An explanation of the analogous roles of the penis and clitoris (proposed by Cohen and Cohen) is a very useful strategy for educating patients and helping them to understand the relationship of intercourse and penile and clitoris stimulation with orgasm. The simple model (see FIG. 116.1) can be shown to patients to explain, for example, why some women are unable to achieve orgasm by intercourse alone, especially using the conventional missionary position.3 It can readily be explained that clitoral stimulation in women is analogous to penile stimulation in men.
Analogous structures in male and female genitalia
Source: Reproduced with permission from G and M Cohen, Canadian Family Physician, 852, 31: 767–713
Female orgasmic difficulties
It is necessary to determine whether the woman has been anorgasmic or can experience orgasms from other activities such as masturbation, or manual or oral stimulation, even though she is non-orgasmic during intercourse. One-third of women may never experience orgasm, but enjoy their sexual relationships despite this.2
A common concern of women is the inability to regularly achieve orgasm through vaginal intercourse, believing there may be a physical cause. It is important to reassure that this is normal, as the majority of women are able to achieve orgasm through clitoral stimulation rather than intercourse.
The use of the Cohen model (see FIG. 116.1) is very helpful in emphasising the importance of clitoral stimulation.
Painful intercourse is a source of considerable distress both physically and psychologically for the sufferer and also for her partner. It may be one of the ‘hidden agenda’ presentations with a vague complaint such as ‘I am uncomfortable down below’. Tact and sensitivity is very important in management.
In particular it is helpful to keep in mind vulval vestibular syndrome, which has subtle physical signs (see CHAPTER 107). Important causes are listed in TABLE 116.6. A common problem encountered is the presence of painful scar tissue following an episiotomy, especially after the first vaginal delivery. Women who experience deep pain with intercourse need a gynaecological referral to assess for pelvic pathology.
Table 116.6Important causes of dyspareunia ||Download (.pdf) Table 116.6 Important causes of dyspareunia
|Pain worse on insertion |
|Physiological—inadequate lubrication |
|Provoked vestibulodynia syndrome |
|Vaginitis in chronic candidiasis |
|Vulvar dermatoses (e.g. dermatitis, psoriasis, lichen planus) |
|Vulvovaginal atrophy (e.g. postmenopausal) |
|Postnatal perineal scarring |
|Incompletely ruptured hymen |
|Pain worse on deep penetration |
|Pelvic adhesions |
|Ovarian and uterine tumours |
Management of dyspareunia involves treating the organic cause and giving appropriate advice about the use of lubricants, including topical oestrogen where indicated. While this may be enough in simpler cases, it does not address the often accompanied fear of penetration,2,7 which can continue even after the cause of dyspareunia is addressed.
Vaginismus is the involuntary contraction of muscles around the introitus (outer third of vagina) in response to and preventing the possibility of penetration. It can be classified as primary or secondary. In primary vaginismus, tampons will probably never have been inserted. It is often related to provoked vestibulodynia (vestibular hypersensitivity—see CHAPTER 107).
A fear of penetration can be the underlying cause and may be associated with fears of internal damage, pregnancy, learned negative attitudes to sex and past sexual trauma. It is not an uncommon cause of unconsummated marriage. The problem may respond to sensitive exploration of fears and education of the anatomy and physiology. Encourage use of lubricant and a comfortable sexual position that the woman can control, usually superior.
Consider referral to specially trained physiotherapists for pelvic floor relaxation and use of vaginal trainers. Vaginal trainers can be inserted at increasing sizes for desensitisation, allowing for progressive vaginal dilation. Expert counselling is necessary if fears remain a barrier to recovery.
The Diagnostic and Statistical Manual of Mental Disorders, fifth edition (DSM-5) defines lack of libido in women as sexual interest/arousal disorder (FSAD), and in men as male hypoactive sexual desire disorder (MSHDD).8 Lack of libido is usually due to a combination of factors including relationship issues, illness, medications, drug and alcohol use, hormonal changes, stress and fatigue. Other sexual difficulties that are treated medically (e.g. erectile dysfunction) may later present with reduced libido, indicating that the underlying relationship factors have not been addressed.
Individuals or couples may benefit from basic sexual counselling from their GP, while others may request input from a sex therapist. If lack of libido is secondary to menopause, a trial of hormonal replacement therapy (HRT) may be useful. Tibolone is an HRT that has been shown to have benefit in managing loss of libido in some women.9 Conclusive evidence in support of other drug therapies is lacking.10
Erectile dysfunction (impotence) is the inability to achieve or maintain an erection of sufficient quality for satisfactory intercourse.
Erectile dysfunction is a common problem. In an Australian study, the overall prevalence of erectile dysfunction was 61% (25% sometimes, 19% usually and 17% had complete erectile dysfunction). More than 20% of healthy men aged 60–65 years with no risk factors had moderate or complete erectile dysfunction.4
Traditionally, the aetiology of erectile dysfunction is classified into organic, psychogenic or mixed. In reality, however, anxiety and depression commonly accompany erectile dysfunction, irrespective of the original aetiology. Consequently, nearly all organic erectile dysfunction will eventually become ‘mixed’.11
psychogenic: related to stress, interpersonal or intrapsychic factors (e.g. depression, marital disharmony, performance anxiety)
neurogenic: disorders affecting the parasympathetic sacral spinal cord (e.g. multiple sclerosis); it usually develops gradually
chronic kidney disease
urological problems (e.g. Peyronie disorder, pelvic trauma and surgery)
Erectile dysfunction may be the first symptom of atherosclerotic disease (e.g. CAD).
The nature of the onset of erectile dysfunction is very important and this includes the nature of the relationship. Of particular importance is a drug history, including alcohol, nicotine, recreational drugs and pharmaceutical agents, particularly antihypertensives (beta blockers and thiazide diuretics), hypolipidaemic agents, antiandrogens (prostate cancer treatment), antidepressants, antipsychotics and H2-receptor antagonists. Ask about nocturnal and early morning erections.
Genitourinary, cardiovascular and neurological examinations are appropriate, although may not reveal the diagnosis. A focused examination should include a rectal examination and examination of the vascular and neurological status of the lower limbs and the genitalia, especially the testicles and penis. Check the cremasteric and bulbocavernosus reflexes.
fasting blood glucose
Other blood tests to consider:
When the aetiology is unclear, specialist testing includes a penile duplex doppler ultrasound using an intracavernosal vasoactive agent.
Address modifiable risk factors, including medications (if feasible), psychosocial issues and lifestyle (see NEAT, CHAPTER 7). Management should comprise appropriate patient education. The partner should be included in the discussions and general management process with an emphasis on bolstering the couple’s self-image, which may have been affected by feelings of rejection or avoidance.
These involve psychotherapy and sex behavioural modification as outlined earlier in this chapter under Basic sexual counselling. Referral to a consultant may be appropriate.
PDE-5 inhibitors: the phosphodiesterase type 5 (PDE-5) inhibitors are the first-line oral medication (see TABLE 116.7). They are about 70% effective but not very effective for neurogenic ED. They do not initiate an erection but enhance whatever erection the man is capable of having. Sexual stimulation is necessary. They are contraindicated if the patient has unstable angina, recent stroke or myocardial infarction. Use with nitrates should be avoided and a nitrate should never be taken within 24 hours of use. The interaction with nitrates can result in a severe and potentially fatal hypotensive response. PDE-5 inhibitors have the potential for side effects, especially headache. Treatment is not considered a failure until a full dose has been trialled 7–8 times.12
Table 116.7Phosphodiesterase type 5 inhibitors11 ||Download (.pdf) Table 116.7 Phosphodiesterase type 5 inhibitors11
| ||Sildenafil (Viagra) ||Tadalafil (Cialis) ||Vardenafil (Levitra) |
|Dosage (mg) ||25, 50, 100 ||5, 10, 20 ||5, 10, 20 |
|Usual starting dose (1 hour pre i/c) ||50 mg ||10 mg ||10 mg |
|Peak effect ||1 hour ||2 hours ||1 hour |
|Half-life (approximately) ||4 hours ||18 hours ||4 hours |
|Class side effects ||Headache, nasal congestion, facial flushing, dyspepsia || || |
|Specific side effects ||Blue vision, diarrhoea ||Myalgia, back pain ||Visual disturbance |
Intracavernosal vasodilator injections are second-line therapy and should be supervised by an experienced practitioner.
Alprostadil intracavernosal injections:
self-administered after supervised teaching (use a penile model if available)
start with a lower dose, 2.5–5 mcg
spontaneous erection in 5-20 minutes
if prolonged erection >2 hours take 120 mg pseudoephedrine orally and have a hot shower—repeat at 4 hours if necessary (provided not hypertensive)
Vacuum constriction devices (VEDs) may have a place in management, where pharmacological therapies have failed or are inappropriate. VEDs are often poorly tolerated in the long term due to side effects such as pain, inability to ejaculate, bruising, ‘hinging’ and paraesthesia.11
An inflatable prosthesis, showing positioning of the components
Premature ejaculation is defined as ‘ejaculation that occurs sooner than desired’ or, more precisely, as ‘persistent or recurrent ejaculation, before, on or shortly after penetration and associated with significant personal distress’. In most cases, this occurs within 1 minute of vaginal penetration. It may not be clearly described by the patient so a careful history is necessary to define the problem. Ensure that the person is not suffering from erectile dysfunction. Both patient and partner may complain about the problem.
There are many approaches to treatment but they are aimed either at prolonged ejaculatory control or at satisfactory sexual activity without preoccupation with ejaculation.
Non-pharmacological treatment includes psychosexual therapy and/or behaviour therapy (including ‘stop-start’ techniques).
SSRIs have also been reported as effective—using dapoxetine 30 mg, sertraline 50 mg or paroxetine 20 mg, all about 3 hours before intercourse.10 Some men may prefer to take SSRIs daily for managing premature ejaculation. Local anaesthetic has been suggested to reduce penile sensation, however this tends to be counterproductive as it reduces sexual pleasure.2