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OSTEOMYELITIS
PRESENTED BY-
Dr. Gurjant Singh (PT), MPT, (Ph.D)
Assistant Professor, MMIPR
DEFINITION OF OSTEOMYELITIS
 Osteo=bone
 Myelo=marrow
 Itis=inflammation
So we can conclude that ostemyelitis is a disease in which
infection of bone marrow occurs.
 Osteomyelitis is an infection of bone & bone
marrow that may be caused by direct
inoculation of an open traumatic wound or by
blood-borne organisms (hematogenous)
CLASSIFICATION
OfOSTEOMYELITIS
 ACC TO DURATION-
 ACUTE OSTEOMYELITIS(Less than 2 weeks)
 SUB-ACUTE OSTEOMYELITIS(Between 2-6 weeks)
 CHRONIC OSTEOMYELITIS(more than 6 week)
 ACC TO ROUTE OF INFECTION(Acc toWaldogel’s)
HEMATOGENOUS(Most common)
DIRECT
CONTIGUITY
 ACC TO HOST RESPONSE
 PYOGENIC
 NON PYOGENIC
Anatomic
Classification
(Cierny-
Mader)1985
1.Medullary
Endosteal
2.Superficial
Localized to surface of
bone, usually 2° to soft
tissue defect.
3.Localized
• Localized sequestra, usually
associated sinus tract
• Bone structurally stable
4.Diffuse
• Permeative process, combination
of I/II/III,
• Commonly unstable
 Infecting microorganisms can
invade by …
 Indirect entry
 Direct entry
INDIRECT ENTRY
 Frequently affects growing bone in boys
<12 years old
 Associated with increased incidence of blunt trauma
 Most common sites of indirect entry ……
 Distal femur
 Proximal tibia
 Humerus
 Radius
Adults with increased risk
 Vascular disorders
 Genitourinary and respiratory infections
 Spread infection from blood to bone
 Vascular-rich bone sites
 Pelvis
 Tibia
 Vertebrae
Direct Entry
 Can occur at any age
 Open wound where microorganisms can gain entry to
body
 May also occur in presence of foreign body
 Implant
 Orthopedic prosthetic device
Direct Entry
 After entry, microorganisms lodge in an area of bone
where circulation slows.
 Usually the metaphysis
 Microorganisms grow causing increased pressure
because most bone is nonexpanding
 Increased pressure leads to ischemia and vascular
compromise of periosteum
Direct Entry
 Eventually, infection passes through bone cortex and
marrow cavity
 Results in cortical devascularization and necrosis
Direct Entry
 Once ischemia occurs, bone dies
 Sequestrum forms
 Devitalized bone separates from living bone .
 Part of periosteum that continues to have a blood
supply forms new bone called involucrum
Etiology and Pathophysiology
 Caused by a variety of microorganisms
 Most common infecting microorganism is Staphylococcus
aureus .
 ORGANISM POSSIBLE PROBLEM
 Staphylococcus aureus Pressure ulcer, penetrating
wound,
open fracture, orthopedic surgery
 Staphylococc Epidermis Indwelling prosthetic device
 Streptococcus viridans Abscessed tooth, gingvial disease

Escherichia coli Urinary tract infection
Mycobacterium tuberculosis Tuberculosis
Neisseria gonorrhoeae Gonorrhea
Pseudomonas sp Puncture wounds, intravenous
drugs
Salmonella sp. Sickle cell disease
Fungi, mycobacterium Immunocompromised host
Escherichia coli Urinary tract infection
Mycobacterium tuberculosis Tuberculosis
Neisseria gonorrhoeae Gonorrhea
Pseudomonas sp Puncture wounds, intravenous
drugs
Salmonella sp. Sickle cell disease
Fungi, mycobacterium Immunocompromised host
PATHOPHYSIOLOGY
Microorganisms enter bone (Phagocytosis).
Lyse bone
Phagocyte contains the infection
Release enzymes
PATHOPHYSIOLOGY
Pus spreads into vascular channels
Raising intraosseous pressure
Impairing blood flow
Chronic ischemic necrosis
Separation of large devascularized fragment
New bone formation
(involucrum)
(Sequestra)
Pathophysiology of Osteomyelitis
Acute Osteomyelitis
Types of Acute Osteomyelitis
I. Hematogenous Osteomyelitis
II. Direct Inoculation Osteomyelitis
Acute Osteomyelitis
Hematogenous Osteomyelitis:
 Bacterial seeding from the blood.
 Seen primarily in Children.
 The most common site is the Metaphysis at the growing
end of Long Bones in Children, and The Vertebrae and
pelvic in Adults.
Acute Osteomyelitis
Direct Inoculation
Osteomyelitis
 Direct contact of the tissue and bacteria as a result of
an Open Fracture or Trauma.
 Tend to involve multiple organisms.
Acute Haematogenous Osteomyelitis
It is an endogenous form of the disease most often affecting
neonates.
Source of infection may be umblicus
Organisms – Staphlococci, Steptococci, E.Coli, Klebsiella,
Pasteurella, Proteus, etc :
Hematogenous-common in children .It is highest in the first
two decades of life. < 5 years of age. In adult-Haematogenous
is less common but they suffered due to debility
disease(diabetes mellitus)drugs(immunosuppresion
Clinical signs – Fever, malaise, non weight bearing lameness,
soft tissue swelling over the involved bone .
Pathophysiology
Septicaemia initiated from focus of infection (umblicus)
Infective emboli enters the nutrient arteries of long bones
The emboli gets entrapped in the end arteries and capillaries of the metaphyseal
area (epiphyseal plate)
Bacterial emboli causes inflammation, microthrombi formation, ischaemia,
bacterial proliferation & necrosis :
Hyperaemia, migration of leucocytes & pus formation
Purulent material travels under pressure in plane of least resistance
Reaches the outer cortex and elevates the periosteum
This compromise cortical blood supply Leads to sequestrum formation
SYMPTOMS
Temperature >102ºF long-lasting pain, Decreased range of motion in the case of joint
involvement. local warmth, tenderness, swelling .
CLINICAL FINDINGS
Within three to seven days- :
Interposed translucent fat planes within muscle are obliterated
by edema fluid.
Periosteal elevation or thickening may represent new bone
formation, pus, or reactive edema from adjacent soft tissue infection .
DIAGNOSIS
 Aspiration of pus and send for culture W.B.C. CRP and ESR
Blood for culture Plain films, bone scintigram, ultrasound,
CT Scan and MRI Even a biopsy all show positive results
 Elevations in the peripheral white blood cell count (WBC),
Erythrocyte sedimentation rate (ESR), and C-reactive
protein (CRP) in children with hematogenous
osteomyelitis are variable and nonspecific Blood culture is
positive in half of cases.
 Laboratory findings: Lytic and sclerosis, indicating chronic
infection. Periosteal new bone formation, with compatible
CLINICAL FINDINGS
Within three to seven days- :
Interposed translucent fat planes within muscle are
obliterated by edema fluid.
Periosteal elevation or thickening may represent new bone
formation, pus, or reactive edema from adjacent soft tissue
infection .
In acute osteomyelitis-
principle of treatment are-
 General supportive treatment Analgesic for relieve pain I/V
fluid(fever with shock, septicaemia)
 Spintage of the affected part
 Antibiotics(oral/intravenous)-It should be started
immediately not waiting for culture of blood and pus
management.
 Drainage-if necesssary
Management and Treatment Of
Acute Osteomyelitis:
 Acute osteomyelitis is an orthopaedic emergency which needs in
patient admission. The management can be discussed as general and
local
 GENERAL MANAGEMENT
• Conservative management is mainstay of treatment. The mneomics
RESTS sums up the conservative line of treatment
• Rest in bed, protect affected part with splints to alleviate pain and
spasm.
• Elevation-of part ,warm and moist packs to reduce swelling.
• Systemic treatment-blood transfusion, iv fluid to correct shock and
hypovolaemia.
• Treatment-with antibiotics to reduce toxicity . Antibiotics given are
penicillins, ciprofloxacin etc.
 Surgery
LOCAL MANAGEMENT
Focus here is on well timed surgery if one of
following indication are present
•Abscess formation
•Severely ill
•Failure to respond to intravenous antibiotics for
more than 48 hrs.
• Exact treatment varies according to the bones
involved, the severity of the infection and the
immune status of the patient.
During acute osteomyelitis following measures are suggested
•Proper splinting of affecting joints in functional positions.
•Limb elevation to control oedema.
•Cryotherapy in initial stages followed by thermotherapy in later
stages .These measure help to reduce pain and spasm.
•Unaffected joints put in active vigorous exercises
•After complete cessation of pain, mild isometrics exercise are
prescribed for affected joints.
•Mobilise joint and strengthen the muscles like active assisted ,
active and resisted exercise after disease is completely arrested.
•Ambulation and weight transfer done slowly commenced
initially with help of assistive advice.
PHYSIOTHERAPY MANAGEMENT
SUB-ACUTE OSTEOMYELITIS
 Is caused by staphylococcus aureus.
 Patient complaint of pain without constitutional
symptoms.
 Temperature may be increased or normal.
 It is not detected until at least two weeks has elapsed.
 Blood culture is positive in 60% of cases
 WBC and ESR raised in 50 % of cases
CAUSES
 Increased host resistances
 Lowered bacterial resistances
 If Anti-biotics are administrated before symptom appear.
A Brodie abscess
is a subacute osteomyelitis with a predilection for the
ends of long bones and the carpus and tarsus. Plain
radiographic findings include the following:
(1) a central area of radiolucency with a surrounding
thick rim of reactive bone sclerosis, which may
persist for months;
(2) pathognomonic tortuous parallel lucent channels
extending toward the growth plate;
(3) a variable degree of periosteal new-bone formation;
and
(4) associated soft-tissue swelling.
A Brodie abscess is characterized
by a double line at the site of the
lesion due to the high signal
intensity of granulation tissue
surrounded by low signal
intensity of bone sclerosis on T2-
weighted MRIs. The lesion has
low-to-intermediate signal
intensity that is outlined by a
hypointense rim on T1-weighted
MRIs.
Treatment of Brodie’s
abscess in the
metaphysis includes
surgical curettage
CLINICAL FEATURES
 pain, limp
 swelling occasionally
 local tenderness
INVESTIGATION
 X ray
 Bone scan
 Biopsy(50%) grow organism
TREATEMENT
 Antibiotics given for 6 month
 Surgery
Chronic osteomyelitis
Chronic osteomyelitis
Is a severe, persistent, and sometimes incapacitating
infection of bone and bone marrow. It is often a
recurring condition because it is difficult to treat
definitively. May arise as a result of an
inappropriately treated acute trauma, soft tissue
spread in the immunosuppressed patient,
diabetics, and i.v drug abusers.
This disease may result from
(1) inadequately treated acute OSM (2) a
hematogenous type of osteomyelitis; (3)
trauma, (4) iatrogenic causes such as joint
replacements and the internal fixation of
fractures; (5) compound fractures; (6)
infection with organisms, such as
Mycobacterium tuberculosis and Treponema
species (syphilis); and (7) contiguous spread
from soft tissues, as in diabetic ulcers or
ulcers in peripheral vascular disease
Clinical presentation
chronic forms of osteomyelitis usually occur in adults.
Generally, these bone infections are secondary to an open
wound, most often an open injury to bone and
surrounding soft tissue. Localized bone pain, erythema
and drainage around the affected area are frequently
present. The cardinal signs of subacute and chronic
osteomyelitis include draining sinus tracts, deformity ,
shortening or lengthning of bones and local signs of
impaired vascularity, range of motion and neurologic
status. The incidence of deep musculoskeletal infection
from open fractures has been reported to be as high as 23
percent.6 Patient factors, such as altered neutrophil
defense, humoral immunity and cell-mediated
immunity, can increase the risk of osteomyelitis
Other forms of chronic osteomyelitis
Tuberculous osteomyelitis of the bone is
secondary 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
TUBERCULOUS
OSTEOMYELITIS
 It is rare in the developed country and common in the
developing and underdeveloped countries of world.
 This disease effect the adolescent and young adult more
often Most frequently involved are spine and bones of
extremities.
 Tuberculosis lesion appear as the focus of bone destruction .
Tuberculosis of spine,potts disease often commences in
vertebral body may be aasociated with compression fracture
and destruction of intervertebral discs producing permanent
damage and paraplegia.
 Extension of caseous material along with pus from the
lumbar vertebrae to the sheaths of psoas muscle produce
psoas abscess or lumbar cold abscess .This abscess when
burst out they form sinus.
 Tuberculosis of spine,Pott’s disease often commense in
vertebral body and may be associated with compression
fracture and destruction of the intervertebral discs,produce
permanent damage and paraplegia.
 Extension of caseous material alongwith pus from the
lumbar vertebrae to sheath of psoas muscle produce psoas
abscess or lumbar cold abscess,this abscess may burst
through skin and form sinus.Long standing cases may
develop systemic amyloidesis.
Laboratory Investigations
• CBC with differential
– Elevated WBC count
– Left shift: Polymorphonucleocytosis
• Blood cultures
• ESR (Normal: < 20 mm/hr)
– Usually elevated > 35mm
• C-Reactive Protein (Normal: < 8 - 10mg/L)
– Elevated > 10mg/L
Diagnostic Imaging
• Plain Radiographs
• Ultrasound
• Radionuclide (Bone) Scans
• C-T Scans
• M R I
Management of
chronic
osteomyelitis
g
GOAL
 Eradication of the infection by achieving a
viable and vascular envoirnment This can
be done by radical debridement by way of
sequestrectomy and resection of scarred
and infected bone and soft tissue.
 Appropriate antibiotic required.
 Reconstruction of both bone and soft
tissue defect may be needed
 Principal of treatment
 Surgery to be undertaken only when fever
and infection has subsided,when living
bone is distinguished from the dead bone .
 When surgery is indicated ,culture is done
and antibiotics is started at least four days
before surgery and is continued for two
weeks.
 Surgery method include Sequestrectomy
and saucerisation.Other methods of
treatment are Open Grafting,hyperbaric
oxygen therapy,closed suction
drainage,amputation is done in very rare
cases.
PHYSIOTHERAPY MANAGEMENT
Measure for chronic osteomyelitis
Here disease has run its course and left back various sequlae like
limb length discrepancies
deformities,scarring etc.Efforts are made to combat these problem
 Limb length discrepancies-corrected by shoe raise and other
method
 Deformities-Corrected by various orthotic devices
 For scar,contractures etc,sustained passive streching of scarred
and contracted tissue.
 Deep ultrasonic massage for adherant scars.
 Strengthening isometrics and isokinetic exercises for the
muscles
 Range of motion exercises like active and passive ones for
affected and non-affected joints
 Assistive devices used for ambulation,weight transfers.
Manifestations of Osteomyelitis
 Cardiovascular effects
 Tachycardia
 GI effects
 Nausea and vomiting
 Anorexia
 MS effects
 Limp in involved extremity
 Localized tenderness
 Integumentary effects
 Drainage and ulceration at involved site
 Swelling, erythema, and warmth at involved site Lymph node
involvement
 Other effects
 High temperature with chills
 Abrupt onset of pain
 Malaise
COMPLICATIONS
Osteomyelitis may result in following complications
 Septicemia
 Acute bacterial arthritis
 Pathologic fractures
 Development of squamous cell carcinoma in
longstanding cases
 Secondary amyloidosis in long standing cases
 Vertebral osteomyelitis may cause vertebral
collapse with paravertebral abscess,cord
Compression and neurological deficits.
Osteomyelitis

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Osteomyelitis

  • 1. OSTEOMYELITIS PRESENTED BY- Dr. Gurjant Singh (PT), MPT, (Ph.D) Assistant Professor, MMIPR
  • 2. DEFINITION OF OSTEOMYELITIS  Osteo=bone  Myelo=marrow  Itis=inflammation So we can conclude that ostemyelitis is a disease in which infection of bone marrow occurs.  Osteomyelitis is an infection of bone & bone marrow that may be caused by direct inoculation of an open traumatic wound or by blood-borne organisms (hematogenous)
  • 3. CLASSIFICATION OfOSTEOMYELITIS  ACC TO DURATION-  ACUTE OSTEOMYELITIS(Less than 2 weeks)  SUB-ACUTE OSTEOMYELITIS(Between 2-6 weeks)  CHRONIC OSTEOMYELITIS(more than 6 week)  ACC TO ROUTE OF INFECTION(Acc toWaldogel’s) HEMATOGENOUS(Most common) DIRECT CONTIGUITY  ACC TO HOST RESPONSE  PYOGENIC  NON PYOGENIC
  • 5. 3.Localized • Localized sequestra, usually associated sinus tract • Bone structurally stable 4.Diffuse • Permeative process, combination of I/II/III, • Commonly unstable
  • 6.  Infecting microorganisms can invade by …  Indirect entry  Direct entry
  • 7. INDIRECT ENTRY  Frequently affects growing bone in boys <12 years old  Associated with increased incidence of blunt trauma  Most common sites of indirect entry ……  Distal femur  Proximal tibia  Humerus  Radius
  • 8. Adults with increased risk  Vascular disorders  Genitourinary and respiratory infections  Spread infection from blood to bone  Vascular-rich bone sites  Pelvis  Tibia  Vertebrae
  • 9. Direct Entry  Can occur at any age  Open wound where microorganisms can gain entry to body  May also occur in presence of foreign body  Implant  Orthopedic prosthetic device
  • 10. Direct Entry  After entry, microorganisms lodge in an area of bone where circulation slows.  Usually the metaphysis  Microorganisms grow causing increased pressure because most bone is nonexpanding  Increased pressure leads to ischemia and vascular compromise of periosteum
  • 11. Direct Entry  Eventually, infection passes through bone cortex and marrow cavity  Results in cortical devascularization and necrosis
  • 12. Direct Entry  Once ischemia occurs, bone dies  Sequestrum forms  Devitalized bone separates from living bone .  Part of periosteum that continues to have a blood supply forms new bone called involucrum
  • 13. Etiology and Pathophysiology  Caused by a variety of microorganisms  Most common infecting microorganism is Staphylococcus aureus .  ORGANISM POSSIBLE PROBLEM  Staphylococcus aureus Pressure ulcer, penetrating wound, open fracture, orthopedic surgery  Staphylococc Epidermis Indwelling prosthetic device  Streptococcus viridans Abscessed tooth, gingvial disease 
  • 14. Escherichia coli Urinary tract infection Mycobacterium tuberculosis Tuberculosis Neisseria gonorrhoeae Gonorrhea Pseudomonas sp Puncture wounds, intravenous drugs Salmonella sp. Sickle cell disease Fungi, mycobacterium Immunocompromised host Escherichia coli Urinary tract infection Mycobacterium tuberculosis Tuberculosis Neisseria gonorrhoeae Gonorrhea Pseudomonas sp Puncture wounds, intravenous drugs Salmonella sp. Sickle cell disease Fungi, mycobacterium Immunocompromised host
  • 15. PATHOPHYSIOLOGY Microorganisms enter bone (Phagocytosis). Lyse bone Phagocyte contains the infection Release enzymes
  • 16. PATHOPHYSIOLOGY Pus spreads into vascular channels Raising intraosseous pressure Impairing blood flow Chronic ischemic necrosis Separation of large devascularized fragment New bone formation (involucrum) (Sequestra)
  • 18. Acute Osteomyelitis Types of Acute Osteomyelitis I. Hematogenous Osteomyelitis II. Direct Inoculation Osteomyelitis
  • 19. Acute Osteomyelitis Hematogenous Osteomyelitis:  Bacterial seeding from the blood.  Seen primarily in Children.  The most common site is the Metaphysis at the growing end of Long Bones in Children, and The Vertebrae and pelvic in Adults.
  • 20. Acute Osteomyelitis Direct Inoculation Osteomyelitis  Direct contact of the tissue and bacteria as a result of an Open Fracture or Trauma.  Tend to involve multiple organisms.
  • 21. Acute Haematogenous Osteomyelitis It is an endogenous form of the disease most often affecting neonates. Source of infection may be umblicus Organisms – Staphlococci, Steptococci, E.Coli, Klebsiella, Pasteurella, Proteus, etc : Hematogenous-common in children .It is highest in the first two decades of life. < 5 years of age. In adult-Haematogenous is less common but they suffered due to debility disease(diabetes mellitus)drugs(immunosuppresion Clinical signs – Fever, malaise, non weight bearing lameness, soft tissue swelling over the involved bone .
  • 22. Pathophysiology Septicaemia initiated from focus of infection (umblicus) Infective emboli enters the nutrient arteries of long bones The emboli gets entrapped in the end arteries and capillaries of the metaphyseal area (epiphyseal plate) Bacterial emboli causes inflammation, microthrombi formation, ischaemia, bacterial proliferation & necrosis : Hyperaemia, migration of leucocytes & pus formation Purulent material travels under pressure in plane of least resistance Reaches the outer cortex and elevates the periosteum This compromise cortical blood supply Leads to sequestrum formation
  • 23. SYMPTOMS Temperature >102ºF long-lasting pain, Decreased range of motion in the case of joint involvement. local warmth, tenderness, swelling . CLINICAL FINDINGS Within three to seven days- : Interposed translucent fat planes within muscle are obliterated by edema fluid. Periosteal elevation or thickening may represent new bone formation, pus, or reactive edema from adjacent soft tissue infection .
  • 24. DIAGNOSIS  Aspiration of pus and send for culture W.B.C. CRP and ESR Blood for culture Plain films, bone scintigram, ultrasound, CT Scan and MRI Even a biopsy all show positive results  Elevations in the peripheral white blood cell count (WBC), Erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP) in children with hematogenous osteomyelitis are variable and nonspecific Blood culture is positive in half of cases.  Laboratory findings: Lytic and sclerosis, indicating chronic infection. Periosteal new bone formation, with compatible
  • 25. CLINICAL FINDINGS Within three to seven days- : Interposed translucent fat planes within muscle are obliterated by edema fluid. Periosteal elevation or thickening may represent new bone formation, pus, or reactive edema from adjacent soft tissue infection .
  • 26. In acute osteomyelitis- principle of treatment are-  General supportive treatment Analgesic for relieve pain I/V fluid(fever with shock, septicaemia)  Spintage of the affected part  Antibiotics(oral/intravenous)-It should be started immediately not waiting for culture of blood and pus management.  Drainage-if necesssary
  • 27. Management and Treatment Of Acute Osteomyelitis:  Acute osteomyelitis is an orthopaedic emergency which needs in patient admission. The management can be discussed as general and local  GENERAL MANAGEMENT • Conservative management is mainstay of treatment. The mneomics RESTS sums up the conservative line of treatment • Rest in bed, protect affected part with splints to alleviate pain and spasm. • Elevation-of part ,warm and moist packs to reduce swelling. • Systemic treatment-blood transfusion, iv fluid to correct shock and hypovolaemia. • Treatment-with antibiotics to reduce toxicity . Antibiotics given are penicillins, ciprofloxacin etc.  Surgery
  • 28. LOCAL MANAGEMENT Focus here is on well timed surgery if one of following indication are present •Abscess formation •Severely ill •Failure to respond to intravenous antibiotics for more than 48 hrs. • Exact treatment varies according to the bones involved, the severity of the infection and the immune status of the patient.
  • 29. During acute osteomyelitis following measures are suggested •Proper splinting of affecting joints in functional positions. •Limb elevation to control oedema. •Cryotherapy in initial stages followed by thermotherapy in later stages .These measure help to reduce pain and spasm. •Unaffected joints put in active vigorous exercises •After complete cessation of pain, mild isometrics exercise are prescribed for affected joints. •Mobilise joint and strengthen the muscles like active assisted , active and resisted exercise after disease is completely arrested. •Ambulation and weight transfer done slowly commenced initially with help of assistive advice. PHYSIOTHERAPY MANAGEMENT
  • 30. SUB-ACUTE OSTEOMYELITIS  Is caused by staphylococcus aureus.  Patient complaint of pain without constitutional symptoms.  Temperature may be increased or normal.  It is not detected until at least two weeks has elapsed.  Blood culture is positive in 60% of cases  WBC and ESR raised in 50 % of cases CAUSES  Increased host resistances  Lowered bacterial resistances  If Anti-biotics are administrated before symptom appear.
  • 31. A Brodie abscess is a subacute osteomyelitis with a predilection for the ends of long bones and the carpus and tarsus. Plain radiographic findings include the following: (1) a central area of radiolucency with a surrounding thick rim of reactive bone sclerosis, which may persist for months; (2) pathognomonic tortuous parallel lucent channels extending toward the growth plate; (3) a variable degree of periosteal new-bone formation; and (4) associated soft-tissue swelling.
  • 32. A Brodie abscess is characterized by a double line at the site of the lesion due to the high signal intensity of granulation tissue surrounded by low signal intensity of bone sclerosis on T2- weighted MRIs. The lesion has low-to-intermediate signal intensity that is outlined by a hypointense rim on T1-weighted MRIs. Treatment of Brodie’s abscess in the metaphysis includes surgical curettage
  • 33. CLINICAL FEATURES  pain, limp  swelling occasionally  local tenderness INVESTIGATION  X ray  Bone scan  Biopsy(50%) grow organism TREATEMENT  Antibiotics given for 6 month  Surgery
  • 35. Chronic osteomyelitis Is a severe, persistent, and sometimes incapacitating infection of bone and bone marrow. It is often a recurring condition because it is difficult to treat definitively. May arise as a result of an inappropriately treated acute trauma, soft tissue spread in the immunosuppressed patient, diabetics, and i.v drug abusers.
  • 36. This disease may result from (1) inadequately treated acute OSM (2) a hematogenous type of osteomyelitis; (3) trauma, (4) iatrogenic causes such as joint replacements and the internal fixation of fractures; (5) compound fractures; (6) infection with organisms, such as Mycobacterium tuberculosis and Treponema species (syphilis); and (7) contiguous spread from soft tissues, as in diabetic ulcers or ulcers in peripheral vascular disease
  • 37. Clinical presentation chronic forms of osteomyelitis usually occur in adults. Generally, these bone infections are secondary to an open wound, most often an open injury to bone and surrounding soft tissue. Localized bone pain, erythema and drainage around the affected area are frequently present. The cardinal signs of subacute and chronic osteomyelitis include draining sinus tracts, deformity , shortening or lengthning of bones and local signs of impaired vascularity, range of motion and neurologic status. The incidence of deep musculoskeletal infection from open fractures has been reported to be as high as 23 percent.6 Patient factors, such as altered neutrophil defense, humoral immunity and cell-mediated immunity, can increase the risk of osteomyelitis
  • 38. Other forms of chronic osteomyelitis Tuberculous osteomyelitis of the bone is secondary 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
  • 39. TUBERCULOUS OSTEOMYELITIS  It is rare in the developed country and common in the developing and underdeveloped countries of world.  This disease effect the adolescent and young adult more often Most frequently involved are spine and bones of extremities.  Tuberculosis lesion appear as the focus of bone destruction . Tuberculosis of spine,potts disease often commences in vertebral body may be aasociated with compression fracture and destruction of intervertebral discs producing permanent damage and paraplegia.  Extension of caseous material along with pus from the lumbar vertebrae to the sheaths of psoas muscle produce psoas abscess or lumbar cold abscess .This abscess when burst out they form sinus.  Tuberculosis of spine,Pott’s disease often commense in vertebral body and may be associated with compression fracture and destruction of the intervertebral discs,produce permanent damage and paraplegia.  Extension of caseous material alongwith pus from the lumbar vertebrae to sheath of psoas muscle produce psoas abscess or lumbar cold abscess,this abscess may burst through skin and form sinus.Long standing cases may develop systemic amyloidesis.
  • 40. Laboratory Investigations • CBC with differential – Elevated WBC count – Left shift: Polymorphonucleocytosis • Blood cultures • ESR (Normal: < 20 mm/hr) – Usually elevated > 35mm • C-Reactive Protein (Normal: < 8 - 10mg/L) – Elevated > 10mg/L
  • 41. Diagnostic Imaging • Plain Radiographs • Ultrasound • Radionuclide (Bone) Scans • C-T Scans • M R I
  • 42. Management of chronic osteomyelitis g GOAL  Eradication of the infection by achieving a viable and vascular envoirnment This can be done by radical debridement by way of sequestrectomy and resection of scarred and infected bone and soft tissue.  Appropriate antibiotic required.  Reconstruction of both bone and soft tissue defect may be needed  Principal of treatment  Surgery to be undertaken only when fever and infection has subsided,when living bone is distinguished from the dead bone .  When surgery is indicated ,culture is done and antibiotics is started at least four days before surgery and is continued for two weeks.  Surgery method include Sequestrectomy and saucerisation.Other methods of treatment are Open Grafting,hyperbaric oxygen therapy,closed suction drainage,amputation is done in very rare cases.
  • 43. PHYSIOTHERAPY MANAGEMENT Measure for chronic osteomyelitis Here disease has run its course and left back various sequlae like limb length discrepancies deformities,scarring etc.Efforts are made to combat these problem  Limb length discrepancies-corrected by shoe raise and other method  Deformities-Corrected by various orthotic devices  For scar,contractures etc,sustained passive streching of scarred and contracted tissue.  Deep ultrasonic massage for adherant scars.  Strengthening isometrics and isokinetic exercises for the muscles  Range of motion exercises like active and passive ones for affected and non-affected joints  Assistive devices used for ambulation,weight transfers.
  • 44. Manifestations of Osteomyelitis  Cardiovascular effects  Tachycardia  GI effects  Nausea and vomiting  Anorexia  MS effects  Limp in involved extremity  Localized tenderness  Integumentary effects  Drainage and ulceration at involved site  Swelling, erythema, and warmth at involved site Lymph node involvement  Other effects  High temperature with chills  Abrupt onset of pain  Malaise
  • 45. COMPLICATIONS Osteomyelitis may result in following complications  Septicemia  Acute bacterial arthritis  Pathologic fractures  Development of squamous cell carcinoma in longstanding cases  Secondary amyloidosis in long standing cases  Vertebral osteomyelitis may cause vertebral collapse with paravertebral abscess,cord Compression and neurological deficits.