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BMF > bone and joint infection > Flashcards

bone and joint infection Flashcards

1
Q

—-Refers to inflammation of the bone or bone marrow
Usually caused by —-
can be — or —

A
  • osteomyletis
  • infection
  • acute ( recent onset ) or chronic ( long term)
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2
Q
  • mechanism of action :
    1- — which is when organism for elsewhere spreads via —
    as. vertebral osteomyelitis
    / discitis in an adult with
    Staph. aureus endocarditis
    2- — organism is directly into — and penetrates the injury , from adjacent focus of infection
A
  • heamotegnous
  • blood
  • contagious
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3
Q
  • heamotagenous osteomlytis :
    1- in children its the emtaohysis of — affected , especially —- and —
    2- in adults it affects –
A
  • long bones
  • tibia and femur
  • vertebea
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4
Q

non homogenous om mechanism can be due to:
1- —- : penetrating injury/bites , contaminated open fractures
2- — : reconstruction of bones , prosthetic material as intra medullary nail , traumatic dental procedure
3- spread from adjacent —– focus as: acute from —– infection or chronic from —

A
  • trauma
  • surgery
  • skin/soft tissue
  • ear or sinus
  • pressure sore or diabetic foot ulcers
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5
Q

causative pathogen in acute om:
- newborn less than 4:
- children from 4 months-4 years and metaphysics of long bones:
- children adolescent so more than 4 years
- adults ( mostly vertebrae) :

A

-S. aureus, group B Streptococcus, E. coli
-S. aureus, group A Streptococcus,
Streptococcus pneumoniae, Kingella kingae [Haemophilus influenzae (if not vaccinated),and Enterobacteriaceae]
-S. aureus (80%), group A Streptococcus
[H influenzae, and Enterobacteriaceae]
In sickle cell disease: non-typhoidal Salmonella
-S. aureus & occasionally Enterobacteriaceae or
Streptococcus spp.
Mycobacterium tuberculosis- endemic areas &
immunocompromised
Brucella spp. (uncommon in Ireland/ UK)

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6
Q

contagious om: pathogenesis:
1- it may be mono microbial or poly microbial
- — most common from eg.cellulitis/ soft tissue infection
- —- more common in children e.g. from ear or sinus infection
- cogualase — : after insertion of metal to stabilise a fracture
- polymicrobial w — : contaminated wound due to trauma, chronic
ulcers

A
  • staph aurus most common
  • streptococci ( Str. pneumoniae, group A strep)
  • -ve staphlyococci
  • gram -ve/anaerobes
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7
Q

chronic om: mechaism
1- usually due to — from —-
2- patient w poor — or multiple —
3- —–
3- —-

A
  • 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
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8
Q

chronic om pathogeen:

A
  • 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
    – IV drug use
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9
Q

pathogenesis of om:
1- bacteria invade —
2- – within the bone increases due to —- ( 1,2 cause acute om)
3- fluid reaches — elevated it and bone —
4- separated periosteum produces —
5- — forms

A
  • bone
  • pressure
  • inflammation and pus
  • periosteum
  • bone dies ( necrotic bone = sequestrum )
  • new bone = involucre
  • sinus tract
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10
Q

clinical features of om:
1- general :
2- local:

A
  • general : ( which are seen in acute)
    – fever
    – malaise
    – anorexia
    – myalgia
  • local:
    – pain
    – tender
    – hot
    – swollen
    ( these above are more seen in acute)
    – restricted motion
    – pseudoparalysis
    – fistula
    – deformity
    ( last 2 are more seen in chronic )
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11
Q

acute vs chronic clinical features
1- acute:
- evolves over —
- no —
- fever , rigours , high acc
- In previously well patients
- If untreated for ≥10 days
(may be reflected by
ongoing clinical features),
get necrotic bone &
chronic osteomyelitis can
occur
2- chronic:
- evolves over:
- patient is —

A
  • days/weeks
  • necrosis/sinus tract
    -Evolves over months/years
    with low-grade
    inflammation, dead bone
    (sequestrum) & fistulous
    tracts
  • Chronic pain
  • Patient systemically well
  • Usually co-morbidities
  • Often relapses despite
    apparently appropriate
    treatment
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12
Q

Non-healing ulcer overlying bone or a chronically
discharging sinus, often a sign of underlying—-

A

chronic om

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13
Q

non microbiology diagnosis :

A
  • 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
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14
Q

microbiological diagnosis include:

A
  • Biopsy of affected bone (not in formalin)
    – Gram stain, culture & susceptibility testing
    – Consider TB culture if chronic
    – PCR: 16S ribosomal RNA
  • Pus/bone & not swab of ulcers/sinuses; may
    grow colonising organisms & not deep
    pathogens
  • Blood cultures if acute OM +/- systemic
    symptoms, e.g. fever
    – Diagnose if the patient is bacteraemic
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15
Q

in microbiological diagnosis:
* Identification of the — essential
to choose the best treatment
* —– is the gold
standard
* In suspected chronic OM, hold antibotics until – biopsy being taken
* A prospective study of bone biopsies showed a
sensitivity for OM of 87% & a specificity of 93%

A
  • causative organism
  • bone biopsy for culture and histology
  • after
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16
Q

management of acute om :
* —- based on infecting organism
– Best response if started within 72h onset of symptoms
* Empiric treatment pending —- results must cover common causative organisms i.e. Staph. aureus
* Antibiotic treatment required for typically —-
– Usually IV for minimum 2-3 weeks followed by oral regimen

A
  • intravenous antibiotics
  • c+s
  • 6 weeks
17
Q

maangeming of acute om in specific treatment:
* If S. aureus:
– —- (MSSA) or —- (if MRSA)
* — may also be required if infected
fractures, delayed diagnosis
* Monitor response to treatment via clinical response/ESR + CRP (1-2 times/week)

A
  • flucloxacillin
  • vancomycin
  • surgery
18
Q

-in chronic om it cant be managed w —- alone
- same principle and treatment depends on — and —
- —- approach
- — debridement to remove necrotic bone if present and send for c+s
- treatment is more – minimum of 3/12 antibiotic therapy ]- success depends on extend of — of necrotic bone

A
  • anitbitotc
  • culture and suscpeitbitly results
  • Multi-disciplinary team (MDT) as : pediatrist radiologist endocrinologist vascular surgeon diabetes nurse specialist tissue viability nurse ad microbiologist/ID physician
  • surgical
  • prolonged
  • removal
19
Q

prevention of om:
1- associated w surgery :
2- contiguous:

A

1-
* Peri-operative precautions to avoid
introducing bacteria into bone
* Appropriate pre-operative prophylaxis
2-
* Pressure sore prevention
* Diabetic foot care

20
Q

—– Inflammation in the joint due to —
* Many other causes of arthritis that are not due to —

A
  • septic arthritis
  • infection
  • infection
21
Q

in septic arthritis:
1- invasion of — by micro organic usually w the extension into the joint space
2- any — agent may cause arthritis and — the most rapidly destructive
3- up to 25% loos of joint after infection is —-
4- pre-disposing factors include :

A
  • synovial memebrane
  • infectious
  • bacteria
  • irreversible
  • Pre-existing joint disease
    – RA: decreased polymorph
    function, with reduced
    chemotaxis
    – OA
  • Prosthetic joints
  • IVDU
  • Diabetes mellitus
  • Ulcerated skin
  • Repeated intra-articular joint
    injection
22
Q

-septic arteries pathogenesis can be:
1- – organisms required to initiate a joint infection — > bacteria trigger an —- —> influx of —- –> release of – and – leads to — —> — subcentral bone loss can be seen within –

A
  • hameotgenous and direct introduction
  • few
  • acute inflammatory synovitis
  • acute and chronic inflammatory cells
  • cytokines and proteases
  • cartlige degradation
  • irreversible
  • days
23
Q

clinical features include:

A
  • Sudden onset of painful, hot swollen joint
  • Joint swelling
    – Knee > hip > shoulder > ankle/wrist
    – Hip more common in children
    – 10-20% polyarticular (2 or 3 joints)
  • More likely in patients with connective tissue disease
  • Fever
  • Source of infection elsewhere in 50%
    – E.g. skin, lungs, bladder
24
Q

causative organism :
1- — : 40-60% of cases
2- — : iv drug use
3- —: if penetrating trauma
age:
neonates —>
- children under 6 —>
- young children —>
- older adults —>

A
  • staph. aureus
  • Pseudomonas spp
  • aerobes
  • E. coli, Grp B streptococcus (bloodstream infecection)
    -children under 6:
    Staph. aureus,
    Strep. pneumoniae,
    Strep. pyogenes (group A strep)
    Kingella kingae
  • young aults: N. gonorrhoeae, Staph. aureus
  • older adults:
    Staph. aureus,
    Strep. pneumoniae,
    Strep. pyogenes,
    Gram negative bacilli (e.g., E. coli)
    Staph. epidermidis– if prosthesis
25
Q

gonococcal septic arthritis :
- septic — or — arthritis
- may occur in association w other disseminated gonococcal infection :

A
  • mono or oligo
    – Migratory polyarthritis
    – Tenosynovitis: wrist, ankles & small
    joints
    – Skin lesions: multiple painless
    macules, papules arms, legs, trunk
    – Fever
26
Q

diagnosis - microbiology

A
  • Joint aspiration to obtain synovial fluid (pre-antibiotics)
  • Microscopy – white cell count (high, predominantly neutrophils)
    – Gram stain (ZN stain) -up to 50% of microscopy positive (25% in
    gonococcal)
    – Microscopy for crystals to rule out gout etc.
  • Culture– up to 90% culture positive
    – 50% in gonococcal
  • PCR
    – Pathogen specific – e.g. gonococcal
    – Pan-bacterial e.g. 16S ribosomal RNA
  • Blood culture, almost 50% positive
  • Urine / genital swabs (if ? gonococcal)
  • Serology only if indicated:
    – Anti-Streptolysin O Titre (ASOT)
    – Brucella
    – Syphilis (rare)
    – Leptospira (rare)
    – Borrelia burgdorferi (Lyme disease)
27
Q

diagnosis - non microbiology :

A
  • Bloods (non-specific)
    – WCC, ESR, CRP
    – Urea and electrolytes, LFTs
  • Diagnostic imaging
    – Plain X-ray
  • Not diagnostic but baseline for assessing future joint
    damage
  • May see effusion
    – MRI – can’t distinguish infection vs. inflammation
    early on
    – May require ultrasound to get fluid specimen
28
Q

treatment:

A
  1. Surgical drainage - remove pus
    – Aspiration
    – Arthroscopic washout
    – Suction drain
  2. IV antibiotics
    – For > 2 wks, then oral for another 2-4 wks
    – Optimum duration unknown
    – e.g. flucloxacillin empirically for native joint pending
    culture & susceptibility
    – Gonococcal arthritis - ceftriaxone
  3. Monitor inflammatory markers (CRP)
29
Q

tuberceuloriss of bone and joints :
- pathogen :
- increased incidence due to —
- found in:
- clinical features include:

A
  • mycobacterium tuberculosis
  • hIV
  • spine T10/11 ( which can cause Potts disease) , hip , knee for weight bearing
  • includes:
  • Slow onset of chronic monoarthritis
  • Usually no systemic symptoms
  • Swelling may be marked, but signs of acute inflammation
    absent or mild
  • Spinal TB
    – Collapse of intravertebral disc
    – Psoas abscess – may spread to groin
    – Paraplegia secondary to pressure on spinal cord
30
Q
  • tuberculosis of bone n joints :
    1- diagnosis:
    2- management
A

1-
* Aspirate
* TB PCR
* ZN / Auramine stain
* Culture
– Synovial fluid culture
positive in 80-90%
* Imaging: see joint
space narrowing &
bone erosions
2-
* Anti-TB drugs usually
eradicate, but may
need surgery
* Prolonged treatment
required for up to 12
months

31
Q

Septic arthritis or OM involving a —- which is total hip replacement and diganosis is complex
managed by :

A
  • prosthetic joint
  • – Surgical drainage/debridement/removal of implant
    – Antimicrobial therapy – usually prolonged (weeks to
    months)

BMF (17 decks)

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