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MSK > Osteomyelitis > Flashcards

Osteomyelitis Flashcards

1
Q

What is osteomyelitis

A

infection localized to bone
inflammatory condition of bone/ bone marrrow caused by an infecting organism, most commonly Staphylococcus aureus.

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2
Q

Epidemiology of osteomyelitis

A

UK incidence:
10 – 100 / 100,000 p/y.
Predominantly Children 80% of acute, haematogenous osteomyelitis
adolescents and adults get contiguous osteomyelitis (often associated with direct trauma)

Older patients: Diabetes mellitus/Peripheral Vascular disease/Arthroplasties
Men more than women

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3
Q

Pathophysiology: 3 routes of transmission for osteomyelitis

A
  • direct inoculation of infection into the bone:
    trauma or surgery,
    polymicrobial or monomicrobial.
  • contact spread of infection to bone:
    from adjacent soft tissues and joints, polymicrobial or monomicrobial,
    older adults: DM, chronic ulcers, vascular disease, arthroplasties / prosthetic material,
  • Haematogenous seeding:
    children (long bones)>adults (vertebrae)
    monomicrobial
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4
Q

Pathogenesis of Osteomyelitis

A
  • Behavioural factors:
    i.e. risk of trauma
  • Vascular supply:
    Arterial disease
    Diabetes mellitus
    Sickle cell disease
  • Pre-existing bone / joint problem:
    Inflammatory arthritis
    Prosthetic material inc arthroplasty
  • Immune deficiency
    Immunosuppressive drugs
    Primary immunodeficiency
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5
Q

Pathogenesis of haematogenous OM

A

Adults:
Usually >50 years
Vertebra > clavicle/pelvis»long bones
Children (85%)
Long bones&raquo_space; vertebra

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6
Q

What is the most common site of infection in long bone haematogenous OM?

A

Metaphysis

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7
Q

Why is the metaphysis the most common site of infection?

A
  • Main blood vessels penetrate the midshaft then go to either end to form vascular loops in the metaphysis.
  • Here blood flow is slower and no endothelial basement membranes are so bacteria can enter the site from the blood
  • capillaries also lack or have inactive phagocytic lining cells which allow growth of microorganisms.
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8
Q

Where are children affected with haematogenous OM spread

A
  • Children, with elongating long bones, the metaphysis is very metabolically active with a large flow of blood predisposing the vasculature to infection.
  • With age, metaphysial blood flow slows.
  • With age vertebrae more vascular so bacterial seeding of verebral endplate more likely
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9
Q

How can lumbar vertebral veins lead to bacteria

A

lumbar vertebral veins communicate with those of the pelvis by valveless anastamoses.

Retrograde flow from urethral , bladder and prostatic infections may be a source of bacteria to these vertebrae

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10
Q

Haematogenous OM in adults

A

Usually >50 years
Vertebra > clavicle/pelvis»long bones

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11
Q

Haematogenous OM in children

A

Long bones&raquo_space; vertebra

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12
Q

People who inject drugs haematogenous OM

A

younger, more often clavicle and pelvis

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13
Q

Who are the people with risk factors for bacteremia

A

central lines, on dialysis
sickle cell disease,
urinary tract infection, urethral catheterization
Similar factors as those for infective endocarditis

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14
Q

S. aureus microbial factors

A

binds host proteins fibronectin, fibrinogen, and collagen
fibronectin binding proteins A and B (FnBPA / FnBPB)
Collagen-binding adhesin (CNA)
can survive intracellularly in cultured macrophages

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15
Q

Which organisms cause OM

A

Staphylococcus aureus,
coagulase-negative staphylococci,
aerobic gram-negative bacilli (30%)
M. tuberculosis
Neisseria gonorrhoeae
Streptococci (skin, oral)
Enterococci (bladder, bowel)
Anaerobes (bowel)
Salmonella in sickle cell anaemia patients

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16
Q

What is the histopathology of osteomyelitis

A

1.inflammatory exudate in the marrow
2. increased intramedullary pressure
3.extension of exudate into the bone cortex
4.rupture through the periosteum
5.Interruption of periosteal blood supply causing necrosis
6. Leaves pieces of separated dead bone
7. New bone forms here

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17
Q

Acute changes of histopathology

A
  • Inflammatory cells
  • Oedema
  • Vascular congestion
  • Small vessel thrombosis
18
Q

Chronic changes of histopathology of OM

A
  • neutrophil exudates
  • lymphocytes & histiocytes
  • Necrotic bone ‘sequestra’
  • new bone formation ‘involucrum’
19
Q

What investigations can we do for OM

A

History
Examination
CRP - raised inflammatory marker
FBC- WCC - high in acute, normal in chronic
U and E
LFTs
HbA1C
MRI - Gold standard
CR
Plain Xray
Nuclear bone scan

20
Q

Symptoms (History)

A

Onset - several days.
dull pain at site of OM
may be aggravated by movement.
- Fever
- Pain
- Overlying redness
- Swelling
- Malaise

21
Q

Signs of clinical OM (Examination)

A

Systemic:
Fever, rigors, sweats, malaise

Local:
Acute OM-
tenderness, warmth, erythema, and swelling
Chronic OM-
tenderness, warmth, erythema, and swelling

PLUS any of
draining sinus tract
deep / large ulcers that fail to heal despite several weeks treatment*
non-healing fractures

22
Q

OM in hip vertebrae or pelvis

A

pain but few other signs or symptoms.

23
Q

OM Vertebral: lumbar > thoracic > cervical

A

Posterior extension - epidural and subdural abscesses or even meningitis.
Extension anteriorly or laterally can lead to paravertebral, retropharyngeal, mediastinal, subphrenic, retroperitoneal, or psoas abscesses.

24
Q

OM Joint - can also present as septic arthritis.

A

when infection breaks through cortex resulting in discharge of pus into the joint (knee, hip, and shoulder).
More common in infants due to patent transphyseal blood vessels and immature growth plate

25
Q

What is shown in a plain x-ray in chronic osteomyelitis

A

cortical erosion,
periosteal reaction,
mixed lucency,
Sclerosis
sequestra
soft tissue swelling

26
Q

Why is an X ray not the best especially in early OM?

A

Poor sensitivity and specificity,

27
Q

Why is MRI good?

A

marrow oedema from 3-5 days
Delineates cortical, bone marrow and soft tissue inflammation

28
Q

How can we make a definitive diagnosis?

A

Microbiology and histology: Bone biopsy
Positive Blood cultures

29
Q

Bone biopsy for OM

A

obtained via sterile technique,
Open bx&raquo_space;> needle bx
2 specimens
Culture
16sRNA PCR may be necessary
Histology showing inflammation and osteonecrosis

30
Q

Positive blood cultures

A

may obviate the need for invasive diagnostic testing if the organism isolated from blood is a pathogen likely to cause osteomyelitis.
+ve in 50% of Acute OM
most useful if hematogenous OM

31
Q

Differential diagnosis for OM

A

Soft tissue infection (Cellulitis and erysipelas)
Charcot joint
Avascular necrosis of bone
Causes: steroid, radiation, or bisphosphonate use.

Gout
uric acid crystals in joint fluid / more acute presentation

Fracture
Bursitis
Malignancy

32
Q

Surgical treatment for OM

A

Debridement (remember Bromfield “we cannot be too early in letting it out”)
Hardware placement or removal

33
Q

Antimicrobial therapy for treatment

A

Initial broad spectrum empirical therapy “start SMART”
S. aureus or MRSA?
gram-negative organisms?
Special population: IVDU/HbSS?

Tailored to culture and sensitivity findings “then FOCUS”.

Bone penetration of drug

Prolonged duration

34
Q

Antibiotics to use

A

Levofloxacin
Ciprofloxacin
Moxifloxacin
Vancomyocin

35
Q

Treatment duration

A

Knowing when to stop treatment is very difficult
6 weeks of IV considered minimum
switch to oral alternatives may work in some situations
Stopping treatment guided by CRP response
failure to respond requires re-imaging

36
Q

TB osteomyelitis

A

May be slower onset
Systemic symptoms
Epidemiology is different from pyogenic OM
Blood Culture less useful
Biopsy essential
Longer treatment 6 months
Caseating Granolumata on histology

37
Q

Risk factors for OM

A
  • Diabetes
  • Old age
  • Peripheral vascular disease
  • Immunocompromise
  • Malnutrition
  • Trauma/ injury
38
Q

Non haematagenous spread

A
  • occurs due to breakdown or removal of the normal protective barriers of skin and soft tissue or contiguous spread (e.g. local skin infection like cellulitis spreading to the bone).
    • Open fractures
    • Skin ulcers
    • Surgery
    • Prosthesis
    • Trauma
    • Animal/ insect bites
39
Q

Haematogenous spread

A

refers to the spread of a pathogen via the blood. Most commonly affects the axial skeleton, primarily the vertebral bones. After the vertebral bones the next most frequently affected sites are other axial bones like the sternum and pelvis.

  • Indwelling intravascular catheter(e.g. Hickman line)
  • Haemodialysis
  • Endocarditis
  • IV drug use
40
Q

Acute osteomyelitis

A
  • Once the bacteria reach the bone they start to proliferate.
    This alerts nearby immune cells - specifically dendritic cells and macrophages - that try to fight off the infection.
    This represents the acute phase of the disease and occurs over a course of weeks.
    The immune cells release chemicals and enzymes that break down bone and cause local destruction.
    Usually acute osteomyelitis comes to a resolution - the immune systemdestroys all of the invading bacteria.
  • If the lesion is not that extensive, and there’s viable bone the osteoblasts and the osteoclasts begin to repair the damage over a period of weeks
41
Q

Chronic osteomyelitis

A
  • affected bone sometimes becomes necrotic and separates from the healthy part of the bone - and that’s called a sequestrum. At the same time, the osteoblasts that originate from the periosteum may form new bone that wraps the sequestrum in place, this is called an involucrum.
  • Cloaca may also form

MSK (20 decks)

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