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CNSLF Micro - Bone & Joint Infections (ii) Osteomyelitis 1 (Acute OM…
CNSLF Micro - Bone & Joint Infections (ii) Osteomyelitis 1
Mechanisms of infection
haematogenous
organism from elsewhere spreads via blood
e.g. vertebral OM/discitis in an adult with S aureus endocarditis
in children affects metaphysis of long bones esp tibia + femur
in adults vertebrae affected
contiguous (shares a common border)
organism directly into bone (e.g. trauma, penetrating injury, bites, contaminated open fracture)
from adjacent skin/soft tissue focus of infection
e.g. acute from ear sinus infection
e.g. chronic from pressure sore (bed-bound), diabetic foot ulcer
surgery (reconstruction of bone, prosthetic material e.g. intra medullary nail, traumatic dental procedure)
may be mono or poly microbial
S aureus = commonest, e.g. from adjacent cellulitis/soft tissue infection
Strep (S pneumo, GAS) more common in children (e.g. from ear or sinus infection)
coag -ve staph e.g. after insertion of metal to stabilise a fracture - produce biofilm so stick to prosthetic material
polymicrobial with gram -ves/anaerobes e.g. contaminated wound due to trauma
Acute OM
usually mono microbial
pathogens in young children (4 months-4 yrs)
S aureus
S pyogenes (GAS pharyngitis, skin + soft tissue, bone)
S pneumo
Kingella Kingae (children under 5)
in sickle cell disease: non-typhoidal salmonella
Hib if not vaccinated
enterobacteriaceae
pathogens in adults
S aureus
TB
more indolent + chronic
endemic areas + immunocompromised
neuro features
systemic upset infrequent
brucella (uncommon in Ire/UK)
occasionally enterobacteriaceae or strep
pathogens in children + adolescents (4yrs-adult)
S aureus (80%)
GAS
Hib
Enterobacteriaceae
pathogens in newborns (<4 months)
S aureus
group B strep
E Coli
features
evolves over days/wks
fever, rigors, high WCC
painful tender bone
no necrosis/fistulae
in previously well patients
if untxed for 10+ days (may be reflected by ongoing clinical features), get necrotic bone + chronic OM can occur
Tx
if S aureus consider adding 2nd anti-staph agent such as oral fusidic acid or flucloxicillin or vanc (if MRSA)
surgery may be required in infected fractures - source control (debridement to remove bioburden)
monitor response to tx via clinical response/ESR + CRP (1-2 times/wk)
Pathogenesis
bacteria invade bone
pressure within bone increases due to inflamm + pus (acute)
if chronic fluid reaches periosteum, elevates it + bone dies (dead necrotic devasced bone) = SEQUESTRUM
separated periosteum produces new bone = INVOLUCRUM
sinus tract forms
Clinical features
general (moreso in acute)
fever
malaise
anorexia
myalgia
anaemia of chronic disease in chronic OM
local
pain, tender, hot, swollen more in acute
fistula + deformity more in chronic
restricted motion
pseudoparalysis
Non-microbiological dx
hx + exam
probe to bone test (to detect chronic OM a/w ulcer)
imaging
plain x-ray may be normal (slow ro change - do serials in chronic)
MRI (see bone oedema early)
bone scan (nuclear) if MRI not possible
blood tests
supportive but not specific
WCC elevated (neutrophilia)
ESR/CRP (inflamm markers)
histology on bone bx
in formalin
pathological not microbiological dx as formalin kills bugs
Management principles
IV (need high serum conc) antibiotics based on infecting organism - best response if started within 72hrs of onset of symptoms
empiric tx pending C+S results must cover common causative organisms i.e. S aureus
antibiotics required for 6 wks, usually IV for min 2-3wks followed by oral
look for improvement: less pain (less analgesia), less signs of inflamm - response should be seen before descalation to oral
Prevention
in surgery
peri-op precautions to avoid introducing bacteria into bone
appropriate pre-op prophylaxis
strict asepsis
instrument sterility
contiguous
pressure sore prevention
diabetic foot care