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Case Reports
 
Peri-renal Urinoma : A Complication of Intravenous Hydrotherapy for Treatment of Small Ureteric Calculus
 
Pankaj N Maheshwari*, Shah Hemendra**, Vikram B Kaushik**, Rajesh Jain**, Vishal P Parmar**
 
In last five years three patients presented with peri-renal urinoma after this mode of unscientific treatment. We report one such case.
 
Introduction

It is a common practice to treat non-obstructive ureteric calculi by ‘hydrotherapy’. Hydrotherapy has meant forced diuresis by intravenous or oral fluids. Patient is hospitalized for three to four days and four to five litres of fluid is given intravenously with diuretics every day in the hope of calculus clearance.
 
Case Report

Thirty eight year old male was diagnosed to have a 6 mm right upper ureteric calculus with mild hydro-ureteronephrosis. He was treated by intravenous hydrotherapy with diuretics and anti spasmodics. He presented 48 hours later with severe renal angle pain and fever. Ultrasonography showed a moderate perirenal collection. Computed tomogram confirmed the diagnosis (Fig. 1).

Patient was hospitalized and Double J ureteric stent was inserted. He was given a broad-spectrum antibiotic cover.

Hydronephrosis and perirenal collection resolved within 3 weeks. The small calculus got evacuated conservatively. Ultrasonography seven days after stent removal showed no perirenal collection.
 
Discussion

It is almost a universal adage that fluids must be forced on patients with stones. An increase in diuresis, however, may reduce the rate of ureteral peristalsis.1 If so, forced ‘hydrotherapy’ may inhibit the ability to pass the stone spontaneously.

Forced diuresis in an obstructed system would generate high intra-renal pressure leading to forniceal tears and perirenal collections. This may have a severe consequence in event of associated urinary infection.


Fig. 1 : Computed Tomogram showing peri-renal urinoma collection.

Our recommendations about conservative management of ureteric calculi are:

  1. Urinary calculi of less than 4 to 5 mm in size usually pass spontaneously;2 they do not require procedural treatment or hospitalization.
  2. Patient is advised to have oral fluids enough to produce 2.5 litres of urine; small amounts of fluids at frequent intervals.
  3. Intravenous forced hydrotherapy does not help in calculus clearance, adds to the cost of treatment, and may cause complications. This may at best be used for a short time to relieve pain during acute colic in a patient who has vomiting.1
  4. Oral forced diuresis has no role in patients with large calculi, significant obstruction and associated urinary infection.3
  5. Antispasmodics relieve pain but may delay calculus clearance as they hamper the ureteric peristaltic activity.4
 
Conclusion
Forced intravenous hydrotherapy is un-scientific, delays calculus clearance and may have significant side effects.
 
References
1. Drach GW. Urinary lithiasis: Etiology, diagnosis and medical management. In Walsh PC, Retik AB, Stamey TA and Vaughan ED editors Campbell’s Urology 6th edition. Philadelphia: WB Saunders Company; 1992 : 2085-2156
2. Irving SO, Calleja R, Lee F, Bullock KN, Wraight P, Doble A. Is the conservative management of ureteric calculi of > 4 mm safe? BJU Int 2000; 85 (6) : 637-40.
3. Ibrahim AI, Shetty SD, Awad RM, Patel KP. Prognostic factors in the conservative treatment of ureteric stones. Br J Urol 1991; 67 (4) : 358-61.
4. Webb DR, Nunn IN, McOmish D, Hare WS. Glucagon and ureteric calculi. Med J Aust 1986; 144 (3) : 124.
 

LESSONS FROM THE WITHDRAWAL OF ROFECOXIB

The history of the development and marketing of non-steroidal anti-inflammatory drugs is both fascinating and frightening.

The first big problem with a new NSAID occurred in the 1980s with benoxaprofen (Opren). But it soon became clear that its use was associated also with novel adverse events, including photosensitivity and hepatotoxicity. The company went on actively marketing the drug until forced to withdraw it when several older people had died of liver failure after using benoxaprofen.

The anti-inflammatory properties of NSAIDs were said to be related to inhibition of COX-2, whereas gastro-intestinal adverse effects occurred because of a COX-1 inhibition.

One of the first NSAIDs to be heavily marketed as a COX-2 selective inhibitor-capable of efficacy without serious toxicity, was celecoxib (Celebrex). Pfizer still promotes this agent on the basis of the CLASS study, despite the fact that this pivotal trial has been discredited, and that doubts have been cast on the selectivity of celecoxib. A subsequent agent was rofecoxib (Vioxx) produced by Merck Sharp and Dohme.

We have three concerns. Firstly, the “Vioxx story” indicates that we urgently need to determine whether the cardiovascular effects of rofecoxib are a class effect applicable to all COX-2 selective inhibitors-and if so, how selective the COX-2 inhibition needs to be to have this adverse effect. Secondly, we believe that the current widespread use of NSAIDs for non-inflammatory pain has to be Reconsidered. Thirdly, we must find ways of preventing further similar episodes.

Paul A Dieppe, Shah Ebrahim, Richard M Martin, Peter Juni, BMJ, 2004; 329 : 867-68.

*Consultant Urologist, Bombay Hospital, Indore, Ex-Chief Urologist RG Stone Clinic, Mumbai; **RG Stone Clinic, Mumbai.