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A 43-year-old male presented to his doctor following the breakup of a long-term relationship. He was very tearful, expressing feelings of loneliness and isolation. He was finding it hard to gain access to his children and was experiencing financial hardship supporting two homes. He had lost his appetite and his sleep pattern was poor. He described frequent episodes of difficulty getting to sleep and early morning wakening. He denied any suicide ideation. The doctor diagnosed depression and prescribed a selective serotonin reuptake inhibitor (SSRI). He gave the man the number of a local counselling service.
On review four weeks later, the patient’s mood had improved somewhat. He noted, however, that he was having difficulty achieving and sustaining an erection. He found this very upsetting and a reflection of his ‘manhood’, which he already believed was poor following his marital breakdown. The doctor, on history and detailed focused examination, diagnosed erectile dysfunction (ED).
Following the exclusion of other causes of ED, the patient’s antidepressant was changed and he was prescribed a phosphodiesterase inhibitor to enhance his erection capacity to use as required. Shortly afterwards, his ED resolved.
Erectile dysfunction (ED) or ‘male impotence’ is a sexual dysfunction characterised by the ‘persistent or recurring inability to achieve and/or maintain an erection sufficient for satisfactory sexual activity’. It is a ‘neuro-vasculo-tissular phenomenon under hormonal control’. Though often perceived in clinical settings as a benign condition, ED is often one of the first clinical manifestations of coronary or peripheral arterial disease and may herald the onset of myocardial infarct or stroke. It is a significant and common medical problem believed to affect 10 per cent of men aged 40-70 years to differing degrees. ED can have a profound effect on the patient’s overall quality-of-life and can be associated with anxiety, depression, loss of self-esteem and self-confidence, and can inhibit interpersonal functioning. Partners too can feel rejected, unattractive, and guilty, feeling that they are to blame.
An erection occurs when blood enters and is retained in sponge-like corpus cavernosum in the penis. The process of erection is initiated by sexual arousal, which is activated in the higher cortical centres of the brain. These centres send signals through a complex neural network via the preoptic and paraventricular area of the hypothalamus. These signals ultimately result in the activation of the parasympathetic nerves in the sacral area, S2-S4. As a consequence of neural stimulation locally, adrenergic tone is inhibited and the nonadrenergic, noncholinergic (NANC) neurotransmitter nitric oxide (NO) is released from the NANC nerves and the endothelial cells. NO increases the level of cyclic guanosine monophosphate (cGMP). This leads to smooth muscle relaxation, increased arterial inflow and veno-occlusion producing the firmness necessary for sexual activity.
Achieving an erection is a very complex event and many chronic illnesses have been implicated in the genesis of ED. These may be classed as structural/anatomical, vasculogenic, neurogenic, hormonal, drug induced, or psychogenic.
Anatomical causes include hypospadias, Peyronie’s disease and micropenis.
Common vasculogenic causes include ischemic heart disease/atherosclerosis, hypertension, diabetes mellitus, dyslipidaemia, and smoking.
Neurogenic causes can be subdivided into central causes and peripheral causes:
– Central causes may be degenerative in nature, such as multiple sclerosis or Parkinson’s disease, stroke, spinal cord damage.
– Peripheral causes include diabetes mellitus and other causes of polyneuropathy. Surgical damage may also result in peripheral nerve damage.
Hormonal causes of ED include hypogonadism, both primary and secondary, hyper and hypothyroidism and hyperprolactinaemia.
Drug-induced causes include antidepressants, such as some SSRIs, antipsychotics, some antihypertensives, anti-androgens, and recreational drugs commonly associated with ED are alcohol, heroin, cocaine, marijuana, and methadone.
Psychogenic causes include lack of arousability and difficulties with sexual intimacy, partner-related or performance-related issues, stress or generalised anxiety disorder.
Psychological causes of ED occur when an erection fails as a consequence of thoughts or feelings rather than physical reasons. ED should only be attributed to psychological illness in the absence of physical causes and represent between 10-20 per cent of all cases of ED. These include anxiety about sexual performance or identity, depression, relationship issues such as guilt, sexual problems in the partner, lack of sex education, history of psychological trauma or abuse, and anxiety/stress disorder with maybe a financial or work component. Always try to identify possible issues regarding sexuality or gender identification.
Lifestyle factors include abuse of alcohol, heroin, cannabis, cocaine, anabolic steroids, and cigarette smoking. ED increases with age and by the age of 70 years, more than 70 per cent of men will be affected to some degree.
Diagnosis of ED is reached by a full and detailed sexual and medical history, including drug use, prescribed and illicit and a physical examination. Certain pertinent questions are very useful:
Duration of ED: did it start gradually or suddenly?
Early morning erection – quality of these – have they changed over time? Firmness of erection. Is it different with different partners, masturbation, oral sex, or with condom use?
Frequency of intercourse – is there difficulty in penetration or loss of erection during coitus?
Is there any new curvature to suggest Peyronie’s disease?
Is there any specific issues regarding desire, arousal, ejaculation, or orgasm?
A detailed medical and psychological history is essential. It is crucial to document relevant comorbidities such as diabetes, peripheral vascular disease (PVD), neurological, liver, or renal disease. A full drug history should be elicited, both prescribed and non-prescribed, including alcohol. Any surgical or trauma to the genital area or spine should be recorded. Time should be given to assessing the patient’s partner relationship should such exist.
Following a detailed history, a full examination, again relevant to the issue at hand, should be undertaken.
How is the patient presenting? What is the general demeanour? Any evidence of blunting of affect or anxiety?
Assessment of the patient’s general health and overall demeanour is important. This includes evidence of secondary sexual characteristics, gynaecomastia if present and hair loss in the axillae or pubic area suggestive of hypogonadism.
Presence or absence of peripheral pulses for evidence of PVD.
Neurological examination particularly assessing saddle sensation and reflexes such as cremasteric reflex.
Testicular exam for hypogonadism and penile examination for fibrous plaques suggestive of Peyronie’s disease.
Rectal examination to assess anal tone and prostate examination for evidence of prostatomegaly.
Abdominal examination for potential organomegaly or signs of renal or liver diseases and cardiovascular examination, which might limit therapeutic options.
If deemed necessary, blood testing for hypogonadism should be arranged: Testosterone, sex hormone binding globulin and prolactin. Screening should also be arranged for hyperthyroidism and hypothyroidism and diabetes: T4/TSH, fasting blood sugar, glucose tolerance test or HbA1c if warranted. A fasting lipid profile might identify atherosclerotic risk while liver and renal function can be assessed with LFT and U+E.
It is estimated that 40 per cent of men over the age of 45 years have low testosterone. The quantitate Androgen Deficiency in the Ageing Male questionnaire (qADAM) was devised in 2010. It is a 10-question questionnaire with a Likert scale of 1-5, where 5 represents the absence of symptoms and 1 the maximal symptoms. The summation of all 10 questions yields a score from 10-50 with 10 being the most symptomatic and 50 the lease symptomatic. The questions asked assess libido, energy level, strength/endurance, enjoyment of life, happiness level, strength of erections, work performance, sleep after dinner, sports ability, lost height. The aADAM correlates well with serum testosterone and is a potential screening tool for androgen deficiency. The results can be followed over time and it is a useful tool to monitor response to testosterone replacement.
The psychology of ED
The psychology of ED is complicated. Many men believe that the ability to get and sustain an erection is crucial for a man to satisfy his partner, a belief also held by many partners. As mentioned, psychological factors are responsible for about 10-20 per cent of all cases of ED. It may be a secondary reaction to an underlying physical cause. In some cases, the psychological effects of ED may stem from childhood abuse or sexual trauma. However, the most common psychological causes of ED include stress, anxiety, guilt, depression, low self-esteem, and indifference. Stress can be job or money-related, or the result of marital/relationship problems. ED is frequently associated with performance anxiety and recurrent anticipatory fear of not achieving an erection becomes a self-fulfilling prophecy. The fear that one’s partner is not being satisfied can lead to guilt. Depression is a common cause of ED and can be very debilitating. Unfortunately for those physicians charged with treating depression, therapeutic options, such as SSRIs, can also cause ED. Low self-esteem can be due to prior episodes of ED (thus a feeling of inadequacy) or can be the result of other issues unrelated to sexual performance. ED may result in indifference to sex, as a result of age or loss of interest in sex.
‘Chem-sex’ refers to the use of recreational drugs during sex. The term ‘slamming’ refers to the use of drugs, often by injection during group sex parties, where partygoers take drugs such as crystal meth or mephadrone to help enhance and prolong sexual activity. The drugs cause an intense high, an increased libido, and prolong the duration of sex often for days. In the recent years, there have been reports of an increase in people accessing addiction services in the UK, particularly in London, to address their chem-sex drug use. The intense highs of crystal meth and mephadrone are followed by intense lows. Users describe staying awake for days at a time while coming down from the drugs, feeling paranoid and depressed. Suicides related to chem-sex drugs have been reported. Where there may not be a physical addiction to crystal meth or methadrone, the psychological addiction is immense and many report that ‘sober sex’; sex without chemicals, is no longer achievable. Without chemicals, ED is a true reality for many. Overuse of pornography can also result in ED where reality cannot match the exaggerated ‘norm’ of onscreen sex. Many men feel totally physically inadequate. Our need for society’s move towards ‘instant gratification’, to have an instant erection and to perform outstandingly, is fuelling our already psychologically challenged patients.
The phosphodiesterase-5 inhibitors (PDE5) should be offered as first-line treatment to the patient unless contraindicated. All three drugs, sildenafil, vardenafil, and talalafil block penile specific PDE5, thereby preventing the breakdown of cGMP. cGMP, as mentioned earlier, leads to smooth muscle relaxation, increased arterial inflow and veno-occlusion producing the firmness necessary for sexual activity. All three drugs are generally well-tolerated. Reported side-effects include headache, flushing, nausea, and nasal stuffiness. Caution is essential in those with a history of cardiovascular disease and PDE5 inhibitors are contraindicated with nitroglicerine, such as, GTN spray or nitrate containing compounds such as amyl nitrate (‘poppers’). It has also been suggested that vardenafil should not be used with drugs that prolong the QTc interval.
As mentioned earlier, low testosterone is surprisingly common. Testosterone supplements, however, are only used for men with low testosterone.
Alprostil is believed to promote intracellular accumulation of cAMP, which results in smooth muscle relaxation. It can be administered intraurethrally or by injection into the corpus cavernosum. For intracorpeal injection, the alprostil is often given with papaverine (a non-specific phosphodiesterase inhibitor) or phentolamine (a competitive, non-selective alpha 1 and alpha 2 adrenorecptor blocker).
Other non-surgical treatments for ED include vacuum constriction devices. Once the erection is achieved under vacuum, a constriction band is applied to the base to the penis. The device is safe but is contraindicated with some blood dyscrasias and for those on warfarin.
Surgical penile prosthesis is another therapeutic option for ED. Saline filled silicone devices which appear natural in the flaccid state and malleable devices are most popular. Satisfaction rates in excess of 90 per cent have been reported.
Successful treatment of ED can be associated with significant improvement in psychological well-being and can greatly improve the quality of relationships. Management includes treating depression and anxiety and changing medication where appropriate. Stopping smoking, exercising, losing weight, controlling blood pressure and improving blood sugar control in diabetics, curtailing excess alcohol, and stopping illicit drug use can all improve ED. Where there is a significant psychological component, psychosexual therapy may play a role. We need to appreciate that mastering the art of gratifying sex takes time and this time may be very variable from man to man. Where organic causes are suspected, there are oral medications, topical and injectable preparations for the penis and finally vacuum constriction devices or surgical implants for the penis.