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MSK > Infective arthritis > Flashcards

Infective arthritis 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

Case study 1
57 year old lady
Severe Rheumatoid Arthritis
On Methotrexate, Prednisolone and Rituximab
Bilateral Knee Replacements 2007
Admitted May 2010
10 day history of L knee pain & swelling
Afebrile, systemically well
Tender, hot, swollen L Knee
Raised inflammatory markers
What investigations did she have?

A

X-Ray L knee joint -unremarkable
Joint aspirate
Fully Sensitive Corynebacterium spp
Identified as Listeria monocytogenes

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3
Q

Case study 1
57 year old lady
Severe Rheumatoid Arthritis
On Methotrexate, Prednisolone and Rituximab
Bilateral Knee Replacements 2007
Admitted May 2010
10 day history of L knee pain & swelling
Afebrile, systemically well
Tender, hot, swollen L Knee
Raised inflammatory markers
What was her management

A

4 weeks later - 1st stage revision
Cement - Gentamicin/Clindamycin with Vancomycin added
Discharged on 6 week course PO Amoxicillin
2nd Stage tissues all negative
Remains well almost 3 years out

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4
Q

Mechanism of infection for 51 year old lady with RA

A

Patient reported diarrhoeal illness 5 months previously. She had eaten soft cheeses after her Christmas Dinner!
Mechanism:
Transient Bacteraemi

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5
Q

Which bacteria is significant in Upper Limbs?

A

Propionibacteria

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6
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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7
Q

Why is it so difficult to treat this?

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
You rely on finding them by Terminal subculture of prolonged broths
They are also very indolent organisms
Seldom cause acute infections
May not significantly raise inflammatory markers

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8
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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9
Q

Risk factors for OM

A
  • Diabetes
  • Old age
  • Peripheral vascular disease
  • Immunocompromise
  • Malnutrition
  • Trauma/ injury
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10
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
NHS
4,224 hospital consultant episodes
80% Require hospital admission
16.2 days mean stay
44,250 hospital bed days

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11
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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12
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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13
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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14
Q

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

A

Metaphysis

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15
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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16
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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17
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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18
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
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19
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
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20
Q

Haematogenous OM in adults

A

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

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21
Q

Haematogenous OM in children

A

Long bones&raquo_space; vertebra

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22
Q

People who inject drugs haematogenous OM

A

younger, more often clavicle and pelvis

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23
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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24
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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25
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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26
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

27
Q

Acute changes of histopathology

A

Inflammatory cells
Oedema
Vascular congestion
Small vessel thrombosis

28
Q

Chronic changes of histopathology of OM

A

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

29
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

30
Q

Symptoms (History)

A

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

31
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

32
Q

OM in hip vertebrae or pelvis

A

pain but few other signs or symptoms.

33
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.

34
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

35
Q

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

A

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

36
Q

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

A

Poor sensitivity and specificity,

37
Q

Why is MRI good?

A

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

38
Q

How can we make a definitive diagnosis?

A

Microbiology and histology: Bone biopsy
Positive Blood cultures

39
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

40
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

41
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

42
Q

Surgical treatment for OM

A

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

43
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

44
Q

Antibiotics to use

A

Levofloxacin
Ciprofloxacin
Moxifloxacin
Vancomyocin

45
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

46
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

47
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
48
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
49
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!

50
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
51
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
52
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
53
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.

54
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.

55
Q

Key presentations for septic arthritis

A

Septic arthitis mainly affects one joint and so should be suspected in all monoarthritic cases. The knee is most commonly affected, but hip, shoulder, wrist and elbow joints are also affected.

56
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
57
Q

Symptoms in septic arthritis

A
  • Difficulty weight bearing
  • Fever
58
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
59
Q

Gold standard investigation for septic arthritis

A

Joint aspiration - MSC

60
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

61
Q

DD for septic arthritis

A

Crystal arthropathies - gout and pseudogout

62
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

63
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.

64
Q

Complications of septic arthritis

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

MSK (20 decks)

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