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Ovid: Oxford Handbook of Urology

Authors: Reynard, John; Brewster, Simon; Biers, Suzanne Title: Oxford Handbook of Urology, 1st Edition Copyright ©2006 Oxford University Press > Table of Contents > Chapter 13 – Disorders of erectile function, ejaculation, and seminal vesicles Chapter 13 Disorders of erectile function, ejaculation, and seminal vesicles P.476
Physiology of erection and ejaculation Innervation 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 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. Mechanism of 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 copora 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 acts to compress the emissary veins which lie within its inner circular and outer longitudinal layers, reducing venous flow even further. Rising intracavernosal pressure and contraction of the ischiocavernosus muscles produces a rigid erection. Following orgasm and ejaculation, vasoconstriction (due to increased sympathetic activity, endothelin, PGF2, and breakdown of cGMP) produces detumescence (Figs. 13.1 and 13.2). Ejaculation Tactile stimulation of the glans penis causes sensory information to travel (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. There is simultaneous closure of the internal urethral sphincter and relaxation of the extrinsic sphincter, directing sperm into the bulbourethra (emission), but preventing sperm 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).

Table 13.1 Phases of erectile process
Phase Term Description
0 Flaccid phase Cavernosal smooth muscle contracted; sinusoids empty; minimal arterial flow
1 Latent (filling) phase Increased pudendal artery flow; penile elongation
2 Tumescent phase Rising intracavernosal pressure; erection forming
3 Full erection phase Increased cavernosal pressure causes penis to become fully erect
4 Rigid erection phase Further increases in pressure + ischiocavernosal muscle contraction
5 Detumescence phase Following ejaculation, sympathetic discharge resumes; there is smooth muscle contraction and vasoconstriction; reduced arterial flow; blood is expelled from sinusoidal spaces
Fig. 13.1 Factors influencing cavernosal smooth muscle
Fig. 13.2 Secondary messenger pathways involved in erection

Impotence: evaluation Definition Impotence (also called erectile dysfunction or ED) describes the persistent inability to achieve or maintain a penile erection sufficent for sexual intercourse. Epidemiology Moderate to severe ED is found in ~10% of men aged 40–70 years. Prevalence increases with age. Aetiology ED is generally divided into psychogenic and organic causes (Table 13.2), although it is often multifactorial. History 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, relationship problems). Medical and surgical: hypertension; cardiac disease; peripheral vascular disease; diabetes mellitus; endocrine or neurological disorders; pelvic surgery, radiotherapy, or trauma (damaging innervation and blood supply to the pelvis and penis). Drugs: enquire about current medications and ED treatments already tried (and 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. The International Index of Erectile Function (IIEF) or ED intensity scale can be used to quantify severity. Examination Full physical examination (CVS, abdomen, neurological); digital rectal examination to assess prostate; external genitalia assessment to document foreskin phimosis and penile 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). Investigation

  • Blood tests—U&E; fasting glucose; PSA; serum testosterone; sex hormone binding globulin; LH/FSH; prolactin; thyroid function test; fasting lipid profile.
  • Nocturnal penile tumescence testing—Rigiscan device contains 2 rings which are placed around base and distal penile shaft to measure tumescence and number, duration, and rigidity of nocturnal erections.
  • Colour Doppler USS—measures arterial peak systolic and end diastolic velocities,1 pre and post intracavernosal injection of PGE1.
Table 13.2 Causes of erectile dysfunction ‘IMPOTENCE’*
Inflammatory Prostatitis
Mechanical Peyronie’s disease
Psychological Depression; anxiety; relationship difficulties; lack of attraction; stress
Occlusive vascular factors Arteriogenic: hypertension; smoking; hyperlipidaemia; diabetes mellitus; peripheral vascular disease
Venogenic: impairment of veno-occlusive mechanism (due to anatomical or degenerative changes)
Trauma Pelvic fracture; spinal cord injury; penile trauma
Extra factors Iatrogenic: pelvic surgery; prostatectomy
Other: increasing age; chronic renal failure; cirrhosis
Neurogenic CNS: multiple sclerosis (MS); Parkinson’s disease; multi-system atrophy; tumour
Spinal cord: spina bifida; MS; syringomyelia; tumour
PNS: pelvic surgery or radiotherapy; peripheral neuropathy (diabetes, alcohol-related)
Chemical Antihypertensives (beta-blockers, thiazides, ACE inhibitors)
Anti-arrhythmics (amiodarone)
Antidepressants (tricyclics, MAOIs, SSRIs)
Anxiolytics (benzodiazepine)
Anti-androgens (finasteride, cyproterone acetate)
LHRH analogues
Anticonvulsants (phenytoin, carbamazepine)
Anti-Parkinson drugs (levodopa)
Statins (atorvastatin)
(Refer to BNF)
Endocrine Hypogonadism; hyperprolactinaemia; hypo and hyperthyroidism; diabetes mellitus
* Note that this list of causes of impotence is not in the order of frequency.
Key: MAOIs = monoamine-oxidase inhibitors; SSRIs = serotonin re-uptake inhibitors; BNF = British National Formulary.
  • Cavernosometry—intracavernosal injection of vasoactive drug followed by saline infusion, the rate of which is proportional to the degree of any venous leaking.
  • Cavernosgraphy—imaging and measurement of blood flow of the penis after intracavernosal injection of contrast and induction of artificial erection; used to identify venous leaks.
  • Penile arteriography

Footnote 1 Normal values: peak systolic velocity >35cm/s; end diastolic velocity <5cm/s. P.481
Impotence: treatment Psychosexual therapy Aims to understand and address underlying psychological issues, and provides information and treatment in the form of sex education, instruction on improving partner communication skills, cognitive therapy, and behavioural therapy (programmed re-learning of couple’s sexual relationship). Oral medication Phosphodiesterase type-5 (PDE5) inhibitors: sildenafil (Viagra); tadalafil (Cialis); vardenafil (Levitra). PDE5 inhibitors enhance cavernosal smooth muscle relaxation and erection by blocking the breakdown of cGMP. Sexual stimulus is still required to initiate events. Side-effects: headache; flushing; visual disturbance. Contraindications: patients taking nitrates; recent myocardial infarction; recent stroke; hypotension; unstable angina. Dopamine receptor agonist: apomorphine (Uprima). Apomorphine is administered sublingually, and acts centrally on dopaminergic receptors in the paraventricular nucleus of the hypothalamus to enhance and co-ordinate the effect of sexual stimuli. Adverse effects: nausea; headache; dizziness. Androgen replacement therapy testosterone replacement is indicated for hypogonadism. It is available in oral, intramuscular, pellet, patch, and gel forms. In older men, it is recommended that PSA is checked before and during treatment. Intraurethral therapy alprostadil (MUSE). Synthetic prostaglandin E1 (PGE1) pellet administered into the urethra via a specialized applicator. Once inserted, the penis is gently rolled to encourage the pellet to dissolve into the urethral mucosa, from where it enters the corpora. Side-effects: penile pain; priapism; local reactions. Intracavernosal therapy alprostadil/Caverjet (synthetic PGE1); papaverine (smooth muscle relaxant) ± phentolamine (α-adrenoceptor agonist). Training of technique and first dose is given by health professional. Needle is inserted at right angles into the corpus cavernosum on the lateral aspects of mid-penile shaft. Adverse effects: pain; priapism; haematoma. Vacuum erection device it contains 3 components: 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. Adverse effects: penile coldness; bruising. Penile prosthesis semi-rigid, malleable, and inflatable penile prostheses are available for surgical implantation into the corpora to provide penile rigidity and sufficient erectile size for sexual intercourse. Side-effects: mechanical failure; erosions; infections. P.483
Treatment options for erectile dysfunction

Organic Psychogenic
Eliminate underlying risk factors Psychosexual counselling ± partner
Oral medication Oral medication
Androgen replacement Intraurethral therapy
Intraurethral therapy Intracavernosal therapy
Intracavernosal therapy
Vacuum devices
Penile prosthesis

Retrograde ejaculation Definition Failure of adequate bladder neck contraction resulting in the propulsion of sperm back into the bladder on ejaculation. Aetiology Secondary to damage or dysfunction of the bladder neck sphincter mechanism. Underlying causes may be neurological (spinal cord injury; 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); transurethral resection of the prostate (TURP); or open prostatectomy. Incidence Retrograde ejaculation following TURP or open prostatectomy occurs in 9 out of 10 men and after BNI, in 1–5 in 10. Presentation ‘Dry’ ejaculation (failure to expel ejaculate fluid from the urethral meatus) and cloudy urine (containing sperm) in the first void after intercourse. Investigation The presence of >10–15 sperm per high-powered field in a post-ejaculate mid-stream urine specimen confirms the diagnosis of retrograde ejaculation. Treatment Medical therapy is initiated in men wishing to preserve fertility, and is only effective in patients who have not had bladder neck surgery. Oral adrenergic drugs may be used to increase the sympathetic tone of the bladder neck smooth muscle sphincter mechanism. Drugs include ephedrine sulphate (25–50mg QDS), pseudoephedrine (60mg QDS) or imipramine (25mg BD). Therapy is often given for 7–10 days prior to a planned ejaculation (co-ordinated with the partner’s ovulation). Alternatively, sperm retrieval may be attempted. 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 intrauterine insemination (IUI) or in vitro fertilization (IVF) treatments. P.485
Peyronie’s disease Definition A benign penile condition characterized by curvature of the penile shaft secondary to the formation of fibrous tissue plaques within the tunica albuginea. Epidemiology Prevalence: ~1%, predominantly affecting men aged 40–60 years. Pathophysiology Dorsal penile plaques are most common (66%). The corpus cavernosus underlying the lesion cannot lengthen fully on erection, resulting in penile curvature. It may be associated with distal flaccidity or an unstable penis (due to cavernosal fibrosis). The disorder has 2 phases:

  • Active phase (1–6 months): painful erections and changing penile deformity.
  • Quiescent phase (9–12 months): disease ‘burns out’. Pain disappears with resolution of inflammation, and there is stabilization of the penile deformity.

Aetiology The exact cause is unknown. 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). Autoimmune disease processes have also been suggested, and there is a reported familial predisposition. Presentation Pain and curvature of the erect penis; hard area (plaque) on penis; erectile dysfunction (30–40%); penile shortening. Associated disorders Dupuytren’s contractures (40%); plantar fascial contracture; tympanosclerosis; previous trauma; diabetes mellitus; arterial disease. Evaluation A full medical and sexual history are taken. Patient’s photographs of the curvature are useful. Assess the location and size of the plaque (is it tender?). Colour Doppler USS is used to assess vascular abnormalities, whereas contrast-enhanced MRI is indicated for complex and extensive cavernosal fibrosis. Management Early disease with active inflammation (<3 months, penile pain, changing deformity) benefits most from medical therapy. Surgery is indicated for a stable, significant deformity (preventing intercourse). Non-mechanical components of erectile dysfunction can be treated conventionally (oral or intracavernosal medications; vacuum device; penile implant).

  • Medical treatments Vitamin E (200mg TDS) for 3 months; tamoxifen 20mg BD for 3 months; colchicine (500mg TDS) for 6 weeks.
  • P.487

  • Extracorporeal shock wave therapy (ESWL) treatment of the plaque.
  • Nesbit’s procedure The penis is degloved via a circumglandular incision. An artificial erection is induced by intracavernosal saline injection. On the opposite side of maximal deformity, an ellipse is excised (a width of 1mm is taken for every 10° of penile curvature), and then closed with sutures. Success rates are 88–94%. Warn the patient that penile shortening of 2–3cm frequently occurs.
  • Plaque incision and grafting Incision of plaque with venous patch insertion to lengthen the affected side (and minimize penile shortening). Success rates 75–96%. Adverse effects: erectile dysfunction 5–12%.

Priapism Definition Prolonged and often painful erection in the absence of a sexual stimulus, lasting >4–6h, which predominantly affects the corpus cavernosa. Epidemiology Peaks in incidence at ages 5–10 and 20–50. Classification

  • Low-flow (ischaemic) priapism Due to veno-occlusion (intracavernosal pressures of 80–120mmHg). More common than high-flow priapism. Manifests as a painful, rigid erection, with absent or low cavernosal blood flow. Ischaemic priapism beyond 4h requires emergency intervention. Blood gas analysis shows hypoxia and acidosis.
  • High-flow (non-ischaemic) priapism Due to unregulated arterial blood flow, presenting with a semi-rigid, painless erection. Blood gas analysis shows similar results to arterial blood.

Aetiology Causes are primary (idiopathic) or secondary (see boxes) including:

  • Intracavernosal injection therapy—PGE1; papaverine
  • Drugs—α-blockers; antidepressants; antipsychotics; psychotrophics; tranquilizers; anxiolytics; anticoagulants; recreational drugs; alcohol excess; total parenteral nutrition
  • Thromboembolic—sickle cell disease (may cause stuttering/recurrent priapism); leukaemia; thalassaemia; fat emboli
  • Malignant infiltration of the corpora cavernosa (e.g. advanced bladder cancer)
  • Neurogenic—spinal cord lesion; autonomic neuropathy; anaesthesia
  • Trauma—penile or perineal injury resulting in cavernosal artery laceration or arterio-venous fistula formation
  • Infection—malaria; rabies; scorpion sting

Pathophysiology 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. Evaluation

  • Serum testing to exclude sickle cell and leukaemia.
  • Cavernous blood samples to determine type of priapism.
  • Colour Doppler ultrasound scan of cavernosal artery and corpora cavernosa. Reduced blood flow in ischaemic priapism; ruptured artery with pooling of blood around injured area in non-ischaemic priapism.

Management Low-flow priapism Aspiration of blood from corpora (50ml portions using a 18–20 gauge butterfly needle) ± intracavernosal injection of α1-adrenergic agonist (phenylephrine 10mg in 19ml saline, injected in 0.5–1ml aliquots every 5 min until detumescence occurs). Monitor BP and pulse during drug P.489
administration. Oral terbutaline may be effective for intracavernosal injection-related cases. Sickle cell disease requires, in addition, aggressive rehydration, oxygenation, analgesia, and haematological input (consider exchange transfusion). High-flow priapism Early stages may respond to a cool bath or icepack (causing vasospasm ± arterial thrombosis). Delayed presentations require arteriography and embolization of the internal pudendal artery. Complications Fibrosis and impotence. Causes of low- and high-flow priapism

Low-flow priapism High-flow priapism
Intracorporeal drug injection Arterio-venous fistula (secondary penile or perineal trauma)
Oral medications (anticoagulants)
Sickle cells disease (recurrent priapism)
Fat embolus
Spinal cord lesion
Autonomic neuropathy
Malignant penile inflammation

Examples of drugs which may cause priapism

α-blockers Prazosin; hydralazine
Antidepressants Sertraline; fluoxetine; lithium
Antipsychotics Clozapine
Psychotrophics Chlorpromazine
Tranquilizers Mesoridazine
Aniolytics Hydroxyzine
Anticoagulants Warfarin; heparin
Recreational drugs Cocaine

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