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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

180
ab d
c
L. P. Martin et al.
Fig. 13.5 T12-L1 Spondylodiscitis in an 87 years-old
male caused by Mycobacterium tubercolosis. (a, b) CT
scan and (c, d) MR images show the infective process in a
the advance of following multidrug chemotherapy
and the good clinical results it obtains, Tuli etal.
introduced the idea of operating only in patients
with specic conditions [50]. These include spinal
instability, severe pain, deformity, recurrent disease or disease that is nonresponsive to chemotherapy, severe neurological weakness, and either
static or progressive neural decits. Surgical intervention should drain existing abscesses, debride
infected tissues, and provide stability to the spine,
as well as correct deformities. As tuberculous
bacilli do not form biolm, it is considered safe to
stabilize them with surgical implants. These can be
done through anterior, posterior, or combined
approaches, depending on vertebral involvement,
location of abscesses, and deformities [33].
Declarations
Author Contributions:
Conceptualization, project administration:
AA, LPM; data curation and formal analysis:
AA, LPM; supervision: PR; writing original
draft: LPM; writing review and editing: AA,
LPM; gures: AA; All authors have read and
agreed to the published version of the
manuscript.
degenerative spinal column that increase the difculty in
assessment of response to therapy
Funding: There was no external funding source
in support of this study.
Institutional Review Board Statement: Not
applicable.
Informed Consent Statement: Written informed
consent was obtained from patients at the time
of admission to our Institute. However, all pic-
tures have been reported anonymized.
Consent for Publication (Include Appropriate
Statements)
We conrm that this chapter, including related
data, gures, and tables, has not been pub-
lished previously, it is not under consideration
for publication elsewhere, and, if accepted, it
will not be published elsewhere in the same
form, in English or in any other language,
without the written consent of the publisher.
Conicts of Interest/Competing Interests
(Include Appropriate Disclosures)
Ruggieri P is a consultant for Stryker and
Exactech (not relevant to the present manu-
script). The other Authors declare that there
are no relationships/conditions/circumstances
that present a potential conict of interest with
the present manuscript

13 Vertebral Osteomyelitis andTuberculosis
181
Availability of Data and Material (Data
Transparency)
Manuscript data are embedded in the text and
fully available on specic request
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Algorithm onTreatment
inFracture-Related Infections
RohanParwani
14
14.1 Introduction
Infection is the most dreaded complication in
orthopedics. As implants have become an important part of orthopedic practice, wound infections, and osteomyelitis have become a common
occurrence [1]. This is especially true after a fracture xation surgery, where the tissue is already
traumatized with injury, and it becomes susceptible to infection. The presence of a dead space
and hematoma provides an active breeding
ground for infection. Also, there might be a direct
contamination from the external environment if
there has been a compound fracture.
The presence of an infection with a fracture is
a double injury to the patient. It prolongs the
rehabilitation time after injury and adds to the
potential costs of treatment to the patient [2]. It
becomes the treating physician’s duty to get the
patient back to his activities as soon as possible.
The physician is faced with conicting dilemmas
and has to navigate through them to get the
patient back to a pre-injury routine as soon as
possible. There are different options available
considering different scenarios. The treatment
needs to be strategized depending on the clinical
R. Parwani (*)
Pediatric Orthopedic Surgeon, Shaishav Children
Orthopedic Hospital, Rajkot, India
Department of Orthopedics, PDU Medical College,
Rajkot, India
scenario, available resources, and nancial freedom of the treating physician. An early infection
in a closed injury is different from a delayed
infection after the fracture is united. In this chapter, we will discuss various factors that inuence
the treatment and then how to decide on the best
possible treatment strategy.
14.2 Factors Inuencing
theTreatment ofFRI
Once a fracture gets infected, we need to identify
and understand at the earliest, the nature and
quantum of the problem to effectively manage it.
The following factors help us understand this.
14.2.1 Establishing anEarly
Diagnosis
We perform multiple trauma surgeries in orthopedics. Not all of them develop infection, but the
ones that do get infected result in a signicant
increase in morbidity and duration of rehabilitation. As such, early and reliable diagnosis of
infection becomes critical because the patient
pays the price in terms of time and nance if the
fracture surgery becomes infected. The diagnosis
needs to be accurate to optimize the use of antibiotics and the need for revision surgery. A consensus article was published by Metsemakers WJ,
© 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_14
183

184
R. Parwani
Morgenstern M, etal. in the Injury Journal and
14.2.2 Primary Injury
Journal of Orthopedic Trauma. The article gives
two sets of criteria to establish the diagnosis of
fracture-related infection [3]. These diagnostic
pointers are divided into two sets of criteria. The
sets consist of suggestive and conrmatory criteria and give indicators of when to start treatment
in anticipation of infection after orthopedic surgery. Suggestive criteria should alert the caregiver team to the possibility of infection and to
start appropriate remedial measures.
Conrmatory criteria indicate established infection and should trigger aggressive management
strategies.
Conrmatory criteria Suggestive criteria
Clinical signs Clinical signs
Fistula Local/systemic (e.g.,
Sinus New-onset joint
Wound breakdown Persistent, increasing,
Purulent drainage or the
presence of pus
Microbiology Laboratory signs
Phenotypically
indistinguishable pathogens
identied by culture from at
least two separate deep
tissue/implant specimens
Histopathology Radiological and/or
Presence of microorganisms
in deep tissue specimens,
conrmed by using specic
staining techniques for
bacteria and fungi presence
of >5PMNs/HPF in
chronic/late-onset cases
(e.g., fracture nonunion)
ESR erythrocyte sedimentation rate, WBC white blood
cell count, CRP C-reactive protein, PMNs polymorphonuclear neutrophils, HPF high-power eld
local redness, swelling,
fever)
effusion
or new-onset wound
drainage
Increased serum
inammatory markers
(ESR, WBC, CRP)
nuclear imaging signs,
microbiology,
pathogenic
microorganisms
identied from a single
deep tissue/implant
specimen
An open or compound injury is more likely to be
infected after xation [4]. The initial injury determines the extent of soft tissue devascularization,
exposure of bone to the external environment, the
type of contamination, and the presence of foreign bodies inside the wound. We can also predict the nature of the infecting organism. The
nature of primary injury inuences not only the
primary management of injury but also the management of subsequent complications. Different
types of compound injuries have different problems. For example, a blast injury involves the
presence of multiple shrapnel and microscopic
contaminants. Therefore, the wound has a high
chance of developing a persistent infection that is
resistant to debridement [5]. The presence of
infection after a blast injury is likely to require
Gram-negative coverage and a more extensive
debridement [6]. On the other end, even a compound injury with bone penetrating the skin
envelope (compound grade 1 tibia fracture) might
be minimally contaminated. If an infection develops after surgery, it can be treated as an infection
after a closed injury. Infection after surgery in a
closed fracture would likely be caused by a
Gram-positive staphylococcal coccus or by a
pathogen present as a result of comorbid conditions [7]. It is less likely to need a soft tissue coverage procedure like ap surgery. A crush injury
or a degloving injury, on the other hand, could
have an intact-looking soft tissue envelope, but
the underlying bone would have been devascularized and likely to turn into sequestrum.
help us predict the nature of the complication and
its further management.
Case 1
ing the nature of primary injury when analyzing
the reason for delayed union.
old child. She sustained a fall from a height of
sixth oor. She had a compound grade 3b shaft of
femur fracture with ipsilateral neck of femur
fracture.
Therefore, knowing the primary injury can
This case shows the benet of consider-
Figure 14.1 shows the trauma scan of 14-year-

14 Algorithm onTreatment inFracture-Related Infections
Fig. 14.1 The trauma
scan of 14-year-old
child. She sustained a
fall from a height of
sixth oor. She had a
compound grade 3b
shaft of femur fracture
with ipsilateral neck of
femur fracture
185
Figure 14.2 shows postoperative X-Ray. We
had xed femur diaphysis fracture with titanium
elastic nailing and the neck femur fracture with a
pediatric dynamic hip screw. She had a routine
post-operative course, the neck of femur fracture
united at 4months, and shaft of femur fracture
showed partial union at 6 months. She was
allowed full weight bearing at 6months.
Figure 14.3 shows X-Ray at 6months.
After waiting for 1year, her knee could not ex
more than 90 degrees and the shaft femur fracture
showed decient posterior cortex union. Figure14.4
shows X-Ray after 1 year of primary surgery.
Considering her primary compound fracture,
despite no postoperative symptoms and signs of
fracture-related infection, we suspected a fracturerelated infection. We opened the fracture site and
sure enough, the bone that had been exposed to the
environment had turned to sequestrum and there
was a low-grade infection. We did debridement,
removed the loose sequestrum, and put in vancomycin and gentamicin-loaded calcium sulfate beads.
No external xator was required since the anterior
Fig. 14.2 Postoperative X-Ray. We had xed femur
diaphysis fracture with titanium elastic nailing and the
neck femur fracture with a pediatric dynamic hip screw.
She had a routine post-operative course, the neck of femur
fracture united at 4 months, and shaft of femur fracture
showed partial union at 6 months. She was allowed full
weight bearing at 6 months

186
R. Parwani
Fig. 14.3 X-Ray at 6 months
Fig. 14.4 X-Ray after 1 year of primary surgery. There is
persistent posterior gap
Fig. 14.5 Last follow up x-ray after debridement and
sequestrectomy
half of the fracture had a solid callus. The patient
recovered well and regained full function.
Figure 14.5 shows the last follow up X-Ray.
14.2.3 Early Versus Late Infection
The duration for which infection is present near the
implant site plays a critical role in determining the
outcome of treatment of fracture-related infection.
This is because of the development of a microscopic structure called biolm [4]. Biolm is a thin
layer of an extracellular matrix made of polymeric
substances excreted by the bacteria themselves [8].
Adherent to this layer are adherent inactive or dormant forms of bacteria. These bacteria are resistant
to antibiotics simply because they are dormant and
surrounded by an extracellular matrix. Various
microbiological studies have demonstrated that
biolms form early after the onset of infection in

(5) Detachment And Reversion To Planktonic
leases
14 Algorithm onTreatment inFracture-Related Infections
187
surgical wound. Therefore, infections should be
treated as early as possible [9, 10].
Acute infections that happen within a short
period of implantation of fracture xation
devices are likely to have planktonic, metabolically active form of bacteria. They are more
likely to be managed successfully with systemic
antibiotics and dead space management. If the
implants are rm, they may be retained for the
time being, till the bone has united [11]. Late
infections are likely to be insidious and associated with biolm formation. Very few antibiotics
are known to effectively penetrate the biolm,
some examples being rifampicin for Grampositive bacteria and uoroquinolones for Gramnegative bacteria [12]. Once a biolm is expected
to be formed, there are very limited options other
than implant removal. If the fracture is not united
by this time, the fracture will have to be stabilized with external xation.
Figure 14.6 shows stages of formation of biolm. Planktonic form is the form when bacteria
are free in tissues and are most likely to be susceptible to antibiotics. Once a mature biolm
forms, usually within 4–6 weeks, the bacteria
have built up defense barriers to evade the host
immune system and antibiotics.
The presence of biolm acts as a source of
chronic infection and inhibits the process of
fracture union. Therefore, once we suspect early
infection after fracture surgery, there is a race
against time to achieve bone union before the
biolm matures. Various studies have examined
the outcome of treatment of early infection with
debridement, antibiotics, and implant retention
(DAIR). Morgensten et al. published a metaanalysis of six studies [13]. They found 86–100%
success rates if this strategy was used within
3weeks of primary surgery. As time progresses
success rates drop off with less than 67% good
outcomes in infections that are more than
10-weeks old. However, it should be noted that,
once an infection has set in, the strategy of DAIR
is only suppressive and not curative, that is, it
only works and buys time till the fracture unites.
The implant almost always has to be removed
after bone union when the function of the limb is
not likely to be hampered [13].
14.2.4 Identifying thePathogen
Various bacteria are known to cause persistent
infection after orthopedic surgery. The source of
bacteria may be from a coexisting chronic illness, it may be a hospital-acquired infection, or
from environmental contamination at the time of
trauma. The identity of the pathogen is required
Plantkonic
(1) Surface adhesion
Fig. 14.6 Biolm formation
Growth Starting A New Cycle
(2) Matrix
production after
forming single layer
(3)Multilayer
microcolony
Biofilm
(4) Mushroom shaped
mature biofilm ..... re
"free bacteria"

188
R. Parwani
to determine the choice of antibiotics. Timely
and accurate identication of the pathogen and
the corresponding drug-resistance characteristics is challenging in chronic infections. Various
microbiological studies have reported a 70–80%
success rate in positively conrming the pathogen [14].
Staphylococcus remains the predominant
causative organism in monomicrobial surgical
site infections after orthopedic surgery [7]. this
bacteria is of particular concern because of its
ability to rapidly develop antibiotic resistance to
evade both the antibiotics and the host immune
response. It is also known to form biolms and
act as a source of persistent infection. It is isolated in up to 60% of orthopedic infections, in
both early and late-onset infections. It is more
likely to cause a purulent discharge, and sinus/
stulas after an orthopedic infection. If staphylococcus is identied, 60–80% of them are likely to
be resistant to penicillin, erythromycin, and uoroquinolone group of antibiotics [7]. Vancomycin
was found to be effective in majority of cases.
Other Gram-positive bacteria, commonly isolated in monomicrobial and polymicrobial infections are staph epidermidis and coagulase-negative
staphylococcus epidermidis [7]. Their antibiotic
susceptibility usually matches the s. aureus species, with vancomycin being regarded as the most
effective antibiotic.
Polymicrobial infections are more likely in
chronic orthopedic infections. Gram-negative
bacilli are more common in this setting and are
likely to be susceptible to the piperacillintazobactam combination. Gram-negative bacilli
are also more likely to be isolated after open fractures, indicating some role of environmental contamination in the development of fracture-related
infection.
united, and the infection has been there for a
signicant duration of time, the implants need
to be replaced with another implant, as a mobile
fracture is not conducive to healing infection in
soft tissues. The presence of infection either in
the implant or soft tissues causes macrophage
apoptosis, inhibits osteoblast differentiation,
and generally inhibits the biology of fracture
healing [15]. Therefore, the presence of a nonunion complicates the treatment of infection and
all options should be carefully reviewed before
planning for treatment. The bone union can
sometimes be difcult to judge on X-ray, especially in cases where we expect a primary bone
union [16]. Advanced methods like CT scans or
appropriate bone scans can be used to give a
better idea of the status of union [17].CT scans
have a low specicity in conrming fracture
union, mainly because of “beam hardening”
artifact from external or internal xation devices
[17]. Bone scan is another important tool, that
can identify the site of infection in the boneimplant interface and help identify if the infection is present at the nonunion site [18].
14.2.5.1 Sequestrum
Sequestrum is dened as a dead bone present in
live bone. It often acts as a source of persistent
infection. Its presence also delays bone union.
Therefore, when considering a revision for
infected nonunion, the sequestrum if present
must be removed. The size of the sequestrum
must be evaluated before surgery and if after
removal, the fracture is further destabilized,
appropriate measures like antibiotic spacer with
or without external xation should be
considered.
14.2.6 Patient Comorbid Factors
14.2.5 Status ofFracture Union
When faced with an infection after trauma surgery, the stage of fracture union plays the most
important role in deciding the future course of
action. Removal of implants may solve all problems in a late infection. But if the bone has not
Any patient undergoing trauma surgery should
have their bio-physiological prole checked.
This is required not only for a safe anesthesia but
also for postoperative care and rehabilitation. The
immunocompetence of the host at the systemic as
well as local soft tissue level plays an important
role in the ability of the host to resist infection.

14 Algorithm onTreatment inFracture-Related Infections
189
The patient is assessed for comorbid factors like
poor nutritional status, obesity, smoking, diabetes, and peripheral vascular disease [19].
Peripheral pulse and sensation should be assessed
in all patients where surgery is planned especially
after infection. We should assess the patient’s
preoperative glycemic control, as during the
physiological stress of surgery, hyperglycemia is
known to be independently associated with poor
clinical outcomes like wound infections [20].
Hyperglycemia induces increased expression of
proinammatory cytokines like TNF, which
inhibit osteoblast activity. Perioperative glycemic
control should be assessed with Hba1c and if
found elevated, appropriate corrective measures
should be started. They should undergo a dietary
as well as endocrine consultation and perioperative insulin should be started if required.
Similarly, obesity, dened as BMI of more than
30 is known to be associated with adverse postoperative outcomes like thromboembolism and
infection. It is not possible or advisable to suggest a drastic weight loss regimen before surgery,
but we should consider it as a contributing
factor.
Multiple investigators have proven the risk
associated with smoking and its relation to fracture union and wound infection rates [21]. A
meta-analysis published by Smolle etal. shows
the signicant risk of orthopedic infections in
fractures of the tibia, hip, calcaneum, elbow, distal femur, and spinal surgery [22]. It might be
best to initiate cessation of smoking in patients
undergoing treatment for fracture-related
infection.
Thus, when considering the treatment of a
patient with a fracture-related infection, the
entire host should be optimized. Depending on
the presence of comorbid conditions, the
patient’s physiology is classied into three categories, according the University of Texas
Medical Branch protocol [23].
Anatomic type
Type I — Medullary osteomyelitis
Type II — Supercial osteomyelitis
Type III — Localized osteomyelitis
Type IV — Diffuse osteomyelitis
Physiologic class
A-host — Good immune system and delivery
B-host — Compromised locally (B
systemically (B
C-host — Requires suppressive or no
Clinical stage
Type+class=clinical stage
Example:
Stage IVB
systemically compromised host
S
treatment minimal disability;
treatment worse than disease; not a
surgical candidate
osteomyelitis=a diffuse lesion in a
S
L
) or
)
14.3 Treatment Options
After identifying the various host factors inuencing the treatment of infection, we can then
start analyzing the various treatment options that
can be offered to the patient. Therefore, we need
to acquaint ourselves with the various treatment
modalities available. Depending on our understanding of indications for different treatment
options we can formulate a cohesive strategy.
14.3.1 Choice ofAntibiotics
Antibiotics will be the mainstay of our treatment
of infection. The choice of antibiotics and duration of antibiotics is determined by the clinical
picture with which the patient presents. In case of
early infection, where only the suggestive criteria
are met, a deep tissue culture should be obtained,
with or without formal debridement of the surgical wound. It has been an international consensus, not to start empirical intravenous antibiotics
without taking deep tissue samples unless the
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