Erectile Dysfunction Screening — Past 6 Months
SHIM / IIEF-5 Questionnaire
1. How do you rate your confidence that you could get and keep an erection?
2. When you had erections with sexual stimulation, how often were your erections hard enough for penetration?
3. During sexual intercourse, how often were you able to maintain your erection after penetrating your partner?
4. During sexual intercourse, how difficult was it to maintain your erection to completion of intercourse?
5. When you attempted sexual intercourse, how often was it satisfactory for you?
Awaiting Responses
Answer all 5 questions about the past 6 months to calculate the SHIM score.
Guidelines & Evidence
Verified
Last Review: 2026
When to Use
Clinical Purpose and Validated Use Cases
The Sexual Health Inventory for Men (SHIM), also known as the IIEF-5, is a validated 5-item abridged version of the International Index of Erectile Function (IIEF-15). It was developed to provide a clinically efficient, psychometrically sound screening and severity-grading instrument for erectile dysfunction (ED) in busy clinical settings where the full 15-item IIEF is impractical. The IIEF-5 assesses erectile function over the preceding 6 months, covering confidence in achieving and maintaining erections, ability to achieve erection with sexual stimulation, ability to maintain erection to completion of intercourse, and overall satisfaction. It does not assess orgasmic function, sexual desire, or intercourse satisfaction — domains covered by the full IIEF-15. The SHIM is validated for use in primary care, urology, endocrinology, cardiology, and psychiatry settings, across multiple languages and cultural contexts, and in clinical trials evaluating ED treatments. It is not a diagnostic instrument for organic versus psychogenic ED — it grades severity and screens for presence of ED, not etiology.
When to Administer the IIEF-5/SHIM
Screening for ED in men presenting with sexual health complaints, decreased libido, or relationship dissatisfaction — IIEF-5 distinguishes ED from low desire or ejaculatory dysfunction
Monitoring treatment response to phosphodiesterase-5 inhibitors (PDE5i: sildenafil, tadalafil, vardenafil, avanafil), intracavernosal injections (ICI), vacuum erection devices (VED), or penile prosthesis
Cardiovascular risk assessment — ED is an independent predictor of major adverse cardiovascular events (MACE); IIEF-5 quantifies ED severity as part of cardiovascular risk stratification (Princeton Consensus Panel III)
Pre- and post-operative assessment in radical prostatectomy, radical cystectomy, pelvic radiation, aortoiliac surgery, or any procedure with risk of cavernous nerve injury
Endocrine evaluation of hypogonadism — IIEF-5 correlates with total testosterone and documents baseline erectile function before testosterone replacement therapy (TRT)
Psychiatric and medication-induced sexual dysfunction screening — antidepressants (SSRIs, SNRIs), antipsychotics, antihypertensives (beta-blockers, thiazides), and androgen deprivation therapy (ADT) all reduce IIEF-5 scores predictably
Diabetes mellitus follow-up — ED occurs in 50–75% of diabetic men and is an early marker of autonomic and vascular neuropathy; annual IIEF-5 is recommended by the International Diabetes Federation
Do NOT use in: men without a sexual partner or sexual activity in the prior 6 months (scores will be artifactually low — questions assume sexual activity occurred), men with priapism or penile anatomic deformity (Peyronie's disease) without adapted scoring interpretation, or as a standalone diagnostic for organic vs psychogenic ED without further evaluation
Epidemiology of Erectile Dysfunction — Why ED Screening Matters
ED affects approximately 322 million men globally (2025 projections), representing a substantial increase from 152 million in 1995. Prevalence increases markedly with age: 12% in men aged 40–49, 22% in 50–59, 30% in 60–69, and 46–68% in men over 70. However, ED is not exclusively a disease of aging — vascular risk factors (hypertension, diabetes, dyslipidemia, obesity, smoking) account for 40–60% of ED cases across all age groups. ED carries significant psychosocial burden: men with ED have 2.5× higher rates of depression, 3× higher rates of relationship dissolution, and lower overall quality-of-life scores independent of comorbid conditions. Critically, ED predicts cardiovascular events by a mean of 2–5 years before the cardiac event — the penis has smaller-diameter arteries (1–2 mm) than coronary arteries (3–4 mm), so atherosclerosis causes erectile impairment before angina or MI. Men with IIEF-5 scores in the Moderate-to-Severe range have a 1.6–2.0× higher risk of incident major adverse cardiovascular events (MACE) after controlling for Framingham risk factors.
Pathophysiology of ED — Mechanistic Categories
| Category | Mechanism | Frequency | Key IIEF-5 Pattern | Distinguishing Clinical Features |
|---|---|---|---|---|
| Vasculogenic (arteriogenic) | Atherosclerosis and endothelial dysfunction of cavernous arteries reduce arterial inflow during arousal. Intracavernous pressure cannot reach systolic blood pressure threshold needed for rigidity. | 40–50% of all ED (most common organic cause) | Gradual onset over months to years. Scores decline progressively. Often better with morning erections (which depend less on arteriogenic inflow and more on nocturnal parasympathetic activity). | Risk factors: hypertension, diabetes, dyslipidemia, smoking, CAD, peripheral arterial disease, obesity. Penile Doppler: peak systolic velocity (PSV) < 25 cm/s after intracavernosal alprostadil injection is diagnostic. |
| Vasculogenic (venogenic) | Failure of veno-occlusion — the corporal sinusoids fail to compress subtunical venules during erection, allowing venous leak. Erection is partially achieved but cannot be sustained. | 15–25% | Patient can achieve initial rigidity but loses erection rapidly. IIEF Q2 (maintain erection) and Q3 (maintain to completion) are most severely depressed. Q1 (confidence) moderate. | Often younger men. Penile Doppler: normal PSV (≥ 25 cm/s) but elevated end-diastolic velocity (EDV ≥ 5 cm/s) after alprostadil. Resistive index (RI) < 0.75 is diagnostic of venous leak. |
| Neurogenic | Disruption of parasympathetic outflow (S2–S4 pelvic nerves, cavernous nerves) impairs nitric oxide (NO) release from endothelium and nitrergic nerve terminals. NO is the obligate mediator of corporal smooth muscle relaxation and erection. | 10–20% | Rapid onset after neurological event. Morning erections disproportionately preserved (centrally mediated) vs stimulus-triggered erections (peripherally mediated via cavernous nerve). Psychogenic erections may be completely absent. | Causes: spinal cord injury (SCI), multiple sclerosis, diabetes (autonomic neuropathy), post-radical prostatectomy, post-pelvic radiation, pudendal nerve entrapment. Biothesiometry/SSEP confirms diagnosis. |
| Endocrine (hypogonadism) | Testosterone modulates central sexual desire (limbic system), peripheral NO synthase expression in cavernous tissue, and smooth muscle cell density. Low testosterone causes reduced libido (often before ED), altered sleep quality, and reduced spontaneous erections. | 8–15% (as primary cause); testosterone deficiency contributes to ED in 25–35% when secondary | Low IIEF-5 accompanied by prominent reduction in desire (IIEF Q15 on full IIEF-15) and reduced spontaneous morning erections. ED may respond poorly to PDE5i alone but responds when TRT is combined. | Morning total testosterone < 300 ng/dL (EAU) or < 350 ng/dL (Endocrine Society). Free testosterone < 65 pg/mL. LH and FSH distinguish primary (testicular failure — LH/FSH elevated) from secondary hypogonadism (pituitary/hypothalamic — LH/FSH normal or low). |
| Psychogenic | Central inhibition of sacral erection centers mediated by cortical, limbic, and autonomic pathways. Catecholamine excess (anxiety) causes corporal smooth muscle contraction via alpha-1 adrenergic receptor activation, opposing erection. | 10–20% (as primary cause); psychological factors contribute in up to 40% of mixed ED | Situational pattern — erections preserved with certain partners or stimuli but absent in others. Morning and nocturnal erections typically preserved (NPTR — nocturnal penile tumescence and rigidity testing). Sudden onset often after identifiable stressor. | Anxiety, depression, relationship conflict, performance anxiety, past sexual trauma. NPTR testing (RigiScan) confirms nocturnal erections — absence suggests organic etiology regardless of IIEF-5 score. Validated psychological tools: HADS, PHQ-9, Beck Depression Inventory. |
| Medication-induced | Multiple mechanisms: antihypertensives reduce perfusion pressure; SSRIs/SNRIs inhibit central dopaminergic arousal; antipsychotics increase prolactin (suppressing GnRH/LH); 5-alpha reductase inhibitors reduce DHT (a peripheral androgen active in cavernous tissue); ADT removes androgenic support for NO synthase expression. | 25% of all ED cases have a contributory medication (not always sole cause) | ED onset temporally related to medication initiation or dose increase. Q1 (confidence) often prominently reduced — performance anxiety secondary to medication effect. Sexual desire may also be reduced. | Antihypertensives: beta-blockers and thiazides are worst offenders. Calcium channel blockers and ACE inhibitors are ED-neutral. SSRIs: paroxetine worst; bupropion least. 5-ARI: finasteride/dutasteride — 2–5% incidence; post-finasteride syndrome debated. |
Related Scores in Practice
In clinical practice, this assessment is frequently evaluated alongside other validated measures. Depending on the patient's presentation and specific diagnostic requirements, you may also need to utilize the Gupi to formulate a comprehensive care plan.
Last Comprehensive Review: 2026