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Osteomyelitis
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GiovanniVicenti, GuglielmoOttaviani,
andBiagioMoretti
36
36.1 Introduction
Osteomyelitis is characterized as bone inammation brought on by an infectious agent [1].
Understanding the etiology of the disease, the
common and uncommon etiological agents, the
principles of anti-infective therapy, and when and
how to perform surgical debridement and reconstructive techniques are all necessary for the successful management of osteomyelitis.
It is difcult to determine the pathophysiology, imaging, and classication of osteomyelitis
because it depends on the patient’s age (child vs.
adult), the duration and intensity of the infection
(acute vs. chronic), the route of spread (hematogenous vs. contiguous focus), the patient’s
immune and vascular status, as well as the
affected area.
36.2 Classication
Osteomyelitis has historically been categorized
using the Waldvogel classication, which was
introduced in 1970 [2]. The source of the infec-
G. Vicenti · G. Ottaviani (*) · B. Moretti
U.O.C Ortopedia e traumatologia, Policlinico di Bari,
Università degli studi di Bari “Aldo Moro”,
Bari, Italy
e-mail: biagio.moretti@uniba.it
tion (hematogenous or contiguous), the existence
of generalized vascular disease, and the length of
the infection were all included in this descriptive
classication system (acute, sub-acute, and
chronic).
The 1977 publication of Ger’s classication
recognized the role of the soft tissue situation in
the surgical decision-making process. This classication categorizes soft tissue conditions as
simple sinus, chronic supercial ulcer, multiple
sinuses, multiple skin-lined sinuses, or multiple
sinuses.
Through the publication of a classication
system that emphasized a more comprehensive
approach to the patient and acknowledged the
signicance of immune competency and the
physiological ability of the host to effect healing,
Cierny and Mader revolutionized our understanding of osteomyelitis in 1984 [3]. This system
included categorization based on the disease’s
anatomical characteristics and the physiological
state of the host (Fig.36.1).
The Cierny and Mader classication however
failed to provide specic, objective criteria
according to which the C-host, whom they
deemed unsuitable for surgery, should be dened.
McPherson etal. attempted to address the shortcomings of the Cierny and Mader host classication system by modifying it to include specic
objective criteria [4].
But several and more articulated classications have been developed.
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023
M. Maruccia et al. (eds.), Pearls and Pitfalls in Skin Ulcer Management,
https://doi.org/10.1007/978-3-031-45453-0_36
405
406
a
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Fig. 36.1 Cierny–
Mader Classication: (a)
medullary osteomyelitis
(early hematogenous);
(b) supercial
osteomyelitis (early
contiguous); (c)
localized osteomyelitis;
and (d) diffuse
osteomyelitis
b
G. Vicenti et al.
c
d
abc
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407
36.3 Pathogenesis
Invasion of the bone by pathogens leads to an
acute reaction by the body and inammatory factors. Microscopic examination of the bone demonstrates the presence of areas of suppurative
inammation in which bacteria and inammatory
cells are deposited. The inammation causes progressive destruction of the bone matrix and subsequent occlusion of blood vessels. As a result,
areas of ischemia are created that contribute to
tissue necrosis. Ischemia also makes it impossible for other inammatory cells and antibiotics to
reach the site of infection. A hypervascularized
rim forms around these areas, which increases
the activity of osteoclasts and osteoblasts resulting in localized osteoporosis and apposition of
new exuberant osseous tissue [5].
36.4 Anatomo-Pathological
Lesions
Four anatomopathological lesions typical of
osteomyelitis are recognized in this process and
deserve to be described (Fig.36.2).
Brodie’s abscess represents a purulent intraosseous collection, often surrounded by a hypervascular orb [6]. It is considered a typical lesion of
acute osteomyelitis even though it manifests over
a period ranging from 1week to 1year and often
the typical symptoms are not associated. By
MRI, a uid lesion, frequently metaphyseal, surrounded by a vascularized orb can be visualized.
Sequestrum, on the other hand, represents the
typical lesion of chronic osteomyelitis [1]. It is an
area of devascularized bone surrounded by an
area of necrosis. As explained earlier this makes
treatment with antibiotics ineffective, as they
cannot reach the site of infection. It can be found
on plain radiographs and, even better, on CT.
Involucrum is the sclerotic area surrounding
the sequestrum [7].
Cloaca, on the other hand, is the break in the
sequestrum that allows communication with the
periosteum and in some cases with the outside,
taking the name stula.
36.5 Pathogens
Osteomyelitis are frequently polymicrobial
infections, especially when caused by contiguity with an ulcer. Hematogenous osteomyelitis,
on the other hand, is usually caused by a single
pathogenic organism. The most frequently isolated pathogen is Staphylococcus aureus. This is
probably due to its numerous virulence factors.
Adhesins allow colonization of implanted tissues and materials. The pathogen has the ability
to evade host defenses and invade cells. It can
also remain viable within host cells, which
Fig. 36.2 Anatomopathological lesions: (a) acute hematogenous osteomielitys (1. nidus); (b) subacute osteomielytis
(2. Brodie’s abscess); and (c) chronic osteomyelitis (3. sinus; 4. sequestrum; 5. stula)
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G. Vicenti et al.
would explain the high rate of recurrence of
infections [8].
Staphylococcus aureus, along with other
bacterial species, is capable of producing biofilm, a highly structured community of sessile
bacteria surrounded by a polymeric extracellular matrix. This structure, which is difficult
for antibiotics to penetrate, surrounds colonies
of bacteria that are metabolically inactive and
therefore less sensitive to their effect [9].
Although some antibiotics have a greater
effect against biofilm, the best therapy is surgical debridement.
36.6 Diagnosis
The diagnosis of osteomyelitis is using a multidisciplinary approach involving laboratory medicine, imaging, and pathology.
Symptomatology is highly variable and
nonspecific. Acute osteomyelitis may be characterized by more obvious symptoms such as
fever, pain, and swelling. Chronic forms, on
the other hand, have more subtle symptomatology; fever may not be present, bone pain,
local swelling, and, in some cases, fistulae are
manifest. Confirmation of osteomyelitis
requires several diagnostic procedures as
described below.
36.6.1 Microbiology
andHistopathology
In any type of osteomyelitis, the identication of
the pathogen is crucial. This can be done by several tools. Blood cultures are diagnostic only in
hematogenous osteomyelitis. The use of local
swabs is now considered obsolete, collecting
samples from the surface of an ulcer or even from
the depth of the ulcer often results in contamination by nonpathogenic microorganisms that have
colonized the site. The suggestion is to take ve
biopsy samples of the deep perilesional tissue,
around the implant or debridement site [10]. All
samples should be analyzed for Gram + and
Gram −.
36.6.2 Laboratory Studies
The use of laboratory tests can be helpful in the
diagnosis and follow-up of osteomyelitis.
Erythrocyte sedimentation rate (ESR) is frequently high but its changes are too slow to allow
adequate follow-up. In contrast, the concentration of C-reactive protein (CRP) is highly sensitive and its kinetics allow the evaluation of the
effectiveness of therapy. In fact, it increases as
early as the rst hours following the acute phase
and decreases in about a week after the start of
effective treatment. The use of these parameters
in combination makes it possible to exponentially increase the sensitivity and specicity of
the tests, moreover with the addition of local
sampling the sensitivity reaches 100% [11]. The
white blood cell count (WBC) may also be normal in chronic osteomyelitis [12]. However, all
of these values, despite being particularly sensitive, are highly nonspecic and, by themselves,
do not allow for a denite diagnosis.
36.6.3 Imaging Procedures
All imaging procedures can be used to complete
the diagnosis of osteomyelitis.
Plain radiography is the basis of diagnosis and
follow-up (Fig.36.3). It allows visualization of
local swelling that occurs as early as 2–3days;
after about 10–12 days, on the other hand, the
presence of a bone defect can be assessed.
Sonography is a useful tool for the evaluation
of osteomyelitis in the acute phase. It allows
excellent visualization of soft tissues, and
because of its low invasiveness it can be used for
the diagnosis of pediatric osteomyelitis [13].
CT allows detailed visualization of bone
structures and surrounding soft tissues, consequently it is a valuable tool for the study of
chronic osteomyelitis. However, it often suffers
from artifacts caused by the simultaneous presence of metal implants [14] (Fig.36.4).MRI, on
the other hand, is ideal for the study of the early
stages of the disease and allows an even more
accurate study of the soft tissues. The presence of
bone edema is a typical sign of osteomyelitis, but
36 Osteomyelitis
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Fig. 36.3 Plain radiography of chronic osteomyelitis showing diffuse osteolysis, periosteal reaction, and soft tissues
involvement
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Fig. 36.4 CT-scan of chronic osteomyelitis showing diffuse osteolysis, osteoporosis, sequestrum, and air bubbles
inside soft tissue
on the other hand, it does not allow for adequate
follow-up as it may persist for months after the
resolution of the disease [15]. Bone scintigraphy
can be used with different types of radiopharma-
ceuticals. Leukocytes labeled with indium-111 or
technetium-99m can be used for early diagnosis
of acute osteomyelitis with high specicity and
high sensitivity.
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G. Vicenti et al.
Positron emission tomography (PET) labeled
with uorine-18-uoro-D-deoxyglucose (FDG)
is a highly sensitive and specic test that combined with CT allows accurate visualization of
lesions [16].
36.7 Treatment
The goal of treatment is always the denitive
eradication of the pathogen, however the options
available are different if the osteomyelitis is acute
or chronic.
36.7.1 Acute Osteomyelitis
The rst line of treatment for acute osteomyelitis
(Fig. 36.5) is always antibiotic therapy [17]. As
mentioned earlier, successful therapy depends on
correct diagnosis and, most importantly, isolation of
the pathogen. To avoid the emergence of resistance,
a consultation with an infectiologist is always recommended and usually the combination of two
antibiotics is chosen. The parameters to be evaluated in the choice of antibiotics are bone-wide distribution, adverse effects, cost, and duration.
36.7.2 Chronic Osteomyelitis
Regarding chronic osteomyelitis, it is now known
that antibiotic therapy alone cannot completely
eradicate the infection. Surgery has therefore
become the cornerstone of treatment.
Fundamental turns out to be the study of the
patient and classication of the disease. The classication most commonly used nowadays is the
Cierny–Mader classication, which in addition
to local conditions, allows us to divide the host
into three classes: host-A healthy patients with
low perioperative risk; host-B patients with local
or systemic immunologic changes; and host-C
patients in whom treatment may be more dangerous than the disease. After accurately studying
the location of the disease and the patient’s
comorbidities, one should try to correct the
immunological status of the patient: nutritional
status should be optimized, and metabolic alterations and anemia should be corrected. To allow
proper wound healing after surgical resection,
one must ascertain the patient’s vascular status
(by pulsoximetry, Doppler, or CT angiography)
and correct it when possible.Salvage surgery
involves an extensive debridement of bone and
soft tissue, and resection surgery tries to maintain
Fig. 36.5 Clinical progression of acute osteomyelitis: (a) 1day; (b) 3days; and (c) 4days
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bone stability. Resection of the osteomyelitis
focus should be radical and include healthy margins (“tumor-like resection”), it is always better
to remove a few more segments than less [18].
However, the extent of resection may cause instability of the treated skeletal segment, leading to
an advancement in the Cierny–Mader classication from stage III to IV, in which case additional
therapies are necessary. The various options
allow the bone defect to be lled acutely or by
multi-step treatments. In acute, it is possible to
ll the defect by the placement of an autologous
graft, this can be taken from numerous anatomical sites and may or may not be associated with
vascularized pedicles and soft tissue aps. If,
however, a high risk of acute recurrence remains,
it is possible to reclaim the osteomyelitis focus
by placing a cement spacer to ll the defect, as
described by Masquelet [19]. The technique
describes the use of a simple poly-methylmethacrylate (PMMA) spacer; however, it can be
fortied with antibiotics to increase its eradicating power and decrease the rate of recurrence.
Retention of the PMMA spacer within the defect
for at least 4–6 weeks causes a “foreign body
reaction” that leads to the formation of a highly
vascularized “pseudomembrane.” The second
step involves the incision of the “pseudomembrane,” the removal of the PMMA spacer, and
placement of bone grafts in what is called a “biological chamber.” A 2016 meta-analysis by an
Italian group of 17 papers (between 2000 and
2016) analyzed variables from 427 patients. An
89.7% union rate was reported with 91.1% eradication of infection in bone defects between 0.6
and 26cm [20]. Another technique, described by
Ilizarov [21] in the 1970s, allows for the simultaneous treatment of bone and soft tissue defects
and is called distractional osteogenesis. Through
the use of a circular external xation system,
devised by the author himself, it is possible to
resect large bone segments while still maintaining limb stability and still allowing load bearing.
Then an osteotomy is made at the metaphyseal
site, and again thanks to Ilizarov’s “apparatus,” it
is possible to ll the defect by progressive distraction of the bony callus, creating a “regenerate” following the principles of distraction
osteogenesis. The most recent meta-analyses
report a cure rate of 97.26%, with unsatisfactory
results in less than 10% of cases [22]. The refracture rate reported in the literature is less than 5%,
but increases as bone decit increases [23].
36.7.3 Foot Infections
Diabetes frequently results in foot infections.
About 20% of diabetic foot infections are complicated by the involvement of the underlying
bone, which typically results from contiguous
spreading from overlaying soft-tissue infection.
This signicantly raises the risk of lower
extremity amputation. Deep wounds, peripheral
neuropathy, Charcot’s arthropathy, vascular
insufciency, poor glycemic control, and immunological dysfunction are among the risk factors
for diabetic foot osteomyelitis (Fig.36.6). The
choice of treatment is inuenced by the presence of an associated vascular disorder and the
presence of adjacent ulcers. Antibiotic treatment
following debridement has demonstrated good
outcomes in patients with good tissue oxygenation [24]. Pressure-off-loading surgical techniques such as hammertoe correction or Achilles
tendon lengthening can help prevent ulcers and
decrease their recurrence. If the extent of osteomyelitis requires larger resections, minor amputations (digit, trans metatarsal, and Chopart
joint) may be opted for to continue to allow
loading on the residual limb. Amputations below
the knee or thigh may be considered in severe
cases complicated by severe vascular insufciency. Of great importance is the correct staging of the host (A, B, or C) and proper patient
information.
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Fig. 36.6 Clinical and radiographic assessment of chronic osteomyelitis of the foot
G. Vicenti et al.
36.8 Conclusions
Osteomyelitis is a common clinical problem
with an increased incidence correlated mainly
with diabetes-related foot infections. Successful
treatment depends on accurate diagnosis, correct staging of the disease and the host, and collaboration of multiple specialists. Antibiotic
therapy is rst line in the treatment of acute
osteomyelitis, while it is adjuvant in the treatment of chronic disease in which surgery is still
the gold standard.
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Part VII
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Plastic Surgery: When and How
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