Erectile Dysfunction following Radical Prostatectomy: A Review

Abstract

Radical prostatectomy remains the gold-standard treatment for localised prostate cancer. Despite the widespread introduction of nerve-sparing techniques, post-operative erectile dysfunction (ED) is still a significant source of morbidity. There are multiple approaches to prevent and treat ED. Recent refinements to surgical technique attempt to minimise disruption to the prostatic neural and arterial supply. A greater understanding of the factors affecting ED has also enabled the first multi-variate risk stratification model, thereby potentially improving awareness of pre-operative risk. Numerous on-demand treatments are available, including phosphodiesterase type 5 inhibitors, intracavernous/transurethral alprostadil, vacuum erection devices and combination therapy with multiple agents. As our understanding of the aetiology improves, attempts to manipulate the molecular mechanisms underpinning ED are also being investigated. In addition, early pharmacological rehabilitation is used to preserve cavernosal smooth muscle function until intra-operative neurapraxia resolves, although the optimum regimen is yet to be defined. Currently, much work is ongoing to improve our understanding and treatment of post-prostatectomy ED. We review the current status and recent advances in this field.

Erectile Dysfunction in Pelvic Cancer Survivors and Current Management Options

“…Anatomical descriptions of pelvic nerves have helped to shape our understanding of the impact of pelvic surgery on sexual function. Damage—whether transection, thermal, ischemic, or traction related—to parasympathetic nerves along their path from the spinal cord to the penis will affect erectile function, while damage to sympathetic nerves will affect ejaculation [ 3 , 4 ].…”

“…After pelvic surgery, nocturnal erections are absent due to temporary or permanent injury to the cavernous nerve [ 3 , 4 ]. The absence of erections decreases cavernous oxygenation, promoting smooth muscle apoptosis, collagen deposition, and fibrosis.…”

“…The absence of erections decreases cavernous oxygenation, promoting smooth muscle apoptosis, collagen deposition, and fibrosis. These fibrotic changes disable compression of the emissary veins running under Buck’s fascia, leading to veno-occlusive dysfunction and (venous leak) ED [ 3 , 4 , 8 , 9 ].…”

“…Penile denervation in rats has been demonstrated to initiate smooth muscle apoptosis in the cavernous tissue, an outcome which is likely due to the loss of growth factors produced by the cavernous nerve [ 4 , 10 ].…”

“…Vascular dysfunction can also be the result of cavernous artery insufficiency [ 4 ]. Erectile tissue requires oxygenation to maintain its integrity and interruption of arterial flow, particularly disruption to the accessory pudendal arteries (present in 4–75% of men) [ 11 ] that run parallel to the NVB, can affect potency.…”