Osteomyelitis
Osteomyelitis
Osteomyelitis
• Def : Infection of bone characterized by progressive inflammatory
destruction and apposition of new bone
• Risk factors :
• recent trauma or surgery
• immunocompromised patients
• illicit IV drug use
• poor vascular supply
• systemic conditions such as diabetes and sickle cell
• peripheral neuropathy
Classification
• In infants - infection often extends through the physis into the epiphysis and then into the
joint.
• In older children - the physis is a barrier to direct spread but where the metaphysis is partly
intracapsular pus may discharge through the periosteum into the joint.
• In adults - the abscess is more likely to spread within the medullary cavity. Vertebral infection
may spread through the end-plate and the intervertebral disc into adjacent vertebral body.
Pathophysiology
3. Necrosis (by the end of the week)
• The rising intraosseous pressure, vascular stasis, infective thrombosis and periosteal stripping
increasingly compromise the blood supply bone death. Bacterial toxins and leucocytic
enzymes also may play their part in the advancing tissue destruction.
• With the gradual ingrowth of granulation tissue the boundary between dead and living bone
becomes defined sequestrum (piece of dead bone separated from the sound bone in necrosis)
• Macrophages and lymphocytes arrive in increasing numbers and the debris is slowly removed by
a combination of phagocytosis and osteoclastic resorption. However, larger sequestra remain
entombed in cavities of bone, inaccessible to either final destruction or repair.
Pathophysiology
4. New Bone Formation (by the 2nd week)
• New bone forms is laid down beneath the stripped-up periosteum.
• With time the new bone thickens to form an involucrum (new bone enclosing the infected tissue and
sequestra)
• If the infection persists, pus may continue to discharge through perforations (cloacae) in the
involucrum and track by sinuses to the skin surfaces. The condition is now established as a
chronic osteomyelitis.
Pathophysiology
5. Resolution and Healing
• If infection is controlled and intraosseous pressure released at an early stage, progression to
chronic osteomyelitis can be aborted. But when infection has progressed to the stage of septic
thrombosis and death of bone it almost inevitably passes into a state of chronic osteomyelitis .
• The bone around the zone of infection is at first osteoporotic (probably d/t hyperemia). With
healing, there is fibrosis and appositional new bone formation; this, together with the periosteal
reaction, results in sclerosis and thickening of the bone.
• Remodelling may restore the normal contours of the bone, but the bone may be left permanently
deformed.
Pathobiology
• Biofilm formation
• Planktonic bacteria attach to an inert substrate and undergo apoptosis to create a matrix for
biofilm
• Biofilm is characterized by bacteria entering a no-growth, or sessile, phase, which makes
them even more resistant to antibiotics that depend on replication to carry out their effect
• biofilm is then made of an extracellular polymeric substance or exopolysaccharide
• antibiotics are less effective due to difficulty penetrating the biofilm and bacteria lowering
their metabolic rate
Clinical Features
ACUTE
• Pain & tenderness over affected bone
• Fever
• Joint movement is restricted and even the gentlest manipulation is painful. However, the
neighbouring joint may not be infected but may be distended with clear fluid good range of
movement is retained
CHRONIC
• Pain, redness and tenderness have recurred (a ‘flare’), or with a discharging sinus
• Fever
• Long-standing cases - tissues are thickenend and often puckered or folded in where a scar or
sinus is attached to the underlying bone
• Seropurulent discharge and excoriation of the surrounding skin
Investigation
1. X-ray (Diagnostic imaging)
• Normal during the first 10 days
• By the end of the 2nd week → periosteal new bone formation (classic x-ray sign of pyogenic
osteomyelitis)
• Later → patchy rarefaction of the metaphysis surrounded by sclerosis ± sequestra
• Ragged appearance of bone destruction and healing
2. Radioisotope scanning
• 99mTc-HDP scans show increased activity in both the perfusion phase and the bone phase. Such
scans are useful for showing up hidden foci of infection.
Investigation
3. FBP
• WBC
• [Hb]
• ESR
• Antistaphycoccal titres
4. Blood culture
5. Aspiration from the metaphyseal subperiosteal abscess or the adjacent joint. Even if no pus is
found, a smear of the aspirate is examined immediately for cells and organisms - gram-stain,
C&S.
Investigation
6. CT
• assist in diagnosis and surgical planning by identifying necrotic bone
7. MRI
• assists in the diagnosis and surgical planning
• best test for diagnosing early osteomyelitis and localizing infection
• T2 sequences will show bone and soft tissue edema
• Findings : penumbra sign
• T1 - dark central abscess with bright internal wall and dark external sclerotic rim
Management
1. Antibiotic therapy
• Empirical antibiotics first, change when C&S returns