture.

Volume

9

Issue

Supplement_1

First Page

A536

Last Page

A537

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