The pathophysiology of ED after radical prostatectomy involves three factors: namely, neural injury, vascular injury, and smooth muscle damage. It is well appreciated by every urologist that thermal injury to the cavernous nerves result in permanent loss of erectile function after surgery. What is less appreciated is the concept that traction on the nerves may in fact be just as deleterious. In a recent study, Masterson et al. demonstrated that alteration in technique, whereby the Foley catheter is no longer used as a retired retraction tool to maximize tension on the lateral pedicles, resulted in a significant improvement in erectile function post-prostatectomy. Furthermore, Mullerad et al. demonstrated in the cavernous nerve injury model that exposure of the cavernous nerves without any direct injury results in an ED in a rat model. Thus, it appears that even the most minor neural trauma may in fact result in at least short-term erectile problems. The consequences of neuropraxia are several fold: it has been well documented by several centers that smooth muscle and endothelium undergo structural changes in response to cavernous nerve injury. User et al. have shown that bilateral and unilateral cavernous neurectomy resulted in early smooth muscle apoptosis. In this analysis, apoptosis was maximal at 2–7 days after surgery. Of note, in this analysis the smooth muscle apoptosis appeared to be clustered in the subtunical area. It was suggested by the authors that this may in fact be a contributor to the development of venous leak postprostatectomy. We have shown in our cavernous nerve crush injury model that crush injury can cause apoptosis in both smooth muscle and endothelium in a more delayed fash-ion compared to neurectomy model. Another consequence of neuropraxia is alterations in smooth muscle: collagen ratios. In response to nerve injury, the smooth muscle undergoes collagenization. Neural injury has been shown to be associated with upregulation of collagen types I and III as well as upregulation of fibrogenic cytokines, such as TGF-beta. Klein et al. showed using electron microscopy that cavernous nerve injury results in endothelial cell retraction. Given the importance of both corporal smooth muscle and endothelium for the purposes of erection, it is easy to see how neuropraxia-induced erectile tissue alterations may be deleterious to long-term erectile function recovery.

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Vascular injury revolves around damage to accessory pudendal arteries (APAs). These arteries are variable in their incidence in the literature depending on what kind of series is assessed, whether it is an operative series, an angiographic series, or a cadaveric series. APAs are super diaphragmatic arteries that lie above the levator ani and are predisposed to injury at the time of radical prostatectomy. Their origin is variable coming from femoral, obturator, vesicle, or iliac arteries. These arteries can be visualized on preoperative endorectal MRI or on preoperative CT scan. Cadaveric studies have the highest incidence of APAs. Probably, the most important study is that of Breza et al. In this study, 10 cadavers underwent extensive pelvic dissection, and the arterial anatomy was defined in detail. In this analysis, 7 of the 10 cadavers had APAs found. In seven cadavers, the APAs were the major source of arterial inflow into the penis, and one cadaver had APAs as the sole source of inflow into the corpora cavernosa. Droupy et al. have shown in a small study using transrectal and transperineal ultrasound that these arteries are functional. Nine of 12 patients studied had periprostatic arteries coursing forward toward the penis. Upon intracavernosal injection the hemodynamic changes that were seen in the cavernosal arteries were mirrored in the periprostatic arteries suggesting that the APAs were functional. Rogers et al. have shown that APA preservation at the time of open radical prostatectomy translates into an improvement in an erectile function recovery and possibly even shortening of the time to recovery of erections.

I have already alluded to the concept that neuropraxia results in smooth muscle alterations. It is likely that this is amplified by the absence of erections. If one thinks of muscle within the body, whether it is skeletal or smooth in nature, muscles require some form of exercise to maintain integrity and health. Viagraaustraliaau.com can help you to live completely sexual life. Given the fact that we obtain three to six erections each night, it is easy to see how going a prolonged period of time without erections may in fact lead to erectile tissue damage.