Physiology of penile erection, pathophysiology evaluation of erectile dysfunction

1. PHYSIOLOGY OF ERECTION,
PATHOPHYSIOLOGY,
MANAGEMENT OF ERECTILE
DYSFUNCTION

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

13. Penile Components and Their
Function
during Penile Erection

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

24. Stimulation of the
parasympathetic nerves
(S2 – S4)
stimulation of the
sympathetic trunk
(T11 – L2)
Erection Detumescence

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.

44. cAMP and
cGMP, activate
their specific
protein
kinases which
leads to

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

46. PATHOPHYSIOLOGY OF
ERECTILE DYSFUNCTION

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

50. Causes (I.M.P.O.T.E.N.C.E.)
Inflammatory Prostatitis, urethritis
Mechanical Peyronie’s Disease, chordee
Psychological Depression, performance anxiety, stress
Occlusive vascular
Art: Hypertension, smoking, hyperlipidemia, DM.,
peripheral vascular disease
Ven: venous occlusion due to anatomical / degenerative
changes
Trauma Pelvic fracture, 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-
parkinson drugs, LHRH analogues
Extra factors Prostatectomy, old age, CRF, cirrhosis

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

60. Mechanism of Vascular Erectile
Dysfunction

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

64. Effect of Antihypertensive Agents
on Sexual Function

65. Other drugs

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

78. EVALUATION

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.

86. PHARMACOLOGIC CAVERNOSOGRAPHY
After penile # communication between
CC & CS seen 27-year-old man with primary ED, venous
leakage from crura

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.

100. TREATMENT OF
ERECTILE
DYSFUNCTION

101. Introduction
3 Sentinel events - Treatment of ED
Inflatable prosthesis -1973
Intracavernous therapy- 1982
PDE5 Inhibitors -1998

102. Treatment Modalities Available
Life style modification
Pharmacotherapy
Surgery

103. LIFE STYLE CHANGES
1. Obesity ↓ caloric Intake
↑ Physical Activity
2. Smoking -Stop Smoking
3. Hypercholesterolemia -Drugs
4. Bicycle Riding - Avoid

104. MEDICATION CHANGES
Non specific Blocker Alpha 1 Antagonist
Anti Hypertensive
Methyldopa Ca channel Blockers
Reserpine ACE Inhibitors
Thiazide
Spironolactone Substitution
Depression
SSRI Drug holidays
MAO Inhibitors SSRI dosage reduction
Tricyclic Antidepressants PDE inhibitors

105.  Pelvic Floor Muscle Exercise
Psychosexual Therapy

106. HORMONAL THERAPY
 Thyroid
 Adrenal
 Hypothalamic dysfunction
 Hypogonadism
 Hyperprolactnemia

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.

109.  CONTRAINDICATIONS
1. Breast carcinoma.
2. Prostate carcinoma.
 PREPARATION
1. Testosterone
2. DHT
3. DHEA

110. TESTOSTERONE
PREPARATIONS
1. Injectable
2. Transdermal
3. Buccal
4. Pellet
5. Oral

111.  IDEAL PREPARATION
1. Plasma levels to be achieved –24h.
2. Normal diurnal pattern.

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

117.  Testosterone Undecanote (TU)
Partially taken up by lymphatic system
40mg / 3times /day.

118.  DHT
Pure androgen
Testosterone –Aromatization – Estradiol
-Gynaecomastia
Effect on Prostate.
 DHT Gel →125 to 250mg / day.

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.

122.  FOLLOW UP
1. Periodic Hb, Hematocrit level
2. LFT
3. Lipid profile
4. P/R, PSA –every 6 months.

123.  Hyperprolactinemia/ ED
1. Avoid offending drugs – Estrogen,
Morphine,
Neuroleptics
2. Prolactian secreting Adenoma -
Bromocriptine
Neurosurgery

124. PHARMACOLOGIC THERAPY
1. Peripherally Acting Agents
2. Centrally Acting Drugs

125. Peripherally Acting Agents
1. Oral Therapy
2. Intracavernous Injection
3. Intraurethral
4. Transdermal

126. PHOSPHODIESTERASE TYPE 5
INHIBITORS

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

132.  Low - < 3 risk factors
 Intermediate - 3< risk factors
 High risk
Unstable or refractory Angina pectoris
Uncontrolled HT
CCF (Class 3/ 4 )
Recent MI < 2 Wks
Arrhythmias
Obstructive cardiomyopathy

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.

135.  INTRACAVERNOUS INJECTIONS
1. Papaverine
2. Alpha Adrenergic Antagonist
Phentolamine, Moxisylyte
3. Alprostadil
4. Combination Therapy
Papaverine + Phentolamine
Papaverine + Phentolamine
+Alprostadil

136.  Papaverine
Alkaloid
Inhibitory effect on PDE
↑C AMP &↑ Cyclic GMP
Blocks voltage dependent Ca
channels
Impair calcium influx
→Penile erection

137.  Dosage: 7.5 -60mg
 Advantage : Low cost & stable at room
temperature
 Disadvantage: Priapism -33%
Corporeal Fibrosis 1% to 33%

138. Alpha –Adrenergic Antagonist
 Phentolamine Methylate
Blocks pre junctional Alpha 2 Receptor
Dose : 0.1 -1ml
Advantage: More potent
 Adverse effect:
Hypotension
Reflex Tachycardia
Nasal congestion
GIT Upsets

139.  Alprostadil – Prostaglandin E1
Smooth muscle relaxation
Vasodilatation
Inhibition of platelet aggregation
 Dose: 1-60mg
 Adverse effect
Pain at the Injection site
Pain during Erection
Hematoma, Ecchymosis
Priapism 1-3%

140.  Combination Therapy
Papaverine 30mg + Phentolamine 0.5mg
(self Injection)
 Response Rate
Armstrong and associates
1. vasculogenic -48%
2. Psychogenic -93%
3. Neurogenic -92%
4. Diabetic -68%
5. Idiopathic -63%
6. Traumatic -60%
7. Alcohol related -68%
8. Drug related -75%

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

145. Contraindications:
Sickle cell disease
Schizophrenia
Psychiatric disorders
Severe systemic disease
Pt on Anticoagulant or Antiplatelet Therapy
Compress the Inj site for 7 to 10 mts

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

155. Surgical treatment
 Prosthetic surgery
 Vascular surgery

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

160. Approaches
Infrapubic Approaches PenoScrotal
Approaches
Advantages Reservoir placement
under direct vision
Better corporeal
exposure
No dorsal nerve
injury
Better Pump
fixation possible
Disadvantages Limited corporeal
exposure
Dorsal nerve injury

161. Surgical procedure
 Out patient procedure
 Spinal or General Anesthesia
 Supine position
 Penoscrotal Approach

162. 2 cm corporotomy
Corporal Exposure
Corporal dilation – 8 mm dilator → 16 mm (proximally)
14mm (distally)

163. Distal measurement
Proximal measurement

164. Appropriate cylinder selection
12,15,18,21cm
Distal cylinder insertion –
Furlow cylinder

165. Proximal portion cylinder insertion
Cylinder placed in its place

166. Corporotomy closure
Pump placement - Incision through dartos
Deep septal subdartos pouch for
pump

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.

172. COMPLICATIONS
 Infections
 Perforation and Erosion
 Poor Glans support
 Over sized cylinder or Rod
 Pump complications
 Auto inflation

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

181. Prosthetic Surgery Results
 Efficacy: 83% of Men/ 70% partners
1. Satisfied
2. Psychosexual well being

182. Vascular surgery
Advantages:
Restores fully natural erection for
longer period without external mechanical
devices, vasoactive medications or internal
prosthesis

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

184. Surgical technique
Penile Arterial Revascularization
 Dorsal artery dissection
 Harvesting of inferior epigastric artery
 Micro vascular anastomosis

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)