An initial approach to medical therapy should consider reversible medical problems that may contribute to erectile dysfunction. Included in this should be assessment of the possibility of medication-induced erectile dysfunction with consideration for reduction of polypharmacy and/or substitution of medications with lower probability of inducing erectile dysfunction.
To examine what is known about the demographics, etiology, risk factors, pathophysiology, diagnostic assessment, treatments (both generic and cause-specific), and the understanding of their consequences by the public and the medical community, the National Institute of Diabetes and Digestive and Kidney Diseases and the Office of Medical Applications of Research of the National Institutes of Health, in conjunction with the National Institute of Neurological Disorders and Stroke and the National Institute on Aging, convened a consensus development conference on male impotence on December 7-9, 1992. After 1 1/2 days of presentations by experts in the relevant fields involved with male sexual dysfunction and erectile impotence or dysfunction, a consensus panel comprised of representatives from urology, geriatrics, medicine, endocrinology, psychiatry, psychology, nursing, epidemiology, biostatistics, basic sciences, and the public considered the evidence and developed answers to the questions that follow.
The laboratory results should be discussed with the patient and, if possible, with his sexual partner. This educational process allows a review of the basic aspects of the anatomy and physiology of the sexual response and an explanation of the possible etiology and associated risk factors (eg, smoking and the use of various medications). Treatment options and their benefits and risks should be discussed. This type of dialogue allows the patient and physician to cooperate in developing an optimal management strategy.
Risks associated with injection therapy including bleeding, pain with injection, penile pain, priapism, and corporal fibrosis (scarring inside of the corpora cavernosa). There is also concern that repetitive injections in the same area could cause scar tissue to build up in the tunica albuginea that could create penile curvature. Thus, doctors recommended that one alternate sides with injection and perform injections no more frequent than every other day.
Three forms of penile prostheses are available for patients who fail with or refuse other forms of therapy: semirigid, malleable, and inflatable. The effectiveness, complications, and acceptability vary among the three types of prostheses, with the main problems being mechanical failure, infection, and erosions. Silicone particle shedding has been reported, including migration to regional lymph nodes; however, no clinically identifiable problems have been reported as a result of the silicone particles. There is a risk of the need for reoperation with all devices. Although the inflatable prostheses may yield a more physiologically natural appearance, they have had a higher rate of failure requiring reoperation. Men with diabetes mellitus, spinal cord injuries, or urinary tract infections have an increased risk of prosthesis-associated infection. This form of treatment may not be appropriate in patients with severe penile corporal fibrosis, or severe medical illness. Circumcision may be required for patients with phimosis and balanitis.
The symptoms of erectile dysfunction include difficulty achieving an erection, trouble maintaining an erection, and a reduced interest in sex. Because male sexual arousal is a fairly complex process, it can sometimes be difficult to identify a specific cause. Arousal starts in the brain but it also involves the nerves, muscles, and blood vessels and can be impacted by hormones and emotions. If a problem develops with any of these things, erectile dysfunction could be the consequence.
In men, erectile dysfunction can be defined as being a persistent inability to get or keep an erection that is firm enough to attain sexual satisfaction. It should not be confused with the occasional incident when this occurs, which is an experience common to the vast majority of men for various reasons. These can include having had too much alcohol to drink, being overly-anxious about a new sexual partner, or being worried about current events in your life. The issue would only be classed as Erectile Dysfunction if it keeps happening again and again. Again, an erection once attained should be hard enough and last long enough to be satisfactory. Other conditions, like premature ejaculation, may interfere in this process but these are different problems, and would be treated differently.
Since endothelial dysfunction, CVD and ED are closely associated in epidemiological studies, the question for clinicians is whether to recommend the man presenting with ED undergo a cardiovascular (CV) evaluation. Clearly, based on numerous studies, ED can be considered at least a ‘marker’ for possible further vascular disease or CVD.15 In their report, Vlachopoulos and coworkers make the point that the man presenting with ED, the clinician, is offered an opportunity to attempt to improve the health of the man by addressing lifestyle modification, and consider further vascular evaluation owing to the clear relationship between endothelial dysfunction, ED and CVD.19

Performance anxiety can be another cause of impotence. If a person wasn’t able to achieve an erection in the past, he may fear he won’t be able to achieve an erection in the future. A person may also find he can’t achieve an erection with a certain partner. Someone with ED related to performance anxiety may be able to have full erections when masturbating or when sleeping, yet he isn’t able to maintain an erection during intercourse.

How’s this for a win-win: The more sex you have, the less likely you are to suffer from erectile dysfunction, according to a 2008 study published in The American Journal of Medicine. Men aged 55-75 who reported having sex less than once per week had twice the incidence of erectile dysfunction (there were 79 cases of ED per 1,000) as men who have sex once a week (32 cases of ED per 1,000). But if you really want to up your odds, shoot for three times per week (only 16 cases of ED per 1,000). Can you really argue with science, or a perscription to have more sex?
Medications: Many common medicines produce erectile dysfunction as a side effect. Medicines that can cause erectile dysfunction include many used to treat high blood pressure, antihistamines, antidepressants, tranquilizers, and appetite suppressants. Examples of common medicines that can cause erectile dysfunction include propranolol (Inderal) or other beta-blockers, hydrochlorothiazide, digoxin (Lanoxin), amitriptyline (Elavil), famotidine (Pepcid), cimetidine (Tagamet), metoclopramide (Reglan), naproxen, indomethacin (Indocin), lithium (Eskalith, Lithobid), verapamil (Calan, Verelan, Isoptin), phenytoin (Dilantin), gemfibrozil (Lopid), amphetamine/dextroamphetamine (Adderall), and phentermine. Prostate cancer medications that lower testosterone levels such as leuprolide (Lupron) may affect erectile function. Some chemotherapies such as cyclophosphamide (Cytoxan) may affect erectile function.
Metabolism (breakdown) of vardenafil can be slowed by aging, liver disease, and concurrent use of certain medications (such as erythromycin [an antibiotic], ketoconazole [Nizoral, a medication for fungal/yeast infections], and protease inhibitors [medications used to treat AIDS]). Slowed breakdown allows vardenafil to accumulate in the body and potentially increase the risk for side effects. Therefore, in men over 65 years of age with liver disease, or who are also taking medication(s) that can slow the breakdown of vardenafil, the doctor will initiate vardenafil at low doses to avoid its accumulation. For example,
Before delving into the causes and solutions to erectile dysfunction, it’s first important to understand how erections work. The penis is mostly comprised or fibrous tissue that fills with blood upon arousal. This is what causes an erection, and after arousal is finished, blood drains back out into the body and the penis becomes flaccid. Men can have erections for no discernible reason throughout the day, but when sexual stimulation occurs, rather through contact, visual, audible, or mental stimulation, the potential for achieving an erection increases.
Because of the difficulty in defining the clinical entity of erectile dysfunction, there have been a variety of entry criteria for patients in therapeutic trials. Similarly, the ability to assess efficacy of therapeutic interventions is impaired by the lack of clear and quantifiable criteria of erectile dysfunction. General considerations for treatment follow:

The drugs work best in combination with sex therapy. Several studies have shown this. There’s more to satisfying sex than just an erection. The quality of the relationship is crucial, especially if sex has been a sore point or if the couple hasn’t had much for a while. To find a sex therapist near you, visit the American Association of Sex Educators, Counselors, and Therapists, the Society for Sex Therapy and Research, or the American Board of Sexology.
Factors that mediate contraction in the penis include noradrenaline, endothelin-1, neuropeptide Y, prostanoids, angiotensin II, and others not yet identified. Factors that mediate relaxation include acetylcholine, nitric oxide (NO), vasoactive intestinal polypeptide, pituitary adenylyl cyclase–activating peptide, calcitonin gene–related peptide, adrenomedullin, adenosine triphosphate, and adenosine prostanoids.

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.
Sildenafil (Viagra) was the first oral phosphodiesterase type 5 (PDE5) inhibitor approved by the FDA in the United States for the treatment of erectile dysfunction (it is not approved for women). Sildenafil inhibits PDE5, which is an enzyme that destroys cGMP. By inhibiting the destruction of cGMP by PDE5, sildenafil allows cGMP to accumulate. The cGMP in turn prolongs relaxation of the smooth muscle of the corpora cavernosa. Relaxation of the corpora cavernosa smooth muscle allows blood to flow into the penis resulting in increased engorgement of the penis. In short, sildenafil increases blood flow into the penis and decreases blood flow out of the penis.
In a prospective, multicenter, single-armed study of ED patients who exhibited a suboptimal response to PDE5 inhibitors, the investigators found that percutaneous implantation of zotarolimus-eluting stents in focal atherosclerotic lesions was both safe and feasible and was associated with clinically meaningful improvement on subjective and objective measures of erectile function. [3]
This statement is more than five years old and is provided solely for historical purposes. Due to the cumulative nature of medical research, new knowledge has inevitably accumulated in this subject area in the time since the statement was initially prepared. Thus some of the material is likely to be out of date, and at worst simply wrong. For reliable, current information on this and other health topics, we recommend consulting the National Institutes of Health's MedlinePlus http://www.nlm.nih.gov/medlineplus/.
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