Osteomyelitis

OSTEOMYELITIS
DR. GAJANAN PANDIT

DEFINITION
Osteomyelitis is defined as an inflammation of the
bone caused by an infecting organism.
The infection may be limited to a single portion of
the bone or may involve numerous regions such as
the marrow, cortex, periosteum, and the surrounding
soft tissue.
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OSTEOMYELITIS

CLASSIFICATION
Classification of osteomyelitis is based on numerous
criteria, such as
Based on duration of symptoms.
Based on mechanism of infection.
Based on the host response to disease.
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CLASSIFICATION
Based on duration of symptoms.
Acute
Subacute
Chronic
The time limits defining these classes are arbitrary.
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CLASSIFICATION
Based on mechanism of infection.
Exogenous
Hematogenous
Exogenous osteomyelitis is caused by open fractures,
surgery (iatrogenic), or contiguous spread from
infected local tissue.
The hematogenous form results from bacteremia.
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CLASSIFICATION
Based on the host response to disease.
Pyogenic
Nonpyogenic
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Bacterial Associations
7
Hematogenous osteomyelitis is most commonly
caused by S. aureus.
In the past, Haemophilus influenzae type B (HiB)
was a common organism in children, but the advent
of HiB vaccine has made it a rare cause.
Causes of osteomyelitis due to direct inoculation,
such as into an open fracture, will be influenced by
the environment in which the injury occurred. For
example, injuries occurring in water may lead to
infection with Aeromonas or Plesiomonas.
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8
Nail puncture wounds of the foot, particularly
through a tennis shoe, are associated with infection
with Pseudomonas aeruginosa
Underlying medical conditions of the host also
influence the expected microbiology. Intravenous
drug users may have P. aeruginosa and other
gram-negative bacilli as causes of their
osteomyelitis
Patients with sickle cell disease are prone to
the development of Salmonella osteomyelitis.

9
Osteomyelitis caused by fungal infections is more
likely to be seen in immunocompromised hosts.
Diabetic foot infections leading to osteomyelitis
often are polymicrobial, often involving anaerobes
and gram-positive and gram-negative aerobic bacilli.
Patients infected with the human immunodeficiency
virus (HIV) are at risk for a variety of unusual
infections, including atypical mycobacteria.

ACUTE HEMATOGENOUS OSTEOMYELITIS
This is the most common type of bone infection and
usually is seen in children.
It is more common in males in all age groups.
It is caused by a bacteremia which is common
occurrence in children.
Bacteriological seeding of bone is generally
associated with other factors such as localized
trauma, chronic illness, malnutrition, or an
inadequate immune system.
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OSTEOMYELITIS

ACUTE HEMATOGENOUS OSTEOMYELITIS
In children, the infection generally involves the
metaphysis of rapidly growing bone.
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OSTEOMYELITIS

CAUSES FOR MORE INCIDENCE OF
METAPHYSEAL OSTEOMYELITIS
1. Hair pin bend vessels in metaphysis.
2. Increased vascularity to metaphysis causing
pooling of blood. It has been aptly called ‘a lake of
blood’.
3. Immature cells of metaphysis due to high turnover.
4. Relative lack of phagocytosis.
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OSTEOMYELITIS

CAUSES FOR MORE INCIDENCE OF
METAPHYSEAL OSTEOMYELITIS
5. Presence of degenerating cartilage cells which act
as a good culture media.
6. Presence of end arteries in metaphysis.
7. More prone to trauma.
8. Presence of single endothelial lining in
metaphyseal arteries.
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OSTEOMYELITIS

Pathogenesis
14
Introduction of bacteria.
Infective embolus enters the nutrient artery.
Trapped in small calibre vessels.
Active hyperemia.
Exudate and debris.
Increased pressure in bone.
Exudate travels along the paths of least resistence.
Subperiosteal abscess.
Sequestrum.

DIAGNOSIS
A diagnosis of acute osteomyelitis should be considered an
emergency.
The presenting signs and symptoms may vary with the
severity of the infection.
Symptoms include fever and chills, general malaise,
irritability, pain, and swelling.
With lower extremity involvement, there is either a
limp or an inability to bear weight.
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OSTEOMYELITIS

DIAGNOSIS
An infant with upper extremity involvement may exhibit
pseudoparalysis; older children and adults with upper
extremity involvement complain of pain on movement or
use of the extremity.
It is important to localize the point of maximum
tenderness, which is usually warm and swollen. In children
it is generally in the metaphyseal region.
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OSTEOMYELITIS

DIAGNOSIS
It is also important to evaluate the adjoining joint for
evidence of septic arthritis, which can occur as an
extension of the adjoining osteomyelitis.
Osteomyelitis involving the
 neck of the femur,
 talus, and
 humeral head often leads to sepsis of the joint because
these foci are located within the joint capsule.
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DIAGNOSIS
Once the point of maximum tenderness is localized,
aspirate the area, and send the pus or fluid obtained for
Gram stain, culture, and sensitivity studies.
If tuberculosis or a fungal infection is suspected, obtain an
acid-fast stain and tuberculosis and fungal cultures.
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OSTEOMYELITIS

DIAGNOSIS
When a joint effusion is present or joint involvement is
suspected, aspirate the joint and confirm with an
arthrogram.
The arthrogram helps document the location of the
aspiration and is useful for positive as well as for negative
aspirations, since it may also identify joint capsule rupture.
Aspiration of the hip joint under ultrasound guidance is
very helpful in children and adults.
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OSTEOMYELITIS

DIAGNOSIS
The white blood cell count is generally elevated,
depending on the severity of the infection, with an increase
in immature or band cells.
The erythrocyte sedimentation rate and the C-reactive
protein are usually elevated.
Obtain blood cultures in all cases of acute hematogenous
osteomyelitis and in chronic osteomyelitis exacerbated by
fever and bacteremia.
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OSTEOMYELITIS

DIAGNOSIS
Roentgenograms taken early in the disease process
generally show soft-tissue swelling. Bony changes are not
present until 7–10 days after the onset of infection.
Radionuclide bone scanning using radioactive-labeled
isotopes, such as technetium-99m and, more specifically,
gallium citrate-67 and indium-111-labeled white blood
cells, is helpful in localizing the area of involvement and in
helping diagnose the condition.
Aspiration is used for the diagnosis, especially when there
is no drainage or sinuses, and in some cases bone biopsy
may be necessary.
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OSTEOMYELITIS

DIAGNOSIS
Magnetic resonance imaging (MRI) has added a new
dimension to the diagnosis, localization, and
characterization of the extent of infection.
T1- and T2-weighted images are the initial screening
techniques for diagnosing osteomyelitis.
The MR finding in osteomyelitis on T1-weighted image
sequences is a low signal intensity due to a dark marrow
signal and an increased signal intensity due to a bright
marrow signal on the T2-weighted image sequences. MRI
has decreased the need for bone scanning and provides
more useful information.
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OSTEOMYELITIS

DIAGNOSIS
Sinograms are done whenever there is a sinus tract or
open draining area from which the depth and extent of the
infection can be determined.
Abscessograms are done whenever an abscess is present
and frank pus is aspirated. The abscessogram will help
outline the extent of the abscess cavity.
MRI, computed tomographic scanning, and radiographic
tomogram are all useful tools in evaluating osteomyelitis.
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OSTEOMYELITIS

Radiographic Pathogenesis
The earliest signs of bone infection are soft-tissue
edema and loss of fascial planes. (seen within 24 to
48 hours of the onset of infection)
The earliest changes in the bone are evidence of a
destructive lytic lesion. (seen within 7 to 10 days after
the onset of infection), and a positive radionuclide
bone scan.
Within 2 to 6 weeks, there is progressive destruction
of cortical and medullary bone, an increased
endosteal sclerosis indicating reactive new bone
formation, and a periosteal reaction.
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OSTEOMYELITIS

Radiographic Pathogenesis
26
In 6 to 8 weeks, sequestra indicating areas of
necrotic bone usually become apparent; they are
surrounded by a dense involucrum, representing a
sheath of periosteal new bone.

DIFFERENTIAL DIAGNOSIS
27
Acute Rheumatism:
onset- gradual, pain- less acute, articular, swelling
confined to joint, affects more than one joint at the
same time and is ‘flitting’ in nature.
Erysipelas:
Less pain and general toxemia.
Haemophilia:
Bleeding diathesis should be looked for.

DIFFERENTIAL DIAGNOSIS
28
Cellulitis:
No intense pain and general malaise is less.
Acute Pyogenic Arthritis:
Features related to joint.
Ewing’s tumour or Osteosarcoma:
Much less intense general illness.

PRINCIPLES OF TREATMENT OF ACUTE
OSTEOMYELITIS (Proposed by NADE)
1. An appropriate antibiotic is effective before pus
formation.
2. Antibiotics do not sterilize avascular tissues or abscesses,
and such areas require surgical drainage.
3. If such removal is effective, antibiotics should prevent
their reformation, and primary wound closure should be
safe.
4. Surgery should not damage further already ischemic bone
and soft tissue; and
5. Antibiotics should be continued after surgery.
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OSTEOMYELITIS

INDICATIONS FOR SURGERY IN ACUTE
HEMATOGENOUS OSTEOMYELITIS
1. Presence of an abscess requiring drainage.
2. Failure of the patient to improve despite appropriate
intravenous antibiotics.
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OSTEOMYELITIS

Subacute Hematogenous Osteomyelitis
31
More insidous onset.
Lacks severity of symptoms.
Diagnosis usually delayed.
Temperature is only mildly elevated.
Mild to moderate pain.
Usually positive radiographs and bone scan.
Often confused with malignancy.

32
The indolent course is related to
Increased host resistence.
Decreased bacterial virulence.
Administration of antibiotics before onset of
symptoms.

Classification:
Gledhill and modified by
Roberts et. al.
Type I
Central metaphyseal
lesion.
DD: Langerhans’ cell
histiocytosis, Brodie
abscess.
33

Classification:
Roberts et. al.
Type II
Eccentric metaphyseal
lesion with cortical
erosion.
DD: Eosinophilic
granuloma, osteogenic
sarcoma.
34

Classification:
Roberts et. al.
Type III
Diaphyseal cortical
lesion.
DD: Osteiod osteoma
35

Classification:
Roberts et. al.
Type IV:
Diaphyseal lesion with
periosteal new bone
formation, but without
bony lesion.
DD: Ewings sarcoma.
36

Classification:
Roberts et. al.
Type V:
Primary subacute
epiphyseal osteomyelitis
DD: Chondroblastoma.
37

Classification:
Roberts et. al.
Type VI:
Subacute osteomyelitis
crossing physis to involve
metaphysis and
epiphysis.
DD: Tuberculosis,
osteogenic sarcoma
38

39
Diagnosis must be established by an open biopsy and
culture.
Treatment consists of biopsy and curretage followed
by treatment with appropriate antibiotics.

Brodie Abscess
40
Localized form of subacute osteomyelitis.
Involves long bones of lower extremity.
C/f: intermittent pain of long duration, local
tenderness.
X-rays:- lytic lesion with a rim of sclerotic bone.
T/t: open biopsy with curettage.

CHRONIC OSTEOMYELITIS
The hallmark of chronic osteomyelitis is infected
dead bone within a compromised soft-tissue
envelope.
The infected foci within the bone is surrounded by
sclerotic, relatively avascular bone covered by a
thickened periosteum and scarred muscle and
subcutaneous tissue.
This avascular envelope of scar issue leaves systemic
antibiotics essentially ineffective.
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OSTEOMYELITIS

CLASSIFICATION:
Cierny and Mader classification based on
Physiological criteria and,
Anatomical criteria
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OSTEOMYELITIS

Physiological criteria: are divided into 3 classes
based on three types of host:
Class A hosts have a normal response to infection
and surgery.
Class B hosts are compromised and have deficient
wound healing capabilities.
Class C hosts, the results of treatment are
potentially more damaging than the present
condition.
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OSTEOMYELITIS

Anatomical criteria:
Type I: Medullary
Is characterised by
endosteal disease.
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OSTEOMYELITIS

Type II: Superficial
Limited to surface of the
bone.
Infection is secondary to
a coverage defect.
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OSTEOMYELITIS

Type III: Localized
Stable, well demarcated
lesion characterised by
full thickness cortical
sequestration and
cavitation.
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OSTEOMYELITIS

Type IV: Diffuse
Lesion creates
mechanical instability,
either at presentation or
after appropriate
treatment.
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OSTEOMYELITIS

Radiographic Findings
48
Early stages- Moth – eaten appearance.
Elevation of periosteum with subperiosteal
laminations of new bone.
Sharply delineated areas of dense bone with
surrounding decalcification.
Gradually, necrotic dense area is sorrounded by
white ring of involucrum.

Sclerosing Osteomyelitis of Garre
49
Chronic form of disease in which the bone is
thickened and distended.
Abscesses and sequestra are absent.
Intermittent pain of moderate intensity and usually
long duration.
Swelling and tenderness.
X-ray: expanded bone with generalized sclerosis.
T/t: Fenestration of sclerotic bone and antibiotics.

TREATMENT:
Surgery for chronic osteomyelitis consists of
sequestrectomy and resection of scarred and infected
bone and soft tissue.
The goal of surgery is eradication of the infection by
achieving a viable and vascular environment.
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OSTEOMYELITIS

SEQUESTRECTOMY AND CURETTAGE
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AFTERTREATMENT:
Protection of limb
Antibiotics
Management of dead space.
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OSTEOMYELITIS

METHODS OF DEAD SPACE MANAGEMENT
PAPINEAU CANCELLOUS GRAFT
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OSTEOMYELITIS

LOCAL CLOSURE
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OSTEOMYELITIS

MYOPLASTY
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OSTEOMYELITIS

FREE BONE TRANSFER
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OSTEOMYELITIS

USE OF BONE TRANSPORT
ILIZAROV TECHNIQUE
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OSTEOMYELITIS

OPEN BONE GRAFTING
Papineau et. al. described an open bone grafting
technique for the treatment of chronic osteomyelitis.
Based on following principles:
1. Granulation tissue markedly resists infection.
2.Autogenous cancellous bone grafts are rapidly
revascularized and are resistant to infection.
3.The infected area is completely excised.
4.Adequate drainage is provided.
5.Adequate immobilization is provided and
6.Antibiotics are used for prolonged periods.
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OSTEOMYELITIS

Papineau technique
The surgery is divided into three stages:
1. DEBRIDEMENT
2.CANCELLOUS AUTOGRAFTING:- posterior iliac
crest, 3 to 4 cm long.
3.SKIN CLOSURE
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OSTEOMYELITIS

Papineau technique
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OSTEOMYELITIS

Polymethylmethacrylate Antibiotic Bead Chains
Commonly used.
Rationale
Bead pouch technique when primary closure not
possible.
Aminoglycosides most commonly employed.
Short term(10 days), long term(80 days) or
permanent implantation.
Rationale for removal.
Technique.
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OSTEOMYELITIS

Biodegradable Antibiotic Delivery System
Advantage over PMMA:- no second procedure,
osteoinductive and osteoconductive property.
E.g. of carriers: BMP+ cancellous bone,
Demineralised bone matrix(DBM) + CaSo4, CaPO4,
Hydroxyappetite.
Problem with calcium based carriers.
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OSTEOMYELITIS

Other modalities
Soft tissue transfer.
Ilizarov technique.
Hyperbaric Oxygen Transfer.
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OSTEOMYELITIS

Complications
Growth disturbances.
Pathological fracture.
Muscle contractures.
Secondary septicemia.
Epithelioma.
Joint stiffness.
Amyloidosis.
66

SURGICAL CONSIDERATIONS
TOURNIQUETS
Apply a tourniquet whenever possible except in patients
with sickle cell disease or significant peripheral vascular
disease.
The tourniquet improves hemostasis and thus facilitates
identification of the infection process.
In acute cases with swelling, cellulitis, or abscess
formation, elevate the extremity for several minutes
before inflating the tourniquet.
In chronic osteomyelitis without significant cellulitis or
abscess formation, use an elastic bandage to extravasate
the extremity before inflating the tourniquet
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OSTEOMYELITIS

DEBRIDEMENT
Thorough debridement of all sequestra and necrotic and
desiccated bone is essential.
Do not remove viable infected bone, so as not to create
large bony defects. It is not necessary to debride viable
infected bone.
Clinically dried out, exposed, desiccated bone is darker
than normal and should be debrided. Necrotic bone that
has not been exposed may appear at surgery more
yellowish than viable bone, which is whitish. The main
finding is that viable bone bleeds, whereas necrotic bone
does not.
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DEBRIDEMENT
Use of an osteotome to superficially shave the outer
cortex of the questionable bone results in small areas
of punctate bleeding.
Some bone that may have been exposed to air may
be viable; in these cases, the exposed outer cortex
should be debrided with an osteotome down to good
bleeding bone.
Evacuate all pus and abscess, and remove all necrotic
and infected soft tissue.
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OSTEOMYELITIS

IRRIGATION
Use copious amounts of irrigating fluid, which
cleanses the area of purulent exudate, loose soft
tissue, and bony fragments, and decreases the
bacterial count.
Recommended:- 2 L of antibiotic solution containing
50,000 units of bacitracin and 1 million units of
polymyxin per liter as the final irrigating solution.
Other antibiotics can be used for topical irrigation as
well.
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WOUND MANAGEMENT
The decision to leave a wound open or to close it requires
careful judgment. In the majority of acute infections, and in
all cases in which there is associated abscess formation with
cellulitis and swelling, the wound should be left open.
In some cases of early postoperative infection, the wound may
be closed over drainage tubes, as long as the wound is
thoroughly clean and the infection is not anaerobic.
In cases of chronic osteomyelitis in which there is no
significant cellulitis or abscess formation and in which the
wound has been adequately debrided and converted to a clean
wound, the wound may be closed over drainage tubes.
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WOUND MANAGEMENT
In some cases in which bone or metal will be exposed
if the wound is left open, a partial closure over the
bone or metal may be desirable, as long as an
adequate pathway has been provided for drainage.
When there is any doubt, it is safest to leave the
wound open.
If the wound is closed, the wound site must be
examined daily for any signs of infection; if such
signs appear, the wound must be opened.
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WOUND MANAGEMENT
Many wounds heal nicely by secondary intention. In the case
of large wounds or when delayed closure is preferable, do not
attempt closure until two criteria are met.
First, the wound should appear clinically healthy, with clean
granulating tissue and without any purulent exudate or
necrotic tissue. If infected necrotic tissues are present,
redebride the wound until it appears healthy.
Second, once the clinical appearance of the wound is clean,
take quantitative tissue cultures and do Gram stains. Wounds
with either a positive Gram stain or quantitative tissue
cultures with a bacterial count greater than 10-5 organisms
should never be closed. (A positive Gram stain implies a
bacterial count of greater than 10-5 organisms.)
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OSTEOMYELITIS

WOUND MANAGEMENT
These wounds should be considered infected and reassessed
for further surgical debridement and the appropriateness of
the systemic antibiotic therapy.
In secondary closure of wounds, it is important to redebride
the wound at the time of closure and to do en bloc resection of
the granulating tissue for several reasons.
First, although the bacterial count is low, these tissues should
still be considered contaminated; debridement will further
reduce the bacterial count and thereby diminish the chance of
infection.
Second, debridement allows for cleaner, healthier tissue to be
approximated by wound closure or covered by muscle
transfer.
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OSTEOMYELITIS

DRAINS
When the wounds are closed, Silastic or polyethylene drains may be
used.
Remove the suction drain in 48–72 hours. The drain allows the
removal of all hematoma and tissue fluid, and the collapse of the
potential dead space. The drains should be removed under sterile
conditions and the tip cut off and sent for culture and sensitivity
tests.
The drain tends to attract whatever bacteria are present because it is
a foreign body and because tissue fluids are removed through it.
In general, a positive culture of the drain tip is a bad prognostic
sign: It means that bacteria remain behind.
Monitor the clinical course and wound site closely; if any clinical
signs of wound infection reappear, it may be necessary to consider
redebridement and reassessment of antibiotic therapy.
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OSTEOMYELITIS

WOUND PACKING
The purpose of leaving a wound open is to allow drainage.
Make certain, therefore, when packing wounds with gauze or
other materials, that packing does not obstruct drainage. If it
does, the purulent exudate will be retained in the wound,
possibly causing tissue breakdown and necrosis with
secondary cellulitis or even abscess formation.
It is best to put wicks perpendicular to the open wound to
allow free drainage. Wicks can be either povidone-iodine
(Betadine)-soaked gauze, plain gauze, or fine-mesh gauze. The
size varies with the size of the wound. The ends of the wicks
should always protrude through the skin edges to allow easy
access and removal and to prevent retention.
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OSTEOMYELITIS

PRINCIPLES OF TREATMENT OF INFECTED
UNUNITED FRACTURES AND NONUNIONS
The principles of treatment are infection control,
stabilization of the fracture, soft-tissue coverage, and
bone graft of ununited fractures and large bone defects.
Infection control includes irrigation and debridement,
culture and sensitivities, and antibiotic therapy. In
chronic osteomyelitis, obtain aerobic, anaerobic, and
fungal cultures. Recent studies have advocated taking of
multiple deep cultures from purulent material, soft
tissue, and bone
Stabilization of the ununited fracture or nonunion is
essential. Soft-tissue coverage may require the use of
local muscle flaps and free vascularized muscle flaps for
soft-tissue defects or an inadequate soft-tissue envelope
after control of the osteomyelitis.
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OSTEOMYELITIS

PRINCIPLES OF TREATMENT OF INFECTED
UNUNITED FRACTURES AND NONUNIONS
Local muscle flaps and free vascularized muscle transfers
also help by bringing in a new blood supply, which is
important in host defense mechanisms, antibiotic
delivery, and osseous and soft-tissue healing. For the
tibia, use the gastrocnemius muscle for proximal-third
defects, the soleus for middle-third, and for the distal-third,
free vascularized muscle transfers.
For local muscle transfers, it is important to assess the
muscle preoperatively and not to transfer damaged
muscle. Also avoid using crushed or badly damaged
muscle, as flap necrosis or flap complications may result.
In these cases, use free vascularized tissue transfer. Do
preoperative angiograms on patients whose vascular
status has been altered from any cause.
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Osteomyelitis

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