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Increased Susceptibility to Infection Related to Extent of Burn Injury

Increased Susceptibility to Infection Related to Extent of Burn Injury Abstract • A model of burn wound sepsis in which the mortality caused by infection was significantly greater after a 60% total body surface area (TBSA) burn than after a 30% TBSA burn was developed in the rat. In rats that sustained a 60% TBSA burn (30% partial plus 30% full thickness), the 30% TBSA partial-thickness burn that was inoculated with Pseudomonas aeruginosa strain 59-1244 developed invasive wound infection (>105 colony-forming units per gram of tissue). Infection did not develop in rats that had a 30% TBSA partial-thickness burn inoculated, without additional injury. The additional burn in the rats with a 60% TBSA burn seemed to affect the development of infection in the partial-thickness wound and the overall outcome by a mechanism other than by infection of the full-thickness wound itself. Autopsy confirmed that mortality was caused by sepsis. (Arch Surg 1984;119:183-188) References 1. Walker HL, Mason AD Jr: A standard animal burn . J Trauma 1968;8: 1049-1051.Crossref 2. Teplitz C, Davis D, Mason AD Jr, et al: Pseudomonas burn wound sepsis: I. Pathogenesis of experimental Pseudomonas burn wound sepsis . J Surg Res 1964;4:200-216.Crossref 3. Lindberg RB, Moncrief JA, Mason AD Jr: Control of experimental and clinical burn wound sepsis by topical application of Sulfamylon compounds . Ann NY Acad Sci 1968;150:950-960.Crossref 4. McManus AT, McLeod CG Jr, Mason AD Jr: Experimental Proteus mirabilis burn surface infection . Arch Surg 1982;117:187-191.Crossref 5. McCabe WP, Rebuck JW, Kelley AP Jr, et al: Leukocyte response as a monitor of immunodepression in burn patients . Arch Surg 1973;106:155-159.Crossref 6. Warden GD, Mason AD Jr, Pruitt BA Jr: Evaluation of leukocyte chemotaxis in vitro in thermally injured patients . J Clin Invest 1974;54: 1001-1004.Crossref 7. McManus AT: Examination of Altered Neutrophil Function in a Burned Rat Model, thesis. University of Texas Graduate School of Biomedical Sciences, San Antonio, 1980. 8. Davis JM, Dineen P, Gallin JI: Neutrophil degranulation and abnormal chemotaxis after thermal injury . J Immunol 1980;124:1467-1471. 9. Center DM, Soter NA, Wasserman SI, et al: Inhibition of neutrophil chemotaxis in association with experimental angioedema in patients with cold urticaria: A model of chemotactic deactivation in vivo . Clin Exp Immunol 1979;35:112-118. 10. Yurt RW: Role of the mast cell in trauma , in Dineen P, Hildrick-Smith G (eds): The Surgical Wound . Philadelphia, Lea & Febiger, 1981, pp 37-62. 11. Bjornson AB, Altemeier WA, Bjornson HS, et al: Host defense against opportunist microorganisms following trauma: I. Studies to determine the association between changes in humoral components of host defense and septicemia in burned patients . Ann Surg 1978;188:93.Crossref 12. Bjornson AB, Altemeier WA, Bjornson HS: Complement, opsonins, and the immune response to bacterial infection in burned patients . Ann Surg 1980;191:323-329.Crossref 13. Christou NV, Meakins JL: Neutrophil function in surgical patients: Two inhibitors of granulocyte chemotaxis associated with sepsis . J Surg Res 1979;26:355-364.Crossref http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Archives of Surgery American Medical Association

Increased Susceptibility to Infection Related to Extent of Burn Injury

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Publisher
American Medical Association
Copyright
Copyright © 1984 American Medical Association. All Rights Reserved.
ISSN
0004-0010
eISSN
1538-3644
DOI
10.1001/archsurg.1984.01390140047008
Publisher site
See Article on Publisher Site

Abstract

Abstract • A model of burn wound sepsis in which the mortality caused by infection was significantly greater after a 60% total body surface area (TBSA) burn than after a 30% TBSA burn was developed in the rat. In rats that sustained a 60% TBSA burn (30% partial plus 30% full thickness), the 30% TBSA partial-thickness burn that was inoculated with Pseudomonas aeruginosa strain 59-1244 developed invasive wound infection (>105 colony-forming units per gram of tissue). Infection did not develop in rats that had a 30% TBSA partial-thickness burn inoculated, without additional injury. The additional burn in the rats with a 60% TBSA burn seemed to affect the development of infection in the partial-thickness wound and the overall outcome by a mechanism other than by infection of the full-thickness wound itself. Autopsy confirmed that mortality was caused by sepsis. (Arch Surg 1984;119:183-188) References 1. Walker HL, Mason AD Jr: A standard animal burn . J Trauma 1968;8: 1049-1051.Crossref 2. Teplitz C, Davis D, Mason AD Jr, et al: Pseudomonas burn wound sepsis: I. Pathogenesis of experimental Pseudomonas burn wound sepsis . J Surg Res 1964;4:200-216.Crossref 3. Lindberg RB, Moncrief JA, Mason AD Jr: Control of experimental and clinical burn wound sepsis by topical application of Sulfamylon compounds . Ann NY Acad Sci 1968;150:950-960.Crossref 4. McManus AT, McLeod CG Jr, Mason AD Jr: Experimental Proteus mirabilis burn surface infection . Arch Surg 1982;117:187-191.Crossref 5. McCabe WP, Rebuck JW, Kelley AP Jr, et al: Leukocyte response as a monitor of immunodepression in burn patients . Arch Surg 1973;106:155-159.Crossref 6. Warden GD, Mason AD Jr, Pruitt BA Jr: Evaluation of leukocyte chemotaxis in vitro in thermally injured patients . J Clin Invest 1974;54: 1001-1004.Crossref 7. McManus AT: Examination of Altered Neutrophil Function in a Burned Rat Model, thesis. University of Texas Graduate School of Biomedical Sciences, San Antonio, 1980. 8. Davis JM, Dineen P, Gallin JI: Neutrophil degranulation and abnormal chemotaxis after thermal injury . J Immunol 1980;124:1467-1471. 9. Center DM, Soter NA, Wasserman SI, et al: Inhibition of neutrophil chemotaxis in association with experimental angioedema in patients with cold urticaria: A model of chemotactic deactivation in vivo . Clin Exp Immunol 1979;35:112-118. 10. Yurt RW: Role of the mast cell in trauma , in Dineen P, Hildrick-Smith G (eds): The Surgical Wound . Philadelphia, Lea & Febiger, 1981, pp 37-62. 11. Bjornson AB, Altemeier WA, Bjornson HS, et al: Host defense against opportunist microorganisms following trauma: I. Studies to determine the association between changes in humoral components of host defense and septicemia in burned patients . Ann Surg 1978;188:93.Crossref 12. Bjornson AB, Altemeier WA, Bjornson HS: Complement, opsonins, and the immune response to bacterial infection in burned patients . Ann Surg 1980;191:323-329.Crossref 13. Christou NV, Meakins JL: Neutrophil function in surgical patients: Two inhibitors of granulocyte chemotaxis associated with sepsis . J Surg Res 1979;26:355-364.Crossref

Journal

Archives of SurgeryAmerican Medical Association

Published: Feb 1, 1984

References