Abstract
Cyclophosphamide (cytoxan) is an alkylating agent used extensively in the chemotherapy of leukemia, lymphomas, and selected solid tumors. Experimentally, cyclophosphamide is currently used for the treatment of steroid-resistant nephrosis in children. The drug is inert as administered orally or systemically but is metabolized to form a potent cytotoxic agent that is excreted in the urine. Adverse reactions include leukopenia, anorexia, nausea, vomiting, alopecia, vesical fibrosis, and sterile hemorrhagic cystitis. It is this last complication that may reach such severe proportions that hemorrhage cannot be controlled by conventional means. The usual cyclophosphamide cystitis is characterized by dysuria, urgency, and gross or microscopic hematuria. Approximately 7% of patients undergoing cyclophosphamide therapy develop this complication. 1,2 Cystoscopically, the bladder appears edematous and hyperemic, with multiple punctate hemorrhagic areas. Histologically, telangiectasia of subepithelial blood vessels can be found. In the great majority of cases a spontaneous remission of the hemorrhage will result with cessation of the drug and forced hydration, 3–8 but occasionally more aggressive measures must be taken to control the bleeding. Local fulgeration with the resectoscope or ball-tip electrode is usually unsuccessful, probably due to the further local mucosal breakdown with the fulgerating current. Suprapubic placement of a cystostomy tube will make irrigations more effective. Bilateral ureteral catheterizations or nephrostomies may be used to divert the cytotoxic urine. Division of the hypogastric vessels is ineffective. Unfortunately, urinary diversion into an ileal conduit may be the only means of control for this severe complication. 9–11
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