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OSTEOMYELITIS
ACUTE OSSTEOMYELITISCHRONIC OSTEOMYELITIS
OSTEOMYELITISDEFINITION : inflammation of the boneOsteo= bone, myelitis= inflammation of the marrow
• Bone becomes infected either through1. haematogenous spread of organisms, or,2. secondary to a contiguous focus of infection. (invasion from a
skin puncture, operation or open fracture)
Contiguous-focus osteomyelitis:• bone infection with relatively normal vascularity and • bone infection with generalized vascular insufficiency (eg:
diabetic foot)
• Acute or chronic.
Anatomy of the bone
EPIDEMIOLOGY• Osteomyelitis affects about 2 in 10,000 people.• In children long bones • In adults vertebrae, feet, and the pelvis• Risk factors are recent trauma diabetes Hemodialysis IV drug abuse People who had splenectomy.
SKIN ABRASION, BOIL, SEPTIC TOOTH
HEMATOGENOUS SPREAD OF
ORGANISMIMPLANTED AT BONE
INFECTION OF ADJACENT
JOINT/SOFT TISSUEEXTENSIO
N TO THE BONE
PENETRATING WOUND, OPEN FRACTURE,
SURGERY TRAUMATIC AND IATROGHENIC
IMPLANTATION
SOURCES OF INFECTIONS
ACUTE HEMATOGENOUS OMPATHOGENESIS
• Bloodstream is invaded, perhaps from minor skin abrasion or boil or in the newborn from an infected umbilical cord
• In adults source of infection – arterial line or dirty needle and syringe
MICROBIAL INVASION
Organism usually settles in the metaphysis possibly because of – highly vascular hairpin arrangement of capillaries slows down the rate of blood flow (sluggish blood flow) has relatively fewer phagocytic cells than the physis or diaphysis thin cortex
• Terminal branches of metaphyseal artery form
loops at growth plate and enter irregular
afferent venous sinusoid. Blood flow
slowed and turbulent, predispose to bacterial seeding plus, lining cell
have little/no phagocytic action made it
favourable for bacteria.
Epiphysis
Looped capillary
Venous sinusoid
Metaphyseal artery
Foci of osteomyelitis
MICROBIAL INVASION
1)TRIGGER ACUTE INFLAMMATION
•Vascular congestion•Fluid exudation•PMN leukocyte infiltration
INCREASE INTRAOSSEOUS PRESSURE
intense pain and obstruction of blood flow
Growth plate
periosteum
2)SUPPURATION(2ND DAY)
Pus appears in the medulla and spread along Volkmann’s canals and elevate periosteum to forms a sub-periosteal abscess then spread along shaft• The pus can spread from here back into the bone, into an adjacent joint or into the soft tissues.
In infants, infxn often extends into epiphysis and thence into the joint. In older children the physis is a barrier to direct spread but where metaphysis is partly intracapsular (e.g. hip, shoulder, or elbow) pus may discharge through periosteum into the joint.
3)NECROSIS (END OF WEEK)
Rising intraosseous pressure, vascular stasis, infective thrombosis and periosteal stripping compromise the blood supply to the bone resulting in bone death and formation of a sequestrum.
4)NEW BONE FORMATION
At 10-14 days new bone forms from the deep layer of the stripped periosteum. With time, new bone thickens to form involucrum enclosing infected tissue and sequestra.
sequestrum
involucrum
Medullary cavity
5)RESOLUTION
if infection is controlled and intraosseous pressure released, the bone will heal
If infection persist, pus may discharge through
perforation in involucrum and track by sinus to the skin surface.
The condition is now established as a chronic
osteomyelitis
Over 90% of acute osteomyelitis cases are caused by Staphylococcus aureus but Streptococcus pyogenes and Haemophilus influenzae may also cause acute infection of the bone although infection with Haemophilus inflenzae is rare following the widespread use of the Hib vaccine. Pseudomonas aeruginosa is often isolated from intravenous drug abusers with vertebral osteomyelitis.
Aetiological agents
ACUTE HEMATOGENOUS OM
CLINICAL FEATURES
• In child, presented withpain, malaise and feverH/o preceding skin lesion, injury, sore throatLimb is held stillRestricted joint movementLocal redness, swelling, warmth and edema-
presence of pus
• In infant,Fails to thrive, drowsy and irritableh/o birth difficulties or umbilical artery
cathetherizationMetaphyseal tenderness and resistance to
joint movementLook for other sites – multiple infections
In adult, commonest site of hematogenous spread is spine – backache, mild fever
INVESTIGATIONBLOOD• FBC – leucocytosis• ESR AND CRP – elevated (CRP is a measurement of the acute phase response and is
especially useful in monitoring the course of treatment of acute osteomyelitis because it normalizes much sooner than the ESR.)
• Blood C&S
ASPIRATION AND BIOPSY aspiration of pus from subperiosteal abscess or the adjacent
joint send for bacteriological examination and sensitivity to antibiotics
IMAGING
1)Plain Radiograph or tomography (changes may lag by 10-14 days) – Early changes
• soft tissue swelling, blurring of fat plane and periosteal reaction – Intermediate changes
• bone destruction (ill defined lytic lesion)• Cloaca• Osteopenia
– Late Changes • Sequestrum formation • Involucrum and bony sclerosis
2. Nuclear medicine – Bone scan – can be confirmed earlier (48 hours)
• Technitium 99m-labeled phosphonate• Galium 67-labeled citrate• Indium-labeled leucocyte
– Increased uptake of tracer in bone scans and white cell scans.
– High sensitivity but other processes such as arthritis and soft tissue infection can appear similar. (lower specificity)
Increased uptake of radiopharmaceutical in the right femur just above the knee joint. Plain film reveals a large lytic area
Acute Osteomyelitis
Bone scan Radiograph of knee
Bone scans, both anterior (A) and lateral (B), showing the accumulation of radioactive tracer at the right ankle (arrow). This focal accumulation is characteristic of osteomyelitis.
Acute Osteomyelitis
Bone Scan of the foot
3. Magnetic Resonance Imaging (MR) – Demonstrate OM as early as isotope scanning– High sensitivity but other processes such as
fractures and tumors can be similar in appearance. – Excellent for demonstrating associated soft tissue
infection4. Computed Tomography
– Demostrate change in subacute and chronic OM• Sequestra• Cloacae• Periostitis• Soft tissue masses
5. Culture of fluoroscopically or CT guided aspirate • Confirm infection• Determine which organism is causing the infection • When the organism is isolated, then treat the patient with the
single appropriate antibiotic. – Lesion must first be visible with some form of imaging – Failure to grow an organism is common, especially if
patient has been treated with antibiotics – A positive culture gives a definitive diagnosis and identifies
organism and sensitivities
Complications
• Chronic OM • Bone abscess (pocket of pus) • Bone necrosis (bone death) • Spread of infection to the joint-septic arthritis other bones – metastatic osteomyelitis• Inflammation of soft tissue (cellulitis) • Growth disturbance if physis is damaged- leads to
shortening, deformity• Sepsis
TREATMENT
• PRINCIPLES OF TREATMENTProvide analgesia and general supportive
measuresTo rest the affected partTo initiate antibiotic treatmentTo undertake surgical eradication of pus and
necrotic tissue
1)ANTIBIOTICSInitially the choice of antibiotics based on examination and
best guess at the most likely pathogenMore appropriate drug can be subtitued once organism is
identify
Older children and previously fits adultProbably have staphylococcal infectionAntibiotic -intravenous flucloxacillin and fusidic acid ( may be
changed once results of sensitivity are known) -continued until there is clinical and laboratory evidence
of improvement (usually for 1-2 weeks) - followed by oral antibiotic for another 2-3 weeks
• Children under 4 years oldHigh incidence of haemophilus infectionAntibiotic: third generation cephalosporin 2)ANALGESICS- paracetamol3) SPLINTAGE Complete bed rest is essential.Splint could be used but should not conceal
affected area.
4)DRAINAGEIf antibiotics given early, drainage may not be
necessaryIf subperiosteal abscess can be detected, or if pyrexia
and local tenderness persists >24 hr after tretment with adequate antibiotics, the pus should be let out.
About 30% of patient with confirmed OM are likely to need an operation
5)FOLLOW UPOnce infection subsided, movement are encouragedto look for recurrence of infection