Thomas Mulligan and Michael P. Feloney

Outline

Male sexuality: Age-associated changes

As men age, their sexual function changes. The frequency of intercourse and the prevalence of any sexual activity decrease. Young married men report intercourse 3 to 4 times per week, whereas only 7% of men aged 60 to 69 and 2% of those older than age 70 report this same frequency (Level of Evidence A).^1,2 However, sexual interest often persists despite decreased activity. Factors contributing to a man’s decreased sexual activity include poor health, decreased partner availability, decreased libido, and erectile dysfunction (ED). Though aging is associated with changes in sexual behavior and response (e.g., refractory period between erections is longer),³ erectile failure is not a part of healthy aging but rather is caused by age-associated disease (e.g., peripheral arterial disease) or treatment (e.g., radical prostatectomy for prostate cancer) (Level of Evidence B).⁴

Erectile physiology and dysfunction

In brief, testosterone, mental health, and an attractive partner stimulate libido. Fantasy as well as visual, tactile, or other erotic stimuli trigger neural impulses from the brain or spinal cord to the penis. Neural impulses cause release of neurotransmitters (e.g., nitric oxide, cGMP), which induce arterial vasodilation. Increasing arterial inflow dilates the corpora cavernosa, which impedes venous outflow. As the intrapenile (i.e., intracavernosal) pressure equilibrates to mean arterial pressure, the penis becomes rigid as blood is trapped in the penis.

ED, the inability to maintain an erection adequate for sexual intercourse, is the most common sexual problem of older men. The prevalence of ED increases with age; by 70 years of age, 67% of men have ED.⁵ The common causes of ED in older men are outlined in Table 32-1.

The most common cause (30% to 50%) of ED in older men is vascular disease (Level of Evidence A).⁶ Risk of vascular ED increases with traditional vascular risk factors (e.g., diabetes mellitus,⁷ hypertension, hyperlipidemia, and smoking).^8,9 Obstruction from atherosclerotic arterial disease impedes the intracavernosal blood flow and pressure needed to achieve a rigid erection. Venous leakage¹⁰ leading to vascular ED can result from Peyronie’s disease, arteriovenous fistula, or trauma-induced communication between the glans and the corpora. In anxious men who have excessive adrenergic-constrictor tone and in men with injured parasympathetic dilator nerves, ED can result from insufficient relaxation of trabecular smooth muscle.

The second most common cause of ED in older men is neurologic (17% to 37%).¹⁰ Disorders that affect the parasympathetic sacral spinal cord or the peripheral efferent fibers to the penis impair penile smooth muscle relaxation and prevent the vasodilation necessary for erection. In patients with prostate cancer, all forms of (curative) treatment frequently cause neurogenic erectile failure (brachytherapy or external radiation, 50%; radical prostatectomy with nerve sparing, 45% to 80%) (Level of Evidence B).⁴ Common health problems such as diabetes mellitus and stroke can cause autonomic dysfunction,¹¹ and surgical procedures such as prostatectomy, cystectomy, and proctocolectomy commonly disrupt the autonomic nerve supply to the penis, resulting in postoperative ED.

Many medications are associated with erectile dysfunction.¹² Medications with anticholinergic effects, such as antidepressants, antipsychotics, and antihistamines, can cause ED by blocking parasympathetic-mediated vasodilation and trabecular smooth muscle relaxation. Almost all antihypertensive agents have been associated with ED; of these, clonidine and thiazide diuretics have higher incidence rates,^13,14 whereas angiotensin-converting enzyme (ACE) inhibitors and angiotensin-receptor blockers have lower incidence rates (Level of Evidence B).^15,16 Numerous over-the-counter medications can cause ED. Cimetidine acts as an antiandrogen¹⁷ and increases prolactin secretion; thus it has been associated with loss of libido and erectile failure. Ranitidine can also increase prolactin secretion, although less commonly than does cimetidine.

The prevalence of psychogenic ED correlates inversely with age. Common causes¹⁸ of psychogenic ED include performance anxiety, fear of sexually transmitted diseases, and “widower’s syndrome,”¹⁹ in which the man involved in a new relationship feels guilt as a defense against subconscious unfaithfulness to his deceased spouse. A patient suffering only from “widower’s syndrome” should be able to achieve rigid erections with masturbation.

Hypogonadism, hypothyroidism, and hyperprolactinemia have been associated with ED. However, less than 5% of ED is caused by endocrine abnormalities.²⁰ Thus endocrine evaluation of men with ED but intact libido is of limited value (Level of Evidence B). Even men with castrate levels of testosterone can attain erections in response to direct penile stimulation. It may be that erection from direct penile stimulation is less androgen dependent, whereas erection from fantasy is more androgen dependent. Thus testosterone plays a large role in libido and a smaller role in ED.²¹

Therefore, if a man has complaints of low libido (more likely the man’s spouse urged him to seek evaluation for this problem), assessment of serum testosterone is warranted. Ideally, blood should be obtained in the morning to account for circadian rhythm and the result carefully interpreted. For example, a serum total testosterone concentration less than 200 ng/dL in a symptomatic man strongly suggests hypogonadism that will likely respond to treatment. A serum total testosterone concentration less than 300 ng/dL in a symptomatic man likely also represents hypogonadism but response to treatment is less predictable.

Evaluation of erectile dysfunction

Sexual history should clarify whether the problem consists of decreased libido, inadequate erections, or orgasmic failure. The onset and duration of ED, the presence or absence of sleep-associated erections, and the associated decline in libido are clues to the likely cause.

Sudden onset (in the absence of pelvic surgery) suggests psychogenic or drug-induced ED. A psychogenic cause is likely if there is a sudden onset but retention of sleep-associated erections or if erections with masturbation are intact (Level of Evidence A).²² If sudden-onset erectile failure is accompanied by lack of sleep-associated erections and lack of erection with masturbation, temporal association with new medication should be investigated. A gradual onset of ED associated with loss of libido suggests hypogonadism. Gradual onset associated with intact libido (the most common presentation) suggests vascular, neurogenic, or other organic causes.

Medical history is directed at discerning those factors likely to be contributing to ED. Vascular risk factors include diabetes mellitus, hypertension, coronary artery disease, peripheral arterial disease, hyperlipidemia, and smoking. Neurogenic risk factors include diabetes mellitus; history of pelvic injury, surgery, or radiation; and spinal injury or surgery. A complete medication review, including over-the-counter medications, is essential. Finally, the history should assess 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.

On physical examination, attention should be paid to signs of vascular, neurologic, or endocrine diseases. A femoral bruit and diminished (or absent) pedal pulses suggest an arterial etiology. Palpation of penile plaques (i.e., Peyronie’s disease) suggests venous etiology. Orthostatic hypotension and loss of the bulbocavernosus reflex suggest neurologic etiology. Small testes and gynecomastia suggest hypogonadism or hyperprolactinemia.

Laboratory evaluations should target relevant comorbid conditions such as diabetes mellitus and vascular disease or disorders suggested by the physical examination. The measurement of serum testosterone should be considered in men with low libido.

An at-home therapeutic trial of a phosphodiesterase inhibitor (sildenafil or vardenafil) is considered first-line evaluation and treatment.²³ The initial dose should be low (sildenafil 25 to 50 mg or vardenafil 5 to 10 mg) in men suspected of having neurogenic ED. A poor response suggests vasculogenic ED. Further therapeutic trial with sildenafil at 100 mg or vardenafil at 20 mg may prove to be effective.

More extensive diagnostic testing is not commonly used. The penile-brachial pressure index²⁴

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