Burn Wound Infections Workup
- Author: Jairo A Fonseca, MD; Chief Editor: Pranatharthi Haran Chandrasekar, MBBS, MD more...
Diagnosis of wound infection should focus on a careful physical examination that is performed frequently by personnel trained in the management of burns.
Laboratory tests or changes in laboratory values such as white blood cell (WBC) count, neutrophil percentage, erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP) level are of low yield in detecting or predicting burn infections because of the inflammatory response associated with the burn itself.
Laboratory examinations are useful for the initial risk assessment. Low prealbumin levels (100-150 mg/L) in burned patients are associated with a higher incidence of sepsis and organ dysfunction, lengthier stays, decreased ability of wound healing, and a higher mortality rate.[8, 23, 24]
In patients with suspected wound infections, procalcitonin (PCT) levels of 0.56 ng/mL have a reported sensitivity of 75% and a specificity of 80% when compared with quantitative swab culture. Although these levels cannot be considered diagnostic, they should prompt the physician to start searching for an infectious source. In the only study that has compared PCT to American Burn Association (ABA) criteria for diagnosing sepsis, PCT was found to have potential utility in diagnosing sepsis in the burned patient. A threshold of 1.5 ng/mL had a sensitivity of 88% and specificity of 92% to diagnose septic complications in burned patients, with high levels found to be an independent predictor of mortality. Without strong evidence to support a PCT threshold in burned patients, one recommendation is that PCT be obtained at admission and then monitored routinely to detect acute changes to guide the start of empirical antibiotic therapy. PCT may also have a role in monitoring response to antimicrobial therapy, as appropriate antimicrobial therapy is associated with a reduction in PCT levels by the third day of treatment. In contrast, patients who died of multiple organ failure secondary to sepsis had PCT levels that remained elevated despite treatment.
Diagnosis of a burn wound infection relies on clinical examination as outlined above (see Clinical) and culture data, including the following:
Quantitative biopsy can be used to confirm infection but is not reliable. This procedure is useful in identifying the infecting pathogen.
Quantitative swab is of limited value but may aid in identifying the infecting pathogen.
Tissue histopathology allows for quantification and evaluation of infection depth and involvement of non-burned skin.
The use of routine wound cultures as part of surveillance procedures has been proposed to provide early identification of organisms colonizing the wound, to monitor response to therapy, to guide empiric therapy, and to evaluate for nosocomial transmission. However, this has not been shown to improve patient outcomes, and routine application has been brought into question.
Ono et al (2015) demonstrated that, among cases of local infection with Staphylococcus species, the burn wound exudate pH rises prior to the onset of clinical signs of local infection.
No imaging studies have been identified as useful for detecting wound infections.
Multiple biopsy samples from several areas of the burn wound should be obtained and sent for histopathology and microbiological workup of the pathogens and their resistance profiles.
After cleaning the wound with isopropyl alcohol, 2 parallel incisions 1-2 cm in length and 1.5 cm apart with a depth to obtain a portion of the underlying fat are made in the skin. Alternatively, biopsy samples typically weighing 0.02-0.5 g may be obtained with a 3-mm punch-biopsy technique.
Biopsy is a commonly bypassed procedure because of technical difficulty within the microbiology section working up these types of samples or a lack of local histopathological expertise.
Bacteria are most commonly detected using Gram or hematoxylin and eosin (H&E) stains.
Fungi may be visualized on periodic acid-Schiff (PAS) or Gomori methenamine silver (GMS) staining, but recovery in culture is required for definitive identification. Note the following:
Aspergillus-like morphology - Presence of parallel-walled, branching, septate hyphae may indicate Aspergillus species, Fusarium species, phaeohyphomycetes, or other molds
Mucor-like morphology (mucormycosis) - Presence of wide, ribbonlike, rarely septate hyphae most commonly denotes Mucorales (eg, Rhizopus, Mucor, Rhizomucor, Absidia)
Yeast-like morphology - Presence of budding yeasts or rounded yeast-like structures; many yeasts, including most Candida species, also produce hyphae and pseudohyphae in tissue
Herpes simplex virus can be isolated via identification of inclusions on light or electron microscopy or other viral particles on biopsy specimen or lesion scraping.
Various stages are used to diagnose burn wound infections.
Stage I is colonization and includes the following substages:
Superficial - Microorganisms present only on burn wound surface
Penetrating - Variable depth of microbial penetration of eschar
Proliferating - Variable level of microbial proliferation at nonviable–viable tissue interface (subeschar space)
Stage II is invasion and includes the following substages:
Microinvasion - Microorganisms present in viable tissue immediately subjacent to subeschar space
Deep invasion - Penetration of microorganisms to variable depth and expanse within viable subcutaneous tissue
Microvascular involvement - Microorganisms within small blood vessels and lymphatics (thrombosis of vessels is common)
Latenser BA, Miller SF, Bessey PQ, et al. National Burn Repository 2006: a ten-year review. J Burn Care Res. 2007 Sep-Oct. 28(5):635-58. [Medline].
Gomez R, Murray CK, Hospenthal DR, Cancio LC, Renz EM, Holcomb JB, et al. Causes of mortality by autopsy findings of combat casualties and civilian patients admitted to a burn unit. J Am Coll Surg. 2009 Mar. 208 (3):348-54. [Medline].
Church D, Elsayed S, Reid O, Winston B, Lindsay R. Burn wound infections. Clin Microbiol Rev. 2006 Apr. 19(2):403-34. [Medline].
Keen EF 3rd, Robinson BJ, Hospenthal DR, et al. Prevalence of multidrug-resistant organisms recovered at a military burn center. Burns. September 2010. 36:819-25. [Medline].
Albrecht MC, Griffith ME, Murray CK, Chung KK, Horvath EE, Ward JA. Impact of Acinetobacter infection on the mortality of burn patients. J Am Coll Surg. October 2006. 203:546-50. [Medline].
Horvath EE, Murray CK, Vaughan GM, et al. Fungal wound infection (not colonization) is independently associated with mortality in burn patients. Ann Surg. 2007 Jun. 245(6):978-85. [Medline]. [Full Text].
Sarabahi S, Tiwari VK, Arora S, Capoor MR, Pandey A. Changing pattern of fungal infection in burn patients. Burns. 2012 Jun. 38(4):520-8. [Medline].
Kasten KR, Makley AT, Kagan RJ. Update on the critical care management of severe burns. J Intensive Care Med. 2011 Jul-Aug. 26(4):223-36. [Medline].
Rowan MP, Cancio LC, Elster EA, Burmeister DM, Rose LF, Natesan S, et al. Burn wound healing and treatment: review and advancements. Crit Care. 2015 Jun 12. 19:243. [Medline].
Keen EF 3rd, Robinson BJ, Hospenthal DR, et al. Incidence and bacteriology of burn infections at a military burn center. Burns. 2010 Jun. 36(4):461-8. [Medline].
Kennedy P, Brammah S, Wills E. Burns, biofilm and a new appraisal of burn wound sepsis. Burns. 2010 Feb. 36(1):49-56. [Medline].
Schofield CM, Murray CK, Horvath EE, et al. Correlation of culture with histopathology in fungal burn wound colonization and infection. Burns. 2007 May. 33(3):341-6. [Medline].
Regules JA, Carlson MD, Wolf SE, Murray CK. Analysis of anaerobic blood cultures in burned patients. Burns. 2007 Aug. 33(5):561-4. [Medline].
American Burn Association. Burn Incidence and Treatment in the United States: 2016. Available at http://www.ameriburn.org/resources_factsheet.php. Accessed: 04/17/2016.
Peck M, Pressman MA. The correlation between burn mortality rates from fire and flame and economic status of countries. Burns. 2013 Sep. 39 (6):1054-9. [Medline].
Mistry RM, Pasisi L, Chong S, Stewart J, She RB. Socioeconomic deprivation and burns. Burns. 2010 May. 36(3):403-8. [Medline].
Mayhall CG. The epidemiology of burn wound infections: then and now. Clin Infect Dis. 2003 Aug 15. 37(4):543-50. [Medline].
Greenhalgh DG, Saffle JR, Holmes JH 4th, Gamelli RL, Palmieri TL, Horton JW. American Burn Association consensus conference to define sepsis and infection in burns. J Burn Care Res. 2007 Nov-Dec. 28(6):776-90. [Medline].
Kaiser ML, Thompson DJ, Malinoski D, Lane C, Cinat ME. Epidemiology and risk factors for hospital-acquired methicillin-resistant Staphylococcus aureus among burn patients. J Burn Care Res. 2011 May-Jun. 32(3):429-34. [Medline].
Shankar R, Melstrom KA Jr, Gamelli RL. Inflammation and sepsis: past, present, and the future. J Burn Care Res. 2007 Jul-Aug. 28(4):566-71. [Medline].
Schultz L, Walker SA, Elligsen M, Walker SE, Simor A, Mubareka S, et al. Identification of predictors of early infection in acute burn patients. Burns. 2013 Nov. 39 (7):1355-66. [Medline].
Murray CK, Hoffmaster RM, Schmit DR, Hospenthal DR, Ward JA, Cancio LC. Evaluation of white blood cell count, neutrophil percentage, and elevated temperature as predictors of bloodstream infection in burn patients. Arch Surg. 2007 Jul. 142(7):639-42. [Medline].
Rodriguez NA, Jeschke MG, Williams FN, Kamolz LP, Herndon DN. Nutrition in burns: Galveston contributions. JPEN J Parenter Enteral Nutr. 2011 Nov. 35(6):704-14. [Medline].
Eljaiek R, Dubois MJ. Hypoalbuminemia in the first 24h of admission is associated with organ dysfunction in burned patients. Burns. 2013 Feb. 39 (1):113-8. [Medline].
Lavrentieva A, Papadopoulou S, Kioumis J, Kaimakamis E, Bitzani M. PCT as a diagnostic and prognostic tool in burn patients. Whether time course has a role in monitoring sepsis treatment. Burns. 2012 May. 38(3):356-63. [Medline].
Mann EA, Wood GL, Wade CE. Use of procalcitonin for the detection of sepsis in the critically ill burn patient: a systematic review of the literature. Burns. 2011 Jun. 37(4):549-58. [Medline].
Uppal SK, Ram S, Kwatra B, Garg S, Gupta R. Comparative evaluation of surface swab and quantitative full thickness wound biopsy culture in burn patients. Burns. 2007 Jun. 33(4):460-3. [Medline].
Ono S, Imai R, Ida Y, Shibata D, Komiya T, Matsumura H. Increased wound pH as an indicator of local wound infection in second degree burns. Burns. 2015 Jun. 41 (4):820-4. [Medline].
Lundy JB, Chung KK, Pamplin JC, Ainsworth CR, Jeng JC, Friedman BC. Update on Severe Burn Management for the Intensivist. J Intensive Care Med. 2015 Jun 24. [Medline].
Sevgi M, Toklu A, Vecchio D, Hamblin MR. Topical antimicrobials for burn infections - an update. Recent Pat Antiinfect Drug Discov. 2013 Dec. 8 (3):161-97. [Medline].
Barajas-Nava LA, López-Alcalde J, Roqué i Figuls M, Solà I, Bonfill Cosp X. Antibiotic prophylaxis for preventing burn wound infection. Cochrane Database Syst Rev. 2013 Jun 6. 6:CD008738. [Medline].
Azzopardi EA, Azzopardi E, Camilleri L, Villapalos J, Boyce DE, Dziewulski P, et al. Gram negative wound infection in hospitalised adult burn patients--systematic review and metanalysis-. PLoS One. 2014. 9 (4):e95042. [Medline].
D'Avignon LC, Hogan BK, Murray CK, Loo FL, Hospenthal DR, Cancio LC, et al. Contribution of bacterial and viral infections to attributable mortality in patients with severe burns: an autopsy series. Burns. 2010 Sep. 36 (6):773-9. [Medline].
Azzopardi EA, Boyce DE, Thomas DW, Dickson WA. Colistin in burn intensive care: back to the future?. Burns. 2013 Feb. 39 (1):7-15. [Medline].
Chong SJ, Ahmed S, Tay JM, Song C, Tan TT. 5 year analysis of bacteriology culture in a tropical burns ICU. Burns. 2011 Dec. 37(8):1349-53. [Medline].
Pidcoke HF, Wade CE, Wolf SE. Insulin and the burned patient. Crit Care Med. 2007 Sep. 35(9 Suppl):S524-30. [Medline].
Breederveld RS, Tuinebreijer WE. Recombinant human growth hormone for treating burns and donor sites. Cochrane Database Syst Rev. 2014 Sep 15. 9:CD008990. [Medline].
Wolf SE. Nutrition and metabolism in burns: state of the science, 2007. J Burn Care Res. 2007 Jul-Aug. 28(4):572-6. [Medline].
Vicic VK, Radman M, Kovacic V. Early initiation of enteral nutrition improves outcomes in burn disease. Asia Pac J Clin Nutr. 2013. 22 (4):543-7. [Medline].
Abdullahi A, Jeschke MG. Nutrition and anabolic pharmacotherapies in the care of burn patients. Nutr Clin Pract. 2014 Oct. 29 (5):621-30. [Medline].
Melinyshyn A, Callum J, Jeschke MC, Cartotto R. Albumin supplementation for hypoalbuminemia following burns: unnecessary and costly!. J Burn Care Res. 2013 Jan-Feb. 34 (1):8-17. [Medline].
Lin JJ, Chung XJ, Yang CY, Lau HL. A meta-analysis of trials using the intention to treat principle for glutamine supplementation in critically ill patients with burn. Burns. 2013 Jun. 39 (4):565-70. [Medline].
Esselman PC. Burn rehabilitation: an overview. Arch Phys Med Rehabil. 2007 Dec. 88(12 Suppl 2):S3-6. [Medline].
Ong YS, Samuel M, Song C. Meta-analysis of early excision of burns. Burns. 2006 Mar. 32(2):145-50. [Medline].
Ciofi Silva CL, Rossi LA, Canini SR, Gonçalves N, Furuya RK. Site of catheter insertion in burn patients and infection: a systematic review. Burns. 2014 May. 40 (3):365-73. [Medline].