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MsK > Infective arthrits > Flashcards

Infective arthrits Flashcards

1
Q

What organisms are involved in (Prosthetic Joint) infections

A

CNS 27%
Enterococcus 14%
Staph aureus 25%
MRSA 7%
Others as well

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2
Q

Which bacteria is significant in Upper Limbs?

A

Propionibacteria

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3
Q

Why is propionibacteria more significant in the upper limbs?

A

They are colonisers of humans from the above the waist

Can even be shed by blinking the eyes

Therefore may represent more of a threat in upper limb prostheses and Spines

Suspect they are a very significant pathogen of upper limb surgery

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4
Q

Why is it so difficult to treat propniobacteria?

A

-Because they are slow growing!
-Even contaminants take 7 days to grow
-Longer when causing clinical infection (Upper limb and spines)
-Because they rarely turn a broth cloudy
-Frequently don’t trigger blood culture detection systems

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5
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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6
Q

Epidemiology of osteomyelitis

A

UK incidence:
10 – 100 / 100,000 p/y.
Predominantly Children 80% of acute, haematogenous osteomyelitis

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7
Q

Pathophysiology: 3 routes of transmission for osteomyelitis

A

direct inoculation of infection into the bone:
trauma or surgery,
polymicrobial or monomicrobial.

contiguous 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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8
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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9
Q

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

A

Metaphysis

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10
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 endothelial basement membranes are absent predisposing to transition of bacteria from the blood to this site.

capillaries also lack or have inactive phagocytic lining cells which allow growth of microorganisms.

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11
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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12
Q

Haematogenous OM in children

A

Long bones&raquo_space; vertebra

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13
Q

People who inject drugs haematogenous OM

A

younger, more often clavicle and pelvis

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14
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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15
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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16
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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17
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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18
Q

Chronic changes of histopathology of OM

A

neutrophil exudates
lymphocytes & histiocytes
Necrotic bone ‘sequestra’
new bone formation ‘involucrum’

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19
Q

What investigations can we do for OM

A
  • Fbc
  • esr
  • crp
  • blood culture
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20
Q

Symptoms (History)

A

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

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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

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22
Q

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

A

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

23
Q

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

A

Poor sensitivity and specificity,

24
Q

Why is MRI good?

A

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

25
Q

How can we make a definitive diagnosis?

A

Microbiology and histology: Bone biopsy
Positive Blood cultures

26
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

27
Q

Positive blood cultures

A

+ve in 50% of Acute OM
most useful if hematogenous OM

28
Q

Differential diagnosis for OM

A

Charcot joint!!!!
Avascular necrosis of bone
Causes: steroid, radiation, or bisphosphonate use.

Gout
uric acid crystals in joint fluid / more acute

29
Q

Surgical treatment for OM

A

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

30
Q

Antimicrobial therapy for treatment

A

Dependant on bacteria

Vancomycin + teicoplannin for MRSA and S aureus
Fusidic acid for s aureus
Flucoxacillin for salmonella

31
Q

Antibiotics to use

A

Levofloxacin
Ciprofloxacin
Moxifloxacin
Vancomyocin

32
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

33
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

34
Q

Risk factors for OM

A
  • Diabetes
  • Old age
  • Peripheral vascular disease
  • Immunocompromise
  • Malnutrition
  • Trauma/ injury
35
Q

Non haematagenous spread can occur through ?

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
36
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
37
Q

What occurs in Acute osteomyelitis

A
  • arrival of bacteria at the bone causes proliferation
  • activates an immune response with dendritic and macrophage cells
  • enzymes released to break down bone
  • acute usually comes to a resolution
  • osteoclasts and osteoblasts repair the damage over a few weeks
38
Q

What is a sequestrum

A
  • affected bone sometimes becomes necrotic and separates from the healthy part of the bone - and that’s called a sequestrum.
39
Q

What is septic arthritis

A

defined as the infection of 1 or more joints caused by pathogenic inoculation of microbes. It occurs either by direct inoculation or via haematogenous spread. It is a medical emergency!

40
Q

Epidemiology of septic arthritis

A
  • Septic arthritis is a rare but potentially devastating condition, affecting 5 per 100,000 people each year in the developed world
  • Increases with age - 45% over 65 yrs
41
Q

Aetiology of septic arthritis

A
  • Staphylococcus aureus - the most common cause in all age groups
  • Staphylococcus epidermidis - prosthetic joints
  • Streptococcus pyogenes - children under 5 years old
  • Neisseria gonorrhoeae - young, sexually-active adults
  • Pseudomonas aeruginosa - immunosuppressed, eldery and IV drug abuse
  • Escherichia coli - immunosuppressed, eldery and IV drug abuse
42
Q

RF for septic arthritis

A
  • Underlying joint disease:10-fold increased risk; conditions such as rheumatoid arthritis, osteoarthritis and gout
  • Intravenous drug use:transfer of pathogenic organisms into the bloodstream
  • Immunocompromised:elderly, diabetes, HIV
  • Prosthetic joint
  • Recent joint surgery
43
Q

Why is septic arthritis a medical emergency?

A

due to the risk of permanent joint destruction, osteomyelitis and sepsis. It is most commonly caused by a bacterial infection, with the microbes either invading the joint directly or via the bloodstream from other sites of infection.

44
Q

What are 90% of cases caused by for septic arthritis

A

90% of cases are caused bystaphylococci or streptococci, often as a complication of other pathologies such as cellulitis, chronic osteomyelitis, or drug abuse. Fungal and viral causes are rare.

45
Q

Key presentations for septic arthritis

A

Hot swollen painful restrictedjoint
Most commonly at the knee

46
Q

Signs for septic arthritis

A
  • Hot, tender, erythematous, swollen joint
    • In the elderly and immunosuppressed and in RA the articular signs may be muted
  • Very limited range of movement
47
Q

Symptoms in septic arthritis

A
  • Difficulty weight bearing
  • Fever
48
Q

1st line investigation for septic arthritis

A
  • FBC: leukocytosis
  • CRP and ESR: elevated due to inflammation and used for monitoring response to treatment
  • Blood cultures: should be performed onallpatients before commencing antibiotics
  • Joint aspiration (arthrocentesis): definitive investigation
    Plain Xray
    US or MRI
49
Q

Gold standard investigation for septic arthritis

A

Joint aspiration - MSC

50
Q

Scoring criteria for septic arthritis

A

Kocher criteria has been used in the diagnosis of septic arthritis. A score of 2 suggests a 40% probability and a score of 3 suggests a 93% probability.

Non weight bearing 1
Temp > 38.5 1
ESR > 40mm/hr 1
WCC >12x10(9)/L 1

51
Q

DD for septic arthritis

A

Crystal arthropathies - gout and pseudogout

52
Q

Management for Septic arthritis

A

IV antibiotics for 2 weeks followed by oral antibiotics for 4 weeks. Broad spectrum antibiotics should be given urgently and then tailored once the causative agent has been identified.
- Empirical therapy: flucloxacillin is first-line
- Penicillin allergy: clindamycin
- Suspected or confirmed MRSA: vancomycin
- Gonococcal arthritis or gram-negative infection: cefotaxime or ceftriaxone
- Joint drainage
- Aspiration
- Arthroscopic drainage
- Open drainage

53
Q

Monitoring septic arthritis

A

After resolution of the acute illness, the patient should be followed up on at least one occasion to confirm complete recovery and to check for the presence of joint damage.

54
Q

Complications of septic arthritis

A
  • Osteomyelitis: the spread of infection from the joint to the surrounding bone
  • Permanent joint destruction
  • Sepsis

MsK (14 decks)

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