Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / @xirurgi_2025 / @xirurgi_2025 - 344 - файл
.pdf
15 Managing Soft Tissue Infection intheDiabetic Foot: Cultures, Drugs, andSource Control
197
effects; thus plasma concentrations must be monitored, especially in patients with renal impairment
and/or previous history of seizure disorders. The
combination of piperacillin and the BLI tazobactam can cover P. aeruginosa, E. faecalis, and strict
anaerobes, as well. This broad-spectrum antibiotic
should be limited to the moderate and severe DFIs
in conjunction with amikacin in cases of septic
shock to both enhance the bactericidal activity and
augment the antibacterial coverage to extendedspectrum beta-lactamases (ESBL)-producing
GNB.The Food and Drug Administration (FDA)
has approved piperacillin-tazobactam for the treatment of complicated SST DFIs but not for diabetic
foot osteomyelitis. Among the carbapenems,
ertapenem has broad-spectrum bactericidal activity directed against a wide spectrum of Grampositive cocci, GNB, and anaerobes, except
enterococci and Pseudomonas sp. (which differs
from imipenem and meropenem), and its use is
approved by the FDA for treating DFIs [29]. It is
effective against ESBL and AmpC-producing bacteria. Confusion and/or seizures may occur especially in elderly patients with renal insufciency.
The main advantage of ertapenem is its long
half-life which allows for once-daily dosing via
intravenous/intramuscular/subcutaneous administration. Prolonged infusions, including continuous
infusion of beta-lactam agents, are likely to maximize the time that serum concentrations remain
above the MIC of the bacteria within the infected
sites about the time-dependent activity of betalactam agents.
Doxycycline is a bacteriostatic tetracycline
antibiotic with broad coverage against Grampositive bacteria including most MRSA strains,
GNB including Klebsiella sp., E. coli, some
Enterobacter strains, and Clostridium sp. The
overall tolerance of doxycycline is good with
only a few cases of pruritus, photosensitization,
few cases of diarrhea, and exceptional lupusinduced reactions reported. The drug is contraindicated in patients with esophageal lesions, liver
cirrhosis, and portal hypertension due to the risk
of hemorrhage. Doxycycline does not need renal
or body weight dosing.
Clindamycin is a member of the macrolide
family with a bacteriostatic effect directed against
both Gram-positive (streptococci and staphylococci) and anaerobic bacteria but no activity
against GNB.The activity of clindamycin against
some strict anaerobes such as Bacteroides spp.
has decreased these last years, making it no longer appropriate as empiric antibiotic treatment in
cases where anaerobes may potentially be
involved. The D-test should be available for
detecting inducible resistance to clindamycin,
especially in the case of MRSA-related DFIs.
Clindamycin may modify taste (bitter or metallic) and is frequently associated with diarrhea,
including Clostridium difcile infections, especially in fragile and elderly patients. Clindamycin
does not require adaptation to renal function.
Metronidazole has a very broad anti- anaerobic
spectrum of activity except for Cutibacterium
acnes, complete oral bioavailability, and excellent tissue diffusion. The use of this antibiotic
may however result in peripheral neuropathy and
toxic encephalopathy, especially with a treatment
duration longer than 2weeks. In addition, patients
should be cautioned not to drink alcohol while
taking metronidazole due to the risk of tachycardia, palpitations, nausea, and vomiting (disulram effect).
Fluoroquinolones are concentrationdependent bactericidal antibiotics with good coverage against GNB and Gram-positive bacteria,
including Streptococcus spp. and E. faecalis, for
levooxacin, moxioxacin, and even some
uoroquinolone- resistant staphylococci for the
new agent delaoxacin. These agents achieve
excellent tissue diffusion and high oral bioavailability (levooxacin) but are limited in the treatment of SST DFIs given the risk of selection of
resistant mutants, especially with staphylococci,
and should probably be reserved for the treatment
of diabetic foot osteomyelitis (DFO).
Choice andAdaptation
oftheAntimicrobial Therapy
Some propositions inspired by the 2019 updated
IWGDF guidelines for the empiric antibiotic regimens are presented in Table15.1.
The use of microbiological results is another
important step in the management of DFIs. These
results are usually available within 3 days of sam-
198
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
Table 15.1 Empiric antibiotic regimens for non-osteomyelitic soft tissue diabetic foot infections
Additional factors Usual pathogen(s) Potential empirical regimens
Mild (grade 1) infections
No complicating
features
β-lactam allergy or
intolerance
Recent antibiotic
exposure
High risk for MRSA MRSA Linezolid; TMP-SMX; doxycycline; macrolide
Moderate to severe (grade 2 and 3) infections
No complicating
features
Recent antibiotics GPC±GNB
Macerated ulcer or
warm climate
Ischemic limb/
necrosis/gas forming
MRSA and multi-resistant GNB
MRSA risk factors MRSA Consider adding, or substituting with, glycopeptides;
MDR GNR risk
factors
Highly resistant GNB
risk factors
Inspired by 2019 IWGDF guidelines
“Usual pathogens” refers to isolates from an infected foot ulcer, not just colonization at another site
Antibiotics should be at the usual recommended doses for serious infections. Where more than one agent is listed, only
one of them should be prescribed, unless otherwise indicated
Consider modifying doses of agents selected for patients with comorbidities such as azotemia, liver dysfunction, and
obesity when required according to the recommendations for each molecule
Oral antibiotic agents should generally not be used for severe infections, except as follow-on (switch) after initial parenteral therapy
Fluoroquinolones (FQ) and Rifampin may ease the emergence of resistant mutants and should be restricted to osteomyelitis complicating DFIs (authors’ personal opinion)
βL-βLaseI: β-lactam, β-lactamase inhibitor; βL-βLaseI 1: amoxicillin/clavulanate, ampicillin/sulbactam; βL-βLaseI 2:
ticarcillin/clavulanate, piperacillin/tazobactam; doxy: doxycycline; ESBL: extended-spectrum β-lactamase-producing
organism; FQ: uoroquinolone with good activity against aerobic gram-positive cocci (e.g., levooxacin, moxioxacin
or delaoxacin); gen: generation; GNB: Gram-negative bacilli; GPC: Gram-positive cocci (Staphylococcus aureus and
β-hemolytic streptococci); group 1 carbapenem: ertapenem; group 2 carbapenem: imipenem, meropenem; ceph: cephalosporin; MRSA: methicillin-resistant S. aureus; S-S pen: semisynthetic penicillinase-resistant penicillin; cipro: antipseudomonal uoroquinolone, e.g., ciprooxacin: TMP-SMX, trimethoprim/sulfamethoxazole
GPC S-S pen; 1st-gen. cephalosporin
GPC Clindamycin; FQ; TMP-SMX; doxycycline
GPC+GNB
GPC±GNB
GNB, including P.
aeruginosa
GPC±GNB±strict
anaerobes
ESBL Carbapenems; FQ; aminoglycoside and colistin
GNB, carbapenemasesproducing rods
βL-βLaseI-1; TMP-SMX; FQ
βL-βLaseI-1; 1st, 2nd, 3rd-gen. cephalosporin
βL-βLaseI-1, 2nd, 3rd gen. cephalosporin; group 1
carbapenem (depends on prior therapy; seek advice)
βL-βLaseI-2; S-S pen+ceftazidime or cefepime;
ciprooxacin; group 2 carbapenem
βL-βLaseI-1 or 2; group 2 carbapenem; 2nd/3rd gen.
cephalosporin+clindamycin or metronidazole
linezolid; daptomycin; fusidic acid; TMP-SMX
New βL-βLaseI (ceftazidime-avibactam); cederocol
E. Senneville and R. Deldar
pling and the patient’s situation should be
assessed at that time. If signs of infection have
decreased, treatment should be maintained unless
the spectrum of the initial antibiotic regimen is
too broad and, therefore, should be reduced (deescalation). On the contrary, in the event of a
favorable outcome but resistant bacteria have
been identied, the treatment should not be modied given the limited accuracy of most ulcer
sampling techniques. In cases of an unfavorable
outcome and before broadening the antibacterial
spectrum of treatment, a non-microbiological
cause of failure should be sought such as poor
adherence to treatment, presence of deep collection, improper or no off-loading of the foot ulcer,
etc. Alternatively, when the infection resolves
under an antibiotic regimen that does not cover
the microorganisms identied from the ulcer, the
treatment should not be modied unless the
infection worsens.
15 Managing Soft Tissue Infection intheDiabetic Foot: Cultures, Drugs, andSource Control
199
Biolm andSoft Tissue Infections
oftheDiabetic Foot
While acute DFIs due to metabolically active
planktonic bacteria involve a direct hostcontrolled response to virulence expression,
chronic episodes mostly related to polymicrobial
biolms involve an inefcient inammatory
response [30]. Biolm formation is a complex
process that involves different communities of
microorganisms that are embedded in an
extracellular matrix made of glycoproteins, polysaccharides, proteins, and deoxyribonucleic acids
[31]. The biolm structure differs from one DFU
to another, given the multiple different microorganisms potentially involved. The consequences
of biolm formation are globally deleterious for
the wound healing process and the response to
antibiotic therapy by impairing antibiotic contact
with bacteria and their antibacterial activity given
the reduced metabolism of the microorganisms
present in the biolm environment. The production of degradative enzymes results in an inammatory response which is depicted by some
experts as a biolm-related infection [32]. The
frustrated host immune response results in
chronic inammation (depicted by some authors
as “chronic biolm infection”) which delays
ulcer healing and creates tissue damage [30, 33].
Given the limitation of this phenomenon in a
wound, topical administration of various agents
with antimicrobial activity and antibiolm
effect has been assessed. Overall, randomized
controlled data on the effectiveness and safety
of topical antimicrobial for DFI is limited and
has not proven convincing efcacy. The IWGDF
suggests against using any currently available
topical antimicrobial agent for treating a mild
DFI [2, 34]. Topical antimicrobial agents can
impact the microbial load and composition of
non-healing DFUs but are unlikely to signicantly improve the healing process [35]. On the
contrary, both chemical biolm disruptors and
wound debridement have shown efcacy in
improving non- healing DFUs [35, 36]. The high
prevalence of genes carrying resistance to most
antibiotics (e.g., beta-lactams, macrolides, aminoglycosides, and tetracyclines) in DFUs may
explain the absence of signicant effect of anti-
biotic agents on the microbial diversity in healed
versus non- healed wounds, especially when
used topically [37, 38]. Topical antibiotic treatment of infected DFUs with gentamicin-laden
sponges showed no benecial effects [39, 40].
Topical cadexomer iodine, which combines a
broad-spectrum antimicrobial and antibiolm
effect, is efcacious in a recent meta-analysis on
the treatment of chronic wounds, including
DFUs [41].
Resolution ofInfection
While the denition of successful management
of SSTs can easily be based on the resolution of
clinical signs of inammation, including inammatory biomarkers, and not on microbiological
cure, the issue is much more challenging for
DFO.Given the high rate of recurrence of DFO,
it is generally recommended to evaluate the
results of DFO at least 1 year after the end of
treatment.
The origin of DFIs being a foot wound in
almost all cases and the prevention of a recurrent
foot ulcer are of utmost importance (see Chap. 8).
References
1. Jneid J, Cassir N, Schuldiner S, Jourdan N, Sotto A,
Lavigne JP, La Scola B. Exploring the microbiota of
diabetic foot infections with culturomics. Front Cell
Infect Microbiol. 2018;8:282.
2. Lipsky BA, Senneville E, Abbas ZG, Aragón-Sánchez
J, Diggle M, Embil JM, etal. Guidelines on the diagnosis and treatment of foot infection in persons with
diabetes (IWGDF 2019 update). Diabetes Metab Res
Rev. 2020;36:1–24.
3. Hobizal KB, Wukich DK.Diabetic foot infections:
current concept review. Diabet Foot Ankle. 2012;3:3.
4. Dowd SE, Wolcott RD, Sun Y, McKeehan T, Smith E,
Rhoads D. Polymicrobial nature of chronic diabetic
foot ulcer biolm infections determined using bacterial tag encoded FLX amplicon pyrosequencing (bTEFAP). PLoS One. 2008;3:e33.
5. Ngba Essebe C, Visvikis O, Fines-Guyon M, Vergne
A, Cattoir V, Lecoustumier A, Lemichez E, Sotto
A, Lavigne JP, Dunyach-Remy C. Decrease of
Staphylococcus aureus virulence by Helcococcus
kunzii in a Caenorhabditis elegans model. Front Cell
Infect Microbiol. 2017;7:77.
200
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
E. Senneville and R. Deldar
6. Lavigne JP, Sotto A, Dunyach-Remy C, Lipsky
BA. New molecular techniques to study the skin
microbiota of diabetic foot ulcers. Adv Wound Care.
2015;4:38–49.
7. Lipsky BA, Armstrong DG, Citron DM, Tice AD,
Morgenstern DE, Abramson MA. Ertapenem versus piperacillin/tazobactam for diabetic foot infections (SIDESTEP): a prospective, randomized,
controlled, double-blinded, multicenter trial. Lancet.
2005;366(9498):1695–703.
8. Hatipoglu M, Mutluoglu M, Turhan V, Uzun G,
Lipsky BA, Turk-Day Study Group, Sevim E,
Demiraslan H, Eryilmaz E, Ozuguz C, Memis A, Ay
H, Arda B, Uysal S, Motor VK, Kader C, Erturk A,
Coskun O, Duygu F, Guler S, Altay FA, Ogutlu A,
Bolukcu S, Yildiz S, Kandemir O, Aslaner H, Polat
A, Karahocagil MK, Yasar KK, Sehmen E, Kilic S,
Sunbul M, Gencer S, Bozkurt F, Yanik T, Oztoprak
N, Batirel A, Sozen H, Kilic I, Celik I, Ay B, Tosun S,
Kadanali A, Çomoglu S, Denk A, Hosoglu S, Aydin O,
Elaldi N, Akalin S, Kandemir B, Akbulut A, Demirdal
T, Balik R, Azak E, Sengoz G. Causative pathogens
and antibiotic resistance in diabetic foot infections: a
prospective multi-center study. J Diabetes Complicat.
2016;30(5):910–6.
9. Noor S, Zubair M, Ahmad J.Diabetic foot ulcer—a
review on pathophysiology, classication and microbial etiology. Diabetes Metab Syndr. 2015;9:192–9.
10. Rahim K, Saleha S, Zhu X, Huo L, Basit A, Franco
OL. Bacterial contribution in chronicity of wounds.
Microb Ecol. 2017;73:710–21.
11. Liu C, Ponsero AJ, Armstrong DG, Lipsky BA,
Hurwitz BL.The dynamic wound microbiome. BMC
Med. 2020;18(1):358.
12. Radzieta M, Sadeghpour-Heravi F, Peters TJ, Hu
H, Vickery K, Jeffries T, Dickson HG, Schwarzer
S, Jensen SO, Malone M. A multiomics approach
to identify host-microbe alterations associated with
infection severity in diabetic foot infections: a pilot
study. NPJ Biolms Microbiomes. 2021;7(1):29.
13. Kumar D, Banerjee T, Chakravarty J, Singh SK,
Dwivedi A, Tilak R.Identication, antifungal resistance prole, in vitro biolm formation and ultrastructural characteristics of Candida species isolated
from diabetic foot patients in Northern India. Indian J
Med Microbiol. 2016;34:308–14.
14. Pouget C, Gustave CA, Ngba-Essebe C, Laurent F,
Lemichez E, Tristan A, Sotto A, Dunyach-Rémy C,
Lavigne JP. Adaptation of Staphylococcus aureus in
a medium mimicking a diabetic foot environment.
Toxins (Basel). 2021;13(3):230.
15. Guilhen C, Forestier C, Balestrino D.Biolm dispersal: multiple elaborate strategies for dissemination
of bacteria with unique properties. Mol Microbiol.
2017;105:188–210.
16. James GA, Swogger E, Wolcott R, Pulcini
ED, Secor P, Sestrich J, Costerton JW, Stewart
P.Biolms in chronic wounds. Wound Repair Regen.
2008;16:37–44.
17. Abbas M, Uçkay I, Lipsky BA. In diabetic foot
infections, antibiotics are to treat infection, not
to heal wounds. Expert Opin Pharmacother.
2015;16(6):821–32.
18. Gardner SE, Haleem A, Jao YL, Hillis SL, Femino JE,
Phisitkul P, Heilmann KP, Lehman SM, Franciscus
CL.Cultures of diabetic foot ulcers without clinical
signs of infection do not predict outcomes. Diabetes
Care. 2014;37(10):2693–701.
19. Nelson A, Wright-Hughes A, Backhouse MR, etal.
CODIFI (Concordance in Diabetic Foot Ulcer
Infection): a cross-sectional study of wound swab
versus tissue sampling in infected diabetic foot ulcers
in England. BMJ Open. 2018;8:e019437.
20. Levine N, Robert B, Lindberg R, Mason A, Basil A,
Pruitt B, Colonel MC.The quantitative swab culture
and smear: a quick, simple method for determining the number of viable aerobic bacteria on open
wounds. J Trauma. 1976;16(2):89–94.
21. Abbas ZG, Lutale JK, Alonso MM, Archibald
LK.The utility of Gram stains and culture in the management of limb ulcers in persons with diabetes. Int
Wound J. 2012;9(6):677–82.
22. Lin SY, Lin NY, Huang YY, Hsieh CC, Huang
YC. Methicillin-resistant Staphylococcus aureus
nasal carriage and infection among patients with
a diabetic foot ulcer. J Microbiol Immunol Infect.
2020;53(2):292–9.
23. Dunyach-Remy C, Courtais-Coulon C, DeMattei C,
Jourdan N, Schuldiner S, Sultan A, Carrière C, Alonso
S, Sotto A, Lavigne JP.The link between nasal carriage of Staphylococcus aureus and infected diabetic
foot ulcers. Diabetes Metab. 2017;43(2):167–71.
24. Zakariah NA, Bajuri MY, Hassan R, Ismail Z,
Md Mansor M, Othman H, Nasruddin DN. Is
Procalcitonin more superior to hs-CRP in the diagnosis of infection in diabetic foot ulcers? Malays J
Pathol. 2020;42(1):77–84.
25. Armstrong DG, Perales TA, Murff RT, Edelson GW,
Welchon JG. Value of white blood cell count with
differential in the acute diabetic foot infection. J Am
Podiatr Med Assoc. 1996;86(5):224–7.
26. Uçkay I, Aragon-Sanchez J, Lew D, Lipsky
BA.Diabetic foot infections: what have we learned
in the last 30 years? Int J Infect Dis. 2015;40:81–91.
27. Lauf L, Ozsvar Z, Mitha I, Regöly-Mérei J, Embil JM,
Cooper A, etal. Phase 3 study comparing tigecycline
and ertapenem in patients with diabetic foot infections
with and without osteomyelitis. Diagn Microbiol
Infect Dis. 2014;78:469–80.
28. Rybak MJ, Le J, Lodise T, Levine D, Bradley J, Liu C,
Mueller B, Pai M, Wong-Beringer A, Rotschafer JC,
Rodvold K, Maples HD, Lomaestro BM.Executive
summary: therapeutic monitoring of vancomycin
for serious methicillin-resistant Staphylococcus
aureus infections: a revised consensus guideline and
review of the American Society of Health-System
Pharmacists, the Infectious Diseases Society of
America, the Pediatric Infectious Diseases Society,
15 Managing Soft Tissue Infection intheDiabetic Foot: Cultures, Drugs, andSource Control
201
and the Society of Infectious Diseases Pharmacists. J
Pediatr Infect Dis Soc. 2020;9(3):281–4.
29. Edmonds M. The treatment of diabetic foot infections: focus on ertapenem. Vasc Health Risk Manag.
2009;5:949–63.
30. Moser C, Pedersen HT, Lerche CJ, Kolpen M,
Line L, Thomsen K, Høiby N, Jensen PØ. Biolms
and host response—helpful or harmful. APMIS.
2017;125(4):320–38.
31. Percival SL, McCarty SM, Lipsky B.Biolms and
wounds: an overview of the evidence. Adv Wound
Care. 2015;4:373–81.
32. Rodríguez-Rodríguez N, Martínez-Jiménez I,
García-Ojalvo A, Mendoza-Mari Y, Guillén-Nieto
G, Armstrong DG, Berlanga-Acosta J.Wound chronicity, impaired immunity and infection in diabetic
patients. MEDICC Rev. 2021;24(1):44–58.
33. Wolcott RD, Rhoads DD, Dowd SE. Biolms
and chronic wound inammation. J Wound Care.
2008;17(8):333–41.
34. Dumville JC, Lipsky BA, Hoey C, Cruciani M,
Fiscon M, Xia J. Topical antimicrobial agents for
treating foot ulcers in people with diabetes. Cochrane
Database Syst Rev. 2017;6(6):CD011038.
35. Malone M, Radzieta M, Schwarzer S, Jensen SO,
Lavery LA. Efcacy of a topical concentrated
surfactant gel on microbial communities in nonhealing diabetic foot ulcers with chronic biolm
infections: a proof-of-concept study. Int Wound J.
2021;18(4):457–66.
36. Kim D, Namen Ii W, Moore J, Buchanan M, Hayes
V, Myntti MF, Hakaim A. Clinical assessment of
a biolm- disrupting agent for the management of
chronic wounds compared with standard of care: a
therapeutic approach. Wounds. 2018;30(5):120–30.
37. Wang G, Sweren E, Liu H, Wier E, Alphonse MP,
Chen R, Islam N, Li A, Xue Y, Chen J, Park S, Chen
Y, Lee S, Wang Y, Wang S, Archer NK, Andrews
W, Kane MA, Dare E, Reddy SK, Hu Z, Grice EA,
Miller LS, Garza LA. Bacteria induce skin regeneration via IL-1β signaling. Cell Host Microbe.
2021;29(5):777–91.
38. Kalan LR, Meisel JS, Loesche MA, Horwinski J,
Soaita I, Chen X, Uberoi A, Gardner SE, Grice
EA.Strain- and species-level variation in the microbiome of diabetic wounds is associated with clinical
outcomes and therapeutic efcacy. Cell Host Microbe.
2019;25(5):641–55.
39. Uçkay I, Kressmann B, Malacarne S, Toumanova
A, Jaafar J, Lew D, Lipsky BA.A randomized, controlled study to investigate the efcacy and safety of
a topical gentamicin-collagen sponge in combination
with systemic antibiotic therapy in diabetic patients
with a moderate or severe foot ulcer infection. BMC
Infect Dis. 2018;18(1):361.
40. Uçkay I, Kressmann B, Di Tommaso S, Portela M,
Alwan H, Vuagnat H, Maître S, Paoli C, Lipsky BA.A
randomized controlled trial of the safety and efcacy
of a topical gentamicin-collagen sponge in diabetic
patients with a mild foot ulcer infection. SAGE Open
Med. 2018;6:2050312118773950.
41. Woo K, Dowsett C, Costa B, Ebohon S, Woodmansey
EJ, Malone M.Efcacy of topical cadexomer iodine
treatment in chronic wounds: systematic review
and meta-analysis of comparative clinical trials. Int
Wound J. 2021;18(5):586–97.
Surgical Management ofDiabetic
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
Foot Infection andOsteomyelitis
VenuKavarthapu andJavierAragónSánchez
16
Introduction
Foot infection in people with diabetes is a dramatic complication. The most common point of
entry of the infection to the foot is an ulcer that
often is due to associated neuropathy, peripheral
arterial disease, or both complications of diabetes. It is estimated that 40–80% of diabetic foot
ulcers (DFUs) become infected at any moment
during their clinical course [1]. The epidemiology of foot complications showed an increased
trend of diabetic foot infections (DFI), including
osteomyelitis (OM) and necrotising fasciitis
despite an 8-year decrease in the trend of DFUs
[2]. Infection is known to increase the costs associated with the treatment, often due to the need
for patients’ admission [3]. Factors related to
infection, such as depth, OM, and severity, will
condition the short-term outcomes in terms of
mortality and amputations [4]. Severe infections
carry a high rate of limb loss at 29.6% [5]. DFIs
also carry a readmission rate of about 10% [6, 7]
to 24% [8], due to recurrence of infection. Finally,
long-term mortality is high in this group of pre-
V. Kavarthapu (*)
King’s College Hospital, London, UK
e-mail: venu.kavarthapu@nhs.net
J. A. Sánchez
Department of Surgery and Diabetic Foot Unit,
Hospital La Paloma,
Las Palmas de Gran Canaria, Spain
sentations; one study reported a gure of 51.7%
of mortality in a 6.5-year follow-up study [9].
Clinical Assessment
andClassications
A detailed and systematic clinical assessment of
a patient with diabetes and foot infection by the
surgeon is crucial for successful management. In
the presence of diabetic peripheral neuropathy,
the local and systemic clinical signs are often
subtle, and it is critical that the clinical assessment is performed in a structured manner that
included appropriate history and clinical examination and supplemented with relevant investigations. This allows the surgeon and the
multidisciplinary team decide if the patient
requires an emergency procedure or delayed surgery after a period of conservative management
with antibiotics. Surgery should not be delayed in
rapidly spreading and deep infections because
these are not well tolerated by patients with diabetes and the risk of progression to diabetic foot
attack is high. That is especially true in cases of
severe infections which are associated with an
inammatory systemic response [10].
Some diabetic foot infections are not only
limb, but life threatening, and such presentations
are often best managed in a multidisciplinary
setup. Sometimes, a timely minor amputation
needs to be considered for prevention of a major
© Springer Nature Switzerland AG 2023
C. E. Attinger, J. S. Steinberg (eds.), Functional Limb Salvage,
https://doi.org/10.1007/978-3-031-27725-2_16
203
204
V. Kavarthapu and J. A. Sánchez
amputation, and a major amputation for saving
the patient’s life. Limb salvage can sometimes be
difcult when surgery is inadvertently delayed
because it allows the infection to proliferate and
destroy tissues beyond recovery and a timely surgical intervention is the key [11–13]. That is
especially true in cases of deep tissue infections,
dened as those below the fascia [14]. Prompt
surgical treatment including extensive use of
revascularisation may reduce the need for aboveankle amputations [13, 15–17]. Such presentations are best managed by a multidisciplinary
diabetic foot team (MDFT) that has access to
specialist diabetic foot surgeons that can perform
surgery in a timely manner and offer functional
limb salvage. The maxim ‘time is tissue’ is totally
true in cases of DFIs with associated signicant
ischemia. Another key point is deciding if the
patients require admission or can be treated in an
ambulatory basis. For these reasons, it is important to perform a detailed clinical assessment,
determine the grade, and classify the type of
infection in patients with diabetes.
DFIs are classied according to their severity,
by International Working Group on the Diabetic
Foot (IWGDF) as mild, moderate, and severe
[18] and this classication has later been validated [5]. IWGDF classies DFI presentations
that have associated systemic manifestations (of
the systemic inammatory response syndrome)
as severe infections [10] and recommends considering hospitalisation for severe DFIs, and
those with a moderate infections that are complex
or associated with key relevant morbidities [10].
Admission is also necessary in cases of failure of
outpatient management, when the patient is
unable or unwilling to comply with outpatientbased treatment, there is a need for more complex
dressing changes than patient/caregivers can provide or when a careful, continuous observation is
needed [10]. However, the current evidence on
the protocol recommended for the need for hospitalisation is low [19].
From a pathological point of view, DFIs can
be classied into two main groups: soft tissue and
bone infections although it is very usual to nd
both types together [20–22]. Soft tissue infections are then classied as cellulitis, abscesses,
tenosynovitis, and necrotising soft tissue infections (necrotising cellulitis, necrotising fasciitis,
necrotising tenosynovitis, and myonecrosis),
including diabetic foot attack (DFA) [23, 24].
Deep abscesses and deep necrotising soft tissue
infections always require surgery and admission.
The infection committee of the International
Working Group on Diabetic Foot (IWGDF) has
recently suggested modifying the classication
of the severity of the infection. They proposed
adding ‘(O)’ to moderate and severe infections
groups that have an associated diagnosis of diabetic foot osteomyelitis (DFO) [10].
Another DFI classication commonly used is
from Infectious Diseases Society of America
(IDSA). This classies the DFIs as group 1 with
no infection, group 2 as mild soft tissue infection
(STI), group 3 as moderate or severe STI, and
group 4 is moderate or severe bone infection
[25]. Studies have shown that patients with DFO
had worse outcomes, more surgeries including
amputations, longer hospitalisations, higher rates
of recurrent infection and readmission than
patients with moderate and severe STI [25]. DFO
has frequently been reported as a risk factor for
amputation and poor outcomes [4, 8, 26] and for
that reason suspecting osteomyelitis is critical at
the initial clinical evaluation. However, it has
recently been reported that in cases of surgical
diabetic foot infections, the presence of bone
infection was not associated with worse prognosis [27].
The management of DFO may be different
from those infections involving exclusively soft
tissues. Osteomyelitis should be suspected in
wounds that extended to a bone or joint and in
cases in which the patient has previous history of
a wound and recurrent ulcers [28]. Checking the
depth of the infection after removing infected
callus and tissue slough is important. However, it
has been reported that nearly 90% of the wounds
in one series were not evaluated for involvement
of underlying structures [29]. Instrumental evaluation is very useful for determining depth and
detecting stulous tracks, cavities, and bone
involvement. A blunt, 14.0-cm, 5F, stainless steel
eye probe [30] or a metal forceps (Halstedmosquito) [31, 32] is gently introduced through
16 Surgical Management ofDiabetic Foot Infection andOsteomyelitis
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
205
the wound and the probe-to-bone (PTB) is considered ‘positive’ if bone (a hard or gritty surface) is palpable. PTB test had a sensitivity of
0.95, a specicity of 0.93, positive predictive
value of 0.97, and a negative predictive value of
0.83in advanced cases of infections in one study
[33]. A systematic review reported a pooled sensitivity of the PTB test of 87% (95% CI, 75–93%),
specicity of 83% (CI, 65–93%), positive
predictive value (PPV) of 98%, and negative predictive value (NPV) of 70% [34]. We can summarise that a positive PTB test in advance cases
reinforces the suspicion of DFO.
The location of the point of entry of the infection in the foot is very important to predict the
infection spread in deep tissue planes and compartments. Suppuration through the ulcer while
palpating at a location distant from the ulcer is
consistent with a spreading infection. In some
presentations, the index ulcer is located on the
plantar aspect and there is cellulitis and uctuation on the dorsum of the foot. In such cases, it is
frequent that the infection had involved the bone
migrating from a high-pressure plantar area to
the low-pressure dorsal area. For this reason, it is
uncommon that infections arising on the dorsal
aspect of the foot spread to the plantar area.
Presence of tissue necrosis is a worrying sign in
such infections, especially when the patient has a
good distal blood supply. In such cases, the surgeon should suspect the existence of a necrotising soft tissue infection [23, 24] that often
resulting in raised pressure inside the foot’s
compartments.
The initial imaging study to evaluate a DFI
infection is weightbearing plain radiographs of
the foot in two standard views. It permits to detect
any foreign body, free gas in soft tissues, and
bone involvement. The reported sensitivity of
plain radiography in the diagnosis of osteomyelitis is usually low, especially in early stages of
infection [35, 36]. In cases of high suspicion of
DFO and an X-ray without pathological ndings,
a sequential X-ray studies may be useful. That is
due to the fact that bone abnormalities can only
be detected at least 2–4 weeks after the onset of
bone infection when signicant bone resorption
is evident [37]. Advanced imaging studies are
needed not only for diagnosing DFO, but also
detecting the soft tissue involvement and spread
of the infection in deep tissue planes. Magnetic
resonance imaging (MRI) has been suggested as
the most useful imaging study to evaluate both
deep soft tissue infections and osteomyelitis [38].
However, the exact role of advanced imaging
studies to plan the surgery and determine the
level of bone resection has still not been claried.
Some studies on DFO reported that the extent of
infection could have been overestimated on an
MRI [39]. Furthermore, preoperative MRI in
cases of DFO in ischaemic feet may be less effective for distinguishing osteomyelitis from reactive bone marrow oedema in cases of neuropathic
ulcers [40].
Applied Anatomy ofDiabetic Foot
Infection
It is essential that the treating surgeon has a good
understanding of the compartmental anatomy of
the foot. The foot is divided into rigid compartments and when an infection penetrates into a
compartment, this can lead to raised compartment pressures resulting in a compartmental syndrome. When the compartmental pressure
exceeds the capillary pressure, necrosis of deep
tissues including muscle and tendons appears.
Bacterial growth, toxins, and leucocyte response
may also induce necrosis by direct tissular damage and producing a neutrophilic vasculitis leading to secondary thrombosis and local ischemic
changes. These factors increase the extension of
tissular death. Another consequence is that antibiotics cannot penetrate to the infection site due
to capillary blockage.
The oor of the compartments is formed by
plantar aponeurosis, which is attached to the calcaneus and spread distally to the toes. There are
three plantar compartments: medial, lateral, and
central. The medial and lateral compartments are
separated from the central compartments by the
medial and lateral intermuscular septum. The
interosseus compartment is located between the
metatarsal bones and contains the interossei muscles. Finally, the dorsal compartment located on
206
V. Kavarthapu and J. A. Sánchez
the dorsal aspect of the foot that contains a thin
layer of subcutaneous tissue and the extensor tendons. Infections of the rst toe spread along the
medial compartment, those involving second to
fourth toes spread along the central compartment,
and of the fth toe spread along the lateral compartment. Sometimes, in cases of infections without appropriate treatment the infection breaks the
septum and may involve the adjacent
compartment. Furthermore, the infection may
migrate from the plantar to dorsal compartment
through the interosseous compartment. Increasing
pressure into the interosseous compartment
results in thrombosis of the blood vessels leading
to toe necrosis even in well vascularised feet.
The forefoot, involving the phalanxes and
metatarsal heads, is the most frequent location of
diabetic foot osteomyelitis [23, 41]. A surgical
series demonstrated that osteomyelitis was
located at the forefoot in 90% of the cases, at the
midfoot in 5%, and at the rear foot in another 5%
of the cases [23]. Others have reported higher gures of mid- and rear foot osteomyelitis [42]. In
the case that a joint is involved, the infection produces a septic arthritis. If the infection progresses,
then infection spreads to the cartilage and adjacent bone. The tip of the toes has neither joint nor
tendon attachments and ulcers located in this area
can easily reach the bone because only subcutaneous tissue lies between the skin and periosteum. Bone prominences from lateral deformities
such as the medial eminence from bunions are
also high-risk locations for ulceration and
osteomyelitis.
debridement is methodical and provides consistent and complete resection of the infected and
necrotic tissue to achieve infection clearance.
Red–amber–green (RAG) model of surgical
debridement provides a structured model for the
performing surgeon to achieve this [43]. The
RAG model highlights the importance of understanding different zones of infection spread and
promotes the surgeon achieve full infection clearance. The infected diabetic foot has a central
zone of active infection with tissue necrosis that
is recognised as the ‘red zone’. This is surrounded
by an area of reactive tissue—a relatively avascular and brous tissue that potentially harbours
small pockets of infections within it, considered
as the ‘amber zone’. Outside this area is the
‘green zone’ that contains normal and healthy tissue that has a full healing potential. The RAG
model recommends removal of all tissue in the
red and amber zones, until the green zone is
reached circumferentially. This principle is applicable to bone debridement as well.
The internal spread of diabetic foot infection
is often along the tissue planes, from the zones/
compartments of high pressure to low pressure.
This is frequently seen along the tendon sheaths
and this route is recognised as the ‘superhighway’ for the spread. It is critical that these
tissue planes and tendon sheaths are probed,
explored, and laid open during debridement so
that all areas of necrotic and reactive tissue are
excised. Such infections with extensive tissue
spread often require repeat surgical debridement
as some of the tissue in the amber and green
zones and the edge if resection die back.
Principles ofSurgical Debridement
ofDiabetic Foot Infections
The aim of surgical management of infected diabetic foot is to achieve complete infection eradication while retaining all healthy and non-infected
tissue. This is accomplished by attaining infection clearance through surgical removal of all
infected tissues, followed by eradication of
retained pathogens in the surrounding normal
looking tissues by providing targeted antibiotic
therapy. It is critical that the technique of surgical
Clean Margins inSurgical Treatment
ofDFO
It is critical that during exostectomy and amputation procedures for DFO presentations, all of
the infected bone is excised. Residual infection
in the proximal bone margins after undergoing
amputation for osteomyelitis may be associated
with a worse prognosis after surgical treatment
of DFO.Usually, the surgeon decides the location at which osteotomy is carried out based on
16 Surgical Management ofDiabetic Foot Infection andOsteomyelitis
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
207
the intraoperative inspection of the bone. Bone
appearance, its consistency, the presence of
vascular thrombosis, fracture pus, and discolouration are considered by the surgeon to
choose the location of osteotomy and the extent
of bone resection. Bone biopsy is taken from
the edges of bone resection for microbiological
and histological studies. It has recently been
suggested a standardised surgical dictation
regarding bone appearance based on density,
anatomic structure, vascular thrombosis,
colour, and draining sinus [44]. However, some
reports highlight that those ndings may be
inaccurate. One group of authors reported that
35.1% of patients had positive margins (dened
by histopathology) in a retrospective cohort.
Residual osteomyelitis at the proximal margin
was associated with a higher rate of treatment
failure, despite the longer duration of antibiotic
therapy. A retrospective observational study
involving 27 patients with DFO showed that the
overall rate of residual osteomyelitis (based on
intraoperative bone culture) was 40.7%. Nine
out of 11 patients (81.8%) with positive margins had poor outcomes [45]. Other authors
found that patients in which proximal bone
specimens had a positive culture were more
likely to undergo repeat surgical intervention.
However, the authors stated that the reason for,
and benet of, this additional surgery was
unclear [46]. Guidelines suggest that it could be
useful obtaining a specimen of bone for culture
(and, if possible, histopathology) at the stump
of the resected bone to administer post-resection antibiotic therapy if positive [10]. However,
the evidence is weak for the moment and the
denitive role of proximal culture, histopathology, or both to guide a reintervention is not well
stated. Regarding postoperative antibiotic therapy, a retrospective series reported that immediate postoperative stopping of antibiotics after
amputation in the absence of residual infection
was not a risk factor of failure of the treatment
[47]. In cases in which residual infections are
apparent after surgery of DFO, a period of 3
weeks was non- inferior to 6 weeks of postoperative antibiotic therapy in a recent randomised
clinical trial [48].
Surgical Management ofForefoot
Osteomyelitis
The forefoot is the most frequent location of
osteomyelitis in the diabetic foot. Forefoot
includes toes, metatarsal bones, interphalangeal and metatarsophalangeals joints. Forefoot
osteomyelitis that does not respond to local
debridement and targeted antibiotic administration is usually treated by means of some
type of amputations [42]. The most common
amputations performed to remove infected
bone and soft tissues in diabetic patients with
forefoot osteomyelitis are toe, ray, and transmetatarsal resections [49]. Conservative surgery in which the infected bone and non-viable
soft tissue are removed without performing any
type of amputation is an accepted alternative to
amputation in some presentations [23, 50, 51].
However, the impact of this type of surgery on
the quality of life and long-term recurrences
when comparing with minor amputations has
not been addressed. Some conservative surgeries, as an alternative to toe amputation, have
been described. Osteomyelitis of the tip of the
minor toes can easily be removed through the
ulcer. This procedure can be carried out combined with percutaneous exor tenotomy to
reduce the deformity of the toe [52, 53]. When
the interphalangeal joint of lesser toes is
involved by the infection, a resection arthroplasty can be considered [23, 54–56]. In a
series of 72 toes, a group of authors reported
successful outcome of excision arthroplasty
for infected IPJs by performing extensive
debridement of bone and soft tissues, thorough
irrigation of the wound, and stabilisation of IPJ
using a Kirschner wire. Just three cases in this
series underwent toe amputations and no proximal spreading of the infection was observed in
any other cases during the follow-up period.
Open arthroplasties leaving the postoperative
wound to heal by secondary intention has also
been described in cases of diabetic foot osteomyelitis [55, 57, 58].
Neuropathic plantar ulcers under the metatarsal head may become complicated by osteomyelitis. In such cases, amputation of the toe
Соседние файлы в папке @xirurgi_2025