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 / Библиотека им академика М.И. Перельмана / Книга_5205_Библиотеки_им_академика_М_И_Перельмана.pdf
X
- •Foreword
- •Preface
- •Contents
- •2.3 Diagnostic Modalities
- •2.4 Antibiotic Stewardship Principles
- •1.1 Historical Background
- •1.2 Epidemiology
- •1.4 Management
- •1.5 Conclusion
- •References
- •2.1 Introduction
- •2.5 Surgical Management
- •Bibliography
- •3.1 Introduction
- •3.2 Pharmacokinetics
- •3.3 Fluoroquinolones
- •3.6 Cephalosporins
- •3.7 Ceftobiprole
- •3.9 Linezolid
- •3.11 Daptomycin
- •3.12 Fosfomycin
- •3.15 Conclusion
- •References
- •4.1 Aetiology
- •4.1.2 Risk Factors
- •4.1.2.2 Bacteria
- •4.1.2.3 Other Causative Agents
- •4.2 Negative Pressure Wound Therapy
- •4.2.1 Summary
- •References
- •5: Bacterial Resistance
- •5.1 Introduction
- •5.3.1 Antibiotic Destruction
- •5.3.4 Target Replacement or Target Bypass
- •5.3.5 Target Site Alteration
- •References
- •6.1 Blood Chemistry Tests
- •References
- •7.1 Introduction
- •7.2 New Diagnostic Tools
- •7.2.1 Serological Tests
- •7.2.1.1 D-dimer
- •7.2.1.2 Fibrinogen
- •7.2.1.3 Neutrophil-to-Lymphocyte Ratio
- •7.2.1.4 Procalcitonin
- •7.2.2 Synovial Tests
- •7.2.2.1 Mass Spectrometry
- •7.2.2.2 Alpha Defensin
- •7.2.2.3 Synovial C-Reactive Protein
- •7.2.2.4 Synovial Interlukin-6
- •7.2.2.5 Calprotectin
- •7.2.3.1 Culture Sonication
- •7.3 Conclusion
- •References
- •8.1 Introduction
- •8.2 Etiology
- •8.4 Clinical Diagnosis
- •8.5 Laboratory Investigations
- •8.6 Biopsy
- •8.7 Radiological Investigations
- •8.8 Medical Management
- •8.8.1 Acute Osteomyelitis
- •8.8.2 Septic Arthritis
- •8.9 Pyomyositis
- •8.10 Surgical Management
- •8.11 Acute Osteomyelitis
- •8.12 Septic Arthritis
- •8.13 Complications
- •8.14 Chronic Osteomyelitis
- •8.15 Pathological Fractures
- •8.16 Post-infective Segmental Bone Loss
- •8.17 Post-infective Physeal Growth Arrest
- •8.18 Post-septic Hip Sequelae
- •8.19 Summary
- •References
- •9.2 Locations
- •Bibliography
- •10: Chronic Osteomyelitis
- •10.1 Introduction
- •10.2 Etiology
- •10.3 Epidemiology
- •10.4 Pathophysiology
- •10.7 Laboratory Test
- •10.8 Diagnostic Radiology
- •10.11 The Host
- •10.12 The Disease
- •10.13 Treatment
- •10.14 Systemic Antibiotic Therapy
- •10.15 Local Antibiotic Depots
- •10.16 Surgical Treatment
- •10.18 Soft Tissue Coverage
- •11.1.6 Imaging
- •11.2 Risk Factors
- •11.3 Common Species
- •10.20 Results
- •10.21 Summary
- •References
- •11.1 Diagnosis
- •11.1.2 Labs
- •11.1.3 Synovial Fluid
- •11.1.4 Culture
- •11.1.5 Histopathology
- •11.4.1 Soft Tissue
- •11.4.2 Bone
- •11.4.3 Joint
- •11.4.4 Periprosthetic
- •References
- •Further Readings
- •12.6 Conclusion
- •12.7 Biography
- •References
- •13.1 Vertebral Osteomyelitis
- •13.1.1 History
- •13.1.2 Epidemiology
- •13.1.3 Pathophysiology
- •13.1.4 Most Common Manifestations
- •13.1.5 Diagnosis
- •13.1.6 Imaging Studies
- •13.1.7 Treatment
- •13.2 Vertebral Tuberculosis
- •13.2.1 History
- •13.2.2 Epidemiology
- •13.2.3 Pathophysiology
- •13.2.4 Most Common Manifestations
- •13.2.5 Pediatric Spinal Tuberculosis
- •13.2.6 Diagnosis
- •13.2.7 Treatment
- •References
- •14.1 Introduction
- •14.2.2 Primary Injury
- •14.2.3 Early Versus Late Infection
- •14.2.5.1 Sequestrum
- •14.2.6 Patient Comorbid Factors
- •14.3 Treatment Options
- •14.3.3 Soft Tissue Coverage
- •14.3.4 External Fixation
- •14.3.5 Antibiotic Loaded Cement/Bioceramics
- •14.3.6 Membrane-Induced Osteogenesis (Masquelet Technique)
- •References
- •15.1 Introduction
- •15.1.1 Conservative Approach
- •15.1.2 Reconstructive Approach
- •15.2 Pedicled Flaps
- •15.2.1 Rectus Abdominis Musculocutaneous Flap
- •15.2.1.1 Surgical Technique
- •15.2.3 Gastrocnemius Flap
- •15.2.3.1 Surgical Technique
- •15.2.4 Soleus Flap
- •15.2.4.1 Surgical Technique
- •15.2.5 Vascularized Fibula Flap
- •15.2.5.1 Surgical Technique
- •15.2.6.1 Surgical Technique
- •15.2.7 Sural Flap
- •15.2.7.1 Surgical Technique
- •15.3 Microsurgical Flaps
- •15.3.1 Anterolateral Thigh Flap
- •15.3.1.1 Surgical Technique
- •15.3.2 Latissimus Dorsi Muscle Flap
- •15.3.2.1 Surgical Technique
- •15.3.3 Gracilis Free-Flap
- •15.3.3.1 Surgical Technique
- •References
- •16: Diabetic Foot Osteomyelitis (DFO)
- •16.1 Introduction
- •16.3.3 Radiographic Examinations
- •16.3.3.1 X-ray
- •16.3.3.2 MRI
- •16.3.3.3 PET-CT
- •16.3.4 Biopsy
- •16.4.1 Antibiotics Therapy
- •16.4.2 Conservative Surgery
- •16.4.3 Aggressive Surgery
- •References
- •17.1.1 Osteoradionecrosis (ORN)
- •17.1.1.1 Prevalence
- •17.1.1.3 Management
- •17.1.2 Risk Prediction
- •17.1.2.1 Conclusion
- •17.1.3.1 Medications
- •17.1.3.3 Patients At-Risk
- •17.2 Pathophysiology
- •17.2.1 Bone Remodeling Inhibition
- •17.2.3 Angiogenesis Inhibition
- •17.2.4 Acquired Immune Dysfunction
- •17.3.2 Local Factors
- •17.3.2.1 Dentoalveolar Procedures
- •17.3.2.2 Anatomic Factors
- •17.3.2.3 Concomitant Oral Disease
- •17.3.2.4 Treatment Goals
- •17.3.3 MRONJ Prevention Strategies
- •17.3.4 Treatment Strategies
- •17.3.4.1 Nonoperative Therapy
- •17.3.5 Operative Therapy
- •17.3.6.1 Pulpitis
- •17.3.6.2 Acute Apical Periodontitis (Periapical Abscess)
- •17.3.6.3 Periapical Granuloma
- •17.3.6.4 Periapical Cyst
- •17.3.7.3 Garre’s Sclerosing Osteomyelitis
- •References
- •18.1 Introduction
- •18.2 Risk Factors
- •18.3 Evidence-Based Preventive Measures
- •18.3.1 Preoperative Measures
- •18.3.1.1 Surgical Hand Preparation
- •18.3.1.5 Preoperative Bathing or Showering
- •18.3.1.6 Preoperative Skin Preparation
- •18.3.1.7 Hair Removal
- •18.3.1.8 Glycemic Control
- •18.3.2 Intraoperative Measures
- •18.3.2.2 Second Dose Antibiotic
- •18.3.2.3 Incisional Wound Irrigation
- •18.3.2.4 Perioperative Oxygenation
- •18.3.2.8 Behavioral Aspects
- •18.3.3 Postoperative Measures
- •18.3.3.1 Postsurgical Wound Care
- •18.3.3.2 Postoperative Antibiotics
- •References
- •19: Periprosthetic Joint Infection: General Aspects
- •19.2 “Local” Patient Risk Factors
- •19.4.1 Presurgical
- •19.4.2 Intraoperative
- •19.4.3 Post-operative
- •19.4.3.1 “Mechanical” Thromboembolic Prophylaxis [101, 102]
- •References
- •20: Low-Grade Periprosthetic Infections
- •20.1 Diagnosis
- •20.3 Outcomes
- •20.4 Conclusion
- •References
- •21.1 Introduction
- •21.5.1 Multidisciplinary Approach
- •21.5.2 Surgical Strategies
- •21.5.3 Other Therapeutic Strategies
- •References
- •22.1.1 Introduction
- •22.2 PJI After Shoulder Arthroplasty
- •22.2.1 Epidemiology
- •22.2.2 Risk Factors
- •22.2.3.2 Diagnostic Criteria
- •22.2.3.3 Clinical Presentation
- •22.2.3.4 Radiology
- •22.2.3.6 Synovial Aspirate
- •22.2.4 Management
- •22.2.4.1 Prevention
- •22.2.4.2 Treatment
- •Implant Retention
- •One-Stage Revision Arthroplasty
- •Two-Stage Revision Arthroplasty
- •Antibiotic Spacer
- •Resection Arthroplasty
- •22.3 PJI after Elbow Arthroplasty
- •22.3.2 Risk Factors
- •22.3.3 Diagnosis
- •22.3.4 Treatment
- •22.3.4.1 Implant Retention
- •22.3.4.2 One-Stage Revision Arthroplasty
- •22.3.4.3 Two-Stage Revision Arthroplasty
- •22.3.4.4 Salvage Procedures
- •References
- •23.1 Introduction
- •23.2 Epidemiology
- •23.3 Pathophysiology
- •23.4 Etiology
- •23.6 Diagnosis
- •23.6.1 Lab Test
- •23.6.2 Imaging
- •23.6.3 Cultures
- •23.7 Risk Factors
- •23.8 Surgical Treatment
- •23.8.2 One-Stage Revision Surgery
- •23.8.3 Two-Stage Revision Surgery
- •23.9 Conclusions
- •References
- •24.1 Introduction
- •24.2 Knee
- •24.2.1 Overview
- •24.2.3 Static Spacers
- •24.2.4 Static Versus Articulating Spacers
- •24.2.5 Distal Femoral or Proximal Tibial Replacement Infection
- •24.2.6 Stage 1 Arthrodesis Spacers
- •24.2.7 Articulating DFR/PTR Spacers
- •24.3 Hip
- •24.3.1 Static Spacers
- •24.3.2 Articulating Spacers
- •References
- •25: Native Hip Joint Infection
- •25.1 Introduction
- •25.2.1 Epidemiology
- •25.2.2 Etiology
- •25.2.3 Clinical Presentation
- •25.2.4 Diagnosis
- •25.2.6 Treatment
- •25.3 Infection Following Hip Preservation Surgery
- •25.3.1 Hip Arthroscopy
- •25.3.1.1 Epidemiology
- •25.3.1.2 Diagnosis
- •25.3.1.4 Treatment
- •25.3.2 Periacetabular Osteotomy
- •25.3.2.1 Epidemiology
- •25.3.2.2 Diagnosis
- •25.3.2.4 Treatment
- •25.3.3 Surgical Hip Dislocation
- •25.3.3.1 Epidemiology
- •25.4.1 Epidemiology
- •25.4.2 Diagnosis
- •25.4.3 Treatment
- •References
- •26: Infective Complications After Trauma Surgeries
- •26.1 Introduction
- •26.3 Epidemiology
- •26.4 Risk Factors
- •26.5 Pathogenesis
- •26.8 Treatment
- •26.8.1 Radical Debridement
- •26.8.2 Implant Handling
- •26.9 Local Antimicrobial Therapy
- •26.9.1.1 Ilizarov Technique
- •26.9.1.2 The Masquelet Technique
- •26.9.1.4 3D Printing
- •26.12.1 Pre-operative Measures
- •26.12.1.1 Skin Preparation Solutions
- •26.12.1.2 Skin Hair Management
- •26.12.2 Peri-operative Management
- •26.12.2.1 Drapes
- •26.12.2.2 Double Gloving
- •26.12.2.3 Antibiotics Coated Implants
- •References
- •27: Infective Complications After Open Fractures
- •27.1 Introduction
- •27.2 Epidemiology
- •27.3 Pathophysiology
- •27.4 Risk Factors
- •27.5.1 Laboratory Examination
- •27.5.2 Imaging Procedures
- •27.6 Nuclear Imaging
- •27.7 Microbiology
- •27.8 Molecular Technologies
- •27.9 Histopathology
- •Irrigation
- •27.10.1.2 Appropriate Intravenous Antibiotics
- •Timing
- •Local Antibiotics
- •27.10.1.3 Meticulous Injury Zone Excision (Debridement)
- •Irrigation
- •27.10.1.4 Fracture Stabilization
- •27.10.1.5 Second Look
- •27.10.1.6 Soft Tissue Closure
- •27.10.2.1 Advantages
- •References
- •28.1 Introduction
- •References
- •29: Infective Complications After Spinal Instrumentation
- •29.1 Introduction
- •29.4 Diagnosis
- •29.5 Treatment
- •29.7 Conclusions
- •References

22
against MRSA/methicillin-resistant
M. Trevenzoli et al.
right sternum and 0.82±0.28 for the left sternum
[18]. Ratios close to unity in the two investigations indicate that exposure to microbiologically
active linezolid is comparable in bone interstitial
uid and plasma. The greater AUC ratio obtained
from microdialysis, when contrasted with concentration ratios obtained from bone homogenate, aligns with linezolid’s limited tendency to
form chelate complexes with the bone inorganic
matrix.
In other words, linezolid penetrates bone well,
and the quantity of linezolid in bone is similar to
the amount in blood plasma, meaning that linezolid can be effective in treating bone infections.
3.10 Trimetoprim/
Sulfametoxazole
Cotrimoxazole also penetrates bone tissue, with a
bone-to-serum ratio that is higher in cancellous
bone (0.30) than in cortical bone (0.20) [31].
Interestingly, the synovial uid-to-serum ratio for
cotrimoxazole is even higher, at 0.61 for sulfamethoxazole and 0.74 for trimethoprim [32].
3.11 Daptomycin
Daptomycin penetrates well into bone in diabetic
foot infections [33]. In one study, researchers
measured daptomycin concentrations in the interstitial uid of metatarsal bone and plasma in
patients with diabetic foot infections. They determined that the average ratio of daptomycin concentrations in bone to plasma was 1.08, suggesting
that daptomycin penetrates well into the bone tissue where infection is most likely to occur. This
is remarkable given that daptomycin is highly
bound to plasma proteins (about 90%) and has a
high molecular weight.
Another study that measured the total area
under the curve (AUC) of daptomycin in bone
and plasma found much lower concentration
ratios (0.095 for thigh bone and 0.082 for shin
bone) [34]. This difference in results is likely
because the rst study measured unbound daptomycin concentrations, while the second study
measured total daptomycin concentrations. Since
daptomycin is highly bound to plasma proteins,
the total daptomycin concentration in bone will
be lower than the unbound plasma daptomycin
concentration.
Overall, the evidence indicates that daptomycin penetrates well into bone in diabetic foot
infections.
3.12 Fosfomycin
Fosfomycin penetrates bone tissue well. In a
study of chronic osteomyelitis patients, the
bone:serum ratio of fosfomycin was determined
to be 0.43 [35]. This means that the fosfomycin
concentration in bone is about 43% of the concentration in serum.
A single dose of 100 mg/kg of fosfomycin
resulted in a mean AUC
of 511.0±100.7mg∙h/
0–12
kg in bone in patients with diabetic foot infections [35]. The AUC
measures the cumulative
0–12
drug exposure over 12h.
The optimal PK/PD target for fosfomycin
Staphylococcus epidermidis (MRSE) is an
AUC
h/minimum inhibitory concentration
0–24
(MIC) ratio > 250. This means that the total
amount of drug exposure over 24h should be at
least 250 times the MIC of the bacteria.
A dosing regimen of fosfomycin 200mg/kg
q24h (16g/day in a 70kg patient) should achieve
optimal PK/PD target attainment at the infection
site against MRSA/MRSE with an MIC value up
to 4mg/L.This is well below the clinical breakpoint of 32mg/L, which means that the bacteria
are still susceptible to the antibiotic at this concentration. Therefore, fosfomycin should not be
utilized as a monotherapy [20].
3.13 Glycopeptides
andLipoglycopeptides
Glycopeptides, such as vancomycin and dalbavancin, penetrate bone tissue to some extent, but
the degree of penetration varies according to the
bone type and the specic glycopeptide.

3 Optimizing Antibiotic Treatment ofBone andJoint Infections: Pharmacokinetics andPharmacodynamics
23
A recent study determined that the ratio of
vancomycin concentrations in cancellous bone to
plasma was 0.45, while the ratio for cortical bone
was 0.17. This indicates that vancomycin penetrates cancellous bone better than cortical bone.
A single dose of 1000 mg of dalbavancin
resulted in a mean bone concentration of
4.1±1.6mg/kg at 14days in subjects undergoing
elective orthopedic interventions.
A dosing regimen of 1500 mg + 1500 mg
1 week apart is anticipated to result in a C
min
(minimum concentration) of >8.04 mg/L for
around 5–6weeks. This is considered to be the
optimal PK/PD target attainment (fAUC/MIC
>111.1) against MRSA and/or MRSE isolates
with a MIC value up to the clinical breakpoint of
0.125mg/L [36–38]. Therefore, dalbavancin can
reach high enough concentrations in bone and
synovial uid to be effective against MRSA and
MRSE infections. A dosing regimen of
1500mg+1500mg 1week apart is anticipated
to maintain these high concentrations for around
5–6weeks [20].
Overall, the evidence indicates that glycopeptides do penetrate bone tissue, but the degree of
penetration varies according to the bone type and
the specic glycopeptide. More research is
needed to better understand the bone penetration
of glycopeptides and to identify the optimal dosage and schedule for treating bone infections.
3.14 Pharmacodynamics
andMonte Carlo Simulations
Pharmacodynamics (PD) studies how drugs
impact biological systems. In the context of antibiotic therapy, PD involves studying the link
between drug concentrations and the desired
therapeutic effect [5].
For beta-lactam antibiotics, the key PD parameter is the T> MIC (time above the minimum
inhibitory concentration). The T > MIC is the
time during which the drug concentration surpasses the MIC of the bacteria being treated. In
the case of other antibiotics, like uoroquinolones, the key PD parameter is the area under the
concentration-time curve above the MIC (fAUC/
MIC). The fAUC/MIC is the total amount of drug
exposure above the MIC over a given time period
[5].
In bone penetration studies, it is not always
possible to perform a PD analysis since bone
penetration data is often sparse, with a small
number of samples collected from each patient.
Additionally, bone penetration data is often collected simultaneously for all patients. This complicates the comparison between the drug’s bone
concentration and the MIC of the bacteria being
treated.
Overall, PD analysis of bone penetration data
can be challenging, but it is important to report
the approaches and assumptions used in bone
penetration studies. This allows other researchers
to understand the study’s limitations and interpret
the results carefully. Population PK modeling is a
more sophisticated approach to analyzing bone
penetration data and can provide estimates of the
average and individual bone penetration
parameters.
Population modeling is a powerful instrument
for analyzing bone penetration data. It can
account for both the average penetration and its
variability between subjects. This information
can be used for predicting the expected
concentration- time proles for different dosage
regimens and to estimate the probability of
achieving a PK/PD target.
One example of how population modeling has
been utilized to study bone penetration is the
work of Landersdorfer CB et al [39]. These
researchers developed a population PK model for
moxioxacin in bone and serum. They then used
the model for predicting the probability of achieving PK/PD targets for positive microbiological
and clinical outcomes in osteomyelitis patients.
Simulation results suggested that a dose of
400 mg moxioxacin administered one time a
day would achieve a≥90% probability of target
attainment for MICs up to 0.375mg/L in cancellous bone and serum and 0.5 mg/L in cortical
bone [39].
This is a promising result, but it is worth noting that the model relied on data from a small
number of patients and that clinical trials are
needed to validate the results. Additionally, the

24
M. Trevenzoli et al.
PK/PD targets used in the simulation were
derived from data on ciprooxacin, not moxioxacin. Therefore, it is important to interpret the
ndings with caution.
Although population modeling is a valuable
tool for studying bone penetration and for predicting the probability of achieving PK/PD targets, it is important to conduct well-designed
clinical studies to collect high-quality bone penetration data that herald clinical outcomes.
3.15 Conclusion
In the context of BJIs, the PK/PD antimicrobial
prole is particularly important to get clinical
success.
(a) One of the key challenges in treating BJIs is
that antibiotics can have difculty penetrating bone and joint tissue. This is due to several factors, including the dense bone matrix,
the existence of biolms, and the limited
blood supply to some areas of bone. As a
result, it is important to choose antibiotics
that have good bone and joint penetration
and ask for an orthopedic consultation to get
surgical toilette to optimize the action of the
antimicrobial therapy.
(b) Another important PK/PD consideration for
BJIs is the time-dependent or dose- dependent
elimination of bacteria. This implies that
some antibiotics, such as beta-lactams, are
more effective at killing bacteria when they
are maintained at an elevated concentration
for a long period. Conversely, dosedependent molecules like uoroquinolones
or aminoglycosides require more attention to
the appropriateness of the individual dosage
than to the maintenance of an adequate
plasma level. Anyway, whatever the mechanism of action, it is important to achieve and
maintain adequate concentrations of the molecule at the infection site.
(c) Lastly, the spectrum of activity of antibiotics
when choosing treatment for BJIs must be
considered. The spectrum of activity refers to
the range of bacteria that an antibiotic is
effective against. For BJIs, it is important to
choose, at least initially, an antibiotic that has
a spectrum of activity against the most prevalent pathogens, taking into account that
Gram-positive bacteria are the most frequently involved.
(d) In addition to the PK/PD considerations
listed above, it is also important to individualize antibiotic treatment for BJIs according
to the patient’s clinical condition, clinical
compliance, the possibility of an allergic
response, or the concomitant therapies with
their relative interactions.
Treating an infection means treating the
patient globally; the use of knowledge relating to
the metabolism of the antibiotic must not make
us forget the empathy that must be sought with
the patient to establish a strong therapeutic
alliance.
References
1. Lew DP, Waldvogel FA. Osteomyelitis. Lancet.
2004;364(9431):369–79. https://doi.org/10.1016/
S0140- 6736(04)16727- 5.
2. Zimmerli W, Ochsner PE. Management of infection associated with prosthetic joints. Infection.
2003;31(2):99–108. https://doi.org/10.1007/
s15010- 002- 3079- 9.
3. Florencio-Silva R, Sasso GR, Sasso-Cerri E, Simoes
MJ, Cerri PS. Biology of bone tissue: structure,
function, and factors that inuence bone cells.
Biomed Res Int. 2015;2015:421746. https://doi.
org/10.1155/2015/421746.
4. Jevon M, Guo C, Ma B, Mordan N, Nair SP,
Harris M, et al. Mechanisms of internalization of
Staphylococcus aureus by cultured human osteoblasts. Infect Immun. 1999;67(5):2677–81. https://
doi.org/10.1128/IAI.67.5.2677- 2681.1999.
5. Landersdorfer CB, Bulitta JB, Kinzig M, Holzgrabe U,
Sorgel F.Penetration of antibacterials into bone: pharmacokinetic, pharmacodynamic and bioanalytical considerations. Clin Pharmacokinet. 2009;48(2):89–124.
https://doi.org/10.2165/00003088- 200948020- 00002.
6. Landersdorfer CB, Kinzig M, Hohl R, Kempf P, Nation
RL, Sorgel F.Physiologically based population pharmacokinetic modeling approach for ciprooxacin in
bone of patients undergoing orthopedic surgery. ACS
Pharmacol Transl Sci. 2020;3(3):444–54. https://doi.
org/10.1021/acsptsci.0c00045.
7. Sorensen TS, Colding H, Schroeder E, Rosdahl
VT. The penetration of cefazolin, erythromy-

3 Optimizing Antibiotic Treatment ofBone andJoint Infections: Pharmacokinetics andPharmacodynamics
25
cin and methicillin into human bone tissue. Acta
Orthop Scand. 1978;49(6):549–53. https://doi.
org/10.3109/17453677808993236.
8. Malizia T, Batoni G, Ghelardi E, Baschiera F, Graziani
F, Blandizzi C, et al. Interaction between piroxicam
and azithromycin during distribution to human periodontal tissues. J Periodontol. 2001;72(9):1151–6.
https://doi.org/10.1902/jop.2000.72.9.1151.
9. Malizia T, Tejada MR, Ghelardi E, Senesi S, Gabriele
M, Giuca MR, etal. Periodontal tissue disposition of
azithromycin. J Periodontol. 1997;68(12):1206–9.
https://doi.org/10.1902/jop.1997.68.12.1206.
10. Rodvold KA, Gotfried MH, Cwik M, Korth-Bradley
JM, Dukart G, Ellis-Grosse EJ. Serum, tissue
and body uid concentrations of tigecycline after
a single 100 mg dose. J Antimicrob Chemother.
2006;58(6):1221–9. https://doi.org/10.1093/jac/
dkl403.
11. Ji AJ, Saunders JP, Amorusi P, Wadgaonkar ND,
O'Leary K, Leal M, et al. A sensitive human bone
assay for quantitation of tigecycline using LC/MS/
MS. J Pharm Biomed Anal. 2008;48(3):866–75.
https://doi.org/10.1016/j.jpba.2008.06.020.
12. Bhattacharya I, Gotfried MH, Ji AJ, Saunders JP,
Gourley I, Diehl A, etal. Reassessment of tigecycline bone concentrations in volunteers undergoing
elective orthopedic procedures. J Clin Pharmacol.
2014;54(1):70–4. https://doi.org/10.1002/jcph.201.
13. Tottrup M, Soballe K, Bibby BM, Hardlei TF, Hansen
P, Fuursted K, et al. Bone, subcutaneous tissue and
plasma pharmacokinetics of cefuroxime in total
knee replacement patients – a randomized controlled trial comparing continuous and short-term
infusion. APMIS. 2019;127(12):779–88. https://doi.
org/10.1111/apm.12996.
14. Lovering AM, Walsh TR, Bannister GC, MacGowan
AP. The penetration of ceftriaxone and cefamandole into bone, fat and haematoma and relevance of
serum protein binding to their penetration into bone.
J Antimicrob Chemother. 2001;47(4):483–6. https://
doi.org/10.1093/jac/47.4.483.
15. Gergs U, Clauss T, Ihlefeld D, Weiss M, Ponicke K,
Hofmann GO, etal. Pharmacokinetics of ceftriaxone
in plasma and bone of patients undergoing hip or knee
surgery. J Pharm Pharmacol. 2014;66(11):1552–8.
https://doi.org/10.1111/jphp.12282.
16. Garazzino S, Aprato A, Baietto L, D'Avolio A, Maiello
A, De Rosa FG, etal. Ceftriaxone bone penetration in
patients with septic non-union of the tibia. Int J Infect
Dis. 2011;15(6):e415–21. https://doi.org/10.1016/j.
ijid.2011.03.003.
17. Zeller V, Durand F, Kitzis MD, Lhotellier L, Ziza JM,
Mamoudy P, etal. Continuous cefazolin infusion to
treat bone and joint infections: clinical efcacy, feasibility, safety, and serum and bone concentrations.
Antimicrob Agents Chemother. 2009;53(3):883–7.
https://doi.org/10.1128/AAC.00389- 08.
18. Andreas M, Zeitlinger M, Wisser W, Jaeger W, MaierSalamon A, Thalhammer F, etal. Cefazolin and linezolid penetration into sternal cancellous bone during
coronary artery bypass grafting. Eur J Cardiothorac
Surg. 2015;48(5):758–64. https://doi.org/10.1093/
ejcts/ezu491.
19. Azanza Perea JR, Sadaba Diaz de Rada
B. Ceftobiprole: pharmacokinetics and PK/PD prole. Rev Esp Quimioter. 2019;32(Suppl 3):11–6.
20. Gatti M, Tedeschi S, Zamparini E, Pea F, Viale
P. Pharmacokinetic and pharmacodynamic considerations for optimizing antimicrobial therapy used
to treat bone and joint infections: an evidence-based
algorithmic approach. Expert Opin Drug Metab
Toxicol. 2023;19(8):511–35. https://doi.org/10.1080/
17425255.2023.2255525.
21. Incavo SJ, Ronchetti PJ, Choi JH, Wu H, Kinzig M,
Sorgel F.Penetration of piperacillin-tazobactam into
cancellous and cortical bone tissues. Antimicrob
Agents Chemother. 1994;38(4):905–7. https://doi.
org/10.1128/AAC.38.4.905.
22. Boselli E, Breilh D, Debon R, Duo F, Bel JC,
Saux MC, etal. Penetration of piperacillin/tazobactam (4 g/500 mg) into synovial tissue. J Chemother.
2002;14(1):54–8. https://doi.org/10.1179/
joc.2002.14.1.54.
23. Al-Nawas B, Kinzig-Schippers M, Soergel F, Shah
PM. Concentrations of piperacillin-tazobactam
in human jaw and hip bone. J Craniomaxillofac
Surg. 2008;36(8):468–72. https://doi.org/10.1016/j.
jcms.2008.06.003.
24. Landersdorfer CB, Kinzig M, Bulitta JB, Hennig FF,
Holzgrabe U, Sorgel F, et al. Bone penetration of
amoxicillin and clavulanic acid evaluated by population pharmacokinetics and Monte Carlo simulation.
Antimicrob Agents Chemother. 2009;53(6):2569–78.
https://doi.org/10.1128/AAC.01119- 08.
25. Torkington MS, Davison MJ, Wheelwright EF,
Jenkins PJ, Anthony I, Lovering AM, etal. Bone penetration of intravenous ucloxacillin and gentamicin
as antibiotic prophylaxis during total hip and knee
arthroplasty. Bone Joint J. 2017;99-B(3):358–64.
https://doi.org/10.1302/0301- 620X.99B3.BJJ2016- 0328.R1.
26. Chambers J, Page-Sharp M, Salman S, Dyer J,
Davis TME, Batty KT, et al. Ertapenem for osteoarticular infections in obese patients: a pharmacokinetic study of plasma and bone concentrations. Eur
J Clin Pharmacol. 2019;75(4):511–7. https://doi.
org/10.1007/s00228- 018- 2597- z.
27. Lovering AM, Zhang J, Bannister GC, Lankester BJ,
Brown JH, Narendra G, etal. Penetration of linezolid
into bone, fat, muscle and haematoma of patients
undergoing routine hip replacement. J Antimicrob
Chemother. 2002;50(1):73–7. https://doi.org/10.1093/
jac/dkf066.
28. Rana B, Butcher I, Grigoris P, Murnaghan C,
Seaton RA, Tobin CM. Linezolid penetration into
osteo-articular tissues. J Antimicrob Chemother.
2002;50(5):747–50. https://doi.org/10.1093/jac/
dkf207.
29. Kutscha-Lissberg F, Hebler U, Muhr G, Koller
M.Linezolid penetration into bone and joint tissues

26
M. Trevenzoli et al.
infected with methicillin-resistant staphylococci.
Antimicrob Agents Chemother. 2003;47(12):3964–6.
https://doi.org/10.1128/AAC.47.12.3964- 3966.2003.
30. Traunmuller F, Schintler MV, Spendel S, Popovic
M, Mauric O, Scharnagl E, etal. Linezolid concentrations in infected soft tissue and bone following
repetitive doses in diabetic patients with bacterial foot
infections. Int J Antimicrob Agents. 2010;36(1):84–6.
https://doi.org/10.1016/j.ijantimicag.2010.03.007.
31. Saux MC, Le Rebeller A, Leng B, Mintrosse J.Bone
diffusion of trimethoprim and sulfamethoxazole high
pressure liquid chromatography (HPLC) (author's
transl). Pathol Biol (Paris). 1982;30(6):385–8.
32. Sattar MA, Cawley MI, Holt JE, Sankey MG, Kaye
CM. The penetration of trimethoprim and sulphamethoxazole into synovial uid. J Antimicrob
Chemother. 1983;12(3):229–33. https://doi.
org/10.1093/jac/12.3.229.
33. Traunmuller F, Schintler MV, Metzler J, Spendel S,
Mauric O, Popovic M, et al. Soft tissue and bone
penetration abilities of daptomycin in diabetic
patients with bacterial foot infections. J Antimicrob
Chemother. 2010;65(6):1252–7. https://doi.
org/10.1093/jac/dkq109.
34. Montange D, Berthier F, Leclerc G, Serre A, Jeunet L,
Berard M, etal. Penetration of daptomycin into bone
and synovial uid in joint replacement. Antimicrob
Agents Chemother. 2014;58(7):3991–6. https://doi.
org/10.1128/AAC.02344- 14.
35. Schintler MV, Traunmuller F, Metzler J, Kreuzwirt G,
Spendel S, Mauric O, etal. High fosfomycin concen-
trations in bone and peripheral soft tissue in diabetic
patients presenting with bacterial foot infection. J
Antimicrob Chemother. 2009;64(3):574–8. https://
doi.org/10.1093/jac/dkp230.
36. Dunne MW, Puttagunta S, Sprenger CR, Rubino C,
Van Wart S, Baldassarre J. Extended-duration dosing and distribution of dalbavancin into bone and
articular tissue. Antimicrob Agents Chemother.
2015;59(4):1849–55. https://doi.org/10.1128/
AAC.04550- 14.
37. Cojutti PG, Rinaldi M, Zamparini E, Rossi N,
Tedeschi S, Conti M, etal. Population pharmacokinetics of dalbavancin and dosing consideration for
optimal treatment of adult patients with staphylococcal osteoarticular infections. Antimicrob Agents
Chemother. 2023;65(5):e02260-20. https://doi.
org/10.1128/AAC.02260- 20.
38. Cojutti PG, Tedeschi S, Gatti M, Zamparini E,
Meschiari M, Siega PD, etal. Population pharmacokinetic and Pharmacodynamic analysis of Dalbavancin
for long-term treatment of subacute and/or chronic
infectious diseases: the major role of therapeutic
drug monitoring. Antibiotics (Basel). 2022;11(8):996.
https://doi.org/10.3390/antibiotics11080996.
39. Landersdorfer CB, Kinzig M, Hennig FF, Bulitta
JB, Holzgrabe U, Drusano GL, et al. Penetration
of moxioxacin into bone evaluated by Monte
Carlo simulation. Antimicrob Agents Chemother.
2009;53(5):2074–81. https://doi.org/10.1128/
AAC.01056- 08.

Aetiology andPathogenesis:
Causative Agents
FranziskaZiegenhain andGerroltNicoJukema
4
Bone, joint and soft tissue infections in orthopaedic and trauma infections are a devastating incident in the treatment of patients, generating
signicant disease burden and a high nancial
impact [1, 2]. Understanding the aetiology and
pathogenesis is critical for prevention and reducing patients’ threats as well as improving treatment of these infections. The different factors
contributing to the occurrence of bone and joint
infections are complex and impact one another
signicantly. Patient’s general and local (soft) tissue factors, as well as the pathogens, inuence
the outcome and the course of treatment. This
chapter concentrates on outlining the aetiology
and pathogenesis of bone and joint infections,
and will give some considerations about their
treatment in trauma surgery.
4.1 Aetiology
4.1.1 Denition
The Centers for Disease Control and Prevention
(CDC) dene a surgical site infection (SSI) as an
infection that occurs in a part of the body that has
undergone surgery. Infections can be divided into
F. Ziegenhain · G. N. Jukema (*)
Department of Trauma Surgery, University Hospital
Zurich, Zurich, Switzerland
e-mail: Franziska.ziegenhain@usz.ch; GerroltNico.
Jukema@usz.ch
supercial wound infections and deep infections
that involve organs and or bones and joints.
Infection following and involving implanted
hardware forms a separate subgroup [3].
4.1.2 Risk Factors
4.1.2.1 Patient-Specic Risk Factors
Different risk factors of the patient that inuence
the occurrence of bone and joint infections have
been described over the years [4, 5]. Systemic as
well as local conditions have a tremendous
impact. Patients with systemic diseases that inuence the immune system are at a signicantly
higher risk of developing osteomyelitis and or
septic arthritis. These diseases include metabolic
conditions like diabetes, arteriosclerosis and obesity, as well as immunodeciencies like HIV,
immunosuppressant medications and malignancies. Diabetes mellitus is hereby of special interest, as up to 20% of these patients suffer from
diabetic foot syndrome with osteomyelitis [6].
Substance abuse, especially smoking and alcoholism, are known risk factors as well [7, 8].
These patients tend to have impaired wound healing. Depending on the degree of the abuse, noncompliance is also a patient factor to take into
consideration. Some of these conditions are
accessible for optimising preoperatively, if time
allows [9]. Prior to elective surgery, these at-risk
patients should be treated by an interdisciplinary
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2025
P. Ruggieri et al. (eds.), Bone and Joint Infections, https://doi.org/10.1007/978-3-031-96383-4_4
27

28
F. Ziegenhain and G. N. Jukema
team. Elective surgery should, when possible, be
postponed until the pre-existing conditions are
improved. Medication of patients with known
diabetes and suboptimal glucose sugar levels
should be adjusted preoperatively whenever possible to reach normal glucose levels, and therefore reduce the risk of infection.
Local status, i.e. reduced blood circulation
(e.g. in patients with arteriosclerosis), closed
damaged soft tissue (classication according to
Tscherne-Oestern [10]) and open fractures (classication according to Gustilo-Anderson [11,
12]) are related to the occurrence of infections of
the bone and joints. The importance of acknowledging the local soft tissues and treating fractures
with extensive soft tissue accordingly is reected
in the multitude of scores and denitions. The
Tscherne-Oestern and Gustilo-Anderson classications are widely used to describe the soft tissue
injury in combination with a fracture. They provide the surgeon with a tool to estimate the level
of tissue damage and treat the patient accordingly. This is especially important as open fractures have a signicantly higher rate of
infections.
The initial management, meaning a carefully
carried out debridement by the most skilled surgeon available and initial (perioperative) antibiotic therapy where needed, determines the course
of the healing process. In general, in case of an
open fracture, every wound should have a surgical debridement with lavage in the operating
room under sterile conditions as soon as possible
after admission [13]. In cases with extended soft
tissue damage, negative pressure wound therapy
can support a favorable outcome in the treatment
of extensive soft tissue damage, especially as it
benets the local circulation and the reduction of
bacterial growth. The number of patients who are
initially more in need of (free) ap plastic surgery can be successfully reduced by staged application of negative pressure wound therapy.
The complex interaction between host factors
and local infection for the course of the disease is
reected in the classication that was proposed in
1985 by Cierny and Mader [4, 14]. Factors that
are taken into account to determine the host class
are systemic factors like malnutrition, renal fail-
ure, diabetes mellitus, immunodeciency, alcohol or tobacco abuse, extreme age and hypoxia,
among others. For local factors, compromising
conditions such as lymphedema, vascular disease, scarring, nerve damage, radiation disease
and major vessel compromise are recognised to
have a major inuence on outcome.
4.1.2.2 Bacteria
Staphylococcus aureus
Staphylococcus aureus is the most commonly
found pathogen in bone and joint infections. This
is due to its high virulence and ubiquitous occurrence. Several cell-associated and extracellular
factors contribute to this. Staphylococcus aureus
produces several adhesions that allow it to attach
to tissue as well as foreign body surfaces [15].
After adhesion, the bacteria produces factors like
protein A, coagulase and other capsular polysaccharides that shield the pathogen from the human
immune system [16–18]. This biolm forms an
almost impossible to penetrate wall for the human
immune system and antibiotic treatment, and
thus protects the embedded bacteria. It also protects the bacteria from mechanical disruption
during surgical debridement. With various exotoxins and hydrolases, S. aureus causes damage
and ultimately (necrotic) destruction of the
infected tissue [19, 20] and is uniquely adapted to
survive in the skeletal structure. Next to biolm
formation, the bacteria can inltrate cells. Studies
have shown inltration of osteoclasts and osteocytes by bacterial species [21, 22]. The activation
of osteoclasts leads to further bone loss, and the
survival of the cells might support long-term colonisation. With its high virulence and ability to
form colonies, S. aureus promotes the formation
of abscesses in bone infections. The forming
necrotic tissue protects the bacteria further from
clearance by antibiotic agents and neutrophil
cells [23, 24]. The combination of these various
mechanisms to spread and survive in the skeletal
system explains the predominance of S. aureus in
bone and joint infections.
4.1.2.3 Other Causative Agents
While S.aureus is the most prevalent bacteria in
bone and joint infections, other commonly found

4 Aetiology andPathogenesis: Causative Agents
29
bacteria include strepto- and pneumococcus species. Depending on the location and cause of the
infection, different bacterial species will be
involved.
Especially in nosocomial infections, multiresistant bacteria like methicillin-resistant
Staphylococcus aureus (MRSA), Pseudomonas
and Enterobacteria can be found [25]. These
pathogens present their own unique challenges,
as antibiotic treatment is often complicated for
treatment of these particular infections.
Preferably, these patients should be treated in
specialised centres by an experienced, multidisciplinary team.
Implant-associated bone and joint infections
become particularly challenging if biolmgenerating bacteria are involved. Next to
Staphylococcus aureus, Pseudomonas aeruginosa and Staphylococcus epididermidis are able
to form biolms and hence expand their virulence [26–28].
Different body regions also play a role in the
different microbiomes that are found. Mixed
infections are predominantly prevalent in the
face, oral region and pelvis due to the common
local skin ora. M. tuberculosis is more frequently found in infections of the spine [29].
If a pre-existing infection of an organ system
is the cause of bone or joint infections, bacteria
are typically the same as primarily found in those
infections. Antibiotic treatment should be adapted
accordingly if there is suspicion of (ongoing)
systemic spread of the primary infection like bacteremia or sepsis.
As bacteria and antibiotic resistance proles
vary in between countries and even between hospitals in a country, it is highly recommended to
follow the local anti-infective guidelines for initial treatment and to adapt antibiotic therapy as
soon as the causative agents are identied according to their resistance pattern.
Properly carrying out of sampling is of essence
to provide adequate antibiotic treatment
(Table4.1).
4.1.2.4 Path ofInfection
In general, two different pathways of infection
are distinguished. Endogen infections, mostly
caused by haematogenous and septic spreading,
are frequently showing monobacterial colonisation. The origin is usually a bacterial infection
like tonsillitis, a soft tissue infection or, for example a visceral organ infection like an appendicitis.
They are more regularly found in children and
Table 4.1 Overview of the most common bacteria found in different types of bone and joint infections [6, 29–34]
Type of infection Commonly found bacteria Polymicrobial infections Gram-negative infections
Post-traumatic/fracture
related
Haematogenous infections Staphylococcus aureus
Vertebral infections Staphylococcus aureus
Implant-related infections Staphylococcus aureus
Staphylococcus aureus
Staphyloccocus
epididermidis
Streptococcus spp.
Pseudomonas spp.
Enterobacteria spp.
Streptococcus spp.
Pseudomonas spp.
Staphylococcus
epididermidis
Streptococcus spp.
Enterococccus spp.
Diphtheroids
Pseudomonas spp.
Enterobacteriaceae spp.
Staphylococcus
epididermidis
>20% app. 20%
app. 20% >10%
>15% >10%
>10% >5%

30
F. Ziegenhain and G. N. Jukema
young adolescents [35]. Metaphyseal bone with
its extensive blood supply and low blood ow
rate is especially susceptible for bacterial attachment and growth of the germs. Depending on the
age of the individual, spreading of the infection
to the joint is possible. It is less likely in children
over the age of 2 years with open epiphyseal
plates and normally no shared blood supply of
the meta- and epiphysis [36]. Children under the
age of approximately two and adults can suffer
from a spreading per continuitatem towards the
joint, resulting in septic arthritis [37].
In contrast, exogen osteitis and septic arthritis
are often multibacterial infections after trauma as
well as iatrogenic after surgeries (e.g. surgical
site infection). For that reason, treatment is often
challenging and requires a different approach
[38].
In post-traumatic infections, details about
patient’s injury are critical for prevention and
successful treatment of infection. For example,
injuries in the farming environment with contaminated wounds need different antibiotic therapy
[39]. Knowledge of these exceptions and where
to expect different bacterial species are essential
for clinical management. International and local
antibiotic guidelines should be considered.
Patients with pre-existing conditions are at higher
risk of developing bone and joint infections after
trauma due to their compromised immune system
[5]. Close surveillance and early intervention are
key to successful treatment.
Iatrogenic infections after surgical intervention (so-called surgical site infections) were
reduced signicantly over the last years by the
implementation of several preventive measures
(for example, the perioperative administration of
an antibiotic drug [40, 41
]. Similar to posttraumatic infections, in elective surgery pathogens are introduced to the bone and or joint from
the skin/outside. Therefore, skin-related species
like Staphylococcus aureus are frequently found
in these infections. Normally, in an acute surgical
site infection, local symptoms like swelling, redness and painful tenderness are present, sometimes with generalised symptoms like fever.
Laboratory examination shows elevated inammatory markers correlating to the response of the
immune system. If an infection after orthopaedic
and trauma surgery cannot be treated successfully in the acute and early phase, it eventually
becomes a chronic infection, with formation of
infected (granulation) tissue, osteonecrosis and
stulae at the surgical site [34, 42, 43].
4.1.3 Acute Osteomyelitis
andSeptic Arthritis
By denition of the CDC acute bone and joint
infections after surgery are limited to a time
period of 30 (acute onset) to up to 90 days
within 1year if an implant is in place (late onset
[3]). In the early stage, patients normally complain of local symptoms like redness, swelling,
pain at the operation site and systemic reactions
like fever, fatigue and general sickness. The
onset is typically within a short time period.
Wounds might present with secretion and possibly pus. As already stated, the critical incident
in bone infection is the development of a biolm, especially if osteosynthesis hardware or
prosthesis with plastic components are in situ
[27]. Biolm prevents an effective antibiotic
treatment and builds a hard-to-penetrate layer
for the human (cellular) immune system and
antibiotic drugs to destroy bacteria. The denitive formation of this biolm occurs early after
the start of infection, over the time of days to
weeks, so the timeframe is essential in the successful treatment of these infections. An acute
infection leads to a quick and strong immune
response. Histologic ndings include erosions
and destruction of bone and neutrophils [44].
Underlying conditions such as diabetes benet
the rapid expansion of the infection due to lack
of adequate perfusion and reduced immune
response [5]. In fracture-related infections,
inadequate xation and/or soft tissue damage
favor the occurrence of an acute or ongoing persistent infection like osteomyelitis. This is
aggravated in patients with extensive soft tissue
damage and according to Gustilo Anderson’s
Classication in Grade II and III open fractures.
To reduce the risk of an acute or an ongoing
infection, adequate wound and soft tissue man-

4 Aetiology andPathogenesis: Causative Agents
31
agement from the early start in open fracture
treatment, for example with negative pressure
wound therapy, is mandatory [45].
4.1.4 Chronic Osteomyelitis
andSeptic Arthritis
Chronic infections of the bone and/or joint are
dened by an onset of more than 30days after a
surgery [3]. A chronic infection can occur after
an insufciently treated acute infection. The
residual bacteria eventually causes the formation
of granulation tissue, sequesters and osteonecrosis. Persistent secretion often results in the formation of chronic stulas [42]. If the infection is
fracture and/or implant-related, non-union of the
fracture can occur [46]. In some cases, the only
clinical and radiological sign of a chronic osseous infection can be a non-union at the fracture
site. The clinician treating the patient should
always be alerted by the absence of fracture
union, especially in patients with underlying diseases and or history of extensive soft tissue damage at the fracture site. Histopathological ndings
include formation of granulation tissue, periosteal reaction and broplasia [38, 47].
together with the foams, is covered with an occlusive semipermeable wound drape and connected
with a negative pressure machine. This negative
wound pressure system at the wound site stimulates the local blood perfusion and will reduce
soft tissue edema [52]. The local blood ow is
stimulated and the immune system of the injured
patient can be more effective in its action against
a local infection and consequently can reduce the
systemic sequelae of a local infection. Especially,
the negative wound pressure therapy with instillation technique has proven to be strongly effective in reducing the risk of recurrent infections in
trauma and orthopaedic patients with (recurrent)
soft tissue and bone infections [48, 53]. Even in
cases with implanted hip and knee prosthesis
with acute infection, the installation technique
with an antiseptic polyhexanide solution (0.04%)
was favorable in retaining the prosthesis in acute
infections [52].
Case Report
A 17-year-old man suffered a grade IIIB open
comminuted patella fracture during holidays
abroad in a motorbike accident (Fig.4.1), with
severe putrid arthritis of the knee joint. Initial
4.2 Negative Pressure Wound Therapy
Especially in Grade II and III open fractures
according to Gustilo Anderson, the risk of an
acute or later, a chronic infection is higher and
related to the extent of damage and loss of soft
tissues.
Chronic infection will develop more easily if
the local vascularisation of soft tissue and bone is
compromised. To reduce the initial bacterial burden in an open trauma wound and/or fracture and
to reduce the risk of an ongoing infection, modern techniques like negative pressure wound therapy can support a faster and better clinical
outcome [48–51]. By use of two different types
of reticulated foam with different physical and
mechanical properties (polyurethane or polyvinylalcohol foam) in the wound, the wound,
Fig. 4.1 Comminuted and dislocated patella fracture
Соседние файлы в папке Библиотека им академика М.И. Перельмана
