Osteomyelitis Flashcards

Acute and chronic osteomyelitis

1
Q

What are the types of osteomyelitis?

A

Acute
Chronic
Specific e.g. TB
Non-specific - most common

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Who is most likely affected by acute osteomyelitis?

A
  • Mostly children (different ages)
  • Boys > girls
  • History of trauma (minor)
  • In adults - history other disease e.g diabetes, rheum arthritis, immune compromise, long-term steroid treatment, sickle cell
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the sources of infection in acute osteomyelitis?

A
  • Haematogenous spread - occurs in children and the elderly
  • Local spread from contiguous site of infection - trauma (open fracture), bone surgery (ORIF), joint replacement
  • Secondary to vascular insufficiency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are sources of infection in acute osteomyelitis specific to infants, children and adults?

A
  • Infants - infected umbilical cord
  • Children - boil, tonsillitis, skin abrasions
  • Adults - UTI, arterial line
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the causative organisms of acute osteomyelitis in infants (<1 year)?

A
  • Staph aureus - most common
  • Group B streptococci
  • E. coli
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the causative organisms of acute osteomyelitis in older children?

A
  • Staph aureus
  • Strep pyogenes
  • Haemophilus influenzae
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the causative organisms of acute osteomyelitis in adults?

A
  • Staph aureus
  • Pseudomonas aeroginosa (esp. secondary to penetrating foot injuries, IVDAs) - particularly in immunosuppressed adults, trainer foot
  • Coagulase negative staphylococci (prostheses) •Propionibacterium spp (prostheses) - shoulder replacement
  • Mycobacterium tuberculosis - uncommon in UK but in the increase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the causative organisms in AO associated with diabetic foot and pressure sores?

A

Mixed infection including anaerobes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the causative organism in AO associated with sickle cell disease?

A

Salmonella spp. (species)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the causative organisms in AO associated with fishermen and filleters?

A

Mycobacterium marinum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the causative organisms in AO associated with debilitating illness, HIV & AIDS, long-term antibiotic therapy, extensive GI surgery and malignancy?

A

Candida

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the causative organisms acute vertebral osteomyelitis?

A
  • Staph aureus

* TB (uncommon and slower onset)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the causative organisms in AO associated with butchers?

A

Brucella

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

When can proteus mirabilis be a cause of AO ?

A

Joint replacement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Where does acute osteomyelitis tend to be found in long bones?

A
  • At the end of long bones - metaphysis (where the growth plate is):
  • Distal femur
  • Proximal tibia
  • Proximal humerus

n.b. adults do also have a metaphysis region of long bones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the feature of the joints affected by AO?

A

They are joints with intra-articular metaphysis

e.g. hip and elbow (radial head)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Describe the pathological sequence of acute osteomyelitis

A
  1. Starts at metaphysis - role of trauma? metaphysial injuries are not uncommon in children - lead to stasis
  2. Vascular stasis - leads to venous congestion and arterial thrombosis - organism can inhabit area
  3. Acute inflammation follows - causes increase of pressure
  4. Suppuration (pus production)
  5. Release of pressure - ruptures into medullary cavity, beneath the periosteum or into the joint (if nearby)
  6. Necrosis of bone (sequestrum)
  7. New bone formation (involucrum - shell of new bone that form - common in staph a infection)
  8. Resolution (if not - chronic osteomyelitis)
18
Q

What are the clinical features of AO in an infant?

A
  • May be minimal signs, or may be very ill
  • Failure to thrive
  • Possibly drowsy or irritable
  • Metaphyseal tenderness + swelling - chubby legs prevent this and and by the time this occurs, pus is rupturing into the periosteal area
  • Decrease ROM - range of motion
  • Positional change
  • Commonest around the knee
  • Often have multiple sites
19
Q

What are the clinical features of AO in a child?

A
  • Severe pain - able to communicate
  • Reluctant to move - neighbouring joints held flexed, not weight bearing, may be tender
  • Fever (swinging pyrexia) •Tachycardia
  • Malaise (fatigue, nausea, vomiting, fretful)
  • Toxaemia
20
Q

What are the clinical features of AO in an 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 (esp. ORIF) - so in younger age group
  • Mixture of organisms
21
Q

What tests should you perform for diagnosis of suspected acute osteomyelitis?

A
  • History and clinical examination (pulse + temp.)
  • FBC + diff WBC (patients usually have a neutrophil leucocytosis in response to infection)
  • ESR (may not be raised very early infections), CRP
  • Blood cultures x3 (at peak of temperature - 60% +ve)
  • U&Es – ill, dehydrated
22
Q

What tests should you perform for diagnosis of suspected acute osteomyelitis cont.?

A
  • X-ray (normal in the first 10-14 days)
  • Ultrasound - demonstrates sub-periosteal pus if it exists
  • Aspiration (of pus)
  • Isotope Bone Scan (Tc-99, Gallium-67) - taken up by bone as an alternative to calcium, increased turnover due to infection will light up
  • Labelled white cell scan (Indium-111) - white cells labelled and re-injected and go to area of infection
  • MRI
23
Q

What will you find on radiographs/x-rays of AO?

A
  • Early radiographs - minimal changes
  • 10-20 days - periosteal changes
  • Medullary changes - lytic areas
  • Late - osteonecrosis (sequestrum)
  • Late - periosteal new bone (involucrum)
24
Q

What scan can be used to image AO and how do early and late phases of AO manifest on them?

A
  • Technetium-99m labelled diphosphonate
  • Gallium 67 citrate delayed imaging
  • Indium-111 labelled WBC scan
  • MRI
  • From early to late phases of AO, the areas “lit up” by the scan enlarge
  • Growth plates are more biologically active than the surrounding bone to show up darker when using Technetium
25
How can AO be diagnosed using microbiology (for treatment)?
* Blood cultures in haematogenous osteomyelitis and septic arthritis * Local spread acute osteomyelitis blood cultures tend to be negative but are taken anyway * Bone biopsy/aspiration -drill biopsy * Tissue or swabs from up to 5 sites around implant at debridement in prosthetic infections * Sinus tract and superficial swab (pus finding a way to the surface) results may be misleading (skin contaminants)
26
Name 5 main differential diagnoses for AO
* Scute septic arthritis * Acute inflammatory arthritis * Trauma (fracture, dislocation, etc.) * Transient synovitis (“irritable hip”) * Soft tissue infection
27
Name 4 rarer differential diagnoses for AO
* Sickle cell crisis * Gaucher's disease - fat build-up in organs * Rheumatic fever * Haemophilia
28
Which soft tissue infections can be differential diagnoses of AO?
* Cellulitis - (deep) infection of subcutaneous tissues (Group A Strep) * Erysipelas - superficial infection with red, raised plaque (Group A Strep) * Necrotising fasciitis - aggressive fascial infection (Group A Strep, Clostridia) * Gas gangrene - grossly contaminated trauma (Clostridium perfringens) * Toxic shock syndrome - secondary wound colonisation (Staph aureus)
29
How is AO treated?
* Supportive treatment for pain and dehydration – general care, analgesia * Rest & splintage * Antibiotics * Surgery
30
What is the route of antibiotics used in AO?
•Start with IV and switch to oral (in consultation with a microbiologist) around the 7-10 day mark (up to 2 weeks)
31
For what duration are antibiotics used in AO?
•4-6 weeks - depends on response and ESR
32
Which antiobiotics are used to treat AO?
* Empirical use of flucloxacillin and benzyl penicillin (while waiting for microbiological results) * Infection most likely to be Staph A or Strep
33
Without antibiotics, what is the prognosis of AO?
* Mortality - 70% | * Chronicity - 80% of survivors
34
Which qualities are required of the antibiotics used in the treatment of AO?
* Spectrum of activity * Penetration to bone * Safety fro long term admininstration
35
Why can antibiotics fail?
* Drug resistance – e.g. beta-lactamases (MRSA) * Bacterial persistence - ‘dormant’ bacteria in dead bone - bacteria can sit for many years * Poor host defences - IDDM, alcoholism * Poor drug absorption * Drug inactivation by host flora * Poor tissue penetration
36
When is surgery indicated in treatment of AO?
* Treatment with simple antibiotics can only be done in the earliest stages (first 24hr) * Aspiration of pus for diagnosis and culture - antibiotics cannot reach pus-filled cavities so must aspirate * Abscess drainage - multiple drill holes and then closed to avoid sinus * Debridement of dead/infected/contaminated tissue * 24-48hr - pus is forming, treat with antibiotics but if this does not work (continued pyrexia) continue to operate * Operate, drain, lavage * Infected joint replacement * one stage revision - take out dead tissue and put joint back in again * two stage revision - take out dead tissue and fill hole with something that releases antibiotics (usually cement0 and go back at a later date and put in a joint replacement * patients too unwell for surgery - treat on long term antibiotics
37
What are the complications of acute AO?
* Septicaemia, death * Metastatic infection * Pathological fracture * Septic arthritis - pus perforates into the joint * Altered bone growth * Chronic osteomyelitis
38
When can chronic osteomyelitis occur?
•May follow acute osteomyelitis * May start de novo: * following an operation * following an open fracture * immunosuppressed, diabetic, elderly, drug abusers •Repeated breakdown of "healed" wounds
39
What are the causative organisms of chronic osteomyelitis?
* Often a mixed infection * Usually same organism(s) each flare-up * Mostly: * staph aureus * e. coli * strep pyogenes * proteus
40
What are the pathological features of chronic osteomyelitis?
* Cavities, possibly sinuses * Dead bone (retained sequestra) - bone comes out * Involucrum * Histological picture is one of chronic inflammation
41
What are the complications of chronic osteomyelitis?
* Chronically discharging sinus + flare-ups * Ongoing (metastatic) infection (abscesses) * Pathological fracture * Growth disturbance + deformities * Squamous cell carcinoma (0.07%)
42
How is chronic osteomyelitis treated?
* Long-term antibiotics * local (gentamicin cement/beads, collatamp) * systemic (orally/ IV/ home AB) * Eradicate bone infection - surgically (multiple operations) * Treat soft tissue problems * Deformity correction * Massive reconstruction * Amputation (how many operations/years later?)