Pressure Ulcers and Infection - Understanding Clinical Features

Author(s): 
Christina Lindholm, RN, PhD

K nown since antiquity, pressure ulcers represent substantial morbidity, major costs to society, and great human suffering.1,2 In one 3-month follow-up study of patients with pressure ulcers,3 a mortality rate of 35% was noted. Addressing infection - always a consideration - has been complicated by the relatively new problem of methicillin-resistant Staphylococcus aureus (MRSA) with a reported incidence as high as 30% and bacteremia occurring in 4% in hospitalized patients,4 along with vancomycin-resistant enterococci (VRE) in chronic wounds. Such findings have encouraged clinicians to focus on the microbiology of pressure ulcers. This article examines the role of bacteria in pressure ulcers and discusses the reliability of clinical signs and symptoms associated with infection.
In one study, incidence of decubitus ulcer infection was reported to be 1.4 per 1,000 ulcer days.5 An average of 2.4 organisms grew from surface swabs of ulcers. Anaerobes were isolated from 14% of the cultures. Aspirates from clinically noninfected ulcers had bacteria isolated in 30% of specimens. Two-thirds of the organisms isolated were considered potentially pathogenic. However, the clinical diagnosis of infection in pressure ulcers remains unclear.
In a Swedish survey study6 that explored qualitative swabbing technique for identification of micro-organisms in pressure ulcers in various facilities (ie, a university hospital, primary care, and community institutions including nursing homes and homes for the elderly), numerous species were identified (see Table 1). The purposes of this study were to investigate presence of micro-organisms in pressure ulcers, to assess antimicrobial resistance of bacteria, and to determine the frequency of antibiotic treatment in pressure ulcers. The total number of isolates resistant to antibiotics was low. No enterococcal or staphylococcal isolate was resistant to vancomycin. No pressure ulcer (N = 117) harbored any MRSA. Of the total number of tested isolates (all wounds, N = 694), 10.9% of the Pseudomonas aeruginosa species were resistant to ciprofloxacin. Almost 60% of patients with pressure ulcers were treated with antibiotics at the time of the study and within the previous 6 months. The most common antibiotic treatment was quinolones. This figure seems high in comparison with the reported incidence of clinical infections,5 especially because reducing the use of antibiotics for chronic ulcers is strongly recommended7 due to the risk of developing antibiotic-resistant strains of bacterial species and the potential environmental hazards.

Clinical Infection: Surgical Sites versus Pressure Ulcers
Postoperative wounds are assessed for infection according to the Centers for Disease Control's (CDC) definition.8 The CDC defines a superficial surgical site infection (SSI) as one involving skin and subcutaneus tissues. A deep SSI is defined as one involving muscle or fascia. An organ/space SSI is defined as an infection involving any part of the anatomy, other than the incision, that was opened or manipulated during the operative procedure. The diagnosis should be made by positive cultures from the incision or by clinical evidence of infection, such as purulent discharge from the wound incision within 30 days of the operative procedure.8
In pressure ulcers and other chronic wounds, however, the definition of wound infection is less clear. The classical signs - "dolor, rubor, calor, and tumor" - are not likely to cover all aspects of infection in a pressure ulcer. Clinicians have suggested that "purulent exudate, delayed healing, discoloration of granulation tissue, pocketing at the wound base, foul odor, and wound breakdown" should be added.9
Clinical signs and symptoms.
* Increasing pain (dolor) is caused by activation of plasma-derived mediators, especially bradykinin, near tiny unmyelinated nerve fiber endings.

References: 

1. Miller H, Delozier J. Cost implications of the pressure ulcer treatment guideline. Columbia, Md. Center for Health Policy Studies; 1994. Contract No 282-91-007.
2. Haalboom JR. Pressure ulcers (Letter). Lancet. 1998;352:9127:581.
3. Lindholm C, Bergsten A, Berglund E. Chronic wounds - prevalence, demography and nursing care in 694 patients. A survey study of Uppsala County, Sweden. Journal of Wound Care. 1999;8(1):5-10.
4. Roghmann MC, Siddiqui A, Plaisance K, Standiford H. MRSA colonization and the risk of MRSA bacteraemia in hospitalized patients with chronic ulcers. J Hosp Infect. 2001;47(2):98-103.
5. Nicolle LE, Orr P, Duckworth H, Brunka J, Kennedy J, Murray BUD, Harding GKM. Prospective study of decubitus ulcers in two long-term care facilities. Canadian Journal of Infection Control. 1994;9(2):35-38.
6. Tammelin A, Lindholm C, Hambraeus A. Chronic ulcers and antibiotic treatment. Journal of Wound Care. 1998;7(9):435-437.
7. Wistrom J, Lindholm C, Melhus A, Lundgren C, Hansson C. Aktuella synpunkter pa infektioner och antibiotikabehandling vid bensar. Lakartidningen. 1999;96(1-2):42-46.
8. Horan TC, Gaynes RP, Martone WJ, Jarvis WR, Emori TG. CDC definitions of nosocomila infections, 1992. A modification of CDC definitions of surgical wound infections. American Journal Infection Control. 1992;20:271-274.
9. Cutting KF, Harding KG. Criteria for identifying wound infection. Journal of Wound Care. 1994;3(4):198-201.
10. Majno G, Joris I. Cells, Tissues and Disease: Principles of General Pathology. Cambridge, Mass.: Blackwell Science;1996.
11. Takiwaki H, Jorgen S. Measurement of erythema and melanin indices. In: Serup J, Jemec GBE (eds). Handbook of Non-invasive Methods and the Skin. Boca Raton, Fla.: CRP Press;1995.
12. Bates-Jensen BM, Vredevoe DL, Brecht ML. Validity and reliability of the pressure sore status tool. Decubitus. 1992;5(6):20-28.
13. Gardner S, Frantz R, Trola C, et al. A tool to assess clinical signs and symptoms of localized infection in chronic wounds: development and reliability. Ostomy/Wound Management. 2001;47(1):40-47.
14. Zimmerli W, Gallin JI. Pus potassium. Inflammation. 1988;12:37-43.
15. Bergstrom N, Allman RM, Carlson CE, et al. Clinical Practice Guideline Number 15: Treatment of Pressure Ulcers. Rockville, Md.:US Department of Health and Human Service. Agency for Health Care Policy and Research; 1994. ACHPR Publication No 95-0652.
16. Hunt TK, Jawetz E, Hutchinsson MB, Dunphy EJ. A new model for the study of wound infection. J Trauma. 1967;7:298-306.
17. Gilchrist B. Infection and culturing, In: Krasner D, Kane D, eds. Chronic Wound Care: A Clinical Source Book for Healthcare Professionals, 2nd ed. Wayne, Pa.: Health Management Publications;1997:109-114.
18. Marks J, Harding KG, Hughes LE. Pilonidal sinus excision: healing by open granulation. Br J Surg. 1985;72:637-640.
19. Sapico FL, Ginunas VJ, Thornhill-Joynes M, Canawati HN, Capen DA, Klein NE. Quantitative microbiology of pressure sores in different stages of healing. Diagn Microbiol Infect Dis. 1986;5:31-38.
20. Hunt TK. The physiology of wound healing. Ann Emerg Med. 1988;17(12):2-10.
21. Landis JR, Koch GG. The measurement of observer agreement for categorical data. Biometrics. 1977;33:159-174.



Post new comment

  • Web page addresses and e-mail addresses turn into links automatically.
  • Lines and paragraphs break automatically.
  • Use to create page breaks.

More information about formatting options

Image CAPTCHA
Enter the characters shown in the image.