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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

7 New Diagnostic Tools fortheDiagnosis ofPeriprosthetic Joint Infection
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57. Sigmund IK, Holinka J, Sevelda F, Staats K,
Heisinger S, Kubista B, etal. Performance of automated multiplex polymerase chain reaction (mPCR)
using synovial uid in the diagnosis of native
joint septic arthritis in adults. Bone Joint J. 2019
Mar;101-B(3):288–96.
58. Fenollar F, Roux V, Stein A, Drancourt M, Raoult
D.Analysis of 525 samples to determine the usefulness of PCR amplication and sequencing of the 16S
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J Clin Microbiol. 2006 Mar;44(3):1018–28.
59. Tarabichi M, Alvand A, Shohat N, Goswami K,
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thetic joint infection: the utility of next-generation
sequencing. Arthroplast Today. 2018 Mar;4(1):20–3.
60. Tarabichi M, Shohat N, Goswami K, Parvizi J. Can
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Feb;100-B(2):127–33.
61. Goswami K, Clarkson S, Phillips CD, Dennis DA,
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Silibovsky R, Belden K, et al. Diagnosis of periprosthetic joint infection: the potential of nextgeneration sequencing. J Bone Joint Surg Am. 2018
Jan 17;100(2):147–54.

Osteoarticular Infections
inChildren
AshokN.Johari, AshishS.Ranade,
andRaashidAnjum
8
8.1 Introduction
Musculoskeletal infections in pediatric patients
present a wide range of conditions, including
osteomyelitis, septic arthritis, pyomyositis,
abscess, or a combination of these. With the
advent of newer investigative modalities, the
diagnosis of unusual and subtle infections has
increased. The advances in diagnosis and treatment of pediatric musculoskeletal infections
have led to decreased morbidity and mortality,
however, they still pose a signicant risk of
morbidity and mortality, especially in developing countries [1, 2]. The reported incidence of
musculoskeletal infections in children is 2–13
per 100,000 of the population in developed
nations and up to 200 cases/100000of the population in developing countries with no clear sex
predilection [3–5]. There are many studies that
report a decrease in the incidence of pediatric
musculoskeletal infection over a period of time,
and many other studies report the opposite [6,
7]. The incidence of septic arthritis alone in the
pediatric age group is reported to be
5.5–12/100000 children, and an increased pro-
pensity of males compared to females, up to
three times, is seen. The most common joint to
be affected in septic arthritis is the hip, followed
by knee, and more than 20% of cases can have
multiple joint involvement at the same time
[8–10]. With the advances in diagnostics, the
incidence of pediatric osteoarticular infection
has increased. Early diagnosis and management
are of pivotal signicance for an optimum outcome. Delay in diagnosis is not infrequent,
especially in developing countries, due to late
presentation, lack of resources, variability in
presentation, late or injudicious management,
etc., and this is associated with potentially disabling morbidities like limb length discrepancies, angular deformities, and other growth
disturbances. The optimum management of
musculoskeletal infections in the pediatric age
group warrants a coordinated approach between
the orthopedic surgeon, radiologist, microbiologist, pediatrician, and allied services [11].
A. N. Johari (*)
Children’s Orthopaedic Centre, Mumbai, India
A. S. Ranade
Deenanath Mangeshkar Hospital, Pune, India
R. Anjum
All India Institute of Medical Sciences, Jammu, India
© 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_8
77

78
A. N. Johari et al.
8.2 Etiology
Table 8.1 Shows commonly encountered microorgan-
isms in different age groups
The most common mode of infection is hematogenous spread from a symptomatic or asymptomatic bacteremia or secondary to the contiguous
source of infection or a direct inoculation [12].
The commonest microorganism causing acute
osteomyelitis or septic arthritis in children is
Staphylococcus aureus, accounting for 60–90%
of cases irrespective of the age group, followed
by Streptococcus species and Gram-negative
organisms in a small subset of patients (<5%). In
neonates, the incidence of Group B Streptococcus
sepsis is increased, whereas the incidence of
cases with H. inuenzae has signicantly
decreased due to the universal immunization for
the same. Salmonella sp. should be considered in
osteomyelitis of the diaphyseal region and in
patients with sickle cell disease. Other commonly
encountered bacteria causing infections in the
pediatric age group include Kingella kingae,
Streptococcus pyogenes, Mycobacterium tuberculosis, atypical mycobacteria, and N. gonorrhea; however, this is not an exhaustive list, and
there are many reports of infection with uncommon microbial agents. In recent years, the incidence of methicillin-resistant Staphylococcus
aureus (MRSA) has increased, and the incidence
stands at 9–30% as per the published literature
[13]. Panton–Valentin Leucocidin (PVL) producing strains of Staphylococcus aureus are responsible for extensive tissue necrosis. PVL is a
cytotoxin that can be produced by different
strains of both methicillin-sensitive
Staphylococcus aureus
(MSSA) and methicillinresistant S. aureus (MRSA) [14]. In a study from
Europe, the incidence of PVL-producing strains
was found to be 18.6% [15]. The common microorganisms causing musculoskeletal infections at
different ages are presented in Table8.1. This is
not an exhaustive list and shows only the common pathogens.
Age of child Microorganisms Empirical antibiotics
Neonates
(0–4weeks)
1month–4
months
4months to
04years
>04years Staphylococcus
Sickle cell
patients
Group A and B
Streptococcus sp.,
Staphylococcus
aureus,
Enterobacter sp.
Staphylococcus
aureus,
Klebsiella
pneumoniae,
Streptococcus
pyogenes,
Kingella kingae,
E. coli,
Enterobacter sp.
Staphylococcus
aureus,
Group A
Streptococcus sp.,
Kingella kingae,
Enterobacter sp.
aureus,
H. inuenzae,
Enterobacter sp.
Group A B
haemolytic
Streptococcus
Staphylococcus
aureus,
Salmonella sp.
(Pathognomonic)
First/Second
generation
Cephalosporin or
Oxacillin +
Gentamicin
First/Second
generation
Cephalosporin
Clindamycin
First/Second
generation
Cephalosporin.
Clindamycin
First/Second
generation
Cephalosporin or
Ampicillin
Clindamycin
First/Second
generation
Cephalosporin or
Ampicillin or
Chloramphenicol

8 Osteoarticular Infections inChildren
79
8.3 Investigative Modalities
inOsteoarticular Infections
inChildren
The diagnosis of musculoskeletal infections in
children is mainly clinical, based on the signs and
symptoms as discussed in the subsequent section,
and test parameters supplement the clinical diagnosis. However, taking an appropriate history and
performing an accurate examination of the child
is a challenging task, and the surgeon needs to be
extremely perceptive to gather as much information as possible.
8.4 Clinical Diagnosis
The clinical presentation of a child with musculoskeletal infection depends upon the type of
infection (osteomyelitis/septic arthritis/pyomyositis), the site of infection, virulence of the causative agent, immune status, and age of the child
[16]. The common presenting symptoms and
signs are pain, fever, inability to bear weight,
local warmth, erythema, tenderness, reduced
mobility of the affected part, and sick general
condition. However, it is not necessary to have all
the signs and symptoms in each patient, and there
can be a variable presentation. An antecedent history of minor trauma is often present in many
cases and should be enquired about. Neonates
and infants do not have a fully developed immune
system, and the presenting symptoms can be subtle in such cases. A high index of suspicion is
required to avoid delays in diagnosis and treatment. A similar subtle presentation is seen in
children with immunodeciency syndromes,
malnourishment, and concomitant comorbid conditions like HIV or Tuberculosis. Dartnell J etal.
in a systematic review of more than 12,000 cases
of pediatric musculoskeletal infections noted the
most common clinical feature as localized pain
(seen in 81%); local rise of temperature, swelling
and tenderness in 70%, fever in 62%, and
restricted mobility in 50% of cases [2].
8.5 Laboratory Investigations
The investigations that should be obtained in a
suspected case of musculoskeletal infection
include a complete blood count with erythrocyte sedimentation rate and a differential leucocyte count. The leucocyte count is generally
elevated with increased neutrophil count; however, in subacute infections in neonates and
children with immunodeciency, the values can
be within normal range. C-reactive protein
(CRP), an acute phase reactant, is a sensitive
marker of acute infection and should be
obtained; it is the single most important independent predictor of infection. An attempt
should be made to obtain a tissue/uid sample
wherever possible for culture, sensitivity, and
Gram staining. The British Orthopaedic
Association and British Society for Children’s
Orthopaedic Surgery recommend that microbiology samples should be taken prior to antibiotic therapy, but this should not delay treatment
in sick children [17]. Dartnell J etal. in a systematic review on acute osteomyelitis noted an
increased white blood cell (WBC) count in 36%
of children on presentation, raised C-reactive
protein (CRP) in 81%, and elevated erythrocyte
sedimentation rate (ESR) in 91% of cases [2].
The laboratory markers supplement the clinical
suspicion or diagnosis of infection and are not
denitive per se. More recently, procalcitonin
has emerged as a sensitive and specic indicator of infection; it has a normal range of
<0.1 ng/ml and levels above 0.4 ng/ml are
highly indicative of infection [18, 19].
Kocher (1999) laid down criteria for the diagnosis of septic arthritis of hip and to differentiate
it from a benign transient synovitis of hip [20].
The original criteria included the following
parameters
1. Inability to bear weight
2. Temperature>38° C
3. WBC>12,000/mm
4. ESR>40mm/hr
3

80
A. N. Johari et al.
The probability of having septic arthritis of
hip increased to more than 90% when three or
more criteria were met. Caird et al. modied
Kocher’s criteria to include a CRP level of more
than 20mg/l. The addition of CRP level increased
the positive predictability of infection to more
than 97% when all the parameters were met.
Moreover, the authors noted a CRP level of more
than 20mg/l to be the most signicant independent predictor of infection [21]. Despite the relevance of this criteria, there are certain drawbacks
too; it can be applied to the hip joint only and is
unable to differentiate between osteomyelitis of
acetabulum from septic arthritis of hip joint. In
any case, it is serving the intended purpose very
well. Copley etal. developed a severity of illness
score for patients of acute hematogenous osteomyelitis based on clinical, laboratory, and radiographic parameters to help objectively assess the
severity and stratify the patients [22]. It comprised of three categories, mild (0–3), moderate
[4–6], and severe (>7). The authors further noted
severity of illness scoring system to be accurate
with respect to physician panel assessment in
88%, 60%, and 78% for mild, moderate, and
severe categories, respectively. The detailed
parameters of severity of illness scoring system
are presented in Table8.2. Mignemi etal. devised
a three-tier classication system that can be
applied to all pediatric musculoskeletal infections in the emergency department for stratication [23]. It is based on the severity of infection
and degree of dissemination. The operational
denitions of the three classes are shown in
Table8.3. There is a need for further research on
predictive algorithms and scoring systems for
their application at large in different ethnicities
and geographic areas [24]. In a study by Hollmig
ST etal., the authors noted that the children older
than 8years with an elevated CRP level at admission had a signicantly increased risk of deep
vein thrombosis (DVT) (40%) [25].
Table 8.2 Copley’s severity of illness score [22] for
acute hematogenous osteomyelitis patients
S. no Parameter Score
1. CRP initial
< 10
10–15
> 15
2. CRP 48h
< 5
5–10
>10
3. CRP 96h
< 5
5–10
>10
4. Respiratory rate
> 125% of midrange normal
< 125% of midrange normal
5. Febrile days on antibiotics
< 2
> 2
6. ICU admission
No
Yes
7. Disseminated disease
No
Yes
Mild (0–3), Moderate (4–6), and Severe>7
0
1
2
0
1
2
0
1
2
1
0
0
1
0
1
0
1
Table 8.3
Inammation Local Infection Dissemination
All of the following must be true
(if available)
1. Negative blood culture.
2. Negative local culture.
3. Not fullling the criteria for
a
cell count >50,000, grossly purulent
Three-tier stratication system for pediatric musculoskeletal infections by Mignemi etal. [23]
For two or more anatomic sites, at
least one of the following must be
true
1. Imaging diagnostic for
osteomyelitis or
pyomyositis.
2. Local culture positive and/
or tissue or uid consistent
with infection
3. Two or more positive blood
cultures.
4. Thromboembolic disease.
local and disseminated types.
One of the following must be true
1. Imaging diagnostic for
single-site osteomyelitis or
pyomyositis.
2. Local culture positive and/
or tissue/uid consistent
with infection
3. Criteria for disseminated
type are not met.
a
.
a
.

8 Osteoarticular Infections inChildren
81
8.6 Biopsy
In cases where denitive diagnosis remains elusive, a bone or tissue biopsy may be necessary.
Biopsy allows for direct examination of affected
tissues, facilitating identication of pathogens
and guiding appropriate treatment strategies.
8.7 Radiological Investigations
Radiographs The X-rays show no ndings for
the initial 1week or 10days, except for possible
changes or distortion in soft tissue planes. The
radiologic changes of osteomyelitis like bone
lysis, periosteal reaction, and increased joint
space can be seen at 2weeks.
Ultrasonography
done to localize an abscess, to assess the extent of
soft tissue involvement, and in aspiration of joint;
however, it is a highly operator-dependent investigation modality and cannot detect changes in
the bone.
An ultrasonogram can be
and the nal delayed phase after 2–4 h.
Musculoskeletal infections cause a focal absorption in the delayed phase, which is attributed to
the increased activity of osteoblasts; however, it
can be tricky, especially if the hotspot localizes
close to a physis. The disadvantages of bone
scan are the lack of details on the size of collection, exposure to ionising radiation, and falsenegative results that may occur in subperiosteal
abscess [29].
Computerised Tomograms (CT) The use of
CT in acute pediatric musculoskeletal infections
is limited because of increased exposure of ionizing radiation to the child and its low sensitivity
and specicity compared to magnetic resonance
imaging. It has a role in chronic osteomyelitis to
plan surgery and assess the sequestrum/involucrum status. Judicious use of investigations
should be done to supplement the clinical diagnosis of musculoskeletal infection.
8.8 Medical Management
Magnetic Resonance Imaging (MRI) MRI is
the investigation of choice to assess the extent of
bone changes and any soft tissue collection; it is
a highly sensitive modality in the early course of
infection. The MRI shows infection as a low signal intensity on T1-weighted images and
increased signal intensity on T2-weighted and
short tau inversion recovery (STIR) images
[26–28]. The contrast-enhanced MRI is not routinely ordered for every case, but is useful for
localizing an intramedullary or muscular abscess.
In addition to the diagnosis of musculoskeletal
conditions, MRI also helps in surgical planning,
like approach and localizing any associated
pyomyositis.
Nuclear Scans
Another diagnostic modality
which can be useful, especially in multisite
infections or when the local signs are minimal, is
bone scintigraphy or technetium 99-scan (
99m
Tc),
which can pick up the physiologically active
bone areas as a hot spot. It is triphasic having an
initial ow phase followed by blood pool phase
8.8.1 Acute Osteomyelitis
It is the most common infection of bone in the
pediatric age group. The most common mode of
infection is hematogenous spread, and it affects
the metaphyseal region of bone owing to the hairpin bend arrangement of vessels, sluggish ow of
blood, rich vascularity, and being a physiologically active site. Treatment of acute osteomyelitis
involves general care of the child, selection and
administration of an appropriate antibiotic, rest to
the affected part, and surgery when indicated. An
attempt should be made to obtain a tissue/uid
sample for culture and sensitivity prior to starting
empirical treatment with broad-spectrum antibiotics. However, it should not delay the onset of
treatment in sick cases, where antibiotics, as per
the local hospital/institution policy, are started
immediately without waiting for the culture and
sensitivity tests. Obtaining a blood sample for
culture at the time of intravenous cannula application is a safe practice without causing any
delay in institution of treatment. An algorithmic

82
A. N. Johari et al.
approach to the management of acute osteomyelitis of the proximal tibia/distal femur is presented in Flowchart 8.1. The duration of the
antibiotic course in acute osteomyelitis is generally 6weeks, with initial 2weeks of intravenous
antibiotics followed by oral route. The time
period for shifting to oral antibiotics is also not
clearly dened and should be based on the recovery of patient manifested by clinical improvement of signs and symptoms and a decrease in
laboratory parameter like CRP and ESR.There
are many studies in the literature evaluating the
outcome of a short course (<3weeks) versus a
traditional 6-week antibiotic regimen in acute
osteomyelitis with no signicant differences [30,
31]. However, the authors recommended to pro-
long the duration in vertebral osteomyelitis and
severe infections caused by MRSA.The decision
to intervene surgically should be based on the
clinical condition of the patient. Surgery, which
may include abscess drainage and debridement is
indicated when there is a large abscess collection,
subperiosteal abscess, failure of nonoperative
treatment (IV antibiotics), and formation of
abscess while on conservative treatment [32]. An
algorithmic approach to management of acute
osteomyelitis of distal femur/proximal tibia is
8.8.2 Septic Arthritis
Septic arthritis is an acute inammation of the
joint which is mostly hematogenous in origin or
secondary to transmission from an adjacent
source of infection like osteomyelitis. The
metaphyseal vessels in children younger than
2 years of age cross the physis and can cause
septic arthritis early in the course of osteomyelitis especially in joints where metaphyseal part is
intracapsular like hip and shoulder. Although
septic arthritis can affect any joint, it most commonly affects the hip and knee joints. Unlike
acute osteomyelitis, septic arthritis warrants an
urgent decompression to prevent rapid joint
destruction due to acute inammatory response,
Acute OM Proximal Tibia/
Distal Femur
Stabilize the child/ send blood
and tissue culture when
possible
Start empirical antibiotics/ to be
changed based on culture
sensitivity report
SurgeryNon-Operative
1. Child stable
2 Improvement on empirical
antibiotics
3 No collection
Flowchart 8.1 An algorithmic approach to operative and nonoperative treatment of acute osteomyelitis of the proximal tibia/distal femur
I. Child Sick
2. Subperiosteal Abscess
3 No improvement with
non-operative

8 Osteoarticular Infections inChildren
83
bacterial toxins, and release of cartilagedegrading enzymes. Wherever possible, an
attempt should be made to obtain joint uid/pus
for culture sensitivity testing before starting antibiotics; however, it should not delay the start of
treatment. The choice of empirical antibiotic is
mostly dependent upon local susceptibility pattern and institutional policy, generally, a
third- generation cephalosporin or a broadspectrum antibiotic covering the likely causative
microbes should be started. Joint decompression
should be done at the earliest to prevent joint
destruction. Decompression can be done through
an open arthrotomy or arthroscopically, although
there are no signicant differences in the outcome, an open arthrotomy is the preferred technique by most surgeons. The antibiotics are
continued for 2–4weeks with regular checks on
clinical improvement, inammatory markers,
and cell counts. The transition from parenteral to
oral antibiotics is a grey area with no welldened guidelines; the decision depends upon
improvement in symptoms and reducing markers and is taken on a case-to-case basis. If the
symptoms persist, there should be a repeat
decompression with debridement, and antibiotics should be started as per the culture report. A
regular follow- up is needed to check the condition of the joint and any growth arrest in the long
term.
8.9 Pyomyositis
Pyomyositis is an acute inammation of the striated muscles, often associated with a history of
minor trauma. The incidence was initially higher
in the tropical regions, but now the incidence is
increasing in the temperate regions as well. Most
cases are secondary to hematogenous spread, but
why a localized muscle is involved is still unclear.
A likely mechanism can be a local trauma to the
muscle, leading to the release of iron from the
myoglobin, which can provide an opportunity for
the bacteria to grow and cause a localized abscess
in the muscle. The pyomyositis presents in a similar way like septic arthritis or osteomyelitis with
fever, pain, inability to move the part, localized
tenderness, local swelling, warmth, erythema,
and often a history of trauma. The most common
site of pyomyositis is the iliopsoas muscle, followed by the thigh muscles. In almost 30% of
cases in the tropics, it can present at multiple sites
at the same time. The investigations are done on
the same lines, an X-ray is taken to rule out any
bone involvement, ultrasonography is a reliable
modality for the diagnosis of pyomyositis, but
MRI is the gold standard for localizing the infection and simultaneously ruling out any bone or
joint involvement, including neoplasms. The
treatment of pyomyositis is based on the presence
of abscess and associated systemic symptoms or
sepsis. Prior to the formation of a collection,
which is labelled as Stage I, it can be managed
nonoperatively with broad-spectrum antibiotics,
keeping in view the regional susceptibility pattern and institutional guidelines. In Stage II, there
is a frank abscess collection which warrants an
early decompression and antibiotics as per the
hospital policy, which can be altered as per the
culture and sensitivity. The Stage III has sepsis
and systemic symptoms and is taken up as an
orthopedic emergency warranting an urgent
decompression, IV antibiotics, and intensive care
unit (ICU) care of the patient [31, 33, 34].
The treatment or detailed review of each and
every pediatric musculoskeletal infection, like
vertebral osteomyelitis, diskitis, skeletal tuberculosis, and low-grade chronic infections like brucellosis, is extensive and beyond the scope of this
chapter. We have tried to discuss the brief outline
and approach toward musculoskeletal infections
in children.
8.10 Surgical Management
The treatment of musculoskeletal infection is
demanding, and often multidisciplinary care is
required. Despite variability in treatment protocols, the treatment principles that remain ubiquitous are organism identication, correct antibiotic
selection and delivery of the antibiotics, and prevention of ongoing tissue damage.

84
A. N. Johari et al.
8.11 Acute Osteomyelitis
Although a vast majority of acute osteomyelitis is
treated medically, surgical treatment is necessary
for a select few. The indications for surgery are
the presence of abscess (subperiosteal/soft tissue
abscess/intramedullary abscess), acute osteomyelitis with concomitant septic arthritis and/or
pyomyositis, complex infections as per the new
classication, and for osteomyelitis cases that
show no improvement despite 48–72h of antibiotic treatment. [35, 36] In addition to clinical
examination, imaging (USG and MRI) helps to
determine the extent of the disease. Imaging is
also useful in deciding on the site and extent of
incision.
The surgical treatment entails removal of
necrotic tissue that facilitates antibiotics reaching
the site of infection, and washout to reduce the
bacterial load to halt the infection spread, obtaining cultures and tissue for histopathological exam
(Fig.8.1a–d). This debridement and washout are
many times combined with drilling a hole in the
bone or making a bone window for draining the
intramedullary abscess. The surgical approach
depends on the bone involved. After surgical
treatment, a drain may be used if the collection is
large. After the surgical procedure, the affected
extremity is protected with a splint, and medical
management is continued. The clinical condition
of the child and the inammatory laboratory
parameters are monitored. A repeat surgical procedure may be needed if there is a worsening in
the condition of the child. Although the treatment
is straightforward, there are several controversies
regarding surgical procedures: the best approach
to debride, the extent of debridement, the role of
repeat surgery, and the use of drains. Also, the
role of bone drilling has been debated. It remains
unknown whether bone drilling should be done
for every case of acute osteomyelitis or if it
should be offered to a select few. In addition, the
optimal way to create a bone window, its size,
and its location in the bone (round or trough
shape) remains unknown. [36, 37] The role of
local drug delivery systems is emerging. The
local drug delivery system offers the advantage
of higher drug concentration at the site of infection and avoids systemic toxicity. In addition, it
helps with dead space management. A recent
study compared surgery along with antibioticloaded calcium sulphate to surgery without a
local drug delivery system. The rst group had a
faster fall in CRP (4.8±2.5 versus 13 +/−9.6days.
[38] Although promising early results, more evidence is needed to dene the role of local drug
delivery systems in treating acute osteomyelitis.
Also, there are no clear evidence-based recommendations for postoperative care, including the
duration of extremity immobilization, and when
to return to sports from the viewpoint of pathological fracture prevention. After the index procedure, secondary procedures are often required.
The reported rate of secondary procedures is
15–33% [39, 40]. Typically, the indications for
secondary or repeat procedures are persistent
pain, MRSA infection, and worsening clinical
condition of the patient and lab parameters. The
treatment principles for repeat surgical procedures remain the same.

8 Osteoarticular Infections inChildren
85
a
b
c
Fig. 8.1
(a) An 1-year old with discharging sinus and
abscess over the left forearm. His CRP and ESR were
raised, and the total leucocyte count was 21,000/cmm. He
was treated with debridement and washout. The cultures
grew Methicillin-sensitive Staphylococcus aureus. The
histopathology showed changes suggestive of tuberculous
osteomyelitis. Diagnosis of tuberculous osteomyelitis
with super-added staphylococcal osteomyelitis was made.
(b) Radiograph at 6-month follow-up. The patient was on
antituberculosis treatment and a removable forearm splint.
(c) Radiographs at 18-month follow-up showing resolution of the lytic lesion. (d) Radiographs and clinical pictures at 6-year- follow-up showing slightly short ulna and
completely healed bony lesion
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