The second option is a prosthesis or penile implant: a kind of hydraulic device surgically implanted in the penis. The prostheses consist of two rods that fit inside the penis, a pump that sits inside the scrotum next to the testicles, and a little reservoir that houses fluid that sits under the groin muscles. When a person wants to be intimate, they pump up the prostheses; afterward, they can use a button to reverse it.
The initial step in evaluating ED is a thorough sexual history and physical exam. The history can help in distinguishing between the primary and psychogenic causes. It is important to explore the onset, progression, and duration of the problem. If a man gives a history of “no sexual problems until one night,” the problem is most likely related to performance anxiety, disaffection, or an emotional problem. Aside from these causes, only radical prostatectomy or other overt genital tract trauma causes a sudden loss of male sexual function.
Oral medicines: The best known ED medications are the Big Three: Viagra (sildenafil citrate, made by Pfizer, Inc.), Levitra (vardenafil HCl, made by Bayer and GlaxoSmithKline), and Cialis (tadalafil, made by Eli Lilly). The three are chemically very similar, and all have proven very effective. Because they are effective, convenient, and relatively inexpensive (about nine dollars per pill), these medicines have become the treatment of choice for most men experiencing ED.
In most healthy men, some of the drug will remain in the body for more than two days after a single dose of tadalafil. Metabolism (clearing of the drug from the body) of tadalafil can be slowed by liver disease, kidney disease, and concurrent use of certain medications (such as erythromycin, ketoconazole, and protease inhibitors). Slowed breakdown allows tadalafil to stay in the body longer and potentially increase the risk for side effects. Therefore, doctors have to lower the dose and frequency of tadalafil in the following examples:
Instead of injecting a medicine, some men insert a suppository of alprostadil into the urethra. A suppository is a solid piece of medicine that you insert into your body where it dissolves. A health care professional will prescribe a prefilled applicator for you to insert the pellet about an inch into your urethra. An erection will begin within 8 to 10 minutes and may last 30 to 60 minutes.
Intraurethral alprostadil (Muse) provides a less invasive alternative to intrapenile injection. It is a pellet that is inserted 5–10 min before intercourse, and its effects last for 1 h. The response rate is ∼50–60%. It can be used twice daily but is not recommended for use with pregnant partners. Complications of priapism and penile fibrosis are less common than after alprostadil given by penile injection. The cost is ∼$18–24 per treatment.
Unconventional CV risk factors, such as impaired erections during masturbation and reduced flaccid acceleration, are interesting parameters to implement in Sexual Medicine context, because they can help fill the gap of information on CV risk, left by the conventional risk factors (the so-called residual risk) (38). However, it should be recognized that not all the healthcare professionals who deal with the complaint of ED (i.e., general practitioners, diabetologists, cardiologists, sport physicians, nurses, etc.) have the facilities or competence for the specific assessment of these parameters. In contexts different than Sexual Medicine and Andrology, the assessment of conventional risk factors is certainly more convenient. Metabolic syndrome (MetS) represents a cluster of metabolic derangements easily and commonly evaluated in several different medical contexts. In a population of more than 600 subjects attending the Sexual Medicine and Andrology Unit of the University of Florence for ED, the presence of MetS was associated with an increased incidence of MACE during 4.3 years of follow-up in younger (first tertile of age: 18–52 years) (Figure 3, Panel A and B) but not in middle aged and older men (second and third tertiles of age: 53–60 and 61–88 years, respectively) (Figure 3, Panel B). Similar to MetS, the algorithms for estimating the risk of developing MACE are easily computed and they take into account factors largely available in a clinical setting. In Europe, the most commonly used algorithm is the SCORE, which takes into account age, smoking habits, systolic blood pressure and total cholesterol (26). These parameters are introduced in a calculation tool that returns the 10-year risk of developing the first MACE. The same estimated risk rate can obviously be derived from different combinations and extent of the single risk factors and, as aforementioned, age has a heavy weight in the amount of risk, even when the other parameters are normal. For overcoming this overestimation, the concept of vascular age, based on the predicted CV risk, has been introduced. Vascular age of a subjects with a specific CV risk profile corresponds to the chronological age of a subjects who has the same estimated risk but only due to chronological age, because of the absence of the other modifiable risk factors (i.e., a non-smoker, normotensive and normocholesterolemic subject) (39,40). Vascular age carries the advantage of easily and directly communicating the concept of high relative risk to patients, in particular to younger ones, who are by definition at low absolute risk (“Your CV risk is the same of a man that is 15 years older than you”). Based on this interesting and useful concept of vascular age, we recently studied the clinical consequences of having a high discrepancy between the estimated vascular and the actual chronological age in our population of men consulting for ED. In our sample, a greater difference between vascular and chronological age was associated with higher glucose and triglyceride levels as well as with impaired penile colour Doppler ultrasound parameters, suggesting a CV impairment (41). When evaluating the subset of men for whom information on incident MACE during a mean follow-up of 4.3 years was available, a greater difference between vascular and chronological age was associated with the incidence of MACE in younger, but not in older men (42).
Not only can guilt affect your ability to perform sexually, but so can low self-esteem. The correlation between erectile dysfunction and low self-esteem seems obvious from one direction – an inability to perform in the bedroom can cause you to feel bad about yourself. But how does low self-esteem cause ED? Self-esteem is defined as, “confidence in one’s own worth or abilities.”
High cholesterol and triglyceride levels increase the risk of cardiovascular disease. Getting your cholesterol and triglyceride levels in an optimal range will help protect your heart and blood vessels. Cholesterol management may include lifestyle interventions (diet and exercise) as well as medications to get your total cholesterol, LDL, HDL, and triglycerides in an optimal range.
This initial release of NO causes rapid and short-term increases in penile blood flow and short-term relaxation of the penile smooth muscle, initiating an erection. The resulting expansion of penile blood vessels and smooth-muscle relaxation allows more blood to flow into the penis. This increased blood flow (shear stress) activates the eNOS in penile blood vessels causing sustained NO release, continued relaxation and full erection.
PDE 5 inhibitors are broken down primarily by enzyme, cytochrome P450enzyme CYP3A4. Medications that decrease or increase the activity of CYP3A4 may affect levels and effectiveness of PDE 5 inhibitors. Such drugs include medications for the treatment of HIV (protease inhibitors) and the antifungal medications ketoconazole and itraconazole. Thus caution is recommended.
As a starting point, consider the National Health and Social Life Survey, which was the first nationally representative sex survey conducted in the United States . The data were collected in 1992 from thousands of Americans aged 18-59. As part of this survey, male participants were asked whether they’d had trouble maintaining or achieving an erection any time in the last year, to which they provided a simple yes/no answer.
These are among the most challenging patients seen in urology practice today: a young, healthy man with neither systemic disease nor a history of trauma, who has complaints of ED (Table 2). These men often have co-morbid diagnoses, such as anxiety, depression, or mood disorders, which make the issue of ED more complex for both the patient and the urologist (12). The psychological burden of ED in these young men is more pronounced than it might be in older men as this is the phase of life during which many men expect to be highly sexually active (4). These young men are usually technologically savvy and may have scrutinized much of the readily available information on the internet regarding ED. Often they arrive to clinic armed with an understanding of the diagnostic evaluation that may be offered to further investigate the etiology of their concerns. This makes the evaluation and treatment of these men more challenging since additional diagnostic testing is often not indicated after a thorough history and physical examination. In many cases, they may have self-diagnosed and self-treated based on the information that they obtained prior to seeing a physician. Many of these men will see multiple urologists on their quest to find a pathophysiology that they can accept, and many have unrealistic expectations of a rapid cure or a surgical cure.
Penile implants: This treatment involves permanent implantation of flexible rods or similar devices into the penis. Simple versions have the disadvantage of giving the user a permanent erection. The latest (and most expensive) device consists of inflatable rods activated by a tiny pump and switch in the scrotum. Squeezing the scrotum stiffens the penis, whether the person is aroused or not. The penis itself remains flaccid, however, so the diameter and length are usually less than a natural erection, and hardness is lacking, although it's sufficient for intercourse.
ED has been for long time considered a problem mainly related to psychological conditions and distress. Accordingly, until phosphodiesterase type 5 inhibitors (PDE5i) were introduced, psychoanalysis and cognitive-behavioural therapy were the only option for ED. In the last few decades, ED has been recognized as a clinical consequence of several different organic diseases and the importance of vascular health in erectile function has been so emphasized that ED is now considered not only the result of vascular impairment, but also a harbinger of forthcoming cardiovascular (CV) events (17). Despite the increasing attention of research towards organic mechanisms and conditions leading to ED, it is now known that considering this symptom as entirely due to organic disorders, is as imprecise as considering it only secondary to psychological conditions. In fact, this pathogenetic dichotomy is now obsolete (1,18,19), because it is now known that ED is a multidimensional disorder deriving from the interaction of different components related to organic conditions, relational context and psychological status (20,21). Even when only one of these components is involved in the initial development of erectile impairment, eventually the other ones will appear, thus further worsening ED (21-23). The multidimensional nature of ED is still not fully accepted by health care professionals when dealing with young patients. In fact, complaints of ED in young men is often underestimated and attributed to transient and self-limiting psychological conditions, such as performance anxiety. Young patients are often reassured without any further medical investigations, including physical exam. However, organic disorders, as well as relational and psychological or psychiatric conditions, can be meaningful in determining ED in younger men. In a population of subjects seeking medical care at the Sexual Medicine and Andrology Unit of the University of Florence for sexual dysfunction, the first tertile of age (n=1,873 subjects) represents younger subjects (18–44 years). Pathogenetic components of ED in our sample are investigated by the Structured Interview on Erectile Dysfunction (SIEDY), a structured interview including 13 questions, whose answers, organized in a Likert scale, provide three scales, one for the organic subdomain [(SIEDY Scale 1); (22)], one for the relational subdomain [(SIEDY Scale 2); (23)] and one for the intrapsychic subdomain [(SIEDY Scale 3); (21)]. According to these scale scores, organic, relational and intrapsychic conditions are all significant risk factors for ED in younger patients of our population (Figure 2).
Your ability to orgasm is not connected to the prostate gland, although a man who has had a radical prostatectomy will have a dry orgasm with no ejaculation. As long as you have normal skin sensation, you should be able to have an orgasm with the right sexual stimulation. This means that treating your ED should allow you to resume a normal, healthy sex life.
In some cases, however, these drugs may be unsuitable for patients with heart disease. If you are considering one of these drugs and you have heart disease, as many diabetics do, be sure to tell your doctor. In rare cases, the pills may create “priapism,” a prolonged and painful erection lasting six hours or more (although reversible with prompt medical attention).