Systemic Antimicrobial Therapies for Pressure Ulcers

Marco Romanelli, MD, PhD; Antonio Magliaro, MD; Diego Mastronicola, MD; and Salvatore Siani, MD

I n chronic wounds, an altered balance among the number of organisms present, their virulence, and host resistance leads to bacterial infection. Infected chronic wounds may manifest with a friable bright red granulating wound bed, localized pain, increased wound size, perilesional warmth and tenderness, erythema on the surrounding skin, malodorous base, and increased wound exudate. The final outcome of infected wounds depends on a balance between factors that promote further complications or lead to their resolution. Wound infection in the geriatric population merits especially assiduous control and rapid intervention because it adversely affects patients' psychological, functional, and medical status. Patients may fear that infection will progress, causing severe psychological distress due to pain or altered appearance; they may experience a rapid decline of their already compromised functional status.
Simple bacterial wound infections often are treated according to their morphological appearance and to clinical experience because only a few pathogens are involved (see Figure 1). Treatment of critical lesions such as infected pressure ulcers or foot ulcers in a person with diabetes once involved administering oral or parenteral antibiotics among normal hosts. Usually, patients with deeper infections are sicker and require more vigorous intervention. Intravenous antibiotics are often prescribed after hospital admission in these cases; surgical drainage and rapid debridement are necessary when the infectious process is deep, extending down to fascia or muscle (see Figure 2). In recent decades, with a dramatic development of several groups of antimicrobial agents, the clinician has been faced with a long list of new antibiotics1 that may be lacking meaningful comparative information. Because of the large number of new agents in clinical practice, terms such as "new generation" antibiotics are commonly used.

Pressure ulcers are commonly colonized by several organisms in the absence of clinical signs of infection (see Table 1). When infection is present, the significance of laboratory tests must be critically evaluated and drug susceptibility tests must be considered according to the clinician's experience and the evidence base from the literature.2 On the other hand, some organisms that once had predictable antibiotic susceptibility characteristics now have become resistant.3 The rapid emergence of antibiotic-resistant bacteria has been highlighted by Colsky et al4 in an ongoing surveillance of patients with complicated skin infections that required hospitalization. In this study, 50% of Staphylococcus aureus isolates from chronic wounds was resistant to oxacillin, with 36% of Pseudomonas isolates resistant to ciprofloxacin. A comparison between these data and previous data obtained by the same authors for the same group of patients5 demonstrated an increasing trend in antibiotic resistance for different species of bacteria involved in soft and deep skin infections.

Clinical Response
A favorable clinical outcome is achieved in infected pressure ulcers when the patient is in stable condition and systemic treatment is established together with good local care (ie, a combination of surgical debridement and exudate control). The antimicrobial drug regimen must be adjusted according to the clinical response of the patient. If marked discrepancies are evident between drug susceptibility tests and clinical response, the following possibilities must be considered: inappropriate selection of drug dosage or route of administration, the emergence of drug-resistant bacteria, and the additional participation of micro-organisms not previously detected.


1. Lampiris HW, Maddix DS. Clinical use of antimicrobial agents. In: Katzung BG (ed). Basic and Clinical Pharmacology, 7th ed. New York, NY: Appleton and Lange;1998.
2. Kertesz D, Chow AW. Infected pressure and diabetic ulcers. Clin Geriatr. 1992;8:835-852.
3. Murray BE. Can antibiotic resistance be controlled? N Engl J Med. 1994;330:229-1230.
4. Colsky AS, Kirsner RS, Kerdel FA. Analysis of antibiotic susceptibilities of skin wound flora in hospitalized dermatology patients. Arch Dermatol. 1998;134:1006-1009.
5. Teng P, Falanga V, Kerdel FA. The microbiological evaluation of leg ulcers and infected dermatoses in patients requiring hospitalization. Wounds. 1993;5(3):133-136.
6. Bergstrom N, Braden B. A prospective study: pressure sore risk among institutionalized elderly. J Am Geriatric Soc. 1992;40:747-758.
7. Darouiche RO, Landon GC, Klima M, Musher DM, Markowsky J. Osteomyelitis associated with pressure sores. Arch Intern Med. 1994;154:753-758.
8. Deloach ED, DiBenedetto RJ, Womble L, Gilley JD. The treatment of osteomyelitis underlying pressure ulcers. Decubitus. 1992;5(6):32-41.
9. Kac G, Buu-Hoi A, Herisson E, Biancardini P, Debure C. Methicillin-resistant Staphylococcus aureus nosocomial acquisition and carrier state in a wound care center. Arch Dermatol. 2000;136: 735-739.
10. Jones RN. Impact of changing pathogens and antimicrobial susceptibility patterns in the treatment of serious infections in hospitalized patients. Am J Med.1996;100(suppl):3S-12 S.
11. Krukowski ZH, Matheson NA. Ten years computerized audit of infection after general surgery. Br J Surg. 1988;75: 857-861.
12. Kunin CM. Resistance to antimicrobial drugs: a worldwide calamity. Ann Intern Med. 1993;118:557-561.
13. Gold HS, Moellering RC. Antimicrobial-drug resistance. N Engl J Med. 1996;335:1445-1453.
14. Neu HC, Duma RJ, Jones RN, et al. Antibiotic resistance: epidemiology and therapeutics. Diagn Microbiol Infect Dis. 1992;15:53S-60S.
15. Darouiche RO, Raad II, Heard SO, et al. A comparison of two antimicrobial-impregnated central venous catheters. N Engl J Med. 1999;340:1-8.
16. Marrier RL. Role of imipenem/cilastatin in the treatment of soft tissue infections. Am J Med.
17. Gould IM, Hudson M, Morris J, et al. Imipenem versus standard therapy in the treatment of serious soft tissue infections. Drugs Exp Clin Res. 1988;14:555-558.
18. Neu HC. Aztreonam: the first monobactam. Med Clin North Am. 1988;72:555-566.
19. Brewer NS, Hellinger WC. The monobactams. Mayo Clin Proc. 1991;66:1152-1157.
20. Swab EA, Sugarman AA, Stern M. Oral bioavailability of monobactam aztreonam (SQ 26,776) in healthy subjects. Antimicrob Agents Chemother. 1983;23:548-550.
21. Donowitz GR, Mandell GL. Beta-lactam antibiotics. Part 2. N Eng J Med. 1988;318:490-500.
22. Fassberder M, Lode H, Schaberg T, et al. Pharmacokinetics of new oral cephalosporins, including a new carbacephem. Clin Infect Dis. 1993;16:646-653.
23. Johnson JD. The cephalosporins in dermatologic practice. Int J Dermatol. 1986;25:427-430.
24. Parish LC, Witkowski JA. Cephalosporin therapy in dermatologic practice. Clin Dermatol. 1992;9:459-469.
25. Derrick CW, Reilly K. The role of cephalexin in the treatment of skin and soft tissue infections. Postgrad Med J. 1983;59(suppl 5):43-46.
26. Gordin FM, Wofsy CB, Mills J. Once-daily ceftriaxone for skin and soft tissue infections. Antimicrob Agent Chemother. 1985;27:648-649.
27. Adkinson NF Jr, Saxon A, Spence MR, et al. Cross allergenicity and immunogenicity of aztreonam. Rev Infect Dis. 1985;74:613-621.
28. Saxon A, Beall GN, Rohr AS, et al. Immediate hypersensitivity reactions to beta-lactam antibiotics. Ann Intern Med. 1987;107:204-215.
29. Lopez AJ, O'Keefe P, Morrissey M, et al. Ceftriaxone-induced cholelithiasis. Ann Intern Med. 1991;115:712-714.
30. Parish LC, Witkowski JA. The quinolones and dermatologic practice. Int J Dermatol. 1987;2:351-256.
31. Smith JW, Nichols RL. Comparison of oral fleroxacin with oral amoxicillin/clavulanate in the treatment of infections of the skin and soft tissue. Am J Med. 1993;94:1505-1545.
32. Neuman M. Clinical pharmacokinetics of the newer antimicrobial 4-quinolones. Clin Pharmacokinet.1988;14:96-121.
33. Vancomycin-resistant Staphylococcus aureus: a real and present danger? Infection. 2002;Jun;30(3):118-124.
34. Weinbren M, Struthers K. Emergence of Staphylococcus aureus (MRSA) with reduced susceptibility teicoplanin during therapy. J Antimicrob Chemother. 2002;Aug;50(2):306-307.
35. Stevens DL. Teicoplanin for skin and soft tissue infections: an open study and a randomized, comparative trial versus cefazolin. J Infect Chemother. 1999 Mar;5(1):40-45.
36. Bochud-Gabellon I, Regamey C. Teicoplanin, a new antibiotic effective against gram-positive bacterial infections of the skin and soft tissues. Dermatologica. 1988;176(1):29-38.

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