Ralph_edit.qxp 26/2/08 9:57 am Page 61
Management of Priapism
with a lowering of the PDE-5 functional set point. Therefore, when
Table 1: Aetiology of Low-flow Priapism
neuronally derived NO mediates smooth muscle relaxation, there is
insufficient PDE-5 available to degrade it. Combined with the impaired pro-
contractile effects of Rho-kinase in the corpus cavernosum, the overall
Idiopathic 30% risk
balance is towards unregulated smooth muscle relaxation.
7 Haematological Sickle cell disease
Stuttering (Recurrent) Priapism
Although poorly understood, this condition is common in patients with
sickle cell disease, although idiopathic stuttering priapism is now also
increasingly recognised. This condition usually occurs nocturnally, then Clozapine
there is a failure of detumescence on waking. Erections become painful
if the duration of the erection exceeds one hour. In sickle cell patients,
the erections are associated with the development of ischaemia.
Intracavernosal injections Papaverine 5% risk
However, recurrent priapism may also be a manifestation of short-lived
high-flow episodes. This condition may represent the early phase of a
Malignancy Metastatic prostate cancer
disease continuum that culminates in a refractory case of low-flow
priapism requiring medical or surgical intervention.
Neurological Cauda equina
Management of Priapism
Figure 1: Phalloarteriogram Showing an Arterial Fistula in a
Case of High-flow Priapism
Management of High-flow Priapism
Although patients present with less pain due to the presence of
normoxic blood within the corpus cavernosum, the persisting erection
can remain troublesome. Differentiating this condition from low-flow
priapism is a priority, and is aided by a good clinical history combined
with Doppler studies that show increased arterial blood flow to the
penis. The blood is well oxygenated and the risk of ischaemic damage
with eventual corporal fibrosis and impotence is low. Potency is reported
to be preserved in 77–86% of patients with long-term follow-up.
Arteriography combined with superselective embolisation using
absorbable material, e.g. gelfoam, is the treatment of choice in this
condition (see Figure 1).
In the presence of fistulae at the base of the
corpora, duplex ultrasound-guided compression can also be successful in
reversing the high-flow priapism. Open arterial ligation using
intraoperative ultrasound techniques has also been described.
Management of Low-flow Priapism
The initial management involves the administration of analgaesia. As the
duration of the erection increases, the tissue becomes increasingly hypoxic
and acidotic, which results in painful stimuli via nociceptors in the penis,
and opioid analgaesia is often required.
Once adequate pain relief has
been administered, aspiration of stagnant corporal blood is performed.
Figure 2: Al-Ghorab Shunt
Using a large-gauge needle and local anaesthesia, corporal blood is
aspirated by inserting the needle directly into the corpus cavernosum. The
blood appears deoxygenated and viscous. In some instances, this in itself
may resolve the problem if veno-occlusion is successfully reversed and
reperfusion allows penile detumescence.
The aspirated blood is sent
for biochemical analysis in order to determine the pO
and pH. This helps
to verify that this is indeed a low-flow priapism (as opposed to a high-flow
However, this simple procedure may not completely resolve
the problem and additional measures are sometimes required.
The next step involves the instillation of α-adrenergic agonists to induce
contraction of the corpus cavernosum and the helicine arteries. This reduces
the volume of stagnated blood and relieves pressure on the subtunical
venules, ultimately leading to detumescence. However, the cavernosal
smooth muscle may still fail to contract due to the metabolic alteration in
the immediate microenvironment of the corporal smooth muscle.
EUROPEAN GENITO-URINARY DISEASE 2007 61