6.6 Treatment of underlying disease

The drainage of any obstruction in the urinary tract and the removal of foreign bodies, such as urinary catheters or stones, may by themselves cause resolution of symptoms and lead to recovery.

Empirical initial treatment should provide broad antimicrobial coverage and should later be adapted on the basis of culture results. The antibacterial treatment options are summarized in Appendix 2.

6.6.1 Adjunctive measures (7)

• Management of fluid and electrolyte balance is a crucial aspect of patient care in sepsis syndrome, particularly when the clinical course is complicated by shock.

• Sympathomimetic amines have been widely used to treat the haemodynamic complications of shock. Alternative agents, such as isoproterenol, dopamine and dobutamine, have mainly replaced noradrenaline.

• Corticosteroids are thought to be beneficial as adjunctive therapy in Gram-negative infections, particularly those complicated by shock.

• Anticoagulation, particularly heparinization, to treat septicaemic states associated with disseminated intravascular coagulation is logical.

• Granulocyte transfusions were once popular for the treatment of infections in neutropenic subjects. Use of recombinant colony-stimulating factors, such as G-CSF and GM-CSF, has mainly replaced WBC transfusions.

• Naloxone, an antagonist of opiates and (3-endorphins, has been shown to reverse the course of endotoxic and hypovolaemic shock.

6.7 Conclusion

Sepsis syndrome in urology remains a severe situation with a mortality rate as high as 20-60%. Early recognition of the symptoms may decrease mortality by timely treatment of the urinary tract disorder, e.g. obstruction, lithiasis. Adequate measures to ensure life-support and appropriate antibiotic treatment are the best approaches to improving patient survival. Prevention of sepsis syndrome is dependent on good practice to avoid nosocomial infections, using antibiotic prophylaxis and therapy in a logical and well-accepted manner.

6.8 References

1. Carlet J, Dumay MF, Gottot S, Gouin F, Pappo M.

Guide pour la prevention des Infections Nosocomiales en reanimation. Arnette Ed Paris 1994: 41-53.

2. Recommendations for prevention of nosocomial pneumonia.

The Hospital Infection Control Practices Advisory Committee Center for Disease Control. Atlanta, GA, 1993

3. Measley RE, Levison ME.

Host defense mechanisms in the pathogenesis of UTI. Med Clin N Am 1991; 75: 275-286.

4. Sobel JD.

Bacterial etiologic agents in the pathogenesis of UTI. Med Clin N Am 1991; 75: 253-273.

5. Olszyna DP, Prins JM, Buis B, Van-Deventer SJ, Speelman P, Van der Poll T.

Levels of inhibitors of tumor necrosis factor alpha and interleukin 1 (in urine and sera of patients with urosepsis). Infect Immun 1998; 66: 3527-3534.

6. Carson CC.

Antimicrobial prophylaxis in genitourinary surgery. In: Antibiotic Therapy in Urology. Mulholland SG (ed). Philadelphia: 1996, pp. 71-89.

7. Lowell S.

Principles and Practice of Infectious Diseases, 4th edition. Mandell, Douglas and Bennetts, 1995, Volume I, 56, pp. 690-701.

8. Rosser CJ, Bare RL, Meredith JW.

UTIs in the critically ill patient with a urinary catheter. Am J Surg 1999; 177: 287-290.

9. Paradisi F, Corti G, Mangani V.

Urosepsis in the critical care unit. Crit Care Clin 1998; 14: 165-180.

10. Degroot-Kosolcharoen J, Guse R, Jones JM.

Evaluation of a urinary catheter with a preconnected closed drainage bag. Infect Control Hosp Epidemiol 1988; 9: 72-76.

11. Garibaldi RA.

Catheter-associated UTI. Curr Opin Infect Dis 1992; 5: 517-523.

12. MacFarlane D.

Prevention and treatment of catheter-associated UTIs. J Infect 1985; 10: 96-106.

13. Persky L, Liesen D, Yangco B.

Reduced urosepsis in a veterans' hospital. Urology 1992; 39: 443-445.

14. Riedl CR, Plas E, Hubner WA, Zimmer H, Ulrich W, Pfluger H. Bacterial colonization of ureteral stents. Eur Urol 1999; 36: 53-59.

7. URETHRITIS

7.1 Definition

Primary urethritis has to be differentiated from secondary urethritis, which may be found in patients with indwelling catheters or urethral strictures and can be caused by uropathogens or by staphylococci. Besides infective causes of urethritis, chemical, mechanical and non-infective inflammatory causes also have to be considered, such as Reiter's, Behget's and Wegener's diseases (1). Only primary urethritis will be discussed in this Chapter (2).

7.2 Epidemiology

From a therapeutic and clinical point of view, gonorrhoeal urethritis has to be differentiated from non-specific urethritis. Non-specific urethritis is much more frequent in Central Europe than gonorrhoeal urethritis. There is a correlation between promiscuity and low socio-economic status on one side and the frequency of N. gonorrhoeae and С trachomatis on the other. Infection is spread by sexual contact.

7.3 Pathogens

Pathogens include N. gonorrhoeae, C. trachomatis, Mycoplasma genitalium and T. vaginalis. The frequency of the different species varies between patient populations (3-7). Mycoplasma hominis probably does not cause urethritis, while Ureaplasma urealyticum is an infrequent cause. In most cases, the clinical evidence of Mycoplasma or Ureaplasma represents an asymptomatic colonization of the urogenital tract.

7.4 Route of infection and pathogenesis

Causative agents either remain extracellularly on the epithelial layer or penetrate into the epithelium (Л/. gonorrhoeae, С trachomatis) and thus cause a pyogenic infection. Originating from urethritis, chlamydiae and gonococci can spread further and can cause epididymitis in the male or cervicitis, endometritis and salpingitis in the female.

7.5 Clinical course

Purulent discharge and alguria are symptoms of urethritis, but many infections of the urethra are asymptomatic.

7.6 Diagnosis

A Gram stain of a urethral discharge or a urethral smear showing more than five leucocytes per high power field (x 1,000) and, eventually, gonococci located intracellularly as Gram-negative diplococci, indicate pyogenic urethritis. A positive leucocyte esterase test or > 10 leucocytes per high power field (x 400) in the first voiding urine specimen are diagnostic. In all patients with urethritis, and where sexual transmission is suspected, the aim should be to identify the pathogenic organisms. If an amplification system is used for identifying the pathogens, the first voiding urine specimen can be taken instead of a urethral smear. Trichomonas can usually be identified microscopically.