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.
Erectile dysfunction (ED) is one of the most common conditions affecting middle-aged and older men. Nearly every primary care physician, internist and geriatrician will be called upon to manage this condition or to make referrals to urologists, endocrinologists and cardiologists who will assist in the treatment of ED. This article will briefly discuss the diagnosis and management of ED. In addition, emerging concepts in ED management will be discussed, such as the use of testosterone to treat ED, the role of the endothelium in men with ED and treating the partner of the man with ED. Finally, future potential therapies for ED will be discussed.

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.
#7 You’re way too distracted. It’s not exactly sexy to try and screw while your newborn/parents/relatives/friends are perched in the next room. If you’re distracted by a loud TV, knocks at the door, or your phone going off while you’re trying to go down on your partner, it’s going to make it an aggravating sexual experience. Not exactly ideal grounds for getting an erection.
Depression and anxiety: Psychological factors may be responsible for erectile dysfunction. These factors include stress, anxiety, guilt, depression, widower syndrome, low self-esteem, posttraumatic stress disorder, and fear of sexual failure (performance anxiety). It is also worth noting that many medications used for treatment of depression and other psychiatric disorders may cause erectile dysfunction or ejaculatory problems.
In a prospective study from the Prostate Cancer Prevention Trial database, Thompson et al reported that men presenting with ED had a significantly higher chance of developing a cardiovascular event over a 7-year follow-up period. [55] The hazard ratio was 1.45, which is in the range of risk associated with current smoking or a family history of MI.

ED can be caused by either physical and/or psychological factors like stress, anxiety, or depression. Importantly, ED can be the first sign of heart or other health conditions, including cardiovascular disease and diabetes. We offer the optional order of a lab test to investigate whether you might have more serious underlying health problems. Our doctors can order investigative labs in all the states we operate in apart from AZ, NY, NJ and RI. You’ll need to go to a Quest Diagnostics center to have these tests done. When we get the test results back, we can help you understand what they mean.
The Prostate Cancer Prevention Trial was a landmark study by Thompson et al that prospectively assessed the time to developing CVD after the diagnosis of ED. There were 4247 men with no ED at study entry; 2420 developed incident ED (defined as the first report of ED of any grade) over 5 years. Those men that developed ED had a 1.45-fold higher probability of experiencing a CV event compared with men who did not develop ED.27
Among their findings, the panel concluded that (1) the term "erectile dysfunction" should replace the term "impotence"; (2) the likelihood of erectile dysfunction increases with age but is not an inevitable consequence of aging; (3) embarrassment of patients and reluctance of both patients and health care providers to discuss sexual matters candidly contribute to underdiagnosis of erectile dysfunction; (4) many cases of erectile dysfunction can be successfully managed with appropriately selected therapy; (5) the diagnosis and treatment of erectile dysfunction must be specific and responsive to the individual patient's needs and that compliance as well as the desires and expectations of both the patient and partner are important considerations in selecting appropriate therapy; (6) education of health care providers and the public on aspects of human sexuality, sexual dysfunction, and the availability of successful treatments is essential; and (7) erectile dysfunction is an important public health problem deserving of increased support for basic science investigation and applied research.
Constriction of the trabecular smooth muscle and helicine arteries induced by sympathetic innervation makes the penis flaccid, with blood pressure in the cavernosal sinuses of the penis near venous pressure. Acetylcholine is thought to decrease sympathetic tone. This may be important in a permissive sense for adequate trabecular smooth muscle relaxation and consequent effective action of other mediators in achieving sufficient inflow of blood into the lacunar spaces. When the trabecular smooth muscle relaxes and helicine arteries dilate in response to parasympathetic stimulation and decreased sympathetic tone, increased blood flow fills the cavernous spaces, increasing the pressure within these spaces so that the penis becomes erect. As the venules are compressed against the tunica albuginea, penile pressure approaches arterial pressure, causing rigidity. Once this state is achieved, arterial inflow is reduced to a level that matches venous outflow.
Some men should not take PDE5 inhibitors. They can cause hypotension (abnormally low blood pressure that can lead to fainting and even shock) when given to patients who are taking nitrates (medications taken for heart disease). Therefore, patients taking nitrates daily should not take any of the PDE5 inhibitors. Nitrates relieve angina (chest pain due to insufficient blood supply to the heart muscle because of narrowing of the coronary arteries); these include nitroglycerine tablets, patches, ointments, sprays, and pastes, as well as isosorbide dinitrate and isosorbide mononitrate. Other nitrates such as amyl nitrate and butyl nitrate also are in some recreational drugs called "poppers."
The rumors are true. Having too much to drink can interfere with a man’s ability to have an erection. According to Everyday Health, alcohol is a depressant. This means that, along with dampening your ability to think, speak, and move efficiently, it can also dampen mood, decrease sexual desire, and make it difficult for a man to achieve erection or reach an orgasm. This is because alcohol decreases blood flow to the penis. That not only may reduce a man’s ability to have an erection, but even if he is lucky enough to get it hard, alcohol can reduce the intensity of his orgasm.

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.

Appallingly little is known about the prevalence of erectile dysfunction in the United States and how this prevalence varies according to individual characteristics (age, race, ethnicity, socioeconomic status, and concomitant diseases and conditions). Data on erectile dysfunction available from the 1940's applied to the present U.S. male population produce an estimate of erectile dysfunction prevalence of 7 million.
The first line and by far the most common treatment today is with the prescription drug sildenafil citrate, sold under the brand name Viagra. An estimated 20 million prescriptions for the pill have been filled since it was approved by the FDA in March 1998. It is also the most effective treatment with a success rate of more than 60%. The drug boosts levels of a substance called cyclic GMP, which is responsible for widening the blood vessels of the penis. In clinical studies, Viagra produced headaches in 16% of men who took it, and other side effects included flushing, indigestion, and stuffy nose.
Despite the accumulation of a substantial body of scientific information about erectile dysfunction, large segments of the public -- as well as the health professions -- remain relatively uninformed, or -- even worse -- misinformed, about much of what is known. This lack of information, added to a pervasive reluctance of physicians to deal candidly with sexual matters, has resulted in patients being denied the benefits of treatment for their sexual concerns. Although they might wish doctors would ask them questions about their sexual lives, patients, for their part, are too often inhibited from initiating such discussions themselves. Improving both public and professional knowledge about erectile dysfunction will serve to remove those barriers and will foster more open communication and more effective treatment of this condition.
After the history, physical examination, and laboratory testing, a clinical impression can be obtained of a primarily psychogenic, organic, or mixed etiology for erectile dysfunction. Patients with primary or associated psychogenic factors may be offered further psychologic evaluation, and patients with endocrine abnormalities may be referred to an endocrinologist to evaluate the possibility of a pituitary lesion or hypogonadism. Unless previously diagnosed, suspicion of neurologic deficit may be further assessed by complete neurologic evaluation. No further diagnostic tests appear necessary for those patients who favor noninvasive treatment (e.g., vacuum constrictive devices, or pharmacologic injection therapy). Patients who do not respond satisfactorily to these noninvasive treatments may be candidates for penile implant surgery or further diagnostic testing for possible additional invasive therapies.

Surgery to repair arteries (penile arterial reconstructive surgery) can reduce impotence caused by obstructions that block the flow of blood to the penis. The best candidates for such surgery are young men with discrete blockage of an artery because of a physical injury to the pubic area or a fracture of the pelvis. The procedure is less successful in older men with widespread blockage of arteries.
Erectile dysfunction (ED), also known as impotence, is the inability to achieve or sustain a hard enough erection for satisfactory completion of sexual activity. Erectile dysfunction is different from other health conditions that interfere with male sexual function, such as lack of sexual desire (decreased libido) and problems with ejaculation release of the fluid from the penis (ejaculatory dysfunction) and orgasm/climax (orgasmic dysfunction), and penile curvature (Peyronie's disease), although these problems may also be present. ED affects about 50% of men age 40 and over. This article focuses on the evaluation and treatment of erectile dysfunction.
You’ve heard of—and probably experienced—the numbing effect alcohol has on your mind, body, and (unfortunately) penis. If you fail to rise to the occasion on a regular basis and you're drinking has gone from occassional weekend binge to a Monday through Friday ordeal, consider cutting back—way back. Heavy drinking proportionately increases your risk of ED, according to research from the Indian Journal of Psychiatry.

The time the dose should be taken and how long the effects last depend on the medication used. The most common side effect of these medications is a headache. However, there is a potential for certain dangerous drug interactions. Anyone prescribed this medication must let his doctor know about any medications he's on, and especially if he's taking nitrates (e.g., nitroglycerin spray, nitroglycerin pills, or nitroglycerin patch) for heart problems.
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.
It is important for clinicians prescribing these drugs to make the patient aware of the action of the drugs especially the fact that they do not result in an immediate erection, and that they do not cause an erection without sexual stimulation. There is frequently a great expectation when men begin using these drugs and it is wise to temper their enthusiasm and explain they do not work immediately, and may not work every time, but also let the patient know that if these drugs do not work, there are other options.
The appropriate evaluation of all men with erectile dysfunction should include a medical and detailed sexual history (including practices and techniques), a physical examination, a psycho-social evaluation, and basic laboratory studies. When available, a multidisciplinary approach to this evaluation may be desirable. In selected patients, further physiologic or invasive studies may be indicated. A sensitive sexual history, including expectations and motivations, should be obtained from the patient (and sexual partner whenever possible) in an interview conducted by an interested physician or another specially trained professional. A written patient questionnaire may be helpful but is not a substitute for the interview. The sexual history is needed to accurately define the patient's specific complaint and to distinguish between true erectile dysfunction, changes in sexual desire, and orgasmic or ejaculatory disturbances. The patient should be asked specifically about perceptions of his erectile dysfunction, including the nature of onset, frequency, quality, and duration of erections; the presence of nocturnal or morning erections; and his ability to achieve sexual satisfaction. Psychosocial factors related to erectile dysfunction should be probed, including specific situational circumstances, performance anxiety, the nature of sexual relationships, details of current sexual techniques, expectations, motivation for treatment, and the presence of specific discord in the patient's relationship with his sexual partner. The sexual partner's own expectations and perceptions should also be sought since they may have important bearing on diagnosis and treatment recommendations.
Me? I'm in my 60's and never had ED, not even once. And never failed to have a good orgasm with sexual activity. Unfortunately, I think it has created too much of a contrast to my wife, who has never had an orgasm, and now in menopause has given up and won't even let me touch her sexually (hugging and kissing is fine, but that's as far as she'll let me go).
That means that as an adult, you need to activate the opposing parasympathetic system through sexually exciting visuals, thoughts and touches to get an erection going. But this nerve transmission is disrupted if you're stressed, anxious or distracted. The latter because you simply don't develop enough total stimulation of your genitals to get an erection, and the former because stress and anxiety all increase adrenaline – a key transmitter in the inhibiting sympathetic nervous system. They quite literally sabotage your erection.
In some cases, ED can be a warning sign of more serious disease. One study suggests ED is a strong predictor of heart attack, stroke, and death from cardiovascular disease. The researchers say all men diagnosed with ED should be evaluated for cardiovascular disease. This does not mean every man with ED will develop heart disease, or that every man with heart disease has ED, but patients should be aware of the link.
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