Pressure Ulcers and Infection - Understanding Clinical Features

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. Bradykinin is reported to be 50 times more potent than histamine and serotonin in eliciting pain. The exception is patients with neuropathy.10 * Erythema (rubor) is the result of the actions of vasoactive mediators (eg, histamine) produced in response to micro-organisms or to any damage to mast cells in connective tissue. Arterioles dilate and flow and pressure increases in the capillary beds. Normally empty capillaries fill with blood carrying oxyhemoglobin.11 * Edema (tumor) occurs from the extravasation of fluid from intravascular to extravascular space. Fluid accumulates in the tissue, and mediators such as histamine, bradykinine, and leukotrienes leak out. Late extravasation (after 12 to 18 hours) is related to cytokines (eg, IL-1 and TNF-a) and leads to a persistent inflammation. The clinical feature of edema in pressure ulcers is taut and shiny skin surrounding the ulcer.12 Excessive accumulation of fluid causes the appearance of pitting edema in the periulcer area.13 * Heat (calor) is due to increased blood flow to periulcer area. Blood from the body core is substantially warmer than the skin temperature.13 * Purulent exudate is rich in white blood cells (eg, neutrophils and macrophages). This type of exudate is common in infections produced by strongly chemotactic bacteria (eg, S. aureus), is rich in potassium, and more acidic than plasma.14 Described as a healthy and vigorous response to bacterial invasion, purulent exudate is white and often has a creamy consistency. In contrast, serous exudate is protein-rich, fluid-like serum that lacks fibrinogen (unlike plasma) and contains activated clotting products. It also contains platelet factors and few leucocytes. It is thin and clear in color.13 Assessing pressure ulcers may be complicated by some modern dressings that may interact with the wound exudate. * Delayed healing is defined as "lack of progress toward wound closure and no decrease in wound size."13 Bergstrom et al15 postulated that chronic wounds should show some evidence of healing within 2 to 4 weeks. If this time limit is exceeded, infection should be suspected. * Discoloration of granulation tissue is described as excessive angiogenetic responses and edematous granulation tissue caused by invading micro-organisms. It also has been described as "pale or dusky in color (compared with normal 'beefy' red color of healthy granulation tissue)."16 * Friable granulation tissue reflects the excessive angiogenetic responses caused by the heavy bioburden.16 It bleeds spontaneously or with light pressure such as gentle manipulation with a sterile cotton-tipped applicator.17 * Pocketing at the base of wound where the wound base is irregular with walls dividing the base into "compartments" is sometimes seen. This phenomenon may be caused by lack of granulation tissue around islands of infection18 or a "lack of granulation tissue along some areas of the wound bed and is presented as recessed areas."13 * Foul odor is usually caused by Gram-negative bacilli. Pseudomonas species have another specific odor, and anaerobic bacteria cause an acrid or putrid odor. Foul odor is always associated with the presence of anaerobes19; the combination of anaerobic and aerobic bacteria is believed to be the most common cause of foul odor. * Wound breakdown has been described as faulty collagen formation caused by high bioburden.20 The result can be seen clinically as loss of tissue. It also has been described as "defects in epithelial tissue that has recently migrated over part of the wound."13 Using the Signs and Symptoms Checklist The reliability of a Clinical Signs and Symptoms Checklist (CSSC) has been tested in a study13 aimed at identifying a structured instrument for the assessment of clinical infection in chronic wounds. A panel of six experts examined content validity. The definitions of the parameters in the CSSC were carefully described. Five nurse observers were trained until 100% agreement with the principal investigator was obtained. Training was performed in up to five practice wounds. The study included 36 subjects (52% with pressure ulcers). The nurses practiced palpation, observation, and manipulation methods to assess the wounds. Tissue biopsies were taken for quantitative analysis: >105 organisms/g of tissue, or the presence of beta-hemolytic Streptococci signified infection. Inter-rater reliability (percent of agreement) was studied. Two independent assessments were performed using Kappa statistics and total percent agreement, occurrence, and non-occurrence percent agreement were measured. Cohen's Kappa agreement was used according to the Landis definition.21 The results showed excellent reliability for pain, edema, delayed healing, wound breakdown, and friable tissue (Kappa > 0.80), and substantial agreement for erythema, discoloration, serous exudate, and purulent exudate (see Table 2). Foul odor and heat received moderate reliability. No patient showed any signs of pocketing. The results suggested that training nurses in assessment of clinical infection in chronic wounds and the timing of assessment in relation to dressing changes and wound cleansing are essential. It also was concluded that the CSSC may improve clinical skill and accuracy in identifying specific signs and symptoms of infection in chronic wounds. The study results contributed to knowledge of clinical infection assessment in chronic wounds. Incorporating a structured approach to infection monitoring, such as using the CSSC, may improve clinical skill and accuracy in identifying specific signs and symptoms of infection.13 More studies are needed to precisely identify which signs or combination of signs are most indicative of infection.13 Using a more structured approach to the identification of clinical infection will allow antibiotics to be prescribed to patients with a higher degree of precision. Conclusion Bacterial colonization, contamination, and infection of pressure ulcers is a serious consideration because some patients will develop bacteremia which can become fatal. A delicate balance exists between prescribing antibiotics and addressing the risks of developing antibiotic-resistant strains. The high incidence of MRSA in some institutions is worrisome. The definitions used for postoperative infections cannot be duplicated in pressure ulcers. Gardner et al13 astutely recognized other signs and symptoms of infection such as pain, edema, delayed wound healing, wound breakdown, and friable tissue demonstrated excellent diagnostic reliability; whereas erythema, discoloration, serous exudate and purulent exudate showed substantial agreement, and foul odor and heat received moderate reliability. More study is needed to ascertain even more precise means of assessing infection to ensure appropriate treatment and subsequent healing.

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.

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