Prepared by Dr. Daghan KOYUNCU
Septic arthritis can be defined as the infection of the joint space. The incidence is higher in the first years of life. It can be diagnosed with history, physical examination, laboratory studies and imaging. It is an acute surgical emergency and it needs to be diagnosed and treated rapidly.
Epidemiology
0.25% of the hospitalizations among children.
Most of the pediatric septic arthritis patients (50%) are < 2y.
More common in boys than girls (2/1).
Hip>knee>ankle>elbow>wrist>shoulder
Staph. Aureus is the most common pathogen. Other possible pathogens: Group B streptococcus, K.kingae, H. influenzae, N. gonorrhea
| Age | Common organism | Empirical antibiotics |
| <12 months | Staphylococcus spp., group B streptoccus | 1st gen cephalosporins |
| 6m-5y | Staphylococcus spp., H. influenzae | 2nd-3rd gen cephalosporins |
| 5-12y | Staphylococcus aureus | 1st gen cephalosporins |
| 12-18y | S. aureus, N. gonorrhea | Oxacillin/cephalosporin |
Table 1: Common organisms in septic arthiris, by age, and their treatment choices
Pathophysiology
Hematogenous seeding is the most common cause. Especially upper respiratory tract illnesses, sinusitis, otitis media.
Other causes are penetrating injuries (direct inoculation) and extension from adjacent bone (osteomyelitis)
In neonates, transphyseal vessels allow the spread of microorganisms into joints with intraarticular metaphysis (hip, elbow, shoulder, ankle, NOT knee)
Bacterial entry to the joint causes an inflammatory cascade which eventually destructs the articular cartilage. Macrophages, neutrophils, cytokines such as IL-1, IL-6 and TNF-α causes cartilage damage starting from 2 to 5 days of the onset.
Evaluation
History:
Acute onset of pain, atraumatic limitation of the extremity
Ill appearing, “septic” child
Physical examination:
Vitals – to rule out hemodynamic instability
Swelling, erythema, tenderness to touch, warmth
Range of motion – pain with passive motion, the patient doesn’t want to actively move the extremity
The presence of warm joint which is painful during passive ROM suggests septic arthritis, while passive ROM doesn’t cause symptoms for osteomyelitis.
Lab tests and imaging:
CBC, CRP, ESR, procalcitonin, blood cultures
WBC – elevated, with >80% neutrophil rate
ESR – elevated, >40 mm/hr
CRP – >20 mg/l for septic patients; if <20, alternative diagnosis is possible
X-rays – septic arthritis may cause joint space widening
USG – can be used for the patients with hip symptoms, to evaluate hip effusion
MRI – demonstrates joint effusion
Kocher criteria are used for the diagnosis of pediatric septic arthritis. ESR, fever, non-weight bearing and higher WBC count are the components.
| Kocher criteria | 4 predictors | 99.6% |
| History of Fever | 3 predictors | 93.1% |
| History of Non-weight bearing | 2 predictors | 40% |
| WBC>12000 cells/mL | 1 predictor | 3% |
| ESR>40mm/h | 0 predictor | 0.2% |
Table 2: Kocher criteria and the possibility of the diagnosis for the number of predictors present
Hip aspiration:
Definitive modality for the diagnosis
Blind aspiration is not suggested. Aspiration should be performed with ultrasonography or an arthrogram.
The aspiration material should be sent for Gram stain, culture, cell count, glucose and protein studies
WBC>50000/mm3, neutrophil predominance, high protein content, low glucose content (< 33% of serum glucose) are found in septic arthritis.
Differential diagnosis:
Transient synovitis – previous URTI/GI infection history, no fever, acute joint pain and inability to bear weight, no toxic appearance, CRP<20mg/L
Osteomyelitis – fever, pain with weight bearing, no pain with joint ROM, x-ray findings
JIA, rheumatic fever, Kawasaki syndrome, avascular necrosis, SCFE, trauma, Lyme arthritis, Legg-Calve-Perthes syndrome
Treatment:
Antibiotic treatment:
For Neisseria infections, antibiotic treatment (ceftriaxone) without debridement can be used for app. 4 weeks.
Surgery: Debridement & irrigation
Aspiration and lavage/repeated aspiration/arthroscopy/open arthrotomy with iv antibiotics
Arthroscopy – ability to see the joint space, remove synovitis, easier rehab as it is a minimal invasive approach
Arthrotomy – most commonly used
Better results – debridement in the first 4 days
Complications:
Sepsis, premature arthritis, femoral head destruction, physeal arrest, growth disturbance, joint stiffness, persistent infection
Delay in treatment – the most important factor for the prognosis
Poor results are associated with delay in definitive treatment >5 days, osteomyelitis of the proximal femur
OSTEOMYELITIS
Epidemiology:
Mostly seen in the metaphysis of long bones (%75).
Femur>tibia>humerus
8-10 in 100000 in developed countries, up to 80 in 100000 in developing countries
Especially affects younger children, <5 years
Pathophysiology:
Mostly hematogenous seeding. Otitis media, pharyngitis, sinusitis cause bacteremia.
Bacterial penetration to metaphyseal region with nutrient arteries. Those arteries form loops adjacent to physis. This causes blood stasis, turbulent blood flow; thus, helping bacterial penetration.
<18 months, transphyseal circulation is viable. This may allow bacterial penetration to epiphysis causing epiphyseal damage and septic arthritis.
In chronic infection, it can reach subperiosteal space, metaphyseal or direct inoculation and can disseminate through cambium. Fibrous periosteum is separated from the bone due to purulent material accumulation. This detachment of the periosteum can cause bone ischemia sequestrum
New bone formation involucrum
Most common pathogens – S. aureus, K. kingae, S. pyogenes, S. pneumoniae
Classification:
Acute hematogenous osteomyelitis – <2 weeks, sudden onset of symptoms
Subacute osteomyelitis – > 2 weeks, masked findings
Chronic osteomyelitis – >1 month, up to years. Caused by the failure to treat AHO
Cierny-Mader classification – anatomic type and host status. Limited adaptability as most pediatric patients are normal hosts.
Subacute osteomyelitis is classified by Gledhill and Roberts et al.
| Type IA | Metaphyseal lucency without marginal sclerosis |
| Type IB | Metaphyseal lucency with surrounding reactive bone, Brodie abscess |
| Type II | Metaphyseal lucency with cortical erosion |
| Type III | Localized diaphyseal erosion with periosteal reaction |
| Type IV | Diaphyseal lesion with subperiosteal bone formation |
| Type V | Epiphyseal lesion |
| Type VI | Vertebral lesion, diskitis |
Table 3: Subacute osteomyelitis classification by Gledhill and Roberts et al.
Evaluation:
History and physical examination:
Neonates – lack of movement, visible swelling
Older children – limb pain, inability to bear weight, fever
Recent infection history, trauma history
Swollen, erythematous, tender limb
Lab tests and imaging:
CBC, CRP, ESR, procalcitonin, blood cultures
X-ray, MRI with and without contrast, three phase body scan, CT scan
X-ray – osteolysis, sequestrum, involucrum, bone defect
MRI – abscess formation, bone infarction
Aspiration – for chronic osteomyelitis, from sinus orifice, after cleaning the orifice with povidone iodine
Biopsy – aerobic, anaerobic, fungal cultures. Always send to pathology, possible Ewing sarcoma or osteosarcoma diagnosis
For subacute osteomyelitis, biopsy after 6 weeks antibiotic treatment.
Treatment:
Antibiotic therapy:
For AHO – first line of the treatment. Start with iv antibiotics (3-14 days) and after symptoms regress and CRP decrease to normal values switch to oral antibiotics if available.
Begin with empiric antibiotics, switch to microorganism specific antibiotics after culture results.
Treatment duration is 4-8 weeks.
For chronic osteomyelitis, combination with surgical debridement is suggested.
Rifampin is used as a supplement to the antistaphylococcal antibiotics – bactericidal action.
Treatment duration is 6-9 months.
Surgery:
For AHO – surgical debridement if subperiosteal/intraosseous abscess is present, limited response to antibiotics
For chronic osteomyelitis – sequestrum removal, abscess drainage, granulation tissue debridement
Debridement of all nonviable, devitalized tissues is essential. Bone debridement should be done until cancellous bleeding, paprika sign, is seen.
Antibiotic impregnated PMMA beads can be used to achieve local antibiotic release and reduce dead space.
If no cortex continuity after debridement – external stabilization is needed.
If extensive bone defect is present – reconstructive procedures such as bone grafting, vascularized fibula grafting or bone transport with Ilizarov method can be performed.
Complications:
AHO:
Chronic infection, septic arthritis, growth disturbance, DVT, pulmonary embolism, avascular necrosis, deformity, adverse drug reactions
Septic arthritis – especially in bones with intraarticular metaphysis
Growth disturbance – bar formation, mostly central and diffuse. Hard to resect. May cause severe limb length discrepancies.
DVT – especially as a part of disseminated staphylococcal infection. Panton-Valentine lekocidin in MRSA infections is responsible.
Chronic osteomyelitis:
Recurrence in 20-30% of patients. Aggressive debridement needs to be performed in order to prevent recurrences.
Osteopenia, angular deformity, joint stiffness, pin site infections.
References:
References:
