Defined as high-flow and low flow types with other terms of nonischemic and ischemic type priapism, respectively.
Priapism results in 5.3 emergency department visits for 100,000 patient years in the US.
Refers to a prolonged penile erection, typically greater than four hours duration, that lasts beyond or is unrelated to sexual stimulation.
Erections associated with ischemic priapism were typically persistently painful, while those associated with non-ischemic priapism are nearly always painless.
Prompt evaluation and treatment can prevent tissue injury, fibrosis, and irreversible erectile dysfunction.
Establishing whether the corporate cavernosa are fully rigid, with sparing of the corporate spongiosum and glans penis, suggesting ischemic priapism,or less than fully rigid, the latter, being more typical of nonischemic priapism.
Measuring corpus cavernosum blood gas can establish ischemic versus nonischemic priapism.
The duration determines the outcome.
Urgent intervention within 6 to 12 hours of onset to is required to prevent permanent erectile dysfunction, penilefibrosis, and penile shortening.
Two main types exist: ischemic and nonischemic, and distinguishing the correct type is essential for management.
Ischemic priapism is also known as Veno occlusive or low-flow priapism and accounts for 95% of cases.
Ischemic priapism is characterized by venous congestion, increased inttracorporal pressure and little or no arterial inflow.
With ischemic priapism patients typically present with pain in the penis, a rigid corpora cavernosa, and dark appearing blood on penile aspiration with abnormalities on cavernous blood gas analysis of acidemia, hypoxia, and hypercapnia.
The most common ischemic priapism etiologies are: sickle cell disease and other hemoglobinopathies, alcohol abuse, recreational drug abuse, vasoactive medications, particularly antihypertensives, antipsychotics, antidepressants, and intracavernosal therapies for erectile dysfunction.
Up to 42% of men with sickle cell disease experience priapism during their lifetime.
Rarely ischemic priapism can be associated with GU tract malignancies, hematologic dyscrasia such as polycythemia, leukemia, and anesthesia general and regional, and spinal cord injury.
Penile ultrasound can distinguish high-flow priapism from no-flow lesions but poorly differentiates low-flow type abnormalities.
Low-flow type priapism requires immediate treatment.
Ischemic priapism is a urologic emergency and has significant potential for complications over time, with rates of erectile dysfunction as high as 90% if ischemic priapism lasts more than 24 hours.
In low-flow priapism penile aspiration of the corpora cavernosa is both a diagnostic and therapeutic measure by decreasing intracorporeal pressure.
Low-flow type disease indicates an interruption in blood flow with corporeal blood similar to venous blood on oxygen and pH content.
In low-flow priapism measures are taken to prevent tissue injury from vascular stasis and to restore normal blood flow.
Management of an acute episode of ischemic priapism includes penile aspiration of old blood, intracavernosal alphaadrenergic agonist injections such as phenylephrine, and surgical shunting procedures if necessary.
Surgical procedures create fistulas to promote drainage of deoxygenated blood from the corpora cavernosa.
Distal shunts are preferred over proximal shunts and is associated with lower risk of complications such as erectile dysfunction.
Infusion of penile phenylephrine in low-flow disease can relieve symptoms.
Treatment is usually with intracavernosal phenylephrine injections.
If conservative measures do not relieve symptoms a Winter shunt, creation of 1-2 fistulas between the glans penis and the corpora cavernosa, is performed in low-flow disease.
Supportive therapy in patients with sickle cell associated disease includes alkalinization, hydration and the use of analgesics.
Embolization of the cavernosal artery can alleviate symptoms of high-flow priapism.
Non-ischemic priapism is referred to as arterial or high-flow priapism.
Nonischemic priapism is caused by increased arterial blood flow into the corpora cavernosa that overwhelms the venous drainage system but does not create an ischemic environment.
With nonischemic priapism the penis is nontender and partially tumescent.
Penile aspiration reveals right red blood and blood gas analysis resembles that of arterial blood without acidemia or hypoxemia.
The most common precipitating etiology of non-ischemic priapism is peroneal trauma, which can cause vascular injury to the internal pudendal artery or its branches.
Non-ischemic priapism does not require emergent treatment and patients can be observed for a spontaneous resolution that occurs in more than 2/3 of cases.
Selective arterial embolization can be performed for persistent symptoms.
Recurrent episodes of ischemic priapism may occur, and such patients need hematologic evaluation to rule out sickle cell disease or other the blood dyscrasias.
Therapies/treatments to prevent recurrent ischemic priapism include hormonal antiandrogens, five alpha-reductase inhibitors, Gonadotropin releasing hormone agonists and non-hormonal therapies including gabapentin, baclofen, digoxin, and phosphodiesterase type five inhibitors.
Hormonal agents for priapism can suppress testosterone levels and their effects-antiandrogens block binding to androgen receptors while gonadotropin releasing hormone agonists downregulate the release of gonadotropins from the pituitary gland.
Ketoconazole, an antifungal agent, inhibits androgen synthesis in the adrenal cortex and testicular Leydig cells with a rapid onset and short half-life.
Ketoconazole plus corticosteroids for recurrent ischemic priapism had a resolution rate of symptoms of 94%.
The tumescence rates are is high is 93% with rapid first line therapies intracavernosal phenylephrine with aspiration and 70 to 92% report preserved erectile function afterward.