9. Wound, bone and joint infections Flashcards

1
Q

In 2011, what percentage of HAIs were SSIs?

A

15.7%

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2
Q

What major pathogens cause SSIs?

A

Staphylococcus aureus (MSSA and MRSA), E. coli, Pseudomonas aeruginosa

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3
Q

If a surgical site is contaminated with ??? per gram of tissue, the risk of SSI is increased.

A

> 10^5 microorganisms per gram of tissue

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4
Q

• The dose of contaminating material required to cause infection is MUCH LOWER if?

A

If there is foreign material present (e.g. silk suture)

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5
Q

What are the three levels of SSIs?

A

Superficial incisional, deep incisional and organ/space infection

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6
Q

What does a superficial incisional SSI involve?

A

Skin and subcutaneous tissues

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7
Q

What does a deep incisional SSI involve?

A

Fascial and muscle layers

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8
Q

What does organ/space infection involve?

A

Any part of the anatomy other than the incision

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9
Q

Case 1: admitted in February 2012, with a subarachnoid and subdural haemorrhage after a fall. Decompressive craniectomy. April 2012 - cranioplasty with titanium plate. October 2012 - admitted with large subdural collection with midline shift. Later, abscess evacuation and titanium plates were removed. Underneath there was severe infection with 1-1.5 cm thick pus. (See images in notes). What is the infection?

A

It is a Gram-positive coccus which is haemolytic. This is MRSA. This patient’s pus grew MRSA

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10
Q

How is MRSA treated (as in case 1)?

A

IV Linezolid

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11
Q

What are pre-operative risk factors of SSIs?

A

Age, all remote infection (e.g. UTI, pneumonia), underlying illness (ASA >= 3, diabetes), malnutrition, low serum albumin, radiotherapy and steroids, rheumatoid arthritis (stop DMARDs 4 weeks before to 8 weeks after operation), obesity, and smoking.

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12
Q

Why is obesity a risk factor for SSIs?

A

Adipose tissue is poorly vascularised, poor oxygenation and access of immune system to these tissues increases risk of SSIs, risk increased by 2 to 7 in patients with BMI > 35

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13
Q

Why is smoking a risk factor for SSIs?

A

Nicotine delays wound healing, peripheral vascular disease (reduced blood supply to the site of operation), encourage stopping smoking

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14
Q

What can be done to prevent SSIs pre-operatively?

A

Consider pre-operative risk factors, pre-operative showering, hair removal (using electric clipper), nasal decontamination (S. aureus is carried in nostrils of 20-30%), antibiotic prophylaxis (bactericidal concentration established)

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15
Q

What can be done to prevent SSI intra-operatively?

A

Surgical personal with symptoms of transmissable infection should inform occupational health, limit no. of people in theatre, ventilation (positive pressure), sterilisation of surgical instruments, skin preparation (trust recommendation: chlorhexidine in 70% alcohol), asepsis and surgical technique, normothermia, oxygenation

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16
Q

Why normothermia?

A

Hypothermia increases risk of SSIs by vasoconstriction, decreasing oxygen delivery.

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17
Q

Incidence of septic arthritis

A

2-10/100,000

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18
Q

Who is septic arthritis more common in?

A

In patients with rheumatoid arthritis

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19
Q

Mortality of septic arthritis

A

7-15%

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20
Q

Morbidity of septic arthritis

A

50%

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21
Q

Risk factors of septic arthritis

A

Rheumatoid arthritis, osteoarthritis, crystal arthritis, joint prosthesis, IVDU, diabetes, chronic renal disease, chronic liver disease, immunosuppression (e.g. steroids), trauma - intra-articular injection, penetrating injury

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22
Q

What is the pathophysiology of septic arthritis?

A

Organisms adhere to the synovium. Bacterial proliferation in the synovial fluid leads to generation of a host inflammatory response. Joint damage leads to exposure of host derived protein (e.g. fibronectin) to which bacteria can adhere.

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23
Q

How does S. aureus cause septic arthritis?

A

Staphylococcus aureus has receptors such as fibronectin-binding protein that recognise selected host proteins

24
Q

How does Kingella kingae cause septic arthritis?

A

Kingella kingae synovial adherence is via bacterial pili

25
What is cytotoxin PVL that some strains of S. aureus produce?
Panton-Valentine Leukocidin - associated with fulminant infection
26
What is a host factor that causes cartilage and bone damage, which can lead to septic arthritis?
Leucocyte derived proteases and cytokines can cause cartilage and bone damage
27
Why does raised intra-articular pressure lead to septic arthritis?
Raised intra-articular pressure can impede capillary blood flow and lead to cartilage and bone ischaemia and necrosis
28
Why does genetic deletion of macrophage-derived cytokines cause septic arthritis?
Genetic deletion of macrophage-derived cytokines can reduce the host-response in S. aureus sepsis in animal models
29
What increases the severity of staphylococcus joint disease in knockout mice?
Absence of IL-10
30
What are causative organisms of septic arthritis?
Staphylococcus aureus (46%), Streptococci (22% - S. pyognenes, S. pneumoniae, S. agalactiae), Gram-negative organisms (E. coli, H. influenzae, Neisseria gonorrhoeae, Salmonella), Coagulase-negative staphylococci (4%)
31
What are rare causes of septic arthritis?
Lyme disease, brucellosis, mycobacteria, fungi
32
What are clinical features of septic arthritis?
1-2 week Hx of red, painful, swollen joint with restricted movement, monoarticular in 90%, knee is involved in 50%. Patients with rheumatoid arthritis may show more subtle signs of joint infection
33
What investigations for septic arthritis?
Blood culture, synovial fluid aspiration, ESR, CRP, USS, CT, MRI
34
Negative culture excludes septic arthritis, true or false?
FALSE
35
What synovial count is traditionally used to suggest septic arthritis?
> 50,000 WBC/mL
36
What do you look for in an USS when investigating septic arthritis?
Confirm effusion and guide aspiration
37
What do you look for in a CT when investigating septic arthritis?
Check for erosive bone change, periarticular soft tissue extension
38
What do you look for in an MRI when investigating septic arthritis?
joint effusion, articular cartilage destruction, abscess, contiguous osteomyelitis
39
How is septic arthritis treated?
1. ANTIBIOTICS - No data on optimum duration of treatment (4-6 weeks is usually given). This is done via OPAT (outpatient parenteral antimicrobial therapy). 2. Drainage of the joint.
40
What are causes of vertebral osteomyelitis?
Acute haematogenous spread (bacteraemia); exogenous - implantation during disc surgery
41
What are causative organisms of vertebral osteomyelitis?
Staphylococcus aureus (48.3%); Coagulase-negative staphylococcus; Gram-negative rods; Streptococcus
42
What is the localisation of vertebral osteomyelitis?
LUMBAR (43.1%), cervical, cervico-thoracic
43
What are symptoms of vertebral osteomyelitis?
Back pain, fever, neurological impairment
44
What are investigations of vertebral osteomyelitis?
MRI (90% sensitive), blood cultures, CT-guided/open biopsy
45
What is the treatment of vertebral osteomyelitis?
Antibiotics for at least 6 weeks, longer treatment may be needed if undrained abscess/implant-associated
46
Resistant Salmonella how do you treat it?
Ciprofloxacin -> (cipro resistant) -> ceftriaxone + azithromycin for 6 months -> (persists) -> meropenem and azithromycin, switched to ceftriaxone and azithromycin -> debridement and stabilisation of spine
47
How does chronic osteomyelitis present?
Pain, Brodies abscess, sinus tract
48
How is chronic osteomyelitis diagnosed?
MRI, bone biopsy for culture and histology
49
How is chronic osteomyelitis treated?
Radical debridement down to living bone and remove sequestra (dead bone tissue) and infected bone and soft tissue
50
What techniques are used to treat chronic osteomyelitis?
Lautenbach technique and Papineau technique
51
What is the Lautenbach technique?
• Debridement and collection of multiple samples for culture and histology • All foreign prosthetic material is removed • Debridement is done all the way down to healthy bleeding bone (check using osteoscopy) • Double lumen irrigation system is introduced through a subcutaneous tunnel (see notes)
52
What is the Papineau technique?
* Complete excision of infected tissue and necrotic bone * This is followed by open cancellous bone grafting of the osseous defect * Split skin grafting is used to close the wound * Success rate of 89-93%
53
What are clinical features of prosthetic joint infection?
Pain, patient complain that the joint was 'never right' after the operation, early failure, sinus tract
54
What organisms cause prosthetic joint infection?
Gram-positive cocci (Coagulase-negative staphylococci is MORE COMMON than S. aureus, Streptococci, Enterococci), aerobic Gram-negative bacilli (Enterobacteriaceae, Pseudomonas aeruginosa), anaerobes, polymicrobial, culture-negative, fungi
55
How is prosthetic joint infection diagnosed?
Radiology (loosening along cement-bone infection), CRP (>13.5 for prosthetic knee joint infection, >5 for prosthetic hip joint infection), joint aspiration (> 1700 WCC/mL - knee, 4200 WCC/mL - hip), intraoperative microbiological sampling (5 sites, >= 3 specimens yield identical organisms is highly suggestive of PJI)
56
Treatment of PJI - single stage revision?
* Remove all foreign material and dead bone * Change gloves and drapes etc. * Re-implant the new prosthesis with antibiotic impregnated cement and give IV antibiotics
57
Treatment of PJI - two stage revision?
* Remove prosthesis and put in a spacer (to take up the space of the prosthesis) * Take samples for microbiology and histology * Period of IV antibiotics (for 6 weeks) then stop antibiotics for 2 weeks * Re-debride and sample at second stage * Re-implantation with antibiotic impregnated cement * NO further antibiotics needed if the samples are clear * If antibiotics are required, OPAT is used