Lecture - Bone and Joint Infections Flashcards

1
Q

Osteomyelitis:

  1. What is it and what structures may it involve?
  2. What are the three characteristics to classify it?
A
  1. It’s an inflammatory process of the bone that is secondary to infection (doesn’t have to be bacterial). It may involve periosteum, medullary cavity, compact or cancellous bone.
  2. DURATION (acute, subacute, chronic), ROUTE OF INFECTION (haematogenous aka through blood or exogenous aka outside of bone) and HOST RESPONSE (pyogenic or granulomatous aka where you form a granuloma?)
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2
Q

Osteomyelitis #2:

  1. What is the first route of infection?
  2. Why is haematogenous most common in children?
  3. Is it mono microbial or polymicrobial?
  4. What is the second route of infection?
  5. Why is it contiguous?
  6. Whereabouts in diabetics does it occur?
  7. Is it mono microbial or polymicrobial?
A
  1. Haematogenous = Organism in blood and then gets into bone
  2. Children - rich vascualr supply to ends (metaphysis). When BV come to supply, they become convoluted and thus vascular stasis so easier for organism to leave blood and get into bone. It’s just about the blood supply to growing bone
  3. Monomicrobial aka caused by single bacterial species - only one organism involved
  4. Exogenous - means it’s from outside of bone. It’s where it’s direct inoculation of the bone by the organism - might have been trauma, surgery etc.
  5. Contiguous aka it can be a local infection near bone that spread.
  6. Feet in diabetics - poor vasuclar supply in lower leg so will have ulcers etc so bacteria can spread
  7. Polymicrobial: Contingious infections of these sorts are often () aka a mix of bacteria causing infection
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3
Q

What are the two causes of (acute) osteomyelitis in terms of organisms that cause it?

A
  1. Haematogenous (aka caused by spread into blood). To some extent, the causes of these are specific to certain age groups. Staph aureus causes it haematogenous-ly in all three (newborns, children an adults)
  2. Direct inoculation/contiguous: also staph aureus to remember here
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4
Q

Osteomyelitis acute #3:

  1. What are 5 risk factors for it?
A
  1. IMMUNOSUPPRESSION
    - AGE (children/elderly - At risk bc either their immune system just developing or as age - immune fucntion tends to decline)
    - PVD: Peripheral vascular disease aka look at blood supply to bone annnnnd look at smokers because that damages vessels or something
    - CHRONIC JOINT DISEASE: like RA - make joint very inflammed and leaky so organism can get into joint (chronic joint inflam can cause osteomyelitis) and then spread
    - RECENT BONE SURGERY/REPLACEMENT/TRAUMA - provides route to enter
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5
Q

Osteomyelitis acute #4:

  1. Clinically, where do children get osteomyelitis and what sort of symptoms can you see? Are there more or less dramatic symptoms in infants?
  2. Where will you see it in adults? What sort of symptoms?
A
  1. Metaphysis (ends) of long bones. Symptoms are like severe pain, swelling, heat, redness, pseudoparalysis (wont wanna use limb that’s infected). Can happen in neonates and infants so they show generalised response aka period of lethargy and drowsy etc so can be challenege to see hwo seriois it is since they dont verbalise
  2. Spine, pelvis - will feel backache. It’s onset is less acute in adults than in kids but you still get paid, redness, swelling, fever etc
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6
Q

What’re complications that can occur in osteomyelitis? (acute)

A
  • Spesis (organism can get into blood)
  • Metastatic infection (Once in blood, it can travel to distant site or organ and then get eg abcess in other organ)
  • septic arthritis (It could result in osteomyelitis or other way around)
  • pathological fracture bc so much bone gets eaten away
  • Chronic osteomyelitis
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7
Q

What’s the pathogenesis for osteomyelitis? (5) acute

A
  1. Inflammation: Infection (aka inflammation) in inelastic bone so pressure just keeps building so occulusion of blood flow and get ischaemia and necrosis. Osteolysis by enzymes collagenase and elastase released by immune cells
  2. Suppuration: pus formation and leak through sinus in chronic infection
  3. Sequestrum = Area of devitalised bone where no blood supply given
  4. Involcrum = it’s healing - you form new bone (sometimes may occur over sequestrum). Sequestrm gets reaborbed and you get healing and things get to normal buuuuut sometimes sequestrum gets left behind and that cna become source of reactivation of osteomyelitis later down the track
  5. Resolution or progression to complication
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8
Q

Three ways to diagnose osteomyelitis? (acute)

A
  1. Culture/stain: Get some sort of pus from the site of infection

Culturing any sort of the draining pus through since but its not a good correlation of what’s in pus and what’s causing infection unless you find staph aureus in pus then it’s most likely the thing causing the infection but otherwise dont culture the pus coming out

Sometimes cant isolate the organism

Blood culutre also good sample if cant find organism in osteomyleitis

Have a smear of pus (inflam cells) and can fee firbrin etc and see gram +ve cocci in clusters

This can direct initial antimicrobial therapy

Also, best results if taken before antimicrobial therapy

Can even see leukocytosis and raised CRP

  1. Bone scans: Radioactive isotope gets incorported into bone/sites of infection so useful bc can diagnose very early osteomyelitis aka within a few dyas of onset of infection (x rays not useful earlier) but slight drawback that get false positives if other infections cause the test to be positive and not the one in the bone
  2. Imaging studies: x-rays take a long time aka 10-14 days before osteomyelitis visible in x-ray and by then, 40% less bone so not good for trying to diagnose early infection.

CT scans useful for bones which are difficult to x ray but need at least 1 week

MRI is useful for early diagnosis but it’s hard to access

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9
Q

What’re the two treatments for osteomyelitis? (acute)

A
  1. MEDICAL: Needs rapid (empric) treatment so treat with antimicrobial before even know what the organism is. Once get culture, need to target the organism specifically (antimicrobial stewardship) not killing off anything else

Need prolonged therapy which can then be changed to oral therpay (from IV) so long course of drug to treat these infections. Children you can give oral only but combination of oral and IV Is good when you’ve establish the thing

  1. SURGICAL: Debridement to remove any foreign objects or necrotic bone. Amputation in diabetics but that’s extreme
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10
Q

Subacute osteomyelitis:

  1. What abscess can you get?
  2. What age group does it generally occur in?
  3. What’s the diagnosis? (2)
  4. What about treatment? (2)
A
  1. Brodie’s abscess - localised osteomyelitis (staph aureus abscess in bone)
  2. Happens generally in adults with few clinical signs and little to no pain - might persist over the years
  3. Aspiration or biopsy of abscess (only half the cases will grow). Or x-ray: Useful in this instance bc it’s a long standing process and have lots of damange to bone (can see abcess in pic on right)
  4. Long course antimicrobials or surgical debridement
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11
Q

Chronic osteomyelitis

  1. Two ways it can arise?
  2. Poly or mono microbial?
  3. Pyogenic or granulomatous?
  4. Two ways to diagnose
  5. Treatment (2)
A
  1. Sequestrum can act as a source of infection or it can arise post-surgical treatment.
  2. DIfferent to acute form bc this is poly-microbial (caused by mix of different bac)
  3. Gramulomatous (TB, syphilis)
  4. Diagnosis = Culture staining or imaging (use x ray bc looking at big destruction of bone)
  5. Long course antimicrobial therapy or surgical debridement (sequestrectomy)
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12
Q

Septic arthritis #1:

  1. What is it?
  2. What three things is it characterised by?
A
  1. Invasion of the joint by pathogen which produces arthritis. Bacteria are most damaging but fungi or virus can also cause it. Acute/chronic disease can also cause it
  2. Colonisation of synovial fluid, influx of inflammatory/immune cells, erosion of synovial membrane (Produce fluid and then damage synovial membrane with I think enzymes etc?)
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13
Q

What’s the cause for acute vs chronic septic arthritis?

A

Actue: 60-80% staph aureus

Chronic: HIV, Rubella, TB, syphillis, fungi (Candida)

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14
Q

Septic arthritis #2:

  1. Increasing incidence in what cause?
  2. What are some risk factors for it?
A
  1. Joint surgery/replacement: bc potential target for some microbes
    - if early onset (less than 3 months post-implant) then staph aureus
    - if 3-24 months then staph epidermidis (bc it makes biofilms on foreign surfaces) REMEMBER THIS
    - More than 24 months: haematogenous spread
  2. Previously damaged joints (RA, grout etc) so existing inflammation or damage to defence mechanisms
    - Immunosuppression
    - Male
    - More than 65
    - Joint replacement surgery
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15
Q

What’re the clinical symptoms of septic arthritis?

A

Acute, acid onset of inflammation and swelling

Severe arthralgia (joint pain)

  • Pseudoparalysis
  • Low-grade fever
  • Monoarticular
  • Could be polyarticular if staph aureus or gonoccus
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16
Q

What are routes of entry for septic arthritis to develop and what are complications following it?

A

-Direct inoculation,
- infection of periarticular tissue (infection around joint so get contiguous spread),
-haematogenous spread
(so like, same as osteomyelitis really)

Complications:

  • spesis
  • osteomyelitis
  • joint destruction (Acute bacterial forms can do a lot of damage to joint so need to recognise)
17
Q

How to diagnose septic arthritis? (5)

A
  1. Aspiration of synovial fluid (Arthrocentesis is the clinical procedure of using a syringe to collect synovial fluid from a joint capsule). Obviously not practical if joint is deep or small synovial space but can see appearance of aspirate (turbid, yellow, decreased viscosity).
  2. Gram stain - just for direct initial antimicrobial therapy
  3. Culture - non-gonococcal cases are usually positive unless antibiotics administered (Most caused by aures so grow in various agar)
  4. Blood culture - Esp if have systemic signs (though not likely)
  5. Imaging studies: x-ray, ultrasound - Bc can see destruction of joint as a result of infection
18
Q

What’s the treatment for septic arthritis?

A

Medical and surgical: both on the lines of osteomyelitis

Medical: Need empirical IV therapy. Change the therapy when sensitivities are known

Surgical: Aspiration, removal of prosthesis or debridement

19
Q

Reactive arthritis:

  1. What is it?
  2. What is the triad of symptoms (that may not always be present)?
  3. It has a strong association with HLA-B27, what does this mean?
A
  1. It’s an autoimmune disease in joints (also inflam process in joint but not direct infection of joint - this is autoimmune response in joint as a result of infection elsewhere ) - sequelae to genitourinary (infection from chlamydia) or GI infection
  2. Urethritis/cervictis, uveitis/conjuctivits, inflammatory arthritis of large joints
  3. It is a halo-type of MHC class 1 type molecule. So a certain amount of people express this MHC class 1 molecue. So 65-96% of people with reactive arthritis have expressed the HLA-B27 molecule
20
Q

What’s the pathogenesis of reactive arthritis?

  • how many weeks after infection does it begin?
  • inflammation of?
  • mechanisms
A

initial infection is usually resolved so this is developing some weeks after it so often people dont make this connection

You can inflammation in joints, skin, mucous membranes and eyes

Mechanisms are unknown but this it’s cross-reactive AB so when you make AB against chlamydia, they cause damage to joint etc

21
Q

What’s the diagnosis and treatment of reactive arthritis?

A

Diagnosis: culture from urethra, cervix or throat (try to find chlamydia bc other consequences too), culture faeces, HLA-B27 typing (synovial fluid is sterile- no point in culture)

Treatment: self-limning (takes 3-12 months to resolve), recurrence is common, have antimicrobials to remove aetiological agent (not to treat arthritis but to get rid of e.g. chlamydia), anti-inflammatory drugs etc (NSAIDs, DMARDs) to treat symptoms