The document discusses the physiology of penile erection and the pathophysiology and management of erectile dysfunction. It covers the historical understanding of erection from ancient times through modern discoveries. Key points include that erection is caused by arterial inflow exceeding venous outflow due to relaxation of penile smooth muscle and compression of veins. Nitric oxide and phosphodiesterases play important roles. Erection involves reflex, psychogenic and nocturnal types triggered by various neural pathways and neurotransmitters like nitric oxide and endothelin.
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Physiology of penile erection, pathophysiology evaluation & management of ed
2. Historical Aspects
First description of erectile dysfunction dates
from about 2000 BC and was set down on
egyptian papyrus.
Two types:
natural - the man is incapable of accomplishing sex
supernatural - evil charms and spells.
Hippocrates ascribed it to excessive
horseback riding.
Aristotle- three nerves carry spirit and
energy to the penis, erection is produced by
influx of air
3. Leonardo da Vinci (1504) noted a large
amount of blood in the erect penis of hanged
men and doubted on the concept of the air-filled
penis
Leonardo da Vinci –
“The penis does not obey the order of its master,
who tries to erect or shrink it at will. Instead, the
penis erects freely while its master is asleep. The
penis must be said to have its own mind, by any
stretch of the imagination.”
4. In 1585 Ambroise Pare gave an accurate
account of penile anatomy and concept of
erection
Pare wrote - “When the man becomes
inflamed with lust and desire, blood rushes
into the male member and causes it to become
erect”
Many theories have since been added to
explain the hemodynamic events during
erection and detumescence
In the 19th century, venous occlusion was
thought to be the main factor in achieving and
5. Much of the current understanding of erectile
physiology wasn’t gained until the 1980s and
1990s
An important breakthrough in the understanding
of neural influences was the identification of
nitric oxide (NO) as the major neurotransmitter
for erection and of phosphodiesterases (PDEs)
for detumescence.
The importance of ion channels (potassium and
calcium) and Rho/ Rho kinase pathways in
contraction and relaxation of smooth muscle
6. Functional Anatomy of the
Penis
Composed of three cylindrical structures: the
paired corpora cavernosa and the corpus
spongiosum (which houses the urethra),
covered by a loose subcutaneous layer and skin
7. Tunica Albuginea
Tunica affords great
flexibility, rigidity, and tissue
strength to the penis
Tunica covering of the
corpora cavernosa-
bilayered structure
•inner circular and outer longitudinal layers of the tunica
albuginea, as well as the intracavernous pillars that act
as struts to augment the septum and provide essential
support to the erectile tissue.
•The longitudinal layer is absent in the ventral groove
housing the corpus spongiosum.
8. External Penile Support
2 ligamentous structures:
1. fundiform ligament arises from Colles‘ fascia and
is lateral, superficial, and not adherent to the
tunica albuginea of the corpora cavernosa.
2. suspensory ligament
9. Fundiform ligament fundiform
ligament
It runs from the level of
the pubic bone, laterally
around the sides of
the penis like a sling,
and then unites at the
base of the penis
before going to
the septum of
the scrotum.
10. Suspensory ligament
suspensory ligament
arises from Buck's
fascia and consists of
two lateral bundles and
one median bundle,
which circumscribe the
dorsal vein of the
penis. Its main function
is to attach the tunica
albuginea to the pubis
and thus it provides
support for the mobile
portion of the penis.
11. Corpora Cavernosa
The corpora cavernosa comprise two
spongy, paired cylinders contained in the
thick envelope of the tunica albuginea
They are supported by a fibrous skeleton
that includes the tunica albuginea, the
septum, the intracavernous pillars, the
intracavernous fibrous framework, and the
periarterial and perineural fibrous sheath
12. Septum between the two corpora cavernosa is
incomplete
Flaccid state, the blood slowly diffuses from
the central to the peripheral sinusoids and the
blood gas levels are similar to those of venous
blood.
Erect, the rapid entry of arterial blood to both
the central and the peripheral sinusoids
changes the intracavernous blood gas levels
to those of arterial blood
14. Arteries
The internal pudendal artery
becomes the common penile
artery after giving off a
branch to the perineum
Later 3 branches
Dorsal artery is responsible
for engorgement of the glans
during erection
The cavernous artery effects
tumescence of the corpus
cavernosum
15. Veins
tiny venules from corpora form
the subtunical venous plexus
and exit as the emissary veins
superficial dorsal vein drains
into saphenous veins
deep dorsal vein drain into
periprostatic venous plexus
cavernous and crural veins join
periurethral veins to form the
internal pudendal veins
16. Hemodynamics and Mechanism of
Erection and Detumescence
Corpora Cavernosa
In the flaccid state, smooth muscles are
tonically contracted, allowing only a small
amount of arterial flow for nutritional
purposes
Sexual stimulation triggers release of
neurotransmitters from the cavernous
nerve terminals. This results in relaxation
of these smooth muscles and the
following events
17. Phases of erection:
1. dilation of the arterioles and arteries by increased
blood flow
2. trapping of the incoming blood by the expanding
sinusoids
3. compression of the subtunical venous plexuses,
reducing venous outflow
18. 4. stretching of the tunica to its capacity, which
occludes the emissary veins (decreases
venous outflow to a minimum)
5. an increase in PO2 (to about 90 mm Hg) and
intracavernous pressure (around 100 mm
Hg), which raises the penis to the erect state
6. a further pressure increase (to several
hundred millimeters of mercury) with
contraction of the ischiocavernosus muscles
19. Phases of detumescence
1. initial detumescence – transient intracorporeal
pressure increase, indicating the beginning of
smooth muscle contraction against a closed
venous system
2. slow detumescence - slow pressure decrease,
suggesting a slow reopening of the venous
channels with resumption of the basal level of
arterial flow
3. fast detumescence - fast pressure decrease with
fully restored venous outflow capacity
20. Blood flow and intracavernous pressure changes
during the seven phases of penile erection and
detumescence
0 - flaccid; 1- latent; 2 - tumescence; 3 - full erection; 4 - rigid
erection;
5 - initial detumescence; 6 - slow detumescence; 7 - fast
21. Hemodynamics of Corpus
Spongiosum and Glans Penis
During erection, the arterial flow increases in a similar
manner however, the pressure in the corpus
spongiosum and glans is only one third to one half that
in the corpora cavernosa- No outer longitudinal tunic
layer (no venous occlusion)
22. Neuroanatomy and
Neurophysiology of Penile Erection
Peripheral Pathways
Innervation of penis - both
autonomic (sympathetic and
parasympathetic)
and somatic (sensory and motor)
Sympathetic and parasympathetic nerves
merge to form the cavernous nerves - effect the
neurovascular events during erection and
detumescence
Somatic nerves- 1° responsible for sensation
and the contraction of the bulbo/ischio-
23. Autonomic Pathways
Sympathetic pathway originates from the 11th
thoracic to the 2nd lumbar spinal segments
Parasympathetic pathway arises from S2-S4
Cavernous nerves are branches of the pelvic
plexus that innervate the penis
cavernous nerves are easily damaged during
radical excision of the rectum, bladder, and
prostate
25. Somatic Pathways
The somatosensory pathway originates at the
sensory receptors in the penile skin, glans, and
urethra and within the corpus cavernosum
The free nerve endings are derived from thin
myelinated Aδ and unmyelinated C fibers
Nerve fibers converge to form bundles of the
dorsal nerve of the penis, which become the
pudendal nerve
Onuf's nucleus in the 2nd to 4th sacral spinal
segments is the center of somatomotor penile
innervation
Contraction of the ischiocavernosus muscles
produces the rigid-erection phase. Rhythmic
26. Supraspinal pathways and
centers
Visually evoked sexual arousal has 3
components associated with neuroanatomic
regions:
1. perceptual-cognitive component that recognizes the
visual stimuli and is performed in the bilateral inferior
temporal cortices;
2. emotional/ motivational component that processes
sensory information with motivational states and is
performed in the right insula, right inferior frontal
cortex, and left cingulate cortex (paralimbic areas);
and
3. physiologic component that coordinates the
endocrine and autonomic functions and is performed
in the left anterior cingulate cortex.
29. 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.
30. 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.
Psychogenic erection is absent in patients with
lesions above T9.
Sacral spinal cord injury retain psychogenic
erectile ability even though reflexogenic erection
31. 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.
32. Neurotransmitters
α-Adrenergic nerve fibers and receptors
- norepinephrine has generally been
accepted as the principal neurotransmitter to
control penile flaccidity and detumescence
Endothelin, a potent vasoconstrictor produced
by the endothelial cells, has also been
suggested to be a mediator for detumescence
33. Flaccidity and Detumescence
Intracorporeal smooth muscle remain in a
semicontracted (flaccid) state due to three factors:
1. Intrinsic myogenic activity
2. Adrenergic neurotransmission
3. Endothelium-derived contracting factors such as angiotensin
II, PGF2α, and endothelins
Detumescence after erection may be a result of
cessation of NO release,
the breakdown of cGMP by phosphodiesterases, or
sympathetic discharge during ejaculation
34. Erection
NO released from nonadrenergic,
noncholinergic neurotransmission and from
the endothelium is the principal
neurotransmitter mediating penile erection
NO increases the production of cGMP, which
in turn relaxes the cavernous smooth muscle
35. Central Neurotransmitters and
Neural Hormones
A variety of neurotransmitters (dopamine,
norepinephrine, 5-HT, and oxytocin) and
neural hormones (oxytocin, prolactin)
have been implicated in regulation of
sexual function.
37. Molecular Mechanism of Smooth
Muscle Contraction
Smooth muscle contraction and relaxation
are regulated by intracellular free calcium
acting through calmodulin.
38. Norepinephrine, endothelins and PGF2α activate receptors on
smooth muscle cells to initiate the cascade of reactions that
result in elevation of intracellular calcium concentrations
40. Latch State
Smooth muscle has the ability to maintain tension for
prolonged periods with minimal energy expenditure.
This efficiency has been termed the latch state and is
critical for sustaining the “basal” tone of the smooth
muscle.
It has been proposed that dephosphorylated myosin
remains bound to actin in the high-affinity state.
Others have proposed that calponin binds actin and
myosin to stabilize cross-bridge interactions and slow
the rate of detachment.
41. Molecular Mechanism of Smooth
Muscle Relaxation
process of relaxation requires a decreased
intracellular Ca2+ concentration and increased
myosin light-chain phosphatase activity.
43. Calmodulin then dissociates from myosin
light-chain kinase and inactivates it.
Myosin is dephosphorylated by myosin light-
chain phosphatase and detaches from the
actin filament, and the muscle relaxes.
Another mechanism of smooth muscle
relaxation is through cyclic adenosine
monophosphate (cAMP) and cGMP, which
are the two major second messengers
involved in smooth muscle relaxation.
45. KEY POINTS: SMOOTH MUSCLE
RELAXATION CAUSES ERECTION
Relaxation of the cavernous smooth muscle is the key to
penile erection.
Nitric oxide release initiates the erection process, and helps
maintain erection.
Upon entering the smooth muscle cells, NO stimulates the
production of cGMP.
Cyclic GMP activates protein kinase G, which in turn opens
potassium channels and closes calcium channels.
Low cytosolic calcium favors smooth muscle relaxation.
The smooth muscle regains its tone when cGMP is
degraded by phosphodiesterase
47. SO WHAT IS ERECTILE
DYSFUNCTION ?
The persistent inability to achieve or maintain
a penile erection sufficient for sexual
intercourse
48. Incidence and Epidemiology
35% of married men aged 60 years and older suffer from
erectile impotence
MMAS (Massachusetts Male Aging Study) study, between
the ages of 40 and 70 years, the probability of
• complete ED was from 5.1% to 15%,
• moderate dysfunction was from 17% to 34%, and
• mild dysfunction was about 17%.
NHSLS (National Health and Social Life Survey) study
revealed the prevalance rates for ED at
• 7% for ages 18 to 29 years, 9% for ages 30 to 39,
• 11% for ages 40 to 49, and 18% for ages 50 to 59.
Worldwide prevalence of ED, 24 international studies were
reported between 1993 and 2003
- Before age 40 the rate was 1% to 9%
- From 40 to 59 it ranged from 2 - 9% to as high
as 20 - 30%
49. Risk Factors for ED
General health status
Diabetes mellitus
Cardiovascular disease
Concurrence of other GU diseases
Psychiatric or psychological disorders
Chronic diseases
Smoking
Medications
Hormonal factors also serve as well-defined risk factors
51. Classification of Erectile
Dysfunction
Organic Psychogenic
1. Vasculogenic
A. Arteriogenic
B. Cavernosal
C. Mixed
1. Generalized
A. Generalized unresponsiveness
1. Primary lack of sexual arousability
2. Aging-related decline in sexual arousability
B. Generalized inhibition
1. Chronic disorder of sexual intimacy
2. Neurogenic 2. Situational
A. Partner-related
1. Lack of arousability in specific relationship
2. Lack of arousability owing to sexual object
preference
3. High central inhibition owing to partner conflict or
threat
B. Performance-related
1. Associated with other sexual dysfunction/s (e.g.,
rapid ejaculation)
2. Situational performance anxiety (e.g., fear of failure)
C. Psychologic distress or adjustment related
1. Associated with negative mood state (e.g.,
3. Anatomic
4. Endocrinologic
52. Functional classification of
impotence
It is unlikely for an individual patient’s impotence to derive solely
from one source. Most cases have a psychogenic component of
varying degree, and systemic diseases and pharmacologic effects
can be concomitant and causative
53. Psychogenic
Previously, psychogenic impotence was believed to be
most common, thought to affect 90% of impotent men
Two possible mechanisms have been proposed to
explain the inhibition of erection in psychogenic
dysfunction:
1. direct inhibition of the spinal erection center by the brain as an
exaggeration of the normal suprasacral inhibition
2. excessive sympathetic outflow or elevated peripheral
catecholamine levels
54. Neurogenic
10% to 19% of ED is neurogenic
MPOA, the PVN, and the hippocampus are important
integration centers for sexual drive and erection, and
pathologic processes in these regions, such as
Parkinson's disease, stroke, encephalitis, or temporal
lobe epilepsy, are often associated with ED.
In men with a spinal cord injury, its nature, location, and
extent largely determine erectile function
Reflexogenic erection is preserved in 95% of patients
with complete upper cord lesions
Introduction of nerve-sparing radical prostatectomy has
reduced the incidence of impotence from 100% to 30 -
50%
55. In cases of pelvic fracture, ED can be a result
of cavernous nerve injury or vascular
insufficiency or both.
In men with posterior urethral injury, early
realignment has been associated with better
potency preservation rate relative to delayed
anastomosis (ED rate 34% vs. 42%)
(Mouraviev et al, 2005).
56. In diabetics, impairment of neurogenic and
endothelium-dependent relaxation results in
inadequate NO release (Saenz de Tejada et al,
1989a).
A corpus cavernosum electromyograph has
been developed and refined for diagnosis of
various conditions affecting the penis
(including autonomic neuropathy), but the
clinical utility of this device is still under
investigation
57. Endocrinologic
Hypogonadism is a frequent finding in the impotent
population
Mulligan and Schmitt (1993) concluded that
testosterone
1. enhances sexual interest
2. increases the frequency of sexual acts
3. increases the frequency of nocturnal erections but has
little or no effect on fantasy-induced or visually stimulated
erections
Hypogonadotropic hypogonadism can be congenital
or caused by a tumor or injury
Hypergonadotropic hypogonadism may result from a
tumor, injury, surgery, or mumps orchitis
Hyperprolactinemia from a pituitary adenoma or drugs,
results in both reproductive and sexual dysfunction
58. Arteriogenic
Atherosclerotic or traumatic arterial occlusive disease
decrease the perfusion pressure and
arterial flow to the sinusoidal spaces
increases time to maximal erection
and decreases the rigidity of the erect
penis
59. Common risk factors associated with arterial
insufficiency include
hypertension,
hyperlipidemia,
cigarette smoking,
diabetes mellitus,
blunt perineal or pelvic trauma,
pelvic irradiation
Focal stenosis of the common penile artery is
most often seen in young patients who have
sustained blunt pelvic or perineal trauma
Long-distance cycling is also a risk factor for
vasculogenic and neurogenic ED
61. Cavernous (Venogenic)
Failure of adequate venous occlusion has been
proposed as one of the most common causes of
vasculogenic impotence
Veno-occlusive dysfunction may result from a variety
of pathophysiologic processes:
1. Degenerative tunical changes (Peyronie's disease, old age,
and diabetes) or traumatic injury to the tunica albuginea (penile
fracture) can impair the compression of the subtunical and
emissary veins
2. Structural alterations in the fibroelastic components of the
trabeculae, cavernous smooth muscle, and endothelium may
result in venous leakage
3. Insufficient trabecular smooth muscle relaxation can cause
inadequate sinusoidal expansion and insufficient compression of
62. Antihypertensive Agents
Diuretics- Thiazides showed a significant increase in ED
when compared with placebo
Treatment of Mild Hypertension Study (TOMHS), in which the
prevalence of ED at 2 years in men taking low-dose thiazide was twice
that of those taking placebo or alternative agents (Grimm et al, 1997).
β-Adrenergic Blockers- 10% of adrenoceptors in the penile
tissue are of the β type, and their stimulation is thought to
mediate relaxation
β antagonists also exert an inhibitory effect within the CNS, perhaps
leading to lowered sex hormone levels
nonselective drugs such as propranolol were associated with a higher
prevalence of ED than placebo or ACE inhibitor.
Newer agents with higher selectivity for the β1 adrenoceptor, such as
acebutolol, have shown a substantial reduction in ED
63. Antihypertensive Agents
α-Adrenoceptor Blockers- positive effect on
erection for α antagonists, particularly those acting
on the α1 receptor - drugs such as doxazosin were
not associated with complaints of ED
Angiotensin-Converting Enzyme Inhibitors-
ACE inhibitor captopril did not cause any
significant adverse effect on sexual function
Angiotensin II receptor antagonists, have a
beneficial effect on sexual dysfunction
Calcium Channel Blockers- no adverse effect on
erection
66. Diabetes Mellitus
Common chronic disease, affecting 0.5% to 2%
worldwide
Prevalence of ED is three times higher in diabetic men
(28% versus 9.6%) occurs at an earlier age and
increases with disease duration.
In 12% of diabetic men, deterioration of sexual function
can be the first symptom.
The presence of ED is associated with more than 14
times higher risk for silent coronary artery disease,
higher major cardiovascular morbidity, and mortality in
diabetic men.
67. Chronic Renal Failure
Sexual dysfunction has been reported in 20%
to 50% of men with chronic renal failure
among men receiving hemodialysis - 45%
prevalence of self-reported severe ED
Uremia decreases NO bioavailability
Automonic neuropathy is common
complication of ESRD
68. Iatrogenic impotence :
Radical prostatectomy 43% to 100%
Perineal prostatectomy for benign 29%
APR - 15% to 100%
External sphincterotomy 2% to 49% .
Nerve-sparing radical prostatectomy reduced
the incidence 100% to 30%-50%
Pelvic fracture, ED result of cavernous n’ injury
or vascular insufficiency or both .
69. Other diseases
severe pulmonary disease (fear aggravating
dyspnea during sexual intercourse)
angina, heart failure, or myocardial infarction
can become impotent from anxiety,
depression, or arterial insufficiency
Liver cirrhosis,
scleroderma,
cachexia
70. Primary Erectile Dysfunction
Primary ED refers to a lifelong inability to initiate or
maintain erections, beginning with the first sexual
encounter
It is almost always due to psychologic factors (guilt,
fear of intimacy, depression, severe anxiety)
Physical cause resulting from mal-development of the
penis or the blood and nerve supply
Micropenis- self explanatory
71. MEDICAL HISTORY
Evaluate role of underlying medical conditions (e.g.,
atherosclerosis, DM) and comorbidities.
Assess potential role of medication.
Past H/O: Prostatectomy, APR, Pelvic trauma.
Differentiate potential organic and psychogenic causes .
72. Characteristic
Organic Psychogenic
Onset Gradual Acute
Circumstances Global Situational
Course Constant Varying
Noncoital erection Poor Rigid
Psychosexual problem Secondary Long history
Partner problem Secondary At onset
Anxiety and fear Secondary Primary
73. SEXUAL HISTORY
Interview conducted face-to-face.
Ensure pt trust, comfort, and openness.
Ascertain severity, onset, and duration of problem, as well as
presence of concomitant medical or psychosocial factors.
Determine presenting complaint is primary sexual problem or other
aspects (desire, ejaculation, orgasm) are involved.
74. PSYCHOSOCIAL HISTORY
Assess pt's past & present partner relationships.
Sexual dysfunction may affect pt's self-esteem and
coping ability, social relationships and occupational
performance.
Ensure pt is involving in monogamous, heterosexual
relationship.
Organic and psychogenic factors often coexist.
75. PHYSICAL EXAMINATION
Screening for medical risk factors or sec sexual
characteristics,
Assessment of CVS, CNS, and genital systems.
Obvious cause (e.g., micropenis, chordee, Peyronie's
plaque.
Test for genital & perineal sensation and
bulbocavernosus reflex (BCR) useful in assessing
possible neurogenic impotence .
76. LAB TESTS
Fasting glucose, lipids & testosterone.
Optional : indicated by history & P/E .
( Prolactin, LH, FSH, Thyroid function.)
PSA measured >50 yrs age ,F/H ca prostate
77. Indications for specialized
evaluation
Primary ED (not caused by organic disease or psychogenic
disorder).
Young patients with a history of pelvic or perineal trauma,
who could benefit from potentially curative revascularisation
surgery or angioplasty.
Patients with penile deformities that might require surgical
correction (e.g., Peyronie’s disease, congenital penile
curvature).
Patients with complex psychiatric or psychosexual disorders.
Patients with complex endocrine disorders.
Specific tests may be indicated at the request of the patient
or his partner.
Medico-legal reasons (e.g., implantation of penile prosthesis
to document end stage ED, sexual abuse
79. VASCULAR
Most commonly performed diagnostic procedure.
Intracavernous inj of vasodilator - genital / Audiovisual
sexual stimulation, and assessment of erection by an
observer.
It bypass neurologic & hormonal influences evaluate
vascular status of penis directly .
COMBINED INTRACAVERNOUS INJECTION AND STIMULATION (CIS)
80. CIS
False-neg in 20% with borderline arterial inflow.
False-positive occur most commonly because of pt
anxiety, needle phobia, or inadequate dosage.
Pt should not leave until penis becomes flaccid
spontaneously or by injection of phenylephrine.
500 μg/mL, given 1 mL every 3 to 5 minutes until
detumescence.
81. DUPLEX ULTRASONOGRAPHY
CIS & blood flow measurement by duplex U/S .
Each cavernous artery assessed.
Cavernous arterial diameters recorded.
PSV <25 cm/s - sensitivity of 100% & specificity of 95% -
severe artery insuff. (Normal PSV35cm/s)
Severe unilateral cavernous artery insufficiency -
asymmetry of PSV > 10 cm/s.
82. Vascular ED, cavernous artery dia increase is usually <
75% & luminal dia rarely exceeds 0.7 mm .
Anxiety or fear of inj lead to poor erection, scanning
repeated after stimulation / redosing.
83. Duplex U/S in Veno-occlusive
Dysfunction
High systolic flow (>25 cm/s PSV) and persistent end-
diastolic flow velocity(>5 cm/s) accompanied by quick
detumescence after self-stimulation.
RI = PSV - EDV/PSV.
During tumescence until full rigidity, diastolic flow is
antegrade RI remains <1.
RI >0.9 associated with normal results during DICC in
90% .
RI < 0.75 associated with venous leakage 95%.
84. DYNAMIC INFUSION CAVERNOSOMETRY
AND CAVERNOSOGRAPHY (DICC)
Simultaneous saline infusion and intracavernous pressure
monitoring to assess penile outflow system.
Intracavernous inj , followed by measurement of maintenance flow
rate, pressure drop
Flow rate required to maintain erection at intracavernous pressure of
> 100 mmHg is < 3 to 5 ml/min.
Pressure decrease in 30sec from 150mmHg is < 45 mmHg.
85. PHARMACOLOGIC
CAVERNOSOGRAPHY
Cavernosography done after cavernosometry.
Opacification of corpora cavernosa but minimal / no
visualization of veins or corpus spongiosum- N
Reserved for young men - candidates for penile vascular
surgery - pelvic trauma or primary ED.
87. PHARMACOLOGIC ARTERIOGRAPHY
Best indication is young pt with ED sec to traumatic a’ disruption or
perineal compression injury.
Intracavernous inj of vasodil agent followed by selective cannulation
of internal pudendal a’ and inj of contrast.
Anatomy and radiographic appearance of internal pudendal, and
penile arteries evaluated.
patent common penile, dorsal, and cavernous
arteries
nonvisualization of common penile artery
and its branches
88. HISTORICAL AND INVESTIGATIONAL
EVALUATIONS OF PENILE BLOOD FLOW
PENILE BRACHIAL PRESSURE INDEX: PBI 0.7 or
less indicate arteriogenic impotence .
PENILE PLETHYSMOGRAPHY (Penile Pulse Volume
Recording):
Vasculogenic ED, waveform - slow upstroke, low rounded peak,
slow down stroke, no dicrotic notch.
INFRARED SPECTROPHOTOMETRY : quantitative
measurements of vascular physiology of penile erection.
89. INVESTIGATIONAL …
RADIOISOTOPIC PENOGRAPHY: 99mTc-labeled RBCs to
quantify changes in penile blood volume after injection of vasoactive
substance .
MAGNETIC RESONANCE ANGIOGRAPHY : localize disease
processes from IIA down to int pudendal arteries .
CAVERNOUS SMOOTH MUSCLE CONTENT: At present,
cavernous biopsy for diagnosis of ED remains controversial
90. NEUROLOGIC
Specialized test for neurologic ED unnecessary.
Young age ,acute onset, normal/ excellent response on
PDE-5 inhibitors –N.ED.
Nerve conduction velocity studies, biothesiometry,
bulbocavernosus EMG, corpus cavernosus EMG –lack
sensitivity & reliability.
Penile thermal sensory testing - promising tool for
diagnosis of neurogenic ED .
91. PSYCHOLOGIC
Diagnostic interview mainstay of evaluation.
Current sexual problem and its history
Deeper causes of sexual dysfunction
Relationship &
Psychiatric symptoms.
Immediate causes –
fear of failure
performance anxiety
insufficient sexual stimulation
loss of attraction
relationship conflicts.
“Deeper” causes of psychogenic ED- unresolved
parental attachments, sexual identity, sexual trauma, and
cultural-religious taboos .
92. Minnesota Multiphasic Personality Inventory (MMPI)-2 is a
valuable tool for assessing pt's personality & its relevance to sexual
dysfunction.
Beck Depression Inventory is a self-reported test score above 18
considered indicative of significant clinical depression .
Short Marital Adjustment Test (for married couples) Dyadic
Adjustment Inventory (for unmarried people) to determine overall
relationship quality .
Psychological consultation is not indicated for most pts, very
useful in men with deep-seated psychological problems.
93. PSYCHOPHYSIOLOGIC
Nocturnal penile tumescence (NPT) monitoring - Halverson
Stamp test :Ring of postage stamps placed around the base of
penis ,at night break.
Sleep laboratory nocturnal penile tumescence and rigidity (NPTR);
RigiScan;
Documented presence of a full erection indicates neurovascular
axis is functionally intact -cause of ED is most likely psychogenic.
94. NPTR
Obscure cause of ED
No response to therapy
Planned surgical treatment
Legally sensitive case
Measurement of drug effects in placebo-controlled trials
Suspected psychogenic cause
Advantages - freedom from psychologic influences, ability to detect
sleep-related abnormalities.
Disadvantages of NPT evaluation - it is age dependent and costly,
ideally done with RigiScan in a sleep center.
95. NPTR …
Devices measure no of episodes, tumescence (strain gauges),
maximal penile rigidity, and duration of N.E.
Electroencephalography, electro-oculography, and EMG, with nasal
air flow, and O2 saturation to document REM sleep and hypoxia
(sleep apnea).
Pt is awakened during maximal tumescence, erection is
photographed and axial rigidity measured at tip of penis.
96. RIGISCAN
First automated, portable NPTR
recording.
Combines monitoring of radial
rigidity, tumescence, no & duration of
erectile events with portable sys -
used at home.
Collect data 3 separate nights for
maximum of 10 hrs/night
Consist of two loops: one is placed at
base of penis & other at coronal
sulcus. By constricting the loops,
device records penile tumescence &
radial rigidity at penile base and tip.
Measurement (initialization) first done
in office 15- 20 mts.
97. RIGISCAN RESULT ANALYSIS…
Radial rigidity > 70% - non buckling erection, and rigidity of < 40%
represents a flaccid penis.
Normal NPTR : 4-5 erectile episodes / night
Mean duration > 30 mts
↑ in circumference of > 3 cm at base and > 2 cm at tip
Maximal rigidity above 70% at both base & tip.
98. TWO EPISODES OF WELL-
SUSTAINED, COMPLETELY RIGID
NOCTURNAL ERECTIONS
TWO EPISODES OF POORLY
SUSTAINED, POORLY RIGID
NOCTURNAL ERECTIONS
RigiScan
99. SUMMARY
Medical and sexual history, physical examination, and basic laboratory
tests done regardless of treatment.
Oral medication, transurethral therapy- no further testing.
Intracavernous injection – CIS.
Venous –CIS, Duplex U/S , DICC.
Arterial / combined arterial & venous - CIS , Duplex U/S DICC &
pharmacologic arteriography.
Specialized neurologic procedures lack sensitivity & specificity-not
widely used or generally recommended .
Pts with complicated endocrine or psychiatric disorders referred for
specialized consultation and evaluation.
107. TESTOTERONE
RATIONALE:
Adequate amount of testosterone –essential.
Production of Nitric Acid synthase
Release of Nitric Oxide.
Increase GMP –Arteriolar dilation
Relaxation of corporeal
smooth muscle
108. Testosterone level below critical level –penile
erectile mechanism blunted or fails.
Critical androgen level – to be determined.
Combination of ED & Hypotestosteronemia –
Trial of supplemental androgen justified.
Normal value → 160 -500ng /dl.
112. Injectables:
Testosterone cypionate
Testosterone Enanthate.
Route: Deep IM
Dose: 200 to 250mg every 2w
Effect :
Supraphysiologic level - 72h.
Subphysiologic level - 10 -12days.
Supraphysiologic level –well Being Increase/ libido↑
Subphysiological level – Unpleasant Desire/ libido
↓
113. Transdermal:
Morning
Simulates normal circadian level
Patch:
Testoderm - 4 to 6mg – Scrotal patch.
Testoderm TTS - 5mg – Arm, Back Upper
Buttocks.
Androderm 2.5 or 5mg patch.
Adverse Effects:
Itching
Skin Irritation
Dermatitis
114. Gel
Androgel 1% - 50mg, 75mg, 100mg
Once daily -Morning
Pellets:
75mg of Testosterone / pellet
2 to 6 pellets (Subcutaneous)
Every 3 to 6 months
115. BUCCAL:
Adhere to Gum tissue above the Incisor.
30mg Testosterone.
Twice daily.
116. ORAL
First pass metabolism (liver)- Metabolically
inactive
200mg/ day.
Large dose toxic
Hepatitis
Cholestatic Jaundice
Hepatoma
Hepatocarcinoma
119. HCG
Every 3 months
Total & Free testosterone →Increase 50%
above
basal
Adequacy/ clinical End points of testosterone
Determination of plasma testosterone –
before next dose
Marginal Synergistic Effect -Testosterone +
PDE -5 inhibitors
120. Adverse Effects of Androgen
Therapy
Supra physiological level of Testosterone →↓
LH/ ↓ FSH –Infertility.
Breast Tenderness, Gynaecomastia
Erythrocytosis
Induce or worsen sleep Apnea
↑LDH
↓HDL -cardiovascular risk
↑ Thromboxane A2 & Platelet Aggregation
121. Androgen Replacement →Not induce
prostate cancer in normal prostate but
Exacerbation of occult cancer?
P/R, PSA,(TRUS Biopsy selected cases) –
Before Therapy.
127. PDE 5 Inhibitors:
Do not increase the NO level
Inhibit the breakdown of CGMP
So Enhances Erection
But without sexual stimulation –Inhibitors are
ineffective
128. PDE 5 inhibitors in special situation
PDE 5 inhibitors in DM is Effective
Improvement in ED and intercourse
satisfaction (IIEF) after 6 months of treatment
But relapse to nearly pretreatment level at 12
months (penson etal 2003)
129. Adverse Effects
PDE -5 inhibitors in other organs & Other
PDE inhibitors
Headache
Dyspepsia
Flushing
Myalgia & Back pain
Rhinitis
Visual disturbances – PDE -6 inhibitors
-Nonarteritic anterior ischemic optic
neuropathy (NAION)
130. PDE INHIBITORS/ CVS
PRINCETON CONSENSUS PANEL
TO evaluate the degree of risk associated with
sexual activity.
1. Low
2. Intermediate
3. High risk
131. Cardiovascular Risk Factors
Age
Male
Hypertension
DM
Smoking
Hyperlipidemia
Sedentary lifestyle
Family H/O –Premature coronary artery disease
133. PDE inhibitors not indicated
Myocardial infarction within previous 90 days
Un stable Angina or Angina during sexual
intercourse.
Class 2 or Great heart failure in previous 6 months.
Uncontrolled arrhythmias
Hypotension <90/ 50 mm Hg.
Uncontrolled HT > 170/ 100 mm Hg.
134. PDE inhibitors not indicated
Stroke within previous 6 months
Retinitis pigmentosa.
Tendency to develop priapism [Sickle cell
Anaemia, Leukemia].
Severe kidney or Hepatic dysfunction – Dose
adjustments.
141. Trimix
Papaverine 2.5ml (30mg/ ml)
Phentolamine 0.5ml (5mg/ ml)
Alprostadil 0.05ml (500ug/ml)
Triple drug combination
As effective as Alprostadil alone lower
Incidence of
painful erection.
Indications:
PGE1 or Papaverine + Phentolamine
Therapy
Failure
Penile pain with PGE1
142. Other drug combination
VIP – 30ug + Phentolamine –(0.5 to 2mg)
CGRP 5ug + Alprostadil -10Ug
Quadmix
Papaverine 30mg/ ml
Phentolamine 2mg /ml
PGE1 20ug/ ml
Forskolin 1000ug/ ml
Ind: Triple therapy failure
143. Adverse effects:
Priapism – Alprostadil -5 times lower than
Papaverine or Papaverine + Phentolamine
Fibrosis - Alprostadil 10 times lower than
Papaverine or Papaverine + Phentolamine
144. How to administer
First injection under supervision
1dose – small dose
Increase incremental dose to achieve
sufficient erection
Goal :
To achieve adequate erection for
sexual intercourse but last for less than 1 hour
146. PDE 5 inhibitor + Intracavernous Injection
FDA not approved
Sildenafil + Trimix
(2/3 of Intracavernous injection failure)
147. INTRAURETHRAL THERAPY
PGE1 - Alprostadil
Mechanism of Action:
Inserted into Urethra – drug absorption by
corpus spongiosum → transportation to corpus
cavernosum (venous channels – circumflex,
emissary veins) → penile erection
148. MUSE – Medicated Urethral system
Semisolid pellet (3×1mm)
Administration into distal Urethra (3cm)
by a
applicator
Efficacy office trial →65%% successful
intercourse
Adverse effects
Penile pain
Hypotension
Syncope
149. Transdermal Therapy
Topiglan →PGE, (0.5 to 2mg) + Transdermal
permeation enhancer
AlproxTD –Enhancer driver Alprostadil gel
Limitation
Audiovisual / Tactile stimulation to achieve
erection.
150. Centrally Acting Drugs
Yohimbine –Alpha 2 antagonist
Trazadone –Antidepressant
Apomorphine –Dopaminergic Agonist
AUA –No efficacy of Yohimbine over placebo in
organic
ED
In severe ED – Trazadone no more effective
than placebo
Sublingual Apomorphine approved by
European authority.
151. Melanocortin Receptor Agonist (MC4R)
Modulate Erectile function / sexual
behaviour
Melaotan 11 - Subcutaneous 0.025mg/ kg
Intranasal PT- 141 (Melanocortin analog).
152. Vacuum constriction device :
Plastic cylinder
connected directly or by
a tubing to vacuum
generating source
(Manual or battery
operated)
After penis
engorgement by the
negative pressure
,Constriction ring
applied to the base of
penis to maintain
erection
Ring should not be
placed not longer than
30 mts
153. Erection different from normal erection
Useful : Malfunctioning penile prosthesis
Severe vascular insufficiency
( Intracavernous injection + VCD)
Not Useful:
Severe venous insufficiency
Arterial insufficiency
Fibrosis secondary to priapism
Infection
154. Patient satisfaction rate 68 to 83 %
Complications:
Penile pain
Numbness
Difficulty in ejaculation
Ecchymosis
Petechiae
156. Prosthetic surgery
Not considered
Situational ED
ED following conflict
ED due to reversible cause
157. Ideal Prosthesis:
That provide its recipient with a
penis that provides as closely as possible
normal penile flaccidity and erection
158. Penile Prosthesis Type
Prosthesis Type American Medical
system
Mentor
Corporation
Semirigid rod AMS Malleable600 Acu form
Positionable DuraII
Two –piece
inflatable
AMS Ambicor
Three piece
inflatable
AMS 700CX
AMS 700CXM
AMS 700uLTREX
159. Two piece inflatable penile prosthesis AMS
Ambicor
Three piece inflatable penile prosthesis
Mentor Titan
Three piece inflatable penile prosthesis
AMS Ultrex 700
167. Pump with tube placed in the pouch
All 3 tubes transposed
168. Connection between Pump and Cylinder
established
Reservoir placement in the Retropubic space
Through penoscrotal incision
169. Entry into Retropubic space through
External inguinal ring
Empty reservoir inserted into prevesical
space
Reservoir filled with normal saline ( 65 ml
)
Wound closed with suction drain
170. POST OF CARE
Urethral catheter, suction drain removed –
Nextday
Antibiotics -1 week
Oral Narcotics – 1week and then NSAIDS
Avoid lifting Heavy weight and heavy exercise to
prevent – Displacement of the reservoir
Ask the pt to keep penis over the lower
abdomen – To prevent ventral curvature of
penis.
171. After 1 month →Instruct to cycle the device.
Permission to begin coitus →When Inflation
without discomfort.
173. INFECTION
INCIDENCE: First time 1-3%
Revision surgery 7-18%
PREVENTION:
Treat UTI or cutaneous infection before
implantation surgery.
Shaving of operative area just before
surgery –To avoid bacterial colonization
Preparation of operative site for 10mts.
174. Broad spectrum antibiotics – 1h before surgery.
Paper drapes instead of cloth drapes
Prosthetic submerged in Antibiotic solution
175. INFECTION
Early: First few weeks following implantation.
Late: 6months to 1-2Y
Early: Gram negative Bacteria
Late: Staphylococcus epidermidis
Treatment:
1. Appropriate Antibiotics
2. Removal of Prosthesis
176. Reimplantation:
As soon as possible after device removal
Usually 2 to 3 months
Advantages:
Early Fibrosis →Easier to dilate
Scar contraction less
177. PERFORATION/ EROSION
Perforation – Intra operative event
Erosion – Post operatively
Perforation: 1. Crural perforation
2. Urethral perforation
Crural perforation:
More common with smaller dilator
Large dilator used to dilate the correct Tract
In distal dilation –Cross over to opposite side
may
occur.
178. Urethral perforation:
Abandon the procedure Urethral Catheter left in place
for 7 to 10 days.
Erosion:
Erosion into meatus or through glans
Treatment:
Removal – To avoid Infection
If erosion occurs one rod –Removal of that rod only.
Coitus possible with only one rod.
179. Poor Glans Support:
-Drooping appearance of Glans
-SST deformity (Deformity –Supersonic
transport while take off and landing)
Due to –Inadequate distal dilation
-Too short cylinders
Correction:
Re insert the longer cylinder
Dorsal plication.
180. Over sized cylinder or Rod
Pain
Erosion
Correction : Reoperation /smaller one
Pump complication: Pump migration
Correction: Revision –Relocation
Autoinflation: With physical activity
183. Principle of the surgery:
↑ Arterial flow in the cavernosal bed
↓Outflow –Venous surgery
Ideal candidate for arterial surgery
Young and psychologically stable
Without vascular risk factors –DM,HT,
Coronary heart
disease
185. Penile Arterial
Revascularization
Doppler USG
Common iliac arteriogram- To demonstrate the
adequacy of donor artery ( Inferior epigastric
artery)
Selective pudental arteriogram- To identify
lesion site
186. Anastomosis:
Between inferior epigastric artery and
dorsal penile artery
Between inferior epigastric artery and
Deep dorsal vein
Superficial femoral artery + Dorsal
penile artery (Saphenous vein graft)
187. GA or SA
Supine with legs abducted position
Preparation of the abdomen & Genitalia
Bladder catheterization
Doppler probe – Monitor the dorsal artery and
to check runoff into revascularized vessel
188. Midline incision
Dissection of inferior
epigastric vessel
Anastomosis inferior
epigastric artery & dorsal
artery –End to Side
Anastomosis
Inferior epigastric artery &
Deep Dorsal Vein
End to End
189. COMPLICATIONS
Penile edema
Superficial ecchymosis/ bruising of penile
shaft/ scrotum
Penile Numbness –returns 12 to 18 months
after surgery
Penile shortening -20%
190. Penile shortening from severe scar
entrapment –Relaxing Z plasty.
Glans hyperemia →Deep dorsal vein
arterializations - Surgical Exploration and
ligation of communication vessels
Results:
long term success rate 50 to 60%
191. Penile venous surgery
Criteria to recommend surgery
Short duration erection or tumescence only
with sexual stimulation
Failure with pharmacotherapy
Normal cavernous artery
Faulty veno occlusive mechanism( Infusion
pump or gravity pharmacocavernosometry)
No medical contraindication to the surgery
192. A. Peripenile anterior scrotal
incision
B. &
C. – Eversion penile tissue
D. - Ligation communicating
veins
E. Release of suspensory
ligament
F. Dissection of the veins/ Deep
dorsal vein ligation
G. Distal dissection
Communicating veins ligated
193. COMPLICATION
IMMEDIATE:
Penile and scrotal skin bruising
Penile edema
Pain from nocturnal erection
Wound infections
Hematuria
Long term complication:
Decreased penile sensation –returns 7 to 9
months
Penile shortening – 20 to 30%
Results: Long term success 25% (After
12months)
Editor's Notes
Skin, superficial dartos, deep buck’s fascia
The membranous layer of the superficial fascia of the perineum (Colles' fascia) is the deeper layer (membranous layer) of the superficial perineal fascia. It is thin, aponeurotic in structure, and of considerable strength, serving to bind down the muscles of the root of the penis. Colles' fascia emerges from the perineal membrane, which divides the base of the penis from the prostate. Colles' fascia emerges from the inferior side of the perineal membrane and continues along the ventral (inferior) penis without covering the scrotum. It separates the skin and subcutaneous fat from the superficial perineal pouch.
Arises from Colles fascia and is superficial
Conglomeration of sinusoids
The sinusoids are larger & tunica is thinner in spongiosum
The blood supply of the penis is mainly derived from the pudendal artery (a branch of the internal iliac artery). The pudendal artery becomes the penile artery at the root of the penis. This artery then branches to give three main branches:
Dorsal artery
Cavernosal artery
Bulbo urethral artery
Distally they form a vascular ring near the glans
Apart from internal pudendal artery accessory artery arise from external iliac, obturator, vesical & femoral artery
Multiple superficial veins run subcutaneously and unite near the root of the penis to form a single (or paired) superficial dorsal vein, which drains into the saphenous veins. Occasionally, the superficial dorsal vein may also drain a portion of the corpora cavernosa.
The emissary veins from corpus cavernosum and spongiosum drain dorsally to deep dorsal laterally to circumflex and ventrally to periurethral veins. Emissary veins join to form cavernous & crural vein which join with internal pudendal vein
α-Adrenergic nerve fibers and receptors have been demonstrated in the cavernous trabeculae and surrounding the cavernous arteries, and norepinephrine has generally been accepted as the principal neurotransmitter to keep the penis in the flaccid state
Nitric oxide
The consensus is that NO derived from neuronal nitric oxide synthase (nNOS) in the nitrergic nerves is responsible for the initiation, whereby NO from endothelial nitric oxide synthase (eNOS) contributes to the maintenance of smooth muscle relaxation and erection
Vasoactive intestinal peptide
In contrast to many other smooth muscles, corpus cavernosum smooth muscle is in a contracted state most of the time.
calcium-binding messenger protein
Myosin light-chain kinase
plasma membrane contain Ca,Mg-ATPases that remove Ca2+ from the cytosol. Na+/Ca2+ exchangers are also located on the plasma membrane. Receptor- and voltage-operated Ca2+ channels close resulting in a reduced Ca2+ entry into the cell.
opening of potassium channels and hyperpolarisation, 2. closing of calcium channels, 3. sequestration of intracellular calcium by the endoplasmic reticulum.
Smooth muscle regains its tone cGMP is degraded by phosphodiesterase
MPOA- medial preoptic area PVN- paraventricular nucleus
Increased prolactin inhibits GnRH inhibits testosterone production
Hyperthyroidism with decreased libido
Hypothyroidism due to low testosterone
Long distance cycling is also a risk factor for vasculogenic & neurogenic ED
receptor complexity and interrelationship of pathways within the CNS make it extremely likely that neurons and ganglia involved in sexual functioning will be affected by psychotropic drugs, leading to functional changes that may be positive or negative
Cigarette smoking may induce vasoconstriction and penile venous leakage because of its contractile effect on the cavernous smooth muscle
EAU
EAu
alprostadil alone Prostaglandin Analog and Prostaglandin E1 Agonis (Caverject or Edex, 10 to 20 μg), a combination of papaverine and phentolamine (Bimix, 0.3 mL),
(27 to 29 gauge), which is inserted at the lateral base of the penis directly into the corpus cavernosum for medication delivery. After needle withdrawal, manual compression is applied to the injection site for 5 minutes to prevent local hematoma formation. The assessment is done periodically subsequently with rating of both rigidity and duration of response. Repeated dosing may be performed if the initial erectile response is poor. Return to penile flaccidity is required before allowing the patient to leave the office, and if detumescence does not occur spontaneously in approximately an hour after dosing, intracavernosal injection of a diluted phenylephrine solution (500 μg/mL)
Peak systolic velocity
changes in diameter and flow waveform in the cavernous arteries induced by intracavernous injection of prostaglandin E1 in a potent young man as demonstrated by duplex ultrasound. Forceful concentric pulsations are particularly noticeable during full erection.
Resistive index
Dynamic infusion caversonometry
The testing is indicated for select patients who are suspected of having a site-specific vasculogenic leak resulting from perineal or pelvic trauma or who have had lifelong ED (primary ED). When used, it generally precedes consideration for corrective penile vascular surgery.
Nocturnal penile tumescence and rigidity
Buckling resistance of 500 g is considered minimum for vaginal penetration; 1.5 kg is considered complete rigidity.
DYNAMIC INFUSION CAVERNOSOMETRY AND CAVERNOSOGRAPHY (DICC
Monoamine oxidase
Phospodiestrase inhibitiors
nonsmoker, nondiabetic, absence of venous leakage, and radiographic confirmation of stenosis of the internal pudendal artery (Hellstrom et al, 2010; Sohn et al, 2013). The highest success rates are reported in young men (less than 30 years of age) with isolated arterial stenosis following perineal or pelvic trauma