Urology Nurses Online:  ARTICLES

Statistics indicate that there are an estimated 10 million impotent men in the United States.¹ In 1985, impotence accounted for 400,000 outpatient visits, 30,000 hospital admissions, and the expenditure of 146 million health care dollars.² The prevalence of impotence increases as men age, with 1.9% of men affected at age 40 years and 25% of men affected at age 65 years.³

The focus of this article is to discuss the prevalence of impotence after a radical prostatectomy for the treatment of prostate cancer. For many years it was assumed that most men who underwent radical prostatectomy would be impotent after surgery. Indeed, early literature reports the rate of impotence at 90% to 100% after surgical intervention.⁴ The reason for this high rate of impotence was the focus of research by Walsh et al.,⁵ in which they identified nerve damage as a contributing factor to postoperative impotence and described the nerve-sparing prostatectomy.
 

Since 1983 the nerve-sparing prostatectomy has become popular, and the incidence of impotence after radical prostatectomy has decreased. Figure 1 illustrates findings reported in three research studies about incidence rates after nerve-sparing radical prostatectomy for prostate cancer. ^6-8

DEFINITION OF IMPOTENCE

Impotence is described as "the consistent inability to achieve or sustain an erection of sufficient rigidity for sexual intercourse."¹ There are degrees of impotence ranging from a partial decrease in penile rigidity to complete erectile failure. This definition is restricted to the erectile capability of the male penis and does not address the problems of libido, ejaculation, and orgasm. The National Institutes of Health Consensus Conference on impotence recommended use of the term erectile dysfunction to define the inability of a male to have an erection as part of the entire process of sexual function.⁹
 

Impotence is a complex phenomenon that can originate from endocrinologic, psychogenic, vasculogenic, neurogenic, drug induced, age-related, or disease-related (diabetes and cardiovascular disease) factors. Impotence is also a common sequela after radical pelvic surgery, which is the specific focus of this article.⁴

PHYSIOLOGY OF ERECTION

To understand the process of why impotence occurs after a radical prostatectomy, it is important to review penile anatomy and the neurovascular physiology of a normal erection. An erection is a neurovascular phenomenon requiring intact pudendal and cavernous nerves, arteries, and veins. These structures have been localized anatomically as neurovascular bundles. The bundles are paired and run lateral to the pelvic fascia outside the prostatic capsule.¹⁰
 

The penile anatomy is composed of the corpus spongiosum, which contains the urethra and two columns of erectile tissue known as the corpora cavernosa. The corpora cavernosa is composed of spongelike tissue that has the ability to expand, allowing the penis to become engorged with blood for an erection. The main penile blood supply flows from the paired internal pudendal arteries to the penile artery. The cavernous and urethral arteries are two of several branches that branch from the penile artery to supply the penis with blood. Blood empties from the corpora cavernosa by way of several venous branches that form the internal pudendal veins.⁴
 

The neural innervation of the penis begins with sensory receptors in he penile skin. As these receptors are stimulated, they carry the somatosensory impulses along the cavernous nerves to the internal pudendal nerve and on to the spinal cord, thus controlling the sympathetic and parasympathetic innervation to the penis.¹⁰ Parasympathetic input causes relaxation of penile smooth muscle and dilation of the cavernosal arteries, allowing blood to engorge the corpora. These enlarged corpora exert pressure on penile veins, reducing the escape of blood from the penis and thus maintaining the erection. Sympathetic input reduces arterial flow to the penis and increases venous outflow, causing the penis to return to a flaccid state and ending the erection.¹
 

NERVE-SPARING PROSTATECTOMY 

Impotence after a radical prostatectomy results from damage during the surgical procedure to either nerves or blood vessels that supply the penis. Walsh et al.⁵ were the leaders in describing the physiology of why men became impotent after radical prostatectomy. They studied the anatomy of neural innervation to the penis and localized the internal pudendal and cavernous nerves as part of the neurovascular bundles responsible for an erection. Hence Walsh et al.⁵ pioneered the nerve-sparing prostatectomy in 1983. Before this time, during radical prostatectomy the neurovascular bundles were torn or cut and left in place because their importance was not appreciated.¹¹ This technique led to the high rate of postoperative impotence (90% to 100%) reported before 1983. After the description of Walsh's new surgical technique in 1983, the nerve-sparing prostatectomy was adopted by surgeons to preserve potency. During a nerve-sparing prostatectomy the prostate is excised with careful dissection to preserve the neurovascular bundles and cavernous nerves.⁷ As the nerve-sparing prostatectomy began to be used, the incidence of impotence was significantly reduced.⁴
 

The nerve-sparing prostatectomy did not completely abolish postoperative impotence in all patients, even with the preservation of both nerve bundles. This result suggested that postoperative impotence may be due to factors other than neural injury and led to further research concerning the role of penile vascular injury as the cause of impotence after a radical prostatectomy.⁴ As stated previously, the primary blood supply to the penis is from the internal pudendal arteries. Any disruption in the blood supply may cause impotence. Accessory branches to the internal pudendal artery arise from the obturator, inferior vesical, and superior vesical arteries. These branches are divided during radical prostatectomy, and this maneuver may compromise the arterial supply to the corpora cavernosa.¹² This disruption in penile blood supply during a radical prostatectomy contributes to the physiology of impotence after surgery.
 
A descriptive correlational study by Aboseif et al.⁴ examined the role of vascular injury as a cause of postoperative impotence. The researchers used pharmacologic testing to define impotence after surgery. A patient was considered potent in this study through a positive response to the vasoactive substance in the office which, as a result, did not rule out impotence related to neural damage. Reliability of the testing was increased by detailed preoperative and postoperative evaluation of each patient. This evaluation allowed the researchers to compare erectile function and penile blood flow for each of the 20 subjects before and after surgery, noting changes within each patient. Forty percent of the patients in the study had erectile and vascular changes after surgery. This result was demonstrated by a decreased erection and a reduction in the penile blood flow after surgery. Despite threats to validity and reliability such as a small sample size, 90% of the sample being older than 60 years, and lack of control for variables such as diabetes and cardiovascular disease, the results of this study suggest that vascular damage may be part of the cause of impotence after radical prostatectomy.
 

MEASUREMENT OF IMPOTENCE

The diagnostic workup for impotence should be individualized according to the patient's situation. Although impotence can be measured by several diagnostic procedures, there is no universally agreed upon diagnostic evaluation for all impotent men.³
 

To determine whether the patient has vasculogenic impotence from vascular damage during prostatectomy, pharmacologic testing may be used.¹⁰ Testing is completed with the use of vasoactive substances such as papaverine or prostaglandin E1. A rubber band is placed at the base of the penis, and a vasoactive substance is injected into the corpus cavernosum, causing relaxation of the smooth muscle and increased arterial blood flow. A normal rigid erection should develop within 5 to 10 minutes. If a full erection develops within 15 minutes and lasts longer than 30 minutes, vasculogenic impotence can be ruled out. Ultrasonography can also be used during pharmacologic testing to assess the diameter of the cavernosal arteries and penile blood flow during an erection.¹ This procedure may be useful after a radical prostatectomy to determine whether damage to the neurovascular bundle during surgery has affected blood flow to the penis.
 

Several factors can influence pharmacologic testing, which may limit reliability and validity of the test. First, stress or anxiety may increase vasoconstrictive input to the penis and prevent an erection during testing. Therefore the negative results from a single injection cannot be conclusive of vascular damage. Second, there has not been a standardized vasoactive drug or dose established for all testing. Nor are there standard measurements to monitor the erectile response during testing.¹ These factors affect the equivalence of testing and allow for variability between researchers. The reliability and validity of pharmacologic testing may be increased if each patient is evaluated by the same person with the same vasoactive agent and in the same setting.
 

FACTORS AFFECTING POSTPROSTATECTOMY 

There are common factors that influence the rate of impotence after a radical prostatectomy. Three factors that correlate with the rate of impotence after a radical prostatectomy have been identified: age, stage of tumor, and surgical technique (the ability to preserve the neurovascular bundles).^7,8,11 The prevalence of impotence will be discussed in relation to these three correlates.

Several studies reported that the rate of impotence after radical prostatectomy is affected by the age of the patient.^6-8 The increasing age of the patient was correlated with an increased rate of impotence after surgery. A study of 503 men revealed an impotence rate of 9% in men younger than 50 years old, 25% in men 50 to 60 years old, 42% in men 60 to 70 years old, and 75% of men older than 70 years.⁵ Another study of 145 patients who underwent a bilateral nerve-sparing prostatectomy revealed impotence rates of 19% for patients 40 to 59 years old, 43% for those 60 to 69 years, and 67% of those 70 to 79 years old.⁷ Walsh's study of 250 men (1987) found impotence rates of 19% for men 40 to 49 years old, 16% for men 50 to 59 years old, 40% for men 60 to 69 years old, and 67% for men 70 to 79 years old.⁸ Figure 2 illustrates the trend that with advancing age the rate of impotence also increases.

There is also a correlation between the rate of impotence in a patient and the stage of the prostatic tumor. Research studies have demonstrated that as the stage of tumor progresses from being organ-confined (stages A and B) to having extracapsular extension (stage C and D), the rate of impotence also increases. Catalona and Bigg⁷ showed this correlation to be statistically significant in their study of 145 men. Impotence rates after surgery for men of all ages were 28% for those with stage A and B tumors compared with 49% for those with stage C and D tumors. Quinlan et al.⁸ also studied the influence of clinical stage of tumor on impotence. Overall rates of impotence for those with stage B tumors were 30% and for those with stage C and D tumors were 38%. In Walsh's⁶ study of 250 patients he identified impotence rates of 25% for patients with organ-confined tumors and 50% for patients with tumors with extracapsular extension. Figure 3 illustrates the comparison of impotence rates in relation to stage of tumor.
 

The third factor identified to have a correlation to the rate of impotence is the surgical technique, or the ability to preserve the neurovascular bundles. The primary goal during a radical prostatectomy is complete tumor excision. Therefore, depending on the size and extension of the tumor, it is not always possible to preserve both neurovascular bundles. Research has demonstrated the rate of impotence is correlated with preservation or excision of the neurovascular bundles. In Catalona and Bigg's⁷ study of those patients who had bilateral nerve-sparing prostatectomies, 37% were impotent after surgery compared with a 61% impotence rate for those who underwent a unilateral nerve-sparing prostatectomy. In those patients who had both neurovascular bundles excised, 95% were impotent after surgery. In a study in which patients had both neurovascular bundles preserved, 24% were impotent compared with a 44% impotence rate, with one neurovascular bundle being preserved and a 100% impotence rate of the patients who had both neurovascular bundles excised.⁸ The influence of surgical technique on impotence after surgery is summarized in Figure 4.

In summary, a review of research shows an increased rate of impotence with advancing age,
increasing stage of tumor, and excision of neurovascular bundles. Depending on the patient's age, stage of cancer, and surgical technique, impotence rates range from 9% to 100% after surgery.^6-8 The average overall rate of impotence after a radical prostatectomy is 34%.
 

NURSING IMPLICATIONS 

Impotence can have a profound effect on the sense of well-being of patients with prostate cancer. Because of these high percentages and potential effects on the patient, it is very important that patients be informed of the possibility of impotence after surgery. For this to occur, health care providers must be educated on the percentages of postoperative impotence and include this in their patient teaching. Nurses should also take the initiative to discuss impotence after surgery with patients and assist them with surgical and nonsurgical treatment options, if desired.
 

Treatment for impotence can be hindered because of the patient's discomfort in discussing the issue and hesitance of the health care provider to mention it.⁹ Through increased teaching about impotence patients will be informed before they undergo surgery and know what to expect after surgery. If they become impotent, they will feel more at ease to discuss this with their health care providers and find a treatment option that works for them.
 

The concerns of patients with impotence and the effects of impotence after surgery are observed on a urology unit almost daily. As health care providers we must do our part to positively affect the care for the impotent patient. This can be done through patient teaching before and after surgery and by providing information about treatment options available for impotence. The implementation of these interventions by health care providers will result in positive outcomes for the patient undergoing radical prostatectomy.
 
 
 

REFERENCES  
 

1. Krane R, Goldstein I, Tejada I. Impotence. N Engl J Med 1989; 321:1648-56.
2. Feldman H, Goldstein I, Hatzichristou D, Krane R, McKinlay J. Impotence and its medical and psychosocial correlates: results of the Massachusetts male aging study. J Urol 1994; 151:54-61.
3. Goldstein I, Krane R. Diagnosis and therapy of erectile dysfunction. In: Walsh PC, Gittes RF, Perlmutter A, Stamey TA, editors. Campbell's Urology. Philadelphia: WB Saunders Co; 1992. p. 3033-67.
4. Aboseif S, Shinohara K, Breza J, Benard F, Narayan P. Role of penile vascular injury in erectile dysfunction after radical prostatectomy. Br J Urol 1994; 73:75-82.
5. Walsh P, Lepor H, Eggleston J. Radical prostatectomy with preservation of sexual function: anatomical and pathological considerations. Prostate 1983; 4:473-7.
6. Walsh P. Radical prostatectomy, preservation of sexual function, cancer control. Urol Clin North Am 1987; 14:663-73.
7. Catalona W, Bigg S. Nerve-sparing radical prostatectomy: evaluation of results after 250 patients. J Urol 1990; 143:538-44.
8. Quinlan D, Epstein J, Carter B, Walsh P. Sexual function following radical prostatectomy: Influence of preservation of neurovascular bundles. J Urol 1991; 145:998-1002.
9. NIH Consensus Conference. Impotence- NIH Consensus Development Panel on Impotence. JAMA 1993; 270:83-90.
10. Lue T. Impotence after prostatectomy. Urol Clin North Am 1990; 17:613-20.
11. Walsh P, Partin A, Epstein J. Cancer control and quality of life following anatomical radical retropubic prostatectomy: results at 10 years. J Urol 1994:152; 1831-6.
12. Walsh P. Radical retropubic prostatectomy. In: Walsh PC, Gittes RF, Perlmutter AD, Stamey TA, editors. Campbell's urology. Philadelphia: WB Saunders Co; 1992: p. 2884-6.