You are on page 1of 74

Dr.

Izaak Zoelkarnain Akbar


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.
Common clinical problem
Defined as a progressive infection of
the bone that results in inflammatory
destruction of the bone, bone
necrosis and new bone formation
Classification by pathogenesis and
chronicity
Early diagnosis is difficult
Delay in diagnosis leads to
decreased cure rates and increased
rates of complication and morbidity
The relapse of a previously treated or
The term acute osteomyelitis is untreated infection is considered a sign
used clinically to signify a of chronic disease. Clinical signs
persisting for more than 10 days correlate
newly recognized bone
roughly with the development of necrotic
infection. Patients usually
bone and chronic osteomyelitis. The
present within several days to clinical pattern may evolve over months
one week after the onset of or even years and is characterized by
symptoms. In addition to local lowgrade inflammation; the presence of

signs of inflammation and pus, microorganisms,and sequestra ; a


compromised soft-tissue envelope;and
infection, patients have signs
sometimes a fistula.
of systemic illness
Sequestrum :
is a devitalized avascular
segment of bone, surrounded, by pus
/infected granulation tissue and is more
dense than surrounding bone .Because of
avascularity , sequestrum does not
decalcify , is more radio opaque and heavy ,
so sinks in water
Its outer surface is usually jagged / irregular
due to erosive process by proteolytic
enzymes in granulation tissue
Involucrum :
is derived from the word volvere
i.e. to wrap .It is the result of reactive
new bone formed by periosteal
reaction , in an attempt to wall off the
infection by forming a thick tense wall
It is jagged on its inner surface
but smooth on its outer surface

.)
Cloacae :

are single or multiple openings in


involucrum and are caused by rupture
of periosteum due to pus under
tension .
Exudates , sequestra are extruded
through the cloacae on the surface

.)
According to the duration of the
disease
acute
chronic
On the basis of the pathogenesis
hematogenous
secondary to a contiguous focus of
infection
associated with peripheral vascular disease
Acute Osteo Sub-Acute Osteo Chronic Osteo
Begins with marrow Occurs in abnormal bone Occurs after inadequate tx or in
edema, cellular infiltration or after inadequate pts with altered immunity
and vascular engorgement antibiotics
Distinguishing feature is
May progress to necrosis Localized pyogenic necrotic bone surrounded by
and abscess formation process granulation tissue

Spread within the Commonly appears as a Interruption of blood supply


intramedullary cavity well-defined osteolytic necrosis devitalized bone
extension through cortex metaphyseal lesion fragments (sequestra)
by Havers and Volkmans (Brodies abscess) with a
canals subperiosteal sclerotic margin that fades
A thick sheath of new periosteal
space periosteum peripherally (fuzzy
sclerotic margin) bone can develop around the
soft tissues sequestra (involucrum)
S. aureus is most common
Rupture of joint space Fistula tract formation
septic arthritis pathogen

Sharp interface between normal


and diseased marrow
Age (adult v. child)
Site (foot, vertebra, long bone)
Source (trauma/surgery, hematogenous, or
contiguous spread/cellulitis,)
Presence or absence of foreign body (hardware)
Acute vs. chronic
Severity
Comorbidity (e.g., diabetic, sickle cell)
Organism

10
PATHOPHYSIOLOGY

Hematogenous Osteomyelitis

Contiguous-Focus Osteomyelitis

Peripheral Vascular Disease-associat


PATHOPHYSIOLOGY
Microorganisms enter bone (Phagocytosis).

Phagocyte contains the infection

Release enzymes

Lyse bone
PATHOPHYSIOLOGY
Bacteria escape host defenses by:

Adhering tightly to damage bone

Persisting in osteoblasts

Protective polysaccharide-rich biofil


PATHOPHYSIOLOGY
Pus spreads into vascular channels

Raising intraosseous pressure

Impairing blood flow

Chronic ischemic necrosis

Separation of large devascularized fragment


(Sequestra)

New bone formation


(involucrum)
PATHOLOGY
Acute Infiltration of PMNs
Congested or thrombosed vessels

Chronic Necrotic bone


Absence of living osteocyte
Mononuclear cells predominate
Granulation & fibrous tissue
Hematogenous
Osteomyelitis
HEMATOGENOUS OSTEPMYELITIS

Rapidly growing bone

Children:
Long bone, Femur, Tibia, Humerus

Older patients: Vertebral bone


HEMATOGENOUS OSTEOMYELITIS

Neonate & infant < 1 year old

Septic arthritis is common.

Growth deformities is common.

Soft tissue involvement is common.


HEMATOGENOUS OSTEOMYELITIS
Children: 1 16 years old

Most frequent in the metaphysis of long bone.

Slugging blood flow through a


sinusoidal venous system.

Deficency of phagocytic cells.

Poor collateral circulation

Susceptibility of this region to trauma.


HEMATOGENOUS OSTEOMYELITIS
Children: 1 16 years old

History of antecedent trauma in 30%

Involucrum

Sequestration

Associated septic arthritis


HEMATOGENOUS OSTEOMYELITIS
Adult

Less common

Spread infection to joint space.

Vertebral Osteomyelitis is common> 50y


HEMATOGENOUS OSTEOMYELITIS

Special consideration
Sickle cell disease
Injection drug users (IDUs)
Hemodialysis
HIV/AIDS
Immunosuppression
Prosthetic orthopedic device
HEMATOGENOUS OSTEOMYELITIS

Microbiologic features
Staphylococci Aureus, Epidermidis
Streptococci Group A & B
Haemophilus influenzae
Gram-negative enteric bacilli
Anaerobes
Polymicrobial
Mycobacterial
Fungi
HEMATOGENOUS OSTEOMYELITIS

Clinical manifestation
Classic presentation: Sudden onset
Usually presentation: Slow, insidious

High fever, Night sweats


Fatigue, Anorexia, Weight loss
Restriction of movement
Local edema, Erythema, & Tenderrnes
HEMATOGENOUS OSTEOMYELITIS

Differentials

Cellulitis
Gas gangrene
Neoplasm
Aseptic bone infection
Clenched fist
osteomyelitis
HEMATOGENOUS OSTEOMYELITIS
Diagnosis & work-up
Lab study:
WBC May be elevated, Usually normal

{C-Reactive Protein (CRP)


Erythrocyte Sedimentation Rate
(Usually is elevated at presentation
Falls with successful therapy)

Blood culture
( Acute osteomyelitis + ve > 50% )
HEMATOGENOUS OSTEOMYELITIS
Diagnosis & work-up
Imaging
Radiology:
Normal
Soft tissue swelling
Periosteal elevation
Lytic change
Sclerotic changew
HEMATOGENOUS OSTEOMYELITIS
Diagnosis & work-up
Imaging
MRI:
Early detection
Superior to plan X ray & CT Scan &
radionuclide bone scan in slected
anatomic location.
Sensitivity 90 100%
HEMATOGENOUS OSTEOMYELITIS
Diagnosis & work-up
Imaging
Radionuclide bone scan:
A 3-phase bone scan ( Technetium 99m )

Positive as early as 24 h after


onset of symptom

False positive Tumor, osteonecrosis


Artheritis, Cellulitis,
Abscess
HEMATOGENOUS OSTEOMYELITIS
Diagnosis & work-up
Imaging
CT Scan:
Useful in evaluation of Spinal, pe
Sternum, Calcaneus

Provides exellent images of bone c

Is used for biopsy localization


Os + gaz in diabetic foot
Septic arthritis
Of
Right hip
HEMATOGENOUS OSTEOMYELITIS
Diagnosis & work-up
Ultrasonography
Simple & inexpensive

Demonstration anomaly 1 2 days after onset

Soft tissue abscess, Fluid collection, &


Periosteal elevation

It allows for aspiration

It doesnt allow for evaluation of bone cortex


HEMATOGENOUS OSTEOMYELITIS
Diagnosis & work-up
Neddle Aspiration or Open biopsy:

From: Soft tissue collection


Subperiosteal abscess
Intraosseos lesions

For: Smear
Culture
Pathology
TREATMENT
Initial treatment shoud be aggressive.

Inadequate therapy Chronic disease


Parenteral
Antibiotic use:
High doses
Good penetration in bone
Full course
Empiric therapy
Surgery
TREATMENT
Empiric Initial Therapy
Neonate S.aureus PRP +
Infant<2 y G ve bacilli Cefotaxime

Children S.aureus PRP +


H.Infenza Ceftriaxone

Adult S.aureus PRP or


1st ceph
TREATMENT
Monitoring Therapeutic Response

1.Symptoms & Signs

2.ESR & CRP

3.Radiography

4.Serial Bone Scan?


TREATMENT
Indication for Surgery

Diagnostic
Hip joint involvement
Neurologic complication
Poor or no response to IV therapy
Sequestration
SURGICAL MANAGEMENT

General principles of surgical therapy include


1.To remove dead , devitalized and infected bone
2.To obliterate any dead space left after
debridement
3. To obtain soft tissue coverage of exposed bone
PROGNOSIS
Is related to:
Causative organisms

Duration of symptoms & sign

Patient age

Duration of antibiotic therapy


COMPLICATION
Bone abscess
Bacteremia

Fracture
Loosing of the prosthetic implant

Overlying soft-tissue cellulitis


Draining soft-tissue tract
Septic Osteomyelitis

Osteomyelitis Scar
Osteomyelitis Deformity of the Forearm
Plain radiograph of the
tibia and fibula in a 14
y/o patient
demonstrating a
pathologic fracture of
the proximal fibula with
periosteal reaction and
erosion of the cortical
bone secondary to
subacute osteomyelitis
CONTIGUOUS-FOCUS
OSTEOMYELITIS
Contiguous-focus Osteomyelitis

Clinical setting:

Postoperative infection

Contamination of bone

Contiguous soft tissue infection

Puncture wounds
Contiguous-focus Osteomyelitis

Microbiologic features
Staphylococci Aureus, Epidermidis

Gram-negative bacteria

Anaerobic infection

Unusual organisms Clostridia, Nocardia


Contiguous-focus Osteomyelitis
Diagnosis
Leukocyte count
Blood culture (infrequently positive)

ESR & CRP


Radiologic evaluation

Technetium bone scan


Open bone biopsy

Culture of wound & draining sinuses??


Contiguous-focus Osteomyelitis
Treatment
Surgery is essential.

Antibiotics Specific
Duration
ASSOCIATED WITH
PERIPHERAL VASCULAR DISEASE
Clinical Features
erythema and drainage
either no pain (if there is advanced neuropathy) or excruciating pain
(if the destruction of bone has been acute).
patients are afebrile,
present with an ulcer without evidence of surrounding inflammation.
The ulcer size (> 2 cm2) and depth (> 3 mm) are predictive of the
likelihood of bone involvement. If bone can be felt with a sterile blunt
probe, the likelihood of osteomyelitis is high.
a high ESR, especially if it is over 70 mm/hour, is helpful in making
the diagnosis of osteomyelitis
Found almost exclusively in the feet in
patients with a long history of diabetes
mellitus and peripheral neuropathy.
Bone involvement usually occurs after an
extension of soft tissue infection involving a
plantar ulcer.
ETIOLOGY
Most infections are polymicrobial
S. aureus remains the most common
pathogen
others include Enterococcus faecalis,
group B streptococci,
Enterobacteriaceae, anaerobic
bacteria (especially peptococci,
peptostreptococci, and Bacteroides
species), and P. aeruginosa
Vertebral
Osteomyelitis
Risk factors:
Male
Age > 50
IVDU
Etiology
Virtually always hematogenous
Lumbar more common then
cervical
59

Localized pain and tenderness
Diagnosis often missed or
delayed

60

Plain films
MRI best
CT-guided needle
biopsy

61
Staph Aureus in about 50%
Other organisms:
Gram negative aerobes
Streptococcus sp.
Tuberculosis
Pseudomonas and candida
in IVDU 62
6 to 12 weeks IV antibiotics if
medical treatment alone
Surgical treatment indicated if
abscess
cord compression
failure of medical treatment
Can follow CRP for reoccurrence or
failure of treatment response
63
Risk factors:
Male
Age > 50
IVDU
Etiology
Virtually always hematogenous
Lumbar more common then
cervical 64
Modality of choice for initial evaluation
Advantages
Inexpensive
Exclude other conditions
May help guide further work-up
Disadvantages
Often normal for the first 10 to 21
days of infection
Sensitivity: 43-75%
Specificity: 75-83%
Earliest finding deep soft
tissue swelling
Active infection for 1-2 weeks
bone destruction and
periosteal reaction
Localized osteoporosis
Pathologic fracture
Infectious
Arthritis
Infectious arthritis can generally be divided
into two categories:
Pyogenic or septic arthritis
Most commonly caused by Staphylococcus
aureus, Neisseria gonorrhea, Klebsiella
pneumoniae, Candida albicans, and
Serratia marcescens

Non-pyogenic arthritis
Most commonly caused by tuberculosis or
fungal infections including actinomycosis,
cryptococcosis,
coccidioidomycosis,histoplasmosis, and
sporotrichosis
Infectious agents can enter the joint space in
several ways

Direct invasion of the synovial membrane


Penetrating wound
Post-surgical following joint replacement

Infection of adjacent soft tissue

Hematogenous spread from a blood borne


infection

Spread from a focus of osteomyelitis in


adjacent bone
Modality of choice for initial evaluation of
suspected joint infections
Diagnosis can be made when characteristic findings
are present
Early plain film findings:
Periarticular osteoporosis
Soft tissue swelling
Joint effusion
Joint space loss
Later plain film findings:
Periosteal reaction
Marginal and central erosions and destruction of
subchondral bone
Subluxation or dislocation
Intra-articular bony ankylosis
Gas formation within the joint
capsule can be seen with infection
by:
E coli, Serratia, Clostridium perfringens

In patients with hip or knee joint


arthroplasties the infected joint
reveals:
Joint fluid
Loosening of the prosthesis components
Bone erosion around the prosthesis
A: AP film shows erosion around tibial
component and loosening of the
prosthesis. Note also osteolytic changes
at lateral and medial femoral condyles. B:
Lateral shows fullness of suprapatellar
bursa caused by large joint fluid. Note
lucencies and bone resorptions around
femoral and tibial components.
Examination of the aspirated fluid
revealed Staphylococcus aureus.
57-year-old man with cellulitis and
septic arthritis of the
metatarsophalangeal joint of the fifth
toe. Note destruction of the joint and
gas formation in the soft tissues. The
aspiration biopsy revealed
Clostridium perfringens.
A 53-year-old man with infectious arthritis of the
right hip joint. A: A radiograph demonstrates
narrowing of the joint and articular erosions. B: An
arthrogram was performed mainly to obtain fluid for
bacteriologic examination, which revealed
Staphylococcus aureus. The imaging study shows
destruction of articular cartilage and hypertrophic
changes of the synovium.