Osteomyelitis Epidemiology Osteomyelitis and suppurative arthritis are most

Osteomyelitis

Epidemiology. • Osteomyelitis and suppurative arthritis are most common in young children – 1/3 cases < 2 y/o – 1/2 cases < 5 y/o • boys : girls, usually 2: 1 • 1/3 cases have minor, closed trauma

Etiology. • A microbial etiology is confirmed in about 3/4 of cases of osteomyelitis • Staphylococcus aureus – the most common infecting organism in all age groups • Group B streptococcus and gram-negative enteric bacilli – prominent pathogens in neonates • group A streptococcus – less than 10% of all cases • After 6 yr of age, most are S. aureus

Etiology. • Exclusive. – puncture wounds of the foot: Pseudomonas aeruginosa – sickle cell anemia: Salmonella and S. aureus • other consideration: – penetrating injuries: atypical mycobacteria – Fungal infections usually occur as part of multisystem disseminated disease – Candida osteomyelitis sometimes occursin neonates with indwelling vascular catheters • Primary viral infections of bones--> rare; – but complain of arthralgia or arthritis may be due to immune responce

Pathogenesis • In newborns and young infants: – transphyseal blood vessels connect the metaphysis and epiphysis – common for pus from the metaphysis joint space • latter part of the first year of life, the physis forms – obliterating the transphyseal blood vessels • later childhood the periosteum becomes more adherent, – favoring pus to decompress through the periosteum • growth plate closes in late adolescence – begins in the diaphysis, and can spread to the entire intramedullary canal

Pathogenesis. • In the metaphysis, nutrient arteries branch into nonanastomosing capillaries under the physis, which make a sharp loop before entering venous sinusoids draining into the marrow • bacterial focus established --> phagocytes --> inflammatory exudates --> metaphyseal space-Halverson system and Volkmann canals) --> subperiosteal space --> impairing blood supply to the cortex and metaphysis

Clinical Manifestations. • signs and symptoms highly dependent on the age, • earliest signs and symptoms are often subtle • latent period of 10 to 12 days between the time of onset of clinical symptoms and the development of definite radiographic changes in bone. • Neonates: – pseudoparalysis – Half of do not have fever , may not appear ill

Clinical Manifestations. • Older infants and children – fever, pain, and localizing signs such as edema, erythema, and warmth – limp or refusal to walk • Local swelling and redness with osteomyelitis may mean that the infection has spread out of the metaphysis into the subperiosteal space, representing a secondary soft tissue inflammatory response

Clinical Manifestations.

Clinical Manifestations. • upper extremities account for one fourth of all cases. Flat bones are less commonly • Several bones or joints are infected in fewer than 10% of cases – exceptions are gonococcal infections and osteomyelitis in neonates • two or more bones are involved in almost half of the cases

Diagnosis. • Take samples: – Aspiration of the infected site for Gram stain and culture • steel needle is needed to penetrate the cortex into the metaphysis. • If pus is encountered in the subperiosteal space, there is no need to go farther. – If gonococcus is suspected, • cervical, and throat cultures should also be obtained – blood culture should be performed

Diagnosis. • Other Lab. Exam – no specific laboratory tests for osteomyelitis – CBC/DC, ESR, CRP--> very sensitive but not specific – normal test results cannot r/o osteomyelitis – can monitor dz progress

Diagnosis. • RADIOGRAPHIC EVALUATION. • Plain Radiographs. – Within 72 hours of onset of symptoms of osteomyelitis – soft tissue technique, displacement or obliteration of the normal fat planes adjacent to deep muscle – compared to the opposite extremity, – can show displacement of the deep muscle

Diagnosis. • • Examination obtained 10 days after the onset B: Repeat examination 1 week

Diagnosis. • Plain Radiographs. – minimal amount of periosteal new-bone formation laid down parallel to the outer margin of the cortex – The actual disease process is usually much more extensive than showed by radiograph

Diagnosis. • Examination 7 days after the onset • 3 months later shows extensive new-bone formation

Diagnosis. • Ultrasonography. – detecting joint effusion and fluid collection in the soft tissue and subperiosteal regions – may guide localization for aspiration or drainage.

Diagnosis. • Computed Tomography and Magnetic Resonance Imaging. – CT is ideal for detecting gas in soft tissues – Increased attenuation occurs within the bone marrow early in the disease due to edema and pus

Diagnosis. • MRI is the best radiologic imaging technique for the identification of abscesses and for differentiation between bone and soft tissue infection – acute osteomyelitis, purulent debris and edema appear dark with decreased signal intensity on T 1 weighted images opposite is seen in T 2 weighted images – for possible surgical intervention – MRI is particularly useful in the evaluation of vertebral osteomyelitis and diskitis clear delineation

Diagnosis. • MRI – MRI does not reliably distinguish osteomyelitis from noninfectious bone marrow edema – not sensitive to changes within the cortex

Diagnosis. • Radionuclide Studies. – be valuable especially if multiple foci are suspected – Technetium-99 methylene diphosphonate (99 m Tc), which accumulates in areas of increased bone turnover – 99 m. Tc 3 phase perfusion, blood pool, and delayed images – Any areas of increased blood flow or inflammation cause increased uptake of 99 m Tc in the • first phase (5– 10? min) and • second phase (2– 4? hr), • but osteomyelitis causes increased uptake of 99 m Tc in the third phase (24? hr)

Diagnosis. • Radionuclide Studies. – sensitivity (84– 100%) and specificity (70– 96%) – can detect osteomyelitis within 24– 48? hr after onset of symptoms – Gallium-67 uptake, Indium-111 leukocytes is more specific for infection – sensitivity in neonates is much lower owing to poor bone mineralization

Treatment. • Optimal treatment of skeletal infections requires collaborative efforts of pediatricians, orthopedic surgeons, radiologists, and physiatrists • one should not wait for the development of radiographic evidence of disease before treatment • empirical antibiotic – antistaphylococcal penicillin, such as nafcillin or oxacillin, and a broad-spectrum cephalosporin, such as cefotaxime – aminoglycoside may be take place of cephalosporin • but reduced antibacterial activity in sites with decreased oxygen tension and low p. H

Treatment • In infants and children younger than 5 yr of age – Cefuroxime • After 5 yr of age and in the absence of special circumstances – nafcillin or cefazolin • With sickle cell disease , gram-negative enteric bacteria are common – broad-spectrum cephalosporin such as cefotaxime or ceftriaxone

Treatment • When the pathogen is identified, appropriate adjustments in antibiotics are made • If a pathogen is not identified and a patient's condition is not improving – re-aspiration or biopsy – Recheck diagnosis

Treatment • Duration of antibiotic (1) the patient shows prompt resolution of signs and symptoms (within 5– 7 days) and (2) the ESR has normalized; a total of 4– 6 wk of therapy may be required – S. aureus or gram-negative bacillary infections, the minimum duration of antibiotics is 21 days – group A streptococcus, S. pneumoniae, or H. influenzae type b, antibiotics minimum of 10– 14 days – Pseudomonas postoperative need total of 7 d treatment – Immunocompromised, mycobacterial or fungal infection patients generally require prolonged courses

Treatment • Oral route – Changing antibiotics from the intravenous route to oral administration when a patient's condition has stabilized, generally after 1 wk – serum bactericidal titers, or Schlichter titers, 45– 60? min after a dose of suspension or 60– 90? min after a capsule or tablet. • A serum bactericidal titer of 1: 8 or more is considered desirable – ß-lactam drugs for staphylococcal or streptococcal infection, a dosage 2~3 times that used for other infections is prescribed

Treatment • SURGICAL THERAPY. – When frank pus is obtained from subperiosteal or metaphyseal aspiration a surgical drainage procedure is usually indicated. – penetrating injury and when a retained foreign body – Infection of the hip is considered a surgical emergency – chronic osteomyelitis consists of surgical removal of sinus tracts and sequestrum Antibiotic therapy is continued for several months until clinical and radiographic

Prognosis. • Failure to improve or worsening by 72? hr requires review of the appropriateness of the antibiotic therapy • CRP typically normalizes within 7 days after start of treatment; ESR typically rises for 5– 7 days, then falls slowly; dropping sharply after 10– 14 d • Recurrence of disease and development of chronic infection after treatment < 10% of patients • initiation of medical and surgical therapy < 1 wk of onset of symptoms better prognosis

SUBACUTE AND CHRONIC OSTEOMYELITIS • Bone Abscess – lucency area surrounded by an irregular zone of dense sclerosis. – The overlying cortex is usually thickened by periosteal new-bone formation

SUBACUTE AND CHRONIC OSTEOMYELITIS • Involucrum and Sequestrum Formation – Sequestra become avascular by losing their • periosteal supply: periosteum is stripped, elevated from cortex • intramedullary supply: infection causes vascular thrombosis • areas of dense bone surrounded by zones of lucency

SUBACUTE AND CHRONIC OSTEOMYELITIS – involucrum is a shell of bone formed by the periosteum that surrounds and encloaks a sequestrum – Involucrum and sequestrum formation in osteomyelitis more common in children than in adults – MRI: • focus of active infection is similar to that of a bone abscess, low on T 1, higher than marrow on T 2, surrounded by a low-intensity rim on both

DIFFERENTIAL DIAGNOSIS. • • • trauma Neuroblastoma Primary bone tumors Cellulitis DVT

• Cellulitis – skin infection, soft-tissue swelling is superficial and does not involve the deeper tissues adjacent to the bone.

Neuroblastoma – arises from sympathetic nervous tissue, often within the adrenal gland. – A palpable mass in the abdomen may be the first evidence – metastatic neuroblastoma is the most common malignant-appearing tumor before the age of 1 year in bone tumor – Calcification often is visible within the primary tumor

Neuroblastoma • X-ray – cranial sutures are spread – In the skull: Thin, whisker-like calcifications frequently extend out and inward – long tubular bones: • moth-eaten, and the cortex often eroded • Periosteal new-bone formation may parallel the cortex or form thin spiculations at right angles to the cortex – Ewing's tumor, neuroblastoma, and leukemia, may have a similar radiographic appearance, particularly in the long bones.

Neuroblastoma

Neuroblastoma

Ewing's tumor • malignant tumor arising in the red bone marrow and closely related histologically to reticulum cell sarcoma • Mostly: 5 ~ 25 y/o ; rarely after 30 y/o; male> female • long bones, extremities, femur, metaphysis – Exception: > 20 y/o, flat bones > long bones • Metastasize easy, multiple lesions may be present • symptoms : pain, swelling; often fever and leukocytosis, like osteomyelitis

Ewing's tumor • (L) Laminated, onionskin, periosteal new-bone formation • (R) permeative destruction and a well-defined, laminated Codman's triangle

Ewing's tumor • X-ray – permeative, poorly marginated, destructive lesion that perforates the cortex – overlaid by a laminated, , onionskin periosteal reaction – Others may find: Codman's triangles, Fine spicules, – In the long bones, differentiation of Ewing's tumor and osteomyelitis may be difficult