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首页> 外文期刊>ANZ journal of surgery >Phenoxybenzamine in the management of neuropathic bladder following spinal cord injury.
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Phenoxybenzamine in the management of neuropathic bladder following spinal cord injury.

机译：苯氧基苯扎明治疗脊髓损伤后的神经性膀胱。

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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.
机译：背景：本研究旨在显示苯氧基苯扎明对尽管最初接受膀胱训练但仍无法通过令人满意的排尿功能而没有导管的脊髓损伤患者的神经性膀胱的临床和尿动力学影响。方法：对46例脊髓损伤的患者进行苯氧苄明的药理处理。它通过轻敲或粗线作为治疗神经性膀胱功能障碍的辅助手段，该功能导致膀胱排空失败，从而使残余尿量＜100 mL。苯氧苯甲胺的起始剂量为每天10 mg，每3天增加10 mg，至每天30 mg;维持3周至6个月（平均39天）。治疗前残留尿量在100到1050 mL之间（平均：360 mL）。随访期为12到36个月（平均16个月）。结果：五名患者（11％）由于治疗不足或随访不足而被排除在外。反射（上运动神经元）膀胱的19例患者（41％）显示了膀胱排空的改善。最大尿道闭合压力降低，介于10至32厘米水柱之间（平均：22厘米水柱）。 22位患者（48％）没有反应，需要采取其他措施，包括经尿道手术（n = 19）。其中九项失败涉及屈曲性（下运动神经元）膀胱，七项失败涉及反射性膀胱，其出口非常紧，尿道关闭压力大于50厘米水柱。六项失败涉及反射性膀胱，这些膀胱缺乏足够强的逼尿肌收缩能力，无法对腹部的拍打做出平衡的膀胱。通过施用拟副交感神经药实现了应答。具有不受抑制的逼尿肌收缩的神经性膀胱对苯氧基苯扎明反应良好。结论：在存在逼尿肌膀胱收缩的情况下，苯氧基苯扎明被证明可用于降低脊髓损伤后的膀胱出口阻力。它可用于控制逼尿肌括约肌功能障碍和自主神经反射亢进。可能由于外部括约肌的横纹肌成分痉挛发展，因此在弯曲膀胱中没有用。膀胱颈（括约肌内部）功能障碍的存在可能会改变或取消其作用。

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