bone infections Flashcards
(19 cards)
Mechanisms of infection of osteomyelitis
how do the organisms spread
haematogenous eg staph aureus endocarditis-> vertebral osteomyelitis (Adults)
children -> metaphysis of long bones affected
contiguous ; organism directly on bone via trauma or from adjacent focus of infection
USUALLY monomicrobial
Causative agents in children of acute osteomyelitis
Children Metaphysis of long bones • Staphylococcus aureus (commonest) • Streptococcus species – e.g. Strep. pyogenes (“group A strep”) or Strep. pneumoniae • Kingella kingae (children <5) • In sickle cell disease: nontyphoidal Salmonella
Causative agent in adults of acute osteomyelitis
Adults Mostly vertebrae • Staphylococcus aureus (commonest) • Mycobacterium tuberculosis endemic areas & immunocompromised neurological features, systemic upset infrequent • Brucella spp. (uncommon in Ireland/ UK)
What is the mech of action for contiguous method of spread for organisms in osteomyelitis
• Trauma
– Penetrating injury/ bites
– Contaminated open fracture
• Surgery
– Reconstruction of bone
– Prosthetic material e.g. intra-medullary nail
– Traumatic dental procedure
• Spread from adjacent skin/ soft tissue focus
– e.g. acute, from ear, sinus infection
– e.g. chronic, from pressure sore/ diabetic foot ulcer
Causative agents for contiguous osteomyelitis
May be monomicrobial or polymicrobial
• Staphylococcus aureus (commonest) e.g.
from adjacent cellulitis/ soft tissue infection
• Streptococci (Str. pneumoniae, group A strep)- more
common in children e.g. from ear or sinus infection
• Coagulase negative staphylococci e.g. after
insertion of metal to stabilise a fracture
• Polymicrobial with Gram negatives/anaerobes, e.g.
contaminated wound due to trauma
What are the causative agents of acute osteomyelitis in relation to age groups?
newborns <4 months= Staph aureus, group B strep , E coli
children (4 months to 4 years) = Staph aureus, Group A strep , strep pneumo, kingella kingae, H influenzae , Enterobacteriaceae
children, adolescents (>4 years to adult) - Staph aureus, Group A strep , H influenzae, Enterobacteriaceae
adults - staph aureus and occassionally enterobacteriaceae/strep
Pathogenesis of acute OM
• Bacteria invade bone
• Pressure within bone
increases due to
inflammation & pus
Pathogenesis of chronic OM
• Fluid reaches periosteum, elevates it & bone dies (dead necrotic bone= sequestrum) • Separated periosteum produces new bone = involucrum • Sinus tract forms
Mechanism of chronic OM
• Usually due to contiguous spread from pressure
sore/ diabetic foot ulcer
• Patients with poor mobility, multiple comorbidities
• Diabetes mellitus, peripheral vascular disease
• Non-acute presentation, usually present for some
time at diagnosis
Define chronic OM
• Usually polymicrobial (> 1 organism), e.g. S. aureus
plus Gram negative bacilli plus anaerobes- organisms
that colonise ulcers
• Staphylococcus aureus (>50% cases)
• Anaerobes (10-20%) including Bacteroides/
Actinomyces
• Gram negative bacilli, i.e. Pseudomonas aeruginosa,
E. coli, Klebsiella spp.
– Nosocomial infection
– Open wound/fracture
– May complicate trauma or surgery
– IVDU
Clinical features of OM
• General – fever – malaise – anorexia – myalgia more often seen in acute OM • Local – pain – tender – hot – swollen – restricted motion – pseudoparalysis – fistula – deformity more common in chronic OM
Differentiate acute vs chronic OM clinical features
Acute • Evolves over days/weeks • Fever, rigors, high WCC • Painful tender bone • No necrosis/ fistulae • In previously well patients • If untreated for ≥10 days (may be reflected by ongoing clinical features), get necrotic bone & chronic osteomyelitis can occur
Chronic • Evolves over months/years with lowgrade inflammation, dead bone (sequestrum) & fistulous tracts • Chronic pain • Patient systemically well • Usually co-morbidities • Often relapses despite apparently appropriate treatment
dx of OM non micro
• History & examination • Probe-to-bone test (chronic osteomyelitis associated with an ulcer) • Imaging, plain X-ray, may be normal, MRI, see bone oedema early, bone scan (nuclear) if MRI not possible • Blood tests (non-specific) –White cell count (elevated, neutrophilia) – Inflammatory markers • ESR, CRP • Histology on bone biopsy (in formalin) –Pathological (not microbiological) diagnosis
dx of OM micro
finding the causative agent
• Bone biopsy for culture & histology is the
gold standard
• In suspected chronic OM, hold antibiotics until
after biopsy being taken
• Biopsy of affected bone (not in formalin)
– Gram stain, culture & susceptibility testing
– Consider TB culture if chronic
• Molecular, 16S ribosomal RNA
• Blood cultures if acute OM +/- systemic
symptoms, e.g. fever
– Diagnose if the patient is bacteraemic
what is chronic osteomyelitis a./w
non healing ulcer w chronic discharge
Management of acute OM
• Intravenous antibiotic based on infecting organism – best response if started within
72h onset of symptoms
• Empiric treatment pending C+S results must
cover common causative organisms i.e.
Staph. aureus
• Antibiotic treatment required for 6 weeks,
usually IV for minimum 2-3 weeks followed
by oral regimen
• If S. aureus: consider adding a 2nd antistaphylococcal
agent such as oral fusidic
acid to flucloxacillin or vancomycin (if
MRSA)
• Surgery may also be required if infected
fractures, delayed diagnosis
• Monitor response to treatment via clinical
response/ ESR + CRP (1-2 times/week)
Management of OM
• Same principle, i.e. treatment based on
culture & susceptibility results
• Cannot be managed with antibiotics alone
• Multi-disciplinary team (MDT) approach
• Surgical debridement to remove necrotic
bone if present- send for C&S
• Treatment more prolonged – minimum 3/12
antibiotic therapy; success depends on
extent of removal of necrotic bone
MDT for chronic OM
tissue viability nurse vascular surgeon podiatrist diabetes nurse specialist endocrinologist micro radio
Prevention of OM
Associated with surgery • Peri-operative precautions to avoid introducing bacteria into bone • Appropriate pre-operative prophylaxis Contiguous • Pressure sore prevention • Diabetic foot care
