Impotence
Louis Kuritzky
Approach
Impotence, defined as the consistent inability to get or maintain an erection sufficient for intercourse, is a patient-defined diagnosis. Because up to one-third of men aged more than 65 years have erectile dysfunction (ED), sheer volume merits accurate clinical definition. The role of the clinician is to confirm impotence, rule out correctable secondary causes, and expeditiously restore sexual function. Although current consensus suggests the term impotence should be replaced with ED because of the alleged pejorative connotations of the former, clinicians should feel comfortable using either term. In fact, technical terms that might cause confusion or be discordant with the patient’s educational or cultural status should be particularly avoided.
Having self-diagnosed impotence, men usually are seeking restoration of sexual function, not further confirmation of the diagnosis. Most healthy men will occasionally experience an isolated episode of inability to perform sexually as a result of fatigue, depression, boredom, anxiety, sleep deprivation, or relationship conflict, but do not fit the consistent portion of the definition. To encourage hopefulness, explain at the outset that essentially 100% of men may have sexual function restored using currently available treatments. Impotence is broadly divided into psychogenic and organic categories, although often a substantial degree of overlap is seen (1).
A. Psychogenic impotence can reflect depression, relationship conflict, performance anxiety, or partner-directed hostility. The history is definitive in most cases. Sudden, complete loss of function, situation or partner variability, and maintenance of morning or masturbatory erections are typical. Good rigid morning erections indicate an intact erectile circuitry sufficient for sexual responsivity, hence circumstantial erectile capacity is psychogenic. Occasionally, patients with dysfunctions other than impotence will seek advice, for instance believing that premature ejaculation is impotence. In such cases, corrective education combined with appropriate attention to the alternate diagnosis is the logical next step.
B. Organic sexual dysfunction is characterized by incremental loss of erectile function. In middle age, men with organic ED note reduced erectile turgidity, increasing requirement for tactile stimulation to produce an erection, and a lengthening refractory period (i.e., the amount of time after ejaculation required before the male is receptive to restimulation and erection). Such stepwise loss of sexual function corroborates organicity.
Most organic impotence is on a vascular basis. Because integrity of the endothelium is necessary to provide adequate dilation of the sinusoids of the corpora cavernosa via the arteries supplying the penis, predictably, disorders causing endothelial dysfunction are associated with ED. For instance, diabetes causes a marked shift “to the left” in the incidence of impotence, so that by age 30, almost one of seven men who are diabetic manifest erectile insufficiency (Chapter 14.1). Unfortunately, improved glycemic control rarely reverses the endothelial or neurologic pathologies sufficient to fully restore erectile function. Smoking, hypertension, atherosclerosis, hyperlipidemia, and peripheral vascular disease all impair endothelial function and, hence, induce ED. Unless a correctable cause of impotence is suspected, it is usually unnecessary to determine the exact underlying cause. On the other hand, all the commonly used treatment tools (i.e., vacuum constriction pumps, intracavernosal injection, intraurethral prostaglandin, sildenafil) can be used, regardless of the underlying cause.
History
A. Basic history. Although written questionnaires may elicit sexual dysfunction, most patients prefer to communicate such issues in the privacy of verbal communication with their primary care provider. For the initial inquiry, simply ask: “Are you sexually active?” For sexual dysfunction evaluation, gender orientation is not relevant to diagnosis or therapy, so that whether the patient is homosexual, heterosexual, or bisexual has no distinct bearing on the diagnostic or therapeutic direction. For persons who are not sexually active, next determine whether this is a matter of choice or an obstacle that prevents sexual activity (e.g., lack of partner, ED, physical disorder).
For persons who are sexually active, a series of follow-up questions will uncover most relevant psychosexual pathology. Begin with: “How would you rate your sex life on a scale of 1 to 10?” If the response is 10, sexual dysfunction is decidedly unlikely. However, most individuals respond, “Oh, about a 7.” Follow with, “What would have to be different to change your sex life from a 7 to a 10?” This forced-choice inquiry often produces responses which directly indicate problematic underlying issues: “Well, if I could just get a good erection.” “If my erection could last more than 30 seconds.” “If my partner didn’t always pick a fight with me and then expect to have sex.”
For impotent men, their response is usually direct and simple, indicating an inability to get or maintain an erection. Follow-up questions should determine the duration and nature of onset. Absence of morning erections should be sought, as this typifies organic impotence. Men who are much more likely to have psychogenic ED are those who report sudden, complete loss of sexual function, or “circumstantial” impotence, for example, (a) good function with one partner, but not another; (b) good erections with masturbation but not with interactive sex; (c) good morning erections, but not at times of interactive sex; or (d) overt anxiety or relationship conflict. Because organic ED generally leads to psychological consequences, many patients suffer a combination of psychogenic and organic impotence.
B. Inquiry about libido is a crucial diagnostic point for testosterone deficiency. Testosterone is necessary for libido, but not erections. Men who present with good libido have only a remote possibility of having testosterone deficiency.
C. A medication history should be taken for all men complaining of impotence, recalling that most medication-induced impotence is evident by the temporal relationship between onset of impotence and medication initiation. On the other hand, agents such as thiazides can produce impotence after months of use. Similarly, some antidepressants can produce sexual dysfunction either early or after weeks of therapy. The relationship of medications to impotence can often be clarified by a drug holiday.
Physical examination
Although physical examination is usually not enlightening, general agreement is seen that the genitals should be examined for evidence of overt testicular atrophy, and the penis for Peyronie’s disease. In the latter, inflammatory plaques in the corpora cavernosa produce an area of limited expansile capacity, with subsequent penile deviation on erection which can prevent intromission. A rectal examination to document rectal sensation as well as tone can be complemented by the bulbocavernosus reflex. This reflex is elicited by briskly squeezing the glans penis in one hand while a single digit from the other is in the rectum. A normal examination, indicating an intact reflex arc, is manifest as a rectal contraction in response to the glans squeeze. Prostate examination is pertinent at this point, in the event testosterone therapy is required.
Testing
Reasonable screening tests for impotence include a complete blood cell count, testosterone level, and a urinalysis. If testosterone is low, luteinizing hormone and follicle stimulating hormone levels should be measured, as an increase in either of these indicates gonadal failure, for which testosterone replacement is indicated; a decrease, however, indicates hypothalamic or pituitary insufficiency, necessitating central nervous system imaging to rule out a mass lesion. Similarly, low testosterone merits a serum prolactin level, as elevations of prolactin result in testosterone suppression. Other diagnostic testing, such as penile Doppler flow or nocturnal penile tumescence testing, add little to the options for therapy, but much to the expense.
Diagnostic assessment
In primary care, 98% of patients will have no testosterone deficiency, prolactin excess, or physical abnormalities (1). Such patients should be reassured that although they have no readily correctable cause for their impotence, effective therapy can be immediately begun. Patients who fail to respond to the standard tools for potency restoration (oral agents, vacuum constriction devices, and so on), or who desire more definitive delineation of their underlying pathology (as might be determined by Doppler studies) should be referred to specialty diagnostic centers.
Reference
1. Kuritzky L, Ahmed O, Kosch S. Management of impotence in primary care. Compr Ther 1998;24(3):137–146.
Book Source Details
- Book Title: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter
- Author(s): Robert B. Taylor (editor)
- Year of Publication: 2000
- Copyright Details: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, Copyright © 2000 Lippincott Williams & Wilkins.
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Copyright Details: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, Copyright © 2008 Williams & Wilkins.
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