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Acute Osteomyelitis
Subacute Osteomyelitis Chronic Osteomyelitis Septic Arthritis
What is Osteomyelitis?
It is Inflammatory process of the bone and its structures secondary to infection
Acute Osteomyelitis
Hematogenous osteomyelitis:
Bacterial seeding from the blood. occurs primarily in children. The most common site is the rapidly growing and highly vascular metaphysis of growing bones. Despite its name, may have a slow clinical development and insidious onset.
Direct contact of the tissue and bacteria during trauma or surgery, spread from a contiguous focus of infection. Clinically:
More localized than those of hematogenous osteomyelitis Tend to involve multiple organisms.
Risk factors:
Diabetes mellitus Sickle cell disease Acquired immune deficiency syndrome (AIDS) IV drug abuse Alcoholism Chronic steroid use Immunosuppression Chronic joint disease. The presence of a prosthetic orthopedic device Any recent orthopedic surgery Open fracture.
Epidemiology
Incidence is higher in developing countries compared to developed ones. Morbidity results from its complications. Male-to-female ratio is approximately 2:1 Acute hematogenous osteomyelitis is primarily a disease in children. Spinal osteomyelitis is more common in persons older than 45 years.
Causative Organisms
Acute hematogenous osteomyelitis :
Newborns (younger than 4 mo): S .aureus, Enterobacter species, and group A and B Streptococcus species Children (aged 4 mo to 4 y): S. aureus, group A Streptococcus species, Haemophilus influenzae, and Enterobacter species
Cont
Children, adolescents (aged 4 y to adult):S .aureus (80%), group A Streptococcus species, H. influenzae, and Enterobacter species Adult: S .aureus and occasionally Enterobacter or Streptococcus species
Causative Organisms
Direct osteomyelitis :
Generally: S aureus, Enterobacter species, and Pseudomonas species . Puncture wound through an athletic shoe: S aureus and Pseudomonas species. Sickle cell disease - S aureus and Salmonellae species.
Pathology
Inflammation: Suppuration:
Volkmann canals, subperiosteal abcess, spread along the shaft, re-enter the bone or burst into the soft tissue Neonates: extends to the epiphysis Older children: confined to the metaphysis.
Resolution
Bone thickens to form an involucrum enclosing the infected tissue an sequestra. Perforation may occur (cloacae) and become converted to chronic osteomyelitis
Bone destruction of head of 2nd metatarsal with periosteal new bone formation characteristic of osteomyelitis
Complications:
Spread:
To the joints: septic arthritis To other bones: metastatic osteomyelitis
Growth disturbance and deformities. Persistent infection. Fracture. Loosening of the prosthetic implant . Overlying soft-tissue cellulitis.
Clinical Approach
History
Physical examination Investigations
Hematogenous osteomyelitis: usually slow insidious progression of symptoms. Direct osteomyelitis: generally more localized, with prominent signs and symptoms. General symptoms of osteomyelitis include the following:
Hematogenous long-bone osteomyelitis
1. 2. 3. 4. 5. 6.
History
Abrupt onset of high fever (fever is present in only 50% of neonates with osteomyelitis) Fatigue Irritability Malaise Restriction of movement . Local edema, erythema, and tenderness
Insidious onset History of an acute bacteremic episode May be associated with contiguous vascular insufficiency Local edema, erythema, and tenderness
Physical examination
Findings at physical examination may include the following:
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3. 4. 5. 6.
Fever (present in only 50% of neonates) . Edema . Warmth . Fluctuance . Tenderness to palpation . Reduction in the use of the extremity .
Investigations
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Lab studies
CBC: leucocytosis
The C-reactive protein level usually is elevated (nonspecific but more useful than ESR). ESR usually is elevated (90%) nonspecific.
Aspiration of the pus from the subperiosteal abscess and culture, and test sensitivity for antibiotics Blood culture results are positive in only 50%
X-Ray:
Radiological studies
First sign is soft-tissue edema at 3-5 days after infection. Bony changes are not evident for 14-21 days:
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2. 3.
early radiographic signs of refraction of the metaphysis and periosteal new bone formation increasing ragged if treatment is delayed sclerosis and thickening of the bone at healing
Approximately 40-50% focal bone loss is necessary to cause detectable lucency on plain films.
Plain-film radiograph showing osteomyelitis of the second metacarpal (arrow). Periosteal elevation, cortical disruption and medullary involvement are present.
The above X-ray of the left ankle of a 10-year-old boy shows lucency in the tibial metaphysis secondary to acute hematogenous osteomyelitis (AHO).
The above X-ray of the right ankle of a 10-year-old boy shows lucency in the tibial metaphysis secondary to acute hematogenous osteomyelitis (AHO).
MRI :
Radiological studies
Early detection and surgical localization of osteomyelitis. Sensitivity ranges from 90-100%.
A 3-phase bone scan with technetium 99m is probably the initial imaging modality of choice Show increase activity but it is a non specific sign of inflamation.
This MRI sagittal section shows the same AHO lesions with the right lesion extending into the growth plate.
Bone scans, both anterior (A) and lateral (B), showing the accumulation of radioactive tracer at the right ankle (arrow). This focal accumulation is characteristic of osteomyelitis.
Radiological studies
CT scan (spinal vertebral lesions, complex anatomy: pelvis, sternum, and calcaneus) Ultrasound
In children with acute osteomyelitis. May demonstrate changes as early as 1-2 days after onset of symptoms. Abnormalities include soft tissue abscess or fluid collection and periosteal elevation. Ultrasonography allows for ultrasound-guided aspiration. It does not allow for evaluation of bone cortex
Diagnosis
Purulent material on aspiration of affected bone. Positive findings of bone tissue or blood culture. Localized classic physical findings of bony tenderness, with overlying soft-tissue erythema or edema. Positive radiological imaging study.
Treatment
Principles of treatment:
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Analgesia an general supportive measures. Rest of the affected part Antibiotic treatment. Surgical eradication of pus and necrotic tissue.
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Treatment
Antibiotic treatment:
Start with IV antibiotics for 1-2 weeks then oral for 3-6 weeks. Take cultures to detect the organism and its sensitivity pattern. Start empirical treatment before the results came back, then modify it according to the results.
Treatment
Antibiotic choices:
Older children and adults (staph infection): fluloxacillin and fusidic acid. MRSA: Vancomycin Children younger than 4 year-old or those with gram negative organisms: 3rd generation cephalosporins. Heroin addicts and immuno-compromised patients: more specific antibiotics.
Cont
Sickle cell anemia and osteomyelitis: fluoroquinolone antibiotic (not in children). A 3rd cephalosporin (eg, ceftriaxone) is an alternative choice.
Nail puncture occurs through an athletic shoe (S aureus and Pseudomonas aeruginosa): ceftazidime or cefepime. Ciprofloxacin is an alternative treatment.
Trauma (S aureus, coliform bacilli, and Pseudomonas aeruginosa): nafcillin and ciprofloxacin. Alternatives include vancomycin and a 3rd cephalosporin with antipseudomonal activity.
Drainage:
Treatment
Subperiosteal abscess Pyrexia and local tenderness more than 24 hour after adequate antibiotic treatment.
Prevention
Improve immunity.
Post-traumatic infection (regular wound dressing for established infection):
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Debridement of open fractures. Stabilization of fractures. Antibiotics. Closure of exposed bone surfaces.
Postoperative infection:
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