OSTEOMYELITIS

GROUP 2
Roanne Telgt
Ashley Dudhnath
Imran Shareef Syed
OBJECTIVES

❏ Introduction ❏ Diagnosis

❏ Epidemiology ❏ Differential diagnosis

❏ Etiology ❏ Management

❏ Classification ❏ Outcomes

❏ Clinical features ❏ Prognosis

INTRODUCTION

❏ Bone and bone marrow infection caused by an infecting agent with

progressive inflammatory destruction
❏ It can be classified as:
➢ Acute, sub- acute or chronic
➢ Based on Cierny-Mader classification
 EPIDEMIOLOGY

❏ Overall incidence of osteomyelitis is greater in developing countries

❏ Hematogenous osteomyelitis is more common in children and adolescence (>50% in
children ≤5 years old) while exogenous osteomyelitis is more common in adults
❏ Approx. 20% of adults with osteomyelitis have hematogenous spread (mostly vertebral
osteomyelitis) with male predominance
❏ Overall incidence of vertebral osteomyelitis is believed to have ↑ over the years due to IV
drug users, higher rates of nosocomial infections after instrumentation and the ↑ age of
the population
ETIOLOGY- ROUTES OF INFECTION
❏ Hematogenous osteomyelitis : originated or transported by blood
➢ Most common etiology in children
➢ In adults the vertebrae are the most common site of hematogenous
osteomyelitis
➢ Most commonly caused by a single pathogen that results in
hematogenous dissemination
❏ Exogenous osteomyelitis:
➢ Usually due to multiple pathogens
➢ Posttraumatic: direct inoculation eg open fractures, penetrating injuries
➢ Contiguous spread: from adjacent tissues eg foot ulcer in diabetic
patients
➢ Iatrogenic: eg placement of infected prosthetics
ETIOLOGY- PATHOGENS
ETIOLOGY- RISK FACTORS

❏ Local:
➢ Poor tissue perfusion
➢ Open fractures
➢ Severe soft tissue injury/ recent trauma

❏ Systemic:
➢ Impaired immunocompetence
➢ Systemic diseases
➢ IV drug use

❏ Microbial:
➢ Highly virulent pathogens
CLASSIFICATION

❏ Due to duration of infection

➢ Acute: within two weeks
➢ Sub-acute: within one to several months
➢ Chronic: longer than several months
❏ Due to Cierny-Mader classification:
Based on the extent of bone infection and immunological status of
the host. Used for classification of chronic osteomyelitis
 CIERNY-MADER CLASSIFICATION
Anatomy
Type 1: Medullary osteomyelitis
Type 2: Superficial osteomyelitis
Type 3: Localized osteomyelitis
Type 4: Diffused osteomyelitis

Host status
Type A: Normal physiological host
Type B(l): Local compromise
Type B(s): Systemic compromise
Type B(sl): Both systemic and local compromise
Type C: treatment morbidity is worse than current condition
SUBTYPES- VERTEBRAL OSTEOMYELITIS

❏ Most often due to infection with Staphylococcus aureus in patients > 50

y/o, have infective endocarditis, diabetes, sickle cell anemia,
degenerative spine disease, spinal surgery, IV drug user or
immunocompromised
❏ Can be caused by direct inoculation or hematogenous seeding of a
distant infectious focus
❏ Classified based on causative agent:
➢ Pyogenic ( staph aureus, enterobacteriaceae, pseudomonas, streptococci)
➢ Tuberculous spondylitis
SUBTYPES - BRODIE ABSCESS AND SYPHILITIC OSTEOMYELITIS

❏ Brodie abscess
➢ Subacute osteomyelitis with a chronic intraosseous abscess that usually
affects the distal femur and proximal tibia
➢ Patients are usually asymptomatic or only mild symptoms and localized
pain
❏ Syphilitic osteomyelitis
➢ Associated with tertiary syphilis in adults
➢ Features include diffuse periostitis (with sabre tibia) / localized gummata
with sequestra, sinus formation, and pathological fractures
SUBTYPES- MYCOTIC OSTEOMYELITIS

❏ Typically seen in immunocompromised patients

❏ Usually occurs as spread from primary lung infections
❏ Features include bone granulomas, necrosis, and suppuration present
without worsening acute illness
PATHOPHYSIOLOGY

❏ Bacteria reaches the bone →proliferation and recruitment of immune

cells → ACUTE OSTEOMYELITIS → repair

OR

 ACUTE OSTEOMYELISTIS → continued destruction of bone and bone

necrosis → CRONIC OSTEOMYELITIS
 CLINICAL FEATURES
ACUTE:
 Children: severe pain, malaise, fever, if left untreated; toxemia. The child will
refuse to move affected limb or even have it touched/ handled.
 Infant: failure to thrive, drowsiness and irritability. Suspicion should be aroused by
a history of birth difficulties, umbilical artery catheterization or a site of infection
such as an inflamed intravenous infusion point or even a heel puncture.
 Adults: the commonest site for hematogenous infection is the thoracolumbar
spine. There may be a history of some urological procedure followed by a mild
fever and backache. There maybe some local tenderness over affected area. In
very elderly pts or in those immunocompromised, systemic features are mild and
the diagnosis maybe missed.
SUBACUTE:
The patient is usually a child or adolescent that presents with pain
near one of the large joints for several weeks to months. They may
have a limp, slight swelling, muscle wasting and local tenderness.
The temperature is normal and there is little to suggest an infection.
CHRONIC:
The patient presents because pain, pyrexia, redness and tenderness
have recurred (a ‘flare’), or with a discharging sinus. In longstanding
cases the tissues are thickened and often puckered or folded inwards
where a scar or sinus adheres to the underlying bone. There may be a
seropurulent discharge and excoriation of the surrounding skin.
DIAGNOSTIC TOOLS IMAGING
Plain X-ray
• Ultrasound- may detect a subperiosteal collection of fluid in the early
stages of osteomyelitis, but it cannot distinguish between a
haematoma and pus.

• MRI- It is the best method of demonstrating bone marrow

inflammation. It is extremely sensitive, even in the early phase of bone
infection, and can therefore assist in differentiating between soft-tissue
infection and osteomyelitis.

• Radionuclide scanning
LABORATORY TESTING

 The most certain way to confirm the clinical diagnosis is to aspirate

pus or fluid from the metaphyseal subperiosteal abscess, the
extraosseous soft tissues or an adjacent joint. Gram stain may help to
identify the type of infection and assist with the initial choice of
antibiotics.
 CRP and ESR values are elevated within 12-24 hours and 24-48 hours
respectively, after the onset of symptoms. WBC count rises and
hemoglobin concentration maybe diminished.
DIFFERENTIAL DIAGNOSIS

 Cellulitis
 Acute suppurative arthritis
 Acute Rheumatism
Streptococcal necrotizing myositis
 Sickle cell crisis
 Gaucher’s disease
 MANAGEMENT (ANTIBIOTICS)
 Intravenous antibiotics (for 4-6 weeks in acute vs > 8 weeks in chronic)
 Empirical therapy start immediately after collecting sample for culture (must cover
Staphylococcal aureus).
• MSSA (Nafcillin and Oxacillin), MRSA (Vancomycin and Clindamycin) and add
cefazoline/fluoroquinolones
 Culture specific
• IV drug user/Foot injury -> Pseudomonas aeruginosa (cephalosporins and /or
fluoroquinolones)
• Prosthetics /catheter -> Staphylococcus epidermidis (vancomycin)
• Sickle cell patients -> Salmonella (fluroquinolones)
• History of tuberculosis -> Mycobacterium tuberculosis (Anti-mycobacterial therapy)
• Cat/dog bite -> Pasteurella multocida (penicillin G)
COMPLICATIONS
 If left untreated or in case of chronic cases:
• Acute to chronic progression
• Pathologic fractures
• Limb(s) shortening, deformity and/or nonunion
• Septic arthritis (seen in children < 8 years old)
• Bone sarcoma
• Squamous cell carcinoma
• Septicemia
• Infective endocarditis
• Systemic amyloidosis (osteoblasts secrete IL-6)
 MANAGEMENT (SURGICAL)
 Surgical debridement
• Expose the INVOLUCRUM
• Remove the SEQUESTRUM
• Saucerize the bone
• Fill the cavity with bone chips, cement spacer
and/or muscle flap. Contains antibiotic-eluting
polymethyl- methacrylate (PMMA) beads.
 Drainage of abscess (sub-periosteal, epidural etc.)
 Masquelet technique
• After 6-8 weeks replace cement with bone graft
(membrane) which secrete BMP-2 and VEGF
 However in very aggressive and recurrent life-threatening cases amputation can be done to
save the life.
OUTCOMES

 Look for the falling levels of ESR and CRP for successful therapy
(but not specific)
 Possible nerve/vessel damage during aggressive surgical
management or from infection itself leads to functional deficits.
PROGNOSIS

 Poor prognosis if it turns into chronic osteomyelitis (due to deeper

penetration).
 30% chances of recurrence.
REFERENCES & THANK YOU

1. Apley’s System of Orthopedics and Fractures Ninth Edition

2. Current Diagnosis and Treatment in Orthopedics Fifth Edition
3. Amboss- Osteomyelitis
4. Medscape- Osteomyelitis
5. Orthobullets- osteomyelitis
6. Oxford handbook of clinical surgery- 4th edition
7. Toronto notes 2020