Bone and Soft Tissue Infections Flashcards

1
Q

In what forms can osteomyelitis occur?

A
  • Acute vs chronic

- Specific (e.g. TB) vs non-specific (most common)

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2
Q

Who is usually affected by acute osteomyelitis?

A
  • Mostly children
  • M>F
  • History of trauma (minor)
  • Other disease: diabetes, rheumatoid arthritis, immune compromise, long term steroid treatment, sickle cell
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3
Q

What the infection in acute osteomyelitis spread?

A
  • Haematogenous spread – children and elderly
  • Local spread from contiguous site of infection: trauma (open fracture), bone surgery (ORIF), joint replacement
  • Secondary to vascular insufficiency
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4
Q

What is a source of infection of osteomyelitis in infants?

A

Infected umbilical cord

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5
Q

What is a source of infection of osteomyelitis in children?

A
  • Boils
  • Tonsillitis
  • Skin abrasions
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6
Q

What is a source of infection of osteomyelitis in adults?

A
  • UTI

- Arterial line

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7
Q

What are the most common infecting organisms of acute osteomyelitis in infants <1 year?

A
  • Staph aureus
  • Group B streptococci
  • E.coli
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8
Q

What are the most common infecting organisms of acute osteomyelitis in older children?

A
  • Staph aureus
  • Strep pyogenes
  • Haemophilus influenzae
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9
Q

What are the most common infecting organisms of acute osteomyelitis in adults?

A
  • Staph aureus
  • Coagulase negative staphylococci (prostheses), Propionibacterium spp (prostheses)
  • Mycobacterium tuberculosis
  • Pseudomonas aeroginosa (esp. secondary to penetrating foot injuries, IVDAs)
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10
Q

Give examples of specific acute osteomyelitis causing organisms and their associated at risk populations.

A

Mixed infection including anaerobes
-Diabetic foot and pressure sores

Salmonella spp.
-Sickle cell disease

Mycobacteriumm marinum
-Fishermen and filleters

Candida
-Debilitating illness including HIV/AIDs

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11
Q

What site are usually affected by acute osteomyelitis?

A

Long bones: Metaphysis

  • Distal femur
  • Proximal tibia
  • Proximal humerus

Joints with intra-articular metaphysis

  • Hip
  • Elbow (radial head)
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12
Q

What is the pathophysiology of acute osteomyelitis?

A
  • Starts at metaphysis
  • Vascular stasis (venous congestion+ arterial thrombosis)
  • Acute inflammation: increased pressure
  • Suppuration
  • Release of pressure (medulla, sub-periosteal, into joint)
  • Necrosis of bone (sequestrum)
  • New bone formation (involucrum)
  • Resolution, or not (chronic osteomyelitis)
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13
Q

What is the clinical presentation of acute osteomyelitis in the infant?

A
  • May be minimal signs, or may be very ill
  • Failure to thrive
  • Possibly. drowsy or irritable
  • Metaphyseal tenderness + swelling
  • Decrease ROM
  • Positional change
  • Commonest around the knee
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14
Q

What is the clinical presentation of acute osteomyelitis in the child?

A
  • Severe pain
  • Reluctant to move (neighbouring joints held flexed); not weight bearing
  • May be tender fever (swinging pyrexia) + tachycardia
  • Malaise (fatigue, nausea, vomiting – “nae weel” - fretful
  • Toxaemia
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15
Q

What is the clinical presentation of a acute osteomyelitis in the adult?

A

-Primary OM seen commonly in thoracolumbar spine
-Backache
-History of UTI or urological procedure
elderly, diabetic, immunocompromised
-Secondary OM much more common
-Often after open fracture, surgery (especially ORIF)
-Mixture of organisms

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16
Q

How is acute osteomyelitis diagnosed?

A
  • History and clinical examination (pulse + temp.)
  • FBC + diff WBC (neutrophil leucocytosis)
  • ESR, CRP
  • Blood cultures x3 (at peak of temperature 60% +ve)
  • U&Es – ill, dehydrated
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17
Q

What is the differential diagnosis for acute osteomyelitis?

A
  • Acute septic arthritis
  • Acute inflammatory -Arthritis
  • Trauma (fracture, dislocation, etc.)
  • Transient synovitis (“irritable hip”)
  • Rare (sickle cell crisis, Gauchers disease, rheumatic fever, haemophilia)
  • Soft tissue infection
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18
Q

What soft tissue infections are included in the differential diagnosis of acute osteomyelitis?

A
  • Cellulitis - (deep) infection of subcutaneous tissues (Gp A Strep)
  • Erysipelas - superficial infection with red, raised plaque (Gp A Strep)
  • Necrotising fasciitis - aggressive fascial infection (Gp A Strep, Clostridia)
  • Gas gangrene - grossly contaminated trauma (Clostridium perfringens)
  • Toxic shock syndrome - secondary wound colonisation (Staph aureus)
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19
Q

How is acute osteomyelitis diagnosed?

A

-X-ray (normal in the first 10-14 days)
-Ultrasound
-Aspiration
-Isotope Bone Scan (Tc-99, Gallium-67)
labelled white cell scan (Indium-111)
-MRI

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20
Q

What is seen on radiographs of acute osteomyelitis?

A
  • Early radiographs minimal changes
  • 10-20 days early periosteal changes
  • Medullary changes: lytic areas
  • Late osteonecrosis: sequestrum
  • Late periosteal new bone: involucrum
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21
Q

What scan are used in acute osteomyelitis?

A
  • Technetium-99m labelled diphosphonate
  • Gallium 67 citrate delayed imaging
  • Indium-111 labelled WBC scan
  • MRI
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22
Q

What is involved in the microbiological diagnosis of acute osteomyelitis?

A
  • Blood cultures in haematogenous osteomyelitis and septic arthritis
  • Bone biopsy
  • Tissue or swabs from up to 5 sites around implant at debridement in prosthetic infections
  • sinus tract and superficial swab results may be misleading (skin contaminants)
23
Q

How is acute osteomyelitis treated?

A
  • Supportive treatment for pain and dehydration including general care and analgesia
  • Rest and splintage
  • Antibiotics (route dependent on patient, duration 4-6 weeks depending on response, choice empirical (Fluclox, and Benzylpen) while waiting)
  • Surgery
24
Q

What is choice of antibiotic dependent on in acute osteomyelitis?

A
  • Spectrum of activity
  • Penetration to bone
  • Safety for long term administration
25
Q

Why might antibiotics fail in acute osteomyelitis?

A
  • Drug resistance – e.g. lactamases
  • Bacterial persistence - ‘dormant’ bacteria in dead bone
  • Poor host defences - IDDM, alcoholism…
  • Poor drug absorption
  • Drug inactivation by host flora
  • Poor tissue penetration
26
Q

What are the indications for surgery in acute osteomyelitis?

A
  • Aspiration of pus for diagnosis & culture
  • Abscess drainage (multiple drill-holes, primary closure to avoid sinus)
  • Debridement of dead/infected /contaminated tissue
  • Refractory to non-operative Rx >24..48 hrs
27
Q

What are the possible complications of acute osteomyelitis?

A
  • Septicemia, death
  • Metastatic infection
  • Pathological fracture
  • Septic arthritis
  • Altered bone growth
  • Chronic osteomyelitis
28
Q

How might chronic osteomyelitis originate?

A
  • May follow acute osteomyelitis (rare in children)

- May start de novo following surgery, open fracture or in immunosuppressed, diabetic, IVDU and elderly patients

29
Q

How is chronic osteomyelitis characterised?

A

Repeated breakdown of healed wounds

30
Q

What organisms are involved in chronic osteomyelitis?

A
  • Often mixed infection
  • Usually same organism(s) each flare-up
  • Mostly Staph. Aureus, E. Coli, Strep. pyogenes, Proteus
31
Q

What is the pathophysiology of chronic osteomyelitis/

A
  • Cavities, poss. sinus(es)
  • Dead bone (retained sequestra)
  • Involucrum
  • Histological picture is one of chronic inflammation
32
Q

What are the possible complications of chronic osteomyelitis?

A
  • Chronically discharging sinus + flare-ups
  • Ongoing (metastatic) infection (abscesses)
  • Pathological fracture
  • Growth disturbance + deformities
  • Squamous cell carcinoma (0.07%)
33
Q

What are the treatment options for chronic osteomyelitis?

A

Long-term antibiotics?(either local (gentamicin cement/beads, collatamp) or systemic (orally/ IV/ home AB))

  • Eradicate bone infection- surgically (multiple operations)
  • Treat soft tissue problems
  • Deformity correction?
  • Massive reconstruction?
  • Amputation?
34
Q

What are the possible routes of infection in acute septic arthritis?

A
  • Haematogenous
  • eruption of bone abscess
  • Direct invasion (penetrating wound, intra-articular injury, arthroscopy)
35
Q

What are organisms are commonly implicated in acute septic arthritis?

A
  • Staphylococcus aureus
  • Haemophilus influenzae
  • Streptococcus pyogenes
  • E. coli
36
Q

What is the pathophysiology behind acute septic arthritis?

A
  • Acute synovitis with purulent joint effusion
  • Articular cartilage attacked by bacterial toxin and cellular enzyme
  • Complete destruction of the articular cartilage
37
Q

What is the sequelae of acute septic arthritis?

A
Complete recovery 
OR
Partial loss of the articular cartilage and subsequent OA
OR
Fibrous or bony anklyosis
38
Q

How do neonates with acute septic arthritis often present?

A

Picture of septicaemia

  • Irritability
  • Resistant to movement
  • Ill
39
Q

How do children and adults often present with acute septic arthritis?

A

Acute pain in single large joint

  • Reluctant to move the joint (any movement – c.f. bursitis where RoM OK)
  • Increase temp. and pulse
  • Increase tenderness
40
Q

What is important to note about adults with septic arthritis?

A
  • Often involves superficial joint (knee, ankle, wrist)
  • Rare in healthy adult
  • May be delayed diagnosis
41
Q

How is acute septic arthritis investigated?

A
  • FBC, WBC, ESR, CRP, blood cultures
  • X ray
  • Ultrasound
  • Aspiration
42
Q

What is the most common cause of septic arthritis in adults?

A

Infected joint replacements

43
Q

What is the most common organism implicated in infected joint replacements?

A

Staph aureus

44
Q

What are the outcomes of an infected joint replacement?

A
  • Death
  • Amputation
  • Removal of arthroplasty
45
Q

What is the differential diagnosis for acute septic arthritis?

A
  • Acute osteomyelitis
  • Trauma
  • Irritable joint
  • Haemophilia
  • Rheumatic fever
  • Gout
  • Gaucher’s disease
46
Q

How is acute septic arthritis treated?

A
  • General supportive measures
  • Antibiotics (3-4 weeks)
  • Surgical drainage & lavage -
47
Q

How is bone tuberculosis classified?

A
  • Extra-articular (epiphyseal / bones with haemodynamic marrow)
  • intra-articular (large joints)
  • Vertebral body

Multiple lesions in 1/3 of patients

48
Q

What are the clinical features of bone tuberculosis?

A
  • Insidious onset & general ill health
  • Contact with TB
  • Pain (esp. at night), swelling, loss of weight
  • Low grade pyrexia
  • Joint swelling
  • Decrease ROM
  • Ankylosis
  • Deformity
49
Q

What is the pathophysiology behind bone tuberculosis?

A
  • Primary complex (in lung or the gut)
  • Secondary spread
  • Tuberculous granuloma
  • Note the role of nutrition and other disease (HIV/AIDs)
50
Q

How does spinal tuberculosis present?

A
  • Little pain

- Present with abscess or kyphosis

51
Q

How is bone tuberculosis diagnosed?

A
  • Long history
  • Involvement of single joint
  • Marked thickening of the synovium
  • Marked muscle wasting
  • Periarticular osteoporosis
52
Q

How is bone tuberculosis investigated?

A
  • FBC, ESR
  • Mantoux test
  • Sputum/urine culture
  • X-Ray (soft tissue swelling, periarticular osteopenia, articular space narrowing)
  • Joint aspiration and biopsy (AAFB identified in 10-20%, culture + in 50% of cases)
53
Q

What is the differential diagnosis for bone tuberculosis?

A
  • Transient synovitis
  • Monoarticular RA
  • Haemorrhagic arthritis
  • Pyogenic arthritis
  • Tumour
54
Q

How is bone tuberculosis treated?

A

Chemotherapy

  • Rifampicin, ethambutol and isoniazid 8 weeks
  • Rifampicin and isoniazid further 6-12 months
  • Rest and splintage
  • Operative drainage rarely necessary