function. The most commonly used therapy was
injection based, perhaps suggesting that other
effective modalities for post-RP therapy would shift
this dynamic. Physicians familiar with sexual
medicine as a discipline are more likely to imple-
ment post-RP therapy targeted at preservation of
erectile function, supporting the role for increased
awareness of this concept.
Given the impact of RP on erectile function, it is
prudent for physicians to implement strategies
related to minimizing and reversing post-RP ED.
This requires both a thorough understanding of the
pathogenesis of post-RP ED and the role of various
therapies to mechanistically impact the process.
Clinically, physicians require treatment strategies
and assessment tools to capture response and
synthesize the literature on the various modalities
of post-RP therapy targeted for recovery of erectile
function. We discuss the clinical strategies designed
to overcome the non-surgical factors believed to
precipitate the development of post-RP ED. Addi-
tionally, we present some commonly used validated
instruments that are useful to define baseline
erectile function and follow response to therapy.
Physiologic mechanism of post-RP ED
RP is believed to impact long-term erectile function
by interfering with the neurological mechanisms
that facilitate cavernosal oxygenation. While the
mechanism of such neurological disruption or
trauma (neuropraxis) is not entirely clear, hypoth-
eses include direct trauma during surgery (for
example retraction injury), damage from tissue
electrocautery, disruption of the neural vasculature
and generalized local inflammation associated with
the procedure.
Regardless of the etiology of this
neurological damage, the functional consequences
of impaired parasympathetic penile function man-
ifest themselves as ED.
This neuropraxia results in a post-procedural ED
with associated cavernosal hypoxia.
Whereas this
issue underlies early post-operative ED, fibrosis
ensues and is marked by the presence of transform-
ing growth factor
, a marker of chronic inflamma-
tion and fibrosis.
Additionally, anti-fibrotic
mediators such as prostaglandin E1 (PGE1) and
cyclic adenosine monophosphate are under-repre-
sented during this process. Therefore, while neuro-
permanently damages cavernosal function and pro-
duces chronic ED. Furthermore, this destructive
cycle leads to cavernosal smooth muscle apop-
In response to these hypoxic conditions,
the tissues upregulate the nitric oxide pathway,
mediated by inducible nitric oxide synthase and
cyclic guanosine monophosphate to attempt to
improve penile blood flow.
Clinically, the impact of this chronic inflamma-
tory response to cavernosal hypoxia is manifested by
long-term collagen deposition and reduced smooth
In addition to vaso-occlusive disease,
venous leak develops due to the reduction in
corporal elasticity. Over time, these patients present
with increasing rates of ED. Therefore, while
occasional use erectogenic pharmacotherapy will
likely produce a transient erection, especially early
after surgery, there is long-term deterioration of
the normal physiologic processes involved in this
This broad overview of mechanisms predisposing
post-RP patients to ED suggests multiple points of
intervention to prevent the development of ED in
these patients. Most importantly, tissue oxygenation
may reduce the prevalence of chronic inflammation
and cavernosal fibrosis. Interestingly, hyperbaric
oxygen therapy in an animal model of cavernous
nerve injury has not been shown to significantly
reverse or minimize this process, suggesting that
there are multiple mechanisms involved.
darily, cytokine mediators of tissue fibrosis and
inflammation are targets for pharmacotherapy aimed
at preserving cavernosal tissue integrity. The con-
cept of erectile preservation (EP) is premised on
minimizing the factors that impair long-term erectile
function. Therefore, therapeutic strategies must
target the aforementioned mechanisms to provide
patients with optimal functional outcomes.
Rationale for erectogenic
pharmacotherapy in RP patients
The use of erectogenic agents after prostatectomy
has traditionally been referred to as penile rehabi-
litation. However, rehabilitation implies the reversal
of functional deterioration. In contrast, the objective
in patients with a planned RP is the preservation of
pre-operative erectile function. In fact, several
programs that initiate the use of erectogenic phar-
macotherapy in this patient population begin in the
weeks before surgery.
For this reason, the program
is referred to as EP rather than penile rehabilitation.
Perhaps, these terms are similar in their intent but
the term ‘EP’ suggests the desired outcome to
patients (for example a short-term therapeutic bridge
directed toward the recovery of natural erections)
and the urologic team to promote awareness and
compliance. Additionally, the protocol allows pa-
tients to have medication-assisted erections regard-
less of natural erectile capacity, thus preserving
erectile function throughout their recovery.
Phosphodiesterase-5 inhibitors
The use of phosphodiesterase-5 (PDE-5) inhibitors
is, in general, the most common therapy offered to
Review and treatment protocol: erectile preservation for RP patients
DJ Moskovic
et al
International Journal of Impotence Research