Dr. med. Dirk Manski

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Review literature: (Serel and Melman, 2000).

Definition of Priapism

Priapism is an unwanted persisting penile erection, which lasts at least 2 h without sexual stimulation. Priapism is associated with the risk of erectile tissue damage.

The name priapism is derived from Priapus, the Greek god of fertility.

Epidemiology of Priapism

The incidence of priapism is about 1–3/100 000. Intracavernosal pharmacotherapy and sickle cell disease are strong risk factors. Age groups at special risk are children between 5–10 years (sickle cell disease) and men between 20–50 years (medication and drugs), but priapism can be possible at any age.

Causes (Etiology) of Priapism

Idiopathic Priapism (30%):

The failure of the physiological detumescence is unclear.

Priapism Induced by Medication and Drugs (20%):

Cocaine, alcohol, painkillers, psychiatric drugs, anesthetics, anticonvulsants or antihypertensives may cause priapism. The antagonism of α1-receptors prevents the smooth muscle contraction of the erectile tissue and thus the detumescence. Phosphodiesterase inhibitors are only a rare cause for priapism.

Sickle Cell disease (10–20%):

A vaso-occlusive crisis is caused by sickling of the red blood cells; the crisis is induced by manipulation or nocturnal hypoventilation and results in a decreased venous outflow and ischemic priapism. Ischemia increases the sickling of the red blood cells worsens the impaired venous outflow. The lifelong risk in homozygous sickle cell disease of suffering a priapism is 40–90%.

Intracavernous Pharmacotherapy:

Older preparations of the intracavernous pharmacotherapy, such as papaverine (opium alkaloid) and phentolamine (alpha-Blocker), cause more often priapism than pharmacotherapy with prostaglandin E1. About 1% of men treated with prostaglandin E1 experience priapism.

Neurological diseases:

Spinal cord compression (lumbar stenosis, herniated disc) or rarely spinal anesthesia can cause priapism.

Malignant Neoplasms:

Tumor infiltration results in venous compression and may cause priapism. Generally rare, tumors causing priapism are leukemia, prostate cancer, renal cell carcinoma, melanoma and inflammatory pelvic tumors.

Priapism due to Trauma:

A blunt perineal trauma or puncture of the erectile tissue may cause injury to arteries in the corpus cavernosum. The increase of arterial flow may exceed the venous capacities and a non-ischemic priapism results.

Rare Causes of Priapism:

Long-lasting sexual activity, insect bites, parenteral nutrition (caused by fast infusion of highly concentrated fat).

Pathophysiology and Clinical Manifestations of Priapism

Ischemic (Low-Flow) Priapism

The failure of the physiological detumescence causes the persistence of the erection, which is tight and painful. The pressure within the erectile tissue is higher than the diastolic blood pressure (80–120 mmHg), an insufficient blood flow leads to ischemia. Ischemia causes paralysis of the smooth muscle cells in the erectile tissue and creates a vicious circle. The high fibrinolytic activity in the erectile tissue prevents the formation of thrombi. An irreversible damage of the erectile tissue with fibrotic healing is probable after 12 hours of ischemic priapism.

Non-Ischemic (High-Flow) Priapism

The increased arterial inflow is higher than the maximum venous outflow. There is no risk of ischemic damage to the erectile tissue. The erection in non-ischemic priapism is less tense and less painful.

Diagnostic Work-Up of Priapism

Laboratory Tests:

Cavernous Aspiration with Blood Gas Sampling:

Blood gas testing from aspirated blood of the corpus cavernosum is essential to differentiate between high- or low-flow priapism using the oxygen concentration, carbon dioxide concentration and acidosis. High-flow priapism is likely to show arterial blood gas values (pO2 >70 mmHg, no acidosis, pCO2 <50 mmHg). Patients with low-flow priapism have typically venous or ischemic blood gas values (pO2 <40 mmHg, acidosis, pCO2 >60 mmHg).

Doppler-Ultrasound of the Penis:

Treatment of Priapism

Therapeutic Blood Aspiration:

After blood gas sampling to differentiate between low-flow and high-flow priapism, further aspiration of blood allows the injection of drugs with α-adrenergic activity (see below).

α-adrenergic Drugs:

After therapeutic blood aspiration, fractional intracavernosal injection of α-adrenergic drugs, e.g. highly diluted epinephrine or norepinephrine, are done to promote smooth muscle contraction. Control of the arterial blood pressure is important, repeated injection are possible if no hypertension is present. After incomplete detumescence, cooling and intermittent compression of the penis with a child's blood pressure cuff may improve the clinical situation.

Additional Treatment of Priapism in Sickle Cell Disease:

Surgical Treatment of Ischemic Priapism:

If conservative treatment of ischemic priapism fails, implementation of a surgical shunt between corpus spongiosum and corpus cavernosum is necessary immediately.

Winter shunt:

Invasive technique of first choice with a high success rate. Puncture of the corpus cavernosum (both sides) through the glans with a thick peripheral venous catheter or biopsy true-cut needle leads to a temporary shunt. Aspiration of the blood and flushing of the corpus cavernosum with alpha-adrenergic agonists is also possible (Winter, 1976).

Ebbehoj shunt:

Analogous to the Winter shunt, a scalpel stitch opens the corpus cavernosum through the glans on either side. The glans is closed with a thin monofiliament suture (Ebbehoj, 1974).

Al-Ghorab shunt:

Do a transverse incision of the glans distal to the sulcus. A circular incision of the tunica albuginea of the corpora cavernosa is done. Close the glans incision with thin monofiliament sutures (Ercole and others, 1981).

Bulbar cavernospongiosal shunt:

Last resort, if distal shunting fails. Exposure of the bulbar corpus spongiosum and corpus cavernosum. Bilateral side-to-side anastomosis after oval excision of the tunica albuginea of the two corpora.

Treatment of High-Flow Priapism:

Spontaneous resolution of high-flow priapism is likely (60%), ice packs may help in spontaneous thrombosis of the ruptured artery. If conservative treatment fails, selective embolization of internal pudendal artery is the next step. The last treatment option is the surgical ligation of the ruptured artery, which can be identified with intraoperative Doppler ultrasonography.

Prognosis after Priapism

Erectile dysfunction results in up to 50–90%, if surgical treatment is necessary. Rarely, a syndrome of recurrent low-flow priapism evolves, which is explained by endothelial changes.

Index: 1–9 A B C D E F G H I J K L M N O P Q R S T U V W X Y Z


Ebbehoj 1974 EBBEHOJ, J.:
A new operation for priapism.
In: Scand J Plast Reconstr Surg
8 (1974), Nr. 3, S. 241–2

Ercole u.a. 1981 ERCOLE, C. J. ; PONTES, J. E. ; PIERCE, Jr.:
Changing surgical concepts in the treatment of priapism.
In: J Urol
125 (1981), Nr. 2, S. 210–1

Melman und Serels 2000 MELMAN, A. ; SERELS, S.:
In: Int J Impot Res
12 Suppl 4 (2000), S. S133–9

Winter 1976 WINTER, C. C.:
Cure of idiopathic priapism: new procedure for creating fistula between glans penis and corpora cavernosa.
In: Urology
8 (1976), Nr. 4, S. 389–91

  Deutsche Version: Priapismus