Letters to the Editor

RE: NEPHROVESICAL SUBCUTANEOUS STENT: ANALTERNATIVE TO PERMANENT NEPHROSTOMY

I. Nissenkorn and Yehoshua GdorJ Urol, 163: 528–530, 2000

To the Editor. Percutaneous nephrostomy is an accepted method ofpalliative treatment for patients with end stage renal failure, septic pyelo-nephritis or hydronephrosis causing intolerable pain secondary to malig-nant ureteral obstruction in whom conventional ureteral stenting hasfailed.1 Recently, a number of reports on different extra-anatomic stentsused subcutaneously to deviate urine from kidney to bladder have beenpublished.2

We used a subcutaneous urinary diversion stent set in 5 patients. Im-planting or later replacing a stent of 2 parts connected with a plugginginterface seems to be simpler but our experience shows that the 10.2FrDouble J* stent can be implanted or replaced easily.3 We report our meth-ods.

Implantation can be performed in a 3 to 4 step subcutaneous tunneling.For urgent cases we performed common percutaneous nephrostomy, whichcan be replaced by an extra-anatomic stent following stabilization of thepatient. We used a guide wire to replace a previously placed percutaneousdrain with an extra-anatomic stent. In uremic cases the sonographicallysuperior kidney should be drained percutaneously and can be replacedwith an extra-anatomic stent after a definitive decrease of biochemicalparameters. Before extra-anatomic stent implantation the patient shouldbe infection-free, that is urine culture negative. The procedure is alsoappropriate in patients without uremia who have pyonephrosis or severepain caused by an obstructed ureter. In these cases a nephrostomy tubeshould be inserted first and after bacteriological, biochemical and clinicalstabilization replacement with an extra-anatomic stent can be performed.The distal part of an extra-anatomic stent can be inserted into a cachecticpatient by revealing the bladder wall through a small incision for thecatheter instead of a puncture. The bladder wall is closed and sealed by a“Z” suture. Tight closing of cutaneous entry points is necessary. Afterimplantation of the stent biochemical, bacteriological and radiological mon-itoring as well as urine sediment analysis should be performed every 3weeks. Administration of low doses of norfloxacin for 3 to 4 weeks can helpprevent biofilm formation around and in the stent.4 After implantation ofan extra-anatomic stent patients should be checked regularly by a urolo-gist.

Respectfully,Akos Pytel, Joseph G. Szekely and Laszlo M. FarkasDepartment of UrologyUniversity Medical School PecsMunkacsy M. u. 2.H-7621 PecsHungary

1. Feng, M. I., Bellman, G. C. and Shapiro, C. E.: Management ofureteral obstruction secondary to pelvic malignancies. J En-dourol, 13: 521, 1999

2. Minhas, S., Irving, H. C., Lloyd, S. N. et al: Extra-anatomic stents inureteric obstruction: experience and complications. BJU Int, 84:762, 1999

3. Lingam, K., Paterson, P. J., Lingam, M. K. et al: Subcutaneousurinary diversion: an alternative to percutaneous nephros-tomy. J Urol, 152: 70, 1994

4. Wollin, T. A., Tieszer, C., Riddel, J. V. et al: Bacterial biofilmformation, encrustation, and antibiotic adsorption to ureteralstents indwelling in humans. J Endourol, 12: 101, 1998

RE: A NEW DIRECT TEST OF BLADDER PERMEABILITY

D. R. Erickson, N. Herb, S. Ordille, N. Harmon andV. P. Bhavanandan

J Urol, 164: 419–422, 2000

To the Editor. We agree with the authors that increased urothelialpermeability has an essential role in interstitial cystitis. However, we

question whether urothelial permeability has a direct association withurothelial glucosaminoglycan deficit as postulated by some. The glu-cosaminoglycan deficit lies at the root of damage, however caused, tothe urothelial cells that produce glucosaminoglycans, resulting in anenhanced susceptibility to infection.1 High susceptibility to infectionand disappearance of active transurothelial sodium-transport2 also im-ply a glucosaminoglycan deficit after sympathetic block, for examplecomplete upper motor lesion. In contrast, a glucosaminoglycan deficitcauses sympathetic overactivity in interstitial cystitis to stimulate theurothelial cells to produce compensatory glucosaminoglycans.3 In thiscontext more nitric oxide from urothelial cells and tachykinins from Cfiber nerve endings are released than is required for normal urgecontrol,4, 5 resulting in increased permeability of the urothelium andsuburothelial vessels, already at low filling volumes. As a consequenceof increased transurothelial transfer of urinary potassium, thesechanges are accompanied, in contrast to normal urge control, not byhyperemia but by relative ischemia.6 This hemodynamic thrust rever-sal is the key issue of the chronically progressive course of interstitialcystitis. The sympathetic overactivity slackens in some end stages, andthe reduced release of nitric oxide and tachykinins normalizes urothe-lial permeability. Similar to the only case of cystometric megalocystisreported by the authors, none of our patients with complete upper orlower motor lesions demonstrated any evidence of increased urothelialpermeability.

Recently, Teichman and Nielsen-Omeis reported that in patientswith interstitial cystitis glucosaminoglycan substitution with intraves-ical heparin or oral sodium pentosanpolysulfate as well as tricyclicantidepressants were successful therapy measures, especially in thosewith a positive potassium leak test (increased urothelial permeability).7This finding is in agreement with our clinical experience. Successfultherapy eliminates the primary cause of sympathetic overactivity, re-sulting in normalization of urothelial permeability and vesical circula-tion.6 The presence of increased permeability does not confirm a diag-nosis of interstitial cystitis but its absence should prevent attendingurologists from instituting a frustrating glucosaminoglycan substitu-tion. In light of the frequently painful bladder spasms triggered by 0.4M. potassium chloride, we find it legitimate to suggest the new perme-ability test reported by the authors. However, for general clinical use,this test is too costly and time-consuming, and bladder distention isunnecessary for a diagnosis. Instead of 0.4 we use 0.2 M. potassiumchloride in comparison to isotonic sodium chloride to measure maxi-mum capacity, and consider a greater than 15% reduction in maximumcapacity caused by potassium chloride as potassium leakage. We haveevaluated differences up to 80%. We have not observed painful bladderspasms with 0.2 M. potassium chloride. We believe that a suspectedincrease in urothelial permeability can be verified in a short time by aninfusion set, appropriate solutions, a catheter and a measuring cup aswell as with bladder to blood tracer tests.

Respectfully,G. HohlbruggerDepartment of UrologyUniversity of InnsbruckA-6020 InnsbruckAustria

and

C. R. RiedlDepartment of UrologyMunicipal Hospital LainzA-1134 ViennaAustria

1. Parsons, C. L., Mulholland, S. G. and Habibullah, A.: Antibacterialactivity of bladder surface mucin duplicated by exogenous glycos-aminoglycan (heparin). Infect Immun, 24: 552, 1979

2. Hohlbrugger, G. and Madersbacher, H.: Transurothelial electri-cal potential differences in the human bladder after spinalcord injury. Proc Int Continence Soc, 11: 122, 1981

3. Stein, P. C., Torri, A. and Parsons, C. L.: Elevated urinarynorepinephrine in interstitial cystitis. Urology, 53: 1140, 1999* Medical Engineering Corp., New York, New York.

0022-5347/01/1653-0914/0THE JOURNAL OF UROLOGY® Vol. 165, 914–915, March 2001Copyright © 2001 by AMERICAN UROLOGICAL ASSOCIATION, INC.® Printed in U.S.A.

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