Infections Flashcards

1
Q

Increased resistance of infection due to what?

A
  • staph aureus: increased resistance via plasmids
  • 50% of strains have plasmid mediated resistance
  • biofilm: increasingly common in staph species, very common in pseudomonas
  • major cause of nosocomial infections
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2
Q

Compromise of homeostasis in MSK infection?

A
  • once altered, bacteria can enter body
  • ex: surgical incision: enviro is compromised by diminished blood fow, O2 tension and fbs
  • infection must be contained b/f hematogenous or contiguous spread can occur
  • blood supply: one of the most impt factors of homeostasis - mult. studies show as blood flow is reduced, risk of infection increases
  • warming an extremity increases microcirculation and vasodilation = increase concentrations of abx
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3
Q

Diff types of trauma and assoc infection?

A
  • osseous trauma: periosteal injury, microvascular and macrovascular compromise, bacteria have an affinity for the exposed binding sites
  • glycocalyx capsule: composed of fibrous exopolysaccharides w/in biofilm
  • impair NL immune fxn and abx penetration
  • biofilm doesn’t just effect foreign material, it can act similarly w/ deviated bone
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4
Q

Factors that increase host susceptibility of infections?

A
  • factors that decreases local immune response: decreased blood flow (PAD, venous stasis, smoking, radiation), neuropathy, trauma, meds (NSAIDs, Rh, steroids)
  • factors that decrease systemic immune response: renal and liver Dz, DM, EtOH, Rh Dzs, immunocompromised states, malnutrition
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5
Q

Dx modalities used in d MSK infections?

A

** gold std is culture of suspected fluid or tissues
clinical:
-primary tool, esp initially
- PE, Hx
- pts often present w/ pain, warmth, swelling, redness and refusal to bear weight (kids esp)
- other sxs: fever, chills, night sweats, nausea, vomiting and loss of jt motion
- serology: CBC w/ diff, ESR, CRP, blood cultures (2 sep sites), gram stain, frozen section, PCR

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6
Q

Normal WBC, ESR, and CRP - means what % chance of no infection?

A
  • 95% chance no infections
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7
Q

When do ESR and CRP elevate?

A
  • ESR: elevates w/in 2 days of infection and will continue to rise for next 3-5 after approp tx
  • CRP: elevates w/in 6 hrs, peaks at 48 hrs, returns to NL 1 wk after approp tx, more sensitive, best indicator for dx and for monitoring tx
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8
Q

Use of gram stain in dx infection?

A
  • becoming more historical
  • good for tailoring of specific abx
  • can be normal even in obvious infection
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9
Q

Use of IL-6 for dx MSK infections?

A
  • new lit shows this can be helpful, esp in periprosthetic infections
  • realistically not many labs have this capability and it is quite expensive
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10
Q

Use of plain films for MSK infection - what can you see?

A
  • always start here!
  • soft tissue swelling, loss of tissue planes are earliest findings
  • bony changes (must have at least 40% bone loss to see on film) usually seen late in course of infection or in setting of chronic infections
  • brodies abscess: infection of the bone
  • ** infection is great mimicker w/ plain films, should always remain on ddx list
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11
Q

use of bone scan in MSK infections?

A
  • next step after plain films, vague test
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12
Q

Other scans used in MSK infections?

A
  • indium 111 leukocyte nuclear scan
  • gallium citrate scan
  • PET scan
  • expensive and time consuming
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13
Q

Use of MRI in MSK infections?

A
  • often used
  • can be highly sensitive**
  • expensive
  • normal bone marrow = high signal on T1
  • low T1 signal could be indicative of infection
  • useful for anatomy findings: abscess (US and CT are better), sinus tracts
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14
Q

MSK infections in adults are most common in what pts?

- diff types of osteomyeltitis?

A
  • MC in pts w/ open fxs, DM foot infection, or recent surgery

types:

  • hematogenous (transferred by the blood): ex - vertebral osteomyelitis
  • contiguous focus (caused by prior infection): subdivided based on presence or absence of vascular insufficiency
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15
Q

Alt classification to MSK infections in adults?

A

describes anatomic involvement:

  • stage 1: medullary
  • stage 2: superficial
  • stage 3: localized
  • stage 4: diffuse

describes the host:

  • normal
  • compromised
  • tx worse than the disease
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16
Q

Hematogenous osteomyelitis:
How common is it?
MC site, bacteria?
Presentation?

A
  • 20% of all adult pts
  • more common in males
  • vertebrae is MC site, followed by long bones, pelvis and clavicle
  • S. aureus is MC bacteria
  • pts present w/ pain and constitutional sxs (fever, chills, swelling, erythema) either acutely or long standing
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17
Q

Vertebral osteomyelitis:
- common in what age group?
Sites, bacteria? Presentation?

A
  • over 50 yo (1-2% are kids 7.5yo)
  • death is rare
  • may involve 2 adjacent vertebrae and the disk (diskitis)
  • lumbar is MC 45%, thoracic 35%, cervical 20%
  • S. aureus is MC
  • pseudomonas in IV drug users, stepping on nail
  • pts present w/ fever, pain over area for 3 wks to 3 months
  • meningitis and abscesses can result w/ motor/sensory deficits occurring in 15% of pts
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18
Q

What is contiguous focused osteomyelitis? Occur in what cases? What can this lead to?

A
  • w/o generalized vasc insufficiency can be caused by trauma w/ direct contact to bone, infection spread from soft tissue, or by nosocomial infection
  • ORIF, prosthetics, open Fxs, chronic soft tissue infections
  • S. aureus is MC bacteria
  • infection occurs about 1 month after the primary cause of infection
  • pts report pain and fever w/ drainage of the area
  • leads to decreased bone stability, necrosis, and soft tissue damage
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19
Q

Causes of contiguous focus osteomyelitis w/ general vascular insufficiency?

A
  • diabetics
  • small bones of the feet
  • mult bugs: staph, strep, enterococcus, G bacilli
  • present w/ ulcers, multiple foot problems all due to peripheral neuropathy and small vessel disease
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20
Q

What is the number 1 predictor for chronic osteomyelitis? How does pt present? Tx?

A
  • h/o osteo
  • pts have recurrence of pain, fever, drainage, erythema, and swelling
  • abx alone isn’t usually helpful
  • nidus of infection must be removed
  • w/ prolonged infection can develop squamous cell carcinoma (Marjolin’s ulcer) or amyloidosis
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21
Q

Osteomyelitis is known as what?

A
  • the great mimicker, always have in Ddx
22
Q

General tx guidelines for osteomyelitis?

A
  • tx w/ abx and surgery: adequate drainage, debridement, dead space management, maintenance of blood supply and wound care
  • tx systemic issues: nutrition, smoking (includes all nicotine)
  • abx for 4-6 wks
  • longer than 6 wks hasn’t been shown to be more efficacious
23
Q

Tx of specific stages of MSK infections?

A
  • stage 1 medullary: 4 wk abx
  • stage 2 superficial: 2 wks of abx 100% effective in NL host, 79% effective in compromised host
  • stage 3 localized and stage 4 diffuse: 4-6 wk abx 98% effective in NL host, less so in compromised host
24
Q

Abx therapy used if surgical tx isn’t an option?

A
  • suppressive abx therapy should be initiated
  • rifampin and fluoroquinolone or bactrim for 6 mos
  • if this fails then life long suppression
25
Q

Mainstay tx of osteomyelitis?

A
  • surgical debridement
  • complete when bone bleeds “paprika sign” this ensures the nidus has been removed
  • if it dead it must be removed
  • bony defects can be filled w/ autograft, or spanned w/ external fixation
  • abx impregnanted beads
    local delivery method that allow high concentrations of abx that are not generally absorbed systemically.
    Used to fill dead space, removed after several weeks, newer carriers are absorbed over time and may not have to be removed
  • abx pumps can also be used
26
Q

Tx of infection in setting of a fx?

A
  • stabilized infected fx is better than a non-stabilized fx
  • fx can and will heal in setting of an infection
  • all hardware doesn’t have to be removed immediately. Implants can be removed after fx has united along w/ debridement
  • alt to internal fixation are external fixators: often takes 8+ months but good healing rates
27
Q

Tx of soft tissue injury?

A
  • open fxs should be thought of as soft tissue injuries that happen to have a broken bone, this is especially true of high energy injuries
  • approp coverage encourages healing:
    negative pressure wound dressings, flaps, skin grafts, avoid secondary intention if at all possible
28
Q

When is HBO therapy used? What does it do?

A
  • shown to be useful for chronic osteomyelitis and soft tissue infections
  • promotes collagen formation and angiogenesis
  • increases O2 tension in soft tissues
  • success of around 85% in one study
  • expensive, reqrs mult tx sessions
29
Q

Routes that septic OA can occur? Predisposing factors? MC site?

A
  • blood, trauma, contiguous spread, IV drug use
  • predisposing factors: DM, Rh, steroid use, HIV, malignancy, age
  • knee is MC
30
Q

Pathophys of adult septic arthritis?

A
  • bacteria destroy synovial cell lining
  • glycosaminoglycan is destroyed: loss of fluid retention ability of the cartilage
  • increase inflammatory response
  • destruction of cartilage
31
Q

MC organisms in Adult septic arthritis?

A
  • N. gonorrhea was the MC
  • S. aureus now thought to be more common due to IV drug use
  • S. aureus is MC non-gonococcal organism: over 40% MRSA
  • other common bacteria: E coli, pseudomonas
  • fungal infections can be seen in HIV positive pts
32
Q

MC sites of adult septic arthritis? Presentation?

A
  • knee MC 52%
  • hip 22%
  • shoulder, ankle: 12%
  • wrist 10%
  • present w/ warm swollen and painful jt
33
Q

Dx adult septic arthritis?

A
  • infectious blood work (CBC, ESR, CRP)
  • aspiration is gold std:
    send for cell ct w/ diff (most impt), crystals, gram stain, Cxs
  • WBC over 50,000 equals infection and high PMN count (90%) - early infection
  • if first aspiration is less than 50K and you continue to be clinically suspicious then repeat aspirations as much as needed
34
Q

Tx of adult septic arthritis?

A
  • surgical emergency
  • abx immediately: tailor as cultures return - tx for 6 wks
  • arthrotomy and surgical debridement (open or arthroscopic)
  • concurrent tx w/ NSAIDs has been shown to decrease cartilage damage
35
Q

Ped osteomyelitis occurs mainly where? Most common spread?

A
  • occurs mainly in high vascular areas at metaphyseal epiphyseal area
  • hematogenous spread MC
  • 1/5000
  • 50% of cases kid is less than 5
  • 68% of cases involve the long bones
  • 90% of time occurs w/ single site of infection
36
Q

Most common bugs in peds osteomyelitis?

A
  • S aureus MC: 61-89%
  • Group A strep: 10%
  • H flu 3-7%
  • other causes:
    kingella kingae, presents w/ URI, salmonella - sickle cell pts, bartonella henselae -cat scratch disease, P aeruoginosa - puncture wounds of feet.
37
Q

PP of MSK infections in peds?

A
  • usually occurs in metaphysis due to large vascularity and low flow rate
  • neonates: periosteum is thin, thus infection can perforate and allow spread to surrounding tissues and jts. This leads to septic arthritis and growth plate abnormalities (hips and shoulder MC)
  • infants: infection and spread becomes more rare due to metaphyseal capillary atrophy
  • kids: spread limited by thickening of cortex
38
Q

Dx osteomyelitis in peds pt? Presentation at diff ages?

A
  • any kid w/ fever and limb pain for 3 days need to be eval
  • neonates: pseudoparalysis, pain w/ palpation, swelling, decreased appetite
  • infants, toddlers, and young kids: FUO, limp or NWB, swelling, warmth, erythema
  • older kids and adolescents: report constant pain that is well localized, fever
- dx: 
36-55% will have + blood cxs
plain xray limited use
**US for hip infections
MRI useful: can increase sensitivity w/ gadolinium
39
Q

Tx of osteomyelitis?

A
  • mainstay: abx, occasional decompression and drainage of infected area (can do w/ 14 g needle)
  • abx need to cover staph and GBS
  • tailor coverage as cultures return
  • IV or oral abx for 4-6 wks
  • follow tx w/ CRP
  • be aware of side effects
40
Q

Tx of chronic osteomyelitis?

A
  • 20% of pts w/ acute hematogenous osteomyelitis
  • occurs after inadequate tx of primary infection
  • tx w/ I and D followed by 6-12 months of abx
  • debridement must remove sequestra and intramedullary purulence
41
Q

Peds septic arthritis:
MC age?
MC site, spread, bug?

A
  • 5-12 cases/100,000 kids
  • peaks in kids younger than 3
  • 80% involve the hip
  • septic OA is seeded by contiguous spread
  • bacteria enter jt rapidly due to vascular nature of synovium and lack of basement membrane
  • S aureus is most common
  • in neonate think GBS and gram - bacilli
42
Q

Presentation of peds septic arthritis?

A
  • fever, edema, erythema, effusion, refusal to ambulate, pseudo-paralysis
  • hip infection: flexed, abducted, external rotation, severe pain w/ PROM and rotation
  • pts usually present after 72 hrs
  • more difficult to detect in neonates
43
Q

Dx peds septic arthritis?

A
  • infectious blood work: highly sensitive
  • plain xray: useful to r/o other dxs (fx, perthes, SCFE)
  • gold std is hip aspiration (impractical)
  • hip US*** (good to do bilateral hips so you have a normal comparison
44
Q

Tx of peds septic arthritis?

A
  • similar to adult
  • abx immediately and tailor as cultures return: duration of at least 3 wks
  • surgical drainage of septic jts on an emergent basis
  • follow tx w/ inflammatory markers
  • long term f/u for potential growth plate disturbances
45
Q

MC bugs of periprosthetic infections? How do these occur?

A
  • occurs 1-2% of pts
  • S aureus and S epidermadis MC
  • occur by:
    direct contact during surgery, after surgery (draining incision), hematogenous inoculation
46
Q

Dx periprosthetic infections?

A
  • sxs: pain is 1st indicator, not changed by activity levels or WB, stiffenss, chronic drainage
  • infectious labs: CBC w/ diff, ESR, CRP: if normal then not infected, if 1/3 abnormal than aspirate the jt
  • aspiration: cell ct most impt: normal is less than 1,700 w/ less than 65% leukocytes, if over 1700 and 65% then 94-97% sensitive and 88-98% specific for periprosthetic infection
  • don’t trust gram stains or cultures
  • plain XRs may show progressive radiolucent lines around prosthetic (late finding)
  • bone scan can demonstarate a hot spot: doesn’t normalize for at least 18 m after surgery, can use as a serial test to access for change
  • indium-111 scan: increases accuracy but can produce false +’s
47
Q

Short vs long term periprosthetic infections?

A
  • short: less than 4-6 wks after surgery, acute hematogenous spread
  • long term: greater than 4-6 wks after surgery, no specific iniciting event w/in recent time frame
  • chronic pain preceding the dx of periprosthetic infection
48
Q

Should only abx be used to tx periprosthetic infection?

A
  • no, terrible idea!
  • only used in pts who are so systemically ill that they can’t tolerate surgery
  • successful in less than 18% of pts
49
Q

Single stage revision tx for periprosthetic infections?

A
  • used for short term infections
  • surgical debridement w/ removal of all easily removed components, mechanical scrubbing of retained components and replacement of removed components
  • abx for 6 wks:
    IV and oral, followed by single oral therapy for at least 1 yr
50
Q

2 stage revision tx for periprosthetic infection?

A
  • long term infections (longer than 6 wks)
  • surgical debridement and removal of all components and fbs (q little of cement and suture)
  • placement of an abx cement spacer
  • abx for 6 wks as described for single stage
  • abx holiday and eval w/ infectious blood work
  • if normal than return to surgery for revision arthroplasty
  • year of oral abx
51
Q

Alt tx for periproshetic infections? Prevention?

A
  • amputation: recommended if life threatening sepsis, mult failed revisions, or persistent severe pain
  • fusion: for TKA, high fxning pt, single jt, young pt, loss of extensor mechanism
  • prevention:
    oral abx prophylaxis for life of pt for all invasive procedures (dentist), single dose amoxicillin, cephalosporin, or clindamycin