Infective arthritis Flashcards

(64 cards)

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
Which organisms cause OM
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
26
What is the histopathology of osteomyelitis
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
Acute changes of histopathology
Inflammatory cells Oedema Vascular congestion Small vessel thrombosis
28
Chronic changes of histopathology of OM
neutrophil exudates lymphocytes & histiocytes Necrotic bone ‘sequestra’ new bone formation ‘involucrum’
29
What investigations can we do for OM
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
Symptoms (History)
Onset - several days. dull pain at site of OM may be aggravated by movement. - **Fever** - **Pain** - **Overlying redness** - **Swelling** - **Malaise**
31
Signs of clinical OM (Examination)
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
OM in hip vertebrae or pelvis
pain but few other signs or symptoms.
33
OM Vertebral: lumbar > thoracic > cervical
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
OM Joint - can also present as septic arthritis.
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
What is shown in a plain x-ray in chronic osteomyelitis
cortical erosion, periosteal reaction, mixed lucency, Sclerosis sequestra soft tissue swelling
36
Why is an X ray not the best especially in early OM?
Poor sensitivity and specificity,
37
Why is MRI good?
marrow oedema from 3-5 days Delineates cortical, bone marrow and soft tissue inflammation
38
How can we make a definitive diagnosis?
Microbiology and histology: Bone biopsy Positive Blood cultures
39
Bone biopsy for OM
obtained via sterile technique, Open bx >>> needle bx 2 specimens Culture 16sRNA PCR may be necessary Histology showing inflammation and osteonecrosis
40
Positive blood cultures
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
Differential diagnosis for OM
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
Surgical treatment for OM
Debridement (remember Bromfield “we cannot be too early in letting it out”) Hardware placement or removal
43
Antimicrobial therapy for treatment
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
Antibiotics to use
Levofloxacin Ciprofloxacin Moxifloxacin Vancomyocin
45
Treatment duration
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
TB osteomyelitis
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
Acute osteomyelitis
- 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 system destroys 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
Chronic osteomyelitis
- 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
What is septic arthritis
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
Epidemiology of septic arthritis
- 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
Aetiology of septic arthritis
- **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
RF for septic arthritis
- **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
Why is septic arthritis a medical emergency?
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
What are 90% of cases caused by for septic arthritis
90% of cases are caused by staphylococci or streptococci, often as a complication of other pathologies such as cellulitis, chronic osteomyelitis, or drug abuse. Fungal and viral causes are rare.
55
Key presentations for septic arthritis
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
Signs for septic arthritis
- 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
Symptoms in septic arthritis
- Difficulty weight bearing - Fever
58
1st line investigation for septic arthritis
- **FBC**: leukocytosis - **CRP and ESR**: elevated due to inflammation and used for monitoring response to treatment - **Blood cultures**: should be performed on **all** patients before commencing antibiotics - **Joint aspiration (arthrocentesis):** definitive investigation Plain Xray US or MRI
59
Gold standard investigation for septic arthritis
Joint aspiration - MSC
60
Scoring criteria for septic arthritis
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
DD for septic arthritis
Crystal arthropathies - gout and pseudogout
62
Management for Septic arthritis
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
Monitoring septic arthritis
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
Complications of septic arthritis
- **Osteomyelitis**: the spread of infection from the joint to the surrounding bone - **Permanent joint destruction** - **Sepsis**