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ERECTILE DYSFUNCTION
Place stress on your relationship?
ANATOMY OF THE PENIS
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.
BLOOD SUPPLY OF THE PENIS
 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.
• Venous drainage is both intra + extra cavernosal
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.
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.
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
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.
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.
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.
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.
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
• This triggers increased arterial blood flow
into sinusoidal spaces, relaxation of
cavernosal smooth muscle, and opening of
vascular spaces
 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
PHYSIOLOGY
 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).
 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
 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.
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.
PHASES OF ERECTION
Phase Term Description
0 Flaccid phase Cavernosal smooth ms contracted; sinusoids
empty; minimal arterial flow
1 Latent (filling)
phase
Increased pudendal artery flow; penile
elongation
2 Tumescent phase Rising intracavernosal pressure; erection
forming
3 Full erection
phase
Increased cavernosal pressure (100 mmHg)
causes penis to become full erect
4 Rigid erection
phase
Further increases in pressure (to several
hundred mmHg) + ischiocavernosal muscle
contraction
5 Detumescence
phase
Following ejaculation, sympathetic discharge
resumes; there is smooth muscle contraction
and vasonstriction; reduced arterial flow; blood
is expelled from sinusoidal spaces
SO WHAT IS IMPOTENCE OR ERECTILE
DYSFUNCTION?
The persistent inability to achieve or maintain a penile
erection sufficient for sexual intercourse
 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?
I.M.P.O.T.E.N.C.E
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
For details see: Siroky,
Mike B. Handbook of
Urology 2003
 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.
 In the majority of impotent men, erectile impairment
has both a psychological and an organic basis.
ED caused exclusively by
emotional stress or psychiatric
disease = 10% - 50% of all
cases
Psychogenic ED
Caused exclusively by
vascular, neurologic,
endocrine, or other physical
disease = 50% - 80%
Organic ED
How to diagnose & evaluate ED?
 History
 Examination
 Investigation
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
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.
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
INVESTIGATION
 LAB:
 Recommended: Fasting glucose, lipid profile,
hormonal profile
 Others: thyroid, PSA, prolactin
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
 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
 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.
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.
 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.
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
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
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
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
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
Erectile Dysfunction Treatment Information by Premier Men's Medical Center

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Erectile Dysfunction Treatment Information by Premier Men's Medical Center

  • 1. ERECTILE DYSFUNCTION Place stress on your relationship?
  • 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.
  • 4.
  • 5. BLOOD SUPPLY OF THE PENIS  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. • Venous drainage is both intra + extra cavernosal
  • 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.
  • 10.
  • 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
  • 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) phase Increased pudendal artery flow; penile elongation 2 Tumescent phase Rising intracavernosal pressure; erection forming 3 Full erection phase Increased cavernosal pressure (100 mmHg) causes penis to become full erect 4 Rigid erection phase Further increases in pressure (to several hundred mmHg) + ischiocavernosal muscle contraction 5 Detumescence phase Following ejaculation, sympathetic discharge 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. I.M.P.O.T.E.N.C.E 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 For details see: Siroky, Mike B. Handbook of Urology 2003
  • 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.  In the majority of impotent men, erectile impairment has both a psychological and an organic basis. ED caused exclusively by emotional stress or psychiatric disease = 10% - 50% of all cases Psychogenic ED Caused exclusively by vascular, neurologic, endocrine, or other physical disease = 50% - 80% Organic ED
  • 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