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Phase II: Musculoskeletal > Infection > Flashcards

Flashcards in Infection Deck (46):

Name 4 local factors that increase susceptibility to infection of bones and joints

Articular steroid injection
Large wound area and depth
Poor perfusion
Distal anatomical location
Necrotic tissue
Foreign body
Chronic bone or joint disease


Name 4 systemic factors that increase susceptibility to infection of bones and joints

Age: children and elderly
General illness
Diabetes mellitus
Sickle-cell anaemia*
Alcohol excess
Rheumatoid disease


Describe the features of acute pyogenic infection

Formation of pus often localised in an abscess
Abscess may extend infection along tissue directly, or spread via lymphatics (lymphangitis and lymphadenopathy) or blood (bacteraemia and septicaemia).

Systemic reaction due to enzymes and toxins.


Describe the features of chronic infection

May occur after acute infection
Less acute systemic effects, but may be more debilitating
Lymphadenopathy, splenomegaly, and tissue wasting


Outline the treatment principles of bone and joint infections

Analgesia and supportive measures
Rest the affected part
Initiate antibiotics
Drainage of pus and debridement of necrotic tissue
Stabilise bone if fractured
Maintain soft tissue and skin cover


What is typically the causative organism of acute osteomyelitis?

Staph aureus
Less often: Strep pyogenes, Strep pneumoniae, or H. influenzae (children)

If sickle-cell: Salmonella typhi


Which patient group is most affected by acute osteomyelitis?

Children over age of 4 years


What is the most common location of acute osteomyelitis in children?

Metaphysis of long bones
Most often at the proximal or distal end of the femur, or the proximal end of the tibia

N.B. in infants, acute osteomyelitis can also reach the epiphysis due to presence of anastomoses.


Describe the pathological changes of acute osteomyelitis

1. Acute inflammation: intense pain, obstructed blood flow
2. Suppuration: subperiosteal abscess formation
-may spread along shaft and re-enter bone, or spread to soft tissues
-infants: may spread to epiphysis and joint
3. Necrosis: usually seen by 1 week
-stasis, periosteal stripping, thrombosis
-bone fragments can act as foreign bodies
4. New bone formation: involucrum encases infection
-if infection persists ➔ chronic osteomyelitis
5. Resolution
-requires infection to be controlled and intraosseous pressure to be release at an early stage
-may result in overall thickening of bone


Describe the clinical features of acute osteomyelitis in children

Severe pain: limb held still
Systemic: fever, malaise, irritability, lethargy
Tenderness over involved bone
Decreased range of motion in adjacent joints

Later: red, swollen, warm ➔ pus formation (suppuration)


Describe the clinical features of acute osteomyelitis in infants and neonates

Infants and neonates may present with misleadingly mild symptoms: failure to thrive, drowsy, irritable
May have metaphyseal tenderness and resistance to joint movements
Always look at other sites, as multi infection is not uncommon.


Name 2 aspects of the history that would increase suspicion of acute osteomyelitis in neonates

Birth difficulties
Umbilical artery catheterisation


Name and explain 2 consequences of acute osteomyelitis in infants within 1st year of life

Growth retardation and deformity

Metaphysis-epiphysis anastomoses present in 1st year of life, allow haematogenous spread to epiphysis.


Where is the commonest location of acute osteomyelitis in adults? What clinical features would suggest this?

Suspicious features: back pain and a mild fever


How is acute osteomyelitis confirmed?

Fine needle aspiration and culture


How is acute osteomyelitis investigated?

Aspirate pus from subperiosteal abscess or joint*
Culture for cells and organisms
Raised WBC and ESR
MRI*: 90-100% sensitivity
X-ray: normal for first 2 weeks


Explain the treatment of acute osteomyelitis

Blood and aspirate samples sent for culture
Supportive: bed rest, splint, analgesia

Prompt antibiotics if pus found on aspiration
Empirical antibiotics: Flucloxacillin or clindamycin
Continue antibiotics for 4-6 weeks
Children should initially receive 2 weeks of IV antibiotics

Abscess drainage
Surgical debringement

Outpatient follow-up*: crucial to check for recurrence


State 3 complications of acute osteomyelitis

Spread: septic arthritic or metastatic osteomyelitis
Pathological fractures
Growth disturbance/deformity if epiphysis involved
Persistent infection ➔ chronic osteomyelitis


Describe the clinical features of subacute osteomyelitis

Common in distal femur, and proximal and distal tibia
Pain near one of larger joints for several weeks


What classic radiographic sign is indicative of subacute osteomyelitis?

Brodie abscess: small oval cavity surrounded by sclerotic bone

Most be explored as can be mistaken for osteoid osteoma or bone tumour if large


What is the commonest causative organism of post-traumatic osteomyelitis?

Staph aureus
Others: E. coli, Proteus mirabilis, Pseudomonas aeruginosa


Describe the clinical features of post-traumatic osteomyelitis

Pain and swelling over fracture site
May have purulent discharge


What are the common causes of chronic osteomyelitis?

Following open fracture or operation
Less common nowadays after acute osteomyelitis


Name 2 typically causative organisms of chronic osteomyelitis

Staph aureus
E. coli
Strep pyogenes
Proteus mirabilis: soil
Pseudomonas aeruginosa
Strep epidermidis: surgical implants


Describe the clinical features of chronic osteomyelitis

Recurrent pain, redness, and tenderness at affected site
Healed and discharging sinus


What x-ray features are seen with chronic osteomyelitis?

Bone rarefaction (thinning) surrounded by dense sclerosis and cortical thickening


Outline the treatment options for chronic osteomyelitis

If seldom relapses: conservative management
-Rest, dressing, and antibiotics for 4-6 weeks

Drainage of any acute abscess

Refractory or frequent relapses: surgery
-excision of infected/devitalised bone
-Ilizarov method after bone transport ➔ bone union


What is the usual causative organism of septic arthritis?

Staph aureus
Children aged 1-4: H. influenzae if not vaccinated


Explain the pathology of septic arthritis

Joint invaded by:
-a penetrating wound
-eruption of adjacent bone abscess
-distal haematogenous spread


Describe the clinical features of septic arthritis in children

Acute severe pain and swelling of single joint
-Commonly hip (children)
-Unable to weight bear
Swinging fever
Red, swollen, tender joint: often flexed
Restricted movement due to pain and spasm


Describe the clinical features of septic arthritis in infants

Emphasis on septicaemia rather than joint pain
Irritable and refuses to feed
Rapid pulse +/- fever
Local warm, tender joints: resistant to movement
Examine umbilical cord and IV access sites


Describe the clinical features of septic arthritis in adults

Acute severe pain and swelling of single joint
-Commonly knee (adults)
-Unable to weight bear
Mild fever
Red, swollen, tender joint: often flexed
Restricted movement due to pain and spasm
Unable to weight bear


How does the presentation of septic arthritis differ in adults with rheumatoid arthritis?

Patients with rheumatoid arthritis, especially on corticosteroids, may develop a 'silent' joint infection.

Suspect septic arthritis if unexplained deterioration in patient's general condition.


What x-ray changes are seen with septic arthritis?

First 2 weeks of bacterial arthritis:
Soft-tissue swelling
Widening of joint space
Periarticular osteoporosis

Later: joint space narrowing and signs of bone destruction


How is a diagnosis of septic arthritis confirmed?

Joint aspiration and culture*
Blood culture positive in 50%
WBC, CRP, and ESR are suggestive


Name 3 differentials of septic arthritis

Osteomyelitis near joint: may be indistinguishable, safest to assume both osteomyelitis and septic arthritis present

Acute haemarthrosis (trauma or haemophilia): blood on joint aspiration

Transient synovitis: clinical features less acute

Gout/CPPD: presence of urate or pyrophosphate crystals


Name 2 complications of septic arthritis

Avascular necrosis
Epiphyseal destruction ➔ pseudoarthrosis
Growth disturbance/deformity
Ankylosis: stiffening and immobility due to fusion


What is the treatment for septic arthritis

Joint aspiration and examination
Antibiotics STAT: flucloxacillin 4-6 weeks
Joint rested and splinted
-if hip: abducted and 30 degrees flexed
Drainage and wash-out of joint

Encourage movement afterwards if cartilage intact
Otherwise, immobilise joint in optimum position whilst ankylosis occurs


What percentage of TB patients present with skeletal involvement?



Which patient groups are most commonly affected by skeletal TB?

Endemic: pulmonary TB in children and young adults
Non-endemic: chronic disease, or immunosuppressed


Explain the pathology of skeletal TB

Infection reaches the skeleton by haematogenous seeding from lungs or intestine.
Chronic inflammation ➔ caseating granuloma
Cold abscess
Chronic sinus, may have secondary pyogenic infection


Describe the progression of vertebral TB

Vertebral TB usually begins in the anterior part of the vertebral body near the intervertebral disc.

Later invasion into intervertebral disc, with subsequent collapse forwards ➔ sharp angulation of spine (gibbus deformity)


Describe the progression of joint TB

Joint TB may start in synovium or nearby metaphysis. If untreated, it will destroy the articular cartilage and cause fibrous ankylosis.


Describe the clinical features of skeletal TB

Tuberculosis arthritis (1%): affects spine (50%), hip or knee (30%). Fever, night sweats, weight loss.

Pott's disease (TB spondylitis): Back pain, lower limb weakness, kyphosis. Fever, night sweats, weight loss.


How is skeletal TB treated?

Anti-tubercular drugs:
2 months: Rifampicin, Isoniazid (+pyridoxine), Pyrazinamide, Ethambutol
Additional 4 months: Rifampicin, Isoniazid (+pyridoxine)

Dose is weight-dependent


What monitoring is required whilst on anti-tubercular treatment?

LFTs: 'R.I.P.' all can cause hepatitis
Visual acuity: 'E.' can cause optic neuritis