Priapism is a pathologic condition of prolonged penile erection that persists beyond, or is unrelated to sexual stimulation. The word priapism is derived from the Greek word Priapus, a fertility god who was described as having a giant phallus. Priapsim is a significant medical condition that requires emergent evaluation and management.
There are two basic types of priapism:
A. Ischemic Priapism
The pathophysiology of ischemic priapism involves an imbalance of the vasoconstrictive and vasorelaxing mechanisms, resulting in a closed penile compartment syndrome. The ischemia results from hypoxia, hypercapnia and acidosis, and leads to cavernosal muscle dysfunction. Later, atrophy with subsequent corporal fibrosis occurs.
Ischemic (venoocclusive) priapism is the most common priapism. Patients present with painful, rigid, prolonged erections beyond several hours. There is high intracavernosal pressure due to the occlusion of blood leaving the erectile muscle and no fresh arterial inflow. The ischemia is progressive with time, and may lead to loss of erectile function and fibrosis if not treated in a timely and effective manner.
B. Arterial (non-ischemic) Priapism
Arterial (non-ischemic) priapism is a less common form, often resulting from trauma, with unregulated high cavernosal blood inflow. The penis is usually painless and not fully rigid. Duplex Doppler flow ultrasound scan can establish the diagnosis. It can be observed, and generally does not need immediate medical therapy. If the priapism persists, selective angiography and embolization may be necessary to treat the arterial-lacunar fistula.
Etiology (Causes) of Ischemic Priapism
1. Pharmaceutical agents used in the treatment of erectile dysfunction (80% of cases), such as tadalafil and vardenifil, as well as penile injection with vasoactive agents such PGE1, papaverine or combinations.
2. Antihypertensive medications such as phenoxybenzamine, labetalol, and prazosin can induce priapism due to their a-adrenergic blocking activity, preventing or delaying physiologic detumescence.
3. Anticoagulants such as heparin and warfarin, which can cause a relative hypercoagulable state occurring after therapy is discontinued.
4. Tricyclic antidepressants such as Trazodone and benzodiazepines. Antipsychotic medications such as phenothiazines and risperidone, as well as illicit drugs such as cocaine and marijuana can result in priapism.
5. Hematological disorders like sickle cell disease, thalassemia, polycythemia, etc.
6. Malignancies such as leukemia, multiple myeloma and many metastatic cancers.
Diagnosis and Treatment of Ischemic Priapism
After getting pertinent history and performing an examination confirming the state of priapism (painful rigid erection usually not involving the glans), the general diagnostic tests recommended include complete blood count with differential, platelet count, urine analysis, and drug screening if indicated. Intravenous fluids, penile block, and analgesic medication can be administered, followed by needle aspiration of corporal blood. In patients with sickle cell disease, alkalization and oxygen supplement should be administered.
Intracorporeal injection of an alpha agonist such as phenylephrine (1 mg or 1 ml drawn from bottle and add 9 ml normal saline) can be done. Use a 27 gauge needle to inject 0.3ml to 0.5 ml per injection into the corporal cavernosa, and repeat in 10 to 15 minutes, up to a maximum of 1.5 ml, while monitoring patient vital signs.
Corporal irrigation using a 16-18 gauge needle inserted perpendicularly into the corpora can be done, using 20-30 ml normal saline until bright red blood is obtained. This helps to restore the oxygenated blood flow back into corporal tissue.
If these treatments are successful, penile detumescence is achieved, and the penis is then wrapped with an elastic bandage to keep the flaccid state and prevent spontaneous return of priapism. The patient is monitored for several hours until stable to be discharged. If partial success is achieved, a Doppler duplex ultrasound evaluation can be helpful, and the patient should be kept for observation.
If conservative therapy does not achieve prompt detumescence, surgical shunting performed by urologist should be considered as soon as possible. In general, if the duration of priapism is less than 24 hours, there is about 90% chance of returning the erectile function to the baseline state before priapism, in contrast to only 20 % for prolonged priapism over several days.
Although the incidence of priapism is not common (about 1 in 100,000 persons/year), patients with priapism often present to healthcare providers other than urologists, such as personal physicians, urgent healthcare clinics and emergency rooms.
As the potential for serious complications from priapism is on the rise, largely as a result of the use of erectile dysfunction medication, healthcare providers must be aware of the potentially serious risks and complications if treatment is delayed or improperly performed. Timely diagnosis and treatment is essential. A good knowledge of this condition, with proper and timely treatment can result in successful resolution, and avoid serious adverse outcomes and potential medical legal issues.
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