Osteomyelitis
Mbanga John Md,Mmed
Orthopaedic surgeon
MZRH
Osteomyelitis
Nelaton (1834) : coined osteomyelitis
The root words osteon (bone) and myelo
(marrow) are combined with itis
(inflammation) to define the clinical state
in which bone is infected with
microorganisms.
Introduction
Osteomyelitis is an inflammation of bone
caused by an infecting organism.
It may remain localized, or it may spread
through the bone to involve the marrow,
cortex, periosteum, and soft tissue
surrounding the bone.
Classification
Attempts to classify are based on
(1) the duration and type of symptoms
(2)the mechanism of infection
(3)the type of host response
Osteomyelitis
Based on the duration and type of
symptoms
Acute: <2weeks Early acute
Late acute(4-5days)
Subacute: 2weeks— Less virulent – more
6weeks immune
Chronic: >6 weeks
Classified according to mechanism
Osteomyelitis may be
1. Exogenous(trauma, surgery
(iatrogenic), or a contiguous infection)
2. Hematogenous (bacteremia)
Etiology
In infants: In children over one
Staphylococcus
Staphylococcus year of age:
aureus is common
aureus Staphylococcus
organism isolated.2
Streptococcus aureus,
agalactiae Streptococcus
Escherichia coli pyogenes
Haemophilus
influenzae1
Single pathogenic organism hematogenous osteomyelitis,
Multiple organisms direct inoculation or contiguous focus
infection.
Staphylococcus aureus ---most commonly isolated pathogen.
1.Song KM, Sloboda JF. Acute hematogenous osteomyelitis in children. J Am Acad Orthop Surg.
gram-negative bacilli and anaerobic organisms are also frequently isolated
2001;9:166-75
2.Lew DP, Waldvogel FA. Osteomyelitis. N Engl J Med. 1997;336:999-1007
Organisms Isolated in Bacterial
Organism
Osteomyelitis
Comments
Staphylococcus aureus Organism most often isolated in all types of
osteomyelitis
Coagulase-negative staphylococci Foreign-body–associated infection
or Propionibacterium species
Enterobacteriaceae species Common in nosocomial infections and
orPseudomonas aeruginosa punchured wounds
Streptococci or anaerobic bacteria
Associated with bites, fist injuries caused by
contact with another person’s mouth,
diabetic foot lesions, decubitus ulcers
Salmonella species
orStreptococcus pneumoniae Sickle cell disease
Lew DP, Waldvogel FA. Osteomyelitis. N Engl J Med 1997;336:999-1007 .
Epidemiology
Incidence of infection increases with increase in grade of
compounding (Guistilo, Anderson) :
Approx. 2% for type I and type II
Approx. 10% to 50% for type III
The tibia most common site for infection.
Pathogenesis: Hematogenous
spread usually
involves the
metaphysis of long
bones in children or
the vertebral bodies
in adults
Direct inoculation of
microorganisms into
bone penetrating Microorganism
s in bone Osteomyelitis
injuries and surgical
contamination are most
common causes
Contiguous focus of
infection seen in patients
with severe vascular
disease.
Pathology:
– sharp hairpin turns
– flow becomes considerably slower
and more turbulent
Pathogenesis
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
These are end-artery branches of the nutrient artery
Pathology
acute inflammatory response due to infection
tissue necrosis, breakdown of bone
Obstruction
Avascular necrosis of bone
Squestra formation
Chronic osteomyelitis
Pathology:
The involucrum is the sheath of reactive,
new, immature, subperiosteal bone that
forms around the sequestrum, effectively
sealing it off the blood stream just like a
wall of abscess.
The involucrum is irregular and is
often perforated by openings.
The involucrum may gradually
increase in density and thickness to
form part or all of a new diaphysis.
local signs
calor, rubor, dolor, tumor
Heat, red, pain or tenderness, swelling
Initially, the lesion is within the medually cavity, there is no
swelling, soft tissue is also normal.
The merely sign is deep tenderness.
Localized finger-tip tenderness is felt over or around the
metaphysis.
it is necessary to palpate carefully all metaphysic areas to
determine local tenderness, pseudoparalysis
Clinical
features
During the period of inactivity, no symptoms are present.
Only Skin-thin, dark, scarred, poor nourished, past sinus, an
ulceration that is not easily heal
Muscles-wasting contracture, atrophy
Joint-stiffness
Bone-thick, sclerotic,
often contains abscess cavity
X-ray findings
X-ray films are negative within 1-2 weeks
Careful comparison with the opposite side may show
abnormal soft tissue shadows.
It must be stressed that x-ray appearances are normal in the
acute phase. There are 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.
X-ray findings
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
Bonakdarpour A, Gaines VD (1983) The radiology of osteomyelitis. Orthop
Clin North Am 14:21–33
X-ray findings
1. Localized osteopaenia and trabecular destruction are
early signs of a suppurative acute process in the bone.
2. The type and extent of cortical destruction is variable . A
wide spectrum is encountered, ranging from a solitary
radiolucency to irregular, multiple radiolucencies (mottling)
to a permeative pattern. The individual lesions are
generally indistinct and irregular in outline.
X-ray findings
3. Lamellated periosteal reactions are invariably present .
4. The reparative phase during therapy is characterized by
endosteal and periosteal new bone formation, development of
surrounding sclerosis and sometimes large osteosclerotic
areas.
5. Soft tissue changes, such as swelling and obliteration of
tissue planes, are rarely of diagnostic value in adults.
6. In newborns and infants, however, loss of normal fat planes
within days of the onset of symptoms may be an early sign of
soft tissue swelling. In this age group lamellated periosteal
changes are generally discernible before any bone
destruction. A late manifestation is the ballooned metaphysis,
sometimes with involvement of the epiphysis.
Differential diagnosis:
Tuberculosis –
Thin watery d/s
Undermining ,bluish discoloration
Diaphyseal involv. More common
H/o pulm. T.B.
Often multifocal
Soft tissue infection
absence of bony changes
Ewing sarcoma
radiological d/d
acute presentation
Bx is diagnostic.
Foreign body
Osteoid osteoma
Histiocytic eosinophilic granuloma
Garre’s osteomyelitis
Treatment
1. General treatment: nutritional
therapy or general supportive treatment
by taking enough caloric, protein,
vitamin etc.
2. Antibiotic therapy
3. Surgical treatment
4. Immobilization
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
Nade S. Antibiotics in the management of acute haematogenous
osteomyelitis and acute septic arthritis in infancy and childhood. Aust New
Zealand J Surg. 1978;48:78–80
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
Complications
Chronic osteomyelitis- 2% in >3wks, 19% in < 3wks
Septic arthritis
Growth disturbance
Septicemia
DVT
Pulmonary embolism
Ramos OM: Chronic osteomylitis in children. Paedi Infe Dis J 2002; 21:431
SUBACUTE HEMATOGENOUS
OSTEOMYELITIS
More insidious onset and lacks the severity of
symptoms
Diagnosis typically is delayed for more than 2 weeks.
a pathogen is identified only 60% of the time
S. aureus and Staphylococcus epidermidis
The diagnosis often must be established by an open
biopsy and culture
Brodie’s abcess
Bone abscess containing pus or jelly like
granulation tissue surrounded by a zone
of sclerosis
Age 11-20 yrs, metaphyseal area,
usually upper tibia or lower femur
Deep boring pain, worse at night,
relieved by rest
Circular or oval luscency surrounded by
zone of sclerosis
Treatment:
Conservative if no doubt - rest + antibiotic
for 6 wks.
if no response – surgical evacuation &
curettage, if large cavity - packed with
cancellous bone graft
Chronic Osteomyelitis of the Femur
Chronic osteomyelitis
If any of sequestrum, abscess cavity, sinus tract or
cloaca is present.
Hematogenous infection with an organism of low virulence
may be present by chronic onset.
Infection introduced through an external wound usually
causing a chronic osteomyelitis.
It is due to the fact that the causative organism can lie
dormant in avascular necrotic areas occasionally becoming
reactive from a flare up.
Classification
The two most widely used in the medical literature and in
clinical practice are those presented by :
Waldvogel et al-
Osteomyelitis is described as either acute or chronic,
depending on the absence or presence of dead bone.
Osteomyelitis is also classified according to the
source of the infection:
hematogenous when it originates from a bacteremia
contiguous focus when it originates from an infection
in nearby tissue
A third category in this classification is osteomyelitis
in the presence of vascular insufficiency.
Classification
Cierny et al -
Includes four anatomic stages
Stage-1, or medullary, osteomyelitis is confined to
the medullary cavity of the bone.
Stage-2, or superficial, osteomyelitis involves only
the cortical bone.
Stage-3, or localized, osteomyelitis usually involves
both cortical and medullary bone but does not
involve the entire diameter of the bone.
Stage-4, or diffuse, osteomyelitis involves the entire
thickness of the bone, with loss of stability.
Classification
With this system, a patient with osteomyelitis is classified
as an A, B, or C host.
An “A” host has no systemic or local compromising
factors.
A “B” host is affected by one or more compromising
factors.
Bs-systemic compromise
Bl-local compromise
Bls-both sys and local compromise
A “C” host is so severely compromised that the radical
treatment necessary would have an unacceptable risk-
benefit ratio (Table I).
Clinical features
During the period of inactivity, no symptoms are present.
Only Skin-thin, dark, scarred, poor nourished, past sinus, an
ulceration that is not easily to heal
Muscles-wasting contracture, atrophy
Joint-stiffness
Bone-thick, sclerotic,
often contain abscess cavity
PERIOSTEAL NEW BONE
FORMATION
SEQUESTRUM
INVOLUCRUM
ANTIBIOTICS
IV antibiotics
Nafcillin/oxacillin/nafcillin with rifampcin
Vancomycin/ampicillin/cefazolin/ceftriaxone
Clindamycin/sulbactum/piperacillin/tazobactam
ORAL antibiotics
Clindamycin/rifampcin/cotrimoxazole
Fluoroquinolones in gram –ve organisms
Linezolid-oral & IV antibiotics—MRSA
To wait is to invite
disaster.
Surgical treatment
Bone Debridement:
The goal of debridement is to leave healthy, viable tissue.
Débridement of bone is done until punctate bleeding is
noted, giving rise to the term the paprika sign.
Copious irrigation with 10 to 14 L of normal saline.
Pulsatile lavage using fluid pressures 50-70 pounds per
square inch and 800 pulses per min.
The extent of resection is important in B hosts as B
hosts treated with marginal resection (i.e., with a clearance
margin of <5 mm) found to have a higher rate of
recurrence than normal hosts.A
Repeated debridements may be required.
A.Simpson AH, Deakin M, Latham JM. Chronic osteomyelitis. The effect of
the extent of surgical resection on infection-free survival. J Bone Joint Surg
Br. 2001;83:403-7.
Sequestrectomy and curettage. A, Affected bone is exposed, and sequestrum
is removed. B, All infected matter is removed. C, Wound is either packed
open or closed loosely over drains.
When to do sequestrectomy?
Early sequestrectomy Delayed sequestrectomy
- Eradicate infection Wait till sufficient involucrum
-Better environment for has formed before doing a
periosteum to respond sequestrectomy to mimimize the
risk of fracture, deformity &
segmental loss
In either case it is critical to preserve the
involucrum
preferable to wait at least 3-6 months before
performing a sequestrectomy
Saucerization
Extension of surgical
debridement
Debrided wounds left open
widely through excision of
overhanging soft tissue and
bone
Wounds drain freely
Abscesses do not form
Limited to areas where it
causes acceptable loss of
function e.g. Tibia and
femur
May require stabilization
Muscle flaps
Increases the blood supply to that area.
Superior to skin flaps .
Obliterates dead space in irregularly
contoured osseous cavity.
Resistance to recurrent sepsis.
Gastocnemius most common -covers proximal
1/3 of tibia , knee, distal 1/5 of femur.
Not used in –distal 1/3 tibia, midfoot,
forefoot.
Cross leg flaps-prolonged immobilization,
exposes normal extremity to infection.
Indications :
Adjacent soft tissue cannot cover the area.
Area should anatomically permit transportation
of a local muscle flap without compromising its
neurovascular bundle.
Debridement procedure hasn’t compromised the
mechanical integrity of osseous structures.
Gross purulence has been eliminated.
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