Osteomyelitis
History
• Disease was known since the times of Hippocrates (460-370 B.C.)
• Bromfield (1773) – “Abcessus in medulla”
• John hunter (1834)- recognized the mechanism of sequestrum
formation by describing it as a pocket of dead cortical bone within an
abscess.
• Louise Pasteur (1840s) had implicated microbes in furuncles,
osteomyelitis and puerperal fever. He had described osteomyelitis as
“a boil of the bone marrow”.
• Nelaton is credited with introducing the term “osteomyelitis” in 1844.
• Ogston was meanwhile researching on staphylococcus. (1884)
• Prior to the introduction of penicillin in 1940, the management of
acute osteomyelitis was based on the principles of the American
surgeon, Winnett Orr (1877–1956). He advocated incisions which were
large enough to expose the whole diseased areas of the bone. All
necrotic bone was to be removed with “saucerisation” of the resulting
cavity.
One of the classifications for osteomyelitis,
although no longer commonly used, is based on
time
• <2weeks – acute osteomyelitis
• >6weeks – chronic osteomyelitis
• 2-6 weeks – subacute osteomyelitis
Classification
Acute Osteomyelitis
• Acute osteomyelitis is a rapidly destructive
pyogenic infection, usually haematogenous in
origin, occurring most commonly in infants
and children; it starts in a metaphysis of an
actively growing long bone and runs a
fulminating septic course that may terminate
fatally.
Pathogenesis
Hematogenous osteomyelitis:
• occurs in children < 15 years of age although adults can have
this disease
• occurs in the metaphysis of the long bones.
– sharp hairpin turns
– flow becomes considerably slower and more turbulent
– decreased activity of macrophages
– Frequent trauma (locus minoris resistantae)
– Precarious blood supply.
Diaphysial osteomyelitis :
– Earlier metaphysis but due to growth becomes diaphyseal mostly
in children.
– Direct trauma to diaphysis
– Tubercular
• ETIOLOGY-
– Age: infancy and childhood
– Sex: Male predisposition 4:1
– Trauma: history of direct blow frequently elicited
– Location: Metaphysis of long bone (m/c upper end
of tibia and lower end of femur)
– Poor nutrition
– Unhygienic surroundings
– Antecedent locus of infection- eg. Boils, tonsillitis.
Causative organisms
• Although many organisms can cause
osteomyelitis, it can be classified into two
– Bacterial pyogenic osteomyelitis
– Tuberculous osteomyelitis
In pyogenic infections, the periosteal reaction is
marked. However in tuberculous osteomyelitis, the
local reactions are not marked (with the exception of
Spina ventosa)
• Bacterial pyogenic osteomyelitis is most
commonly caused by Staphylococcus aureus in all
age groups. However some exceptions are
present-
– In patients of haemoglobinopathies, most common
organism is Salmonella. (several symmetrical bones
are involved)
– In patients on prolonged parenteral therapy, most
commonly fungal infection is found
– In IV drug abusers – Pseudomonas
– In osteomyelitis following animal bite- Pasteurella
– In osteomyelitis following human bite- Eikenella
One organism – Hematogenous route of infection
Multiple organisms – Exogenous route of infection
*Needle Licker’s osteomyelitis
Why is S. Aureus the 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) ----- 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.
• Panton valentine leucocidin toxin has been asso. with
occurrence of DVT in MRSA infections.
Clinical Picture
• Heat, red, pain or tenderness, swelling
• Initially, the lesion is within the medullary cavity, there is no
swelling, soft tissue is also normal.
• The mere sign is deep tenderness.
• Localized finger-tip tenderness is felt over or around the
metaphysis.
• It is necessary to palpate carefully all metaphysial areas to
determine local tenderness, pseudoparalysis.
• An increase effusion in the adjacent joint proves in most
cases to be a sympathetic synovitis with sterile clear fluid.
• hip, shoulder, ankle; these joints can develop septic
arthritis by extension of osteomyelitis.
• A lighting up of infection is manifested by aching pain that
is worse at night.
• In later stage, a sinus may open on skin and starts to
exudate purulent material and small sequestra.
Differential diagnosis
– Rheumatic fever-less acute, Polyarticular, confined to joints, no effect of
antibiotics, dramatic response to salicylates & ACTH.
– Ewing sarcoma- fever, leukocytosis, subperiosteal bone deposition present. But
diaphysial & diffused; less intense constitutional symptoms. Radiosensitive, biopsy diagnostic.
– Acute suppurative arthritis- joint fluid earlier; decreased ROM; ms.
spasm; purulent synovial fluid on aspiration.
Laboratory findings
• The white blood cell count will show a marked
leucocytosis as high as 30,000 or more.
• Raised CRP and ESR.
• Blood culture positive in 30-50% of infants and
children.
• The blood culture demonstrates the presence of
bacteremia, the blood must be taken when the
patient has a chill, especially when there is a
spiking temperature.
• Aspiration. The point of maximal tenderness
should be aspirated with a large-bore needle.
Radiological Findings
– Radiographs are negative within first 7-10 days. x-ray
appearances are of little value in making the early diagnosis. By
the time there is x-ray evidence of bone destruction, the patient
has entered the chronic phase of the disease.
– Careful comparison with the opposite side may show abnormal
soft tissue shadows.
– It takes from 10 to 21 days for an osseous lesion to become
visible on conventional radiography, because a 30–50%
reduction of bone density must occur before radiographic
change is apparent.
– Lamellated periosteal reactions are invariably present . The
reparative phase during therapy is characterized by endosteal
and periosteal new bone formation, development of
surrounding sclerosis and sometimes large osteosclerotic areas.
Ultrasonography
• Ultrasound cannot directly access bone marrow
abnormalities present in osteomyelitis but can
document osteomyelitis indirectly by identifying
periosseous soft tissue abnormalities.
• The very first sonographic sign, seen even before
any periosteal reaction, is edematous swelling of
the deep soft tissues
Bone Scan
• Radioisotopic bone scanning is valuable in early
localization (within 48 hrs) of bone infection.
• The specificity of radioactive isotopic imaging
techniques have improved in the evaluation of
musculoskeletal infection.
• Technitium-99m imaging is very sensitive , it is
the choice for acute hematogenous
osteomyelitis, the overall accuracy being 92%.
Magnetic resonance imaging
• Magnetic resonance imaging has very high sensitivity
and specificity. It is gradually becoming the
investigation of choice for acute hematogenous
osteomyelitis.
• Advantage:
– Useful for differentiating between bone and soft-tissue
infection.
– Helpful in surgical planning.
• Disadvantage:
– A metallic implant in the region of interest may produce
focal artifacts.
– False positives in tumors and healing fractures.
Treatment
• Antibiotics-penicillin & cephalosporins; now clinda & vanco. 5-7 days IV, oral for 4-6 wk
• Drainage
• Conservative – can wait for 48 hours
Nade’s indications for surgery
• 1. Abscess formation
• 2. Severely ill & moribund child with features of
acute osteomyelitis
• 3. Failure to respond to IV antibiotics for >48 hrs
•Nade’s principles
•  Antibiotic is effective before pus forms
•  Antibiotic cannot sterilise avacular tissue
•  Antibiotic prevents reformation of pus once
removed
•  Pus removal restores periosteum---- restores
blood flow
•  Antibiotic should be continued after surgery
Complications
• Bone abscess
• Septic Arthritis
• Septicaemia
• Fracture
• Growth arrest
• Overlying soft-tissue cellulitis
• Thrombophlebitis
• Chronic osteomyelitis
Chronic Osteomyelitis
• The Cierny-Mader anatomic types of adult osteomyelitis. (A) Type 1 is
intramedullary osteomyelitis, where the nidus is endosteal. (B) Type 2
indicates superficial osteomyelitis, which is limited to the surface of the
bone. (C) Type 3 is termed localized osteomyelitis, in which the full
thickness of the cortex of the bone is involved. This type of osteomyelitis
often requires complex dead space management and osseous stabilization
after debridement. (D) Type 4 is diffuse osteomyelitis involving the entire
circumference of the bone. These lesions are mechanically unstable and
require complex reconstruction.
Physiologic host
A Host
Normal host. Normal immune system.
Normal vascularity.
B Host Bs: systemic compromise
Bl: local compromise
Bsl: systemic and local compromise
C Host
Treatment morbidity worse than present
condition with low prognosis for cure.
Radiological findings
Etymology
– sequester in Latin means standing apart.
– involucrum is derived from Latin word involvō,
meaning a sheath that covers or envelopes.
• Antibiotics- most workers prefer IV antibiotics
for 5-7 days followed by 4-6 weeks of oral
antibiotics after surgery.
• Oral antibiotics commonly used-
fluoroquonolones, linezolid, trimethoprim.
• For MRSA- doxy and clinda
• For anaerobic infections- Metronidazole.
Treatment
• Surgery –
• Sequestrectomy and saucerisation – check
radiology for 6-8 weeks, see for involucrum
covering atleast 2/3rd of the diameter of the
bone. Debride till paprika sign.
• Closed irrigation and suction- mild detergent
instilled, preventing formation of penicillinase.
When to do sequestrectomy?
Early sequestrectomy
• - Eradicate infection
• -Better environment for periosteum to respond
Delayed sequestrectomy
• Wait till sufficient involucrum has
formed before doing a sequestrectomy
to mimimize the risk of fracture,
deformity & segmental loss
• Wound is left open EXCEPT:
• a) Compromised hosts (Class B host); ankle,
hand, spine
• b) Type II lesions (primary soft tissue
reconstruction and/or host alteration)
• c) Minimal necrosis osteomyelitis
• Papineau technique: Cavity is packed with small
cancellous bone graft (preferably autogenous)
mixed with an antibiotic and fibrin sealant
• Primary closure with transferred tissue: In muscle
flap transfer, a suitable large wad of muscle with
its blood supply intact can be mobilized and laid
into the cavity. The surface is later closed with a
split-skin graft
• Primary closure with antibiotic impregnated beads:
Porous gentamicin-impregnated PMMA beads are
used to sterilize the cavity. It is easier but less
successful. Furthermore, they are extremely
difficult to be removed if not taken out by 2-3
weeks
Reconstruction of bone & soft-tissue defect
Subacute Osteomyelitis
• Subacute osteomyelitis is defined as a chronic
infection of the bone characterized by a lack
of systemic manifestations.
• Pain is the most common symptom, and has
been present for months before the first OPD
visit.
• Difference between sub acute osteomyelitis
and other types of osteomyelitis
– No sinus
– Immunity of individual is normal
– Organism has low virulence
• Examples of sub acute osteomyelitis-
– BROADIES ABSCESS
– SCLEROSING OSTEOMYELITIS OF GARRE
• Brodie’s abcess
• ESR, CRP normal
• m/c - staph aureus
culture often
negative.
• Sclerosing
osteomyelitis of Garre
• Excessive involucrum
formed by
oversensitive
periosteum.
• No abscess cavity.
Thank You

Osteomyelitis

  • 1.
  • 2.
    History • Disease wasknown since the times of Hippocrates (460-370 B.C.) • Bromfield (1773) – “Abcessus in medulla” • John hunter (1834)- recognized the mechanism of sequestrum formation by describing it as a pocket of dead cortical bone within an abscess. • Louise Pasteur (1840s) had implicated microbes in furuncles, osteomyelitis and puerperal fever. He had described osteomyelitis as “a boil of the bone marrow”. • Nelaton is credited with introducing the term “osteomyelitis” in 1844. • Ogston was meanwhile researching on staphylococcus. (1884) • Prior to the introduction of penicillin in 1940, the management of acute osteomyelitis was based on the principles of the American surgeon, Winnett Orr (1877–1956). He advocated incisions which were large enough to expose the whole diseased areas of the bone. All necrotic bone was to be removed with “saucerisation” of the resulting cavity.
  • 3.
    One of theclassifications for osteomyelitis, although no longer commonly used, is based on time • <2weeks – acute osteomyelitis • >6weeks – chronic osteomyelitis • 2-6 weeks – subacute osteomyelitis Classification
  • 4.
    Acute Osteomyelitis • Acuteosteomyelitis is a rapidly destructive pyogenic infection, usually haematogenous in origin, occurring most commonly in infants and children; it starts in a metaphysis of an actively growing long bone and runs a fulminating septic course that may terminate fatally.
  • 5.
    Pathogenesis Hematogenous osteomyelitis: • occursin children < 15 years of age although adults can have this disease • occurs in the metaphysis of the long bones. – sharp hairpin turns – flow becomes considerably slower and more turbulent – decreased activity of macrophages – Frequent trauma (locus minoris resistantae) – Precarious blood supply. Diaphysial osteomyelitis : – Earlier metaphysis but due to growth becomes diaphyseal mostly in children. – Direct trauma to diaphysis – Tubercular
  • 6.
    • ETIOLOGY- – Age:infancy and childhood – Sex: Male predisposition 4:1 – Trauma: history of direct blow frequently elicited – Location: Metaphysis of long bone (m/c upper end of tibia and lower end of femur) – Poor nutrition – Unhygienic surroundings – Antecedent locus of infection- eg. Boils, tonsillitis.
  • 7.
    Causative organisms • Althoughmany organisms can cause osteomyelitis, it can be classified into two – Bacterial pyogenic osteomyelitis – Tuberculous osteomyelitis In pyogenic infections, the periosteal reaction is marked. However in tuberculous osteomyelitis, the local reactions are not marked (with the exception of Spina ventosa)
  • 8.
    • Bacterial pyogenicosteomyelitis is most commonly caused by Staphylococcus aureus in all age groups. However some exceptions are present- – In patients of haemoglobinopathies, most common organism is Salmonella. (several symmetrical bones are involved) – In patients on prolonged parenteral therapy, most commonly fungal infection is found – In IV drug abusers – Pseudomonas – In osteomyelitis following animal bite- Pasteurella – In osteomyelitis following human bite- Eikenella One organism – Hematogenous route of infection Multiple organisms – Exogenous route of infection
  • 9.
  • 10.
    Why is S.Aureus the 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) ----- 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. • Panton valentine leucocidin toxin has been asso. with occurrence of DVT in MRSA infections.
  • 11.
    Clinical Picture • Heat,red, pain or tenderness, swelling • Initially, the lesion is within the medullary cavity, there is no swelling, soft tissue is also normal. • The mere sign is deep tenderness. • Localized finger-tip tenderness is felt over or around the metaphysis. • It is necessary to palpate carefully all metaphysial areas to determine local tenderness, pseudoparalysis. • An increase effusion in the adjacent joint proves in most cases to be a sympathetic synovitis with sterile clear fluid. • hip, shoulder, ankle; these joints can develop septic arthritis by extension of osteomyelitis. • A lighting up of infection is manifested by aching pain that is worse at night. • In later stage, a sinus may open on skin and starts to exudate purulent material and small sequestra.
  • 12.
    Differential diagnosis – Rheumaticfever-less acute, Polyarticular, confined to joints, no effect of antibiotics, dramatic response to salicylates & ACTH. – Ewing sarcoma- fever, leukocytosis, subperiosteal bone deposition present. But diaphysial & diffused; less intense constitutional symptoms. Radiosensitive, biopsy diagnostic. – Acute suppurative arthritis- joint fluid earlier; decreased ROM; ms. spasm; purulent synovial fluid on aspiration.
  • 13.
    Laboratory findings • Thewhite blood cell count will show a marked leucocytosis as high as 30,000 or more. • Raised CRP and ESR. • Blood culture positive in 30-50% of infants and children. • The blood culture demonstrates the presence of bacteremia, the blood must be taken when the patient has a chill, especially when there is a spiking temperature. • Aspiration. The point of maximal tenderness should be aspirated with a large-bore needle.
  • 14.
    Radiological Findings – Radiographsare negative within first 7-10 days. x-ray appearances are of little value in making the early diagnosis. By the time there is x-ray evidence of bone destruction, the patient has entered the chronic phase of the disease. – Careful comparison with the opposite side may show abnormal soft tissue shadows. – It takes from 10 to 21 days for an osseous lesion to become visible on conventional radiography, because a 30–50% reduction of bone density must occur before radiographic change is apparent. – Lamellated periosteal reactions are invariably present . The reparative phase during therapy is characterized by endosteal and periosteal new bone formation, development of surrounding sclerosis and sometimes large osteosclerotic areas.
  • 15.
    Ultrasonography • Ultrasound cannotdirectly access bone marrow abnormalities present in osteomyelitis but can document osteomyelitis indirectly by identifying periosseous soft tissue abnormalities. • The very first sonographic sign, seen even before any periosteal reaction, is edematous swelling of the deep soft tissues
  • 16.
    Bone Scan • Radioisotopicbone scanning is valuable in early localization (within 48 hrs) of bone infection. • The specificity of radioactive isotopic imaging techniques have improved in the evaluation of musculoskeletal infection. • Technitium-99m imaging is very sensitive , it is the choice for acute hematogenous osteomyelitis, the overall accuracy being 92%.
  • 17.
    Magnetic resonance imaging •Magnetic resonance imaging has very high sensitivity and specificity. It is gradually becoming the investigation of choice for acute hematogenous osteomyelitis. • Advantage: – Useful for differentiating between bone and soft-tissue infection. – Helpful in surgical planning. • Disadvantage: – A metallic implant in the region of interest may produce focal artifacts. – False positives in tumors and healing fractures.
  • 18.
    Treatment • Antibiotics-penicillin &cephalosporins; now clinda & vanco. 5-7 days IV, oral for 4-6 wk • Drainage • Conservative – can wait for 48 hours Nade’s indications for surgery • 1. Abscess formation • 2. Severely ill & moribund child with features of acute osteomyelitis • 3. Failure to respond to IV antibiotics for >48 hrs
  • 19.
    •Nade’s principles • Antibiotic is effective before pus forms •  Antibiotic cannot sterilise avacular tissue •  Antibiotic prevents reformation of pus once removed •  Pus removal restores periosteum---- restores blood flow •  Antibiotic should be continued after surgery
  • 20.
    Complications • Bone abscess •Septic Arthritis • Septicaemia • Fracture • Growth arrest • Overlying soft-tissue cellulitis • Thrombophlebitis • Chronic osteomyelitis
  • 21.
  • 22.
    • The Cierny-Maderanatomic types of adult osteomyelitis. (A) Type 1 is intramedullary osteomyelitis, where the nidus is endosteal. (B) Type 2 indicates superficial osteomyelitis, which is limited to the surface of the bone. (C) Type 3 is termed localized osteomyelitis, in which the full thickness of the cortex of the bone is involved. This type of osteomyelitis often requires complex dead space management and osseous stabilization after debridement. (D) Type 4 is diffuse osteomyelitis involving the entire circumference of the bone. These lesions are mechanically unstable and require complex reconstruction.
  • 23.
    Physiologic host A Host Normalhost. Normal immune system. Normal vascularity. B Host Bs: systemic compromise Bl: local compromise Bsl: systemic and local compromise C Host Treatment morbidity worse than present condition with low prognosis for cure.
  • 24.
  • 25.
    Etymology – sequester inLatin means standing apart. – involucrum is derived from Latin word involvō, meaning a sheath that covers or envelopes.
  • 28.
    • Antibiotics- mostworkers prefer IV antibiotics for 5-7 days followed by 4-6 weeks of oral antibiotics after surgery. • Oral antibiotics commonly used- fluoroquonolones, linezolid, trimethoprim. • For MRSA- doxy and clinda • For anaerobic infections- Metronidazole. Treatment
  • 33.
    • Surgery – •Sequestrectomy and saucerisation – check radiology for 6-8 weeks, see for involucrum covering atleast 2/3rd of the diameter of the bone. Debride till paprika sign. • Closed irrigation and suction- mild detergent instilled, preventing formation of penicillinase.
  • 35.
    When to dosequestrectomy? Early sequestrectomy • - Eradicate infection • -Better environment for periosteum to respond Delayed sequestrectomy • Wait till sufficient involucrum has formed before doing a sequestrectomy to mimimize the risk of fracture, deformity & segmental loss
  • 36.
    • Wound isleft open EXCEPT: • a) Compromised hosts (Class B host); ankle, hand, spine • b) Type II lesions (primary soft tissue reconstruction and/or host alteration) • c) Minimal necrosis osteomyelitis
  • 37.
    • Papineau technique:Cavity is packed with small cancellous bone graft (preferably autogenous) mixed with an antibiotic and fibrin sealant • Primary closure with transferred tissue: In muscle flap transfer, a suitable large wad of muscle with its blood supply intact can be mobilized and laid into the cavity. The surface is later closed with a split-skin graft • Primary closure with antibiotic impregnated beads: Porous gentamicin-impregnated PMMA beads are used to sterilize the cavity. It is easier but less successful. Furthermore, they are extremely difficult to be removed if not taken out by 2-3 weeks Reconstruction of bone & soft-tissue defect
  • 39.
    Subacute Osteomyelitis • Subacuteosteomyelitis is defined as a chronic infection of the bone characterized by a lack of systemic manifestations. • Pain is the most common symptom, and has been present for months before the first OPD visit.
  • 40.
    • Difference betweensub acute osteomyelitis and other types of osteomyelitis – No sinus – Immunity of individual is normal – Organism has low virulence • Examples of sub acute osteomyelitis- – BROADIES ABSCESS – SCLEROSING OSTEOMYELITIS OF GARRE
  • 41.
    • Brodie’s abcess •ESR, CRP normal • m/c - staph aureus culture often negative.
  • 42.
    • Sclerosing osteomyelitis ofGarre • Excessive involucrum formed by oversensitive periosteum. • No abscess cavity.
  • 43.