Osteomyelitis Akut Dan Kronik

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ACUTE AND

CHRONIC
OSTEOMYELITIS
DEFINITION

 Inflammation of the bone caused


by an infecting organism
HISTORY

In the early 1900’s about 20% of


patients with osteomyelitis died
and patients who survived had
significant morbidity.
Introduction-
• Oldest known evidence of
osteomyelitis fractured spine of
dimetrodon permian reptile 291-250
million years ago

• Hippocrates 460-370 BC infection


after fracture

• Nelaton credited with introducing


the term osteomyelitis in 1844 4
INTRODUCTION
 The key to successful management is
early diagnosis and appropriate
surgical and antimicrobial
treatment.
 A multi disciplinary approach is
required, involving an orthopaedic
surgeon, an infectious disease
specialist, and a plastic surgeon in
complex cases with significant soft
tissue loss.
CLASSIFICATION
1) The duration - acute, subacute and
chronic

2) Mechanism of infection – exogenous


or hematogenous

3) The type of host response to the


infection- pyogenic or non pyogenic
ACUTE HEMATOGENOUS
OSTEOMYELITIS
 Most common type of bone
infection, usually seen in children
 Decrease in incidence, could be due
to higher standard of living and
improved hygiene.
 Bimodal distribution- younger than 2
years, and 8-12 years
 More common in males
ACUTE HEMATOGENOUS OSTEOMYELITIS-
CAUSES
 Caused by a bacteraemia

 Bacteriological seeding of bone


generally is associated with
other factors such as localized
trauma, chronic illness,
malnutrition or an inadequate
immune system.
ACUTE HEMATOGENOUS OSTEOMYELITIS
PATHOPHYSIOLOGY

 In children the infection generally


involves the metaphyses of rapidly
growing long bones

 Bacterial seeding leads to an


inflammatory reaction which can
cause local ischaemic necrosis of bone
and subsequent abscess formation
ACUTE HEMATOGENOUS OSTEOMYELITIS
PATHOPHYSIOLOGY
 As the abscess enlarges,
intramedullary pressure increases
causing cortical ischaemia, which
may allow purulent material to
escape through the cortex into the
subperoisteal space.
ACUTE HEMATOGENOUS OSTEOMYELITIS
PATHOPHYSIOLOGY

 A subperisoteal abscess then


develops

 If left untreated this process


eventually results in extensive
sequetra formation and chronic
osteomyelitis
ACUTE HEMATOGENOUS OSTEOMYELITIS
PATHOPHYSIOLOGY

 In children younger than 2 years,


blood vessels cross the physis, thus
epiphysis may be involved

 Limb shortening or angular


deformity may occur
ACUTE HEMATOGENOUS OSTEOMYELITIS
PATHOPHYSIOLOGY
 Joint may be involved in some cases-
hip joint most common, especially
for intraarticular physes- proximal
humerus,radial neck, distal fibula

 Metaphysis has relatively fewer


phagocytic cells than the physis or
diaphysis, hence more infection here
ACUTE HEMATOGENOUS OSTEOMYELITIS
PATHOPHYSIOLOGY
 In children older than 2 years the
physis effectively acts as a barrier to
the spread of a metaphyseal abscess

 Metaphyseal cortex thicker, hence


diaphysis more at risk

 After physes are closed acute


hematogenous osteomyelitis is much
less common
ACUTE HEMATOGENOUS OSTEOMYELITIS
PATHOPHYSIOLOGY
 After the physes are closed,
infection can extend directly from
the metaphysis into the epiphysis
and involve the joint

 Septic arthritis resulting from acute


hematogenous osteomyelitis
generally is seen only in infants and
adults.
ACUTE HEMATOGENOUS OSTEOMYELITIS
MICROBIAL PATTERN
 Staphylococcus aureus most common
in older children and adults
 Gram negative bacteria- increasing
trend- vertebral
 Pseudomonas most common in
intravenous drug abusers
 Salmonella in sicke cell
 Fungal infections in chronically ill
patients on long term intravenous
therapy.
ACUTE HEMATOGENOUS OSTEOMYELITIS
MICROBIAL PATTERN
 Infants- staph aureus most common
but group B streptococcus and gram
negative coliforms

 Prematures staph aureus andgram


negative organisms

 Hemophilus influenzae primarily in


children 6 months to 4 years old,
incidence decreased dramatically by
ACUTE HEMATOGENOUS OSTEOMYELITIS
MICROBIAL PATTERN
Ngetich, 2002 found that of children
presenting with haematogenous
osteomyelitis in Kenyatta national
hospital the commonest isolated
organism was staphylococcus aureus
accounting for 29 (60.4%)of the
cases, 15 (60%) of these were MRSA
strains
ACUTE HEMATOGENOUS OSTEOMYELITIS
DIAGNOSIS
 History and physical examination
Fever and malaise
Pain and local tenderness
Sweliing
Compartment syndrome in children
ACUTE HEMATOGENOUS OSTEOMYELITIS
DIAGNOSIS
 Laboratory tests
White blood cell count
Erythrocyte sedimentation rate
C-reactive protein
 checked very 2- 3 days post

treatment initiation
Aspiration for suspected abscess
ACUTE HEMATOGENOUS OSTEOMYELITIS
DIAGNOSIS

 Plain radiographs

 Technetium-99m bone scan +/- MRI


RADIOGRAPHS
 Soft tissue swelling

 Periosteal reaction

 Bony destruction
(10-12 days)
BONE SCAN

Can confirm
diagnosis
24-48 hrs after
onset
ACUTE HEMATOGENOUS OSTEOMYELITIS
TREATMENT
 Surgery and antibiotic treatment are
complementary, in some cases
antibiotics alone may cure the
disease.

 Choice of antibiotics is based on the


highest bacteriocidal activity, the
least toxicity and the lowest cost
ACUTE HEMATOGENOUS OSTEOMYELITIS
TREATMENT
 Nade’s 5 principles of treatment
1. An appropriate antibiotic is
effective before pus formation

2. Antibiotics do not sterilize


avascular tissues or abscesses
and such areas require surgical
removal
ACUTE HEMATOGENOUS OSTEOMYELITIS
TREATMENT- NADES PRINCIPLES

3. If such removal is effective,


antibiotics should prevent their
reformation and primary wound
closure should be safe

4. Surgery should not damage already


ischaemic bone and soft tissue

5. Antibiotics should be continued after


surgery
ACUTE HEMATOGENOUS OSTEOMYELITIS
TREATMENT

 The two main indications for surgery in


acute hematogenous osteomyelitis are:
1. The presence of an abscess requiring
drainage
2. Failure of the patient to improve
despite appropriate intravenous
antibiotic treatment
ACUTE HEMATOGENOUS OSTEOMYELITIS
TREATMENT- SURGERY
 The objective of surgery is to drain any
abscess cavity and remove all non viable or
necrotic tissue
 Subperiosteal abscess in an infant-several
small holes drilled through the cortex into
the medullary canal
 If intramedullary pus is found, a small
window of bone is removed
 Skin is closed loosely over drains and the
limb splinted
ACUTE HEMATOGENOUS OSTEOMYELITIS
TREATMENT

 Generally a 6 week course of


intravenous antibiotics is given

 Orthopedic and infectious


disease followup is continued for
at least 1 year
SUBACUTE HEMATOGENOUS
OSTEOMYELITIS

 More insidious onset and lacks


severity of symptoms

 Indolent course hence diagnosis


delayed for more than two
weeks.
SUBACUTE HEMATOGENOUS OSTEOMYELITIS
CLINICAL FEATURES
 The indolent course of subacute
osteomyelitis is due to:
increased host resistance
decreased bacterial virulence
administration of antibiotics before the
onset of symptoms
 Systemic signs and symptoms are minimal
 Temperature is only mildly elevated
 Mild to moderate pain
SUBACUTE HEMATOGENOUS OSTEOMYELITIS
INVESTIGATIONS
 White blood cell counts are generally normal

 ESR is elevated in only 50% of patients

 Blood cultures are usually negative

 Plain radiographs and bone scans generally


are positive
SUBACUTE HEMATOGENOUS OSTEOMYELITIS
INVESTIGATIONS

 S. Aureus and Staphylococcus


epidermidis are the predominant
organisms identified in subacute
osteomyelitis
SUBACUTE HEMATOGENOUS OSTEOMYELITIS
BRODIE ABSCESS

 Localized form of subacute


osteomyelitis occuring most
commonly in the long bones of the
lower extremeties

 Intermittent pain of long duration is


most times the presenting
compliant, along with tenderness
over the affected area
BRODIE ABSCESS
SUBACUTE HEMATOGENOUS OSTEOMYELITIS
BRODIE ABSCESS
 On plain radiographs appears as a lytic lesion
with a rim of sclerotic bone

 S aureus is cultured in 50% of patients and in


20% the culture is negative

 The condition requires open biopsy with


curetage to make the diagnosis

 The wound should be closed loosely over a


drain
SUBACUTE HEMATOGENOUS OSTEOMYELITIS
GLEDHILL CLASSIFICATION
SUBACUTE HEMATOGENOUS OSTEOMYELITIS
TREATMENT
 Biopsy and curettage followed by treatment
with appropriate antibiotics for all lesions
that seem to be aggressive

 For lesions that seem to be a simple abscess


in the epiphysis or metaphysis biopsy is not
recommended- IV antibiotics for 48 hrs
followed by a 6 week course of oral
antibiotics
CHRONIC OSTEOMYELITIS
 Hallmark is infected dead bone
within a compromised soft tissue
envelope

 The infected foci within the bone


are surrounded by sclerotic,
relatively avascular bone covered
by a thickened periosteum and
scarred muscle and subcutaneous
tissue
COM

 Sinus track cultures usually do not


corelate with cultures obtained at
bone biopsy
COM IN KNH

 2008-=108
 2009 =79
 2010-=99
 2011-=79
 2012= 53
CLASSIFICATION OF COM
ANATOMICAL CLASSIFICATION
CLASSIFICATION OF COM
DIAGNOSIS COM

 Based on
Clinical
 laboratory and
 imaging studies
CLINICAL EVALUATION COM

 Skin and soft tissue integrity


 Tenderness
 Bone stability
 Neurovascular status of limb
 Presence of sinus
LABORATORY COM
 Erythrocyte sedimentation rate
 C reactive protein
 WBC count only elevated in 35%
 Biopsy for histological and
microbiological evaluation
Staphyloccocus species
Anaerobes and gram negative
bacilli
ORGANISMS IN COM
 Girasi, 1981 found that the
commonest organisms found at the
orthopaedic unit at Kenyatta
national hospital, then in kabete
was staphylococcus aureus which
was resistant to penicillin and
ampicillin
IMAGING STUDIES IN COM
 Plain X rays
Cortical destruction
Periosteal reaction
Sequestra
Sinography
SINOGRAPHY
IMAGING -

 Isotopic bone scanning more useful


in acute than in chronic
osteomyelitis

 Gallium scans increased uptake in


areas where leucocytes and bacteria
accumulate. Normal scan excludes
osteomyelitis
COM IMAGING

 CT Scan
Identifying sequestra
Definition of cortical bone and
surrounding soft tissues
COM IMAGING
 MRI
Shows margins of bone and soft
tissue oedema
Evaluate recurrence of infection
after 1 year
Rim sign- well defined rim of high
signal intensity surrounding the
focus of active disease
Sinus tracks and cellulitis
TREATMENT OF COM
 Surgical treatment mainstay
Sequestrectomy
Resection of scarred and infected
bone and soft tissue
Radical debridement
Resection margins >5mm
SURGICAL TREATMENT OF COM
 Adequate debridement leaves a dead
space that needs to be managed to avoid
recurrence, or bony instability
Skin grafts,
Muscle and myocutaneous flaps
Free bone transfer
Papineau technique
Hyperbaric oxygen therapy
Vacuum dressing
TREATMENT OF COM
 Antibiotic duration is controversial
6 week is the traditional duration
1 week IV, 6 weeks of oral therapy
Antibiotic polymethyl methacrylate
(PMMA) beads as a temporary filler of
dead space
Biodegradable antibiotic delivery system
RESECTION OR EXCISION FOR
COM

 Resection of a segment of affected


bone may be necessary to control
infection

 With techniques of bone and soft


tissue transport, massive resections
can be performed and reconstructed
without significant disability.
RESECTION OR EXCISION FOR
COM
AMPUTATION FOR
OSTEOMYELITIS
 Amputation indications include
Arterial insufficiency
Major nerve paralysis
Non functional limb-stiffness,
contracture
Malignant change
 Prevalence of maliganacy arising from
COM reported as 0.2 to 1.6% of cases.
 Most are squamous cell carcinoma, also
reticulum cell carcinoma,fibrosarcoma
SCLEROSING OSTEOMYELITIS OF
GARRE’

 Bone is thickened and distended,


but abscesses and sequestra are
absent.

 Cause unknown

 Thought to caused by a low grade,


possibly anaerobic bacterium
SCLEROSING OSTEOMYELITIS
OF GARRE’
REFERENCES
 Canale Terry and Beaty James (2007) Campbell’s Operative
Orthopaedics, Philadelphia, Mosby
 Ben Mbonye-Girasi (1981) Mode of Presentation and End
results of Management of Haematogenous Osteomyelitis at
the Orthopaedic Unit Kenyatta National Hospital over a
Five Year Period. Nairobi : unpublished masters in
medicine project, School of Medicine, University of Nairobi
 Issac K Ngetich (2002) A Study of Haematogenous
Osteomyelitis in Children in Kenyatta National Hospital
Kenya. Nairobi : unpublished masters in medicine project,
School of Medicine, University of Nairobi
 Lewis R P, Sutter V L and Finegold S M (1978) Bone
Infections Involving Anaerobic Bacteria. Baltimore pub med
PMID 207946

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