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C A S E R E P O R T Open Access
Recurrent priapism in the setting of
cannabis use
Sebastian Montgomery
1
, Kristal Sirju
1
, Joseph Bear
1,2
, Latha Ganti
1,3*
and John Shivdat
1,3
Abstract
Priapism (persistent and painful erection of the penis) is a notable urological emergency, with over 90% of those
remaining erect for 24 h losing sexual function. Drug-induced priapism is common in the adult population, with
intracavernosal injectables for erectile dysfunction topping the list. A variety of illicit drugs associated with priapism
have been described; however, we are not aware of any other case reports showing cannabis alone as the inciting
factor. Here, we present a case of a healthy 32-year-old African American man with a history of stuttering
(recurrent) priapism secondary to mild cannabis substance use without comorbid substance use, licit or illicit.
Introduction
Priapism is defined by an erection that persists for
longer than four hours that is not related to sexual
stimulation. It is divided into two main groups, ische-
mic or low-flow and non-ischemic or high-flow priap-
ism. The majority of cases encountered in the
emergency department are ischemic priapism, which
results from failed relaxation of cavernosal smooth
muscle (Broderick et al., 1994). To the patient, the
risk of priapism is obvious, as ischemic priapism can
cause serious complications, as the blood trapped in
the penis is deprived of oxygen. When an erection
lasts longer than four hours, this hypoxemic environ-
ment can lead to damage to the penile tissue, with
notable destruction obvious at twelve hours (Spycher
et al., 1986). As a result, untreated priapism can cause
permanent loss of sexual function and must be
treated as a urological emergency. Priapism itself has
a bimodal distribution, with the majority of childhood
cases involving sickle cell anemia and adult cases with
known etiology involving intracavernosal injections.
Drug-induced priapism has long been proposed to
include PDE-5 inhibitors, anticoagulants, antihyper-
tensives, antidepressants, alpha-blockers, and recre-
ational drugs (most notably cocaine). We conducted a
PubMed search with priapism and cannabis
(cannabinoid, cannabis), limiting it to English lan-
guage articles in adults. No publication year limit was
imposed. No case reports were found that described
priapism in the setting of cannabis use without con-
current medical disease or drug use. Of the four pre-
viously published case reports linking cannabis use to
priapism, this is the first that we are aware of that
excluded all other well-established causes of priapism.
Case report
We present the case of a healthy 32-year-old African
American man who presents to the emergency depart-
ment with persistent erection for six hrs not related to
sexual activity. Notably, the patient had been seen two
weeks prior in our emergency department for a persist-
ent erection lasting twelve hrs. At that time he under-
went a needle aspiration with phenylephrine injection
leading to successful detumescence. He admitted to
smoking cannabis several nights per week for the past
six months, including within the two hour period prior
to each presenting episode of priapism. During this time,
the patient had four or more episodes of a persistent
erection lasting close to four hours that were self-
resolving. He reported a previous full outpatient evalu-
ation for sickle cell trait and anemia as a teenager that
was negative, and denied any known relatives with sickle
cell disease or trait. He admitted a history of cannabis
use at age sixteen and seventeen, during which time he
had recurrent priapism lasting less than four hours and
never requiring medical treatment. He quit cannabis use
in his twenties, and during this period did not have any
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* Correspondence: lathagantimd@gmail.com
1
Coliseum Medical Centers/ Mercer University, 350 Hospital Drive, 31217
Macon, Georgia, United States
3
Envision Physician Services, Nashville, Tennessee, United States
Full list of author information is available at the end of the article
Journal of Cannabi
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Montgomery et al. Journal of Cannabis Research (2020) 2:7
https://doi.org/10.1186/s42238-020-0015-8
episodes of priapism. He denied any history of psychi-
atric disease and took no prescribed or over-the-counter
medications, specifically denying psychiatric medications
or blood pressure medications. On physical exam, the
patient was mildly hypertensive with an erect, swollen,
and tender penis. A repeat needle aspiration with (1000
mcg total) of phenylephrine was completed, again result-
ing in successful detumescence. A urine drug screen was
consistent with cannabis use without other drug use. A
complete blood count revealed no anemia and a normal
mean corpuscular volume. The patient was again re-
ferred to urology and internal medicine on an outpatient
basis for further workup; however he was lost to follow-
up in this period.
Discussion
This case report examines the first known case of
cannabis-associated priapism in a patient where all other
known causes of priapism have been excluded. While
cannabis use has already been noted in educational
sources and textbooks as a potential cause of priapism,
an electronic literature review was only able to identify
four distinct cases of cannabis use coinciding with priap-
ism, none of which were convincingly able to prove can-
nabis was the sole cause (Reichman, 2013). In the first
two papers, the patients had cannabis use and concur-
rent sickle cell trait (Matta et al., 2014; Birnbaum and
Pinzone, 2008). Sickle cell disease itself is the number
one cause of secondary priapism in children ages five to
ten years old (Banos et al., 1989). The third report notes
cannabis and 3,4-methylenedioxymethamphetamine
(MDMA or ecstasy) use prior to the episode of priapism,
with MDMA already having been proven a cause of pri-
apism (Tran et al., 2008). The fourth case report notes
concurrent insulin dependent diabetes mellitus, cocaine
use, and anabolic steroid use, with cocaine and diabetes
each previously described causes of priapism (Evans
et al., 2016). An additional report gives supporting evi-
dence that synthetic cannabinoids, which are 100 times
more potent activators of the same cannabinoid type 1
receptor (CB1R) as THC, can cause priapism (Ortac
et al., 2018; Wiley et al., 2014). If synthetic cannabinoids
can cause priapism, plant cannabis, affecting the same
CB1R, would also be capable to potentiate this reaction.
In total, there are over 400 psychoactive compounds
in cannabis. Of these, delta-9-tetrahydrocannabinol, or
THC, is both found in the highest quantities and the pri-
mary psychoactive compound (Atakan, 2012). THC in-
teracts with the two primary cannabinoid receptors,
Cannabinoid type 1 receptor and cannabinoid type 2 re-
ceptor (CB2R). THC primarily interacts with CB1R, with
its major psychoactive effects due to CB1R’s presence in
the central nervous system’s basal ganglia, limbic system,
hippocampus, and cerebellum; however, CB1R can also
be found throughout the peripheral body, notably in the
peripheral nervous system, uterus, testicular tissues, and
vasculature (Russo and Guy, 2006; Pagotto et al., 2006;
Pertwee, 2006). It is possible that the sympathetic block-
age thought to occur as a result of cannabinoid activity
limits the ability of the thoracolumbar sympathetic path-
way to cause detumescence or that the now unopposed
sacral parasympathetic activity that initiated the erection
increases the risk for priapism (Dean and Lue, 2005). Al-
ternatively, cannabinoids direct vascular effects could
potentiate the unrelenting erection notable in priapism.
A third possible effect of more chronic cannabis
use involves the thrombogenic effects caused by in-
creased platelet activation (Randall, 2007). There is
noted expression of CB1R and CB2R on platelets and
during THC use there is a measurable increase in
platelet expression of glycoprotein IIb-IIIa and P-
selectin, resulting in greater platelet activation
(Deusch et al., 2004). This culminates in a 4.8-fold in-
crease in myocardial infarction in the 60 min after
THC use (Mittleman et al., 2001). These factors to-
gether could lead to thrombotic causes of priapism,
similar to that noted in sickle cell patients. Our pa-
tient has a direct, albeit circumstantial, connection
between his recurrent (stuttering) priapism and can-
nabis use. He notes recurrent priapism when heavily
using cannabis at age sixteen and seventeen. These
episodes each lasted under four hours and resolved
without medical intervention or medical examination.
When the patient stopped using cannabis at age
eighteen, his priapism resided, with no notable epi-
sodes in his twenties. He once again resumed his use
of cannabis over six months ago and noted at least a
dozen episodes that self-resolved in under four hours
at home. The abstinence and subsequent use of can-
nabis were the only appreciable factors in this pa-
tient’s battle with recurrent unwanted erections.
Conclusion
In conclusion, cannabis use is a likely cause for priapism
in our patient. He had no medical history other than
mild hypertension, he took no medications, and used
only cannabis, supported by his urinary drug screen.
Further, his history exhibited a convincing correlation
between his cannabis use and his episodes of recurrent
priapism. Because cannabis is the most widely used illicit
substance, its link to priapism suggests it may soon be-
come more prominent within the emergency department
(Ortac et al., 2018).
Abbreviations
CB1R: Cannabinoid type 1 receptor; CB2R: Cannabinoid type 2 receptor;
ED: Emergency department; PDE: Phosphodiesterase;
THC: Tetrahydrocannabinol
Montgomery et al. Journal of Cannabis Research (2020) 2:7 Page 2 of 3
Acknowledgements
None.
Authors’contributions
SM, KS, and JS saw the patient. SM drafted the manuscript, and all authors
contributed substantially to its revision. JS takes responsibility for the paper
as a whole. All authors read and approved the final manuscript.
Funding
N/A
Availability of data and materials
N/A (retrospective chart review)
Ethics approval and consent to participate
Written informed consent was obtained from the patient.
Consent for publication
Written informed consent was obtained from the patient.
Competing interests
The authors declare that they have no competing interests.
Author details
1
Coliseum Medical Centers/ Mercer University, 350 Hospital Drive, 31217
Macon, Georgia, United States.
2
Southeastern Urology Associates, Macon,
Georgia, United States.
3
Envision Physician Services, Nashville, Tennessee,
United States.
Received: 19 March 2019 Accepted: 19 January 2020
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