Cover
Title Page
List of contributors
Foreword
CHAPTER 1: Epidemiology of male sexual dysfunction
1. Erectile dysfunction
2. Premature ejaculation
3. Peyronie’s disease
4. Hypogonadism
5. References
CHAPTER 2: Physiology of ejaculation
1. Introduction
2. The spinal cord and the brain of male rats
3. Peripheral nerves and ejaculation
4. Emission and the autonomic nervous system
5. Expulsion and the somatic nervous system
6. The central nervous system and ejaculation
7. Orgasm
8. References
CHAPTER 3: Physiology of penile erection
1. Functional anatomy
2. Hemodynamics of penile erection and detumescence
3. Neurophysiology of erections
4. Smooth muscle physiology
5. Summary
6. Further reading
CHAPTER 4: Anatomy of penile erection
1. Introduction
2. Penile anatomy
3. Neuroanatomy of penile erection
4. Hemodynamics and physiology of male erection
5. Molecular mechanisms of penile erection
6. Conclusions
7. References
CHAPTER 5: Endocrinology of male sexual dysfunction
1. Introduction
2. Central organization of sexual function
3. The kisspeptin‐GPR54‐neurokinin B pathway and regulation of GnRH release
4. Effect of gonadotropins at testicular level
5. Testosterone action in male sexual function
6. Endocrine disorders
7. Late‐onset hypogonadism
8. Treatment of sexual dysfunction associated with endocrinopathy
9. References
CHAPTER 6: Pharmacology of drugs used for the treatment of erectile dysfunction
1. Introduction
2. Oral agents
3. Intracavernosal agents
4. Other agents
5. Summary
6. References
CHAPTER 7: Pharmacology of drugs used in premature ejaculation
1. “Selective” neurotransmitter reuptake inhibitors
2. Use of locally active agents
3. Other potential “broad spectrum” approaches
4. Coming next?
5. Summary
6. References
CHAPTER 8: Cardiovascular risk and erectile dysfunction
1. Erectile dysfunction and cardiovascular disease: examining the link
2. The temporal relationship
3. Prediction of CVD events and mortality
4. Methods of evaluating the risk
5. Conclusion
6. A final thought…
7. References
CHAPTER 9: The evaluation of the patient with erectile dysfunction
1. Introduction
2. Sexual history
3. The physical examination
4. Questionnaires
5. Current guidelines
6. Laboratory investigations in the man presenting with ED: the key role of the GP
7. Specialist investigations
8. Penile abnormalities
9. Patient/partner education – consultation and referrals
10. Indications for secondary referral
11. Problems associated with prescribed drugs
12. The role of lifestyle modification
13. Current prescribing issues in ED
14. The role of testosterone replacement in ED
15. Conclusion
16. References
CHAPTER 10: Endocrinological investigation of men with erectile dysfunction
1. Introduction
2. Hypogonadism
3. Prolactin
4. Thyroid hormones
5. Other hormones
6. Obesity
7. Type 2 diabetes mellitus
8. Conclusion
9. References
CHAPTER 11: Duplex ultrasonography and its role in the assessment of male sexual dysfunction
1. Introduction
2. Uses of penile Doppler
3. Penile ultrasonographic anatomy
4. Standard operating technique
5. How to scan
6. Findings
7. References
CHAPTER 12: MRI in men with sexual dysfunction
1. Introduction
2. Scanning protocol and radiological anatomy
3. Penile fracture
4. Priapism
5. Fibrosis and Peyronie’s disease
6. Penile implants
7. Other conditions
8. References
CHAPTER 13: The metabolic syndrome and ED
1. Introduction
2. The metabolic syndrome: a cluster of findings increasing the risk of type 2 DM and CVD: its relationship to ED
3. Novel biomarkers (metabolic and imaging) to clarify CVS risk in the ED patient
4. Conclusion
5. References
CHAPTER 14: Psychological assessment of patients with ED
1. Introduction
2. Psychosocial impact of ED
3. Psychological assessment of patients with ED
4. Making referrals
5. Questionnaires
6. References
CHAPTER 15: Nocturnal penile tumescence study
1. Introduction
2. Investigation
3. Conclusion
4. References
CHAPTER 16: Psychosexual therapy for male sexual dysfunction
1. Introduction
2. Psychosexual therapy
3. Treatments
4. Erectile dysfunction: case examples using sex therapy techniques
5. Ejaculatory dysfunction
6. PLISSIT: a sexuality assessment and intervention tool
7. Conclusion
8. References
CHAPTER 17: Treatment of premature ejaculation and ejaculatory disorders
1. Introduction
2. Definition of premature ejaculation
3. Epidemiology and etiology of premature ejaculation
4. Treatment of premature ejaculation
5. Anejaculation
6. Delayed ejaculation
7. Retrograde ejaculation
8. Painful ejaculation
9. References
CHAPTER 18: Erectile dysfunction and infertility
1. Differences and common links between male infertility and erectile dysfunction
2. The impact of infertility on erectile dysfunction
3. Overview of the evaluation of erectile dysfunction
4. Treatment considerations for erectile dysfunction
5. Erectile dysfunction treatment for infertile men
6. Conclusion
7. References
CHAPTER 19: Drug therapy for erectile dysfunction
1. General approach to drug therapy
2. Pharmacological therapies
3. Intracavernosal injection therapy
4. Intraurethral therapy
5. Topical therapies
6. Future therapies for erectile dysfunction
7. Conclusion
8. References
CHAPTER 20: Priapism
1. Epidemiology and pathophysiology of priapism
2. Clinical assessment of the patient with priapism
3. Management of priapism
4. Conclusions
5. References
CHAPTER 21: Management of erectile dysfunction after pelvic surgery
1. Introduction
2. Mechanisms of erectile dysfunction
3. Treatment of erectile dysfunction
4. Conclusion
5. References
CHAPTER 22: Management of erectile dysfunction in men with diabetes
1. Introduction
2. Pathophysiology
3. Assessment and investigation
4. Treatment
5. Conclusion
6. References
CHAPTER 23: Management of erectile dysfunction in neurological patients
1. Neurological disorders and sexual dysfunction
2. Management of ED in the neurological patient
3. Conclusion
4. Acknowlegdements
5. References
CHAPTER 24: Non‐surgical therapy for Peyronie’s disease
1. Oral therapies in Peyronie’s disease
2. Topical agents
3. Injectable agents
4. Mechanical devices
5. Conclusion
6. References
CHAPTER 25: Micropenis and penile dysmorphobia: diagnosis, management, outcomes, and future developments in the field
1. Introduction
2. Causes of micropenis
3. Congenital micropenis
4. Assessment
5. Acquired micropenis
6. Treating micropenis
7. Techniques for the future
8. Penile dysmorphobia
9. References
CHAPTER 26: Surgical treatment of Peyronie’s disease
1. Introduction
2. Etiology and pathogenesis
3. Course of the disease
4. Diagnosis and evaluation
5. Medical treatment
6. Surgical treatment
7. Conclusion
8. References
CHAPTER 27: Penile implant surgery
1. Introduction
2. Indications
3. Types of prostheses
4. Preoperative counseling and surgical planning
5. Surgical technique
6. Complications
7. Outcomes
8. Conclusion
9. References
CHAPTER 28: Vascular surgery for erectile dysfunction
1. Introduction
2. Penile vascular anatomy
3. Arterial revascularization
4. Surgery for corporal veno‐occlusive dysfunction (CVOD)
5. Endovascular techniques
6. Conclusion
7. References
CHAPTER 29: Penile cancer
1. Introduction
2. Penile preserving surgery (PPS)
3. Carcinoma in situ (Tis) and non‐invasive verrucous carcinoma (Ta)
4. Tumor invading the subepithelium (T1) or corpus spongiosum (T2)
5. Tumor invading the corpus cavernosum (T2) or the urethra (T3)
6. Tumor invading adjacent structures (T4)
7. Summary
8. References
CHAPTER 30: Penile reconstruction and trauma
1. Introduction
2. Surgical principles
3. Skin grafting
4. Glans resurfacing of the penis
5. Male genital lichen sclerosus (LS)/balanitis xerotica obliterans (BXO)
6. Technique of glans resurfacing and SSG
7. Buried penis
8. Male genital lymphedema
9. Peyronie’s disease
10. Reconstruction following trauma
11. Summary
12. References
CHAPTER 31: Disorders of sex development
1. Introduction
2. Gonadal dysgenesis
3. Failure of androgen synthesis or receptors
4. Anti‐müllerian syndrome
5. Other anatomical disorders
6. Testicular regression syndromes
7. Other chromosomal anomalies
8. References
CHAPTER 32: Sexual dysfunction and prostate cancer therapy
1. Introduction
2. Sexual dysfunction
3. Preoperative sexual function and treatment – can outcome be predicted?
4. Radical prostatectomy
5. Penile rehabilitation after radical prostatectomy
6. Radiotherapy and brachytherapy
7. Androgen deprivation therapy (ADT)
8. Active surveillance
9. Ablative therapy
10. Conclusion
11. References
CHAPTER 33: Assessment and management of the male to female transgender patient
1. Background
2. Legislation and guidelines
3. The UK pathway
4. Male‐to‐female genital reconstructive surgery
5. Surgical complications
6. Non‐genital surgery
7. Follow‐up and patient satisfaction
8. References
Index
End User License Agreement

List of Tables

Chapter 05
1. Table 5.1 Classification of disorders that may be associated with endocrine and sexual dysfunction.
2. Table 5.2 Conditions associated with alterations in sex hormone‐binding globulin (SHBG) concentrations.
Chapter 06
1. Table 6.1 Affinity and selectivity of the phosphodiesterase type 5 (PDE5) inhibitors.
2. Table 6.2 Tissue distribution of the phosphodiesterase enzymes.
3. Table 6.3 Pharmacokinetics of the PDE5 inhibitors.
Chapter 08
1. Table 8.1 Erectile dysfunction (ED) predicts coronary events.² The younger the age group, the greater the cardiovascular risk from ED. In men in their 40s who have ED at baseline, cardiovascular risk over a 10‐year follow‐up is 50‐fold greater than men who have normal erections.
2. Table 8.2 Artery size and atherothrombosis. A significant restriction to flow in the penile arteries may be subclinical in larger vessels.
3. Table 8.3 Relative risk of increased events and mortality: erectile dysfunction (ED vs no ED).
Chapter 09
1. Table 9.1 Relative risks for men with erectile dysfunction.
2. Table 9.2 Further investigations to evaluate the man with erectile dysfunction (ED).
Chapter 10
1. Table 10.1 More and less specific clinical, biochemical, and instrumental parameters associated with hypogonadism.
Chapter 12
1. Table 12.1 Common MR sequences used in imaging the penis.
Chapter 14
1. Table 14.1 Scales that measure anxiety and distress.
Chapter 16
1. Table 16.1 Checklist for assessment of premature ejaculation (PE).
2. Table 16.2 Checklist for assessment of delayed ejaculation (DE).
Chapter 17
1. Table 17.1 Summary of the symptoms of the four premature ejaculation (PE) syndromes used in the classification of men with complaints of PE.¹⁵
2. Table 17.2 Treatment options for the management of premature ejaculation (PE).
3. Table 17.3 Causes of retarded ejaculation.⁶³
4. Table 17.4 Adjunctive pharmacotherapy for SSRI‐induced retarded ejaculation.⁶⁴
Chapter 18
1. Table 18.1 Causes and distribution of male infertility.
2. Table 18.2 Classification of causes of erectile dysfunction.
3. Table 18.3 Etiologies common to male infertility and erectile dysfunction (ED).
Chapter 19
1. Table 19.1 Selection of drugs reported to cause erectile dysfunction as a side effect.
2. Table 19.2 Characteristics of three major phosphodiesterase inhibitors.
3. Table 19.3 Management of phosphodiesterase‐5 (PDE5) inhibitor non‐responders.
4. Table 19.4 Adverse events and efficacy reporting.
5. Table 19.5 Common drug therapies for erectile dysfunction.
6. Table 19.6 Contraindications to erectile dysfunction medications.
Chapter 20
1. Table 20.1 Etiology of ischemic priapism.
2. Table 20.2 Blood gas values.
Chapter 21
1. Table 21.1 Pharmacokinetics of phosphodiesterase type 5 inhibitors (PDE5i).
2. Table 21.2 Characteristics of erectile aids.
Chapter 22
1. Table 22.1 Pharmacokinetic data for sildenafil, tadalafil, and vardenafil.
Chapter 23
1. Table 23.1 The multidimensional nature of sexual dysfunction following neurological disease. Adapted from (6)
2. Table 23.2 Medications used in the management of neurological symptoms may contribute to sexual dysfunction. Adapted from (17)
Chapter 24
1. Table 24.1 Vascular risk factors in Peyronie’s disease.
Chapter 25
1. Table 25.1 Etiology of micropenis.
2. Table 25.2 Penile dimensions for normal adults.
3. Table 25.3 Mean stretched penile length (cm) in normal children.
Chapter 27
1. Table 27.1 Available penile prostheses.
Chapter 29
1. Table 29.1 Factors involved in deciding on the most appropriate method of treating the primary penile lesion tailored to the individual.
2. Table 29.2 Treatment options by stage: oncological outcome and effect on sexual function.
Chapter 30
1. Table 30.1 Techniques used to bridge soft tissue defects during reconstruction.
2. Table 30.2 Outcomes for glans resurfacing for lichen sclerosus (LS).
3. Table 30.3 The etiology and techniques of increasing relative penile length as a treatment for buried penis.
Chapter 31
1. Table 31.1 Classification of disorders of sex development (DSD).
2. Table 31.2 Sexual Function with a small penis.

List of Illustrations

Chapter 03
1. Figure 3.1 Pathways regulating smooth muscle contraction, which leads to detumescence.
2. Figure 3.2 Cellular pathways regulating smooth muscle relaxation necessary for tumescence.
Chapter 04
1. Figure 4.1 Ventral view of penile anatomy. The corpus spongiosum contains the urethra and lies within the groove between the two corpora cavernosa. The bulbar and urethral arteries are the first branches of the penile artery. The dorsal artery and nerve course lateral to the dorsal vein of the penis.
2. Figure 4.2 Cross‐sectional view of penile anatomy. The three erectile bodies (two corpora cavernosa and midline corpus spongiosum) are surrounded by the tunica albuginea, which is composed of an inner circular layer and an outer longitudinal layer. The subsequent layers of the penis from deep to superficial are penile fascia, deep (Buck’s) fascia, superficial (dartos fascia), and skin. The superficial dorsal vein courses through dartos fascia, and the deep dorsal vein runs through Buck’s fascia.
3. Figure 4.3 Molecular mechanisms of penile smooth muscle relaxation. Nitric oxide is released from endothelial cells (eNOS) and neurons (nNOS). NO diffuses to the cytoplasm of smooth muscle cells leading to activation of its intracellular receptor, guanylyl cyclase. This binding activates guanylyl cyclase leading to the conversion of guanosine triphosphate (GTP) to cyclic guanosine monophosphate (cGMP). Through cGMP‐specific protein kinases cytosolic calcium levels decrease, leading to cavernosal smooth muscle relaxation. PDE5, phosphodiesterase type 5.
Chapter 05
1. Figure 5.1 Schematic diagram of the hypothalamic‐pituitary‐gonadal axis showing neural systems that regulate gonadotropin‐releasing hormone (GnRH) secretion and feedback of gonadal steroid hormones at the level of the hypothalamus and pituitary. CNS, central nervous system; CRH, corticotropin‐releasing hormone; FSH, follicle‐stimulating hormone; GABA, gamma‐aminobutyric acid; GALP, galanin‐like peptide; LH, luteinizing hormone; NE, norepinephrine; NPY, neuropeptide Y.
2. Figure 5.2 Schematic diagram showing the neuroanatomy of the kisspeptin‐GnRH pathway and the relationship between KNDy neurons and GnRH neurons in humans. Kisspeptin signals directly to the gonadotropin‐releasing hormone (GnRH) neurons, which express kisspeptin receptor. The location of kisspeptin neuron populations within the hypothalamus is species specific, residing within the preoptic area (POA) and the infundibular nucleus in humans. Kisspeptin neurons in the infundibular nucleus co‐express neurokinin B and dynorphin (KNDy neurons), which via neurokinin B receptor and kappa opioid peptide receptor autosynaptically regulate pulsatile kisspeptin secretion, with neurokinin B being stimulatory and dynorphin inhibitory. In humans, KNDy neurons in the infundibular nucleus relay both negative (red) and positive (green) sex steroid feedback. The role of the POA kisspeptin population in mediating sex steroid feedback in humans is incompletely explored. ME, median eminence; –, stimulatory; 2, inhibitory; ERα, estrogen receptor alpha; PR, progesterone receptor; Kiss1/KiSS1, kisspeptin; NKB, neurokinin B; Dyn, dynorphin. LH, luteinizing hormone; FSH, follicle‐stimulating hormone.
3. Figure 5.3 Production, transport, and metabolism of biologically active androgens. Testosterone is predominantly derived from the testis and is mainly bound to transport proteins in the circulation. In peripheral tissues it is metabolized or converted to other active steroids such as dihydrotestosterone or estradiol.
4. Figure 5.4 Schematic representation of the biochemical events leading to a) penile flaccidity or b) erection. a) Penile flaccidity: Noradrenaline (NA) binding generates inositol 1,4,5‐trisphosphate (InsP₃), which, by increasing intracellular calcium (Ca²⁺) levels, activates Ca²⁺‐sensitive chloride channels (CLCAs), resulting in membrane depolarization with the diffusion of the stimulus to the neighboring cells and the opening of voltage‐operated channels (VOC). The increased Ca²⁺ flow promotes, through calmodulin, activation of myosin light chain (MLC) kinase (MLCK) and cell contraction. Cell contraction is also obtained by altering the Ca²⁺ sensitivity through a NA‐induced activation of a second pathway, RhoA/ROCK, which increases, through a series of kinase activations, the sensitivity of MLC to Ca²⁺. Testosterone is considered to negatively regulate the latter event. b) Penile erection: Nitric oxide (NO) diffuses into smooth muscle cells (SMC) and activates a soluble guanylate cyclase (sGC), which in turn transforms guanosine triphosphate (GTP) into cyclic guanosine monophosphate (cGMP). Cyclic GMP activates protein kinase G (PKG), which through the indicated pathways, finally decreases intracellular Ca²+ levels, leading to relaxation. Phosphodiesterase type 5 (PDE5) metabolizes cGMP into GMP, thereby limiting its effects. Testosterone enhances PDE5 activity. Other abbreviations: CPI‐17, protein phosphatase 1 regulatory, subunit 14A; eNOS, endothelial nitric oxide synthase; GAP, GTPase activating protein; GEF, guanine nucleotide exchange factor; MLCP, myosin light chain phosphatase; nNOS, neuronal nitric oxide synthase; PLC, phospholipase C; RhoA, Ras homolog gene family member A; ROCK, Rho‐associated coiled‐coil containing protein kinase; SR, sarcoplasmic reticulum.
5. Figure 5.5 Hypogonadism due to alterations in the hypothalamic‐pituitary‐testicular axis. a) Primary hypogonadism due to testicular disease. Classically, this results in both androgen deficiency and impairment of sperm production and elevated luteinizing hormone (LH) and follicle‐stimulating hormone (FSH) levels (hypergonadotrophic hypogonadism) due to loss of negative feedback regulation of gonadotropins. GnRH, gonadotropin‐releasing hormone; T, testosterone. b) Secondary hypogonadism due to hypothalamic and/or pituitary disease. This manifests as both androgen deficiency and impairment of sperm production and inappropriately normal or low LH and FSH levels (hypogonadotrophic hypogonadism).
6. Figure 5.6 Macroadenoma of the pituitary, with large suprasellar extension, causing secondary hypogonadism, and other features of hypopituitarism.
7. Figure 5.7 Clinical features of hypogonadism. A 32‐year‐old man with severe androgen deficiency caused by Kallmann’s syndrome (hypogonadotrophic hypogonadism and anosmia) who presented with poor sexual function, sparsity of body hair, and poorly developed secondary sexual characteristics and 3 cc testes. Luteinizing hormone <1.0; follicle‐stimulating hormone 0.4; testosterone level 1.2 U/L.
8. Figure 5.8 Right‐sided macroprolactinoma with extension into the right cavernous sinus causing a right sixth nerve palsy, and galactorrhea. Prolactin 33,400 mU/L (nomolar range <360).
9. Figure 5.9 Hypothalamo‐pituitary‐testicular axis and potential sites of therapeutic disruption. AR, androgen receptor; DHT, dihydrotestosterone; LH, luteinizing hormone; LHRH, luteinizing hormone releasing hormone.
10. Figure 5.10 Investigation and management of suspected hypogonadism. FSH, follicle‐stimulating hormone; GnRH, gonadotropin‐releasing hormone; hCG, human chorionic gonadotropin; LH, luteinizing hormone; MRI, magnetic resonance imaging; T, testosterone.
Chapter 07
1. Figure 7.1 The neurophysiology of ejaculation in the human male. ACh, acetylcholine; Bulbospongiosus muscle; D2, dopamine D2 receptors; 5‐HT, 5‐hydroxytryptamine (serotonin) receptors; NA; NO, nitric oxide; OT, oxytocin receptors.
Chapter 08
1. Figure 8.1 Angiogram identifies critical right coronary artery stenosis.
2. Figure 8.2 Successful stent insertion into right coronary artery as shown in Figure 8.1.
3. Figure 8.3 Algorithm for assessing cardiovascular disease (CVD) following a diagnosis of erectile dysfunction. Cardiac Computed Tomography Angiograph (CCTA).
Chapter 09
1. Figure 9.1 Management of erectile dysfunction (ED) in all men with ED, especially those with known cardiovascular disease. ^aSexual activity is equivalent to walking 1 mile on the flat in 20 minutes or briskly climbing two flights of stairs in 10 seconds. ^bSexual activity is equivalent to 4 minutes of the Bruce treadmill protocol.
2. Figure 9.2 Algorithm for androgen therapy in a man presenting with erectile dysfunction (ED). PDE5I, phosphodiesterase type 5 inhibitor; T, testosterone.
Chapter 10
1. Figure 10.1 Prevalence of endocrinological problems as derived from a consecutive series of 4388 subjects seeking medical care for sexual dysfunction at our unit between 2000 and 2013. Hyperprolactinemia (circulating prolactin levels >420 mU/L or 20 ng/mL) was considered mild (prolactin levels 420–735 mU/L, or 20–35 ng/mL) or severe (prolactin levels >735 mU/L, or 35 ng/mL) as previously reported.^18,19 Gonadal status was identified according to the European Male Aging Study criteria: normal or eugonadal (testosterone ≥10.5 nmol/L and luteinizing hormone ≤9.4 U/L); secondary hypogonadism (testosterone <10.5 nmol/L and luteinizing hormone ≤9.4 U/L); primary hypogonadism (testosterone <10.5 nmol/L and luteinizing hormone >9.4 U/L); and compensated hypogonadism (testosterone ≥10.5 nmol/L and luteinizing hormone >9.4 U/L).⁹ Subclinical hypo‐ and hyperthyroidism were defined when TSH values were outside the reference ranges (0.4–4.5 mU/L) with normal free thyroid hormones. Overt hypo‐ and hyperthyroidism were defined when both TSH and free thyroid hormone values were outside the reference ranges.
2. Figure 10.2 Algorithm for the diagnosis of testosterone deficiency. PRL, prolactin; cFT, calculated free testosterone; TT, total testosterone; LH, luteinizing hormone; SHBG, sex hormone‐binding globulin.
Chapter 11
1. Figure 11.1 Longitudinal image of the penis at the level of the penoscrotal junction (evident by the slight dorsal curvature of the penis) showing an accessory cavernosal artery that, in this patient, forms the dominant supply to the penis (red arrow). This was discovered after abnormally low values for peak systolic velocity (PSV) were seen at the level of the crura in the setting of a normal erection, illustrating the importance of looking for accessory vessels. Also visible (white arrow) is the dorsal artery, which lies outside of the tunica.
2. Figure 11.2 a) Axial image of the flaccid penis at the midshaft level immediately following intracorporal injection of alprostadil showing increased echogenic material within the corporal tissue close to the ventral tunica. This should not be confused with calcified plaque, and reinforces the importance of scanning preinjection. b) Axial image of the same patient at the same level 15 minutes later demonstrating almost complete dispersal of the drug (scattered echogenic foci in the left corpus are all that remain).
3. Figure 11.3 a‐f Clockwise from top left. a) Longitudinal and b) axial: B‐mode ultrasound of the distal penis showing a classical appearing non‐calcified plaque on the dorsal tunical surface that appears as a focus of thickening (defined by the calipers). c) Longitudinal view of the midshaft showing a dorsal curvature cause by a non‐calcified plaque (defined by arrows). d) Axial view of the midshaft demonstrating fibrosis of the right corpus cavernosum as shown by the reduced caliber compared to the left and the focus of increased echogenicity. e) Longitudinal view of the midshaft showing marked wasting of the corpus caused by a combination of tunica plaque and intracorporal fibrosis. f) Axial ultrasound of the midshaft showing two adjacent calcified plaques with post‐acoustic shadowing involving the ventral tunica and septum (defined by calipers 1 and 2).
4. Figure 11.4 Waveforms. ED, end diastole; EDV, end‐diastolic velocity; PS, peak systole; PSV, peak systolic velocity.
5. Figure 11.5 a) Longitudinal view of the cavernosal artery 30 minutes post‐injection of alprostadil showing a normal peak systolic velocity (97 cm/s) but with sustained, high end‐diastolic velocity of 30 cm/s (low resistance) suggestive of veno‐occlusive dysfunction. The patient had 70% tumescence. b) Cavernosography in the same patient revealed early filling of the periprostatic plexus and pelvic veins consistent with a venous leak.
6. Figure 11.6 a) Longitudinal view of the penis at the penoscrotal junction showing a large fistula between the main cavernosal artery and the venous sinusoids as demonstrated by a focal area of turbulent flow in the corporal substance. Spectral trace shows both high peak systolic and high end‐diastolic velocities consistent with a low resistance pattern seen in non‐ischemic priapism. b) Longitudinal view at the level of the penoscrotal junction demonstrating the classically described ischemic waveform, which is low flow and high resistance. The calipers are positioned over the main cavernosal artery. The expanded corpora indicate tumescence, and the heterogeneity suggests early fibrosis. c) Longitudinal view of the penis in a second patient with ischemic priapism. This demonstrates very high peak systolic velocity (1.5 m/s) but crucially there is reversed flow in diastole, which clearly distinguishes it from both the high‐flow, low‐resistance waveform in image a (non‐ischemic priapism) and image b (classical ischemic priapism).
Chapter 12
1. Figure 12.1 a) T2 sagittal and b) T1 post‐contrast images in a man with low‐flow priapism. Note in a) the normal corrugations (short white arrow) and the normal urethra (black arrow). Also, Buck’s fascia (long white arrow) is seen as a slightly higher signal layer than the adjacent (deeper) tunica albuginea. The T2 image shows low signal in the corpus cavernosum proximally, and high signal distally, but this does not correlate with the degree of infarction. For this, the post‐contrast image b) obtained at 8 min is necessary: it shows generally no enhancement in the corpora cavernosa (long arrows), except around the proximal cavernosal arteries (short white arrows). The patient went on to have a penile implant the same week, with a good functional outcome.
2. Figure 12.2 a) T2 axial and b) sagittal images of a penile implant. a) This shows the two cavernosal components (long white arrows) lying in the left corpus cavernosum (true crossover). Note the periarterial post‐priapism fibrosis in the right corpus cavernosum (black arrow) and the normal urethra (short white arrow). The sagittal image in b) shows a “kink” at the point where the right cavernosal component crosses over to the left (long white arrow).
Chapter 15
1. Figure 15.1 A normal NPT trace.
2. Figure 15.2 An abnormal NPT trace.
Chapter 16
1. Figure 16.1 Annon’s PLISSIT model.
Chapter 18
1. Figure 18.1 Algorithm for the diagnostic evaluation of erectile dysfunction (ED).
2. Figure 18.2 Princeton III Consensus Panel recommendations for management of erectile dysfunction (ED) in cardiovascular disease (CVD). ^aSexual activity is equivalent to walking one mile on flat surface in 20 minutes or briskly climbing two flights of stairs in 10 seconds. ^bSexual activity is equivalent to four minutes of the Bruce treadmill protocol. Low‐risk patients are those able to perform exercise of moderate intensity without symptoms. This group also includes patients with a history of successful revascularization, asymptomatic controlled hypertension, mild valvular dysfunction, and left ventricular dysfunction (New York Heart Association (NYHA) class I and II). High‐risk patients are those with moderate to severe cardiac symptoms, including unstable angina pectoris, uncontrolled hypertension, congestive heart failure (NYHA class IV), recent myocardial infarction (MI; <2 weeks), high‐risk arrhythmia, severe cardiomyopathy, and moderate to severe valve disease.
3. Figure 18.3 Treatment algorithm for management of erectile dysfunction (ED). BPH, benign prostatic hyperplasia; LUTS, lower urinary tract symptoms; PDE5i,phosphodiesterase type 5 inhibitor; VED, vacuum erection device.
Chapter 21
1. Figure 21.1 Pathophysiology of erectile dysfunction (ED) after pelvic surgery.
Chapter 22
1. Figure 22.1 The International Index of Erectile Function 5 (IIEF‐5) assessment tool.
2. Figure 22.2 Investigation of the diabetic patient with erectile dysfunction (ED).
3. Figure 22.3 Photo of vacuum device with different sized cylinders and constriction rings.
4. Figure 22.4 Treatment algorithm for erectile dysfunction (ED).
Chapter 24
1. Figure 24.1 The pathophysiological theories for Peyronie’s disease.
Chapter 26
1. Figure 26.1 A surgical algorithm for the treatment of Peyronie’s disease.
Chapter 27
1. Figure 27.1 Typical setup for an inflatable penile prosthesis (IPP) placement with the AMS 700 LGX device.
2. Figure 27.2 Cylinder erosion.
3. Figure 27.3 SST (“supersonic transporter”)deformity.
4. Figure 27.4 Reservoir placement in a patient with a previous robotic assisted laparoscopic prostatectomy (RALP) led to deep venous thrombosis after obstructing the right external iliac vein.
Chapter 28
1. Figure 28.1 Penile vascular anatomy. CIA, common iliac artery; EIA, external iliac artery; IIA, internal iliac artery; IPA, internal pudendal artery.
Chapter 29
1. Figure 29.1 Post operative appearance after total glans resurfacing.
Chapter 30
1. Figure 30.1 The technique of glans resurfacing for (a) balanitis xerotica obliterans (BXO) and (b) carcinoma in situ. (c) After excision of the glans epithelium. (d) Following skin grafting, the long‐term outcome.
2. Figure 30.2 Release of the buried penis in an obese patient with phimosis due to lichen sclerosus (LS) affecting the penile shaft skin. a) Preoperatively, despite losing approximately 20 kg, the patient still had a significant pre‐pubic fat pad. b) A wide incision is used to excise the pre‐pubic fat pad; c) excision of the LS‐affected skin resulted in exposure of the penile shaft, which was amenable to a thick SSG (d).
3. Figure 30.3 Treatment of a fractured penis (a) with a bilateral corporal and urethral injury (b). Repair of the corporal defect and urethra (c), through the midline peno‐scrotal incision (d) obviates the need for a circumcision and degloving of the penis.

List of contributors

James Bellringer
Parkside Hospital
London, UK

Catherine Benedict
Memorial Sloan Kettering Cancer Center
New York, USA

Pierre‐Marc G. Bouloux
The Royal Free Hospital
London, UK

Gerald Brock
St Joseph’s Health Sciences Centre; and Lawson Health Research Institute
London, ON, Canada

Culley Carson
University of North Carolina
Chapel Hill, NC, USA

Lizzie Chandra
St James Hospital, Leeds Teaching Hospitals NHS Trust
Leeds, UK

Kelly A. Chiles
George Washington University
Washington, DC, USA

Eric Chung
Princess Alexandra Hospital
Brisbane, Queensland, Australia

Giovanni Corona
Maggiore‐Bellaria Hospital Bologna, Italy

Victoria Dawson
University Hospital Southampton
Southampton, UK

Ian Eardley
Leeds Teaching Hospital Trust
Leeds, UK

Mark Emberton
University College Hospital
London, UK

Francisco J. Garcia
University of Western Ontario;
St Joseph’s Health Sciences Centre;
Lawson Health Research Institute
London, ON, Canada

Angela Gregory
Nottingham University Hospital
Nottingham, UK

Geoffrey Hackett
University of Bedfordshire, Luton, UK
Good Hope Hospital,
Sutton Coldfield, UK

Paul K. Hegarty
Mater Private Hospital
Mahon, Cork, Ireland

Wayne J.G. Hellstrom
Tulane University
New Orleans, LA, USA

Graham Jackson
Guy’s and St Thomas’ Hospitals NHS Trust
London, UK

Salim Janmohamed
University College London
London, UK

Ates Kadioglu
Istanbul Faculty of Medicine, Istanbul University
Istanbul, Turkey

Jas Kalsi
Frimley Health NHS Foundation Trust and Imperial College
Healthcare, London, UK

Oliver Kayes
St James Hospital, Leeds Teaching Hospitals NHS Trust
Leeds, UK

Mohit Khera
Baylor College of Medicine
Houston, TX, USA

Michael Kirby
The Prostate Centre
London, UK

Alex Kirkham
University College Hospital London
London, UK

Stephen Larsen
University College Hospital London
London, UK

Chi‐Ying Li
University College Hospital London
London, UK

Marc Lucky
Aintree University Hospital
Liverpool, UK

Tom F. Lue
University of California
San Francisco, CA, USA

Mario Maggi
University of Florence
Florence, Italy

Martin Miner
Brown University
Providence, RI, USA

Suks Minhas
University College Hospital
London, UK

Caroline Moore
University College Hospital
London, UK

John Mulhall
Memorial Sloan Kettering Cancer Center
New York, NY, USA

Asif Muneer
University College Hospital London
London, UK

Christian J. Nelson
Memorial Sloan Kettering Cancer Center
New York, USA

Jalesh N. Panicker
The National Hospital for Neurology and Neurosurgery and UCL Institute of Neurology
London, UK

Alexander W. Pastuszak
Baylor College of Medicine
Houston, TX, USA

Mark Paulos
Brown University
Providence, RI, USA

David Ralph
University College Hospital London
London, UK

Tina G. Rashid
Charing Cross Hospital
London, UK

Rowland Rees
University Hospital Southampton
Southampton, UK

Ashley Ridout
University College Hospital
London, UK

Emre Salabas
Istanbul Faculty of Medicine, Istanbul University
Istanbul, Turkey

Varun Sahdev
University College Hospital London
London, UK

Patrick Selph
University of Alabama at Birmingham
Birmingham, AL, USA

Majid Shabbir
Guy’s Hospital
London, UK

Alan Shindel
UC Davis
Sacramento, CA, USA

C.J. Shukla
Western General Hospital, NHS Lothian
Edinburgh, UK

Vikram Soni
Baylor College of Medicine
Houston, TX, USA

Conrad von Stempel
University College Hospital
London, UK

Raanan Tal
Rambam Healthcare Campus
Haifa, Israel

Ronny B.W. Tan
Tan Tock Seng Hospital, Singapore

Phillip Thomas
Brighton and Sussex University Hospitals NHS Trust, Brighton, UK
Parkside Hospital, London, UK

Katarina Ivana Tudor
Department of Neurology, University Hospital Center Zagreb
Zagreb, Croatia

Linda Vignozzi
University of Florence, Florence, Italy

Marcel D. Waldinger
Drexel University College of Medicine
Philadelphia, PA, USA

Miles Walkden
University College Hospital
London, UK

Dan Wood
University College Hospital
London, UK

Michael Grant Wyllie
Global Pharma Consulting
Banbury, UK

Tet Yap
St George’s Hospital
London, UK

Andrew Yates
Leeds & York Partnership NHS Foundation Trust
Leeds General Infirmary
Leeds, UK

Lindsay Yuh
UC Davis
Sacramento, CA, USA

Uwais B. Zaid
University of California
San Francisco, USA

Xiaoyu Zhang
University of California
San Francisco, USA

Male Sexual Dysfunction

A Clinical Guide

List of contributors

Foreword