Osteomielita Lb.eng

8/12/2019 Osteomielita Lb.eng

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Osteomyelitis


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Osteomyelitis

Inflammation of bone and marrow

Types

Pyogenic osteomyelitisTuberculous osteomyelitis


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Pyogenic

Osteomyelitis


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Pyogenic osteomyelitis

Always caused by bacteria

Routes of infection

Hematogenous spread Extension from a contiguous site

Direct implantation


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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


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Morphology

Acute

Subacute

Chronic


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Organisms once localized in bone

Bacteria proliferate and induce inflammatory reaction and cause celldeath.

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 theperiosteum

Subperiosteal abscess

Segmental bone necrosissequestrum (dead piece of bone)

Rupture of periosteum leads to an abscess in the surrounding softtissue and the formation of draining sinus.


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Over time, host response develops

After first week of infection chronic inflammatory cellsbecome more numerous

Cytokines from leukocytes stimulates osteoclastic boneresorptioningrowth of fibrous tissuedeposition ofreactive bone in the periphery

Reactive woven or lamellar bone which forms sleeve of

living tissue surrounding dead bone is called asinvolucrum.


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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


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PATHOLOGY

Acute Infiltration of PMNsCongested or thrombosed vessels

Chronic Necrotic boneAbsence of living osteocyteMixed inflmmatory cells

predominateGranulation & fibrous tissue


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Osteomyelitis-gross & microscopy


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Sequestrum (necrotic bone)


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Involucrum (new bone)


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Osteomyelitis of the tibia of a

young child. Numerousabscesses in the bone show

as radiolucency.
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HEMATOGENOUS OSTEOMYELITIS

Clinical manifestationClassic presentation: Sudden onset

High fever, Night sweatsFatigue, Anorexia, Weight lossRestriction of movement

Local edema, Erythema, & Tenderrness
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lenched fistosteomyelitis
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Diagnosis & work-upLab study:

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% )

{


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Diagnosis & work-up

ImagingRadiology:NormalSoft tissue swellingPeriosteal elevationLytic changeSclerotic change


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Complications of chronic osteomyelitis:

1) Deformities of bones:

2) Pathological fractures.

3) Systemic effectssuch as chronic fever & fatigue.

4)

Amyloidosis of the AA type(secondaryamyloidosis).This can get further deposited in thekidney, liver & blood vessels.

5) Squamous cell carcinoma of the skin:The skin atthe edges of the draining sinus tracts may undergo

malignant transformation over time.6) Sepsis

7) Rarely sarcoma in the infected bone


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Specific forms of chronic osteomyelitis

Forms of chronic osteomyelitis include:

Brodie abscess,

Tuberculous osteomyelitis,

Osteomyelitis of congenital syphilis, and Osteomyelitis of acquired syphilis.


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TB osteomyelitis:

Dissemination of tuberculosis outside the lungscan lead to the appearance of skeletal TB:

Skeletal Tuberculosis:

Tuberculous osteomyelitis involves mainly thethoracic and lumbar vertebrae (known as Pottdisease) followed by knee and hip.

There is extensive necrosis and bony destruction

with compressed fractures (with kyphosis) andextension to soft tissues, including psoas "cold"abscess.


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Tuberculous osteomyelitis of the bone is secondaryhematogenous 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 acold abscess at a distant site (eg: psoas abscess in caseof spinal tuberculosis).


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Spinal tuberculosis. Magnetic resonance imaging of the spinerevealing osteomyelitis involving T10 and T11 vertebral bodies

and disc space (A; arrow) and an adjacent multiloculated

paravertebral abscess (B; arrow).


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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.


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Syphilitic osteomyelitis:

The transplacental spread of spirochetes from motherto the fetus results in congenital syphilis.

Long bones, such as the tibia, are mainly affected.

Congenital syphilis has 2 forms:

Periosteitis and osteochonditis.


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Regarding acquired syphilis, bone lesions are manifestations oftertiary syphilis.

Gummatous lesions appear as discrete punched-out radiolucentlesions 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.


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Sabre tibia

Osteomielita Lb.eng

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