madman
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Erectile dysfunction is defined as the recurring inability to achieve and maintain a satisfactory erection for sexual intercourse associated with relevant life impairment. The underlying etiologies may be manifold and complex. Currently, vascular etiologies are highly prevalent, especially amongst elderly men. Of special interest, especially venogenic causes are of increasing relevance. Therapeutic options comprise risk factor modification, pharmacotherapy, surgical treatment, and endovascular treatment. Especially endovascular treatment options have recently increased in popularity including transcatheter embolization procedures for veno-occlusive dysfunction.
INTRODUCTION
The definition of erectile dysfunction or impotence is described as the recurring inability to achieve and maintain a satisfactory erection for sexual intercourse (1). The etiologies of erectile dysfunction may be manifold and complex (2). Potential underlying etiologies can be either psychogenic or organic. Psychogenic etiologies of erectile dysfunction may include depression, anxiety, and partner-related difficulties. On the other hand, organic erectile dysfunction can be due to vasculogenic, endocrinologic, neurogenic, iatrogenic, and structural components.
Regarding vascular etiologies of erectile dysfunction, a regular erectile function depends on adequate arterial inflow as well as venous outflow occlusion. Both arterial inflow stenosis or impaired venous outflow occlusion compromises the filling of the corporeal bodies. Either problem, namely compromised arterial inflow or venous leakage, may result in vasculogenic erectile dysfunction (3).
In younger patients with arteriogenic erectile dysfunctions, it was previously reported that blunt pelvic trauma may cause endothelial dysfunction with reactive atherosclerosis resulting in focal arterial stenosis of the distal internal pudendal artery passing through Alcock’s canal. In this location, the internal pudendal artery is highly susceptible to blunt mechanical trauma due to compression against the ischio-pubic ramus (4). On the contrary, older patients with arteriogenic erectile dysfunction tend to have a more diffuse atherosclerotic disease. In this patient population, erectile dysfunction may be secondary to potential plaque formation in all arterial vasculature involved with penile tumescence (5)
In patients with venogenic erectile dysfunction, veno-occlusive dysfunction was recognized as the underlying cause in most cases (Box 1). Veno-occlusive dysfunction may result from age or injury-related changes to the tunica albuginea, cavernosal smooth muscle dysfunction from structural alterations, excessive adrenergic input, or from shunts created during priapism episodes and subsequent repair (6, 7). Although the underlying mechanisms of veno-occlusive dysfunction are not yet fully understood, several conditions such as age, diabetes, prostatectomy, pelvic radiation, and androgen deprivation therapy appear to be potential risk factors (8). Of interest, the average age of patients with venogenic erectile dysfunction was found to be significantly lower (51 years) than that of patients with arteriogenic erectile dysfunction (59 years) (9).
Most studies have shown an increase in the prevalence of vasculogenic erectile dysfunction with aging (7, 10).Therefore, Wespes et al. hypothesize that the erectile dysfunction of aging may be the result of atherosclerosis-induced cavernosal ischaemia leading to cavernosal fibrosis and subsequent venoocclusive dysfunction concluding that erectile dysfunction due to aging appears to be a slowly progressive disorder and that it may be wise for patients to seek medical intervention earlier rather than later (11).
Therapeutic options comprise risk factor modification, pharmacotherapy, surgical treatment, and endovascular treatment (9). Especially endovascular treatment options have recently increased in popularity including transcatheter embolization procedures for veno-occlusive dysfunction. This chapter outlines diagnosis and endovascular treatment of erectile dysfunction due to venous leakage including study results eliding a systematic analysis.
DIAGNOSIS
*Duplex Ultrasound
*Cavernosometry
*Cavernosography
*Computed Tomography Cavernosography
ENDOVASCULAR TREATMENT
*Antegrade Approach via Deep Dorsal Penile Vein
*Retrograde Transfemoral Venous Approach
SUMMARY AND CONCLUSION
In patients with erectile dysfunction, vasculogenic etiologies need to be considered if other causes such as neurogenic, psychogenic, and hormonal could be excluded (24). Vasculogenic etiologies include either arteriogenic or venogenic causes. Venogenic erectile dysfunction is due to veno-occlusive disease, also called “venous leak,” with incomplete relaxation of corporeal smooth muscle during arterial inflow and insufficient occlusion of venous outflow tracts. Dean et al. report that veno-occlusive disease may be due to multiple factors such as degenerative changes or injury of tunica albuginea, impaired relaxation of corporeal smooth muscles, venous shunting, and excessive adrenergic tone in anxious individuals (25).
In patients with veno-occlusive dysfunction, endovascular treatment with transcatheter embolization of venous leaks is performed to an increasing degree. The preferred access route for transcatheter embolization is the deep dorsal vein with or without surgical exposure (7). Alternatively, access routes via common femoral veins have been used (18). Most notably, liquid embolic materials with low viscosity such as a combination of N-butyl-2-cyanoacrylate and ethiodized oil mixed in 1:1– 1:3 ratios depending on the quantity, size, and location of venous leaks are used for embolization and preferably causing venous inflammation, thrombosis, and fibrosis. Valsalva maneuver is required to avoid unintentional migration of glue with potential non-target embolization. If required, fibered coils may be used in advance in order to prevent the expansion of glue through veins with fast outflow e.g., into femoral or iliac veins. Coils should be oversized up to 50% of the actual vein diameter to prevent inadvertent coil migration. Technical success rates range between 86 and 97%. Technical failures were due to failed direct deep dorsal vein puncture or failed access to periprostatic veins via the femoral approach. In previous studies, complication rates were low (5.2%) consisting mainly of minor complications (9). However, symptomatic pulmonary embolism as a formidable major complication occurred in two patients (<1%). Follow-up is performed using a pharmacologic color Doppler exam combined with the IIEF-6 questionnaire. The average clinical success rate in a recent meta-analysis was 59.5% ranging from 21.9 to 100% (9).
In conclusion, endovascular treatment is a promising approach in patients with erectile dysfunction due to veno-occlusive dysfunction which is increasingly utilized. Endovascular therapy with embolization of venous leaks is minimally invasive and may provide a safe alternative to surgical management. Further studies are needed to more adequately determine its role within the complex framework of the manifold causes of erectile dysfunction.
INTRODUCTION
The definition of erectile dysfunction or impotence is described as the recurring inability to achieve and maintain a satisfactory erection for sexual intercourse (1). The etiologies of erectile dysfunction may be manifold and complex (2). Potential underlying etiologies can be either psychogenic or organic. Psychogenic etiologies of erectile dysfunction may include depression, anxiety, and partner-related difficulties. On the other hand, organic erectile dysfunction can be due to vasculogenic, endocrinologic, neurogenic, iatrogenic, and structural components.
Regarding vascular etiologies of erectile dysfunction, a regular erectile function depends on adequate arterial inflow as well as venous outflow occlusion. Both arterial inflow stenosis or impaired venous outflow occlusion compromises the filling of the corporeal bodies. Either problem, namely compromised arterial inflow or venous leakage, may result in vasculogenic erectile dysfunction (3).
In younger patients with arteriogenic erectile dysfunctions, it was previously reported that blunt pelvic trauma may cause endothelial dysfunction with reactive atherosclerosis resulting in focal arterial stenosis of the distal internal pudendal artery passing through Alcock’s canal. In this location, the internal pudendal artery is highly susceptible to blunt mechanical trauma due to compression against the ischio-pubic ramus (4). On the contrary, older patients with arteriogenic erectile dysfunction tend to have a more diffuse atherosclerotic disease. In this patient population, erectile dysfunction may be secondary to potential plaque formation in all arterial vasculature involved with penile tumescence (5)
In patients with venogenic erectile dysfunction, veno-occlusive dysfunction was recognized as the underlying cause in most cases (Box 1). Veno-occlusive dysfunction may result from age or injury-related changes to the tunica albuginea, cavernosal smooth muscle dysfunction from structural alterations, excessive adrenergic input, or from shunts created during priapism episodes and subsequent repair (6, 7). Although the underlying mechanisms of veno-occlusive dysfunction are not yet fully understood, several conditions such as age, diabetes, prostatectomy, pelvic radiation, and androgen deprivation therapy appear to be potential risk factors (8). Of interest, the average age of patients with venogenic erectile dysfunction was found to be significantly lower (51 years) than that of patients with arteriogenic erectile dysfunction (59 years) (9).
Most studies have shown an increase in the prevalence of vasculogenic erectile dysfunction with aging (7, 10).Therefore, Wespes et al. hypothesize that the erectile dysfunction of aging may be the result of atherosclerosis-induced cavernosal ischaemia leading to cavernosal fibrosis and subsequent venoocclusive dysfunction concluding that erectile dysfunction due to aging appears to be a slowly progressive disorder and that it may be wise for patients to seek medical intervention earlier rather than later (11).
Therapeutic options comprise risk factor modification, pharmacotherapy, surgical treatment, and endovascular treatment (9). Especially endovascular treatment options have recently increased in popularity including transcatheter embolization procedures for veno-occlusive dysfunction. This chapter outlines diagnosis and endovascular treatment of erectile dysfunction due to venous leakage including study results eliding a systematic analysis.
DIAGNOSIS
*Duplex Ultrasound
*Cavernosometry
*Cavernosography
*Computed Tomography Cavernosography
ENDOVASCULAR TREATMENT
*Antegrade Approach via Deep Dorsal Penile Vein
*Retrograde Transfemoral Venous Approach
SUMMARY AND CONCLUSION
In patients with erectile dysfunction, vasculogenic etiologies need to be considered if other causes such as neurogenic, psychogenic, and hormonal could be excluded (24). Vasculogenic etiologies include either arteriogenic or venogenic causes. Venogenic erectile dysfunction is due to veno-occlusive disease, also called “venous leak,” with incomplete relaxation of corporeal smooth muscle during arterial inflow and insufficient occlusion of venous outflow tracts. Dean et al. report that veno-occlusive disease may be due to multiple factors such as degenerative changes or injury of tunica albuginea, impaired relaxation of corporeal smooth muscles, venous shunting, and excessive adrenergic tone in anxious individuals (25).
In patients with veno-occlusive dysfunction, endovascular treatment with transcatheter embolization of venous leaks is performed to an increasing degree. The preferred access route for transcatheter embolization is the deep dorsal vein with or without surgical exposure (7). Alternatively, access routes via common femoral veins have been used (18). Most notably, liquid embolic materials with low viscosity such as a combination of N-butyl-2-cyanoacrylate and ethiodized oil mixed in 1:1– 1:3 ratios depending on the quantity, size, and location of venous leaks are used for embolization and preferably causing venous inflammation, thrombosis, and fibrosis. Valsalva maneuver is required to avoid unintentional migration of glue with potential non-target embolization. If required, fibered coils may be used in advance in order to prevent the expansion of glue through veins with fast outflow e.g., into femoral or iliac veins. Coils should be oversized up to 50% of the actual vein diameter to prevent inadvertent coil migration. Technical success rates range between 86 and 97%. Technical failures were due to failed direct deep dorsal vein puncture or failed access to periprostatic veins via the femoral approach. In previous studies, complication rates were low (5.2%) consisting mainly of minor complications (9). However, symptomatic pulmonary embolism as a formidable major complication occurred in two patients (<1%). Follow-up is performed using a pharmacologic color Doppler exam combined with the IIEF-6 questionnaire. The average clinical success rate in a recent meta-analysis was 59.5% ranging from 21.9 to 100% (9).
In conclusion, endovascular treatment is a promising approach in patients with erectile dysfunction due to veno-occlusive dysfunction which is increasingly utilized. Endovascular therapy with embolization of venous leaks is minimally invasive and may provide a safe alternative to surgical management. Further studies are needed to more adequately determine its role within the complex framework of the manifold causes of erectile dysfunction.
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