Erectile dysfunction (ED) has replaced the term impotence to define the inability to achieve and maintain an erection satisfactory for sexual performance. Many international epidemiologic studies over the past decade have reported on the incidence and prevalence of ED in the male population (Table 1). Based on extrapolated data from the Massachusetts Male Aging Study (MMAS), ED affects some 20-30 million American men most of whom are older than 50 years. It has been estimated by this study that 5% of men in their 40s, 10% of men in their 60s, and 20% of men in their 70s will have complete erectile dysfunction. This epidemiologic study of a homogeneous suburban Boston community surveyed 1709 men and reported 52% of men aged 40-70 years had some degree of ED. Of these, 10% had complete ED, 25% moderate and 17% minimal. The prevalence of erectile dysfunction increased with age with moderate and complete ED increasing most markedly. The percentages of erectile dysfunction were increased further by the addition of risk factors for ED especially those for vascular disease including history of cardiac disease, antihypertensive or vasoactive drug use and tobacco use. From 1987 to 1997, 847 of 1297 men at risk for ED and without initial erectile dysfunction at baseline were followed longitudinally for additional evaluation. In this homogeneous group of white suburban American men, the incidence of ED was found to be 25.9 cases per 1000 man years with annual incidence rates increasing with each decade. Incidence was 12.4 cases per 1000 man years for men age 40-49 years, 29.8 for men age 50-59 years, and 46.4 for men age 60-69 years. The age-adjusted risk for erectile dysfunction in this group of men was higher when risk factors were added. Diabetics had a risk of 50.7 per 1000 man years, treated heart disease 58.3, and treated hypertension 42.5. The authors estimated that the number of new cases of ED in white American men of the same age group would be approximately 617,715 within each patient group.
Population Age (years) % affected
Cologne, Germany 30-80 19.2
Spain 25-70 18.9
Perth, Australia 40-69
33.9
Krimpen, the Netherlands 50-78 11.0
London, UK 16-78 19.0
European and international studies have likewise demonstrated similar prevalence to that of the MMAS. Spector and Boyle reported 32% of British men had difficulty obtaining an erection, 20% with difficulty maintaining erection. In a younger group of men aged 18-29 years from Denmark, Fugl-Meyer and Fugl-Meyer reported a 5% prevalence of ED even in these younger individuals.
Until the early 1980s, erectile dysfunction was suspected to be principally psychological in nature. It was widely published in the 1970s that more than 90% of men with 'impotence' had a psychological basis for their condition. Pioneering studies in the past two decades have elucidated the physiology of erectile function and its pathophysiology. These studies have changed the understanding of ED and erectile physiology. Penile function as elucidated by these studies is a complex process requiring a combination of neurological, endocrinological, psychological factors, and the vascular system for satisfactory function. The causes of ED are, therefore, frequently overlapping and multifactorial. In order to understand the causes and treatment for erectile dysfunction, it is important to review the penile anatomy and physiology of erectile function.
Anatomy of the penis
The penis is a specialized vascular organ composed of complex vascular tissue responsive to neurological impulses that create penile rigidity. The penis is composed of two paired corpora cavernosa and a third cylindrical corpus spongiosum that contains the urethra and is contiguous with the glans penis. The corpora cavernosa or penile erectile bodies are surrounded by a thick fibrous sheath (tunica albuginea) that is relatively non-distensible, composed of elastic fibers and collagen that support and maintain the rigidity of erectile function. Surrounding the tunica albuginea is a second gossamer layer of fascia called Buck's fascia. Within these functional Structures courses a complex vascular sinusoidal network of spongy tissue that activates erection. While the corpora cavernosa are generally considered to be separate cylinders, there is no clear septum between the two corpora and the distal portion of the penis and free vascular cross-communication occurs. The corpora themselves are composed of sinusoids made up of smooth muscle tissue and lined by endothelial cells. The corpora spongiosum is composed of similar spongy tissue but is surrounded by a less rigid thinner tunica albuginea resulting in less rigidity on activation. The blood supply of the corpora cavemosa originates from the internal iliac arteries and courses to the internal pudendal arteries that terminate in the arterioles to the penis. These small penile arteries include the dorsal artery to the penis outside the tunica albuginea, the bulbo-urethral artery that travels within the corpus spongiosum lateral to the urethra and the central cavernosal arteries that travel in the central portion of each of the paired corpora cavernosa and supply the blood for erection. A proximal perineal branch of the pudendal artery provides blood supply to the perineal skin and scrotum. The dorsal artery of the penis is responsible for the blood supply of the penile skin and glans penis and contributes little to erectile function. The cavernosal arteries on the other hand enter the corpora cavernosum at the hilum of each corpus cavernosum and give rise to multiple small helicine arteries that drain directly into the vascular lacunar spaces of the corpus cavernosum. Accessory pudendal arteries may also provide blood supply to the penis. These variable arteries may originate from the obturator artery, inferior pudendal artery, iliac trunk, or inferior gluteal artery and frequently lie close to the capsule of the prostate.
Venous drainage of the penis is important both anatomically and functionally. The lacunar spaces or vascular sinusoids of the corpora cavernosa drain through subtunical veins beneath the tunica albuginea into the emissary veins by way of the deep dorsal vein of the penis. The deep dorsal vein culminates in the periprostatic venous plexus superior and lateral to the prostate. The superficial dorsal penile vein lies above Buck's fascia and provides drainage predominantly for the penile skin culminating in the saphenous vein. The proximal penile shaft and proximal corpus cavernosum drains through veins exiting the crura of the corpora cavernosa termed the crural veins that join to form the internal pudendal vein. As with most venous systems, the venous drainage of the penis is variable and complex and has multiple intercommunications.
Sinusoidal smooth muscle is contracted and blood flows from the internal pudendal arteries via the cavernosal arteries and the helicine arteries to the lacunar spaces and out through the open emissary veins; during erection the smooth muscle of the sinusoids relaxes allowing blood to flow into the lacunar spaces. The resultant pressure compresses the emissary veins beneath the rigid tunica albuginea, reducing venous outflow.
The nerve supply to the penis controls not only sensation,
but also vascular supply to the penis. A pair of sympathetic nerves from S2-4
nerve roots Cavernosal artery primarily control erectile function while the
sympathetic nerves from T 11 -1-2 control detumescence and also contribute to
ejaculation and emission. These autonomic nerve fibers form the pelvic plexus of
nerves and enter the penis within the cavernous nerves that course lateral and
inferior to the prostate. It is these nerves that are preserved during
nerve
sparing radical prostatectomy. In addition to the autonomic nervous system,
peripheral nerves form sensory and motor elements through a reflex are in the
sacral spinal cord at Onuf's nucleus.
Peripheral nerves containing sensory elements are also responsible for erectile
function especially maintenance of erection. Ultimate central nervous system
control is likely initiated in the hypothalamus in the medial pre-optic area
that integrates psychological and tactile stimuli.
Excitatory stimuli from the central nervous system pass through the autonomic nervous system and produce erections through a variety of neurotransmitters. Many neurotransmitters including acetylcholine (ACh) and vasoactive intestinal polypeptide (VIP) contribute to erectile function.6 The most important neurotransmitter in the corpora cavernosa is nitric oxide (NO). NO functions via the cyclic guanosine monophosphate (cGMP) system. It is is produced from the precursor L-arginine by the enzyme nitric oxide synthase (NOS). The secondary transmitter cGMP is ultimately responsible for smooth muscle relaxation in the corpus cavernosum and producing erection. The relaxation is mediated by calcium efflux from the smooth muscle cell. cGMP is broken down in the corpus cavernosum smooth muscle cell by the enzyme phosphodiesterase (PDE) with subsequent detumescence. The most active PDE in the corpus cavernosum is type 5 (PDE-5). Additional smooth muscle relaxation occurs through a secondary pathway mediated by cyclic adenosine monophosphate (cAMP). cAMP, which can be stimulated by prostaglandin E1 (PGE1), VIP, or papaverine assists the primary eGMP system.
Once a central nervous system or tactile stimulus has occurred, secretion of NO is initiated and smooth muscle sinusoids of the corpus cavernosum begin to relax. Initial stimuli produce dilation and relaxation of the central cavernosal artery and the helicine arterials that produce increased influx of blood to the lacunar spaces of the corpora cavernosa. As this increased flow and downstream relaxation continues, the lacunar spaces or sinusoids fill with blood, increase in size, and produce decreases in venous outflow by compressing the subtunical venous channels against the tunica albuginea producing a high-pressure rigid erection. Rigidity is increased to a level beyond that of the abdominal aorta from the contraction of the perineal muscles especially the bulbocavernosus and ischtocavernosus muscles. At the conclusion of sexual activity, psychological and physical stimuli diminish, smooth muscle sympathic tone increases, vasoconstriction occurs, cGMP is broken down by PDE-5 and detumescence occurs.
History of systemic diseases that are
known ED risk
factors should be carefully elicited. The diagnosis of erectile dysfunction
begins with a thorough evaluation of history, and physical, and laboratory
studies. The sexual history is important and leads the physician to understand
the causes, risk factors
for erectile dysfunction, and ultimately treatment choices for a man with ED.
The general history of a man presenting with ED should include metabolic
diseases, trauma, surgical procedures, smoking and general health questions.
Current medications, recreational drug and alcohol use, and activity level
should be recorded. The specific sexual history should differentiate between
primary ED (the patient has had no previous erections during his life) and
secondary ED (erections were present, but have been lost after previous normal
sexual function). Ejaculatory dysfunction, diminished libido, and changes in
orgasm should also be asked for. Onset of ED is also critically important as
sudden onset is more commonly psychogenic or postsurgical while gradual onset ED
is more commonly associated with metabolic diseases such as diabetes, vascular
disease, hypercholesterolemia and hypertension. It is important to identify ED
during masturbation, with other partners, and morning and nocturnal erections.
The last successful intercourse should be queried, as well as interpersonal
difficulties with partners, lifestyle changes, stress, anxiety and possible
depression. Psychogenic ED is common and is caused by psychological problems
such as performance anxiety characterized by fear of erectile failure,
depression, obsessive compulsive disorder, psychiatric disorders as well as
marital problems. Cultural problems with understanding sexual function have also
been elucidated in many patients with strong religious beliefs or culture
differences.
ED may be associated with the medications used to treat various chronic
conditions as well as non-prescription medications. Systemic diseases that are
risk factors for erectile dysfunction are predominantly vascular diseases, but
also include coronary artery disease, peripheral vascular disease, diabetes
mellitus, renal failure, hypercholesterolemia, neurologic abnormalities
including trauma and back surgery, psychiatric diagnoses, drug, alcohol and
tobacco abuse. Surgical procedures associated with erectile dysfunction include
radical pelvic surgery such as abdominal perineal resection, radical
prostatectomy, pelvic trauma and pelvic radiation therapy. Symptom scores such
as the International Index of Erectile Function (IIEF), or its short form - the Sexual
Health Inventory for Men - (SHIM), may be helpful in measuring ED and following
patients on therapy. The shorter SHIM may be most helpful in screening men prior
to initiating treatment.
Psychotropic: Benzodiazepines, Amphetamines, Barbiturates, Opiates, Tranquillizers (Phenothiazines - Butyrophenones - Thioxanthenes) Antidepressants (MAO inhibitors - Tricyclics - Serotonin re-uptake inhibitors)
Antihypertensives: Diuretics (thiazides, spironolactone) Vasodilators Sympatholytics (methyidopa, reserpine) Beta blockers (propranolol, atenolol) Ganglion blockers (guanethidine)
Anticholinergics: Atropine Diphenhydramine
Androgenic agents: HRH agonists Anti-androgens Oestrogen
Recreational agents: Alcohol Marijuana Nicotine Cocaine
Others: Clofibrate Cimetidine Digoxin 4 Indomethacin MAO, monoamine
oxidase; LHRH, luteinizing hormone-releasing hormone.
Diabetes mellitus
Cardiovascular disease
Spinal cord injury
Cigarette smoking
Depression
Atherosclerosis
Hypertension
Pelvic surgery/trauma
Merectile dysfunctionications
Arthritis
Peripheral vascular disease
Renal failure
Substance abuse
Endocrine abnormalities
Peptic ulcer disease
Physical examination of men with genitourinary abnormalities should include a general physical examination with special attention to secondary sexual characteristics and genital development. The penis must be carefully examined to identify abnormalities such as micropenis, Peyronie's disease, hypospadias or penile malignancy. Testicular examination may reveal soft, small, atrophic testes, absent testes, or testicular masses. Unusual genetic syndromes such as Klinefelter's syndrome or Kallmarm's syndrome may also be suspected. Vascular disease can be assessed by examination of peripheral pulses and a focused neurologic examination will help demonstrate decreased perineal, penile or suprapubic sensation. A bulbocavernosus reflex may be elicited to identify peripheral neuropathies and other neurogenic abnormalities associated with erectile dysfunction. Digital rectal examination of the prostate is important as significant prostatitis and benign prostatic hyperplasia with lower urinary tract symptoms may be associated with ED. Examination may also reveal prostatic carcinoma or other abnormalities of the prostate or rectum.
Laboratory studies to assist in the elucidation of treatable causes of erectile dysfunction and any underlying undiagnosed metabolic condition are critical prior to initiating treatment. Urinalysis may identify glycosuria associated with undiagnosed diabetes mellitus or urinary infection. Scrum studies should include Serum testosterone, glucose, creatinine and fasting lipid profile. If serum total testosterone is low, additional measurements free testosterone, bioavailable testosterone, luteinizing hormone (LH) and prolactin may be helpful in differentiating pituitary from testicular hormonal abnormalities if present. In patients with significant renal failure and dialysis prolactin levels are essential. Since hypogonadism and hyperprolactinemia result in erectile dysfunction in only 17-35% of men these studies are frequently unfruitful. They do, however, identify clearly treatable forms of ED and may be helpful in patients who are otherwise treatment failures. Hormonal evaluations are best carried out with morning evaluations since diurnal testosterone variation in normal physiologic excretion results in the highest testosterone value between 8 and 10 in the morning. Late afternoon testosterone may be borderline or low because of this diurnal variation. Primary or hypogonadotrophic hypogonadism is frequently associated with elevation in the pituitary hormones LH and follicle -stimulating hormone (FSH). The majority of patients with low testosterone from androgen deficiency in the aging male (ADAM) have isolated decreases in serum testosterone associated with testicular testosterone deficiencies termed hypogonadotrophic hypogonadism. Patients with clear deficiencies in testosterone may benefit from testosterone replacement therapy.
Additional studies
In patients where ED is not clearly elucidated through history and physical examination and in whom knowledge of etiology is important for counseling, medico-legal decision making, or surgical procedures, additional, more sophisticated, testing can be suggested in selected patients. Psychogenic ED can be differentiated in some patients using nocturnal penile tumescence monitoring. While this study is currently not frequently done, it continues to be helpful for some patients with medico-legal issues associated with their ED and also to eliminate the possibility of psychogenic erectile dysfunction. The association of nocturnal erections with rapid eye movement (REM) or dream sleep has been well established. The RigiScan device has been used in nocturnal tumescence monitoring not only for the presence or absence of ED but also to evaluate duration and rigidity. This device can be used at home in the patient's own bedroom to decrease anxiety and promote valid interpretation.
Clear and concise evaluation of blood flow to the penis and penile arterial function may be helpful in patients in whom oral medications have failed or prior to surgery in patients with perineal trauma or Peyronie's disease. An injection in the office of a pharmaco-active agent may provide helpful diagnostic information in some patients. However, Doppler blood flow studies with a pharmaco-active agent injection are better. Agents such as papaverine, phentolamine, and PGE1 have been userectile dysfunction for both diagnosis and treatment of ED since the early 1980s. Virag and associates first identified the use of vasoactive agent papaverine in a pharmacologic screening procedure. PGE1 is most often userectile dysfunction today for both diagnostic and therapeutic injections for the production of erection. It produces significant vasodilation in the corpus cavernosum and in normal patients is associated with significant penile erection. A 20 gg dose of PGE1 can be injected into a single corpus cavernosum to provide full erection within 10-20 minutes and erectile maintenance for at least 15 minutes without penile or psychological stimulation. A normal result following injection indicates normal vascular physiology and adequate arterial flow with an intact venoocclusive mechanism and suggests a psychogenic, neurogenic or endocrine cause for the ED. Because of significant contractile stimuli from adrenergic discharge, however, normal erection may not occur even in patients with normal physiology. Duplex Doppler ultrasound imaging facilitates the evaluation and provides additional information about arterial flow beyond simple visualization of erection after injection. Not only can these studies measure blood flow velocity in the cavernosal arteries in both contracted and relaxed states, but also venoocclusive abnormalities can be identified.
In patients in whom significant venoocclusive abnormalities are suspected and must be docurnented, cavernosometry and cavernosography may be performed after the injection of PGE1 along with an infusion of normal saline and, subsequently, radiographic contrast material into the corpora cavernosa and identifying pressure to obtain and maintain an erection and subsequent areas of venous leakage on fluoroscopic, evaluation. While these studies are rarely done today as venous leak surgery and venous ligation surgery are infrequently used in patients with ED, they may be helpful in some selected patients.
In young men with significant perineal trauma and a suspicion of decreased penile blood flow from cavernosal artery occlusion, abnormal Doppler blood flow studies can be followed by penile angiography. These studies are also performed after an injection of PGE1 into the corpus cavernosum. They can document single or multiple small areas of occlusion that can be treated with penile revascularization surgery. While candidates for this surgery are rare, in young men with isolated trauma-produced lesions in the pudendal arteries, a successful result can frequently be achieved.
When investigating erectile dysfunction and questioning patients regarding their erectile function, it is important to identify risk factors. Additionally, recent studies have documented the coexistence of lower urinary tract symptoms, benign prostatic hyperplasia and ED. This unique risk factor for ED appears to progress independent of age and other risk factors. Treatment of lower urinary tract symptoms appears to improve ED whether it is medical or surgical. Indeed many of the u.-adrenergic blocking agents will facilitate erectile function. Antihypertensive medications, and indeed hypertension and agents such as hydrochlorothiazide and thiazide diuretics are likely to produce ED. Agents most likely to facilitate erections and satisfactorily treat hypertension include angiotensin receptor blockers (ARBs), angiotensin-converting enzyme (ACE) inhibitors, calcium channel blockers, and selective ot-blocking agents. Medications for the treatment of depression, especially the selective serotonin release inhibitors (SSRI) can produce decreases in erectile function as well as ejaculatory dysfunction. The metabolic syndrome (consisting of obesity, insulin resistance, hypercholesterolemia, and often obstructive sleep apnea), can also be associated with ED. Treatment of these risk factors may limit the progression, reverse some of the effects of ED, and facilitate the results of treatment.
Management and therapy
The process of care model for treatment of ED and the World Health Organization consensus conference have both suggested initial treatment be focused at lifestyle changes and management of current medications. Smoking cessation, managing diabetes, decreasing cholesterol, and treating hypertension may improve erectile function and facilitate medical treatment. Modifying antihypertensive medications to include 'erection hospitable agents' such as ot-blockers, ACE inhibitors, calcium channel blockers, and ARBs may maintain control of hypertension with restoration and maintenance of erectile function. Patients with low testosterone should receive injectable or topical testosterone supplements. If depression or relationship issues are significant problems, sexual counseling or psychiatric therapy may be helpful in addition to pharmacologic treatment. Office counseling with patient and partner may facilitate understanding and probable causes of the erectile dysfunction treatment alternatives, and expectations. Indeed, recent evidence has supported improvement of erectile function with sexual counseling.
First-line therapy
If lifestyle changes and medication modifications fail to improve erectile function, safe, effective oral agents are available for the treatment of ED. The introduction of sildenafil in 1998 revolutionalized the treatment of ED by providing an effective, safe method for restoring erectile function with minimal side effects and adverse events. Sildenafil as well as tadalafil and vardenafil are selective PDE-5 inhibitors that facilitate cGMP and subsequent corpus cavernosal smooth muscle relaxation. Improvement in erectile function occurs as quickly as 15 minutes after a dose and is maximum at 60 minutes following ingestion of sildenafil and vardenafil. Tadalafil, a longer-acting agent is active longer than the 4 hours for sildenafil and vardenafil with a half life of 17.5 hours. Sildenafil now has five years of clinical experience and is usually begun at 50 mg although for most patients doses of 100 mg are required for satisfactory results. First and second doses may not be effective as multiple doses and studies have demonstrated that as many as eight trials may be necessary for full success and effectiveness. Adverse events include headache, dyspepsia, facial flushing, blue vision and rhinitis. In subgroup studies, sildenafil has been reported to significantly improve erectile function compared with placebo in patients with both type 1 and type 2 diabetes with and without complications, spinal cord injury, hypercholesterolemia, depression, hypertension, cardiac disease, and patients following radical prostatectomy. In patients with psychogenic ED also the results are excellent.
While sildenafil is effective for ED of virtually all types of etiology and severity, it is least effective in patients with severe vascular disease - as are all oral agents. Tadalafil and vardenafil have fewer published clinical and basic science studies to document effectiveness and tolerability. The data available, however, demonstrate excellent effectiveness in similar subgroups of patients as sildenafil. Side effects are similar, but blue vision is reduced with both newer agents. Tadalafil, however, appears to cause less rhinitis but back pain in some selected patients. All three PDE-5 inhibiting agents are safe and effective in all groups of patients except those being treated with nitrates for coronary artery and cardiovascular disease, in these patients, the additive blood pressure lowering effects may produce produce profound hypotension. Additionally, care must be taken in co-administering beta-blocking agents since some select groups of patients may report dizziness and hypotension.
Other oral agents have previously been used with some limited success. Prior to the introduction of sildenafil, yohimbine, a presynaptic blocking agent was widely used as an oral agent. This medication, which often produces erectile function especially in combination with other erectogenic agents, has demonstrated minimal improvement in placebo controlled trials. Its side effect of significant hypertension limits its use to patients with cardiovascular disease. Trazodone, a non-SSRI antidepressant, has been tried as an oral agent for ED but only with limited success.
Central nervous system acting agents are available and in development. Apomorphine has been approved in Europe as an oral treatment of ED. This non-opiate dopamine agonist has its predominant effects in the hypothalamus. The sublingual preparation currently used produced erectile function within 30 minutes of administration in both double-blind placebo controlled studies and postmarketing reports. Its effectiveness while less than PDE-5 inhibitors is significantly better than placebo with side effects including nausea, vomiting, and in a small minority of patients, syncope. The success of this agent has spurred investigation of other agents for the treatment of erectile dysfunction. Melanotan or melatonin stimulating hormone (MSH) has also been demonstrated to be effective in selected patients with both organic and psychogenic ED.
Second-line therapy
In patients in whom first-line agents or changes in lifestyle fail to improve erectile function and who are motivated to continue with therapeutic alternatives, second-line therapy is available. This includes intracavernosal injection therapy, vacuum erection device therapy and intraurethral and topical medication administration.
Management and therapy
Intracavernosal injection was first given in the 1980s using phenoxybenzamine with improvement in erectile function in both organically and psychogenically impotent men. Subsequent development of combination therapy with PGE1, phentolamine, and papaverine have increased the effectiveness, comfort and safety of injection therapy. Currently PM or alprostadil is administered at doses of 2.5-5 mg. Patients with significant vasculogenic ED require higher starting and maintenance doses. After an initial in-office titration to a dose that produces a firm erection satisfactory for sexual intercourse that lasts no longer than 60 minutes many men may require at-home dosage adjustment. If erections persist for more than 4 hours, patients should be advised to go to the emergency room for treatment with an c1-agonist such as intracavernosal phenylephrine or aspiration therapy. While this complication is rare, early treatment will preserve future erectile function and allow patients to continue with injection therapy. If initial treatment with intracavernosal PM is ineffective or produces excessive penile pain, combination of papaverine with or without phentolamine and PGE1 may produce satisfactory erectile function with less penile discomfort. Side effects from this combination are similar to PGE1 alone and include prolonged erections, priapism, corpus cavernosurn fibrosus, and occasional transient hypotension. The most common adverse event, however, is penile pain most commonly seen with PG111.27 This complication occurs after approximately 20% of injections. Other complications such as hematoma, edema and corpus cavernosum fibrosis occur in less than 5% of patients.
Despite initial success rates in excess of 70% with these injection techniques, few patients continue injection therapy for more than 3-4 years. The reasons for discontinuation include inadequate erectile function, penile pain, poor patient partner satisfaction and anxiety. Several series have reported less than 50% continuation rate at 60 months.
Other alternatives include topical or transurethral PGE1 (alprostadil). The medicated urethral system for erection (MUSE), is available in 250, 500 or 1000 mg strength. Its effectiveness is approximately 30% in large clinical studies. A small applicator with a pellet of PGE1 is placed approximately 2 cm in the urethra. After the pellet is deposited and the applicator removed the patient stimulates the urethra to allow PGE1 to enter the corpus cavernosa. Erection occurs within 10-15 minutes and is maintained for as long as 40 minutes. Rare side effects include prolonged erection, priapism, but significant penile pain, aching, and urethral burning can occur. While this agent is an excellent addition to patients with penile prosthesis for further engorgement and is useful as combination therapy with PDE-5 oral agents, its success as a single agent in patients with severe erectile dysfunction has been disappointing. Newer formulations using a topical administration of PGE1 have completed clinical trials with success greater than that of MUSE and with similar adverse events. The agents may be useful in some patients as primary therapy or in future helpful as combination treatment. These alternatives while less effective than direct injection eliminate the need for needles and injections, and may be more acceptable to many patients.
Vacuum constriction device
Vacuum constriction devices have been available since the early twentieth century when they were first patented in 1972 by Dr Otto Lederer. They have been medically prescribed since the 1980s. These devices aspirate blood into the penis using a vacuum tube placed around the penis producing engorgement of the corpus cavernosum with trabecular smooth muscle relaxation. The blood is maintained within the corpus cavernosum by use of a constricting band placed at the base of the penis to maintain venous stasis without decreased arterial inflow. Although these devices produce rigid erectile function satisfactory to as many as 80% of patients, they may be uncomfortable, obstruct ejaculation, and produce other noxious side effects.
Application of the vacuum device includes placement of a
vacuum chamber or cylinder over the penis with occlusion at the penile base
(Fig. 27.4). The closed end is attached to a vacuum pump and the constriction
band is placed on the proximal portion of the open cylinder. The cylinder is
then sealed to the skin at the base of the penis and the vacuum pump activated.
Once an erection has been established, the constriction ring is slipped from the
proximal cylinder onto the base of the penis to maintain the erection. Usually
this can be maintained for up to 30 minutes before discomfort and edema require
removal of the constriction ring. Patients should not use the vacuum erection
device if they have hematologic abnormalities which require anticoagulant use,
or leukaemia or sickle cell disease.