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J Urol. 2003 Jun;169(6):2173-6.

The incidence and causes of erectile dysfunction after pelvic fractures associated with posterior urethral disruption.

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1
Department of Urology, Hebrew University Hadassah Medical Center, Jerusalem, Israel.

Abstract

PURPOSE:

Erectile dysfunction is a common sequel of pelvic fractures, particularly those associated with posterior urethral injury when it can be neurogenic or arteriogenic due to damage to the cavernous nerves or branches of the pudendal arteries. We studied erectile function of patients with posterior urethral injuries due to pelvic fractures.

MATERIALS AND METHODS:

Patients referred for posterior urethral reconstruction and strictures due to pelvic fractures were evaluated before reconstruction. All patients underwent nocturnal penile tumescence testing, and if those results were abnormal, penile duplex ultrasound with intracavernous injection was performed. Patients with normal vascular function on duplex ultrasound were diagnosed with neurogenic erectile dysfunction. Those patients with abnormal arterial function on duplex ultrasound underwent arteriography to further define the extent and location of arterial damage.

RESULTS:

The study included 25 consecutive patients with posterior urethral strictures and a mean age of 28.6 years. Of the patients 18 (72%) had erectile dysfunction as demonstrated by nocturnal penile tumescence and all underwent penile duplex ultrasound. Ultrasound confirmed normal vascular response in 13 of the 18 patients and they were diagnosed with probable neurogenic erectile dysfunction. The remaining 5 patients (28%) with erectile dysfunction had an abnormal arterial response, and significant arterial pathology was confirmed by arteriography.

CONCLUSIONS:

Erectile dysfunction is common in patients with pelvic fractures associated with urethral injury. We believe that erectile function should be assessed and documented in such patients before attempting urethroplasty. In the majority of these patients erectile dysfunction is caused by disruption of the cavernous nerves with sparing of arterial inflow.

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