(Iv) Osteomyelitis: Mini-Symposium: Pathology

MINI-SYMPOSIUM: PATHOLOGY
(iv) Osteomyelitis resistant to infection; in experimental models, it is necessary to

cause injury or bone death prior to inoculation with a large
number of bacteria to induce osteomyelitis. It has been postu-
Martin McNally
lated that minor bone injury may cause intramedullary hae-
Kugan Nagarajah morrhage, predisposing to the deposition of bacteria in
haematogenous osteomyelitis. Additionally the tortuous blood
vessels in the metaphyses of the long bones may undergo
thrombosis, slowing blood flow and causing bacterial seeding.
Abstract Injury and thrombosis expose many proteins (clotting cascade,
Osteomyelitis causes bone death, soft-tissue compromise, functional
matrix components and damaged cell proteins). Staphylococcus
impairment and systemic illness and considerable morbidity. There are
aureus and other organisms can adhere to these via specific
several distinct forms which present considerable management chal-
binding sites, allowing colonization of the tissues.
lenges. Recent advances have led to new powerful techniques for the
Acute haematogenous osteomyelitis is usually seen in pre-
eradication of infection and restoration of function. Surgery remains
pubertal children or the elderly. It has a rapid onset of symptoms,
central to treatment for chronic osteomyelitis and some acute presenta-
with localized pain, pyrexia and malaise. 30% of children have
tions. However, multi-disciplinary working is essential to achieve satisfac-
a history of recent minor injury to the site of infection. Signs of
tory outcomes.
bacteraemia (rigours, vomiting, and prostration) are present in half
of the patients. The infection is most often in the metaphysis of
Keywords acute; chronic; dead space management; debridement; a long bone (distal femur and proximal tibia are common), begin-
ilizarov reconstruction; infected non-union; osteomyelitis; posttraumatic ning in the medulla but spreading rapidly to involve cortex with
sinus formation, sub-periosteal abscess formation and soft-tissue
extension. In young children, the infection may spread to the adja-
Introduction cent joint and present as a septic arthritis. Spread of the infection
with periosteal stripping causes local ischaemia and further micro-
Acute and chronic bone infections are common worldwide, but in
vascular thrombosis and tissue death. The appearance of dead bone
developed countries the pattern of disease is changing. The inci-
signals the end of the acute phase of the condition.
dence of haematogenous infection is alling, while bone infections
Brodie’s abscess is a medullary, haematogenous osteomyelitis
arising from surgical intervention, injury, peripheral vascular
with a sub-acute presentation. The central bone abscess is often
disease and the sequelae of diabetes are increasing. Additionally,
surrounded by dense new bone (medullary involucrum) which
intravenous drug abuse and immuno-compromised patients due to
probably prevents sinus formation (Figure 2a and b).
HIV and cytotoxic therapy have given rise to new challenges. Contiguous osteomyelitis occurs when a pathogen enters the
The advent of effective antimicrobial therapy in the 1940s radi- bone from an adjacent infective source. This may follow an open
cally improved the outcome for many patients with severe infec- fracture, a bone operation, a skin ulcer or a pressure sore. It can
tions. However, there are only a few occasions when antibiotics occur in any bone and is more commonly seen in adults, particu-
alone are adequate treatment for osteomyelitis; in the majority of larly in those with concomitant disease (diabetes with foot ulcers,
cases treatment still requires surgery with adjunctive antibiotics. paraplegia with pressure sores, peripheral arterial or venous
While acute osteomyelitis can produce major systemic illness insufficiency with ulceration, or fracture with internal fixation). It
with potential mortality, chronic osteomyelitis, with persistent may present acutely, within days of an injury or operation, or may
sinus drainage, chronic ill health and on-going pain results in have a more insidious onset producing extensive bone involve-
unemployment, social isolation and recurrent need for medical ment over many weeks or months in a debilitated patient. Unlike
treatment and a high risk of depression and other mental illness. haematogenous osteomyelitis, contiguous osteomyelitis always
compromises the surrounding soft tissues and may cause cortical
Definitions (Figure 1) bone death prior to medullary infection.
Osteomyelitis is an inflammatory condition of bone caused by Chronic osteomyelitis (Figures 3 and 4) may begin as acute
an infecting organism. It is usually limited to a single bone but, haematogenous or contiguous disease. The key feature of chronicity
rarely can be multifocal. Osteitis describes infection affecting is the presence of dead bone. Extensive periosteal stripping,
only cortical bone; osteomyelitis implies that the cortex and medullary ischaemia with intravascular thrombosis and activation
medulla are involved. of inflammatory cells all contribute to bone death. Small areas of
Haematogenous osteomyelitis is due to blood-borne spread of dead bone may be absorbed or revascularized but inflammatory
bacteria to a focus in a bone. Normal healthy bone is very macrophages can cause separation of larger dead bone fragments or
sequestra. These may move to the surface along sinus tracts, to be
discharged with pus and allowing, at least temporarily, resolution of
Martin McNally MD FRCSEd FRCS(Orth) Consultant in Limb Reconstruction, the infection. The surrounding bone may react with new bone
The Bone Infection Unit, Nuffield Orthopaedic Centre, Windmill Road, formation within the medulla or under the elevated periosteum,
Oxford OX3 7LD, United Kingdom and Honorary Senior Clinical Lecturer, producing an involucrum. In time, this can replace almost all of
University of Oxford, United Kingdom. a long bone. Reactivation of infection may then occur with openings
forming in the involucrum or cortex, (cloacae) allowing further
Kugan Nagarajah MB MSc FRCS(T þ O) Clinical Fellow in Limb Recon- discharge of pus from cutaneous sinuses. This cycle of reactivation,
struction Nuffield Orthopaedic Centre, United Kingdom. discharge with symptoms, partial resolution with skin healing and
ORTHOPAEDICS AND TRAUMA 24:6 416 Ó 2010 Elsevier Ltd. All rights reserved.
Figure 1 Schematic diagram of the evolution of bone infection from acute medullary disease to chronic osteomyelitis with dead bone, involucrum, sinuses
and discharge.
then relapse may proceed for many years. However, most large infecting organism (haematogenous or contiguous focus) or by
sequestra remain trapped within the bone. In some cases, an open the cultured organism. However these classifications are not
sinus may continue to drain permanently from an area of deep helpful to determine treatment regimen or prognosis.
infection. This tends to reduce pain and systemic upset but there is In 1983 Cierny and Mader, a surgeon and a physician (internal
a risk of the development of squamous carcinoma (Marjolin’s Ulcer) medicine specialist) designed a classification for chronic osteo-
in the wall of a chronic active sinus (Figure 5). myelitis based on four anatomical types of the disease (I to IV) in
Chronic sclerosing osteomyelitis (of Garre) is a rare form the bone and three physiological groups of patients (A, B and C).
which causes pain and many of the features of chronic bone This has been widely applied and shown to be useful prognos-
infection but does not develop sinuses or purulent discharge and tically with modern treatment. It can also be used, with some
is invariably culture-negative. It may affect more than one bone caveats, in acute infections.
when it is also known as chronic multifocal osteomyelitis. While It emphasizes the importance of considering the whole patient
it has been regarded as a benign self-limiting condition in adult not just the local disease as not to do so courts early recurrence of
life, pain may persist for many years. infection and treatment failure.
An understanding of the general physiological status of the
Classification patient is important to define those who will cope well with
treatment, particularly extensive surgery or prolonged recon-
Osteomyelitis can be sub-divided into groups based on the speed struction and highlights areas of dysfunction which can be
of onset of symptoms (acute and chronic), the source of the optimized prior to treatment to improve the potential for wound
Figure 2 a Coronal MRI showing typical medullary high signal around an area of dense medullary new bone in a Brodie’s abscess. b Transverse section of
the same lesion showing the double medullary nidus and no extramedullary involvement.
and bone healing, eradication of infection and functional or general condition which may convert them to A- or B-
restoration. hosts.
Group A host is a healthy patient with no concomitant
conditions which would impair the response to stress, surgery,
infection or antimicrobial therapy.
Conditions which affect the outcome of treatment of
Group B hosts have impairments which directly affect the
osteomyelitis
ability to heal wounds or reduce the efficacy of drug treatment or
Local factors in the limb (Bl-host) Systemic factors (Bs-host)
prevent appropriate surgery.
These are sub-divided into Arterial ischaemia Malnutrition
Group Bl hosts who have local conditions in the affected limb. Venous insufficiency Diabetes
Group Bs hosts who have systemic co-morbidity. Previous surgery Smoking
Group Bls hosts who have both. DVT IV drug abuse
Group C-hosts are of two types. Firstly, those who are mori- Lymphoedema Hypoxia
bund with chronic infection or other disease and in whom Radiation fibrosis Renal/liver failure
treatment of the infection would not improve survival or Tissue scarring Immuno-suppression
quality of life. Treatment of the osteomyelitis in these patients Retained foreign material/implants Malignancy
is usually not indicated. Secondly are patients who have few Osteoporosis Sickle-cell disease
symptoms from their chronic infections. In some of these, the Compartment syndrome Drug allergies
morbidity from extensive treatment to eradicate infection may Obesity Mental illness
be greater than the inconvenience of the condition. Such C-
hosts may continue with quiescent infection for many years
without definitive intervention but should be followed up
regularly. The anatomic classification of osteomyelitis is based on the
Patients should only be placed in Group C after careful specific distribution of infected bone in the limb. There are four
consideration and the decision is taken jointly with the types, each of which tends to be related to a particular aetiology
patient. Surgeons must not forget that the status of a patient of infection.
can change. A-hosts can develop conditions which affect Type I: (Figure 6a and b) medullary osteomyelitis involves only
treatment and C-hosts can have fluctuations in their infection medullary and endosteal bone. It is mostly a haematogenous
Figure 3 Extensive chronic osteomyelitis with medullary sequestra, cavi-

tation around these and involucrum formation around all of the humeral
diaphysis.
Figure 4 MRI demonstrates all of the features of chronic osteomyelitis.

There is medullary necrosis with abscess formation, breech of the cortex
infection which can present acutely or chronically. It is uncommon through a medial cloaca producing a circumferential sub-periosteal
in adults, occurring mainly in the immuno-compromised, after abscess. The middle third of the femur shows mature involucrum and
bacteraemia or those with sickle-cell disease. Brodie’s’ abscess is below this, the cortex has abnormal signal, suggesting that it is dead and
a sub-acute form. will become a sequestrum.
The lesion is well demonstrated on MRI and plain X-ray.
While the soft-tissue envelope is often inflamed, it is usually
infection-free and will tolerate surgery well. The host state is infected. The endosteal surface and the medullary bone are
important in preventing recurrence and wound breakdown after unaffected and remain healthy. There is almost always a visible
surgery. soft-tissue defect which may be larger or smaller than the area of
Type II: superficial osteomyelitis is a contiguous infection dead bone. Cortical disease is difficult to identify on MRI but CT
which often arises in the base of a varicose ulcer or other skin may show areas of cortex which look abnormal or which are
breach. Exposed bone after open fractures, deep burns and about to separate from the underlying bone.
arterial or pressure ulcers can also go on to type II infections Type III: localized osteomyelitis is currently the most common
(Figure 7a and b). Only the outer part of the bone cortex is form of osteomyelitis. There is involvement of the medullary
(Figure 8a and b) often follows fractures with internal fixation or

after haematogenous osteomyelitis with multiple cloacae and
extension from the medulla to the cortex and soft tissues. The
typical type III osteomyelitis will have an area of dead cortical
bone which may form a sequestrum with medullary pus and
further deep dead bone.
In infected tibial fractures, the muscle attachments and good
blood supply of the postero-lateral part of the bone may preserve
this cortex, producing a type III osteomyelitis of the anterior and
medial bone. Anterior subcutaneous cortical fragments which
have been stripped of periosteum by injury or surgery will form
sequestra. Healing of the fracture at the back of the tibia may
progress, but with persistent infection draining through surgical
wounds or sinuses at the front.
Investigation of type III infection is primarily with plain X-rays
and MRI (if there are no implants). MRI can show the muscle
attachments around cortical bone which may allow an assess-
ment of potential viability prior to surgery. CT will show dead
bone fragments in infected fractures and can be very helpful in
planning exposure for surgical resection of the dead tissue, pro-
tecting the viable stable segment. Care must be taken not to
excise healthy bone in order to access deep infection, thus
creating an unstable bone after resection or a bone which is at
high risk of fracture.
Note: after removal of an infected fracture fixation plate, it is
tempting to assume that infection may be restricted to the metal-
work and the cortex under the plate, i.e. a type II osteomyelitis.
However residual organisms in the medulla around screw tracks
can cause early recurrence of infection after metal removal. Thus
it is safer to assume that these cases are type III diseases and
Figure 5 This large ulcerating sinus had been present for many years. The require excision of the screw tracks and any deep collections.
patient refused treatment of the underlying osteomyelitis but biopsy of Type IV: diffuse osteomyelitis shares all of the features of the
the ulcer edge revealed a squamous carcinoma. previous types with the cardinal addition of skeletal instability. It
comprises all infected fracture non-unions (Figure 9) and many
bone and cortex limited to part of the circumference of the bone. haematogenous infections with circumferential cortical extension
This is important, as it leaves a healthy portion of the bone to and extensive sub-periosteal abscess formation. Longstanding
maintain stability across the zone of infection. Type III disease cases of chronic sclerosing osteomyelitis may also have diffuse
a Clinical appearance of a type I medullary osteomyelitis. The swelling is not flucuant and there are no sinuses. b MRI confirmation of the clinical
staging with infection limited to the medulla. The inner surface of the cortex has separated at the back forming a small sequestrum of dead bone.
Figure 6
a A deep ulcer over the subcutaneous border of the tibia communicates with a small area of dead cortical bone, causing persistent discharge and
failure of wound healing despite prolonged dressings. b MRI cannot easily demonstrate dead cortical bone. In this case, foreign material in the
tissues adjacent to the bone and loss of the thickness of the postero-medial corner of the tibia suggest type II osteomyelitis.
Figure 7
involvement. In all type IV cases, segmental resection of the bone Aeromonas sp. (water borne infection), Brucella, Burkholderia
will be required to achieve an infection-free limb. (Melioidosis) and Borellia burgdorferi (Lyme disease).
Haematogenous Mycobacterium tuberculosis infection of the
bones accounts for one in 50 of all cases of tuberculosis world-
Pathology
wide, half affecting the vertebral bodies, mainly in the thoracic
S. aureus can cause all types of osteomyelitis and it is the causal spine. 60% of those with TB osteomyelitis will also have extra-
organism in over one-third of acute cases and half of all vertebral osseous disease. M. tuberculosis bone infection requires biopsy
infections. While recently hospitalized MRSA infection may be for confirmation of the diagnosis (by ZiehleNeilsen staining on
present but the majority of staphylococci remain meticillin sensitive. histology or prolonged bacterial culture). Most cases can be
S. aureus is the commonest organism in acute osteomyelitis, treated with multi-drug antibiotic regimens alone and surgery is
followed by Enterococci, Enterobacteriacae, Streptococci and reserved for those with neurological complications in the spine or
anaerobic bacteria. Haematogenous disease in children may also to provide stability to the skeleton.
be caused by H. influenzae, in those who are not immunized. Bacteria attach to the surface of dead bone by a series of
Contiguous infections arising from injury or after surgery often complex cellular interactions, mediated by bacterial adhesins.
have a polymicrobial culture. S. aureus predominates but coagu- These surface components recognize host proteins which are
lase-negative staphylococci, Propionobacterium acnes and Gram- present on the dead bone (or coating implants). Once attached,
negative bacilli are all common, especially in implant-related the bacteria produce a polysaccharide extracellular matrix.
infection. Clostridia, and Nocardia may all infect contaminated Within this matrix, micro-colonies develop and mature. This
open fractures. Pseudomonas aeruginosa is the commonest combination of ordered colonies in polysaccharide ‘slime’ is
organism after puncture wounds to the foot and multi-drug resis- known as a biofilm. Many bacteria can form biofilms; those
tant Pseudomonas sp. are now a concern in many units. formed by S. aureus, coagulase-negative staphylococci and Pseu-
In drug addicts and the immuno-compromised, atypical domonas species in orthopaedic infections have been extensively
organisms can be cultured. In such cases, specific culture for studied. Within a biofilm, there is enhanced cellecell signalling
fungi (Aspergillus and Candida), Bartonella and Mycobacteria (quorum sensing) which allows maintenance and further
may be necessary. In HIV and AIDS, bone and joint infection is production of the biofilm. It can also initiate separation of biofilm
the third most common infective presentation after respiratory fragments with spread of the infection. S. aureus has been shown
and cerebral infections; a wide range of organisms have been to express a number of virulence factors, can invade living cells
described. and survive inside osteoblasts.
Sickle-cell disease is characterized by recurrent hypoxic crises Organisms may enter a ‘resting state’ (small colony variants)
which produce extensive bone infarcts which may become with very little metabolic activity, becoming highly resistant to
infected, usually with Salmonella but often with S. aureus or antibiotics. The sensitivity of a culture in the laboratory on an
Streptococcus pneumoniae. agar plate may bear no relationship to the ability of the same
There are many other specific infections related to occupation antibiotic to kill bacteria in a biofilm or living as small colony
or endemic disease. These include Mycobacterium marinum, variants in dead tissue. These mechanisms allow bacteria to
Figure 9 This fracture exhibits diffuse type IV osteomyelitis with bone

lysis, fixation failure, soft-tissue infection and discharging sinuses. The
medial cortex, under the plate was found to be necrotic at debridement.
be signs of old healed sinuses, active discharging sinuses, soft-

a & b Coronal and axial MRI of a typical type III osteomyelitis of
the distal ulna. The medulla and radial side of the cortex are tissue abscesses, or scars from previous surgery or injury.
involved with bone lysis, abscess formation and periosteal Chronic osteomyelitis can produce long-term ill health with
elevation. The muscles on the ulnar side are well attached to the weight loss, malaise, fatigue or depressed mood. Acute systemic
cortical bone, which was seen to be alive at operation. upset is less common but pyrexia, sweating attacks and anorexia
are associated with flare-ups of the disease (Figure 9).
Figure 8 There are no specific blood tests to confirm the diagnosis of
bone infection. In acute cases, the white-cell count, ESR and CRP
levels are usually raised but are often normal in chronic infec-
tion. If the patient is pyrexial, blood cultures can be useful and
avoid contact with the host immune system and antibiotics,
should always be taken in acute osteomyelitis. Atypical infection
explaining the failure of antimicrobial therapy alone in the
with Brucella, Bartonella or Spirochaetes (syphilis and yaws) can
treatment of established chronic osteomyelitis.
be diagnosed with blood serology.
Diagnosis
Imaging
The diagnosis of any bone infection is primarily clinical. Pain, Plain radiology remains the initial investigation of choice. In the
unilateral localized swelling, erythema and increased limb early phase of acute osteomyelitis, i.e. the first 2e3 days, plain X-
temperature are common features in acute disease. Systemic rays may be normal but over 6e7 days successively localized
upset is variable and may be absent, even in severe acute oste- osteopenia, bone destruction, cortical breaches, periosteal reac-
omyelitis, but most children with acute infection will have tion and a developing involucrum will become apparent. Visible
pyrexia at some point. sequestra may appear at around 10 days. Over several weeks, the
Chronic infection may be more difficult to diagnose. Pain is whole bone will become generally osteopenic due to disuse. Any
the most common symptom but may be rather diffuse or non- area of cortical bone which remains without osteopenia is likely
specific and is usually not related to activity. Signs may be subtle, to be avascular.
with minimal swelling, a small patch of increased temperature or Ultrasound scanning is invaluable for early identification of
local tenderness. In established chronic osteomyelitis, there may soft-tissue abscesses and joint effusions. It also allows guided
biopsy of infected areas and limited drainage of painful sub- may well be the method of diagnosis in the future but is not
periosteal collections. universally accepted at present.
Computed tomography (CT) is a sensitive test for bone
destruction. Fine cut CT can define small sequestra and aid in the Histology
design of surgical approaches to excise disease but it has little Histological assessment of deep tissue supports the microbiolog-
place in the initial diagnosis of infection. ical diagnosis. Some infections, such as tuberculosis and actino-
Isotope scanning has been advocated with bone tropic mycosis can be directly diagnosed by histology alone. In acute
isotopes (99mTc), labelled white cells, labelled antibodies, and infection, direct microscopy with Gram staining of aspirated fluid
antibiotics. These tests are non-specific and are inferior to other gives a rapid indication of the type of organism present (e.g. Gram-
forms of imaging. positive cocci) but continued treatment should be based on full
Magnetic Resonance Imaging (MRI) is the single most effec- culture results with antibiotic sensitivities.
tive investigation in bone infection. It can demonstrate early In chronic osteomyelitis, organisms are rarely seen on Gram
inflammatory change, define the extent of infection, show stain and this test can be omitted. Histology can confirm the
sequestra and sinus tracts and identify infective foci remote from diagnosis of osteomyelitis in cases with negative cultures by the
the presenting region (Figure 5). It is limited by the presence of demonstration of acute and chronic inflammatory cells, dead
metal implants and requires considerable skill in interpretation of bone, active bone resorption and remodelling and the presence of
chronic osteomyelitis. Cortical bone is black on all MRI small sequestra.
sequences. Dead or infected cortical bone is also black. MRI
diagnosis of cortical osteomyelitis is based on the changes in the Treatment of osteomyelitis
surrounding tissues but small areas of infected cortical bone can General considerations
be missed. dentification of the aetiology of infection, disease classification
While MRI is very sensitive, it can over-estimate the extent of and an understanding of the pathogenesis of the condition allows
medullary infection in the acute phase due to widespread bone planning of treatment for individual patients. There is no single
oedema obscuring the margins of the active infection. Addition- antibiotic regimen or surgical procedure which is appropriate for
ally post-operative MRI changes may persist for months or years all patients.
and can be difficult to distinguish from recurrent infection. The first decision in the management of osteomyelitis is the
location of that treatment. Patients should be treated in centres
Bacteriology which can deal with the many and varied co-morbidities in B-
The gold standard diagnostic test is microbiological culture of the hosts and provide the full range of surgical options necessary to
infecting organism from more than one deep specimen, taken tackle complex infections. Type IV, diffuse osteomyelitis and
with strict aseptic precautions in a patient who has not received many infected fractures should only be treated by dedicated bone
any antimicrobial agent for at least 10 days. infection teams. There is increasing evidence that patients with
Culture of superficial swabs or fluid from sinuses has been bone and joint infection are better treated in a multi-disciplinary
shown to be misleading and has a poor correlation with deep unit. In our Bone Infection Unit, all new patients are assessed
tissue flora. Thus the choice of antibiotic should not be based on jointly by an infectious diseases physician and a limb recon-
superficial cultures. struction surgeon specializing in bone infection. Imaging and
Aspiration of deep fluid collections, guided percutaneous bone bone biopsy are performed by dedicated musculoskeletal radi-
biopsies and blood cultures may all be useful, particularly in paedi- ologists. Plastic surgeons, vascular surgeons and other specialists
atric acute infection and diabetic foot infections and in acute disease, are involved as required. Follow-up after surgery is arranged
these may give early diagnosis allowing treatment with antibiotics with the team above, together with clinical nurse specialists who
alone. However in chronic osteomyelitis, and implant-related infec- assist with home intravenous therapy, Ilizarov reconstruction
tion, percutaneous biopsy may often be negative as organisms can be and wound care.
distributed sparsely throughout the area of abnormal tissue.
Prolonged cultures for aerobic and anaerobic organisms of at Acute osteomyelitis
least 7 days are essential in bone infection. Some fastidious bacteria It is only appropriate to treat acute bone infection solely with
associated with implant-related infections, such as Propionobacteria antibiotics in the following circumstances:
may require 2 weeks in culture while Mycobacteria may take even Diagnosis confirmed within a few days of the onset of
longer. It is important to warn the laboratory of any unusual clinical symptoms
features which might prompt specific culture techniques for atypical No dead bone or abscess seen on imaging
organisms. Low temperature cultures may be needed for some Rapid systemic response to drug treatment
Mycobacteria and immuno-compromised patients should have No adjacent septic arthritis
cultures for fungi and other unusual organisms. Tuberculous osteomyelitis
Harvest of organisms from specimens may be enhanced by Vertebral osteomyelitis without cord compression
sonication. This utilizes ultrasound to liberate organisms from In such cases, treatment must begin urgently. Blood cultures are
biofilms and improve positive culture rates. It may be especially taken and high dose intravenous antibiotic is given which should
valuable in low-grade implant infections where the micro- be active against S. aureus, Streptococci and Gram-negative rods
organism load may be small. such as E. coli. Cephalosporins, Clindamycin or a combination of
Some laboratories are now advocating the use of specific Flucloxacillin and Gentamicin may be used. Vancomycin should
genetic probes for identification of bacterial DNA and RNA. This be substituted if there is the possibility of MRSA infection.
The limb should be splinted, good analgesia given and any co- Treatment is tailored to the needs of each patient but there are
morbidities addressed. some basic principles:
Treatment should be modified after cultures are obtained and
Pre-operative
continued for at least 4 weeks. IV antibiotics can be converted to
Patient assessment and clinical staging of disease (IA, IVBs,
oral therapy after 72 h if the patient remains apyrexial, the limb
etc.)
condition has improved, there is no sign of abscess or skin
Full discussion of all treatment options with potential
breakdown, the organism is sensitive to oral antibiotics and
complications and choice of appropriate and acceptable plan
compliance with treatment can be relied upon.
Diagnostic tests for general health and limb condition (blood
If there is not a rapid clinical response, the limb deteriorates, or
tests, scanning, angiography, guided biopsy)
there is imaging evidence of progression of disease, then surgery is
Optimization of B-hosts and treatment of co-morbidities
indicated to prevent bone destruction and the onset of chronic
osteomyelitis. Operative
Acute mycobacterial osteomyelitis requires targeted multi- Limited exposure for multiple, uncontaminated bone
drug therapy, guided by local infectious disease protocols and sampling
treatment should continue for many months. Debridement and excision of all affected tissue
Intravenous antibiotics after sampling
Chronic osteomyelitis Bone stabilization
Chronic bone infection is characterized by the presence of dead Dead space management
bone colonized by bacteria in a state preventing eradication by Soft-tissue cover
antibiotics alone. Therefore definitive treatment aimed at cure of
the infection must include surgery. Post-operative
As with any condition, management is based on an evaluation of Functional rehabilitation
the effects of the disease, the benefits of treatment and the associated Continued antimicrobial therapy guided by culture results
risks. As full cure of chronic osteomyelitis may involve complex Monitoring for early recurrence or adverse events
surgery with complications, antimicrobial drug reactions, staged Second-stage reconstruction
reconstruction and prolonged time in treatment and rehabilitation, Optimization of patients with complex or multiple co-morbidities
an approach which arrests current symptoms, but with the potential can be challenging and, as surgeons often lack the necessary
for later recurrence, may be more acceptable for some patients. skills to manage many of the medical problems faced by patients
In C-hosts it is reasonable to withhold treatment or just to with chronic osteomyelitis these are better managed by infec-
treat flare-ups of symptoms with short courses of antibiotics. tious disease specialists. Nutritional problems, smoking and drug
Guided biopsy of the infected bone may assist in the selection of misuse should be addressed and any drugs with adverse effects,
appropriate antimicrobial therapy. However, on occasion such on wound or bone healing such as steroids, non-steroidal anti-
patients may elect to have limited surgery and prolonged anti- inflammatories, cytotoxics, etc. should be stopped if possible.
biotic suppression to keep symptoms at a low level, rather than Additionally all antibiotics should be stopped at least 10 days
have surgery aimed at disease eradication, for example in prior to surgery, to allow the best chance of bacterial culture
implant-related infections this can be effective over many years. from deep specimens at operation.
However, the choice of antibiotic regimen can be difficult. As part of the active management of concomitant disease,
Drugs with high bone bioavailability are needed. Clindamycin or anaemia and coagulopathy should be addressed. In sickle-cell
ciprofloxacin with rifampicin has been advocated when the disease, a high sickle-cell fraction (>70%) may necessitate exchange
organism is sensitive. Rifampicin has very high bone penetration transfusion to permit safe anaesthesia and to prevent further bone
but should never be used alone. infarcts and wound ischaemia after surgery. Blood glucose control in
Curative limb salvage surgery for chronic osteomyelitis diabetic patients may require pre-operative in-patient treatment as
should only be considered if the likely outcome is better than chronic infection can make blood glucose levels erratic.
amputation. With current techniques, this is now often the case As the vascular supply of the affected limb is critical in deter-
and the earlier rather nihilistic view of surgery for bone infection mining the outcome of surgery, significant arterial occlusion or
is unwarranted. Nonetheless some patients may chose amputa- venous insufficiency may require vascular reconstruction prior to
tion after consideration of the treatment options as they believe definitive treatment of the osteomyelitis. If an arterial bypass or
this will give them a quicker resolution of the infection and early angioplasty is performed, infection surgery can be delayed for up to
return to work. For below-knee amputation this may be correct, 3 months to allow optimal reperfusion of the tissues.
but in one large study amputation failed to cure the infection in In HIV patients, antiviral therapy should be reviewed to
9% of cases. reduce viral load to the lowest possible level.
The outcome of surgery is dependant on the physiological status
of the patient and the duration of the infection. Repeated sub- Operative treatment
optimal antibiotic treatment without surgery encourages microbial A tourniquet should be used if possible. Surgical exposure should
resistance and limits the choice of drugs available after surgery. be planned to minimize damage to unaffected tissues while
Definitive treatment should not be unduly delayed, particu- allowing access to the dead bone for sampling. Collection of
larly in infected fractures and non-unions, where bone instability specimens is performed through a small surgical approach;
can cause increased soft-tissue compromise, extension of the multiple deep samples are taken (usually at least four for bacteri-
infection and further bone death. ology culture and two for histology) from the bone and adjacent
tissue as early as possible in the operation to avoid contamination reconstruction lest concerns about the size of the evolving defect
from the patient’s skin and surrounding surfaces but samples prevent adequate resection of the disease.
should not be taken from around a sinus. Each sample is taken with Type IV infections require a segmental resection to eradicate
a fresh instrument (knife, curette, osteotome or bone nibbler) the infected zone. This should be planned to include the involved
which has not been used in any other part of the operation and has soft tissues and skin, protecting the neurovascular structures. It
not touched the patient’s skin. Samples for bacteriology should be is often helpful to apply an external fixator prior to excision to
sent to the laboratory as soon as sampling is complete and the provide stability during surgery and to maintain limb alignment.
laboratory should be warned if any special culture techniques are There is no evidence that antibiotic solutions are superior to
required or atypical organisms are suspected. antiseptics in wound washing but mild detergents have been
If a sinus has been present for many years, this should be shown to be effective in bacterial removal.
excised and sent for histological review to exclude squamous Thus after the excision, the wound is washed with 0.05%
carcinoma. aqueous chlorhexidine which has good antibacterial activity and
After specimens have been taken the infected area must be is gentle on the living tissues rather than hydrogen peroxide
fully exposed to allow radical excision of all infected tissue. which kills host cells or iodine based solutions which are inac-
When planning a radical excision, it is helpful to think of the tivated by contact with blood (Figure 10).
procedure in two stages. Firstly, the limb is laid open to assess The sterile drapes are then replaced and surgical gloves are
the extent of the disease and the limits of the required resection. changed. All contaminated instruments are removed. The tour-
Secondly, the affected tissue is removed by a systematic excision, niquet is released and the pattern of exposed bone bleeding is
starting at one end of the infection and progressing to the other observed. Any small area which does not display punctate
rather than piece-meal removal of tissue without fully under- bleeding (paprika or nutmeg sign) requires further resection.
standing the extent of the disease and with a high risk of leaving Then intravenous antibiotics are given. Our preference is for
infected tissue behind. vancomycin and meropenem initially as these cover most Gram
In general skin and indurated subcutaneous tissue around positive and negative organisms, including MRSA and most
sinuses should be removed as such skin heals poorly. Sinuses anaerobes. Our recent study showed that one-third of organisms
should be excised with an ellipse of skin and are followed down cultured from 166 cases of osteomyelitis were resistant to the
through the deep tissue to a cloaca in the bone. They rarely usual empirical penicillin-based antibiotic regimens.
traverse healthy muscle, rather passing between muscle groups.
Hence they may have long tortuous courses. Dead space management
In type I osteomyelitis, the medullary disease is best While soft-tissue abscess drainage allows the cavity to collapse,
approached through a cortical window in the metaphysis to removing the void previously occupied by pus, bone removal of
reduce the risk of post-operative fracture. The window is infected tissue leaves a rigid-walled space which will rapidly fill
opened using a slow-speed cooled drill and sharp osteotomes. with blood, an ideal culture medium for bacteria. Thus managing
The medullary contents are removed and the canal reamed to such a dead space is essential. The best void filler is living tissue
above and below the lesion. There is often a layer of dead bone which can be from the surrounding muscles by either local rota-
around the inside of the cortex (endosteal sequestrum) which tion/transposition flaps or from distant sites using free vascular-
should be removed back to healthy cortex. This can be ach- ized muscles or bone grafts. There is evidence that muscle flaps
ieved with an osteotome or chisel. Some surgeons prefer to use perform better in osteomyelitis surgery than skin or
a bone burr but care must be taken to avoid thermal necrosis of
the underlying cortex, with the potential for later new
sequestration. If the disease is confined to the isthmus of the
bone, reaming from one end may allow full excision without
a cortical window.
In type II osteomyelitis, the surrounding skin usually needs to
be removed back to a healthy surface of cortical bone which can
be identified because the periosteum will be vascular and nor-
mally adherent to the bone surface. The involved cortex is dis-
coloured and brittle. This should be removed with a chisel to
a bleeding surface, but it may not be necessary to remove the full
thickness of the cortex.
Treatment of type III osteomyelitis involves a combination of
the above techniques. The debridement and excision must be
carefully planned to avoid removing the healthy section of bone
which maintains stability. If this is at risk of fracture during
resection, an external fixator should be applied prior to excision
which must be performed methodically. The medulla and Figure 10 A fully excised Type III osteomyelitis of the tibia. All of the
unstable and scarred surrounding skin has been removed down to
endosteum are cleared together with cortical sequestra, sub-
healthy soft-tissue which can contribute to healing. The cortical window
periosteal abscesses, compromised soft tissues and scarred skin. has been extended to resect all dead bone but the periosteum has not
While the final defect may be large, at this stage it is important to been stripped from the adjacent living cortex. The medullary disease has
focus on tissue removal, rather than thinking ahead to the been cleared and normal bone bleeding observed.
fasciocutaneous flaps. Such flaps provide enhanced blood flow to

the bone; deliver parenteral antibiotics and are resistant to
bacterial colonization (Figure 11). However, if a muscle is placed
in a type III defect, little bone growth can be expected which may
mean there is a permanent fracture risk necessitating delayed
secondary bone grafting to the defect after elevation of the muscle
flap.
Voids can also be filled with an antibiotic-loaded carrier to
deliver high concentrations of antimicrobial directly to the site of
the infection. Most will elute the drug at therapeutic levels for
several weeks. Absorbable and non-absorbable carriers are
available. Originally, Klemm described the use of poly-methyl-
methacrylate (PMMA) beads as a carrier for Gentamicin. These
are provided on wire strings and can be moulded to fit into many
spaces. They can be placed with the end of the string protruding
from the wound for gradual removal (one bead per day starting
after 2e3 days) or can be buried in the bone, permanently, or for
later removal during secondary reconstruction (Figure 12a).
PMMA can also be formed into antibiotic-loaded rods to fill the
whole medullary cavity of the long bones or it can be implanted
as a temporary block spacer across joints or the diaphysis
pending staged bone defect management. PMMA is available
ready mixed with Gentamicin or vancomycin. Other antibiotics
can be added but must be heat stable up to at least 70 C.
Recently, a range of absorbable carriers has been developed.
Collagen carriers with Gentamicin and calcium sulphate pellets
with 4% Tobramicin are produced commercially. Calcium
sulphate can be hand mixed and combined with almost any anti-
biotic as it does not heat up to any extent during curing. It can be
used in a wide variety of bone spaces and dissolves at a predictable a PMMA Gentamicin beads provide high levels of local antibiotics
rate giving very high antibiotic levels for up to 8 weeks within bone defects. These beads will be buried in the bone, to be
(Figure 12b). Additionally there is some evidence that it is osteo- removed at a later second-stage reconstruction. b Calcium
conductive, allowing bone ingrowth into the resection defect. sulphate pellets with tobramycin provide an absorbable antibiotic
Dissolving carriers all share the problem of fluid production delivery system, which avoids the need for removal.
during dissolution which may cause wound leakage for several
weeks. In our experience, this is proportional to the volume of Figure 12
carrier implanted.
As type I osteomyelitis defects are intramedullary, they are

not accessible to filling with muscle. However, they are ideal for
an antibiotic carrier, either as absorbable pellets or a PMMA
antibiotic-loaded rod.
Some authors have advocated the use of continuous suction-
irrigation with antibiotic fluid through implanted tubing within the
medullary canal in these cases. This technique requires prolonged
hospitalization and is much more expensive than an implanted
antibiotic carrier. It is hard to support its use when there are many
more convenient ways of antibiotic delivery for the patient.
The superficial parts of type III defects are usually amenable
to muscle flap filling but the deeper parts of the defect may be
narrow. We often fill the medullary canal with calcium sulphate
pellets and lay the muscle over these. The Papineau technique
described in 1973 of radical excision and space filling using
autogenous bone graft chips followed by repeated dressings over
many weeks epithelializes with poor quality skin. This technique
is rarely indicated today.
Figure 11 This latissimus dorsi muscle will be used to fill the dead space Type IV segmental defects can be managed in a variety of
as a free tissue transfer. The posterior tibial vessels have been exposed ways which are often combined with elements of the bone
after excision of infection and copious irrigation. reconstruction and stabilization. The simplest method is to
acutely shorten the limb to allow bone contact and eliminate the
dead space which may also aid wound closure. It is safe to
acutely shorten the tibia by up to 4 cm, the femur by 6 cm and the
humerus by 5 cm, providing the remaining tissues are supple and
there are no tight scars around neurovascular bundles. This is
our procedure of choice in the elderly type B-host or in those who
will not tolerate prolonged reconstruction. In type A-hosts, acute
shortening can be combined with re-lengthening through a cor-
ticotomy outside the area of infection (bifocal com-
pressionedistraction). Our practice is to delay the corticotomy
for 6 weeks in patients with very active infection, or where there
has been an intramedullary nail crossing the site of infection and
corticotomy (Figure 13aee).
Large segmental defects can be managed in either one or two
stages. Single stage reconstruction with vascularized fibular
grafting, which may be combined with a muscle flap, is a highly
effective treatment but is high risk and is best reserved for type
A-hosts or type Bs-hosts where the systemic compromise can be
well controlled in the initial phase of treatment. Ilizarov bone
transport may be a safer technique in terms of achieving an
infection-free functional limb with a lower risk of failure and
amputation. It is a demanding technique which requires careful
attention to detail during the surgery and pro-active involvement
during distraction to avoid complications and is only possible if
there is sufficient bone available to create the transport segment.
It can be combined with muscle flaps and absorbable antibiotic
carriers, but bone transport around a free muscle flap must be
planned carefully to prevent injury to the flap vascular pedicle
during transport.
Staged reconstruction in type IV osteomyelitis is becoming
more popular, particularly in the USA. The resection defect is
filled with a temporary antibiotic spacer or antibiotic-coated
implant prior to skin closure. Then, at a later date, the definitive
reconstruction is performed in healthy, infection-free tissue
with combinations of bone grafts, implants and permanent
spacers.
Masquelet has described an interesting staged reconstruction
in type IV osteomyelitis. After segmental resection, the defect is
filled with a large PMMA spacer and the soft tissues closed over
it. Over several weeks, a membrane is induced to form around
the spacer, which Masquelet believes is osteoinductive. After
6e8 weeks, the spacer is removed and bone graft packed into the
defect and the membrane is closed tightly around the graft. Over
many months, the graft is incorporated and remodelled.
Bone stabilization
a Segmental resection of type IV osteomyelitis of the tibia. The
Stability is an absolute requirement for eradication of infection.
proximal end has been fully resected but the distal cut is within the
In type IV disease it is obvious that bone will require fixation but region of dead bone and further excision will be needed. b The
in all types of osteomyelitis the potential for fracture after exci- tibia has been stabilized in an Ilizarov circular fixator and the bone
sion must be considered and, if necessary, prevented. acutely shortened to eliminate the dead space. The remaining
A stable limb is also essential for active rehabilitation in the bone has good periosteal cover. The soft-tissue defect will be filled
post-operative period as many type B-hosts do not tolerate bed with a free gracilis muscle flap. c Early post-operative radiograph
with good distal bone contact. A proximal corticotomy is being
rest or limited mobility well. Thus fixation should promote early
distracted to restore limb length. d & e Lateral and AP radiographs
weight-bearing and limb use. In most cases, this is best provided of the completed reconstruction with restoration of the tibial bone
by an external fixator bridging the bone defect (Figure 14). Fix- and no signs of on-going infection.
ator pins must be placed outside the area of infection. This may
involve crossing a joint to achieve adequate stability. External Figure 13
fixator placement should be planned before surgery to allow
a plastic surgeon to access vessels for micro-vascular
usually at 7 days but in some instances, as described above,

prolonged cultures are needed. However, there is inadequate
evidence in the literature to strongly advocate any particular
regimen.
In type IV osteomyelitis, with a segmental resection, the
residual bacterial load may be low and a very short course of
parenteral antibiotic in hospital may be all that is required. In
contrast, a patient who has been bacteraemic, with a grossly
swollen, infected limb may require much longer treatment. It is
our experience that extensive soft-tissue reconstructions heal
better with prolonged antibiotic therapy.
The choice of antimicrobial should be made with an infec-
tious disease specialist team, but in general MRSA infection is
Figure 14 Monolateral external fixator bridging a defect after excision of
best treated with intravenous vancomycin or teicoplanin.
a type III infection. This dead space was filled with calcium sulphate
pellets and has formed some medullary new bone as the pellets have Sensitive staphylococci and streptococci can be managed with
dissolved. ceftriaxone once per day. Anaerobes may require clindamycin
and Pseudomonas an aminoglycoside or ciprofloxacin. We
prefer two drugs in combination where possible to reduce the
anastomosis for muscle flaps or skin transposition for dead space risk of bacterial resistance, but there are many other drug
filling or skin closure. Ilizarov circular fixators are particularly combinations.
useful in this regard. There is no consensus worldwide on the method of delivery or
There is an increasing interest in the use of antibiotic-coated the duration of antibiotics but most centres advise at least 6
internal fixation devices in osteomyelitis. They can only be used weeks of treatment, beginning with some IV antibiotic and
safely when the surgeon is confident that a complete excision of continuing with oral drugs. Antibiotics can be given intrave-
the infected tissue has been performed and there is good soft- nously for prolonged periods using long intravenous lines. The
tissue cover over the implant but even with these restrictions, vast majority of our patients have these inserted to allow
success rates have been shown to fall by around 6% at 2 years parenteral therapy at home. After 2e6 weeks of IV therapy,
when internal fixation is used in the reconstruction. patients will usually continue with oral therapy for a further 6
weeks.
Soft-tissue cover In up to one-third of cases, the laboratory will be unable to
In the past it was common to leave infected wounds open. With culture significant organisms from operative specimens. Post-
better understanding of the disease process and better excision and operative antibiotic choice can then be difficult. The choice must
powerful techniques for soft-tissue reconstruction, it is now include a drug with activity against S. aureus but beyond this, the
unusual to leave a patient with an open wound except when the aetiology of the infection and patient characteristics (sickle-cell
wound would close directly after excision without the need for disease, HIV, etc.) may help in defining an appropriate regimen.
extensive reconstruction but for the tissues being indurated and
stiff. In such cases, a few days of elevation and antibiotics may allow Prognosis and outcome
the tissues to settle with a simpler second stage delayed closure. Management of osteomyelitis in dedicated units, which provide
If it is usually possible to close the wound directly without all of the necessary skills is associated with high success rates
tension in femoral, humeral and spinal disease. Around the and patient satisfaction scores. There are now numerous pub-
pelvis, bone resection of the iliac wings or ischiae will often lished case series reporting in excess of 95% infection-free limbs
allow direct closure, but extensive pressure ulcers or sinuses may at 2 years or more after treatment. A few long-term studies have
preclude closure. If necessary muscle flaps used for dead space shown that more than 90% maintain this result at more than 5
filling are covered with split skin grafts. When healed, they are years.
robust and resistant to injury and can be safely elevated to allow That said, it is difficult to state that any individual patient has
second-stage surgery. been cured of their infection but most have prolonged disease-
Vacuum-assisted closure has been widely applied to many free intervals and die of other causes before relapse. We recently
wound types, but has a very limited place in osteomyelitis. It reviewed 344 of our patients. Overall 98.5% were infection-free
should not be used on discharging sinuses with on-going deep at 2 years, falling to 92% at 4 years and 90% at 8 years.
bone infection as it wastes time prior to definitive treatment. It Cierny has shown in a series of 1966 patients that outcome is
may be indicated in those with extensive soft-tissue defects after determined by host type. Primary treatment was successful in
surgery, who are not suitable for free tissue transfer (Bl-hosts). 96% of type A-hosts and 73% of type B-hosts. Retreatment of
the failed cases gave a 95% success rate at 2 years for both
Antimicrobial therapy groups.
The initial IV antibiotics must be continued until a definitive Recurrence of infection may occur early or late. Early relapse
regimen based on positive cultures can be determined. Our is usually seen shortly after stopping antibiotics and can be
practice is to continue IV meropenem for 3e4 days and then stop treated by repeated surgery. It has been shown that most patients
if no Gram-negative organisms have been isolated. IV vanco- who will relapse have symptoms within the first 2 years after
mycin is continued until final culture results are obtained. This is surgery but a few can return many years later.
There are many potential complications of treatment. In type Kacaoglu M, Eralp L, Rashid HU, Sen C, Bilsel K. Reconstruction of
IVB patients multiple operations are common with significant segmental bone defects due to chronic osteomyelitis with use of an
risks of flap failure, non-union, systemic upset and antimicrobial external fixator and an intramedullary nail. J Bone Joint Surg Am 2006;
drug intolerance. More extensive surgery presents a higher risk 88: 2137e45.
for the patient and the lowest risk strategy should always be Klemm KW. Antibiotic bead chains. Clin Orthop 1993; 295: 63e76.
chosen. Lazzarini L, Lipsky BA, Mader JT. Antibiotic treatment of osteomyelitis:
Success in treatment is not measured only by the infection- what have we learned from 30 years of clinical trials? Int J Infect Dis
free interval. Functional outcome has recently been studied in 2005; 9: 127e38.
patients undergoing treatment for chronic osteomyelitis. In Lazzarini L, Mader JT, Calhoun JH. Osteomyelitis in long bones. J Bone
a series with a 94% cure rate, Short Musculoskeletal Functional Joint Surg Am 2004; 86-A: 2305e18.
Assessment (SMFA) scores were within one standard deviation Lew DP, Waldvogel FA. Osteomyelitis. Lancet 2004; 364: 369e79.
of those in the normal population. A Masquelet AC, Begue T. The concept of induced membrane for recon-
struction of long bone defects. Orthop Clin N Am 2010; 41: 27e37.
McCarthy JJ, Dormans JP, Kozin SH, Pizzutillo PD. Musculoskeletal infec-
tions in children. J Bone Joint Surg Am 2004; 86-A: 850e63.
FURTHER READING McKee MD, Wild LM, Schemitsch EH, Waddell JP. The use of an antibiotic-
Akinyoola AL, Adegbehingbe OO, Aboderin AO. Therapeutic decision in impregnated, osteoconductive, bioabsorbable bone substitute in the
chronic osteomyelitis: sinus track culture versus intraoperative bone treatment of infected long bone defects: early results of a prospective
culture. Arch Orthop Trauma Surg 2009; 129: 449e53. trial. J Orthop Trauma 2002; 16: 622e7.
Beuerlein MJ, McKee MD. Calcium sulfates: what is the evidence? J Orthop McNally MA, Small JO, Tofighi HG, Mollan RAB. Two stage management
Trauma 2010; 24(suppl 1): S46e51. of chronic osteomyelitis of the long bones. J Bone Joint Surg Br
Chang W, Colangeli M, Colangeli S, Di Bella C, Gozzi E, Donati D. Adult 1993; 75-B: 375e80.
osteomyelitis: debridement versus debridement plus Osteoset T Papineau L-J. L’excision-greffe avec fermeture retardee deliberee dans
pellets. Acta Orthop Belg 2007; 73: 238e43. l’osteomyelite chronique. La Nouvelle Presse Medicale 1973; 2:
Cierny III G, Mader JT, Pennick JJ. A clinical staging system for adult 2753e5.
osteomyelitis. Clin Orthop 2003; 414: 7e24. Sheehy SH, Atkins BA, Bejon P, et al. The microbiology of chronic oste-
Cierny III G, DiPasquale D. Treatment of chronic infection. J Am Acad omyelitis: prevalence of resistance to common empirical antimicrobial
Orthop Surg 2006; 14: S105e110. regimens. J Infect 2010; 60: 338e43.
Costerton W, Veeh R, Shirtliff M, Pasmore M, Post C, Ehrlich G. The Thonse R, Conway J. Antibiotic cement-coated interlocking nails for the
application of biofilm science to the study and control of chronic treatment of infected non-unions and segmental bone defects. J
bacterial infections. J Clin Invest 2003; 112: 1466e77. Orthop Trauma 2007; 21: 258e68.
Egol KA, Singh JR, Nwosu U. Functional outcome in patients treated for chronic Tramputz A, Zimmerli W. Diagnosis and treatment of infections associated
post-traumatic osteomyelitis. Bull NYU Hosp Jt Dis 2009; 67: 313e7. with fracture-fixation devices. Injury 2006; 37: S59e66.
Gristina AG, Costerton JW. Bacterial adherence and the glycocalyx and their role Ziran BH, Rao N, Hall RA. A dedicated team approach enhances outcomes
in musculoskeletal infection. Orthop Clin North Am 1984; 15: 517e35. of osteomyelitis treatment. Clin Orthop 2003; 414: 31e6.

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MINI-SYMPOSIUM: PATHOLOGY

(iv) Osteomyelitis resistant to infection; in experimental models, it is necessary to

Figure 3 Extensive chronic osteomyelitis with medullary sequestra, cavi-

Figure 4 MRI demonstrates all of the features of chronic osteomyelitis.

(Figure 8a and b) often follows fractures with internal fixation or

Figure 9 This fracture exhibits diffuse type IV osteomyelitis with bone

be signs of old healed sinuses, active discharging sinuses, soft-

fasciocutaneous flaps. Such flaps provide enhanced blood flow to

As type I osteomyelitis defects are intramedullary, they are

usually at 7 days but in some instances, as described above,

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