Management of Osteomyelitis Flashcards

1
Q

is it more common for odontogenic infections to spread to soft tissue/fascial spaces or osseous structures

A

soft tissue/fascial spaces

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2
Q

what is osteomyelitis

A

inflammation and infection of the bone marrow with a tendency to progression

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3
Q

where does osteomyelitis start

A

in the medullary bone and then continues to involve adjacent cortical plates and often periosteum - more frequently seen in the mandible

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4
Q

what happens if osteomyelitis is untreated

A

it progresses from inflammatory destruction of bone, to necrosis (sequestra)

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5
Q

in the oral region, osteomyelitis is usually a result of:

A

bacterial infection secondary to odontogenic infections and trauma

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6
Q

which jaw is osteomyelitis incidence higher in and why

A

mandible due to dense, poorly vascularized cortical plates

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7
Q

maxillary bone is:

A

much less dense with excellent blood supply

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8
Q

describe the mandible

A

-predominantly supplied by inferior alveolar neurovascular bundle
- overlying cortical plate is thick

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9
Q

describe the maxilla

A
  • much more vascular than mandible as it receives blood supply from several arteries
  • less dense than mandible
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10
Q

describe the course of osteomyelitis

A

indolent, yet progressive and persistent course

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11
Q

what are the immuno compromised status factors that can predispose to osteomyelitis

A
  • DM
  • malignancy
  • AIDS
  • patients taking chronic steroids, and chemotherapeutic agents
  • patients on immunosuppressants
  • tuberculosis
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12
Q

what are the conditions that affect the jaw vascularity

A
  • H/O irradiation treatment
  • advanced osteoporosis
  • osteopetrosis
  • late stage cemento osseous dysplasia
  • osteitis deformans (paget disease)
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13
Q

osteomyelitis is primarily the result of:

A

odontogenic infections or trauma which cause inoculation of bacteria into the jaws
- results in an inflammatory cascade that is usually self limiting in the healthy patient
- with progression the condition is considered pathologic

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14
Q

what is the pathogenesis of osteomyelitis

A
  • infection and associated inflammation (edema) spreads into marrow spaces and causes compression of blood vessels and therefore causes severe compromise of blood supply
  • pus travels through haversian and volkaman’s canal and accumulation beneath the periosteum and elevating it from cortex and thereby reducing the blood supply
  • ultimately cortical bone perforates, compromising periosteal blood supply as well
  • reduced blood supply causes necrosis of the bone
  • small section of necrotic bone may get completely lysed while large get localized and get separated from the shell of new bone by bed of granulation tissue
  • the dead bone is surrounded by the new viable bone this is called involucrum
  • then pus penetrate the periosteum and mucosal and cutaneous fistulate develop and thereby discharging the purulent pus
  • intraoral or extraoral fistulas develop
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15
Q

what happens after an extraoral fistula

A

bacteria then proliferates as normal blood borne defenses do not reach the tissue and the osteomyelitis process spreads until it is stopped by surgery and medical treatment

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16
Q

what is the microbiology of osteomyelitis

A
  • usually a mixed infection when involving the jaws
  • alpha hemolytic streptococci and anaerobic bacteria (peptostreptococcus, fusobacterium, prevotella) recognized as prime pathologic species for osteomyelitis of the jaws
  • osteomyelitis of the long bones usually caused by staphylococcus aureus
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17
Q

what are the classifications of acute osteomyelitis

A
  • contiguous focus
  • progressive
  • hematogenous
  • suppurative vs non suppurative
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18
Q

what is contiguous focus

A

the result of the spread of infection from an adjacent soft tissue focus such as wound, laceration, abscess, post operative infection

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19
Q

what is hematogeous acute osteomyelitis

A

spread to the bone from a source through bloodstream

20
Q

what are the classifications for chronic osteomyelitis

A
  • recurrent multifocal
  • garre’s
  • suppurative or nonsuppurative
  • chronic sclerosing
  • chronic refractory osteomyelitis
21
Q

what is garre’s chronic osteomyelitis

A

proliferative periostitis, periostitis ossificans

22
Q

what is the clinical presentation of osteomyelitis

A

-pain
-swelling and erythema of overlying tissues
- adenopathy
- fever
- paresthesia of the inferior alveolar nerve
- trisumus
- malaise
- fistulas

23
Q

in the acute phases of osteomyelitis it is common to see _____ but uncommon in the chronic phase

A

leukocytosis

24
Q

_______ are sensitive indicators of inflammation but non specific

A

elevated erythrocyte sedimentation rate and C-reactive protein

25
Q

radiographic images are not as good as clinical presentation because

A

cortical involvement is required for any change to be evident

26
Q

acute osteomyelitis appears _____ radiographically

A

normal

27
Q

when will destruction be visible on radiograph

A

until at least 30-60% of destruction of mineralized portion of bone takes places

27
Q

what is the presentation of chronic osteomyelitis on radiograph

A

moth eaten appearance

28
Q

what radiograph is initially recommended for dx of osteomyelitis and why

A

pano because it is easily obtainable and gives information of possible sources and progression

29
Q

what is the standard for imaging for osteomyelitis and why

A

CT scans
- provide 3 dimensional views
- require 30-50% demineralization before changes are seen
- allow assessment of the cortices

30
Q

what does an MRI tell about osteomyelitis

A
  • it can assist in early dx by detection of bone marrow changes prior to cortical involvement
  • bone marrow changes and soft tissue changes are seen more accurately in MRI when compared to a CT scan
31
Q

what is a technetium bone scan

A

more sensitive than plain film imaging in detecting early infections and may be positive as early as three days

32
Q

what is the downside of bone scnas

A

they are sensitive for bone turnover but are not specific for osteomyelitis
- there is a high incidence of false positive osteomyelitis nuclear medicine studies of soft tissue infections

33
Q

what interventions are required for tx of osteomyelitsi

A
  • medical and surgical interventions
  • medical therapy alone will not suffice and only delay appropriate treatment
  • tissues from the affected site should be sent for microbiological exam ,culture, and sensitivity, and histopathological exam
  • immunocompromised states should be controlled medically to achieve optimum response to therapy
34
Q

begin empiric antibiotic treatment based on:

A

gram stain( microbiological exam) results

35
Q

how long is AB therapy indicated for osteomyelitis

A

6 weeks

36
Q

what ABs are used

A

carbapenems, cephalosporins, fluoroquinolones, clindamycin, metronidazole, or combination therapy

37
Q

when would HBO therapy be considered

A

for chronic refractory osteomyelitis

38
Q

what is chronic refractory osteomyelitis

A

a persistent or recurrent bone infection lasting longer than 6 months despite surgical and medical treatment

39
Q

what happens in HBO therapy

A

placing a pt in a chamber where they breathe 100% oxygen at increased atmospheric pressure
- consists of 90 minute sessions for 5 days per week for 20-60 treatments based on their condition

40
Q

what is the MOA for HBO

A
  • enhances leukocyte oxidative killing
  • neo angiogenesis
  • osteogenesis
  • synergistic antibiotic activity
41
Q

what is a sequestrectomy

A
  • the removal of infection and avascular pieces of bone
  • since the sequestrum is avascular, ABs will not be able to penetrate it
42
Q

what is sauceriztion

A

involves the removal of adjacent bony cortices and open packing to permit healing by secondary intention after the infected bone has been removed
- the margins of the bone which lodge the sequestra are trimmed down to create a saucer shaped defect instead of a deep hollow cavity
- this saucer shaped defect cant accumulate a large clot

43
Q

what is decortication and what is the key element

A
  • involves removal of the dense, chronically infected and poorly vascularized bony cortex and placement of the vascular periosteum adjacent to the medullary bone to allow increased blood flow and healing in the affected area
  • key element is cutting back to healthy bleeding bone - clinical judgement
44
Q

may support weakened mandible using:

A

external fixation, reconstruction plate or MMF

45
Q

segmental resection is a last resort following:

A

multiple attempts at more conservative debridement

46
Q
A