Dysfunction - STA HealthCare Communications

Focus on CME at the
University of Toronto

Treating

Erectile

Dysfunction

It was previously thought that erectile dysfunction (ED) was essentially a
psychologic disorder. Increasingly, however, sophisticated medical
examinations are now able to determine physical causes for ED.

By Magdy M. Hassouna, PhD, MD, FRCPC

E rectile dysfunction (ED) is defined as the lying organic cause.2 ED also encompasses disor-
inability to achieve or maintain an erection ders in ejaculation and orgasm.
sufficient for satisfactory sexual function.1 It was
previously thought that ED was essentially a psy- How Common Is It?
chologic disorder. Recently, however, the majority
of men with ED have been found to have an under- Kinsey et al reported the results of a survey con-
ducted on 15,781 men. The survey suggested that
Dr. Hassouna is associate professor of surgery the prevalence of ED was less than 1% in men
(urology), University of Toronto, and urologist, under age 30, 6.7% in men between the ages of
The Toronto Hospital — Western Division, Ontario. 45 to 55, and 25% in men above 65 years.3

The Massachusetts Male Aging Study (MMAS)
was a cross-sectional community-based random-
sample survey in men aged 40 to 70. The study was
conducted between 1987 and 1989 in 11 cities
around Boston. Although the sample population

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Erectile Dysfunction

Erection Theories of Yesteryear Another study showed evidence that the
prevalence of ED was significantly associated
Many theories have with age (p < 0.001), and correlated with a lower
attempted to explain the quality of life (P < 0.001).6
erectile process. The
presence of intravascular Mechanisms of Erection
protrusions (i.e., pollsters)
was first proposed in Neuroanatomy. The neural mechanisms
1869.7 It was postulated responsible for erections in men are still poor-
that an erection was the ly understood. It is known, however, that
result of active there are two kinds of penile erections:
contraction and reflexogenic and psychogenic.
relaxation of these Peripherally, the penis is innervated by both
“cushions” or
muscular divisions of the autonomic nervous system, as
protrusions in well as the somatic sensory nerves through the
the afferent and pudendal nerve. The pudenal nerve arises from
efferent penile vasculature, the S2-S4 segments of the spinal cord in Onuf’s
and that tumescence was nucleus, and supplies the skin of the dorsal, and
produced by the shunting of the lateral aspects of the shaft and the glans.
arterial blood to cavernous Other sensory contribution comes from the
spaces as a result of the ilioinguinal nerve; this nerve particularly affects
concomitant relaxation of the skin of the ventral base of the penis and the
arterial pollsters and the anterior part of the scrotum. The parasympathet-
contraction of the venous
pollsters. In more detailed ic innervation to the penis originates as pregan-
animal studies and in studies glionic fibers from the intermediolateral
on young human males, Newman et al did nuclei in the S2-S4 spinal segments. Nerve
not find any pollsters, and suggested that
pollsters may represent a response to fibers form a plexus that courses laterally in the
aging.8 endopelvic fascia close to the hypogastric ves-
sels, terminating beside the rectum into the
was less than the cohort in Kinsey’s study, the pelvic plexus. Branches from the plexus inner-
MMAS addressed several pertinent questions vate the urinary bladder, lower ureter, seminal
related to sexuality in aging men.4 The study vesicles, prostate, rectum and urethra.
showed that the prevalence of ED in this popula-
tion was 52%. The projected number of men Two critical branches (called the cavernous
who will be affected by ED for the year 2005 is nerves) have been implicated in the mechanisms
more than 50 million men between the ages of of erection. The cavernous nerves travel along
40 and 70.5 the posterolateral aspects of the prostate to the
corpora cavernosa. At the base of the prostate,
the cavernous nerves are located lateral to the
capsule of the prostate. Distally, the cavernous
nerves are at the five and seven o’clock position
near the apex of the prostate. The sympathetic
innervation of the penis is derived from the tho-

212 The Canadian Journal of CME / November 2001

Erectile Dysfunction

racolumbar portion of the spinal cord (specifi- In the flaccid state, the arterioles are constricted
cally T11-L2). The efferent fibers run through and the sinusoids are contracted; together, they exert
the retroperitoneum towards the hypogastric maximum resistance against arterial flow, allowing
plexus. These nerves contribute to the pelvic only a small amount of blood to enter the corpora for
plexus and the cavernous nerves, and are respon- nutritional purposes. The venules in the periphery of
sible for emission and ejaculation. the corpora run between the corpora and the adja-
cent sinusoidal wall, while the larger intermediary
The arterial supply of the penis is derived venules run between the sinusoidal wall and the
from the internal pudendal artery. This artery tunica albuginea for some distance before exiting as
branches from the ischiopudendal trunk of the the emissary veins. When the sinusoids are contract-
internal iliac artery, which contributes to the ed (in the flaccid state), these venules drain freely to
vascular supply of the prostate. the extra penile veins. During erection, the smooth
muscles of the sinusoids and arterioles relax,
Hemodynamics of Erection increasing sinusoidal compliance and causing
peripheral resistance to decrease to a minimum; this
The past decade had witnessed a surge in the
understanding of the physiology of erection. This Intensive investigations have
knowledge has tremendously aided researchers settled some of the controversy
who are investigating methods to treat ED, and
has helped design some treatment options, partic- regarding the mechanism of
ularly vasoactive drugs. erection. During erection, there is
an increase in arterial blood-flow,
Extensive investigations in animal models9 and sinusoidal relaxation and venous
human volunteers10 have settled some of the con-
troversy regarding the mechanism of erection (see resistance.
sidebar). During erection, there is an increase in
arterial blood-flow, sinusoidal relaxation and results in a sudden increase in the arterial flow, dila-
venous resistance, resulting in turgidity of the cor- tion of the arterial tree and a filling of the sinusoids.
pora cavernosa and corpus spongiosum (i.e., vas- Dilation of the arterial tree allows blood to rush in,
cular or full-erection phase). Subsequent contrac- and permits transmission of about 80% of the sys-
tion of the bulbocavernosus and ischiocavernosus tolic pressure to the sinusoidal spaces. This high
muscles either spontaneously or reflexively com- intracavernous pressure converts a soft flaccid organ
presses the proximal corpora, culminating in cav- to a blood-distended erect penis.11,12
ernosal rigidity and further engorgement of the
glans penis; this is commonly seen during mastur- Distension of the sinusoids within a limited space
bation or intercourse (i.e., skeletal muscle or rigid- (because of a relatively indistendable tunica albug-
erection phase). In full erection, the pressure in the inea) results in a compression of the small venules
corpora cavernosa is approximately 90 mmHg to between the sinusoids. Further expansion of the
100 mmHg, while the pressure in the glans penis sinusoids during full erection compresses the inter-
is 40 mmHg to 50 mmHg. In the rigid-erection mediary venules between the sinusoidal wall and the
phase, compression of the blood-distended corpo-
ra can increase the intracavernous pressure well
above the systolic pressure.11

The Canadian Journal of CME / November 2001 213

Erectile Dysfunction

25 1 2 3 4 3 5 6 Phase

Pudendal arterial
flow (mL/min)

Intracorporeal pressure 0
(cm H2O) 200

100

0
Cavernous Nerve

Pudendal Nerve

Figure 1. Arterial blood flow and intracavernous pressure changes during the different phases of penile erection in experimental animals

tunica albuginea. Stretching of the tunica albuginea The Six Phases
also compresses the emissary veins. These actions of Penile Erection
reduce the venous capacity to a minimum, efficient-
ly obtaining and maintaining erection in the corpora Based on the actions of the arterial, venous and
cavernosa without diverting too much cardiac out- sinusoidal systems, Lue et al described six phases
put for penile erection. In contrast, the glans penis of penile erection (Figure 1).11,12
(with no tunica albuginea) remains flaccid during
the erection. Flaccid phase. In the flaccid state, only a mini-
mal amount of blood flow enters the corpora cav-

214 The Canadian Journal of CME / November 2001

Erectile Dysfunction

ernosa for nutritional purposes. The pH, PCO2 and The blood flow diminishes to the level it had dur-
PO2 of blood from the corpora cavernosa are at lev- ing the flaccid phase, and a large portion of blood is
els maintained in venous blood. High-resolution expelled from the sinusoidal spaces. The penis
ultrasound and doppler study in humans show that returns to its flaccid length and girth.
the paired cavernous arteries at the base of the penis
have an average inner diameter of 0.05 cm. Peak Why Erectile Dysfunction?
velocity of blood flow is usually 15 cm/second, or is
not detectable. Penile erection is a complex physiologic
response that is dependent on the integration of
Latent (filling) phase. There is increased blood psychogenic, endocrine, vascular and neuro-
flow in the internal pudendal artery during both the genic mechanisms. Disturbance of one or more
systolic and the diastolic phases, without an increase of these mechanisms will result in erectile dys-
in intracavernous pressure. The penis shows slight
elongation and fullness. The highest blood-flow rate Men with primary psychogenic
occurs during this phase, with a peak flow velocity impotence often come from
over 30 cm/second and a two-fold dilation of the
cavernous arteries. sexually repressed backgrounds,
where sex
Tumescence phase. The penis rapidly expands
and elongates to its maximum capacity. The intra- was not discussed or was treated
cavernous pressure continues to increase, and, sub- as sinful and immoral.
sequently, blood inflow decreases.
function. The individual causes are many, and
Full-erection phase. During this phase, the intra- each cause may work by more than one mecha-
cavernous pressure can rise to as much as 85% of nism (e.g., diabetes mellitus can cause ED
the systolic pressure, and becomes more steady. through vascular and neurologic causes).
Blood flow in the internal pudendal artery is less Additionally, several mechanisms or causes may
than the blood flow during the tumescence phase. work simultaneously in a cumulative fashion to
Although the venous channels are mostly com- produce severe erectile dysfunction. The report-
pressed, the venous flow is slightly higher than what ed incidence of impotence varies with age,
it is during the flaccid state, and blood gases of the affecting 5% of men who are 40 to 49 years old,
intracavernous blood are maintained at the same and 85% of 80-year-old men.13
level as in the arterial side.
Psychogenic Factors:
Skeletal or rigid-erection phase. As a result of How Important are They?
the contraction of the ischiocavernosus muscles, the
intracavernous pressure rises well above the systolic In the past, psychogenic factors were considered
pressure, causing rigid erection. During this phase, to be very important in causing ED; more than
there is almost no blood flow through the cavernous 90% of impotent patients were diagnosed to be
artery. The short duration of this phase, however, psychogenic.14 Increasingly, sophisticated med-
prevents the development of ischemia.

Detumescence phase. After ejaculation or the
cessation of erotic stimuli, sympathetic tonic dis-
charge resumes, resulting in the contraction of the
smooth muscles around the sinusoids and arterioles.

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Erectile Dysfunction

ical examinations are now able to determine individual with ED confirmed the diagnosis in
physical causes for dysfunctions that, in the past, 82% of cases, and changed the diagnosis in 18%
would have been diagnosed as having a psy- of the cases. Studies regarding the partner’s
chogenic base. In a systematic, multidiscipli- impact on treatment showed that in 42% of the
nary, multidimensional assessment of a large cases, there was no change in the chosen treat-
number of impotent men, an organic cause was ment modality, in 18% of the cases, there was a
found in 35.9% of men, a psychogenic cause was change of treatment due to a change in diagnosis
found in 38.3%, and multiple or indeterminate and in 40% of the cases, there was a change in
causes in 28.8% of men.15 the chosen treatment modality, even though the
diagnosis was confirmed.17
Men with primary psychogenic impotence
often come from sexually repressed back- The Endocrine Factor
grounds, where sex was not discussed or was
treated as sinful and immoral. Generally, anxiety The prevalence of endocrine disorders in a popu-
and depression are believed to be the major lation of impotent men is not clear, but is estimat-
causes of psychogenic sexual dysfunction. These ed to be between 5% and 35%.18 Many hormones
may affect sexual performance, but androgens and
The prevalence of endocrine prolactin play the most important role.19
disorders in a population of
impotent men is estimated to be Testosterone, the principal androgen in the
male, is secreted primarily by the testicular Leydig
between 5% cells. The adrenals also secrete some testosterone.
and 35%. Testosterone secreted by Leydig cells is regulated
by the hypothalamus and the pituitary gland
emotions may be the result of nonsexual con- through the hypothalamic pituitary gonadal axis.
cerns, or may be specific to the sexual situation. Testosterone affects its target tissues either direct-
The presence of anxiety and depression may be ly or after it has been intracellularly converted to
a result of impotence, as well as a precipitating dihydrotestosterone (DHT). Although the effects
factor for ED.16 It must be stressed that identify- of both androgens (testosterone and DHT) are well
ing a possible psychologic factor does not mean established, their role and the level required for
that this factor is the sole cause of impotence. normal erectile physiology and sexual behavior
are still being investigated.20
Psychologic evaluation is important in both
the diagnosis and treatment of sexual dysfunc- Some studies have demonstrated that castrated
tion. The interview and the questionnaire are two and hypogonadal men were able to maintain sexual
tools typically used for this evaluation. It is activity. It was found that androgen replacement in
helpful to interview the couple together as well hypogonadal individuals had a significant effect on
as apart, in case there is information one would sexual behavior and activity that was dose-
rather not share with the other.16 Some studies dependent, and could not be reproduced by placebo.
have shown that interviewing the partner of the Hypogonadal men who received an androgen
replacement experienced a return of libido, mood
elevation and restoration of ejaculation. For men
with erectile potency, the situation is more com-
plex. It appears that the physiologic capacity for

216 The Canadian Journal of CME / November 2001

Erectile Dysfunction

erection is less sensitive to androgen withdrawal Erection is essentially a
than are sexual interest and sexual activity.
Androgen-dependent spontaneous erection (diurnal hemodynamic process; vascular
and nocturnal) is markedly suppressed in hypogo- diseases are, therefore, the
nadism, and is restored by androgen replacement. leading causes of erectile
In contrast, erections in response to erotic films are dysfunction. In the majority of
unaffected by androgen replacement, despite the cases, intervention is successful.
marked effects of androgen on sexual interest and
behavior. The central process leading to sponta- an increase in the estradiol production rate and
neous erections is androgen-dependent, whereas the a decrease in its metabolic clearance, resulting
mechanism leading to erection in response to a cer- in an elevation of serum estradiol. The Leydig
tain type of external erotic stimuli remains intact cells may be inhibited by the high estradiol lev-
despite androgen deficiency. Although the els and/or by circulating antibodies to thyroid-
importance of androgens for normal sexual stimulating hormone. The decreased libido seen
interest and activity has been established, the in patients with hyperthyroidism may be due to
amount of androgens required for both basal and the hypermetabolic effects of thyroxine or the
optimal function is still unknown, and may have increased level of circulating estrogen.23
vary by individual. Not only may the circulating Individuals with hyperthyroidism also com-
level of testosterone be important, but there may
also be more basic physiologic mechanisms
working at the molecular level (i.e., receptor site
activation).21

Prolactin has a complex relationship with
gonadotropins. In men with hyperprolactinemia
and testosterone deficiency, serum Luteinizing
hormone (LH) levels are inappropriately low,
indicating the failure of the hypothalamic pitu-
itary axis to respond to a reduced amount of
testosterone. Prolactin also appears to inhibit
gonadotropin-releasing hormone (GnRH).
Individuals with prolactin-secreting tumors
respond to an infusion of GnRH by increasing
the level of LH. In addition, GnRH may have a
direct effect on the central nervous system.
Some of the most common causes of hyperpro-
lactinemia include pituitary tumors, primary
hypothyriodism and drug-related and idiopathic
factors.22

Abnormalities in the thyroid hormone may
alter the hypothalamic pituitary gonadal axis,
resulting in ED. Hypothyroidism causes both

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Erectile Dysfunction

plain of sexual dysfunction. In these patients, mellitus, blunt perineal or pelvic trauma and
testosterone secretion is decreased, and the pelvic irradiation.24
metabolic transformation of testosterone shifts
towards etiocholanolone rather than andros- Veno-occlusive disorders or venogenic impo-
terone. The elevated serum prolactin levels in tence could be defined as occurring when the
individuals with primary hypothyroidism penile arterial inflow is less than venous out-
(mediated by the feedback-induced thy- flow. When tests such as dynamic infusion cav-
rotropin-releasing hormone [TRH]) may also ernosometry and cavernosography are per-
contribute to impotence. formed on men with vasculogenic impotence,
about 55% to 88% of the men are found to have
The incidence of decreased libido and potency a venous leak. For practical purposes, however,
in acromegalic individuals with elevated levels of venogenic impotence could be defined as occur-
growth hormone is as high as 50%, due to hypo- ring only when excessive venous outflow pre-
thalamic pituitary dysfunction and increased vents full erection in the presence of normal
serum prolactin.21 arterial blood flow.25

Peripheral Vascular Disease: Neurologic Factors
A Leading Cause of ED
Neurologic impotence is said to exist if a neuro-
Erection is essentially a hemodynamic process; pathic process (either central or peripheral)
vascular diseases are therefore the leading caus- results in failure to initiate the arteriolar and
es of erectile dysfunction. In the majority of lacunar smooth-muscle relaxation that facilitates
cases, intervention is successful. Alteration in the hemodynamic alteration associated with
the flow of blood to (arterial) and from (venous) penile erection. Neurogenic factors have been
the penis are the two mechanisms by which vas- estimated to be the sole or major contributing fac-
cular impotence occurs. Decreased arterial flow tor in 10% to 20% of all organically impotent men.
to the penis may be due to various causes. The The pelvic cavernous nerve complex is the major
most well known cause is Leriche’s syndrome, pathway for neurologic control of penile erection.
or thrombotic obliteration of the aortic bifurca- Impairment of this pathway or other neurologic
tion, with resultant pain and claudication of the pathways that utilize the pelvic cavernous nerve as
hips and thighs, and, in males, impotence. the final common pathway will result in neuro-
Atherosclerotic and traumatic arterial occlusive genic impotence. These pathways include the dor-
diseases of the hypogastric cavernous arterial sal-nerve afferent pathway (both peripherally and
bed can decrease the perfusion pressure and the centrally), as well as the poorly described efferent
arterial flow to the lacunar spaces, thus decreas- pathway.26
ing the rigidity of the erect penis and increasing
the time to maximal erection. Fibrosis, calcifica- Neurologic causes of impotence are most com-
tion and obliteration of the small cavernous ves- monly peripheral neuropathy, spinal-cord lesions
sels (which may occur with aging) have the same or lesions of the cerebral hemisphere. Peripheral
effect. Common risk factors associated with neuropathy may result from a variety of causes;
arterial insufficiency include hypertension, the most important cause is diabetes mellitus.
hyperlipedemia, cigarette smoking, diabetes Patients with chronic renal failure (particularly
those undergoing hemodialysis) are frequently
impotent. Even though uremic neuropathy may

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Erectile Dysfunction

contribute to impotence through Schwan’s cell Table 1
dysfunction, the hormonal abnormalities associat-
ed with uremia are most likely the primary cause. Evaluation of Erectile Dysfunction
Amyloidosis, with involvement of the autonomic
nervous system, can cause neurogenic impotence, • Sexual function questionnaire
especially the familial type. Multiple sclerosis is • Gatrointestinal disease or surgery
characterized by a loss of myelin in the white mat- • Pelvic or spinal trauma
ter of the brain, brain stem and spinal cord. The • Vascular or endocrine diseases
impact of MS on potency is variable, affecting • Neurologic diseases
35% to 43% of MS patients The severity of impo- • Sleep disorders
tence is directly related to the duration of the dis- • Marital and sexual history
ease, but in several patients, sexual potency tend- • Medications
ed to remit and relapse. Other causes of spinal- • Tobacco and alcohol consumption
cord lesions that can affect potency include those
accompanying syphilis (tabes dorsalis), spina bifida,
syringomyelia, amyotrophic lateral sclerosis and
compression from a herniated disk or tumor.

Diabetes Mellitus (DM) morning erection signals a more organic cause for
and Erectile Function the ED. The patient should be asked to describe the
problem in his terms: Is it consistent with the same
The prevalence of erectile dysfunction in men sexual partner or does it vary if more than one part-
with DM ranges from 35% to 75%, and is two to ner is involved? The patient should also be encour-
five times higher than the prevalence of ED in aged to relate the frequency of the problem and the
healthy control subjects. ED occurs 10 to 15 years frequency of sexual encounters that were not satis-
earlier in diabetic patients than in nondiabetic factory. One should also ask the patient about his
ones, and is often an early complication of DM. libido and sexual gratification during the orgasm.
Some studies report that impotence may often be
the only symptom that leads to the discovery of 2. Circumstances surrounding the ED. The subtle
unrecognized DM.27 onset of ED should always point to the possibility of
an organic cause. Physicians should inquire about
Evaluation for Erectile any changes in the general health of the patient to
Dysfunction rule out an associated disease.

History and physical examination. When taking a 3. Medical history. Special interest should
patient’s history, the physician should emphasize the always be paid to the medication the patient is
following issues (Table 1): taking. The majority of antihypertensive drugs
are associated with variable degrees of ED.
1. Duration of the ED. An onset of short duration Antipsychotic drugs are also associated with
should always point to the possibility of a psy- ejaculation disorders, particularly delayed ejacu-
chogenic background. The lack of nocturnal and lation and lack of libido. The patient should

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Erectile Dysfunction

understand that he should not voluntarily inter- What Specific Tests Should
rupt the treatment because of any side effects he Be Performed?
may experience. Every effort should be made to
substitute the offending drug with another drug Laboratory tests are needed only if the diagnosis
that has fewer side effects. of hypogonadism cannot be confirmed during the
history and the physical examination. These tests
As previously mentioned, diabetes mellitus is should not be ordered indiscriminantly, since they
associated with ED. have not been proven to be cost-effective.

4. Surgical history. ED usually occurs follow- Specific tests should be requested if the diagno-
ing extensive pelvic surgery. Radical prostatecto- sis is unclear or if the patient requests a full inves-
my is notoriously associated with ED in more tigation for a litigation problem.
than 50% of cases. Other pelvic surgeries
(e.g., abdomino-perineal resection of the rectum, Color duplex Doppler penile ultrasound is a rel-
surgery of the retroperitoneum, extensive frac- atively noninvasive test that can detect changes in
ture for the pelvic girdle) are known to cause ED. the arterial and venous penile blood flow. When
performed in conjunction with the intracavernosal
With a better understanding of the injection of a vasoactive agent, this test helps pre-
mechanisms of hemodynamics dict the patient response to local therapy.
involved in erection, several
different methods have been Diurnal penile tumescence has gained popular-
proposed to help restore penile ity because of its simplicity and reproducibility.
erection. This test involves the study of the erection and
rigidity by a Rigiscan® under erotic visual stimu-
In the physical examination, physicians lation.
should emphasize the general habitus and the
degree of masculinization of the patient (such as Cavernosometry-caverosography should be
secondary sexual characteristics [e.g., pubic performed to diagnose the possibility of a veno-
hair, gynecomastia]) as part of the evaluation of occlusive disease. Currently, these tests are not
the endocrinal status. commonly ordered, due to their invasiveness and
poor yield.
Local examination involves an estimation of
the consistency, size and location of the testes, Penile electrophysiologic studies such as con-
looking for any possible anomalies. The penile duction velocity and cortical-evoked potentials are
size and any abnormal fibrosis should be docu- very sophisticated tests used to uncover any
mented. Occasionally, a Polaroid® picture changes in the penile innervation in patients with
depicting the penis in an erect state is a very peripheral neuropathy. These studies are also help-
effective method to assess the degree of curva- ful in medico-legal cases to document any subtle
ture for future reference. damage to the penile innervation.

Pudendal arteriography is usually reserved for
patients with localized arterial blockage, and is
often performed prior to surgical arterialization of
the penis.

Office injection of a vasoactive drug in a cumu-
lative dose is a very cost-efficient method of
assessing the patient’s response. A full rigid erec-

220 The Canadian Journal of CME / November 2001

Erectile Dysfunction

tion after 10 to 15 minutes and lasting 30 minutes is local bruising. Use of this device necessitates
indicative of a vascular disorder that is not major.28 patient education and support.29

Treatment of Erectile Systemic oral drugs. The presence of silde-
Dysfunction nafil has changed the way ED is treated.
Sildenafil is a potent inhibitor to cyclic GMP,
The treatment of ED has taken a major turn dur- and therefore increases the penile response to
ing the last two decades. With a better under- sexual stimulation. There have been several
standing of the mechanisms of hemodynamics studies confirming the efficacy and safety of
involved in erection, several different methods sildenafil in patients with variable etiologies of
have been proposed to help restore penile erec- ED.30,31,32
tion.
The main side effects of sildenafil are
Vasoactive local drugs. The principle behind headache, flushing, dyspepsia and visual distur-
the application of vasoactive drugs is to induce a bances.
sudden decrease in the vascular resistance in the
cavernous bodies. The resulting sinusoidal Surgical treatment. The demand for surgical
relaxation will enable blood to pool in the cor- implantation of a penile prosthesis has declined
pora cavernosa to induce rigidity. in the recent years with the introduction of less
invasive and efficient ways of restoring erection.
For practical purposes, there are three drugs Penile implants can be divided into two general
available that can be used alone or in combina- types: nonhydraulic (semirigid) and hydraulic.
tion: papaverine, phentolamine and The surgical principle is to dilate the cavernous
prostaglandin E1 PGE1. tissue and to replace it with two cylinders of ade-
quate length and girth. The surgery is invasive
After the basic examination and tests have and carries a risk of complications. The patient
been conducted, intracavernosal administration should understand the limitations and the possi-
of these drugs should be presented to the patient ble complications of penile implants.
as a treatment option. The patient should be
made aware of the limitations, side effects and Conclusion
long-term complications of this therapy. The
recently introduced intraurethral-installed PGE1 Management of ED should include a proper
(Muse®) has been embraced for its simplicity in evaluation of the patient’s symptoms. Special
delivering the drug. The price and the inconsis- investigation tests should be tailored to the indi-
tency of response are the main drawbacks of the vidual patient’s needs. Invasive tests should be
therapy. reserved according to the patient’s desire, and in
medicolegal cases. In the majority of cases,
Vacuum constriction device. The principle treating the underlying cause of ED is not prac-
behind this device is to create a vacuum around tical or feasible. The treating physician should
the penis using a specially designed cylinder, discuss the different treatment options with the
resulting in blood pooling in the corpora caver- patient and provide the treatment that is accept-
nosa. An elastic band is applied around the base able to the patient. CME
of the penis to maintain the rigidity. Proponents
of this device praise its simplicity and efficiency.
Complications are usually minor, in the form of

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Erectile Dysfunction

References in impotence. Urology 1986; 27(6):499.
1. NIH Consensus Development Panel on Impotence: NIH 19. Krane RJ, Goldeteis I, Saenz de Tejada I: Impotence. N

Consensus Conference on Impotence. JAMA 1993; Engl J Med 1989; 321(24):1648.
270(1):83. 20. McClure RD: Endocrine evaluation and therapy. In:
2. Foreman MM, Doherty PC: Experimental approaches to
the development of pharmacological therapies for erectile Tanagho EA, Lue TF (eds.) Contemporary management
dysfunction. In: Riley A, M Peet M, Wilson C (eds). of impotence and infertility. 1st edition. Williams &
Sexual Pharmacology. Oxford, Oxford Medical Wilkins, Baltimore, 1988, p. 84.
Publications, 1993, p. 87-113. 21. Shakeback NE, Bancroft J, Davidson DW: Androgen
3. Kinsey AC, Pomeroy WB, Martin CE: Sexual behaviour replacement with oral testosterone enanthoate
in the human male. W.B. Saunders, Philadelphia, 1948. inhypogonadal men: a double blind randomized study.
4. Feldman HA, Goldstein I, Hatzichristou D, et al: Clin Endocrinol 1981; 14:49.
Impotence and its medical and psychological correlates: 22. McClure RD: Endocrine evaluation and therapy for
Results of the Massachusetts Male Aging Study. J Urol erectile dysfunction. Urol Clin North Am 1988; 15(1):53.
1994; 151(1):54. 23. Kidd GS, Glass AR, Vigersky RA:The hypothalamic
5. United States Bureau of the Census: Statistical Abstract pituitary-testicular axis in thyrotoxicosis. J Clin
of the United States 1992, 112th ed. Washington, DC, Endocrinol Metab 1979; 48(5):98.
1992. 24. Virag R, Bovilly P, Frydman D: Is impotence an arterial
6. Jonler M, Moon T, Brannan W, et al: The effect of age, disorder? A study of arterial risk factors in 440 impotent
ethnicity and geographical location on impotence and men. Lancet 1981; 1(8213):181.
quality of life. Br J Urol 1995; 75(5):651. 25. Lue TF: Treatment of venogenic impotence. In: Tanagho
7. Aboseif SR, Lue TF: Hemodynamics of penile erection. EA, Lue TF, McClure RD (eds). Contemporary
Urol Clin North Am 1988; 15(1):1. management of impotence and fertility. 1st edition.
8. Newman HF, Northup JD, Devlin J: Mechanism of Williams & Wilkins, Baltimore, 1988, p. 175.
human penile erection. Investig Urol 1964; 1:350. 26. Goldstein I, Saenz de Tejada I, Blanco R, et al:
9. Lue TF, Takamura T, Schmidt RA, et al: Hemodynamics Neurogenic impotence: Pharmacologic approach. In:
of erection in the monkey. J Urol 1983; 130(6):1237. Tanagho EA, Lue TF, McClure RD (eds). Contemporary
10. Shiari M, Ishii N, Mitsukawa S, et al: Hemodynamic management of impotence and fertility. 1st edition.
mechanism of erection in the human penis. Arch Androl Williams & Wilkins, Baltimore, 1988, p. 47.
1978; 1:345. 27. Boller F, Frank E: Clinical syndromes. In: Boller F,
11. Lue TF, Tanagho EA: Physiology of erection and Frank E (eds). Sexual dysfunction in neurological
pharmacological management of impotence. J Urol 1987; disorders: Diagnosis, management and rehabilitation.
137(5):829. Raven Press, New York, 1982, p. 33.
12. Saenz de Tejada I, Goldstein I, Blanco R, et al: Smooth 28. Lue TF: Impotence: a patient goal-directed approach to
muscles of the corpora cavernosa: role in penile erection. treatment. World J Urol 1991; 8(2):67.
Surgical Forum 1985; 36:623. 29. Cookson MS, Nadig PW: Long-term results with the
13. Kaneko S, Bradley WE: Evaluation of erectile vacuum constriction device. J Urol 1993; 149(2):290.
dysfunction with continuous monitoring of penile 30. Goldstein I, Lue TF, Padma-Nathan H, et al: Oral
rigidity. J Urol 1986; 136(5):1026. sildenafil in the reatment of erectile dysfunction. N Engl
14. Spark RF, White RA, Connolly PB: Impotence is not always J Med 1998; 338(20):1397.
psychogenic: insight into hypothalamic-pitutary-gonadal 31. Morales A, Gingell C, Collins M, et al: Clinical safety of
oral sidenafil in the treatment of erectile dysfunction. Int
dysfunction. JAMA 1980; 243(8):750. J Impot Res 1998; 10(2):69.
15. Nickel C, Morales A, Condra M, et al: Endocrine dysfunction 32. Zippe CD, Kedia AW, Kedia K, et al: Treatment of
erectile dysfunction after radical prostatectomy with
in impotence: incidence, significance and cost-effectiveness. sildenafil citrate. Urology 1998; 52(6):963.
J Urol 1984; 132(1):40.
16. Smith AD: Psychogenic factors in the multidisciplinary
evaluation and treatment of erectile dysfunction. Urol Clin
North Am 1988; 15(1):41.
17. Teifer L, Melman A: Interview of wives: A necessary
adjuvant in the evaluation of impotence. Sex Disabil 1983;
6:167.
18. Maatman TJ, Montague DK: Routine endocrine screening

222 The Canadian Journal of CME / November 2001