International Journal of Impotence Research (2003) 15, Suppl 5, S80–S85

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Priapism pathophysiology: clues to prevention

AL Burnett1*
1
Department of Urology, The James Buchanan Brady Urological Institute, The Johns Hopkins Hospital, Baltimore,
Maryland, USA

Priapism, in which penile erection persists in the absence of sexual excitation, is an enigmatic yet
devastating erectile disorder. Current endeavors to manage the disorder suffer from a poor
fundamental knowledge of the etiology and pathogenesis of priapism. These endeavors have
remained essentially reactive, which commonly fail to avert its pathological consequences of
erectile tissue damage and erectile disability, not to mention its psychological toll. The role of
preventative management seems paramount with respect to priapism. As a prerequisite to
formulating prevention strategies, gaining understanding of its pathogenic features and likely
pathophysiologic mechanisms is viewed to be quite important. This review combined an analysis of
clinicopathologic reports as well as a summary of clinical and basic science investigations on the
subject to date. These assessments support the basic classification of priapism into low-flow
(ischemic) and high-flow (nonischemic) hemodynamic categories, resulting from venous outflow
occlusion and unregulated arterial overflow of the penis, respectively. In addition, consistent with
the hypothesis that dysregulative physiology of penile erection accounts for some presentations of
priapism, several plausible molecular mechanisms influencing the functional state of the erectile
tissue are discussed. Current progress in the field suggests prevention possibilities using androgenic
suppressive therapy, adrenergic agonist therapies, and effectors of the nitric oxide-dependent
erection regulatory pathway in the penis. New ideas for prevention may emerge from targeting
molecular mechanisms involved in regulating erectile tissue function.
International Journal of Impotence Research (2003) 15, Suppl 5, S80–S85. doi:10.1038/sj.ijir.3901077

Keywords: priapism; etiology; pathogenesis; penis; erection

Introduction interventions offered subsequent to the onset of

Priapism, defined as prolonged penile erection in
the absence of sexual stimulation, probably repre-
sents the greatest challenge in therapeutic manage-
ment among erectile disorders. The disorder has an
obscure etiology and often unpredictably affects
select individuals without a clear pathogenic basis.
Furthermore, it may cause significant physical and
psychological debilitation, commonly rendering
complete impotence in a young man who before its
occurrence was sexually intact. Finally, treatments
offered for the disorder often are administered too
late to redress the problem fully or restore normal
erectile function.
Conventional treatments in the field are mostly
reactive, administered usually after the priapic
episode has already happened. The knowledge that
*Correspondence: AL Burnett, MD, The Johns Hopkins
Hospital, 600 North Wolfe Street, Marburg 407, Baltimore,
MD 21287-2411, USA.
E-mail: aburnett@jhmi.edu
priapism are frequently inadequate emphasizes the
role of prevention of the problem. However, while
the optimal therapy for this disorder may be its
prevention, the key element in this management
practice is having a sound understanding about the
pathogenic basis of the disorder. At this time,
scientific ignorance persists in this regard. Such
fundamental questions require resolution: What
causes priapism? Who is most susceptible? Are
there predisposing factors or conditions pertaining
to its onset or recurrence? Is there scientific
evidence for a pathophysiologic mechanism that
can be targeted for preventive treatment?
To advance prevention objectives, further under-
standing about the pathophysiology of priapism is
required. Insights, both now and in the future, will
draw from clinical study as well as from basic
science investigation in this field. Clinical study
relates to epidemiologic approaches as well as to
observations from procedures used to treat the
disorder. Basic science investigation relates to
unraveling the molecular determinants of the dis-
order, akin to the type of progress made recently in
the field of erectile dysfunction. In this essay, we

discuss the pathophysiology of priapism, with
emphasis on these subject areas. The essay con-
cludes with the postulate that priapism results from
derangements in the complex, integrative control
system involved in normal penile erection, from
which new preventive strategies can be considered.
Abnormal penile blood flow
Frank Hinman Sr1 can be credited with providing an
early, comprehensive study of the pathophysiology
of priapism. He understood the effects of and gave
primary relevance to ‘mechanical’ disturbances
involving the penile circulation, which he asso-
ciated with ‘thrombosis of the veins of the corpora’.
He identified the relationship to priapism of such
clinical conditions as pelvic abscess formation,
penile tumorous growths, perineal or genital injury,
and hematologic dyscrasias. His description pro-
vided the foundation for the concept of low-flow,
ischemic priapism, in which a veno-occlusive
pathology is believed to be a major cause of
priapism.
Distinctive veno-occlusive pathologies include
(see Table 1): sickle cell disease, which is associated
with sickled erythrocytes producing a sludge ef-
fect;2,3 parenteral hyperalimentation particularly
combined with fat emulsion, which is associated
with increased intravascular viscosity, stimulated
blood coagulability, or the development of fat
embolism;4,5 hemodialysis, which is associated with
increased intravascular viscosity as a consequence
of hemoconcentration and hypovolemia following
treatment;6 intracavernosal heparin administration,
which is associated with increased blood coagul-
ability paradoxically on the basis of its stimulating
platelet aggregation;7 local primary or metastatic
neoplastic processes, which are associated with
direct tumor infiltration and obstruction;8–11 and
Table 1 Conditions associated with low-flow priapism
Sickle cell disease and other hemoglobinopathies
Vasoactive drugs
Neoplastic disease (local or metastatic)
Penis
Urethra
Prostate
Bladder
Kidney
Gastrointestinal tract
Hematologic dyscrasias
Leukemia
Polycythemia
Traumatic injury
Hyperlipidic parenteral nutrition
Hemodialysis
Heparin treatment
Fabry’s disease
Neurologic conditions
Priapism prevention
AL Burnett
S81
Table 2 Conditions associated with high-flow priapism
Traumatic arteriocavernous fistula
Vasoactive drugs
Penile revascularization surgery
Neurologic conditions
hematologic dyscrasias, which are also associated
with tumor infiltration and obstruction from hema-
togenous spread.8,9
An additional concept for priapism resulting from
disturbed blood flow is high-flow, nonischemic
priapism, in which arterial overflow is considered
to be pathogenic.12,13 Trauma seems to be the
primary basis for this entity, either commonly from
blunt trauma to the perineum or genitalia14–16 or
from vascular laceration such as that resulting from
needle passage with intracavernosal pharmacother-
apy17 (see Table 2). Following trauma, the penile
vasculature is structurally damaged, which permits
uncontrolled blood entry and filling within the
corpora cavernosa. Commonly, a fistula forms
between arterial inflow vessels and the venous and
sinusoidal outflow circulation of the penis. Penile
arterial revascularization surgery for arteriogenic
impotence provides another setting for the compli-
cation of high-flow priapism.18,19
Abnormal erection neuroregulation
A ‘neural’ variant of priapism was initially sup-
ported by Hinman Sr, who recognized that a
substantial number of patients presenting with
priapism exhibit neurologic disease.1 He suggested
that this form of priapism affected ‘erectile centers’
of the nervous system and included infections such
as syphilis, brain tumors, epilepsy, intoxication, and
brain and spinal cord injury as causative factors.1
Several mechanisms have been proposed to explain
how these neurologic diseases cause priapism,
mostly in line with concepts related to the neuror-
egulatory basis for penile erections. One explanation
pertains to abnormal activation of neural reflexo-
genic mechanisms involved in erection following
genital stimulation.20–24 Another explanation relates
to disturbances in central neurotransmission that
mediates penile erection.25 Knowledge of the tradi-
tional autonomic sympathetic nervous system that
mediates detumescence and penile flaccidity has
supported the general belief that pathogenic failure
of this system could readily predispose to the
development of priapism.26,27
Priapism variants
Priapism variants are worth examining briefly to
acknowledge that they do not readily fit the contexts
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 Priapism prevention
AL Burnett
S82
of the classically described hemodynamic disorders.
In addition, as unique priapism presentations, their
consideration may reveal pathogenic aspects about
the disorder. Idiopathic priapism, which according
to some investigators constitutes as much as half of
all registered cases,28–30 has long been recognized as
priapism occurring without a discernible clinical
association. The variant has been associated with
sporadic previous priapism episodes and particu-
larly with erections that are sustained for prolonged
durations of sexual activity.26,28–31 Nocturnal erec-
tions have also been associated.1,26 ‘Stuttering’
priapism, familiarly observed as frequently recur-
ring priapism episodes in men with sickle cell
disease,32 has been associated with sleep and sexual
arousal.32–34 It is interesting that these episodes bear
no relationship to other vaso-occlusive crises char-
acteristic of sickle cell disease35,36 and may not
always predispose to complete erectile dysfunc-
tion.32,33,35
Refractory priapism, in reference to the recurrent
erectile state that follows aspiration or incision of
the corpora cavernosa for ischemic priap-
ism,2,31,37,38 has long been recognized but poorly
understood. Some have contended that the blood
flow pattern resembles high-flow priapism based on
radiographic study, in the absence of an arterial-
cavernosal fistula.37–40 High-flow priapism has been
clinically assessed in priapism related to medical
diseases including Fabry’s disease41 and sickle cell
disease.37 Drug-induced priapism, which as sug-
gested implies a medication-related phenomenon,
represents another variant that has resulted from use
of alpha-adrenergic antihypertensives, psychotropic
agents, antidepressant medications, cocaine, and
pharmacotherapeutic agents for erectile dysfunc-
tion.42–56 The mechanism of action is contended to
relate to peripheral and central signaling pathways
stimulated by the offending drug that produce
corporal smooth muscle relaxation.
Clinical study
Besides observations of drug effectors of priapism,
clinical assessments of the corrective effects of
therapeutic prospects for the disorder have contrib-
uted to understanding its pathophysiology. Pharma-
ceutical approaches described to offer benefit
include: intracorporal thrombolytic agents, which
would support the pathogenic roles of blood stasis
and thrombosis,57,58 oral diethylstilbestrol, which
by exerting antiandrogenic effects would imply that
androgens permit aberrant penile erection;35 sys-
temic injections of gonadotropin-releasing hormone
analogues, which because they are also anti-andro-
genic would further hypotheses about the patho-
genic role of androgens;59,60 lidocaine as a penile
anesthetic block, which is considered to work by
International Journal of Impotence Research
blunting sensory input conveyed in the dorsal nerve
of the penis of reflexive erectile pathways;61 oral
and intracorporal alpha-adrenergic agonists,
which exert contractile effects on erectile tissue,
thus indicating the likely pathogenic role of uncon-
trolled non-adrenergic factors;24,60,62,63 intracorpor-
al methylene blue, an antagonist of the nitric oxide/
cyclic guanosine monophosphate/protein kinase G
effector mechanism of corporal smooth muscle
relaxation, pointing to a possible pathogenic role
of this biochemical pathway.64,65
Basic science investigation
Basic research in the field has consisted mainly of
identifying and evaluating animal models featuring
priapic behavior and molecular studies that suggest
possible mechanisms for the disorder. Transgenic
mouse models of sickle cell disease display priap-
ism supporting the idea that disturbed penile
vascular homeostasis associated with the hematolo-
gic disease is pathophysiologic.66 A mouse model of
senility syndrome exhibits priapism, understood to
occur on the basis of degeneration of medullary
reticular formation neurons that normally inhibit
male spinal sexual reflexes.67 Mice lacking the genes
for both neuronal and endothelial nitric oxide
synthases display phasic erectile activity, indicating
that the altered nitric oxide release affects the
control mechanisms associated with penile erec-
tion.68 After induction of prolonged erections or
conditions of priapism in isolated cavernosal tissue
experimentally in animals, the cavernosal tissue
loses responsiveness to adrenergically stimulated
tissue contraction,69,70 undergoes destructive meta-
bolism via lipid peroxidation,71 and increases
expression of the tissue fibrosis marker transforming
growth factor beta.72
Dysregulatory mechanisms
Since many regulatory factors are now known to
influence the functional state of the cavernosal
tissue, it is not surprising to consider that situations
in which any of these factors go awry may lead to the
development of priapism. This reference to erectile
regulatory factors involved in priapism could apply
to factors involved in corporal smooth muscle
responses that operate somehow in a dysfunctional
manner or to factors activated under the pathologi-
cal conditions of priapism that adversely affect
erectile tissue physiology. Dysregulatory mechan-
isms of erectile tissue function may be associated
with idiopathic, stuttering, and other divergent
presentations of priapism, conceivably distin-

guished from the origins of classic hemodynamic
types of priapism.
The current description of mediators and signal
transduction pathways involved in penile erection
suggests several scientifically plausible mechanisms
that may contribute to the pathophysiology of
priapism. Such mechanisms include: physiologic
increases in oxygen tension within the cavernosal
tissue, which stimulate corporal smooth muscle cell
production and release of vasorelaxant substances
while inhibiting the production and release of
vasoconstrictive substances;73,74 heightened andro-
genic milieu, which promotes corporal neuromus-
cular transmission of penile erection;75 altered
composition of myosin isoforms and the extent of
myosin phosphorylation in the corporal smooth
musculature, which determines its level of basal
tone;76,77 abnormal expression levels of ion chan-
nels and gap junctions in corporal smooth muscle
cells, which could affect the tonicity and synchro-
nicity of these cells;78 aberrant nitric oxide regula-
tion in the penis, which has been correlated with
supraphysiologic erectile responses;68,79 intracor-
poral blood flow-related ‘shear stress’ forces that
activate endothelial-based biochemical pathways
sustaining penile erection.80
Prevention strategies
The development of prevention strategies for priap-
ism expectedly will revolve around surveillance and
early implementation of effective therapies. Indivi-
duals at risk for ischemic priapism, such as the
hemodialysis patient or the patient with a hemato-
logic dyscrasia, should be cautioned about the
possible occurrence of the disorder under these
circumstances while understandably basic attempts
are undertaken to remedy the presumed causative
etiology. Given the high level of alertness under
these circumstances, standard therapies for manage-
ment of the veno-occlusive pathology should be
readily available. The risk of priapism with vasoac-
tive pharmacotherapy for erectile dysfunction
should be reduced with proper counseling regarding
this risk and considerations for in-office test dosing,
particularly for local or combined pharmacothera-
pies, to establish the best dose that would limit the
risk subsequently.
Notwithstanding cases of unprecedented is-
chemic priapism, high-risk groups such as those
with sickle cell disease manifesting ‘stuttering’
priapism and those exhibiting recurrent ‘idiopathic’
or neurologic priapism may be considered to have
the greatest relevance for prevention efforts. These
presentations arguably constitute the most clinically
vexatious settings for priapism and would seem to
benefit most from taking advance measures against
the disorder. After all, these individuals fit a
Priapism prevention
AL Burnett
S83
predictable pattern of progression to erectile tissue
destruction in which, it would seem, clinical
opportunities exist to gain disease control. Pre-
sently, current pharmacologic treatment successes
support the roles of androgenic suppressive
agents,59,60 adrenergic agonist therapies,24,60,62,63
and effectors of the nitric oxide-dependent erection
regulatory pathway in the penis such as methylene
blue.64,65 As promising as these therapies have been,
they still warrant certain considerations such as
when they should be administered, whether they
can be administered with minimal penile trauma
and without causing adverse extra-penile effects,
and whether they can be offered with a regimen that
does not impair natural erections long term.
For the future, systematic development and
application of therapies may result from improved
understanding of the role of dysregulatory mechan-
isms of penile erection. This charge is consistent
with current objectives to better understand the
molecular mechanisms associated with the erectile
tissue response. Therapies are anticipated that will
target mechanisms involved in neurovascular trans-
mission unique to the penis, corporal smooth
muscle physiology, and biochemical regulation of
erectile responses.
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