Erectile dysfunction is caused by problems with blood flow to the penis, nerve signals in the body, hormone levels, or psychological issues. During arousal, signals from the brain cause blood vessels in the penis to widen and let in more blood, making the penis hard. The veins are then compressed to maintain the erection. Common causes of erectile dysfunction include diseases like diabetes or damage to the nerves, blood vessels, muscles, or tissues of the penis. A doctor can diagnose erectile dysfunction through a medical history, physical exam, and tests. Treatments may include oral medications, counseling, injections, devices, or surgery.

1. ERECTILE DYSFUNCTION
No laughing matter..

2. ANATOMY OF THE PENIS

3. BLOOD SUPPLY OF THE PENIS
 Is from the internal pudendal artery, which
enters the perineum through Alcock’s canal and
gives rise to 4 terminal branches
1. Dorsal art.
 supplies penile skin and glans and contributes little to
erectile function
2. Cavernosal art.
 within the corpora, branches into helicine arterioles
3. Bulbar art.
4. Scrotal art.

5. BLOOD SUPPLY OF THE PENIS
• Venous drainage is both intra + extra cavernosal
 Intracavernosal drainage:
helicine arterioles drain into
vascular lacunar spaces of
corp. cavernosum  which
empty into subtunical v.
emissary v., pierce tunica
albuginea  deep dorsal v.

6. BLOOD SUPPLY OF THE PENIS
 Extracavernosal drainage: is via 3 routes
1. Deep dorsal v. – drains distal corpora
into santorini’s vesicoprostatic venous
plexus
2. Cavernosal and crural v. – drains prox.
corpora into santorini’s plexus and int.
pudendal v.
3. Superficial dorsal v. – drains blood from
penile skin, glans and communicates
with deep dorsal v.

7. NERVE SUPPLY OF THE PENIS
 Autonomic
 Paraympathetic nerves from S2-4 nerve roots
primarily control erectile function while the
sympathetic nerves from T11-L2 control
detumescence and also contribute to ejaculation and
emission.
 These autonomic nerve fibers form the pelvic plexus
of nerves and enter the penis within the cavernosal
nerves that course lateral and inferior to the
prostate.
 N.B. It is these nerves that are preserved during nerve
sparing radical prostatectomy.

8. NERVE SUPPLY OF THE PENIS
 Somatic
 Peripheral nerves (dorsal penile and pudendal n.) form
sensory and motor elements through a reflex arc in the sacral
spinal cord at Onuf's nucleus (S2-4).
 Peripheral nerves containing sensory elements are also
responsible for erectile function, as they innervate the ischio
and bulbo cavernosus muscles of the penis

9. NERVE SUPPLY OF THE PENIS
 Central
 Ultimate central nervous system control is likely
initiated in the hypothalamus in the medial pre-optic
area that integrates psychological and tactile stimuli.

11. TYPES OF ERECTION
Reflexogenic erection:
A genital stimulation leads to a
reflexogenic erection. Afferent signal pass
via the pudendal nerve to the sacral
erection center, this sends the efferent
signal via the inferior hypogastric plexus.
 The reflexogenic erection is largely
independent of cortical influences, as this
kind of erection can remain intact after
cervical or thoracic spinal cord injuries.

12. Psychogenic erection:
 The cortical processing of sensory, visual,
auditory stimuli or fantasies are triggers for an
erection.
 The cortical centers influence the sacral erection
centers, which cause the erection via activation of
the inferior hypogastric plexus.

13. Nocturnal erection:
 Occurs during the REM sleeping phase and can
be measured during sleeping studies (Nocturnal
penile tumescence = NPT).
 Typical for the psychogenic impotence is the
existence of NPT, in contrast to serious
vascular erectile dysfunction.
 Sympathetic centers mediate nocturnal erections,
the existence of NPT still cannot rule out damage
to the sacral parasympathetic erection center.

14. REVIEW MECHANISM OF ERECTION:
What happens to the penis during arousal?
 Audiovisual or tactile stimuli  activate
nuclei of spinal erection center T11-L2 and
S2-4
• Signals relayed via
cavernosal n. to erectile
tissue of corpora cavernosa
activating the veno-occlusive
mechanism

15. • This triggers increased arterial blood flow
into sinusoidal spaces, relaxation of
cavernosal smooth muscle, and opening of
vascular spaces

16.  The result: Blood expands the sinusoidal spaces which
compresses the subtunical venous plexuses against the
tunica albuginea decreasing the venous outflow, and
further compressing the emissary veins

17. PHYSIOLOGY

18.  Excitatory stimuli from the CNS produce erections
through a variety of neurotransmitters.
 Many neurotransmitters including acetylcholine (ACh)
and vasoactive intestinal polypeptide (VIP) contribute
to erectile function.
 The most important neurotransmitter in the corpora
cavernosa is nitric oxide (NO).

19.  Following sexual stimulation, acetyl choline triggers
the release of nitric oxide from endothelial cells,
and diffuses into the corporal smooth muscle.
 Nitric oxide (NO) is a gas that acts as a vasodilating
agent, inducing smooth ms relaxation via (guanylate
cyclase) the cGMP system.
 Therefore, NO  arteries dilate  fills the corpora
spongiosum and cavernosa with blood = erection

20.  cGMP is broken down by phosphodiesterase type 5 (PDE5).
 When this occurs the Ca2+ increases in concentration in the
cell, resulting in contraction of the smooth muscle cells and
detumescence.
 N.B. Sildenafil ('Viagra') is a PDE5 inhibitor, and allows for
erections to be maintained in response to stimuli, but does not
initiate erection.

21. ERECTION VS. DETUMESCENCE
 Stimulation of the pelvic plexus and the
cavernous nerves (Parasympathetic fibers )
through tactile sensory stimuli to the penis,
releases acetylcholine, which enhances penile
blood flow and smooth muscle relaxation, thus
inducing erection
 Sympathetic (adrenergic) fibers and
norepinephrine neurotransmission help to
maintain the penis in its flaccid state.
 norepinephrine, activates alpha-adrenergic
receptors that produce vasoconstriction of the penile
vasculature and decompression of penile venules,
which result in detumescence.

22. PHASES OF ERECTION
Phase Term Description
0 Flaccid phase Cavernosal smooth ms contracted; sinusoids
empty; minimal arterial flow
1 Latent (filling) Increased pudendal artery flow; penile
phase elongation
2 Tumescent phase Rising intracavernosal pressure; erection
forming
3 Full erection Increased cavernosal pressure (100 mmHg)
phase causes penis to become full erect
4 Rigid erection Further increases in pressure (to several
phase hundred mmHg) + ischiocavernosal muscle
contraction
5 Detumescence Following ejaculation, sympathetic discharge
phase resumes; there is smooth muscle contraction
and vasonstriction; reduced arterial flow; blood
is expelled from sinusoidal spaces

23. SO WHAT IS IMPOTENCE OR ERECTILE
DYSFUNCTION?
The persistent inability to achieve or maintain a penile
erection sufficient for sexual intercourse

24.  ED affects about 10% of men aged 40-70 years,
and prevalence increases with age
 Primary ED (ie, the man has never been able to
attain or sustain erections) is rare and is almost
always due to psychologic factors (guilt, fear of
intimacy, depression, severe anxiety) or
clinically obvious anatomic abnormalities.
 Most often, ED is secondary (ie, a man who
previously could attain and sustain erections no
longer can). Over 80% = have an organic
etiology. However, in many men with organic
disease, ED leads to secondary psychologic
difficulties that compound the problem.
What is the aetiology of ED?

25. For details see: Siroky,
Mike B. Handbook of
I.M.P.O.T.E.N.C.E Urology 2003
Inflammatory Prostatitis, urethritis
Mechanical Peyronie’s Disease, chordee
Psychological Depression, performance anxiety, stress, relationship
difficulties
Occlusive vascular Art: Hypertension, smoking, hyperlipidemia, DM.,
peripheral vascular disease
Ven: venous occlusion due to anatomical or
degenerative changes
Trauma Pelvic fracture, SC inj, penile trauma
Endocrine Hypogonadism, hyperprolactinemia, hypo +
hyperthyroidism
Neurologic Parkinsons, multiple sclerosis, spina bifida, pelvic
surgery, peripheral neuropathy
Chemical Anti-HTN, anti-arrhythmics, antidepressants,
anxiolytics, anti-androgens, anticonvulsants, alcohol,
marijuana, anti-parkonson drugs, LHRH analogues
Extra factors Prostatectomy, old age, CRF, cirrhosis

26.  ED is more prevalent among patients with
atherosclerotic peripheral vascular disease,
hypertension, diabetes mellitus (75% of diabetic pts),
hypercholesterolemia, and heart disease and among
men who smoke cigarettes.
Psychogenic ED Organic ED
ED caused exclusively by Caused exclusively by
emotional stress or psychiatric vascular, neurologic,
disease = 10% - 50% of all endocrine, or other physical
cases disease = 50% - 80%
 In the majority of impotent men, erectile impairment
has both a psychological and an organic basis.

27. How to diagnose & evaluate ED?
 History
 Examination
 Investigation

28. HISTORY
 Sexual
 Some symptoms suggest psychogenic ED, and others suggest
organic disease.
 A psychogenic cause is suggested by the sudden onset of ED
or the presence of ED under some circumstances but complete
erection at other times.
 In contrast, gradual deterioration of erectile quality over
months or years with preservation of libido suggests organic
disease.
 Psychological Evaluation

29. HISTORY
 Medical
 Inquiries should be made about: DM, HTN, smoking,
hypercholesterolemia, and hyperlipidemia as well as
about liver, renal, vascular, neurologic, psychiatric,
and endocrine disease.
 Surgical History
 Abdominal, pelvic, perineal
 Drug History
 Androgenic substances are associated with decreased
serum testosterone levels and decreased libido.

30. EXAMINATION
 Full Physical
 Body habitus, 2ndry sexual characteristics
 CVS, abdomen, neurological (bulbocavernosus reflex
is used to assess integrity of S2-4)
 External Genitalia
 Penis: Phimosis, penile lesions
 Testis: size, consistency
 DRE

31. INVESTIGATION
 LAB:
 Recommended: Fasting glucose, lipid profile,
hormonal profile
 Others: thyroid, PSA, prolactin

32. INVESTIGATION
 Specialized Evaluations:
 Indicated for failure of ttt, peyronie’s disease, 1ry ED,
history of surgery/trauma, complicated endocrine or
neuropsychiatric disorder
A. Vascular Evaluation
B. Neurologic Evaluation
C. Psychologic Evaluation
D. Hormonal Evaluation

33.  1st line vascular evaluation: Intracavernosal
injection
 Allows bypass of neurologic and hormonal influences,
directly evaluates penile blood flow
 Alprostadil (10 – 20 μg) alone, or a combination of
papaverine + phentolamine (ie Bimix), or all three (ie
Trimix).
 Compress needle site manually to prevent hematoma

34.  2nd line vascular evaluation:
 Duplex U/S: measures penile blood flow; most
reliable and least invasive assessment of ED
 Color Doppler U/S: measures arterial peak systolic
velocity value (N:>35 cm/s) and end diastolic velocity
(N:<5 cm/s)
 Cavernosography: measures penile blood flow
following intracavernosal inj of contrast and
induction of artificial erection. Can identify venous
leakage.

35. Venous leak (veno-occlusive
insufficiency).
Bilateral (a and b) Doppler
waveforms of the cavernosal
arteries at 25 min post-injection of
prostaglandin E demonstrate a
high peak systolic velocity (>40
cm/s), which excludes arterial
insufficiency as a cause of erectile
dysfunction in this patient.
However, a persistent diastolic flow
velocity of more than 5 cm/s is
suggestive of venous leak.

36.  2nd line vascular evaluation:
 Selective Penile Arteriography: to specifically assess a
defective/ruptured branch of cavernous art.
A. Arterial phase of right pudendal arteriography demonstrating obvious
extravasation (arrow) at right penile artery.
B. Venous phase image of right pudendal arteriography demonstrating
expansion of extravasation (arrow) and opacified penile veins.

37. TREATMENT
 Psychosexual therapy
 Aims to understand and address the underlying
psychological issues following proper evaluation
 Instructs the pt on information regarding sex
education, partner communication and sexual
behavioral therapy

38. TREATMENT
 Oral Medication
PDE5 (phosphodiesterase type-5) inhibitors (ex.
Sildenafil = viagra, tadalafil = cialis, vardenafil =
levitra)
 Blocks the breakdown of cGMP, thus maintaining
erection
 Sexual stimulation is still needed to initiate erection
 Adverse Effects: headache, visual disturbance
 Contraindication: pts on nitrates, recent MI, recent
stroke, unstable angina

39. TREATMENT
 Androgen Replacement Therapy: indicated for
hypogonadism. Available in oral, IM, patch & gel
forms. In older men, PSA must be checked before
and during ttt.
 Intraurethral pellet therapy: using a synthetic
PGE-1 pellet administered into the urethra.
Unavailable in Egypt.
 Intracavernosal therapy: Alprostadil/Caverjet
(synthetic PGE1) enhances cavernosal smooth
muscle relaxation. The needle is inserted at right
angles into the corpus cavernosum on the lateral
aspect of the penile shaft. A/E = priapism, pain,
hematoma

40. TREATMENT
 Alternative therapy
 Vacuum erection device: uses vacuum chamber, pump and
constriction device to increase blood flow into the penis and
maintain rigidity via constriction band

41. TREATMENT
 Alternative therapy
 Penile prosthesis: may be semi-rigid, malleable or
inflatable.
 Inserted surgically into the corpora to provide sufficient
size & rigidity for sexual intercourse. A/E = erosion,
infection, mechanical failure

42. …THANK YOU