Priapism is an abnormal penile erection which is generally not initiated by sexual stimulation and doesn’t lead to ejaculation lasting more than 6 hours in a case of ischemic priapism. It is an urgent medical condition that requires evaluation and often rapid treatment to avoid loss of erectile function. The priapism may result either from  reduction or loss of the normal venous outflow from the penis=veno-occlusive, ischemic, anoxic or low-flow priapism  or abnormal arterial inflow into the penis= arterial, non-ischemic or high-flow priapism.

 v  Low flow (veno-occlusive) priapism is most common form and is characterized by full, rigid and painful erection. It is associated with stasis of blood within the corpora cavernosa(corpus cavernosum) due to obstruction of the venous outflow. If lasts 4 hours or more it is considered as compartment syndrome which requires emergency medical intervention. Etiological factors include: Drugs (Therapeutic intracorporal injection of Papaverine (5%) and Prostaglandin E1 for erectile dysfunction. Psychotropic agents (Trazodone, Thioridazine, Chlorpromazine) -> block the normal smooth muscle contraction required to induce detumescence. Antihypertensives (Prazosin, Ca-channel blockers) -> smooth muscle relaxation. Recreational drugs (Cocaine, Ectasy). Anticoagulants (Heparin, Warfarin)-> cessation of therapy. Androgens (Testosterone, GnRH) – high doses in hypogonadal men). Hematological (Sickle cell disease -> commonest cause of priapism in children. Sickle cell trait -> when blood flow through penis is low -> sickle cells become more rigid and sludge within sinusoids causing intraluminal obstruction of venous outflow -> priapism, usually during sleep lasting less than 3 hours. Thalassemia. Myeloma –rare. Leukemia – rare). Neurological (Lumbar disc disease – rare, self-limiting. Cerebrovascular disease – rare, self-limiting. Epilepsy – rare, self-limiting. Spinal cord stenosis). Others (Amyloidosis. Genitourinary tract infections. Tumors of prostate and bladder -> obstruction of venous outflow. Fabry’s disease. Vasculitis)

v  High flow (arterial) priapism is less common form. It is not emergency -> penile venous outflow remains intact and the cavernosal tissue remains well oxygenated. It is caused by unregulated cavernous arterial inflow. Erection is usually painless and not fully rigid and intercourse may be possible. Patients may urinate spontaneously. Etiological factors include: Secondary to blunt trauma to the penis or perineum, leading to a laceration of the cavernosal artery or one of its branches. Penile revascularization which involve direct anastomosis of the inferior epigastric artery onto the corpora (Michal I operation) can also lead to priapism

 v  The physician must initially distinguish arterial from veno-occlusive priapism. A complete medical history and physical examination are the cornerstones of accurate diagnosis and effective treatment. The history should include medications, trauma and predisposing risk factors. Severity of pain is a fairly reliable predictor of low-flow priapism. High-flow priapism is suggested by penile or perineal trauma. Laboratory studies should include screening for psychoactive drugs and metabolites of cocaine. Also include reticulocyte count, urinalysis, complete blood count, platelets and differential white blood count. Urological management after these basic measures includes assessment of corporal blood flow status with corporal aspirate and visual inspection by blood colour and consistency. Penile angiography is indicated in a case of high-flow priapism to localize affected vessels.

v  Management include: Pain control -> dorsal nerve block, circumferential penile block, subcutaneous local penile shaft block, oral or i.v conscious sedation for pediatric patients. Aspiration of 50ml of blood through large needle and irrigation with warm, heparinised saline. Injection into cavernosa or infusion of α-adrenoceptor agonist (phenylephrine) ,,200μg,, to promote detumescence. If ineffective 500μg. Most patients will respond to it and resolve priapism within 20 minutes. Treatment of underlying causes -> sickle cell disease with exchange transfusion, myeloma with plasmapheresis, leukemia with local radiotherapy. Surgical management is done if previous methods fail. A number of procedures have been described, all of which have the same principle, namely shunting of the cavernosal blood to a low-pressure vascular system. The simplest technique has been described by Winter. Following a penile block, a Trucut needle is inserted through the glans penis into the corpora cavernosa. The aim is to remove a piece of the tunica albuginea with the Trucut needle, thereby creating a communication between the cavernosal tissue and the spongiosal tissue of the glans penis. An alternative procedure involves a direct anastomosis between the corpora and the spongiosal tissue. This is achieved via a middle incision over the urethra in the perineum, where the spongiosal tissue is thickest and there is less risk of urethral injury. A 1-2 cm diameter segment of the tunica albuginea is removed and the penis is squeezed to empty it of the priapistic blood. The corpus cavernosum is then anastomosed onto a similar window in the surface of the corpus spongiosum. Because of the communication between the corpora, the anastomosis is only necessary unilaterally. Given the potential risk to the urethra involved with the corporo-spongiosal shunt, the technique of corporo-saphenous shunting can be used in these cases unresponsive to Winter’s technique. In cases where treatment is delayed, corporal fibrosis ensues. The only therapeutic option in such patients is insertion of a penile prosthesis, which may be tehcnically demanding for the surgeon.

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