INFECTIONS OF THE BONES

AND JOINTS
Dr. Mohd Hezery Harun
Orthopaedic & Trauma Surgeon
Department of Orthopaedics UPM
 Definition
Infection- invasion of the body by pathogenic
microorganisms and their multiplication which can
lead to tissue damage and diseases

Osteomyelitis- infection of bone tissue

Septic arthritis- infection of joints

Microorganisms- bacterial, viral, fungal, TB

 What makes bone infection differs
from others?

• Rigid compartments- less tolerance to built up

pressure
• More susceptible to vascular damage and cell death
• Lead to tissue necrosis
 Factors predisposing to infection:
• Malnutrition
• Diabetes Mellitus
• Steroid
• Immune deficiency
• venous stasis in the limbs
• Peripheral vascular disease
• Loss of sensibility
• Trauma
 Processes of infection

• Inflammation
• Necrosis
• Healing (new bone formed)
• Remodelling / Ankylosis
 Osteomyelitis

- Progressive disease of
bone if not treated
- Can involve one /
multiple sites
- Periosteum,
medullary cavity
and/or cortical bone
can be affected
 Classification
• Duration
– Acute
– Subacute
– Chronic

• Route of infection
– Haematogenous
– Exogenous/ direct inoculation
– In diabetics (poor blood supply and non-healing
ulcers)

• Host response
– Pyogenic
– Granulomatous
 Pathology
• Acute inflammatory reaction with vascular
congestion
• Rise in intra-osseous pressure causing intense
Inflammation pain

• At 2-3 days pus forms within bone & forces its

way to forms sub-periosteal abscess
Suppuration
• Pus can spread from here back into bone, into
adjacent joint or into soft tissues

• At 7 days, rising pressure, vascular stasis,

Necrosis infective thrombosis & periosteal stripping
compromise blood supply to bone -> bone
death -> sequestrum
New bone formation
• At 10-14 days this forms from deep surface of
stripped periosteum forming involucrum

Resolution
• With release of pressure & appropriate
antibiotics healing can occur
 Osteomyelitis (haematogenous)

- Secondary to bacteremia
- Predilection for metaphysis
- Non-anastomosing terminal branches of nutrient artery twist back before
entering sinusoidal veins
- Relative vascular stasis & lack of phagocytes favors bacterial colonization
Osteomyelitis (haematogenous)

• Preceeded by bacteraemia (seeding

of bacteria into blood)
• Source – throat, gums, urinary tract,
skin
• Seen in children and elderly
 Osteomyelitis (direct spread)

- Open injuries
- Perforating injuries
- Operative procedure
 Osteomyelitis (direct spread)

Open injuries
Perforating injuries
Operative
procedure
 Osteomyelitis (Etiology)
Type Common pathogens
Haematogenous

Infant (<1 y.o.) Staphylococcus aureus

Streptococcus agalactiae
Escherichia coli
Children (1-16 y.o.) Staphylococcus aureus
Sreptococcus pyogenes
Haemophilus influenzae
Adults (>16 y.o.) Staphylococcus aureus
Coag neg Staphylococci
Gm negatives : E coli, Pseudomonas
Direct spread

Depends on primary site of infection Staphylococcus aureus

Streptococcus pyogenes
Enterococcus
Coag neg Staphylococci
Gm negatives
Anaerobes
Diabetic foot Staphylococcus aureus
Streptococci
Gm negatives (Pseudomonas, Proteus)
Anaerobes
 Epidemiology
• Haematogenous OM
usually in children
single site
50% Pre-school age
incidence 1:5000 (children); 1:1000
(neonates)
• Direct spread
usually in adults
commonly after open fractures / punctures
• Spinal OM
Age group >45 y.o.
Lumbar > thoracic > cervical (rare)
Batson’s prevertebral plexus
 Batson’s
prevertebral plexus
 Manifestations
• Acute OM : fever, chills, malaise, localised
pain at involved region

• Chronic OM : fever (+/-), discharging

sinus, deformity

• Spine OM : fever, back pain (localised),

tenderness
 Diagnosis

• History
• Physical examination
• Lab investigations
• Radiological investigations
• Special tests
 Lab parameters in OM

PARAMETERS Acute OM Chronic OM Diabetics

Full blood count TWCC  TWCC  TWCC /

Hb  Hb  Hb 

ESR and CRP   

(used in monitoring Rx)
– C-reactive protein
• elevated in 98% of patients with acute hematogenous
osteomyelitis
• becomes elevated within 6 hours
• most sensitive to monitor therapeutic response
• declines rapidly as the clinical picture improves
• CRP is the best indicator of early treatment success and
normalizes within a week
• failure of the C-reactive protein to decline after 48 to
72 hours of treatment should indicate that treatment
may need to be altered
 Radiological Investigations
• X-rays
- not sensitive for acute OM (usually after 2-3
weeks)
- periosteal elevation
- soft tissue swelling
- osteolytic lesion
- Chronic OM
- sclerosis
- sequestra
- involucrum
Acute OM
 Chronic OM
Involucrum (B)

Cloacae (D)

Sequestrum (E)
Vertebral OM
 CT scan and MRI
• CT – more sensitive than plain films

• Can determine extent of bone involvement

*crucial in deciding how much debridement
to do

• MRI – can detect early changes in bone, more

sensitive than CT
 CT scan

MRI
MRI
 Culture and sensitivity
(to identify organism and adjust Rx)

• Blood – can be +ve in acute OM

• Deep tissue – from needle biopsy or
during surgical debridement
- should also be sent for HPE
- inflammatory cells /
granuloma
• Sinus specimen – non-representative
• Children – empirical mostly, needle
biopsy not done
 Osteomyelitis
(Principles of Treatment)
• Empirical antibiotics (to cover the most likely
organism) – should be adjusted once C&S
available
• Splinting (Acute OM)
• Analgesics (pain relief)
• Physiotherapy (once pain )
» Range of motion of affected joint
» Muscle strengthening
 Osteomyelitis
(Principles of Treatment)
• Antibiotics
• Given intravenously for 4-6 weeks
• Staphylococcus aureus – Cloxacillin
• Streptococcus – Penicillin
• Gram negatives – Gentamycin / Ciprofloxacin
• Anaerobes – Metronidazole / Clindamycin
• Diabetics – broad spectrum
(Cephalosporins/Combination antibiotics)
 Osteomyelitis
(Principles of Treatment)
• Chronic OM
Surgical debridement needed
- obtain deep tissue for culture
- remove dead tissue until healthy tissue seen
- sequestrectomy
- + reaming of canal
- washout (10L normal saline)
- flap coverage may be needed

For persistent case – amputation may

be performed
Chronic OM
Debridement
Debridement and flap cover
DM with Non-healing Ulcer and Severe
OM
DM with Non-healing Ulcer and
Severe OM
 Septic arthritis

• Serious bacterial infection of the joint

• If not treated early – significant damage to the
joint surface – disability
• Can affect any age – clinical pictures differ
• Confusion – sterile reactive inflammatory
arthritis (similar presentation)
 Septic arthritis (epidemiology)

• 1/3 will have significant joint damage – subsequent

OA / ankylosis
• Staph aureus – causes more damage than others
• 45% - over 65 y.o., 56% - male, 50% has underlying
chronic joint disease (OA, RA)
• Knee (50%), hip (20%), shoulder (8%), ankle (7%),
wrist (7%)
• Children – hip (60%), knee (35%)
 Septic arthritis

• Commonest organism – Staph aureus

• Others :
- Neisseria gonorrhoeae – young sexually active
adults
(gonococcal arthritis)
- Streptococci – very young or very old
- Gram negative bacilli – elderly
- Polymicrobial – post-trauma, diabetics
 Septic arthritis (Etiology)
Type Common pathogens
Haematogenous

Infant (<1 y.o.) Staphylococcus aureus

Streptococcus agalactiae
Escherichia coli
Children (1-16 y.o.) Staphylococcus aureus
Sreptococcus pyogenes
Haemophilus influenzae
Adults (>16 y.o.) Staphylococcus aureus
Coag neg Staphylococci
Gm negatives : E coli, Pseudomonas
Direct spread

Depends on primary site of infection Staphylococcus aureus

Streptococcus pyogenes
Enterococcus
Coag neg Staphylococci
Gm negatives
Anaerobes
Diabetic foot Staphylococcus aureus
Streptococci
Gm negatives (Pseudomonas, Proteus)
Anaerobes
 Septic arthritis (pathogenesis)

Haemtogenous spread Infected periarticular tissue

(OM, ulcers)

Joint

Infected prosthesis

Direct innoculation
(penetrating injuries, gunshots)
 Manifestations
• fever
• joint pain, usually severe
• joint swelling
• redness
• warmth
• limited use of extremity
• guarding or protecting of affected
joint
• children – irritability, refusal to feed,
pseudoparalysis
Septic arthritis
 Organism in
Septic Arthritis joint
(Pathogenesis)
Bacterial
Acute
products
inflammatory
reaction

Release of cytokines and other

products by PMNs

Cartilage
damage

Joint space
narrowing
 Diagnosis

• History
• Physical examination
• Lab investigations
• Radiological investigations
• Special tests
 Kocher criteria
• Special for hip septic arthritis
• Includes
1. Non weight bearing
2. Fever
3. ESR >40
4. WBC >12000
• Significant
– 4/4- 99% SA
– 3/4- 93%
– 2/4- 40%
– 1/4- 3%
Lab parameters in SA
PARAMETERS

Full blood count TWCC 

ESR and CRP 

(used in monitoring Rx)
X-ray
X-ray
 Others

• Blood culture – useful

• Joint aspiration – synovial fluid analysis, culture
and sensitivity
• Bone scan – increased uptake in affected joint
Joint aspiration
 Synovial fluid analysis in SA
Parameter Normal Inflammatory Septic
joint arthritis (Gout) arthritis

White cell count <2,000 2,000 – 80,000 > 80,000

(per l)

Glucose Serum < Serum << Serum

Protein Serum Serum >> Serum

Appearance Clear Thick yellow Greenish

turbid
 Treatment
• Antibiotics – according to the most
probable organism (3-4 weeks)
» Staph aureus – Cloxacillin
» Streptococcus - Penicillin
» Gonococcal – Ceftriaxone for 24-48H then oral
antibiotics for 7-10 days
• Analgesics (pain relief)
• Drainage – arthrotomy and lavage
• Splinting – acute stage (prevent
contracture)
• Physiotherapy (ROM, muscle
strengthening) – once pain 
Arthrotomy
 Complications

• Sepsis
• Joint damage – osteoarthritis
• Ankylosis (fused joint)
• OM
• Pathological dislocation (hip)
Thank You