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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

86
d
Fig. 8.1 (continued)
A. N. Johari et al.
8.12 Septic Arthritis
In contrast to acute hematogenous osteomyelitis,
septic arthritis always necessitates surgical treatment. The treatment principles are decompression of the joint, washout of inammatory uid,
and debridement to decrease the bacterial load.
The indications for surgical treatment are conrmed or clinical diagnosis of septic arthritis.
Joint aspiration and synovial uid analysis
remain an excellent tool for diagnosing septic
arthritis. However, the facilities for joint aspiration and synovial uid analysis may not be available universally. It is recommended to diagnose
septic arthritis based on clinical and laboratory
parameters. [41, 42] The diagnosis of septic
arthritis warrants urgent surgical treatment.
Delays give rise to sequelae (Fig.8.2a–h).
When to do the surgery?
It is recommended to do the surgery at the
earliest. [43] The duration between the onset of
symptoms and the drainage procedure has a
bearing on outcomes. Guidelines recommend
doing the joint decompression on an emergent
basis, but it remains unknown whether delaying
it by a few hours makes any difference. It
remains unknown whether doing the procedure
in the middle of the night versus doing it in the
morning makes any difference in the outcomes.
A delay of more than 24h has shown poor outcomes. The treatment of late-presenting septic
arthritis remains problematic. It has been shown
to have suboptimal outcomes and poor results.
[44–47] This highlights the need for early diagnosis and appropriate referral. This is crucial
for saving the joint and to achieve good results.
The arthrotomy and washout can be done by
different means, although an open arthrotomy and
washout remain the most commonly used
approach. Surgical treatment of septic arthritis can
be achieved via open arthrotomy, needle aspiration
(one-time or repeated procedures), or arthroscopic
washout. Various factors need to be taken into consideration while choosing the best option. These
factors include the age of the patient, size of the
joint involved, availability of instruments and personnel in addition to training, and comfort level of
the surgeon performing the procedure. [48–51].

8 Osteoarticular Infections inChildren
87
The hip joint is the most commonly involved
joint for septic arthritis. Hip joint septic arthritis
can be treated via open arthrotomy using an anterior or medial approach. With the anterior
approach, an anterior incision is made and the
interval between sartorius and tensor fascia lata is
identied. Through this interval, the rectus femoris is split to expose the anterior hip capsule. A
small window is made in the capsule to open the
hip joint. The tissue is sent for culture and histopathology. Wash is given using normal saline. It
is important to open the joint and identify the
femoral head for complete decompression of the
joint. A suction drain may be used for the hip
joint and removed after it stops draining.
However, there are other approaches, such as
needle aspiration or hip arthroscopy, for treating
a
septic arthritis of the hip. The European Society
guidelines advocate surgeon preference depending on his/her experience. [52].
Needle aspiration, although a simple technique, carries the risk of inadequate drainage.
However, needle aspiration remains a minimally
invasive alternative, especially in neonates or if
the child is medically unt to undergo a longer
procedure. Similarly, hip arthroscopy offers an
alternative to open arthrotomy. It is possible to do
debridement and also obtain tissue for histopathological examination. El Sayed prospectively
compared arthroscopy versus open arthrotomy
and showed that the results are similar in both
procedures. The hospital duration was signicantly shorter in the arthroscopy group compared
to the open arthrotomy group (3.8 days versus
Fig. 8.2 (a and b): An 8-year old had febrile illness and
pain in the left hip which started on the sixth March 2020.
He was diagnosed to have multiorgan sepsis, septic arthritis of left hip with left femoral vein thrombosis. Antibiotics
and thrombolytics were started. He was operated 15days
later, on the 21st March 2020, for hip decompression. (c)
7months from onset, avascular necrosis of the femoral
epiphysis with hinged abduction is visible. No treatment
was given. (d) A year since the onset of infection, the
hinged abduction is very visible on the X-ray and MRI.An
arthrogram was done along with an adductor tenotomy,
and the hip was contained in a hip spica at another centre.
(e) 3months after the adductor tenotomy, the hip appears
contained. (f) 1 year and 8 months since the adductor
tenotomy, the hip remains contained. (g) Functionally, the
child is doing well and is able to sit cross-legged and can
also do the split. (h) Status of the hip on X-ray nearly
3years and 11months since the onset

88
A. N. Johari et al.
b
c
Fig. 8.2 (continued)

8 Osteoarticular Infections inChildren
d
89
e
Fig. 8.2 (continued)

90
A. N. Johari et al.
f
g
h
Fig. 8.2 (continued)

8 Osteoarticular Infections inChildren
91
6.4days). [51] Although a promising approach,
hip arthroscopy requires special equipment and
training, which may be unavailable routinely.
The minimally invasive procedures may offer
several advantages, such as smaller incisions,
shorter hospital stays, and better parental acceptance. The minimally invasive approaches have
been fraught with the risk of incomplete joint
drainage requiring repeat procedures. Studies have
shown this risk to be almost ve times higher with
minimally invasive procedures such as needle
aspiration and arthroscopy. In recently published
systematic reviews, the risk of redo surgery after
open arthrotomy is 3%, arthrocentesis is 15%, and
arthroscopy is 14%. [53, 54] This highlights the
evolving role of minimally invasive procedures
and calls for identifying the correct indications
that might minimize the risk of repeat procedures.
8.13 Complications
Pediatric musculoskeletal infections can lead to
complications. These complications may affect
the physeal growth plate, segment of a bone, or the
joint and may signicantly burden the individual,
parental, and healthcare resources. Complications
or post-infective sequelae may have long-term
effects as they affect growth and can create deformity. There could be physical and psychological
consequences leading to disability. In many cases,
multiple complex surgeries might be necessary.
The exact prevalence of complications is not
clear. The risk factors for the development of
complications are infections with MRSA and
other highly virulent organisms, complex infections (septic arthritis with osteomyelitis), delay in
the treatment, younger children, and positive
blood cultures indicating disseminated infection.
[39] In addition to a delay in diagnosis, inadequate or inappropriate treatment, and lack of a
multidisciplinary care team have been shown to
lead to a high prevalence of musculoskeletal
infection sequelae. [55–57]. Also, increasing virulence, antibiotic resistance, and changes in epidemiology contribute to adverse outcomes. [58, 59].
A study by McNeil has shown that infection
with Accessory Gene Regulator (AGR) III S.
aureus, duration of fever >4days after admission,
and delayed source control were associated with
a signicant increase in complications of osteoarticular infections. [60, 61] A-score and C-scores
were developed to predict complications. [55]
A-score can predict complications within
6weeks and C-score variables can be used to predict complications at/after 12weeks. [Tables 8.4
and 8.5] Vij etal. have shown that the A-score,
along with clinical judgment, can be useful in
determining optimal timing for early care decisions such as the transition to oral antibiotics, the
need for further intervention, and discharge. The
C-score can be useful while considering the decision specic to the development of chronic osteomyelitis and the need for antibiotics beyond
12weeks, and to rule out pathological fracture or
avascular necrosis. [62].
Complications of pediatric musculoskeletal
infection can be acute or chronic, as listed in
Table8.6. [56, 58, 60, 63, 64] [Table8.6]
Table 8.4 A-score variables
Presence of a bone abscess 2
Temperature≥38°C for more than 48h from
the start of antibiotics
Suppurative arthritis 3
Presence of disseminated disease, presence of DVT,
septic pulmonary embolism, and endocarditis
Delayed source control (surgical intervention
after 3days)
Maximum score 15
Table 8.5
CRP≥100mg/L at 2–4days after starting
antibiotics
Presence of disseminated disease 1
Occurrence of bone debridement 2
Maximum score 4
Table 8.6
in children
Acute complications Chronic complications
Multifocal osteomyelitis Chronic osteomyelitis
Septicemia Pathological fracture
Venous
thromboembolism
Septic shock Joint destruction
Compartment syndrome Physeal growth arrest and
Death Sequestrum, bone loss
C-score variables
Complications of musculoskeletal infections
Osteonecrosis
its sequelae
Malignant transformation
2
4
4
1

92
A. N. Johari et al.
8.14 Chronic Osteomyelitis
Chronic osteomyelitis is a long-standing infection characterized by radiographic evidence of
dead necrotic bone (sequestrum), reactive new
bone formation (involucrum), and signs of longstanding infection. It is associated with repeated
episodes of symptoms of infection. In osteomyelitis, 20% form sequestra. [64].
Chronic osteomyelitis poses therapeutic challenges such as the presence of infected bone and/
or soft tissue, focal or segmental bone loss, soft
tissue loss, physeal damage, joint contracture,
and pathological fracture. The commonly used
classication systems are the Beit CURE classication and the Cierny–Mader classication. The
Beit CURE classication can guide treatment
selection. [65, 66] The treatment of this complex
problem is multidisciplinary and can vary
depending on several host and surgeon factors.
The treatment principles include host optimization, antibiotic therapy (systemic antibiotics and/
or local antibiotic drug delivery system), and surgical treatment. The surgical treatment involves
radical debridement followed by dead space
management and the management of focal/segmental bone defects. The local antibiotics delivery systems using various materials have shown
encouraging results. [67, 68] Fig.8.3a–d.
The management principles for treating
chronic sequelae of a pediatric musculoskeletal
infection are as follows: [37]
• Prevention—early diagnosis and the right
treatment—get it right.
• Team approach.
• Comprehensive evaluation—not to miss out
on multiple sites of infection, especially in
neonates and young children.
• Planning the treatment.
• Creating a problem list.
• Priority list for each problem.
• Taking into consideration family expectations,
resources, and surgeon capabilities.
• Discussing reconstructive as well as prosthetic
options in detail.
• Biology preservation.
• Follow-up till skeletal maturity and beyond.

a
8 Osteoarticular Infections inChildren
93
b
c
Fig. 8.3
(a). Radiographs and MRI of an 8-year-old girl
with chronic osteomyelitis of the right distal femur. She
was having recurrent pain, swelling in the right thigh, and
fever. (b
surgery radiographs. Patient was treated with debridement
through a bone window and placement of a local drug
) Immediate postoperative and 1-month post-
delivery system (Vancomycin added to Calcium sulfate).
(c) Radiographs at 6-month follow-up showing complete
absorption of the Calcium sulfate and no signs of recurrence of the infection. (d) Radiographs and clinical pictures at 30-month follow-up showing no signs of
recurrence and full knee range of motion

94
A. N. Johari et al.
d
Fig. 8.3 (continued)
8.15 Pathological Fractures
The reported incidence of pathological fractures
is 3–5% [69, 70]. The reported risk factors for
pathological fractures are infection with a virulent strain (PVL, MRSA, or AGR group III
Staphylococcus aureus), prolonged fever, more
than three debridements, bacteraemia, extent on
bone involvement >45% on radiographs at
6 weeks, large subperiosteal abscess, involvement of > two-third length of the bone on the
initial MRI and a sharp transitional zone
between diseased and normal bone marrow on
initial MRI. [30, 38] Inadequate drainage of an
intraosseous abscess can be a risk factor. Also, a
slot created for bone debridement can act as a
stress riser for the development of pathological
fractures. It is important to create a slot/window
with a small width on the non-tension side of the
bone to minimize the risk of pathological fracture. [71–73] The treatment is nonoperative in
the majority of cases. Debridement followed by
fracture stabilization is necessary for some
cases. [70].

8 Osteoarticular Infections inChildren
95
8.16 Post-infective Segmental Bone Loss
Post-infective segmental bone loss develops due
to resorption of bone or destruction of the bone
due to infection. Another possibility is during
aggressive debridement, after the removal of
sequestrum with a weak involucrum done to
eradicate infection. [73] The incidence of postinfective bone gap development is 20% [65].
Bone gap management is a daunting task and
often needs complex reconstructive surgical
treatment. Many times, it may require plastic surgical intervention. The treatment principles
include eradication of the infection, optimization
of the host condition, soft tissue cover, alignment
of the bone segments, dead space management,
enhancement of bone healing, achieving bony
stability, posttreatment rehabilitation, and protection of the new bone. [74–76]. In general, smaller
defects (< 6cm) can be managed with autologous
bone graft and acute shortening. Larger defects
need acute or gradual bone transport, induced
membrane technique, or bular graft placement
(vascularized or non-vascularized). [74–83].
8.17 Post-infective Physeal Growth Arrest
The incidence of post-infective physeal growth
arrest is 7–20%. It is more common in the distal
and proximal femur. [84] The growth arrest leads
to a total or partial closure of the epiphyseal
growth plate, leading to limb shortening and/or
angular deformity. The severity of the deformity
depends on the age of the child and the anatomic
location of the physis involved. In general, a
peripheral physeal bar involving a smaller area
of the physis, and at least 2 years of growth
remaining, can be treated with physeal bar resection and fat graft interposition. It is recommended to do simultaneous osteotomy if the
deformity is >15 degrees [85, 86]. Physeodesis
to be offered if the physeal bar involves >50% of
the physeal area and/or the growth remaining is
less than 2years. The associated leg length discrepancy will need to be treated. Figure8.4a–c
The outcomes of post-infective bar resection are
unfavorable as compared to posttraumatic bars.
[85, 86].
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