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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

366
A. Albani-Forneris et al.
inammatory reaction, the blood ow decreases
causing anoxia of the cartilage [9].
25.2.2 Etiology
In adults the most common causes of SA of the
hip joint are gram-positive organisms, being
Staphylococcus aureus responsible for about
37–56% of cases, especially in those patients suffering from uncontrolled diabetes or rheumatoid
arthritis (prevalence of up to 80% of infections).
In the latter group, polyarticular infections caused
by this bacterium are more prevalent. The
increase in cases of methicillin-resistant
Staphylococcus aureus (MRSA) strains, whose
sensitivity to antibiotics varies according to the
communities and in-hospital infections, is currently a cause for concern [3, 9]. Streptococcus
pyogenes (group A—Beta-haemolytic) is second
in frequency (8–16% of cases). In patients with
immunodeciency, and gastrointestinal or urinary tract infections, it is important to consider
group B, C, and G streptococci as potential
offending organisms. Gram-negative bacilli
should also be suspected in immunocompromised patients, as well as in the elderly population and intravenous drug users [10]. Following
inclusion in the immunization schedule, the incidence of Haemophilus inuenzae-joint infections
has decreased considerably in the neonatal and
pediatric population [11], as has in the adult population as well.
Mycobacterium tuberculosis-joint infections
are rare (2%), with chronic and silent presentations being the most common types, exhibiting
progressive, late symptoms similar to those of
primary osteoarthritis. Only about 50% of these
patients are found to have thoracic radiographs
with signs of tuberculosis infection. Therefore,
its diagnosis is late and advanced joint damage is
commonly seen [12].
Gonococcal septic arthritis was the main cause
of septic arthritis in young adults in the 80’s;
today its prevalence has fallen to 1% or less.
Some believe, however, that its incidence may
increase due to antibiotic resistance and current
sexual behaviors [13]. Women are mainly
affected, usually presenting with migratory polyarthritis. The isolation of gonococcus in cultures
is approximately 50%. Fortunately, treatment is
usually effective, and joint sequelae are rare [14].
25.2.3 Clinical Presentation
The clinical presentation of septic hip arthritis
can vary depending on age, the underlying cause
of the infection, the patient’s general health, and
immune status. However, some common signs
and symptoms of septic hip arthritis are: (i) pain
in the groin area, which is usually the most prominent symptom, is often severe, constant and
worsens with movement; (ii) fever, although
chills and high fever are unusual; (iii) limited
range of motion and stiffness; and (iiii) swelling
and local redness, with the adjacent skin being
warm. Weight-bearing is usually difcult with
the affected leg, with patients usually limping or
needing walking assistance. In some cases,
patients with septic hip arthritis are also likely to
experience systemic symptoms such as fatigue,
malaise, and loss of appetite. Due to joint effusion, the hip is usually exed, abducted, and
externally rotated, a position in which the joint
capsule has greater volume [10, 13].
25.2.4 Diagnosis
The gold standard for the diagnosis of native hip
arthritis is the conrmation of an offending
organism in the synovial uid by culture, for
which it is of paramount importance to perform
an arthrocentesis (i.e., hip joint aspiration) prior
to antibiotic treatment. The synovial uid (SF)
white blood-cell count (WBC) is usually
>50,000 cells/mm3 but its reported sensitivity
ranges from 53 to 100% with a specicity of
66%-97%. The polymorphonuclear leukocyte
ratio >90% has shown a sensitivity of 42–82%
and specicity of 67–89% [15]. Gram stain usually provides rapid results but its low sensitivity
of 45% limits its utility [16].
Elevated inammatory markers such as
C-reactive protein (CRP), erythrosedimentation

25 Native Hip Joint Infection
367
rate (ESD) in addition to serum WBC
>10,000 cells/mm3 are non-specic for the
diagnosis of septic arthritis, however, they are
very sensitive, and when correlated with the
patient's clinical picture and a synovial uid
WBC value of >50,000cells/mm3 the specicity increases and the combined sensitivity
reaches almost 100% [17]. Measurement of
CRP in synovial uid is as useful as serum
measurement, although it increases the specicity. Serum CRP >20mg/l is a strong independent risk factor for septic arthritis (odds ratio
81.9, p< 0.001) [18]. On the other hand, the
synovial CRP threshold seems to be around
10mg/l [19], similar to what has been described
for cases with periprosthetic joint infection
[20]. Recent studies have shown that the synovial uid and serum neutrophil-to- lymphocyte
ratio (SF- and SR-NLR), with a cut-off value of
25, had 78% sensitivity and 81% specicity in
the diagnosis of native hip arthritis. It seems to
be a very useful tool for diagnosis at no additional cost [21]. However, these results should
be validated in prospective studies.
Diagnostic imaging studies focus on identifying inammation, adjacent tissue involvement,
and joint damage. Sometimes, they are not able
to accurately differentiate whether it is an infectious or non-infectious cause. Ultrasonography
can evidence an increase in joint uid with very
low specicity but is very helpful in performing a
guided and safe arthrocentesis, which is almost
always needed. Radiographic images are useful
when compared with previous radiographs if they
are available, initially a widening of the joint
space and fat pad displacement can be visualized,
but in cases of late diagnosis, joint erosion and
space narrowing can be seen.
In cases where adjacent bone involvement is
suspected, magnetic resonance imaging (MRI)
is useful for diagnosis and for assessing the
extent of infection in adjacent tissue (Fig.25.1).
The area of the edema and inammation may
help the surgeon guide the extent of the debridement [22].
25.2.5 Dierential Diagnoses
When diagnosing SA it is important to consider
other differential diagnoses of pathologies with
acute mono- or oligo-articular involvement, such
as crystalloid arthritis, reactive arthritis, rheumatoid arthritis, and Lyme disease. Intra-articular
accumulation of monosodium urate crystals
(gout) or calcium pyrophosphate (pseudogout)
can produce symptoms similar to SA, thus being
the main diagnosis to be excluded. The diagnosis
is conrmed by direct visualization of crystals by
polarized light microscopy in synovial uid. In
patients with gout, high serum urate levels, the
presence of tophi as well as rst metatarsophalangeal joint involvement are useful to clinically
assess the diagnosis. However, the intra-articular
presence of crystals or the absence of positive
cultures does not denitively exclude the diagnosis of SA [23, 24].
Reactive arthritis occurs in patients with a history of gastrointestinal or genitourinary infections, usually after 2–4weeks. Joint symptoms
are caused by bacteria that share the characteristic of being intracellular organisms, such as
Chlamydia trachomatis (which has genitourinary
transmission). In these situations, treatment
should be symptomatic and the use of broadspectrum antibiotics is not recommended [25].
When symptoms are symmetrical and polyarticular, with three or more joints involved, often
affecting the joints of the hands and is associated
with morning stiffness, the diagnosis of rheumatoid arthritis should be considered [26]. However,
these patients are at increased risk for SA and
therefore should be suspected in cases that present with acute monoarticular symptoms.
Patients presenting with joint swelling and
pain who are inhabitants of or recent travelers
to areas where Lyme disease is endemic should
be suspected of B. burgdorferi infection. The
history of a slowly expanding skin lesion (ery-
thema migrans) at the site of a tick bite orients
the diagnosis which can be conrmed by serology [27].

368
Fig. 25.1 Radiographic
and magnetic resonance
imaging (MRI) of a
57-year-old female, with
a history of acute
myeloid leukemia under
prolonged treatment
with immunosuppressive
drugs. The patient
presented with fever and
severe pain in both hips
that increased with
weight bearing (she was
unable to walk).
Radiographs did not
show any acute
pathology. MRI revealed
abundant effusion,
cartilage erosion and
signs of atypical
insufciency fractures of
both hips. Positive
cultures for Klebsiella
pneumoniae after
bilateral hip joint
aspiration
A. Albani-Forneris et al.

25 Native Hip Joint Infection
369
25.2.6 Treatment
Septic arthritis is an orthopedic emergency, and
should not be delayed since its aggressive behavior leads to irreversible osteoarticular damage in
the short-term. Antibiotic treatment must always
be accompanied by surgical debridement of the
joint. Empirical antibiotic treatment must start
immediately without waiting for culture results.
Only after the offending germ has been identied, the antibiotic therapy should be targeted to
the specic germ. Surgical debridement can be
performed either open or arthroscopically. Hip
arthroscopy has proven to be a safe treatment
option for patients with acute native infection
[28]. However, this requires specic equipment
to be available at the orthopedic theater, as well
as specic surgical training and skills. For this
reason, the authors of this chapter recommend
performing the surgical debridement in an open
fashion, through a minimally invasive direct anterior (Hueter) approach, which provides straightforward access to the joint.
Given the high prevalence of methicillinresistant Staphylococcus aureus (MRSA) in the
community, an antibiotic effective against
MRSA, such as vancomycin, should always be
included [29]. Only in areas where methicillinsensitive strains are prevalent, cefazolin can be
used empirically. Patients with risk factors for
gram-negative bacteria such as those immunosuppressed, intravenous drug users, elderly, or
critically ill patients would benet from the
empirical use of antibiotics effective against
these germs. Under suspicion of disseminated
gonococcal disease, ceftriaxone should be used.
The duration of the antibiotic treatment is determined by the causal germ in case it is
identied.
If SA is diagnosed in a late scenario or chronically, then the benet of debridement and antibiotherapy remains unclear. Therefore, when
the hip joint presents with space narrowing at
index diagnosis or it has advanced cartilage
damage upon complementary imaging, one- or
two-stage total hip arthroplasty should be considered. Patients with a history of native joint
infections are at higher risk of periprosthetic
joint infection (PJI), especially smokers. Sultan
etal. showed that in patients with a history of
treated same- joint native septic arthritis, the
proportion of PJI was ve of 62 patients (8%).
The Kaplan-Meier analysis demonstrated overall survivorship free from PJI of 92% at
14.5 ± 1.14 years (95% condence interval
[CI]=12.3–16.8years) [30]. Surprisingly, failures were reported in the knee joint only,
whereas no cases of hips with previous native
hip arthritis had to be reoperated. However, it
has also been shown that less than a 1-year quiescent period after septic arthritis has been associated with 38-times increased risk and 22-times
risk for post-THA PJI, at 0 and 6months and 6
and 12 months, respectively [31]. Despite
patients undergoing THA 6months after their
septic arthritis treatment having a decreased risk
(compared to those between 0 and 6months),
the risks of further infection thereafter are still
high. Therefore, the authors of this chapter suggest doing a two-stage arthroplasty with an
articulating spacer in between to perform the
most aggressive debridement possible. Often,
delayed septic arthritis is diagnosed in patients
with a systemic infection that will have prolonged hospitalization times. Functional spacers
(Kiwi-type spacers) are especially useful in critically ill patients in which the time to the second
stage remains unknown [32] (Fig.25.2).

370
Fig. 25.2 Image of functional femoral spacer assembled to a polished stem, coated with antibiotic-loaded cement; and
postoperative radiographs of implanted bilateral functional spacers
A. Albani-Forneris et al.
25.3 Infection Following Hip Preservation Surgery
25.3.1 Hip Arthroscopy
25.3.1.1 Epidemiology
The overall estimated incidence of septic arthritis after hip arthroscopy is less than 1% [33],
ranging from 0% to 1.2% [34, 35]. Although the
frequency of this complication is higher in the
knee and the shoulder, the native hip is not an
exception. In very rare cases, abdominal or
scrotal infection may develop after uid effusion into those compartments in case increased
articular pressure is needed to perform the
arthroscopy [36].
The history of intra-articular anesthetic, cortisone injection, or contrast agents for enhanced
computed tomography or magnetic resonance
imaging, increases the risk of joint infection.
After analyzing a large administrative database,
Wang etal. dened the risk of post-hip arthroscopy infection by separating the population into
three groups based on the interval between
preoperative injection and ipsilateral hip arthros-
copy: <3months, 3–6months, 6–12months [35].
In this study, preoperative hip injection within
3months of hip arthroscopy was associated with
a higher risk of postoperative infection as compared to both privately insured and medicare controls (2.16%, odds ratio [OR] 6.1, P<.001; and
2.80%, OR 1.99, P=.037, respectively). This 2to 6-fold risk was not associated with any other
demographic risk factor.
Nonetheless, some other factors such as obesity, inammatory arthritis, chronic kidney disease, coronary artery disease, and depression
have been associated with post-hip arthroscopy
acute infection [37–40]. These factors, however,
had been associated with overall complications
and 30-day readmissions and not specically
with postoperative infection.
Surprisingly, the addition of hip arthroscopy
as an adjuvant procedure to other hip preservation surgeries such as periacetabular osteotomy
has not increased the complication rate of both
procedures when performed in isolation [41]. In a
prospective series of 248 hips analyzed by
Sabbag etal. [41] the authors described 3 cases
with postoperative infection and 1 additional case
which required haematoma exploration, being

25 Native Hip Joint Infection
371
such incidence below or in line with previously
described prevalence percentages of post-hip
arthroscopy infection.
Despite hip arthroscopy being increasingly
indicated and performed in the last 20years, evidence of antibiotic prophylaxis for this procedure has been under-reported [42]. In a recent
systematic review including 9 studies, which
comprised 592 patients, only 390 received routine antibiotic prophylaxis, while 160 patients
did not and 42 received prophylaxis only if an
additional implant was used [42]. This calls for
the development of Delphi-based guidelines on
antibiotic prophylaxis in hip arthroscopy specically. Despite being based on an arthroplastydriven study [43], the authors of this chapter
believe that prophylaxis should always be done
intravenously during anesthetic induction with
cefazolin, whenever possible. We believe that
one prophylactic dose of antibiotics is as effective as multiple doses [44, 45].
25.3.1.2 Diagnosis
Diagnosis of an acute infection following hip
arthroscopy is usually straightforward. Although
fever and chills may be absent, pain (when loading or rotating the hip) and persistent wound
drainage with elevated C-reactive protein and
erythrosedimentation rate are usually present. If
in doubt, hip joint aspiration should be performed
to obtain appropriate samples for culture, cytologic analysis (including percentage of polymorphonuclears and synovial C-reactive protein),
and physicochemical analysis. Whether doubt
persists following this algorithm, an open
debridement to obtain further samples should be
performed.
If diagnosis is performed after 4–6weeks, the
infection can be considered as chronic, with an
increased risk of failure of an eventual irrigation
and debridement procedure. In this scenario, the
senior author strongly recommends performing a
magnetic resonance imaging (STIR volume) [46]
to discard osteomyelitis and further plan a one- or
two-stage primary total hip replacement. This
helps determine the exact extension of the
intraosseous edema, being useful for preopera-
tive planning so that all regions affected by the
infection can be resected.
25.3.1.3 Dierential Diagnoses
Several situations may mimic an acute hip infection, although none of them usually presents with
excruciating pain and wound drainage. The following diagnoses should be strongly considered:
• Nerve damage, especially to the femorocutaneous or pudendal nerves
• Fluid extravasation, which may be associated
with massive wound drainage [47]
• Complex regional pain syndrome, previously
described after hip surgery [48]
• Ganglion cyst arising from the hip joint [49]
• Femoral neck fracture (prevalence, 0.08% to
0.12%) [50]
25.3.1.4 Treatment
In case of an acute infection, the authors of this
chapter suggest performing an open instead of
arthroscopic debridement through an extensile
anterior (Hueter) approach. This enables the surgeon to remove all brotic and necrotic, infected
tissue while preserving the vascularity of the
femoral head provided by the deep rami of the
medial femoral circumex artery. A ‘bikini’-type
incision can be performed connecting the anterolateral and mid-anterior portals in the most supercial plane, while the deeper dissection must be
done following the Hueter interval to reach the
hip joint.
There is, however, room for the indication of
arthroscopic treatment following an infected hip
arthroscopy [28, 51]. Lee etal. reported 9 patients
with native septic arthritis treated with
arthroscopic debridement without major complications and with only one of them with infection
relapse at a mean follow-up of 19.4months [52].
From the senior author’s point of view, arthroscopy can be especially better for treating infected
hip arthroscopy in the pediatric population, for
being less invasive and having good-to-excellent
functional and infection-free results at a minimum 2-year follow-up [53].

372
A. Albani-Forneris et al.
If a chronic infection is diagnosed, a primary
total hip arthroplasty is advocated, either in one or
two stages. In this scenario, there is no room for
an arthroscopic approach. Preferably, two stages
are recommended in order to perform a wide
debridement in the rst stage, with the removal of
all infected tissue including capsule, synovium,
subcutaneous tissue, and bone. If a posterior or a
lateral approach is chosen, the authors of this
chapter strongly recommend performing an anterior debridement at least through the arthroscopic
portals, since the infection is supposed to be ante-
riorly ’grounded’. Otherwise, an anterior approach
is preferred to excise the previous scars and
remove a sinus tract, if any. A case example is
shown in Figs.25.3, 25.4 and 25.5.
25.3.2 Periacetabular Osteotomy
25.3.2.1 Epidemiology
The rst description of the surgical technique and
outcomes of periacetabular osteotomy (PAO) was
performed by Ganz in 1988 [54]. Since that
Fig. 25.3 Radiographic and magnetic resonance imaging
(MRI) of a 26-year-old male who underwent right hip
arthroscopy due to femoroacetabular impingement at
another institution 1month before referral to our institution. The patient presented with excruciating pain, inabil-
ity to walk independently, and persistent wound drainage.
Radiographs evidenced chondral collapse with joint space
narrowing, while revealing massive effusion associated
with an anterior collection as well as bony acetabular and
femoral head edema

25 Native Hip Joint Infection
373
Fig. 25.4 Intraoperative images show massive drainage
of pus after performing an anterior approach joining both
arthroscopic portals, followed by resection of a compro-
report, the development of this technique has
been globalized and the indication has
substantially increased in the past 20 years, as
has the development of fellowship training in hip
preservation surgery. It has been further shown
that the more this procedure is performed, the
fewer complications are seen, especially after the
rst 40 PAOs [55]. In this concise report performed by Novais etal. that analyzed the surgeon’s learning curve, the three infections
detected (out of 81 cases, 3.7%) were associated
with extended surgical procedure time since the
median operative time was 320 minutes.
In a series of 238 PAOs operated between
1994 and 2008, only 3 cases (1.26%) developed a
deep infection that required open debridement
[56]. In a prospective multicenter study of 205
consecutive unilateral periacetabular osteotomies
performed at seven institutions by ten surgeons,
Zaltz et al. reported 2 patients (0.97%) that
required incision and drainage of a deep infec-
mised femoral head with chondral delamination and
implantation of an antibiotic-loaded spacer
tion, one of which required a primary hip replacement years after the PAO [57]. Likewise, in a
systematic review performed by Ali and Malviya
[58], the incidence of supercial infection was
1.03%, whereas deep infections represented
0.69%. While minimally invasive procedures had
not been associated with neither infection nor
wound complications, abductor-sparing modied
Smith-Petersen and two-incision approaches
were the most associated with this complication.
25.3.2.2 Diagnosis
Even though there is no specic research study
focusing on how to make an accurate diagnosis
of deep infection following hip preservation surgery, any wound with erythema and persistent
drainage should be inspected and eventually
explored. In the ‘Hip Arthroscopy’ section, the
authors suggest ordering blood work and performing aspiration of any suspicious collection if
there is any doubt.

374
A. Albani-Forneris et al.
Fig. 25.5 After 5weeks of the rst stage and following
normalization of the serum biomarkers, the patient underwent implantation of a short femoral neck-preserving
cementless stem and a cementless acetabular component
25.3.2.3 Classication
In 2012, Sink etal. published a modied DindoClavien classication adapted for hip preservation surgery to better classify complications
following surgery, with good-to-excellent intraand inter-observer reliability [59]. This has been
further validated for the pediatric population
undergoing hip preservation surgery [60].
In this classication, a supercial infection is
classied as grade 1, ‘without clinical relevance’.
On the other hand, a deep wound infection can be
classied as grade 2 if it only requires medical
treatment, or grade 3 if it needs ‘surgical therapy
or unplanned hospitalization’. The following
table (Table 25.1) depicts the Dindo-Clavien
with a ceramic-on-polyethylene bearing surface. The gure depicts both radiographic and intraoperative images
(right hip)
classication adjusted for PAO and other hippreserving surgeries [59, 61].
25.3.2.4 Treatment
A supercial wound infection following PAO can
be safely treated with oral antibiotics and observation. On the other hand, surgical debridement
is the gold standard for the treatment of a deep
infection. Sometimes, a new osteotomy of the
anterior-superior iliac spine is needed to evacuate
uid collection lying medially to the inner table.
Oral antibiotherapy is usually indicated unless a
multi-drug resistant bacteria is isolated, in which
case intravenous administration of antibiotics
may be needed.

25 Native Hip Joint Infection
375
Table 25.1 Dindo-Clavien classication adjusted for
PAO and other hip-preserving surgeries
Grade Complication
1. Complication without
clinical relevance
2. Complications treated with
conservative or medical
therapy (outpatient)
3. Complication treated with
surgery, intervention, or
requiring unplanned
readmission
4. Life-threatening
complication, requirement of
intensive care unit, or
requirement of salvage
procedure (total hip
replacement), or
complication not treatable
with potential for permanent
disability
5. Death –
Urinary tract
infection
Supercial wound
infection
Heterotopic
ossications grades
1–2 (Brooker)
Postoperative fever
Paraesthesia of
femoro-cutaneous
nerve
Transient
neuropraxia of the
femoral or sciatic
nerves
Blood loss (>5
blood conserves
administered)
Avulsion of the
anterior-superior
iliac spine
Trochanteric
delayed union
Stress fracture of
the ischium
Deep wound
infection
Haematoma
requiring evacuation
Migration of the
acetabular fragment
Revision surgery for
non-union
Heterotopic
ossication grades
3–4 (Brooker)
Intra-articular
osteotomy (fracture)
Trochanteric
non-union
Deep vein
thrombosis
Conversion to total
hip replacement
(necrosis of the
acetabular fragment
or femoral head)
Permanent nerve
injury
Pulmonary
embolism
Organ dysfunction
25.3.3 Surgical Hip Dislocation
25.3.3.1 Epidemiology
Infection following surgical hip dislocation
(SHD) is also a rare complication. In the rst
series described with this technique, no infections were reported in 213 hips [62]. In a retrospective multicenter study of complications
following SHD on 334 hips carried out before the
publication of Sink etal.’s classication of complications, only one (0.3%) deep infection was
found (treated with surgical debridement),
whereas two supercial wound infections (0.6%)
were diagnosed (and treated with observation
only) [63]. In other series, surgical site infections
were reported to be as high as 3.8% [64]. In the
setting of complex hip deformities, such complications are reported to be more prevalent, given
the extended surgical time required for appropriate correction [65]: supercial infection, 4.34%;
and deep infection, 2.17%.
When performing SHD for the treatment of
femoral head fractures, infection may arise and
be as high as 3.2%, being the most common complication following surgical treatment [66].
However, the modernization of this technique has
led to almost zero infections in cases where this
technique was performed by fellowship-trained
surgeons [67].
25.3.3.2 Classication, Diagnosis
andTreatment
The authors of the chapter suggest reading the
previous section (‘Periacetabular osteotomy’),
since classication, diagnosis, and treatment are
the same.
25.4 Infection Following Plating
or Nailing ofaPrevious Hip
Fracture
25.4.1 Epidemiology
Infection following failed xation after hip fracture is not uncommon despite many of them
being treated with minimally invasive approaches,
especially because such fractures occur in a very
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