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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

9 Osteoarticular Infections inAdults
107
Fig. 9.6 The trend of hospitalizations for bone tuberculosis at the Putti hospital in Cortina in the years. The x-axis
represents years from 1976 to 1995, and the y-axis represents the number of patients, ranging from 0 to 200. The
chart shows a general decline in the number of patients
over the years, with uctuations
Fig. 9.7 Pie chart illustating the percentage of localizations of tuberculous bone infections (specic) in different
part froma 1975 to 2015, totaling 4.473 cases, especially
joint. The largest segment is Spondylitis at 45.2%, followed by Coxitis at 16.9% and Gonylitis at 15.3%
Fig. 9.8 Pie chart illustrating the percentage of localizations of non- tuberculous bone infections (nonspecic)
cases from 1980 to 2015, totaling 3.713 cases. The most
important localizations involve the long bones and less so
the joints, including prosthetics
Table 9.1
highlighting characteristics of MB Atypical
Ruyon group organism
I (photochromogens) M. marinum
II (scotochromogens) M. szulgai
III (nonchromogens) M. intracellulare
IV (rapid growers) M. chelonei
The different laboratory microbiological
M. kansaii
M. gordonae
M. malmoense
M. xeopi, M. terrae
M. fortuitum
Fig. 9.9 Intradermal
Mantoux reaction. Is it a
subcutaneous
inoculation and on the
right positive reaction on
the test

108
F. Da Rin de Lorenzo
Fig. 9.10 Tine test. It is a system that olready has the
puried protein of the Mycobacterium inside it and is
applied directly tothe skin
Pyogenic infections are generally caused and
decreasing in percentage by:
• Staphylococcus aureus
• Staphylococcus epidermidis
• Gram-negative ora
• Pyocyanus or Pseudomonas aeruginosa
• Anaerobes
• Rarely Mycetes
The history in specic forms is not always helpful
unless the patient does not work in contact with meat
(e.g., butchers), has not recently had a pulmonary
tuberculosis episode, has not come into contact with a
tuberculosis patient, or does not come from areas
where tuberculosis is endemic. It should be considered that many patients have a calcied primary tuberculosis complex without any symptoms but have a
positive Mantoux (Fig.9.9) or Tine test (Fig.9.10).
The latter is a test consisting of a special disk equipped
with four tips previously immersed in a solution of
puried bacillary extracts completely free of toxic
action; the length of the tips is such as to inoculate a
standardized number of units of puried protein derivative, called PPD, into the dermis; after 48h the inoculation point is examined, where, in the event of a
positive reaction, an erythematous inltrate of proportional extension appears to individual sensitivity.
The tuberculin reaction becomes positive
4–6weeks after infection.
There is also the “Quantiferon” test [14, 15]. It
is a venous blood sample that is placed in test
tubes, which detects the quantity of interferon
gamma cytokine released following stimulation
Table 9.2
ease and nontuberculous bone disease
Anamnesis 10/30 12/19
Clinic 10/30 14/19
Radiographic situation 10/30 6/19
RMN scintigraphy
With marked leukocytes 12/19
Laboratory 6/30 19/19
Mantoux or tine test 28/30 ///////
Cultural examination 5/30 19/19
Biopsy/histology 19/30 ///////
Table 9.3
ease and non-tuberculous bone disease
Pain Insidious Acute
Fistolae Yes (attention
Edema Yes Yes
Thermotouch No Yes
Reddened skin No Yes
Functional
limitation
Deformity Yes Yes
Laboratory Very altered * Very
* TB test (hematologic)—lcs (pus a/o secreted)
** V.E.S.—PCR—Fibrinogen - Complete blood count with
formula
Comparison between tuberculous bone dis-
Specic
(tbc)
Comparison between tuberculous bone dis-
Specic Nonspecic
overinfection)
Yes Yes
Nonspecic
(piogenic)
Yes
altered **
of T lymphocytes with two specic TB antigens
(ESAT-6 and CFP-10) [16–18]. In fact, the laboratory tests are normally different; in the tuberculous form, the erythrocyte sedimentation rate
(ESR) and the PCR can be normal unless there is
a nonspecic superinfection. Therefore, the tests
are the TB test (hematological) and the LCx (in
the pus or in the pulmonary secretion). However,
ESR, C-reactive protein (CRP), and brinogen for
nonspecic forms are important. The biopsy as
well as the culture examination is very important.
We compared 30 cases of tuberculous arthritis
with 19 cases of pyogenic hematogenous arthritis
(Table 9.2) and we took into consideration, by
comparing them, the different characteristics [16,
19]. The medical history is important in the two
pathologies, especially if there was a previous
tuberculous episode, if the hygienic conditions
are reduced, if the patient has come into contact

9 Osteoarticular Infections inAdults
Fig. 9.11 Typical tuberculoma with central caseous
necrosis with the presence of Langerhans cells
Fig. 9.12 Culture of pus containing Staphylococcus
aureus
with a positive person, or if he has risk factors
that also concern the pyogenic forms.
The clinic (Table 9.3) highlights how the
tuberculous form does not have important septic
signs, in fact it does not present the classic signs
of inammation (color, rubor, and dolor et functio lesa) being a “cold” condition, the opposite of
the pyogenic pathology. Scintigraphy with
marked autologous leukocytes is fundamental for
the pyogenic form and less so for the tuberculous
form which can, however, give us false positives.
The laboratory with the classic signs of infection
is derisive for the pyogenic forms, less so for the
tuberculous ones. Generally, ESR, PCR, and
Fibrinogen were altered in all pyogenic forms
only in 1/3 in tuberculous ones. Mantoux and
Tine tests were positive in 28 cases. It should be
considered that the two cases were anergic subjects and therefore not immunologically active.
The culture examination did not allow us to isolate the mycobacterium in almost all cases but with
109
the biopsy (Fig.9.11) we managed to obtain all the
diagnoses for the tuberculous forms while the culture examination (Fig.9.12) for the pyogenic forms
highlighted 100% of the cases. However, it must be
considered that the negativity of the culture test is
not an indication of the absence of infection which
will be considered after having carried out the
entire set of assessments. In fact, the diagnosis is
not the outcome of a single piece of data but the
overall data collected.
Continuing the clinical comparison between the
two pathological forms, rst of all, the big difference
is the phlogistic aspect, which in the tuberculous
form does not present redness and is not hot to the
touch, as are the abscesses, which by denition are
dened as “cold.” Something completely different
for nonspecic forms. The TBC forms appear today,
so much modied in comparison with classical
tables that it is difcult to differentiate the two forms.
It is easy to have over-infections in TBC forms or
combinations of mixed forms, especially in the
super-infections of phytolized tuberculous forms.
Laboratory tests are fundamental for the diagnosis of tuberculosis and are the hematological
one, the Tb test (A 60) Serological diagnosis of
tbc—IgA, IgM, IgG counts (80% positive) [17]
and in the search for mycobacterium antigens in
pus or in the pulmonary secretion which is LCx
amplication mycobacteria’s gene (Ligase reaction at chain) (100% of validity and results are
available in 7days) [18]. The radiographic appearance of a tuberculous arthritic form can be divided
into four stages (Figs.9.13, 9.14, 9.15, and 9.16).
Fig. 9.13 A radiographic example of stage 1 tubercular
arthritis of the elbow with demineralization caused by
inammation of the synovial membrane

110
F. Da Rin de Lorenzo
Stage 1
Fig. 9.14 In the stage 2 is evident narrowing of the articular space due to initial destruction of the cartilage. In this
stage, the synovial membrane will hypertrophy and will
ll the articular space; bone erosion develops at the sites
where the articular capsule is attached
Stage 2
Stage 3
Fig. 9.16 In the stage 4 the further joint destruction with
disruption of the anatomical prole
Fig. 9.15 In the stage 3 the entire joint is affected and
presents many bone lesions, and the articular space is narrowing without serious anatomical destruction of the
articulation. In this stage, the joint space is lled with
hypertrophic synovial membrane and pus. The articular
cartilage, the capsule, and the ligaments are destroyed.
There could also be abscesses and stulas
Fig. 9.17 An apparently normal X-ray....
Stage 4
A radiological test that can help identify a
focus is the CT scan (Figs.9.17 and 9.18), especially in certain areas such as the pelvis or spine
or as in the following case, where the focus was
able to be localized in correspondence with the
olecranon area.

9 Osteoarticular Infections inAdults
111
Fig. 9.20 … but on MRI, there are epiphyseal septic foci
Fig. 9.18 … but the CT images showing a focus in the
olecranon site
Fig. 9.19 An apparently normal X-ray of the shoulder …
Fig. 9.21 A scintigraphy with autologous labeled leuko-
cytes showing septic arthritis of the left elbow while the
right elbow is normal
Nuclear magnetic resonance (MRI) (Figs.9.19
and 9.20) [19] is very important because it allows
us to identify any septic foci as in the following
case, where on the X-ray everything appears normal and instead on the MRI some epiphyseal foci
appear.
Furthermore, scintigraphy (Fig. 9.21) with
autologous labeled leukocytes.
It should be considered that these radiological
tests (conventional radiography, CT scan, MRI,
and scintigraphy with technetium) are not specic for the differential diagnosis between the
various joint septic forms, but indicate the presence of a septic focus and not the type of infection.
The most important test for a differential diagnosis is endoarticular aspiration and biopsy.

112
F. Da Rin de Lorenzo
Fig. 9.22 An example of a tuberculous form of the wrist treated with cortisone for the diagnosis of rheumatoid arthritis
that has evolved into carpitis [19. 22]
The biopsy can be performed in joints such as
the hip, knee, ankle, shoulder, and wrist, even
arthroscopically, which allows the precise collection of any material from the site of the focus, but
9.1 Antibiotic Therapy
forOsteoarticular
Tuberculosis (Table9.4) [22]
also capsular parts.
The differential diagnosis [20, 21] in tubercu-
losis pathology is made above all on a percentage
basis, from top to bottom, with:
In our experience, we have adopted a local and a
general therapy. The rst consists of 3-weekcycles
on alternate days where the antibiotic is introduced into the affected joint by inltration, which
• Non-tuberculous mycobacteria
• Pyogenic arthritis
• Rheumatoid arthritis (Fig.9.22) [19].
• Osteomyelitis
• Fungal arthritis
• Viral infections
• Sero-negative arthritis
• Gout
• Pseudodogout
is removed from the general therapy [23–26].
The general therapy is daily, being a therapy with
various antibiotics. Therefore, isonicotinic acid,
ethambutol, and streptomycin are used to inltrate while rifampicin (600mg) is given orally in
the morning on an empty stomach with a glass of
water to avoid enzymatic induction, which creates drug-induced hepatitis. Recently, it is common to give Rifater ® which contains 50mg of
isoniazid, 120mg of rifampicin, and 300mg of
We must always suspect a tuberculous form
when faced with an X-ray with osteopenia, a
reduction in the joint rim, and possibly if there
are irregularities on the joint edges, such as nail
marks (Phemister’s Triad) [4, 18].
pyrazinamide. It is used to administer 3–6 tablets
per day, which must be taken all together on an
empty stomach and 1–2 h before meals with a
little water. This description of antibiotic therapy
concerns adults.

9 Osteoarticular Infections inAdults
113
Table 9.4
Drug
Isoniazid 5 (4–6) 300 10 (8–12) 900
Rifampicin 10 (8–12) 600 10 (8–12) 600
Pyrazinamide 25 (20–30) – 35 (30–40) –
Ethambutol 15 (15–20) – 30 (25–35) –
Streptomycin
a
Patients aged over 60years may not be able to tolerate more than 500–750mg daily, so some guidelines recommend
reduction of the dose to 10mg/kg per day in patients in this age group (2). Patients weighing less than 50kg may not
tolearate doses above 500–750mg daily (WHO Model Formulary 2008, www.who.int/selection_medicines/list/en/)
are obviously not the same. Antibiotic therapy
can last from 6months to 18months.
ney function must be checked because these antibiotics can cause damage to the optic nerve [27] and/
or acoustic and renal and hepatic dysfunction.
is very important because there are some forms
that are resistant to common antituberculosis
drugs but sensitive to antibiotics used for pyogenic forms [22]. We will now deal with some
localizations, always comparing the tuberculous
forms with the pyogenic ones.
Recommended doses of rst line antituberculosis drugs for adult
Recommended dose
Daily 3 times per week
Dose and range
(mg/kg body weight)
a
15 (12–18) 15 (12–18) 1000
For children, the dosages and antibiotic drugs
Maximum
(mg)
acute forms generally consists of an arthrotomy,
associated with surgical cleaning, especially of
the soft parts, and the application of drains for
Visual and auditory function and liver and kid-
continuous washing for 7–10 days (Fig. 9.25).
On the same occasion, samples can be taken for
histological examination and analysis of the collected liquid.
Table 9.4 The antibiogram of mycobacterium
started immediately while awaiting the results of
the culture tests and the antibiogram associated
with anti-inammatories and antipyretics. Bear in
mind that the results of the samples, if it is tuberculosis, can be obtained even after 10–15days.
Rest, the use of braces to avoid direct load which
Dose and range
(mg/kg body weight)
Daily maximum
(mg)
Treatment with broad-spectrum antibiotics is
must be maintained for at least a month. In our
experience we have used, in cases in which a pos-
9.2 Locations
sible joint collapse was suspected, mobilizations
with trans-skeletal traction, in others cases of
9.2.1 Tuberculous Arthritis
oftheHip (Coxitis) 16.9% TB
and8.6% Pyogenic [28–34]
active and passive mobilizations with the help of
the physiotherapist. If the diagnosis results in a
tuberculous form, antibiotic therapy (multidrug
therapy) [1] must be started immediately and conFor diagnosis, in addition to what has been seen
previously, it is important to carry out an arthrocentesis which, as we have said, needs to be
ultrasound- guided (Figs. 9.23 and 9.24), as the
joint is in depth and it is also useful if you want to
reach a possible outbreak or spill.
The symptoms of septic arthritis usually
appear rapidly and include acute pain in the groin
region, swelling and local heat associated with
evening fever but chills, tiredness, and generalized weakness, inability to move the limb may
also be present, and the inability to walk with
weight on the affected limb. The treatment of
tinued for at least a year. Instead, if it is a form, for
example, staphylococcal, the therapy, usually with
two antibiotics, must be continued for 6–8weeks,
the same treatment if we are faced with a mycobacterium resistant to antitubercular drugs.
Infection of a joint at a young age very often
leads, if not treated with the utmost urgency, to
the complete destruction of the joint itself. The
reinfection rate on prostheses applied in septic
arthritis if caused by Gram-negative germs is
20%. In TB of 40%, therefore, we believe that the
objective is to perform the prosthesis in two
stages [35]. In tuberculous forms, as the biolm

114
Fig. 9.23 Ultrasound that highlights an abscess near the femoral epiphysis, that can be aspirated under ultrasound
guidance
F. Da Rin de Lorenzo
Fig. 9.24 The aspiration of the material that will be
examined
is missing, it is possible to restore the prosthesis
in one stage [35–40] but we prefer to do it in two
stages, trying to save the bone structures as much
as possible [33]. For the prosthesis of pyogenic
septic arthritis, once an irreparable lesion has
been created in the joint, we intervene by applying a prosthesis and as we have said in our experience, we do it in two stages.
If we carry out an excellent surgical cleaning,
we are a little more economical because we want to
maintain the vascularization of the neck as much as
possible as highlighted in the following case:
A 35-year-old male patient who complained
of severe pain and was treated with antibiotics
Fig. 9.25 Arthrotomy and surgical cleaning with application of drains for continuous washing. A DAIR on a the
tubercular form
without carrying out emptying and drainage and
also favoring weight bearing, and, therefore, as a
result, we had osteolysis of the cup and lysis of
the epiphyseal area (Fig.9.26a–b). Upon arthrocentesis, it was found to be Mycobacterium hom-
inis. Blood tests showed an ESR of 28 and CRP
was normal.

9 Osteoarticular Infections inAdults
a b
115
Pelvis
Destroyed
cartilage
Fig. 9.26a–b (Fig.9.26a) An X-ray showing septic arthritis and the drawing (Fig.9.26b) reproducing the pathological
condition of the hip arthritis
Infected
synovial fluid
Femur
Joint capsule
After two cycles of general and local antibiotic therapy, it was decided to carry out the prosthetic surgery in two stages. Therefore, removal
of the femoral epiphysis, cleaning and reaming of
the cotyle. Cleaning of the remaining part of the
neck and multiple samples, both in the central
areas and in the remaining neck, for culture
examination and antibiogram. A self-made spacer
was then applied with the addition of two antituberculosis drugs:
Rifampicin………10%
Streptomycin……5%
(The percentage is related to 40 g of polymethylmethacrylate powder)
Radiographic data to consider is the osteopenia of the hip and epiphyseal wormholes, as well
as reduction of the joint rim (Phemister’s Triad)
(Fig.9.27) [32, 33].
After 60days with negative culture tests, negative laboratory tests, and an almost normal local
clinical appearance, the second surgical stage is
performed: removal of the spacer (Fig.9.28) and
application prosthesis (Fig.9.29).
Also, on this occasion, samples are taken for
culture and antibiogram examination, and the
spacer is sent to the laboratory to carry out the
microbiological research test with dithiothreitol,
which did not reveal any germs or mycobacteria.
Another case of a 45-year-old male patient
presenting with coxalgia that arose after a 10-day
feverish period with episodes of 40° resistant to
antipyretics and antibiotics given by his doctor.
Fig. 9.27 Radiographic appearance with the antibiotic
spacer
Fig. 9.28 Surgical removal of the antibiotic spacer
Laboratory tests reveal a signicant alteration of
ESR, CRP, and brinogen as well as an increase
in neutrophils.

116
F. Da Rin de Lorenzo
Fig. 9.31 X-ray of surgical cleaning and application of
antibiotic spacer
Fig. 9.29 X-ray 10 years later, the result remained
unchanged, and the tuberculosis has never reactivated
Fig. 9.30 X-ray of suspected septic arthritis of the right
hip but only if we nd the germ we understand wath type
of infection it is and its sensitivity to antibiotics
The differential diagnosis includes tuberculosis, arthrosis, or chondrolysis, but see the comparison with the contralateral hip (Fig.9.30). The
arthrocentesis performed resulted in a pyogenic
form due to Staphylococcus aureus.
Therefore, after a period of remediation, we
decided to intervene in two stages.
Application of antibiotic spacer (Fig. 9.31)
added with antibiotics according to the sensitivity of the antibiogram:
Vancomycin….0.10% Imipenem………0.5%
Cefotaxime…….0.5%, always in realtion to
the cement powerd.
After 4 weeks, still under local and general
antibiotic therapy, the spacer was removed and
the neck-sparing prosthesis was applied
(Figs.9.32 and 9.33).
Why did we use the neck-sparing prosthesis?
Because its characteristic is to save the neck
bone, but also to leave good vascularity, as can be
seen from Drawing 9.1.
This would help the arrival of antibiotics and
cells predisposed to the immunological action
against germs, especially at the site of
implantation of the stem on the resected edge,
where the previous infection was located.
Some other considerations must be added
regarding tuberculosis of the hip, namely that it is
a disease that does not produce biolm, so much
so that some authors apply the prosthesis at one
time even if the infection is active because they
believe that after having done a resection, careful
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