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MM Test 4 > B6.078 Osteomyelitis > Flashcards

B6.078 Osteomyelitis Flashcards

1
Q

anatomic types of osteomyelitis

A

stage 1: medullary
stage 2: superficial
stage 3: localized
stage 4: diffuse

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2
Q

physiologic classes of osteomyelitis

A 
A host: normal
B host (s) : systemic compromise
B host (l) : localized compromise
B host (sl): systemic and local compromise
C host: treatment worse than disease
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3
Q

systemic factors that affect osteomyelitis

A 
malnutrition
renal or hepatic failure
DM
chronic hypoxia
immune disease
malignancy
extremes of age
immunosuppression or immune deficiency
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4
Q

local factors that affect osteomyelitis

A 
chronic lymphedema
major vessel compromise
small vessel compromise
vasculitis
venous stasis
extensive scarring
radiation fibrosis
neuropathy
tobacco abuse
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5
Q

pathogenesis of osteomyelitis

A

compromised bone allows for bacterial attachment

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6
Q

mediators of microbial adhesion

A

hematoma
fibrin
platelets
fibronectin

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7
Q

forces that mediate adhesion of bacteria to bone

A

van der walls
hydrophobic interactions between small molecules
polysaccharide polymers

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8
Q

bacterial progression of osteomyelitis

A

disruption of periosteum allows for blood collection around damaged bone
disruption of blood flow occurs within cortical bone
bone becomes walled off by bacteria/biofilm and no longer viable
over time, bone can extrude out of sinus tract

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9
Q

what do bacteria in osteomyelitis release?

A

extracellular toxins
bacterial antigens / enzymes
this leads to recruitment of additional immune cells

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10
Q

what causes the damage in osteomyelitis

A

immune response

granular enzymes can degrade bone and cartilage substrates such as collagen and elastin, leading to bone degradation

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11
Q

granular enzymes

A

serine proteases
endogenous oxidants
metalloproteinases

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12
Q

pathogenesis of osteomyelitis

A
  1. pus spreads into vascular channels
  2. increased intraosseous pressure, decreased blood flow, decreased pH, decreased O2
  3. ischemic necrosis
  4. formation of devascularized fragments
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13
Q

what is hematogenous osteomyelitis

A

osteomyelitis spread via blood

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14
Q

where does hematogenous osteomyelitis occur

A

metaphyses of long bones in children

vertebrae of adults

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15
Q

why does hematogenous myelitis occur in metaphyses in children

A

non anastomosing capillary ends make sharp loops near growth plate
-blood pools and allows for movement of bacteria
metaphyseal capillaries lack phagocytic lining cells
sinusoidal veins contain functionally inactive phagocytic cells

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16
Q

is acute vs chronic osteo an applicable designation

A

not really

areas of micronecrosis must be removed regardless of the acuity or chronicity of an uncontrolled infection

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17
Q

how to diagnose osteomyelitis

A

isolate organism from bone
histo evidence of inflammation and osteonecrosis
exception: in hematogenous osteomyelitis blood cultures and radiographic evidence may be sufficient

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18
Q

how to do a bone culture

A

take before abx initiated or once a person has been off abx for a sufficient period of time

  • bone cultures taken during debridement surgery are preferred
  • deep bone biopsy
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19
Q

lab findings in osteomyelitis

A

non-specific
leukocytosis (acute): rarely >15,000
in chronic, WBC usually normal
increased ESR and CRP

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20
Q

can you culture the drainage from the sinus tract

A

no, multiple other colonizing bacteria

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21
Q

when can you see changes on xray in osteomyelitis?

A

1st visible change in bone: 2-3 weeks
lytic changes: weeks to months
need loss of 30-50% of bone mineralization to see changes

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22
Q

early changes on imaging

A

soft tissue swelling
periosteal thickening, or elevation or both
focal osteopenia
loss of trabecular architecture

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23
Q

later changes on imaging

A

diffuse osteopenia / lytic changes

24
Q

benefits of CT in imaging osteo

A 
high spatial resolution
exceptional cortical bone density
small foci intraosseous gas
tiny foreign bodies
involucrum / sequestration formation
25
Q

benefits of bone scintigraphy in imaging osteo

A

MDP pools in areas with good blood flow
positive in 24-48 hours after onset of disease
can detect multiple areas of involvement
good sensitivity

26
Q

mechanisms of bone scintigraphy

A

absorption on crystal surfaces
binding to organic matrix
preferentially incorporated into metabolically active bone

27
Q

normal bone scintigraphy

A

rapid redistribution throughout extracellular fluid
over several hours, >50% accumulates in bone, remainder in urine
symmetrical pattern

28
Q

benefits of MRI in imaging osteo

A

exquisite bone and soft tissue detail
high sens and spec
best imaging technique

29
Q

early osteo on MRI

A

poor definition soft tissue planes
no cortical thickening
interface normal / abnormal marrow difficult to appreciate

30
Q

chronic osteo on MRI

A

cortical thickening
good distinction between normal / abnormal marrow
Gd T1 enhanced images > no enhancement with devitalized sequestered tissue

31
Q

treatment of osteo in adults (non hematogenous)

A

surgical disease

4-6 weeks parenteral abx + surgery

32
Q

principals of osteo treatment

A 
debride necrotic tissue
obliterate dead space
stabilization
soft-tissue coverage
restore effective blood supply
33
Q

treatment of osteo in children (hematogenous)

A

4 wks therapy ( 2 IV and 2 po)

34
Q

how long doe sit take bone to revascularize after debridement

A

3-4 weeks

35
Q

what does a lack of osseous incorporation of joint after hardware placement signify

A

sign of early infection

36
Q

black halo around hardware on xray

A

bony lysis / death

usually result of infection

37
Q

growth of biofilm

A
  1. attachment
  2. growth within EPS (extracellular polymeric substances) to form complex 3D structures that contain nutrients
  3. dispersal of metabolically active bacteria from inside biofilm
38
Q

why cant antimicrobials treat biofilms well?

A

resistance to phagocytosis
slowed metabolism of pathogens within biofilms
decreased penetration of antimicrobial into biofilm

39
Q

discuss bacterial gene expression changes in biofilm states

A

12% genes differentially expressed

6% upregulated, 6% downregulated

40
Q

downregulated genes within biofilm bacteria

A 
translation, transcription
adhesion factors
aerobic production of energy
phenol soluble modulins
*stop dividing to be elusive to abx, and transition to anaerobic state to decrease metabolic activity)
41
Q

upregulated genes within biofilm bacteria

A 
chaperones and stress factors
fermentation
global regulators
resistance factors
osmoprotection
*keep organisms alive/viable long term in decreased metabolic state*
42
Q

why cant we cure chronic osteo with abx alone?

A

abx fairly ineffective against sessile organisms in biofilm
biofilm can act as a diffusion barrier to slow down the infiltration of some antimicrobial agents
biofilm protects host from phagocytic clearance
reactive chlorine species may be deactivated in the surface layers of biofilm before deeper dissemination into lower layers

43
Q

what is bone cement?

A

polymerized polymethylmethacrylate
drug delivery device (antibiotics can be added to cement)
fills dead space
exothermic reaction limits abx options

44
Q

use of rifampin in osteo

A

controversial
has bactericidal activity, concentrates intracellularly and penetrates biofilm
may be benefits for use in treatments of prosthetic device infections

45
Q

benefits of increased O2 tension

A

lethal effect on strict anaerobes
augments oxygen dependent intracellular killing mechanisms
benefits not clear in osteo, reserved for select really bad disease or as an adjunct to suppressive therapy

46
Q

osteo in the setting of vascular insufficiency

A

distal extremity most commonly involved
usually diabetics (peripheral neuropathy)
usually polymicrobial
adequate blood flow required for healing

47
Q

clinical presentation of osteo in vascular insufficiency

A

pain often absent
fever / systemic symptoms often lacking
poor distal pulses

48
Q

pathogenesis of vertebral osteomyelitis

A

typically hematogenous seeding via arterial blood supply
vertebral bone = highly vascular marrow with relatively high-volume blood flow compared to adult long bones
arterial anastomoses extend into intervertebral discs > with age, end anastomoses regress, terminate in endplates
blood flow sluggish near endplates

49
Q

characterize vertebral osteo

A

increasing incidence with age
s. aureus most common
GNRs - 30% (e.coli)

50
Q

locations of vertebral osteo

A

lumbar - 50%
thoracic - 35%
cervical - less common
sacrum - more typical with contiguous infection

51
Q

diagnosis of vertebral osteo

A

usually a single organism present
blood cultures positive 50-70%, obviating need for biopsy
MRI very sensitive for discitis, epidural abscess, marrow edema, etc. (can estimate degree of bony destruction)

52
Q

treatment of vertebral osteo

A

6 weeks of parenteral or highly bioavailable oral therapy for most patients

53
Q

factors associated with poor outcomes in vertebral osteo

A 
multidisc disease
epidural abscess
lack of surgical therapy
s. aureus
old age
extensive bony destruction
54
Q

indications for surgery in vertebral osteo

A

progressive neuro deficits
progressive deformity / spinal instability
persistent or recurrent bloodstream infection
worsening pain despite appropriate therapy

55
Q

follow up MRI in vertebral osteo

A

not routinely recommended if improving

only in patients with poor clinical response

MM Test 4 (20 decks)

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