Erectile Dysfunction in Older Men
Case Presentation
A 72-year-old male who is a retired CEO of a major company and a long-time patient complains of erectile dysfunction (ED) on a routine office visit. He was married for 30 years when his wife died of cancer three years ago. He was depressed initially and often thought of his late wife. On the insistence of his children and friends, he began to socialize again and recently met an attractive female, with whom he started an intimate relationship. However, he failed to obtain sufficient erection at the moments that mattered. He feels very frustrated and seeks help. The patient currently acts as a consultant to several companies, exercises daily, and is an avid golfer and an active member of his country club. He has a history of coronary artery disease with a myocardial infarction five years ago, well-controlled hypertension for the last ten years, diabetes mellitus for 15 years, benign prostatic hypertrophy, exertional angina, and hyperlipidemia. He is taking the following medications: enalapril; aspirin; isosorbide mononitrate; doxazosin; lovastatin; and insulin glargine. His physical examination is unremarkable except for diminished peripheral pulses, and he appears to be in good spirits.
Discussion
An erection is initiated by the parasympathetic division of the autonomous nervous system and is accomplished by engorgement of corpora cavernosa with venous blood in response to various physiological stimuli, resulting in hardening, swelling, and enlargement of the penis as a prelude to sexual intercourse. This hemodynamic event results primarily from relaxation of smooth muscles of the arterial vasculature, distension of the corpora cavernosa and the surrounding sinuses, and compression of the venules influenced by the neurotransmitter nitric oxide released by the endothelial lining. Nitric oxide eventually increases the tissue concentration of a potent smooth muscle relaxant cyclic guanosine monophosphate (cGMP), which is ultimately neutralized by the enzyme phosphodiesterase-5 (PDE-5).
Aging affects the sexuality of men in various manners. A man’s sexual response begins to slow down after age 30. However, a man’s sexual drive is more likely to be affected by his health and his attitude about sex and intimacy than by his age. An aging man may find that it takes longer to achieve an erection. His erection may not be as firm or as large as it used to be. The amount of ejaculate may be smaller. The loss of erection after orgasm may happen more quickly, or it may take longer before an erection is again possible. Some men may find that they need more foreplay.
Stages of sexual response also change with aging. There is delayed erection, decreased tensing of the scrotal sac, and loss of testicular elevation during the excitement phase. The plateau stage is prolonged, and pre-ejaculatory secretion is decreased. Orgasm is diminished in duration and intensity, characterized by decreased quantity and force of seminal emission. There is rapid detumescence and testicular descent during the resolution phase. The refractory period between erections is also prolonged.
The frequency of sexual intercourse and the prevalence of engaging in any sexual activity also decrease. Young men report having intercourse two to three times per week, whereas only 7% of men age 60-69 years and 2% of those age 70 years and older report the same frequency. Fifty percent to 80% of men age 60-70 years engage in any sexual activity, a prevalence rate that declines to 15-25% among those age 80 years and older.1
A man’s level of sexual activity, interest, and enjoyment in younger years often determines his sexual behavior with aging. In most healthy adults, pleasure and interest in sex do not diminish with age. However, sexual interest often persists despite decreased activity, and a healthy man with good blood flow to his penis will be able to have erections that are firm enough for intercourse throughout his entire life. Factors contributing to a man’s decreased sexual activity and sexual intercourse include social issues, partner availability, physical limitations, poor health, medications, medical conditions including decreased libido, and ED.
Erectile dysfunction is the consistent inability to achieve or maintain an erection that is adequate for successful and sustained vaginal penetration. ED is not a part of healthy aging. Although the incidence of ED increases with age, it is difficult to gauge the real prevalence of ED due to difficulty in getting confirmation from a lot of men.2 Almost 50% of men over age 40 years have some sort of sexual dysfunction, but only one-third of them report ED. By 70 years of age, two-thirds of men have ED. ED can be a result of physiologic changes of aging; cultural, social, and psychological factors; health status including physical limitations, chronic diseases, and medications; or a combination thereof. About one-fifth of ED cases can be due to psychological factors such as stress, depression, anxiety, or apathy. Other psychogenic causes include relationship conflicts, performance anxiety, childhood sexual abuse, fear of sexually transmitted diseases, and widower’s syndrome. Chronic medical conditions such as vascular, neurological, or other systemic diseases can account for as much as three-fourths of ED cases. Vascular disease is the most common cause of ED in older men, the risk for which increases with smoking, hypertension, atherosclerotic disease, hyperlipidemia, and diabetes. ED is a marker of peripheral vascular disease portending major vascular events such as stroke or myocardial infarction. Neurological causes including stroke, spinal cord injuries, and Parkinson’s disease are the next most common causes of ED. Disorders that affect the parasympathetic sacral spinal cord or the peripheral efferent autonomic fibers to the penis impair penile smooth muscle relaxation and prevent the vasodilation necessary for erection. Common health problems such as diabetes mellitus, stroke, and Parkinson’s disease or surgical procedures such as radical prostatectomy, transurethral prostatectomy, cystoprostatectomy, and proctocolectomy may result in autonomic dysfunction leading to ED. Other diseases that contribute to ED are hypogonadism, hyperthyroidism, hypothyroidism, and hyperprolactinemia. The following medications/substances commonly used in elderly males may also contribute to ED: anticholinergics, antidepressants, antipsychotics, and antihistamines; nearly all antihypertensive agents, especially beta-blockers, clonidine, and thiazide diuretics; over-the-counter medications such as cimetidine and ranitidine; and alcohol.
Evaluation of ED entails thorough medical and sexual history, including inadequate erections, decrease in libido or orgasmic failure, onset and duration of ED, as well as presence or absence of sleep-associated erections and associated decline in libido.3 Sudden onset suggests psychogenic or drug-induced ED. A gradual onset of ED associated with loss of libido suggests hypogonadism. Medical history should address vascular risk factors including diabetes mellitus, hypertension, coronary artery disease, peripheral arterial disease, hyperlipidemia, alcohol use, and smoking. Neurogenic risk factors including diabetes mellitus, history of pelvic injury or surgery, spinal injury or surgery, Parkinson’s disease, multiple sclerosis, and alcoholism should be evaluated carefully. Extensive medication review, including over-the-counter medications, should be performed. Psychosocial history should be explored in detail, including the patient’s relationship with the sexual partner, the partner’s health and attitude toward sex, economic or social stresses, living situation, alcohol use, and affective disorders.
Physical examination should emphasize upon signs of vascular or neurologic diseases, including palpation of peripheral pulses, signs of autonomic neuropathy, and loss of the cremasteric and bulbocavernosus reflexes. The genital examination should include retraction of the prepuce for phimosis, examination of the glans penis for balanitis, palpation of the penis for Peyronie’s plaques, assessment for testicular atrophy, and a thorough prostate exam. A loss of secondary sexual characteristics, the presence of small testes, and gynecomastia suggest hypogonadism resulting in diminished libido.
Laboratory evaluation must emphasize urinalysis, cholesterol level, and serum testosterone concentration. If the serum testosterone is low, further hormonal evaluation may be done using free testosterone, luteinizing hormone, and prolactin serum concentrations. Measurement of free testosterone alone is not reliable enough and should not be used as the sole diagnostic criterion. It should be measured early in the morning, and low values must be verified at least once more, at least one week later. Other diagnostic screening tools include intracavernous injection of a vasoactive drug such as papaverine or prostaglandin E1 (PGE1), nocturnal penile tumescence testing, penile brachial pressure index, penile arteriography, Doppler ultrasound, and dynamic infusion cavernosometry.
There are a number of treatment options available for ED4 (Table I). Sex therapy and counseling can be effective in treating ED resulting from psychogenic causes such as stress, depression, or anxiety. It may take a few weeks to be effective and may require ongoing periodic supporting sessions. The effect may last for years. Use of a vacuum device is yet another noninvasive and safe means of achieving an erection, especially when medications or other surgical interventions are contraindicated. The onset of effect is within 5 minutes that lasts for about 30 minutes. Common adverse effects of a vacuum device include: petechiae; coldness, bruising, and reddening of the penis; and painful ejaculation. PDE-5 inhibitors are the oral medications used to treat ED and include sildenafil, vardenafil, and tadalafil.5 There is a wide range for onset, duration, and dosing of the various medications. See Table II for specific information on each. The common adverse effects include headache, back pain, flushing, rhinitis, dyspepsia, and transient color blindness. They are contraindicated in patients using nitrates, for risk of potentiating fatal episodes of hypotension. Alpha-blockers are also contraindicated for the same reason, except with sildenafil and tadalafil that can be used with 0.4 mg of tamsulosin. The medicated urethral system for erection (MUSE) involves intrauretheral administration of alprostadil 250-1000 μg, with an onset of effect of 10 minutes and duration of effect of 60-90 minutes. Adverse effects include penile pain or burning and hypotension.
There is much controversy over the use of intracavernosal administration of papaverine, PGE1, or phentolamine for treating ED when other treatments are ineffective or contraindicated. See Table I for specific information. Various kinds of penile prostheses are also available to address ED. They are implanted surgically and may need to be replaced in five to ten years. They are associated with infection, erosion, or mechanical failure.
Case Conclusion
After detailed discussion with the patient and careful consideration of his clinical conditions, medications, age, and lifestyle, a number of treatment options were considered. Sex therapy and counseling were excluded due to lack of obvious psychogenic causes such as stress, depression, or anxiety. PDE-5 inhibitor treatment was contraindicated because of the patient’s use of nitrates for risk of potentiating fatal episodes of hypotension. Due to the same reason, MUSE also was not an option. Intracavernosal administration of papaverine, PGE1, or phentolamine, usually an option of last resort, was also excluded due to high rates of complications such as fibrosis. The best option for his situation appeared to be a vacuum device. The patient was carefully explained the use of the device and the common adverse effects that he may encounter. On the first couple of follow-up visits, he expressed his unhappiness regarding the clumsy process he had to go through, but he did achieve positive results. After using it a few times, the patient became used to the vacuum device and was very satisfied with the results. He was eventually able to establish a successful relationship.
The author reports no relevant financial relationships.
Dr. Sharma is Site Medical Director, Prison Health Services, Manhattan Detention Complex, and Attending Geriatrician, Jewish Home Lifecare, New York, NY.
References
1. Mulligan T, Reddy S, Gulur PV, Godschalk M. Disorders of male sexual function. Clin Geriatr Med 2003;19(3):473-481, v.
2. Nicolosi A, Buvat J, Glasser DB, et al; GSSAB Investigators’ Group. Sexual behaviour, sexual dysfunctions and related help seeking patterns in middle-aged and elderly Europeans: The global study of sexual attitudes and behaviors. World J Urol 2006;24:423-428. Published Online: July 19, 2006.
3. Seftel AD. From aspiration to achievement: Assessment and noninvasive treatment of erectile dysfunction in aging man. J Am Geriatr Soc 2005;53:119-130.
4. Gholami SS, Graziottin TM, Lue TF. The treatment of erectile dysfunction in the elderly. Curr Urol Rep 2001;2:1-2.
5. Müller A, Smith L, Parker M, Mulhall JP. Analysis of the efficacy and safety of sildenafil citrate in the geriatric population. BJU Int 2007;100:117-121.