infection of bone

1. BONE & JOINT
INFECTION

2. ACUTE OSTEOMYELITIS
• DENOTES INFECTION OF CORTICAL
BONE & BONE MARROW
• ETIOPATHOGENESIS
• HAEMATOGENOUS SPREAD FROM
DISTANT FOCI
• DIRECT INVASION FROM INFECTED
WOUND OR JOINT
• ORGANISM –bacteria-most commonly
STAPH AUREUS.

3. CLINICAL FEATURES
SEEN 7-10 DAYS AFTER ONSET OF
INFECTION
PAIN, FEVER,CHILL
SOFT TISSUE SWELLING,
REDNESS

4. X-RAY FINDING
 SWELLING WITH EDEMA &BLURRING
OF FAT PLANES
 SMALL SINGLE OR MULTIPLE LUCENCY
AFFECTING METAPHYSES
 ELAVATION OF PERIOSTEUM
&LAYERED NEW BONE FORM
 PERIOSTEAL REACTION –LAMELLAR
 OSTEOPENIA IN SURROUNDING BONE
DUE TO HYPERAEMIA

5. MRI FINDINGS
 HIGHLY SENSITIVE
 IMAGING MODALITY OF CHOICE IN EARLY STAGE
 SHOWS LOW SIGNAL INTENSITY ON TI &HIGH
SIGNAL INTENSITY ON T2 &FAT SUPPRESSED &
STIR SEQ
 SHOWS POST CONTRAST ENHANCEMENT
 INTRAOSSEOUS,SUBPERIOSTEAL & SOFT TISSUE
ABCESS IF PRESENT APPEAR AS WELL
CIRCUMSCRIBED AREA OF LOW SIGNAL ON T1 HIGH
SIGNAL ON T2 &SHOWING RIM ENHANCEMENT

6. USG
 SHOWS COLLECTION OF FLUID IN THE
AREA BENEATH PERIOSTEUM

7. BRODIES ABCESS
 A SUBACUTE LOCALISED TYPE OF
OSTEOMYELITIS,FOUND IN CANCELLOUS
TISSUE NEAR END OF BONE.
 CAUSED BY ORGANISMS OF LOW
VIRULENCE .
 ON XRAY-WELL CIRCUMCSRIBED AREA
OF BONE DESTRUCTION HAS A
SURROUNDING ZONE OF REACTIVE
SCLEROSIS SOMETIMES ACCOMPANIED
BY PERIOSTEAL REACTION

8.  CT DEMONSTATES CENTRAL
NECROSIS & SEQUESTRATION OF THE
LESION WITH LOCAL SURROUNDING
SCLEROSIS
 MRI SHOWS HYPERINTENSE NIDUS ON
T2 WITH SCLEROTIC RIM.

9. CHRONIC
OSTEOMYELITIS
 RESULTS FROM INADEQUATELY
TREATED OSTEOMYELITIS
 FROM INFECTION FOLLOWING
COMPOUND FRACTURE
 IATROGENIC CAUSE –JT
REPLACEMENT &INTERNAL FIXATION
OF FRACTURE
 INFECTION WITH MYCO.
TUBERCULOSIS &TREP PALLIDUM

10. CLINICAL FEATURES
 PAIN ,LOCAL SWELLING
 PUS DISCHARGE &SINUS FORMATION
 SYSTEMIC SYMPTOMS-FEVER &
MALAISE

11. PATHOGENESIS
 DIRECT INVASION OF SYNOVIAL
MEMBRANE BYPENETRATING
WOUND,POSTSURGICAL JOINT
REPLACEMENT
 INFECTION OF ADJACENT TISSUE
 HEMATOGENOUS SPREAD FROM
BLOOD BORNE INFECTION
 SPREAD FROM OSTEOMYELITIS

12. FEATURES OF CHRONIC
OSTEOMYELITIS
 INVOLUCRUM-THICK PERIOSTEUM
AROUND INFECTED BONE
 SEQUESTRUM- PIECE OF DEAD
INFECTED BONE
 CLOACAE-OPENING IN CORTEX
THROUGH WHICH PUS ESCAPE

13. X RAY FINDINGS
SCLEROTIC & LUCENT AREA ADMIXED
WITH BONE THICKENING
IRREGULARITIES & DEFORMITIES
SEQUESTRUM REMAIN AS AVASCULAR
ISOLATED SEGMENT DENSER THAN
SURROUNDING BONE
SINUS TRACT – SEEN AS ALUCENT TRACK
EXTENDING IN CONTIGUITY FROM
MEDULLARY CAVITY WITH DISRUPTION
OF CORTEX.

14. CT FINDINGS
 CT ADDS GREATER ANATOMICAL
DETAIL TO CHANGES IN CHRONIC
OSTEOMYELITIS
 SEQUESTRA REMAIN AS HIGH
ATTENUATION SPICULES OF BONE IN
AREAS OF OSTEOLYSIS
 CLOACAE, PERIOSTITIS & LOCAL SOFT
TISSUE MASSES ARE WELL DEPICTED

15. MRI
 DEVITALISED BONE SHOW LOSS OF
SIGNAL & DOES NOT ENHANCE .
 SINUS TRACT SEEN AS A LINEAR AREA
OF LOW SIGNAL ON T1W & HIGH
SIGNAL ON T2W & STIR IMAGES.
 SOFT TISSUE INFLAMMATION SEEN AS
BRIGHT SIGNAL ON T2, SHOWING
ENHANCEMENT AFTER CONTRAST

16. SCLEROSING
OSTEOMYELITIS OF GARRE
 A RARE TYPE OF CHRONIC
OSTEOMYELITIS IN CHILDREN &YOUNG
ADULTS PRESENTING WITH INSIDIOUS
ONSET OF PAIN
 SYMPTOMS RECUR AT INTERVALS & THE
SUBSIDE GRADUALLY
 RADIOLOGICAL APPEARANCE IS THAT OF
INTENSE SLEROSIS RESULTING IN
THICKENED BONE.AREAS OF FRANK
BONE DESTRUCTION RARE

17. PYOGENIC ARTHRITIS
 ARTHRITIS OF INFECTIVE ORIGIN
 MOST COMMONLY BY STAPHYLOCOCCUS,
STREPTOCOCCUS

18. PATHOGENESIS
 FORMn OF PUS IN BONE DEPRIVES LOCAL CORTEX
& MEDULLA OF BLOOD SUPPLY
 DEAD BONE RESORBED BY GRANULATION TISSUE
 PIECES OF BONE NOT RESORBED REMAIN AS
SEQUESTRA
 SEQUESTRA BEING DEVITALISED REMAIN DENSER
THAN SURROUNDING BONE
 INVOLUCRUM FORM BENEATH VITAL PERIOSTEUM
ELEVATED BY PUS
 IN AREA OF DEAD PERIOSTEUM, DEFECTS IN
INVOLUCRUM OCCURS-RESULTING IN CLOACA
 CLOACA ALLOW PUS & SEQUESTRUM TO ESCAPE
VIA SINUS

19. IMAGING
 XRAY
 ARTHROGRAPHY
 USG
 CT
 MRI

20. XRAY
 MODALITY OF CHOICE FOR INITIAL EVALUATION
 EARLY FINDINGS-JOINT EFFUSION,SOFT
TISSUE SWELLING,PERIARTICULAR
OSTEOPOROSIS DUE TOHYPERAEMIA,
 LATE FINDINGS-MARGINAL &CENTRAL EROSION
OF SUBCHONDRAL
BONE,SUBLUXATION,DISLOCATION,JOINT
SPACE REDUCTION&BONY ANKYLOSIS

21. ARTHROGRAPHY
 RADIOGRAPHS OBTAINED AFTER CONTRAST
INJECTION REVEAL-
 DESTRUCTION OF ARTICULAR CARTILAGE
 HYPERTROPHY OF SYNOVIUM
 IRREGULAR JOINT CAPSULE IN CHRONIC
INFECTION

22. ULTRASOUND
 SENSITIVE TECHNIQUE FOR
DEMONSTRATING EFFUSION

23. CT
 USED TO GUIDE JOINT ASPIRATION
 CT FINDINGS INCLUDE-JOINT
EFFUSION,IRREGULARITY
&NARROWING OF JOINT ,SOFT TISSUE
SWELLING, SUBBCHONDRAL BONE
DESTRUCTION &ARTICULAR EROSION

24. MRI
OVERTLY SENSITIVE HOWEVER
EXPENSIVE
EARLY STAGE SHOWS DISTENSION OF
JOINT WITH FLUID WHICH APPEARS
HYPERINTENSE ON T2
LATER STAGE SHOWS CARTILAGE
DESTRUCTION,JT SPACE
REDUCTION,SPREAD OF INFECTION
TO ADJACENT BONE &SOFT TISSUE

25. POTT”S SPINE
 MOSTFREQUENT SITE OF BONE
INVOLVEMENT BY TUBERCULOSIS
 DEFINED AS AN INFECTION BY
mycobacterium tuberculosis. OF ONE OR
MORE OF THE EXTRADURAL
COMPONENTS OF SPINE-
VERTEBRA,IV DISC,PARASPINAL SOFT
TISSUE &EPIDURAL SPACE.

26. PATHOGENESIS
 SPREAD USUALLY BY THE HEMATOGENOUS
ROUTE BY PERIVERTEBRAL ARTERIAL OR
VENOUS PLEXUS, ARTERIAL BEING MORE
COMMON
 INFECTION BEGINS IN CANCELLOUS AREA OF
VERTEBRAL BODY, COMMONLY IN PARADISCAL
LOCATION.VERTEBRA BECOMES SOFT & EASILY
COMPRESSED TO PRODUCE WEDGING OR
COLLAPSE.DISC RESIST INFECTION UNTIL LATE
AS DISC IS AVASCULAR

27. CLINICAL FEATURES
 CAN OCCUR AT ANY AGE, BUT
MAJORITY <30 YRS
 FEVER,MALAISE , NIGHT SWEATS
 PERSISTENT SPINAL PAIN, LOCAL
TENDERNESS,LIMITATION OF SPINAL
MOBILITY
 LOWER THORACIC &LUMBER
VERTEBRA MOST COMMONLY
AFFECTED FOLLOWED BYMID
THORACIC & CERVICAL VERTEBRA

28. CLINICAL FEATURES cont
 PARAPLEGIA-EARLY ONSET DUE TO
CORD EDEMA ,CORD COMPRESSION BY
EPIDURAL ABCESS OR GRANULATION
TISSUE,PATHOLOGICAL SUBLUXATION
OR DISLOCATION,SEQUESTERED BONE
OR DISC FRAGMENTS
LATE ONSET DUE TO DURAL FIBROSIS,
SEVERE KYPHOSCOLIOTIC
DEFORMITY,SPINAL CANAL STENOSIS&
SEQUESTRA FROM VERTEBRAL BODY

29. XRAY
 USUAL INITIAL INVESTIGATION BUT
OFTEN NEGATIVE IN EALY DISEASE.
 DEPENDING ON LOCATION FINDINGS
ON XRAY-
PARADISCAL –MOST COMMON TYPE
BEGIN IN ANTERIOR PART OF
VERTEBRAL
SUPERIOR INFERIOR ADJACENT TO
ENDPLATE

30. XRAY FINDINGS contd
 DEMINERALISATION & LOSS OF
DEFINITION OF DENSE MARGIN OF
ENDPLATE WITH LITTLE PERIOSTEAL
REACTION OR SCLEROSIS
 AS INFECTION SPREADS, ADJACENT IV
DISC GETS INVOLVED WITH NARROWING
OF DISC SPACE
 WITH FURTHER PROGRESSION ATERIOR
WEDGING OR COLLAPSE OCCUR
RESULTING IN KYPHOSIS

31.  STARTS IN CENTRAL PART OF
VERTEBRAL BODY
 SHOWS A LYTIC AREA WITH ABSENCE
OF NORMAL TRABECULAE IN CENTRAL
PORTION AWAY FROM DISC MARGIN
 GRADUALLY ENLARGES CAUSING
BALLOONING OF VERTEBRAL BODY.
 IN LATER STAGE CONCENTRIC
COLLAPSE OCCUR RESEMBLING
VERTEBRA PLANA
 DISC SPACE MINIMALLY AFFECT

32. APPENDICEAL OR NEURAL ARCH
NEURAL ARCH INVOLVEMENT IN 2-30%OF
CASES IN CONTIGUITY WITH VERTEBRAL
BODY INVOLVEMENT
COMMONLY AFFECTS CERVICAL & UPPER
DORSAL SPINE
TENDENCY TOWARDS PEDICLE &LAMINA
INVOLVEMENT
XRAY SHOWS PEDICULAR OR LAMINA
DESTRUCTION, EROSION OF ADJACENT
RIBS OR POSTERIOR CORTEX OF
VERTEBRAL BODY WITH RELATIVE SPARING

33.  ABCESS
PRODUCE SOFT TISSUE OPACITY ON XRAY
,OPACITY OFTEN BILATERAL .
GLOBULAR ABCESS DENOTES PUS UNDER
TENSION
ABCESS IN CERVICAL REGION CAUSE
WIDENING OF PREVERTEBRAL TISSUE
DORSAL SPINE ABCESSS CAUSE LATERAL
DISPACEMENT OF POSTEROMEDIAL PLEURAL
LINE
IN LUMBER REGION ABCESS SEEN TO TRACK
ALONG PSOAS PRODUCING BULGING OF
PSOAS OTLINE ON XRAY

34. CT
 HELPS IN EARLY DETECTION OF BONE
&SOFT TISSUE
 BETTER ANATOMIC LOCALISATION &
CHARACTERISATION OF LESION.
 PROVIDE GUIDANCE FOR BIOPSY &
SURGICAL APPROACH
 HOWEVER LESS USEFUL THAN MRI AS
EARLY INFLAMMATORY CHANGES ARE
NOT WELL DEPICTED,SOFT TISSUES
POORLY DELINEATED

35. CT FINDINGS
 ON CT 4 PATTERNS DESCRIBED
FRAGMENTARY- 47%,MOST COMMON SHOWS
NUMEROUS SMALL BONE FRAGMENTS IN SOFT
TISSUE MASS
OSTEOLYTIC- 33%
SUBPERIOSTEAL-10%
WELL DEFINED LYTIC WITH SCLEROTIC MARGIN
OBLITERATION OF FAT PLANE IS SEEN IN ABCESS
FORMATION.
DISC SPACE NARROWING, KYPHOSIS & CHANGES
SEEN ON XRAY WELL DEPICTED

36. MRI
HAS HIGH SENSITIVITY OF EARLY BONE
INVOLVEMENT & EDEMA, FOR
ASSESMENT OF SPINAL CORD OR
NEURAL INVOLVEMENT INCLUDING
ENDPLATE CHANGES & MARROW
INFILTRATION.
SKIP BONE LESIONS,
EPIDURAL,MENINGEAL &CORD
INVOLVEMENT MORE CLEARLY

37. MRI FINDINGS
 T1W IMAGE SHOWS HETEROGENOUS DECREASE
SIGNAL INTENSITY IN AFFECTED VERTEBRA &LOSS OF
CORTICAL DEFINITION
 ON T2W IMAGE HETEROGENOUS INCREASED SIGNAL
INTENSITY
 PARASPINAL SOFT TISSUE MASSES SEEN WITH LOSS
OF SIGNAL INTENSITY SHOWING POSTCONTRAST
THICK RIM ENHANCEMENT.
ON T2 PARASPINAL MASS APPEAR HYPERINTENSE
EPIDURAL EXTENSION WELL DEPCTED SEEN IN ABOUT
60% INVOLVED VERTEBRA.
POST CONTRAST FAT SUPPRESSED T1 SEQ BEST TO
DEMONSTRATEMENINGEAL & EPIDURAL INFLAMMATORY
SOFT TISSUE

38. TUBERCULAR ARTHRITIS
 TUBERCULAR ARTHRITIS USUALLY
AFFECTS MAJOR JOINTS – HIP & KNEE
 MULTIFOCAL INFECTION RARE
 INFECTION MAY BE SYNOVIAL OR
SECONDARY TO BONE DISEASE.THE
LATTER FACILITATED AS EPIPHYSEAL
PLATE OFFER LITTLE RESISTENCE.

39. TUBERCULOSIS OF HIP
 LESIONS COMMONLY ARISE IN
ACETABULUM, SYNOVIUM, FEMORAL
EPIPHYSIS OR METAPHYSISSPREAD
OR SPREAD FROM FOCI IN GREATER
TROCHANTER OR ISCHIUM.

40. STAGE OF SYNOVITIS
 IN EARLY SYNOVITIS . SOFT TISSUE
SWELLING & JOINT WIDENING OCCUR DUE
TO EFFUSION
 PT PRESENTS WITH IRRITABLE HIP
 DISPLACEMENT OF FAT PLANES & POSIVE
OBTURATOR SIGN DUE TO FLEXION
DEFORMITY
 FIRST RADIOLOGICAL SIGN MAY BE
JUXTAARTICULAR OSTEOPOROSIS

41. STAGE OF ARTHRITIS
 DEFORMITY OF HIP JOINT IS PRESENT
 IN ADDITION TO OSTEOPOROSIS LOCALISE
EROSION SEEN IN PERIARTICULAR REGION
 DESTRUCTION OF ARTICULAR CARTILAGE
LEADS TO EROSION OF ACETABULAR
MARGIN & FEMORAL HEAD WITH
REDUCTION OF JOINT SPACE.

42. STAGE OF ADVANCED
ARTHRITIS
 WITH FURTHR PROGRESSUION .
DESTRUCTION OF , CAPSULE & LIGAMENTS
OCCUR
RTICULAR CARTILAGE, ACETABULUM,
FEMORAL HEAD