Osteomyelitis Flashcards
What is osteomyelitis
infection localized to bone
inflammatory condition of bone/ bone marrrow caused by an infecting organism, most commonly Staphylococcus aureus.
Epidemiology of osteomyelitis
UK incidence:
10 – 100 / 100,000 p/y.
Predominantly Children 80% of acute, haematogenous osteomyelitis
adolescents and adults get contiguous osteomyelitis (often associated with direct trauma)
Older patients: Diabetes mellitus/Peripheral Vascular disease/Arthroplasties
Men more than women
Pathophysiology: 3 routes of transmission for osteomyelitis
- direct inoculation of infection into the bone:
trauma or surgery,
polymicrobial or monomicrobial. - contact spread of infection to bone:
from adjacent soft tissues and joints, polymicrobial or monomicrobial,
older adults: DM, chronic ulcers, vascular disease, arthroplasties / prosthetic material, - Haematogenous seeding:
children (long bones)>adults (vertebrae)
monomicrobial
Pathogenesis of Osteomyelitis
- Behavioural factors:
i.e. risk of trauma - Vascular supply:
Arterial disease
Diabetes mellitus
Sickle cell disease - Pre-existing bone / joint problem:
Inflammatory arthritis
Prosthetic material inc arthroplasty - Immune deficiency
Immunosuppressive drugs
Primary immunodeficiency
Pathogenesis of haematogenous OM
Adults:
Usually >50 years
Vertebra > clavicle/pelvis»long bones
Children (85%)
Long bones»_space; vertebra
What is the most common site of infection in long bone haematogenous OM?
Metaphysis
Why is the metaphysis the most common site of infection?
- Main blood vessels penetrate the midshaft then go to either end to form vascular loops in the metaphysis.
- Here blood flow is slower and no endothelial basement membranes are so bacteria can enter the site from the blood
- capillaries also lack or have inactive phagocytic lining cells which allow growth of microorganisms.
Where are children affected with haematogenous OM spread
- Children, with elongating long bones, the metaphysis is very metabolically active with a large flow of blood predisposing the vasculature to infection.
- With age, metaphysial blood flow slows.
- With age vertebrae more vascular so bacterial seeding of verebral endplate more likely
How can lumbar vertebral veins lead to bacteria
lumbar vertebral veins communicate with those of the pelvis by valveless anastamoses.
Retrograde flow from urethral , bladder and prostatic infections may be a source of bacteria to these vertebrae
Haematogenous OM in adults
Usually >50 years
Vertebra > clavicle/pelvis»long bones
Haematogenous OM in children
Long bones»_space; vertebra
People who inject drugs haematogenous OM
younger, more often clavicle and pelvis
Who are the people with risk factors for bacteremia
central lines, on dialysis
sickle cell disease,
urinary tract infection, urethral catheterization
Similar factors as those for infective endocarditis
S. aureus microbial factors
binds host proteins fibronectin, fibrinogen, and collagen
fibronectin binding proteins A and B (FnBPA / FnBPB)
Collagen-binding adhesin (CNA)
can survive intracellularly in cultured macrophages
Which organisms cause OM
Staphylococcus aureus,
coagulase-negative staphylococci,
aerobic gram-negative bacilli (30%)
M. tuberculosis
Neisseria gonorrhoeae
Streptococci (skin, oral)
Enterococci (bladder, bowel)
Anaerobes (bowel)
Salmonella in sickle cell anaemia patients
What is the histopathology of osteomyelitis
1.inflammatory exudate in the marrow
2. increased intramedullary pressure
3.extension of exudate into the bone cortex
4.rupture through the periosteum
5.Interruption of periosteal blood supply causing necrosis
6. Leaves pieces of separated dead bone
7. New bone forms here
Acute changes of histopathology
- Inflammatory cells
- Oedema
- Vascular congestion
- Small vessel thrombosis
Chronic changes of histopathology of OM
- neutrophil exudates
- lymphocytes & histiocytes
- Necrotic bone ‘sequestra’
- new bone formation ‘involucrum’
What investigations can we do for OM
History
Examination
CRP - raised inflammatory marker
FBC- WCC - high in acute, normal in chronic
U and E
LFTs
HbA1C
MRI - Gold standard
CR
Plain Xray
Nuclear bone scan
Symptoms (History)
Onset - several days.
dull pain at site of OM
may be aggravated by movement.
- Fever
- Pain
- Overlying redness
- Swelling
- Malaise
Signs of clinical OM (Examination)
Systemic:
Fever, rigors, sweats, malaise
Local:
Acute OM-
tenderness, warmth, erythema, and swelling
Chronic OM-
tenderness, warmth, erythema, and swelling
PLUS any of
draining sinus tract
deep / large ulcers that fail to heal despite several weeks treatment*
non-healing fractures
OM in hip vertebrae or pelvis
pain but few other signs or symptoms.
OM Vertebral: lumbar > thoracic > cervical
Posterior extension - epidural and subdural abscesses or even meningitis.
Extension anteriorly or laterally can lead to paravertebral, retropharyngeal, mediastinal, subphrenic, retroperitoneal, or psoas abscesses.
OM Joint - can also present as septic arthritis.
when infection breaks through cortex resulting in discharge of pus into the joint (knee, hip, and shoulder).
More common in infants due to patent transphyseal blood vessels and immature growth plate
What is shown in a plain x-ray in chronic osteomyelitis
cortical erosion,
periosteal reaction,
mixed lucency,
Sclerosis
sequestra
soft tissue swelling
Why is an X ray not the best especially in early OM?
Poor sensitivity and specificity,
Why is MRI good?
marrow oedema from 3-5 days
Delineates cortical, bone marrow and soft tissue inflammation
How can we make a definitive diagnosis?
Microbiology and histology: Bone biopsy
Positive Blood cultures
Bone biopsy for OM
obtained via sterile technique,
Open bx»_space;> needle bx
2 specimens
Culture
16sRNA PCR may be necessary
Histology showing inflammation and osteonecrosis
Positive blood cultures
may obviate the need for invasive diagnostic testing if the organism isolated from blood is a pathogen likely to cause osteomyelitis.
+ve in 50% of Acute OM
most useful if hematogenous OM
Differential diagnosis for OM
Soft tissue infection (Cellulitis and erysipelas)
Charcot joint
Avascular necrosis of bone
Causes: steroid, radiation, or bisphosphonate use.
Gout
uric acid crystals in joint fluid / more acute presentation
Fracture
Bursitis
Malignancy
Surgical treatment for OM
Debridement (remember Bromfield “we cannot be too early in letting it out”)
Hardware placement or removal
Antimicrobial therapy for treatment
Initial broad spectrum empirical therapy “start SMART”
S. aureus or MRSA?
gram-negative organisms?
Special population: IVDU/HbSS?
Tailored to culture and sensitivity findings “then FOCUS”.
Bone penetration of drug
Prolonged duration
Antibiotics to use
Levofloxacin
Ciprofloxacin
Moxifloxacin
Vancomyocin
Treatment duration
Knowing when to stop treatment is very difficult
6 weeks of IV considered minimum
switch to oral alternatives may work in some situations
Stopping treatment guided by CRP response
failure to respond requires re-imaging
TB osteomyelitis
May be slower onset
Systemic symptoms
Epidemiology is different from pyogenic OM
Blood Culture less useful
Biopsy essential
Longer treatment 6 months
Caseating Granolumata on histology
Risk factors for OM
- Diabetes
- Old age
- Peripheral vascular disease
- Immunocompromise
- Malnutrition
- Trauma/ injury
Non haematagenous spread
- occurs due to breakdown or removal of the normal protective barriers of skin and soft tissue or contiguous spread (e.g. local skin infection like cellulitis spreading to the bone).
- Open fractures
- Skin ulcers
- Surgery
- Prosthesis
- Trauma
- Animal/ insect bites
Haematogenous spread
refers to the spread of a pathogen via the blood. Most commonly affects the axial skeleton, primarily the vertebral bones. After the vertebral bones the next most frequently affected sites are other axial bones like the sternum and pelvis.
- Indwelling intravascular catheter(e.g. Hickman line)
- Haemodialysis
- Endocarditis
- IV drug use
Acute osteomyelitis
- Once the bacteria reach the bone they start to proliferate.
This alerts nearby immune cells - specifically dendritic cells and macrophages - that try to fight off the infection.
This represents the acute phase of the disease and occurs over a course of weeks.
The immune cells release chemicals and enzymes that break down bone and cause local destruction.
Usually acute osteomyelitis comes to a resolution - the immune systemdestroys all of the invading bacteria. - If the lesion is not that extensive, and there’s viable bone the osteoblasts and the osteoclasts begin to repair the damage over a period of weeks
Chronic osteomyelitis
- affected bone sometimes becomes necrotic and separates from the healthy part of the bone - and that’s called a sequestrum. At the same time, the osteoblasts that originate from the periosteum may form new bone that wraps the sequestrum in place, this is called an involucrum.
- Cloaca may also form
