Overactive Bladder: Neurogenic

Fig. 4.1

Urodynamic tracing for 39-year-old man with T6 SCI

Findings

The urodynamic tracing demonstrates the filling phase. The patient’s bladder was emptied by catheterization after he was unable to void; therefore, no PFS is included. The first evidence of neurogenic detrusor overactivity was noted at a bladder volume of 120 mL. The amplitude of detrusor contraction was >100 cm H₂O (Laborie urodynamic machines are usually not accurately calibrated above a contraction strength of 100 cm H₂O). The type of neurogenic detrusor overactivity was phasic. The increased EMG activity during each episode of detrusor overactivity was suggestive of detrusor external sphincter dyssynergia (DESD) . Small volume UUI was demonstrated with each detrusor contraction (not registered on the flow curve but noted by the clinician performing the evaluation). The compliance was within normal limits at this low bladder capacity.

The corresponding fluoroscopy images demonstrated evidence of detrusor trabeculation with bilateral bladder diverticula (Fig. 4.2). There was no vesicoureteral reflux seen on this exam. Although no voiding phase was captured, the bladder trabeculation and bladder diverticula suggest high-pressure voiding consistent with DESD .

Fig. 4.2

Fluoroscopic image from filling phase for 39-year-old man with T6 SCI demonstrating bladder diverticula

4.2.1.5 Treatment Options

In order to avoid high-pressure voiding and to improve his urinary incontinence, the patient was taught to perform clean intermittent catheterization and was placed on a daily anti-muscarinic. Intradetrusor injection of onabotulinumtoxinA would be an appropriate treatment modality to add to CIC if he continues to have urinary incontinence between catheterizations. Augmentation cystoplasty would be reserved for refractory UUI after he had failed onabotulinumtoxinA treatment .

4.2.2 Patient 2

4.2.2.1 History

The patient is a 64-year-old woman with a past medical history significant for hypertension and hypothyroidism. Approximately 1 year ago, she began to experience a gait disturbance and a hand tremor. She developed a shuffling gait and increased limb rigidity. Her mobility was significantly impaired and her family had suggested she start to use a rolling walker. She also began to complain of urinary urgency, frequency, and worsening urinary incontinence. Although she had had infrequent episodes of stress urinary incontinence for many years, she began to wear pads on a daily basis due to urinary incontinence associated with urgency and not enough warning time to get to the bathroom. She does not complain of difficulty emptying her bladder. She admits that she does not keep herself well hydrated, but she has a habit of sipping on coffee throughout the day. Her neurologist has diagnosed her with Parkinson’s disease and has started her on carbidopa/levodopa. She presents to her urologist since her worsening incontinence is having a negative impact on her quality of life .

4.2.2.2 Physical Examination

General: alert, oriented, and in no apparent distress. Ambulating with assistance of family member. Mild bilateral hand tremor
Abdomen: soft, nontender, and nondistended. No palpable bladder. No costovertebral tenderness bilaterally. Laparoscopic port site scars from previous cholecystectomy
Genitourinary: evidence of postmenopausal vaginal atrophy. Urethral hypermobility but no urinary incontinence with Valsalva maneuvers. No pelvic organ prolapse
Neurologic: cogwheel rigidity of bilateral lower extremities. Intact perineal sensation and bulbocavernosus reflex
Bladder scan: 30 mL after void

4.2.2.3 Labwork/Other Studies

Serum creatinine: 0.6 mg/dL
Renal and bladder ultrasound: symmetric kidneys with no hydronephrosis and no evidence of calculi or renal scarring, normal appearing bladder

4.2.2.4 UDS

See Fig. 4.3.

Fig. 4.3

Urodynamic tracing for 64-year-old woman with Parkinson’s disease

Findings

A slow infusion rate of 10 mL/min was used to minimize the provocative nature of bladder infusion. Her first bladder sensation was noted at only 13 mL. Starting at a low bladder volume of approximately 20 mL, the patient began to demonstrate phasic neurogenic detrusor overactivity . The maximum amplitude of detrusor contraction was 55 cm H₂O, and the patient experienced associated UUI with each episode of detrusor overactivity. The increased EMG activity during each episode of detrusor overactivity is consistent with a guarding reflex.

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