Abstract and Introduction
Abstract
A cohort of 20 patients with delayed priapism who underwent treatment at the Emergency Department of our academic referral centers between January 2002 and April 2010 was studied. Of these, 16 cases suffered from a low-flow priapism. A total of 6 cases were managed non-surgically, 10 required shunt surgery, and of these 5 were treated by early penile prosthesis surgery. Prostheses were easily implanted in all patients with a mean operative time of 94 min. No intraoperative complications and no infection were registered. All patients with an inflatable prosthesis complained a reduction in penile sensibility that lasted 3 months. All patients were satisfied with the results of surgery (International Index of Erectile Function Questionnaire-5, Q5 mean value 4), and all were successfully engaging in satisfactory sexual intercourses. No significant loss of penile length, neither apical erosion nor extrusion was recorded. Early insertion of a penile prosthesis is a simple and safe procedure in patients with ischemic priapism, which failed to respond to conservative management. Early insertion of a prosthesis helps to maintain adequate penile length, resolve priapism and, in the long term, it results in high satisfaction rates.
Introduction
Ischemic priapism is a relatively rare sexual-function-threatening andrological emergency, with an incidence of 1.5 per 100 000 person-year. Ischemic priapism can occur at all ages, from newborn to elderly, with an undesirable, rigid and painful erection, which persists in the absence of sexual stimulation, not being relieved by either ejaculation or orgasm.
American Urological Association guidelines define priapism as a persistent penile erection, of >4 h in duration, that continues hours beyond, or is unrelated to, sexual stimulation. Typically, only the corpora cavernosa are affected. Ischemic (veno-occlusive, low flow) priapism is a non-sexual, persistent erection characterized by little or no cavernous blood flow and abnormal cavernous blood gases (hypoxic, hypercarbic and acidotic). The corpora cavernosa are rigid and tender to palpation. Patients typically report pain. A variety of etiological factors may contribute to failure of the detumescence mechanism in this condition. Ischemic priapism is an emergency. Resolution of ischemic priapism is characterized by the penis returning to a flaccid, non-painful state. However, in many cases, persistent penile edema, ecchymosis and partial erections can occur, and it may mimic unresolved priapism. Resolution of priapism can be verified by measurement of cavernous blood gases or blood flow measurement by color duplex ultrasonography.
In the long term, up to 25% of patients with ischemic priapisms induce erectile dysfunction.
Indeed, especially when priapism is not adequately and promptly treated, histopathological changes drive the cavernosal tissue toward irreversible fibrosis. This usually happens after 48 h, along with the necrosis of the vasa and corpora cavernosa smooth muscle cells, and with the consequent transformation those smooth muscle cells into fibroblast-like cells. It is not clear at which absolute time point such damages become unreversible; moreover, it may also vary according to the etiology of ischemic priapism and the degree of the pre-existing damage of the corpus cavernosum smooth muscles. In this context, it has been demonstrated that after 6 consecutive hours of ischemia, acidosis, glucopenia, hypoxia, hypercapnia and anoxia occur. Both in vitro and in vivo models have shown that anoxia and glucopenia may function as two independent damaging factors to the corpora cavernosa smooth muscles. Finally, there is experimental evidence that irreversible histopathological alterations are caused by the combination of a state of acidosis, glucopenia and hypoxia that last for >4 h.
From the therapeutic standpoint, the initial management is conservative, and involves exercise, aspiration and intracorporal injection of α-adrenergic agonists, in order to obtain the smooth muscle relaxation, blood outflow and prompt penile detumescence.
A successful outcome of the conservative approach relies on the actual duration of the episode of priapism, being surely more effective (even with the injection of relatively high doses of α-adrenergic agonists) for episodes lasting <24 h. Episodes either lasting >24 h or not responsive to conservative approaches require more aggressive therapeutic strategies, such as shunt surgery.
However, there is no universal consensus about the management of delayed presentations of ischemic priapisms or medical refractory priapism.
In general, α-adrenergic agonists should be used in all patients, irrespective of the time of presentation, whereas shunt surgery should be offered to the cases of ischemic priapism lasting ≤72 h, starting with a distal shunt (Winter, Al-Ghorab, Ebbehoj or more recent Brant shunt) and performing a proximal shunt (Quackels, Barry or Grayhack shunt) in cases of distal shunt failure. In this context, the longer the veno-occlusive priapism event, the greater the chance of permanent erectile dysfunction.
There is a group of patients who do not respond to the shunt surgery. In these latter men, and in patients with either a delayed presentation or a severe long lasting condition, erectile dysfunction has to be treated by an elective penile prosthesis surgery in order to contrast the devastating consequences, such as fibrosis and penile shortening.
Likewise, these two groups could benefit by an immediate penile prosthesis implantation, the former group firstly to resolve the dramatic priapic episode, and overall to resume erectile functioning. Thus, early penile prosthesis insertion offers some advantages, including (a) the resolution of the episode of priapism, (b) the treatment for the inevitable erectile dysfunction and (c) the prevention of penile shortening due to severe fibrosis.
These observations prompted us to present our experience in the treatment of refractory ischemic priapism with early inflatable penile prosthesis insertion.