Male Sexual Dysfunction
Clinical Snapshot
Erectile dysfunction (ED) is the persistent inability to achieve or maintain an erection sufficient for satisfactory sexual activity, on all or almost all attempts.[1] It is common, has vascular, neurogenic, structural, hormonal, and psychogenic causes that frequently coexist, and is far more than a quality-of-life issue: vascular ED often precedes the clinical diagnosis of coronary artery disease, so its presence should prompt a genuine cardiovascular risk assessment, not just a prescription.[2] This chapter focuses on the assessment and stepwise pharmacologic management of ED — phosphodiesterase type 5 (PDE5) inhibitors as first-line therapy, the essential nitrate-interaction safety check, second-line options when PDE5 inhibitors fail or are contraindicated, and testosterone replacement therapy for confirmed hypogonadism — with brief, distinct coverage of premature ejaculation, delayed ejaculation, and low sexual desire, since more than one of these conditions can be present in the same patient and a focused sexual history is needed to tell them apart.
Recognize the Condition
Erectile dysfunction
ED is classified by underlying mechanism, since this shapes both workup and counselling.
Categories of erectile dysfunction
Organic
Vasculogenic (the most common organic cause, sharing risk factors with cardiovascular disease), neurogenic (multiple sclerosis, Parkinson disease, spinal cord injury, diabetic neuropathy, pelvic surgery/radiation damaging autonomic nerves), structural (Peyronie disease, penile fracture, prior priapism), or hormonal (testosterone deficiency, hyperprolactinemia). Affects all erections, including nocturnal/morning and self-stimulated erections.
Psychogenic
Generalized or situational; related to performance anxiety, depression, relationship distress, or other psychosocial stressors. Erections that are firmer with self-stimulation or on waking than with a partner point toward this category.
Mixed
The most common overall pattern in clinical practice — an organic predisposition compounded by secondary performance anxiety once erections first become unreliable.
Premature ejaculation
Ejaculation that occurs sooner than desired with a sense of lack of control, causing distress. Lifelong premature ejaculation is present from a person's first sexual experiences, typically with ejaculation within about 1-2 minutes of penetration nearly every time; acquired premature ejaculation is a clinically significant reduction in ejaculatory latency from a patient's own previous pattern, with associated distress.[3]
Delayed ejaculation
A marked delay in, or inability to achieve, ejaculation despite adequate sexual stimulation and the desire to ejaculate. Uncommon before age 50, with incidence increasing with age.
Male hypoactive sexual desire disorder
A persistent or recurrent lack of sexual thoughts, fantasies, and desire that causes distress. Depression, low testosterone, anxiety, insomnia, and insufficient physical activity are commonly associated.
More than one of these conditions can be present in the same patient at once — a focused sexual history covering desire, erection, ejaculation, and satisfaction is needed to identify all of them, since treating only the presenting complaint risks leaving a coexisting condition unaddressed.
Risk Factors
- Advancing age.
- Cardiovascular risk factors that overlap heavily with vasculogenic ED: diabetes mellitus, dyslipidemia, hypertension, obesity, metabolic syndrome, sedentary lifestyle, and smoking.
- Pelvic or prostate surgery (radical prostatectomy), pelvic radiation therapy, pelvic trauma, or penile fracture.
- Neurologic disease — multiple sclerosis, Parkinson disease, spinal cord injury, diabetic neuropathy.
- Peyronie disease and other structural penile abnormalities.
- Lower urinary tract symptoms/benign prostatic hyperplasia and chronic prostatitis/chronic pelvic pain syndrome.
- Psychological factors — depression, anxiety, performance anxiety, relationship distress.
- Testosterone deficiency.
- Alcohol use, both acute intoxication and chronic heavy use; cannabis use.
- Medications — a major and frequently overlooked cause. Always review the medication list as part of the workup; the table below reproduces the drug classes most consistently associated with each type of male sexual dysfunction.
Medication-associated male sexual dysfunction
| Sexual disorder | Drug classes/agents associated |
|---|---|
| Erectile dysfunction | 5-alpha reductase inhibitors, acetazolamide, alcohol (acute or chronic use), alpha-blockers, anti-androgens, barbiturates, carbamazepine, cimetidine, clofibrate, clonidine, digoxin, GnRH analogues, ketoconazole, lithium, MAOIs, metoclopramide, opioids, phenothiazines, phenytoin, spironolactone, SSRIs, thiazide diuretics, tricyclic antidepressants |
| Delayed ejaculation | 5-alpha reductase inhibitors, alpha-blockers, antipsychotics, SSRIs |
| Male hypoactive sexual desire disorder | 5-alpha reductase inhibitors, alcohol (chronic use), anti-androgens, barbiturates, beta-blockers, carbamazepine, GnRH analogues, ketoconazole, MAOIs, opioids, phenytoin, spironolactone, SSRIs, tricyclic antidepressants |
Abbreviations: GnRH = gonadotropin-releasing hormone; MAOI = monoamine oxidase inhibitor; SSRI = selective serotonin reuptake inhibitor. When a temporal link is plausible, discuss an alternative agent or dose adjustment with the prescriber before assuming the sexual dysfunction is unrelated to therapy.
Red Flags & Refer
Refer or escalate urgently for any of the following:
- Priapism — a persistent, often painful erection lasting over 4 hours, unrelated to sexual stimulation or desire — is a true urologic emergency requiring immediate care; permanent penile damage can result without treatment within hours. It is most commonly precipitated by intracavernosal injection therapy.
- Use of any nitrate — regular or intermittent, including recreational nitrite ("poppers") use — is an absolute contraindication to PDE5 inhibitor therapy; the combination can cause severe, potentially fatal hypotension. Confirm nitrate status before every PDE5 inhibitor prescription or dispense.
- Chest pain, dyspnea, dizziness, or palpitations occurring during or after sexual activity — assess cardiovascular risk before continuing or starting any ED therapy.
- High cardiovascular risk features — unstable or refractory angina, uncontrolled hypertension, decompensated heart failure, a recent myocardial infarction or stroke, or a high-risk arrhythmia — defer ED treatment and refer for cardiology stabilization before resuming sexual activity or starting any therapy.[2]
- Sudden, painless vision loss or sudden hearing loss in a patient taking a PDE5 inhibitor — discontinue the drug and refer immediately.
Assessment & Diagnosis
History
- A focused sexual history distinguishing ED, premature ejaculation, delayed ejaculation, and low desire, including onset (lifelong vs. acquired), whether it is generalized or situational, and erection quality with self-stimulation and on waking versus with a partner.
- Medical, surgical, and psychiatric history, including pelvic/prostate surgery or radiation, pelvic trauma, and previously tried treatments.
- A complete medication review against the table in Risk Factors, plus tobacco, alcohol, cannabis, and other substance use.
- Screening for comorbid sexual conditions — premature ejaculation, delayed ejaculation, low desire, and Peyronie disease — since their presence changes management.
- Partner involvement in the history, when possible — it improves both assessment accuracy and treatment outcomes.
Physical examination
- Cardiovascular signs suggesting vascular disease — bruits, hypertension, poor peripheral pulses, heart failure.
- Neurologic signs suggesting an irreversible neurogenic cause.
- Signs of hypogonadism — reduced body/facial hair, gynecomastia, small or atrophic testes.
- Genital examination for penile plaques/curvature (Peyronie disease) and testicular size/consistency.
Laboratory testing
- Fasting glucose or A1c and a lipid profile in suspected vasculogenic or idiopathic ED, to identify occult diabetes and dyslipidemia.[1]
- Morning total testosterone in patients with symptoms of testosterone deficiency (low desire, fatigue) or an unsatisfactory response to a PDE5 inhibitor.[1] Diagnose testosterone deficiency only after two total testosterone measurements, both drawn before 11 a.m. after an overnight fast on separate days, showing a level under 300 ng/dL (approximately under 10.4 nmol/L) together with compatible symptoms or signs.[4] If testosterone is low, check LH; if LH is low or low-normal, check prolactin.[4]
- Screening questionnaires support diagnosis and follow-up but are not a substitute for laboratory testing, and are not a validated tool for deciding who is a candidate for testosterone therapy.[4]
When testing is not indicated
Specialized testing — nocturnal penile tumescence and penile duplex ultrasound — provides little information beyond a detailed history and should be reserved for sub-specialist use in conflicting histories or medico-legal cases; it is not part of routine ED assessment.[1]
Cardiovascular risk stratification before treating ED
ED is an independent cardiovascular risk marker, and every patient starting ED therapy should be stratified before treatment using a framework such as the Princeton IV Consensus.[2]
Princeton IV cardiovascular risk categories
Low risk
Achieves 5 metabolic equivalents (METs) on exercise testing without ischemia, controlled hypertension, minimal heart failure symptoms (NYHA class I-II), successful prior revascularization, or mild valve disease. Manage in primary care — any first-line ED therapy can be considered.
Intermediate risk
Moderate angina, a recent myocardial infarction (2-8 weeks prior), NYHA class III heart failure, prior stroke, or peripheral artery disease. Obtain cardiology evaluation and exercise testing (e.g., 4 minutes of a standard Bruce protocol without symptoms) before starting ED therapy; restratify to low or high risk based on the result.
High risk
NYHA class IV heart failure, uncontrolled hypertension, unstable or refractory angina, a recent untreated myocardial infarction, or a high-risk arrhythmia. Defer all ED treatment until the cardiac condition is stabilized, and manage jointly with cardiology.
Coronary artery calcium scoring is a reasonable adjunct for further risk assessment in men with ED and no known cardiovascular disease who fall in a borderline-to-intermediate risk category.[2]
Validated questionnaires
The International Index of Erectile Function (IIEF) and its abridged 5-item version (IIEF-5, also called the Sexual Health Inventory for Men, SHIM) are validated tools that support diagnosis and track response to treatment without replacing a detailed history. The abridged version scores 5 domains — confidence in achieving an erection, erection firmness for penetration, ability to maintain an erection until completion of intercourse, difficulty maintaining an erection, and satisfaction with intercourse — each from 1 (or 0, if there was no sexual activity) to 5, for a total score of 5-25.
| IIEF-5 (SHIM) score | Severity |
|---|---|
| 22-25 | No erectile dysfunction |
| 17-21 | Mild |
| 12-16 | Mild to moderate |
| 8-11 | Moderate |
| 5-7 | Severe |
The clinically meaningful change in score depends on baseline severity — a smaller absolute change is meaningful in mild ED than in severe ED — so use the score to track trend and treatment response in an individual patient rather than as a single pass/fail cutoff.[1]
Treatment Targets
- Achieve and maintain an erection sufficient for satisfactory sexual activity, using the lowest effective dose or least invasive option that works for the patient.
- Identify and correct reversible contributing factors — causative medications, uncontrolled diabetes/hypertension/dyslipidemia, and lifestyle factors — alongside, not instead of, pharmacologic therapy.
- Use the ED assessment as an opportunity for cardiovascular risk-factor review, given the link between vasculogenic ED and cardiovascular disease.
- Confirm testosterone deficiency biochemically before treating it, and treat it on its own merits (sexual and non-sexual symptoms) rather than as a substitute for standard ED therapy.
- Address the psychological and relationship dimension of sexual dysfunction alongside any organic cause, involving the partner where appropriate.
- For premature ejaculation, delayed ejaculation, and low sexual desire — achieve a pattern and degree of sexual satisfaction that is acceptable to the patient and their partner, combining behavioural and pharmacologic approaches as needed.
Choose Initial Treatment
Erectile dysfunction
1st line a PDE5 inhibitor (sildenafil, tadalafil, or vardenafil) for essentially all patients with ED, given strong efficacy and safety evidence across a wide range of causes.[1]
Stratify cardiovascular risk before starting — treat low-risk patients in primary care; obtain cardiology evaluation for intermediate-risk patients before starting therapy; defer all ED treatment in high-risk patients until the cardiac condition is stabilized (see Assessment & Diagnosis).[2]
Absolute contraindication — never combine with nitrates any regular or intermittent nitrate use, including recreational nitrites, rules out PDE5 inhibitor therapy entirely; do not attempt to work around the interaction by timing doses apart in a patient who needs ongoing nitrate therapy — refer for an alternative anti-anginal strategy instead.
Choice among the three PDE5 inhibitors is driven by patient preference for duration of action and dosing pattern rather than by preferential efficacy — see Pharmacologic Treatment Options and Drug Tables for comparative dosing. Tadalafil may be taken on-demand or once daily; there is no clinically meaningful efficacy difference between the two regimens, so the choice is a shared decision based on spontaneity, frequency of sexual activity, and cost.[1]
2nd line — use when PDE5 inhibitors fail after a genuinely adequate trial, or are contraindicated intracavernosal alprostadil (the most effective second-line pharmacologic option), a vacuum erection device, or intraurethral alprostadil.[1]
Special situation — confirmed testosterone deficiency add testosterone replacement therapy only after biochemical confirmation (two low morning fasting levels plus symptoms). Testosterone alone is not an effective treatment for ED in a man with a normal testosterone level, and even in confirmed hypogonadism, testosterone monotherapy produces at best a modest improvement in erectile function — its main role is treating the broader syndrome of testosterone deficiency, with a possible adjunctive role added to a PDE5 inhibitor in men with low-to-low-normal testosterone who have not responded to the PDE5 inhibitor alone.[1]
Premature ejaculation
1st line a topical penile anesthetic, a daily SSRI, or on-demand clomipramine, each a reasonable first choice depending on patient preference for on-demand versus regular dosing.[3]
Testosterone deficiency (independent of ED)
Treat confirmed testosterone deficiency with testosterone replacement therapy for its own indication (low desire, fatigue, reduced bone/muscle mass) once contraindications are excluded (see Special Populations) — this is a distinct treatment decision from ED management, even though the two frequently overlap.
Non-Pharmacologic Treatment
Lifestyle measures (erectile dysfunction)
- Increase physical activity/exercise — supported by evidence as improving erectile function, and a reasonable recommendation given its safety, low cost, and broader cardiovascular benefit.[1]
- Smoking cessation, and reducing alcohol and cannabis consumption.
- Weight management and dietary changes, particularly with comorbid obesity or metabolic syndrome.
- L-arginine and citrulline (nitric oxide synthase substrates) have limited supporting evidence and are not currently recommended.[1]
Psychological and relationship counselling
- Offer early referral for sexual counselling, especially when a psychogenic component is suspected — cognitive behavioural therapy or mindfulness-based approaches can be sufficient for situational ED.
- Address sexual avoidance directly: making time and context for intimacy, reintroducing affectionate/sexual communication throughout the day, and normalizing a broader range of sexual activity beyond penetrative intercourse.
- Involve the partner in assessment and counselling whenever possible — it improves both diagnostic accuracy and treatment outcomes, and sexual dysfunction affects the couple, not only the patient.
- Combining psychological treatment with a PDE5 inhibitor is common in practice and appears more effective than either approach alone.
Vacuum erection device
Creates negative pressure to draw blood into the penis, trapped by a constriction ring at the base to maintain firmness; safe for up to 30 minutes once the ring is applied — the ring must be removed by 30 minutes. There is a learning curve, and some patients cannot tolerate the degree of constriction required. It has no absolute contraindications, making it a reasonable option for patients who cannot use or have contraindications to pharmacologic therapy, though caution is reasonable in patients on anticoagulation or with a bleeding disorder given the local trauma potential.[1]
Low-intensity shockwave therapy — not currently recommended
Despite being widely offered, including by non-urologists, low-intensity shockwave therapy is not Health Canada or FDA approved for ED, and current evidence does not support a clinically meaningful benefit — do not present it as an evidence-based option outside of a clinical trial.[1]
Investigational regenerative therapies
Stem cell therapy, platelet-rich plasma, and amniotic fluid matrices are being studied for ED but remain experimental; do not recommend them outside of a clinical trial.[1]
Premature ejaculation — behavioural techniques
- Stop-start technique: pause stimulation on reaching moderate arousal, repeated several times before allowing ejaculation, to build tolerance of higher arousal states.
- Squeeze technique: a firm squeeze to the glans at the point of stopping — most clinicians do not recommend adding the squeeze given the discomfort involved, and the stop-start technique alone is generally preferred.
- Referral for sex therapy/relationship counselling, particularly when premature ejaculation is affecting a partnered relationship.
- Combining behavioural techniques with pharmacotherapy is recommended to prolong benefit and allow eventual dose reduction.
Special Populations
Adolescents
ED is uncommon before age 50 and rare in adolescence; a young patient presenting with generalized, lifelong ED should be referred for specialist evaluation rather than managed with a standard stepwise approach, since a structural or congenital vascular cause is more likely.
Renal impairment
Reduce the starting dose of all three PDE5 inhibitors in significant renal impairment (see Drug Tables for specifics); tadalafil is not recommended in severe renal impairment.
Hepatic impairment
Reduce the starting dose of all three PDE5 inhibitors in hepatic impairment; tadalafil is not recommended in severe hepatic impairment.
Older adults
Start PDE5 inhibitors at the lower end of the dose range in patients over 65. Cardiovascular risk stratification (see Assessment & Diagnosis) is especially important in this group, and polypharmacy increases the chance of an unrecognized nitrate or interacting antihypertensive.
Fertility-desiring patients
Do not prescribe exogenous testosterone to a man who is currently trying to conceive — it suppresses spermatogenesis and can produce severe oligospermia or azoospermia.[4] Men with testosterone deficiency who want to preserve fertility should be referred for options that raise endogenous testosterone instead (human chorionic gonadotropin, selective estrogen receptor modulators, or aromatase inhibitors, alone or combined) — specialist-directed.[4]
Prostate cancer history
Testosterone therapy is not appropriate in men with untreated or active prostate cancer. In men with a history of treated, localized prostate cancer with favourable pathology and an undetectable PSA, testosterone therapy can be considered on an individualized basis with urology/oncology involvement rather than treated as an automatic exclusion.[4]
Post-radical-prostatectomy erectile dysfunction
Do not default to a scheduled, prophylactic (penile rehabilitation) PDE5 inhibitor regimen after radical prostatectomy — current evidence does not support a meaningful benefit over treating ED as it presents.[1]
Monitoring & Follow-Up
PDE5 inhibitor therapy
At follow-up, confirm an adequate trial before concluding a drug has failed — correct dose, correct timing relative to food and sexual activity, and adequate sexual stimulation. Reassess cardiovascular risk periodically, particularly if new symptoms or risk factors emerge.
Testosterone replacement therapy
- Hemoglobin/hematocrit at baseline, then at 3-6 months, then annually — a hematocrit reaching 54% or higher on treatment warrants dose reduction or temporary discontinuation.[4]
- PSA and digital rectal exam at baseline in men over 40, then per shared decision-making using standard prostate-cancer-screening guidance.[4]
- Testosterone level rechecked once the patient is established on a stable dosing regimen (timing depends on formulation — e.g., partway through the interval between doses for short-acting injectable esters), then every 6-12 months once the target range is reached, approximately 450-600 ng/dL (15.6-20.8 nmol/L).[4][5]
- Discuss stopping therapy if the patient does not feel meaningfully better after 3-6 months despite achieving target testosterone levels — persistence of symptoms at target levels suggests testosterone deficiency was not the (sole) cause.[4]
Premature ejaculation, delayed ejaculation, and low desire
Reassess response and tolerability at follow-up, and adjust regimen (on-demand versus daily dosing, dose) as needed. When using an SSRI or clomipramine for premature ejaculation, counsel that delayed ejaculation and reduced desire are expected — and here, therapeutically useful — effects, distinct from an unwanted adverse effect in other indications.
Common Errors to Avoid
- Prescribing or dispensing a PDE5 inhibitor without asking about nitrate use, including intermittent and recreational nitrite use.
- Treating ED with testosterone therapy alone without confirming deficiency on two separate morning fasting measurements plus compatible symptoms.
- Assuming ED is purely psychological, or purely organic, without a history that genuinely covers both.
- Missing a medication cause because the causative drug was started long before the ED complaint was raised — always cross-check the current medication list.
- Not counselling on the high-fat-meal delay with sildenafil, or on the need for adequate sexual stimulation regardless of which PDE5 inhibitor is used — none of them produce an erection without arousal.
- Presenting low-intensity shockwave therapy as an evidence-based option — current evidence does not support it and it is not Health Canada or FDA approved for this use.
- Continuing testosterone therapy indefinitely without rechecking hematocrit, PSA, and testosterone levels on schedule.
- Prescribing exogenous testosterone to a man who is actively trying to conceive.
- Not asking about cardiovascular symptoms with exertion or sexual activity before starting any ED therapy.
- Treating only the presenting complaint without screening for a coexisting sexual dysfunction — ED, premature ejaculation, delayed ejaculation, and low desire frequently overlap.
Clinical Decision Algorithm
Drug Tables
How to use this table: Doses are adult doses and require patient-specific confirmation (renal/hepatic function, weight, allergy history). Pediatric dosing is weight-based per the current product monograph unless stated. Drug pricing is intentionally omitted. Select any drug name to open its complete Pharmasist Drug Database page.
PDE5 Inhibitors — 1st line
First-line for essentially all erectile dysfunction. Absolute contraindication: any nitrate use. Use caution with alpha-blockers (additive hypotension) and strong CYP3A4 inhibitors/inducers.
| Drug | Dosage | Adverse effects | Comments |
|---|---|---|---|
| Sildenafil | On-demand: 50 mg PO 30-60 min before sexual activity (range 25-100 mg) Maximum frequency: 1 dose per 24 hours Reduced starting dose: 25 mg if over 65 years, hepatic/renal impairment, or concurrent CYP3A4 inhibitor | Headache, flushing, dyspepsia, nasal congestion, transient visual disturbance (blue-tinge, blurred vision, light sensitivity), rare priapism, rare sudden vision/hearing loss | Take on an empty stomach or after a low-fat meal — a high-fat meal delays absorption and reduces peak effect.[1] |
| Tadalafil | On-demand: 10 mg PO 30-60 min before sexual activity (range 5-20 mg) Maximum frequency, on-demand: 1 dose per 24-48 hours Daily dosing: 2.5-5 mg PO once daily Renal/hepatic impairment: Reduce starting dose; not recommended in severe renal or severe hepatic impairment | Headache, flushing, dyspepsia, back pain, myalgia, rare priapism, rare sudden vision/hearing loss | Longest duration of action of the three PDE5 inhibitors; no food-timing restriction. Also used at a lower daily dose for lower urinary tract symptoms in a separate context; this table covers ED dosing only. |
| Vardenafil | On-demand: 10 mg PO 30-60 min before sexual activity (range 5-20 mg) Maximum frequency: 1 dose per 24 hours Reduced starting dose: 5 mg if over 65 years, hepatic impairment, or concurrent CYP3A4 inhibitor | Headache, flushing, dyspepsia, rhinitis, rare QT prolongation, rare priapism, rare sudden vision/hearing loss | Avoid combining with other QT-prolonging antiarrhythmics (e.g., quinidine, procainamide, amiodarone, sotalol). A high-fat meal delays peak concentration. |
Adjunctive folic acid 5 mg PO daily has limited trial evidence for improving PDE5 inhibitor response specifically in men with diabetes-related ED and is not a substitute for standard therapy or diabetes management.[6]
Prostaglandin E1 (PGE1) Analogues — 2nd line
Used when PDE5 inhibitors fail after an adequate trial or are contraindicated. Dosing is individualized during in-office titration by the prescriber, not the pharmacist.
| Drug | Dosage | Adverse effects | Comments |
|---|---|---|---|
| Alprostadil, intracavernosal injection | Neurogenic ED, starting dose: 1.25-2.5 mcg, titrated by small increments as directed Vascular/psychogenic/mixed ED, starting dose: 2.5 mcg, titrated to response Maximum: Up to 60 mcg in severe vascular ED, per in-office titration | Penile pain, hematoma, ecchymosis, corporal fibrosis with repeated use, priapism | Onset 5-10 minutes; erection duration up to about 1 hour. Use no more than once daily, or 3 times weekly at least 24 hours apart. Requires a teaching session on injection technique and sterile handling.[1] |
| Alprostadil, intraurethral pellet (MUSE) | Dosing: Individualized in-office titration; use no more than once per 24-hour period | Penile pain, dizziness, syncope (rare), priapism (rare) | A distinct product from the intracavernosal injection above — not linked to the Drug Database's alprostadil entry, which specifically covers the injectable (Caverject) formulation. An in-office trial is needed to confirm efficacy, since retrograde absorption to the corpora is unpredictable and depends on individual venous anatomy.[1] |
Androgen Replacement — special situation, confirmed testosterone deficiency only
Never a substitute for standard ED therapy in a man with a normal testosterone level. Confirm deficiency (two low morning fasting levels plus symptoms) before starting; exclude untreated prostate/breast cancer, a current desire for fertility, and a baseline hematocrit over 50% first.
| Drug | Dosage | Adverse effects | Comments |
|---|---|---|---|
| Testosterone cypionate | Initial: 50-100 mg IM once weekly, or 100-200 mg IM every 2 weeks Target level: Approximately 450-600 ng/dL (15.6-20.8 nmol/L) | Erythrocytosis, acne, gynecomastia/breast tenderness, mood changes, suppressed spermatogenesis, worsening sleep apnea | Intramuscular oil-based ester. Adjust dose/frequency based on trough testosterone level.[4] |
| Testosterone enanthate | Initial: 50-100 mg IM once weekly, or 100-200 mg IM every 2 weeks Target level: Approximately 450-600 ng/dL (15.6-20.8 nmol/L) | Erythrocytosis, acne, gynecomastia/breast tenderness, mood changes, suppressed spermatogenesis, worsening sleep apnea | Intramuscular oil-based ester, essentially interchangeable with cypionate. Adjust dose/frequency based on trough testosterone level. |
Premature Ejaculation — SSRIs (off-label)
Regular daily dosing is more effective than on-demand dosing and may take 2-3 weeks for full benefit; on-demand dosing gives more timing flexibility for infrequent sexual activity.
| Drug | Dosage | Adverse effects | Comments |
|---|---|---|---|
| Citalopram | Daily: 20-40 mg PO once daily On-demand: 20-40 mg PO 3-6 hours before sexual activity | Nausea, fatigue, decreased libido, delayed ejaculation (the desired effect here), dose-dependent QT prolongation | [3] |
| Paroxetine | Daily: 10-40 mg PO once daily On-demand: 10-40 mg PO 3-6 hours before sexual activity | Nausea, fatigue, decreased libido, delayed ejaculation (the desired effect here), discontinuation symptoms if stopped abruptly | |
| Sertraline | Daily: 50-200 mg PO once daily On-demand: 50-200 mg PO 3-6 hours before sexual activity | Nausea, fatigue, decreased libido, delayed ejaculation (the desired effect here), GI upset |
Premature Ejaculation — tricyclic (off-label)
| Drug | Dosage | Adverse effects | Comments |
|---|---|---|---|
| Clomipramine | On-demand: 25 mg PO 4-24 hours before sexual activity (range 25-50 mg) Daily: 10-30 mg PO once daily | Dry mouth, sedation, nausea, orthostatic hypotension | On-demand dosing gives timing flexibility; move to daily dosing if on-demand 25 mg is inadequate. |
Premature Ejaculation — topical and other adjuncts
| Drug | Dosage | Adverse effects | Comments |
|---|---|---|---|
| Topical lidocaine/prilocaine anesthetic | Application: Applied to the glans approximately 20-30 minutes before sexual activity, per product-specific directions | Local numbness; possible transfer to and numbness in a receptive partner | Not linked to a Drug Database entry — the existing lidocaine-prilocaine monograph is the dental Oraqix periodontal gel and the bare lidocaine monograph is the injectable formulation; neither represents the topical genital anesthetic product used here. Advise removing (wiping off or washing) or using a condom before penetration to limit partner numbness.[3] |
| Tramadol | On-demand: Per current product-specific dosing guidance, used only under specialist direction | Nausea, dizziness, sedation, dependence risk with regular use, seizure risk at high doses or with interacting drugs | Reserve for patients who have failed first-line topical anesthetic/SSRI/clomipramine therapy; discuss the dependence risk of using an opioid for a non-analgesic indication explicitly before prescribing.[3] |
Compounded alprostadil combined with papaverine and phentolamine (informally known as "Trimix") is more effective than alprostadil alone but is not Health Canada approved and is prescribed only by specialists experienced in intracavernosal therapy — not included as a standard table row above.[1]
Evidence note: Comparative PDE5 inhibitor dosing and second-line therapy content reflect the CUA 2021 Canadian guideline, cross-checked against the AUA 2018 erectile dysfunction guideline.[7] Testosterone dosing and monitoring reflect the AUA Testosterone Deficiency guideline. Premature ejaculation dosing reflects the AUA/SMSNA 2022 ejaculation disorders guideline.
References
- Canadian Urological Association guideline: Erectile dysfunction — Canadian Urological Association Journal (Domes T, Najafabadi BT, Roberts M, et al.). Can Urol Assoc J 2021;15(10):310-322
- The Princeton IV Consensus recommendations for the management of erectile dysfunction and cardiovascular disease — Mayo Clinic Proceedings (Kohler TS, Kloner RA, Rosen RC, et al.). Mayo Clin Proc 2024
- Disorders of Ejaculation: An AUA/SMSNA Guideline — Journal of Urology, American Urological Association/Sexual Medicine Society of North America (Shindel AW, Althof SE, Carrier S, et al.). J Urol 2022;207(3):504-512
- Evaluation and Management of Testosterone Deficiency: AUA Guideline — Journal of Urology, American Urological Association (Mulhall JP, Trost LW, Brannigan RE, et al.). J Urol 2018;200(2):423-432
- Update to the Testosterone Guideline — Journal of Urology, American Urological Association (Trost L). J Urol 2024;211(4):608-610
- Assessment of the efficacy of combination therapy with folic acid and tadalafil for the management of erectile dysfunction in men with type 2 diabetes mellitus — Journal of Sexual Medicine (Hamidi Madani A, Asadolahzade A, Mokhtari G, et al.). J Sex Med 2013;10(4):1146-1150
- Erectile Dysfunction: AUA Guideline — Journal of Urology, American Urological Association (Burnett AL, Nehra A, Breau RH, et al.). J Urol 2018;200(3):633-641
Professional reference only. Apply clinical judgment and verify patient-specific decisions against current authoritative guidance and product information.