{'fraction_non_alphanumeric': 0.027309236947791166, 'fraction_numerical': 0.018473895582329317, 'mean_word_length': 5.27455919395466, 'pattern_counts': {'":': 0, '<': 1, '<?xml version=': 0, '>': 1, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Phenoxybenzamine in the management of neuropathic bladder following spinal cord injury.

BACKGROUND
The present study aims to show the clinical and urodynamic effects of phenoxybenzamine on the neuropathic bladder of spinal cord-injured patients who failed to be free of catheter by attaining satisfactory voiding function, despite initial bladder training.


METHODS
Forty-six spinal cord-injured patients were subjected to pharmacological manipulation with phenoxybenzamine. It was used as an adjunct in the management of neuropathic bladder dysfunction that caused failure of the bladder to empty, by tapping or crede to achieve satisfactory residual urine volume of < 100 mL. Phenoxybenzamine was started with a dose of 10 mg daily, increased by 10 mg every 3 days to a dose of 30 mg daily; this was maintained from 3 weeks to 6 months (mean: 39 days). The pre-treatment residual urine volume ranged between 100 and 1050 mL (mean: 360 mL). Follow-up periods ranged between 12 and 36 months (mean: 16 months).


RESULTS
Five patients (11%) were excluded due to either inadequate treatment or inadequate follow-up. Nineteen patients (41%) with reflex (upper motor neurone) bladders showed improvement of bladder evacuation. There was a reduction of the maximum urethral closure pressure, which ranged between 10 and 32 cm of water (mean: 22 cm). Twenty-two patients (48%) did not respond, requiring other measures to be taken which included transurethral surgery (n = 19). Nine of the failures involved areflex (lower motor neurone) bladders, and seven failures involved reflex bladders with an extremely tight outlet and urethral closure pressure of > 50 cm of water. Six failures involved reflex bladders that were lacking strong enough detrusor contractions to attain a balanced bladder responsive to abdominal tapping; response was achieved by administration of a parasympatheticomimetic drug. Neuropathic bladders with uninhibited detrusor contractions responded well to phenoxybenzamine.


CONCLUSIONS
Phenoxybenzamine proved useful in reducing bladder outlet resistance after spinal cord injury, provided that detrusor bladder contractions were present. It is useful in controlling detrusor-sphincter dyssynergia and autonomic hyperreflexia. It was not useful in areflex bladders, perhaps due to the development of spasticity of the striated muscle component of the external sphincter. The presence of bladder neck (internal sphincter) dysfunction may modify or abolish its effect.