OSTEOMYELITIS DEFINITION : inflammation of the bone Osteo= bone, myelitis= inflammation of the marrow Bone becomes infected either through haematogenous spread of organisms, or, 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.
EPIDEMIOLOGY Osteomyelitis affects about 2 in 10,000 people. In childrenlong bones In adults vertebrae, feet, and the pelvis Risk factors are recent trauma diabetes Hemodialysis IV drug abuse People who had splenectomy.
SOURCES OF INFECTIONS INFECTION OF ADJACENT JOINT/SOFT TISSUEEXTENSION TO THE BONE PENETRATING WOUND, OPEN FRACTURE, SURGERY TRAUMATIC AND IATROGHENIC IMPLANTATION SKIN ABRASION, BOIL, SEPTIC TOOTH HEMATOGENOUS SPREAD OF ORGANISMIMPLANTED AT BONE
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
Foci of osteomyelitis Epiphysis 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. Looped capillary Venous sinusoid Metaphyseal artery
INCREASE INTRAOSSEOUS PRESSURE intense pain and obstruction of blood flow
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. Growth plate periosteum 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 intraosseouspressure, vascular stasis, infective thrombosis and periostealstripping compromise the blood supply to the bone resulting in bone death and formation of a sequestrum. 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. 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 aureusbut Streptococcus pyogenesandHaemophilusinfluenzaemay also cause acute infection of the bone although infection with Haemophilusinflenzae is rare following the widespread use of the Hib vaccine. Pseudomonas aeruginosais often isolated from intravenous drug abusers with vertebral osteomyelitis. Aetiological agents
In adult, commonest site of hematogenous spread is spine – backache, mild fever
INVESTIGATION BLOOD 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)
Acute Osteomyelitis Bone scan Radiograph of knee Increased uptake of radiopharmaceutical in the right femur just above the knee joint. Plain film reveals a large lytic area
Acute Osteomyelitis Bone Scan of the foot 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.
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 infection 4.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
-intravenous flucloxacillinand 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