# 43 Infection of the bones and joints

# ACKNOWLEDGEMENTS

ACKNOWLEDGEMENTS

Dr Philip Bejon and Dr Philipa Matthews contributed to earlier versions of  this chapter, and I remain grateful for their input. ACKNOWLEDGEMENTS

Dr Philip Bejon and Dr Philipa Matthews contributed to earlier versions of  this chapter, and I remain grateful for their input. ACKNOWLEDGEMENTS

Dr Philip Bejon and Dr Philipa Matthews contributed to earlier versions of  this chapter, and I remain grateful for their input.

# ACUTE OSTEOMYELITIS

ACUTE OSTEOMYELITIS

This presents like septic arthritis with a short history of  pain, swelling, loss of  function and systemic upset. In adults, the vertebral column is the commonest site; in children, long bones are most frequently a ff ected. In young children, a fever and refusal to weight-bear may be the only clues. ACUTE OSTEOMYELITIS

This presents like septic arthritis with a short history of  pain, swelling, loss of  function and systemic upset. In adults, the vertebral column is the commonest site; in children, long bones are most frequently a ff ected. In young children, a fever and refusal to weight-bear may be the only clues. ACUTE OSTEOMYELITIS

This presents like septic arthritis with a short history of  pain, swelling, loss of  function and systemic upset. In adults, the vertebral column is the commonest site; in children, long bones are most frequently a ff ected. In young children, a fever and refusal to weight-bear may be the only clues.

# ANTIMICROBIAL THERAPY FOR PROSTHETIC JOINT INFECTI

ANTIMICROBIAL THERAPY FOR PROSTHETIC JOINT INFECTION AND FRACTURE-RELATED INFECTION

Following surgical sampling, empiric broad-spectrum intra venous antibiotic therapy (e.g. vancomycin and meropenem) should be given. This can be rationalised when culture results are available. In culture-negative cases, ongoing therapy to co ver the most likely pathogens should be instituted. surgical approach, with 6 weeks for those in whom prosthetic material is completely removed versus 6 months for pa tients undergoing a ‘DAIR’ strategy , and prolonged (occasionally lifelong) treatment for patients in whom all other options are contraindicated or intolerable. In a few patients, the best ther - apy is no intervention, when chronic low-grade symptoms are well controlled and preferable to the risks of  either surgery or long-term antibiotic therapy . The antibiotic regimen should be planned with the advice of  a microbiologist and supervised carefully to promote com - pliance and to detect and manage side e ff ects . Monitoring of the joint is largely on clinical grounds; biomarkers including CRP ar e not predictive of  tr eatment failure. Serial radiographs are helpful to detect progressive bone loss, which may be an indicator of  recurrent active infection and can predispose to periprosthetic fracture and implant loosening. ANTIMICROBIAL THERAPY FOR PROSTHETIC JOINT INFECTION AND FRACTURE-RELATED INFECTION

Following surgical sampling, empiric broad-spectrum intra venous antibiotic therapy (e.g. vancomycin and meropenem) should be given. This can be rationalised when culture results are available. In culture-negative cases, ongoing therapy to co ver the most likely pathogens should be instituted. surgical approach, with 6 weeks for those in whom prosthetic material is completely removed versus 6 months for pa tients undergoing a ‘DAIR’ strategy , and prolonged (occasionally lifelong) treatment for patients in whom all other options are contraindicated or intolerable. In a few patients, the best ther - apy is no intervention, when chronic low-grade symptoms are well controlled and preferable to the risks of  either surgery or long-term antibiotic therapy . The antibiotic regimen should be planned with the advice of  a microbiologist and supervised carefully to promote com - pliance and to detect and manage side e ff ects . Monitoring of the joint is largely on clinical grounds; biomarkers including CRP ar e not predictive of  tr eatment failure. Serial radiographs are helpful to detect progressive bone loss, which may be an indicator of  recurrent active infection and can predispose to periprosthetic fracture and implant loosening.

# ANTIMICROBIAL THERAPY FOR PROSTHETIC JOINT INFECTION AND FRACTURE-RELATED INFECTION

ANTIMICROBIAL THERAPY FOR PROSTHETIC JOINT INFECTION AND FRACTURE-RELATED INFECTION

Following surgical sampling, empiric broad-spectrum intra venous antibiotic therapy (e.g. vancomycin and meropenem) should be given. This can be rationalised when culture results are available. In culture-negative cases, ongoing therapy to co ver the most likely pathogens should be instituted. surgical approach, with 6 weeks for those in whom prosthetic material is completely removed versus 6 months for pa tients undergoing a ‘DAIR’ strategy , and prolonged (occasionally lifelong) treatment for patients in whom all other options are contraindicated or intolerable. In a few patients, the best ther - apy is no intervention, when chronic low-grade symptoms are well controlled and preferable to the risks of  either surgery or long-term antibiotic therapy . The antibiotic regimen should be planned with the advice of  a microbiologist and supervised carefully to promote com - pliance and to detect and manage side e ff ects . Monitoring of the joint is largely on clinical grounds; biomarkers including CRP ar e not predictive of  tr eatment failure. Serial radiographs are helpful to detect progressive bone loss, which may be an indicator of  recurrent active infection and can predispose to periprosthetic fracture and implant loosening.

# Antibiotic therapy

Antibiotic therapy

Patients with septic shock, or with rapidly advancing local or systemic signs of  infection, should receive prompt empiric antibiotic therapy . When delay in antibiotics would be unsafe, blood cultures, local aspiration of  pus or radiologically guided biopsy may give valuable culture material immediately prior to starting antibiotics. In most cases, it is safe to delay antibiotics until definitive operative microbiological samples have been taken, particu - larly in chronic or implant-related infections. For patients who should be made; if  safe to do so, antibiotics should be stopped at least 2 weeks before biopsy or surgery . Local guidelines should be followed, but most hospitals rec ommend a ‘community-acquired’ level of  cover using an agent such as co-amoxiclav . Additional antibiotics to cover resistant Gram-positive organisms (e.g. vancomycin for methicillin resistant S. aureus [MRSA]) are considered if  there has been significant prior hospital exposure or if  the patient is known to be colonised with these organisms. Cover for resistant Gram-negative organisms (e.g. meropenem for Pseudomonas considered in certain settings, including severe diabetic foot infection. In the past, prolonged intravenous antibiotic courses (i.e. 4–6 weeks of  treatment) were often recommended. The recent OVIV A trial has shown that oral therapy is equally e ff ective, providing tha t the organism(s) is susceptible and the patient can tolerate the chosen antibiotic. Summary box 43.4 Antibiotics for osteomyelitis /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF 

Septic shock needs treatment without delay, with antibiotics
chosen empirically based on local guidelines
In clinically stable patients, antibiotics should be delayed until
specimens have been taken
In elective surgery for osteomyelitis, antibiotics should be
stopped at least 2 weeks in advance
Agents such as co-amoxiclav or ceftriaxone are appropriate
for most community-acquired infection
Vancomycin or meropenem may be indicated for resistant
species
Oral therapy is effective if susceptible organisms are cultured

Antibiotic therapy

Patients with septic shock, or with rapidly advancing local or systemic signs of  infection, should receive prompt empiric antibiotic therapy . When delay in antibiotics would be unsafe, blood cultures, local aspiration of  pus or radiologically guided biopsy may give valuable culture material immediately prior to starting antibiotics. In most cases, it is safe to delay antibiotics until definitive operative microbiological samples have been taken, particu - larly in chronic or implant-related infections. For patients who should be made; if  safe to do so, antibiotics should be stopped at least 2 weeks before biopsy or surgery . Local guidelines should be followed, but most hospitals rec ommend a ‘community-acquired’ level of  cover using an agent such as co-amoxiclav . Additional antibiotics to cover resistant Gram-positive organisms (e.g. vancomycin for methicillin resistant S. aureus [MRSA]) are considered if  there has been significant prior hospital exposure or if  the patient is known to be colonised with these organisms. Cover for resistant Gram-negative organisms (e.g. meropenem for Pseudomonas considered in certain settings, including severe diabetic foot infection. In the past, prolonged intravenous antibiotic courses (i.e. 4–6 weeks of  treatment) were often recommended. The recent OVIV A trial has shown that oral therapy is equally e ff ective, providing tha t the organism(s) is susceptible and the patient can tolerate the chosen antibiotic. Summary box 43.4 Antibiotics for osteomyelitis /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF 

Septic shock needs treatment without delay, with antibiotics
chosen empirically based on local guidelines
In clinically stable patients, antibiotics should be delayed until
specimens have been taken
In elective surgery for osteomyelitis, antibiotics should be
stopped at least 2 weeks in advance
Agents such as co-amoxiclav or ceftriaxone are appropriate
for most community-acquired infection
Vancomycin or meropenem may be indicated for resistant
species
Oral therapy is effective if susceptible organisms are cultured

Antibiotic therapy

Patients with septic shock, or with rapidly advancing local or systemic signs of  infection, should receive prompt empiric antibiotic therapy . When delay in antibiotics would be unsafe, blood cultures, local aspiration of  pus or radiologically guided biopsy may give valuable culture material immediately prior to starting antibiotics. In most cases, it is safe to delay antibiotics until definitive operative microbiological samples have been taken, particu - larly in chronic or implant-related infections. For patients who should be made; if  safe to do so, antibiotics should be stopped at least 2 weeks before biopsy or surgery . Local guidelines should be followed, but most hospitals rec ommend a ‘community-acquired’ level of  cover using an agent such as co-amoxiclav . Additional antibiotics to cover resistant Gram-positive organisms (e.g. vancomycin for methicillin resistant S. aureus [MRSA]) are considered if  there has been significant prior hospital exposure or if  the patient is known to be colonised with these organisms. Cover for resistant Gram-negative organisms (e.g. meropenem for Pseudomonas considered in certain settings, including severe diabetic foot infection. In the past, prolonged intravenous antibiotic courses (i.e. 4–6 weeks of  treatment) were often recommended. The recent OVIV A trial has shown that oral therapy is equally e ff ective, providing tha t the organism(s) is susceptible and the patient can tolerate the chosen antibiotic. Summary box 43.4 Antibiotics for osteomyelitis /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF 

Septic shock needs treatment without delay, with antibiotics
chosen empirically based on local guidelines
In clinically stable patients, antibiotics should be delayed until
specimens have been taken
In elective surgery for osteomyelitis, antibiotics should be
stopped at least 2 weeks in advance
Agents such as co-amoxiclav or ceftriaxone are appropriate
for most community-acquired infection
Vancomycin or meropenem may be indicated for resistant
species
Oral therapy is effective if susceptible organisms are cultured

# CHRONIC OSTEOMYELITIS

CHRONIC OSTEOMYELITIS

This is a serious condition that may a ff ect the patient for decades. Chronic bone infection is best treated within a dedi - cated multidisciplinary team that has the skills to deal with all aspects of  the condition, the associated comorbidities and the range of  surgical reconstructive options. CHRONIC OSTEOMYELITIS

This is a serious condition that may a ff ect the patient for decades. Chronic bone infection is best treated within a dedi - cated multidisciplinary team that has the skills to deal with all aspects of  the condition, the associated comorbidities and the range of  surgical reconstructive options. CHRONIC OSTEOMYELITIS

This is a serious condition that may a ff ect the patient for decades. Chronic bone infection is best treated within a dedi - cated multidisciplinary team that has the skills to deal with all aspects of  the condition, the associated comorbidities and the range of  surgical reconstructive options.

# Clinical features

Clinical features

Most patients present after an acute or subacute history with a single hot, swollen, painful joint. In children, there is often a history of  recent minor trauma. The joint is held immobile in the ‘position of comfort’, with ‘pseudoparalysis’ in neonates. Sidney Ringer , 1835–1910, Professor of  Clinical Medicine, University College Hospital, London, UK. /uni25CF /uni25CF - /uni25CF /uni25CF /uni25CF - /uni25CF /uni25CF ) is There is severe pain if  any attempt is made to move the a ff ected joint actively or passively . In children and adults, the knee joint is most frequently a ff ected, whereas in neonates it is the hip. Fever and other systemic signs are usually present, but their absence does not rule out the diagnosis. Fever is absent in about one-third of  cases. 

Extremes of age
Underlying joint abnormality, especially rheumatoid arthritis
Immunocompromise (e.g. diabetes mellitus, HIV infection,
immunosuppressive therapy)
Joint instrumentation (e.g. steroid injection, arthroscopy)
Intravenous drug abuse
Indwelling central venous catheter
Bacteraemia (especially
Staphylococcus aureus
)
HIV, human immunode
/f_i
ciency virus.

Clinical features

PJIs may present early (within 3 months of  surgery), in a delayed manner (3–24 months from surgery) or late (after 2 /uni00A0 years). /uni25CF Early infections are acquired at surgery and are usually caused by virulent organisms (e.g. S. aureus ). They present with a discharging wound, cellulitis, pain, inflammation and swelling. /uni25CF Delayed infections are more characteristically due to low-virulence organisms (e.g. coagulase-negative staphylo cocci or cutibacteria). André Gächter , contemporary , Swiss orthopaedic surgeon. . The - /uni25CF Late infections are more likely to present with an indo - lent clinical syndrome of  joint discomfort or mechanical dysfunction (‘start-up’ symptoms are particularly charac - teristic), with or without a discharging sinus. Late presen - tations are usually due to haematogenous infection of  a pre viously uninfected joint, from bacteraemia. The source may indicate the microbiology (e.g. pneumococci from re - spiratory origin, Salmonella spp. from the gut, Escherichia coli from the urinary tract). 

(b)
Figure 43.4
(a)
Septic arthritis of the hip in a person who injects drugs.
This was untreated for several weeks, resulting in destruction of the
joint surface.
(b)
The same hip after 9 months without treatment. The
proximal femur and acetabulum have been grossly eroded by infection.

Clinical features

Most patients present after an acute or subacute history with a single hot, swollen, painful joint. In children, there is often a history of  recent minor trauma. The joint is held immobile in the ‘position of comfort’, with ‘pseudoparalysis’ in neonates. Sidney Ringer , 1835–1910, Professor of  Clinical Medicine, University College Hospital, London, UK. /uni25CF /uni25CF - /uni25CF /uni25CF /uni25CF - /uni25CF /uni25CF ) is There is severe pain if  any attempt is made to move the a ff ected joint actively or passively . In children and adults, the knee joint is most frequently a ff ected, whereas in neonates it is the hip. Fever and other systemic signs are usually present, but their absence does not rule out the diagnosis. Fever is absent in about one-third of  cases. 

Extremes of age
Underlying joint abnormality, especially rheumatoid arthritis
Immunocompromise (e.g. diabetes mellitus, HIV infection,
immunosuppressive therapy)
Joint instrumentation (e.g. steroid injection, arthroscopy)
Intravenous drug abuse
Indwelling central venous catheter
Bacteraemia (especially
Staphylococcus aureus
)
HIV, human immunode
/f_i
ciency virus.

Clinical features

PJIs may present early (within 3 months of  surgery), in a delayed manner (3–24 months from surgery) or late (after 2 /uni00A0 years). /uni25CF Early infections are acquired at surgery and are usually caused by virulent organisms (e.g. S. aureus ). They present with a discharging wound, cellulitis, pain, inflammation and swelling. /uni25CF Delayed infections are more characteristically due to low-virulence organisms (e.g. coagulase-negative staphylo cocci or cutibacteria). André Gächter , contemporary , Swiss orthopaedic surgeon. . The - /uni25CF Late infections are more likely to present with an indo - lent clinical syndrome of  joint discomfort or mechanical dysfunction (‘start-up’ symptoms are particularly charac - teristic), with or without a discharging sinus. Late presen - tations are usually due to haematogenous infection of  a pre viously uninfected joint, from bacteraemia. The source may indicate the microbiology (e.g. pneumococci from re - spiratory origin, Salmonella spp. from the gut, Escherichia coli from the urinary tract). 

(b)
Figure 43.4
(a)
Septic arthritis of the hip in a person who injects drugs.
This was untreated for several weeks, resulting in destruction of the
joint surface.
(b)
The same hip after 9 months without treatment. The
proximal femur and acetabulum have been grossly eroded by infection.

Clinical features

Most patients present after an acute or subacute history with a single hot, swollen, painful joint. In children, there is often a history of  recent minor trauma. The joint is held immobile in the ‘position of comfort’, with ‘pseudoparalysis’ in neonates. Sidney Ringer , 1835–1910, Professor of  Clinical Medicine, University College Hospital, London, UK. /uni25CF /uni25CF - /uni25CF /uni25CF /uni25CF - /uni25CF /uni25CF ) is There is severe pain if  any attempt is made to move the a ff ected joint actively or passively . In children and adults, the knee joint is most frequently a ff ected, whereas in neonates it is the hip. Fever and other systemic signs are usually present, but their absence does not rule out the diagnosis. Fever is absent in about one-third of  cases. 

Extremes of age
Underlying joint abnormality, especially rheumatoid arthritis
Immunocompromise (e.g. diabetes mellitus, HIV infection,
immunosuppressive therapy)
Joint instrumentation (e.g. steroid injection, arthroscopy)
Intravenous drug abuse
Indwelling central venous catheter
Bacteraemia (especially
Staphylococcus aureus
)
HIV, human immunode
/f_i
ciency virus.

Clinical features

PJIs may present early (within 3 months of  surgery), in a delayed manner (3–24 months from surgery) or late (after 2 /uni00A0 years). /uni25CF Early infections are acquired at surgery and are usually caused by virulent organisms (e.g. S. aureus ). They present with a discharging wound, cellulitis, pain, inflammation and swelling. /uni25CF Delayed infections are more characteristically due to low-virulence organisms (e.g. coagulase-negative staphylo cocci or cutibacteria). André Gächter , contemporary , Swiss orthopaedic surgeon. . The - /uni25CF Late infections are more likely to present with an indo - lent clinical syndrome of  joint discomfort or mechanical dysfunction (‘start-up’ symptoms are particularly charac - teristic), with or without a discharging sinus. Late presen - tations are usually due to haematogenous infection of  a pre viously uninfected joint, from bacteraemia. The source may indicate the microbiology (e.g. pneumococci from re - spiratory origin, Salmonella spp. from the gut, Escherichia coli from the urinary tract). 

(b)
Figure 43.4
(a)
Septic arthritis of the hip in a person who injects drugs.
This was untreated for several weeks, resulting in destruction of the
joint surface.
(b)
The same hip after 9 months without treatment. The
proximal femur and acetabulum have been grossly eroded by infection.

# DIABETIC FOOT INFECTION

DIABETIC FOOT INFECTION

The global prevalence of  diabetes has increased exponentially in recent years. Foot infections are a leading cause of  hospital admissions in this group, with an annual incidence of  foot complications of  1–2% per year owing to the combined influ - ence of  macro- and microvascular insu ffi ciency , mechanical disruption, peripheral and autonomic neuropathy , immune defects and impaired tissue healing. Ulceration of  the calca - neum and bones of  the foref oot is common ( Figure 43.11 ) and will result in amputation in up to one-fifth of  cases. Infection begins as invasion of  bacteria into the com - promised tissues and will rapidly spread to deep structures. Diagnosis is made on the clinical signs and symptoms of  local inflammation and systemic upset. The presence of a wound/ ulcer, spreading cellulitis, fevers or critical ischaemia indicate a e infection and the need for urgent treatment. more sever Blood tests are frequently unhelpful, as inflammatory mark - ers may be normal or only mildly raised. Plain radiographs may show evidence of  osteomyelitis but can be normal (par - ticularly ear ly in infection). MRI is the most sensitive imaging modality for diagnosis of bone involvement. Superficial swabs - - - terials - 

The
Figure 43.11
A severe diabetic foot infection, with marked infection,
necrosis and tissue loss. The patient was neuropathic and had ankle
and hindfoot deformity. The foot was salvaged with a corrective triple
fusion of the hindfoot, excision of the infected ulcer, antibiotic therapy
and primary closure of the lateral soft tissues.

mining the organisms responsible for underlying deep-seated infection. A combination of  the ‘probe-to-bone’ test with ele vated inflammatory markers and abnormal plain radiographs confirms the diagnosis. The aetiological agents of  diabetic f oot infection are the same as for bone infection in non-diabetic individuals, namely S. aureus , β -haemolytic streptococci and aerobic Gram-negative bacilli. Pseudomonas is over-represented, and empirical therapy for severe infections should include cover for this organism. Anaerobes may also be present and addition of  metronidazole (particularly for abscesses and/or devitalised tissue) should be considered. Surgical debridement is required for collections, necrotic areas or more extensive osteomyelitis. Thought should be given to distinguishing superficial osteitis, resulting from loss of  soft-tissue cover (often in association with v ascular compro mise), from more extensive bone involvement. In the former, biopsy and antibiotic therapy may be of  limited importance and optimising glycaemic control, improving vascular supply and relieving pressur e, with appropriate footwear, much more important. This approach may avoid more extensive tissue loss or later amputation. Many patients with diabetes with foot infection have sig nificant vascular compromise and neuropathy , which makes healing after surgery unreliable. A full vascular assessment is mandatory in those with poor peripheral pulses. Proximal angioplasty or bypass surgery may impro ve distal vascularity to a level where infection surgery in the foot may be more successful. Amputation is not an easy option in diabetic foot disease and wound healing can be problematic. In general, excision should be adequate to remove all infected material and excess bone may need to be resected to allow tension-fr ee skin clo sure. If  there is extensive peripheral neuropathy , a below-knee amputation in an area with better sensation may be more appropriate. Summary box 43.10 Diabetic foot infection /uni25CF /uni25CF /uni25CF /uni25CF 

The most important risk factor for osteomyelitis is the
presence of a foot ulcer
Ulcer swabs are not reliable in determining the pathogens
responsible for osteomyelitis
Bone biopsy for culture should be considered in extensive/
complex infection but may not be necessary in mild disease
In severe disease, surgical debridement of collections and/
or necrotic tissue is required, followed by antibiotics tailored
according to culture results

DIABETIC FOOT INFECTION

The global prevalence of  diabetes has increased exponentially in recent years. Foot infections are a leading cause of  hospital admissions in this group, with an annual incidence of  foot complications of  1–2% per year owing to the combined influ - ence of  macro- and microvascular insu ffi ciency , mechanical disruption, peripheral and autonomic neuropathy , immune defects and impaired tissue healing. Ulceration of  the calca - neum and bones of  the foref oot is common ( Figure 43.11 ) and will result in amputation in up to one-fifth of  cases. Infection begins as invasion of  bacteria into the com - promised tissues and will rapidly spread to deep structures. Diagnosis is made on the clinical signs and symptoms of  local inflammation and systemic upset. The presence of a wound/ ulcer, spreading cellulitis, fevers or critical ischaemia indicate a e infection and the need for urgent treatment. more sever Blood tests are frequently unhelpful, as inflammatory mark - ers may be normal or only mildly raised. Plain radiographs may show evidence of  osteomyelitis but can be normal (par - ticularly ear ly in infection). MRI is the most sensitive imaging modality for diagnosis of bone involvement. Superficial swabs - - - terials - 

The
Figure 43.11
A severe diabetic foot infection, with marked infection,
necrosis and tissue loss. The patient was neuropathic and had ankle
and hindfoot deformity. The foot was salvaged with a corrective triple
fusion of the hindfoot, excision of the infected ulcer, antibiotic therapy
and primary closure of the lateral soft tissues.

mining the organisms responsible for underlying deep-seated infection. A combination of  the ‘probe-to-bone’ test with ele vated inflammatory markers and abnormal plain radiographs confirms the diagnosis. The aetiological agents of  diabetic f oot infection are the same as for bone infection in non-diabetic individuals, namely S. aureus , β -haemolytic streptococci and aerobic Gram-negative bacilli. Pseudomonas is over-represented, and empirical therapy for severe infections should include cover for this organism. Anaerobes may also be present and addition of  metronidazole (particularly for abscesses and/or devitalised tissue) should be considered. Surgical debridement is required for collections, necrotic areas or more extensive osteomyelitis. Thought should be given to distinguishing superficial osteitis, resulting from loss of  soft-tissue cover (often in association with v ascular compro mise), from more extensive bone involvement. In the former, biopsy and antibiotic therapy may be of  limited importance and optimising glycaemic control, improving vascular supply and relieving pressur e, with appropriate footwear, much more important. This approach may avoid more extensive tissue loss or later amputation. Many patients with diabetes with foot infection have sig nificant vascular compromise and neuropathy , which makes healing after surgery unreliable. A full vascular assessment is mandatory in those with poor peripheral pulses. Proximal angioplasty or bypass surgery may impro ve distal vascularity to a level where infection surgery in the foot may be more successful. Amputation is not an easy option in diabetic foot disease and wound healing can be problematic. In general, excision should be adequate to remove all infected material and excess bone may need to be resected to allow tension-fr ee skin clo sure. If  there is extensive peripheral neuropathy , a below-knee amputation in an area with better sensation may be more appropriate. Summary box 43.10 Diabetic foot infection /uni25CF /uni25CF /uni25CF /uni25CF 

The most important risk factor for osteomyelitis is the
presence of a foot ulcer
Ulcer swabs are not reliable in determining the pathogens
responsible for osteomyelitis
Bone biopsy for culture should be considered in extensive/
complex infection but may not be necessary in mild disease
In severe disease, surgical debridement of collections and/
or necrotic tissue is required, followed by antibiotics tailored
according to culture results

DIABETIC FOOT INFECTION

The global prevalence of  diabetes has increased exponentially in recent years. Foot infections are a leading cause of  hospital admissions in this group, with an annual incidence of  foot complications of  1–2% per year owing to the combined influ - ence of  macro- and microvascular insu ffi ciency , mechanical disruption, peripheral and autonomic neuropathy , immune defects and impaired tissue healing. Ulceration of  the calca - neum and bones of  the foref oot is common ( Figure 43.11 ) and will result in amputation in up to one-fifth of  cases. Infection begins as invasion of  bacteria into the com - promised tissues and will rapidly spread to deep structures. Diagnosis is made on the clinical signs and symptoms of  local inflammation and systemic upset. The presence of a wound/ ulcer, spreading cellulitis, fevers or critical ischaemia indicate a e infection and the need for urgent treatment. more sever Blood tests are frequently unhelpful, as inflammatory mark - ers may be normal or only mildly raised. Plain radiographs may show evidence of  osteomyelitis but can be normal (par - ticularly ear ly in infection). MRI is the most sensitive imaging modality for diagnosis of bone involvement. Superficial swabs - - - terials - 

The
Figure 43.11
A severe diabetic foot infection, with marked infection,
necrosis and tissue loss. The patient was neuropathic and had ankle
and hindfoot deformity. The foot was salvaged with a corrective triple
fusion of the hindfoot, excision of the infected ulcer, antibiotic therapy
and primary closure of the lateral soft tissues.

mining the organisms responsible for underlying deep-seated infection. A combination of  the ‘probe-to-bone’ test with ele vated inflammatory markers and abnormal plain radiographs confirms the diagnosis. The aetiological agents of  diabetic f oot infection are the same as for bone infection in non-diabetic individuals, namely S. aureus , β -haemolytic streptococci and aerobic Gram-negative bacilli. Pseudomonas is over-represented, and empirical therapy for severe infections should include cover for this organism. Anaerobes may also be present and addition of  metronidazole (particularly for abscesses and/or devitalised tissue) should be considered. Surgical debridement is required for collections, necrotic areas or more extensive osteomyelitis. Thought should be given to distinguishing superficial osteitis, resulting from loss of  soft-tissue cover (often in association with v ascular compro mise), from more extensive bone involvement. In the former, biopsy and antibiotic therapy may be of  limited importance and optimising glycaemic control, improving vascular supply and relieving pressur e, with appropriate footwear, much more important. This approach may avoid more extensive tissue loss or later amputation. Many patients with diabetes with foot infection have sig nificant vascular compromise and neuropathy , which makes healing after surgery unreliable. A full vascular assessment is mandatory in those with poor peripheral pulses. Proximal angioplasty or bypass surgery may impro ve distal vascularity to a level where infection surgery in the foot may be more successful. Amputation is not an easy option in diabetic foot disease and wound healing can be problematic. In general, excision should be adequate to remove all infected material and excess bone may need to be resected to allow tension-fr ee skin clo sure. If  there is extensive peripheral neuropathy , a below-knee amputation in an area with better sensation may be more appropriate. Summary box 43.10 Diabetic foot infection /uni25CF /uni25CF /uni25CF /uni25CF 

The most important risk factor for osteomyelitis is the
presence of a foot ulcer
Ulcer swabs are not reliable in determining the pathogens
responsible for osteomyelitis
Bone biopsy for culture should be considered in extensive/
complex infection but may not be necessary in mild disease
In severe disease, surgical debridement of collections and/
or necrotic tissue is required, followed by antibiotics tailored
according to culture results

# Diagnosis

Diagnosis

Clinical - Diagnosis is predominantly clinical with confirmation using other tests, as outlined below . Biomarkers Raised inflammatory markers (erythrocyte sedimentation rate [ESR], C-reactive protein [CRP] and white cell count [WCC]) are characteristic of  acute infection, but they are neither su ffi ciently sensitive nor su ffi ciently specific to rule infection in or out. Recently , new synovial fluid markers ( α -defensin and calprotectin) have shown high accuracy in diagnosis of  PJI. Imaging Plain radiographs can demonstrate dead bone, periosteal reaction, involucrum formation and loosening of  implants. However, they are often normal in the first few days of  infec - tion. A normal radiograph does not exclude infection. Over time, radiographs will show progressive implant loosening, bone lysis or sequestration in chronic osteomyelitis. Ultrasonography is ideal for identifying soft-tissue collec - tions and joint e ff usions and can be used to guide bone biopsy and aspiration. Computed tomography (CT) scans are helpful in assessing bone union of infected fractures. Small sequestra and cortical erosions are best seen with CT and these scans can be used to plan surgery for excision of  dead bone ( Figure 43.3a ). Isotope bone scans are of  very limited value as they are non-specific and give no information that may guide diagno 18 sis or treatment. The combination of F-fluorodeoxyglucose 18 positron emission tomography ( FDG-PET) with a CT scan allows localisation of  active infection in chronic osteomyelitis 18 and may facilitate planning of  surgery . FDG-PET/CT is not specific to infection and so cannot reliably distinguish infective from aseptic loosening around implants. Magnetic resonance imaging (MRI) scanning is the investi gation of  choice, in the absence of  metal implants. It is highly sensitive and specific, showing all components of  the disease ( Figure 43.3b ). However, it can overestimate the extent of infection when ther e is widespread reactive oedema. α β Microbiological diagnosis Good treatment starts with a reliable microbiological diagno - sis. Superficial swabs from wounds or spontaneously draining - pus are unreliable. Cultures from these do not reflect the pathogens in the bone. Microbiological samples may be falsely negative if antibiotics are given first. Synovial tissue samples are particularly important in producing a higher diagnostic yield for infection with mycobacteria or fungi. In chronic infections, particularly those involving pros - thetic material, multiple biopsy samples are needed. It is rec - - ommended to take at least five tissue samples; each one with a separate, sterile instrument. Samples should be promptly transferred to the laboratory with clinical details of  the infec - tion. Cultur e should be maintained for at least 10 days in mus - culoskeletal infections to allow identification of  slow-growing 

Classi
/f_i
cation of
Group(s) of organisms
infection
Gram positive
Staphylococci
Streptococci
Cutibacteria
Enterococci
Gram negative
Enterobacteriaceae
Pseudomonas
spp.
Kingella kingae
Haemophilus
spp.
Neisseria
spp.
Others
Fungi, especially
Candida
spp.
Mycobacterium tuberculosis
Atypical mycobacteria
(
Mycobacterium marinum,
Mycobacterium ulcerans
)
Mixed
Any combination of the above
organisms
‘Culture negative’
No growth from cultures,
but diagnosis of infection
made on clinical/radiological/
histopathological grounds
GI, gastrointestinal; HIV, human immunode
/f_i
ciency virus.
Examples of speci
/f_i
c organisms and context in which infection occurs
Staphylococcus aureus
(commonest across all settings)
Coagulase-negative staphylococci (common in implant-associated infection)
-Haemolytic streptococci, including
Streptococcus pneumoniae,
Streptococcus milleri
group and
Streptococcus viridans
(in implant-associated
infection)
-Haemolytic streptococci (e.g.
Streptococcus pyogenes, Streptococcus
agalactiae
)
Increasingly recognised in implant-associated infection and septic arthritis of
the shoulder
Common in diabetic foot infection and chronic osteomyelitis
Escherichia coli
(especially at extremes of age)
Klebsiella
spp.
Salmonella
spp. (particularly associated with sickle cell disease)
Associated with diabetic foot infections, osteomyelitis underlying chronic
wounds/ulcers, patients heavily exposed to a hospital environment and/or prior
antibiotics
Common cause of septic arthritis in children under 4 years
Haemophilus in
/f_l
uenzae
(consider in non-immunised children)
Neisseria meningitidis
Neisseria gonorrhoeae
(consider risk factors for sexually transmitted infection)
Cause infection in immunocompromised and/or heavily antibiotic-exposed
hosts. Common after prolonged use of negative-pressure wound therapy
Present without pulmonary disease
Geographical distribution
Common with HIV
May be a component of disseminated infection in HIV-infected patients; also
cause post-surgical infection in immunocompetent hosts
More common after trauma, recurrent surgery and with poor wound healing
and sinuses, or resulting from contiguous spread from an infected source (e.g.
skin, GI tract)
Most common in patients who have had recent antimicrobial exposure prior to
surgical sampling

organisms such as C. acnes . A positive tissue diagnosis is con firmed when phenotypically identical organisms are cultured from at least two of  the five tissue samples. A single positive culture may suggest infection. It is also possible to culture organisms from remo implants that have been subjected to ultrasonic vibration to disrupt biofilm (sonication). Summary box 43.3 Principles of diagnosis /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF The histological diagnosis of  infection (rather than other sources of  inflammation) depends on identifying organisms on a Gram stain or the presence of  a neutrophilic infiltrate. Histology can directly diagnose tuberculosis and atypical mycobacterial osteomyelitis (caseating and non-caseating granulomas), actinomycosis and fungal hyphae. The presence of  five or more polymorphonuclear neutrophils per high- powered field is diagnostic in fracture-related joint infections and PJIs. Histology is valuable in confirming the presence of infection in culture-negative cases. 

(b)
Figure 43.3
(a)
T ransverse computed tomography scan of the femur
with a central sequestrum, sinus and cortical bone erosion.
(b)
netic resonance imaging scan of the same femur with better resolution
of the medullary infection and soft-tissue involvement.
ESR and CRP are neither sensitive nor speci
/f_i
c in making a
diagnosis of bone infection
Plain radiographs may be normal in the early phase
Ultrasonography is valuable for identifying
/f_l
uid/pus collections
MRI is usually the investigation of choice
Super
/f_i
cial swabs are of no value in identifying the organism
causing deep infection
If the patient is on antibiotics, cultures may be falsely negative
Multiple biopsy specimens should be obtained to optimise
microbiological diagnosis
A neutrophil in
/f_i
ltrate on histology can con
/f_i
rm infection

Diagnosis

Aspiration and/or biopsy of intra-articular fluid or tissue will allow a Gram stain to be performed (although this is positive in only about one-third of infected cases). Culture of a causative organism from synovial fluid is diagnostic (positive in 80–90%) but results are delayed by the time taken to grow and identify the organism in the laboratory . A high WCC in joint fluid 3 (e.g. 50–150 /uni00A0 000 cells/mm ), with a neutrophil predominance (>90%), is characteristic of  infection. However, other inflam - matory conditions can also cause a raised cell count, and crystals may be seen in infected joints as well as in gout or pseudogout. The limited sensitivity of  direct microscopy and Gram stain and the time taken to obtain a positive culture should not delay early treatment for the infection. The decision to perform a sur gical washout and give antibiotics should be based on the clinical picture. Summary box 43.5 Presentation of septic arthritis /uni25CF /uni25CF ). /uni25CF - /uni25CF - 

Children may be toxic and febrile but adults may have only a
low-grade fever
Usually symptoms affect only one joint, often with pre-existing
arthropathy
The joint is swollen and held in a characteristic ‘position of
comfort’
Any
movement causes extreme pain

Diagnosis

Infection should be suspected in any patient with a leaking wound over an implant, unresolved pain or new pain around a previously pain-free implant. Routine blood tests may be - helpful in acute infection but are often falsely reassuring. The European Bone and Joint Infection Society (EBJIS) has produced diagnostic criteria for PJI. Infection is confirmed if  there is a sinus communicating with the joint or there is a high synovial fluid WCC (>3000/µL), a positive microbiologi cal culture or positive histology (more than five polymorphs per high-power field) ( Figure 43.5 ) Plain radiographs may show features of  loosening of  a chronically infected prosthesis, and ultrasound ma y identify associated collections. Nuclear scans cannot reliably distinguish aseptic loosening from PJI. 

Infection unlikely
All findings negative
A
B
Clinical
A
Clear alternative reason for
Clinical features
implant dysfunction
C-reactive protein
B
Laboratory
• Leukocyte count ≤1500
Synovial fluid
• PMN ≤65%
• All cultures negative
Microbiology
• No growth on sonication
Histology
Negative
C
Radiology
Negative 3-phase isotope
Nuclear imaging
bone scan
Figure 43.5
The European Bone and Joint Infection Society de
/f_i
nition of prosthetic joint infection. CFU, colony-forming unit; CRP , C-reactive
protein; HPF , high-power
/f_i
eld; PMN, polymorphonuclear cells. (Reproduced with permission from McNally MA, Sousa R, Wouthuyzen-Bakker
M
et al
. Infographic: The EBJIS de
/f_i
nition of prosthetic joint infection: a practical guide for clinicians.

Diagnosis

- In the early phase (2–3 days) radiographs may be normal but MRI will show bone oedema and periosteal elevation. After 5–7 days, plain radiographs may show subtle abnormality with osteopenia and periosteal new bone formation. WCC and CRP are often elevated in the early phase. Treatment should not be delayed pending investigations. Diagnosis

Plain radiographs can delineate soft-tissue swelling, subperi - osteal reaction, bone destruction and sequestra. CT scans are good for cortical bone imaging ( Figure 43.8 ). MRI is the imag - ing test of  choice (see General principles of orthopaedic infection ). Blood tests are often normal in chronic osteomy - e from deep elitis. Confirmation of  the diagnosis is with cultur 18 surgical samples and histology . FDG-PET CT scanning can be helpful for surgical planning. 

Figure 43.8
showing diaphyseal chronic osteomyelitis.
clearly shows the sequestration of the lateral cortex and overlying
new bone formation (involucrum).

Diagnosis

Clinical - Diagnosis is predominantly clinical with confirmation using other tests, as outlined below . Biomarkers Raised inflammatory markers (erythrocyte sedimentation rate [ESR], C-reactive protein [CRP] and white cell count [WCC]) are characteristic of  acute infection, but they are neither su ffi ciently sensitive nor su ffi ciently specific to rule infection in or out. Recently , new synovial fluid markers ( α -defensin and calprotectin) have shown high accuracy in diagnosis of  PJI. Imaging Plain radiographs can demonstrate dead bone, periosteal reaction, involucrum formation and loosening of  implants. However, they are often normal in the first few days of  infec - tion. A normal radiograph does not exclude infection. Over time, radiographs will show progressive implant loosening, bone lysis or sequestration in chronic osteomyelitis. Ultrasonography is ideal for identifying soft-tissue collec - tions and joint e ff usions and can be used to guide bone biopsy and aspiration. Computed tomography (CT) scans are helpful in assessing bone union of infected fractures. Small sequestra and cortical erosions are best seen with CT and these scans can be used to plan surgery for excision of  dead bone ( Figure 43.3a ). Isotope bone scans are of  very limited value as they are non-specific and give no information that may guide diagno 18 sis or treatment. The combination of F-fluorodeoxyglucose 18 positron emission tomography ( FDG-PET) with a CT scan allows localisation of  active infection in chronic osteomyelitis 18 and may facilitate planning of  surgery . FDG-PET/CT is not specific to infection and so cannot reliably distinguish infective from aseptic loosening around implants. Magnetic resonance imaging (MRI) scanning is the investi gation of  choice, in the absence of  metal implants. It is highly sensitive and specific, showing all components of  the disease ( Figure 43.3b ). However, it can overestimate the extent of infection when ther e is widespread reactive oedema. α β Microbiological diagnosis Good treatment starts with a reliable microbiological diagno - sis. Superficial swabs from wounds or spontaneously draining - pus are unreliable. Cultures from these do not reflect the pathogens in the bone. Microbiological samples may be falsely negative if antibiotics are given first. Synovial tissue samples are particularly important in producing a higher diagnostic yield for infection with mycobacteria or fungi. In chronic infections, particularly those involving pros - thetic material, multiple biopsy samples are needed. It is rec - - ommended to take at least five tissue samples; each one with a separate, sterile instrument. Samples should be promptly transferred to the laboratory with clinical details of  the infec - tion. Cultur e should be maintained for at least 10 days in mus - culoskeletal infections to allow identification of  slow-growing 

Classi
/f_i
cation of
Group(s) of organisms
infection
Gram positive
Staphylococci
Streptococci
Cutibacteria
Enterococci
Gram negative
Enterobacteriaceae
Pseudomonas
spp.
Kingella kingae
Haemophilus
spp.
Neisseria
spp.
Others
Fungi, especially
Candida
spp.
Mycobacterium tuberculosis
Atypical mycobacteria
(
Mycobacterium marinum,
Mycobacterium ulcerans
)
Mixed
Any combination of the above
organisms
‘Culture negative’
No growth from cultures,
but diagnosis of infection
made on clinical/radiological/
histopathological grounds
GI, gastrointestinal; HIV, human immunode
/f_i
ciency virus.
Examples of speci
/f_i
c organisms and context in which infection occurs
Staphylococcus aureus
(commonest across all settings)
Coagulase-negative staphylococci (common in implant-associated infection)
-Haemolytic streptococci, including
Streptococcus pneumoniae,
Streptococcus milleri
group and
Streptococcus viridans
(in implant-associated
infection)
-Haemolytic streptococci (e.g.
Streptococcus pyogenes, Streptococcus
agalactiae
)
Increasingly recognised in implant-associated infection and septic arthritis of
the shoulder
Common in diabetic foot infection and chronic osteomyelitis
Escherichia coli
(especially at extremes of age)
Klebsiella
spp.
Salmonella
spp. (particularly associated with sickle cell disease)
Associated with diabetic foot infections, osteomyelitis underlying chronic
wounds/ulcers, patients heavily exposed to a hospital environment and/or prior
antibiotics
Common cause of septic arthritis in children under 4 years
Haemophilus in
/f_l
uenzae
(consider in non-immunised children)
Neisseria meningitidis
Neisseria gonorrhoeae
(consider risk factors for sexually transmitted infection)
Cause infection in immunocompromised and/or heavily antibiotic-exposed
hosts. Common after prolonged use of negative-pressure wound therapy
Present without pulmonary disease
Geographical distribution
Common with HIV
May be a component of disseminated infection in HIV-infected patients; also
cause post-surgical infection in immunocompetent hosts
More common after trauma, recurrent surgery and with poor wound healing
and sinuses, or resulting from contiguous spread from an infected source (e.g.
skin, GI tract)
Most common in patients who have had recent antimicrobial exposure prior to
surgical sampling

organisms such as C. acnes . A positive tissue diagnosis is con firmed when phenotypically identical organisms are cultured from at least two of  the five tissue samples. A single positive culture may suggest infection. It is also possible to culture organisms from remo implants that have been subjected to ultrasonic vibration to disrupt biofilm (sonication). Summary box 43.3 Principles of diagnosis /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF The histological diagnosis of  infection (rather than other sources of  inflammation) depends on identifying organisms on a Gram stain or the presence of  a neutrophilic infiltrate. Histology can directly diagnose tuberculosis and atypical mycobacterial osteomyelitis (caseating and non-caseating granulomas), actinomycosis and fungal hyphae. The presence of  five or more polymorphonuclear neutrophils per high- powered field is diagnostic in fracture-related joint infections and PJIs. Histology is valuable in confirming the presence of infection in culture-negative cases. 

(b)
Figure 43.3
(a)
T ransverse computed tomography scan of the femur
with a central sequestrum, sinus and cortical bone erosion.
(b)
netic resonance imaging scan of the same femur with better resolution
of the medullary infection and soft-tissue involvement.
ESR and CRP are neither sensitive nor speci
/f_i
c in making a
diagnosis of bone infection
Plain radiographs may be normal in the early phase
Ultrasonography is valuable for identifying
/f_l
uid/pus collections
MRI is usually the investigation of choice
Super
/f_i
cial swabs are of no value in identifying the organism
causing deep infection
If the patient is on antibiotics, cultures may be falsely negative
Multiple biopsy specimens should be obtained to optimise
microbiological diagnosis
A neutrophil in
/f_i
ltrate on histology can con
/f_i
rm infection

Diagnosis

Aspiration and/or biopsy of intra-articular fluid or tissue will allow a Gram stain to be performed (although this is positive in only about one-third of infected cases). Culture of a causative organism from synovial fluid is diagnostic (positive in 80–90%) but results are delayed by the time taken to grow and identify the organism in the laboratory . A high WCC in joint fluid 3 (e.g. 50–150 /uni00A0 000 cells/mm ), with a neutrophil predominance (>90%), is characteristic of  infection. However, other inflam - matory conditions can also cause a raised cell count, and crystals may be seen in infected joints as well as in gout or pseudogout. The limited sensitivity of  direct microscopy and Gram stain and the time taken to obtain a positive culture should not delay early treatment for the infection. The decision to perform a sur gical washout and give antibiotics should be based on the clinical picture. Summary box 43.5 Presentation of septic arthritis /uni25CF /uni25CF ). /uni25CF - /uni25CF - 

Children may be toxic and febrile but adults may have only a
low-grade fever
Usually symptoms affect only one joint, often with pre-existing
arthropathy
The joint is swollen and held in a characteristic ‘position of
comfort’
Any
movement causes extreme pain

Diagnosis

Infection should be suspected in any patient with a leaking wound over an implant, unresolved pain or new pain around a previously pain-free implant. Routine blood tests may be - helpful in acute infection but are often falsely reassuring. The European Bone and Joint Infection Society (EBJIS) has produced diagnostic criteria for PJI. Infection is confirmed if  there is a sinus communicating with the joint or there is a high synovial fluid WCC (>3000/µL), a positive microbiologi cal culture or positive histology (more than five polymorphs per high-power field) ( Figure 43.5 ) Plain radiographs may show features of  loosening of  a chronically infected prosthesis, and ultrasound ma y identify associated collections. Nuclear scans cannot reliably distinguish aseptic loosening from PJI. 

Infection unlikely
All findings negative
A
B
Clinical
A
Clear alternative reason for
Clinical features
implant dysfunction
C-reactive protein
B
Laboratory
• Leukocyte count ≤1500
Synovial fluid
• PMN ≤65%
• All cultures negative
Microbiology
• No growth on sonication
Histology
Negative
C
Radiology
Negative 3-phase isotope
Nuclear imaging
bone scan
Figure 43.5
The European Bone and Joint Infection Society de
/f_i
nition of prosthetic joint infection. CFU, colony-forming unit; CRP , C-reactive
protein; HPF , high-power
/f_i
eld; PMN, polymorphonuclear cells. (Reproduced with permission from McNally MA, Sousa R, Wouthuyzen-Bakker
M
et al
. Infographic: The EBJIS de
/f_i
nition of prosthetic joint infection: a practical guide for clinicians.

Diagnosis

- In the early phase (2–3 days) radiographs may be normal but MRI will show bone oedema and periosteal elevation. After 5–7 days, plain radiographs may show subtle abnormality with osteopenia and periosteal new bone formation. WCC and CRP are often elevated in the early phase. Treatment should not be delayed pending investigations. Diagnosis

Plain radiographs can delineate soft-tissue swelling, subperi - osteal reaction, bone destruction and sequestra. CT scans are good for cortical bone imaging ( Figure 43.8 ). MRI is the imag - ing test of  choice (see General principles of orthopaedic infection ). Blood tests are often normal in chronic osteomy - e from deep elitis. Confirmation of  the diagnosis is with cultur 18 surgical samples and histology . FDG-PET CT scanning can be helpful for surgical planning. 

Figure 43.8
showing diaphyseal chronic osteomyelitis.
clearly shows the sequestration of the lateral cortex and overlying
new bone formation (involucrum).

Diagnosis

Clinical - Diagnosis is predominantly clinical with confirmation using other tests, as outlined below . Biomarkers Raised inflammatory markers (erythrocyte sedimentation rate [ESR], C-reactive protein [CRP] and white cell count [WCC]) are characteristic of  acute infection, but they are neither su ffi ciently sensitive nor su ffi ciently specific to rule infection in or out. Recently , new synovial fluid markers ( α -defensin and calprotectin) have shown high accuracy in diagnosis of  PJI. Imaging Plain radiographs can demonstrate dead bone, periosteal reaction, involucrum formation and loosening of  implants. However, they are often normal in the first few days of  infec - tion. A normal radiograph does not exclude infection. Over time, radiographs will show progressive implant loosening, bone lysis or sequestration in chronic osteomyelitis. Ultrasonography is ideal for identifying soft-tissue collec - tions and joint e ff usions and can be used to guide bone biopsy and aspiration. Computed tomography (CT) scans are helpful in assessing bone union of infected fractures. Small sequestra and cortical erosions are best seen with CT and these scans can be used to plan surgery for excision of  dead bone ( Figure 43.3a ). Isotope bone scans are of  very limited value as they are non-specific and give no information that may guide diagno 18 sis or treatment. The combination of F-fluorodeoxyglucose 18 positron emission tomography ( FDG-PET) with a CT scan allows localisation of  active infection in chronic osteomyelitis 18 and may facilitate planning of  surgery . FDG-PET/CT is not specific to infection and so cannot reliably distinguish infective from aseptic loosening around implants. Magnetic resonance imaging (MRI) scanning is the investi gation of  choice, in the absence of  metal implants. It is highly sensitive and specific, showing all components of  the disease ( Figure 43.3b ). However, it can overestimate the extent of infection when ther e is widespread reactive oedema. α β Microbiological diagnosis Good treatment starts with a reliable microbiological diagno - sis. Superficial swabs from wounds or spontaneously draining - pus are unreliable. Cultures from these do not reflect the pathogens in the bone. Microbiological samples may be falsely negative if antibiotics are given first. Synovial tissue samples are particularly important in producing a higher diagnostic yield for infection with mycobacteria or fungi. In chronic infections, particularly those involving pros - thetic material, multiple biopsy samples are needed. It is rec - - ommended to take at least five tissue samples; each one with a separate, sterile instrument. Samples should be promptly transferred to the laboratory with clinical details of  the infec - tion. Cultur e should be maintained for at least 10 days in mus - culoskeletal infections to allow identification of  slow-growing 

Classi
/f_i
cation of
Group(s) of organisms
infection
Gram positive
Staphylococci
Streptococci
Cutibacteria
Enterococci
Gram negative
Enterobacteriaceae
Pseudomonas
spp.
Kingella kingae
Haemophilus
spp.
Neisseria
spp.
Others
Fungi, especially
Candida
spp.
Mycobacterium tuberculosis
Atypical mycobacteria
(
Mycobacterium marinum,
Mycobacterium ulcerans
)
Mixed
Any combination of the above
organisms
‘Culture negative’
No growth from cultures,
but diagnosis of infection
made on clinical/radiological/
histopathological grounds
GI, gastrointestinal; HIV, human immunode
/f_i
ciency virus.
Examples of speci
/f_i
c organisms and context in which infection occurs
Staphylococcus aureus
(commonest across all settings)
Coagulase-negative staphylococci (common in implant-associated infection)
-Haemolytic streptococci, including
Streptococcus pneumoniae,
Streptococcus milleri
group and
Streptococcus viridans
(in implant-associated
infection)
-Haemolytic streptococci (e.g.
Streptococcus pyogenes, Streptococcus
agalactiae
)
Increasingly recognised in implant-associated infection and septic arthritis of
the shoulder
Common in diabetic foot infection and chronic osteomyelitis
Escherichia coli
(especially at extremes of age)
Klebsiella
spp.
Salmonella
spp. (particularly associated with sickle cell disease)
Associated with diabetic foot infections, osteomyelitis underlying chronic
wounds/ulcers, patients heavily exposed to a hospital environment and/or prior
antibiotics
Common cause of septic arthritis in children under 4 years
Haemophilus in
/f_l
uenzae
(consider in non-immunised children)
Neisseria meningitidis
Neisseria gonorrhoeae
(consider risk factors for sexually transmitted infection)
Cause infection in immunocompromised and/or heavily antibiotic-exposed
hosts. Common after prolonged use of negative-pressure wound therapy
Present without pulmonary disease
Geographical distribution
Common with HIV
May be a component of disseminated infection in HIV-infected patients; also
cause post-surgical infection in immunocompetent hosts
More common after trauma, recurrent surgery and with poor wound healing
and sinuses, or resulting from contiguous spread from an infected source (e.g.
skin, GI tract)
Most common in patients who have had recent antimicrobial exposure prior to
surgical sampling

organisms such as C. acnes . A positive tissue diagnosis is con firmed when phenotypically identical organisms are cultured from at least two of  the five tissue samples. A single positive culture may suggest infection. It is also possible to culture organisms from remo implants that have been subjected to ultrasonic vibration to disrupt biofilm (sonication). Summary box 43.3 Principles of diagnosis /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF The histological diagnosis of  infection (rather than other sources of  inflammation) depends on identifying organisms on a Gram stain or the presence of  a neutrophilic infiltrate. Histology can directly diagnose tuberculosis and atypical mycobacterial osteomyelitis (caseating and non-caseating granulomas), actinomycosis and fungal hyphae. The presence of  five or more polymorphonuclear neutrophils per high- powered field is diagnostic in fracture-related joint infections and PJIs. Histology is valuable in confirming the presence of infection in culture-negative cases. 

(b)
Figure 43.3
(a)
T ransverse computed tomography scan of the femur
with a central sequestrum, sinus and cortical bone erosion.
(b)
netic resonance imaging scan of the same femur with better resolution
of the medullary infection and soft-tissue involvement.
ESR and CRP are neither sensitive nor speci
/f_i
c in making a
diagnosis of bone infection
Plain radiographs may be normal in the early phase
Ultrasonography is valuable for identifying
/f_l
uid/pus collections
MRI is usually the investigation of choice
Super
/f_i
cial swabs are of no value in identifying the organism
causing deep infection
If the patient is on antibiotics, cultures may be falsely negative
Multiple biopsy specimens should be obtained to optimise
microbiological diagnosis
A neutrophil in
/f_i
ltrate on histology can con
/f_i
rm infection

Diagnosis

Aspiration and/or biopsy of intra-articular fluid or tissue will allow a Gram stain to be performed (although this is positive in only about one-third of infected cases). Culture of a causative organism from synovial fluid is diagnostic (positive in 80–90%) but results are delayed by the time taken to grow and identify the organism in the laboratory . A high WCC in joint fluid 3 (e.g. 50–150 /uni00A0 000 cells/mm ), with a neutrophil predominance (>90%), is characteristic of  infection. However, other inflam - matory conditions can also cause a raised cell count, and crystals may be seen in infected joints as well as in gout or pseudogout. The limited sensitivity of  direct microscopy and Gram stain and the time taken to obtain a positive culture should not delay early treatment for the infection. The decision to perform a sur gical washout and give antibiotics should be based on the clinical picture. Summary box 43.5 Presentation of septic arthritis /uni25CF /uni25CF ). /uni25CF - /uni25CF - 

Children may be toxic and febrile but adults may have only a
low-grade fever
Usually symptoms affect only one joint, often with pre-existing
arthropathy
The joint is swollen and held in a characteristic ‘position of
comfort’
Any
movement causes extreme pain

Diagnosis

Infection should be suspected in any patient with a leaking wound over an implant, unresolved pain or new pain around a previously pain-free implant. Routine blood tests may be - helpful in acute infection but are often falsely reassuring. The European Bone and Joint Infection Society (EBJIS) has produced diagnostic criteria for PJI. Infection is confirmed if  there is a sinus communicating with the joint or there is a high synovial fluid WCC (>3000/µL), a positive microbiologi cal culture or positive histology (more than five polymorphs per high-power field) ( Figure 43.5 ) Plain radiographs may show features of  loosening of  a chronically infected prosthesis, and ultrasound ma y identify associated collections. Nuclear scans cannot reliably distinguish aseptic loosening from PJI. 

Infection unlikely
All findings negative
A
B
Clinical
A
Clear alternative reason for
Clinical features
implant dysfunction
C-reactive protein
B
Laboratory
• Leukocyte count ≤1500
Synovial fluid
• PMN ≤65%
• All cultures negative
Microbiology
• No growth on sonication
Histology
Negative
C
Radiology
Negative 3-phase isotope
Nuclear imaging
bone scan
Figure 43.5
The European Bone and Joint Infection Society de
/f_i
nition of prosthetic joint infection. CFU, colony-forming unit; CRP , C-reactive
protein; HPF , high-power
/f_i
eld; PMN, polymorphonuclear cells. (Reproduced with permission from McNally MA, Sousa R, Wouthuyzen-Bakker
M
et al
. Infographic: The EBJIS de
/f_i
nition of prosthetic joint infection: a practical guide for clinicians.

Diagnosis

- In the early phase (2–3 days) radiographs may be normal but MRI will show bone oedema and periosteal elevation. After 5–7 days, plain radiographs may show subtle abnormality with osteopenia and periosteal new bone formation. WCC and CRP are often elevated in the early phase. Treatment should not be delayed pending investigations. Diagnosis

Plain radiographs can delineate soft-tissue swelling, subperi - osteal reaction, bone destruction and sequestra. CT scans are good for cortical bone imaging ( Figure 43.8 ). MRI is the imag - ing test of  choice (see General principles of orthopaedic infection ). Blood tests are often normal in chronic osteomy - e from deep elitis. Confirmation of  the diagnosis is with cultur 18 surgical samples and histology . FDG-PET CT scanning can be helpful for surgical planning. 

Figure 43.8
showing diaphyseal chronic osteomyelitis.
clearly shows the sequestration of the lateral cortex and overlying
new bone formation (involucrum).

# EPIDEMIOLOGY

EPIDEMIOLOGY

The pattern of  bone infection is changing, and the incidence is increasing. Bone and joint infection a ff ects around 1 per 10 /uni00A0 000 children across the world. Inadequate initial treatment generates chronic infections in up to one-third of  cases. In the developed world, bone infection is frequently seen after injury or surgery (contiguous focus osteomyelitis) and is often implant related ( Figure 43.1 ). Increasing life expectancy , obesity , medical comorbidities (diabetes, peripheral vascular disease, immunocompromise) and increased rates of  bone surgery contribute to a group of  patients with increased susceptibility to infection. Prosthetic joint replacement is a highly successful therapy for joint disease but is complicated by infection in at least 1% of  cases. It was estimated that joint replacement generated more than 70 /uni00A0 000 new cases of  prosthetic joint infection (PJI) in the USA in 2020. These are di ffi cult and expensive to treat, myelos , - - - 

Treatment of infection of native bones and joints
•
Treatment of fracture-related and prosthetic joint
•
infections
Figure 43.1
This open fracture of the tibia was treated with internal
/f_i
xation using a plate. An early fracture-related infection developed,
with skin breakdown and exposure of the metalwork.

fracture has decreased but increased use of  internal fixation has increased the prevalence of  post-traumatic bone infection overall. This will produce a significant economic burden for healthcare providers in the future. Summary box 43.1 Epidemiology of bone infection /uni25CF /uni25CF /uni25CF 

Bone and joint infections from haematogenous spread remain
common worldwide
The increased use of implants for joint replacement and
fracture
/f_i
xation are an important source of new infections
Immunocompromised patients are another increasing source
(e.g. diabetes, cancer treatment)

EPIDEMIOLOGY

The pattern of  bone infection is changing, and the incidence is increasing. Bone and joint infection a ff ects around 1 per 10 /uni00A0 000 children across the world. Inadequate initial treatment generates chronic infections in up to one-third of  cases. In the developed world, bone infection is frequently seen after injury or surgery (contiguous focus osteomyelitis) and is often implant related ( Figure 43.1 ). Increasing life expectancy , obesity , medical comorbidities (diabetes, peripheral vascular disease, immunocompromise) and increased rates of  bone surgery contribute to a group of  patients with increased susceptibility to infection. Prosthetic joint replacement is a highly successful therapy for joint disease but is complicated by infection in at least 1% of  cases. It was estimated that joint replacement generated more than 70 /uni00A0 000 new cases of  prosthetic joint infection (PJI) in the USA in 2020. These are di ffi cult and expensive to treat, myelos , - - - 

Treatment of infection of native bones and joints
•
Treatment of fracture-related and prosthetic joint
•
infections
Figure 43.1
This open fracture of the tibia was treated with internal
/f_i
xation using a plate. An early fracture-related infection developed,
with skin breakdown and exposure of the metalwork.

fracture has decreased but increased use of  internal fixation has increased the prevalence of  post-traumatic bone infection overall. This will produce a significant economic burden for healthcare providers in the future. Summary box 43.1 Epidemiology of bone infection /uni25CF /uni25CF /uni25CF 

Bone and joint infections from haematogenous spread remain
common worldwide
The increased use of implants for joint replacement and
fracture
/f_i
xation are an important source of new infections
Immunocompromised patients are another increasing source
(e.g. diabetes, cancer treatment)

EPIDEMIOLOGY

The pattern of  bone infection is changing, and the incidence is increasing. Bone and joint infection a ff ects around 1 per 10 /uni00A0 000 children across the world. Inadequate initial treatment generates chronic infections in up to one-third of  cases. In the developed world, bone infection is frequently seen after injury or surgery (contiguous focus osteomyelitis) and is often implant related ( Figure 43.1 ). Increasing life expectancy , obesity , medical comorbidities (diabetes, peripheral vascular disease, immunocompromise) and increased rates of  bone surgery contribute to a group of  patients with increased susceptibility to infection. Prosthetic joint replacement is a highly successful therapy for joint disease but is complicated by infection in at least 1% of  cases. It was estimated that joint replacement generated more than 70 /uni00A0 000 new cases of  prosthetic joint infection (PJI) in the USA in 2020. These are di ffi cult and expensive to treat, myelos , - - - 

Treatment of infection of native bones and joints
•
Treatment of fracture-related and prosthetic joint
•
infections
Figure 43.1
This open fracture of the tibia was treated with internal
/f_i
xation using a plate. An early fracture-related infection developed,
with skin breakdown and exposure of the metalwork.

fracture has decreased but increased use of  internal fixation has increased the prevalence of  post-traumatic bone infection overall. This will produce a significant economic burden for healthcare providers in the future. Summary box 43.1 Epidemiology of bone infection /uni25CF /uni25CF /uni25CF 

Bone and joint infections from haematogenous spread remain
common worldwide
The increased use of implants for joint replacement and
fracture
/f_i
xation are an important source of new infections
Immunocompromised patients are another increasing source
(e.g. diabetes, cancer treatment)

# FRACTURE-RELATED INFECTION

FRACTURE-RELATED INFECTION

Infection complicates around 3–5% of  all fracture fixations. Open tibia fractures are a high-risk group with up to 25% becoming infected after fixation. Calcaneal fractures and ankle fracture fixation in the elderly also have high infection rates. Many of  the principles outlined above for PJI can be applied to infections associated with metalwork used to fix fractures. There are several clinical scenarios which must be addressed: /uni25CF Unhealed fracture with stable fixation . This is usually seen early after fixation and can be managed with deep sampling, debridement of infected tissues and man agement of dead spaces (often with local antibiotic carriers) (‘DAIR’ approach). It is extremely important to provide good soft-tissue cover over the fracture. In the tibia, this will most often require a plastic surgical reconstruction. After debridement, systemic antibiotics must be given to suppress infection until bone union. /uni25CF Healed fracture with infected implant . In these cases, the implant can be removed, but there should still be a careful debridement, deep sampling, dead space man agement and soft-tissue cover. /uni25CF Unhealed fracture with unstable fixation bility is essential for bone healing and eradication of  in fection. If  the implant is not stable, it should be removed and replaced by an external fixator. Radical excision of the infected fracture is needed and the resulting defect may present a major reconstructive c hallenge ( Figure 43.7 Recently , antibiotic-coated locking nails have been used to restabilise infected fractures with some success. FRACTURE-RELATED INFECTION

Infection complicates around 3–5% of  all fracture fixations. Open tibia fractures are a high-risk group with up to 25% becoming infected after fixation. Calcaneal fractures and ankle fracture fixation in the elderly also have high infection rates. Many of  the principles outlined above for PJI can be applied to infections associated with metalwork used to fix fractures. There are several clinical scenarios which must be addressed: /uni25CF Unhealed fracture with stable fixation . This is usually seen early after fixation and can be managed with deep sampling, debridement of infected tissues and man agement of dead spaces (often with local antibiotic carriers) (‘DAIR’ approach). It is extremely important to provide good soft-tissue cover over the fracture. In the tibia, this will most often require a plastic surgical reconstruction. After debridement, systemic antibiotics must be given to suppress infection until bone union. /uni25CF Healed fracture with infected implant . In these cases, the implant can be removed, but there should still be a careful debridement, deep sampling, dead space man agement and soft-tissue cover. /uni25CF Unhealed fracture with unstable fixation bility is essential for bone healing and eradication of  in fection. If  the implant is not stable, it should be removed and replaced by an external fixator. Radical excision of the infected fracture is needed and the resulting defect may present a major reconstructive c hallenge ( Figure 43.7 Recently , antibiotic-coated locking nails have been used to restabilise infected fractures with some success. FRACTURE-RELATED INFECTION

Infection complicates around 3–5% of  all fracture fixations. Open tibia fractures are a high-risk group with up to 25% becoming infected after fixation. Calcaneal fractures and ankle fracture fixation in the elderly also have high infection rates. Many of  the principles outlined above for PJI can be applied to infections associated with metalwork used to fix fractures. There are several clinical scenarios which must be addressed: /uni25CF Unhealed fracture with stable fixation . This is usually seen early after fixation and can be managed with deep sampling, debridement of infected tissues and man agement of dead spaces (often with local antibiotic carriers) (‘DAIR’ approach). It is extremely important to provide good soft-tissue cover over the fracture. In the tibia, this will most often require a plastic surgical reconstruction. After debridement, systemic antibiotics must be given to suppress infection until bone union. /uni25CF Healed fracture with infected implant . In these cases, the implant can be removed, but there should still be a careful debridement, deep sampling, dead space man agement and soft-tissue cover. /uni25CF Unhealed fracture with unstable fixation bility is essential for bone healing and eradication of  in fection. If  the implant is not stable, it should be removed and replaced by an external fixator. Radical excision of the infected fracture is needed and the resulting defect may present a major reconstructive c hallenge ( Figure 43.7 Recently , antibiotic-coated locking nails have been used to restabilise infected fractures with some success.

# FURTHER READING

FURTHER READING

Coakley G, Mathews C, Field M et al . BSR & BHPR, BOA, RCGP and BSAC guidelines for management of  the hot swollen joint. Rheumatology 2006; 54 : 1039–41. Dudareva M, Hotchen AJ, Ferguson J et al . The microbiology of osteomyelitis: changes over ten years. J Infection 2019; 79 : 189–98. Ferguson J, Athanasou N, Diefenbeck M, McNally MA. Radiographic and histological analysis of  a synthetic bone graft substitute eluting gentamicin in the treatment of  chronic osteomyelitis. J Bone Joint Infect 2019; 4 (2): 76–84. Hotchen AJ, Dudareva M, Corrigan RA et al . Can we predict outcome after treatment of  long bone osteomyelitis? A study of  patient- reported quality of  life, stratified with the BACH classification. Bone Joint J 2020; 102-B (11): 1587–96. EFORT Open Rev 2017; 2 (1): 7–12. Li H-K, Rombach I, Zambellas R et al . Oral versus intravenous - antibiotics for bone and joint infection. N Engl J Med 2019; 380 : - 425–36. Lipsky BA, Senneville E, Abbas ZG et al . Guidelines on the diagnosis and treatment of  foot infection in persons with diabetes (IWGDF 2019 update). Diabetes Metab Res Rev 2020; 36 (S1): e3280. McNally MA. Osteomyelitis. In: Chen AF (ed.). Management of orthopaedic infections: a practical guide . New Y ork, NY: Thieme, 2021: ch. 5, 61–87. McNally MA, Ferguson JY , Lau ACK et al . Single-stage treatment of chronic osteomyelitis with a new absorbable, gentamicin-loaded, calcium sulphate/hydroxyapatite biocomposite. Bone Joint J 2016; 98-B : 1289–96. McNally M, Govaert G, Dudareva M et al . Definition and diagnosis of fracture-related infection. EFORT Open Rev 2020; 5 : 614–19. McNally MA, Sousa R, Wouthuyzen-Bakker M et al . The EBJIS definition of  prosthetic joint infection: a practical guide for clinicians. Bone Joint J 2021; 103-B (1): 18–25. Metsemakers W-J, Morgenstern, M, Senneville E et al . General treatment principles for fracture-related infection: recommendations from an international expert group. Arch Orthop Trauma Surg 2020; 140 (8): 1013–27. Middleton R, Khan T , Alvand A. Update on the diagnosis and management of  prosthetic joint infection in hip and knee arthroplasty . Bone Joint 360 2019; 8 (4): 5–13. Mifsud M, Ferguson JY , Stubbs DA et al . Simultaneous debridement, Ilizarov reconstruction and free muscle flaps in the management of complex tibial infection. J Bone Joint Infect 2020; 6 : 63–72. FURTHER READING

Coakley G, Mathews C, Field M et al . BSR & BHPR, BOA, RCGP and BSAC guidelines for management of  the hot swollen joint. Rheumatology 2006; 54 : 1039–41. Dudareva M, Hotchen AJ, Ferguson J et al . The microbiology of osteomyelitis: changes over ten years. J Infection 2019; 79 : 189–98. Ferguson J, Athanasou N, Diefenbeck M, McNally MA. Radiographic and histological analysis of  a synthetic bone graft substitute eluting gentamicin in the treatment of  chronic osteomyelitis. J Bone Joint Infect 2019; 4 (2): 76–84. Hotchen AJ, Dudareva M, Corrigan RA et al . Can we predict outcome after treatment of  long bone osteomyelitis? A study of  patient- reported quality of  life, stratified with the BACH classification. Bone Joint J 2020; 102-B (11): 1587–96. EFORT Open Rev 2017; 2 (1): 7–12. Li H-K, Rombach I, Zambellas R et al . Oral versus intravenous - antibiotics for bone and joint infection. N Engl J Med 2019; 380 : - 425–36. Lipsky BA, Senneville E, Abbas ZG et al . Guidelines on the diagnosis and treatment of  foot infection in persons with diabetes (IWGDF 2019 update). Diabetes Metab Res Rev 2020; 36 (S1): e3280. McNally MA. Osteomyelitis. In: Chen AF (ed.). Management of orthopaedic infections: a practical guide . New Y ork, NY: Thieme, 2021: ch. 5, 61–87. McNally MA, Ferguson JY , Lau ACK et al . Single-stage treatment of chronic osteomyelitis with a new absorbable, gentamicin-loaded, calcium sulphate/hydroxyapatite biocomposite. Bone Joint J 2016; 98-B : 1289–96. McNally M, Govaert G, Dudareva M et al . Definition and diagnosis of fracture-related infection. EFORT Open Rev 2020; 5 : 614–19. McNally MA, Sousa R, Wouthuyzen-Bakker M et al . The EBJIS definition of  prosthetic joint infection: a practical guide for clinicians. Bone Joint J 2021; 103-B (1): 18–25. Metsemakers W-J, Morgenstern, M, Senneville E et al . General treatment principles for fracture-related infection: recommendations from an international expert group. Arch Orthop Trauma Surg 2020; 140 (8): 1013–27. Middleton R, Khan T , Alvand A. Update on the diagnosis and management of  prosthetic joint infection in hip and knee arthroplasty . Bone Joint 360 2019; 8 (4): 5–13. Mifsud M, Ferguson JY , Stubbs DA et al . Simultaneous debridement, Ilizarov reconstruction and free muscle flaps in the management of complex tibial infection. J Bone Joint Infect 2020; 6 : 63–72. FURTHER READING

Coakley G, Mathews C, Field M et al . BSR & BHPR, BOA, RCGP and BSAC guidelines for management of  the hot swollen joint. Rheumatology 2006; 54 : 1039–41. Dudareva M, Hotchen AJ, Ferguson J et al . The microbiology of osteomyelitis: changes over ten years. J Infection 2019; 79 : 189–98. Ferguson J, Athanasou N, Diefenbeck M, McNally MA. Radiographic and histological analysis of  a synthetic bone graft substitute eluting gentamicin in the treatment of  chronic osteomyelitis. J Bone Joint Infect 2019; 4 (2): 76–84. Hotchen AJ, Dudareva M, Corrigan RA et al . Can we predict outcome after treatment of  long bone osteomyelitis? A study of  patient- reported quality of  life, stratified with the BACH classification. Bone Joint J 2020; 102-B (11): 1587–96. EFORT Open Rev 2017; 2 (1): 7–12. Li H-K, Rombach I, Zambellas R et al . Oral versus intravenous - antibiotics for bone and joint infection. N Engl J Med 2019; 380 : - 425–36. Lipsky BA, Senneville E, Abbas ZG et al . Guidelines on the diagnosis and treatment of  foot infection in persons with diabetes (IWGDF 2019 update). Diabetes Metab Res Rev 2020; 36 (S1): e3280. McNally MA. Osteomyelitis. In: Chen AF (ed.). Management of orthopaedic infections: a practical guide . New Y ork, NY: Thieme, 2021: ch. 5, 61–87. McNally MA, Ferguson JY , Lau ACK et al . Single-stage treatment of chronic osteomyelitis with a new absorbable, gentamicin-loaded, calcium sulphate/hydroxyapatite biocomposite. Bone Joint J 2016; 98-B : 1289–96. McNally M, Govaert G, Dudareva M et al . Definition and diagnosis of fracture-related infection. EFORT Open Rev 2020; 5 : 614–19. McNally MA, Sousa R, Wouthuyzen-Bakker M et al . The EBJIS definition of  prosthetic joint infection: a practical guide for clinicians. Bone Joint J 2021; 103-B (1): 18–25. Metsemakers W-J, Morgenstern, M, Senneville E et al . General treatment principles for fracture-related infection: recommendations from an international expert group. Arch Orthop Trauma Surg 2020; 140 (8): 1013–27. Middleton R, Khan T , Alvand A. Update on the diagnosis and management of  prosthetic joint infection in hip and knee arthroplasty . Bone Joint 360 2019; 8 (4): 5–13. Mifsud M, Ferguson JY , Stubbs DA et al . Simultaneous debridement, Ilizarov reconstruction and free muscle flaps in the management of complex tibial infection. J Bone Joint Infect 2020; 6 : 63–72.

# GENERAL PRINCIPLES OF ORTHOPAEDIC INFECTION Pathol

GENERAL PRINCIPLES OF ORTHOPAEDIC INFECTION Pathology

Bone infection has all the elements of  any inflammatory condi tion but bone produces some specific pathological features. Acute osteomyelitis occurs when pathogenic organisms cause infection, leading to inflammation in the bone and surround ing tissues. The medullary bone may form abscesses and pus ma y track through the cortex to form periosteal elevation and soft-tissue extension. This process will devascularise the cortical bone, causing bone death – the characteristic featur of  chronic osteomyelitis. Bacteria can adhere to dead bone or implant surfaces, forming a complex community enveloped in a polysaccha ride matrix, known as a biofilm. These bacteria alter their metabolic state, making them mor e resistant both to the host immune system and to antibiotics. Toxins and lytic enzymes ly damage to articular cartilage. from bacteria cause ear Hans Christian Joachim Gram , 1853–1938, Professor of  Medicine, Copenhagen, Denmark. dead fragments of  bone (sequestration) and forming sinuses to drain pus and discharge small bone fragments. New bone is laid down around the infection from the periosteum (involu - crum) ( Figure 43.2 ). In septic arthritis, infection may follow direct ingress of bacteria after injury or surgery , or may result from discharge of  an adjacent acute osteom yelitis into the joint. Particularly in neonates or the elderly , bacteraemia may infect a previously normal joint. Summary box 43.2 Pathology of bone infection /uni25CF /uni25CF /uni25CF 

(a)
(b)
Figure 43.2
(a)
Radiograph of chronic
infection of the femur with a large central
sequestrum and well-developed involucrum.
(b)
The sequestrum that was removed from the
mid-femur at surgery.
Bacteria infecting bone form a resistant bio
/f_i
lm on dead bone
and implant surfaces
Infected bone dies and forms a sequestrum
The periosteum around lays down new bone – an involucrum

GENERAL PRINCIPLES OF ORTHOPAEDIC INFECTION Pathology

Bone infection has all the elements of  any inflammatory condi tion but bone produces some specific pathological features. Acute osteomyelitis occurs when pathogenic organisms cause infection, leading to inflammation in the bone and surround ing tissues. The medullary bone may form abscesses and pus ma y track through the cortex to form periosteal elevation and soft-tissue extension. This process will devascularise the cortical bone, causing bone death – the characteristic featur of  chronic osteomyelitis. Bacteria can adhere to dead bone or implant surfaces, forming a complex community enveloped in a polysaccha ride matrix, known as a biofilm. These bacteria alter their metabolic state, making them mor e resistant both to the host immune system and to antibiotics. Toxins and lytic enzymes ly damage to articular cartilage. from bacteria cause ear Hans Christian Joachim Gram , 1853–1938, Professor of  Medicine, Copenhagen, Denmark. dead fragments of  bone (sequestration) and forming sinuses to drain pus and discharge small bone fragments. New bone is laid down around the infection from the periosteum (involu - crum) ( Figure 43.2 ). In septic arthritis, infection may follow direct ingress of bacteria after injury or surgery , or may result from discharge of  an adjacent acute osteom yelitis into the joint. Particularly in neonates or the elderly , bacteraemia may infect a previously normal joint. Summary box 43.2 Pathology of bone infection /uni25CF /uni25CF /uni25CF 

(a)
(b)
Figure 43.2
(a)
Radiograph of chronic
infection of the femur with a large central
sequestrum and well-developed involucrum.
(b)
The sequestrum that was removed from the
mid-femur at surgery.
Bacteria infecting bone form a resistant bio
/f_i
lm on dead bone
and implant surfaces
Infected bone dies and forms a sequestrum
The periosteum around lays down new bone – an involucrum

# GENERAL PRINCIPLES OF ORTHOPAEDIC INFECTION Pathology

GENERAL PRINCIPLES OF ORTHOPAEDIC INFECTION Pathology

Bone infection has all the elements of  any inflammatory condi tion but bone produces some specific pathological features. Acute osteomyelitis occurs when pathogenic organisms cause infection, leading to inflammation in the bone and surround ing tissues. The medullary bone may form abscesses and pus ma y track through the cortex to form periosteal elevation and soft-tissue extension. This process will devascularise the cortical bone, causing bone death – the characteristic featur of  chronic osteomyelitis. Bacteria can adhere to dead bone or implant surfaces, forming a complex community enveloped in a polysaccha ride matrix, known as a biofilm. These bacteria alter their metabolic state, making them mor e resistant both to the host immune system and to antibiotics. Toxins and lytic enzymes ly damage to articular cartilage. from bacteria cause ear Hans Christian Joachim Gram , 1853–1938, Professor of  Medicine, Copenhagen, Denmark. dead fragments of  bone (sequestration) and forming sinuses to drain pus and discharge small bone fragments. New bone is laid down around the infection from the periosteum (involu - crum) ( Figure 43.2 ). In septic arthritis, infection may follow direct ingress of bacteria after injury or surgery , or may result from discharge of  an adjacent acute osteom yelitis into the joint. Particularly in neonates or the elderly , bacteraemia may infect a previously normal joint. Summary box 43.2 Pathology of bone infection /uni25CF /uni25CF /uni25CF 

(a)
(b)
Figure 43.2
(a)
Radiograph of chronic
infection of the femur with a large central
sequestrum and well-developed involucrum.
(b)
The sequestrum that was removed from the
mid-femur at surgery.
Bacteria infecting bone form a resistant bio
/f_i
lm on dead bone
and implant surfaces
Infected bone dies and forms a sequestrum
The periosteum around lays down new bone – an involucrum

# Introduction

INTRODUCTION

Osteomyelitis is an old disease, identified in dinosaur bones, early hominids and skeletons from ancient civilisations. It is named from the components of  the disease ( osteo , bone; marrow; itis , inflammation; Greek) and is caused by bacterial invasion of  the bone. Worldwide, acute infection of  bones and joints remains common in children. In adults, open fractures and orthopaedic implant surgery produce a large number of severe infections each year. Orthopaedic infection can present acutely , with major sys temic upset, local inflammation and purulence, or insidiously , with gradual bone destruction leading to loss of  function and slowly evolving local symptoms, with or without systemic fea tures. Bone and joint infections cause a substantial burden of complex morbidity . Acute infections can be life- or limb-threat ening, w hile chronic disease may produce pr olonged disability , pain and ill-health. This has major implications for patient mental health and social interactions.

# Learning objectives

Learning objectives

To understand: Characteristic features of septic arthritis, acute and • chronic osteomyelitis and implant infections Diagnostic principles in bone and joint infection • Learning objectives

To understand: Characteristic features of septic arthritis, acute and • chronic osteomyelitis and implant infections Diagnostic principles in bone and joint infection • Learning objectives

To understand: Characteristic features of septic arthritis, acute and • chronic osteomyelitis and implant infections Diagnostic principles in bone and joint infection •

# MUSCULOSKELETAL INFECTION CAUSED BY MYCOBACTERIA

MUSCULOSKELETAL INFECTION CAUSED BY MYCOBACTERIA

Tuberculous arthritis/osteomyelitis remains prevalent in low- and middle-income countries. There is now a resur gence across the world as a consequence of  migration and immunocompromise (including human immunodeficiency tuberculosis . Around half  of  all cases a ff ect the spine, typically - manifesting as para-discal infection but also causing discitis and vertebral osteomyelitis. Native joint infection typically presents with monoarticular pain in a weight-bearing joint. For optimal management of  tuberculosis, the patient must be referred to a specialist multidisciplinary team for input that includes the following components. /uni25CF Baseline screening for HIV and other blood-borne viruses. /uni25CF Assessment for other sites of  mycobacterial infection. /uni25CF Measurement of  baseline renal and liver function, to be repeated at intervals throughout treatment. Drug-induced hepatitis is the commonest serious side e ff ect that may re - quire temporary withdrawal or alteration of  therapy . /uni25CF Baseline and follow-up testing of  hearing (if  injectable agents to be used) and colour vision (if  ethambutol to be - used). /uni25CF Consideration of  any potential drug interactions (rifampi - cin is a potent inducer of  the cytochrome P450 system; it can interact with many classes of drug, including anticon - vulsants, antiretroviral therapy , anticoagulants, antibiotics and antifungals). /uni25CF Institution of  appropriate infection control precautions - and contact tracing. /uni25CF Appropriate education and support to optimise adherence to therapy . /uni25CF Prescription of  an appropriate combination of  drug ther - apy . /uni25CF For fully sensitive M. tuberculosis , the preferred regimen is oral rifampicin, isoniazid, pyrazinamide and etham - butol for 2 months, followed by rifampicin and isonia - zid for a further 4 months. /uni25CF Worldwide, there is an increase in the prevalence of - drug-resistant tuberculosis, classified as multidrug re - sistant (MDR) and extensively drug resistant (XDR). Infection with these organisms requires a treatment regimen that includes an injectable agent (typically ami - kacin, kanamycin or capreomycin) together with oral agents selected according to the susceptibility profile of the isolate (these may include cycloserine, ethionamide, para-aminosalicylic acid [PAS], fluoroquinolones and linezolid). Prolongation of  therapy is r equired, and side e ff ects/toxicity are common. /uni25CF Surgery is only recommended to decompress or stabilise the spine and occasionally to confirm the diagnosis by tis - sue biopsy . Non-tuberculous mycobacteria are ubiquitous environmen - tal organisms. They are best recognised as agents of  disease in patients with underlying immunocompromise (including HIV , diabetes and organ transplantation) or other risk factors for introduction of  infection (such as penetrating trauma or the presence of  a pr osthesis). However, they may occasionally also cause infection in hosts without obvious risk factors. Treatment can be di ffi cult; these organisms are resistant to the standard agents used for first line antituberculous therapy; surgery to debride and drain sites of infection can therefore be - particularly important to reduce the bacterial burden. There is no single standardised drug regimen or duration, so choice of and length of  treatment depends on the location of  disease; extent of  surgical debridement; the identification and pheno typic characteristics of  the organism; and the patient’s underly ing condition, presence of  immunocompromise and response to therapy . As for treatment of M. tuberculosis , expert medical oversight is crucial throughout treatment. MUSCULOSKELETAL INFECTION CAUSED BY MYCOBACTERIA

Tuberculous arthritis/osteomyelitis remains prevalent in low- and middle-income countries. There is now a resur gence across the world as a consequence of  migration and immunocompromise (including human immunodeficiency tuberculosis . Around half  of  all cases a ff ect the spine, typically - manifesting as para-discal infection but also causing discitis and vertebral osteomyelitis. Native joint infection typically presents with monoarticular pain in a weight-bearing joint. For optimal management of  tuberculosis, the patient must be referred to a specialist multidisciplinary team for input that includes the following components. /uni25CF Baseline screening for HIV and other blood-borne viruses. /uni25CF Assessment for other sites of  mycobacterial infection. /uni25CF Measurement of  baseline renal and liver function, to be repeated at intervals throughout treatment. Drug-induced hepatitis is the commonest serious side e ff ect that may re - quire temporary withdrawal or alteration of  therapy . /uni25CF Baseline and follow-up testing of  hearing (if  injectable agents to be used) and colour vision (if  ethambutol to be - used). /uni25CF Consideration of  any potential drug interactions (rifampi - cin is a potent inducer of  the cytochrome P450 system; it can interact with many classes of drug, including anticon - vulsants, antiretroviral therapy , anticoagulants, antibiotics and antifungals). /uni25CF Institution of  appropriate infection control precautions - and contact tracing. /uni25CF Appropriate education and support to optimise adherence to therapy . /uni25CF Prescription of  an appropriate combination of  drug ther - apy . /uni25CF For fully sensitive M. tuberculosis , the preferred regimen is oral rifampicin, isoniazid, pyrazinamide and etham - butol for 2 months, followed by rifampicin and isonia - zid for a further 4 months. /uni25CF Worldwide, there is an increase in the prevalence of - drug-resistant tuberculosis, classified as multidrug re - sistant (MDR) and extensively drug resistant (XDR). Infection with these organisms requires a treatment regimen that includes an injectable agent (typically ami - kacin, kanamycin or capreomycin) together with oral agents selected according to the susceptibility profile of the isolate (these may include cycloserine, ethionamide, para-aminosalicylic acid [PAS], fluoroquinolones and linezolid). Prolongation of  therapy is r equired, and side e ff ects/toxicity are common. /uni25CF Surgery is only recommended to decompress or stabilise the spine and occasionally to confirm the diagnosis by tis - sue biopsy . Non-tuberculous mycobacteria are ubiquitous environmen - tal organisms. They are best recognised as agents of  disease in patients with underlying immunocompromise (including HIV , diabetes and organ transplantation) or other risk factors for introduction of  infection (such as penetrating trauma or the presence of  a pr osthesis). However, they may occasionally also cause infection in hosts without obvious risk factors. Treatment can be di ffi cult; these organisms are resistant to the standard agents used for first line antituberculous therapy; surgery to debride and drain sites of infection can therefore be - particularly important to reduce the bacterial burden. There is no single standardised drug regimen or duration, so choice of and length of  treatment depends on the location of  disease; extent of  surgical debridement; the identification and pheno typic characteristics of  the organism; and the patient’s underly ing condition, presence of  immunocompromise and response to therapy . As for treatment of M. tuberculosis , expert medical oversight is crucial throughout treatment. MUSCULOSKELETAL INFECTION CAUSED BY MYCOBACTERIA

Tuberculous arthritis/osteomyelitis remains prevalent in low- and middle-income countries. There is now a resur gence across the world as a consequence of  migration and immunocompromise (including human immunodeficiency tuberculosis . Around half  of  all cases a ff ect the spine, typically - manifesting as para-discal infection but also causing discitis and vertebral osteomyelitis. Native joint infection typically presents with monoarticular pain in a weight-bearing joint. For optimal management of  tuberculosis, the patient must be referred to a specialist multidisciplinary team for input that includes the following components. /uni25CF Baseline screening for HIV and other blood-borne viruses. /uni25CF Assessment for other sites of  mycobacterial infection. /uni25CF Measurement of  baseline renal and liver function, to be repeated at intervals throughout treatment. Drug-induced hepatitis is the commonest serious side e ff ect that may re - quire temporary withdrawal or alteration of  therapy . /uni25CF Baseline and follow-up testing of  hearing (if  injectable agents to be used) and colour vision (if  ethambutol to be - used). /uni25CF Consideration of  any potential drug interactions (rifampi - cin is a potent inducer of  the cytochrome P450 system; it can interact with many classes of drug, including anticon - vulsants, antiretroviral therapy , anticoagulants, antibiotics and antifungals). /uni25CF Institution of  appropriate infection control precautions - and contact tracing. /uni25CF Appropriate education and support to optimise adherence to therapy . /uni25CF Prescription of  an appropriate combination of  drug ther - apy . /uni25CF For fully sensitive M. tuberculosis , the preferred regimen is oral rifampicin, isoniazid, pyrazinamide and etham - butol for 2 months, followed by rifampicin and isonia - zid for a further 4 months. /uni25CF Worldwide, there is an increase in the prevalence of - drug-resistant tuberculosis, classified as multidrug re - sistant (MDR) and extensively drug resistant (XDR). Infection with these organisms requires a treatment regimen that includes an injectable agent (typically ami - kacin, kanamycin or capreomycin) together with oral agents selected according to the susceptibility profile of the isolate (these may include cycloserine, ethionamide, para-aminosalicylic acid [PAS], fluoroquinolones and linezolid). Prolongation of  therapy is r equired, and side e ff ects/toxicity are common. /uni25CF Surgery is only recommended to decompress or stabilise the spine and occasionally to confirm the diagnosis by tis - sue biopsy . Non-tuberculous mycobacteria are ubiquitous environmen - tal organisms. They are best recognised as agents of  disease in patients with underlying immunocompromise (including HIV , diabetes and organ transplantation) or other risk factors for introduction of  infection (such as penetrating trauma or the presence of  a pr osthesis). However, they may occasionally also cause infection in hosts without obvious risk factors. Treatment can be di ffi cult; these organisms are resistant to the standard agents used for first line antituberculous therapy; surgery to debride and drain sites of infection can therefore be - particularly important to reduce the bacterial burden. There is no single standardised drug regimen or duration, so choice of and length of  treatment depends on the location of  disease; extent of  surgical debridement; the identification and pheno typic characteristics of  the organism; and the patient’s underly ing condition, presence of  immunocompromise and response to therapy . As for treatment of M. tuberculosis , expert medical oversight is crucial throughout treatment.

# Management

Management

Successful treatment requires accurate diagnosis and a multi - disciplinary approach to deliver a package of  care, summarised as follows: /uni25CF Preoperative: /uni25CF patient assessment and clinical staging of  disease; /uni25CF full discussion of  all treatment options with potential complications; /uni25CF diagnostic tests for general health; /uni25CF optimisation of  patients and treatment of  comorbid - ities. /uni25CF Operative: /uni25CF exposure for multiple, deep bone sampling; /uni25CF excision of  all a ff ected tissue; /uni25CF intravenous antibiotics after sampling; /uni25CF bone stabilisation, if  necessary; /uni25CF dead-space management; /uni25CF soft-tissue cover, which may include plastic surgery . /uni25CF Postoperative: /uni25CF functional rehabilitation; /uni25CF continued antimicrobial therapy guided by culture re - sults, with regular clinical monitoring. - The principles listed above dictate that a range of  surgical and medical specialists will be needed to treat patients with bone and joint infections. If  the patient is systemically well, ved tions, optimise patient there is often time to complete investiga health and plan interventions. Complex infections should be referred early to centres that specialise in these cases. Atten - tion to diabetes control, peripheral vascular disease, nutrition and smoking cessation is essential. Many patients will benefit from psychological support or at least good counselling around the di ffi culties of  eradicating infection and the components of treatment. 

Mag
-

Management

Surgical management Medical treatment alone is rarely indicated in joint sepsis. Prompt surgical drainage is a priority to avoid further damage to the cartilage. Arthroscopic washout is commonly performed but it may be di ffi cult to remove loculated areas of infection. Washout should be with Ringer’s solution or of  the risk of  chondrolysis. There should be a low threshold for open arthrotomy , particularly if  a joint is not settling. A synovectomy is recommended if  there is major synovial thickening, aggressive synovitis or subchondral erosions seen on radiology (Gächter stages 3 and 4). Inadequate clearance may lead to chronic infection with destruction of  the joint ( Figure 43.4 ). Treatment may then require joint excision, joint fusion or staged joint replacement. Medical management Antibiotics are usually given for 3–6 weeks (beginning with intravenous therapy). There are sparse data to guide duration. Longer courses should be considered if  the infection is slow to resolve, if  more than one washout is required, if  the patient is bacteraemic and/or if  the infection is caused by S. aureus choice of  antibiotics is as given in Summary box 43.4 . Summary box 43.6 Native joint septic arthritis /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF 

Most common at extremes of age, in patients with rheumatoid
arthritis and in association with immunocompromise
Most commonly affects hips in neonates and knees in adults
and children
The commonest pathogen is
S. aureus
Joints should be aspirated for microbiology before starting
antibiotics, if safe to do so
Management is prompt surgical joint washout, followed by
3–6 weeks of antibiotics

Management

A multidisciplinary approach is required, including ortho paedics, plastic surgery , infectious diseases/microbiology , α pharmacy , nursing, occupational therapy and physiotherapy , centred on the patient’s understanding and wishes regarding their condition. Many patients have other medical comorbid - ities tha t should also be addressed and optimised. PJI can be - associated with a range of  emotional, psychological and mental health issues, ranging from anger about surgical complications to depression arising from chronic symptoms, lack of function and prolonged hospitalisation. T he choice of  surgical strategy for prosthetic joints can be categorised as: /uni25CF salvage of  an infected implant; /uni25CF removal of  the infected implant with or without reimplan - - tation. 

Infection likely
Infection con
/f_i
rmed
Two positive findings
Any positive finding
or
or
C
A
B
C
A
A
B
• Early radiographic
loosening
Sinus tract communication
• Wound-healing problems
with the joint +/–
• Recent fever/bacteraemia
visualisation of prosthesis
• Purulence around
prosthesis
• CRP >10mg/L
• Leukocyte count >3000
• Leukocyte count >1500
• PMN >80%
• PMN >65%
• Positive
-defensin
• Single positive culture
• ≥2 positive samples with
(aspiration or
the same microorganism
intraoperative)
• >50 CFU/mL of any
• > 1 CFU/mL any
organism on sonication
organism on sonication
• Presence of ≥5
Presence of ≥5 neutrophils
neutrophils in ≥5 HPFs
in a single HPF
• Visible microorganisms
Positive white blood cell
labelled scintigraphy
Bone Joint J
2021;
103-B
(1): 16–17.)

determine this (i.e. salvage for early infection versus removal and revision for late infection). Others regard any firmly fixed implant as potentially salvageable, irrespective of  the timing (and there are now several studies showing that this is feasi ble). However, it is agreed that loose infected implants should always be removed ( Figure 43.6 ). Furthermore, it is essential to achieve soft-tissue cover of  bone and pr osthetic material. This may be di ffi cult around the knee, requiring local muscle flaps. Management options can be divided into the following broad approaches. /uni25CF Debridement, antibiotics and implant reten tion - ‘DAIR’ . This can only be undertaken if the pros thesis is well fixed. DAIR is not a form of  washout as all infected soft tissue and necrotic bone must be fully excised and modular components exchanged. This cannot be achieved by arthroscopic surgery . Good soft-tissue cov is essential. Following debridement, the patient is treated with long-term antibiotics (frequently 6 weeks of  intra venous therapy followed by 6 months or more of  oral anti biotics). Prolonged infection-free intervals can be achieved in 80% of  patients but success with this strategy may be lower in infections caused by S. aureus or with multiresis tant organisms. /uni25CF Two-stage joint revision surgery . A thorough ex cision is undertaken and all cement and loose foreign ma terial is removed. An antibiotic-impregnated spacer may be implanted (which may be articulating). This is a tem porary measure and cannot withstand full weight-bearing. The patient is treated with oral or intravenous antibiotics, Gathorne Robert Girdlestone , 1881–1950, Nu ffi eld Professor of  Orthopaedics, University of  Oxford, UK, described excision arthroplasty of  the hip for septic arthritis. ed after the course of  antibiotics has been completed. In recent years ther e has been a trend towards shorter inter - vals between stages, often within the 6-week antimicrobial - therapy . /uni25CF Single-stage joint revision surgery . The procedure is the same as above, but removal and reimplantation are undertaken in the same operating session. Healthy soft tissues around the new implant are essential to prevent reinfection. Some centres consider single-stage revisions when less florid signs of  infection are present (i.e. absence of  collections or sinus tracts), or for frail patients for whom - the risk of a second operation is higher. There are no ad - - equate trial data comparing outcomes with the two-stage approach. /uni25CF Joint removal or fusion . When reconstruction options are not technically possible or are ruled out by comorbid er conditions, removal of  the prosthesis without reimplanta - tion may palliate symptoms. An example is the Girdlestone - excision arthroplasty of the hip. In prosthetic infections of - the knee, ankle or wrist, it may be possible to create a joint fusion after pr osthesis removal. This is complex surgery , which may involve major bone reconstruction. Amputa - - tion may be necessary for knee or ankle implants. /uni25CF Suppressive therapy with antibiotics . In patients - who are not medically fit for any operative intervention, or - who choose to decline all surgical options, long-term treat - ment with antibiotics may help to suppress the symptoms - of  infection. There are limited data, but anecdotally the success rate of  this approach is low . 

(a)
Figure 43.6
(a)
Sinus draining from the scar over the lateral side of the hip. This patient had a total hip replacement 14 years before that had
been complicated by a wound haematoma and infection.
(b)
Radiograph of both hips of same patient. Both hips are loose but only the right
side has de
/f_i
nite infection (arrows).
(b)

Prosthetic joint infection /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF 

Well-
/f_i
xed prostheses may be Debrided, treated with
Antibiotics and the Implant Retained (‘DAIR’ approach)
Loose prostheses must be removed
Replacement can be made at the initial surgery (one stage) or
after a delay to allow infection to be eradicated with antibiotics
(two stage)
Multiple surgical samples are crucial for identifying a pathogen
Thorough excision of infected tissue is a key determinant of
outcome
Long-term antibiotics may be used for patients who are not
suitable for major revision surgery

Management

- Acute osteomyelitis can be treated with antibiotics alone, when the diagnosis is made within 2–3 days of  onset of  symptoms, . Sta - there is no dead bone on imaging and there is no adjacent - septic arthritis. Culture results help to guide therapy , so blood cultures should be taken, and radiologically guided sampling should be considered. Empirical intravenous therapy against Gram-positive organisms is given (cephalosporins or flucloxa - ). cillin), adding gentamicin to cover Gram-negative organisms in children under 1 year. The limb should be splinted and good analgesia given. Intravenous antibiotics should be converted to oral therapy , depending on clinical progress and the results of cultures, and therapy is continued for a total of 2–3 weeks. If  the patient does not respond rapidly , if  the limb deteriorates or if  there is imaging evidence of  progression of  disease, surgery is indi - cated to prevent bone destruction and the onset of  chronic osteomyelitis. With prompt treatment, acute bone infection has a good - prognosis with a 90% cure rate. Failure to tr eat adequa tely pro - duces chronicity , with recurrent infection over many years. In children, the adjacent growth plates and joints may be a ff ected with subsequent deformity and joint destruction. Summary box 43.8 Acute osteomyelitis /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF Gavriil Abramovich Ilizarov , 1921–1992, orthopaedic surgeon, Kurgan, Western Siberia, Russia, pioneered this eponymous approach to bone reconstruction in the 1960s for the management of  osteomyelitis, fractures and limb deformities. 

(c)
Figure 43.7
(a)
Radiograph of a complex distal tibia fracture that was internally
/f_i
xed but complicated by deep infection.
plate was loose and grossly infected.
(c)
The plate and all infected tissue was excised. Deep samples were sent for microbiology and histology.
The defect at the lower end was
/f_i
lled with an absorbable antibiotic carrier.
and the skin primarily closed.
Presents in children with toxaemia, fever and unwillingness to
move the limb
May affect the vertebral column in adults, where back pain
may be the only symptom
Radiographs may be normal for up to 1 week so are of limited
value in early diagnosis
MRI is the investigation of choice
WCC and CRP are usually raised
Early diagnosis is treated with high dose intravenous
antibiotics, started empirically and modi
/f_i
ed with culture
results
Late diagnosis and/or failure of medical treatment requires
surgical debridement
(d)
(b)
At operation, the
(d)
The bone was stabilised with an Ilizarov circular external
/f_i
xator

Management

The BACH classification divides patients into ‘uncomplicated’, ‘complex’ and ‘limited options available’ based on the four important features of  the infection ( Figure 43.9 ). These are: the anatomical location in the bone (B), the antimicrobial profile (A), the need for soft-tissue cover (C) and the health of  the host (H). Treatment must always address all four parts of  the classification to achieve good outcomes. All infected unhealed fractures and infected non-unions are complex. As with PJI, comorbidities should be optimised before sur - gery . The interaction between the patient’s health status and the extent of  the bone infection greatly a ff ects the outcome after surgery . In chronic infection, it is essential to address med - ical conditions that ma y impair wound healing (e.g. smoking, peripheral vascular disease, diabetes, steroid use) prior to sur - gery . This approach has been shown to improve cure rates. A joint assessment by an orthopaedic sur geon, plastic surgeon and infectious disease physician will allow good preoperative planning. 

B
one involvement
A
ntimicrobial options
Ax
B1
Unknown/culture negative
Cavitary
ed
involvement
cat
A1
(including medullary,
pli
<4 resistant tests
cortical and
om
≥
80% susceptibility tests
non-segmental
Unc
sensitive
corticomedullary)
A2
B2
>4 resistant tests
Segmental
<80% susceptibility tests
involvement
lex
sensitive
Any infection with
Comp
joint involvement
A3
B3
Sensitivity to either 0 or 1
Whole bone
susceptibility test
involvement
Limited options
Figure 43.9
The BACH classi
/f_i
cation of osteomyelitis.
(a)
Coronal computed tomography scan of the femur
(b)
A transverse section
C
overage of soft tissue
H
ost status
H1
C1
Patient
/f_i
t and well or has
Direct closure possible
well-controlled disease
Plastic surgery expertise
not
required
H2
C1
Patient with either poorly
Direct closure not possible
controlled disease, severe
Plastic surgery expertise
disease or recurrent
required
osteomyelitis
H3
Un
/f_i
t for anaesthetic
Patient declines surgery
Surgery not indicated

In uncomplicated disease, excision of  the dead bone, with local and systemic antibiotics and direct wound closure, is highly e ff ective ( Figure 43.10 ). If  more than one-third of  the cortical circumference is excised, splintage is essential, often with external fixation to prevent fracture. Secondary bone grafting may be needed. When the infection is segmental (BACH complex), or when the soft-tissue envelope cannot be closed directly , major recon struction will be required. Curative resection must be segmen tal and bone stabilisation will always be required. The Ilizarov method, which uses distraction osteogenesis to fill bone defects, is a powerful and successful technique in these cases. It can be combined with free tissue transfer. T his allows reconstruction to proceed in parallel with rehabilitation. After surgery , patients should be given antibiotics. In total segmental excision of  infection a short course may be indicated, but in most chronic infections 6–12 weeks is often advised. If there is any doubt about the adequacy of  removal of  the dead bone , a long antibiotic course will be needed and recurrence will be more likely . In chronic fracture-related infection, anti biotics should continue until fracture union. There is now increasing interest in the use of  local antibiotic absorbable carriers. These can deliver high doses of  antibiotics into the bone, without systemic e ff ects. Some ceramic ma (with hydroxyapatite) can form new bone in the defect, avoid ing the need for secondary bone grafting. Chronic osteomyelitis /uni25CF /uni25CF /uni25CF 

Figure 43.10
(a)
This magnetic resonance imaging scan shows a
BACH uncomplicated medullary osteomyelitis of the femur.
(b)
infected bone has been removed by reaming and the central defect
/f_i
lled with absorbable calcium sulphate pellets with gentamicin.
Chronic disease requires specialist surgery with excision,
stabilisation and reconstruction
Host status should be optimised before surgery
Following surgery, antibiotic therapy is typically continued for
at least 6 weeks

Management

Successful treatment requires accurate diagnosis and a multi - disciplinary approach to deliver a package of  care, summarised as follows: /uni25CF Preoperative: /uni25CF patient assessment and clinical staging of  disease; /uni25CF full discussion of  all treatment options with potential complications; /uni25CF diagnostic tests for general health; /uni25CF optimisation of  patients and treatment of  comorbid - ities. /uni25CF Operative: /uni25CF exposure for multiple, deep bone sampling; /uni25CF excision of  all a ff ected tissue; /uni25CF intravenous antibiotics after sampling; /uni25CF bone stabilisation, if  necessary; /uni25CF dead-space management; /uni25CF soft-tissue cover, which may include plastic surgery . /uni25CF Postoperative: /uni25CF functional rehabilitation; /uni25CF continued antimicrobial therapy guided by culture re - sults, with regular clinical monitoring. - The principles listed above dictate that a range of  surgical and medical specialists will be needed to treat patients with bone and joint infections. If  the patient is systemically well, ved tions, optimise patient there is often time to complete investiga health and plan interventions. Complex infections should be referred early to centres that specialise in these cases. Atten - tion to diabetes control, peripheral vascular disease, nutrition and smoking cessation is essential. Many patients will benefit from psychological support or at least good counselling around the di ffi culties of  eradicating infection and the components of treatment. 

Mag
-

Management

Surgical management Medical treatment alone is rarely indicated in joint sepsis. Prompt surgical drainage is a priority to avoid further damage to the cartilage. Arthroscopic washout is commonly performed but it may be di ffi cult to remove loculated areas of infection. Washout should be with Ringer’s solution or of  the risk of  chondrolysis. There should be a low threshold for open arthrotomy , particularly if  a joint is not settling. A synovectomy is recommended if  there is major synovial thickening, aggressive synovitis or subchondral erosions seen on radiology (Gächter stages 3 and 4). Inadequate clearance may lead to chronic infection with destruction of  the joint ( Figure 43.4 ). Treatment may then require joint excision, joint fusion or staged joint replacement. Medical management Antibiotics are usually given for 3–6 weeks (beginning with intravenous therapy). There are sparse data to guide duration. Longer courses should be considered if  the infection is slow to resolve, if  more than one washout is required, if  the patient is bacteraemic and/or if  the infection is caused by S. aureus choice of  antibiotics is as given in Summary box 43.4 . Summary box 43.6 Native joint septic arthritis /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF 

Most common at extremes of age, in patients with rheumatoid
arthritis and in association with immunocompromise
Most commonly affects hips in neonates and knees in adults
and children
The commonest pathogen is
S. aureus
Joints should be aspirated for microbiology before starting
antibiotics, if safe to do so
Management is prompt surgical joint washout, followed by
3–6 weeks of antibiotics

Management

A multidisciplinary approach is required, including ortho paedics, plastic surgery , infectious diseases/microbiology , α pharmacy , nursing, occupational therapy and physiotherapy , centred on the patient’s understanding and wishes regarding their condition. Many patients have other medical comorbid - ities tha t should also be addressed and optimised. PJI can be - associated with a range of  emotional, psychological and mental health issues, ranging from anger about surgical complications to depression arising from chronic symptoms, lack of function and prolonged hospitalisation. T he choice of  surgical strategy for prosthetic joints can be categorised as: /uni25CF salvage of  an infected implant; /uni25CF removal of  the infected implant with or without reimplan - - tation. 

Infection likely
Infection con
/f_i
rmed
Two positive findings
Any positive finding
or
or
C
A
B
C
A
A
B
• Early radiographic
loosening
Sinus tract communication
• Wound-healing problems
with the joint +/–
• Recent fever/bacteraemia
visualisation of prosthesis
• Purulence around
prosthesis
• CRP >10mg/L
• Leukocyte count >3000
• Leukocyte count >1500
• PMN >80%
• PMN >65%
• Positive
-defensin
• Single positive culture
• ≥2 positive samples with
(aspiration or
the same microorganism
intraoperative)
• >50 CFU/mL of any
• > 1 CFU/mL any
organism on sonication
organism on sonication
• Presence of ≥5
Presence of ≥5 neutrophils
neutrophils in ≥5 HPFs
in a single HPF
• Visible microorganisms
Positive white blood cell
labelled scintigraphy
Bone Joint J
2021;
103-B
(1): 16–17.)

determine this (i.e. salvage for early infection versus removal and revision for late infection). Others regard any firmly fixed implant as potentially salvageable, irrespective of  the timing (and there are now several studies showing that this is feasi ble). However, it is agreed that loose infected implants should always be removed ( Figure 43.6 ). Furthermore, it is essential to achieve soft-tissue cover of  bone and pr osthetic material. This may be di ffi cult around the knee, requiring local muscle flaps. Management options can be divided into the following broad approaches. /uni25CF Debridement, antibiotics and implant reten tion - ‘DAIR’ . This can only be undertaken if the pros thesis is well fixed. DAIR is not a form of  washout as all infected soft tissue and necrotic bone must be fully excised and modular components exchanged. This cannot be achieved by arthroscopic surgery . Good soft-tissue cov is essential. Following debridement, the patient is treated with long-term antibiotics (frequently 6 weeks of  intra venous therapy followed by 6 months or more of  oral anti biotics). Prolonged infection-free intervals can be achieved in 80% of  patients but success with this strategy may be lower in infections caused by S. aureus or with multiresis tant organisms. /uni25CF Two-stage joint revision surgery . A thorough ex cision is undertaken and all cement and loose foreign ma terial is removed. An antibiotic-impregnated spacer may be implanted (which may be articulating). This is a tem porary measure and cannot withstand full weight-bearing. The patient is treated with oral or intravenous antibiotics, Gathorne Robert Girdlestone , 1881–1950, Nu ffi eld Professor of  Orthopaedics, University of  Oxford, UK, described excision arthroplasty of  the hip for septic arthritis. ed after the course of  antibiotics has been completed. In recent years ther e has been a trend towards shorter inter - vals between stages, often within the 6-week antimicrobial - therapy . /uni25CF Single-stage joint revision surgery . The procedure is the same as above, but removal and reimplantation are undertaken in the same operating session. Healthy soft tissues around the new implant are essential to prevent reinfection. Some centres consider single-stage revisions when less florid signs of  infection are present (i.e. absence of  collections or sinus tracts), or for frail patients for whom - the risk of a second operation is higher. There are no ad - - equate trial data comparing outcomes with the two-stage approach. /uni25CF Joint removal or fusion . When reconstruction options are not technically possible or are ruled out by comorbid er conditions, removal of  the prosthesis without reimplanta - tion may palliate symptoms. An example is the Girdlestone - excision arthroplasty of the hip. In prosthetic infections of - the knee, ankle or wrist, it may be possible to create a joint fusion after pr osthesis removal. This is complex surgery , which may involve major bone reconstruction. Amputa - - tion may be necessary for knee or ankle implants. /uni25CF Suppressive therapy with antibiotics . In patients - who are not medically fit for any operative intervention, or - who choose to decline all surgical options, long-term treat - ment with antibiotics may help to suppress the symptoms - of  infection. There are limited data, but anecdotally the success rate of  this approach is low . 

(a)
Figure 43.6
(a)
Sinus draining from the scar over the lateral side of the hip. This patient had a total hip replacement 14 years before that had
been complicated by a wound haematoma and infection.
(b)
Radiograph of both hips of same patient. Both hips are loose but only the right
side has de
/f_i
nite infection (arrows).
(b)

Prosthetic joint infection /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF 

Well-
/f_i
xed prostheses may be Debrided, treated with
Antibiotics and the Implant Retained (‘DAIR’ approach)
Loose prostheses must be removed
Replacement can be made at the initial surgery (one stage) or
after a delay to allow infection to be eradicated with antibiotics
(two stage)
Multiple surgical samples are crucial for identifying a pathogen
Thorough excision of infected tissue is a key determinant of
outcome
Long-term antibiotics may be used for patients who are not
suitable for major revision surgery

Management

- Acute osteomyelitis can be treated with antibiotics alone, when the diagnosis is made within 2–3 days of  onset of  symptoms, . Sta - there is no dead bone on imaging and there is no adjacent - septic arthritis. Culture results help to guide therapy , so blood cultures should be taken, and radiologically guided sampling should be considered. Empirical intravenous therapy against Gram-positive organisms is given (cephalosporins or flucloxa - ). cillin), adding gentamicin to cover Gram-negative organisms in children under 1 year. The limb should be splinted and good analgesia given. Intravenous antibiotics should be converted to oral therapy , depending on clinical progress and the results of cultures, and therapy is continued for a total of 2–3 weeks. If  the patient does not respond rapidly , if  the limb deteriorates or if  there is imaging evidence of  progression of  disease, surgery is indi - cated to prevent bone destruction and the onset of  chronic osteomyelitis. With prompt treatment, acute bone infection has a good - prognosis with a 90% cure rate. Failure to tr eat adequa tely pro - duces chronicity , with recurrent infection over many years. In children, the adjacent growth plates and joints may be a ff ected with subsequent deformity and joint destruction. Summary box 43.8 Acute osteomyelitis /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF Gavriil Abramovich Ilizarov , 1921–1992, orthopaedic surgeon, Kurgan, Western Siberia, Russia, pioneered this eponymous approach to bone reconstruction in the 1960s for the management of  osteomyelitis, fractures and limb deformities. 

(c)
Figure 43.7
(a)
Radiograph of a complex distal tibia fracture that was internally
/f_i
xed but complicated by deep infection.
plate was loose and grossly infected.
(c)
The plate and all infected tissue was excised. Deep samples were sent for microbiology and histology.
The defect at the lower end was
/f_i
lled with an absorbable antibiotic carrier.
and the skin primarily closed.
Presents in children with toxaemia, fever and unwillingness to
move the limb
May affect the vertebral column in adults, where back pain
may be the only symptom
Radiographs may be normal for up to 1 week so are of limited
value in early diagnosis
MRI is the investigation of choice
WCC and CRP are usually raised
Early diagnosis is treated with high dose intravenous
antibiotics, started empirically and modi
/f_i
ed with culture
results
Late diagnosis and/or failure of medical treatment requires
surgical debridement
(d)
(b)
At operation, the
(d)
The bone was stabilised with an Ilizarov circular external
/f_i
xator

Management

The BACH classification divides patients into ‘uncomplicated’, ‘complex’ and ‘limited options available’ based on the four important features of  the infection ( Figure 43.9 ). These are: the anatomical location in the bone (B), the antimicrobial profile (A), the need for soft-tissue cover (C) and the health of  the host (H). Treatment must always address all four parts of  the classification to achieve good outcomes. All infected unhealed fractures and infected non-unions are complex. As with PJI, comorbidities should be optimised before sur - gery . The interaction between the patient’s health status and the extent of  the bone infection greatly a ff ects the outcome after surgery . In chronic infection, it is essential to address med - ical conditions that ma y impair wound healing (e.g. smoking, peripheral vascular disease, diabetes, steroid use) prior to sur - gery . This approach has been shown to improve cure rates. A joint assessment by an orthopaedic sur geon, plastic surgeon and infectious disease physician will allow good preoperative planning. 

B
one involvement
A
ntimicrobial options
Ax
B1
Unknown/culture negative
Cavitary
ed
involvement
cat
A1
(including medullary,
pli
<4 resistant tests
cortical and
om
≥
80% susceptibility tests
non-segmental
Unc
sensitive
corticomedullary)
A2
B2
>4 resistant tests
Segmental
<80% susceptibility tests
involvement
lex
sensitive
Any infection with
Comp
joint involvement
A3
B3
Sensitivity to either 0 or 1
Whole bone
susceptibility test
involvement
Limited options
Figure 43.9
The BACH classi
/f_i
cation of osteomyelitis.
(a)
Coronal computed tomography scan of the femur
(b)
A transverse section
C
overage of soft tissue
H
ost status
H1
C1
Patient
/f_i
t and well or has
Direct closure possible
well-controlled disease
Plastic surgery expertise
not
required
H2
C1
Patient with either poorly
Direct closure not possible
controlled disease, severe
Plastic surgery expertise
disease or recurrent
required
osteomyelitis
H3
Un
/f_i
t for anaesthetic
Patient declines surgery
Surgery not indicated

In uncomplicated disease, excision of  the dead bone, with local and systemic antibiotics and direct wound closure, is highly e ff ective ( Figure 43.10 ). If  more than one-third of  the cortical circumference is excised, splintage is essential, often with external fixation to prevent fracture. Secondary bone grafting may be needed. When the infection is segmental (BACH complex), or when the soft-tissue envelope cannot be closed directly , major recon struction will be required. Curative resection must be segmen tal and bone stabilisation will always be required. The Ilizarov method, which uses distraction osteogenesis to fill bone defects, is a powerful and successful technique in these cases. It can be combined with free tissue transfer. T his allows reconstruction to proceed in parallel with rehabilitation. After surgery , patients should be given antibiotics. In total segmental excision of  infection a short course may be indicated, but in most chronic infections 6–12 weeks is often advised. If there is any doubt about the adequacy of  removal of  the dead bone , a long antibiotic course will be needed and recurrence will be more likely . In chronic fracture-related infection, anti biotics should continue until fracture union. There is now increasing interest in the use of  local antibiotic absorbable carriers. These can deliver high doses of  antibiotics into the bone, without systemic e ff ects. Some ceramic ma (with hydroxyapatite) can form new bone in the defect, avoid ing the need for secondary bone grafting. Chronic osteomyelitis /uni25CF /uni25CF /uni25CF 

Figure 43.10
(a)
This magnetic resonance imaging scan shows a
BACH uncomplicated medullary osteomyelitis of the femur.
(b)
infected bone has been removed by reaming and the central defect
/f_i
lled with absorbable calcium sulphate pellets with gentamicin.
Chronic disease requires specialist surgery with excision,
stabilisation and reconstruction
Host status should be optimised before surgery
Following surgery, antibiotic therapy is typically continued for
at least 6 weeks

Management

Successful treatment requires accurate diagnosis and a multi - disciplinary approach to deliver a package of  care, summarised as follows: /uni25CF Preoperative: /uni25CF patient assessment and clinical staging of  disease; /uni25CF full discussion of  all treatment options with potential complications; /uni25CF diagnostic tests for general health; /uni25CF optimisation of  patients and treatment of  comorbid - ities. /uni25CF Operative: /uni25CF exposure for multiple, deep bone sampling; /uni25CF excision of  all a ff ected tissue; /uni25CF intravenous antibiotics after sampling; /uni25CF bone stabilisation, if  necessary; /uni25CF dead-space management; /uni25CF soft-tissue cover, which may include plastic surgery . /uni25CF Postoperative: /uni25CF functional rehabilitation; /uni25CF continued antimicrobial therapy guided by culture re - sults, with regular clinical monitoring. - The principles listed above dictate that a range of  surgical and medical specialists will be needed to treat patients with bone and joint infections. If  the patient is systemically well, ved tions, optimise patient there is often time to complete investiga health and plan interventions. Complex infections should be referred early to centres that specialise in these cases. Atten - tion to diabetes control, peripheral vascular disease, nutrition and smoking cessation is essential. Many patients will benefit from psychological support or at least good counselling around the di ffi culties of  eradicating infection and the components of treatment. 

Mag
-

Management

Surgical management Medical treatment alone is rarely indicated in joint sepsis. Prompt surgical drainage is a priority to avoid further damage to the cartilage. Arthroscopic washout is commonly performed but it may be di ffi cult to remove loculated areas of infection. Washout should be with Ringer’s solution or of  the risk of  chondrolysis. There should be a low threshold for open arthrotomy , particularly if  a joint is not settling. A synovectomy is recommended if  there is major synovial thickening, aggressive synovitis or subchondral erosions seen on radiology (Gächter stages 3 and 4). Inadequate clearance may lead to chronic infection with destruction of  the joint ( Figure 43.4 ). Treatment may then require joint excision, joint fusion or staged joint replacement. Medical management Antibiotics are usually given for 3–6 weeks (beginning with intravenous therapy). There are sparse data to guide duration. Longer courses should be considered if  the infection is slow to resolve, if  more than one washout is required, if  the patient is bacteraemic and/or if  the infection is caused by S. aureus choice of  antibiotics is as given in Summary box 43.4 . Summary box 43.6 Native joint septic arthritis /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF 

Most common at extremes of age, in patients with rheumatoid
arthritis and in association with immunocompromise
Most commonly affects hips in neonates and knees in adults
and children
The commonest pathogen is
S. aureus
Joints should be aspirated for microbiology before starting
antibiotics, if safe to do so
Management is prompt surgical joint washout, followed by
3–6 weeks of antibiotics

Management

A multidisciplinary approach is required, including ortho paedics, plastic surgery , infectious diseases/microbiology , α pharmacy , nursing, occupational therapy and physiotherapy , centred on the patient’s understanding and wishes regarding their condition. Many patients have other medical comorbid - ities tha t should also be addressed and optimised. PJI can be - associated with a range of  emotional, psychological and mental health issues, ranging from anger about surgical complications to depression arising from chronic symptoms, lack of function and prolonged hospitalisation. T he choice of  surgical strategy for prosthetic joints can be categorised as: /uni25CF salvage of  an infected implant; /uni25CF removal of  the infected implant with or without reimplan - - tation. 

Infection likely
Infection con
/f_i
rmed
Two positive findings
Any positive finding
or
or
C
A
B
C
A
A
B
• Early radiographic
loosening
Sinus tract communication
• Wound-healing problems
with the joint +/–
• Recent fever/bacteraemia
visualisation of prosthesis
• Purulence around
prosthesis
• CRP >10mg/L
• Leukocyte count >3000
• Leukocyte count >1500
• PMN >80%
• PMN >65%
• Positive
-defensin
• Single positive culture
• ≥2 positive samples with
(aspiration or
the same microorganism
intraoperative)
• >50 CFU/mL of any
• > 1 CFU/mL any
organism on sonication
organism on sonication
• Presence of ≥5
Presence of ≥5 neutrophils
neutrophils in ≥5 HPFs
in a single HPF
• Visible microorganisms
Positive white blood cell
labelled scintigraphy
Bone Joint J
2021;
103-B
(1): 16–17.)

determine this (i.e. salvage for early infection versus removal and revision for late infection). Others regard any firmly fixed implant as potentially salvageable, irrespective of  the timing (and there are now several studies showing that this is feasi ble). However, it is agreed that loose infected implants should always be removed ( Figure 43.6 ). Furthermore, it is essential to achieve soft-tissue cover of  bone and pr osthetic material. This may be di ffi cult around the knee, requiring local muscle flaps. Management options can be divided into the following broad approaches. /uni25CF Debridement, antibiotics and implant reten tion - ‘DAIR’ . This can only be undertaken if the pros thesis is well fixed. DAIR is not a form of  washout as all infected soft tissue and necrotic bone must be fully excised and modular components exchanged. This cannot be achieved by arthroscopic surgery . Good soft-tissue cov is essential. Following debridement, the patient is treated with long-term antibiotics (frequently 6 weeks of  intra venous therapy followed by 6 months or more of  oral anti biotics). Prolonged infection-free intervals can be achieved in 80% of  patients but success with this strategy may be lower in infections caused by S. aureus or with multiresis tant organisms. /uni25CF Two-stage joint revision surgery . A thorough ex cision is undertaken and all cement and loose foreign ma terial is removed. An antibiotic-impregnated spacer may be implanted (which may be articulating). This is a tem porary measure and cannot withstand full weight-bearing. The patient is treated with oral or intravenous antibiotics, Gathorne Robert Girdlestone , 1881–1950, Nu ffi eld Professor of  Orthopaedics, University of  Oxford, UK, described excision arthroplasty of  the hip for septic arthritis. ed after the course of  antibiotics has been completed. In recent years ther e has been a trend towards shorter inter - vals between stages, often within the 6-week antimicrobial - therapy . /uni25CF Single-stage joint revision surgery . The procedure is the same as above, but removal and reimplantation are undertaken in the same operating session. Healthy soft tissues around the new implant are essential to prevent reinfection. Some centres consider single-stage revisions when less florid signs of  infection are present (i.e. absence of  collections or sinus tracts), or for frail patients for whom - the risk of a second operation is higher. There are no ad - - equate trial data comparing outcomes with the two-stage approach. /uni25CF Joint removal or fusion . When reconstruction options are not technically possible or are ruled out by comorbid er conditions, removal of  the prosthesis without reimplanta - tion may palliate symptoms. An example is the Girdlestone - excision arthroplasty of the hip. In prosthetic infections of - the knee, ankle or wrist, it may be possible to create a joint fusion after pr osthesis removal. This is complex surgery , which may involve major bone reconstruction. Amputa - - tion may be necessary for knee or ankle implants. /uni25CF Suppressive therapy with antibiotics . In patients - who are not medically fit for any operative intervention, or - who choose to decline all surgical options, long-term treat - ment with antibiotics may help to suppress the symptoms - of  infection. There are limited data, but anecdotally the success rate of  this approach is low . 

(a)
Figure 43.6
(a)
Sinus draining from the scar over the lateral side of the hip. This patient had a total hip replacement 14 years before that had
been complicated by a wound haematoma and infection.
(b)
Radiograph of both hips of same patient. Both hips are loose but only the right
side has de
/f_i
nite infection (arrows).
(b)

Prosthetic joint infection /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF 

Well-
/f_i
xed prostheses may be Debrided, treated with
Antibiotics and the Implant Retained (‘DAIR’ approach)
Loose prostheses must be removed
Replacement can be made at the initial surgery (one stage) or
after a delay to allow infection to be eradicated with antibiotics
(two stage)
Multiple surgical samples are crucial for identifying a pathogen
Thorough excision of infected tissue is a key determinant of
outcome
Long-term antibiotics may be used for patients who are not
suitable for major revision surgery

Management

- Acute osteomyelitis can be treated with antibiotics alone, when the diagnosis is made within 2–3 days of  onset of  symptoms, . Sta - there is no dead bone on imaging and there is no adjacent - septic arthritis. Culture results help to guide therapy , so blood cultures should be taken, and radiologically guided sampling should be considered. Empirical intravenous therapy against Gram-positive organisms is given (cephalosporins or flucloxa - ). cillin), adding gentamicin to cover Gram-negative organisms in children under 1 year. The limb should be splinted and good analgesia given. Intravenous antibiotics should be converted to oral therapy , depending on clinical progress and the results of cultures, and therapy is continued for a total of 2–3 weeks. If  the patient does not respond rapidly , if  the limb deteriorates or if  there is imaging evidence of  progression of  disease, surgery is indi - cated to prevent bone destruction and the onset of  chronic osteomyelitis. With prompt treatment, acute bone infection has a good - prognosis with a 90% cure rate. Failure to tr eat adequa tely pro - duces chronicity , with recurrent infection over many years. In children, the adjacent growth plates and joints may be a ff ected with subsequent deformity and joint destruction. Summary box 43.8 Acute osteomyelitis /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF Gavriil Abramovich Ilizarov , 1921–1992, orthopaedic surgeon, Kurgan, Western Siberia, Russia, pioneered this eponymous approach to bone reconstruction in the 1960s for the management of  osteomyelitis, fractures and limb deformities. 

(c)
Figure 43.7
(a)
Radiograph of a complex distal tibia fracture that was internally
/f_i
xed but complicated by deep infection.
plate was loose and grossly infected.
(c)
The plate and all infected tissue was excised. Deep samples were sent for microbiology and histology.
The defect at the lower end was
/f_i
lled with an absorbable antibiotic carrier.
and the skin primarily closed.
Presents in children with toxaemia, fever and unwillingness to
move the limb
May affect the vertebral column in adults, where back pain
may be the only symptom
Radiographs may be normal for up to 1 week so are of limited
value in early diagnosis
MRI is the investigation of choice
WCC and CRP are usually raised
Early diagnosis is treated with high dose intravenous
antibiotics, started empirically and modi
/f_i
ed with culture
results
Late diagnosis and/or failure of medical treatment requires
surgical debridement
(d)
(b)
At operation, the
(d)
The bone was stabilised with an Ilizarov circular external
/f_i
xator

Management

The BACH classification divides patients into ‘uncomplicated’, ‘complex’ and ‘limited options available’ based on the four important features of  the infection ( Figure 43.9 ). These are: the anatomical location in the bone (B), the antimicrobial profile (A), the need for soft-tissue cover (C) and the health of  the host (H). Treatment must always address all four parts of  the classification to achieve good outcomes. All infected unhealed fractures and infected non-unions are complex. As with PJI, comorbidities should be optimised before sur - gery . The interaction between the patient’s health status and the extent of  the bone infection greatly a ff ects the outcome after surgery . In chronic infection, it is essential to address med - ical conditions that ma y impair wound healing (e.g. smoking, peripheral vascular disease, diabetes, steroid use) prior to sur - gery . This approach has been shown to improve cure rates. A joint assessment by an orthopaedic sur geon, plastic surgeon and infectious disease physician will allow good preoperative planning. 

B
one involvement
A
ntimicrobial options
Ax
B1
Unknown/culture negative
Cavitary
ed
involvement
cat
A1
(including medullary,
pli
<4 resistant tests
cortical and
om
≥
80% susceptibility tests
non-segmental
Unc
sensitive
corticomedullary)
A2
B2
>4 resistant tests
Segmental
<80% susceptibility tests
involvement
lex
sensitive
Any infection with
Comp
joint involvement
A3
B3
Sensitivity to either 0 or 1
Whole bone
susceptibility test
involvement
Limited options
Figure 43.9
The BACH classi
/f_i
cation of osteomyelitis.
(a)
Coronal computed tomography scan of the femur
(b)
A transverse section
C
overage of soft tissue
H
ost status
H1
C1
Patient
/f_i
t and well or has
Direct closure possible
well-controlled disease
Plastic surgery expertise
not
required
H2
C1
Patient with either poorly
Direct closure not possible
controlled disease, severe
Plastic surgery expertise
disease or recurrent
required
osteomyelitis
H3
Un
/f_i
t for anaesthetic
Patient declines surgery
Surgery not indicated

In uncomplicated disease, excision of  the dead bone, with local and systemic antibiotics and direct wound closure, is highly e ff ective ( Figure 43.10 ). If  more than one-third of  the cortical circumference is excised, splintage is essential, often with external fixation to prevent fracture. Secondary bone grafting may be needed. When the infection is segmental (BACH complex), or when the soft-tissue envelope cannot be closed directly , major recon struction will be required. Curative resection must be segmen tal and bone stabilisation will always be required. The Ilizarov method, which uses distraction osteogenesis to fill bone defects, is a powerful and successful technique in these cases. It can be combined with free tissue transfer. T his allows reconstruction to proceed in parallel with rehabilitation. After surgery , patients should be given antibiotics. In total segmental excision of  infection a short course may be indicated, but in most chronic infections 6–12 weeks is often advised. If there is any doubt about the adequacy of  removal of  the dead bone , a long antibiotic course will be needed and recurrence will be more likely . In chronic fracture-related infection, anti biotics should continue until fracture union. There is now increasing interest in the use of  local antibiotic absorbable carriers. These can deliver high doses of  antibiotics into the bone, without systemic e ff ects. Some ceramic ma (with hydroxyapatite) can form new bone in the defect, avoid ing the need for secondary bone grafting. Chronic osteomyelitis /uni25CF /uni25CF /uni25CF 

Figure 43.10
(a)
This magnetic resonance imaging scan shows a
BACH uncomplicated medullary osteomyelitis of the femur.
(b)
infected bone has been removed by reaming and the central defect
/f_i
lled with absorbable calcium sulphate pellets with gentamicin.
Chronic disease requires specialist surgery with excision,
stabilisation and reconstruction
Host status should be optimised before surgery
Following surgery, antibiotic therapy is typically continued for
at least 6 weeks

# Microbiology

Microbiology

Virulent Gram-positive organisms, particularly Staphylococcus - aureus , are the most common cause of  bone or joint infection in native tissue. However, once prosthetic material is implanted, a wide range of organisms can be involved. This includes - organisms with low virulence that are usually considered skin commensals, such as coagulase-negative staphylococci, α -haemolytic streptococci and Cutibacterium acnes ( Table 43.1 ). e Microbiology

Virulent Gram-positive organisms, particularly Staphylococcus - aureus , are the most common cause of  bone or joint infection in native tissue. However, once prosthetic material is implanted, a wide range of organisms can be involved. This includes - organisms with low virulence that are usually considered skin commensals, such as coagulase-negative staphylococci, α -haemolytic streptococci and Cutibacterium acnes ( Table 43.1 ). e Microbiology

Virulent Gram-positive organisms, particularly Staphylococcus - aureus , are the most common cause of  bone or joint infection in native tissue. However, once prosthetic material is implanted, a wide range of organisms can be involved. This includes - organisms with low virulence that are usually considered skin commensals, such as coagulase-negative staphylococci, α -haemolytic streptococci and Cutibacterium acnes ( Table 43.1 ). e

# NATIVE JOINT SEPTIC ARTHRITIS Epidemiology

NATIVE JOINT SEPTIC ARTHRITIS Epidemiology

Bacterial infection of  native joints occurs with an estimated incidence of  4–10 per 100 /uni00A0 000 population per year in western Europe, with higher rates associated with socioeconomic deprivation and in developing countries. The condition most characteristically a ff ects patients at extremes of  age, usually with pre-existing arthropathy or immunocompromise ( Table 43.2 Joint infection may arise as a result of  haematogenous dis semination of  bacteria from another focus (e.g. endocarditis) or may occur as a result of  direct inoculation or local exten sion from an infected source (e.g. traumatic wound or adjacent osteomyelitis). NATIVE JOINT SEPTIC ARTHRITIS Epidemiology

Bacterial infection of  native joints occurs with an estimated incidence of  4–10 per 100 /uni00A0 000 population per year in western Europe, with higher rates associated with socioeconomic deprivation and in developing countries. The condition most characteristically a ff ects patients at extremes of  age, usually with pre-existing arthropathy or immunocompromise ( Table 43.2 Joint infection may arise as a result of  haematogenous dis semination of  bacteria from another focus (e.g. endocarditis) or may occur as a result of  direct inoculation or local exten sion from an infected source (e.g. traumatic wound or adjacent osteomyelitis). NATIVE JOINT SEPTIC ARTHRITIS Epidemiology

Bacterial infection of  native joints occurs with an estimated incidence of  4–10 per 100 /uni00A0 000 population per year in western Europe, with higher rates associated with socioeconomic deprivation and in developing countries. The condition most characteristically a ff ects patients at extremes of  age, usually with pre-existing arthropathy or immunocompromise ( Table 43.2 Joint infection may arise as a result of  haematogenous dis semination of  bacteria from another focus (e.g. endocarditis) or may occur as a result of  direct inoculation or local exten sion from an infected source (e.g. traumatic wound or adjacent osteomyelitis).

# PROSTHETIC JOINT INFECTION Epidemiology

PROSTHETIC JOINT INFECTION Epidemiology

The incidence of  PJI is around 1% per joint per year, with upper limb joints at a higher risk. Infection can be minimised with improved operative practice, prophylactic systemic anti biotics, local antibiotics in cement and the use of  surgical ‘care bundles’. Risk factors include obesity , skin disease, diabetes, malignancy , inflammatory arthritis, prolonged or complicated surgery , revision surger y , fracture and postoperative wound infection or haematoma. PROSTHETIC JOINT INFECTION Epidemiology

The incidence of  PJI is around 1% per joint per year, with upper limb joints at a higher risk. Infection can be minimised with improved operative practice, prophylactic systemic anti biotics, local antibiotics in cement and the use of  surgical ‘care bundles’. Risk factors include obesity , skin disease, diabetes, malignancy , inflammatory arthritis, prolonged or complicated surgery , revision surger y , fracture and postoperative wound infection or haematoma. PROSTHETIC JOINT INFECTION Epidemiology

The incidence of  PJI is around 1% per joint per year, with upper limb joints at a higher risk. Infection can be minimised with improved operative practice, prophylactic systemic anti biotics, local antibiotics in cement and the use of  surgical ‘care bundles’. Risk factors include obesity , skin disease, diabetes, malignancy , inflammatory arthritis, prolonged or complicated surgery , revision surger y , fracture and postoperative wound infection or haematoma.