December 5, 2024

Acute Hematogenous Osteomyelitis is first coined by Reynaud (17th Century) and later popularized by Nelaton (1834)

Acute osteomyelitis

Organisms

  • Staphylococcus aureus (> 70%)
  • Group A B-hemolytic streptococcus (Streptococcus pyogens)
  • Group B streptococcus
  • Alpha hemolytic streptococcus
  • Hemolytic influenza
  • Kingella kinger
  • E.coli, Pseudomonas, Proteus

Why Metaphysis is a common site for abscesses?

  1. Hairpin bend arrangements of arterioles
  2. Relatively less phagocytosis
  3. Sluggish flow
  4. Torturous blood vessels and skimming of bacterias
  5. Dead (apoptotic) and degenerative cartilages cell from physeal plate serve as a medium for bacterial growth
  6. Microfracture and local hematoma common in young active children
  7. Fine vessels in hypertrophic zones of physics may more easily allow bacterias to pass through and adhere to Type I collagen of that area

In infants where there is anastomosis between metaphysics and epiphyseal blood vessels , infection can also reach epiphysis

Cause of Diaphyseal Osteomyelitis:

  1. Long-standing Osteomyelitis in children
  2. Post-traumatic Osteomyelitis
  3. Implant related Osteomyelitis
  4. Tubercular Osteomyelitis
  5. Drug abusers (Heroins addict- Pseudomonas)
  6. Immunocompromised (Fungal)
  7. Salmonella Osteomyelitis (Often bilateral and may be symmetrical)

Morrey’s and Peterson’s criteria for Acute Osteomyelitis

LikelyTypical clinical setting and definite radiographic evidence of osteomyelitis are present and there is a response to antibiotic therapy
ProbableBlood culture (+)in the setting of clinical and radiographic features of osteomyelitis
DefinitePathogen isolated from bone or adjacent soft tissue or there is histological evidence of osteomyelitis

Pathologenesis of Acute Hematogenous Osteomyelitis

  1. Stage of inflammation
  2. Stage of suppuration
  3. Stage of bone necrosis
  4. Stage of reactive new bone formation
  5. Stage of resolution and healing
  6. Stage of Chronicity
Acute Hematogenous Osteomyelitis pathogenesis

Involucrum: Encasing Sequestrum

Sinus: Cloacae in involucrum

Causes of Chronicity of Infection

  1. Presences of unabsorbed and retained sequestra serving a constant source of infection
  2. Unobliterated cavities (dead spaces)
  3. Microbiological shift ( Changes of aerobic cocci to gram-negative/ anaerobic)
  4. Multiple types of bacteria ” mixed infection” and anti-microbial resistance

Periosteal reaction is not seen in

  • HIV associated Osteomyelitis
  • Tubercular Osteomyelitis
  • Long-standing resolving Osteomyelitis

Septic arthritic secondary to acute Osteomyelitis is seen in

  1. In infants < 6 months; the physiological connection between epiphyseal and metaphyseal vasculature through epiphyseal plate
  2. Intraarticular location of metaphysis- proximal humerus, neck of femur, proximal radius, distal fibula in adults

Peltola and Vahuvanen’s criterias

4 criteria

  1. Purulent material on the aspiration of the affected bone
  2. The positive finding of bone tissue or blood culture
  3. Localized classic findings
    • Bony tenderness
    • Overlying soft-tissue edema, erythema
  4. Positive radiological imaging

Diagnostic Imaging

Plain X-Ray

Osteoporosis is a feature of metabolically active, and thus living bone . Segment that fails to become osteoporotic is metabolically inactive and possible dead

USG

CT Scan

Radionucleotide Scanning

SPECT/CT

MRI

Role of 99Tc bone Scintigraphy

It is a screening tool (< 10 % specificity)

  • Phase I: Arterial (flow) phase
  • Phase II: Venous phase
  • Phase III: Focal bone uptake
Phase I + Phase II = Positive
Phase III = Negative
Soft tissue infections
Phase I + Phase II + Phase III = Positive
True bone infections

Ga67 Scintigraphy: For vertebral osteomyelitis

In111 Labeled leukocyte imaging: Else where infection in the body

Leukocyte imaging In111 if used in conjunction with a sulpher colloid scan that delineates areas of normal bone activity whereas a leukocyte scan highlights the involved regions

Incongruences of In111 labeled leukocyte scans and Sulpher colloids scans is highly suggestive of infection

Laboratory Investigations

  • Aspirate Pus
  • Blood Culture (If fever >38°C)
  • CRP (Usually elevated in 12-24 hrs) Normal in (2-4 weeks)
  • ESR in 24 to 48 hrs
  • WBC count: Rises
  • ASO titer may be elevated

Under evaluation

  • IL-6
  • alpha-defensin immunity

Treatment of Acute Hematogenous Osteomyelitis

General Principles of Infection Control

Principles

  1. Appropriate microbial therapy
  2. Surgical drainage if required
  3. Splinting and rest of the affected part
  4. Supportive treatment for pain and dehydration

Injectable antibiotics (after culture sensitivity), CRP level (Normal) (2-4 weeks) + Patient condition improves, then oral antibiotics for next 3-6 weeks

Age groupOrganismsDrugs
Neonates- 6 monthsPenicillin resistance S.aureus
Group B streptococcus
Gram (-) organisms
Flucloxacillin + 3rd generation cephalosporins
Alternatively,
– flucloxacillin
– benzylpenicillin
– gentamycin
6 months – 6 yearsH. influenzaCombination of i.v. flucloxacillin + cefotaxime/ cefuroxime
Older children and previously fit adultsStaphylococcus
Streptococcal
Fusidic acid + I.V. flucloxacillin
Benzylpenicillin (better)
Elderly and previously not fit patientsRisk of Gram (-) infections (Respi, UTI, GI)Flucloxacillin + Second/third cephalosporins
Patients with sickle cell diseaseSalmonella and gram (-) organismsChloramphenicol or 3rd generation cephalosporin + fluoroquinolone (Ciprofloxacin)
Heroin addicts and immunocompromised patientPseudomonas
Proteus or aerobics
3rd generation cephalosporin or fluoroquinolones
Patient considered to be at risk of MRSA
(Previously hospitalized with MRSA, hospitalized)
MRSAIV Vancomycin or teicoplanin +3rd generation cephalosporin

Surgical drainage

If clinical features do not improve within 36 hours of initiating treatment or even earlier if

  • there is a sign of pus (swelling, edema. fluctuation)
  • Pus is aspirated

When there is no pus:

  • Drill a few holes in the bones in various direction

And if the extensive intramedullary abscess

  • Drainage can be achieved by cutting a small window in the cortex

The wound is closed with/ without drain and splinting is applied

Once signs of infection subside, movements are encouraged and the child is allowed to walk with crutches (full weight bearing)

Splinttage

  • Prevents joint contracture
  • Prevents dislocation ( in the hip)- skin traction

General Supportive treatment

  • Intravenous fluids

Complications

  • Epiphyseal damage and altered bone growth
  • Supportive arthritis
  • Metastatic infection
  • Pathological fractures
  • Chronic infections

Biofilms

Biofilms are bacterial colonization and resistance to antibodies are enhanced by the ability of certain microorganisms to adhere to avascular bone surfaces and foreign implants protected from both host defense and antibodies by a protein polysaccharides slime (glycocalyx or biofilm)

Probably teichoic acid (the sweet husk of cells)

Mechanism of biofilms formation
Mechanism of biofilms formation

It significantly protects bacteria from phagocytosis, and recognition helps cling to inert implant material and forms a biofilm that may contain numerous colonies of bacteria safely hidden from host immunity (eg. Streptococcus epidermidis)

Biofilms stimulate the release of PGE2 from monocytes which inhibits T lymphocytes proliferation, B lymphocytes blastogenesis, Immunoglobulins production

Interferes with while cell chemotaxis and degranulation

So, eradication of biofilms forming is impossible

Implants have to be removed for complete eradication of infection

See also: Subacute hematogenous osteomyelitis

See also: Chronic Osteomyelitis

See also: Multifocal Non-suppurative Osteomyelitis and Caffey’s Disease

See also: Septic Arthritis in Infants/ Children