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344 Challenging Concepts in Urological Surgery
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is often a plaque palpable which can become hard, and can be assessed by ultrasound.5 However, the
size and magnitude of the plaque bears no influence on the degree of deformity.6 It is at this stage that
surgical intervention can be considered.
Learning point Psychosexual impact
It is essential that the psychosexual impact of PD on patients is assessed and managed
appropriately. Approximately 48% of men with PD are affected by depression, with 26%
moderately and 22% severely affected, and 81% reporting emotional distress associated with PD.
Four core domains have been identified as being important to men with PD: physical appearance
Expert comment
The presence of ED
It is essential to establish
if ED is present as this will
impact intervention. A trial of
phosphodiesterase type 5 inhibitors
can be given to see if ED can be
improved.
Patients need to be counselled
appropriately as performing
surgical intervention in patients
with refractory ED will render any
repair useless. Such patients can be
considered for penile prosthesis.
and self- image; sexual function and performance; PD- related pain and discomfort; and social
stigmatization and isolation.
Depression has been associated with a twofold increase in sexual problems, namely reduction in
sexual desire, libido, erectile dysfunction (ED), and orgasm. Antidepressants can cause treatmentemergent sexual dysfunction, further affecting overall problems.10 This can result in exacerbation of ED
symptoms in PD.
Expert comment Evaluation of PD
There is currently no internationally accepted standard of evaluation for PD. Current recommendations
in the examination for PD include degree of curvature and stretched penile length, which is equivalent
to erect length.11 This can be with self- photograph, vacuum- assisted erection test, or pharmacologicalinduced erection. The International Index of Erectile Function may be useful but has not been validated
in PD.12 Peyronie’s Disease Questionnaire may be helpful in establishing baseline scores and in
determining change over time (level of evidence 2a).
Ultrasound scan measurement of plaque size is user dependent and inaccurate, and is not
recommended in everyday clinical practice (level of evidence 3).6 Doppler ultrasound scanning can be
used in those with ED, for vascular assessment (level of evidence 2a).
9
7,8
13
14
Clinical tip Erection test
When performing the artificial
erection test, it is best to compress
the base of the penis against the
pubic bone, so as not to miss any
proximal element to the curvature.
A tourniquet can then be used if
proximal disease is excluded.
Clinical tip Mobilization of
the neurovascular bundle
Great care needs to be taken when
mobilizing the neurovascular
bundle in order to avoid
neurovascular complications
such as glans ischaemia. It can be
performed laterally to medially, or
medially to laterally after excising
the dorsal vein.
Given the degree of curvature and waist deformity of the penis, a Nesbit or its alternative penile- shortening procedures was ill- advised due to the degree of penile length
loss, therefore the patient was counselled regarding a Lue procedure, and advised to
stop smoking and continue with his exercise programme while awaiting intervention.
The management of stable PD depends on whether ED is present and penile length
(Figure 35.1).
The operation involved initial circumcision, followed by degloving of the penis
down to the level of Buck’s fascia. Two butterfly needles were inserted from the glans
into the corpora cavernosa. An erection test was then performed with normal saline
and a tourniquet around the base of the penis to further characterize site, plane, and
degree of curvature (Figure 35.2a).
As the site of the curvature and plaque disease was on the dorsal aspect of the
penis at the level of the midshaft, the neurovasculature was mobilized with Buck’s
fascia. This allowed for direct access to the affected tunica albuginea. A modified H
incision was made into the point of maximum curvature of the tunica thereby creating
a window for grafting with bovine collagen Permacol® (Figure 35.2b).
Finally, a repeat erection test was completed after closure of Buck’s fascia to determine if any further corrections were required, with an accepted residual curvature of
up to 10° (Figure 35.2c). The skin was then replaced and sutured closed.
Stable disease
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345Case 35 Peyronie’s disease
Erectile
dysfunction
Treatment responseNo treatment response
Adequate penis length
curvature <60°
absence of special
deformities (hourglass,
hinge)
Penile prosthesis
(remodelling plaque)
Figure 35.1 Surgical algorithm for PD.
Expert comment Congenital penile curvature
Penile curvature can either be congenital or acquired. Congenital penile curvature is rare with an
incidence of <1% and results from disproportionate development of the tunica albuginea of the
corporal bodies, with the most common curvature being ventrally.15 Any intervention is deferred until
after puberty and intervention shares the same principles as PD.
Congenital penile curvature typically affects the entirety of the tunica rather than an affected site with
PD. Surgical correction therefore should take place in specialized centres only with clinicians used to
dealing with challenging cases.
4
Nesbit or plication
procedures
No erectile
dysfunction
Short penis
curvature >60°
presence of special
deformities (hourglass,
hinge)
Tunica lengthening
procedures
Figure 35.2 Intraoperative images of penile straightening surgery (Lue’s). (a) Erection test to characterize
site, plane, and degree of curvature. (b) Modified H incision. (c) Final erection test following closure of
Buck’s fascia.
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Learning point Prevalence and aetiology of PD
PD is a fibrotic disease of the tunica albuginea which results in a focal loss of elasticity at the involved
site of plaque formation. During erection, non- uniform expansion results in curvature at the site due
to loss of longitudinal stretch.
The aetiology of PD is unclear; however, the most widely accepted hypothesis is that of a localized
response to endogenous factors from repetitive microvascular injury or trauma within the bilayer of
the tunica albuginea in genetically susceptible individuals.
process, characterized by remodelling of connective tissue into a dense fibrotic plaque.
The prevalence of PD is 0.4– 9%
typical age at presentation being 55– 60 years. Risk factors include trauma, genetic susceptibility, diabetes,
hypertension, lipid abnormalities, ischaemic cardiomyopathy, ED, smoking, and alcohol excess.
Learning point Non- surgical management of PD
Conservative therapy is predominantly focused towards patients in the early stages of the disease,
when the plaque has not densely fibrosed or calcified. However, the efficacy in distinct patient
populations is yet to be demonstrated.
There are a multitude of treatment options for PD; however, due to the incomplete aetiological
understanding there is a lack of efficacious treatment, and large multicentre series or randomized
controlled trials are lacking.21 Non- surgical treatment modalities have focused on disrupting or reducing
the acute phase process. Options include oral, mechanical, topical, and intralesional therapies (Table 35.1).
While other therapies may have potential benefit in differing stages of PD including potassium
para- aminobenzoate, intralesional and topical verapamil, intralesional interferon, and iontophoresis,
they have not shown sufficient evidence to be recommended.4 Other therapies have shown little
or no benefit such as vitamin E, tamoxifen, colchicine, acetyl esters of carnitine, pentoxifylline,
extracorporeal shockwave lithotripsy, and intralesional steroids and are currently not recommended
by the European Association of Urology.
16
3,20
; this figure may be higher in specific high- risk subgroups, with a
4
4
17,18
This results in a prolonged inflammatory
19
21
Table 35.1 Non- surgical management of PD
Oral Topical Mechanical
Vitamin E
Potassium para- aminobenzoate
Tamoxifen
Colchicine
Verapamil
H- 100 gel
Iontophoresis
Extracorporeal shockwave lithotripsy
Traction device
Vacuum device
Acetyl esters of carnitine
Pentoxifylline
Evidence base Intralesional collagenase Clostridium histolyticum
Intralesional collagenase Clostridium histolyticum (CCH) is the only medical therapy approved by the
US Food and Drug Administration and European Medicines Agency for the treatment of PD with
dorsal or lateral curvature >30°. Two large, randomized, placebo- controlled, double- blind trials
(IMPRESS I and II) have confirmed its efficacy22 with improvement in curvature of 34% versus 18.2%
in placebo. Peyronie’s Disease Questionnaire and International Index of Erectile Function scores
improved and overall satisfaction rates were also higher.
22,23
Significant adverse events related to this
included three corporeal ruptures, all requiring surgical repair, and three haematomas.
The International Consortium on Sexual Medicine guidelines recommend the use of intralesional CCH
should be limited to stable curvature between 30° and 90°, with normal erectile function, and no
underlying hour- glass deformity, plaque calcification, or proximally located plaque at the base of the
penis, level of evidence 2. Clinical trials have not yet established CCH use in ventral curves, or complex
PD effect in these groups.21 Its use during the acute phase is currently under investigation.
24
Evidence base Traction device
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A recent non- randomized controlled trial into the use of traction device in the acute phase of PD
found that there was a mean improvement curvature of the penis of 20° in 55 patients, compared
to 41 patients in the non- intervention group. There was also improved sexual function, reported
pain level, and a reduction in the need for surgical intervention.25 However, in order to attain these
results, it requires commitment from a patient perspective. The traction device needs to be worn for a
minimum of 6 hours a day for 6 months. In practice, this is difficult to achieve, and therefore vacuum
devices are more commonly used despite lack of high- level evidence.
4
Future directions Developments in non- surgical management of PD
Recent development in non- surgical management have included the use of hyaluronic acid, plasma- rich
platelets, H- 100 gel, and combination therapy. Further larger- scale studies are required to assess their
26
efficacy.
There is also increasing evidence for the role of mesenchymal stem cell therapy. This may result in
beneficial effects of local growth and repair, leading to regeneration of tissue. Studies involving rat
models injected with adipose tissue- derived stem cells into tunica albuginea and corpus cavernosum
showed statistically significant results in the improvement of erectile function through prevention of
fibrosis during the acute phase.27 It has also been used in conjunction with interferon and has shown
promising results.28 Very few human studies have been performed to date and with small numbers but
results show that it may be beneficial.
29
Learning point Penile shortening surgery
There have been developments of penile shortening surgery throughout the years, since the
Nesbit procedure was first documented in 1965.30 There are three techniques in current use
for the management of penile curvature. All procedures involve techniques performed on the
convex side of the penis, opposite to the site of plaque formation, in order to achieve penile
straightening.
● Nesbit procedure: excision of a 5– 10 mm elliptical section of the tunica albuginea or
approximately 1 mm for every 10° of curvature.
● Plication Heineke– Mikulicz principle (Yachia or Lemberger): after exposure, single or multiple
longitudinal incisions to the convex side of the penis, with a vertical incision and a horizontal
closure to the tunica, thus applying the Heineke– Mikulicz principle.
● ‘Sixteen- dot’ Lue procedure: parallel plication of the tunica albuginea with non- absorbable
suture under minimal tension. The central point of curvature needs to be established, then 16
(two pairs) or 24 dots (three pairs) are marked at 0.5 cm distance from each other and plicated.
Satisfaction rates in those with normal erectile function preoperatively are 74– 94% for Nesbit
corporoplasty and 52– 98% for plication procedures in patients with PD, while success rates for
penile straightening ranges from 57– 100% to 73– 96% respectively.31 Degrees of complications and
risks vary between the different methods but include penile shortening, ED, change in sensation,
recurrent curvature, palpable sutures, and the potential need for circumcision at the time of
operation.
32
Learning point Penile lengthening procedures
Penile lengthening procedures, as described in the case of our patient, are performed on the concave
side of the penis, and require a graft. While the aim of the procedure is to preserve length, 17– 40% of
patients still experience a degree of shortening over time.
33
A Lue procedure as described, involves either a ‘H’ or double- ‘Y’ incision into the tunica albuginea,
creating a defect on the affected concave side which is grafted. In a recent review of plaque incision
and grafting, successful straightening was reported in 80– 96.4% of patients; however, ED rates were
347Case 35 Peyronie’s disease
Expert comment The aim
of surgical management
The aim of surgical intervention is
to correct the curvature of the penis
in a patient with stable disease,
allowing for sexual intercourse and
improvement in quality of life. It
is usually recommended to wait a
year from the onset of symptoms
before performing any surgical
intervention. There are three types
of surgical strategies available for
patients with PD or congenital
curvature: a penile shortening
procedure, a penile lengthening
procedure, or prosthesis.
Learning point Penile
prosthesis
This is typically reserved for
patients with severe PD, usually
in combination with ED with
or without complex deformity
such as a hinge deformity,
particularly if non- responsive
to phosphodiesterase type 5
inhibitors. Penile prostheses are
often used in conjunction with
grafting or plication techniques
in order to achieve sufficient
correction, where intraoperative
modelling of the penis through
manually bending in the opposite
direction to the curvature is not
4,33
sufficient.
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higher than for penile shortening procedures. The percentage of patients requiring adjunctive therapy
was between 4.6% and 67.4% postoperatively, and 0– 11.8% were unable to achieve erection.34
Factors that are associated with increased rates of ED are excision of plaque, the use of larger grafts,
preoperative ED, age >60 years, and ventral curvature.
Future directions Penile volume- loss deformity
Penile volume- loss deformity is often overlooked, it is reported to be present in 65% of men with PD
curvature and 10– 13% of those with <10° curvature. This can result in global penile length loss, hourglass deformity, unilateral indentation, distal tapering, or proximal or distal girth loss. These changes
alone can result in axial instability, psychological distress, and decreased sexual activity. Volume loss
deformities are often difficult to quantify and are typically not reported in outcome measurements.
Further quantitative investigation is required for the development of volume- restoring therapies.
A final word from the expert
PD is a poorly recognized but fairly common condition primarily affecting the ageing male, with
a peak age of incidence in the early 50s. The pathophysiology has yet to be fully clarified, but
there is an association with vascular risk factors such as diabetes and other fibrotic conditions
such as Dupuytren’s contracture.
It typically has an acute inflammatory phase followed by a chronic and stable phase which
usually plateaus within a year of symptom onset, resulting in fibrosis of the tunica albuginea. It
can present in a similar way to those with a clear history of penile injury.
Symptoms include a palpable lump in the penis, penile pain (in the acute phase), penile
shortening, or ED, but the commonest reason to seek medical attention is a penile curvature
during erection, prohibiting sexual intercourse.
Patient assessment includes taking a clear history of the symptoms, defining the patient’s
main concerns, examining the penis, and a reliable assessment of the degree of curvature or
deformity— either by good photographic evidence or a pharmacologically induced erection
in the clinic. If left alone in the acute phase, there is a 3– 13% chance of improvement of the
curvature and a 30– 50% chance of further progression.
Treatment choices should be directed at the patient’s concerns and priorities. There is no
effective medical therapy that can reverse the fibrosis of PD, and realistic options lie between
mechanical stretching therapy, intratunical injections, or surgery. The evidence for mechanical
stretching therapy such as the vacuum erection device or penile stretchers is low level, and the
success rates low, but the risks are minimal. Rather than just wait, patients may opt to do this in
the early phase of the disease when it is too early to consider surgery.
More recently, level 1 evidence has emerged for the benefits, though modest, of intratunical
injections of CCH (Xiapex®) as an option for those not ready for or not wanting to consider
surgery. On average, a 34% improvement in curvature can be achieved, and the results are better
in the milder curvatures.
Surgery remains a mainstay of treatment for stable disease (>1 year). Curvatures of <60°
can be corrected by shortening the convex side (corporoplasty) by a number of methods
such as excision, plication, or the Heineke– Mikulicz principle. This will cause a geometric
and proportional shortening of the erect penis, and is therefore not advised in curvatures
of >60°. For more severe curvatures, an incision and grafting procedure is advised which
aims to lengthen the shortened concave side, though this is associated with a significant
35
36
complication profile including ED and recurrent curvature. For this reason, a penile prosthesis
https://t.me/med1917
is recommended as the best option where there is a combination of severe curvature and preexisting ED.
Severe PD/ penile fibrosis can be a challenging problem to treat, impossible to reverse, and
often associated with psychological morbidity, so it is vital to manage patient expectations and
counsel patients appropriately from the start.
349Case 35 Peyronie’s disease
References
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of erectile function (IIEF): a multidimensional scale for assessment of erectile dysfunction.
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2013;190(2):627– 634.
14. Hellstrom WJ, Bivalacqua TJ. Peyronie’s disease: etiology, medical, and surgical therapy. J
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15. Yachia D, Beyar M, Aridogan IA, Dascalu S. The incidence of congenital penile curvature. J
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2007;4(6):1527– 1538.
17. Brock G, Hsu GL, Nunes L, von Heyden B, Lue TF. The anatomy of the tunica albuginea in
the normal penis and Peyronie’s disease. J Urol. 1997;157(1):276– 281.
18. Gonzalez- Cadavid NF. Mechanism of penile fibrosis. J Sex Med. 2009;6(3):353– 362.
19. Kumar B, Narang T, Gupta S, Gulati M. A clinic- aetiological and ultrasonographic study of
Peyronie’s disease. Sex Health. 2006;3(2):113– 118.
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20. Schwarzer U, Sommer F, Klotz T, et al. The prevalence of Peyronie’s disease: results of a
large scale survey. BJU Int. 2001;88(7):727– 730.
21. Chung E, Ralph D, Kagiolu A, et al. Evidence- based management of Peyronie’s disease. J
Sex Med. 2016;13(6):905– 923.
22. Gelbard M, Goldstein I, Hellstrom WJ, et al. Clinical efficacy, safety and tolerability of
collagenase clostridium histolyticum for the treatment of Peyronie disease in 2 large doubleblind, randomized, placebo controlled phase 3 studies. J Urol. 2013;190(1):199– 207.
23. Gelbrand M, Lipshultz LI, Tursi J, et al. Phase 2b study of the clinical efficacy and
safety of collagenase Clostridium histolyticum in patients with Peyronie disease. J Urol.
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24. Yang KK, Bennett N. Peyronie’s disease and injectable collagenase Clostridium
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25. Martinez- Salamanca JI, Egui A, Moncada I, et al. Acute phase Peyronie’s disease management with traction device: a non- randomised prospective controlled trial with ultrasound
correlation. J Sex Med. 2014;11(2):506– 515.
26. Randhawa K, Shukla CJ. Non- invasive treatment in management of Peyronie’s disease. Ther
Adv Urol. 2019;11:1– 13.
27. Castiglione F, Hedlund P, Van der Aa F, et al. Intratunical injection of human adipose tissuederived stem cells prevents fibrosis and is associated with improved erectile function in a
rat model of Peyronie’s disease. Eur Urol. 2013;63(3):551– 560.
28. Gocke A, Abd Elmageed ZY, Lasker GF, et al. Intratunical injection of genetically modified
adipose tissue- derived stem cells with human interferon α- 2b for treatment of erectile dysfunction in a rat model of tunica albugineal fibrosis. J Sex Med. 2015;12(7):1533– 1544.
29. Levy JA, Marchand M, Iorio L, Zribi G, Zahalsky MP. Effects of stem cell treatment in
human patients with Peyronie disease. J Am Osteopath Assoc. 2015;115(10):e8– e13.
30. Nesbit RM. Congenital curvature of the phallus: report of three cases with description of
corrective operation. J Urol. 1965;93:230– 232.
31. Çayan S, Aşcı R, Efesoy O, et al. Comparison of patient’s satisfaction and long- term results
of two penile plication techniques: lessons learned from 387 patients with penile curvature.
Urol. 2019;129:106– 112.
32. Ralph D, Gonzalez- Cadavid N, Mirone V, et al. The management of Peyronie’s disease: evidence- based 2010 guidelines. J Sex Med. 2010;7(7):2359– 2374.
33. Gaffney CD, Pagano MJ, Weinberg AC, et al. Lengthening strategies for Peyronie’s disease.
Transl Androl Urol. 2016;5(3):351– 362.
34. Rice P, Somani BK, Rees RW. Twenty years of plaque incision and grafting for Peyronie’s
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36
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CASE
Ejaculatory orgasmic
disorders
Maria Satchi
Expert commentary David Ralph
Case history
A 50- year- old Afro- Caribbean male was referred to a tertiary urology service for investigation and management of an 18- month history of delayed and absent ejaculation
and difficulty reaching orgasm. He felt the time to reach orgasm was prolonged and
this was followed by small volume of ejaculate or more often, a ‘dry ejaculate’. He
was able to achieve a spontaneous erection; however, he felt this was not as rigid as
it had once been. He was most troubled by the reduction or on occasion, absence of
the ejaculate and said that in only one in 20 episodes he would note a small volume
expelled, the rest remained ‘dry’. On the occasion he was able to reach orgasm, he felt
the urine was cloudy.
Expert comment Ejaculation versus orgasm
Ejaculation and orgasm, although linked, are two separate neurophysiological processes that occur
during peak sexual arousal. In the absence of an underlying neurological disorder, ejaculation
typically promotes a state of orgasm. However, ejaculation can occur without orgasm and vice
versa. It is therefore important to view ejaculatory disorders and orgasmic disorders separately with
an understanding of the underlying physiology. During the history taking process ascertain if the
symptoms have been lifelong or acquired, present during masturbation and sexual intercourse and if
situational or consistent. This will help to explore an organic versus psychological cause.
Learning point Physiology of ejaculation
Ejaculation is under control of the autonomic nervous system, predominantly the sympathetic nervous
system, and has been described in two phases: emission and expulsion.
The emission phase can be stimulated by tactile stimulation of the glans penis or by visual or physical
stimulation which is under cerebral control. On activation, sensory information is sent via the dorsal
penile nerve and pudendal nerve which enter the spinal cord at S2– S4 to relay information to the
thalamus and sensory cortex. Central coordination of afferent sensory information is mainly in the
medial preoptic area, paraventricular nucleus, and periaqueductal grey and this plays an important
role in sexual function.
Sympathetic efferent nerve fibres from T10– L2 via the hypogastric nerves reach the pelvic plexus
and stimulate smooth muscle contraction of the epididymis and vas deferens to propel sperm to
reach the prostatic urethra via the ejaculatory ducts along with the glandular secretions from the
seminal vesicles, bulbourethral glands, and prostate to form seminal fluid. Contraction of the internal
urethral sphincter with simultaneous relaxation of the external urethral sphincter prevents retrograde
ejaculation (RE) into the bladder and promotes forward antegrade ejaculation.
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During the expulsion phase, somatosensory information reaches S2– S4 of the spinal cord via the
dorsal penile and pudendal nerves. Onuf’s nucleus in S2– S4 of the spinal cord sends out efferent
somatomotor signals to stimulate rhythmic contraction of the ischiocavernosus and bulbocavernosus
muscle which are under control of the somatic nerves. To achieve antegrade ejaculation, the bladder
neck remains closed.
Prior to this, the patient had no concerns regarding his ability to orgasm or ejaculate. He was unable to identify any specific triggers or new medications that coincided
with the onset of his symptoms. On review of his past medical history, he was a
human immunodeficiency virus (HIV)- positive male, diagnosed 18 years ago with a
consistently undetectable viral load and a CD4 count of 700 cells/ mm3. He had no
prior history of abdominal or pelvic surgery. His only medication was his long- term
antiretroviral medications aciclovir and Eviplera®, a combination of emtricitabine,
rilpivirine, and tenofovir. He was in a stable, loving relationship and could not identify
any psychological stressors or triggers.
Expert comment HIV- positive men
Ejaculatory and orgasmic disorders in HIV- positive men on highly active antiretroviral therapy have
been reported in various studies ranging in prevalence between 24% and 49%. Similarly, other studies
have not found a significant positive association. The evidence regarding an association between
HIV- positive patients and ejaculatory disorders is not robust enough to draw definite conclusions.
Patients with HIV, similar to non- infected individuals, may have other comorbidities and psychosexual
issues that impact sexual function. They should be investigated and managed in the same way.2 This
differentiation can help with diagnosis and streamline management.
1
Learning point Classification of ejaculatory disorders
Ejaculatory disorders should be classified as lifelong where it is noted from the patients first sexual
experiences and lasts throughout, or acquired, where the current problem was preceded by normal
experiences. It should be differentiated from situational or consistent, and if the symptom is present
during masturbation and sexual intercourse. The impact on sexual activity and quality of life should be
noted and this can be done via patient questionnaires to assess the problem objectively.
Ejaculatory disorders can be classified as follows:
● Premature ejaculation (PE): according to the International Society of Sexual Medicine, PE is
the inability to delay ejaculation in the majority of cases of vaginal penetration causing personal
distress. It can be defined as intravaginal ejaculatory latency time of ≤1 minute (in lifelong PE) or a
bothersome reduction in intravaginal ejaculatory latency time to ≤3 minutes (in acquired PE).
● Delayed ejaculation (DE): marked delay or inability to achieve ejaculation where a prolonged period
of stimulation may be required and causes personal distress. There is no defined time period.3.
● Retrograde ejaculation (RE): absence of antegrade ejaculation and can be partial or complete.
Partial RE refers to sperm identified in the post- orgasmic urinalysis associated with an antegrade
ejaculate as well.
● Anejaculation: complete absence of antegrade ejaculation or RE.
Orgasmic disorders can be primary (lifelong) or secondary (acquired). They can be classified as follows:
● Delayed orgasmia (DO): World Health Organization 2nd Consultation on Sexual Dysfunction
defines DO as persistent or recurrent difficulty, delay in, or absence of attaining orgasm after
sufficient sexual stimulation, which causes personal distress.
● Anorgasmia (AO): The International Consultation on Sexual Medicine defines anorgasmia as the
perceived absence of orgasm, independent of the presence of ejaculation.
Learning point Drug history
https://t.me/med1917
A review of drug history is vital as pharmacotherapies can affect sexual function. Antipsychotic
medication that acts to block dopamine receptors in the brain can affect ejaculation causing DE or
RE. Out of the atypical antipsychotics, clozapine, has also been reported to cause RE. Methyldopa
can cause DE. Monoamine oxidase inhibitors and selective serotonin reuptake inhibitors (SSRIs)
that increase serotonin levels, can delay ejaculation and orgasm.4 Alpha- 1- adrenoceptor blockers
can affect ejaculatory volume with tamsulosin having the greatest effect compared to others such as
5
alfuzosin.
Learning point SSRIs
Serotonin (5HT) is thought to inhibit ejaculation. Consequently, SSRIs which inhibit the reuptake
of 5HT in the central nervous system can delay ejaculation and be used in the treatment of PE.6
Dapoxetine is a short- acting SSRI licensed for the use in PE. Other SSRIs such as paroxetine and
fluoxetine and tricyclic antidepressants such as clomipramine have been used; however, these are
unlicensed. These medications should not be used in young patients with bipolar disorder and should
be prescribed with caution in those with depression as there is an increased risk of suicide attempts or
thoughts. It should also not be offered to those trying to conceive as may have unfavourable effects
on sperm parameters. In patients already on an SSRI with DE/ AO, alternatives should be considered if
possible and advice sought from the lead physician.
On review of his social history, the patient had been an ex- smoker for 20 years,
denied any recreational drug use, and consumed 10 units of alcohol per week.
Examination of the external genitalia was normal.
Prior to his referral to the urology department, his general practitioner had organized a thyroid function test, full blood count, renal profile, lipid profile, and testosterone, fasting glucose, and glycated haemoglobin (HbA1c) tests. All blood counts
were within normal limits.
353Case 36 Ejaculatory orgasmic disorders
Learning point Hormonal regulation of ejaculation
Hormones can influence the regulation of ejaculation and therefore should be assessed.
● Testosterone: Elevated testosterone has been associated with PE, and low testosterone with DE and
reduced ejaculate volume. It is thought to play a role through its action on androgen receptors on
the medial preoptic area and pelvic floor muscles.
● Thyroid hormones: hyperthyroidism has been associated with PE, and hypothyroidism with DE.
● Prolactin: hyperprolactinaemia has been associated with anorgasmia and DE, and low levels of
prolactin with PE.3 Hyperprolactinaemia also inhibits gonadotropin- releasing hormone resulting in
decreased testosterone via the hypothalamic- pituitary- gonadal axis.
● Oxytocin: significance is unclear; however, an increase in level is noted after orgasm, reaching
baseline approximately 10 minutes later.
Expert comment Systemic examination for hormonal dysfunction
Examination of this patient should not only focus on the external genitalia but also look for systemic
signs and symptoms of endocrine disturbance. On examination, a loss of muscle mass, central obesity,
loss of body hair, small testes may be suggestive of low testosterone. Gynaecomastia may be seen
in both hypogonadism and hyperprolactinaemia. Patients with hyperthyroidism may have a visible
tremor, sweating and unexplained weight loss whilst those with hypothyroidism may have a history of
weight gain.
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