10
ESSM
Today
Key from Kols:
Priapism
by Evangelos Zacharakis
Evangelos Zacharakis
(PhdfrS, fEcSM, fEaa)
Consultant Urological Surgeon
The Urology Centre, Guy’s Hospital
Great Maze Pond
London, SE1 9RT, UK
Email: evangelos.zacharakis@
doctors.org.uk
Strategies for the management
of ischaemic priapism
The pathophysiology of ischaemic priapism
is still not completely understood although
the initiating mechanisms are likely to be
multifactorial involving central neuronal
pathways, alterations in the corpus caver-
nosum microenvironment, modulation of the
smooth muscle contractile machinery and
aberrant neurotransmitter regulation in the
corpus cavernosum leading to dysregulation
of the smooth muscle.
Introduction
Priapism is defined as a prolonged penile
erection that lasts longer than 4 hours in the
absence of sexual stimulation and remains de-
spite orgasm. It is commonly classified into non
ischaemic (high flow), ischaemic (low flow) and
stuttering (recurrent) subtypes (1-5). Ischemic
priapism is the most common type of priapism
accounting for more than 95% of all episodes.
Obstruction of the penile venous outflow leads
to stasis of blood witin the corpus cavernosum
formatting a a compartment syndrome which
results in the development of hypoxia, acidosis
and glucopenia (6).
Ischemic priapism is a medical emergency as the
progressive ischemia within the cavernosal tissue
is associated with time-dependent changes in
the corporal metabolic environment, which leads
to smooth muscle necrosis. The absolute time
point at which irreversible damage to the corpus
cavernosum smooth muscle occurs is unknown
and may vary according to the aetiology of is-
chemic priapism and the degree of pre-existing
smooth muscle dysfunction. There is evidence,
however, that even after 6 h of ischemia, irre-
versible changes have already started to occur
(7–10). Broderick and Harkaway analysed the
change in the cavernous blood gas alterations in
the pO2, pH and pCO2 during the erection and
found out that fter 240 minutes the cavernous
tissue is no longer perfused by highly oxygen-
ated blood (11). Histologically the components
of the corpus cavernosum undergo progressive
changes as the duration of priapism increases.
In cases where priapism is of a short duration
(less than 12 hours) the tissue consisted of minor
endothelial defects with occasional lymphocytic
infiltration with no alteration in the smooth mus-
cle cells. It is only after 12 to 14 hours of low-
flow priapism that trabecular smooth muscle
cells show the beginning of focal cytoplasmic
transformation which manifests as an increase
in size of the perinuclear cytoplasm, endoplasmic
reticulum, ribosomes and Golgi apparatus. At
between 24 to 48 hours duration widespread
endothelial destruction and exposure of the
basement membrane occurs with subsequent
thrombocyte adherence. In addition to this the
smooth muscle cells undergo a transformation as
described above as well as necrosis. Persistent
blood stasis for longer than two days is asso-
ciated with infiltration of the trabecular tissue
with inflammatory cells and smooth muscle cells
undergoing necrosis or phenotypic change into
fibroblast like cells (12).
Even if left untreated, unless secondary to direct
malignant infiltration of the corpora, the degree
of tumescene tends to subside spontaneously
with time and the necrotic cavernosal tissue un-
dergoes fibrosis, resulting in erectile dysfunction
refractory to medical treatment and in a short-
ened indurated penis (7).
Diagnosis of ischaemic priapism
The diagnosis of ischaemic priapism is based
on the clincial history and examination, radio-
logical imaging and blood gas analysis, whilst
urine toxicology, haematological screening and
abdominal imaging are required to investigate
the underlying cause.
Color Doppler Ultrasonography of the penis is
used to assess the flow in the cavernosal arteries
and corpus cavernosum to differentiate ischae-
mic from non-ischaemic priapism. Penile Doppler
will demonstrate reduced or absent flow within
the cavernosal arteries and impaired perfusion
of the distal corpus cavernosum. However, after
corporal blood aspiration the interpretation of pe-
nile Doppler can be difficult due to aberrant high
flow in segments of the corpus cavernosum (13,
14). Therefore a more reliable investigation to
distinguish between ischaemic and non-ischae-
mic priapism corporal blood gas analysis, which
will typically show ischaemic, venous blood with
pO2 <30mmHg and pCO2 >60 mmHg and pH
<7.25 in cases of low flow priapism. A recent
series of 23 patients, in which the radiological
findings have been correlated with biopsies from
the corpus cavernosum, Gadolinium enhanced
high-definition Magnetic Resonance Imaging
(MRI) of the penis has a sensitivity of 100% when
used to detect the presence of necrosis of the
cavernosal smooth muscle (15). Therefore, this
imaging modality may represent an extremely
useful imaging modality to asses the corporal
tissue viability (Fig 1).
Management of ischaemic priapism
The goal of management of ischemic priapism
involves successful detumescence and prese-
vation of cavernosal smooth muscle function in
order to prevent penile shortening and refractory
erectile dysfunction in the long term.
The initial conservative management of IP, if
the duration of the erection is between 4 to
24 hours, involves ejaculation, vigorous physi-
cal exercise and cold baths with the aim to
stimulate the noradrenergic system to release
cathecolamines, which would stimulate smooth
muscle contaction via sympathomimetics and
induce detumescence.
1) Aspiration and instillation of sympatho-
mimetics
If conservative management fails, the next step
involves aspiration of ischaemic blood from the
corpora cavernosa using 19G ‘butterfly’ needle
through the glans penis and into the corpora or
