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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

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PJI After Shoulder andElbow
Arthroplasty
GeorgHauer, SebastianM.Klim,
andAndreasLeithner
22
22.1 PJI After Shoulder andElbow
Arthroplasty
22.1.1 Introduction
Shoulder and elbow arthroplasty is proving to be
an effective treatment for people suffering from
painful shoulder or elbow arthritis [11, 30, 75].
Periprosthetic joint infection (PJI) after total
shoulder arthroplasty (TSA) and total elbow
arthroplasty (TEA) is rare but can have serious
consequences, potentially resulting in signicant
damage to soft tissues, bone loss, and impaired
functional outcomes [11, 44]. Prompt diagnosis
and appropriate treatment are critical to cure the
infection and minimize extensive damage to bone
and soft tissue.
While a signicant number of knee and hip
replacement operations were performed in
England and Wales in 2021, there were far fewer
shoulder and elbow replacements. According to
the National Joint Registry for England, Wales,
Northern Ireland, and the Isle of Man, approximately 80,000 procedures were performed for
hip and knee joints, respectively. In contrast, the
number of shoulder and elbow replacement sur-
G. Hauer · S. M. Klim (*) · A. Leithner
Department of Orthopaedics and Trauma, Medical
University of Graz, Graz, Austria
e-mail: georg.hauer@medunigraz.at;
Sebastian.klim@medunigraz.at;
Andreas.leithner@medunigraz.at
geries was notably lower, with roughly 5500 and
760 procedures, respectively [42]. Interestingly,
although shoulder PJI is less common [14],
affecting about 1% of patients [5], the treatment
of PJI in the shoulder is particularly more
demanding compared to PJI in other joints [32].
It is associated with higher morbidity and higher
costs [4, 39]. In addition, the incidence of elbow
PJI is higher than for hip or knee arthroplasty,
with reported rates ranging from 1% to 19% [32,
48, 54].
Historically, much of the guidance and expertise related to PJI has been derived from research
and guidelines developed in the eld of lower
limb arthroplasty [49]. Little attention has been
paid to shoulder and elbow PJI, primarily because
TSA and TEA are used less frequently and the
incidence of acute fulminant PJI is relatively low
[21, 81]. To effectively diagnose and assess PJI in
the shoulder and elbow, it is essential to begin the
process with a standardized, and universally
accepted denition. This is particularly important
because of the microbiological differences and
the difculties arising from the increased rates of
positive intraoperative cultures in revision cases
that do not appear to have an infection [2, 21, 29,
36]. Fortunately, in recent years there has been a
marked increase in research efforts focusing on
the complexities and unique factors in this particular area, suggesting that there is increasing
recognition of the particular challenges associated with shoulder and elbow PJI [17].
© 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_22
319

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22.2 PJI After Shoulder Arthroplasty
22.2.1 Epidemiology
The epidemiology of shoulder PJI has been thoroughly investigated, with data collected from
various sources including observational studies
and meta-analyses. In a recent systematic metaanalysis using 105 articles, the pooled PJI incidence following TSA was 0.61% (0.34–0.93)
over a follow-up period of 1.1years [32]. The
authors also found that the PJI incidence was
higher following inverse TSA compared with anatomical TSA.In an arthroplasty register analysis,
the authors described a 1.4% (95% CI 1.2 to 1.6)
ten-year cumulative revision rate due to infection
[38]. The adjusted relative risk of revision surgery
due to infection was about 2.5 times higher for
inverse TSA compared to anatomical TSA.Shah
and colleagues could demonstrate a 2.4% shoulder PJI rate at a mean follow-up of 4.3years for
primary inverse TSA [61]. There was also a tendency for increased infection rates in the revision
surgery groups compared to the primary arthroplasty groups, i.e., in line with other studies [67,
71]. Zumstein etal. published a systematic review
and found that the incidence of PJI after inverse
TSA was 3.8%, a gure comparable to that of
anatomical arthroplasty. Again, the revision group
had a higher infection rate compared to the primary group (5.8% versus 2.9%) [82].
The available studies used a wide range of
follow-up periods and different diagnostic criteria to identify PJI cases. Because of these different approaches, it is difcult to determine the
exact incidence of shoulder PJI based on the
available data. Conducting more comprehensive
studies using generally accepted diagnostic criteria would provide a more reliable estimate of
shoulder PJI incidence.
22.2.2 Risk Factors
The evidence in the present literature lacks uniform consistency, as the studies used different
diagnostic criteria for shoulder PJI, the followup time varied and the number of participants
varied. This variety of factors makes it difcult
to reach reliable conclusions about the risk factors associated with PJI.The likelihood of infection occurring after any type of arthroplasty
depends on several factors related to the patient,
the surgical procedures, and the indication [33].
Regarding the inuence of patient characteristics, there is strong evidence that men show an
increased risk of needing revision surgery due to
PJI [32, 40, 56, 63] and that older age is associated with a decreased risk of joint infection [12,
32, 56, 63]. With each additional year of life, the
risk of infection decreases by 5% [40]. The
increased risk of shoulder PJI in younger patients
remains uncertain [38], while in men it is associated with a higher bacterial load of Cutibacterium
acnes [56].
There is no robust evidence of associations of
other patient characteristics or comorbidities
such as heart failure, obesity, peripheral vascular
disease, chronic lung disease, diabetes mellitus,
liver disease, renal failure, or smoking status with
the risk of PJI following TSR.While some studies indicate a correlation with an elevated risk
associated with these factors [3, 26, 40, 46, 64,
67], others suggest no signicant inuence [32,
40, 62, 63].
Studies demonstrated that revision arthroplasties had signicantly higher infection rates than
primary arthroplasties [12, 67, 71, 82]. In addition, inverse TSA was associated with higher
infection rates compared to conventional shoulder arthroplasty [56, 82]. Studies also found that
previous treatments such as steroid injections
given within 3months prior to arthroplasty and
patients with a history of non-arthroplasty shoulder surgery were associated with an increased
risk of shoulder PJI [12, 76, 77].
The risk of shoulder PJI is complex and
inuenced by several factors. Particular attention should be paid to those at higher risk of PJI
after primary TSR, including younger men and
those with previous shoulder surgery. These
patients should receive appropriate advice and
guidance [32].

22 PJI After Shoulder andElbow Arthroplasty
321
22.2.3 Denition andDiagnosis
22.2.3.1 Denition
With the number of TSA increasing every year,
the incidence of complications requiring revision
surgery has also increased [42]. The COVID-19
pandemic did lead to a decrease in the number of
implantations. However, the numbers are now
expected to exceed those of the previous year
again on an annual basis [42]. It is expected that
the demand for shoulder prostheses will increase
sevenfold in the next 15years [9]. Among the
complications after TSA, PJI is one of the main
causes of implant failure [8, 46, 60]. In the past,
it was challenging to measure the consequences
of shoulder PJI, due to the absence of a precise
and unambiguous denition. In order to create
uniform standards for clinical decision-making
and research reporting, a precise denition of
shoulder PJI was established at the 2018
International Consensus Meeting on Orthopaedic
Infections [21].
An exact and universally accepted denition
of shoulder PJI is of great importance. This denition helps in clinical decision-making and provides a consistent basis for future research
reports. In addition, the adoption of a recognized
denition is the rst fundamental step toward a
rigorously tested diagnostic method [21]. The use
of different PJI denitions among researchers
dealing with shoulder problems has probably led
to different and contradictory conclusions regarding both diagnosis and treatment [27].
When dening infections after prosthetic joint
replacement, there is agreement that a combination of clinical, laboratory, and radiological features should be used to conrm or exclude an
infection [50]. This approach is also appropriate
for shoulder PJI.It has been recognized that certain features of shoulder PJI can be considered as
denite indicators of infection and should be
given more importance in the denition. On the
other hand, some less specic features may indicate infection but may also be present in patients
without infection. As a result, two levels of certainty have been introduced for these diagnostic
features. The criteria can be classied as either
conrmatory (indicating denite infection if ful-
lled) or suggestive (indicating features suggestive of possible infection and warranting further
investigation) [21].
22.2.3.2 Diagnostic Criteria
Despite ongoing debates and uncertainties
regarding the denition and treatment of PJI of
the shoulder, there are cases where the presence
of infection is undeniable. To address this, a subgroup known as “denite PJI” of the shoulder has
been introduced to categorically identify such
cases [21].
Conrmatory Criteria for Shoulder PJI
1. Presence of a sinus tract from the skin surface
to the prosthesis.
2. Gross intra-articular pus.
3. Two positive tissue cultures with phenotypically identical virulent organisms.
Suggestive Criteria for Shoulder PJI.
In cases where there are no conrmatory signs
of infection, the diagnosis of shoulder PJI can be
difcult. To avoid this, a system was introduced
with three categories: probable PJI, possible PJI,
and unlikely PJI.To categorize these cases, minor
criteria with different weights were introduced
(Table22.1) [21].
A score of 6 or higher with an identied organism is considered an indicator of probable shoulder PJI. A score of 6 without an identied
organism indicates possible PJI. Fewer than 6
with one positive culture with a virulent organism
or two positive cultures with a low-virulence
organism indicates possible PJI.Shoulder PJI is
considered unlikely if the cultures are negative or
there is only one positive culture with a lowvirulence organism.
22.2.3.3 Clinical Presentation
The most common initial symptom is pain (86%),
followed by a draining sinus (44%), stiffness
(35%), redness (35%), swelling (32%), fever
(21%), night sweats (9%) and chills (9%) [7].
Non-specic symptoms such as pain and impaired
function play an important role, especially in
cases of late shoulder PJI, when the postoperative
function was normal until that point. In the case
of painful shoulder arthroplasty, conrming a
diagnosis of infection is often difcult and

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G. Hauer et al.
Table 22.1
Minor criteria Weight
Unexpected wound drainage 4
Single positive tissue culture with virulent
organism
Single positive tissue culture with low-
virulence organism
Second positive tissue culture (identical
low-virulence organism)
Humeral loosening 3
Positive frozen section (5 PMNs in ≥5
high-power elds)
Positive preoperative aspirate culture (low or
high virulence)
Elevated synovial neutrophil percentage
(˃80%)
Elevated synovial WBC count
(˃3000 cells/μL)
Elevated ESR (˃30mm/h)
Elevated CRP level (˃10mg/L)
Elevated synovial α-defensin level
Cloudy uid 2
PJI periprosthetic joint infection, PMN polymorphonuclear leukocyte, WBC white blood cell, ESR erythrocyte
sedimentation rate, CRP C-reactive protein
a
Beyond 6weeks from recent surgery
Minor criteria for denition of shoulder PJI
a
a
a
3
1
3
3
3
2
2
2
2
2
components, radiolucent lines, osteolysis, endostal scalloping, and new bone formation [11, 13,
18]. However, these ndings are often absent in
indolent or low-grade infections. Especially if
humeral loosening is found, this should signicantly increase the suspicion of PJI of the shoulder. In their research, Pottinger etal. [53] showed
that loosening of the humeral component and
humeral osteolysis, as seen on plain radiographs,
were associated with a threefold and tenfold
increase in the likelihood of a positive
Cutibacterium acnes culture, respectively.
Computed tomography (CT) can be useful in
assessing bone stock and the current implant conguration, while magnetic resonance imaging
(MRI) can help in assessing possible osteomyelitis or an abscess in the area [18]. Various nuclear
imaging techniques have been introduced to
improve the accuracy of infection diagnosis,
however, they have a limited role in the workup
for shoulder PJI.Three-phase bone scintigraphy
is one of the most frequently used imaging techniques used in the diagnosis of PJI, especially for
evaluating late PJI [25].
requires additional investigations. However, in
such cases, it is important to consider the possibility of infection [18].
Erythema and swelling may indicate infection, but these indicators are usually not specic
enough to denitively diagnose infection. The
presence of fever as a systemic sign of infection
associated with PJI of the shoulder indicates a
more aggressive course of the disease.
Nevertheless, it is noteworthy that fever is rare in
PJI of the shoulder [7].
The only clinical sign that is conrmatory for
shoulder PJI is the presence of a sinus tract even
without other clinical, laboratory, or microbiological ndings. A strong indication of PJI of the
shoulder is also the development of unexpected
wound drainage from a previously dry, healing
wound [18].
22.2.3.4 Radiology
Plain radiographs may be helpful in diagnosing
PJI.Radiographic ndings of concern for PJI of
the shoulder include loosening or migration of
22.2.3.5 Inammatory Markers
Limited research is available regarding the use of
serum erythrocyte sedimentation rate (ESR),
C-reactive protein (CRP), or white blood count
(WBC) for assessing shoulder PJI [41, 70].
Serum ESR, CRP, and WBC have low sensitivity
in the diagnosis of shoulder PJI [18]. Despite
their inclusion in a standard infection investigation, normal values should not be used to denitively exclude infection [18]. Piper et al. [51]
have published thresholds for CRP and ESR
associated with PJI in the shoulder. The optimized ESR cut-off for shoulder arthroplasty has
been set at 26mm/h. This specic ESR cut-off
has shown a sensitivity of 32% and a specicity
of 93% in the diagnosis of shoulder PJI.Similarly,
the optimized CRP cut-off is 7mg/L, with this
value showing a sensitivity of 63% and a specicity of 73% for the detection of shoulder PJI.
22.2.3.6 Synovial Aspirate
A standard examination for the diagnosis of
shoulder PJI is synovial aspiration and analysis.

22 PJI After Shoulder andElbow Arthroplasty
323
Aspiration of synovial uid is mandatory if a distinct uid collection is identied, however, “dry
taps” are often observed in Cutibacterium acnes
infections [6, 7]. Due to the lower virulence of
Cutibacterium acnes, the threshold for an
increased number of leukocytes in the context of a
shoulder, PJI remains unknown and may be lower
than accepted values for other PJIs. Consequently,
the currently accepted leukocyte count thresholds
of >1100–3000 cells/ml with a polymorphonuclear neutrophils (PMN) differentiation of >80%
for chronic hip and knee PJI are unlikely to be
appropriate for the diagnosis of shoulder PJI, as
the bacterial pathogens in the shoulder usually
produce a less severe inammatory response [18].
22.2.3.7 Microbiological Prole
The uniqueness of shoulder PJI lies in the underlying processes, which are primarily due to the
specic microorganisms that colonize the shoulder. The predominant pathogens of surgical site
infections (SSI) and shoulder PJI surgery are usually coagulase-negative Staphylococcus species,
Cutibacterium acnes and Staphylococcus aureus
[24, 31, 56, 63]. Cutibacterium acnes, in particular, has recently emerged as the predominant
cause of PJI in the shoulder [18]. However,
Cutibacterium acnes infection can be particularly
challenging because of its slow and gradual progression, and conrming positive cultures often
necessitates longer incubation periods for samples [10]. A potential disadvantage associated
with the increased sensitivity of prolonged cultures for Cutibacterium acnes is the fact that this
may also carry an increased risk of contamination and false-positive results [16]. Unexpected
positive cultures (UPCs) without clinical or
radiographic signs of infections are a dilemma.
However, the exact denition and management of
UPCs in the context of shoulder arthroplasty
revisions remains unclear, as does the role of
Cutibacterium acnes [18]. Cutibacterium acnes
is the predominant microorganism identied in
most positive UPC cases, however, it remains
uncertain whether the signicance of UPC caused
by one bacterium differs from that of UPC with
another bacterium. Providing semi-quantitative
and quantitative reports of bacterial culture
results (eg, density of bacteria, Cuti [Propi]
score) could be of clinical value in diagnosing
PJI in the shoulder and in assessing the signicance of UPCs [18]. Nevertheless, the lack of
adequately designed studies addressing this issue
makes it difcult to draw denitive conclusions.
22.2.4 Management
22.2.4.1 Prevention
Targeting the microorganisms most likely to
cause shoulder PJI is an important aspect of prophylactic measures. Patients scheduled for TSA
should be prescribed intravenous antibiotics that
are effective against both Gram-positive and
Gram-negative microorganisms [18]. Cefazolin
is the standard antibiotic to be administered.
Patients who are intolerant to beta-lactam antibiotics should be further investigated to determine
if they are eligible for treatment with cefazolin.
In patients with a true hypersensitivity reaction or
side effects that make cefazolin treatment impossible, alternative options such as vancomycin or
clindamycin should be considered [20].
22.2.4.2 Treatment
Treatment strategies for shoulder PJI include
chronic antibiotic treatment, irrigation, and
debridement with or without the exchange of components, one- or two-stage revision procedures,
the use of antibiotic spacers, and resection arthroplasty. These approaches are based on the collective knowledge and literature on hip and knee
arthroplasty [20]. The choice of the most suitable
antibiotic, the method of administration, and the
duration of treatment depend on the surgical therapy concept chosen and the pathogen detection
and should be determined individually after consultation with infectious disease experts [19].
Implant Retention
In acute shoulder PJI, the choice of irrigation and
debridement with retention of components or
replacement of modular components is often
considered practical. It is recommended that
debridement, antibiotics, and implant retention
(DAIR) be considered for shoulder arthroplasty

324
G. Hauer et al.
when infection is conrmed within a 30-day window of symptom onset [7, 20]. However, it is
noteworthy that this strategy is associated with a
reported failure rate of 42% to 63% and less
favourable functional outcomes [7, 19]. Given
these results, the surgeon must carefully weigh
the potential for recurrent infection against the
morbidity associated with implant removal.
One-Stage Revision Arthroplasty
Utilizing the knowledge acquired from managing
knee and hip infections, the concept of singlestage replacement is presented as a viable solution when the responsible microorganism is
clearly identied [19]. This approach offers
advantages such as shorter hospital stays, cost
efciency, shorter antibiotic treatment duration,
and the potential to optimize clinical outcomes
[5]. The criteria for choosing between a one-stage
and a two-stage exchange are currently unclear
[19]. While the pooled data suggest a potential
superiority of the one-stage exchange over the
two-stage approach, it is important to recognize
that this observation could be inuenced by
selection bias and other variables such as the specic pathogen, the antibiotic resistance pattern,
the timing of the infection or diagnostic elements
such as obvious clinical signs of infection [19].
initial phase with less consideration for soft tissue preservation [5, 19].
Antibiotic Spacer
In two-stage revision arthroplasty, an antibioticloaded cement spacer can be used to provide
localized, highly concentrated antibiotic administration. In certain cases, an antibiotic-loaded
cement spacer may also serve as a denitive and
permanent treatment option [7, 19]. The aim is to
eliminate the infection while maintaining a functional, pain-free joint shoulder. Complications of
permanent spacer, however, include erosion of
the glenoid and humeral components, as well as
potential problems associated with spacer fracture and rotation [35].
Resection Arthroplasty
In cases where the patient’s medical comorbidities or technical complexity make revision with a
denitive implant too risky, resection arthroplasty serves as an acceptable salvage procedure
to eradicate shoulder PJI [17]. Although it
achieves a remarkable infection eradication rate
of over 90%, it is usually chosen for patients with
lower functional requirements as it provides less
favourable functional outcomes [5, 57–59].
Two-Stage Revision Arthroplasty
A two-stage replacement arthroplasty, which
includes removal of the implant, irrigation, and
debridement, followed by insertion of an antibiotic spacer and delayed re-implantation, has been
suggested as the “gold standard” for shoulder PJI
[19, 22]. If the microorganism responsible for the
infection is not known, this is strongly recommended. The rst step is to eradicate the infection
after removal of the prosthesis. Usually, a cement
spacer loaded with antibiotics is implanted and
general antibiotics are administered, adjusted
according to the microorganism identied later.
In case of persistent infection, an additive irrigation and debridement procedure may be proposed. In the re-implantation phase, inverse TSA
has become the implant of choice in recent years.
It offers several advantages, including the ability
to perform more extensive debridement in the
06/2021 inverse shoulder prosthesis
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