Hospital Practice

ISSN: 2154-8331 (Print) 2377-1003 (Online) Journal homepage: http://www.tandfonline.com/loi/ihop20

The Case of the Edematous Bladder William B. Seaman To cite this article: William B. Seaman (1978) The Case of the Edematous Bladder, Hospital Practice, 13:4, 195-199, DOI: 10.1080/21548331.1978.11707323 To link to this article: http://dx.doi.org/10.1080/21548331.1978.11707323

Published online: 06 Jul 2016.

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Date: 24 August 2017, At: 16:29

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The Case of the Edematous Bladder

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B. sEAMAN

Columbia-Presbyterian Medical Center

Dysuria, abdominal pain, frequency, and gross hematuria developed in a 52-year-old woman who had been receiving intermittent therapy with a combination of cyclophosphamide, methotrexate, and 5-fluorouracil for 10 months because of an unresectable

carcinoma of the ovary. Cystoscopy revealed evidence of hemorrhagic cystitis. When visualized by intravenous urography, the bladder was contracted, with an irregular mucosa that had a cobblesone or scalloped appearance, which was compatible with marked

Intravenous urograms display small, contracted bladder with scalloped contour and cobblestone mucosal pattern due to sub-

bullous edema secondary to severe cystitis. The cystitis cleared spontaneously following cessation of cyclophosphamide therapy. Cyclophosphamide was developed as a transport form of nitrogen mus(continued on page 19Q)

mucosal edema and hemorrhage in a patient receiving cyclophosphamide forunresectable ovarian carcinoma. llmpital Pradkc April 1978

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tard. It is inactive in vitro and is converted to active metabolites by phosphamidases in the liver microsomes. The active metabolites are then converted to secondary metabolites and are excreted in the urine. It is these primary and secondary urinary metabolites, not those circulating in the blood, that cause the cystitis. Two clinical and pathologic forms of cystitis have been described, acute and chronic. In the acute form, which occurs within 48 hours of a massive intravenous infusion of cyclophosphamide, edema, hemorrhage, and occasional areas of full thickness necrosis may develop. This usually responds to cessation of therapy but may be followed by insidious development of fibrosis and telangiectasia. Roentgenographically, the bladder shows contracture and an irregular cobblestonelike mucosa. The underlying cause is submucosal edema and hemorrhage which produce a scalloped, nodular contour that may be mistaken for tumor invasion. The acute form may follow administration of. the drug by either the oral or intravenous route. ·The chronic form may be asymptomatic and is detected by the presence of microscopic hematuria. Sudden onset of gross painless hematuria may also occur. Elevation of the i~ter­ trigonal ridge, ureteral obstruction, and vesicoureteral reflux can develop. Calcification of the entire bladder wall is a rare end-stage phenomenon. Johnson et al found urinary bladder fibrosis in 10 of 49 autopsied patients who had been on long-term cyclophosphamide therapy. More recently, malignant tumors have been reported. Wall et al have described five patients who received large doses of cyclophosphamide over a long period of time and, after the occurrence of hemorrhagic cystitis, developed invasive, fatal carcinomas of the urinary bladder. Other alkylating agents rarely cause hemorrhagic cystitis, although it has been reported following therapy with cytosine arabinoside. Cyclophosphamide is now also being used in the treatment of nonmalignant diseases, including severe lupus erythematosus, Wegener's granulomatosis, rheuma-

Marked improvement is seen in bladder size following cessation of cyclophOSJihamide therapy. Most other cancer chemotherapeutic agents do not cause hemorrhagic cystitis.

toid arthritis, and the idiopathic nephrotic syndrome. Hemorrhagic cystitis should signal immediate discontinuance of the drug. Giving therapy on an intermittent basis has been recommended as a possible way of avoiding

this complication, but this approach has not been uniformly successful. 0 Dr. Seaman is Professor and Chairman, Department of Radiology, ColumbiaPresbyterian Medical Center, New York.

References Aptekar RG et al: Bladder toxicity with chronic oral cyclophosphamide therapy in non-malignant disease. Arthritis Rheum 16:461, 1973 Berkson BM, Lome LG, Shapiro I: Severe cystitis induced by cyclophosphamide. JAMA ll5:6o5, 1973 Frauas RS, Shackelford CD: Cyclophosphamide cystitis with bladder wall calcification. J Assoc Canad Radioll5:3l4, 1974 Johnson WW, Meadows DC: Urinary blad-

dcr fibrosis and telangiectasia associated with long term cyclophosphamide therapy. N Eng! J Med l84:l9Q, 1971 Renert WA, Berdan WE, Baker DH: Hemorrhagic cystitis and vesicoureteral reflux secondary to cytotoxic therapy for childhood malignancies. Am J Roentgenol 117=664. 1973 Wall RL, Clausen KP: Carcinoma of the urinary bladder in patients receiving cyclophosphamide. N Eng! J Med l93:l71, 1975 Hospital Practke April 1978

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