13 Sexual health

Autonomic: sympathetic nerves originating from T11–L2 and parasympathetic nerves originating from S2–4 join to form the pelvic plexus. The cavernosal nerves are branches of the pelvic plexus (i.e. parasympathetic) that innervate the penis. Parasympathetic stimulation causes erection; sympathetic activity causes ejaculation and detumescence (loss of erection).

Somatic: somatosensory (afferent) information travels via the dorsal penile and pudendal nerves and enters the spinal cord at S2–4. Onuf’s nucleus (segments S2–4) is the somatic centre for efferent (i.e. somatomotor) innervation of the ischiocavernosus and bulbocavernosus muscles of the penis.

Central: medial preoptic area (MPOA) and paraventricular nucleus (PVN) in the hypothalamus are important centres for sexual function and penile erection.

Neuroendocrine signals from the brain, created by audiovisual or tactile stimuli, activate the autonomic nuclei of the spinal erection centre (T11–L2 and S2–4). Signals are relayed via the cavernosal nerve to the erectile tissue of the corpora cavernosa, activating the veno-occlusive mechanism (Table 13.1). This triggers increased arterial blood flow into sinusoidal spaces (secondary to arterial and arteriolar dilatation), relaxation of cavernosal smooth muscle, and opening of the vascular space. The result is expansion of the sinusoidal spaces against the tunica albuginea which compresses the subtunical venous plexuses, decreasing venous outflow. Maximal stretching of the tunica albuginea, which acts to compress the emissary veins that lie within its inner circular and outer longitudinal layers, reduces venous flow even further. Rising intracavernosal pressure and contraction of the ischiocavernosus muscles produce a rigid erection. Following orgasm and ejaculation, vasoconstriction (due to increased sympathetic activity, endothelin, PGF2, and breakdown of cGMP) produces detumescence. Noradrenaline (NA) released from sympathetic nerve terminals in the corpora acts on smooth muscle cell α₁-adrenoceptors, leading to raised intracellular calcium which helps maintain penile flaccidity (Figs. 13.1 and 13.2).

Tactile stimulation of the glans penis sends sensory information (via the pudendal nerve) to the lumbar spinal sympathetic nuclei. Sympathetic efferent signals (travelling in the hypogastric nerve) cause contraction of smooth muscle of the epididymis, vas deferens, and secretory glands, propelling spermatozoa and glandular secretions into the prostatic urethra (emission). There is simultaneous closure of the internal urethral sphincter and relaxation of the extrinsic sphincter, directing sperm into the bulbourethra, but preventing sperm from entering the bladder. Rhythmic

contraction of the bulbocavernosus muscle (somatomotor innervation) leads to the pulsatile emission of the ejaculate from the urethra. During ejaculation, the alkaline prostatic secretion is discharged first, followed by spermatozoa and finally, seminal vesicle secretions (ejaculate volume 2–5mL). The seminal vesicles contribute 2mL, prostate 0.5mL, and Cowper’s glands 0.1mL of the ejaculate. There is an additional vasal and testicular contribution (accounting for around 5–10% of the total ejaculate volume).

Erectile dysfunction (ED) (also called impotence) describes the ‘consistent or recurrent inability to attain and/or maintain a penile erection sufficient for sexual intercourse’.¹

In men aged 40–70y, mild ED is found in 17%, moderate ED in 25%, and complete ED in 10%.² Incidence increases with age, with complete ED affecting ∼15% of men in their 70’s and 30–40% in their 80’s.

ED is generally divided into psychogenic and organic causes (Table 13.2). It is often multifactorial.

Sexual: onset of ED (sudden or gradual); duration of problem; presence of erections (nocturnal, early morning, spontaneous); ability to maintain erections (early collapse, not fully rigid); loss of libido; relationship issues (frequency of intercourse and sexual desire).

Sexual function symptom questionnaires: International Index of Erectile Function (IIEF)—full and short version (IIEF 5) (see

p. 575; Table 13.3); Brief Male Sexual Function Inventory (BMSFI); quality of life questionnaire (QoL-MED).

Medical and surgical: enquire about risk factors, including diabetes mellitus (ED affects 50% overall and 30% of treated diabetics);² cardiovascular disease; hypertension; peripheral vascular disease; endocrine or neurological disorders; pelvic and penile surgery, radiotherapy, or trauma (which damage innervation and blood supply to the pelvis and penis). Intermediate or high risk cardiovascular disease requires further specialist assessment and treatment prior to ED treatment.

Psychosocial: assess for social stresses, anxiety, depression, coping problems, patient expectations, and relationship details.

Drugs: enquire about current medications and ED treatments already tried and their outcome.

Social: smoking, alcohol consumption.

An organic cause is more likely with gradual onset (unless associated with an obvious cause such as surgery where onset is acute); loss of spontaneous erections; intact libido and ejaculatory function; existing medical risk factors and older age groups.

Full physical examination (cardiovascular, abdomen, neurological); BP; DRE to assess the prostate; assess secondary sexual characteristics; external genitalia assessment to document foreskin phimosis, penile deformities and lesions (Peyronie’s plaques); confirm presence, size, and location of testicles. The bulbocavernosus reflex can be performed to test integrity of spinal segments S2–4 (squeezing the glans causes anal sphincter and bulbocavernosal muscle contraction).

Correct any reversible causes (i.e. alter lifestyle, stop smoking, change medication, etc.) (Table 13.2).

Aims to understand and address underlying psychological issues and provides information and treatment in the form of sex education, psychosexual counselling, instruction on improving partner communication skills, cognitive therapy, and behavioural therapy (programmed relearning of couple’s sexual relationship). Pharmacotherapy may be a useful adjuvant.

Phosphodiesterase type-5 (PDE5) inhibitors: first-line therapies which include sildenafil (Viagra^®), tadalafil (Cialis^®), vardenafil (Levitra^®) (Table 13.4). PDE5 inhibitors enhance cavernosal smooth muscle relaxation and erection by blocking the breakdown of cGMP by phosphodiesterase. Sexual stimulus is still required to initiate events. Success is reported in up to 80%. Early use of PDE5 inhibitors following radical prostatectomy can help optimize the return of spontaneous erections (penile rehabilitation).

Contraindications: patients taking nitrates, recent myocardial infarction, recent stroke, hypotension, unstable angina, non-arteritic anterior ischaemic optic nerve neuropathy (NAION). Cautions: intermediate and high risk cardiovascular disease requires cardiac review prior to treatment, use with α-blockers, groups with predisposition to priapism.

Dopamine receptor agonist: apomorphine (Uprima^®), taken sublingually, acts centrally on dopaminergic receptors in the paraventricular nucleus of the hypothalamus to enhance and coordinate the effect of sexual stimuli. Side effects: nausea, headache, dizziness. Not commonly used.

Intraurethral therapy: second-line therapy when oral therapies have been ineffective. A synthetic prostaglandin E1 (PGE1) pellet (alprostadil) is placed into the urethra via a specialized applicator (Medicated Urethral System for Erection (MUSE)^TM device). Once inserted, the penis is gently rolled to encourage the pellet to dissolve into the urethral mucosa from where it enters the corpora. PGE1 acts to increase cAMP within the corporal smooth muscle, resulting in muscle relaxation. Side effects: penile and urethral pain, priapism, local reactions.

Training of technique and first dose is given by a health professional. Needle is inserted at right angles into the corpus cavernosum on the lateral aspects of mid-penile shaft. Discontinuation rates from penile injection techniques are high. Contraindications: sickle cell disease or high-risk candidate for priapism. Adverse effects: pain, priapism, haematoma.

Used when pharmacotherapies have failed. It contains three components: a vacuum chamber, pump, and constriction band. The penis is placed in the chamber and the vacuum created by the pump increases blood flow to the corpora cavernosa to induce an erection. The constriction band is placed onto the base of the penis to retain blood in the corpora and maintain rigidity. Relative contraindication: anticoagulation therapy. Side effects: penile coldness, bruising.

Used in: specialist centres where there is a clear-cut diagnosis of a vascular disorder. Acts to increase arterial inflow and decrease venous outflow. Rarely used now as it is uncommon for success rates to exceed 50%.

Semi-rigid, malleable, and inflatable penile prostheses are available when other therapies have failed or are unsuitable. Also indicated for Peyronie’s disease, trauma, and penile fibrosis (i.e. secondary to priapism). The device is surgically implanted into the corpora to provide penile rigidity and generally has high satisfaction rates, up to 90% (Fig. 13.3). Side effects: infection, erosion, mechanical failure, penile shortening, glans may not fully engorge.

Indicated for hypogonadism and is available in oral, buccal, intramuscular, pellet, transdermal patch, and gel forms. Most guidelines recommend PSA, Hb, and LFT checks before and after starting treatment (see

pp. 596–7). It can improve the results of PDE5 inhibitors in hypogonadal men.

An acquired benign penile condition characterized by deformity of the penile shaft secondary to the formation of a fibrous inelastic scar on the tunica albuginea.¹

Prevalence is 3–9%,¹ predominantly affecting men aged 40–60y.

Histologically, plaques have excessive connective tissue (fibrosis) and increased cellularity with random orientation of collagen fibres. Dorsal penile plaques are most common (66%). The corpus cavernosus underlying the lesion cannot lengthen fully on erection, resulting in penile curvature. The disorder has two phases:

The natural history of Peyronie’s plaques over 18 months is that 40% will progress, 47% will remain stable, and 13% will improve.²

The exact cause is unknown, but it is currently considered to be a wound healing disorder which occurs after penile trauma in genetically predisposed men.¹ It is likely that repeated minor trauma during intercourse causes microvascular injury and bleeding into the tunica, resulting in inflammation and fibrosis (exacerbated by transforming growth factor-β (TGF-β).

Peyronie’s disease may present with penile pain, a palpable lump (plaque), penile curvature, ED (in 40%), a more complex deformity (shortening, indentation, hourglass deformity), or a combination of these features.

Diabetes mellitus (in 30%); ED; arterial disease; Dupuytren’s contractures (25%); plantar fascial contracture; tympanosclerosis; raised cholesterol or triglycerides; hypertension; low testosterone.

A full medical and sexual history (including erectile function) are taken. Patient photographs or outpatient injection of intracavernosal PGE1 can be used to assess the degree of curvature. Assess the location and size of the plaque (is it tender?). Record stretched penile length preoperatively to help advise patients that loss of penile length is partly due to the disease and not all due to the surgical correction. Colour Doppler USS is useful in assessing the plaque and any vascular abnormalities whereas contrast-enhanced MRI is indicated for complex and extensive cavernosal fibrosis.

Early disease with active inflammation (<3 months, penile pain, changing deformity) may benefit from medical therapy. Surgery is indicated for stable, mature disease (present for 12 months; stable for 3 months), with significant deformity preventing intercourse. Non-mechanical components of ED can be treated conventionally (e.g. oral PDE5 inhibitors or intracavernosal pharmacotherapy).

ESWL: has little effect on penile deformity, but may help reduce pain.

Peyronie’s vacuum therapy: exercises using mechanical stretching.

(Box 13.1)

prolonged, unwanted erection, in the absence of sexual desire or stimulus, lasting >4h.

incidence of 1.5 per 100 000,¹ with peaks at ages 5–10 and 20–50.

Causes are primary (idiopathic) or secondary, including:

Priapism lasting for 12h causes trabecular interstitial oedema, followed by destruction of sinusoidal endothelium and exposure of the basement membrane at 24h and sinusoidal thrombi, smooth muscle cell necrosis, and fibrosis at 48h.

Ice packs, cold showers, and exercise may be beneficial in early stages.

Decompress urgently with aspiration of blood from the corpora (5mL portions using a 18–20 gauge butterfly needle until oxygenated red blood is obtained). If no change after 10min, proceed to intracavernosal injection of α1-adrenergic agonist (phenylephrine 100–200mcg (0.5–1mL of a 200mcg/mL solution to a maximum of 1mg)) every 5–10min until detumescence (loss of erection) occurs; see

www.bnf.org). Monitor BP and pulse during drug administration. Oral terbutaline may be effective treatment for intracavernosal injection-related cases. Sickle cell disease requires, in addition, aggressive rehydration, oxygenation, analgesia, and haematological input (consider exchange transfusion).

If aspiration and phenylephrine fails after 1h, surgical intervention is attempted with shunt and biopsy. Following a penile block, the Winter technique places a Trucut biopsy needle through the glans into the corpora cavernosa to remove small pieces of tunica albuginea and allow evacuation of hypoxic blood. Alternatively, a small blade stab incision is made via the glans into the corpora, avoiding the urethra. If there is no response, corporosaphenous shunting can be considered where the long saphenous vein is tunnelled and anastomosed onto the corpora cavernosum.

If this fails or patients present late (after 48–72h), discuss the insertion of a penile prosthesis. This will treat both the priapism and inevitable ED and avoids the difficulty and high complication rates of delayed insertion into a fibrotic penis.

Conservative treatment is recommended in most cases. Traumatic or delayed presentations require arteriography and either selective or internal pudendal artery embolization with autologous blood clot or fat. Ligation of fistula may be required.

Optimize haematological management of sickle cell disease to reduce frequency of attacks. Regular oral alpha agonists such as etylephrine can be helpful and/or androgen suppression (i.e. cyproterone acetate).

Complications: 90% of priapism lasting >24h develop complete ED.

Failure of adequate bladder neck contraction results in the propulsion of sperm back into the bladder on ejaculation.

Acquired causes are due to damage or dysfunction of the bladder neck sphincter mechanism. These include neurological disease (SCI; neuropathy associated with diabetes mellitus; nerve damage after retroperitoneal surgery) or anatomical disruption following transurethral resection of ejaculatory ducts (for obstruction), bladder neck incision (BNI), TURP, or open prostatectomy. Drugs to treat BOO (α-blockers) causes reversible retrograde ejaculation in 5% of men. Congenital causes include bladder exstrophy, ectopic ejaculatory ducts, and spina bifida.

Retrograde ejaculation following TURP or open prostatectomy occurs in 9 out of 10 men and after BNI, in 1–5 in 10.

‘Dry’ ejaculation (failure to expel ejaculate fluid from the urethral meatus) or low ejaculate volume (<1mL) and cloudy urine (containing sperm) in the first void after intercourse.

The presence of >10–15 sperm per high powered field in post-orgasmic urine specimens confirms the diagnosis of retrograde ejaculation.

Medical therapy: is initiated in men wishing to preserve fertility and is only effective in patients who have not had bladder neck surgery. Therapy is often given for 7–10 days prior to a planned ejaculation (coordinated with the partner’s ovulation).

Oral sodium bicarbonate and adjustment of fluid intake is initiated to optimize urine osmolarity and pH and enhance sperm survival. Sperm are collected by gentle urine centrifuge and washed in insemination media in preparation for IUI or IVF treatments.

Premature ejaculation (PE) is classified as lifelong or acquired. The International Society for Sexual Medicine (ISSM) defines lifelong PE as ‘ejaculation which always or nearly always occurs prior to or within one minute of vaginal penetration and the inability to delay ejaculation on all or nearly all vaginal penetrations and negative consequences such as distress, bother, frustration, or avoidance of sexual intimacy’.¹ Related conditions include natural variable PE and PE-like dysfunction.

Detailed medical, sexual, and psychosocial history and physical examination. Establish perceived degree of ejaculatory control, onset, and duration of the problem. Quantitative measures of sexual intercourse include:

Gradual withdrawal of drug therapy can be attempted after 6–8 weeks.

The ISSM defines orgasmic dysfunction as: ‘inability to achieve an orgasm or markedly diminished intensity of orgasmic sensation’ or ‘marked delay of orgasm during any kind of sexual stimulation’.¹ Under this category, they include delayed ejaculation, inhibited ejaculation, retarded (and partially retarded) ejaculation, anejaculation, and anorgasmia.¹

is ‘the persistent or recurrent difficulty, delay in, or absence of attaining orgasm after sexual sufficient stimulation, which causes personal distress’.² It may be lifelong or acquired, global or situational, and the prevalence increases with age (Table 13.7).³

is the complete absence of an antegrade or retrograde ejaculation. There is failure of emission from the seminal vesicles, prostate, and ejaculatory ducts into the urethra. True anejaculation is associated with normal orgasm and is most often due to drug-related causes or central or peripheral nervous system dysfunction (Table 13.7).

is the inability to reach orgasm (which may give rise to anejaculation in men). This is rare. Primary conditions are usually attributed to psychological causes. Secondary causes may be related to drugs or decreased penile sensation (secondary to pudendal nerve dysfunction, seen in peripheral neuropathy associated with diabetes mellitus) (Table 13.7).

A detailed sexual history, including the exact symptoms, duration, related arousal or desire problems, and precipitating factors should be taken. A full medical and drug history identifies any underlying or reversible causes. A focused physical (including external genitalia and palpation for bilateral vasa) and neurological examination (including bulbocavernosus reflex, anal sphincter tone, and perineal sensitivity where appropriate) should be performed. Urine microscopy and culture may identify infection. Post-ejaculatory urinalysis can be performed to exclude retrograde ejaculation. If there is clinical suspicion of possible ejaculatory duct obstruction, consider transrectal USS, vasography, or percutaneous puncture of the seminal vesicles. Cystourethroscopy can be used to assess the ejaculatory ducts and exclude urethral obstruction (urethral stensosis).

General: aim to identify and treat the underlying aetiology and address any infertility issues in men of reproductive age. Patient education and counselling on lifestyle change (i.e. reducing alcohol consumption, attempting sexual intercourse when not tired) are helpful adjuvants. If an organic cause has been excluded, psychosexual therapy is recommended.

Drugs: that facilitate ejaculation by central dopaminergic or antiserotonergic action have been tried, especially in drug-induced anejaculation, although no randomized trials have been carried out for this condition. Examples include: 5-HT receptor antagonists (cyproheptadine); dopaminergic drugs (amantadine, yohimbine); dopamine reuptake inhibitors (bupropion); 5-HT1A receptor agonists (buspirone). The treatment of delayed ejaculation is similar to anejaculation.

Anejaculation: where the aim is to retrieve sperm for ART methods include:

Late-onset hypogonadism (LOH): is defined as ‘a clinical and biochemical syndrome associated with advancing age and characterized by symptoms and a deficiency in serum testosterone levels (below the young healthy adult male reference range). This condition may result in significant detriment in the quality of life and adversely affect the function of multiple organ systems’.¹ It is also known as age-associated testosterone deficiency (TDS).¹

LOH involves components of both primary and secondary hypogonadism (see  p. 596) and a degree of reduced responsiveness of target organs to testosterone and its adrogenic mediators. Ageing decreases the production of LHRH and LH due to effects on the hypothalamus and pituitary. This causes a decline in the both the number of Leydig cells in the testes and their sensitivity to LH so reducing testosterone levels. SHBG binds testosterone and renders it unavailable to most tissues and levels of SHBG increase with age. Along with age-related changes in androgen receptors and altered androgen metabolism, the result is less bioavailable testosterone.

In a normal adult male, the serum testosterone reference range is around 10.4–34.7nmol/L. Testosterone levels show diurnal variation, peaking in early morning and recommendations for testing are:

Symptoms and biochemical evidence of testosterone deficiency indicate the need for testosterone replacement therapy (Fig. 13.5). Where testosterone levels are borderline/normal, but symptoms are present, consider an initial 3-month trial of testosterone and then review (see  p. 597). Residual symptoms may need specific treatment such as PDE5 inhibitors for ED.

For normal testosterone physiology, refer to  p. 552; for normal androgen metabolic pathways, see  p. 684.

Male hypogonadism has been defined as inadequate gonadal function due to deficiencies in gametogenesis and/or the secretion of gonadal hormones. Hypogonadism may be primary (due to abnormal testicular function or testicular response to gonadotrophins) or secondary (due to failure of the hypothalamic–pituitary axis, leading to inadequate gonadotrophic stimulation and reduced testicular testosterone production (Table 13.8). The result is testosterone deficiency.

Hypogonadism and related symptoms caused by low testosterone levels. Symptomatic LOH and primary hypogonadism should be treated with androgens. Patients with secondary hypogonadism may be given LH and FSH or pulsatile LHRH if fertility is required, otherwise they should receive androgen replacement (see  p. 598). The aim is to achieve normal serum testosterone levels.

Testosterone replacement can be given by transdermal patch or gel, intramuscular injection, subdermal implant, buccal, and oral administrations (Table 13.9). Transdermal preparations produce a normal testosterone level with physiological diurnal profile, but they can produce local skin reaction. Intramuscular injections are long-acting, but do not provide normal hormonal circadian rhythm. Oral preparations tend to be less used due to variable pharmacokinetics. Buccal mucoadhesive tablets (Striant^®) produce more reliable testosterone levels, but require twice daily application.

This is characterized by central obesity, insulin resistance, dyslipidaemia, and hypertension, resulting in increased risk of cardiovascular disease and progression to diabetes mellitus. Hypogonadism is frequently associated with metabolic syndrome. There is evidence that testosterone treatment may help some conditions associated with the syndrome and reduce the risk of cardiovascular complications.

Urethritis is inflammation of the urethra. Infective urethritis may present with clear, mucopurulent, or purulent urethral discharge, coloured white, yellow, green, or brown. It can be associated with dysuria and pain at the external urethral meatus or in the penile shaft, which persist between voiding. There may be urinary frequency and urgency. Some infections are asymptomatic.

Assess symptoms, sexual history, and sexual contacts. Examine external genitalia for testicular or epididymal tenderness, discharge at the meatus, lymphadenopathy, or skin lesions. Refer to genitourinary medicine for management and to trace and treat contacts.

The diagnosis of urethritis on urethral smear is defined as ≥5 polymorphonuclear leucocytes (PMNL) per high powered field (1000 magnification) or ≥10 PMNL per high powered field (400 times magnification) in the first voiding urine specimen.

is caused by the Gram-negative dipplococcus N. gonorrhoea. Complications include genitourinary tract involvement causing epididymitis. Haematogenous spread of infection to other sites (71%) can cause disseminated gonococcal infection (DGI), manifest initially as tendon or joint pain (see Table 13.10).

is mainly caused by C. trachomatis infection and may be asymptomatic (particularly in women). Specific complications include oculogenital syndrome (NGU and conjunctivitis). Transmission to females results in increased risk of pelvic inflammatory disease, abdominal pain, ectopic pregnancy, infertility, and perinatal infection (see Table 13.10).

Recurrence of symptoms and signs 4–7 days after successful single-dose therapy for GU, caused by a dual urethral infection for which the NGU element was untreated. The most common cause is C. trachomatis. It is recommended an active antichlamydial treatment should be added in to the original gonorrhoea treatment because of this.

is described as the presence of PMNL (≥5 per high powered field at 1000 magnification) in a male urethral smear, in the absence of any proven specific infection.

Infective causes of urethritis with false-negative laboratory results (i.e. missed sexually transmitted infection (STI)).

Urethral swab: culture, Gram stain, and NAAT to exclude STI. Bearing in mind that some cases of NSU may be due to STI with false-negative results, sexual contacts should be traced and antibiotics can often alleviate symptoms. Standard C. trachomatis treatments are usually recommended (azithromycin 1g single oral dose or oral doxycycline 100mg bd 7 days) and are often effective.

This is a condition of uncertain aetiology that only affects women. It manifests as dysuria, frequency, urgency, and suprapubic discomfort without any evidence of infection or urological abnormality to account for the symptoms.

Infection, painful bladder syndrome/interstitial cystitis, urethral diverticulum.

It is a diagnosis of exclusion. Urethral and endocervical swabs should be taken for culture, Gram stain, and NAAT to exclude an STI cause and MSU specimen to examine for UTI. Where indicated, consider cystoscopy to exclude BPS/IC or MRI to investigate for urethral diverticulum.

A course of antibiotics (covering C. trachomatis and anaerobes) can provide symptom relief in some cases, even in the absence of positive cultures. Alkalinization of the urine (potassium citrate, sodium bicarbonate) may help alleviate symptoms.