infections Flashcards

(24 cards)

1
Q

what is septic arthritis

A

intra-articular infection that can eventually lead to a destructive arthropathy if left untreated; it is an orthopedic surgical emergency.

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2
Q

Which joints are commonly affected by septic arthritis?

A

In a descending order, these are: knee, hip, shoulder, elbow, ankle, sternoclavicular and sacroiliac joints (think of IV drug use in the latter two).

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3
Q

Why are the knee, hip and shoulder the most commonly involved joints? in septic

A

Because they have abundant metaphyseal blood supply.

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4
Q

What would predispose to the development of septic arthritis (risk factors)?

A

▪ Advanced age.
▪ Comorbidities: diabetes mellitus, rheumatoid arthritis, immuncompromsied (HIV).
▪ Bacteremia.
▪ Crystal-induced arthritis.
▪ Prosthetic joint.
▪ IV drug use.
▪ Intra-articular injections.

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5
Q

What is the most common organisms are involved in the causation of septic arthritis?

A

Staphylococcus aureus

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6
Q

most common cause in sexually active young adults.

A

Neisseria

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7
Q

causes septic arthritis in sickle cell disease patients.

A

Salmonella

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8
Q

mainly affect the extremes of age (neonates and the elderly), IV drug users and diabetics.

A

Gram-negative bacilli, e.g. E. coli, Klebsiella,

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9
Q

cause arthritis mainly in young infants.

A

Group B streptococci

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10
Q

causes arthritis mainly in IV drug users.

A

Pseudomonas aeruginosa

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11
Q

mainly implicated in prosthetic joint infections.

A

Coagulase-negative staphylococci

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12
Q

arthritis mainly occur in the immunocompromised hosts.

A

Fungal or candidal

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13
Q

What routes are involved in the pathogenesis of septic arthritis?

A

▪ Hematogenous spread (most common route), i.e. bacteremia. blood
▪ Direct inoculation, e.g. trauma or surgery.
▪ Contiguous spread, e.g. from adjacent osteomyelitis - due to arteriolar anastomosis
between epiphysis and synovium.

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14
Q

How would a patient with septic arthritis be investigated?

A

Complete blood count can reveal leukocytosis with a left shift.
▪ Inflammatory markers: ESR and C-RP - help confirm the presence of acute infection
and C-RP is used to monitor response to treatment.
▪ Two sets of blood cultures.
- x-ray of the affected joint (of limited value in diagnosis but to rule out other pathologies as well):

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15
Q

what is gold standard for diagnosis in septic arthritus and to direct antibiotic Rx;

A

Synovial fluid aspiration and analysis

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16
Q

How is septic arthritis treated?

A

▪ Aspirate synovial fluid and send it for analysis.
▪ Start IV empiric antibiotic therapy based on patient’s age, risk factors and gram stain
results: if gram+, starts IV vancomycin; if gram-, starts third generation cephalosporins.
so
▪ Once culture and sensitivity results are obtained, switch to organism-specific
antibiotics that should be continued for 6 to 12 weeks.
▪ Operative management should ensue with open or arthroscopic joint arthrotomy forurgent decompression, debridement, irrigation and surgical drainage.

17
Q

gout

A

-ve burefringent
urate deposition
needle crystal

18
Q

pseudogout

A

+ve bifringent
calcium pyrophosphate
square crytals

19
Q

what is osteomyelitis

A

inflammation of bone caused by an infecting organism withprogressive destruction.

20
Q

What would predispose to the development of osteomyelitis (risk factors)?

A

▪ Recent trauma or surgery or presence of foreign body.
▪ Comorbidities: diabetes mellitus, sickle cell disease, immuncompromsied (HIV).
▪ Vascular insufficiency.
▪ IV drug use.

21
Q

How can osteomyelitis be classified?
▶ It can be classified according to timing into:

A

Acute (within two weeks) hematogenous osteomyelitis; due to bacteremia.
▪ Subacute (from two to six weeks); usually by direct inoculation
▪ Chronic (more than six weeks); due to untreated/inadequately treated disease.

22
Q

What is the mechanism involved in the pathogenies of osteomyelitis

A

Biofilm-producing bacteria introduced by blood/trauma to bone—>
Inflammatory reaction and release of lytic enzymes—->
local ischemic necrosis—->
pus collection and abscess formation—->
increased intramedullary pressure—->
cortical ischemia—->
purulent material escapes through thin cortex into subperiosteal space—-> subperiosteal abscess formation

23
Q

late findi gs in osteomyelitis

A

♦ Periosteal reaction/thickening/elevation (periostitis) - can manifest as Codman’s triangle.
♦ Lytic lesion (due to presence of intraosseous/Brodie’s abscess) with surrounding sclerosis (wouldn’t show until ~50% of the bone matrix is destroyed) - hence, if x-ray is unrevealing, do not exclude diagnosis in the setting of strong clinical suspicion. ♦ Presence of sequestrum, involucrum and cloaca in chronic OM.

24
Q

early changes in osteomyelitis include

A

soft tissue swelling and loss of normal fat planes.