Vacuum erection associated impotence and Peyronie's disease.

PURPOSE: Use of a nonmedical, catalogue type vacuum erection device resulted in a case of vacuum induced vasculogenic impotence and Peyronie's disease. MATERIALS AND METHODS: A 66-year-old potent man used a nonmedical vacuum erection device (cylinder plus a hand pump without a pressure-release valve and a doughnut-shaped ring at the base without tension bands) after having achieved a spontaneous rigid erection. The resultant excessive overinflation of the penis was followed by dorsal curvature, diminished rigidity and decreased erectile maintenance. RESULTS: Physical examination revealed a dorsal mid shaft Peyronie's plaque. Nocturnal penile tumescence testing and office injection testing were abnormal and demonstrated partial, short-lived, dorsally curved erections. Dynamic pharmaco-cavernosometry and pharmaco-cavernosography established vasculogenic impotence with site-specific crural (unrelated to the Peyronie's plaque) veno-occlusive dysfunction and dorsal penile curvature. CONCLUSIONS: Vacuum erection devices create pulling forces on the penis. We estimate that the pulling forces in this case were prohibitively high (approximately 29 pounds) due to absence of a pressure-release valve and to the preexistent erection at vacuum application. These intense pulling forces are hypothesized to have damaged the tunica in the mid shaft (Peyronie's disease) and the crus (veno-occlusive dysfunction), the latter being the site of attachment of the corpora to the ischiopubic ramus and a most likely location for high magnitude pulling forces to exert an abnormal injury effect. The patient underwent a Nesbit plication procedure and presently performs self-injection for satisfactory sexual activity.

Blunt trauma: the pathophysiology of hemodynamic injury leading to erectile dysfunction.

A 9 1/2-year pharmaco-cavernosometry/pharmaco-cavernosography and pharmaco-arteriography study was performed in 131 men with persistent changes in erectile function following blunt pelvic or perineal trauma. The goal was to determine the incidence of hemodynamic impairment, and to characterize the location and pattern of abnormal venous drainage. Corporeal veno-occlusive dysfunction was identified in 62% of the cases and cavernous artery insufficiency in 70%. Pharmaco-cavernosography revealed abnormal venous drainage confined to the proximal corpora in 91% of the cases. Patients with pelvic trauma had significantly more abnormal sites of venous drainage (3 or more sites in 61%) and more severe degrees to which venous structures filled with contrast medium (23% had 3+ degree of luminal filling) than did patients with perineal trauma (61% had 1 or 2 sites of venous drainage and 92% had 1+ or 2+ degree of luminal filling). Pharmaco-arteriography revealed site specific arterial occlusive lesions consistent with the site of impact. Traumatic vasculogenic impotence is hypothesized as being the result of direct impact injury to the fixed proximal corpora and its arterial inflow bed. The exerted perineal impact force is estimated to range from 50 to 500 pounds, depending on the weight of the individual, height of the fall, speed at contact and surface hardness. Traumatic veno-occlusive dysfunction is theorized to be the consequence of focal intracavernous wound repair and permanent focal alterations in erectile tissue compliance. Traumatic vasculogenic impotence afflicts an estimated 600,000 American men of whom 250,000 have sports-related injuries. Future consideration should be given to the development of appropriate protective perineal equipment.