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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5205_Библиотеки_им_академика_М_И_Перельмана.pdf
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- •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

96
A. N. Johari et al.
a
b
Fig. 8.4 (a) An 8-year-old girl who had right knee septic
arthritis and probably right tibial osteomyelitis in early
childhood presented with a right tibial varus deformity
and 4cm shortening. (b) She underwent completion of the
proximal tibial physeodesis, right proximal tibial osteotomy, and tibial lengthening and deformity correction
using a six-axis correction system. (c) Clinical photographs after the frame removal showing correction of the
deformity and leg length equalization. The patient is
under regular follow-up, as she will need another leglength equalization procedure at a later stage

Pre-treatment Post-treatment
Pre-treatment Post-treatment
8 Osteoarticular Infections inChildren
97
Fig. 8.4 (continued)
8.18 Post-septic Hip Sequelae
The complications of septic arthritis of the hip
joint can be varied. They could range from growth
disturbance to complete dislocation of the hip
and/or destruction of the femoral head and neck.
These sequelae are severe if the infection occurs
in a neonate and the treatment is delayed or if
there is a delay in diagnosis or presentation.
Concurrent osteomyelitis and infection with virulent organisms can result in extensive damage to
the epiphysis, physis, and metaphysis of the
proximal femur, resulting in a spectrum of
sequelae. The incidence is approximately 33%
[47, 87, 88]. The sequelae are classied by the
extent of involvement of the proximal femur. The
treatment is complex surgical reconstruction,
depending on the involvement of the proximal
femur and the status of the hip joint. The treatment offered is dependent on the location and
extent of the deformity, the type of deformity,
and the vascularity of the femoral head. In addition to symptoms, the range of motion of the hip,
age of the child, previous surgical scars, and
advanced imaging ndings need to be taken into
consideration to offer the reconstructive option.
[89, 90]. Femoral neck osteomyelitis can give
rise to resorption of the neck and creation of a
pseudarthrosis with coxa vara. Johari etal. have
discussed the management of this condition [91]
as a special group (Group 5) in his classication
of sequelae of septic hips.
8.19 Summary
Pediatric musculoskeletal infections pose a signicant challenge for the growing skeleton. It is
important to diagnose the infection early and
start appropriate, timely treatment to minimize
the complications and have optimal outcomes.

98
A. N. Johari et al.
This will help to avoid disastrous complications
and sequelae. Box 8.1.
Box 8.1 Key Learning Points
• A high index of suspicion is necessary
for early diagnosis of musculoskeletal
infections in children, especially in
neonates.
• Consider obtaining an MRI to dene the
involvement of bone and/or joint and the
soft tissues.
• Indications for surgical intervention are
the presence of subperiosteal/intramedullary/soft tissue abscess and/or septic
arthritis.
• Septic arthritis warrants urgent surgical
decompression of the joint.
• A multidisciplinary approach is desirable for the diagnosis and optimal care
of a child with a musculoskeletal
infection.
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Osteoarticular Infections inAdults
hosst resistance
FerdinandoDaRinde Lorenzo
9
Hematogenous joint infections in adults represent
a relatively low percentage as the major cause of
joint infections is represented by trauma, postsurgical infections, and also local inltrations, which,
in some cases, have been the cause of joint infections. Usually occurs after septicemia or, as with
tuberculosis, from a mostly pulmonary focus. I,
therefore, thought of treating the tuberculous
forms (specic forms), about which little is
known, comparing them with the pyogenic (nonspecic forms), also giving attention to this
pathology which is far from having disappeared
and which presents high resistance to normal antitubercular drugs. Therefore, the tuberculous joint
pathology will be described comparing it with the
pyogenic form, highlighting the differences both
in diagnosis and in treatment. A typical arthritis in
adults is bone tuberculosis which represents
approximately 5% of secondary extrapulmonary
localizations (Figs.9.1 and 9.2) [1–4]. In the case
of vertebral localization, especially the dorsal
one, the infection sometimes occurs due to contiguity from a pulmonary focus. But the “vertebral”
topic will not be discussed in this chapter.
Latest tuberculosis estimate: worldwide there
were nearly 9 million new cases of tuberculosis
and 1.4 million cases of tuberculosis with bone
involvement. The World Health Organization
F. Da Rin de Lorenzo (*)
Codivilla-Putti Institutes, National Reference Center
for the diagnosis and treatment of bone infections,
Cortina d’Ampezzo (BL), Italy
(WHO) declared TB a global public health emergency in 1993 (Fig.9.3) [1, 5, 6].
The arrival of emigrants, especially from
Africa, has brought this disease back to Italy,
even though most of the subjects come from
Eastern Europe (Fig.9.4).
Before entering into the diagnosis of the infections, it is important to highlight that there are, in
all cases, risk factors that can increase infections.
The general risk factors [9–12] concern the
patient’s condition rather than the virulence of
the germ:
Septic risk factors
• Poor personal hygiene and an overcrowded
environment
• Pathologies with immunodeciencies (HIV
infection: the virus that causes AIDS)
• Corticosteroid therapy (e.g., A.R.)
• Oncological pathologies
• Diabetes mellitus
• Reduced nutritional status
• Older age
• Obesity
• Organ Transplants
• Silicosis
• Skin disorders and/or open wounds
• Smokers (recommended to quit 6 weeks
before the eventual intervention)
• Drug intake and alcohol abuse
contaminant bacterial load virulence
© 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_9
103

104
Fig. 9.1 The
relationship between
Mycobacterium
tuberculosis and humans
is a complex and
delicate balance and is a
persistent disease. The
lymphatic system and
the typical localization
F. Da Rin de Lorenzo
A classication of bone infections identies
the nonspecic forms (OsteomyelitisOsteoarthritis) with the specic forms (mostly
tuberculous) (Fig.9.5).
Over the years, cases have decreased in our
Institute, and nowadays we treat around 40 cases
per year in total of all bone localizations (Fig.9.6).
Out of a total of 4473 cases, these are the
percentages of localizations (Fig.9.7) [8] that
remain unchanged to this day, with the prevalence of vertebral localizations followed by the
hip and knee.
A different percentage in the pyogenic forms
out of a total of 3713 cases (Fig.9.8) that affect the
joints as the long bones are normally affected more.
Types of the most frequently encountered typical
and atypical mycobacteria (MB) (Table9.1) [13]:
- Typical:
Mycobacterium tuberculosis hominis (B.K.)
Mycobacterium bovis e avium
- Atypical:
Mycobacterium kansaii
Mycobacterium marinum
Mycobacterium scrofolaceum
Mycobacterium avescens
Mycobacterium avium complex
Mycobacterium xenopi
Mycobacterium fortuitum
Mycobacterium chelone

9 Osteoarticular Infections inAdults
105
Fig. 9.2 Area chart displaying trends in disease incidence
from 1991 to 2003, categorized into decreasing, emerging,
and persisting diseases. The left column shows decreasing
diseaseslike Polio and HIV in the US, with incidence per
100.000. The middle column highlights emerging diseases
suchas Avian Inuenza and SARS, with varying scales.
The right column presents persisting diseases like
Tuberculosis and Malaria, measured in millions. Blue
areas represent cases, and red lines indicate deaths. The
chart includes specic labels for diseases and region, with
a legend for color coding.Deaths (990,000 among HIVnegative people and 430,000 HIV-associated TB
deaths). The latestestimates are that there were almost
nine million new cases in 2011 and 1.4 million
boneTB.The World Health Organization (WHO) declared
TB a global public health emergency in 1993. [5, 6]
Fig. 9.3 World map illustrating estimated new TB incidence rates, per 100.000 population by country, 2013 [1, 5, 6]

106
Percentage of total TB case in foreigners
1999 2000 2001 2002 2003
Percentage of TB case in foreigners by continemt of origin
2004 2005 2006 2007 2008
+
–
F. Da Rin de Lorenzo
60
50
40
30
20
10
0
from 1999 to 2008
Europe
Americas
Fig. 9.4 Line chart showing the percentage of tuberculosis
(TB) cases in foreigners by continent of orig froma 1999 to
2008 in Italy. The chart includes data for Europe, Asia, Africa
and the Americas, with trend lines for Europe and Africa.
The y-axis represents the percentage of total TB cases in foreigners, ranging from 0 to 60%. The x-axis covers the years
BONE
INFECTIONS
Asia
Trend Europe
Africa
Trend Africa
1999 to 2008. There has been an improvement regarding the
trend from Africa; however, the trend from Europe is negative with an increase of 3–5% Asia and Americas remain
relatively stable [5–9]. Before entering into the diagnosis of
the infection, it is important to highlight that there are, in all
cases, risk factors that can increase infections
TUBERCOLOSIS
(extrapulmonary)
5-7%
SECONDARY
-Pulmonary
PRIMARY
processes
- By continuity
- By continuity
HEMATOGENE
IATROGENE
ACUTE
CHRONIC
CHRONIC
Fig. 9.5 Classication of bone infections: A owchart
illustrating the classication of bone infections. The diagram begins with “Bone Infections” at the top, then
branches out into Tuberculosis (ExtrapulmonaryOsseous) 5-7%” and Osteomyelitis-Osteoarthritis.
Tuberculosis is then classied into primary, secondary
(pulmonary processes by continuity, by contiguity) and
OSTEOMYELITIS
OSTEOARTHRITIS
CHRONIC
<AB INITIO>
POST-TRAUMATIC
O.M. OF <GARRE>
SECONDARY
ABSCESS
OF <BRODIE>
nally chronic forms. Osteomyelitis and osteoarthritis are
classied as acute or chronic “ab initio” such as Garrè’s
sclerosing osteomyelitis or Brodie’s abscess. Acute forms
are divided into hematogenous, post-traumatic, iatrogenic
and secondary to a nearby focus. All of these forms can
become chronic. The owchart uses different colors to
distinguish the different forms
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