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MICRO - Abbie > 9. Wound, bone and joint infections > Flashcards

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
Q

What is cytotoxin PVL that some strains of S. aureus produce?

A

Panton-Valentine Leukocidin - associated with fulminant infection

26
Q

What is a host factor that causes cartilage and bone damage, which can lead to septic arthritis?

A

Leucocyte derived proteases and cytokines can cause cartilage and bone damage

27
Q

Why does raised intra-articular pressure lead to septic arthritis?

A

Raised intra-articular pressure can impede capillary blood flow and lead to cartilage and bone ischaemia and necrosis

28
Q

Why does genetic deletion of macrophage-derived cytokines cause septic arthritis?

A

Genetic deletion of macrophage-derived cytokines can reduce the host-response in S. aureus sepsis in animal models

29
Q

What increases the severity of staphylococcus joint disease in knockout mice?

A

Absence of IL-10

30
Q

What are causative organisms of septic arthritis?

A

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
Q

What are rare causes of septic arthritis?

A

Lyme disease, brucellosis, mycobacteria, fungi

32
Q

What are clinical features of septic arthritis?

A

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
Q

What investigations for septic arthritis?

A

Blood culture, synovial fluid aspiration, ESR, CRP, USS, CT, MRI

34
Q

Negative culture excludes septic arthritis, true or false?

A

FALSE

35
Q

What synovial count is traditionally used to suggest septic arthritis?

A

> 50,000 WBC/mL

36
Q

What do you look for in an USS when investigating septic arthritis?

A

Confirm effusion and guide aspiration

37
Q

What do you look for in a CT when investigating septic arthritis?

A

Check for erosive bone change, periarticular soft tissue extension

38
Q

What do you look for in an MRI when investigating septic arthritis?

A

joint effusion, articular cartilage destruction, abscess, contiguous osteomyelitis

39
Q

How is septic arthritis treated?

A
  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
Q

What are causes of vertebral osteomyelitis?

A

Acute haematogenous spread (bacteraemia); exogenous - implantation during disc surgery

41
Q

What are causative organisms of vertebral osteomyelitis?

A

Staphylococcus aureus (48.3%); Coagulase-negative staphylococcus; Gram-negative rods; Streptococcus

42
Q

What is the localisation of vertebral osteomyelitis?

A

LUMBAR (43.1%), cervical, cervico-thoracic

43
Q

What are symptoms of vertebral osteomyelitis?

A

Back pain, fever, neurological impairment

44
Q

What are investigations of vertebral osteomyelitis?

A

MRI (90% sensitive), blood cultures, CT-guided/open biopsy

45
Q

What is the treatment of vertebral osteomyelitis?

A

Antibiotics for at least 6 weeks, longer treatment may be needed if undrained abscess/implant-associated

46
Q

Resistant Salmonella how do you treat it?

A

Ciprofloxacin -> (cipro resistant) -> ceftriaxone + azithromycin for 6 months -> (persists) -> meropenem and azithromycin, switched to ceftriaxone and azithromycin -> debridement and stabilisation of spine

47
Q

How does chronic osteomyelitis present?

A

Pain, Brodies abscess, sinus tract

48
Q

How is chronic osteomyelitis diagnosed?

A

MRI, bone biopsy for culture and histology

49
Q

How is chronic osteomyelitis treated?

A

Radical debridement down to living bone and remove sequestra (dead bone tissue) and infected bone and soft tissue

50
Q

What techniques are used to treat chronic osteomyelitis?

A

Lautenbach technique and Papineau technique

51
Q

What is the Lautenbach technique?

A

• 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
Q

What is the Papineau technique?

A
  • 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
Q

What are clinical features of prosthetic joint infection?

A

Pain, patient complain that the joint was ‘never right’ after the operation, early failure, sinus tract

54
Q

What organisms cause prosthetic joint infection?

A

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
Q

How is prosthetic joint infection diagnosed?

A

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
Q

Treatment of PJI - single stage revision?

A
  • 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
Q

Treatment of PJI - two stage revision?

A
  • 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

MICRO - Abbie (19 decks)

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