Chronic pyogenic osteomyelitis- etiology, pathogenesis,

1. Presented By-
Dr.Punit Gaurav
1st year Post Graduate
Dept. of Orthopaedics

2. TOPICS TO BE COVERED
• Introduction
• Causes
• Pathogenesis
• Pathology
• Roentgenology
• Diagnosis
• Differential Diagnosis

3. INTRODUCTION
 Nelaton (1834) : coined osteomyelitis
 Definition: “ A severe,persistent and incapacitating
infection of bone and bone marrow ”.
 Chronic osteomyelitis is often defined as the presence
of ongoing bone infection for longer than 3 weeks in the
presence of devitalized bone.

4.  Osteomyelitis (osteo- derived from the Greek
word osteon, meaning bone, myelo- meaning
meaning marrow, and -itis meaning
inflammation) simply means an infection of the
infection of the bone or bone marrow.
marrow.
 Infection mainly involves
- Marrow spaces
- Haversian canals
- Subperiosteal Spaces

5.  Bone is involved secondarily.
 Hallmark of chronic osteomyelitis is infected dead
bone within a compromised soft-tissue envelope.
 Infected foci within the bone are surrounded by
sclerotic, relatively avascular bone covered by a
thickened periosteum and scarred muscle and
subcutaneous tissue.

6.  This avascular envelope of scar tissue leaves
systemic antibiotics essentially ineffective.
 Secondary infections are common, and sinus
track cultures usually do not correlate with
cultures obtained at bone biopsy.

7.  Multiple organisms may
grow from cultures taken
from sinus tracks and from
open biopsy specimens of
surrounding soft tissue and
bone.

8.  Osteomyelitis occurs when an adequate
number of a sufficiently virulent organism
overcomes the host's natural defenses
(inflammatory and immune responses)
and establishes a focus of infection, for
example; local skeletal factors also play a
role in the development of infection

9.  Relative absence of
phagocytic cells in the
metaphyses of bones in
children may explain why
acute hematogenous
osteomyelitis is more
common in this location.

10. Factors responsible for chronicity
 Local factors: Cavity, Sequestrum, Sinus, Foreign body, Degree
of bone necrosis.
 General: Nutritional status of the involved tissues, vascular
disease, DM, low immunity.
 Organism: Virulence.
 Treatment: Appropriateness and compliance.
 Risk factors: Penetrating trauma, prosthesis, Animal bite.

11. ETIOLOGY

12. ORGANISMS CAUSING POSSIBLE PROBLEM
1)Staphylococcus aureus
Pressure ulcer, penetrating wound, open
fracture, orthopedic surgery, vascular
insufficiency disorder.
2)Staphylococcus epidermidis
Indwelling prosthetic device.
3)Streptococcus viridans
Abscessed tooth, gingival disease.
4)Escherichia coli
Urinary tract infection.

13. 5)Mycobacterium tuberculosis
Tuberculosis
6)Neisseria gonorrhoeae
Gonorrhea
7)Pseudomonas sp.
Puncture wounds, intravenous drugs
8)Salmonella sp.
Sickle cell disease
9)Fungi, mycobacteria
Immunocompromised host

14. According To Age:
1)Infants < 1yr :
Gr. B streptococci, S. aureus, E.coli
2) 1-16 yrs :
S. aureus, S. pyogens, H.influenzae
3) > 16 yrs :
S.aureus, S epidermidis, Gram –ve Bacilli

15. WHY STAPHYLOCOCCUS MOST
COMMON?
 S.aureus and S.epidermis elements of normal skin
flora
 S.aureus increased affinity for host proteins
(traumatised bone)
 Enzymes (coagulase, surface factor A) hampers
hosts immune response .
 Inactive “L” forms dormant for years
 “Biofilm” (polysaccharide “slime” layer) increases
bacterial adherence to any substrate .
 Large variety of adhesive proteins and
glycoproteins mediate binding with bone
components.

16. PATHOGENESIS

17. BACTERIAL RESISTANCE BY BIOFILM
 Most infections encountered in orthopaedics
are related to BIOFILM(A coherent cluster of
bacterial cells imbedded in a matrix—which
are more tolerant to most anti-microbials and
the host defence than planktonic bacterial
cells forming bacteria.)

18.  First, the bacteria need to find an inert surface (e.g., implant or dead
tissue).
 Implants or dead tissue that have been integrated by the host with some
type of surface are not inert and will resist colonization.
 Then, the colonization process will continue until mature colonies are
formed.
 Once mature, the colonies can change based on environmental signals or
signals between colonies

20. Hematogenous spread
usually involves the
metaphysis of long
bones in children or the
vertebral bodies in
adults
Direct inoculation of
microorganisms into
bone
penetrating injuries
and
surgical
contamination are
most common causes
Contiguous focus of
infection
seen in patients with
severe
vascular disease.
Microorganism
s
in bone
Osteomyelitis

21.  Whatever may be the inciting cause the bacteria
reaches the metaphysis of rapidly growing bone &
provokes an inflammatory response.
 Why metaphysis is involved?
1. Infected embolus is trapped in U-shaped small end
arteries located predominantly in metaphyseal region
2. Relative lack of phagocytosis activity in
metaphyseal region
3. Highly vascularised region ---minor trauma—
hemorrhage ----locus minoris resistantae---excellent
culture medium.

22.  Sharp hairpin turns
 Flow becomes considerably
slower and more turbulent.
 Relatively fewer phagocytic
cells than physis and
metaphysis.

23. EVOLUTION
 Described by Trueta in 1959.
 3 stages-
1) Stage I : Boil in the Bone
with pain which is
severe,constant,with
tenderness.

24.  Stage II-
The signs and symptoms become more
marked and the general symptoms of
inlmmation appear.

25.  Stage III-
The inflammation spreads
outward and produces
subperiosteal inflammatory
collection- so called sub
periosteal abscess.

26. These are end-artery branches of the nutrient artery
Acute inflammatory response due to infection
Tissue necrosis, breakdown of bone
Obstruction
Avascular necrosis of bone
Chronic osteomyelitis

28. THE INFLAMMATORY RESPONSE TO
OSTEOMYELITIS:
 Prostaglandin-E production has been shown to be five to
thirty fold higher in infected bone than in normal bone.
- postulated to be responsible for bone resorption and
sequestrum formation.
 Effective phagocytosis is defense in patients with
osteomyelitis
 Intramedullary oxygen tensions important for phagocytic
function
- oxygen tensions of <30 mm Hg impair normal phagocytic
function

29.  In any infection of bone , there is an attempt at repair,
that if incomplete, it results in chronic persistence of
infection.
 This repair is accomplised by hyperemia of the
surrounding tissue , which effects the decalcification of
the bone.
 Granulation tissue forms and carries in osteoclasts n
osteoblasts.

30.  Necrotic cancellous bone is readily absorbed
and replaced by new bone.
 Dead cortex is gradually absorbed about its
surface and is detached from living bone to
form a sequestrum.(this requires several
months).

31. PATHOLOGY
 The most common site is
lower femoral metaphysis.
 Other sites - upper tibial
-upper femoral
-upper humeral
metaphyis

32. Pathologic features of chronic osteomyelitis
 SEQUESTRUM – is a piece
of dead bone ,surrounded
by infected granulation
tissue trying to “eat” the
sequestrum away.
 Appears pale having
smooth inner surface and a
rough outer.

33. Different types of SEQUESTRA
TYPES DISEASE
TUBULAR PYOGENIC
RING EXTERNAL FIXATORS
BLACK ACTINOMYCOSIS
CORALLIFORM PERTHE'S DISEASE
COKE TUBERCULOSIS
SANDY TUBERCULOSIS
FEATHERY SYPHILIS

34.  When SEQUESTRUM IS COMPLETE, it
lies in the free cavity and is LESS
attacked by granulation tissue and is
absorbed more slowly.
 Meanwhile , the surrounding living
bone attempts to wall off the
infection by forming a thick , dense
wall , the INVOLUCRUM.
 INVOLUCRUM is the dense sclerotic
bone overlying the sequestrum.

35.  An Involucrum usually has multiple
openings , the cloacae , through
which exudate , bone debris , and
sequestra find exit and pass through
sinus tracts to the surface.
 CONSTANT DESTRUCTION of
neighboring soft tissue leads to THIN
skin which is easily traumatised , skin
epithelium grows inwards to line the
sinus tract.

37.  In chronic osteomyelitis of long
standing ,multiple cavities and
sequestra exist throughout the
bone.
 The shaft becomes thickened ,
irregular and deformed.

40. Factors affecting physiological class
Systemic Factors Local Factors
 Malnutrition
 Renal,Livere failure
 Alcohol abuse
 Immune deficiency
 Chronic Hypoxia
 Malignancy
 Diabetes Mellitus
 Extremes of ages
 Steroid therapy
 Tobacco abuse
 Chronic Lymphedema
 Venous stasis
 Major vessel compromise
 Arteritis
 Extensive scarring
 Radtion fibrosis

42. USE OF THIS CLASSIFICATION
- To decide whether treatment should be
1) Simple or Complex
2) Curative or Palliative
3) Limb sparing or Ablative

43. CLINICAL PICTURE
 DURING THE PERIOD OF
INACTIVITY:
- Usually no symptoms
- Skin over the focus is dusky, thin,
scarred, poorly nourished
- Break in the skin causes ulceration
that heals slowly
- Muscles are scarred & leads to
contractures of the adjacent joints.

44.  DURING ACUTE EXACERBATION
- Aching pain worsening at night,
overlying soft tissue becomes
edematous, warm redddened & tender
- Patient is febrile
- As infection progresses, sinus may
open up & drain extruding small
sequestrum at intervals

45. - Intervals between flare ups may
be months or years.
- Flare ups may be due to poor
general condition & lowered
resistance.
- Recurrent toxemia will eventually
cause debilitary & sometimes fatal.

46. DIAGNOSIS
 The diagnosis is based on
Clinical ,
Laboratory and
Imaging studies.
 The “GOLD STANDARD” is to obtain a biopsy
specimen for histological and microbiological
evaluation of the infected bone.

47. CLINICAL
 Physical examination should be
focused on integrity of skin and soft
tissue .
 Determination of area of tenderness.
 Assessing bone stability.
 And evaluation of neuro vascular
status of the limb.

48. LABORATORY
 Lab studies generally are
nonspecific and give no indication
for severity of the infection.
 ESR and C- Reactive protein are
elevated in most patients.
 But WBC’S elevated in only 35%.

49.  The white blood cell count will show a marked
leucocytosis as high as 20,000 or more.
 Peak elevation of the ESR occurs at 3 to 5 days
after infection and returns to normal
approximately 3 weeks after treatment is begun.
 CRP increases within 6 hours of infection, reaches
a peak elevation 2 days after infection, and returns
to normal within 1 week after adequate treatment
has begun.

50. CULTURAL STUDIES
 Key to the successful
management of osteomyelitis is
the isolation of the involved
pathogens before the initiation of
antibiotics.
 Cultures of superficial wounds or
sinus tracks should not be relied
on because they have been shown
to be poor indicators of deep
infection and usually are
polymicrobial.

51.  The preferred specimen in
most bacterial and yeast
infections is aspirated fluid
(joint or purulent fluid).
 A deep wound biopsy or a
curetted specimen after leaning
the wound is acceptable.

52. RADIOLOGY

53.  Multiple imaging technique are available to evaluate
chronic osteomyelitis ,however no technique can
absolutely confirm or exclude presence of osteomyelitis.
 Imaging should be done to confirm the diagnosis and
prepare for surgery.
 Initial plain radiographs to be performed it yields
valuable information.

54. PLAIN RADIOGRAPH
 Earliest changes are swelling
of the soft tissue, periosteal
thickening and/or elevation,
and focal osteopenia.
 More diagnostic lytic changes
are delayed and are associated
with subacute and chronic
osteomyelitis.

55. USG
 May detect a subperiosteal
collection of fluid in Early
stages of osteomyelitis.
 To establish if joint effusion
is present.
 To localise needle aspiration.

56. Sinography
 Sinography can be preformed if a
sinus track is present.
 Roentgenograms made in two
planes after injection of radiopaque
liquid into sinus.
 Helpful in locating focus of infection
in chronic osteomyelitis.
 A valuable adjunct to surgical
planning

57. RADIONUCLEOTIDE SCAN
Isotopic bone scanning is more useful in acute
osteomyelitis than chronic osteomyelitis.
 Most common is 99mTc phosphate, which can detect
osteomyelitis.

58.  Three-phase bone scan consists of
(1)Flow phase- shows blood flow
(2)Immediate or equilibrium - shows relative flow and
distribution of radio isotope into extracellular matrix
(3) Delayed phase-shows osteoblastic activity
 Osteomyelitis shows increase uptake in all three phase

59. MRI
 MRI has very high sensitivity and specificity for
the diagnosis of osteomyelitis.
 Classic findings of osteomyelitis on MRI are a
decrease in the normally high marrow signal on
T1 images and a normal or increased signal on
T2 images.

60.  May reveal a well defined rim of
high signal intensity surrounding
the focus of active disease (RIM
SIGN).
 The reported abnormal images
reflect an increase in water
content, resulting from edema in
the marrow cavity.

61.  Marrow fat is replaced by edema and cellular
infiltrates that are lower in signal than fat on T1
images and higher in signal than fat on T2 and
STIR image.

62. CT SCAN
 CT provides excellent
definition of cortical bone
and a fair evaluation of the
surrounding soft tissues and
is especially useful in
identifying sequestra.

63. DIFFERENTIAL DIAGNOSIS
 TUBERCULOSIS OF BONE-
-Thin watery discharge
-Undermining Bluish discolouration,
-Diaphyseal involvement more common
-H/o Pulmonary TB
-Often Multifocal
 SOFT TISSUE INFECTION
-Absence of bony changes

64.  EWING SARCOMA
-Radiological D/D
-Acute presentation
-Biopsy is diagnostic
 OSTEONECROSIS
 OSTEOID OSTEOMA
 HISTIOCYTIC EOSINOPHILIC GRANULOMA
 GARRE'S OSTEOMYELITIS

65. REFERENCES
 CAMPBELL’S OPERATIVE ORTHOPAEDICS,14th
edition
 Apley and Solomon’s System of Orthopaedics
and Trauma 10th Edition
 Kulkarni's Textbook Of Orthopedics And Trauma
3rd edition
 Turek’s Orthopaedics Principles and Their
Applications 7th edition.