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Define Erectile Dysfunction: it’s physiological, social, and psychological causes. Give an analysis of the treatment programmes available and assess the likely outcomes of treatment
Erectile dysfunction (ED) is defined as the inability of the male to attain and maintain erection of the penis sufficient to permit satisfactory sexual intercourse. In the United States alone, it is estimated that ED afflicts 30 million men, but only 10% have received treatment1. The MAELS (Men’s Attitudes to Life Events and Sexuality) study were carried out to identify prevalence of erectile dysfunction and related health issues in the general male population in Europe, North and South America which includes eight countries (United States, United Kingdom, Germany, France, Italy, Spain, Mexico, and Brazil). MAELS study involved 2912 men and overall prevalence of ED in the MALES sample was 16%. The MALES study concluded that, high prevalence rates of ED and its association with co-morbid medical conditions, such as diabetes and depression, 58% of ED sufferers consult a physician about their problem and only 16% of men with self-reported ED maintain their use of oral therapy2
In Nicoloci et al study it was estimated that, the prevalence of ED varied across the included four countries, but it was common in all of them and increased in prevalence and severity with age. Despite national variations in prevalence, uniform associations were found between ED and medical conditions and lifestyle habits3. As the world’s population continues to increase and to live longer, it is predicted that 322 million men worldwide will suffer from this disorder by the year 20254.
Penile erection occurs as a function of trabecular smooth muscle relaxation and a subsequent increase in blood flow to lacunar spaces, which results in engorgement of the penis and restriction of venous drainage. Relaxation of the smooth muscle in the corpus cavernosum relies on the coordination of several central and peripheral nervous system signaling pathways. A change from primarily sympathetic to parasympathetic activity in the penis causes nitric oxide, the principal mediator of penile erections, to be released from endothelial cells lining the blood vessels and sinusoids of the corpus cavernosum and from nonadrenergic, noncholinergic nitric oxide- producing neurons5. Nitric oxide then diffuses across smooth muscle cell membranes and activates soluble guanylate cyclase, causing accumulation of cyclic guanosine monophosphate (cGMP) and resulting in a cascade of events that leads to the relaxation of smooth muscle and to an erection5, 6.
Mills et al hypothesized that the nitric oxide/protein kinase G pathway controls erection by not only lowering Ca21 but also by inhibiting the Rho-kinase pathway7. Detumescence is initiated by sympathetic stimulation, which is followed by ejaculation, contraction of cavernosal smooth muscle, and a return to penile flaccidity5.
Two hypotheses are believed most likely to play a role in the pathology of ED. The first considers metabolic imbalances between contractile (norepinephrine, endothelin, and prostanoids) and relaxatory factors (vasoactive intestinal polypeptide and nitric oxide) in the corpus cavernosum as the reason for ED8. The other focuses on a structural basis of the condition, such as an imbalance between trabecular smooth muscle and connective tissue and a possible role for corpus cavernosum hypoxemia in tissue fibrosis. The greater prevalence and severity of ED that occurs with aging may be a consequence of a shifting in the structural or metabolic balance in some men8. In addition, several medical conditions (diabetes, vascular disease and chronic diseases such as hepatic failure, renal failure and dialysis), medications or certain types of injury/surgery are believed to contribute to the development and maintenance of erectile dysfunction9. The aetiology of erectile dysfunction involves multiple psychogenic and organic factors, the causes and management of the same are described in this literature.
Figure 1: Anatomy and Mechanism of Penile Erection10.
Erectile dysfunction can be classified as psychogenic, organic (neurogenic, hormonal, arterial, cavernosal, or drug-induced), or mixed psychogenic and organic. The mixed psychogenic and organic form of erectile dysfunction is the most common10. Health (NIH) Consensus Conference on Impotence reported that approximately 75% of ED cases had physical rather than psychological etiologies1.
Psychogenic Erectile Dysfunction
Performance anxiety, a strained relationship, lack of sexual arousability, and overt psychiatric disorder such as depression and schizophrenia are the common causes of psychogenic erectile dysfunction10. The strong association between depressive symptoms and erectile dysfunction has been confirmed in study carried out by Aroujo et al. Moderate to complete erectile dysfunction is 1.82 times more likely in those who exhibit depressive symptomatology compared with those who do not. This association is independent of both age and Para-aging factors (e.g. Demographic, anthropometric, and lifestyle factors, health status, medication use, hormones commonly associated with age). Depressed individuals may be overly critical of them or have the tendency to self-focus, such behaviours in the context of sexual relations, may lead to performance anxiety, which may inhibit the man’s ability to obtain an erection. This relationship may manifest itself through the effect of depression on libido or sexual desire11. Decreased libido is the main problem reported in men with schizophrenia. Men who were treated with neuroleptic drug, associated with improve restoration of sexual desire but lead to difficulties with erection, orgasm and sexual satisfaction12.
Organic Erectile Dysfunction
Neurogenic Erectile Dysfunction
Penile erection is neurovascular event, in which hypothalamic and limbic pathways play an important role in the integration and control of reproductive and sexual functions. The medial preoptic area, paraventricular nucleus, and anterior hypothalamic regions modulate erections and coordinate autonomic events associated with sexual responses13. Neurologic disorders include compromised central neural pathways, such as Parkinson’s disease, Alzheimer’s disease, multiple sclerosis, stroke and cerebral trauma often cause erectile dysfunction by decreasing libido or preventing the initiation of an erection. Peripheral neural pathways disorders, such as spinal cord injury, pelvic injury also cause erectile dysfunction but the degree of erectile function depends largely on the nature, location, and extent of the lesion. Sensory involvement of the genitalia is essential to achieve and maintain reflexogenic erection, and this becomes more important as the effect of psychological stimuli abates with age10.
Vascular Causes of Erectile Dysfunction
Common risk factors associated with generalized penile arterial insufficiency include hypertension, hyperlipidemia, cigarette smoking, and diabetes mellitus. In diabetes, induced erectile dysfunction appears is due to the glycation end-product (AGEs) and increased level of oxygen free radicals, impaired nitric oxide synthesis, increased endothelin and endothelin-B receptor binding sites, up-regulated RhoA/Rho-kinase pathway, neuropathic damage and impaired cGMP-dependant protein kinase-1 (PKG-1)14. In study of arterial risk factors in 440 impotent male, 34% men had hyperlipidemia. Hyperlipidemia is a risk factor for the development of coronary artery disease and erectile dysfunction. Hyperlipidemia contributes to the development of atherosclerotic vessel disease, both in the coronary arteries and arterial blood supply of the penis. In study carried out by Virag and colleague, it was reported that penile vascular changes have been demonstrated in impotent patient with elevated serum lipids15.
In men with hypertension, erectile function is impaired mainly by the arterial stenotic lesions associated with increased blood pressure. In one study it was demonstrated that hypertension duration, hypertension severity and age constitute significant determinants of erectile dysfunction in patient with essential hypertension. Hypertension duration affected significantly erectile function that is 0-3 years: 14%, 3-6 years: 28%, >6 years: 60%, x2 = 21.37 – p<0.001. Hypertension severity was significantly related to erectile dysfunction (stage 1 hypertension: 24%, Stage 2 hypertension: 44.6%, x2 = 19.4 – p< 0.001. Erectile dysfunction was more frequent in older subjects (<50 years: 19.7%, >50years: 43.2%, x2 = 22.0 – p<0.001)16.
Focal stenosis of the common penile or cavernous artery most often occurs in men who have sustained blunt pelvic or perineal trauma. Levine and colleague study shown that the incidence of arterial lesions in the distal internal pudendal or common penile artery was significantly higher in patients with blunt pelvic trauma (92%) than in those with blunt perineal trauma (35%)17. Failure of the veins to close during an erection that is veno-occlusive dysfunction can cause erectile dysfunction. Veno-occlusive dysfunction may be caused by the development of large venous channels draining the corpora cavernosa, degenerative changes to the tunica albuginea due to peyronie’s disease, old age, diabetes mellitus or traumatic injury due to penile fracture18.
Structural alterations in the fibroelastic components of the trabeculae, cavernous smooth muscle, and endothelium may result in venous leak. Acquired venous shunts—the result of operative correction of priapism—may cause persistent glans/cavernosum or cavernosum/spongiosum shunting19.
Hormonal Causes of Erectile Dysfunction
Androgen influences the growth and development of the male reproductive tract and secondary sex characteristics. Its deficiency decreases nocturnal erections and libido. In one study it was demonstrated that erection in response to visual stimulation is preserved in men with hypogonadism. Erections to fantasy were significantly smaller and slower to develop in the hypogonadal men and did show significant improvement during androgen replacement. These results suggest that erections to certain types of stimuli are relatively independent of androgens, whereas the response to fantasy may be androgen dependent20.
Hyperprolactemia may be drug induced, or due to pituitary adenoma and chronic renal failure21. It results in reproductive and sexual dysfunction because prolactin inhibits central dopaminergic activity and therefore the secretion of gonadotropin-releasing hormone, resulting in hypogonadotropic hypogonadism. Symptoms may include loss of libido, erectile dysfunction10.
ED also may be associated with both the hyperthyroid and the hypothyroid state. Hyperthyroidism is commonly associated with diminished libido, which may be caused by the increased circulating estrogen levels, and less often with ED. In hypothyroidism, low testosterone secretion and elevated prolactin levels contribute to ED19.
Drug-Induced Erectile Dysfunction
Many drugs have been reported to cause erectile dysfunction. Central neurotransmitter pathways, including serotonergic, noradrenergic, and dopaminergic pathways involved in sexual function, may be disturbed by antipsychotic, antidepressant, and centrally acting antihypertensive drugs. Diuretics like thiazide have traditionally been reported to produce erectile dysfunction but the cause is unknown. Spironolactone which is known to exert an anti-androgen effect and it can cause erectile failure, gynecomastia and a decrease in libido10.
Approach to diagnosis and treatment of Erectile Dysfunction10
Diagnosis of erectile dysfunction
A thorough history taking is the important aspect of a patient’s assessment. If it indicates the possibility of the psychiatric problem, this problem should be addressed before treatment for erectile dysfunction. Some time psychosocial history may reveal deep-seated psychological problems or relationship conflicts that can be successfully treated by mental health professionals. Erectile dysfunction is occasionally the presenting symptom of a number of diseases such a hypertension, spinal cord injury, diabetes mellitus, coronary artery disease, pituitary adenoma and hyperlipidemia. Therefore detail history taking is important and patient should undergo physical examination and appropriate laboratory tests should be performed to find out these diseases.
The physical examination should include evaluation of the breasts, hair distribution, penis, and testes; palpation of the femoral and pedal pulses; blood pressure and testing of genital and perineal sensation10. Further examination or referral may be appropriate where indicated by age or findings in the historyespecially regarding cardiovascular, neurological, endocrine, and urinary systems22.
Recommended laboratory tests include urinalysis, a complete blood count, and measurements of serum glucose, creatinine, cholesterol, triglycerides, and testosterone while the patient is fasting. If the man’s serum testosterone concentration is low, serum free (or bioavailable) testosterone, prolactin, and luteinizing hormone should be measured. Liver function is also associated with erectile dysfunction hence liver function test should be done22, 10.
Psychosexual therapy and Education
Psychotherapist should provide education about normal sexual physiology and pathology. Behavioural interventions may reduce anxiety and desensitization. Counselling may reduce fear and anxiety which will improve sexual communication and create realistic expectation for sex. Discuss further diagnostic tests and treatment option with patient and his partner.
Modify Lifestyle factors such as obesity, smoking, alcohol consumption, and lack of exercise. Early adoption of healthy lifestyle may be best approach to reducing the burden of erectile dysfunction on the health and well-being of older men23.
Erectile dysfunction due to hypogonadism may be present in up to 30% of male elderly population and in about 2/3rd of cases is responsive to androgen replacement therapy24. In patients with arteriogenic ED and low-normal androgen levels, short-term testosterone administration increases T and FT levels and improves the erectile response to sildenafil likely by increasing arterial inflow to the penis during sexual stimulation25.
Phosphodiesterases (PDEs) are a super family of hydrolytic enzymes that plays a critical role in regulating physiological processes by terminating signal transduction through their hydrolytic action on cyclic nucleotides26. PDE-5 is an enzyme found in trabecular smooth muscle. It catalyzes the degradation of cGMP, which results in an elevated cytosolic calcium concentration and smooth-muscle contraction. PDE-5 inhibitors, therefore, block this biochemical pathway to promote erection27.
PDE5 inhibitors are contingent on the presence of cGMP in the smooth muscle cell. In the presence of sexual stimulation, the PDE inhibitors will reinforce the normal cellular signals that increase cyclic nucleotide concentrations by blocking cyclic nucleotide hydrolysis, thereby facilitating the initiation and maintenance of an erection28. PDE-5 inhibitors promote vasodilation, therefore should not be given to patients taking nitrates, they inherently have the potential to cause hypotension27.
First line treatment for erectile dysfunction is with PDEs 5 unless contraindicated. There are currently three oral Phosphodiesterases inhibitors are available sildenafil citrate, vardenafil and tadalafil. There are number of published study have supported their efficacy in the treatment of erectile dysfunction. Sidenafil citrate is selective inhibitor of Phosphodiesterases type 5, which inactivates cyclic GMP. When sexual stimulation releases nitric oxide into the penile smooth muscle, inhibition of Phosphodiesterases type 5 by sildenafil causes a marked elevation of cyclic GMP concentrations in the glans penis, corpus cavernosum, and corpus spongiosum, resulting in increased smooth-muscle relaxation and better erection. Sildenafil has no effect on the penis in the absence of sexual stimulation, when the concentrations of nitric oxide and cyclic GMP are low10.
Pharmacokinetic characteristic of PED-5 inhibitors27
The assisted erection obtained with a vacuum device is different from an erection obtained normally, in that there is no initial relaxation of the sinus smooth muscle within the corpora cavernosa. Instead all tissue of the penis becomes engorged with trapped blood, which has been drawn into the penis by the action of negative pressure. Thus Vacuum constriction devices (VCDs) provide passive engorgement of the corpora cavernosa in conjunction with a constrictor ring placed in the root of the penis to retain blood within the corpora. The penis may become slightly cool or numb and may become slightly bluish in colour or numb and may become slightly bluish in colour due to cyanosis. Efficacy of vacuum therapy in term of erection satisfactory for intercourse is 90% regardless of the aetiology of impotence29.
Intracavernosal-injection therapy is an important therapeutic option for men with erectile dysfunction of various causes and who does not responding to oral drugs. It does not involve surgery or devices and has reproducible erection responses and tolerable side effects. Physiologic mechanisms that relax penile smooth muscle and elicit erections are mimicked by vasoactive drugs administered intracavernosally that directly relax the smooth muscle30.
The most commonly used intracavernous drugs in the United States are alprostadil and a combination of papaverine, phentolamine, and alprostadil (trimix)10. The erection appears 5-15 min and lasts according to the dose injected. Efficacy rates for intrcavernous alprostadil of >70% are presented in general ED populations and patient subgroups (eg, diabetes or cardiovascular disease) with reported sexual activity after 94% of the injections and satisfaction rates of 87-93.5% in patients and 86-90.3% in partners31. Men must receive appropriate training and education by medical personnel before beginning home injections. The goal is to achieve an erection that is adequate for sexual intercourse but does not last for more than one hour10. Complications of intracavernous alprostadil include penile pain, prolonged erections, priapism, and fibrosis31.
Priapism is preventable through careful dose adjustment. To prevent fibrosis, we routinely instruct men to compress the injection site for 5 minutes (up to 10 minutes in men taking an anticoagulant drug). Intracavernous injection therapy is contraindicated in men with sickle cell anaemia, schizophrenia or other severe psychiatric disorders, or severe venous leakage10. After 6 h of erection, patients are advised to consult the doctor to avoid any damage to the intracavernous muscle, which would provoke permanent impotence. When this problem occurs, the dose is usually reduced for the next injection under blood pressure monitoring31.
Prostaglandin E1 is an endogenous unsaturated 20-carbon fatty-acid derivative of arachidonic acid, and alprostadil is a more stable, synthetic form of prostaglandin E110.
Intraurethral alprostadil has been developed and marketed by Vivus (Menlo Park, California). The mechanism of action of transurethral alprostadil is based on its absorption from the urethra and transport throughout the erectile bodies by commmuniting vessels between the corpus spongiosum and the corpora cavernosa32.
The Medicated Transurethral System for Erection (MUSE™) consists of a polypropylene applicator with a hollow stem 3.2 cm long and 3.5 mm in diameter. The tip (3 or 6 mm long) contains a semisolid pellet of medication that is available in four doses, i.e. 125, 250, 500 and 1000 µg. Alprostadil is administered while the subject is seated or standing, by fully inserting the stem of the applicator into the distal urethra. A button is depressed to deposit the pellet. A gentle sideways oscillation of the applicator separates the medicated pellet from the applicator tip. The patient should urinate immediately before administration, because the medicated pellet has been developed specifically to dissolve in the small quantity of urine that remains in the urethra after urination. After removing the applicator, massaging the penis for 30-60 s allows the compound to distribute and be absorbed fully32.
Alprostadil given transurethrally (medicated urethral system for erection (MUSE, AstraZeneca, Kings Langley) has proved efficacy in providing erections adequate for intercourse22.
Penile implants require a surgical procedure for insertion. Penile prostheses are semi-rigid, malleable or inflatable implants, which can be surgically inserted into the penis to allow an erect state. Prostheses should be considered in patients whose impotence has an organic cause and who are unwilling to consider, fail to respond to, or are unable to continue with medical treatment or external devices22.
According to Wespes et al young patients with a history of pelvic or perineal trauma may be benefited from potentially curative vascular surgery33. Some patients with arterial occlusive disease may require arterial reconstructive surgery but careful selection of patient is required. Venous surgery, with extensive ligation of the vein that drains the corpora cavernosa, is sometimes used as the last resort before the implantation of a penile prosthesis in young men with veno-occlusive disease. The results are generally poor as only 30% of patients report long term improvement34.
Outcome of Treatments
Twenty patients was identified with arteriogenic ED by dynamic colour duplex ultrasound (D-CDU) studies, who were having normal sexual desire but testosterone (T) and FT were in the lower quartile of normal range (low-normal) and was not responding to sildenafil treatment (100 mg) on six consecutive attempts. Hence one month treatment of transdermal testosterone was given, which led to a significant increase in T and FT levels (23·7 ± 3·3 SD vs. 12·8 ± 2·1 nmol/l and 473 ± 40·2 vs. 260 ± 18·1 pmol/l, P < 0·01, respectively). In addition testosterone administration induced a significant increase in arterial inflow to cavernous arteries measured by D-CDU (32 ± 3·6 vs. 25·2 ± 4 cm/s, P < 0·05), with no adverse effects. Also, a significant improvement in erectile function domain score at IIEF was found in the androgen but not in the placebo-treated patients (21·8 ± 2·1 vs. 14·4 ± 1·4, P < 0·05) which was associated with significant changes in the GAQ score (80%vs. 10%, P < 0·01)25.
Inhibition of PDE5 results in increased arterial blood flow leading to smooth muscle relaxation, vasodilatation, and penile erection. Three potent selective PDE5 inhibitors are licensed with proven efficacy and safety for the treatment of ED. They are sildenafil citrate, vardenafil and tadalafil, which are considered as first line therapy for erectile dysfunction31. Sildenafil was released in 1998, since that it becomes the drug of choice for most men with erectile dysfunction10.
In Goldstein et al study, the efficacy and safety of sildenafil was evaluated; it was administered as needed in two sequential double-blind studies of men with erectile dysfunction of organic, psychogenic, or mixed causes. 532 men were treated with oral sildenafil (25, 50, or 100 mg) or placebo for 24 week to 32 week. For the men receiving 100 mg of sildenafil, the mean score for the question about achieving erections was 100 percent higher after treatment than at base line (4.0 vs. 2.0 of a possible score of 5). In the last four weeks of treatment in the dose-escalation study, 69 percent of all attempts at sexual intercourse were successful for the men receiving sildenafil, as compared with 22 percent for those receiving placebo (P<0.001). The mean numbers of successful attempts per month were 5.9 for the men receiving sildenafil and 1.5 for those receiving placebo (P<0.001). Increasing doses of sildenafil were associated with improved erectile function but headache, flushing, and dyspepsia were the most common adverse effects in the dose-escalation study, occurring in 6 percent to 18 percent of the men35.
Similarly Hellstrom and colleague carried out randomized, double-blind, placebo-controlled trial to find out efficacy and safety of vardenafil in erectile dysfunction. The results of this study indicated that the vardenafil dosages of 5, 10, and 20 mg were significantly superior to placebo for the treatment of ED, based on the primary study endpoints of the EF domain score of the IIEF and diary-recorded success rates for penetration and maintenance of erection during intercourse. For men those were receiving vardenafil 20 mg, the mean EF domain score increased from 12.8 (moderate, on average) at baseline to 21.4 (mild level of ED, on average) at week 12. The efficacy was maintained over next 14 weeks, resulting in 85% of men using vardenafil 20 mg having reported improved erections at 26 weeks36.
Also in one observational study the outcomes of the patients who took the same therapies (tadalafil, sildenafil, or vardenafil) were compared for the period of 6 months. In nine European countries at 904 sites, 8047 patients were enrolled and out of those, 94% (7560) of them selected either tadalafil (5315), sildenafil (1252), or vardenafil (993) for treatment at baseline. Tadalafil, sildenafil, and vardenafil were therapeutically effective and improved patient satisfaction in the 40-58% of men who completed 6 month of a single therapy. Patients taking tadalafil consistently had numerically higher levels of therapeutic effectiveness and satisfaction compared with patients who took sildenafil or vardenafil37. Phosphodiesterase 5 resulted in a high level of therapeutic effectiveness and patient satisfaction.
Use of the external vacuum device was associated with improvements in men’s and their partner’s sexual functioning. Turner and colleague study assessed the sexual and psychosocial effects of 12 month’s use of an external vacuum device in the treatment of erectile dysfunction. They observed that the external vacuum device produced erections sufficient for intercourse in 87% of the men in sample. These improvements included erections of better quality, increased partner arousal, and increased frequency of orgasm and sexual satisfaction for men and women38.
In Chen et al study, the efficacy of vacuum device was evaluated in the treatment of 32 post- radical prostatectomy patients who fail oral PDE5 inhibitors. They observed 26 (81%) patients out of 32 were successfully treated with vacuum device. 16 (50%) were successfully treated with vacuum device only and 10 (31%) ended up with a combination, 5/10 treated using vacuum device and intracavernosal injection (ICI) and 4/10 using vacuum therapy and 5 phosphodiesterase inhibitors (PDE5i) and one patient using both (VED+ICI and/or VED+PDE5i). There was significant improvement in erectile function, (p<0.001); intercourse satisfaction (p<0.001) and overall satisfaction (p<0.001) domains of the IIEF score39.
In a double-blind, placebo-controlled study with 1511 men, alprostadil was delivered transurethrally and during in-clinic testing, 996 men (65.9%) had erections sufficient for intercourse. Of these men, 961 reported the results of at least one home treatment; 299 of the 461 treated with alprostadil (64.9%) had intercourse successfully at least once, as compared with 93 of the 500 who received placebo (18.6 percent, P<0.001). The most common side effect was mild penile pain40.
In an open-label, dose-escalating study, 249 patients were treated in an outpatient setting; of these patients, 159 (64%) achieved an erection sufficient for intercourse and were randomized (1:1) to either active medication or placebo for home treatment. Of the patients randomized to alprostadil for home treatment, 69% reported intercourse at least once, compared with 11% of patients randomized to placebo (P<0.001). The most common adverse reaction (urethral pain/burning) was reported by 7% of patients in the clinic. Most patients (83%) graded transurethral alprostadil as causing minimal or no discomfort in the clinic. No patient reported priapism or developed penile fibrosis41.
In Linet et al study, the efficacy and safety of alprostadil formulated for intracavernosal treatment for men with erectile dysfunction of vasculogenic, neurogenic, psychogenic, and mixed causes were investigated in three separate prospective studies. In dose-response study of 296 men, observed all doses of alprostadil were superior to placebo and there was a significant dose-response relation (P<0.001), resulting in higher response rates with increasing doses of alprostadil. To study safety and efficacy of injection, six-month self-injection study carried out in 683 men and they observed the men and their partners rated the sexual activity as satisfactory after 87 and 86 percent of the injections, respectively. Some patients reported penile pain, prolonged erection, priapism, penile fibrosis42.
The outcome of the of penile prosthesis surgery for different type of prosthesis with 447 men, who had 504 penile implanted between August 1975 and December 2000 were evaluated in Minervini et al study. Out of 504 penile implants, 393 were malleable, 81 were three-piece inflatable and 30 were self-contained hydraulic prostheses for a mean follow up period of 50 (1-2970) months. The most serious complications observed were infection (8%) and erosion (5%). Overall 89% of men could have sexual intercourse and 81% were satisfied with the result43.
In arterial and/or venous impotence patients, the sexual satisfaction rates with 4 surgical techniques were compared in Wespes et al study. Surgery was performed in 130 patients with vascular erectile dysfunction by 1 surgeon. Out of 130, Two young patients (2%) with traumatic arterial lesions underwent penile revascularization (group 1), while 128 with arterial and/or venous impotence were also treated with surgery, including 11 of 130 (8%) with deep dorsal penile vein resection (group 2), 39 (30%) with arterialization of the deep dorsal penile vein (group 3) and 78 (60%) with penile implants (group 4).
Sexual satisfaction, defined as the possibility of satisfactory sexual intercourse without any additional treatment or pain, was evaluated by patient interview. Out of 130 patients, 111 (85%) participated in the sexual life events interview, including 2 of 2 (100%) in group 1, 7 of 11 (63.6%) in group 2, 33 of 39 (85%) in group 3 and 69 of 78 (88%) in group 4. Mean follow-ups was 50, 48, 46 and 54 months for groups 1 to 4, respectively. The sexual satisfaction rate was 2 of 2 (100%) for penile revascularization, 1 of 7 (14%) for venous resection, 4 of 33 (12%) for arterialization and 64 of 69 (93%) for penile implantation. Complications occurred in 9.5%, 12.5% and 20.5% of the patients in groups 2 to 4, respectively
Except for young patients with traumatic arterial lesions, this study demonstrated the poor sexual satisfaction rate in impotent patients treated with the vasculogenic approach and the high rate of satisfac
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