Evaluation and Management of Sexual Dysfunction in Men and Women PDF

14Evaluation and Management of Sexual Dysfunction in Men and Women JAMES ANAISSIE AND MOHIT KHERA CONTRIBUTORS OF CAMPBELL-WALSH-WEIN, 12TH EDITION Alan W. Shindel, Tom F. Lue, Arthur L. Burnett Ii, Ranjith Ramasamy, Gregory A. Broderick, Chris G. Mcmahon, Matthew J. Mellon, J...

14Evaluation and Management of Sexual Dysfunction in Men and Women JAMES ANAISSIE AND MOHIT KHERA CONTRIBUTORS OF CAMPBELL-WALSH-WEIN, 12TH EDITION Alan W. Shindel, Tom F. Lue, Arthur L. Burnett Ii, Ranjith Ramasamy, Gregory A. Broderick, Chris G. Mcmahon, Matthew J. Mellon, John J. Mulcahy, Allen D. Seftel, Hailiu Yang, Ervin Kocjancic, Valerio Iacovelli, and Omer Acar ERECTILE DYSFUNCTION Epidemiology Erectile dysfunction (ED) is the inability to attain and/or maintain penile erection sufficient for sexual performance or satisfaction. ED affects up to 20% of men worldwide older than 20 years old and wors- ens with age. Prevalence begins at 1%–10% for men younger than 40 years and approaches 50%–100% for men older than 70 years. Medical comorbidities, such as metabolic syndrome and cardiovascu- lar disease, are associated with ED. Lower education and cigarette smoking are additional predictors for developing ED. The inverse is also true, and ED is now considered a sentinel for future risk of car- diovascular disease. The major risk factors for ED are in Table 14.1. Pathophysiology ED and can be broadly separated into psychogenic and organic eti- ologies (Box 14.1), with most having a functional organic disorder. Organic causes include vasculogenic (most common), neurogenic, Downloaded for ahmed eliwa ([email protected]) at Egyptian Knowledge 351 Bank from ClinicalKey.com by Elsevier on November 14, 2022. For personal use only. No other uses without permission. Copyright ©2022. Elsevier Inc. All rights reserved. 352 CHAPTER 14 Evaluation and Management of Sexual Dysfunction Table 14.1 Major Erectile Dysfunction Risk Factors MULTIVARIATE CONDITION ADJUSTED ODDS RATIO Diabetes mellitus 2.9 Hypertension 1.6 Cardiovascular disease 1.1 Hypercholesterolemia 1.0 Benign prostate enlargement 1.6 Obstructive urinary symptoms 2.2 Increased body mass index (.30 kg/m2) 1.5 Physical inactivity 1.5 Current cigarette smoking 1.6 Antidepressant use 9.1 Antihypertensive use 4.0 Data from Francis ME, Kusek JW, Nyberg LM, Eggers PW. The contribution of common medical conditions and drug exposures to erectile dysfunction in adult males. J Urol 2007;178:591-596; and Selvin E, Burnett AL, Platz EA. Prevalence and risk factors for erectile dysfunction in the US. Am J Med 2007;120:151-157. anatomic, and endocrinologic. The metabolic syndrome and its com- ponents cause impaired penile perfusion secondary to generalized atherosclerosis, subsequent increased vascular resistance, vascular tone, and fibrosis. These, in turn, lead to a decline in erectile function. ED can also be secondary to neuronal dysfunction. Because erec- tion is a neurovascular event, any disorder of the brain, spinal cord, or peripheral nerves can negatively impact erectile function. Similarly, iatrogenic damage to the cavernosal nerves and vasculature after radical pelvic surgery or after pelvic fracture may cause ED. Damage to the peripheral nervous system from diabetes mellitus can decrease erectile function. Endocrine disorders such as low serum testosterone, as well as hyperprolactinemia, hyperthyroidism, and hypothyroidism, levels often lead to decreases in erectile function and libido. Last, ED can be drug induced. Many antihypertensive medica- tions can lead to reversible ED, as seen in Table 14.2. Other drug classes correlated with ED include antipsychotics, antidepressants, recreational drugs, and more. Table 14.3 summarizes many of these medications and suggests possible alternatives. Clinical Manifestations ED manifests with marked difficulty in obtaining erections, maintaining them until completion of sexual activity, and/or a Downloaded for ahmed eliwa ([email protected]) at Egyptian Knowledge Bank from ClinicalKey.com by Elsevier on November 14, 2022. For personal use only. No other uses without permission. Copyright ©2022. Elsevier Inc. All rights reserved.  CHAPTER 14 Evaluation and Management of Sexual Dysfunction 353 Box 14.1 Classification of Male Erectile Dysfunction ORGANIC I. Vasculogenic A. Arteriogenic B. Cavernosal C. Mixed II. Neurogenic III. Anatomic IV. Endocrinologic V. Medication induced PSYCHOGENIC I. Generalized A. Generalized unresponsiveness 1. Primary lack of sexual arousability 2. Aging-related decline in sexual arousability B. Generalized inhibition 1. Chronic disorder of sexual intimacy II. Situational A. Partner related 1. Lack of arousability in specific relationship 2. Lack of arousability because of sexual object preference 3. High central inhibition because of partner conflict or threat B. Performance related 1. Associated with other sexual dysfunction (e.g., rapid ejac- ulation) 2. Situational performance anxiety (e.g., fear of failure) C. Psychological distress or adjustment related 1. Associated with negative mood state (e.g., depression) or major life stress (e.g., death of partner) significant decrease in erectile rigidity. Many men have a poor understanding of ED and its symptoms and may confuse ED with decreased libido or disorders of ejaculation. Diagnosis and Testing The diagnosis of ED differs from most urologic diagnoses in that extensive diagnostic procedures are generally not required. Therefore, the diagnosis can be made based on the patient’s re- port of consistent inability to attain and/or maintain an erection Downloaded for ahmed eliwa ([email protected]) at Egyptian Knowledge Bank from ClinicalKey.com by Elsevier on November 14, 2022. For personal use only. No other uses without permission. Copyright ©2022. Elsevier Inc. All rights reserved. 354 CHAPTER 14 Evaluation and Management of Sexual Dysfunction Table 14.2 Effect of Antihypertensive Agents on Sexual Function AGENT EFFECT MECHANISM Diuretics ED (twice as com- Unknown mon as placebo) b-Blocker ED Prejunctional a2-receptor (nonselective) inhibition a1-Blocker Decreases ED rate Failure of sympathetic- but may cause induced (1) closure of alteration of internal sphincter and ejaculation proximal urethra and (2) failure of seminal emission during ejaculation a2-Blocker ED Inhibition of central a2-receptor Angiotensin- Possible reduction converting enzyme in ED inhibitor Angiotensin II Possibly reduction receptor blocker in ED ED, Erectile dysfunction. sufficient for satisfactory sexual intercourse. Several well- validated questionnaires, such as the Index of Erectile Function (IIEF), are useful adjuncts to the patient’s history. The physical exam should focus on the neurologic, cardiovascular, and genital systems. Obvious physical signs of hypogonadism such as small testes or gynecomastia should be noted. (https://www. auanet.org/guidelines/guidelines/erectile-dysfunction-(ed)- guideline) Laboratory tests are not mandatory for diagnosis of ED but can help delineate the etiology. Recommended laboratory tests include serum chemistries, fasting glucose or hemoglobin A1c, complete blood count (CBC), lipid profile, and morning serum total testosterone. Further diagnostic testing such as intracavernosal injection of erectogenic medications with or without penile duplex ultrasonography (PDU) are used at the clinician’s discretion to better characterize the arterial or veno- occlusive mechanisms of ED. Downloaded for ahmed eliwa ([email protected]) at Egyptian Knowledge Bank from ClinicalKey.com by Elsevier on November 14, 2022. For personal use only. No other uses without permission. Copyright ©2022. Elsevier Inc. All rights reserved.  CHAPTER 14 Evaluation and Management of Sexual Dysfunction 355 Table 14.3 D  rug-Induced Erectile Dysfunction and Suggested Alternatives KNOWN TO CAUSE ERECTILE SUGGESTED CLASS DYSFUNCTION ALTERNATIVES Antihypertensives Thiazide diuretics Angiotensin- General b-blockers converting enzyme inhibitors Angiotensin II recep- tor antagonists Selective b-blockers a-Blockers Calcium channel blockers Psychotropics Antipsychotics Newer anxiolytics Antidepressants (bupropion, Anxiolytics buspirone) Antiandrogen Androgen receptor N/A antagonists Luteinizing hormone– releasing hormone agonists 5a-Reductase inhibitors Recreational Tobacco Tobacco cessation drugs Alcohol (large volume) Alcohol in moderate Treatment The most recent American Urological Association (AUA) guide- lines advocate that all therapeutic options for ED be offered, with any being a valid initial therapy. This demonstrates a shift from the traditional escalation from least to most invasive treatments. An algorithm for ED treatment pathways is seen in Fig. 14.1. Lifestyle modification is a primary treatment for ED. Weight loss, diet, exercise, and decrease in cigarette smoking can lead to meaningful improvements in ED. Switching or ceasing a causative medication can lead to significant improvement. The AUA guide- lines also propose a referral to a mental health professional to promote treatment adherence, reduce performance anxiety, and integrate treatments into a sexual relationship. Downloaded for ahmed eliwa ([email protected]) at Egyptian Knowledge Bank from ClinicalKey.com by Elsevier on November 14, 2022. For personal use only. No other uses without permission. Copyright ©2022. Elsevier Inc. All rights reserved. 356 CHAPTER 14 Evaluation and Management of Sexual Dysfunction COUNSEL THE MAN AND PARTNER REGARDING: - The value of psychosocial/relationship cessation) to improve erectile function support from trained professional to and overall health optimize treatment satisfaction - The benefits and risks/burdens of all - The importance of lifestyle change available ED treatments that are not (weight loss, exercise, smoking contraindicated Using a shared decision-making framework, identify appropriate treatmenta based on values and priorities of man and partner Vacuum Intraurethral Intracavernosal Penile prosthesis PDE5i devices (IU) alprostadil injections (ICI) surgery ASSESS OUTCOMES, ADVERSE EVENTS, AND SATISFACTION OF MAN AND PARTNER IF INADEQUATE EFFICACY AND/OR UNACCEPTABLE AEs AND/OR INSUFFICIENT SATISFACTION, THEN ADDRESS AS APPROPRIATE: - Dose adjustments (for PDE5i, IU partner with mental health professional alprostadil, ICI) to refine values and priorities and/or - Revisit instructions to maximize efficacy to address psychosocial or relationship (for all treatments) barriers to successful treatment - Revisit values and priorities of man and - Consider alternate treatment a For men with testosterone deficiency, defined as the presence of symptoms and signs and a total testosterone 36 hours priapism vs. delayed Document erectile function outcomes FIG. 14.2 ​Algorithm for managing ischemic priapism. BP, Blood pressure; ECG, electrocardiogram; HR, heart rate. Vital signs should be monitored because this can cause hypertension, reflex bradycardia, and cardiac arrhythmias. If the above fails, then the next step is creation of a distal corporoglanular shunt, as seen in Fig. 14.3. These include the Winter (large biopsy needle), Ebbehøj (scalpel), and Al-Ghorab (excision of tunica albuginea at the tip of Downloaded for ahmed eliwa ([email protected]) at Egyptian Knowledge Bank from ClinicalKey.com by Elsevier on November 14, 2022. For personal use only. No other uses without permission. Copyright ©2022. Elsevier Inc. All rights reserved.  CHAPTER 14 Evaluation and Management of Sexual Dysfunction 363 A B A B FIG. 14.3 ​(A) Winter shunt. The distal cavernoglanular shunt procedure is created by transglanular placement of a large-bore needle or angiocatheter into the distal glans and corpus cavernosum. (B) Corporal snake maneuver is a modification of the Al-Ghorab shunt. After excision of a 5-mm circular core of distal tunica albuginea, a 7/8 Hegar dilator is inserted down each corporal body through the tunica window.  (B, Copyright Brady Urological Institute. From Burnett AL, Pierorazio PM. Corporal “snake” maneuver: corporoglanular shunt surgical modification for ischemic priapism. J Sex Med 2009;6:1171-1176.) the corpus cavernosum). Proximal shunting using the Quackels or Grayhack procedures may be warranted if more-distal shunting pro- cedures have failed to relieve the priapism. Underlying SCD or blood dyscrasias should be treated concurrently with intracavernous therapy. The mainstay of treatment of nonischemic priapism is observa- tion because many resolve spontaneously. Corporal aspiration has only a diagnostic role. Selective arterial embolization is a treatment option if needed. Surgical management of nonischemic priapism is a last resort and should be performed with intraoperative PDU. Treatment of stuttering priapism is focused on prevention. Systemic therapy with a-adrenergic agonists, PDE5i, terbutaline, digoxin, gonadotropin-releasing hormone, and antiandrogens or self-ICI of phenylephrine can be utilized. DISORDERS OF MALE ORGASM AND EJACULATION Epidemiology Ejaculatory dysfunction (EjD) ranges from premature ejaculation (PE), to delayed ejaculation (DE), to a complete inability to ejaculate. The 2020 AUA PE guidelines (https://www.auanet.org/guidelines/ guidelines/disorders-of-ejaculation) define lifelong PE as poor Downloaded for ahmed eliwa ([email protected]) at Egyptian Knowledge Bank from ClinicalKey.com by Elsevier on November 14, 2022. For personal use only. No other uses without permission. Copyright ©2022. Elsevier Inc. All rights reserved. 364 CHAPTER 14 Evaluation and Management of Sexual Dysfunction ejaculatory control, associated bother, and ejaculation within ,2 minutes of initiation of penetrative sex. Interestingly, although abnormal intravaginal latency times (IVLT) affect only 2.5% of the general male population, a much higher number report having the disorder. The prevalence (20%–30%) varies widely. The prevalence of DE is less clear, with studies suggesting that up to 40% of men are impacted and worsening with age. Retrograde ejaculation (RE) primarily develops after surgical bladder outlet procedures for lower urinary tract symptoms (LUTS). Another common cause of DE is the use or abrupt cessation of selective sero- tonin reuptake inhibitors (SSRIs). Five to 15% of men using SSRIs will have sexual dysfunction, sometimes following the first dose. Other rare disorders of orgasm and ejaculation include orgasmic headache, painful ejaculation, and post orgasmic illness syndrome. Although these are rare, painful ejaculation can occur in up to 25% of men with benign prostatic hypertrophy (BPH)/LUTS. Pathophysiology EjD can be acquired or lifelong, with the latter being secondary to neurobiological and genetic variations. Acquired sexual dys- function is usually secondary to sexual performance anxiety and/or relationship problems. Almost half of all men with ED also complain of PE, likely secondary to “rushing” sex to avoid premature detumescence. DE or absent ejaculation has a wide variety of possible etiologies (Table 14.6). Clinical Manifestations EjD has variable presentations. PE is the most common, in which men have a recurrent pattern of ejaculation within 2 minutes of vaginal penetration that is bothersome to the patient and part- ner. This can either be lifelong or acquired. DE (usually after ,25–30 minutes), anejaculation, and anorgasmia constitute the other end of the spectrum. RE commonly presents after surgical procedures that compromise the bladder neck, such as transure- thral resection of the prostate (TURP). Diagnosis and Testing Lifelong PE is present since the patient’s first sexual experience, whereas, in acquired PE, patients experience IVLT that is markedly reduced from prior sexual encounters. A significant amount of men Downloaded for ahmed eliwa ([email protected]) at Egyptian Knowledge Bank from ClinicalKey.com by Elsevier on November 14, 2022. For personal use only. No other uses without permission. Copyright ©2022. Elsevier Inc. All rights reserved.  CHAPTER 14 Evaluation and Management of Sexual Dysfunction 365 Table 14.6 C  auses of Retrograde Ejaculation, Delayed Ejaculation, Anejaculation, and Anorgasmia Aging man Degeneration of penile afferent nerves Psychogenic Inhibited ejaculation Congenital Müllerian duct cyst Wolffian duct abnormality Prune belly syndrome Anatomic causes Transurethral resection of prostate Bladder neck incision Neurogenic causes Diabetic autonomic neuropathy Multiple sclerosis Spinal cord injury Radical prostatectomy Proctocolectomy Bilateral sympathectomy Abdominal aortic aneurysmectomy Para-aortic lymphadenectomy Infective Urethritis Genitourinary tuberculosis Schistosomiasis Endocrine Hypogonadism Hypothyroidism Medication a-Methyldopa Thiazide diuretics Tricyclic and SSRI antidepressants Phenothiazine Alcohol abuse SSRI, Selective serotonin reuptake inhibitor. who self-report PE fail to satisfy these criteria. Standardized ques- tionnaires can be used as an adjunct to a full history in diagnosis, especially to evaluate for the commonly concurrent presence of ED. Physical exam and labs are of limited utility. All other forms of EjD are similarly diagnosed by history and physical exam. RE may be confirmed by obtaining a postejaculation urine sample for presence of sperm. Other testing should be used as clinically indicated but may be of limited utility. Treatment All men with PE should receive basic psychosexual education or coaching, which is often used in conjunction with pharmaco- logic therapy (Fig. 14.4). First-line medical treatment includes Downloaded for ahmed eliwa ([email protected]) at Egyptian Knowledge Bank from ClinicalKey.com by Elsevier on November 14, 2022. For personal use only. No other uses without permission. Copyright ©2022. Elsevier Inc. All rights reserved.  PE-LIKE Bank from ClinicalKey.com by Elsevier on November 14, 2022. For personal use only. Downloaded for ahmed eliwa ([email protected]) at Egyptian Knowledge 366 CHAPTER 14 Evaluation and Management of Sexual Dysfunction No other uses without permission. Copyright ©2022. Elsevier Inc. All rights reserved. ejactulation Treatment dysfunction Reassurance Patient/partner history No Education Natural Behavioral therapy Yes variable PE Premature ejaculation (PE) Yes Manage primary Yes PE secondary to ED or other sexual dysfunction cause No Acquired PE Lifelong PE Treatment Treatment Behavioral therapy Patient SSRI pharmacotherapy SSRI pharmacotherapy preference Behavioral therapy Combination treatment Combination treatment Attempt graduated withdrawal of drug therapy after 6–8 weeks FIG. 14.4 ​Algorithm for the office management of premature ejaculation. ED, Erectile dysfunction; SSRI, selective serotonin reuptake inhibitor.  CHAPTER 14 Evaluation and Management of Sexual Dysfunction 367 daily SSRIs, on-demand dapoxetine or clomipramine, and topi- cal penile anesthetics. On-demand medications are available but allow for less sexual spontaneity. Tramadol can be recom- mended if the patient has failed first-line therapy. A full list of possible pharmacologic treatments of PE is in Table 14.7. Lastly, ED is commonly associated with PE and should be treated first. Any surgical options for PE are considered experimental. Delayed or absent ejaculation is also treated with psycho- sexual therapy, but pharmacotherapy has very limited success. Table 14.7 in the AUA guidelines on PE lists many medications that may lead to delayed ejaculation and can lead to improvement after cessation. ED should be treated concurrently. Treatment algorithms for DE are in Fig. 14.5. RE has proven difficult to treat, but case reports have shown success with pseudoephedrine and its analogues, tricyclic antidepressants, and bladder neck reconstruction. PEYRONIE DISEASE Epidemiology Peyronie disease (PD), or an abnormal curvature of the penis, is affects 3%–20% of all men. The peak age of onset is in the early 50s. The incidence of symptomatic PD appears to be increasing, likely due to increased awareness and medical visits for ED medications. Pathophysiology PD is currently thought to be a wound-healing disorder of the tunica albuginea that results in contractile scar tissue and resul- tant penile deformity (Fig. 14.6). Unfortunately, the scars in PD do not undergo normal wound healing and thus do not resolve spontaneously. PD appears to go through an active phase during which the scar can grow, resulting in progressive deformity and pain. How- ever, once PD has stabilized (chronic phase), there is usually no further progression. The exact cause has yet to be fully elucidated, but it is thought it may be due to penile trauma or repeated micro- trauma. Genetic predisposition, autoimmune factors, and aberrant wound healing may also contribute. 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Table 14.7 Drug Therapy for Premature Ejaculation (PE) DRUG DOSE DOSING INSTRUCTIONS INDICATION COMMENTS LEVEL OF EVIDENCE Dapoxetine 30–60 mg On demand, 1–3 hours Lifelong PE Approved in.50 High before intercourse Acquired PE countries Paroxetine 10–40 mg Once daily Lifelong PE High Acquired PE Sertraline 50–200 mg Once daily Lifelong PE High Acquired PE Fluoxetine 20–40 mg Once daily Lifelong PE High Acquired PE Citalopram 20–40 mg Once daily Lifelong PE High Acquired PE Clomipramine 12.5–50 mg Once daily Lifelong PE High Acquired PE 12.5–50 mg On demand, 3–4 hours Lifelong PE High before intercourse Acquired PE Tramadol 25–50 mg On demand, 3–4 hours Lifelong PE Potential risk of Low before intercourse Acquired PE opiate addiction Topical lignocaine/ Patient titrated On demand, 20–30 minutes Lifelong PE High prilocaine before intercourse Acquired PE Bank from ClinicalKey.com by Elsevier on November 14, 2022. For personal use only. 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Alprostadil 5–20 mcg Patient administered Lifelong PE Risk of priapism and Very Low intracavernosal injection 5 Acquired PE corporal fibrosis CHAPTER 14 Evaluation and Management of Sexual Dysfunction 369 minutes before intercourse PDE5 inhibitors Sildenafil 25–100 mg On demand, 30–50 minutes Lifelong and Low Tadalafil 10–20 mg before intercourse acquired PE in Vardenafil 10–20 mg men with Avanafil 50–200 mg normal erectile function Lifelong and Improved efficacy if Moderate acquired PE in combined with men with ED SSRI ED, Erectile dysfunction; PDE5, phosphodiesterase type 5; SSRI, selective serotonin reuptake inhibitor. 370 CHAPTER 14 Evaluation and Management of Sexual Dysfunction Delayed ejaculation Failure of emission Anejaculation Neurogenic Anorgasmia Metabolic Drug adverse effect Disease-specific management Never Inhibited male orgasm Psychosexual therapy Inhibited male orgasm Nocturnal/masturbation emissions Is there orgasm? Sometimes Psychosexual therapy Age-related degeneration Reassure/alter sexual technique Always Is there ejaculation? Yes No Are sperm present in urine after orgasm? No Yes Aspermia Retrograde Ejaculatory duct ejaculation obstruction Reassure/educate Pharmacotherapy Surgery FIG. 14.5 ​Algorithm for the office management of delayed ejaculation. A B FIG 14.6 The dot procedure employs no incision. The tunica albuginea is pli- cated with permanent suture using an extended Lembert-type suture placement following four dots per plication. (A) Suture placement for dorsal curve. (B) Suture placement for ventral curve. Downloaded for ahmed eliwa ([email protected]) at Egyptian Knowledge Bank from ClinicalKey.com by Elsevier on November 14, 2022. For personal use only. No other uses without permission. Copyright ©2022. Elsevier Inc. All rights reserved.  CHAPTER 14 Evaluation and Management of Sexual Dysfunction 371 Clinical Manifestations PD usually presents as a gradually worsening penile curvature (typically dorsal), pain with intercourse, and resultant emotional distress. Other common deformities include indentation, hinge effect, or shortening. There is usually an acute phase, lasting 6–18 months with painful erections and worsening deformity, followed by a chronic phase when the plaque stabilizes and pain resolves. Concomitant ED is present in about one third of PD cases. Diagnosis and Testing Although a thorough history is essential for the diagnosis of PD, the physical exam is the most crucial component. (https://www. auanet.org/guidelines/guidelines/peyronies-disease-guideline). To assess for PD, the flaccid penis should be evaluated on stretch to document stretched length and presence of a penile plaque. More important is an evaluation of the erect penis. Per the AUA guide- lines, physicians should perform an in-office ICI erectogenic test with or without PDU to assess for plaque location, size, and char- acteristics as well as degree of curvature or deformity prior to consideration of any form of invasive treatment. Treatment Treatment of PD is predominantly via intralesional injectable (ILI) or surgical therapy. Many oral and topical therapies have been studied, but none has proven effective, and they are thus not recommended. Risks, benefits, and expectations should be outlined. The only ILI therapy approved by the Food and Drug Adminis- tration (FDA) for PD is collagenase clostridium histolyticum (CCH), which degrades the collagen in aberrant PD plaques. CCH is indicated for patients with stable disease, curvature.30 degrees, and intact erectile function. It is administered as serial treatments and often combined with manual modeling (bending of the penis opposite to the site of curvature). Average reduction in curvature is ,35%. Common adverse events include penile ecchymosis, swelling, and pain, with the rare occurrence of corporal rupture. Off-label ILI medications for PD include interferon a-2b or vera- pamil. The patient should be counseled on the potential adverse effects of each off-label treatment. ESWT may improve penile pain but not curvature. Downloaded for ahmed eliwa ([email protected]) at Egyptian Knowledge Bank from ClinicalKey.com by Elsevier on November 14, 2022. For personal use only. No other uses without permission. Copyright ©2022. Elsevier Inc. All rights reserved. 372 CHAPTER 14 Evaluation and Management of Sexual Dysfunction Surgical intervention remains the gold standard for the treat- ment of stable PD. The goal is to make the penis “functionally straight,” generally regarded as #20 degrees of curvature. Choos- ing the correct surgical intervention depends on the degree of deformity. In a penis with curvature ,70 degrees with intact erectile function, tunical plication is recommended. This in- volves shortening of the longer (convex) side of the penis to match the shorter side (Fig. 14.6). It often causes penile shorten- ing. A plaque excision with or without grafting is recommended in men with more complex curvatures or curvatures.70 degrees. Of note, both of these therapies require men to have erectile rigidity adequate for coitus. In men with PD and ED refractory to medical therapy, IPP placement is an effective treatment for both. If deformity exists after IPP placement and manual model- ing, the practitioner can consider additional plication sutures and/or plaque incision and grafting. Several alternative treat- ments exist but lack the clinical evidence for recommendation (Table 14.8). SEXUAL DYSFUNCTION IN FEMALES Epidemiology Female sexual dysfunction (FSD) can take many forms (Table 14.9). Although data are limited, 5.8% of women report symptoms consistent with FSD. Prevalence may be higher, with one study demonstrating that.33% of women reported a new sexual disor- der within the previous 12 months. Hypoactive sexual desire was the most prevalent sexual complaint (21.4%), followed by prob- lems in arousal (11.4%), satisfaction (10.4%), orgasm (8.8%), and lubrication (8.7%). Decreased sexual desire is 20% in women younger than 25 years of age and approaches 70%–80% in women 55–74 years of age. Pathophysiology The pathophysiology of FSD is highly complex and must be consid- ered in a biopsychosocial context. Biologic factors such as common comorbidities and their treatment modalities (e.g., antihyperten- sives) have been associated with FSD (Table 14.10). Pregnancy, breastfeeding, and a postmenopausal state are often associated with decreased libido. Aging is also known to contribute to FSD because Downloaded for ahmed eliwa ([email protected]) at Egyptian Knowledge Bank from ClinicalKey.com by Elsevier on November 14, 2022. For personal use only. No other uses without permission. Copyright ©2022. Elsevier Inc. All rights reserved.  Table 14.8 External Force Application for Peyronie Disease Bank from ClinicalKey.com by Elsevier on November 14, 2022. For personal use only. Downloaded for ahmed eliwa ([email protected]) at Egyptian Knowledge No other uses without permission. Copyright ©2022. Elsevier Inc. All rights reserved. TREATMENT MECHANISM OF ACTION STUDY OUTCOMES ADVERSE EFFECTS Electromotive Bypasses hepatic metabolism, increases Verapamil alone: no benefit Temporary erythema at the CHAPTER 14 Evaluation and Management of Sexual Dysfunction 373 drug adminis- concentration of drug to target tissues Verapamil 1 dexamethasone: decreases electrode site tration compared with topical application alone in plaque volume and penile curvature from 43 to 21 degrees Extracorporeal Direct damage to the penile plaque; Improvements in pain, IIEF-5 score, Local petechiae and shock wave increases vascularity of the targeted area, and mean QoL score; no curvature ecchymoses therapy inducing an inflammatory reaction, reduction resulting in lysis of the plaque and removal by macrophages Penile traction Decreases a-smooth muscle actin; Length increased 0.5–2.0 cm; girth Erythema in the increases matrix metalloproteinases increased 0.5–1.0 cm; curvature balanopreputial sulcus, involved in collagen degradation mean decrease of 20 degrees; pain discomfort decreased; softening or shrinking of plaque; overall satisfaction, 85% Vacuum therapy Unknown; mechanical effects similar to Reduction in angle of curvature by Development of PD, traction have been suggested 5–25 degrees in 21 of 31 patients urethral bleeding, skin necrosis, and penile ecchymosis Radiation Antiinflammatory effects via functional No clinical benefit Possible malignant change, therapy modulation of the adhesion of white increased risk for ED in blood cells to activated endothelial cells older patients and modulation of the induction of nitric oxide synthase in activated macrophages ED, Erectile dysfunction; IIEF, International Index of Erectile Function; PD, Peyronie disease; QoL, quality of life. 374 CHAPTER 14 Evaluation and Management of Sexual Dysfunction Table 14.9 Definitions of Female Sexual Dysfunction DSM-IV-TR DSM-5 Female Sexual Interest Sexual Desire Disorders or Arousal Disorder Hypoactive sexual desire disorder: Lack of or significantly reduced Deficiency or absence of sexual sexual interest or arousal as fantasies and desire for sexual manifested by three of the activity following: Sexual aversion disorder: Aversion 1. Absent or reduced interest in to and active avoidance of sexual activity genital sexual contact with a 2. Absent or reduced sexual or sexual partner erotic thoughts or fantasies 3. No or reduced initiation of Sexual Arousal Disorders sexual activity and unreceptive Female sexual arousal disorder: to partner’s attempts to initiate Persistent or recurrent inability 4. Absent or reduced sexual to attain or to maintain until excitement or pleasure during completion of the sexual sexual activity in almost all or activity, an adequate lubrication- all (75%–100%) sexual swelling response, or sexual encounters excitement 5. Absent or reduced sexual interest or arousal in response to any internal or external sexual or erotic cues (written, verbal, or visual) 6. Absent or reduced genital or nongenital sensations during sexual activity in almost all or all (75%–100%) sexual encounters Orgasmic Disorder Female Orgasmic Disorder Female orgasmic disorder: Presence of either of the following Persistent or recurrent delay in, on all or almost all (75%–100%) or absence of, orgasm after occasions of sexual activity: normal sexual excitement 1. Marked delay in, marked infrequency of, or absence of orgasm 2. Markedly reduced intensity of orgasmic sensations Downloaded for ahmed eliwa ([email protected]) at Egyptian Knowledge Bank from ClinicalKey.com by Elsevier on November 14, 2022. For personal use only. No other uses without permission. Copyright ©2022. Elsevier Inc. All rights reserved.  CHAPTER 14 Evaluation and Management of Sexual Dysfunction 375 Table 14.9 Definitions of Female Sexual Dysfunction—cont’d DSM-IV-TR DSM-5 Genitopelvic Pain Sexual Pain Disorders or Penetration Disorder Dyspareunia: Genital pain that is Persistent or recurrent difficulties associated with sexual inter- with one or more of the following: course 1. Vaginal penetration during Vaginismus: Recurrent or intercourse persistent involuntary 2. Marked vulvovaginal or pelvic contraction of the perineal pain during intercourse or muscles surrounding the outer penetration attempts third of the vagina when vaginal 3. Marked fear or anxiety about penetration with a penis, finger, vulvovaginal or pelvic pain in tampon, or speculum is anticipation of, during, or attempted because of vaginal penetration 4. Marked tensing or tightening of pelvic floor muscles during attempted vaginal penetration Table 14.10 M  edical Conditions That Can Affect Female Sexual Function POSSIBLE IMPACT ON FEMALE MEDICAL CONDITION SEXUAL FUNCTION Coronary artery disease May affect pelvic perfusion, arousal disorder Dermatologic conditions (e.g., lichen Genital pain, problems with sclerosus, lichen planus, eczema) lubrication Diabetes mellitus Low desire Hypertension Low desire Hypothyroidism Problems with lubrication and orgasm Malignancy and its treatment (breast, Problems with desire, arousal, anal, colorectal, bladder, orgasm, and genital pain gynecologic) Neuromuscular disorders, spinal cord Problems with desire, arousal, injury, multiple sclerosis orgasm, and genital pain Parkinson disease, dementia Low desire Urinary incontinence Desire, arousal, and pain domains can be affected Modified from Faubion SS, Rullo JE. Sexual dysfunction in women: a practical approach. Am Fam Physician 2015;92(4):281-288. 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All rights reserved. 376 CHAPTER 14 Evaluation and Management of Sexual Dysfunction Table 14.11 C  lasses and Examples of Medications That Might Be Associated With Low Sexual Desire Anticonvulsants Carbamazepine Phenytoin Primidone Cardiovascular Angiotensin-converting enzyme inhibitors medications Amiodarone b-blockers (atenolol, metoprolol, propranolol) Calcium channel blockers Clonidine Digoxin Diuretics (hydrochlorothiazide, spironolactone) Lipid-lowering agents Hormones Antiandrogens (flutamide) Gonadotropin-releasing hormone agonists Oral contraceptives Analgesics Nonsteroidal antiinflammatory drugs Opiates Psychotropic medi- Antipsychotics cations Anxiolytics (alprazolam, diazepam) Selective serotonin reuptake inhibitors Serotonin norepinephrine reuptake inhibitors Tricyclic antidepressants Illicit drugs Amphetamine Cocaine Heroin Marijuana Others Histamine receptor antagonists Alcohol Indomethacin Ketoconazole Chemotherapeutic agents Modified from Clayton AH, Kingsberg SA, Goldstein I. Evaluation and management of hypoactive sexual desire disorder. Sex Med 2018;6(2):59-74. levels of estrogen and testosterone decline. Many medications can be associated with FSD (Table 14.11). From a psychosocial perspective, it is well known that psychi- atric disorders and their treatments (e.g., SSRIs) can lead to FSD. Sexual abuse and trauma in childhood, as well as problems with body image, are also common contributors. External factors such as religion, culture, relationship factors, career stress, and financial stress can also worsen FSD. Downloaded for ahmed eliwa ([email protected]) at Egyptian Knowledge Bank from ClinicalKey.com by Elsevier on November 14, 2022. For personal use only. No other uses without permission. Copyright ©2022. Elsevier Inc. All rights reserved.  CHAPTER 14 Evaluation and Management of Sexual Dysfunction 377 Clinical Manifestations The most common manifestation of FSD is low desire, followed by low arousal and orgasmic dysfunction. In female sexual interest-arousal disorder (FSID), women present with absent or decreased desire, fantasizing, excitement, and/or pleasure. With female orgasmic disorders, desire may be present, but the patient has absent, delayed, or weak orgasms. The third classifi- cation is genitopelvic pain-penetration disorder, in which there is significant difficulty, distress, and/or pain in achieving or maintaining vaginal penetration. Diagnosis and Testing The main barrier to the proper diagnosis of FSD is that ,20% of women with sexual issues will seek medical treatment, likely secondary to sociocultural barriers. Assessment is best ap- proached by addressing biologic, psychological, sociocultural, and interpersonal factors (Table 14.12). In addition to a thorough Table 14.12 B  iopsychosocial Model of Assessing Sexual (Dys)Function Biologic factors Medications Hormonal status Neurobiology Physical health Aging Psychological factors Depression Anxiety Self-image Substance abuse History of sexual abuse, trauma Sociocultural factors Upbringing Cultural norms and expectations Religious influences Interpersonal factors Relationship status or quality Partner’s sexual function Life stressors Modified from Bitzer J, Giraldi A, Pfaus J. Sexual desire and hypoactive sexual desire disorder in women. Introduction and overview. Standard operating procedure (SOP Part 1). J Sex Med 2013;10(1):36-49; Fugl-Meyer KS, Bohm-Starke N, Damsted Petersen C, et al. Standard operating procedures for female genital sexual pain. J Sex Med 2013;10(1):83-93; Latif EZ, Diamond MP. Arriving at the diagnosis of female sexual dysfunction. Fertil Steril 2013;100(4):898-904. Downloaded for ahmed eliwa ([email protected]) at Egyptian Knowledge Bank from ClinicalKey.com by Elsevier on November 14, 2022. For personal use only. No other uses without permission. Copyright ©2022. Elsevier Inc. All rights reserved. 378 CHAPTER 14 Evaluation and Management of Sexual Dysfunction medical and sexual history, all female patients, regardless of age, should be screened for sexual dysfunction using one of many well-validated questionnaires. Additionally, a history of the sexual partner is often helpful. A thorough physical examination of in- ternal and external pelvic organs must accompany the history. Laboratory testing is rarely indicated. Treatment The treatment of FSD is focused on the psychosocial aspect, with medications available as an adjunct. Addressing modifiable factors such as disease states, medications, and relationships can have a large impact. There are two FDA-approved treatment options for FSID. Flibanserin (Addyi) is taken daily and can increase sexual desire by ,50%. The second option is bremelanotide (Vyleesi), which is ad- ministered intramuscularly 45 minutes before sexual intercourse. Estrogen replacement therapy can reduce many of the symptoms associated with sexual dysfunction, and testosterone therapy can increase desire and satisfaction. A treatment algorithm for FSID is in Fig. 14.7. Female orgasmic disorder (FOD) without sufficient arousal often requires patient and partner psychotherapy with sexual edu- cation. Like FSID, FOD is responsive to hormonal therapy with estrogen or testosterone. If patients have sufficient arousal, on- demand oxytocin can improve rates of orgasm. Female sexual arousal disorder (FSAD) is best treated with hormones, but success has also been noted with the use of PDE5i, prostaglandins, and other medications. Treatment of female per- sistent genital arousal disorder with duloxetine, pregabalin, and varenicline has limited success. Genitopelvic pain and penetration disorder treatments include biofeedback, vaginal dilation, and, in refractory cases, vestibulectomy. Last, almost half of women with LUTS and/or prolapse report some form of sexual dysfunction, and treatment of the underlying disease can lead to significant sexual improvement. Downloaded for ahmed eliwa ([email protected]) at Egyptian Knowledge Bank from ClinicalKey.com by Elsevier on November 14, 2022. For personal use only. No other uses without permission. Copyright ©2022. Elsevier Inc. All rights reserved.  CHAPTER 14 Evaluation and Management of Sexual Dysfunction 379 Routinely screen women for HSDD: direct questioning and/or decreased sexual desire screener If findings are suggestive of HSDD (low desire and associated distress) Further evaluation: sexual history, medical history, psychosocial history, focused physical exam Refer for psychological If HSDD is generalized, intervention if low desire is acquired (i.e., not lifelong), situational and refractory to and not due exclusively to office-based counseling or another medical condition for significant psychiatric or the direct physiological conditions or unresolved effect of a medication or issues related to sexual drug of abuse, consider trauma or abuse pharmacotherapy FDA approved: Currently available flibanserin but off label: transdermal testosterone bupropion Evaluate treatment outcomes (desire, distress, QoL) and continue or adjust treatment accordingly FIG. 14.7 ​Treatment algorithm for hypoactive sexual desire disorder. (Data from Clayton AH, Kingsberg SA, Goldstein I. Evaluation and management of hypoactive sexual desire disorder. Sex Med 2018b;6:59-74.) Downloaded for ahmed eliwa ([email protected]) at Egyptian Knowledge Bank from ClinicalKey.com by Elsevier on November 14, 2022. For personal use only. No other uses without permission. Copyright ©2022. Elsevier Inc. All rights reserved.