REVIEW

A Review of Antipsychotics and Priapism

Thomas Hwang, MD, Tejash Shah, MD, and Hossein Sadeghi-Nejad, MD, FACS

ABSTRACT

Introduction: Pharmacologically induced priapism is now the most common cause of priapism, with approx-
imately 50% of drug-related priapism being attributed to antipsychotic usage. The majority of pharmacologic
priapism is believed to result in ischemic priapism (low flow), which may lead to irreversible complications, such
as erectile dysfunction. It is imperative that prescribing physicians be aware of potentially inciting medications.
Objectives: To identify medications, specifically antipsychotics, associated with priapism and prolonged erec-
tions and understand the rates and treatment of these side effects.
Methods: A PubMed search of all articles available on the database relating to priapism, prolonged erections,
and antipsychotics was performed.
Results: Various typical and atypical antipsychotic drugs (APDs) have been implicated in pharmacologically
induced priapism. In addition to dopaminergic and serotoninergic receptors, APDs have affinities for a wide array
of other receptors in the central nervous system, including histaminergic, noradrenergic, and cholinergic re-
ceptors. Although the exact mechanism is unknown, the most commonly proposed mechanism of priapism
associated with APDs is a-adrenergic blockade in the corpora cavernosa of the penis. Priapism appears in only a
small fraction of men using medications with a1-receptoreblocking properties, indicating differential sensitiv-
ities to the a-blocking effect among men, and/or additional risk factors that may contribute to the development
of priapism. The best predictor for the subsequent development of priapism is a past history of having prolonged
and painless erections. The acute management algorithm of APD-induced priapism is the same as for other causes
of low-flow priapism.
Conclusion: Clinicians should educate patients treated with antipsychotics about the potential for priapism and
its sequelae including permanent erectile dysfunction. Appropriate patient education will raise awareness,
encourage early reporting, and help reduce the long-term consequences associated with priapism through early
intervention. Hwang T, Shah T, Sadeghi-Nejad H. A Review of Antipsychotics and Priapism. Sex Med Rev
2020;XX:XXXeXXX.
Copyright
2020, International Society for Sexual Medicine. Published by Elsevier Inc. All rights reserved.
Key Words: Priapism; Antipsychotics; Prolonged Erections; Medication Side Effects

INTRODUCTION arterial (high-flow or nonischemic) priapism, and stuttering

Priapism is characterized by a prolonged penile erection lasting
more than 4 hours that is unrelated to sexual stimulation or in-
terest.1 Although the incidence of priapism is low in the general
population (0.5e0.9 cases per 100,000 person-years), when
stratified for specific populations with increased baseline risk, such
as those with sickle cell anemia, the rates of priapism significantly
increase.1 Depending on the etiology of priapism, it can be further
classified into ischemic (low-flow or veno-occlusive) priapism,
Received August 1, 2020. Accepted October 13, 2020.
Department of Urology, Rutgers New Jersey Medical School, Newark, NJ,
USA
Copyright ª 2020, International Society for Sexual Medicine. Published by
Elsevier Inc. All rights reserved.
https://doi.org/10.1016/j.sxmr.2020.10.003
(recurrent or intermittent) priapism.1
Ischemic priapism, or low flow priapism, is the most common
form of priapism, accounting for >95% of all priapism episodes.2,3
It is the result of venous occlusion leading to a backup of blood and
decreased cavernous arterial inflow.4 The blockage of fresh blood
induces tissue hypoxia that may lead to irreversible complications of
ischemic penile fibrosis and subsequent erectile dysfunction.4
Ischemic priapism is a urologic emergency that requires a medi-
cal intervention to minimize potentially irreversible consequences.1
The etiology of ischemic priapism is idiopathic in most cases but
has been associated with illicit drugs such as cocaine, hematological
disorders such as sickle-cell anemia, malignancy, and commonly
prescribed medications, including antipsychotic drugs (APDs).1,5
Arterial priapism, or high-flow priapism, is a persistent erection
caused by unregulated cavernous arterial inflow, often secondary

Sex Med Rev 2020;-:1e8 1

2 Hwang et al
to penile trauma or iatrogenic injury.1,4 Arterial priapism is not a
medical emergency as the corporal tissue is adequately
perfused.1,4 Stuttering priapism, or intermittent priapism, in-
volves recurrent painful episodes of prolonged erections, usually
for less than 3 hours.1 Erections are usually self-limited with
intervening periods of detumescence.6
Pharmacologically induced priapism is now the most common
cause of priapism, with approximately 50% of drug-related pri-
apism being attributed to antipsychotic usage.4,7 The majority of
pharmacologic priapism is believed to result in ischemic priapism
(low flow), which may lead to irreversible complications, such as
erectile dysfunction.4 Therefore, it is important that prescribing
physicians be aware of potentially inciting medications. In this
review, we will focus on APDs and its relation to priapism.
MATERIALS AND METHODS
A thorough PubMed search was performed of all articles
available on the database relating to priapism and antipsychotic
medications. The search included case reports, case series, and
reviews. Review articles were cross-referenced to search for
further available detailed individual reports. Additional publica-
tions were reviewed for general background on pathophysiology,
evaluation, and management. Only articles published in English
were considered. The quality of evidence reviewed is limited by
the observational and uncontrolled nature of case reports, case
series, and review articles.
RESULTS
Pharmacology
APDs are often classified as “typical” and “atypical” and are
typically used to treat patients with neuropsychiatric disorders,
particularly, schizophrenia and bipolar disorder, and can help
ameliorate psychosis.4,8 Off label, APDs are used in the treat-
ment of many other ailments, including treatment-resistant
depression, dementia, obsessive-compulsive disorder, aggres-
sion, autism spectrum disorders, sleep disorders, and pervasive
developmental disorders.8 All APDs antagonize dopaminergic
transmission at the dopamine type 2 (D2) receptors in the central
nervous system (CNS) but are heterogeneous as a drug group.9
The functional distinction between classes is based solely on
their ability to cause extrapyramidal symptoms (EPS), including
tardive dyskinesia.8
Typical APDs, or first-generation antipsychotics, are charac-
terized by a strong affinity for the D2 receptors in the CNS.9
Typical APDs are associated with a higher incidence of EPS at
usual clinical dosages than atypical APDs.8 Commonly prescribed
typical antipsychotics include phenothiazines (chlorpromazine,
thioridazine, fluphenazine, perphenazine, mesoridazine, thio-
thixene) and butyrophenones (haloperidol, zuclopenthixol).5
Atypical APDs, or second-generation antipsychotics, are most
accurately described as one that produces minimal EPS at
clinically effective doses.8 Atypical antipsychotics are serotonergic
antagonists at the 5-hydroxytryptamine 2A receptors receptors as
well as being D2 receptor antagonists.10 Commonly prescribed
atypical antipsychotics include clozapine, risperidone, ziprasi-
done, olanzapine, aripiprazole, and quetiapine.5
Both typical and atypical APDs have been implicated in
pharmacologically induced priapism. In addition to dopami-
nergic and serotoninergic receptors, APDs have affinities for a
wide array of other receptors in the CNS, including histamin-
ergic, noradrenergic, and cholinergic receptors.10e12 The
receptor-binding profile of APDs has been published previously
in pharmacological literature and demonstrates the varying af-
finities APDs have for adrenergic receptors, as well as other CNS
receptors. The differing binding affinities between APDs is
proposed to be related to its side effect profile.5,13 Although the
exact mechanism is unknown, the most commonly proposed
mechanism of priapism associated with APDs is a-adrenergic
blockade in the corpora cavernosa of the penis.14
During the flaccid state, the penile arterioles are in a tonic
state of contraction mediated by a-adrenergic activity.15 Induc-
tion of a penile erection is a result of increased sacral para-
sympathetic tone leading to relaxation of the cavernous and
arteriolar smooth muscles.15 The relaxation of smooth muscle
increases blood flow into the arterioles and sinusoids and com-
presses the emissary veins against the tunica albuginea with a
consequent decrease in venous outflow.10,15 The inflow of blood
and decrease in outflow lead to an erection. Detumescence oc-
curs when the process is reversed with sympathetic stimulation
by norepinephrine at a1- and, to a smaller extent, a2-adrenergic
receptors.10 In general, antipsychotics are more potent in
blocking a1-adrenoreceptors than a2-adrenoreceptors.16 APDs
block a1-adrenergic receptors in the corpora cavernosa inhibiting
the sympathetic system that mediates smooth muscle contraction
and detumescence.14,The a-2-blockade exacerbates the a1-
mediated priapism by stimulating the release of nitric
oxideelike substance, a potent muscle relaxant.10 The blockade
of these receptors shifts the penile vascular equilibrium into the
direction of prolonged erection and intracavernosal stasis, which
consequently may result in ischemic priapism. It is important to
note, however, that priapism only appears in a small fraction of
men using medications with a-1 receptor-blocking properties,
indicating differential sensitivity to the a-1 blockade and/or
additional factors that must be present for priapism to manifest.9
Typical vs Atypical Antipsychotics
Priapism with APDs can occur soon after starting APDs, with
chronic APD use, or after a change in dose or addition of another
medication.5,7,17e19 Drug-induced priapism accounts for
~15e41% of all cases, of which antipsychotic-induced priapism
is most commonly implicated.9 The incidence of priapism
relating to APDs has not been estimated in the literature. In
comparison, trazodone has been estimated at between 1 in 1,000
and 1 in 10,000, and it is likely the incidence in antipsychotics is
Sex Med Rev 2020;-:1e8
Antipsychotics and Priapism
lower.5 Priapism associated with APD use may be considered an
idiosyncratic reaction, as there has been no conclusive evidence
of correlation between priapism and the dosage or duration of
APD use.10,20 Andersohn et al21 found a correlation between the
drug affinities for the a1 receptor of different antipsychotics and
their relative propensities for causing priapism. In addition, there
have been reports of increased risk of priapism secondary to
polypharmacy with APDs and one reported case of clitoral
priapism.10,22,23
Approximately 50% of medication-induced priapism cases
are due to APDs, in which phenothiazines are the most
commonly implicated ones.20 Although atypical antipsychotics
were initially thought to be less likely to cause priapism than
their typical counterparts, almost all atypical antipsychotics,
including risperidone, olanzapine, aripiprazole, clozapine, and
quetiapine, have been linked to priapism in the literature.20,24
The potential for any individual antipsychotic to cause pria-
pism is believed to be dependent on their affinity to block
adrenergic receptors.21 Among the older typical antipsychotics,
mesoridazine, chlorpromazine, levomepromazine, thioridazine,
and fluphenazine have the highest propensity to block a1-
adrenoreceptors.21 Within the newer atypical antipsychotics,
ziprasidone, risperidone, clozapine, and quetiapine have a high
affinity.21 However, even among the APDs with reported low
affinity, such as aripiprazole, there have been case reports of
priapism.21,25,26
Historically, among typical antipsychotics, the phenothiazine
class is most commonly implicated to cause priapism.5 In
comparing the pharmacology of phenothiazines to butrophe-
nones, the phenothiazines are low-potency dopamine receptor
antagonists with higher a-adrenergic blockade, whereas butro-
phenones are higher potency D2 antagonists with lower a-
adrenergic blockade.21 In the literature, this is reflected in the
higher number of case reports associated with phenothiazines,
when compared to higher potency D2 antagonists, such as,
haloperidol.5,21
Clozapine was the first atypical antipsychotic to be associated
with priapism and was first reported in 1992. Since that time,
there have been over 10 case reports.5 Clozapine is often used in
patients with schizophrenia who have failed trials with other
drugs and is considered treatment resistant.5 Patients who
develop priapism on clozapine present a challenge to the pre-
scribing psychiatrist. In cases of clozapine-associated priapism,
one patient was attempted to be switched to quetiapine but did
not achieve a good control of his symptoms. Consequently, the
patient requested to restart clozapine despite the risks and was
able to gradually increase his dose with no recurrence of pria-
pism.27 In another case, a 25-year-old patient developed priapism
after 1 year of taking clozapine. His dose was reduced to half his
original dose successfully with no further episodes. However, it is
important to note that his initial episode of priapism had lasted
33 hours, and it is likely the patient was subsequently
impotent.28
Sex Med Rev 2020;-:1e8
3
Risperidone and ziprasidone have the highest affinities for a1-
adrenoreceptors among atypical antipsychotics and have been
associated with priapism in over 20 cases when administered as a
monotherapy or in combination with other drugs.5,21,29
Associated Risk Factors
Priapism appears in only a small fraction of men using med-
ications with a1-receptor blocking properties, indicating differ-
ential sensitivities to the a-blocking effect among men, and/or
additional risk factors that may contribute to the development of
priapism.9,30 The best predictor, however, for the subsequent
development of priapism is a past history of having prolonged
and painless erections. It has been noted that a history of delayed
detumescence is present in approximately 50% of any subse-
quent case of priapism.31 Therefore, it is important to regularly
inquire and counsel the patient taking antipsychotics about the
occurrence of this side effect to increase awareness and to pro-
mote early reporting of symptoms.
Diabetes has been implicated as a possible risk factor for the
development of ischemic priapism in patients using atypical
antipsychotics. In one case report, a 44-year-old man with a 23-
year history of schizophrenia developed priapism when separately
trialed on risperidone and trazodone, quetiapine, and olanzapine.
During this time, his blood sugar was found to be elevated. In
the past, the patient had been on risperidone and trazodone for
2 years, and quetiapine and trazodone for 4 months with no
documented episodes of priapism. During that period, his blood
sugar had been stable. After his diabetes was controlled with
insulin, the patient was stabilized on loxapine.32 The implication
is that there is a possible increased risk of developing priapism in
patients on atypical antipsychotics with elevated blood glucose
levels.32
In theory, polypharmacy may increase the risk of priapism
either through the synergistic effect of combining drugs that can
independently cause priapism or by combining drugs that may
affect another drug’s metabolism.24 The effect of a-adrenergic
antagonism leading to priapism has been demonstrated in men
using other medications with a-antagonistic activity, such as, a-
blockers for the management of blood pressure or lower urinary
tract symptoms (LUTS), and trazodone, an antidepressant.4,33,34
In one case, terazosin, a a-1-selective adrenergic antagonist, was
prescribed to an otherwise healthy male for LUTS. As his dose of
terazosin was titrated from 1 to 5 mg, the duration of his erec-
tions increased from 1 to 3.5 hours. Ultimately, the patient
suffered an acute priapism episode lasting 17.5 hours, and he
subsequently developed postpriapism erectile dysfunction.33
Given the selective action of terazosin on a-adrenergic re-
ceptors, this report gives support to the proposed mechanism of
APD-induced priapism through a-adrenergic blockade.
Although one may expect a high incidence of priapism in pa-
tients using a-blockers, this is not the case. It is proposed that
this may be related to dosage, where there is a greater incidence
of priapism in patients taking a-blockers for hypertension than
4 Hwang et al
for LUTS. It is also likely that there are factors in addition to a-
blockade that plays a role in the development of priapism.4 In
APDs, those with higher affinities for a-adrenergic blockade have
been implicated to have a higher association with priapism and
have been reported with more frequency than their low-a-affinity
counterparts.21 Given the proposed etiology of APD-induced
priapism, the combination of APDs with other medications
with a-blocking properties, such as antidepressants and a-
blockers such as tamsulosin, may increase the risk of
priapism.4,21,35
In many patients with psychotic disorders, the practice of
combining APDs or taking them concurrently with other psy-
chiatric medications such as serotonin-specific reuptake in-
hibitors (SSRIs) is very common and increases the risk of side
effects, thereby making it more difficult to ascertain the
offending agent.9 Combining antipsychotics with SSRIs, highly
active antiretroviral therapy (HAART), and lithium have been
implicated in increasing the risk for priapism through alterations
in drug metabolism.5,22,32
Risperidone is metabolized by the cytochrome P450 (CYP450)
2D6 enzymatic system, and to a lesser extent, 3A4.36 There is some
evidence suggesting that CYP450 enzyme inducers or inhibitors
could impact risperidone plasma levels.37e39 SSRIs inhibit the
CYP450 2D6 system and can lead to a higher plasma level of ris-
peridone, and in turn, a greater a-adrenergic blockade.40 There
have been case reports of priapism developing in patients taking
risperidone concurrently with paroxetine, citalopram, or fluvox-
amine.23,41,42 However, it is important to note that risperidone has
caused priapism even when used as a monotherapy.43
HAART has also been implicated in interacting with anti-
psychotic medications through the alteration of CYP450 en-
zymes leading to increased plasma levels of antipsychotic.22,44
Although case reports exist, there is a paucity of definitive data
regarding interactions between HAART and antipsychotic
medications.
Lithium is not directly associated with priapism, but a number
of cases have occurred in patients taking lithium and risperidone
concurrently.45,46 A suggested mechanism of action is that
lithium acts synergistically to increase a-adrenergic antago-
nism.5,45,46 In one case, a patient had been taking risperidone for
2 years without developing priapism. Once the patient was
started on lithium, he began developing prolonged erections
between 1 and 3 hours. His risperidone was tapered from
1.5 mg/day to 1 mg/day with resolution of symptoms.46
Although it is unclear to what extent polypharmacy increases
the risk of priapism, clinicians must be cognizant of the theo-
retical risk when prescribing drugs that interact metabolically, or
may act synergistically.
Clitoral Priapism
Clitoral priapism has been associated with perineal malig-
nancies and radiation but is much less frequently reported as a
side effect of medications. However, clitoral priapism associated
with antidepressants, including trazodone, nefazodone, cit-
alopram, and bupropion, has been reported.5 Olanzapine is the
only antipsychotic that has been reported in the literature to
cause clitoral priapism.47 In this case, a 27-year-old female with
bipolar disorder was maintained on sodium valproate for
6 months. She developed a manic episode with psychotic features
and was prescribed olanzapine for the first time. 4 weeks after
starting olanzapine, she developed painful swelling of her clitoris.
Olanzapine was discontinued, and the swelling resolved in
2 days. Of note, the patient did not have any clitoris-related
pathology previously in her medical history.47
Acute Evaluation and Treatment
In the evaluation of a patient with acute priapism, a
comprehensive history is the mainstay in diagnosis.2,48 The
history can help determine the underlying type of priapism
(ischemic vs arterial) and should include the duration of erection,
presence and degree of pain, previous episodes of priapism and
method of treatment, current erectile function, use of erectogenic
therapies, medications, recreational drug use, history of sickle cell
disease, hemoglobinopathies, hypercoagulable states, and
trauma.1,2 APD-induced priapism is thought to induce ischemic
priapism, and our review will focus on the treatment of low-flow
priapism.
The physical examination should include the genitalia, peri-
neum, and abdomen.1 The abdominal and perineal examination
may reveal evidence of trauma or malignancy.1 In ischemic pri-
apism, the corpora are fully rigid and tender, but the glans penis
is soft. In comparison, the corpora in arterial priapism are not
fully rigid.1 Laboratory testing should include a complete blood
count, white blood count with blood cell differential, platelet
count, and coagulation profile.2,48 Corporal blood gas analysis is
essential to differentiate arterial and ischemic priapism. In
ischemic priapism, the corporal aspirate will usually reflect pO2
(mmHg) < 30, pCO2 (mmHg) > 60, and pH < 7.25.2
The management of APD-induced ischemic priapism requires
emergent intervention to restore penile flaccidity and prevent
damage to the corpora cavernosa.1 The first step in the man-
agement of ischemic priapism is decompression of the corpora
cavernosa by penile aspiration until fresh red oxygenated blood is
obtained.1 Decompression promotes the recovery of the intra-
corporal blood circulation, which should relieve the penile pain.1
If priapism persists or recurs after penile aspiration, the next step
is intracavernosal injection of sympathomimetic agents.1 Phen-
ylephrine is suggested as the drug of choice because of its high
selectivity for the a1-adrenergic receptor, without concomitant
b-mediated ionotropic and chronotropic cardiac effects.49,50
Phenylephrine is usually diluted in normal saline to a concen-
tration of 100e500 mg/mL and given in 1-ml doses every
3e5 minutes. It is administered directly into the corpus cav-
ernosum with a maximum dosage of 1 mg over 1 hour.1 Patients’
vital signs should be monitored every 15 minutes; side effects of
Sex Med Rev 2020;-:1e8
Antipsychotics and Priapism
sympathomimetic agents include headache, dizziness, hyperten-
sion, reflex bradycardia, tachycardia, palpitations, and irregular
cardiac rhythm.1,51
If detumescence is not achieved after aspiration and intra-
cavernosal injection of a sympathomimetic drug, surgical inter-
vention in the form of penile shunt surgery should be performed
to relieve penile ischemia and avoid corporal fibrosis in priapism
cases 72 hours.2,52,53
The type of shunt procedure performed is selected by the
surgeon’s preference and familiarity. As a rule, it is preferable to
try distal shunts first.1 It is important to note, however, that
prolonged priapism events >36 hours appear to irreversibly
damage erectile tissue structurally and functionally. In these
cases, any shunt procedure may only serve to decrease pain
without preserving erectile function.1
In intractable cases of acute ischemic priapism lasting
>48e72 hours, immediate penile prosthesis surgery has been
recommended.1 Ischemic episodes of that duration will usually
result in complete erectile function impairment and major penile
fibrosis/deformity. By performing immediate prosthesis place-
ment, one may avoid surgical difficulties and complications (eg,
urethral injury, tunical erosions, infection, penile shortening)
associated with corporal fibrosis.54e57
Preventing Future Episodes
After the acute presentation of priapism associated with an
APD, future occurrences may be avoided by discontinuing the
offending medication, decreasing the dosage, or changing to an
APD with a lower affinity for a-adrenergic receptors.5,21 In cases
of stuttering priapism, hormonal manipulation and the use of a-
adrenergic agonists, digoxin, terbutaline, gabapentin, baclofen,
hydroxyurea, or phosphodiesterase type 5 inhibitors have been
reported in the literature.1 Given the proposed mechanism of
APD-induced priapism, the use of a-adrenergic agonists, such as
pseudoephedrine, has been suggested.58 In one case, a 36-year-
old male with schizophrenia had been trialed on several anti-
psychotics, including risperidone, fluphenazine, aripiprazole,
haloperidol, and quetiapine. The patient had poor psychiatric
response to these medications and had developed priapism to
each of these antipsychotics. The patient was started on chlor-
promazine with improvement of his psychiatric symptoms;
however, once the medication was titrated to 400 mg/day, the
patient again developed priapism. The patient’s dose of chlor-
promazine was reduced to 200 mg/day, and he was started on
pseudoephedrine ER 120 mg nightly. The patient did not
develop any further episodes of priapism and was able to sub-
sequently increase his dosage of chlorpromazine to 450 mg/
day.58
DISCUSSION
It is estimated that between 15% and 26% of priapism cases
are associated with the use of antipsychotic medications.59 The
Sex Med Rev 2020;-:1e8
5
most serious complication of priapism is impotence secondary to
ischemia and corporal fibrosis.5 The prognosis is dependent on
the promptness of treatment, but even with treatment, 40e50%
of patients can develop erectile dysfunction and permanent
damage.5,60 On acute presentation of priapism, a urologic
consultation should be obtained on an emergent basis to restore
penile flaccidity.5 Detumescence can normally be achieved
through corporal aspiration and intracavernosal injection of an a-
adrenergic agonist.1
With the increasing use of APDs in various disorders, the
clinician must be conscious of the risk of priapism associated
with these medications, although the overall risk may be low.
Priapism can occur in patients starting APDs, in those who have
been on stable doses for long periods of time, and with the
addition of other medications.5,7,17e19 It has been hypothesized
that APDs with higher affinities for a1-adrenoreceptors have a
higher propensity to cause priapism; however, even APDs with
low a-adrenergic antagonism have been linked to the side ef-
fect.21 It should be mentioned that the incidence of priapism
with APDs is based on published case reports and reported
adverse drug reactions submitted to the US Food and Drug
Administration. As a result, the reported incidence of priapism
with any individual APD may partially be the result of the fre-
quency of use in the population and the length of time the drug
has been on the market. Regardless, baseline risk factors should
be considered when starting a patient on APDs. These include
personal history of prolonged erections, sickle cell anemia, sub-
stance abuse, diabetes, and polypharmacy with drugs that are
independently linked to priapism or may alter the metabolism of
APDs.5
Patients prescribed APDs should be made aware of the po-
tential side effects before the initiation of treatment, as the lack of
awareness may lead to a delay in seeking medical attention or
reduce adherence to their therapy. Sexual dysfunction is preva-
lent in users of antipsychotics and may be attributed to the effects
of this class of medications on a1- and a2-adrenergic, histamine-
H1, and dopaminergic receptors.9 Sexual side effects are espe-
cially important to recognize and address in patients with psy-
chosis, as this patient population is less likely to spontaneously
report these symptoms because of the sensitive nature of the
pathology.9 It is also important to be aware that these side effects
can reduce patient adherence to APDs, a major cause of psy-
chotic relapse and rehospitalization for psychosis.61
Unfortunately, it seems likely that patients starting psycho-
tropic medications will not be counseled appropriately regarding
the side effects of prolonged erections and priapism.62 In a study
performed at the VA New Jersey Health Care System in New
Jersey, all male patients younger than 50 years taking trazodone
were surveyed regarding their counseling before initiating ther-
apy. It was found that only 43 of 229 (18.78%) patients were
informed about the side effects of prolonged erections, 37 of 229
(16.16%) were informed about the risk priapism, and only 17 of
229 (7.42%) patients were asked if they had a history of
6 Hwang et al
prolonged erections or priapism.62 Although the study was
limited to practice patterns at only one veterans affairs hospital,
the findings raised awareness that many patients on psychotropic
medications are likely not being appropriately counseled before
initiating therapy.
After appropriate counseling and with proper monitoring,
patients who report a history of prolonged erections on APDs or
who develop priapism should be switched to another antipsy-
chotic and followed closely. Although there is no preferred
antipsychotic for at-risk patients, medications with lower a-
adrenergic antagonistic properties are likely to have a lower risk
for causing priapism. Other strategies that can be used include
taking pseudoephedrine, an a-adrenergic agonist that has also
been used for cases of stuttering priapism.58
CONCLUSION
It is the responsibility of clinicians to educate patients treated
with antipsychotics about the potential for priapism and its
sequelae including permanent erectile dysfunction. If the patient
develops erectile dysfunction, consulting mental health pro-
fessionals to help manage the feelings of lost masculinity,
depression, guilt, and anxiety is well advised.63 The latter is
particularly relevant because the affected patient may be less
compliant with antipsychotic medication prescriptions in the
future.64 Appropriate patient education will raise awareness,
encourage early reporting, and help reduce the long-term con-
sequences associated with priapism through early intervention.
Corresponding Author: Tejash Shah, MD, Department of
Urology, Rutgers New Jersey Medical School, 185 S Orange
Ave, Newark, NJ 07103, USA. Tel: (973)972-4488; Fax: (973)
972-3892; E-mail: tejash121390@gmail.com
Conflict of Interest: The authors report no conflicts of interest.
Funding: None.
STATEMENT OF AUTHORSHIP
Thomas Hwang: Writing - Original Draft, Formal Analysis;
Conceptualization, Methodology, Investigation, Resources,
Writing - Review & Editing, Funding Acquisition, Project
Administration; Tejash Shah: Writing - Original Draft, Formal
Analysis; Conceptualization, Methodology, Investigation, Re-
sources, Writing - Review & Editing, Funding Acquisition,
Project Administration; Hossein Sadeghi-Nejad: Writing -
Original Draft, Formal Analysis; Conceptualization, Methodol-
ogy, Investigation, Resources, Writing - Review & Editing,
Funding Acquisition, Project Administration.
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