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RB Y2 MSK 02 - Rheumatology > Infections of the Bone > Flashcards

Infections of the Bone Flashcards

1
Q

describe the clinical approach to infection

A

Clinical suspicion – history is key

  • Examination

Confirmation

  • Indirect – CT scan, MRI best
  • Direct – gold standard is bone biopsy
    • Surgical sample, histology
    • Wound swabs/blood cultures (useful in septic patients) are not very helpful

Treatment:

  • Debridement
  • Antimicrobials
    • Await microbial diagnosis
      • Unless acute presentation or sepsis
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2
Q

describe the approach to antimicrobial prescribing

A

await microbial diagnosis, unless acute presentation or sepsis

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3
Q

how will the patient typically present

A
  • Acute illness with extreme pain over affected bone
  • Tenderness, warmth, swelling and erythema of the affected part
  • Unwillingness to move limb
  • Signs of systemic infection
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4
Q

osteomyelitis

A

inflammation of the bone and medullary cavity

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5
Q

where is OM usually seen

A

in the metaphyses of long bones

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6
Q

predisposing conditions

A
  • Sickle cell anaemia
  • IV drug user
  • DM
  • Immunosuppression
  • alcohol excess
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7
Q

how long must the ABx course be

A

minimum 6 weeks

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8
Q

summarise what happens in the bone in osteomyelitis

A

bone necrosis and reactive bone formation

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9
Q

which forms of acute osteomyelitis can progress to chronic?

A

all

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10
Q

how do bacteria cause bone inflammation

A

bacteria lodge in metaphyseal blood vessels and set up an inflammatory reaction in the medullary canal, which spreads through the cortex, elevates the periosteum and may spread locally into an adjacent joint (septic arthritis)or into blood vessels(bacteraemia and septicaemia)

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11
Q

what does interference with bone blood supply cause

A

bone death and formation of sequestrum (dead fragment of bone) embedded in pus/infected granulation tissue

the sequestra are surrounded by sclerotic bone which is relatively avascular

within the bone the Haversian canals become blocked with scar tissue and the bone becomes surrounded by thickened periosteum

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12
Q

why is chronic osteomyelitis so hard to treat

A

due to avascular nature of the sequestra ABx will not travel to site via blood stream

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13
Q

involucrum

A
  • Periosteum lays down a new shell of bone called involucrum surrounding the existing sequesta
  • This is new, immature bone that forms around the seqestrum, effectively sealing it off
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14
Q

why is S Aureus particularly difficult to eradicate

A

can infect osteocytes intracellularly and decreases the activity and viability of osteoblasts

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15
Q

who does an acute osteomyelitis in the absence of recent surgery tend to occur in

A

kids

IC adults

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16
Q

describe 3 mechanisms of acute osteomyelitis in children

A
  • the metaphyses of long bones contain abdundant tortuous vessels with sluggish flow which can result in the accumulation of bacteria and infection spreading towards the epiphysis
  • some metaphyses are intra articular (proximal femur, humerus, radial head and ankle), therefore infection can spread into a joint causing co-existing septic arthritis
  • loosely applied periosteum so an abscess can extend widely along the sub periosteal space
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17
Q

Brodie’s abscess

  • onset
  • who is it usually found in
  • describe the pathology
A

form of localised subacute or chronic osteomyelitis with a more insidious onset

found in children

central cavity containing pus (which may be sterile) lined by granulation tissue and surrounded by reactive bone sclerosis

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18
Q

chronic osteomyelitis

A

develops from an untreated acute osteomyelitis and may be associated with sequestrum and/or involucrum

can be suppressed with ABx and lay dormant for years before reactivating

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19
Q

where does chronic osteomyelitis tend to be in adults

A

axial skeleton (spine or pelvis) or intervertebral disc

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20
Q

what can TB cause

A

chronic osteomyelitis, particularly in the spine through haematogenous spread from primary lung infection

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21
Q

what must one do to the sequestrum in the treatment of osteomyelitis

A

physically remove it

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22
Q

what investigations are useful in chronic osteomyelitis

A

blood tests are not

X ray and MRI are

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23
Q

treatment of chronic osteomyelitis

A

ABx alone wont work

surgery to remove sequestrum and debride

fixation of bone if there is instability

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24
Q

what can diffuse osteomyelitis result in

A

skeletal instability (eg infected non union)

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25
Q

what are the benefits of external fixation if the bone has been shortened by debridement

A

it can be subsequently lengthened

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26
Q

who is at particular risk of OM of the spine

A

poorly controlled DM, IV drug abusers, IC patients

complications of spinal surgery

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27
Q

where is the most common location for osteomyelitis in spine

A

lumbar spine

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28
Q

how do patients with osteomyelitis of the spine present

A
  • insidious onset of back pain which is constant and unremitting
  • paraspinal muscle spasm and spinal tenderness
  • fever and systemic upset
  • severe cases may be associated with neurological deficit
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29
Q

what can eventually happen to vertebra due to osteomyelitis

A

vertebral end plates weaken and eventually collapse leading to kyphosis or vertebra plana

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30
Q

investigations for osteomyelitis in spine

A

MRI - extent of infection and abscess formation

blood cultures - causative organism

endocarditis should be considered

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31
Q

treatment of osteomyelitis of the spine and indications for surgery

A
  • high dose IV ABx after CT guided biopsy to obtain tissue culture
  • indications for surgery are inability to obtain cultures by needle biopsy, no response to ABx, previous vertebral collapse and neurological deficit
  • surgery involves debridement, stabilisation and fusion of adjacent vertebrae
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32
Q

what is the gold standard investigation

A

bone biopsy

MRI

33
Q

normal ABx prescribed

A

flucloxacillin for 6 weeks

34
Q

complications

A
  • Septicemia
  • Acute pyogenic arthritis
  • Growth retardation
  • Chronic osteomyelitis
35
Q

management of open fractures

A
  • Cover wound with dressing
  • Broad spectrum antibiotics (IV)
  • Ensure tetanus immunisation
  • Early debridement in theatre
36
Q

clinical clue for open fracture

A

non union and poor wound healing

37
Q

which patient groups commonly get OM from haematogenous spread

A
  • prepubertal children
  • PWID
  • central lines, dialysis, elderly
38
Q

pathogens implicated in PWID

A
  • Staphylococcus, Streptococci and often unusual pathogens (Pseudomonas, TB, candida, Eikenella Corrodens
39
Q

Eikenlla Corrodens

A
  • causes OM in PWID
  • ‘needle lickers’
40
Q

osteitis pubis

A
  • inflammation over the pubic symphysis
  • presents with localised pain radiating outwards
41
Q

what can predispose one to the bacterial type of Osteitis Pubis

A

urogynaecological procedures

42
Q

what can cause the sterile type of Osteitis Pubis

A
  • complication of invasive (surgery) procedure about the pelvis (can occur up to 18 months later)
  • may occur as an inflammatory process in athletes
43
Q

what is the common causative organism in sickle cell anaemia patients

A

salmonella

44
Q

sickle cell anaemia

A
  • Sickle cell anaemia is an autosomal recessive genetic disorder characterised by the synthesis of defective haemoglobin – HbS.
  • These are deformed and rigid and lead to frequent clotting and thrombosis of blood vessels.
  • The consequence of obstruction is ischemia and infarction.
  • Results in small localised areas of dead tissues.
45
Q

what is the DD of OM in sickle cell anaemia

A

bone infarction

46
Q

are there single or multiple lesions in OM sickle cell anaemia

A
  • can be multifocal
  • seen in the long bones
47
Q

Gaucher’s disease

A
  • lysosomal storage disease in which glucocerebroside accumulates in cells and certain organs eg bones
  • can manifest as a bone crisis (severe bone pain as a result of infarction)
48
Q

which bone does Gaucher’s disease oftne affect

A

the tibia

49
Q

pathogens implicated in Gaucher’s disease

A
  • if just a bone crisis is sterile
  • S Aureus if infected
50
Q

SAPHO

A
  • Synovitis, acne, pustulosis, hyperostosis and osteitis
  • hypertosis means abnormal excessive growth of bone, frequently located in chest wall
  • Osteitis often occurs at sacroiliac joints and spine
51
Q

CRMO

A
  • Autoimmune disease similar to osteomyelitis, but without the infection
  • involves multiple bones at different times
  • may be related to SAPHO
52
Q

diagnosis of SAPHO and CRMO

A
  • History plus culture samples are needed to exclude osteomyelitis
  • Raised inflammatory markers
  • Lytic lesions of X rays
  • Multifocal
53
Q

general symptoms of SAPHO and CRMO

A

can cause fever, weight loss and malaise

54
Q

which bacteria may play a role in SAPHO and CRMO

A

Proprionibacterium

55
Q

which is found in adults and which in kids - SAPHO and CRMO

A
  • SAPHO in adults
  • CRMO in kids
56
Q

Pott’s disease

A

TB in the spine that has spread haematogenously from eg the lungs

57
Q

features of Pott’s disease

A
  • Clinical Features: backache and stiffness of all back movements
  • Eventually leads to caseous necrosis, vertebral collapse and gibbus
  • May be abscess formation
58
Q

what test would you offer in adults with Pott’s

A

HIV

59
Q

planktonic bacteria

A

is free in the blood

60
Q

sessile bacteria

A
  • sits on prosthetic/joint and forms a biofilm
  • phenotypic transformation of sessile bacteria
61
Q

what bacteria are implicated in prosthetic joint infection

A
  • S aureus
  • S epidermidis
  • Propionibacterium acnes
  • E coli
  • Pseudmonas aeruginosa
62
Q

diagnosis of prosthetic joint infection

A
  • culture perioperative tissue
  • CRP
  • radiology
63
Q

coauglase negative staph in infections

A
  • they are part of the normal flora eg epidermidis, so have a low virulence and can only cause infection in the presence of prosthetic material
  • They produce a surface polysaccharide slime which allows them to stick to the materia
64
Q

initial treatment of staph epidermidis

A
  • vancomycin
  • often add rifampicin
65
Q

what happens to the prosthetic joint if it is infected

A
  • Ideally the prosthetic joint is removed if it is causing infection, this can be done in 1 or 2 stages
  • In some elderly people the joint is not removed and is just debrided, but this has a poor prognosis
66
Q

which joint is most commonly affected by septic arthritis

A

knee

67
Q

when must septic arthrtis be considered

A

consider in any acutely inflamed joint as it can destroy a joint in under 24 horus

68
Q

what often causes septic arthritis in sexually active people

A

neisseria gonorrhoea

69
Q

what commonly causes septic arthritis in pre school children

A

H influenzae, rarely seen now due to vaccination

70
Q

diagnosis of septic arthritis

A
  • Clinical picture
  • Urgent joint aspiration for synovial fluid microscopy and culture is the key investigation
  • Blood culture if pyrexial
  • Gout can present in the same way so exclude crystals
71
Q

treatment of septic arthritis

A
  • presumptive flucloxacillin to cover S aureus
  • if under 5 add ceftriaxone for H influenzae
72
Q

pyomyositis

A

Bacterial infection of the skeletal muscles that results in a pus-filled abscess

73
Q

which organisms often cause pymyositis in infected wounds

A

clostridium ones

74
Q

common cause of pymyositis

A

S aureus

75
Q

what is tetanus caused by

A
  • Clostridium tetani
  • Gram positive strictly anaerobic rods
  • Forms spores, which are found in soil etc.
  • The exotoxin causes muscle spasms and rigidity.
76
Q

classical description of tetanus

A
  • locked jaw
  • spasms can be induced by loud noises and bright lights
77
Q
A
78
Q

treatment of tetanus

A
  • Surgical debridement
  • Antitoxin
  • Supportive measures
  • Antibiotics are not that useful as it is due to toxin
  • Survivors are not immune – booster vaccine

RB Y2 MSK 02 - Rheumatology (33 decks)

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