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9 Osteoarticular Infections inAdults
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Chronic Osteomyelitis
YangguanWu andDavidJoseph
10
10.1 Introduction
Chronic osteomyelitis, a long-lasting inammation of the bone and surrounding tissue due to
infection by microorganisms, has been around
for a long time. Evidence of this disease in animals dates back hundreds of millions of years
[3], and discussions about human osteomyelitis
can be traced back to the era of Hippocrates
(460–370 BC). Over the years, various terms
were used to describe bone infection until
Nelaton introduced the term “osteomyelitis” in
1844 [3].
Historically, the treatment for osteomyelitis
prior to 1976 [4–8] involved a series of steps:
sequential debridement, saucing, packing, healing by secondary intention, bypass open bone
grafting, followed by prolonged antibiotic therapy [9–12] and long-term external support using
orthotics and casts [4, 7, 13, 14]. Bone infection
was often tolerated because methods for restoring hard and soft tissue decits were unreliable.
Surgeons were hesitant to remove all infected
segments due to the fear of causing fractures, loss
of function, and even death. As a result, the criteria for selecting patients for limb salvage were
restrictive. Debridement was only intralesional.
Y. Wu (*) · D. Joseph
Department of Orthopedic Surgery, Elmhurst
Hospital Center, Icahn School of Medicine,
NY, New York, USA
e-mail: wuyang@nychhc.org; Josedav@nychhc.org
Deciencies in wound healing and persistent
infections contributed to a low treatment success
rate (50–70%) [4, 7, 14].
However, the treatment of chronic osteomyelitis has evolved rapidly over the past three
decades. The development of methods to counter
biolm formation, a key mechanism in pathogen
colonization of wounds, has been instrumental in
shaping modern treatment protocols [15–29].
With the advent of limb salvage protocols,
more than 90% of patients with chronic osteomyelitis can now be successfully treated [30–31].
This is particularly impressive given the increasing number of patients with multiple comorbidities that affect wound healing.
Innovations in technology have led to new
xation strategies, such as locking plates and retrograde nails, and improved methods of detecting
and isolating biolm pathogens [32–35]. The
development of antimicrobial agents for resistant
pathogen strains and innovative approaches to
open wound treatment, such as vacuum-assisted
closure [36, 37], has broadened the selection criteria for treatment and provided a basis for limb
salvage following debridement [38–43].
The successful use of antibiotic depot protocols before nal reconstruction has ushered in a
new era of treating chronic osteomyelitis with
staged treatment protocols [44–48]. This process
parallels the staging and treatment of musculoskeletal tumors and requires the same precision
and foresight [49–52].
© 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_10
129
130
Y. Wu and D. Joseph
The prospect of successful reconstruction following infection has helped to overcome early
fears of treatment failure among orthopedic surgeons and has provided the condence to perform thorough debridement [53]. The
maintenance or restoration of a competent soft
tissue envelope facilitates re-exposure, contains
and concentrates locally released antibiotics,
revascularizes bone and tendon grafts, and prevents secondary colonization of the wounds.
A currently proposed treatment algorithm for
chronic osteomyelitis includes thorough debridement with local antibiotic depots that preserve
length, safeguard early wound closure, maintain
working dead space, and prepare the wound for
reconstruction [54–60]. This is followed by a
staged reconstruction strategy tailored to the
location, size of soft and bony defects, local soft
tissue and vascular supply, and the patient’s overall physiological status.
10.2 Etiology
The etiology of this condition is multifactorial,
involving a complex interplay of host factors,
microbial pathogens, and environmental inuences. Understanding the underlying causes of
chronic osteomyelitis is crucial for effectively
managing and preventing this challenging disease [61].
Host factors play a signicant role in the
development of chronic osteomyelitis. Patients
with compromised immune systems, such as
those with diabetes, HIV/AIDS, or autoimmune
disorders, are at increased risk of developing
chronic osteomyelitis. Additionally, individuals
with vascular insufciency or peripheral neuropathy are more susceptible to bone infections due
to impaired blood ow and sensation in the
affected area. These host factors create an environment conducive to bacterial colonization and
proliferation within the bone tissue, leading to
chronic inammation and bone destruction [62].
Microbial pathogens are another key component in the etiology of chronic osteomyelitis. The
most common causative agents of chronic osteomyelitis are Staphylococcus aureus and
Pseudomonas aeruginosa, although many other
bacteria, fungi, and even mycobacteria can also
be implicated. These pathogens can enter the
bone tissue through direct trauma, surgical procedures, or hematogenous spread from other sites
of infection. Once inside the bone, the pathogens
form biolms, complex communities of bacteria
encased in a protective matrix that resist host
immune defenses and antibiotic therapy. The
presence of biolms contributes to the chronicity
of osteomyelitis by allowing the bacteria to persist and evade eradication [63].
Environmental inuences, such as poor
wound care, inadequate antibiotic therapy, and
foreign body implantation, can also contribute to
the development of chronic osteomyelitis.
Improper management of acute osteomyelitis or
failure to address underlying risk factors can
lead to the progression of the infection to a
chronic state. Inadequate blood supply to the
affected bone, either due to trauma or underlying
vascular disease, can impair the delivery of
immune cells and antibiotics to the site of infection, further complicating the treatment of
chronic osteomyelitis [64].
10.3 Epidemiology
The epidemiological landscape of osteomyelitis
in the United States is complex and multifaceted
[65–70]. While the incidence remains elusive,
estimates suggest a rate as high as 1in 675 hospital admissions perannum, translating to approximately 50,000 cases yearly. Further studies
indicate an overall incidence of 21.8 cases per
100,000 person-years [66].
Interestingly, the incidence appears disproportionately higher in males, although the underlying reasons for this disparity remain unclear. Age
is another signicant factor, with incidence rates
escalating primarily due to the increased prevalence of comorbid conditions such as diabetes
mellitus and peripheral vascular disease in older
populations [66].
The advent of advanced imaging modalities,
including magnetic resonance imaging (MRI)
and bone scintigraphy, has markedly enhanced
10 Chronic Osteomyelitis
131
our diagnostic capabilities and our understanding
of the infection’s characteristics [67].
In 2004 alone, the United States witnessed
over 110,000 infections stemming from nearly
600,000 articial joint replacements and two million internal fracture xations. The nancial
implications are substantial, with the treatment of
implant-related chronic osteomyelitis (COM)
projected to cost US hospitals $1.62 billion by
2020 [67].
Moreover, the intersection of osteomyelitis
with other conditions presents additional challenges. For instance, chronic diabetic foot ulcers
can become infected and lead to diabetic foot
osteomyelitis, thereby elevating mortality rates
and amputation risks [68].
In summary, osteomyelitis poses a signicant
public health challenge. It burdens the healthcare
system considerably, underscoring the critical
need for early detection strategies and effective
treatment protocols to manage this condition
optimally [69–70].
10.4 Pathophysiology
The pathophysiology of chronic osteomyelitis
involves a complex interplay of host immune
response, bacterial virulence factors, and bone
remodeling processes [61].
The initial stage of chronic osteomyelitis
begins with introduction of bacteria into the bone
tissue through direct trauma, surgery, or hematogenous spread. Once inside the bone, bacteria
adhere to the bone matrix and form biolms [18],
which protect host immune defenses and antibiotics [1, 2]. The biolm structure allows bacteria
to evade phagocytosis by immune cells and
establish a chronic infection within the bone [1,
2, 62–64].
The host immune response to chronic osteomyelitis is characterized by a persistent inammatory reaction involving the recruitment of
immune cells such as neutrophils, macrophages,
and lymphocytes to the site of infection. These
immune cells release pro-inammatory cytokines
and chemokines, leading to further tissue damage
and bone resorption. Chronic inammation also
disrupts the normal bone remodeling process,
impairing bone healing and increasing susceptibility to recurrent infections [62–64].
Bacterial virulence factors play a crucial role
in the pathogenesis of chronic osteomyelitis.
Some bacteria, such as Staphylococcus aureus,
produce toxins and enzymes that facilitate tissue
invasion and immune evasion. These virulence
factors contribute to the formation of biolms
and establish a chronic infection within the bone.
In addition, some bacteria can persist within host
cells, further complicating the treatment of
chronic osteomyelitis [62–64].
Biolms are structured communities of bacteria embedded in a self-produced extracellular
matrix consisting of polysaccharides, proteins,
and nucleic acids. Forming biolms is a critical
factor in the pathogenesis of chronic osteomyelitis, as biolms provide a protective environment
for bacteria, allowing them to evade both the host
immune response and antibiotic treatment [1, 2].
The biolm formation process in chronic
osteomyelitis typically involves several stages,
including the initial attachment of planktonic
bacteria to the bone surface, followed by the proliferation and maturation of the biolm [71]. This
maturation phase is crucial, enhancing the biolm’s structural integrity and antibiotic resistance. Studies have shown that biolms can
signicantly reduce the efcacy of antibiotic
treatments, as the bacteria within biolms exhibit
altered metabolic states and gene expression proles that confer increased resistance [72, 73]. For
instance, S. aureus biolms harbor mutant forms
and minor colony variants that complicate treatment efforts [72].
Moreover, the presence of biolms in osteomyelitis is associated with various clinical challenges, including the need for surgical
intervention to remove infected tissue or implants
[74]. The chronic nature of these infections often
leads to repeated episodes of inammation and
bone destruction, exacerbated by the biolm’s
ability to persist in a dormant state, allowing for
recurrence even after seemingly successful treatment [1, 2, 75, 76]. This persistence is particularly problematic in patients with compromised
immune systems or those with underlying
132
Y. Wu and D. Joseph
conditions such as diabetes, which can predispose them to chronic infections [73].
The pathophysiology of chronic osteomyelitis
also involves alterations in bone metabolism and
remodeling. Chronic inammation and infection
disrupt the balance between bone formation and
resorption, leading to bone destruction and necrosis. The release of inammatory mediators and
cytokines further exacerbates bone loss and
impairs healing. As a result, patients with chronic
osteomyelitis often experience persistent pain,
deformity, and functional impairment [61].
10.5 Clinical Evaluation
andDiagnosis
Diagnosing chronic osteomyelitis requires a thorough history and physical examination, as well as
imaging studies and laboratory tests to conrm
the presence of infection [61].
10.6 History andPhysical
History taking in patients with suspected
chronic osteomyelitis should focus on identifying risk factors for infection, such as recent
trauma, surgery, or the presence of underlying
medical conditions that may predispose to bone
infections. Patients may report persistent pain,
swelling, and drainage from the affected area
and systemic symptoms such as fever, chills,
and malaise. A detailed history of previous
treatments, including antibiotics and surgical
interventions, is essential for further management [61, 62].
Physical examination of patients with chronic
osteomyelitis typically reveals localized tenderness, swelling, and erythema over the affected
bone. Sinus tracts, draining wounds, or exposed
bone may also be noted. In some cases, the
affected limb may be warm to the touch, with
limited range of motion and muscle weakness.
Careful inspection of the skin and soft tissues
surrounding the affected bone is important to
assess for signs of cellulitis or abscess formation
[61, 62, 77].
Physical examination should also include in
the vascular status, deformity, and functional
impairment because of the disease. This information helps clinical decision-making.
10.7 Laboratory Test
The test pertains to the diagnostic procedures
employed in detecting and monitoring osteomyelitis, a bone infection. Here are the key
points [78]:
Complete Blood Counts (CBCs): These are
crucial in detecting acute infections, where an
increase in white blood cells, or leukocytosis, is
observed. However, the white blood cell count
may remain within normal ranges in chronic
osteomyelitis cases.
Inammatory Markers: Erythrocyte
Sedimentation Rate (ESR) and serum C-reactive
protein (CRP) escalate during the acute phase of
infection and postsurgical intervention. These
markers peak on the third and fth days following manipulation, respectively.
Normalization of CRP and ESR: CRP levels
typically revert to baseline within 3weeks, while
ESR normalization is more protracted than
CRP.A resurgence in CRP levels 3days postsurgical intervention or at the commencement of
antibiotic therapy could indicate a relapse or
unsuccessful treatment. These tests play a pivotal
role in diagnosing and monitoring osteomyelitis.
However, it is nonspecic because elevated levels
of both CRP concentration and ESR can occur
due to factors unrelated to osteomyelitis.
Several biomarkers have been studied for their
diagnostic value in chronic osteomyelitis, including interleukin-6 (IL-6), defensins, calmodulin,
and D-dimer [79–82].
IL-6 is a pro-inammatory cytokine that plays
a key role in the immune response to infection
and inammation. Studies have shown that elevated levels of IL-6 are associated with chronic
osteomyelitis, making it a potentially useful biomarker for diagnosing the condition. However,
IL-6 is not specic to osteomyelitis and can be
elevated in other inammatory conditions, limiting its diagnostic value [79].
10 Chronic Osteomyelitis
133
Defensins are antimicrobial peptides that have
been implicated in the pathogenesis of chronic
osteomyelitis. Studies have shown that defensin
levels are elevated in patients with chronic osteomyelitis, suggesting a potential role as a diagnostic biomarker. However, further research is
needed to validate the diagnostic value of defensins in this context [80].
Calmodulin is a calcium-binding protein that
regulates various cellular processes, including
inammation and immune response. Studies
have shown that calmodulin levels are altered in
patients with chronic osteomyelitis, indicating a
potential role as a diagnostic biomarker. However,
more research is needed to establish the diagnostic accuracy of calmodulin in chronic osteomyelitis [81].
D-dimer is a brin degradation product that is
elevated in conditions associated with hypercoagulability and inammation, such as chronic
osteomyelitis. Studies have shown that elevated
D-dimer levels are associated with chronic osteomyelitis, suggesting a potential role as a diagnostic biomarker. However, D-dimer is not specic
to osteomyelitis and can be elevated in other conditions, limiting its diagnostic value [82].
In conclusion, IL-6, defensins, calmodulin,
and D-dimer are promising biomarkers for diagnosing chronic osteomyelitis. However, further
research is needed to validate their diagnostic
accuracy and establish their clinical utility in this
context.
Laboratory results are also important, offering
insights into patient comorbidities that may
impact metabolic, immune, or hematopoietic
function [61].
10.8 Diagnostic Radiology
Radiological Findings: Radiological ndings are
typically inconclusive during the initial 2weeks
of hematogenous osteomyelitis, considered the
disease’s acute phase. A fracture, bone callus, or
surgical implant can obscure the detection of specic infectious indicators. In contrast, during the
late phase of chronic osteomyelitis, there may be
unusually well-localized local bone rarefactions
or lytic lesions following the destruction of
50–75% of the bone matrix. Other abnormalities
that may be observed include visible bone
sequestration, bone sclerosis, neoformation, and
cortical thickening, periosteal reaction, and sinus
tract [77].
Bone Scintigraphy: This diagnostic technique
has proven to be valuable for osteomyelitis
screening and early diagnosis. It utilizes technetium- 99 or indium-labeled white blood cells or
gallium-67, markers of bone marrow activity, to
highlight areas of inammatory activity.
However, there is ongoing debate regarding
which marker would be most sensitive for the
early detection of osteomyelitis [83].
Computed Tomography (CT): CT scans can
help determine how much bone fragment is
involved and extended into soft tissues. CT also
provides a more detailed characterization of bone
sequestration. They offer comprehensive images
of the cortical bone layer, the status of the bone
union, bony integrity, and volume. Incorporating
deep learning into CT imaging has enhanced its
sensitivity and specicity in diagnosing chronic
osteomyelitis [84].
Magnetic Resonance Imaging (MRI): MRI
provides an in-depth study of the extent of the
infection, including its impact on soft tissues.
It enables earlier detection of acute changes
when simple segmental radiographs are normal. In chronic infections, periosteal reactions
can be more accurately veried by visualizing
lamellar thickening or “Codman triangle” formation. MRI is a valuable tool for staging
[85–87].
Positron Emission Tomography (PET) Scan:
PET scan with the 2-[18F]-uoro-2-deoxy-Dglucose (FDG) marker is another promising
imaging modality, with high sensitivity (approximately 95%) and specicity (75–99%). PET
Scan provides 3D precision, which helps target
disease in surgery for complete eradication.
However, this method is limited by its low availability and high cost [88].
134
Y. Wu and D. Joseph
10.9 Bone Biopsy
andIdentication
ofthePathogen
A bone biopsy is recognized as the denitive
method for diagnosing chronic osteomyelitis.
The presence of necrotic bone and the replacement of trabecular bone with brous tissue inltrated by inammatory cells can facilitate the
diagnosis of chronic osteomyelitis, even without
microorganism isolation. However, isolating a
microorganism from a biopsy substantiates the
diagnosis and is pivotal in determining the appropriate systemic antimicrobial therapy [89].
Isolation can be achieved through blood cultures, although this method is only validated in
acute hematogenous osteomyelitis due to its low
yield in a chronic setting. Material obtained from
an open sinus tract or other open wounds by
swabbing may yield misleading results, as the
isolates may include nonpathogenic microorganisms that are colonizing the site [89].
Bone biopsies can be performed percutaneously with the assistance of CT or ultrasonography or via an open biopsy during surgery. Open
biopsy is often preferred due to the low yield of
percutaneous procedures. When bone biopsies
are conducted, it is essential that the samples are
processed for both aerobic and anaerobic cultures. If commonly cultured microorganisms are
absent and the clinical features are compatible,
mycobacterial and fungal culture samples should
also be taken and processed [89].
In chronic osteomyelitis culture, many biopsies yield negative results due to long-term antibiotic use and biolm formation. To maximize
diagnostic yield, it was previously recommended
that antibiotics be stopped 48h to 14days prebiopsy, although there is no consensus on this in
the current literature. The specimens should be
obtained from up to ve sites centered around the
disease nidus at the time of debridement [90].
Sonication of dead bone, surrounding tissue,
and implanted hardware, extending incubation to
at least 14 days, has been reported to increase
microbial isolation yields. Mycobacterial cultures take about 6weeks (approximately one and
a half months) to yield results [35, 91, 92].
Recent studies have focused on molecular
biology approaches to detect microbial colonization. One advantage of molecular methods for
microbial detection is that antibiotic therapy does
not affect their results. Techniques such as nextgeneration sequencing, including 16S rRNA
gene proling, have detected fracture-associated
microbiomes in persistent nonunion in 77% of
patients not detected by traditional culture [93].
Specimens obtained for histopathology, either
by biopsy or during surgery as frozen sections,
are also crucial because the presence of neutrophils in signicant amounts indicates infection.
More than ve neutrophils per high-power eld
indicate infection, with a sensitivity of 43–84%
and specicity of 93–97%. Visualization of granulomatous lesions with positive Ziehl-Neelsen
staining can lead to the diagnosis of mycobacterial infection earlier than culture results [91].
10.10 Classication oftheHost
andDisease
The primary objective of any treatment is to
improve the patient’s quality of life. Factors that
guide patient selection include the effect of the
infection on the patient’s physiological wellbeing and the degree of physical disability caused
by the disease. Pain that results in dysfunction
and recurrent episodes of sepsis are strong indicators for surgical intervention. The CiernyMader classication system, established in 1983,
lays down a pioneering framework for understanding the natural history of osteomyelitis, outlining treatment protocols and predicting
outcomes [3, 19, 61]. This system categorizes the
disease into three host cohorts and four anatomic
types of infection, organized sequentially to
denote disease complexity and its associated
level of treatment strategy [29].
10.11 The Host
The physiological health of a patient is a crucial
factor in determining their eligibility for treatment. A patient must possess the physiological
10 Chronic Osteomyelitis
135
capacity to resist infection, heal surgical wounds,
and withstand the metabolic and psychological
stress of sequential procedures, substantial blood
loss, and extended hospital stays.
Patients are categorized into three physiological classes based on their health status and the
disability caused by their disease (Table10.1):
1. Class A Hosts: These are healthy individuals
with a normal response to stress, trauma, and
infection.
2. Class B Hosts: These patients have comor-
bidities that inherently impair wound healing
and their response to treatment.
3. Class C Hosts: These are patients for whom
the potential morbidity or functional loss
resulting from treatment may exceed the
impact of the disease on their quality of life.
Observation or palliation alone may be the
preferred course of action for such patients
[59, 62, 63]. However, if their condition
improves or advancements in medical technology present a treatment option that out-
Table 10.1 Physiological class: the host
Type Characteristics
A Good immune system and delivery
B Compromised locally (BL) or systemically (BS)
C Requires suppressive or no treatment; Minimal
disability; Treatment worse than disease; Not a
surgical candidate
Factors affecting physiological class
Systemic factors (S) Local factors (L)
Malnutrition Renal or
hepatic failure
Diabetes mellitus Venous stasis
Chronic hypoxia Major vessel
Immune disease Arteritis
Extremes of age Extensive scarring
Immunosuppression
Immune deciency
Tobacco abuse Neuropathic Ulcer
Alcohol abuse
Malignancy
Chronic lymphedema
compromise
radiation brosis
Small-vessel disease
weighs the risks. These patients may be
reevaluated for treatment and reclassied as
Class A or B hosts.
10.12 The Disease
The Chierny-Mader classication system for
osteomyelitis delineates the disease into four distinct types, each escalating in complexity, associated increased level of the treatment modality
(Table10.2):
Type I: This category is characterized by a
sequestered nidus conned to the endosteum.
It may be associated with an isthmic scar,
granulation tissue, sequestered bone (trabeculae and endosteal cortex), or medullary
implants. The enveloping soft tissue may also
be implicated. Predominantly observed in
immunosuppressed adults, this variant of
osteomyelitis is more diaphyseal than
metaphyseal.
Type II: Termed supercial osteomyelitis, the
biolm nidus in this type is exposed on a bony
surface at the base of an atrophic soft tissue
defect [61]. The nidus involves only the supercial part of an otherwise healthy osseous segment and does not extend into the medullary
canal.
Type III: This type is marked by a full-thickness
cortical sequestrum within or adjacent to a
stable osseous segment. The canal, like Type I,
and the soft tissue envelope may be involved,
like Type II, and foreign bodies are common.
Type IV: This permeative form of osteomyelitis
exhibits characteristics of Types I, II, and III
but additionally features instability. The
lesions are either intrinsically unstable or
become unstable following debridement.
Each type necessitates a specic treatment
modality that aligns with the nature and history
of osteomyelitis.
136
Y. Wu and D. Joseph
Table 10.2
Type
I Medullary
II Supercial
III Localized
IV Diffuse
Anatomic type of the chronic osteomyelitis (local disease) and treatment strategy
Description Graph Surgery
Debridement Restoration
Unroong RIA Dead space management: e.g. Abx
Unroong
RIA
Decortication
Unroong
Reaming
Decortication
Sequestrectomy
Unroong
Reaming
Decortication
Sequestrectomy
Stabilization
beads
Soft Tissue Coverage: e.g tissue
transfer
Dead space management Soft tissue
coverage
Bone graft
Dead space management
Soft tissue coverage
Segmental bone restoration
Fixation
10.13 Treatment
Patient selection and decision-making (Fig.10.1):
Selecting a treatment strategy is a complex
process that hinges on various factors. These
include the clinical stage of the disease, the anatomical site of infection, wound characteristics,
and the prociency of the healthcare team.
In instances where curative treatment is contraindicated, untimely, or excessively debilitating for the patient, palliative and suppressive
therapies are employed to enhance patient wellbeing. The potential benets of limb salvage
must signicantly outweigh those of amputation to warrant the associated morbidity and
risk [59, 94, 95].
Limb ablation becomes a consideration when
neither limb salvage nor palliative care is deemed
safe or feasible. This decision-making process is
profoundly inuenced by intrinsic patient conditions or comorbidities, heightening the risk of
treatment failure. Such risk factors can precipitate metabolic deciencies, skin and wound
breakdown, immune deciencies, bacteremia,
and complications associated with excessive
bleeding. Moreover, the presence of multiple
comorbidities can exacerbate these risks [3, 58,
94–97]. Therefore, engaging in these discussions
with a well-informed healthcare team that can
guide these decisions based on the patient’s condition and prognosis is crucial.
Upon determining that a patient is at risk due
to comorbidities, it is imperative to exhaust all
avenues to invoke interventions to optimize the
host response, irrespective of the chosen treatment modality [98, 99]. The preoperative rectication of deciencies in wound healing could
enhance the outcome for a Type B host, making it
10 Chronic Osteomyelitis
137
Fig. 10.1 The diagram depicts the general rule of patient
selection and decision-making. A patient was carefully
evaluated with history and physical, laboratory test, and
diagnostic image. The patient was then divided into three
categories: Type A host is a healthy patient with normal
repose to stress, trauma, and infection. Type A patient is
usually a good candidate for limb salvage. Type B patients
have comorbidities that inherently compromise wound
healing and response to the treatment. Using less invasive
methods should be considered for limb salvage. For type
C patients, the treatment causing morbidity and loss of
function outweighs the patient’s quality of life impacted
by disease. Palliative treatment is chosen. However, after
reversing some comorbidities and/or new technology can
offer a more favorable outcome, C-host can be reclassied to A-host or B-host. Limb salvage is considered.
Amputation is recommended if the patient’s condition is
akin to that of a Type A host [55]. This underscores the importance of comprehensive patient
management, where the focus extends beyond
the primary disease to include overall health optimization [3, 96, 97].
As for surgical intervention, methods with low
morbidity, such as atraumatic exposure, staged
worsening and/or reversal of the adverse comorbidity is
not feasible. Once limb salvage is chosen, A live, clean,
manageable wound is established with thorough debridement, which is followed by pathogen-target antibiotics
and bone stabilization. A single-stage reconstruction with
antibiotic depot can be considered if the patient is healthy,
osseous integrity is adequate with simple treatment, the
wound is clean without sign of infection, and the soft tissue envelop is healthy and pliable (content in broken line).
Otherwise, the I&D, biopsy, and antibiotic depot/spacer
with or without temporized xation can be repeated as
many as possible until a viable, clean, manageable wound
is achieved. A staged denitive reconstruction was then
instituted based on the status of osseous integrity and soft
tissue envelope. Cierny-Madar classication provides
great help in establishing the treatment strategy
(Table10.2)
treatment protocols, and reconstruction unlikely
to require surgical implants, should be considered rst if they provide equivalent results
[11–105]. If internal xation stabilization is an
absolute requirement, the nal reconstruction
may be better staged to follow the interval of
local antibiotics therapy [46, 106, 107].