It is generally agreed that
acute osteomyelitis arises from the presence of a blood borne nidus or embolus
of pathogenic organisms which is deposited by the blood stream in the end
of the metaphysis of a growing bone. Joint infection presumably arises from
a similar nidus being implanted in synovial membrane although it may be associated
with metaphysial bone infection when the joint capsule and synovium pass beyond
the epiphyseal cartilage (e.g. in the hip), and in the neonate (see below).
In neonates there is vascular communication between the metaphysis and the epiphysis, thus osteomyelitis in the metaphysis can easily spread to the epiphysis and give rise to septic arthritis in this age group.
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Osteomyelitis in the newborn -
with a probable pathological hip dislocation. |
In bone the nidus of organisms results in
death of local bone and the early formation of pus (i.e. an abscess). If this
infection is treated early with antibiotics (possibly up to the first three
days) the infection may be controlled but more usually considerable pus appears,
and this passes through the bone and produces a sub-periosteal abscess. If
untreated this will rupture into the soft tissues, or even through the skin.
| Death of bone is usually followed
by the radiographic appearance of one or more sequestrae (fragment/s of
dead bone), and although in young children (and in the absence of any
sinus) these may absorb with adequate antibiotic therapy and appropriate
rest, they more often remain as infected dead material which the body
tries to dissolve and ‘expel’ by pus formation (the chronic
stage). |
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| Sequestration of the radial shaft with massive involucrum. The right hand X-ray is after sequestrectomy. |
Fortunately the periosteum in the region
of the acute bone infection usually remains viable and will produce a shell
of sub-periosteal new bone – the involucrum. This is likely to contain
one or more cloaca (drainage holes) through which pus, and occasionally entire
or small fragments of sequestrae may discharge.
Rarely the local periosteum may have been killed
by the severity of the original infection, or may have been destroyed in an
open fracture. In this situation little or no involucrum will form and this
will make surgical treatment even more difficult.
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| A severe infection may kill the periosteum, resulting in poor or no involucrum formation. | A severe infection may kill the periosteum, resulting in poor or no involucrum formation. |
In acute septic arthritis the infection usually remains within the affected joint which will rapidly fill up with pus. Bacterial and serum enzymes in the pus are responsible for damage to the hyaline cartilage of the joint, although this may not be obvious to the naked eye. Therefore, in the early stages of septic arthritis the cartilage may appear normal. Similarly when a joint destroyed by septic arthritis is explored at a late stage there may appear to be healthy cartilage but this is likely to be fibro-cartilage.
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Chronic osteomyelitis may result from an inadequately or late treated acute infection and is considered to have appeared when there is formation of a sequestrum, hopefully involucrum formation, and discharge of pus. |
Sequestration with some involucrum
formation |
Chronic ostoemyelitis can also arise (as can chronic
septic arthritis) as a result of infection with the tubercle bacillus or with
certain fungi (maduramycosis, actinomycosis). The pathological processes are
similar but microscopically the former will contain the caseation, giant cells,
and epithelial tissue of a tubercle, and in the latter the actual infecting
fungus will be visible under the microscope. Rarely Ziehl-Nielsen staining
will demonstrate acid-fast bacilli. These can more often be cultured by appropriate
means although this can take several weeks. Tuberculous and fungal pus formation
usually results in cold abscesses although superadded secondary bacterial
infection can cause the more classical signs of an acute or sub-acute infection.
These chronic infections result in slow destruction
of bone, and there may be less obvious formation of sequestrae. However, some
fungal infections produce pathogonomic radiological changes, with a ‘radiating’
pattern of new bone formation associated with areas of bone destruction.
An acute bone or joint infection rarely
follows an open injury, but may develop a few days after a joint aspiration,
arthroscopy or open reduction of a fracture and insertion of foreign material
(plates, screws etc. having been used to maintain the reduction). Again the
most common organism is the staphylococcus and these infections are considerably
more likely to occur in immuno-suppressed individuals (HIV/Aids, Steroids
and possibly Non-Steroidal Anti-Inflammatory drugs).
| Thus the decision to open a closed
fracture, or to introduce an instrument into a joint must never be taken
lightly as disaster (and even death) can result. Great care with sterility
is essential (especially in the presence of immune-suppression) and in
many circumstances it is wise to use conservative management to treat
closed fractures, particularly where conditions for operating are not
ideal. |
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| An infected K nail, with somewhat tenuous union. |
The extent of bone destruction resulting
from an acute osteomyelitis can vary enormously, and radiological changes
lag behind what is actually happening in the bone. Thus there may be a real
risk of a pathological fracture in normal looking bone, and limbs may have
to be protected with appropriate splints or traction for many weeks (plaster
gutters are very useful for this, as they can be removed for wound inspection,
and for gentle assisted joint movements), and until there is good clinical
and radiological evidence that adequate healthy bone remains, or has been
formed.