Pre- and postjunctional effects of neuromuscular blocking agents and their antagonists.

A 23-yr-old black man with a history of chronic renal failure secondary to Alport’s syndrome was admitted to this hospital because of priapism. Medications at the time of admission included only propranolol. The patient noted a painful erection after intercourse that persisted for 12 hr until admission. Laboratory findings on admission included blood urea nitrogen 62 mgidl, hemoglobin 10.4 g/dl, and potassium 5.3 mEq/L. Hemoglobin electrophoresis did not reveal sickle cell disease or trait. Initial therapy included ice packs and amyl nitrate inhalation. The priapism persisted and the patient was brought to the operating room. Diazepam (10 mg) followed by ketamine in 50-mg increments to a total of 150 mg was administered without effect on the priapism. Inhalation anesthesia with nitrous oxide and oxygen (3:2) and halothane increasing in 0.5% increments up to 3% was initiated. This too, was ineffective, so 15 min after induction of anesthesia, 1 mg of physostigmine was also administered. We continued the halothane for another 35 min until it was decided to treat the patient surgically. A corpus cavernosa/spongiosum shunt and circumcision was performed. After this procedure, detumescence was only partially achieved. Priapism is caused by obstruction to the outflow of blood from the corpus cavernosa. If obstruction to flow within the corpus cavernosa is prolonged, evacuation of blood becomes more difficult because of increased viscosity and sludging of blood as well as edema formation (2). Initially priapism may be secondary to an autonomic imbalance and then ketamine and physostigmine might be successful if used early for the correction of this condition, but if, as in the present case, treatment is delayed, ketamine and physostigmine may not be successful.