Erectile Dysfunction Algorithm

The full reasoning pathway — treat ED as a cardiovascular warning sign: assess vascular risk and endocrine causes before reaching for a PDE5 inhibitor, address reversible factors, treat, refer and safety-net.StartDecisionInvestigateActionReferStop / Admit

PresentationErectile dysfunction

Onset (gradual = organic; sudden/situational = psychogenic), morning/spontaneous erections, libido, relationship & mood factors, drugs, smoking/alcohol. Examine genitalia, BP, BMI, waist, peripheral pulses.

Step 1 · Safety — ED as a cardiovascular & endocrine flagRed flags?

ED is a marker of cardiovascular disease — assess QRISK, BP, lipids, HbA1c (may precede CV events by 3–5 years)
ED + exertional chest pain → investigate angina before any PDE5 inhibitor
Low libido + headache / visual field defect / gynaecomastia → pituitary tumour
Peyronie's, penile/testicular abnormality, or young man with primary ED

YES — red flag

Stop · escalateInvestigate / escalate

Significant CV risk / suspected angina → assess & manage CV risk (PDE5i contraindicated with nitrates). Very low testosterone / pituitary features → endocrinology.

NO — characterise & treat

Step 2 · InvestigateVascular + endocrine work-up

HbA1c, fasting lipids, morning total testosterone (repeat + add prolactin/LH/FSH/SHBG if low); TFT; QRISK; U&E. Examine for hypogonadism.

Step 3 · which mechanism?

Vasculogenic

Commonest

Cardiovascular risk factors, diabetes, gradual onset, loss of spontaneous erections. ED = endothelial disease.

Endocrine

Hypogonadism / pituitary

Low libido + low morning testosterone (confirm) → hypogonadism; raised prolactin → pituitary; thyroid disease.

Psychogenic / drug-induced

Common

Sudden, situational, preserved morning erections; performance anxiety, depression; drugs (beta-blockers, thiazides, SSRIs, finasteride, opioids).

Step 7 · treat

Step 7 · Action — risk reduction + PDE5 inhibitorTreat the cause and the symptom

First-line: a PDE5 inhibitor (sildenafil/tadalafil) for most, regardless of cause — contraindicated with nitrates/nicorandil; counsel on timing and adequate trials (×4 at max dose before "failure").
Optimise cardiovascular risk — BP, lipids/statin, glycaemic control, and review culprit drugs (switch where possible).
Hypogonadism: testosterone replacement (specialist-guided, after confirming low levels and excluding contraindications).
Psychogenic: psychosexual therapy/relationship support; treat depression.

Step 6 · escalation thresholds

Step 6 · ReferEscalation thresholds

Cardiology / CV risk management ED is a CV risk marker — treat risk; assess angina before PDE5i if symptomatic.
Endocrinology confirmed hypogonadism, raised prolactin/pituitary features.
Urology / psychosexual PDE5i failure (consider intracavernosal/vacuum/implant), Peyronie's, young men with primary ED, suspected structural cause.

Step 8 · lifestyle & modifiable factors

Step 8 · Lifestyle — genuinely improves EDTreat the arteries

Smoking cessation, weight loss, regular exercise (aerobic activity improves erectile function), alcohol reduction, and good glycaemic/BP control all improve ED and CV risk · reduce recreational drugs · address sleep (OSA) · relationship/psychological support; review and switch culprit medications.

Step 9 · review & safety-net

Step 9 · Review & safety-netWhen to come back

Review PDE5i response after adequate trials (correct dose/timing, ×4) before declaring failure; recheck CV risk factors and testosterone if treated. Seek urgent care for chest pain on exertion, or priapism (erection >4 h — urological emergency). Reassess mood and relationship factors at follow-up.

⚠️ ED is a window onto the arteries: new erectile dysfunction often precedes cardiovascular events by years — assess and treat cardiovascular risk, not just the symptom. And never give a PDE5 inhibitor with nitrates or nicorandil.

Safety

Red Flags — Exclude Urgent Underlying Conditions

Done

ED is a vascular symptom — screen for conditions requiring urgent action before treatment.

Priapism Painful erection >4 hours → 999 (ischaemic priapism — permanent ED risk within 24h if untreated)

Sudden onset + cardiovascular symptoms New ED + exertional chest pain, dyspnoea, palpitations → same-day (ACS, undiagnosed HF — exercise tolerance test if stable)

Hypogonadism symptoms + young patient <40y, fatigue, loss of libido, gynaecomastia, infertility → pituitary tumour (MRI, LH/FSH/testosterone/prolactin panel)

Haematospermia + perineal pain Blood in semen, perineal/rectal pain → same-day (prostate/seminal vesicle pathology, prostatitis, rarely malignancy)

Penile deformity + ED Painful erection + curved/deformed penis → Peyronie's disease → urology referral (do not start PDE5 inhibitor without assessment)

Pelvic/perineal trauma Recent pelvic fracture, perineal crush injury, or radical prostatectomy → same-day/urology (urethral injury, post-surgical neuropathy)

Nitrate use If patient on nitrates (GTN, isosorbide) → PDE5 inhibitors absolutely contraindicated. Assess cardiovascular stability before any ED treatment.

Suicidal ideation + ED Depression + sexual dysfunction + hopelessness → immediate mental health assessment. ED is a recognised precipitant of suicide risk in men.

Case-find for prostate cancer ED is a NICE NG12 trigger to offer PSA + DRE. If the prostate feels malignant on DRE or PSA is above the age-specific threshold → 2WW urology.

ED is an independent cardiovascular risk marker — men with ED have a 44% higher risk of major cardiovascular events (MACE) within 10 years (Vlachopoulos et al, JACC 2013). The penile vasculature (1.5-2mm diameter) occludes before coronary arteries (3-4mm) — ED often precedes MI by 2-5 years. Priapism is an emergency: ischaemic priapism lasting >6h causes irreversible corporal fibrosis in >50% of cases. The nitrate-PDE5 inhibitor interaction causes severe hypotension — potentially fatal.

Diagnose

Classify — Organic vs Psychogenic vs Mixed Aetiology

Done

Classification drives management — most ED has a mixed aetiology, but distinguishing predominant cause is essential.

Organic features

Gradual onset, absent nocturnal/morning erections, normal libido, consistent across situations, associated with vascular risk factors (T2DM, HTN, dyslipidaemia, smoking)

Psychogenic features

Sudden onset, normal nocturnal/morning erections (NPT present), situational (occurs with masturbation but not partner), young age, associated with anxiety/depression/relationship conflict

Mixed (most common)

Organic cause with psychological overlay — even purely organic ED causes performance anxiety, perpetuating the problem. Treat both components.

Nocturnal penile tumescence

Ask specifically about morning erections (proxy for NPT). Present = psychogenic strongly favoured. Absent = organic cause more likely. Not 100% reliable.

IIEF-5 Score

International Index of Erectile Function (5 questions, scored 5-25). 5-7 = severe, 8-11 = moderate, 12-16 = mild-moderate, 17-21 = mild, ≥22 = no ED. Use to document severity and monitor response.

Duration / progression

Acute onset after specific event = psychogenic. Gradual progressive worsening over years = organic (vascular, neuropathic). Post-radical prostatectomy = iatrogenic neurogenic.

EAU Guidelines 2023 estimate 50-80% of ED has an organic component. Pure psychogenic ED is now considered less common than previously thought — even in young men, vascular and hormonal screening should be performed. The IIEF-5 is validated, quick (<2 minutes), and allows objective monitoring of treatment response. Psychogenic ED responds well to CBT/psychosexual therapy — combined PDE5 inhibitor + psychotherapy achieves superior outcomes to either alone (NNT ~3).

Diagnose

Targeted History — Cardiovascular, Psychosocial & Medication Review

Done

ED history requires sensitivity. Use PLISSIT model (Permission, Limited Information, Specific Suggestion, Intensive Therapy).

Cardiovascular risk

BP (check today), dyslipidaemia, T2DM (HbA1c), smoking, family history of premature CVD, obesity, physical activity level. ED = 'canary in the coal mine' for CVD.

Medications review

Common causative drugs: beta-blockers (especially atenolol), thiazide diuretics, antidepressants (SSRIs, TCAs, SNRIs), antipsychotics, finasteride, dutasteride, spironolactone, opioids, recreational drugs (cocaine, cannabis, anabolic steroids)

Hormonal symptoms

Loss of libido (hypogonadism), fatigue, gynaecomastia, reduced body hair, testicular atrophy, infertility, hot flushes (hypoandrogenism)

Neurological

MS, Parkinson's, spinal cord injury, peripheral neuropathy (diabetic neuropathy). Pelvic surgery (prostatectomy, rectal surgery, aortoiliac reconstruction).

Psychosocial

Depression (PHQ-9), anxiety (GAD-7), relationship satisfaction, partner's views, past sexual trauma, pornography use, sexual orientation considerations. Work/financial stress.

Lifestyle factors

Cycling (>3h/week perineal pressure = arterial/venous compression). Smoking (endothelial damage). Alcohol (>14u/week). Obesity (aromatisation of testosterone → oestrogen).

Ejaculation / orgasm

Premature ejaculation often co-exists. Absence of ejaculation = retrograde ejaculation (T2DM, alpha-blocker use, post-TURP). Anorgasmia = neurological/psychogenic.

Previous treatment

Previous PDE5 inhibitor trial — which one, dose, how taken (with food?), adequate stimulation? Many 'treatment failures' are administration errors.

SSRIs cause ED in up to 40% of male users — often undisclosed as patients don't connect the medications. Atenolol is the worst offender among beta-blockers (4× greater ED risk vs nebivolol). Finasteride causes persistent sexual dysfunction in ~2% even after stopping (Post-Finasteride Syndrome — controversial but recognised). Cycling >3h/week is associated with 2× increased ED risk due to perineal artery compression. Alcohol — acute: facilitates psychogenic ED; chronic: causes hypogonadism and peripheral neuropathy.

Diagnose

Examination — Cardiovascular, Genital & Hormonal Assessment

Done

Physical examination is essential — do not proceed to treatment without cardiovascular and genital assessment.

Blood pressure

Check both arms. Assess CVD risk — hypertension is a major vascular risk factor for ED. White coat hypertension common; consider ABPM. Target BP <130/80 in men with ED + CVD risk.

Cardiovascular

Heart rate, rhythm, peripheral pulses (femoral, popliteal — absence suggests aortoiliac disease/Leriche syndrome = classic triad of bilateral buttock claudication + ED + absent femoral pulses)

BMI / Waist

Obesity (BMI >30) → reduced free testosterone (SHBG effects + aromatisation). Metabolic syndrome predicts ED risk. Waist >102cm = high risk.

Genitalia

Testicular size/consistency (small, soft = hypogonadism; firm nodule = cancer). Penile plaques (Peyronie's). Phimosis. Hypospadias. Secondary sexual hair. Gynaecomastia.

DRE (if ≥50y or LUTS)

Prostate assessment before starting alpha-blockers or if PSA testing planned. Enlarged/nodular prostate → exclude malignancy before finasteride/dutasteride.

Peripheral neuropathy

Diabetic neuropathy screen — 10g monofilament, vibration sense (128Hz tuning fork). Neuropathy = neurogenic ED component, less responsive to PDE5 inhibitors.

Leriche syndrome (aortoiliac occlusive disease) causes severe neurogenic + vasculogenic ED and is found in <1% of ED patients but is surgical. Absent femoral pulses are pathognomonic. Testicular volume <15ml = hypogonadism (Prader orchidometer measurement). 25% of men with ED have hypogonadism — many are undiagnosed. Peyronie's disease (fibrous plaque causing penile curvature) is present in 5-9% of men with ED and requires specific management (intralesional collagenase, surgery) — PDE5 inhibitors don't treat the underlying condition.

Diagnose

Investigations — Hormonal, Metabolic & Cardiovascular Screening

Done

Screen for treatable underlying causes before initiating PDE5 inhibitor therapy.

All patients Mandatory

Fasting glucose / HbA1c, fasting lipids, U&E/eGFR, FBC. Morning testosterone (8-11am) × 2 if low libido, fatigue, or hypogonadism features

Testosterone interpretation

Total testosterone <8 nmol/L = deficiency (treat). 8-12 nmol/L = borderline (check SHBG, calculate free testosterone). >12 nmol/L = normal. Must be fasting, morning sample

If testosterone low

LH + FSH: High LH/FSH = primary hypogonadism (testicular failure). Low/normal LH/FSH = secondary hypogonadism → MRI pituitary (prolactin, macro-prolactinoma exclusion)

Prolactin

Hyperprolactinaemia (stress, antipsychotics, macroprolactinoma) → suppresses testosterone → ED. Repeat if elevated — exclude stress artefact. If >700 mIU/L → MRI pituitary.

Thyroid

TSH — both hypo and hyperthyroidism cause ED. Hypothyroidism also reduces testosterone synthesis. Check if fatigue or other thyroid features.

PSA (if ≥50y)

Before starting testosterone therapy (contraindicated in active prostate cancer). Discuss PSA testing per NICE guidance. If PSA raised → prostate assessment before hormonal therapy.

Cardiovascular workup

ECG (rhythm, ischaemic changes). QRISK3 score calculation. 24h BP monitoring if hypertensive. Resting ECG and exercise tolerance test if cardiac symptoms before PDE5 inhibitor.

When NOT to investigate

Young healthy man with clearly psychogenic ED (sudden onset, situational, morning erections preserved, identifiable precipitant) — cardiovascular baseline still required but hormonal screen may be deferred.

Testosterone must be measured in the morning (fasting) — levels are 15-25% higher at 8am vs 4pm due to circadian rhythm. Two measurements are required due to day-to-day variability (up to 30%). T2DM is present in 25-35% of men with ED — HbA1c detects undiagnosed T2DM (prevalence 3-6% in general male population, higher with ED). QRISK3 is now preferred over Framingham — the Princeton III Guidelines stratify patients into low/intermediate/high cardiovascular risk before PDE5 inhibitor initiation.

Refer

Referral Criteria — When to Escalate

Done

Most ED is managed in primary care. These presentations require specialist input.

999

Priapism (>4 hours). Haemodynamic instability. Acute coronary syndrome triggered by ED discussion/treatment.

Same-day

Priapism <4 hours (call urology for advice — aspiration may avoid emergency). Suspected acute prostatitis with systemic sepsis. Acute urinary retention.

Urgent 2/52 Urology

Peyronie's disease (penile curvature with ED). Hypospadias affecting sexual function. Post-radical prostatectomy ED (nerve-sparing — early PDE5 inhibitor rehab). Testicular pathology on examination.

Endocrinology

Secondary hypogonadism (low testosterone + low/normal LH/FSH). Prolactin >700 mIU/L or any pituitary mass on MRI. Testosterone deficiency not responding to primary care management.

Psychosexual therapy

Predominantly psychogenic ED. Failed PDE5 inhibitor trial in young man. Relationship conflict. Sexual trauma. Performance anxiety. Prefer non-pharmacological approach.

Cardiology

High cardiovascular risk before PDE5 inhibitor initiation (recent MI <6/52, unstable angina, severe HF, uncontrolled HTN). Needs exercise testing/risk stratification first.

Primary care manage

ED + metabolic risk factors (T2DM, dyslipidaemia, HTN, obesity) — address underlying risks + PDE5 inhibitor. Psychogenic ED with adequate explanation/counselling. ED secondary to medication — switch drug if possible.

Princeton III Consensus Guidelines (2012) stratify cardiovascular risk: LOW risk (stable angina, well-controlled HTN, mild HF) = safe for PDE5 inhibitors. HIGH risk (recent MI <6/52, unstable angina, NYHA Class 3-4 HF, uncontrolled HTN) = defer until stabilised by cardiologist. Post-radical prostatectomy penile rehabilitation with early PDE5 inhibitor use (nerve-sparing procedures) improves long-term erectile recovery by 50% — urology should initiate within weeks of surgery.

Treat

Treatment — PDE5 Inhibitor Ladder & Hormonal Therapy

Done

PDE5 inhibitors are first-line for all organic and mixed ED. Correct underlying cause simultaneously.

On-demand (situational)

Sildenafil 50mg 1st line

Take 30-60 min before sexual activity. Avoid high-fat meal (delays absorption). Titrate to 100mg if inadequate, or reduce to 25mg if side effects. Duration 4-6h.

Spontaneity preferred

Tadalafil 10mg daily

Daily tadalafil (5mg OD) or on-demand (10mg, titrate to 20mg). Duration 36h allows sexual spontaneity. Preferred in daily use, T2DM, post-prostatectomy rehab.

Sildenafil side effects

Vardenafil 10mg

Alternative to sildenafil. Take 25-60 min before activity. Titrate to 20mg. Avoid with class IA/III antiarrhythmics (QT prolongation risk). Check ECG first.

Hypogonadism confirmed

Testosterone replacement

Refer endocrinology for initiation. Testogel 50mg sachet daily (transdermal) or Nebido 1000mg IM every 10-14/52. Improves libido + PDE5 response. Monitor PSA, FBC, testosterone levels.

PDE5 inhibitor CI or fails

Alprostadil 2nd line

Caverject (intracavernosal injection, urology-taught) 5-40mcg or MUSE urethral pellet 125-1000mcg. Effective in >70% of PDE5 failures. Urology to initiate.

All treatments fail

Vacuum erection device

Non-pharmacological. Effective in 60-70%. Useful in cardiovascular disease, anticoagulant use, PDE5 contraindication. Available on NHS prescription. Urology or primary care.

PDE5 teachingMust counsel: require sexual stimulation (not aphrodisiacs), avoid high-fat meals (sildenafil), avoid grapefruit, not take >once/day. Nitrate CI absolute. Allow 4-6 attempts at optimal dose before declaring failure.

Medication switchIf ED caused by beta-blocker → switch to nebivolol (vasodilatory, less ED). SSRI-induced ED → consider mirtazapine or bupropion (lower sexual SE profile). Thiazide → switch to amlodipine/ACE inhibitor.

NHS prescriptionED medications are NHS-prescribable for: T2DM, MS, Parkinson's, polio, prostate cancer, spinal cord injury, renal failure, severe pelvic injury, single gene neurological disease, radical prostatectomy, prostate/rectal cancer treatment.

PDE5 inhibitors have overall efficacy of 65-75% across ED aetiologies (Cochrane meta-analysis, 2009). NNT ~2-3 for improved erection. Tadalafil daily (5mg) is superior to on-demand dosing for T2DM-related and post-prostatectomy ED (earlier penile rehabilitation). 50% of PDE5 'failures' are administration errors — the most common being taken after a high-fat meal (delays sildenafil absorption by 1-2h) or insufficient sexual stimulation. A 4-attempt trial at maximum tolerated dose is required before declaring treatment failure.

Lifestyle

Non-Pharmacological — Lifestyle as Vascular Treatment

Done

Lifestyle modification can restore erectile function without drugs — and reduces cardiovascular risk simultaneously.

Exercise 40 min aerobic exercise × 4/week reduces ED by 30% (RCT, Lamina et al). Improves endothelial function, reduces BMI, raises free testosterone. Most powerful lifestyle intervention.

Weight loss 10% body weight loss restores erectile function in 30% of obese men without medication. Reduces aromatisation of testosterone to oestrogen. Target BMI <25.

Smoking cessation Smoking causes endothelial dysfunction and is an independent risk factor for ED (OR 1.51). Cessation improves ED in 25% within 1 year. Refer to NHS Stop Smoking Service.

Alcohol reduction Chronic excess alcohol → hypogonadism, peripheral neuropathy, testicular atrophy. Target <14 units/week with alcohol-free days. Acute excess causes transient ED even in healthy men.

Mediterranean diet Reduces ED risk by 40% (Esposito et al, JAMA 2004, RCT). Improves endothelial function, reduces insulin resistance. Olive oil, fish, legumes, vegetables, nuts.

Cycling modification >3h/week cycling → perineal pressure compresses pudendal artery. Use ergonomic saddle (no-nose design), padded shorts, standing intervals. Reassess if not improving.

Psychosexual therapy CBT addresses performance anxiety, sensate focus exercises improve intimacy. Combined PDE5 + psychotherapy superior to either alone. Refer if relationship conflict. COSRT-registered therapist.

Sleep hygiene Testosterone secretion occurs predominantly during sleep (REM phase). Obstructive sleep apnoea causes hypogonadism + ED. Screen (STOP-BANG score). CPAP improves testosterone and ED.

The MMAS (Massachusetts Male Ageing Study) showed physical activity reduces ED risk by 30-40%. Esposito's landmark RCT (JAMA 2004) showed Mediterranean diet improved IIEF scores from 13.9 to 17.0 (vs 13.6 to 13.4 in controls — p<0.001). Sleep apnoea affects 15-25% of men with ED — CPAP therapy normalises testosterone levels in 70% of hypogonadal men with OSA. Lifestyle modification addressing all vascular risk factors collectively has greater impact on erectile function than any single drug intervention.

Safety

Follow-Up — Review, Monitoring & Cardiovascular Surveillance

Done

Follow-up has a dual purpose: assess treatment response AND manage cardiovascular risk.

4-6 weeks

Review PDE5 inhibitor response (re-score IIEF-5). Check side effects (flushing, headache, visual changes). Confirm correct administration technique. Address new psychological barriers.

3 months

Reassess QRISK3 if newly initiated antihypertensive/statin. Repeat testosterone if borderline. Weight/BMI/waist circumference. HbA1c if T2DM. Lifestyle progress.

6-12 months

Annual cardiovascular review — BP, lipids, HbA1c, weight, smoking status. IIEF-5 re-score to document outcome. Consider stepping down PDE5 inhibitor dose if lifestyle improvements significant.

On testosterone

Every 3-6 months: testosterone level, haematocrit/FBC (polycythaemia risk — target testosterone 10-25 nmol/L), PSA, BP. Refer if PSA rise >1.4 ng/ml above baseline at any 12-month assessment.

Safety-net 999

Chest pain/dyspnoea during sexual activity → stop sexual activity, call 999. Priapism >4 hours. Any severe adverse drug reaction (syncope after PDE5 + nitrate interaction).

Safety-net same-day

Sudden vision loss or hearing loss after PDE5 inhibitor (rare NAION — non-arteritic ischaemic optic neuropathy — stop PDE5 inhibitor permanently). Priapism <4 hours.

Non-responders

Failed 2 different PDE5 inhibitors at maximum dose → confirm compliance, check testosterone, consider referral to urology (penile Doppler, alprostadil, vacuum device, surgical implant discussion)

Psychological review

If ED persists despite optimal pharmacological treatment → formal psychosexual therapy referral. Partner involvement in therapy improves outcomes. COSRT UK directory.

ED patients have 44% higher rate of major cardiovascular events — every ED consultation is an opportunity for CVD risk reduction. Annual cardiovascular review in men with ED has been shown to detect new-onset T2DM, hypertension, and dyslipidaemia — effectively making ED a 'gateway' to preventive medicine. NAION (non-arteritic ischaemic optic neuropathy) associated with PDE5 inhibitors has estimated incidence of 2.5/100,000 — rare but serious; patients must be warned. Testosterone monitoring for polycythaemia is mandatory — haematocrit >54% requires dose reduction or phlebotomy.