İnfeksiyon: Kronik Yarada Ampirik Sistemik Antibiyotik Kullanımı
Özet
Kronik yaralar zamanla değişen polimikrobiyal bir floraya sahiptir ve tümü bakterilerle kontamine olmaktadır. Yaralarda başlangıçta koagülaz negatif stafilokoklar, streptokoklar ve Staphylococcus aureus gibi cilt florası elemanları saptanırken, ilerleyen dönemlerde gram-negatif basiller ve anaerop mikroorganizmalar eklenmektedir. Lokal veya sistemik enfeksiyon bulgusu olmayan hiçbir kronik yaraya rutin ampirik ya da profilaktik antibiyotik tedavisi önerilmez; antibiyotik kullanımı debridman ve cerrahi drenajın bir alternatifi değildir. Enfeksiyon varlığında, yaradan kantitatif doku kültürü gibi uygun örnekler alınmalı ve süreç mikrobiyolojik olarak desteklenmelidir. Ampirik antibiyotik seçiminde hastanın klinik özellikleri, ek hastalıkları ve lokal direnç verileri dikkate alınmalıdır. Hafif enfeksiyonlarda 1-2 haftalık oral tedavi yeterliyken; yaygın selülit, sistemik bulgular veya oral alım güçlüğü durumunda parenteral tedavi tercih edilmeli ve orta/şiddetli enfeksiyonlarda tedavi en az 4-6 hafta planlanmalıdır. Şiddetli enfeksiyonlarda veya MRSA, ESBL+ gram-negatifler gibi dirençli patojen riskinin yüksek olduğu durumlarda ampirik spektrum bu etkenleri kapsayacak şekilde genişletilmelidir. Tedavi, enfeksiyon bulguları gerilediğinde yara tamamen iyileşmese bile kesilmelidir.
Chronic wounds have a polymicrobial flora changing over time, and all of them become contaminated with bacteria. While skin flora elements like coagulase-negative staphylococci, streptococci, and Staphylococcus aureus are detected initially, gram-negative bacilli and anaerobes are added in later stages. Routine empirical or prophylactic antibiotic therapy is not recommended for any chronic wound without local or systemic signs of infection; antibiotic use is not an alternative to debridement and surgical drainage. In the presence of infection, appropriate samples such as quantitative tissue cultures must be taken and the process should be microbiologically supported. Patient's clinical characteristics, comorbidities, and local resistance data must be considered in empirical antibiotic selection. While a 1-2 week oral therapy is sufficient for mild infections, parenteral therapy should be preferred in case of widespread cellulitis, systemic signs, or difficulty in oral intake, and treatment for moderate/severe infections should be planned for at least 4-6 weeks. In severe infections or when the risk of resistant pathogens like MRSA and ESBL+ gram-negatives is high, the empirical spectrum must be expanded to cover these agents. Treatment should be discontinued when infection signs regress, even if the wound is not completely healed.
Referanslar
Landis SJ. Chronic wound infection and antimicrobial use. Adv Skin Wound Care. 2008;21(11):531-40.
Gjodsbol K, Christensen JJ, Karlsmark T, Jorgensen B, Klein BM, Krogfelt KA. Multiple bacterial species reside in chronic wounds: a longitudinal study. Int Wound J. 2006;3(3), 225-31.
Bowler PG, Davies BJ. The microbiology of acute and chronic wounds. Wounds. 1999;11:72-8.
Morton LM, Phillips TJ. Wound healing and treating wounds. Differential diagnosis and evaluation of chronic wounds. J Am Acad Dermatol. 2016;74(4):589-605.
Schultz GS, Sibbald RG, Falanga V, Ayello EA, Dowsett C, Harding K, Romanelli M, Stacey MC, Teot L, Vanscheidt, W. Wound bed preparation: a systematic approach to wound management. Wound Rep Reg. 2003;11:1-28.
Lipsky BA, Dryden M, Gottrup F, Nathwani D, Seaton RA, Stryja J. Antimicrobial stewardship in wound care: a position paper from the British Society for Antimicrobial Chemotherapy and European Wound Management Association. J Antimicrob Chemother. 2016;71(11):3026-35.
Lipsky BA, Hoey C. Topical antimicrobial threapy for treating chronic wounds. CID. 2009;49(10):1541-49.
Lipsky BA, Berendt AR, Cornia PB, Pile JC, Peters EJ, Armstrong DG, Deery HG, Embil JM, Joseph WS, Karchmer AW, Pinzur MS, Senneville E. 2012 Infectious Diseases Society of America clinical practice guideline for the diagnosis and treatment of diabetic foot infections. CID. 2012;54(12):132-173.
Leekha S, Terrell C, Edson RS. General principles of antimicrobial therapy. Mayo Clin Proc. 2011;86(2):156-67.
Siddiqui AR, Bernstein JM. Chronic wound infection: facts and controversies. Clin Dermatol. 2010;28(5):519-26. METİN İÇİNDE BULUNAMADI
Saltoglu N, Kılıcoglı O, Baktıroglu S, Osar-Siva Z, Aktas S, Altındas M, ... & Engin A. Diagnosis, treatment and prevention of diabetic foot wounds and infections: Turkish consensus report. Klimik Journal. 2015;28(1):2-34.
Serra R, Grande R, Butrico L, Rossi A, Settimio UF, Caroleo B, Amato B, Gallelli L, de Franciscis S. Chronic wound infections: the role of Pseudomonas aeruginosa and Staphylococcus aureus. Expert Rev Anti-infect Therapy. 2015;13(5):605-13.
Ertugrul BM, Lipsky BA, Ture M, Sakarya S. Risk factors for infection with Pseudomonas aureginosa in diabetic foot infections. J AM Podiatr Med Assoc. 2017;107(6):483-89.
Jouhar L, Jaafar RF, Nasreddine R, Itani O, Haddad F, Rizk N, Hoballah JJ. Microbiological profile and antimicrobial resistance among diabetic foot infections in Lebanon. Int Wound J. 2020;17(6):1764-73.
Shahrokh S, Aliye T, Yazdi M, Siavash M, Aminorroaya A. Bacterial Profile and Antimicrobial Resistance Patterns of Infected Diabetic Foot Ulcers in Iran: A Systematic Review and Meta-Analysis of Cross-Sectional Studies. Int J Low Extrem Wounds. 2021:15347346211002715.
Zafra VG, Torres AH, Vázquez EG, Cogollos TS, Jordana MC, Gómez JR, Gómez JG, Martinez AH, Barberán, J. Risk factors for methicillin-resistant Staphylococcus aureus and extended-spectrum ß-lactamase-producing Enterobacterales in patients with diabetic foot infections requiring hospital admission. Rev Esp Quimioter. 2020;33(6):430-5.
Datta P, Chander J, Gupta V, Mohi GK, Attri AK. Evaluation of various risk factors associated with multidrug-resistant organisms isolated from diabetic foot ulcer patients. J Lab Physicians, 2019;11(01):58-62.
Tzaneva V, Mladenova I, Todorova G, Petkov D. (2016). Antibiotic treatment and resistance in chronic wounds of vascular origin. Clujul Med. 2016; 89(3):365-70.
