I. Definitions, etc.

  1. "Impotence" includes libidinal, orgasmic, ejaculatory, or erectile dysfunction
  2. "Erectile dysfunction" (ED) = inability of male to attain and maintain erection sufficient to allow "satisfactory sexual performance" (NIH panel)
  3. Isolated incidents are part of normal fluctuation of sexual function

II. Epidemiology

  1. Epidemiologic study of impotence impeded by cultural stigma, inconsistent use of definitions, etc.
  2. Prevalence
  1. Kinsey found < 1% affected before age 30
  2. Most studies find overall prevalence to be 3-20%
  3. Prevalence increases with age; NIH panel quotes 5% at age 40, 15-25% at age 65 and above
  4. 70-80% of cases of ED are organic in etiology (NIH panel; Ann. Acad. Med. Singapore 21:248, 1992)
  5. About 70% of organic cases are due to vascular (arterial or venous) cause (AFP article)

III. Erectile physiology and pathophysiology

  1. Hormonal, neurologic, vascular, local paracrine, and psychological mechanisms
  2. Spinal reflexes (inc. somatosensory) plus supraspinal mechanisms (inc. cognitive) involved in neural regulation of erection/detumescence
  3. Begins with parasympathetic impulse from S2-4 transmitted through pelvic plexus by cavernous nn. to the "helicine" arterioles within corpus cavernosum
  1. These arterioles are supplied by the cavernous artery, a branch of the the common penile artery which in turn branches off the internal pudendal artery
  1. Nitric oxide (aka endothelial-derived relaxing factor) is released from endothelium of cavernous aa. (and possibly directly from parasympathetic neurons)
  2. NO, through 2nd messenger systems (cGMP and cAMP), induces relaxation of smooth muscle of cavernous artelioles and corpus cavernosum, allowing blood to flow into sinusoidal spaces of corpora cavernosa
  3. As pressure increases in corpori, small emissary veins in nonelastic tunica albuginea become occluded, trapping blood in corpora cavernosa (causing penis to act as a capacitor)
  4. Striated mm (bulbocavernosus and ischiocavernosus) not necessary for erection but may create "super-rigidity" by compressing proximal part of corpora cavernosa, creating intracavernosal pressures in excess of systolic pressure!
  5. Sympathetic impulses input from T10-L2
  1. May result in ejaculation
  2. In combination with decreased parasympathetic tone causes arteriolar and cavernosal smooth mm. relaxation, causing detumescence
  1. Arterial insufficiency will produce ED by interfering with filling of corpus cavernosa
  2. Intrinsic cavernosal sm. mm. dysfunction may play a role in ED
  1. If cavernosal sm. mm. relaxation is incomplete (e.g. in the case of neuropathy), compression of venules in tunica albuginea is incomplete ("veno-occlusive dysfunction," not the same as "venous leak)
  1. "Venous leak" results from congenital venous enlargement, Peyronie's, trauma, etc. Interferes with occlusion of venules of tunica albuginea, resulting in ED, esp. get early loss of erection
  2. Note that the innervation responsible for ejaculation is separate from that responsible for tumescence. Because of this some men with ED will still experience orgasm and ejaculation with a partially tumescent or flaccid penis; this is common in ED due to diabetic neuropathy (see below)

IV. Causes of ED

  1. Almost any systemic illness can cause ED through hormonal, vascular, neurologic, and psychological mechanisms
  2. However, NOT a natural consequence of aging!!
  3. Vascular disease accounts for about 50% of ED in men over 50yo
  1. Vascular surgery (e.g. aortofemoral bypass) can itself cause ED
  2. GI surgery, e.g. APR
  3. Pelvic irradiation
  4. Atherosclerotic peripheral vascular disease, esp. from DM (see below)
  1. Neurologic
  1. Peripheral neuropathy of any cause
  1. DM, through neurologic and vascular mechanisms
  1. Prevalence of ED is about 50% in diabetic adult males
  2. In one series, 15% of previously healthy men presenting with impotence had abnormal glucose tolerance! (AFP article)
  3. Usually starts with inability to maintain erection; libido is preserved
  1. No specific test for peripheral neuropathy of nerves of pelvis
  2. No specific treatment available
  1. Head trauma or surgery
  2. Spinal cord trauma (about 50% prevalence of ED) or surgery
  3. Retroperitoneal or pelvic surgery or trauma (10% ED with TURP)
  4. Pelvic XRT
  5. Prostatitis (?--NIH paper mentions it as a part of hx to get)
  6. n.b. vasectomy is NOT associated with increased risk for ED
  7. CNS causes: MS, CVA, tumors, temporal lobe epilepsy, infection
  1. Endocrine disorders
  1. Hypogonadism (hypotestosteronemia)--Click link for details
  1. Role of androgens in ED is unclear
  1. Hypotestosteronemia occurs in about 5% of men with ED
  2. Individuals with castration levels of testosterone are in many cases still capable of achieving erections triggered by cognitive stimuli
  3. Seems to play more of a role in older men, in whom treatment of hypogonadism seems to have more of an impact on erectile function (Zonszein 1995)
  1. When ass'd with ER, usually accompanied by decreased libido
  1. Hyperprolactinemia
  1. Causes decreased libido and ED, even if mild (20-80 ng/ml)
  2. Causes include prolactinoma, meds (see below), renal failure, and idiopathic
  3. Us. treated w/bromocriptine
  1. Hypothyroidism
  2. Hyperthyroidism
  3. Hypercortisolism (suppresses synthesis of gonadotropins)
  1. Chronic renal failure-unknown mechanism; hormonal factors (e.g. decreased clearance of prolactin) may play a role
  2. Liver failure: more common with EtOH liver disease than other causes
  3. Alzheimer's (not correlated with degree of cognitive impairment or depression!)
  4. COPD-independent of vascular disease
  5. Local penile disease
  1. Peyronie's
  2. "Subclinical fibrosis" (?)
  3. Post-priapism (commonly leads to ED): causes include sickle-cell anemia, certain drugs, trauma, neoplasm, TPN, and intracavernosal injection (mostly papaverine and phentolamine)
  1. Surgery and trauma (see above)
  2. Psychogenic factors
  1. Can create difficulty with either initiation or maintenance of an erection
  2. Probably a component even in men with clear organic etiology; can be a result as well as a cause of ED-"slippery slope" from minor to major erectile dysfunction
  3. Stress
  1. Abnormally high sympathetic tone could conceivably suppress erectogenic effect of parasympathic outflow
  2. One study showed unemployed men were at greater risk for developing ED (J. Sex. Res., 30:43, 1993; cited in Rosen)
  1. Depression (may lead to hormonal alterations as well; see above)
  2. Poor self-image
  3. Performance anxiety, guilt
  4. Relationship difficulties (can be either cause, effect, or both)
  5. Lack of attraction
  6. Fear of STD's and/or pregnancy
  7. Note--Why treat pts w/psychogenic ED with physical txs, e.g. intercavernosal injection?
    1. One series of 153 men treated w/intercavernosal injection and untreated control group of 53 men, all w/ ED of various etiologies. Among the subset of those with psychogenic ED, at 6mo f/u, 84% of those in tx group had return of spont. erectile function c/w 22% of untreated controls (p < 0.001); no such difference in subset with vascular etiology to their ED. In other words, having the "backup" of intercavernosal injection gave pts with psychogenic ED the confidence to resume normal erectile function (McMahon CG. "The return of spontaneous erections after self-injection of prostaglandin E1. Int. J. Impot. Res 4:179, 1992)

V. Drug-induced ED

  1. Mechanisms include CNS sedation or depression, lowering plasma testosterone or raising plasma prolactin levels, lowering blood pressure by any mechanism
  2. Antihypertensives, especially beta-blockers and spironolactone
  1. Other cardiac drugs
  1. Digoxin (decreases serum testost. and increases estradiol levels)
  2. Clofibrate
  3. Gemfibrozil
  4. HMG CoA reductase inhibitors, possibly (J. Clin. Pharm. Ther. 21:89, 1996)
  1. Phenothiazines (increase prolactin levels)
  1. Antidepressants
  1. Tricyclics
  2. Tetracyclics
  3. MAOIs (increase prolactin levels)
  4. Lithium
  5. SSRIs
  1. H2-blockers (act as weak androgen antagonists)
  2. Hormones
  1. Estrogens
  2. Progestins
  3. Corticosteroids (see above)
  4. GNRH agonists
  1. Cytotoxic agents
  1. Cyclophosphamide
  2. Methotrexate
  3. Roferon-A
  1. Anticholinergics
  1. Disopyramide
  2. Anticonvulsants
  1. Miscellaneous
  1. Metoclopramide (increases prolactin levels)
  2. Finasteride
  3. Baclofen
  4. Ketoconazole
  5. Drugs of abuse
  1. Tobacco (independent of vasc. dis.; Am. J. Epidem. 140:1003, 1994)
  2. EtOH
  3. Marijuana (used chronically)
  4. Amphetamines
  5. Opiates (used chronically)
  6. Cocaine (used chronically)

VI. History

  1. Onset, duration of ED
  1. Rapid onset more common with psychogenic cause
  2. Apparent precipitant (random failure, relationship trouble, trauma, depressions, etc.)
  1. Does erection occur at times other than intercourse (at night, in a.m., with masturbation)? What frequency, duration?
  1. If it does, strongly suggests psychogenic; note, however, that unintentional "reflex" erections can occur with spinal cord damage
  1. Is the problem getting or maintaining an erection (latter suggests "venous leak")
  2. Any particular situation where it occurs (e.g. with 1 partner and not another)
  3. Decreased libido? (if so, suggests hypogonadism)
  4. Psychosexual hx (see above IV.L); also
  1. Pt's and partner's goals & expectations
  2. Relationship problems?
  3. Loss of attraction toward partner?
  4. Pt's attitudes toward sex
  5. Current sexual techniques (how rigid is the "script"?)
  6. Other sexual dysfunction, including of desire, orgasm (delayed or premature)
  1. Psychiatric history
  2. Drugs (inc. illicit and OTC)
  3. EtOH history
  4. Spinal or pelvic surgery, trauma, or irradiation
  5. History of neurologic or cardiovascular disease (known CHD, PVD, or HTN; history of smoking) or DM
  6. Other systemic disease (renal, hepatic, thyroid, COPD)
  7. Hx of urologic disease (Peyronie's, priapism)
  8. Previous eval/tx for ED


  1. BP
  2. Signs of atherosclerosis, e.g. bruits, periph. pulses
  3. Thyroid exam
  4. Signs of hypercortisolism
  5. Signs of androgenization
  6. Testicular size/consistency
  7. Penis for Peyronie's placques
  8. Neurologic: perianal sensation, rectal tone, bulbocavernosus (often lost in neurogenic ED)

VIII. Initial lab w/u

  1. Glucose
  2. Testosterone (early am)
  1. Unlike in the female, gonadotropin measurements are not a reliable indicator of gonadal failure; LH tends to remain normal in the hypogonadal male
  2. Confirm with a second draw if the first is low
  1. Prolactin (looking for elevation)-references differ on whether to do routinely or only if testosterone is low
  2. PSA
  3. TSH, BUN/Cr, LFT's if indicated clinically
  4. If testosterone is low, check LH to distinguish between pituitary and gonadal failure

IX. Special diagnostics-rarely necessary; may help guide surgical management (see below)

  1. Noctural penile tumescence testing (NPT, "Rigiscan")
  1. Can document nighttime erections and confirm psychogenic impotence
  2. May be useful is no clear evidence of morning/nocturnal erections and no clear secondary cause
  3. Limited by lack of standards and data on "normals"; falsely abnormal results may be possible in psychogenic ED
  4. Home model now available!
  5. "Postage stamp test" = low-tech alternative
  1. Duplex ultrasonography of penile vasculature
  1. Can identify venous as well as arterial problems
  1. Cavernosography/cavernosometry
  1. Only if contemplating surgical repair of venous system for venous leak or veno-occlusive dysfunction
  1. Pelvic/penile angiography
  1. Only if contemplating surgical revascularization
  1. n,b, B, C, and D have problems of lack of normative data, variable interpretation of results, and poor predictability of therapeutic outcomes of surgery (NIH paper)

X. Treatment-note that most treatments are not highly specific to etiology of ED, so diagnostic workup will often not alter management

  1. General tx principles:
  1. If pt favors noninvasive tx, only eval needed is above hx, px, and initial lab w/u
  2. Involve pt and partner if possible
  3. Treat underlying medical problems and change or d/c meds if indicated (duh)
  4. May combine more than one tx if one tx fails
  1. Although it should be obvious that successful tx improves overall quality of life, this issue has been studied
  1. Self-injection shown in an uncontrolled study over 1y to be ass'd w/ improvement in measures of anxiety and depression (though were normal to start with; Levine et al., J. Sex. Marital Ther. 17:101, 1991)
  2. Another uncontrolled study of 99 pts undergoing self-injection tx showed that 50% reported improvement in overall quality of relationships (unchanged in 45%; worsened in 5%; van Driel et al., Int. J. Impot. Res. 3:95, 1991)
  1. Counseling and sex therapy-not only for those who have purely "psychogenic" ED!
  1. Usual format of sex therapy is counseling for couple plus "homework" assignments (Masters and Johnson approach)
  2. Some, but not much, data to support effectiveness; sometimes it's all that's needed for psychogenic ED
  3. Treat coexisting psychosocial problems (partner relationships, substance abuse, etc.)
  4. Educate about nature of sexual function and explore pt's and partner's expectations
  5. Decrease anxiety and distractions
  6. Increase sexual communication, intimacy, and trust
  7. Shift focus from achieving erection and other performance demands to increasing intimacy & pleasure ("sensate focus")
  1. Yohimbine (Yocon)
  1. Alpha-2-adrenergic antagonist derived from tree bark; site of action unknown
  2. Us. dose 6-30mg TID
  3. Sl. better than placebo in a few controlled trials; 10-40% of men show subjective improvement (AFP article)
  4. 29 pts w/impotence of varying causes randomized to yohimbine 36mg QD x 25d vs. placebo w/crossover; no diff. between drug & placebo for erectile function or libido (Urol. 49:441, 1997)
  5. Meta-analysis of 7 randomized double-blind trials of yohimbine 5-10mg TID vs. placebo; response rates measured by varying methods; in each study was superior to placebo; in aggregate analysis did achieve statistical significance (J. Urol. 159:433, 1998--JW)
  6. Can cause nausea, irritability, HTN
  7. Not FDA-approved; grandfathered in. NIH panel and AUA discourage its use
  1. Other oral agents
  1. Trazodone increases awake penile tumescence responses in control and sexually dysfunctional men; can cause priapism
  2. Pentoxyfylline improves sexual function in patients with vasculogenic erectile dysfunction (Rosen and Leiblum article)
  3. Phosphodiesterase-type-5 inhibitors
  1. Inhibit phosphodiesterase type 5, thus inhibiting the reconversion of cGMP back to GMP which ordinarily terminates the cGMP-mediated relaxation of cavernosal smooth mm (which is stimulated by nitric oxide)
  2. All result in higher likelihood of successful intercourse than placebo, but treatment failures are still common
  3. Must not be given along w/nitrates b/c severe hypotension can result
  4. Side effects include HA, flushing, dyspepsia, and myalgia, diarrhea, rash
  5. High-fat meals interfere with absorption (except Tadalafil)
  6. Sildenafil (Viagra)
    1. Dose = 25-100mg PO 30min before intercourse, max 1x/d
    2. Recc'd dose is 50mg (can go up to 100mg) 1h before intercourse, up to QD. Start at 25mg if > 65yo, hepatic or renal impairment, or on cimetidine, erythromycin, ketoconazole, itraconazole, and mibefradil.
    3. Side effects as above, also transient visual abnormalities (color change or increased sensitivity to light)
  7. Vardenafil (Levitra)
    1. Dose = 2.5-20mg 60min before intercourse, max 1x/day
    2. Similar side f/x  and drug interactions to Sildenafil, except vardenafil may not cause visual changes; MAY cause some mild QT prolongation which sildenafil does not (Med. Lett. 45:78, 2003)
    3. No evidence for quicker onset of clinical action than Sildenafil as of 2003, though marketed as such
  8. Tadalafil (Cialis)
    1. Dose = 5-20mg (start a 10mg except with moderate renal insufficiency or mild-mod hepatic impairment, start at 5mg, max 10mg)
    2. Can increase risk of hypotension in patients on Alpha-blockers
  1. Delquamine PO-a selective alpha-2 antagonist; trials in progress
  2. Papaverine buccal-limited evidence, trials in progress
  3. Apomophine SL (Uprima) 2-4mg
    1. A dopaminergic agonist
    2. Increases activity of hypothalamic neurons involved in regulation of intracavernosal smooth mm. tone
    3. Can cause nausea, hypotension and syncope (about 0.7% incidence for the latter)--risk may be greater with alcohol intake
  1. Testosterone supplementation--See under Hypogonadism (hypotestosteronemia)
  1. Vacuum constriction devices
  1. Hollow cylinder placed over penis
  2. Pump mechanism generates vacuum within cylinder, drawing blood into penis and creating erection
  3. Constricting rubber ring placed first over cylinder and then rolled onto erect penis near base; acts as a tourniquet, effectively trapping blood within corpii caverosa
  4. Save and very effective for all types of ED; only contraindications are h/o priapism and coagulopathy
  5. May impair ejaculation, sometimes uncmofortably
  6. Prob. more difficult to learn than self-injection
  7. User satisfaction about 68% (AFP article); may engender less satisfaction than self-injection (see below)
  8. However, high rate of patient dropout (NIH paper)
  9. One-time cost about $400
  1. Penile (intercavernosal) self-injection
  1. Inject vasodilatory agents directly into corpus cavernosum using 30g needle; first described in 1982, producing smooth mm. relaxation and thus erection
  1. Advantage of local administration of meds, with little systemic effect
  2. Onset us. within 10-15min; Duration tends to be average 1-2h and is dose-related
  3. Dose requirement tends to be lowest in pts with ED due to spinal cord injury and those with psychogenic ED
  4. Tends to work regardless of the cause of ED, though may be less successful in pts with arterial insufficiency
  5. In-office trial at start of therapy is often used to see if it will work
  6. Automatic self-injection devices may be on the way
  7. Study of self-injection vs. vacuum (done at Madigan): 44 pts in a crossover study x 18mos; no sig. diff. in quality of erections; sig. better attainment of orgasm and overall satisfaction of pt & partner w/injections; no sig. diff. in side-effects; 80% were using their assigned modality at end of study (Br. J. Urol. 79:952, 1997)
  1. Dropout rate is high
  1. 49% at 1y in one study (cited in Urol. Clin. N. Am., 22:833, 1995), with loss of efficacy and loss of interest as most common reasons
  2. One 5y followup of 100 pts on various regimens found only 32% continued to use; most of those d/c'd in the first year; most common reasons were desire for a permament modality of therapy, lack of a partner, and feer of needles, rather than ineffectiveness or side f/x; 82% would stil recommend to a friend (Urol. 49:932, 1997)
  1. Contraindications
  1. Poor manual dexterity, visual or cognitive dysfunction (though could train partner to do injections)
  2. Anticoagulant use
  3. Unstable CV disease (b/c of possibility of hypotension)
  1. Papaverine
  1. Causes cavernosal and arteriolar dilatation by increasing intracellular cAMP
  2. Can cause elevation of transaminases though this has evidently cause little clinically relevant hepatic dysfunction
  3. In use alone in doses 5-60mg, rates of "satisfactory" erection ranged from 35-55%, with higher rates among pts with psychogenic ED and younger pts (<60yo as c/w > 60yo); erections lasted mean 90 minutes
  1. Phentolamine
  1. Alpha-adrenergic antagonist
  2. Used ONLY in combination with other drugs (not effective alone)
  3. In combination with papaverine (30mg papaverine + 0.5-1mg phentolamine in most studies), response rates ranged from 69-95%; one head-to-head comparison showed a response rate of 49% vs. 18% with papaverine alone
  1. PGE1 (alprostadil, "Caverject")
  1. Works through a cAMP mechanism
  2. Dose: 1-40ug (us. starting dose 10-20ug)
  3. Response rate about 71% overall across several studies
  4. NEJM 334:873, 1996: set of 3 studies done by Upjohn
  1. Exclusions in all 3 studies: penile deformities, h/o priapism, SSA or SS trait, uncontrolled DM or HTN, HIV
  2. 296 men with ED, mean age 54, randomized to intercavernosal PGE1 (2.5-20ug) vs. placebo; sig. difference in attainment of erection and dose-response relationship seen for success and duration
  3. "Dose-finding study" in 201 men with ED given 1-30ug; min. effective dose was <2ug in 20-25% of those with neurogenic, vasulogenic, and mixed-etiology ED and 38% of those with psychogenic ED
  4. Uncontrolled study of 683 men with ED, mean 58yo; found mean effective dose was 20ug; 87% of injections led to an erection sufficient to have sex; sig. pain occurred in 50% of pts but only 11% of injections; 5% had prolonged erection (4-6h) and 1% had priapism (>6h); 2% developed fibrosis; 31% dropped out (most common reasons: side effects, inefficacy)
  1. Causes more pain than papaverine or phentolamine (see above)
  1. Papaverine, PGE1, and phentolamine ("Tri-Mix")
  1. Each ml containes 18mg papaverine, 0.6mg phentolamine, and 6mg PGE1
  2. In doses 0.25-1ml, response rates ranged from 77-92% in various studies; note that there is little evidence for added effect with > 0.75ml
  3. A randomized crossover study of 228 pts using Tri-Mix vs. PGE1 alone vs. papaverine-phentolamine showed "superiority" of Tri-Mix (Int. J. Impot. Res. 3:113, 1991; cited in Urol. Clin. N. Am., 22:833, 1995; article and details not given)
  4. Another study of 32 men who were "nonresponders" to papaverine-phentolamine in combination received, at different times, either 1ml of Trimix and 40ug PGE1; successful erections occurred in 22% of PGE1 injections and 50% of Trimix; also, pain occurred in 12.5% of Trimix injections but 41% of PGE1 injections (J. Urol. 155:913, 1996)
  5. Cheaper than PGE1 alone: $5 per 0.5ml dose (vs. $40 w/PGE1)
  1. Phenoxybenzamine, thymoxamine, VIP, and calcitonin gene-related peptide have also been used; others are under investigation
  2. Potential complications
  1. Pain with injection
  1. Us. none or very brief with papaverine and phentolamine
  2. With PGE1 alone, "prolonged" pain occurs in 19-34% of pts
  3. With Trimix, "prolonged" pain occurs in around 5%
  1. Priapism
  1. Arbitrarily defined as > 4h duration; some advise tx after 1h
  2. Increased risk of hypoxia and tissue acidosis with increased duration
  3. A case series at Univ. Iowa involving 640 pts found rates of erections lasting > 4h after TRIAL injections in the officeto be 4.3 with papaverine and papaverine-phentolamine combination, 2% with PGE1, 3.5% with papaverine-PGE1 combination, and 1.9% with Trimix.
  4. Note that rates of priapism with home injection tend to be much less (one estimate at 0.3%) b/c the appropriate, i.e. lowest effective, dose has been selected.
  5. Treated with intracavernosal epinephrine or phenylephrine; surgical shunting as a last resort, which may make further intracavernosal injections ineffective
  1. Penile scarring/fibrotic nodules
  1. Fibrotic nodules occurred in 5.4% of pts using papaverine or papaverine-phentolamine in one series
  2. Tri-Mix ass'd with 2-4% risk of nodule formation
  3. PGE1 seems to cause this problem only rarely
  4. Don't seem to be deforming or of functional significance, but usually considered a contraindication to further injection, at least for 1-2mos
  1. Transient hypotension-uncommon
  2. Cavernositis (very rare, only a few case reports, probably more common in diabetics)
  1. Penile prostheses/implants
  1. First one was a piece of human rib in 1930's
  2. Once was the only option; declining now as nonsurgical options emerging
  3. Has the advantage of not requiring any intact erectile mechanisms
  4. Three main types; all are permanent; implanted under local
  1. Inflatable-cosmetically more "natural"-looking but more prone to mechanical failure; more expensive
  1. One study of 80 pts with mean f/u 3y found that 55% had "functional disturbances" and 28% had been removed; most of pts were "satisfied" with results (Europ. Urol. 31:335, 1997)
  1. Malleable-cosmetically less appealing but more reliable; cheaper
  2. Semirigid (older technology)
  1. Complication rate for both about 3% (mechanical failure requiring reoperation; infection, and erosion)
  1. Silicon particle shedding has been reported but no clear clinical result
  1. Highly effective; 90% of users are satisfied (AFP article)
  2. Other modalities (vacuum contriction, intracavernosal injection) probably become ineffective after having an implant
  3. $10,000-$25,000 (higher if pt has multiple medical conditions requiring hospitalization for implantation)
  1. Vascular surgery
  1. Venous (us. ligation): used with venous leakage
  1. No good pre-op tests to predict who'll respond
  2. Long-term f/u shows "decreased effectiveness" (NIH paper)
  1. Arterial revascularization
  1. Favored in pts with congenital or traumatic vascular abnormality; pts with atherosclerotic disease are considered poorer candidates; AUA 1996 guidelines say should be considered "investigational" in pts with atherosclerotic vascular disease (J. Urol 156:2007, 1996)
  2. Preoperative eval. incompletely predicts who'll respond
  1. Topical treatments
  1. Study from Egypt: BMJ 312:1512, 1996
  1. 36 pts with erectile dysfn of varied causes; randomized, placebo-controlled crossover study (cream or placebo, each for 1 week)
  2. Cream composed of aminophylline, isosorbide dinitrate, and co-dergocrine mesylate (a mixture of ergot alkaloids)
  3. 58% reported full erection and satisfactory intercourse with drug; 8% with placebo
  4. 82% with psychogenic or mixed-cause ED had satisfactory results
  5. No side effects noted by pts or partners
  1. Transurethral alprostadil
  1. Semisolid pellet inserted in urethra with plastic applicator
  2. Urology 48:851, 1996
  1. 68 men with long-standing (mean 41mos) ED, mostly organic, randomized to transurethral alprostadil 125, 250, 500, or 1000ug vs. placebo over 2-4 weeks.
  2. 75% on the drug had "full enlargement of the penis"; 49% had erection sufficient for intercourse
  3. Penile pain occurred in 9-18% of administrations, depending on dose
  1. NEJM 336:1, 1997-JW & Am. Med. News
  1. 1,511 men with organic ED aged 30-84 given trial dose of intraurethral alprostadil
  2. Excluded men with paraplegia, poorly controlled DM, sickle cell, or psychogenic ED
  3. 996 (66%) responded to test dose and were included in the study, randomized to drug vs. placebo x 3mos
  4. 65% vs. 19% had successful intercourse at least once
  5. Penile pain occurred in 33% of users (c/w 3% of placebo pts)
  6. 3.3% of in-office doses ass'd w/hypotension
  7. No other adverse effects reported, inc. priapism or penile fibrosis, though some minor adverse effects, inc. urethral burning and minor urethral bleeding and testicular pain
  1. Alprostadil is embryotoxic; not recc'd if partner is pregnant
  1. Nitroglycerin paste-poor results so far