Andrology

Priapism

• Definition: erection persisting > 4 hours beyond, or unrelated to, sexual stimulation
• Classification (3): ischemic · non-ischemic · recurrent (stuttering)

Ischemic vs Non-ischemic

• Stuttering = recurrent ischemic episodes with confirmed ischemia
  • Most commonly sickle cell disease (also the most common cause in children/adolescents)
• EF recovery by time to reversal: <12h ≈100% → 12–24h ≈75% → 24–36h ≈50% → ≥36h ≈0%
  • Duration is the key driver of future ED — the most significant complication of prolonged ischemic priapism
  • Duration vs outcome (exam answer): resolution within 24 h → 78–100% functional erections; beyond 36–48 h → ED > 90% — the shunt type does not change this

Risk factors

• Hematologic:
  • SCD (priapism in 23–89% of homozygous males by age 18)
    • SCD is the dominant cause in young men
  • Thalassemia
  • Hemolytic anemias
  • Leukemia
  • Myeloma
• Medications (9 classes):
  • α-blockers
  • Trazodone/antipsychotics
  • Anticoagulants
  • Antihypertensives
  • Hydroxyzine
  • ADHD agents
  • Recreational (cocaine, alcohol, marijuana)
  • Hormones (testosterone, GnRH)
  • Intracavernosal erectile agents
    • Men ≥ 40: prolonged erection is usually from ED pharmacotherapy, especially intracavernous vasoactive injection
    • Intracavernous alprostadil (trial definitions: prolonged erection 4–6 h, priapism > 6 h): prolonged erection ~5% · priapism ~1%
• Other:
  • GU/pelvic trauma
  • Thrombophilia
  • Metabolic (Fabry, amyloid)
  • Neurogenic
  • Malignant infiltration
• Infectious: malaria
  • Suspect in a febrile man with night sweats from an endemic area
  • Manage as ischemic priapism alongside antimalarials

Diagnosis

• Mandatory: H&P + corporal blood gas (aspiration)
  • Blood gas is the definitive test for ischemic vs high-flow
    • Obtain it even after perineal trauma
• Optional:
  • CBC
  • Hgb electrophoresis
  • Tox screen
  • Penile duplex US only when ischemic vs non-ischemic is indeterminate (not the primary diagnostic test)

History — the elements that change management

• Duration of the erection
• Presence of pain
• Previous episodes and how they were treated
• Baseline erectile function
• Use of erectogenic therapies
• Medications and recreational drugs
• Sickle cell disease, hemoglobinopathies, hypercoagulable states
• Trauma to the pelvis, perineum or penis

Investigations to consider

• Cavernosal blood gas (mandatory)
• CBC
• PT/PTT
• Urine toxicology
• Hemoglobin electrophoresis
• Penile duplex (only if ischemic vs non-ischemic is unclear)

Gas results are sometimes reported in kPa — 1 kPa = 7.5 mmHg.

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Management — Ischemic

Conservative measures are NOT recommended — observation, oral agents and cold packs have no role in established ischemic priapism, and cold compresses are contraindicated in sickle cell disease. Do not delay transfer.

Initial measures

• Monitored bed
• IV access
• Hydration and oxygen
• Analgesia
• ± hematology consult

(Oral terbutaline and pseudoephedrine are described for injection-induced prolonged erection, but are not recommended in established ischemic priapism — go to aspiration.)

(Oral phenylephrine is likewise not recommended — oral terbutaline and phenylephrine are ineffective in acute ischemic priapism > 4 hours.)

• First-line: corporal aspiration ± irrigation ± intracavernosal phenylephrine (aspiration alone resolves ~36%)
  • Why aspiration is the first step: it decompresses the penis, relieves pain and supplies the blood gas (dark "crankcase oil" blood) — diagnostic and therapeutic
  • Erection > 4 h after intracavernous injection = ischemic priapism
    • → aspirate, then intracavernosal phenylephrine promptly
    • Escalate to a shunt exactly as for any ischemic priapism

Aspiration technique

• Penile nerve block first
  • Infiltrate around the entire base of the shaft with 1% lidocaine WITHOUT epinephrine, or bupivacaine without epinephrine
• 19-gauge needle on a large syringe.
  • Insert laterally through the shaft
    • This avoids the corpus spongiosum and urethra ventrally, and the neurovascular bundle dorsally
• Aspirate 20–30 mL from the 2 or 10 o'clock position while milking the shaft.
  • Because the corpora communicate, aspiration on one side is usually enough
• If the initial aspirate is bright red rather than dark venous blood, suspect an arterial cause and treat as high-flow
• Aspirate first to fill the corpora with fresh oxygenated blood before injecting
• Once detumescence is achieved, apply an elastic bandage around the shaft to keep the corpora empty and compress the puncture site

Phenylephrine

• Dilute to 100–500 mcg/mL; supplied as 10 mg in 1 mL, so dilute before use
• Inject at 3 or 9 o'clock near the base
  • 0.5–1.0 mL per dose
  • Doses ≥5 min apart
  • Continue up to 1 hour
• Max ~1 mg (hypertensive stroke reported at cumulative 2 mg); monitor BP/HR
• α-agonist of choice (α1-selective, fewest cardiac effects); off-label
  • i.e., minimal β-mediated inotropic and chronotropic effects
• AE:
  • Hypertension + reflex bradycardia (most common)
  • Headache
  • Dizziness
  • Arrhythmia
• Have atropine ready (0.02–0.05 mg/kg) for reflex bradycardia — involve the ER physician
• Second line epinephrine; third line methylene blue

Surgical shunting

• (only after BOTH α-agonist AND aspiration/irrigation attempted)
• If persistent > 1 hour despite injection + aspiration → surgical shunting
  • Ischemia beyond ~36 h → aspiration + sympathomimetic injection unlikely to work; a shunt is usually needed
  • Post-treatment gas equivocal → color duplex US best confirms resolution
    • Tells resolved ischemia with edema apart from persistent ischemia or conversion to high flow
• Consider for events ≤72 hours; forego shunt if > 72 hours
• Distal first (corporoglanular), with or without tunneling — optimal type undefined
  • Why distal first (e.g., Ebbehoj): less invasive and less postoperative ED than proximal shunts
  • Tunneling slightly improves detumescence but worsens later erectile function
  • Proximal shunting: limited utility — removed as a recommended treatment in the latest AUA priapism guideline update

• AE of shunting (6):
  • Penile edema
  • Hematoma
  • Infection
  • Urethral fistula
  • Penile necrosis
  • PE
• Most likely early complication of a distal shunt: non-ischemic (high-flow) priapism
  • The created fistula + post-ischemic hyperemia
  • Check persistent tumescence with a blood gas
• Persistent erection after a distal (Al-Ghorab) shunt → corporal blood gas (or duplex) to confirm the shunt is open before any redo
  • Squeezing the penile base should detumesce an open shunt
• Redo shunt after early closure → peri-procedural antithrombotic therapy
  • Tunical incision activates clotting in stagnant penile blood
  • 84% ↓ priapism recurrence
  • Regimen: aspirin 325 mg preop → heparin 5,000 IU intraop → aspirin 81 mg + clopidogrel 75 mg for 5 days postop
• Acute ischemic priapism > 36 h → options:
  • Observation/pain control
  • Distal shunt ± tunneling
  • Early penile prosthesis (within 2 weeks)
    • Infection rate <10%
    • Corporal fibrosis not yet established so length preserved
    • > 36 h + failed distal shunt with tunneling → likely complete ED → place the prosthesis early
    • > 48 h with woody induration despite shunts → confirm ongoing ischemia with Doppler + corporal blood gas, then consider an immediate penile prosthesis
    • Insertion after corporal fibrosis has developed is extremely difficult with higher complication rates

Sickle cell disease — acute episode

• Managed like other ischemic priapism — aspiration + intracavernous phenylephrine first
• Hydration, oxygen and exchange transfusion are adjuncts
  • They must not replace penile-directed therapy
• If aspiration + phenylephrine fail → exchange transfusion may ultimately be required
• Never cold saline irrigation
  • May further precipitate sickling in the penis

Management — Stuttering (recurrent ischemic) prevention

• Children should receive alpha agonists (oral and intracavernosal) plus a PDE5 inhibitor
  • No hormonal agents before sexual maturation (LH-RH/GnRH agonists or antagonists, antiandrogens, estrogens)
    • They impair normal maturation and spermatogenesis
• Adults
  • 5α-reductase inhibitors
  • Antiandrogens
    • Hormonal agents work by down-regulating testosterone
      • → hot flashes, gynecomastia, ED, loss of libido, infertility
      • → advise sperm cryopreservation before antiandrogen therapy
  • GnRH agonists
  • Intracavernosal alpha agonists
  • Baclofen
  • Pseudoephedrine
  • PDE5i
    • Daily low-dose sildenafil reduces recurrent episodes — no role in treating an acute episode
  • Home self-injection α-agonist
    • Sexually active man → train in home intracavernosal phenylephrine injection rather than LH-RH agonists (significant testosterone-suppression adverse effects)
  • Ketoconazole + prednisone
• Use alpha agonists with caution in hypertensive patients
• SCD-specific: hydroxyurea, chronic exchange transfusion (reduces episodes — not primary treatment of an acute episode)

Management — Non-ischemic (not an emergency)

• Recognize it: typically after perineal/straddle injury
  • Corporal gas non-hypoxic or Doppler shows high PSV and EDV
• First-line: observation (spontaneous/conservative resolution up to 62%)
  • Reasonable 4-week trial
  • Conservative care: perineal ice + site-specific compression
  • Compression therapy may work, especially in children — continuous compression with a strap-on dressing
  • Tumescence severely bothersome → re-evaluate with penile duplex and consider intervention
  • Second-line: percutaneous fistula embolization
    • Detumescence ~85%, ~80% retain erections, recurrence ~30% (offer a 2nd attempt)
    • Bilateral embolization ↑ ED risk
  • Surgical ligation last resort (transcorporal; most urologists inexperienced)
    • Surgical ligation carries a risk of long-term impotence
• Prolonged erection (≤4 h) after ICI:
  • Distinct from priapism
  • Conservative ± in-office phenylephrine
  • Treat as ischemic only if > 4 h

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Peyronie's Disease

• Definition: acquired fibrosis of the tunica albuginea (TGF-β1) ± pain, deformity (curvature/indentation/hinge/shortening), ED, distress
• Plaque location: dorsal in 60–70% (deviates toward the affected/scarred side)

Things commonly got wrong

• Peyronie's is not rare
• Once it has stabilized, there is usually no further progression
• It does not have a high likelihood of spontaneous resolution
• It is not a disease of only middle-aged men, nor only of white men
• Trauma to the flaccid AND the erect penis can activate the scarring process
• ED is frequently found in men with Peyronie's
• Plaque calcification is NOT an indication of mature, chronic-phase disease
  • Some calcification in about 34% — can appear early; does not predict the need for surgery

Risk factors — "IT DRAG A Crooked Wand"

Infection · Trauma · Diabetes · Radical prostatectomy (11–16%) · increasing Age · Genetic · Autoimmune · Collagen disorders (Dupuytren, plantar fascia/Ledderhose, tympanosclerosis) · aberrant Wound healing

• Hypogonadism → more severe disease; PDE5i are not associated
• Associated conditions:
  • Aging
  • Diabetes
  • ED in 37–58%
  • Psychological distress
  • Radical prostatectomy
  • Hypogonadism
  • Collagen disorders
• Post-radical prostatectomy: 15.9% in one series, at a mean of 13.9 months
• Trauma alone does not cause it
  • None of 193 penile fracture patients developed Peyronie's
  • Buckling microtrauma produces a plaque only in a susceptible host (Dupuytren contracture or family history)

Pathophysiology

• Wound-healing disorder of the tunica albuginea
  • An exuberant scar after penile injury
  • Not premalignant
  • Its association with Dupuytren contracture varies widely between studies
• TGF-β1 = key mediator → activates myofibroblasts → extracellular matrix + type I collagen deposition (pentoxifylline works by blocking this pathway)
• Calcification is driven by activated myofibroblasts:
  • The scar fails to undergo the remodeling phase of wound healing → myofibroblasts persist in the plaque instead of undergoing apoptosis
• Fibrosis sits in the tunica albuginea, not the corpora cavernosa → curvature
  • True corporal fibrosis follows scleroderma, cavernositis or removal of an infected penile prosthesis
• ED is veno-occlusive (venous leak):
  • The inelastic plaque stops the tunica expanding → subtunical venules are not compressed → blood escapes

Natural history

• Pain resolves in ≈90%
  • Untreated: resolves in most men within a year (89% complete resolution)
• Curvature: improves only 12–13%, worsens ≈45%, stable ≈42%
  • Untreated series (exam answer): improves 12% · stable 40% · worsens 48%
  • Exam answer: spontaneous improvement in ≤10% (no more than 13% in natural history studies); full resolution extremely rare; up to 50% worsen
• Active (acute): changing symptoms ± pain, up to 18 months
  • Pain on erection marks the active phase — the scar can grow and the deformity progress
• Stable (chronic): unchanged ≥3 months

Diagnosis

• Mandatory: H&P (penis examined on stretch; baseline stretched length)
  • Also examine the palms (associated collagen vascular disorders)
  • Photos of the erect penis from several angles help show the deformity
• Recommended before invasive treatment: assess erect deformity — ICI ± duplex US (gold standard) or home photographs/protractor
  • Plaque size measurement (calipers or any other method) is inaccurate — the plaque is rarely a discrete lesion
  • US after vasoactive injection best assesses curvature and erectile response

What a complete duplex assessment gives you

• Identification and measurement of plaque calcification
  • A rock-hard plaque suggests calcification but needs imaging, preferably US, to confirm
    • Hyperdense plaque with shadowing behind it
  • Significant calcification → intralesional injection less likely to work
• Objective measurement of the erect deformity — curvature, girth irregularity, hinge effect
• Identification of corporal fibrosis
• Observation of the erectile response to vasoactive injection
• Penile vascular parameters — PSV, EDV, resistive index

PDQ questionnaire

• 15 questions, 3 domains:
  • Psychological and physical symptoms (6 items)
  • Penile pain (3 items)
  • Effects of symptoms (6 items)

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Management — Non-surgical

• Active phase: NSAIDs for pain
  • Painful erections, even with a 60° curve or hourglass deformity → NSAIDs + observation
    • Plication or incision and grafting waits for the stable phase
• Little or no pain, penetration still possible (e.g. 10–20° curve) → reassurance only
  • Review if pain, progression or difficulty with intercourse develops
• ED + normal arterial flow + curve <30° → oral PDE5i first; avoid intracavernosal injection (may worsen the curvature)

Stable phase

• Penile traction — first-line non-invasive; wear ≥3 h/day
• Intralesional + modeling: collagenase · verapamil · interferon α-2b
• ESWT — conditional, for pain only (do NOT use to reduce curvature — may worsen it)
  • AUA: penile pain only, with low overall utility
    • Not recommended for curvature (low-intensity shockwave does not correct it) or plaque size, nor for calcified plaques or hourglass deformity
• Oral agents largely ineffective (vitamin E, tamoxifen, procarbazine not recommended)
  • No oral agent other than NSAIDs is indicated — Potaba included
    • Pentoxifylline and traction are off-label

Oral agents

Intralesional agents

• Poor candidates for verapamil: extensive calcification, curvature > 90°, or ventral curvature — the plaque cannot be adequately infiltrated
• Predictors of verapamil success: age under 40 and curvature > 30°
• Topical verapamil: no consistent benefit

External force

Collagenase (Xiaflex)

• Degrades collagen I & III; reduces curvature + plaque, does not treat pain or ED
• Candidates:
  • Curvature >30° and <90°
  • Intact EF
  • Single dorsal/lateral plaque
  • No hourglass/calcification
    • Untested in hourglass deformity
    • Exam answer: stable disease, 55° curve with mild hourglass, declining surgery → offer intralesional collagenase; if he accepts surgery → plication (or another surgical procedure)
  • No ventral curvature
• IMPRESS: 17° improvement
• AE: corporal rupture (penile fracture), bruising, pain, swelling, hematoma
  • Sudden severe penile pain + swelling after injection (on waking or after sex) → suspect penile fracture (≈0.5%) → penile exploration
    • US may be falsely negative
  • Avoid sex for 2 weeks after collagenase
    • Fracture after intercourse (likely ventral) → add cystoscopy at exploration to exclude urethral injury — not for an expected dorsal fracture
• Plication or grafting can be performed after collagenase without added technical difficulty

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Management — Surgical

Indications (4)

• Stable disease (≥1 yr from onset + ≥3–6 mo stable)
  • EAU (exam answer): stable for 3–6 months, or >9–12 months from onset, before surgical correction
• Deformity preventing intercourse (>30°)
• Failed non-surgical
• Desire for rapid/reliable result

Choice depends on erectile function + deformity severity:

• Hourglass or hinge = complex deformity → tunical lengthening (plaque incision and grafting) even with only a 40° curve
  • Plication cannot correct it
• Penile length a concern (e.g. stable 50° curve, no hourglass/hinge, good PDE5i erections) → incision and grafting rather than plication
• Curve >70° (CUA: >60°) preventing penetration, good PDE5i erections → incision and grafting rather than plication
• Grafting also requires no venous insufficiency on duplex; suits dorsal deformities better than ventral
• ED not adequately treated by PDE5i (e.g. SHIM 15 on sildenafil) → prosthesis with straightening (manual modeling)
  • Straightening alone leaves the ED
  • Straightening surgery is gated on erections adequate for penetration with or without PDE5i
    • → PDE5i failure means prosthesis, even if intracavernosal injections work

Pre-operative consent — set these expectations

• Goal is "functionally straight" — residual curvature under 30°
• Length: more likely shorter with plication than with grafting
• Diminished rigidity: ≥5% in all studies (grafting more than plication); ≥30% if pre-operative erectile quality was suboptimal
• Decreased sensation: typically resolves in 1–6 months; rarely compromises orgasm or ejaculation
• Grafting: rarely gives long-term length gain; de novo ED in up to 50%; penile numbness most likely with lengthening procedures

Technique notes

• Historically the plaque was totally excised
  • This produced large graft onlays with an unacceptably high ED rate.
  • Plaque incision replaced it: a modified-H or double-Y incision at the point of maximum curvature
• Plaque excision and grafting is preferable when the area of maximum deformity is excised, particularly with severe indentation
• Ventral curvatures repaired with grafting have a much higher rate of complete ED
• Prosthesis + significant residual curvature (>30°) → manual modeling (full inflation, force opposite max curvature 90 sec)
  • Urethral injury = most common AE of modeling
    • Most dreaded: urethral injury at the meatus — the cylinder tips extrude under pressure on the distal shaft
  • Modeling works best for untreated Peyronie plaques; less successful for corporal scarring after implant removal
  • If residual curvature still exceeds 30° after modeling, make a relaxing incision in the tunica over the maximum curvature.
    • If the incisional defect is > 2 cm, place a biograft (pericardium or SIS) to prevent cicatrix contracture or prosthesis herniation
  • >60° still remaining after modeling at IPP placement → complete the IPP and add incision and grafting or plication
    • Repeat modeling or switching device is unlikely to help
  • Post-operative prolonged cylinder inflation
    • Keep the device inflated 10–30 minutes daily for 3 months, starting 6 weeks after surgery
  • AMS 700 CX and Titan have the best intrinsic rigidity and best correct curvature associated with tunical scarring
• Dry gangrene of the glans after incision and grafting
  • → most often dorsal artery injury (lies under Buck fascia in the operative field; supplies the glans)
  • Glans supply is normally redundant — dorsal arteries + bulbourethral artery → necrosis only when this dual supply is already compromised
• Superficial external pudendal artery (femoral branch, in the dartos fascia) supplies penile skin independently of the erectile bodies
  • → skin flaps can be raised without compromising corporal perfusion

Predictors of post-operative ED

• Age > 55
• Corporeal veno-occlusive dysfunction with RI < 0.80
• Large tunica defect and graft size
• Ventral curvature
• Curvature > 60°

Graft material

• The ideal graft approximates the strength and elasticity of normal tunica albuginea
  • Minimal morbidity and tissue reaction
  • Readily available
  • Not too thick
  • Pliable and easy to size and suture
  • Inexpensive
  • Infection-resistant
  • Preserves erectile capacity.

Post-operative rehabilitation

• Massage and stretch, nightly PDE5i, traction therapy
  • To prevent shortening and possibly recover length, encourage straight healing, preserve vascular integrity, and encourage partner participation
• Counsel: residual curvature, shortening, ↓rigidity, ↓sensation

Penile fracture

• True fracture = tear in the tunica albuginea → acute loss of erection, eggplant deformity, deviation away from the tear (hematoma mass effect)
• Snap without loss of erection + shaft and scrotal ecchymosis, no hematuria → torn subcutaneous penile vein, not a fracture
  • → observation (no urethral evaluation or exploration needed)

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Erectile Dysfunction

Physiology

• Parasympathetic S2–S4 (cavernosal) → erection/tumescence
  • Autonomic fibers run in the cavernous nerves
    • Terminal branches of the pelvic (inferior hypogastric) plexus, passing posterolateral to the prostate
• Sympathetic T10–L2 → detumescence + emission
• Somatic pudendal (Onuf, S2–S4) → sensation + ischio-/bulbocavernosus contraction
• NO = principal erectile neurotransmitter (nNOS → initiation, eNOS → maintenance) → ↑cGMP → smooth-muscle relaxation
  • PDE5 degrades cGMP
  • nNOS sits in the nitrergic nerves
  • NO activates guanylate cyclase → ↑cGMP → ↓cytosolic calcium via the three mechanisms below
  • PDE5 inhibitors block cGMP degradation — they do not increase its production (production needs NO acting on guanylate cyclase)
  • PDE5, PDE6 and PDE9 hydrolyze only cGMP
    • Every PDE except PDE6 (confined to photoreceptor cells) is present in the corpus cavernosum
• Norepinephrine = principal neurotransmitter of flaccidity (and is high in psychogenic ED)
  • Released by postganglionic sympathetic adrenergic nerves, which keep penile smooth muscle tonically contracted → detumescence
  • Acetylcholine, VIP, cGMP and prostaglandin all promote tumescence

How the smooth muscle actually relaxes

• Flaccidity — NE plus endothelin-derived factors (endothelin, PGF2α) raise intracellular calcium → increased smooth-muscle tone
• Erection — NO raises cGMP and cAMP, which activate protein kinases producing three effects:
  1. Opening of K⁺ channels → hyperpolarization
  2. Sequestration of intracellular calcium into the endoplasmic reticulum
  3. Blockade of calcium influx by inhibiting voltage-gated calcium channels
• The event that initiates detumescence after a normal erection is a transient rise in intracorporal pressure
• Endothelin-1 is the most potent vasoconstrictor
• PGE1 → erection · PGF2α + endothelin + NE → flaccidity

Psychogenic vs reflexogenic erection

• Psychogenic — audiovisual or fantasy.
  • Pathway: brain → T11–12 and S2–4
  • A lesion above T9 abolishes psychogenic erection
  • Psychogenic stimulation alone is not enough for penetration
• Reflexogenic — tactile stimuli to the penis.
  • One tract ascends to the sensory perception area
  • The other goes to the autonomic nuclei in the cord, then the cavernous nerve
  • Rigidity comes mainly through somatic pathways
  • Preserved in 95% of complete upper-cord lesions vs 25% of lower-cord lesions
  • In a complete injury above T12: reflex erection, but no emission and no ejaculation
  • Complete T12 or L1 injury → sacral S2–S4 reflexogenic erections spared, psychogenic erections lost
    • Emission and ejaculation impaired or abolished — they depend on the T12–L2 spinal ejaculation generator
  • Patients with sacral cord injury retain psychogenic erectile ability even though reflexogenic erections are abolished
    • Psychogenic erections survive via T11–T12 sympathetic outflow

Central neurotransmitters

Testosterone

• Enhances sexual interest, frequency of sexual activity and frequency of nocturnal erection
• Relaxes penile artery and cavernous smooth muscle
• The threshold for normal erection is 300 ng/dL (≈10.4 nmol/L)
• Hyperprolactinemia → inhibits dopaminergic activity in the medial preoptic area and suppresses hypothalamic GnRH and pulsatile LH
  • → secondary hypogonadism with low testosterone
  • Also interferes with peripheral testosterone → DHT conversion (may ↓libido independent of testosterone level) and may have a direct contractile effect on cavernosal smooth muscle

Classification

• Organic — "ED VAN": Endocrinologic · Drug-induced · Vasculogenic · Anatomic · Neurogenic · vs psychogenic vs mixed
• Psychogenic clues:
  • Present nocturnal/masturbatory erections
  • Situational
  • Recent stress
  • Performance anxiety

Pathophysiology in three failures

• Venous leak = failure of the tunica albuginea to compress the subtunical and emissary veins (aging, diabetes, Peyronie disease, penile fracture)
  • Not disease of a named draining vein

Risk factors, by adjusted odds ratio

• 93% of men with ED develop it about 24 months before the onset of ischemic heart disease — ED is a sentinel symptom
• Acebutolol (β1-selective) causes less ED; α1-blockers and ARBs enhance erection
• Drug-induced ED:
  • Diuretics (incl. thiazides) and α2-agonists (clonidine, methyldopa) → ED
  • ACE inhibitors, ARBs, α1-blockers and calcium channel blockers are not associated
  • Sudden ED ~2 weeks after starting hydrochlorothiazide → drug-induced
    • Switch to an erection-neutral antihypertensive (e.g. an ARB) rather than stopping treatment — blood pressure must stay controlled
• Spermatotoxins (male reproductive dysfunction):
  • Cimetidine
  • Spironolactone
  • Indinavir
  • Prednisone
  • Lisinopril is not — it may even improve bulk seminal parameters

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Diagnosis

• Mandatory: H&P + morning total testosterone
• diabetes screen (fasting glucose/HbA1c) + lipid panel + questionnaires: SHIM/IIEF-5 (5 items, score 1–25, assesses the past 6 months, >21 = normal erectile function), IIEF (15 items, 5 domains), EHS
• Further labs where indicated: bioavailable testosterone, TFT, LFT, LH, FSH, prolactin, PSA
  • Mildly raised prolactin + normal testosterone → rarely clinically significant
    • Repeat the prolactin first (high interassay variability) before LH, MRI or bromocriptine
  • Low libido + normal exam + adequate testosterone → most common cause is psychological
  • Low testosterone + low or inappropriately normal LH/FSH → check prolactin
    • Then a contrast-enhanced pituitary MRI before testosterone therapy
    • Confirmed hyperprolactinemia → image first, since a prolactinoma is treated with a dopamine agonist
    • Normal prolactin → still image — non-prolactin-secreting pituitary tumors also occur
  • Limited evidence supports pituitary MRI in severe hypogonadism (testosterone < 6 nmol/L, 1.75 ng/mL) with inadequate gonadotropins
  • Free testosterone adds little when total testosterone is very low (e.g. 98 ng/dL) → image the pituitary before starting replacement

History — what to cover

• Partner interview
• Onset and duration
• Number of partners
• Difficulty generating vs maintaining
• Global vs situational
• Constant vs intermittent
• Morning and nocturnal erections
• Rigidity
• Last satisfying intercourse
• Curvature
• Physical capacity
• Desire
• Ejaculation
• Orgasm
• PMHx, PSHx, medications, family and social history

Sexual activity imposes a cardiac stress equivalent to

• Walking 1 mile in 20 minutes
• Briskly climbing 2 flights of stairs in 10 seconds
• 4 minutes of the Bruce treadmill protocol

Princeton classification — cardiac risk before resuming sexual activity

Vascular evaluation, in sequence

1. Combined intracavernosal injection and stimulation (CIS) — first line
   • Positive test = a rigid erection that cannot be bent, appearing within 10 minutes and lasting 30 minutes
   • Good erection after 15 µg alprostadil in a healthy young man → points away from vascular ED → start an oral PDE5 inhibitor (first line) without extensive testing
2. Penile duplex US — second line, and the most accurate vascular test. Assess at 5, 10, 15 and 20 minutes

• A patient with an arteriovenous fistula will NOT have a negative end-diastolic velocity
• EAU normal values (exam answer): PSV > 30 cm/s, EDV < 3 cm/s, RI > 0.8; a PSV < 25–30 cm/s signals arterial insufficiency
• Veno-occlusive pattern: preserved PSV (> 25 cm/s) with a high EDV (> 5 cm/s, e.g. 7) and a low RI → venous leak
• Normal hemodynamics → psychogenic ED
• Tumescence without rigidity after papaverine–phentolamine → values uninterpretable (false positives from anxiety or low vasoactive dose)
  • → repeat with alprostadil before diagnosing arterial insufficiency
• Severe arteriogenic ED (PSV ~11–12 cm/s) in a young man → cardiovascular risk screening and intervention
  • ED in younger men predicts up to a 50-fold rise in future cardiac events
• After pelvic fracture: normal duplex (PSV > 25–30, EDV < 5 cm/s) + normal testosterone + normal pudendal EMG
  • → psychogenic ED → start a PDE5 inhibitor
• Indications for penile duplex:
  • Priapism (persistent or partial erection after treatment for ischemic priapism)
  • Young patient with ED
  • Trauma with ED
  • Refractory ED
  • Peyronie's disease
  • Endocrinopathy
• Dynamic infusion cavernosometry and cavernosography
  • For suspected vasculogenic leak from trauma, or lifelong ED
  • Usually precedes penile vascular surgery
  • Duplex and cavernosometry both assess venous leak (veno-occlusive dysfunction)
    • Duplex also measures arterial inflow
  • Veno-occlusive dysfunction = saline infusion cannot raise intracorporal pressure to mean systolic pressure
    • Or the pressure falls quickly after infusion stops
    • → cavernosography then localizes the leak
  • Both are now historical tests — no longer routinely used
• Penile angiography — young patient with ED secondary to traumatic arterial disruption
• NPTR — reserved for when it will change management

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Management ladder

• 1st: PDE5 inhibitors
• 2nd: ICI / intraurethral alprostadil / vacuum device
• 3rd: surgery (prosthesis)
• Plus conservative throughout: psychosexual counseling, medication change, lifestyle/exercise (~+3 IIEF-EF)
• Treatment is shared decision-making — a patient may decline any non-surgical line and go straight to a prosthesis
• Mixed vasculogenic ED (PSV < 25–30 + EDV > 5 cm/s) that fails or cannot tolerate intracavernosal therapy → penile prosthesis

PDE5 inhibitors — augment but do not induce erection

• Act through the NO pathway (inhibit PDE5 → ↑cGMP) — sexual stimulation is still required
• Absolute CI:
  • Nitrates (precipitous hypotension, no antidote — avoid nitro 24 h sildenafil/vardenafil, 48 h tadalafil, 12 h avanafil)
  • Hypersensitivity
• Relative CI:
  • Severe renal/liver disease
  • Severe cardiac (MI <6 mo)
  • NYHA class II
  • Non-selective α-blockers
  • Anti-arrhythmics (vardenafil — QT)
  • Hereditary retinal disorders (retinitis pigmentosa)
  • History of priapism
  • The MI and hereditary (degenerative) retinal disorder cautions carry an FDA warning
• AE: headache, flushing, dyspepsia, nasal congestion, visual disturbance
  • Class-wide (don't discriminate between agents): headache 7–16%, dyspepsia and flushing 4–10%
    • From PDE5 inhibition in vascular and GI smooth muscle
  • Tadalafil-specific: back pain and myalgia (lower back myalgia attributed to PDE11 inhibition)
    • Can persist into the next day given the long half-life
  • Bothered by an agent-specific side effect (backache, blue-green vision) → switch to another PDE5 inhibitor
• Cross-reactivity: sildenafil and vardenafil hit PDE6 (vardenafil is the most selective); tadalafil hits PDE11
  • Sildenafil is the most likely to cause visual disturbance — blue vision, color blindness — via PDE6
    • NAION (sudden vision loss) is the serious one
  • Diplopia, blurred vision, chromatopsia = retinal PDE6 cross-reactivity
    • Most with sildenafil and vardenafil, rare with tadalafil
    • These need no ophthalmology referral
  • Good sildenafil responder with visual side effects → switch to tadalafil (very little PDE6 affinity)
    • No need to escalate to intraurethral or intracavernosal PGE1
• Initial response rate is 70% — but only 50% in diabetics
• After 7–10 days of daily tadalafil the serum level is maintained
• Drug interactions:
  • Ketoconazole, itraconazole and protease inhibitors (ritonavir) block CYP3A4 → reduce the PDE5i dose
  • Rifampin induces CYP3A4 → higher doses needed
  • Clearance depends on CYP3A4 — indinavir, NNRTIs and macrolides also raise levels → use the lowest starting dose
  • On protease inhibitor–based HIV therapy → intracavernosal alprostadil preferred
    • Acts locally via cAMP, escaping the CYP3A4 interaction shared by every oral PDE5i
• α-blocker co-use (hypotension risk):
  • Sildenafil 25 mg — with an α-blocker (e.g. tamsulosin) at any time
    • 50–100 mg must be separated from any α-blocker by 4 hours
    • The same concern applies to vardenafil
  • Tadalafil — any dose with tamsulosin 0.4 mg
  • Adding tadalafil to an existing α-blocker → patient stable on the α-blocker first, then tadalafil at the lowest recommended dose
  • Starting an α-blocker in a tadalafil user → don't stop tadalafil
    • Lower it to 10 mg on demand (or 2.5 mg daily) and avoid simultaneous dosing

Indications for regular (daily) dosing

• The patient wants spontaneity
• Coexisting LUTS — tadalafil only
• Before prostatectomy, to familiarize the patient
  • The rationale is anti-fibrotic, since the cavernous nerves undergo neuropraxia post-operatively

Post-operative ED rates

• APR → ED from cavernous nerve injury — the nerves run alongside the posterolateral rectum and prostate
• After urethroplasty, loss of libido and anorgasmia are very rare

Intracavernosal injection

• Trimix = alprostadil + papaverine + phentolamine (more pain)
• Bimix = papaverine + phentolamine (more priapism)
• Limit 10 injections/month (fibrosis)
• CI = MAOI, poor dexterity, psych instability, coagulopathy/unstable CV, priapism risk

• Alprostadil (PGE1) is the only FDA-approved agent
  • Raises cAMP
  • Most common side effect is pain
  • Expensive
  • 10–20 µg
  • Single-agent dose range 5–40 µg, onset 5–15 minutes, efficacy > 70%; can be offered at any treatment stage
  • Its cAMP action bypasses the NO–cGMP pathway → still works after PDE5i failure
  • Pain in 50% of patients (11% of injections) — more than with trimix
    • Eases with continued use or added sodium bicarbonate or local anesthetic
  • After pain: prolonged erection 5% · fibrosis 2% · priapism 1%
• Papaverine — vasodilator and non-specific PDE inhibitor (2, 3, 5) → raises cGMP and cAMP
  • Priapism 35%, fibrosis, impaired LFTs
• Phentolamine (α-blocker) maintains the erection — must not be given alone
• The principle of bimix/trimix: lower the dose of each agent to cut side effects, while gaining synergy

MUSE (intraurethral alprostadil)

• Useful for floppy glans syndrome; lower incidence of prolonged erection than ICI
• The option when PDE5i and injections are both unsuitable
  • e.g. clopidogrel coagulopathy or unstable CV disease (relative CIs to ICI)
• Contraindicated in urethral stricture, meatal stenosis, balanitis
• AE
  • Pain
    • Local pain (29–41%) is the commonest adverse event
  • Minor urethral bleeding
  • Priapism
  • Hypotension/hypersensitivity
• Must not be used during unprotected intercourse with a pregnant partner — it may induce uterine contractions — and not in couples trying to conceive

Vacuum device

• The constriction ring must not be left in place longer than 30 minutes
• Venous leak (EDV > 5 cm/s despite adequate vasoactive dosing) → poor response to injections and intraurethral therapy
  • → a man refusing a prosthesis should use a vacuum erection device

Arterial revascularization — candidate criteria

• Under 55 years
• Non-smoker
• Non-diabetic
• No venous leakage
• Radiographic confirmation of internal pudendal artery stenosis
• Highest success in men under 30 with isolated arterial stenosis after perineal or pelvic trauma
• May be considered for pure arteriogenic ED with normal hormonal and neurological status
• Venous reconstructive surgery remains investigational
  • Penile venous ligation is not recommended
    • Currently no role in any setting for veno-occlusive ED
    • Rarely gives lasting benefit and delays more reliable treatment such as a penile prosthesis

Testosterone therapy — erythrocytosis

• Intramuscular injection = the formulation most associated with erythrocytosis and thrombotic risk
  • Hemoglobin and hematocrit rise in direct correlation with testosterone levels
• All men on testosterone need periodic CBCs — first erythrocytosis check at 3 months
• Baseline hematocrit > 50% → consider withholding until the cause is explained
• On-treatment hematocrit ≥ 54% (e.g. 56%) → hold therapy
• Manage by withholding until hematocrit falls
  • → restart at a lower dose or a transdermal preparation, ± therapeutic phlebotomy

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Penile Prosthesis

Types

• Limited dexterity → semirigid
• Prior pelvic surgery (RP, cystectomy, APR) → submuscular reservoir
  • After cystectomy + urinary diversion (exam answer): best option is a 3-piece with an ectopic submuscular reservoir (between rectus and transversalis fascia), avoiding the scarred space of Retzius
• 2-piece when pelvic surgery has restricted the space of Retzius
• Pre-op: stretched penile length ≈ maximal post-op length (counsel re: shortening + glans softening)
• Indications: refractory ED · refractory ED with Peyronie's · priapism lasting > 36 hours

Approaches

Preparation

• Counsel: effectively irreversible
  • After explantation the penis is unlikely to respond reliably to other ED treatments
• Prior successful CABG → counts as low cardiac risk
  • No further cardiovascular evaluation needed
• Good glycemic control
  • One meta-analysis put the cut-off at HbA1c 11
  • Diabetes per se does not appear to raise prosthesis infection risk
• Ask the patient NOT to shave
• 10-minute alcohol-based skin prep
• Gentamicin + vancomycin, or cefazolin + gentamicin, or cefazolin alone
• Post-operative antibiotics for 24 hours only [EAU, AUA]

Operative principles

• Penoscrotal incision → good exposure of the corporotomy sites
• Dilate to 13 mm distally, 12 mm proximally
• Malleable girths: 13, 11, 9.5 mm.
• Inflatable:
  • Standard 18 mm if dilated to 13
  • Narrow base if dilated only to 10
• Reservoir — usually the space of Retzius, after piercing transversalis fascia
  • After radical prostatectomy, placing the reservoir through the inguinal canal into Retzius has caused bowel compression on inflation, requiring surgical intervention
  • Scarred Retzius
    • → risks iliac vessel injury (vessels ~1 inch lateral to the reservoir) and bowel compression near the internal inguinal ring when the reservoir fills
  • Prior Retzius surgery (RP, cystectomy, APR, pelvic fracture with bladder rupture)
    • → reservoir submuscularly or through a separate incision
  • Ectopic alternative — submuscular suprafascial
    • Between rectus above and transversalis fascia below.
    • A finger through the inguinal canal creates a space pointing toward the umbilicus
    • A long nasal speculum, then a double-hinged or ring clamp, develops the cavity 3–4 inches inside the internal inguinal ring
  • Other acceptable sites:
    • Epigastrium via a subcostal incision
    • Deep fat above the abdominal wall fascia in obese men
    • Peritoneal cavity
  • Not a scrotal cavity after orchiectomy
    • Cloverleaf lockout valves can be manipulated through the scrotum → autoinflation
    • The Conceal reservoir is too large
• Pump — anterior sub-dartos, in the most dependent area
• Water-tight corporal closure → drain → pressure dressing → keep the catheter

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Intra-operative troubleshooting

Cross-over

• Remove both cylinders
• Place a large dilator in the common cavity
• Redilate the opposite cavity pointing laterally and place a cylinder in it
• Remove the dilator and place the second cylinder in the original common cavity
• Test by inflating — the Foley should sit midline with both cylinders symmetrical either side
• Prevent:
  • Keep the penis on traction
  • Aim the dilator tip laterally
  • And leave a spacer in the contralateral corpus while its mate is dilated

Corporal perforation

• The most likely site of corporal perforation during placement is the septum
  • The septum is the weakest, fenestrated structure and dilators naturally drift medially → cylinder crossover

Curved erection after cylinder placement

• < 20° is acceptable and should permit intercourse
• > 20° → manual modeling for 90 seconds after clamping the pump tubing with shodded clamps, to protect the pump from back-pressure.
  • Repeatable.
  • Alternatively a Nesbit/plication, or plaque incision and grafting

Blood in the Foley during reservoir placement

• Bladder perforation — from the blind transversalis fascia puncture into the space of Retzius
• Always empty the bladder first

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Post-operative complications

• The commonest post-operative complaint after prosthesis placement is length loss

Penile necrosis

• At risk:
  • Severe cardiovascular disease
  • Diabetes
  • Chronic smoking
  • Previous prosthetic implants
  • Prior pelvic radiation.
• Counsel pre-operatively, especially with two or more.
• When ischemic necrosis is detected, remove the cylinders promptly to take pressure off the penis
  • Conservative debridement.

Cylinder erosion / extrusion

• Remove the cylinder
• Place a spacer cylinder in the opposite corporal body to maintain patency and preserve length
• Replace after 5–6 months, once solid scar has obliterated the erosion tract.
• Cylinder tip eroding through the urethral meatus (exam answer): even if only one tip has eroded, remove all device components wherever the erosion is → allow 8–12 weeks of urethral healing before reimplantation

Autoinflation

• In the obese patient, keep the implant completely deflated during healing so the capsule forms around a larger space.
• If the cylinders are partially filled, the reservoir is not completely full and the smaller capsule limits future expansion → autoinflation.
• Not prevented by weight loss, reservoir location, abstinence, or daily cycling of the device

Oversized cylinders

• Cylinders too long for the corpora buckle inside them on inflation → S-shaped deformity.
• Prevent by choosing cylinders equal to or ~1 cm shorter than the measured corporal length.
• Pain only on inflation, no signs of infection → oversized buckling cylinders (lightning-bolt configuration)
  • → confirm with penile MRI with the prosthesis inflated
  • → then revise to smaller cylinders

Bulge at the base

• Early post-op → corporotomy herniation, repaired without graft
• Years later → cylinder aneurysm from frequent maximal inflation and aggressive use.

Mechanical failure

• > 3 years after implantation → replace the entire device, not just the failed part, as the remaining components share the same wear.
• Revising an uninfected malfunctioning implant carries ~10% infection risk (disturbed biofilm)
  • → ~3% with revision washout (antiseptic irrigation of each implant cavity)

Infection — cause and recognition

• Mostly the patient's own skin flora introduced at surgery:
  • Staphylococcus epidermidis
  • Staphylococcus aureus
  • Candida albicans.
• Rates: 1–3% after primary implantation vs 7–18% after revision
• Biofilm shields the organisms → systemic antibiotics alone fail
  • → remove all components plus any permanent sutures or graft material
• Pus at the incision or on squeezing the pump = definitive sign
  • With fever + leukocytosis → skip salvage and remove every component — retained parts can form abscesses
• Two weeks post-op, persistent penoscrotal pain and swelling, afebrile, WBC 7000/cu mm, clean wound
  • → observe: a non-infected device improves within 7–14 days
  • Early antibiotics can mask a developing infection
  • Imaging does not aid diagnosis
  • Draining a hematoma risks infecting a device that may not be infected

Infection — two options

• Leave the implant out.
  • Irrigation drains in each corporal body, wound closed
  • Antibiotic solution instilled every 8 hours for 3 days.
  • Return in 2–6 months to replace
    • Cylinders are harder to place because of corporal scarring, and the erection will be noticeably shorter
  • Use a vacuum device daily while waiting to limit penile shortening
  • Delayed re-implantation causes secondary corporal fibrosis, decreased penile size and a harder reinsertion
    • Minimize by re-operating 6–12 weeks post-op
• Salvage
  • Remove the infected prosthesis, wash out, immediately replace the device.
  • Successful in 80%
  • Salvage is contraindicated in:
    • Enterococcus
    • Tissue necrosis
    • Sepsis
    • Diabetic ketoacidosis
    • Or cylinder erosion into the urethra
  • Reserve immediate antibiotic-washout salvage for men without sepsis or severe local infection
    • It sidesteps the delayed re-implantation fibrosis above and preserves length and girth

Adhesions block scrotal removal of an infected device's reservoir

• → make a second incision over the reservoir tubing for direct retropubic access
• The entire implant must come out

Antiseptic washes during salvage

• Dilute povidone-iodine 0.35–3.5% in the implant cavities, left 3 minutes
  • Wash out with saline or antibiotic solution
• Eliminate hydrogen peroxide — no antiseptic advantage over povidone-iodine and it can be cytotoxic
• Chlorhexidine may be more effective but the data are insufficient
• Pressure irrigation optional

SST deformity

• Conservative first, pulling the penile skin toward the scrotum.
• If that fails, glans pexy
  • Tack the glans to the distal tunica albuginea with a non-absorbable 3-0 suture.

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Ejaculatory & Orgasmic Dysfunction

• Emission (sympathetic T10–L2) → seminal fluid into prostatic urethra + bladder-neck closure (α-sympathetic)
• Ejection (somatic pudendal S2–S4) → rhythmic bulbocavernosus contraction, antegrade expulsion

Ejaculation potential

• Unlike erectile capacity, the ability to ejaculate increases with descending levels of spinal injury.
  • Fewer than 5% of complete upper motor neuron lesions retain the ability to ejaculate.

Premature Ejaculation (PE)

• Definition (ISSM 2013): ejaculation ≤1 min (lifelong) or bothersome reduction to ≤3 min (acquired) + inability to delay + negative personal consequences
• Lifelong PE is neurologic in etiology.
• Acquired PE
  • Performance anxiety
  • Psychosocial problems
  • ED
  • Chronic prostatitis
  • Recreational drugs
  • Hyperthyroidism
• Treat comorbid ED first.
  • ED + PE → PDE5i alone first (e.g., tadalafil)
    • Restoring erections often resolves the PE
    • With lifelong PE, treating ED and PE together is also appropriate
• 1st: psychosexual therapy (squeeze, stop-start)
• 2nd: pharmacotherapy — "PASTA" (all off-label):
  • PDE5i (only if comorbid ED)
  • Anesthetic topical — 2.5% lidocaine/prilocaine, 20–30 min pre-intercourse, wipe before penetration
  • SSRIs — dapoxetine on-demand

• Paroxetine gives the strongest delay — IELT increases about 8.8-fold.
• But dapoxetine is the only approved oral drug
  • EAU 2026 carries a Strong recommendation for either dapoxetine or a lidocaine/prilocaine spray as first-line in lifelong PE.
  • Only two approved PE agents
    • Dapoxetine (the oral on-demand drug) and lidocaine/prilocaine spray
    • Everything else is off-label (dapoxetine is approved in Europe, not the USA)
  • Dapoxetine — short-acting SSRI, Tmax 1.3 h → IELT 2.5-fold at 30 mg, 3.0-fold at 60 mg
  • Check orthostatic BP and heart rate before starting dapoxetine — 0.1% vasovagal syncope
  • Dapoxetine and lidocaine/prilocaine both fail → next on-demand option is clomipramine
    • The most serotonergic tricyclic and the only second-line agent that can be taken on demand (EAU second line: daily SSRIs or daily/on-demand clomipramine)
• The delay usually appears within 5–10 days of starting treatment
  • Daily SSRIs raise IELT 2.6- to 13.2-fold
    • Full effect takes 2–3 weeks
    • Tachyphylaxis may develop after 6–12 months of chronic use
• SSRIs and tramadol are all contraindicated with MAOIs
• Attempt graduated withdrawal of drug therapy after 6–8 weeks
  • e.g., lifelong PE responding satisfactorily to daily paroxetine → taper, don't stop
    • Sudden cessation or rapid dose reduction risks SSRI withdrawal syndrome

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Delayed Ejaculation / Anejaculation / Anorgasmia

• Delayed ejaculation (DE): latency beyond 25–30 min with distress (most men ejaculate within ~4–10 min)
• Causes:
  • Psychogenic
  • Aging (DM — afferent nerve degeneration)
  • Endocrine (hypothyroidism, hyperprolactinemia)
  • Neurogenic
  • Radical prostatectomy → no ejaculate, orgasm preserved
  • RPLND → anejaculation in non-nerve-sparing; nerve-sparing preserves antegrade in 80–100%
  • SSRIs → ejaculatory dysfunction in ~60%
  • Older man with preserved erections → most likely age
    • Degeneration of penile afferent nerves and Pacinian corpuscles
  • Other leading causes: diabetic autonomic neuropathy · SSRIs or major tranquilizers
    • Diuretics and β-blockers are classic ED-associated drugs, not leading drug causes of DE
• Management:
  • Psychosexual therapy
  • Lifestyle
  • Pharmacotherapy
  • Vibratory stimulation/electroejaculation for SCI (risk of autonomic dysreflexia)
  • Psychogenic DE is the commonest → refer to a sexual-health mental health professional once organic causes are excluded (AUA)

Causes — of retrograde ejaculation, delayed ejaculation, anejaculation and anorgasmia

The diagnostic algorithm — start with: is there orgasm?

• Never → either failure of emission (neurogenic, metabolic, drug side effect → disease-specific management) or inhibited male orgasm (→ psychosexual therapy)
• Sometimes → inhibited male orgasm with nocturnal/masturbatory emissions (→ psychosexual therapy), or age-related degeneration (→ reassure, alter technique)
  • Nocturnal emissions in DE → emission pathway intact → check TSH: hypothyroidism is a reversible endocrine cause strongly associated with DE
• Always → then ask: is there ejaculation?
  • No → are sperm present in the urine after orgasm?
    • No → aspermia — think ejaculatory duct obstruction
    • Yes → retrograde ejaculation — reassure/educate, pharmacotherapy, surgery

Orgasm without any antegrade ejaculate is called aspermia, anejaculation, or dry ejaculation

Drug therapy for delayed ejaculation / anejaculation

• Pseudoephedrine does NOT help delayed ejaculation — it is only for retrograde ejaculation

Retrograde Ejaculation

• RF: bladder-neck surgery (TURP), diabetes
• Dx: post-orgasmic urinalysis for sperm and fructose (vs failure of emission)
  • Indicated when the ejaculate volume is < 1 mL
• Rx: α-agonists (pseudoephedrine, ephedrine, midodrine), imipramine
  • Pseudoephedrine 120 mg every 6 hours the day before coitus, and twice on the day of coitus, produced antegrade ejaculation in 58% of a predominantly diabetic group
  • Imipramine 25 mg BID

Other

• Painful ejaculation:
  • Treat underlying cause (urethritis, BPH, prostatitis/CPPS, seminal vesiculitis, seminal vesicular calculi, EDO)
  • Occurs in 17–23% of men with LUTS/BPH
• Ejaculatory anhedonia:
  • Sufferers may be male or female
  • Aware of orgasm and ejaculation but experience little or no pleasure
  • Assess total and free testosterone, pituitary gonadotropins and prolactin.
    • If there is hyperprolactinemia or secondary hypogonadism, get a pituitary MRI
  • Pharmacotherapy and psychotherapy — cabergoline 0.5–3 mg every 3 days
• Post-orgasmic illness syndrome (POIS):
  • Flu-like myalgia/fatigue within 30 min of orgasm
  • Proposed type-1 hypersensitivity
  • Trial autologous-semen desensitization
• After bulbar urethroplasty: ejaculatory dysfunction is the commonest sexual dysfunction
  • Permanent in up to 20%
  • Semen pooling in the urethra or weak ejaculation, presumed from neourethral tortuosity or bulbocavernosus dysfunction

Post-vasectomy pain syndrome

• Refractory pain with no other identifiable cause → vasectomy reversal (vasovasostomy)
  • Restores vasal patency, relieving the epididymal obstruction and pressure driving the pain
  • Complete relief 34–50% · overall improvement 82–93%
  • Relief may take 3 months or more · reoperation ~20% over 1–9 years