, Ratna Maheshwari2 and Shalin Maheshwari2
(2)
Pediatric Orthopedics, Childrens’ Orthopedic Centre, Mumbai, India
Take-Home Message
A child with bone pain and fever should be assumed to have osteomyelitis until proven otherwise.
Samples should be sent for culture and histology to rule out neoplasm.
Acute hematogenous osteomyelitis without abscess can generally be treated medically.
Most cases of AHO are caused by S aureus. In neonates, the most common organism is group B streptococci.
Because of the prevalence of CA-MRSA, empiric coverage should cover CA-MRSA in most cases.
Susceptibilities and resistant strains of CA-MRSA vary by community, adding importance to aspiration or biopsy for culture.
The metaphyseal blood supply crosses the physis to the epiphysis in children younger than 12–18 months, so severe sequelae are more common.
Preoperative MRI aids surgical planning by delineating the extent of the infection and the location of abscesses.
Definition
Osteomyelitis is an inflammation of the bone.
Two of the following four parameters must be present according to the Peltola and Vahvanen criteria:
Pus aspirated from bone
Positive bone or blood culture
Localized pain, swelling, warmth, and limited ROM of joints
Radiographic changes typical of osteomyelitis
Etiology
Trauma is a common cause of infection.
Staphylococcus aureus still remains the most common organism responsible for acute osteomyelitis; streptococci, Kingella kingae, Gram-negative organisms, and salmonella are far less frequently responsible.
Risk factors for developing acute hematogenous osteomyelitis:
Diabetes mellitus
Chronic renal disease
Hemoglobinopathies
Rheumatoid arthritis
Concurrent varicella infection
Immune compromise
Pathophysiology
Hematogenous spread—usually involves the metaphysis of the long bones
Direct inoculation—penetrating injuries and surgical contamination
From a contiguous focus of infection
Slow blood flow in the capillaries of the metaphysis allows bacteria to exit the vessel walls.
If a sufficient number of bacteria lodge in the bone to overwhelm the local defenses, an infection occurs.
Osteoblast necrosis, activation of osteoclasts, release of inflammatory mediators, recruitment of inflammatory cells, and blood vessel thrombosis cause a purulent exudate.
A subperiosteal abscess forms when the exudate penetrates the porous metaphyseal cortex.
In bones with an intra-articular metaphysis, the exiting exudate can enter the joint and cause an associated septic arthritis.
If pus is not drained and the elevated periosteum remains viable, it will produce new bone over time and involucrum will form.
When both medullary and periosteal blood supplies are compromised, large areas of dead bone or sequestra may be formed.
Evaluation
Clinically acute localized tenderness in the region of the metaphysis of a long bone in the presence of fever should be sufficient grounds to make a tentative diagnosis of acute osteomyelitis. Use of antibiotics may mask the symptoms.
Laboratory findings
Initial blood work should include C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), blood cultures, and white blood cell (WBC) count with differential.
Blood cultures may yield an organism 30 % of the time.
The WBC is elevated in only 25 % of patients.
Diagnostic imaging
Plain radiographs are of little use in the diagnosis of acute osteomyelitis.
In stage I Trueta, there are no plain radiographic changes either in the soft tissue planes or in the bone. In stages II and III, there is loss of definition of soft tissue planes indicative of edema. However, there are still no changes in the bone; bone changes appear 10–14 days after the onset of infection in children.
Ultrasound scanning is useful for the diagnosis of a subperiosteal abscess.
Technetium Tc 99 m bone scan can help localize the focus and will demonstrate a multifocal infection.
MRI detects marrow and soft tissue edema seen early in infection as well as abscesses requiring surgical drainage. It provides good anatomic detail in many planes. In acute osteomyelitis, the low signal intensity in T1 becomes a high signal intensity in T2.
Classification
Trueta divided the clinical stages of acute osteomyelitis into three.
In stage I, there is severe bone pain and profound local tenderness without any soft tissue inflammation.
In stage II, the systemic and local signs are more pronounced; this corresponds to the development of a subperiosteal abscess.
In stage III, there is pus in the soft tissues, and in this stage, it is difficult to distinguish osteomyelitis from cellulitis.
Classification | Description |
|---|---|
Anatomic stage | |
1 | Medullary osteomyelitis |
2 | Superficial osteomyelitis |
3 | Localized osteomyelitis |
4 | Diffuse osteomyelitis |
Physiological host status | |
A | Normal host |
B | Systemic compromise |
Local compromise | |
Systemic and local compromise | |
C | Treatment worse than disease |
Stage 1, or medullary, osteomyelitis is confined to the medullary cavity of the bone.
Stage 2, or superficial, osteomyelitis involves only the cortical bone and most often originates from a direct inoculation or a contiguous focus.
Stage 3, or localized, osteomyelitis usually involves both cortical and medullary bones. In this stage, the bone remains stable, and the infectious process does not involve the entire bone diameter.
Stage 4, or diffuse, osteomyelitis involves the entire thickness of the bone, with loss of stability, as in infected nonunion.Related posts:
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