MANAGEMENT OF ERECTILE DYSFUNCTION · 2020-04-05 · •ERECTILE DYSFUNCTION: Erectile dysfunction...
Transcript of MANAGEMENT OF ERECTILE DYSFUNCTION · 2020-04-05 · •ERECTILE DYSFUNCTION: Erectile dysfunction...
MANAGEMENT OF ERECTILE DYSFUNCTION
• ERECTILE DYSFUNCTION: Erectile dysfunction (ED), defined as the persistent inability to achieve and maintain penile erection sufficient to permit satisfactory sexual performance
• EPIDEMIOLOGY
– Prevalent; 1 in every 10 men
– Frequency & severity varies with age
– Uncommon in young men except those with psychological problem
– More common in middle age & highly prevalent >60years
– Peculiarities in our environment:
• Reluctance in discussing sexual issues
– Consequence:
• Loss of confidence & self esteem, negative feelings & depression.
• TERMINOLOGY
– Erection- Tumescence
– Flaccid- Detumescence
• ANATOMY
• Key organ: paired corpora carvenosa- composed of vascular spaces(multiple lacuna spaces lined by vascular endothelium), smooth muscles & fibro-elastic tissues.
• Arterial supply:
– Carvenosal artery(run centrally in corpus carvenosa giving off multiple helicine arteries)
• NB. Carvenosal art. -a branch of common penile artery derived from perineal art(a branch of internal pudendal art which is a branch of internal iliac art.)
• Venous drainage:
– Deep dorsal vein: drains the distal 2/3rd of corpora carvenosa, corpus spongiosum & glans. It drains into vesico-prostatic plexus
– Carvenosal veins: emissary veins in proximal 1/3rd
join to form 1 or 2 carvenosal veins- drains into internal pudendal vein.
• Innervation:
– 3 sets of nerves involve in penile tumescence & detumescence
– Parasympathetic:
• S2-S4( as nervi erigentes to reach pelvic plexus
• Produces nitric oxide(NO) as neurotransmitter) which causes dilation of the carvenosal tissue
– Sympathetic:
• T10-L2( via hypogastric nerve): causes tonic contraction of the carvenosal smooth muscle.
– Somatic:
• via pudendal nerve: supply propioception & sensory sensation to penile skin & glans penis
• MECHANISM OF ERECTION
• Detumescence phase is maintained by tonic sympathetic discharge with contraction of the smooth muscle of carvenosal tissue- leads to decrease blood flow into the carvenosal tissue
• Tumescence phase: occur by relaxation of carvenosal tissue which allow inflow of blood. Mediated by Nitric oxide (NO)
– Effect of Nitric oxide is terminated by 5-phosphodiesterase enzymes
– Other neurotransmitters involve in tumescence
• Prostaglandin E1: relaxes carvenosal smooth muscle
– Other neurotransmitters involve in detumescence:
• Endothelin 1: vasoconstrictory effect
• maintenance of erection:
– maintained by veno-occlusive mechanism which prevents venous drainage from carvenosal tissue. This is achieved by the high intra-corporeal pressure causing compression of the emissary veins which drain the carvenosal tissue.
• Prevention of coagulation of blood in carvenosal tissue is by prostacylin: prevent coagulation & has anti-platelet aggregation activity.
• PATHOPHYSIOLOGY OF ED
• ORGANIC CAUSES
1. Vascular causes(60%):
A. Arterial insufficiency
– Atherosclerosis of internal iliac artery & carvenosal art.
– Vascular damage from previous pelvic surgery/trauma
B. Veno-occlusive abnormality:
– venous leakage due to decrease distensibility of the carvenosal tissue
C. Intra-carvenosal smooth muscle fibrosis:
• loss of elasticity & distensibility of carvenosal tissue
– Causes
• Neglected priapism
• Peyronie's disease
• Aging process
2. Neurogenic causes:
– CNS: CVA, Parkinson’s disease, multiple sclerosis
– Peripheral Nv: diabetic neuropathy, cauda equinalesion, perineal Nv injury during surgery,
3. Endocrine causes:
– Low testosterone
– hypogonadism
4. Aging :
– Affect distensibility of carvenosal tissue
– Impairs neurogenic erectile function with increase latency to achieve erection
– Decrease in NO synthesis
• 5. Drug Induced:
– Antihypertensive- moduretics, Aldomet, Beta blockers, diuretics
– Anti-psychotics- TCAs
– Some aphrodisiacs
• PSYCHOGENIC CAUSES:
• Anxiety increases sympathetic vasomotor tone of carvenosal tissue(detumescence)
• Depression
• RISK FACTORS
1. Diabetes mellitus: can lead to diabetic neuropathy, damage of blood vessels & autonomic neuropathy
2. Hypertension: damage blood vessels, some anti-hypertensives. e.g. Beta blockers, diuretics
3. Hyperlipideamia: damage peripheral blood vessels
4. Hypercholesterolemia & increased triglyceride associated with ED
5. Smoking: has damaging effect on blood vessels
6. Peyronie's disease: fibrous tissue in tunica albuginea which affect the veno-occlusive mechanism & distensibility of carvenosal tissue
7. Previous surgery: Radical prostatectomy, Abdomino-perineal resection
8. Penile trauma: penile fracture
9. Depression: 90% of depressed men have ED
EVALUATION• HISTORY
– Ascertain the patient’s problem: distinguish ED from loss of libido or premature ejaculation
– Determine the duration, nature of onset, consistency or severity.
– Ascertain sexual gratification of his partner:
• Emphasis on:
–Previous & present relationship
–Attitude of partner towards the problem
–Effect of ED on the relationship
– Ascertain early morning tumescence( help distinguish psychogenic from organic ED. Unlikely to be organic if present).
– Drug history:
• LHRH, flutamide, bicalutamide: loss of libido, ED.
• Anti-hypertensives:
• diuretics: thiazide, spironolactone
• Methyl dopa, clonidine, reserpine
• Beta blockers: atenolol, propanolol
• Hydralazine
• ACEI
• Antidepressant:• TCA: amitriptylline, nortriptyline• Transquilizers: haloperidol, chlorpromazine• Anxiolytics: diazepam• Others: cimetidine, ketoconazole,
metoclopropamide, baclofen
– Systemic disease Hx:• DM• HTN• Vascular disease: intermittent claudication in the
gluteal and calf– Social history: smoking, alcohol, marijuana, nicotine,
opiates, some herbal concoction
– History of previous pelvic surgery/radiation
– History of trauma/pelvic fracture
• PHYSICAL EXAMINATION
• General appearance: may reveal androgen state, obesity
• Chest: gynaecomastia
• Abdomen : DRE: anal tone/ bulbocarvenous reflex- if depressed may be suggestive of neurological disorder
• External genitalia: may detect
– Peyronie’s disease
– Testicular abnormalities
– Loss/ abnormalities of penile sensation
• Extremities: palpate to detect peripheral vascular disease
• INVESTIGATION
• Urinalysis: may be glycosuria in DM
• Fasting blood sugar: elevated in DM
• Liver function test: abnormal values in patient with liver failure /high alcohol intake
• Serum testosterone: low in hypogonadism, post Orchidectomy
• Fasting lipid profile: hypercholesterolemia, increased triglycerides
• SPECIAL INVESTIGATIONS
• Nocturnal penile tumescence testing:
– help differentiate psychogenic from organic causes
– Use snap gauge device or ring of postage stamps
• Diagnostic intra-corporeal injection: induction of artificial erection to:
– Determine the distensibility of carvenosal tissue
– Determine feasibility of use of injection pharmacotherapy in ED treatment
– Drugs used: papaverine, phentolamine, PGE1
• Color duplex Doppler ultrasound assessment of intra-corporeal blood flow:
– done by inducing erection with PGE1 injection & assessing blood flow into the carvenosal tissue
• Dynamic infusion carvenosometry & carvenosography:
– Help to identify venous leakage and intra-corporeal pressure.
• Angiography:
– To determine arterial insufficiency
TREATMENT
• Done step wise: from least invasive to most invasive
• Behavioural modification
– Stop smoking, alcohol, weight loss, physical exercises
• Treat co-morbidities: HTN, DM, statins to lower lipoprotein cholesterol
• Stop use of drugs predisposing to ED
• Psychosexual counseling:
– NB: all patients have psychological component to their problem
• Psychological problem is mostly due to unrealistic expectation by one or both sides of the relationship
• Emphasis is on:
–Understanding of the problem
–Overcoming anxiety
–Teaching communication skills
–Re-learning sexual behaviour
• MEDICAL THERAPIES
• A. ORAL AGENTS:
• α- adrenoceptor antagonist
– Yohimbine HCl: causes corporal vasodilation & erection. Dose 10mg t.d.s
• Side effects: tremulousness, headache, palpitation, increase in BP
– Phentolamine: vasodilators but has narrow safety margin
• Dopamine agonist:
– apomorphine; side effects: persistent yawning, nausea & vomiting
• Serotonin agonist:
– trazodone- has sympatholytic effect . S/E: drowsiness, hypotension
• 5-Phosphodiesterase inhibitors(PDE-5I):
– increases level & effect of NO
– Sidenafil citrate: dose: 25 to 50mg/day; used 1hour before intercourse
• Half life: 3.8hours
• Efficacy: 96%
• S/E: facial flushing. Headache, effect on color vision, GI disturbances,
• Contra-indication: avoid in patients on nitrates: glycerl trinitrate, Nitroprusside- can lead to profound hypotension & cardiac arrest.
– Tadanafil: dose: 10 to 20mg/day
• Half life: 17.5 hours
• contra-indicated in : concomitant use of organic nitrates & α blocker
• S/E: headache, nasal stuffiness, dyspepsia
– Verdenafil HCl: dose 5 to 20mg
• Seems to be more effective in DM & post prostatectomy patient with ED
• Half life: 4.7hours
• S/E: as in sidenafil, prolong QT interval on ECG
• C/I: nitrate therapy & α blocker
• B. TRANSDERMAL DRUG DELIVERY:
– application of paste which contain PGE1 or Papaverine
• C. TRANSURETHRAL CORPOREAL DRUG DELIVERY:
– insertion of drug pellets intra-urethral. e.g PGE1
– S/E”: urethral pain, occasional bleeding & priapism
• D. INTRA-CORPORAL INJECTION:
– Injection of vasodilators into the carvenosal tissue e.g. Papaverine, phentolamine, PGE1
– S/E: priapism, ischemic injury to smooth muscles of carvenosal tissue
• VACUUM DEVICES & CONSTRICTION RING
– Vacuum device suction effects increase arterial inflow while the constriction reduces venous leakages
– S/E: penile bruising, may be uncomfortable, pain at ejaculation
• SURGICAL THERAPY
1. Correction of venous leakage by ligation
2. Arterial re-vacularization of damage arterial supply
3. Implantation of penile prosthesis: insertion of silicon prosthesis into corpora carvenosa
4. Penile enlargement: some attribute ED to small penile size:
• Division of suspensory ligament
• Advanced V-Y plasty of intra-pubic skin.