Sexual Dysfunction in Men and Women. Stanley Zaslau

Chapter 3. Physical Diagnosis and Testing

Aimee E. Rogers, MD

■ Stanley Zaslau, MD, MBA, FACS

 Introduction

 There are many components to a successful sexual act, and dysfunction can occur at any point in the process.

 The sexually competent male must:

 Have desire for his sexual partner (libido)

 Direct blood from the iliac artery into the corpora cavernosa to achieve penile tumescence and rigidity (erection) adequate for penetration

 Discharge sperm and prostatic/seminal vesicle fluid through the urethra (ejaculation)

 Experience a sense of pleasure (orgasm)1

 At any point in time, this process can break down, which results in erectile dysfunction. This can be due to:

 Psychological causes

 Medications

 Hormonal abnormalities

 Neurological issues

 Vasculopathy

 Those issues and the other various etiologies of male sexual dysfunction will be discussed separately. This chapter will focus on physical diagnosis and evaluation of erectile dysfunction with the use of an ever-expanding array of tools, ranging from questionnaires and Doppler ultrasounds to penile arterial blood flow mapping.

 Initial Evaluation

 The evaluation begins with a sexual history and physical examination. The history and physical examination have

been reported to have a 95% sensitivity, but only a 50% specificity in determining the cause of impotence; as a result, additional diagnostic tests are needed to maximize specificity.2

 The sexual history includes important information such can’t as:

 Rapidity of onset of dysfunction

 Duration of dysfunction

 Severity of the problem

 An assessment of risk factors for impotence

 Sexually competent men who suddenly develop symptoms ‘overnight’ are usually those who have a psychogenic component to their sexual dysfunction.

 This is contrasted with men who notice their sexual function fail sporadically, then worsen over time. These men are likely suffering from organic disease, whether it be neurogenic or vascular.

 Another important component of the sexual history is erectile reserve. In men presenting with erectile dysfunction, the presence or absence of spontaneous erections is an important clue to diagnosis.

 Most men experience spontaneous erections during REM sleep, and often wake up with an erection, attesting to the integrity of neurogenic reflexes and corpora cavernosa blood flow.3 Reports of either morning or nocturnal erections can usually be elicited by either the patient or his partner.

 Men who report the lack of either type of spontaneous erection usually suffer from either neurological or vascular disease.

 It’s also important to remember the importance of the patient’s medical history.

 According to Lue and Broderick, the goals of medical history taking are:

 To evaluate the potential role of underlying medical conditions (e.g., atherosclerosis, diabetes) and comorbidities (e.g., depression)

 To differentiate between potential organic and psychogenic causes

 To assess the potential role of medication-induced ED

■ With respect to the final goal of history taking, it is important to remember that some medications, such as some beta-blockers, may contribute to the patient’s sexual dysfunction, and some, such as nitrates, may be contraindicated for use in treatment of erectile dysfunction.4

 The physical examination begins with assessment of the heart, lungs, and abdomen. In addition to the basic physical examination, the evaluation of the sexually dysfunctional male should include the following:

 Evaluation of body habitus and an assessment of secondary sexual characteristics

 A careful assessment of femoral and peripheral pulses as a clue to the presence of vasculogenic disease

 A breast examination to evaluate for possible gynecomastia, indicative of certain genetic syndromes

 Examination of the testicles, noting any atrophy, asymmetry, or masses

 A thorough examination of the penis, looking for evidence of chordee, micropenis, or Peyronie’s plaque

 Testing for genital and perineal sensation, and eliciting the bulbocavernosus reflex (BCR)

 Testing for visual field defects, indicative of a pituitary tumor with resultant hypogonadism

 A patient’s past surgical history may similarly yield insights. Radical pelvic surgery (e.g., prostatectomy, abdominoperineal resection) and pelvic trauma are well known to be associated with erectile dysfunction.5,6

 Laboratory Testing

 Laboratory tests for men with sexual dysfunction usually start with a fasting glucose and lipid profile to assess for any potential medical comorbidities, such as diabetes or hyperlipidemia.

 This is usually followed closely by hormonal profiles, including serum testosterone, prolactin, and thyroid function tests.

 A majority of the time, male sexual dysfunction that stems from a hormonal abnormality is a result of testosterone deficiency, or hypogonadism.

 Hypogonadism in a male refers to a decrease in one or both of the two major functions of the testes: sperm production or testosterone production.7

 These abnormalities can result from dysfunction of the testes, as in primary hypogonadism, or from pituitary or hypothalamic dysfunction, as seen in secondary hypogonadism.

 If the testosterone level is below or at the low limit of normal, the practitioner should then obtain serum concentrations of luteinizing hormone (LH) and follicle-stimulating hormone (FSH). These values allow differentiation between primary (abovenormal FSH/LH) hypogonadism and secondary (normal or reduced FSH/LH) hypogonadism.

 A prolactin level is drawn to rule out any possible dysfunction of the hypothalamic-pituitary axis.

 False elevations of prolactin levels can be seen after large meals, stress, or certain types of drugs.

 Any man with a confirmed diagnosis of hyperprolactinemia (non-drug-induced) should undergo investigation of the hypothalamic-pituitary axis, preferably an MRI, to rule out the presence of a tumor responsible for the hyperprolactinemia.8

 Thyroid function tests are usually performed in order to rule out hyper- or hypothyroidism as a cause of the patient’s sexual dysfunction.

 In men with hyperthyroidism, an increase in serum SHBG concentrations results in high serum total testosterone concentrations, but serum-free (unbound) testosterone concentrations are normal or low.9

 Extragonadal conversion of testosterone to estradiol is increased, which results in elevated serum estradiol concentrations.

 According to Carani et al., these changes can cause:

 Gynecomastia

 Reduced libido

 Erectile dysfunction10

• The same authors found that hypothyroidism also has a negative effect on sexual function. They found that 64% of hypothyroid men evaluated in their multicenter prospective study experienced decreased libido, erectile dysfunction, and delayed ejaculation.

 Noninvasive Methods of Evaluation

 After the history and physical exam are completed, the practitioner’s attention should turn to the noninvasive methods of evaluation of erectile dysfunction.

 This is most commonly in the form of questionnaires and sexual function symptom scores.

 Many ED questionnaires and sexual function profiles have been developed over the years.

 They were initially used to differentiate psychogenic ED from nonpsychogenic ED.

 More recently, a variety of self-report measures for assessing the levels of male sexual function or dysfunction have been created; self-administered questionnaires (SAQs) have seen their greatest use in clinical trials.

 SAQs attempt to quantify sexual interest, performance, and satisfaction.

 The most commonly referenced SAQs include:

 The International Index of Erectile Function (IIEF) by Rosen and associates (1997)

 The Brief Male Sexual Function Inventory (BMSFI) by O’Leary and colleagues (1995)

 The Erectile Dysfunction Inventory for Treatment Satisfaction (EDITS) by Althof and associates (1999)11

 The IIEF is the most widely used SAQ, and it is statistically validated in many languages. Its items address and quantify five domains:

 Erectile function

 Orgasmic function

 Sexual desire

 Intercourse satisfaction

 Overall satisfaction12

 It is important to remember that all sexual inventories rely on self-assessment.

 In 1999, Blander and colleagues demonstrated that SAQs do not differentiate among the various causes of ED (vascular, neurogenic, or psychogenic), and evidence-based assessments such as diagnostic tests are still necessary in patients with complex erectile dysfunction.13

■ Nocturnal penile tumescence (NPT) testing was first described in 1940 by Halverson, who documented nocturnal erections in infants.

 In 1966, Karacan and colleagues were the first to demonstrate that 80% of NPT occurs during rapid eye movement (REM) sleep.

 Total tumescence time during sleep peaks during puberty, when as much as 20% of total sleep time may be spent with an erection.

 In the second decade of life, the average duration of nocturnal erection is 38 minutes. In adults, the average duration of the erectile state is 27 minutes.14

 NPT was initially used by psychologists to study sleep and dreams. Fairly recently, it has been applied to differentiate psychogenic from organic erectile dysfunction.

 Historically, NPT has been measured by a variety of methods.

 The earliest methods include:

 The stamp test (Barry et al., 1980)

 Snap gauges (Diedrich et al., 1992)

 Sleep laboratory nocturnal penile tumescence and rigidity (NPTR)

 The RigiScan (Endocare, Inc., Irvine, California) was introduced in 1985, and it was the first device to provide automated, portable NPT recording.

 Most recently, NPT electrobioimpedance (NEVA American Medical Systems, Inc., Minnetonka, Minnesota) testing has been introduced as the most advanced form of nocturnal penile tumescence testing.

 In its most classic form, NPT consists of nocturnal monitoring devices that measure:

 The number of erectile episodes

 Tumescence (circumference change by strain gauges)

 Maximal penile rigidity

 Duration of nocturnal erections15

 Traditionally, NPT was recorded in conjunction with various other monitoring devices, including electroencephalography, electro-oculography, electromyography (EMG), and oxygen saturation measurements to document REM sleep and the presence or absence of sleep apnea.

 In these evaluations, the patient is awakened during maximal tumescence, and the erection is photographed and axial rigidity measured with a device applied to the tip of the penis.

 In the past, formal NPT evaluations were costly because they needed to be conducted in specially equipped sleep centers with trained observers.16 Recently, NPT testing has been simplified.

 Devices such as the RigiScan provide accurate, reproducible information quantifying the number, duration, tumescence, and radial rigidity of erectile episodes a man experiences as he sleeps in the comfort of his own bed.17

 The RigiScan consists of a recording unit that collects data for three separate nights for a maximum of 10 hours each night.

 The device consists of two loops.

 One is placed at the base of the penis.

 The other is placed at the coronal sulcus.

 Via constriction of the loops, the device records penile tumescence (circumference) and radial rigidity at the penile base and tip.

 A baseline penile circumference is established while the patient is awake prior to the test.

 Penile rigidity is recorded every three minutes by constriction of the loops. If the loop at the base

detects a circumference increase of greater than 10mm, sampling is increased to every 30 seconds.18

 The data generated can be downloaded to provide a graphic index quantifying erectile activity as either normal or impaired.

 Radial rigidity above 70% represents a nonbuckling erection, and a rigidity of less than 40% represents a flaccid penis.

 According to Levine’s study of NPT, the number of erections considered normal is three to six per 8-hour session, lasting an average of 10 to 15 minutes each.19

 In 1992, Cilurzo and colleagues recommended the following as normal NPT recording criteria20:

a. Four to five erectile episodes per night

b. Mean duration of erection longer than 30 minutes

c. An increase in circumference of more than 3 cm at the base and more than 2 cm at the tip

d. Maximal rigidity above 70% at both base and tip

As can be seen from the data presented by Levine19 and Cilurzo20 there is some variability as to normal NPT recording criteria.

Men who are experiencing sexual dysfunction with a normal NPT are considered to have psychogenic erectile dysfunction, whereas those with impaired NPT are considered to have “organic” erectile dysfunction, usually due to vascular or neurological disease. a. In comparison, testosterone-deficient hypogonadal men are still capable of exhibiting some erectile activity during nocturnal penile tumescence studies.21

 Vascular Evaluation

 Vascular evaluation is performed in men with erectile dysfunction in order to diagnose those with arterial and venous occlusive dysfunction.

 Over the years, multiple tests have been developed to identify and quantify arterial and veno-occlusive disease. • This includes:

 Combined intracavernous injection and stimulation (CIS)

 Duplex ultrasound

 Dynamic infusion cavernosometry and cavernosog- raphy (DICC)

 Selective penile angiography

 Traditionally, the first-line evaluation of penile blood flow has been combined intracavernous injection and stimulation (CIS).

 CIS consists of:

 An intracavernous injection of a vasodilator or a combination of two or three vasodilators

 Genital or audiovisual sexual stimulation

 Assessment of the erection by an observer22

 Several intracavernosal injection agents have been used, including:

 Alprostadil alone (Caverject or Edex)

 A combination of papaverine and phentolamine (Bimix)

 A mixture of all three agents (Trimix)

 The technique involves injecting the chosen medication into the corpus cavernosum. The erectile response is periodically evaluated for both rigidity and duration.

 The CIS test is the most commonly performed diagnostic procedure for erectile dysfunction. It allows the clinician to bypass neurological and hormonal influences, and to evaluate the vascular status of the penis directly via observation.23

 The second-line evaluation of penile blood flow is usually duplex ultrasonography (grayscale or color-coded).

Duplex ultrasound consists of high-resolution, real-time ultrasonography and color-pulsed Doppler, which enables the ultrasonographer to visualize the dorsal and cavernous arteries selectively and to perform dynamic blood flow analysis. It is also the best tool available for the diagnosis of high-flow priapism and localization of a ruptured artery.24

 Conclusions

 The initial evaluation of the patient with sexual dysfunction must include a thorough sexual history and physical examination.

 The physical examination has a very high sensitivity but a low specificity thus sometimes requiring additional diagnostic testing to confirm the diagnosis.

 It is important to rule out other silent, but coexisting conditions such as diabetes, and hyperlipidemia.

 Important noninvasive methods of evaluation of ED include questionnaires and sexual function symptom scores.

■ References

1. Spark RF. Evaluation of male sexual dysfunction. UpToDate. 2008.

2. Davis-Joseph B, Tiefer L, Melman A. Accuracy of the initial history and physical examination to establish the etiology of erectile dysfunction. Urology. 1995;45:498.

3. Spark RF. Evaluation of male sexual dysfunction. UpToDate. 2008.

4. Broderick GA, Lue TF. Evaluation and nonsurgical management of erectile dysfunction and premature ejaculation. In: Wein AJ, Kavoussi LR, Novick AC, Partin AW, Peters CA, eds. Campbell-Walsh Urology. Ninth ed. Philadelphia, PA: Saunders Elsevier Company; 2007:750-787.

5. Armenakas NA, McAninch JW, Lue TF, et al. Posttraumatic impotence: magnetic resonance imaging and duplex ultrasound in diagnosis and management. J Urol. 1993; 149: 1272-1275.

6. Walsh PC, Partin AW, Epstein JI. Cancer control and quality of life following anatomical radical retropubic prostatectomy: results at 10 years. J Urol. 1994;152:1831-1836.

7. Snyder, PJ. Clinical features and diagnosis of male hypogonadism. UpToDate. 2009.

8. Broderick GA, Lue TF. Evaluation and nonsurgical management of erectile dysfunction and premature ejaculation. In: Wein AJ, Kavoussi LR, Novick AC, Partin AW, Peters CA, eds. Campbell-Walsh Urology. Ninth ed. Philadelphia, PA: Saunders Elsevier Company; 2007:750-787.

9. Abalovich M, Levalle O, Hermes R, et al. Hypothalamic- pituitary-testicular axis and seminal parameters in hyperthyroid males. Thyroid. 1999;9:857.

10. Carani C, Isidori AM, Granata A, et al. Multicenter study on the prevalence of sexual symptoms in male

hypo- and hyperthyroid patients. J Clin Endocrinol Metab. 2005;90:6472.

11. Broderick GA, Lue TF. Evaluation and nonsurgical management of erectile dysfunction and premature ejaculation. In: Wein AJ, Kavoussi LR, Novick AC, Partin AW, Peters CA, eds. Campbell-Walsh Urology. Ninth ed. Philadelphia, PA: Saunders Elsevier Company; 2007:750-787.

12. Rosen RC, Riley A, Wagner G, et al. The international index of erectile function (IIEF): a multidimensional scale for assessment of erectile dysfunction. Urology. 1997; 49:822-830.

13. Blander DS, Sanchez-Ortiz RF, Broderick GA. Sex inventories: can questionnaires replace erectile dysfunction testing? Urology. 1999;54(4):719-723.

14. Karacan I, Williams RL, Finley WW, Hursch CJ. The effects of naps on nocturnal sleep: influence on the need for stage-1 REM and stage 4 sleep. Biol Psychiatry. 1970;2(4): 391-399.

15. Kessler WO. Nocturnal penile tumescence. Urol Clin North Am. 1988;15(1):81—86.

16. Broderick GA, Lue TF. Evaluation and nonsurgical management of erectile dysfunction and premature ejaculation. In: Wein AJ, Kavoussi LR, Novick AC, Partin AW, Peters CA, eds. Campbell-Walsh Urology. Ninth ed. Philadelphia, PA: Saunders Elsevier Company; 2007:750-787.

17. Bain CL, Guay AT. Reproducibility in measuring nocturnal penile tumescence and rigidity. J Urol. 1992;148:811.

18. Broderick GA, Lue TF. Evaluation and nonsurgical management of erectile dysfunction and premature ejaculation. In: Wein AJ, Kavoussi LR, Novick AC, Partin AW, Peters CA, eds. Campbell-Walsh Urology. Ninth ed. Philadelphia, PA: Saunders Elsevier Company; 2007:750-787.

19. Levine LA, Lenting EL. Use of nocturnal penile tumescence and rigidity in the evaluation of male erectile dysfunction. Urol Clin North Am. 1995;22(4):775-788.

20. Cilurzo P, Canale D, Turchi P, Giorgi PM, Menchini Fabris GF. The Rigiscan system in the diagnosis of male sexual impotence. Arch Ital Urol Nefrol Androl. 1992;64(S2): 81-85.

21. Kwan M, Greenleaf WJ, Mann J, et al. The nature of androgen action on male sexuality: a combined laboratory-selfreport study on hypogonadal men. J Clin Endocrinol Metab. 1983;57:557.

22. Donatucci CF, Lue TF. The combined intracavernous injection and stimulation test: diagnostic accuracy. J Urol. 1992;148(1):61—62.

23. Broderick GA, Lue TF. Evaluation and nonsurgical management of erectile dysfunction and premature ejaculation. In: Wein AJ, Kavoussi LR, Novick AC, Partin AW, Peters CA, eds. Campbell-Walsh Urology. Ninth ed. Philadelphia, PA: Saunders Elsevier Company; 2007:750-787.

24. Broderick GA, Lue TF. Evaluation and nonsurgical management of erectile dysfunction and premature ejaculation. In: Wein AJ, Kavoussi LR, Novick AC, Partin AW, Peters CA, eds. Campbell-Walsh Urology. Ninth ed. Philadelphia, PA: Saunders Elsevier Company; 2007:750-787.



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