Some concise notes from Davidsons
Source of infection: Haematogenous infection, post trauma, post operative
Most likely causative organisms: Staphylococcus, pseudomonas and mycobacterium tuberculosis
Risk factors: Often affects children and adolescents. Diabetes mellitus, compromised immunity (HIV and AIDS). Sickle cell disease (commonly associated with salmonella infection)
Progression of disease: Osteonecrosis leads to fragment of necrotic bone called a sequestrum (often found on any part of a bone but there is preferential targeting of the juxta-epiphyseal regions of long bones adjacent to joints). The cortex is perforated by pus, which stimulates the formation of new bone growth in the periosteum (involucrum), often leading to the development of sinuses that discharge throught the skin.
Presentation: Bone pain, tenderness, malaise, night sweats, pyrexia, adjacent joint may be painful to move. Potential for secondary septic arthritis.
Investigations: MRI best to investigate early changes. X-Ray (shows osteopenia, osteolysis and osteonecrosis). Cultures: open or image guided biopsy or blood cultures.
Osteolysis is the destruction of bone tissue.
Treatment: Parenteral antibiotics for 2 weeks followed by oral antibiotics for 4 weeks. Resection of infected bone and reconstruction is often recquired.
Complications: Secondary amyloidosis, skin malignancy at the at the margin of a discharging sinus. (marjolin’s ulcer).
What are the types of osteomyelitis?
Non-specific (most common)
Who does osteomyelitis commonly affect?
Mostly children (diffrerent ages)
Boys is more common than girls
Someone with a history of trauma
What diseases might predispose someone to osteomyelitis?
Diabetes, rheum arthritis, immune compromise, long-term steroid treatment, sickle cell
What are the different sources of infection for osteomyelitis?
- haematogenous spread – children and elderly
- local spread from contiguous site of infection – trauma (open fracture), bone surgery (ORIF), joint replacement
- secondary to vascular insufficiency
What are the common sources of infection in infants?
Infected umbilical cord
What are the common sources of infections in children?
Boils, tonsilitis, skin abrasions
What are the common sources of infection in adults?
What is the most likely infective organism for infants (less than 1 year)
Strep group B
What are the likely infective organisms for osteomyelitis in older children?
Older children: staph aureus, strep pyogenes, haemophilus influenzae
What is the likely infective organism for osteomyelitis in adults?
−coagulase negative staphylococci (prostheses), Propionibacterium spp (prostheses)
− Mycobacterium tuberculosis
− Pseudomonas aeroginosa (esp. secondary to penetrating foot injuries, IVDAs)
What are the likely organisms to be infecting diabetic foot and pressure sores?
Mixed infection including anaerobes
What is the likely infective organism for sickle cell disease?
What type of bacteria are fishermen and filleters exposed to?
What type of organism is liekly to cause osteomyelitis in HIV and AIDS patients?
What is the pathology of osteomyelitis?
starts at metaphysis – role of trauma?
(venous congestion + arterial thrombosis)
acute inflammation – increased pressure
release of pressure
(medulla, sub-periosteal, into joint)
necrosis of bone (sequestrum)
new bone formation (involucrum)
resolution - or not (chronic osteomyelitis)
Notes from Davidsons: Any part of a bone may be involved but there is preferential targeting of the juxta-epiphyseal regions of long bones adjacent to joints
What are the clinical features on an infant?
may be minimal signs, or may be very ill
failure to thrive
poss. drowsy or irritable
metaphyseal tenderness + swelling
commonest around the knee
What are clinical features in a child of osteomyelitis?
reluctant to move (neighbouring joints held flexed); not weight bearing
may be tender fever (swinging pyrexia) + tachycardia
malaise (fatigue, nausea, vomiting – “nae weel” - fretful
What are the clinical features of osteomyelitis in an adult?
- Primary OM seen commonly in thoracolumbar spine
history of UTI or urological procedure
elderly, diabetic, immunocompromised
Which is more common, primary or secondary OM?
- Secondary OM much more common
- often after open fracture, surgery (esp. ORIF)
- mixture of organisms
Investigations for acute osteomyelitis?
history and clinical examination (pulse + temp.)
FBC + diff WBC (neutrophil leucocytosis)
blood cultures x3 (at peak of temperature – 60% +ve) (blood cultures for haematogenous osteomyelitis and septic arthritis)
U&Es – ill, dehydrated
What is the differential diagnosis for acute OM?
acute septic arthritis
acute inflammatory arthritis
trauma (fracture, dislocation, etc.)
transient synovitis (“irritable hip”)
- sickle cell crisis
- Gaucher’s disease
- rheumatic fever
Soft tissue infection:
−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)
How is the diagnosis of acute OM achieved?
X-ray (normal in the first 10-14 days)
Isotope Bone Scan (Tc-99, Gallium-67)
labelled white cell scan (Indium-111)
What are the features of acute OM on radiographs?
Early - minimal changes
10-20 days - early periosteal changes
Medullary changes - lytic areas
Late osteonecrosis (sequestrum)
Late periosteal new bone (involucrum)
What is the treatment for acute Osteomyelitis?
supportive treatment for pain and dehydration – general care, analgesia
rest & splintage
- route (IV/oral switch – 7-10 days?)
- duration (4-6 wks – depends on response, ESR)
- choice - empirical (Fluclox + BenzylPen) while waiting ( I think this is because staph aureus is a likely causative organism)
When might antibiotics fail?
- drug resistance – e.g. b lactamases
- bacterial persistence - ‘dormant’ bacteria in dead bone
- poor host defences - IDDM, alcoholism…
- poor drug absorption
- drug inactivation by host flora
- poor tissue penetration
So the antibiotics won’t work for the following reasons:
The bacteria - resistant, or persistant (dormant bacteria in dead bone)
The host - Defences are poor, gut flora inactivates drug
The antibiotic - poor absorption, poor tissue penetration
What are the indications for surgery in acute OM?
- 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
So this is done to remove pus, which will be sent off for diagnosis and culture and to drain an abscess. Surgery is used to debride dead/infected/contaminated tissue. OR if non operative therapy isn’t working.
What are the complications of acute OM?
altered bone growth
may follow acute osteomyelitis (now much rarer in children)
may start de novo
following open # (poss. many years earlier)
immunosuppressed, diabetics, elderly, drug abusers, etc.
repeated breakdown of “healed” wounds
What arethe likely causative organisms for osteomyelitis?
often mixed infection
usually same organism(s) each flare-up
mostly Staph. Aureus, E. Coli, Strep. pyogenes, Proteus
cavities, poss. sinus(es)
dead bone (retained sequestra)
histological picture is one of chronic inflammation
What are the complications of chronic OM?
- chronically discharging sinus + flare-ups
- ongoing (metastatic) infection (abscesses)
- pathological fracture
- growth disturbance + deformities
- squamous cell carcinoma (0.07%)
What is the treatment for chronic osteomyelitis?
−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?)
What is the route of infection for septic arthritis?
eruption of bone abscess
penetrating wound (iatrogenic? – joint injection)
What are the common causative organisms for acute septic arthritis?
What is the pathology assocaited with acture septic arthritis (pathway of disease)?
Synovitis (inflammation of the synovial membrane) with purulent joint effusion (increased intra-articular fluid)
Articular cartilage is attacked by bacterial toxin and cellular enzyme
Complete destruction of the articular cartilage
What is the sequalae for acute septic arthritis?
partial loss of the articular cartilage and subsequent OA
fibrous or bony ankylosis
What are the features of septic arthritis in the neonate?
Picture of septicaemia:
resistant to movement
What are the features of acute septic arthritis in a child/adult?
Acute pain in single large joint
reluctant to move the joint (any movement – c.f. bursitis where RoM OK)
increase temp. and pulse
What are the features of acute septic arthrits in an adult?
often involves superficial joint (knee, ankle, wrist)
rare in healthy adult
May be delayed diagnosis
What are the investigations for septic arthritis?
FBC, WBC, ESR, CRP, blood cultures
What is the most common cause of septic arthritis in adults?
Infected joint replacement
rare (1-1.5%) but disaster (death, amputation, removal of arthroplasty)
changing picture of organisms, but Staph still most common
What is the differential diagnosis for acute septic arthritis?
What is the treatment for acute septic arthritis?
general supportive measures
antibiotics (3-4 weeks)
surgical drainage & lavage - emergency (“never let the sun set on pus” ); open or arthroscopic lavage;
infected joint replacements - one stage revision, two stage revision, antibiotics only?
Some concise notes from Davidson’s on septic arthritis:
Most rapid and destructive joint disease.
Source of infection: Haematogenous spread from either skin or upper respiratory tract, infection from either skin or upper respiratory tract, infection from direct puncture wounds or secondary to joint aspiration.
Risk factors: increasing age, pre-exisintg joint disease (RA), joint replacement, diabetes mellitus, immunosuppression, IVDA. RA predisposes infection via route of skin due to maceration of skin between toes.
Clinical features: Mono-arthritis and fever. If previous joint disease then multiple joints may be affected. The joint is usually swollen, hot and red, with pain at rest and on movement. Knee and hip are commonly targetted.
Causative organisms: Adults - staph aureus (especially if there is RA and diabetes. Sexually active adults - disseminated gonococcal infections have the potential to cause mono/oligoarthritis, painful pustular skin lesions may also be present.
What are the classfications of tuberculosis?
- extra-articular(epiphyseal / bones with haemodynamic marrow)
- intra-articular(large joints)
- vertebral body
- multiple lesions in 1/3 of patient
What are the clincal features of bone TB?
Pain especially at night, swelling, loss of weight
Low grade pyrexia
Spinal TB - little pain, present with abscess of kyphosis
What are the diagnostic features of TB?
involvement of single joint
marked thickening of the synovium
marked muscle wasting
What are the investigations for Tuberculosis?
FBC , ESR
Sputum/ urine culture
Xray soft tissue swelling
articular space narrowing
Joint aspiration and biopsy
AAFB identified in 10-20%
culture +vein 50% of cases
What are the differential diagnosis for TB?
What is the treatment for tuberculosis?