ACUTE

OSTEOMYELITIS

Ankit Karki
Resident -1st year
Department of Orthopedics
LMCTH, Palpa
Anatomy

• Parts of Long Bone

Epiphysis
Metaphysis
Diaphysis
Histology of bone
• Basic structural unit of bone
is osteon/ haversian system
Components
1. Haversian canal
2. Lamellae
3. Lacunae
4. Canaliculi
5. Volkman canal
Periosteum
• Outer layer of fibrous tissue
• Inner cambium layer
More vascular, cells
with osteogenic potential
Limiting membrane for bone
and responsible for periosteal
osteogenesis

Endosteum
- Lines walls of bone cavities including
marrow spaces forming inner limiting
membrane
Blood supply of long bone
Introduction
• Inflammation of the bone and bone marrow caused by infecting
organisms
• Nelaton coined
• Osteon- bone
• Myelo- marrow
• itis- inflammation
Multidisciplinary approach
Classification

Duration of symptoms Mechanism of infection

Acute <2 weeks a. Hematogenous: from
Subacute 2weeks- 3month bacteremia
Chronic >3 months b. Exogenous: Open fracture,
surgery, contiguous spread
from infected local tissue
Classification

Kelly’s: Weiland et al:

• Type I: hematogenous OM
• Type II: OM associated with
fracture union
• Type III: OM without fracture
union
• Type IV:post op/ post traumatic
OM
• Type I: Soft tissue infection
• Type II:Circumferential cortical
and endosteal infection
• Type III:Type II + segmental
defect
Acute Pyogenic Osteomyelitis
• Rapidly destructive pyogenic infection
• Hematogenous
• Diagnosed within 2 weeks of onset of symptoms
• Most common type in children
• Metaphyseal involvement
• Also in adult
Etiology
• Common in active growth i.e. bimodal at 2yrs and 8-12 yrs
• M:F= 4:1
• Site: Metaphysis, mainly in children around knee
Risk Factors
• Poor nutrition
• Trauma
• Infections- skin, dental, respiratory, Gi, UTI
• Burns
• Leucocyte and leucopenia dysfunction
• Iatrogenic intervention
• Sickle cell anemia
• Immunosuppressive therapy
 Mode of spread
1. Direct introduction
• Pin prick
• Stab wound
• Injection
• Open fracture or
• An operation
2. Direct spread from contiguous
focus of infection
3. Indirect spread via blood stream
• Respiratory tract infection
• Bowel and genitourinary tract infection
• Nose and throat infection
 Cause
Age group Most common

Younger than 4 month S. aureus, Enterobacter species, group A and B

streptococcus species
4mth to 4yrs age S. aureus, Group A streptococcus; H. influenza
Adolescents S. aureus, group A streptococcus; H influenza;
Enterobacter

Adult S. aureus, rarely Enterorbacter, streptococcus

Sickle cell anemia patients Salmonella species

Iv drug users pseudomonas

Pathogenesis
• Hair pin arrangement of blood
vessels
• Blood flow slowed and turbulent
• Increased vascularity causing
pooling of blood
• Immature cells
• Low oxygen tension
• Lining cells have little or no
phagocytic activity
• Single endothelial lining in
metaphyseal arteries
Another theory
• Hypertrophic zone of physes has fine
blood vessels
• Allows bacteria more easily to pass
through and adhere to type 1
collagen
• In infants
• Anastomoses between metaphyseal
and epiphyseal blood vessels still
present
• Infection can also reach the epiphysis.
Cascade of events
• Infective embolus enters nutrient artery trapped in vessel of small caliber
• Blocks vessels, area of bone become necrotic

• Active hyperemia in vicinity with infiltration of PMN cells which is poured as exudate
• Increased intra osseous pressure due to exudate and debris(intense pain)

• Vessels get compresswed , further necrosis occurs 2nd – 3rd day

• Exudate follows path of least resistance
• Accumulated in sub periosteal spaces to form abscess and damages blood supply
• Perforates and spread to soft tissues
2nd route of spread of infection

• Exudate into medullary cavity destroying marrow

elements, blood supply

• In advanced stages cortex may be surrounded by pus,

depriving blood supply

• Diaphyseal sequestration
3rd Route of spread of infection

• Through physis into joints.

Clinical presentation
• History of trivial trauma
Cardinal features

• Pain
• Fever
• Refusal to bear weight
• Elevated white cell count
• Elevated ESR
• Elevated CRP
Any local swelling or inflammation , painfulness and restricted
movement accompanied by fever should elicit the tentative diagnosis
of acute OM.
Diagnosis of acute osteomyelitis
• PELTOLA AND VAHVANEN’S CRITERIA (2/4 are found)
1. Purulent material on aspiration of the affected bone
2. Positive findings of bone tissue or blood culture
3. Localised classic physical findings
Bony tenderness
Overlying soft tissue edema, erythema
4. Positive radiological imaging
Peltola H. Vahvanen V(1984) A Comparative study of osteomyelitis and purulent
arthritis with specific reference to aetiology and recovery, infection 12:75-79
Morrey and Peterson criteria
• Definite- pathogen isolated from bone or adjacent soft tissue or
histologic evidence of osteomyelitis
• Probable- A blood culture is positive in the setting of clinical and
radiographic features of osteomyelitis
• Likely- Typical clinical setting and definite radiographic evidence of
osteomyelitis are present and there is response to antiobiotic therapy.
 Evaluation
• History and physical examination
• Lab tests:
1. Hb
2. TBC- polymorphonuclear leukocytosis
3. ESR- 60mm in 1 hr
4. CRP- Elevated, acute phase reactant, normalizes much sooner than ESR
5. Blood culture:Bacterial screening with 3 blood cultures at 30 mins interval-
65% isolating organism
6. Aspiration of pus: Subperiosteal space to obtain marrow aspirate, gram
stain, culture and sensitivity
Radiological investigations

X ray
• Sensitivity: 43-75%, specificity: 75-83%
• Timing:
• Soft tissue changes visible within 3 days
• Bone changes visible in 1-2 weeks
• Early findings:
• Bone: osteopenia
• Late findings:
• Bone: cortical erosion, mixed lucency and sclerosis
• Periosteal reaction
• Soft tissue swelling
Evaluation
2. Sinography:
If sinus track is present
Xray in 2 planes after injection into sinus
Locates focus of infection
3. 3 phases bone scan 99m Tc- MDP
• Increased uptake in all 3phases
• Highly sensitive in acute infection
• Poor in presence of neuropathic arthropathy, fracture, tumor
• Gallium scan and Indium 111 labelled leucocyte scan in conjugation
Evaluation
• MRI Scan
As sensitive as bone scan
Detects changes in water content of marrow before disruption of
cortical bone
IOC for vertebral OM
Differential diagnosis
• Rheumatic fever- gradual joint swelling- poly
• Ewing sarcoma- radiological signs
• Acute suppurative arthritis- muscle spasm more marked- limited
movement and effusion
• Cellulitis- no intense pain
• Erysipelas- raised red margin
Management
• Conservative and operative management.
• Antibiotic choice based on highest bactericidal activity, least toxicity
and lower cost
Nade’s principle of treatment of acute OM

• An appropriate antibiotic is effective before pus formation

• Antibiotics do not sterilize avascular tissue or abscess such areas
require surgical removal
• If such removal is effective antibiotics should prevent their
reformation and primary wound closure should be safe
• Surgery should not damage further already ischemic bone and soft
tissues
• Antibiotics to be continued after surgery
Conservative management

• Analgesics and appropriate splinting

• IV fluids, blood transfusion, high protein diet
• Antibiotics
-selection: mostly semi synthetic penicillin or 1 st generation
cephalosporin
-dosage:2-3 times
Gram negative- empirical bacterial coverage
Selection of antibiotics
• Neonates and infants up to 6 months of age: flucloxacillin plus a third generation cephalosporin
like cefotaxime.
• Children 6 months to 6 years of age: intravenous flucloxacillin and cefotaxime or cefuroxime.
• Older children and previously fit adults: intravenous flucloxacillin and fusidic acid.Allergic to
penicillin -- a second- or third-generation cephalosporin.
• Elderly and previously unfit patients: combination of flucloxacillin and a second- or third-
generation cephalosporin.
• Patients with sickle-cell disease: Chloramphenicol was used but now third generation
cephalosporin or a fluoroquinolone like ciprofloxacin.
• Heroin addicts and immunocompromised patients: thirdgeneration cephalosporins or a
fluoroquinolone
• Patients at risk of methicillin-resistant S. aureus (MRSA): intravenous vancomycin (or similar
antibiotic) together with a third-generation cephalosporin.
• End point of treatment- 4-8 weeks
• Combined oral and IV for 6 weeks
• CRP- at 4-5 weeks
If normal- continue antibiotics for 6 weeks
If higher- repeat at 2-3 weeks—if exceeds 12 weeks MRI to R/O any
surgically treatable causes.
Surgical treatment

• Indications
1. Presence of an abscess requiring drainage
2. Failure of patient to improve despite appropriate intravenous
antibiotic treatment.
The objective of surgery is to drain any abscess cavity and remove all
nonviable or necrotic tissue.
Drainage of acute osteomyelitis (TIBIA)
Drainage of acute osteomyelitis (TIBIA)
• Tourniquet whenever possible. Do not exsanguinate the limb in presence of infection.
• Anteromedial incision 5 to 7.5 cm over the affected part of the tibia.
• Periosteum incised longitudinally for drainage of compressed pus
• Drill several holes 4 mm through cortex into the medullary canal.If pus escapes use a
drill to outline a cortical window 1.3 × 2.5 cm, and cortex removed with an
osteotome
• Evacuate the intramedullary pus, and any necrotic tissue.
• Irrigate the cavity with at least 3 L of saline with a pulsatile lavage system with
antibiotics.
• Skin closed loosely over drains, but not with excessive tension on the skin
After drainage
• Long leg posterior slab application with foot in neutral position, ankle
at 90 degrees, knee at 20 degree flexion
• Antibiotics as per sensitivity
• 6 weeks course
• Followup for 1 year
Complications
• Early
1. Septic arthritis
2. Tenosynovitis
3. DVT
4. Multiple pyogenic abscess
5. Antibiotics reactions
• Late
1. Chronic osteomyelitis
2. Pathological fracture
3. Local growth disturbances
4. Premature closure of epiphysis
5. Deformity
Recent advances in osteomyelitis
• Improved pathophysiology of osteomyelitis
Mechanism of bacterial adherence
Biofilm formation
Intracellular infection
Bone destruction
• New therapeutic strategies
Local delivery of antibiotics
Research on new delivery materials with appropriate mechanical properties, low exothermic
reaction, controlled release of antibiotics, and absorbable scalffolding for promoting bone
regeneration
• Prevention, early diagnosis, and innovative treatment such as biofilm disruptors and
immunotherapy.
References
• Campbell’s text book of Orthopedics
• Tachdjian’s pediatric Orthopedics
• Apley’s system of orthopedics and fracture
• BD Chaurasia Anatomy volume 1
• Review article Osteomyelitis: Recent advances in pathophysiology and
therapeutic strategies
Mitchell C. Brt, David W. Anderson, E. Bruce Toby, Jinxi Wang
• THANK YOU