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Erectile Dysfunction - A rising problem Mr C Dawson MS FRCS Consultant Urologist Edith Cavell Hospital Peterborough.

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Presentation on theme: "Erectile Dysfunction - A rising problem Mr C Dawson MS FRCS Consultant Urologist Edith Cavell Hospital Peterborough."— Presentation transcript:

1 Erectile Dysfunction - A rising problem Mr C Dawson MS FRCS Consultant Urologist Edith Cavell Hospital Peterborough

2 Prevalence and significance of E.D. Exact incidence unknown May affect 1 in 10 men Affects 10 million men in US alone, 400,000 OPD visits and 30,000 hospital admissions (1992 figs) Significance to Urologists - Increased public awareness of new treatments has resulted in increase in referrals

3 Definition of Erectile Dysfunction “Inability to achieve and maintain an erection sufficient to allow penetrative sexual intercourse to occur (.... with satisfaction to the patient and his partner)”

4 Myths surrounding E.D. “Nothing can be done” “It’s to be expected at my age, isn’t it?” “Do you think it’s all in my mind doctor?”

5 Erectile Dysfunction and ageing Testosterone levels decline with age Effects of testosterone on erectile capacity is not clear Wide variation in “normal” levels of testosterone Therefore, ageing and reduced testosterone may be independently associated with E.D.

6 Psychological cause? Careful history will usually determine those patients with a psychological element to their E.D. Persistent E.D., especially of insidious onset is more likely to have an organic cause More than 90% of cases of E.D. have an organic basis

7 Mechanism of erection Depends on integrated processes of : – increased arterial inflow to penis – filling of sinusoids of the corpora cavernosa, aided by relaxation of cavernosal smooth muscle – passive occlusion of the venous plexus provides increased resistance to outflow and aids rigidity

8 Mechanism of erection

9 The role of chemical mediators Previously suggested that erection under parasympathetic, and detumescence under sympathetic, control - over simplified view Non-adrenergic non-cholinergic (NANC) mechanisms now believed to be important

10 The role of chemical mediators Nitric oxide (NO) now appears to be the final element in the NANC pathway and may be derived from nerve endings NO raises cyclic GMP levels leading to penile smooth muscle relaxation

11 Pathophysiology of E.D. Robert Krane, BAUS 1996 Arterial insufficiency in E.D. may lead to – hypoxia of the corpora – Imbalance between PGE1 and TGF-B1 – Excess Collagen Deposition – Fibrosis of the corpora cavernosa – Dysfunction of the veno-occlusive mechanism

12 Pathophysiology of E.D. Flaccid state – Hypoxia, increased TGF-B1, and fibrosis Asleep – Nocturnal penile tumescence 3-5x per night, 40 mins per time. Normoxic episodes increase PGE1, decrease collagen, and decrease TGF Established E.D. – Hypoxia all the time; don’t get the benefit of NPT episodes

13 Pathophysiology of E.D. Use it or lose it! More erections = increased normoxia Increased PGE and cAMP Decreased TGF-B ?? decrease fibrosis already present

14 Assessment of the patient with E.D. Careful History Examination Further investigations

15 Points to note in the initial history Duration, ?insidious or acute onset Absence of erections or diminished quality Penetrative SI possible? Able to masturbate? Early morning erections? Libido normal, or decreased Pain or curvature of erection (?Peyronie’s disease) Related psychosocial factors

16 Medical History Chronic systemic medical disease Neurological Problems Previous surgery Vascular risk factors Drug History

17 Physical examination Endocrine – Assessment of secondary sexual characteristics – Examine neck for Thyroid – Gynaecomastia – Size and consistency of testes Neurological – Sensory deficit in sacral dermatomes Vascular – BP, Carotid Bruits, AAA, Foot pulses Local - examine penis for plaques or fibrosis

18 Laboratory Investigations No single diagnostic test FBC, U+E, LFT - to screen systemic medical disorders

19 Role of Hormone evaluation Testosterone affects secondary sex characteristics; effects on erections unclear - If libido is reduced, testosterone should be measured If Testosterone repeatedly low check LH – Low Testosterone and Low LH may indicate hypothalamic or pituitary defect (CT advised) – Low Testosterone and High LH suggests testicular failure Hyperprolactinaemia inhibits LHRH pulse Abnormal thyroid function may cause E.D.

20 Further Management of E.D. Pragmatic approach best, based upon available treatments Diagnostic intracavernosal injection – Normal erection suggests normal vascular dynamics, and precludes further investigation – Poor, or absent, erectile response may be followed by investigations in certain circumstances

21 Further Management of E.D. Medical therapy – “Magic Pill” still sought – Yohimbine - may improve erectile capacity in some men

22 Intracavernosal Pharmacotherapy Papaverine +/- Phentolamine Prostaglandin E1 (Caverject) Combination therapies Requires trained supervision until patient competent to give injection

23 Results of intracavernosal therapy Papaverine alone -30% success rate PGE1 alone - 70% success rate Combination therapies may have success rates of 85-90% Priapism less with PGE1 (0.4% vs 6% for Papaverine Early drop-out rate as high as 50%

24 Vacuum device Less invasive than intracavernous injection Results good - up to 92% success in some series Bruising reported so contraindicated in bleeding diathesis or anticoagulant treatment Expensive for patient to purchase

25 Penile Prosthesis Usually tried only after injections and vacuum device have failed, or for E.D. associated with Peyronie’s disease Rigid, or inflatable types Insertion requires strict asepsis under GA Infection is the most important complication, necessitating removal Erosion of one or both cylinders may occur

26 The Future Better understanding of chemical mediators may lead to pharmacological treatments? - e.g. Sildenafil

27 Conclusions Media attention and public awareness has led to increased referrals Better understanding of mechanism of erection, and pathophysiology of E.D. has rationalised investigation and treatment

28 Conclusions Current management relies on pragmatic approach, and response to intracavernosal injection of PGE Good success rates with either injections or vacuum device. Prosthesis rarely required Future developments likely to radically alter management of this condition


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