Septic arthritis

Dr Taral Nagda

Pediatric Orthopedic Surgeon

www.ipodindia.org

The Guru Mantra

“The risks of delayed drainage far outweigh

the benefits of waiting and watching for a response to antibiotics.”

The Facts and figures

The knowledge of these general facts regarding pattern of involvement may be invaluable in diagnosis of the condition.

1. Septic arthritis is more common than osteomyelitis in infancy and childhood.
2. Most common joints-the hip and knee – 60 % cases
3. Polyarticular in about 5 percent
4. Age group 75 percent occur in children below 5 years

Pathophysiology

The organisms

It has been a traditional teaching that the most common organisms are gram-positive aerobes (80%) and approximately 20% of cases are caused by gram-negative anaerobes with Staphylococcus aureus the most common among the gram positive with less commonly implicated bacteria include  group A and group B streptococci, Streptococcus pneumoniae and Haemophilus influenza. Neonates are more susceptible to group B streptococcal infection.

Over recent years, the microbes isolated in bone and joint infections have changed. In the 1970s and 1980s. The introduction of the Haemophilus influenzae type B vaccine has resulted in a vast reduction in cases secondary to hemophilus, but a number of new organisms have appeared. Recent publications would suggest that perhaps only 40% of infections are the result of S. aureus. We have noticed a  recent upsurge of septic arthritis caused by methicillin-resistant strains of Staphylococcus aureus (MRSA). Although these infections were once thought to be predominantly hospital acquired, but of late, several cases of community-acquired MRSA also have been identified

Diagnosis

Need for an early diagnosis

The damage to the cartilage, growth plate and bone due to avasularity and enzymatic distruction sets in early.The cartilage destruction starts as early as 8 hours following the onset.The avascularity sets in within 24-48 hours of the temponade. The biggest challenge is therefore to control the  infection and drain the joint before the damage takes place

The challenges of diagnosis septic arthritis

-No single test can be relied upon

-Inflamatory markers may be normal or only slightly elevated early in the disease

-The xrays may be normal early in the disaease

-The imaging modalities such as xrays, ultrasound, bone scan  or MRI  suggest a process of inflammation and effusion but can not diagnose septic arthritis

-The laboratory investigations such as blood counts, erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) may help in suggesting that there is an infective process going on but cannot definitely confirm the diagnosis of septic arthritis.

-The only way the joint infection can be conclusively diagnosed is by demonstrating bacteria in

the fluid removed from the joint. However, an organism may only be cultured in approximately 60 percent of cases of true septic arthritis.

-Knee jerk antibiotics may blunt clinical preasentation

– Realizing the limitations of investigations in confirming the diagnosis of septic arthritis, it is imperative that treatment is commenced on the basis of a high index of suspicion. Definitive treatment

should not be withheld for want of confirmatory laboratory tests.

On the basis of a careful clinical examination, a tentative diagnosis of septic arthritis needs to be made. If joint aspiration does not yield fluid with bacteria demonstrable either in a Gram-stained smear or on culture, a presumptive diagnosis may be made with the help of the results of other laboratory tests in conjunction with clinical findings.

Kocher’s cliteria

Kocher et al  identified clinical and laboratory predictors of septic arthritis:

1. history of fever
2. inability to bear weight on the limb
3. ESR _40 mm/hour
4. White blood cell (WBC) count 12 000/mL.

The predicted probability of septic arthritis was 0.2 if none of these predictors was present. This means if none of the factors were present there was only 2 % chance of the condition being septic arthritis

The probability of a diagnosis of septic arthritis was 40, 93.1 and 99.6 percent if two, three or four of these predictors, respectively, were present.

Although Kocher noted these four risk factors and validated these risk factors in a subsequent report,  other centers have found that these four factors may not have as high a predictive value in determining a septic hip as was originally thought. In a recent paper from Melbourne it was noted that a significant number of patients had normal parameters and suggested that clinical acumen still plays a crucial role in management

Cliteria of Jung et al:

The following were identified as were identified as independent multivariate predictors of septic arthritis.

Temperature>37°C

ESR > 20 mm/hour

CRP> 1 mg/dL

WBC> 11 000/mL

An increased joint space>2 mm

Radiology

X-rays are findings are often normal.Look for soft tissue swelling around the joint, widening of the joint space, and displacement of tissue planes.

Ultrasound is very sensitive in detecting joint effusions generated by septic arthritis. It also  can be used to define the extent of septic arthritis and help guide treatment. Sometimes Ultrasound helps to differentiate septic arthritis from other conditions (eg, soft tissue abscesses, tenosynovitis) in which treatment may differ.

MRI Can show changes of marrow edema and help to differentiate between transient synovitis, inflammatory arthritis and septic arthritis by virtue of changes in marrow edema and synovial lining. It can also diagnose additional osteomyelitis. In a recent study markers of SA on MRI included  bone marrow oedema  and absence of T1-weighted and T2-weighted low signal intensity synovial tissue. Furthermore, soft-tissue oedema and reduced contrast enhancement in the epiphyses were more frequent in children with SA.

Differential diagnosis

Conditions that Mimic infection

• Transient synovitis: May be difficult to differentiate early on. The lab reports, presence of mixed echogenesity on US and severity of symptoms and signs point to infective process. When in doubt a joint aspiration should be performed
• Inflamatory arthritis: Fluid out of proportion to symptoms
• Other conditions to keep in mind
  • Malignancies:leukemia, Ewing’s sarcoma, Metastasis
  • Langerhans cell histiocytosis
  • Sickle cell disease and bone infarct
  • Storage disorders: Gaucher disease

Management

Antibiotic therapy

Aim

To control and eradicate the infective process

Which antibiotic

The antibiotic selected should be effective against the organism responsible for the infection. Since

Gram-positive organisms are most frequently responsible for the infection, an antibiotic that is

effective against these organisms should be started empirically. In hospital acquired infection a combination broad spectrum antibiotic is started to be effective against gram positive and gram negative organisms

How long?

In the past it was recommended that treatment with antibiotics should be continued for six weeks.

However, recent studies suggest that the duration of medication may be reduced to four weeks or

less without adverse outcome in the long term

To start with an IV route is preferred  Once the clinical signs improve and CRP levels touch baseline

the antibiotic may be given orally.

Monitoring the treatment

1Clinical parameters: Fever, heart rate, Pain, range of movements,Weight bearing status

2. Lab p[arameters: ESR, TC/DC, CRP Among this CRP is the best indicator of response to therapy.
3. USG to look for reduction in joint effusion
4. Xrays To look for lytic areas and joint position

Failure of CRP to fall by 1 week

1 Recollection

2. Missed multifocal septic arthritis
3. Systemic infection- pneumonitis, pleuritis, pyelonephritis, peritonitis
4. Wrong antibiotic, resistant organism
5. Associated osteomyelitis

Shortened antibiotic course

A recent paper from Melbourne suggests a shortened antibiotic regimen of 3 days Iv antibiotic with 3 week oral antibiotics in patients with childhood septic arthritis and osteomyelitis. After 3 full days of intravenous antibiotics the patients were assessed with regard to converting to oral therapy. An improvement in symptoms (pain, movement), normalization of temperature, and stabilizing CRP were defined as prerequisites for conversion. Persistent pain, fever, and rising inflammatory markers dictated that therapy should continue and that surgical exploration could be indicated. All patients were kept in hospital for 1 day after conversion to oral therapy to ensure tolerance. Oral antibiotics were continued for 3 weeks, usually at half the intravenous dose if tolerated. They found that a temperature of greater than 38.4 on admission and CRP greater than 100 were the best predictor of needing antibiotics for more than 3 days The addition of ESR, WCC, or both did not help in determining which patients will require prolonged therapy. They could successfully convert 59% of patients by day 3 and 86% by day 5 resulting in only 14% of patients requiring intravenous therapy for 6 days or more.

Surgical Intervention

Aim

1. Joint decompression: To reduce temonade, relieve pain and spasm, and obtain sample for smear and culture
2. Joint lavage: To washout the enzymes and debris harmful to joint cartilage

Methods

1. Aspiration and lavage:  Minimally invasive. Repeated joint aspirations are not a good option for hip joint as it does not decompress joint adequately, prolongs antibiotic therapy and hospital stay
2. Arthrotomy:  Allows joint inspection and complete joint clearance. Septic hips in young children are drained anteriorly to avoid disrupting the posterior blood supply to the femoral epiphysis. It is critical to do a definitive capsulotomy. Be sure that the joint is aggressively irrigated and that there is no purulent collection left behind. Some have recommended decompression of the femoral neck if there is associated osteomyelitis that has not decompressed itself into the joint
3. Arthroscopy: All advantages of arthrotomy being minimally invasive

Immobilization of the joint

Aim

To relieve spasm, prevent deformity and instability

Methods

With brace, plaster or traction

Prognosis

Depends on the following factors

-Duration of disease

-Type of organism

-Age of child

-The joint involved

-Intervention

-Associated systemic disorders and immune status

Summary

We recommend high index of suspicion while diagnosing septic arthritis in children and an aggressive treatment approach. Initial investigations include blood cultures, and hematologic markers (WCC, CRP, and ESR) followed by appropriate imaging. Ultrasound should be used to confirm SA and MRI can be used in selected cases. Empirical antibiotics (Amoxycillin Clav combination with amikacin) should be commenced after prompt drainage of joint collections. Further choice of antibiotics will depend on culture report and clinical course. Short antibiotic treatment guided by improvement in clinical parameters and CRP is effective in most cases.

References

Arnold SR, Elias D, Buckingham SC, et al. Changing patterns of acute hematogenous osteomyelitis and septic arthritis: emergence of community-associated methicillin-resistant Staphylococcus aureus. J Pediatr Orthop. 2006;26:703–708

Buxton RA, Moran M. Septic arthritis of the hip in the infant and young child. Curr Orthop. 2003;17:458–464

Caird MS, Flynn JM, Millman JE, et al. Factors distinguishing septic arthritis from transient synovitis of the hip in children. A propective study. J Bone Joint Surg Am. 2006;88(6):1251-1257.

Jagodzinski, Kanwar, Graham K  Prospective Evaluation of a Shortened Regimen of Treatment for Acute Osteomyelitis and Septic Arthritis in Children Journal of Pediatric Orthopaedics Volume 29(5), July/August 2009, pp 518-525

Jung ST, Rowe SM, Moon ES, et al. Significance of laboratory and radiologic findings for differentiating between septic arthritis and transient synovitis of the hip. J Pediatr Orthop. 2003;23(3):368-372.

Kirkhus E, Flatø B, Riise O, Reiseter T, Smith HJ. Differences in MRI findings between subgroups of recent-onset childhood arthritis.Pediatr Radiol. 2010 Dec 7. [Epub ahead of print]

Kocher MS, Mandiga R, Murphy JM, et al. A clinical practice guideline for treatment of septic arthritis in children: efficacy in improving process of care and effect on outcome of septic arthritis of the hip. J Bone Joint Surg Am. 2003;85A(6):994-999.

Kocher MS, Mandiga R, Murphy JM, et al. A clinical practice guideline for treatment of septic arthritis in children: efficacy in improving process of care and effect on outcomes of septic arthritis of the hip. J Bone Joint Surg Am. 2003;85:994–999

Kocher MS, Mandiga R, Zurakowski D, et al. Validation of a clinical prediction rule for the differentiation between septic arthritis and transient synovitis of the hip in children. J Bone Joint Surg Am. 2004;86A(8):1629-1635.

Luhmann SJ, Jones A, Shootman M, et al. Differentiation between septic arthritis and transient synovitis of the hip in children with clinical prediction algorithms. J Bone Joint Surg. 2004;86A:956-962.

Lyon RM, Evanich JD. Culture-negative septic arthritis in children. J Pediatr Orthop. 1999;19:655–659

Moumile K, Merckx J, Glorian C, et al. Bacterial aetiology of acute osteoarticular infections in children. Acta Paediatr Int J Paediatr. 2005;94:419–422.

Vinod MB, Matussek NC, Graham HK, et al. Duration of antibiotics in children with osteomyelitis and septic arthritis. J Paediatr Child Health. 2002;38:363–367