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microbiology > Wound, bone and joint infection > Flashcards

Wound, bone and joint infection Flashcards

1
Q

How common are surgical site infections?

A

15.7% of HAIs are SSIs

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2
Q

What are the major pathogens in SSIs?

A

•Staph.aureus (MSSA and MRSA)•E.coli•Pseudomonas aeruginosa

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3
Q

Describe the pathogenesis of SSIs.

A
  • Contamination of wound at operation•Pathogenicity and innoculum of microorganisms•Host immune response
  • If surgical site is contaminated with

> 10 5 microorganisms per gram of tissue, risk of SSI is increased.

•The dose of contaminating bacteria required to cause infection is much lower if there is foreign material present e.g silk suture

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4
Q

What are the 3 levels of SSIs?

A
  • Superficial incisional- affect skin and subcutaneous tissue•
  • Deep incisional- affect fascial and muscle layers•
  • Organ/space infection- any part of anatomy other than incision
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5
Q
  • Admitted in February 2012, with a subarachnoid and subdural haemorrhage after a fall. Decompressivecraniectomy
  • April 2012. Cranioplasty with titanium plate.•
  • October 2012. Admitted with large subdural collection with midline shift
  • 16.10.12 Abscess evacuation. Titanium plates removed. Underneath there was severe infection with 1-1.5cm thick pus.

What is the most likely causative organism?

A

MRSA - Gram +ve cocci

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6
Q

How is SSI prevention classified?

A

•Pre-operative phase:

  • Age
  • Remote illnesses
  • Underlying illness
  • Obesity
  • Smoking
  • Pre-op shower
  • Hair removal
  • Nasal decontamination
  • Antibiotic Prophylaxis

•Intra-operative phase•

  • Management of infected personnel
  • Theatre traffic
  • Ventilation
  • Sterilisation of surgical instruments
  • Skin preparation
  • Asepsis and surgical technique
  • Normothermia
  • Oxygenation

•Post-operative phase

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7
Q

What is the effect of age on SSI?

A
  • An independent risk factor
  • A direct linear trend of increasing risk until 65 years of age
  • A prospective study examining patient undergoing total hip replacement. Age over 75 was found to be a significant risk factor
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8
Q

What are the underlying illnesses affecting SSIs?

A
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9
Q

What is the role of Obesity in SSIs?

A
  • Adipose tissue is poorly vascularised. Poor oxygenation of tissues and functioning of the immune response increases the risk of SSIs•
  • Risk increased by 2 to 7 in patients with a BMI of 35 or more
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10
Q

What is the role of smoking in SSIs?

A

•Smoking duration and number of cigarettes smoked•Nicotine delays primary wound healing•Peripheral vascular disease•Vasocontrictive effect of reduced oxygen-carrying capacity of blood•Encourage tobacco cessation

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11
Q

What is the role of pre-op showering in SSIs?

A

•Microorganisms colonising the skin may contaminate exposed tissues and cause an SSI••There is no difference in SSI incidence when chlorhexidine or detergent/bar soap is used••Patients should be advised to shower or bath using soap or on the day of surgery or the day before

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12
Q

What is the role of shaving in SSIs?

A
  • Micro-abrasions caused by shaving with a razor may lead to multiplication of bacteria•
  • Use electric clippers on the day of surgery with single-use head
  • Hair should not be removed unless it will interfere with the operation
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13
Q

What is the role of nasal decontamination in SSIs?

A
  • S.aureus is carried in the nares of 20-30%•
  • A multivariate analysis demonstrated that S.aureuscarriage was the most powerful independent risk factor for SSI following cardiothoracic surgery
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14
Q

What is the role of antibiotic prophylaxis in SSIs?

A

•Antibiotic prophylaxis should be given at induction of anaesthesia•Bactericidal concentration of the drug should be established in serum and tissues at time of incision.•Additional doses may be necessary if there has been significant blood loss or if the operation has been prolonged

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15
Q

What is the role of management of infected surgical personnel?

A

•Encourage surgical personnel who have symptoms of a transmissible infection to report to occupational health.

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16
Q

What is the role of theatre traffic in SSIs?

A

•One person sheds 1 billion skin cells per day ; 10% carry bacteria•Microbial load in theatre is related to the number of people present•Theatre personnel should be kept to a minimum

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17
Q

What is the role of ventilation in SSIs?

A

•Maintain positive pressure ventilation•Maintain around 20 air changes per hour (of which at least 3must be fresh air)•Filter all air•Keep operating room doors closed•Consider laminar flow for orthopaedic implant surgery

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18
Q

What is the role of sterilisation of surgical instruments in SSIs?

A

•Sterilise all surgical instruments•Inadequate sterilisation of surgical instruments has resulted in SSI outbreaks

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19
Q

What is the role of skin preparation in SSIs?

A

•When skin is incised microorganisms may contaminate tissues and cause an SSI••Prepare skin at surgical site using antiseptic preparation: povidine-iodine or chlorhexidine.••Chlorhexidine in 70% alcohol is used

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20
Q

What is the role of asepsis and surgical technique is SSIs?

A

•Maintaining effective haemostasis while preserving adequate blood supply, gently handling tissues, avoiding inadvertent entries into hollow viscus, removing devitilised tissues and eradicating dead space.•Adhere to asepsis when placing intravascular devices or epidural catheters

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21
Q

What is the role of normothermia in SSIs?

A

•Mild hypothermia appears to increase the risk of SSIs by causing vasoconstriction, decreased delivery of oxygen to wound space and subsequent impairment of neutrophil function

•In theatre suite: Measure patients temperature before inducing anaesthesia. Start forced air warming if temperature is below 36ºC

Warm intravenous fluid. Warm irrigation fluid

22
Q

What is the role of oxygenation in SSIs?

A

•Maintain optimal oxygenation during surgery, to maintain a haemoglobin saturation of more than 95%•Higher inspired oxygen concentrations in peri-operative period reduces SSIs

23
Q

What is the incidence of septic arthritis? What is mortality and morbidity?

A

•Incidence is 2-10 cases per 100,000•In patients with RA incidence is 28-38 per 100,000 population.•Mortality is 7-15%•Morbidity is 50%

24
Q

What are the RFs for septic arthritis?

A

•Risk factors

Rheumatoid arthritis , osteoarthritis, crystal induced arthritis

Joint prosthesis

Intravenous drug abuse

Diabetes, chronic renal disease, chronic liver disease

Immunosuppression- steroids

Trauma- intra-articular injection, penetrating injury

25
Q

What is the pathophysiology of septic arthritis?

A

•Organisms adhere to the synovial membrane, bacterial proliferation in the synovial fluid with generation of host inflammatory response.•Joint damage leads to exposure of host derived proteins such as fibronectin to which bacteria adhere

26
Q

Describe the pathogenesis of septic arthritis in terms of bacterial factors and host factors.

A

•Bacterial Factors

  • S.aureus* has receptors such as fibronectin binding protein that recognise selected host proteins.
  • Kingella kingae* synovial adherence is via bacterial pili

Some strains produce the cytotoxin PVL ( Panton-Valentine Leucocidin) which have been associated with fulminant infections.

  • Host Factors
  • Leucocyte derived proteases and cytokines can lead to cartilage degradation and bone loss.
  • Raised intra-articular pressure can hamper capillary blood flow and lead to cartilage and bone ischaemia and necrosis.

Genetic deletion of macrophage –derived cytokines (lymphotoxin α, TNFα, interleukin 1 receptor) reduces host protection in S.aureussepsis in animal models

Absence of interleukin10 in knockout mice increases the severity of staphylococcal joint disease.

Genetic variation in expression of these cytokines may lead to differential susceptibility to septic arthritis.

27
Q

What are the causative organisms of septic arthritis?

A

•Staph. aureus 46%

  • Coagulase negative staphylococci 4%

•Streptococci 22%–Streptococcus pyogenes–Streptococcus pneumoniae–Streptococcus agalactiae•Gram negative organisms

  • E.coli
  • Haemophilus influezae
  • Neisseria gonorrhoeae
  • Salmonella

Rare- Lyme, brucellosis, mycobacteria, fungi

28
Q

What are the clinical features of septic arthritis?

A

•1-2 week history of red, painful, swollen restricted joint-Monoarticular in 90%-Knee is involved in 50%

•Patients with rheumatoid arthritis may show more subtle signs of joint infection

29
Q

What are the investigations for septic arthritis?

A

Blood culture before antibiotics are given

Synovial fluid aspiration for microscopy and culture

ESR,CRP

-Traditionally a synovial count> 50,000 cells/mm3 used to suggest septic arthritis

(Negative culture result does not exclude septic arthritis)

30
Q

What imaging can be used for septic arthritis?

A

•X-rays- soft tissue oedema•US- confirm effusion and guide needle aspiration•CT- erosive bone change, periarticular soft tissue extension•MRI- joint effusion, articular cartilage destruction, abscess, contiguous osteomyelitis

31
Q

What is the management of septic arthritis?

A

Antibiotics- iv Cephalosporin or Flucloxacillin

  • may need to add vancomycin if at high risk of MRSA

No data on optimum duration of treatment

Upto 6 weeks of antibiotics may be given

OPAT (outpatient parenteral antibiotic team)

•Drainage- arthoscopic washout

32
Q

How do we classify vertebral osteomyelitis?

A

•Acute haematogenous•Exogenous- after disc surgery

  • implant associated
33
Q

What are the causative organisms of vertebral osteomyelitis?

A

•Causative Organisms

S.aureus-48.3%

CNS- 6.7%

GNR- 23.1%

Strep- 43.1%

34
Q

Where do pathogens localise in vertebral osteomyelitis?

A

•Localisation

cervical- 10.6%

cervico-thoraco-0.4%

lumbar 43.1%

35
Q

What are the symptoms of vertebral osteomyelitis?

A

•Symptoms

Back pain- 86%

Fever- 60%

Neurological impairment 34%

36
Q

How do we diagnose vertebral osteomyelitis?

A

•Diagnosis-MRI: 90% sensitive-Blood cultures-CT/ open biopsy

37
Q

What is the treatment of vertebral osteomyelitis?

A

•Treatment-Six weeks of treatment-Longer treatment if undrained abscesses/implant associated

38
Q

•76 year old man•Admitted with a 4 month history of back pain with radiation down left leg•Weight loss of 25kg over the last 6 months•PMH: fracture right femur 25yrs ago in Kuwait. Metal plate inserted.

Arthritis right knee, Hypertension. Lived in Iraq, Jordan and Singapore. Arrived in UK in 1993.

MRI: discitis of L2/3

Spinal biopsy in September 2010

Tissue sent for culture. Coagulase negative staphylococci grown from enrichment.

Histology : vague granuloma

Empirical anti- tuberculous treatment commenced ( rifater and ethambutol)

Empirical iv ceftriaxone commenced

  • On 11.11.10 anterior L2/3 debridement and stabilisation
  • Tissue- no growth
  • Tissue sent for 16S PCR
  • Serology- lyme, syphilis, brucella

What do you think the causative organism is?

A

Brucella

39
Q

What is this showing?

A

Brucella granuloma

40
Q

How does chronic osteomyelitis present?

A

•Pain•Brodies abscess•Sinus tract

41
Q
A

Bone formation and destruction.

42
Q

How do we diagnose and treat chronic osteomyelitis?

A

•MRI•Bone biopsy for culture and histology

•Radical debridement down to living bone-remove sequestra, and remove infected bone and soft tissue

43
Q

What is the Papineau technique?

A

•Initially described by Papineau in 1973•Complete excision of infected tissue and necrotic bone•Open cancellous bone grafting of the osseous defect.•Split skin grafting for wound closure•Papineau reported a 93 % success rate after treating 180 patients•Panda et al reported a 89% success rate.

44
Q

What are the Signs and symptoms of PJI (prosthetic joint infection)

A

•Pain•Patient complains that the joint was ‘never right’•Early failure•Sinus tract

45
Q

What are the causative organisms of PJI?

A

•Gram positive cocci

  • coagulase negative staphylococci
  • staphylococus aureus
  • Streptococci sp-Enterococci sp

•Aerobic gram negative bacilli-Enterobacteriaceae-Pseudomonas aeruginosa-•Anaerobes•Polymicrobial•Culture negative•Fungi

46
Q

How do we diagnose PJI?

A

•Radiology- loosening•If CRP>13.5 for prosthetic knee joint infection •CRP> 5 for prosthetic hip joint infection•Joint aspiration

If >1700/ml of WCC correlates with knee PJI

If > 4200/ml of WCC correlates with hip PJI

Am J med 2004;117:557-562.

May only get planktonic bacteria in joint fluid, may need to sample bacteria where infection is most likely

47
Q

Describe intraoperative microbiological sampling in PJI.

A

•Tissue specimens from at least 5 sites around the implant•Histopathology – infection defined as >5 neutrophils per high power field.•If 3 or more specimens yield identical organisms, this is highly predictive of infection (sensitivity 65%, specificity 99%)

48
Q

Describe single stage revision.

A

•Remove all foreign material and dead bone••Change gloves, drapes etc••Re-implant new prosthesis with antibiotic impregnated cement and give iv antibiotics .

49
Q

Describe Endo Kilinik single stage revision.

A

Aspirate joint to identify pathogen

Excision of infected tissue , synovectomy

Add antibiotics to bone cement according to culture results

Implantation of a cemented hip or knee prosthesis using antibiotic loaded cement

Give 7-10 days of iv antibiotics

Culture drain tips

Success rate is 89% in 2002

50
Q

Describe 2 stage revision

A

•Remove prosthesis•Take samples for microbiology and histology•Period of iv antibiotics (6weeks). Stop antibiotics for 2 weeks•Re-debride and sample at second stage•Re-implantation with antibiotic impregnated cement•No further antibiotics if samples clear•OPAT

51
Q

•Age- 70yrs old•1994 Right THR; 1998 Revision of acetabular component•X-ray: lysis around distal part of femoral component•Diabetic

What is the most likely pathogen?

A

Coagulase negative staphylococci

microbiology (19 decks)

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