An approach to the diagnosis and management of the impotent patient is presented in Figure 187.1. Apparent and likely causes of impotence should be considered first and, if possible, eliminated before the work-up continues. For instance, observing the patient for a few weeks off offending medication may be all that is necessary to establish the cause of impotence. When no obvious or remediable cause is present, the next step is based on the clinical impression of the likelihood of organic versus psychologic impotence. If the latter is considered more likely, it is perfectly reasonable to refer the patient directly for sexual therapy, with the option of reconsidering the diagnosis if, after appropriate therapy, there is no improvement. While an occasional patient with organic impotence will be misrouted, many more with psychogenic impotence will be spared an unnecessary and costly evaluation for organic causes. When organic impotence is likely, a serum testosterone level is the initial screening test for hypogonadism and should be obtained prior to urologic referral. Patients with low testosterone levels require further endocrine evaluations as depicted in Figure 187.1.
Ejaculatory incompetence, erectile difficulty, erectile dysfunction, erectile failure, frigidity–female Medtalk The inability to achieve or maintain a penile erection adequate for the successful completion of intercourse, terminating in ejaculation; penile erection is mediated by nitric oxide Epidemiology Prevalence of minimal, moderate, and complete impotence in the Massachusetts Male Aging Study was 52%; age is the most important factor; complete impotence ↑ from 5%–age 40 to 15%–age 70; for an erection to achieve a successful outcome, it requires
Studies to further define vasculogenic disorders include pharmacologic duplex grey scale/color ultrasonography, pharmacologic dynamic infusion cavernosometry/ cavernosography, and pharmacologic pelvic/penile angiography. Cavernosometry, duplex ultrasonography, and angiography performed either alone or in conjunction with intracavernous pharmacologic injection of vasodilator agents rely on complete arterial and cavernosal smooth muscle relaxation to evaluate arterial and veno-occlusive function. The clinical effectiveness of these invasive studies is severely limited by several factors, including the lack of normative data, operator dependence, variable interpretation of results, and poor predictability of therapeutic outcomes of arterial and venous surgery. At the present time these studies might best be done in referral centers with specific expertise and interest in investigation of the vascular aspects of erectile dysfunction. Further clinical research is necessary to standardize methodology and interpretation, to obtain control data on normals (as stratified according to age), and to define what constitutes normality in order to assess the value of these tests in their diagnostic accuracy and in their ability to predict treatment outcome in men with erectile dysfunction.
Modern drug therapy for ED made a significant advance in 1983, when British physiologist Giles Brindley dropped his trousers and demonstrated to a shocked Urodynamics Society audience his papaverine-induced erection. The drug Brindley injected into his penis was a non-specific vasodilator, an alpha-blocking agent, and the mechanism of action was clearly corporal smooth muscle relaxation. The effect that Brindley discovered established the fundamentals for the later development of specific, safe, and orally effective drug therapies.[better source needed][better source needed]
Qaseem, A., Snow, V., Denberg, T. D., Casey, D. E., Forciea, M. A., Owens, D. K., & Shekelle, P. (2009). Hormonal testing and pharmacologic treatment of erectile dysfunction: A clinical practice guideline from the American College of Physicians. Annals of internal medicine, 151(9), 639-649. Retrieved from http://annals.org/aim/article/745155/hormonal-testing-pharmacologic-treatment-erectile-dysfunction-clinical-practice-guideline-from