Osteomyelitis is a severe bone infection that can be acute or chronic, with Staphylococcus aureus being the most common cause. Treatment involves antibiotics combined with surgical debridement or drainage of abscesses. The goals of treatment are to eradicate the infection, resolve symptoms, and prevent complications through a multi-disciplinary approach and prolonged antibiotic therapy.

1. Lesson 7
Osteomyelitis
Tsegaye Melaku (BPharm, MSc)
Assistant Professor of Clinical Pharmacy
tsegayemlk@yahoo.com or tsegaye.melaku@ju.edu.et +251913765609December, 2020

2.  Session hits:
– Differentiating acute and chronic infections
– Most frequent pathogens in osteomyelitis
– Treatment protocol ( IV/Oral, duration)
– Monitoring plan
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3.  It is a severe infection of the bone, bone marrow & surrounding soft tissue
 It is progressive infectious process that can involve one or multiple
components of bone
– The periosteum, medullary cavity, and cortical bone.
 Characterized by progressive inflammatory destruction of bone, by
necrosis, and by new bone formation.
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4.  Acute or chronic infection
– Acute: first episode case or symptoms within
2 weeks
– Chronic: disease relapse or symptoms
persisting >2 months
– Characterized by presence of
necrotic bone
 Its Rx & Dx is challenging (complex nature)

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7.  Uncommon disease
 Incidence: 0.4/1,000 children in US
 Vertebral osteomyelitis: in old age
(>50 years)
 Acute hematogenous osteomyelitis
– Bimodal distribution
– Younger than 2 years, and
8- 12 years

8.  Ethiopia
– TASH (COM): Biruk et al, 2006
– Mean age 18 years
– Trauma as cause: 27%
– Most affected Lower limb bones: Tibia, 36%, fibula 22%
and femur 21%
– Etiology: S.aureus
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9.  Duration: Acute, subacute & chronic
– Differing prognoses and are treated in different ways
 Route of infection: hematogenous, contagious & inoculation
– Hematogenous
– Common in children & elderly
– Monomicrobial
– Contagious (with or without vascular insufficiency)
– Infection first begins in an area adjacent to bone spread
to bone
– Common in adult
– Polymicrobial

10.  Direct inoculation
– Trauma
– Open fracture 3-25%
– Surgery
 Contagious can be result of:
– Traumatic injury, penetrating injury, orthopedic surgery, or
– Diabetic or other forms of ischemic or neuropathic ulcer
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11.  Can be classified into four stages based on extent of bone involvement:
– Medullary,
– Superficial (contagious focus/at base of soft tissue)
– Localized(discrete area)
– Diffuse (all regions)
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12.  Essentially reflect their bacteremia incidence as a function of host age
 Can be comorbidity dependent
 Staphylococcus aureus: common cause
– 70% to 80% of bone infections
– ↑MRSA currently

13.  S. aureus -#1 pathogen
– Hematogenous osteomyelitis
– Device related infection
– Opportunistic pathogen
 Antibiotic resistance
– Methicillin resistant S. aureus (MRSA)
– 50% in some regions
– Vancomycin intermediate S. aureus (VISA)
– Vancomycin resistant S. aureus (VRSA)
 Biofilm formation
– Resistant abx/immunity/env’tal stress
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14.  Hematogenous spread (usually 1 organism)
– Infant (<1 year)
– S. aureus, CoNS, GBS, E.coli
– Children & adults (>16 years)
– S. aureus, CoNS, E. Coli, Pseudomonas spp.,Serratia spp.
 Contiguous spread (polymicrobial)
– Microbiology depends on the primary site of infection
– S. Aureus, Streptococcus spp., Enterococcus
– Proteus mirabilis,Pseudomonas spp., Anaerobes
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15.  It depends on mode of infection & patient factors
– Hematogenous /contiguous
– DM/PAD: MRSA, Enterobacteriaceae, & P. aeruginosa
– Sickle cell patients: Salmonella spp.
– Prosthetic implants: CoNS
– Neonates: E. coli or GBS
– Bed sores: polymicrobial
– IVDU: P. aeruginosa
– Fungus: chronically ill patients on long term intravenous therapy
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16.  Bone is normally resistant to infection.
– However, when microorganisms are introduced into bone can cause
osteomyelitis.
 Determinant: microbial &patient-specific factors.
 Bone infected: hematogenous/inoculation/contagious(adjacent site) 
bacteria attachment to tissues & prosthetic material  
inflammation(leukocytes and cytokines)  local edema & ischemia
  bone necrosis.
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17.  Dead bone(due to necrosis)   sequestra (bacteria nidus)  
chronic disease
– Difficult to treat(poor penetration)
– Surgical intervention
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19.  Hematogenous
– Chills, fever, and malaise
– Pain and local swelling
– Localized back pain & tenderness (vertebrae infection)
– Increased ESR, CRP, procalcitonin
– Inflammation, erythema, edema,
– Decreased range of motion
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20.  Contagious
– Increasing pain
– Mild fever and minimal drainage
– Imaging is often difficult to interpret
 A cardinal sign of chronic osteomyelitis
– The formation of a sinus tract (a channel from the infected site to
the skin) with purulent drainage
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21.  CBC
– Usually normal WBC
 Bone biopsy: definitive dx
 Blood cultures: for hematogenous
 Superficial swabs
 History & physical examination
– Fever & malaise
– Pain & local tenderness
– Sweliing
– Compartment syndrome in children
 Normochromic normocytic anemia (anemia of chronic disease)
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22.  Laboratory tests
– WBC, ESR, CRP
– Checked very 2- 3 days post treatment initiation
– Aspiration for suspected abscess
 Plain radiographs (usually used)
– Soft tissue swelling
– Periosteal reaction
– Bony destruction (10-12 days)
 Technetium-99m bone scan +/- MRI
– Confirm dx 24-48 hrs after onset
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23.  Goal
– Resolves signs and symptoms
– Eradicates the microorganism(s)
– Prevents relapses
– Prevents complications such as amputation
 The key to successful management:
– Early diagnosis
– Appropriate surgical & antimicrobial treatment
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24.  A multi-disciplinary approach is required:
– Orthopaedic surgeon
– Infectious disease specialist
– Plastic surgeon (in case significant soft tissue loss)
 Acute: medical (pharmacotherapy)
 Chronic: Surgical intervention + pharmacotherapy

25.  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
3) If such removal is effective, antibiotics should prevent their
reformation and primary wound closure should be safe
4) Surgery should not damage already ischemic bone and soft tissue
5) Antibiotics should be continued after surgery
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26.  Indication for surgery in acute case
– The presence of an abscess requiring drainage
– Failure of the patient to improve despite appropriate IV antibiotic
 Empiric antibiotic therapy is usually avoided.
– Treatment usually continues for 4- 8 weeks or longer
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27.  S. aureus:
– MSSA: Nafcillin or oxacillin 2 g q6h
– MRSA: vancomycin 1 g q12h
 Streptococci:
– Penicillin G 4–6×106 U q6h ; switch to oral clindamycin 600 mg q6h
– Erythromycin 500 mg q6h
– Ceftriaxone 2g q12h
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28.  Enteric Gm(-) organisms:
– Oral ciprofloxacin 750 mg q12h
 Serratia or P. aeruginosa:
– Piperacillin–tazobactam 2–4 g q4h or
– Imipenem 500 mg q6h
 Anaerobes:
– Clindamycin 600mg q6h or
– Metronidazole 500mg q8h
– Amoxicillin–clavulanic acid 1.2g q6h–2.2g q8h
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29.  Support for shorter duration therapy
– Adequate surgical debridement
– Diabetic foot osteomyelitis with good vascular supply,~6 weeks
– Prosthetic joint infection after implant removal, ~4 weeks
– Acute hematogenous osteomyelitis (non-vertebral), ~2-3 weeks
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30.  Groups at risk for failure
– Recurrent infection – PJI requiring multiple surgeries
– Vertebral osteomyelitis
– Undrained abscess, endovascular infection, MRSA,
immunosuppression
– Lower recurrence rates in high risk patients treated with
≥6-8 weeks+
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31.  Individualized duration
– Acute vs chronic infection
– Response to therapy
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32.  Efficacy & safety
 Resolves signs and symptoms
 Symptoms resolution within 2 to 4 days of IV abx
 ↓CRP within 1 week of therapy
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33. 1. Septic arthritis
2. Sepsis and septic shock
3. HIV + OIs
4. TB
5. UTI
6. GI infections
7. Intra abdominal infections
8. Skin and soft tissue infections
9. Surgical prophylaxis
10. Parasitic infections, malaria & NTDs
11. Fungal infections(superficial & disseminated)
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