Osteomyelitis

Osteomyelitis Inflammation of bone and marrow Types Pyogenic osteomyelitis Tuberculous osteomyelitis

Pyogenic Osteomyelitis

Pyogenic osteomyelitis Always caused by bacteria Routes of infection Hematogenous spread Extension from a contiguous site Direct implantation

Causes Staphylococcus aureus in 80% to 90% of cases E.coli, Pseudomonas, and Klebsiella in patients with genitourinary tract infections and IV drug abusers. In neonates: Hemophilus influenza and group B streptococci In patients with sickle cell disease –Salmonella infection

Morphology Acute Subacute Chronic

Organisms once localized in bone Bacteria proliferate and induce inflammatory reaction and cause cell death. Bone undergoes necrosis within first 48 hours Bacteria and inflammation spread within the shaft of the bone and may percolate throughout the haversian systems and reach the periosteum Subperiosteal abscess Segmental bone necrosis sequestrum (dead piece of bone) Rupture of periosteum leads to an abscess in the surrounding soft tissue and the formation of draining sinus.

Over time, host response develops After first week of infection chronic inflammatory cells become more numerous Cytokines from leukocytes stimulates osteoclastic bone resorption ingrowth of fibrous tissue deposition of reactive bone in the periphery Reactive woven or lamellar bone which forms sleeve of living tissue surrounding dead bone is called as involucrum.

Brodie abscess: is a small intraosseous abscess that frequently involves the cortex and is walled off by reactive bone Sclerosing osteomyelitis of Garre: typically develops in jaw and is associated with extensive new bone formation

PATHOLOGY Acute Infiltration of PMNs Congested or thrombosed vessels Chronic  Necrotic bone Absence of living osteocyte Mixed inflmmatory cells predominate Granulation & fibrous tissue

Osteomyelitis-gross & microscopy

Sequestrum (necrotic bone)

Involucrum (new bone)

Osteomyelitis of the tibia of a young child Osteomyelitis of the tibia of a young child. Numerous abscesses in the bone show as radiolucency.

Clinical manifestation HEMATOGENOUS OSTEOMYELITIS Clinical manifestation Classic presentation: Sudden onset High fever, Night sweats Fatigue, Anorexia, Weight loss Restriction of movement Local edema, Erythema, & Tenderrness

Clenched fist osteomyelitis

{ Diagnosis & work-up Lab study: HEMATOGENOUS OSTEOMYELITIS WBC  May be elevated, Usually normal C-Reactive Protein (CRP) Erythrocyte Sedimentation Rate (Usually is elevated at presentation Falls with successful therapy) Blood culture ( Acute osteomyelitis + ve > 50% ) {

Imaging Diagnosis & work-up Radiology: HEMATOGENOUS OSTEOMYELITIS Normal Soft tissue swelling Periosteal elevation Lytic change Sclerotic change

Complications of chronic osteomyelitis: Deformities of bones: Pathological fractures. Systemic effects such as chronic fever & fatigue. Amyloidosis of the AA type (secondary amyloidosis).This can get further deposited in the kidney, liver & blood vessels. Squamous cell carcinoma of the skin: The skin at the edges of the draining sinus tracts may undergo malignant transformation over time. Sepsis Rarely sarcoma in the infected bone

Specific forms of chronic osteomyelitis Forms of chronic osteomyelitis include: Brodie abscess, Tuberculous osteomyelitis, Osteomyelitis of congenital syphilis, and Osteomyelitis of acquired syphilis.

TB osteomyelitis: Dissemination of tuberculosis outside the lungs can lead to the appearance of skeletal TB: Skeletal Tuberculosis: Tuberculous osteomyelitis involves mainly the thoracic and lumbar vertebrae (known as Pott disease) followed by knee and hip. There is extensive necrosis and bony destruction with compressed fractures (with kyphosis) and extension to soft tissues, including psoas "cold" abscess.

Tuberculous osteomyelitis of the bone is secondary hematogenous spread from a primary source in the lung or GI tract. It most commonly occurs in the vertebrae (body) and long bones. Once established, the bacilli provoke a chronic inflammatory reaction. Small patches of caseous necrosis occur, and these coalesce to form larger abscesses. The infection spreads across the epiphysis into the joints. The infection may track along soft tissue to appear as a cold abscess at a distant site (eg: psoas abscess in case of spinal tuberculosis).

Spinal tuberculosis. Magnetic resonance imaging of the spine revealing osteomyelitis involving T10 and T11 vertebral bodies and disc space (A; arrow) and an adjacent multiloculated paravertebral abscess (B; arrow).

Psoas abscess: Computed tomographic scan of the abdomen showing a left iliopsoas abscess (arrow) that likely originated from tuberculous osteomyelitis involving the T12, L1, and L2 vertebrae.

Syphilitic osteomyelitis: The transplacental spread of spirochetes from mother to the fetus results in congenital syphilis. Long bones, such as the tibia, are mainly affected. Congenital syphilis has 2 forms: Periosteitis and osteochonditis.

Regarding acquired syphilis, bone lesions are manifestations of tertiary syphilis. Gummatous lesions appear as discrete punched-out radiolucent lesions in medulla or destructive lesions within the cortex. The surrounding bone is sclerotic, and no discharge is present. Bones frequently affected are those of nose, palate, skull and extremities, especially the long tubular bones such as tibia. Histology : edematous granulation tissue containing numerous plasma cells and necrotic bone.

“Sabre” tibia