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Erectile Dysfunction (Condition)

Erectile dysfunction (ED) is the consistent or recurrent inability to attain or maintain a penile erection sufficient for satisfactory sexual performance.[1] It is one of the most common male sexual dysfunctions, with prevalence estimates of 2–9% at ages 40–49 in one review, while the Massachusetts Male Aging Study found some degree of ED in 39% by age 40; estimates beyond age 70 range from 50–100%.[1] A 1999 modelling projection estimated 322 million cases worldwide by 2025.[2]

For the operative treatment atlas (penile prosthesis, revascularization, Peyronie's surgery as comorbid disease) see Sexual Dysfunction Treatment Atlas. For the pharmacology hubs (PDE5 inhibitors, intracavernosal injection agents, intraurethral alprostadil, testosterone replacement, androgen adjuncts, priapism management) see Sexual Medicine & Andrology.

Pathophysiology​

Erection is a neurovascular event requiring coordination of psychological, endocrine, vascular, and neurological systems. Parasympathetic stimulation triggers release of nitric oxide (NO) from endothelial cells and nonadrenergic noncholinergic neurons, which activates guanylyl cyclase to produce cyclic GMP (cGMP). cGMP causes smooth-muscle relaxation in the corpora cavernosa, increasing arterial inflow and compressing subtunical venules to trap blood and produce rigidity. PDE5 inhibitors prolong this signal by blocking cGMP degradation.[1][3] Burnett and colleagues (1992) localized NO synthase in the rat to penile neurons innervating the corpora cavernosa and to neuronal plexuses in the adventitia of penile arteries; small doses of NO synthase inhibitors abolished electrically stimulated erections.[40]

ED is classified as psychogenic, organic, or mixed, with mixed being most common:[1]

ClassMechanismExamples
VasculogenicArterial insufficiency, corporal veno-occlusive dysfunction (venous leak), sinusoidal fibrosisAtherosclerosis, post-radiation, post-traumatic
NeurogenicCentral or peripheral neural disruptionStroke, MS, spinal-cord injury, diabetic neuropathy, post–radical pelvic surgery
EndocrinologicalTestosterone, prolactin, thyroid axisHypogonadism, hyperprolactinemia, diabetes mellitus
Drug-inducedPharmacologic interference with NO / sympathetic balanceAntihypertensives, SSRIs, antiandrogens, major tranquilizers
PsychogenicPerformance anxiety, depression, relationship dynamicsPsychological factors may occur alone or with organic causes[4]

Risk Factors​

Age is the dominant risk factor; type 2 diabetes mellitus is the second, with ED in 50–75% of diabetic men.[1] Other contributors:[1][4][3]

  • Hypertension. In an outpatient hypertension-center questionnaire study, 68.3% of 104 respondents reported ED; the questionnaire was mailed to 476 men.[42]
  • Dyslipidemia
  • Obesity and metabolic syndrome
  • Sedentary lifestyle
  • Cigarette smoking. In the prospective-cohort subgroup of a meta-analysis, current smoking was associated with higher odds of ED than never smoking (OR 1.51, 95% CI 1.34–1.71).[47]
  • Alcohol and recreational drug use
  • Lower urinary tract symptoms / BPH
  • Depression
  • Prostate-cancer treatment. ED can follow radical prostatectomy, radiation, brachytherapy or focal ablation with high-intensity focused ultrasound (HIFU). AUA/ASTRO requires counseling about sexual risks ; its discussion recommends documenting baseline function.[39] In a selected 92-man focal-HIFU cohort without severe ED before treatment, 36% had severe ED (IIEF-5 ≤7) at 12 months.[26]
  • COVID-19. Proposed vasculogenic mechanism (endothelial nitric-oxide synthase reduction near penile vascular endothelium); one survey found higher ED prevalence in COVID-19-positive than -negative men (28% vs 9%).[27][28]

ED as a Cardiovascular Risk Marker​

Vasculogenic ED and cardiovascular disease (CVD) commonly share endothelial dysfunction and atherosclerosis.[1][5][21] Because penile arteries are smaller-caliber than coronary arteries, the same degree of endothelial dysfunction manifests earlier in erectile tissues.

The Mostafaei 2021 umbrella review of meta-analyses confirmed that ED independently predicts:[6]

OutcomeRelative risk
Cardiovascular disease1.45
Coronary heart disease1.50
Myocardial infarction1.55
Stroke1.36
All-cause mortality1.25

ED can precede symptomatic coronary disease, but the interval and proportion depend on the population studied; the Dong meta-analysis evaluated future cardiovascular risk.[7][3] The current EAU framework incorporates Princeton IV cardiovascular assessment. ED is a risk marker; urgency and referral depend on cardiovascular symptoms and the individual risk assessment.[21]

Diagnostic Evaluation​

Evaluation begins with a sexual, medical and psychosocial history that documents onset, rigidity and duration of stimulated and morning erections, desire, arousal, ejaculation, orgasm, partner context and medication exposure. Examine the genitourinary, endocrine, vascular and neurological systems, including penile deformity and signs of hypogonadism; record blood pressure and BMI or waist circumference if not recently assessed.[9][11][21]

Validated questionnaire — IIEF-5 (Sexual Health Inventory for Men)​

ScoreSeverity
5–7Severe ED
8–11Moderate ED
12–16Mild-to-moderate ED
17–21Mild ED
22–25None

The IIEF-5/SHIM is a validated ED screening tool; the separate six-item IIEF-EF domain described below is used to measure treatment efficacy in many trials.[8][11]

A separate instrument, the six-item Erectile Function domain of the full 15-item IIEF, was scored 6–30 among men who attempted sexual activity in the validation study, with these cutoffs: 26–30 no ED, 22–25 mild, 17–21 mild-to-moderate, 11–16 moderate, 6–10 severe. It is a distinct scale from the 5-item, 25-point IIEF-5/SHIM above, and its cutoffs should not be applied to a SHIM score.[29]

The Erection Hardness Score (EHS) is a simple 4-point patient-reported scale used to establish baseline rigidity and track treatment response in the clinical encounter: 1, penis larger but not hard; 2, hard but not hard enough for penetration; 3, hard enough for penetration but not completely hard; 4, completely hard and fully rigid.[30]

Laboratory testing​

  • Fasting glucose or HbA1c. Diabetes screen
  • Lipid panel. Atherosclerotic risk
  • Morning total testosterone. Confirm a low value on a second early-morning draw; obtain LH to classify confirmed deficiency and free testosterone when total testosterone is borderline or SHBG is altered.[18][25]
  • Selected: prolactin, TSH when clinically indicated[9]

Specialized tests (selected cases)​

  • Nocturnal penile tumescence (NPT). Psychogenic versus organic differentiation. Recorded over 2–3 consecutive nights with penile strain gauges (RigiScan); sleep disruptors (irregular schedule, sleep apnea, restless leg syndrome, PTSD, depression) impair REM sleep independent of erectile capacity, giving a high false-negative rate. A study is generally reliable only when completely normal, with at least one erectile episode of tip rigidity above 60% lasting more than 10 minutes; most abnormal studies fall short of normal criteria without being fully absent, which limits clinical utility, while absent nocturnal erections are nonspecific and cannot establish an organic cause.[31][21]
  • Intracavernosal injection (ICI) test. Gives limited information about vascular status; use dynamic penile duplex when a diagnostic vascular assessment is warranted.[21]
  • Penile duplex Doppler ultrasound. After vasoactive injection, peak systolic velocity assesses arterial inflow (>30 cm/s usually normal), end-diastolic velocity helps assess veno-occlusive function (<3 cm/s usually normal), and resistive index >0.8 is usually normal; anxiety or inadequate vasoactive dosing can produce false-positive vascular findings.[21]
  • Shear wave elastography. Investigational ultrasound measure of corporal stiffness using induced shear waves. In one feasibility study, post-injection measurements distinguished 26 men with arterial ED from 30 with nonvascular ED (AUC 0.81); venogenic classification, cardiovascular-risk prediction and replacement of duplex Doppler were not tested.[32]
  • Cavernosometry or cavernosography. When surgical revascularization is being considered
  • Selective pudendal arteriography. Pre-revascularization in young men with focal post-traumatic disease[9]

Cardiovascular risk assessment​

Assess cardiovascular risk and the safety of sexual activity. The EAU 2026 framework adopts the Princeton IV algorithms, which added coronary artery calcium scoring for cardiovascular risk stratification:[41] for men with predominantly vasculogenic ED and no overt disease, calculate the 2019 ACC/AHA 10-year ASCVD risk (low below 5%, borderline 5% to below 7.5%, intermediate 7.5% to below 20%, high 20% or more) and obtain a coronary artery calcium score in the borderline-to-intermediate group, because the risk score alone can underestimate risk in men aged 40 to 60. Princeton IV proposes lifestyle care for CAC 0; lifestyle care, risk-factor control and a moderate- to high-intensity statin for CAC 1–100; and risk-factor control, a high-intensity statin and preventive-cardiology referral for CAC >100.[41][48] Men with overt cardiovascular symptoms or disease are assessed by exercise capacity, with a stress test when risk is intermediate or indeterminate and cardiology referral when risk is high. The EAU asks that these flowcharts be adapted to local expertise, test availability and cost, and separately keeps the 3rd Princeton recommendations for prescribing PDE5 inhibitors in men with cardiovascular disease.[21] Princeton IV offers a rough functional screen for usual-partner sexual activity: walking one mile on flat ground in 20 minutes or briskly climbing two flights of stairs in about 10 seconds without cardiac symptoms corresponds to about 2–3 METs (coital activity in established couples has been estimated at about 2.5–3.3 METs). More vigorous sexual activity may require 5–6 METs, and indeterminate cardiovascular risk calls for formal assessment rather than reliance on this proxy.[33][34][41]

Treatment​

Treatment uses shared decisions across the available options. The EAU 2026 framework replaces a rigid three-tier ladder with choices based on efficacy, invasiveness, safety and patient preference; the AUA 2018 and ICSM guidance provide additional context.[21][11][12]

1. Lifestyle modification — the foundation​

The AUA guideline recommends counseling men with ED and comorbidities that dietary change and increased physical activity improve overall health and may improve erectile function ; it also advises smoking-cessation counseling.[11] Weight loss, exercise and better control of diabetes, hypertension and dyslipidemia benefit cardiovascular health. The effect on erections is small on average, with clinically important gains in a subset of men.[11][4] A meta-analysis of randomized trials found increased physical activity produced a 3.85-point improvement in IIEF erectile-function scores (95% CI 2.33–5.37).[35] Exercise may also potentiate a PDE5 inhibitor: in a small randomized study, adding a prescribed aerobic exercise regimen (mean 3.4 hours/week, about 22.8 MET-hours/week) to PDE5i therapy produced a higher erectile-function domain score than PDE5i alone at three months (26.8 vs 24.7, P = 0.003), with larger gains also seen in confidence, desire and satisfaction subscales.[36]

2. First-line — oral PDE5 inhibitors​

PDE5 inhibitors are an established first-line pharmacotherapy ; response depends on cause, correct use and the outcome definition.[1][11][12][21] See the PDE5 inhibitors pharmacology hub for the deep dive on mechanisms, dosing, contraindications, and post-RP rehab evidence.

Use the prescribing hub for agent selection, starting doses, adjustment and contraindications. Avoid interpreting an intercourse-attempt success rate as a patient-level cure rate.

Key prescribing principles:

  • Assess apparent nonresponse. If the patient wants to continue a PDE5 inhibitor, allow several properly timed attempts with sexual stimulation; review dose and safe titration, because education and correct use restore response in some men.[12][15][21]
  • Review stimulation, timing, food effects, adherence and safe dose adjustment; patients may select another modality without exhausting every oral regimen.[11][21]
  • Absolute contraindication: concomitant organic nitrates or nitric-oxide donors, including recreational amyl nitrite (poppers) and nicorandil, or the soluble guanylate-cyclase stimulator riociguat, because of severe hypotension risk.[21][52] Nitrate-free intervals and label details are in the PDE5 inhibitors hub.[21][10]
  • With α-blockers, both drugs vasodilate; establish stability on the α-blocker and start the PDE5 inhibitor at its lowest dose. Use caution in patients with autonomic dysfunction.[21][14]
  • Common side effects: headache, flushing, dyspepsia, nasal congestion, visual disturbances.
  • All four agents are effective, but comparative efficacy estimates vary across analyses and doses; select using individual response, onset, duration, adverse effects and daily-versus-on-demand preference.[12][21][49]

3. Injection, intraurethral and device options​

For inadequate oral response, contraindications, or informed preference :[11][15][16][21]

  • Intracavernosal injection (ICI). Alprostadil monotherapy or bimix / trimix / quadmix combinations. ICI is the most reliably effective non-surgical option in PDE5-resistant patients. Risks include penile pain (about half of patients), priapism (about 1% with alprostadil) and penile fibrosis (about 2%). Before home ICI, perform an in-office injection test and instruct patients to return to the office or emergency department for an erection lasting more than four hours .[21][11][38] Combinations containing papaverine carry more priapism risk than alprostadil alone.[21][38] EAU 2026 reports fibrosis in 5–10% with papaverine-containing mixtures versus about 2% with alprostadil alone.[21] See the ICI agents pharmacology hub.
  • Intraurethral alprostadil (MUSE). Less invasive than ICI but typically less effective; useful when ICI is not tolerated. FDA now lists every MUSE strength as discontinued, so US availability cannot be assumed. See intraurethral alprostadil.
  • Vacuum erection device (VED). This non-invasive mechanical option is useful when pharmacotherapy is unsuitable and may preserve penile size during post-RP rehabilitation; it has not demonstrated faster spontaneous erectile-function recovery.[50] EAU 2026 offers it to well-informed patients requesting drug-free treatment : erections satisfactory for intercourse in up to 90% and satisfaction 27–94%, falling to 50–64% continued use at two years; the constriction ring should come off within 30 minutes to avoid skin necrosis, and EAU 2026 calls VEDs contraindicated with bleeding disorders or anticoagulation; AUA 2018 instead advises caution and use of a vacuum limiter, so assess individual bleeding risk.[21][11]
  • Topical MED3000 (Eroxon). FDA authorized this non-prescription, non-medicated topical device in 2023 for men aged 22 years and older. Applied to the glans, its volatile solvents evaporate to produce a cooling-then-warming sensation; nitric-oxide release and smooth-muscle relaxation are proposed, unproven downstream effects. FDA labeling advises against use with penile disease or deformity, damaged penile skin, ingredient allergy, or medical advice to avoid sexual activity; stop use if irritation occurs.[44] In FM71, a 96-man, 24-week randomized open-label study, 59% of MED3000 users versus 83% of tadalafil 5 mg users met the study’s severity-adjusted IIEF-EF response criterion, while 44.9% versus 30.0% of intercourse attempts had a noticeable erection within 10 minutes.[37] FM71 excluded men after radical prostatectomy or Peyronie’s surgery, those with severe uncontrolled diabetes, and prior PDE5-inhibitor nonresponders.[44] The 2.8% MED3000 headache rate came from a separate trial, whereas 19.1% was the tadalafil rate in FM71.[37] Because it is sold without a prescription, men may bypass the clinician visit that would otherwise screen for the cardiovascular and endocrine risk factors ED often signals.[37]

4. Penile prosthesis​

Surgically implanted inflatable or malleable penile prostheses may be selected after discussion of all options, including when other treatment is ineffective or unacceptable; EAU 2026 recommends implantation if other treatments fail or according to patient preference, with full counseling on benefits and harms .[21] EAU 2026 cites series reporting about 92–100% patient and 91–95% partner satisfaction; multicomponent inflatable prostheses (IPPs) are also associated with high satisfaction.[21][9] In a systematic review of 83 studies enrolling 12,132 implant recipients, satisfaction data were available for 9,429 patients and pooled patient satisfaction was 83% (95% CI 80–86%); mean follow-up across the included studies was 47.6 months.[51] AUA advises counseling on postoperative expectations and not operating in the presence of systemic, cutaneous or urinary tract infection.[11] EAU 2026 finds no head-to-head evidence favoring one implant class or approach (level 3) and reports mechanical failure below 5% at five years for modified three-piece devices, survival of 87.2% at five and 76.8% at ten years in a meta-analysis, and infection of 2–3% after primary implantation in low-risk men at high-volume centers (1–2% with coated devices).[21]

For the operative pathway — preoperative evaluation (CURSED), intraoperative setup (no-touch), approaches (PS / IP / SC), reservoir placement (SoR / HSM), models database, infection prevention, revision, and complications — see Penile Implants.

5. Testosterone replacement therapy​

The AUA recommends measuring morning total testosterone in every man with ED .[11] Testosterone deficiency is defined by the AUA as total testosterone below 300 ng/dL on two separate early-morning measurements together with symptoms or signs.[25] In men with confirmed hypogonadism, testosterone replacement improves IIEF erectile-function scores (pooled mean gain about 2.3 IIEF-EF points, below the 4-point threshold assumed by the Cochrane review for its IIEF-EF analysis).[18][19][8] Benefit is greater in men with more severe hypogonadism (total T < 8 nmol/L, about 230 ng/dL) and smaller with diabetes or obesity; in men without deficiency, testosterone has little or no effect on erectile function.[19][8] In the nested TRAVERSE Sexual Function Study, 1,161 men aged 45–80 with low libido, two testosterone values <300 ng/dL, and established or elevated cardiovascular risk were randomized to testosterone gel (n = 587) or placebo gel (n = 574). Testosterone improved the primary sexual-activity score versus placebo at 6 and 12 months, with the effect maintained at 24 months, and improved desire, but not erectile function.[43] TRT may be combined with PDE5 inhibitors for enhanced effect in hypogonadal men with ED: the AUA advises that a PDE5 inhibitor may be more effective combined with testosterone , and that testosterone is not an effective monotherapy for ED.[19][15][11]

The Endocrine Society 2018 guideline recommends against starting testosterone in men planning near-term fertility or with breast or prostate cancer, thrombophilia, untreated severe obstructive sleep apnea, elevated hematocrit, severe LUTS, uncontrolled heart failure, myocardial infarction or stroke within the last six months, an unevaluated palpable prostate nodule or induration, or PSA above 4 ng/mL (above 3 ng/mL at increased risk) without urologic evaluation.[18] For hypogonadal men aged 55 to 69 years with a life expectancy over 10 years who are considering testosterone therapy, the Endocrine Society suggests discussing prostate-cancer risk and monitoring and assessing risk before treatment and 3 to 12 months after starting for those who choose monitoring; for men aged 40 to 69 years at increased prostate-cancer risk, it suggests discussing risk and offering monitoring options (recommendation 2.3).[18] TRAVERSE randomized 5,246 symptomatic men aged 45–80 with two testosterone values below 300 ng/dL and existing or high cardiovascular risk (5,204 in the full analysis). Transdermal testosterone was noninferior to placebo for major adverse cardiovascular events; atrial fibrillation, acute kidney injury and pulmonary embolism occurred more often.[24][20] See the testosterone replacement pharmacology hub for the full framework.

6. Emerging therapies​

  • Low-intensity extracorporeal shockwave therapy (Li-ESWT). Proposed mechanism: neovascularization and tissue regeneration. The 2025 Cochrane review (21 trials, 1,357 men) found low-certainty evidence: the average short-term erectile-function benefit may be too small to be clinically important; longer-term benefit remains uncertain and heterogeneous. EAU offers a weak recommendation for mild vasculogenic ED, PDE5 inhibitor poor responders and patients who decline oral therapy, whereas AUA considers treatment investigational .[21][11]
  • Stem-cell, platelet-rich-plasma (PRP) and botulinum toxin therapy. The AUA classes intracavernosal stem-cell therapy as investigational and PRP as experimental; EAU limits intracavernosal PRP to clinical trials (level 1b for mild improvement, but no recommendation), finds stem-cell data insufficient for a recommendation, and offers no recommendation for botulinum toxin, whose two randomized trials in non-responders were small.[17][11][21]

7. Psychosexual therapy​

Counseling is recommended for men with psychogenic ED, either as monotherapy or in combination with pharmacotherapy. The AUA advises considering referral to a mental health professional for any man treated for ED, to support adherence, reduce performance anxiety and integrate treatment into the sexual relationship .[11] Couples-based therapy is particularly valuable when relationship dynamics contribute. The 2007 Cochrane review found group therapy plus sildenafil superior to sildenafil alone (RR 0.46 for persistence of ED; two trials, 71 men), and one small trial (20 men) favored group therapy over sildenafil on IIEF.[13] See the canonical Psychosexual Therapy page for the full sensate focus / CBT / MBI / PLISSIT framework.

Special Populations​

PopulationKey considerations
Post-radical prostatectomyOffer erectile-function treatment; the AUA advises counseling that early PDE5 inhibitor use may not improve spontaneous, unassisted function.[11] EAU 2026 concurs (penile rehabilitation with PDE5 inhibitors does not increase spontaneous recovery, level 1a), advises that data are inadequate to support any specific rehabilitation regimen , and still suggests starting pro-erectile treatment at the earliest opportunity after prostatectomy or other curative prostate-cancer treatment .[21] REACTT improved assisted function during treatment but did not establish unassisted recovery after washout. Discuss PDE5i, MUSE, ICI, VED and prosthesis according to goals.[23]
Post-pelvic radiationVasculogenic + neurogenic mechanism; PDE5i first-line; ICI / IPP for non-response[21]
Diabetes mellitusHigh prevalence (50–75%); poorer PDE5i response; lower threshold for second-line[16]
Spinal-cord injury / MSNeurogenic mechanism; PDE5i first-line; autonomic-dysreflexia precaution in lesions T6 and above (see Autonomic Dysreflexia)[14]
Cardiovascular diseasePrinceton IV-informed risk stratification; nitrate use is an absolute contraindication to PDE5i[10]
Young men with focal post-traumatic diseaseSelective candidates for penile revascularization (AUA: conditional recommendation for young men with focal arterial occlusion and no generalized vascular or veno-occlusive disease; penile venous surgery is not recommended; EAU 2026 reports 60–70% long-term success after pelvic or perineal trauma, requires confirmation by pharmaco-arteriography, treats veno-occlusive dysfunction as a contraindication and no longer recommends venous ligation)[11][21] — see saphenous vein graft
Peyronie's disease overlapTreat concomitant ED with a PDE5 inhibitor when appropriate. For stable, intercourse-limiting curvature with ED unresponsive to pharmacotherapy, use a penile prosthesis with straightening if needed ; men with adequate rigidity may be candidates for curvature surgery without an implant.[45] See Peyronie's disease.

Prognosis and Key Takeaways​

ED is a treatable condition at all stages. The diagnosis should prompt cardiovascular risk assessment, as it may precede symptomatic CVD by several years (the interval varies by population).[6][1][5][7]

Discuss lifestyle and psychosexual care alongside medication, injection/device therapy and prosthesis. Avoid promising the same success rate across different causes or presenting surgery as a mandatory last step.[11][21]

For the reconstructive urologist, ED management runs in parallel with penile-implant and Peyronie's-disease practice. New ED warrants cardiovascular assessment.[46] Consider referral for cardiac assessment when exercise reserve is inadequate, arteriogenic ED is documented, or Princeton cardiovascular risk is high .[46]

Selected evidence​

Sildenafil pivotal trials · 1998[22]; REACTT · 2014[23].

Erectile dysfunction — key study comparisons
Study and populationComparison and resultsUse and limitations
Sildenafil pivotal trials · 1998

Men with erectile dysfunction of organic, psychogenic or mixed causes.

Randomized n=861

Source and methods: Sildenafil pivotal trials · 1998
Source
Goldstein I et al. Oral Sildenafil in the Treatment of Erectile Dysfunction (1998). DOI: 10.1056/NEJM199805143382001
Design
Two sequential double-blind randomized placebo-controlled trials
Denominators
532 in a 24-week fixed-dose trial; 329 different men in a 12-week flexible-dose trial. The displayed intercourse outcome belongs to the latter.
Follow-up
12 and 24 weeks; a subsequent 32-week extension was open label
Sildenafil vs placebo

Successful intercourse attempts · Final 4 weeks of the 12-week trial

69% of attempts with sildenafil vs 22% with placebo.

P<.001.

Demonstrates on-treatment efficacy.

  • Success measured per intercourse attempt.
REACTT · 2014

Men ≤68 with normal preoperative erectile function undergoing bilateral nerve-sparing radical prostatectomy.

Randomized n=423

Source and methods: REACTT · 2014
Source
Montorsi F et al. Effects of Tadalafil Treatment on Erectile Function Recovery Following Bilateral Nerve-sparing Radical Prostatectomy: A Randomised Placebo-controlled Study (REACTT) (2014). DOI: 10.1016/j.eururo.2013.09.051
Design
Randomized double-blind placebo-controlled trial
Denominators
139 daily tadalafil, 143 on-demand tadalafil, 141 placebo.
Follow-up
9 months treatment, 6-week washout, then open-label extension
Daily or on-demand tadalafil vs placebo

Unassisted IIEF-EF ≥22 after drug washout · 9 months treatment followed by 6-week washout

20.9% daily, 16.9% on-demand, 19.1% placebo.

Odds ratio vs placebo: daily 1.1 (95% CI 0.6–2.1); on-demand 0.9 (0.5–1.7).

PDE5 inhibitors may assist erections after surgery.

  • Selected nerve-sparing postoperative population.

See Also​

Podcasts​

Management of Post-Prostatectomy Erectile Dysfunction
BackTable Urology, Ep. 51 (2022) · Darshan Patel, Mike Hsieh
backtable.com

References​

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