erectile dysfunction

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viagra is a commercial produced medicine conta...

viagra is a commercial produced medicine containing Sildenafil citrate, which is used to treat male erectile dysfunction and pulmonary arterial hypertension. (Photo credit: Wikipedia)

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Erectile dysfunction (ED) is the inability to attain or sustain an erection satisfactory for sexual intercourse. Most erectile dysfunction is related to vascular, neurologic, psychologic, and hormonal disorders; drug use can also be a cause. Evaluation typically includes screening for underlying disorders and measuring testosterone levels. Treatment options include oral phosphodiesterase inhibitors or apomorphine, intraurethral or intracavernosal prostaglandins, mechanical pump devices, and surgical implants.

The term impotence has been replaced by the term erectile dysfunction. In the US, at least 10 to 20 million men > 18 are affected. The prevalence of partial or complete ED is about 50% in men 40 to 70 and increases with aging. However, many men can be successfully treated.

Etiology

Primary ED (ie, the man has never been able to attain or sustain erections) is rare and is almost always due to psychologic factors (guilt, fear of intimacy, depression, severe anxiety) or clinically obvious anatomic abnormalities. Most often, ED is secondary (ie, a man who previously could attain and sustain erections no longer can). Over 80% of secondary ED cases have an organic etiology. However, in many men with organic disease, ED leads to secondary psychologic difficulties that compound the problem. Psychologic factors must be considered in every case.

Psychologic causes may relate to performance anxiety, stress, or a mood disorder (particularly depression). ED may be situational, involving a particular place, time, or partner.

The major organic causes of ED are vascular and neurologic disorders, often stemming from atherosclerosis and diabetes. Complications of surgery, usually prostate surgery, are another common cause. Other causes include hormonal disorders, drugs, and structural disorders of the penis (eg, Peyronie’s disease).

The most common vascular cause is atherosclerosis of penile arteries, often secondary to diabetes. Atherosclerosis and aging decrease the capacity for dilation of arterial blood vessels and smooth muscle relaxation, limiting the amount of blood that can enter the penis. Inadequate impedance of venous outflow (venous leaks) may cause ED or, more commonly, failure to maintain tumescence as long as desired. Venous leaks make it difficult for blood to remain in the penis during erection, so erections occur but cannot be sustained. Priapism, particularly as in sickle cell disease, may damage penile vasculature and lead to ED.

Stroke, partial complex seizures, multiple sclerosis, peripheral and autonomic neuropathies, and spinal cord injuries are among the neurologic causes. Diabetic neuropathy and surgical injury are particularly common causes.

Any endocrinopathy associated with testosterone deficiency (hypogonadism) may decrease libido and cause ED. However, erectile function only rarely improves with normalization of serum testosterone levels.

Numerous drug causes are possible (see Table 1: Male Sexual Dysfunction: Commonly Used Drugs That Can Cause Erectile Dysfunction). Alcohol can cause temporary ED.

Table 1

Commonly Used Drugs That Can Cause Erectile Dysfunction

Class
Drugs

Antihypertensives
β-Blockers, clonidine

, loop diuretics
(probably), spironolactone

, thiazide diuretics

CNS drugs
Alcohol, anxiolytics, cocaine, monoamine oxidase inhibitors, opioids, SSRIs, tricyclic antidepressants

Others
Amphetamines, antiandrogens, anticancer drugs, anticholinergics, cimetidine

,
estrogens

, gonadotropin-releasing hormone
analogs

Of men who have undergone transurethral resection of the prostate, up to 40% can experience problems with erections for reasons that are not clear. ED is more common after more extensive prostatic resection (eg, radical prostatectomy). Prolonged perineal pressure (as occurs during bicycle riding) can cause temporary ED.

Diagnosis

Clinical evaluation

Screening for depression

Testosterone level

Evaluation should include history of drug and alcohol use, smoking, diabetes, hypertension, and atherosclerosis and symptoms of vascular, hormonal, neurologic, and psychologic disorders. It is vital to screen for depression, which may not always be apparent. The Beck Depression Scale or, in older men, the Yesavage Geriatric Depression Scale (see see Approach to the Geriatric Patient: Geriatric Depression Scale (Short Form)) is easy to administer and may be useful. Satisfaction with sexual relationships should also be explored. Partner sexual dysfunction (eg, atrophic vaginitis, depression) must be considered and evaluated.

Examination is focused on the genitals and extragenital signs of hormonal, neurologic, and vascular disorders. Genitals are examined for anomalies, signs of hypogonadism, and fibrous bands or plaques (Peyronie’s disease). Poor rectal tone, perineal sensation, or abnormal anal wink or bulbocavernosus reflexes may indicate neurologic dysfunction. Diminished peripheral pulses suggest vascular dysfunction.

A psychologic cause should be suspected in young healthy men with abrupt onset of ED, particularly if onset is associated with a specific emotional event or if the dysfunction occurs only in certain settings. A history of ED with spontaneous improvement also suggests psychologic origin (psychogenic ED). Men with psychogenic ED usually have normal nocturnal erections and erections upon awakening, whereas men with organic ED often do not.

Laboratory assessment should include measurement of testosterone level; if the level is low or low-normal, follicle-stimulating hormone (FSH) and luteinizing hormone (LH) should be measured (see Male Reproductive Endocrinology and Related Disorders: Diagnosis of primary and secondary hypogonadism). Evaluation for occult diabetes, dyslipidemias, hyperprolactinemia, thyroid disease, and Cushing’s syndrome should be done based on clinical suspicion.

A penile pressure–brachial pressure index (systolic BP in the penis divided by systolic BP in the arm) < 0.6 indicates impaired blood flow to the penis, but this test is seldom done in general clinical practice. Additional invasive or provocative penile tests include duplex ultrasonography before and after injection of a vasoactive drug and cavernosography or cavernosometry; these tests can be considered in some patients, such as those with posttraumatic erectile dysfunction or before penile reconstructive surgery (eg, for Peyronie’s disease).

Treatment

Treatment of cause

Usually an oral phosphodiesterase inhibitor

Sometimes a mechanical device or an intracavernosal or intraurethral prostaglandin

Underlying organic disorders require appropriate treatment. Drugs that are temporally related to onset of ED should be stopped or switched. Depression may require treatment. For all patients, reassurance and education (including of the patient’s partner whenever possible) are important.

For further therapy, noninvasive methods (mechanical devices and drugs) are tried first. All drugs and devices should be tried ≥ 5 times before being considered ineffective.

Mechanical devices: Men who can develop but not sustain an erection may use a constriction ring. As soon as erection occurs, a metal or elastic ring or a leather band with snaps (sold by prescription in pharmacies or OTC in sex paraphernalia stores as a “cock ring”) is placed around the base of the penis, preventing venous outflow. If the man cannot develop an erection, a vacuum device can draw blood into the penis, after which the band or ring is placed at the base of the penis to retain the erection. Bruising of the penis, coldness of the tip of the penis, and lack of spontaneity are some drawbacks to this modality. A constriction ring and vacuum devices might also be useful adjuncts for patients who do not respond satisfactorily to drug therapy.

Drugs: The primary drugs for ED are oral phosphodiesterase inhibitors, oral apomorphine

(not available in the US), and intracavernosal or intraurethral prostaglandins. Almost all patients prefer oral drug therapy to other methods for treating ED.

Oral phosphodiesterase inhibitors selectively inhibit cyclic guanosine monophosphate (cGMP)–specific phosphodiesterase type 5 (PDE5), the predominant phosphodiesterase isoform in the penis. These drugs include sildenafil

, vardenafil

, and tadalafil

. By
increasing cGMP, these drugs enhance the nitric oxide release essential for normal erection. Although vardenafil

and tadalafil

are more selective for the penile vasculature than
sildenafil

, adverse effects of these drugs are similar. Although no clinical trials directly
compare the drugs, all 3 appear to be equally effective (60 to 75%). Sildenafil

dose is 50
mg, although most men respond best to 100 mg. Tadalafil

has a significantly longer
duration of action (24 to 48 h) than sildenafil

and vardenafil

(about 4 to 6 h), which might
lead to more convenient dosing. The usual dosage for tadalafil

and vardenafil

is 5 to 20
mg. All PDE5 inhibitors are generally taken at least 1 h before sexual intercourse. Dosing frequency should not be ≤ 24 h for sildenafil

and vardenafil

and not ≤ 48 h for tadalafil

.
All PDE5 inhibitors cause direct coronary vasodilation and potentiate the hypotensive effects of other nitrates, including those used to treat cardiovascular disease as well as recreational amyl nitrate (“poppers”). Thus, all nitrates are contraindicated for 24 h after the administration of any PDE5 inhibitor. Other adverse effects of PDE5 inhibitors include flushing, visual abnormalities, and headache. Sildenafil

and vardenafil

may cause abnormal color
perception. Tadalafil

use has been linked with myalgias. Some users of PDE5 inhibitors
have rarely developed anterior ischemic optic neuropathy, but whether there is a causal relationship is unclear. Vardenafil

should be administered cautiously and at lower initial
dosages to patients receiving α-blockers, such as prazosin

, doxazosin

, and
tamsulosin

, because of the risk of prolonged hypotension. One study showed that
sildenafil

may be safely administered with doxazosin

.

Apomorphine increases erectile neurogenic signals by CNS mechanisms. It appears to be only moderately effective and can cause nausea, somnolence, and hypotension.

Alprostadil (the prostaglandin PGE1), given via intraurethral insertion or intracavernosal injection, can produce erections with a mean duration of about 60 min. It causes priapism (see Symptoms of Genitourinary Disorders: Priapism) in ≤ 1% and penile pain in about 10%. The intracavernosal dose is adjusted by the physician to minimize priapism; the patient can then self-inject at home. Priapism is less common with intraurethral therapy, but intraurethral therapy is much less effective (50 to 60%) than intracavernosal injection, the most effective pharmacotherapy for erectile dysfunction (80 to 90%). Combination therapy with a PDE5 inhibitor and alprostadil

may be useful for some patients who fail to respond to oral PDE5
inhibitors alone.

Surgery: For patients who do not respond to drug therapy, invasive treatment options include implantation of a penile prosthesis. Prostheses can be rigid plastic rods or hydraulically operated devices. Both involve the risks of general anesthesia, infection, and prosthetic malfunction.

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