This document discusses septic arthritis, which is an infection of the joint space that is often bacterial but can also be fungal or viral. It is a rheumatologic emergency as it can cause rapid joint destruction and significant morbidity. The document covers the pathophysiology, clinical features, diagnosis, treatment and complications of septic arthritis. Joint drainage, antibiotics, and rest are the mainstays of treatment, while complications can include joint destruction and ankylosis if not treated promptly. Prognosis depends on factors like age, joint involved, and treatment delay.
3. INTRODUCTION
• Infection of joint space.
• often bacterial but could be
fungal or viral.
• rheumatologic emergency as
joint destruction occurs rapidly
and can lead to significant
morbidity and mortality.
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4. INTRODUCTION
• Prevalence:range from 8 to 27
%
• a 2007 systematic review that
included a total of 6242
patients with acutely painful
joints showed 653 (10 percent)
had septic arthritis1.
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6. PATHOPHYSIOLOGY
• S aureus is the most common
cause of septic arthritis in all age
groups. Among those aged 15-
50 years, N gonorrhea runs a
close second, especially among
those who are sexually active.
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7. PATHOPHYSIOLOGY
• In the elderly, the
immunocompromised and in
those patients who have had
intravascular devices or urinary
catheters inserted, infection with
a Gram-negative enteric bacillus
is more common.
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10. CLINICAL FEATURES
Usually present with a single
painful swollen joint.
Low grade fever, local rise in
temperature & impaired range of
motion.
The knee is involved in more
than 50 % of cases followed by
hip, shoulder, elbow, ankle &
wrist 2.
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11. CLINICAL FEATURES
20 % of septic joint infections
are polyarticular3.
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16. DIAGNOSIS
X-ray:
The earliest findings are soft
tissue swelling around the
joint and a widened joint
space from joint effusion.
Displacement of adjacent fat
pads may be present,
especially in infants and
children.
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18. DIAGNOSIS
Later, joint-space narrowing
could be found as articular
cartilage is destroyed. Loss
of visualization of the white
cortical line over large areas
of the joint surface soon
ensues as bone destruction
begins to develop.
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19. DIAGNOSIS
Blood cultures are positive in
about 50 percent of cases.
Elevations of CRP are usually
present, though the sensitivity
of the ESR test in patients with
septic arthritis is inconsistent 4,5.
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20. DIAGNOSIS
Computed tomography (CT), or
magnetic resonance imaging
(MRI) are far more sensitive
than plain films in early septic
arthritis.
MRI:
Synovial enhancement and
the presence of a joint effusion
& perisynovial soft tissue
edema.
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24. TREATMENT
General support: analgesics,
antipyretics and joint splintage
for first few days.
Definitive care:
IV antibiotics for initial 1-2
wks followed by oral
antibiotics for 3-4 wks.
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27. TREATMENT
Joint drainage: needle
aspiration or open.
Older children with early
septic arthritis can often be
treated by repeated closed
aspiration ; however, if there
is no improvement within 48
hours, open drainage is
necessary.
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33. FOLLOW UP
• Once general condition is satisfactory
and the joint is no longer painful or
warm, further damage is unlikely.
• If articular cartilage has been
preserved, gentle and gradually
increase active movements.
• If articular cartilage has been
destroyed the aim is splinting to keep
the joint immobile while ankylosis is
awaited.
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34. FOLLOW UP
• If deformity is present,
subsequent osteotomy should
be planned to correct it.
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35. COMPLICATIONS
Partial or complete destruction
of epiphysis.
Retarded growth
Ankylosis
Osteomyelitis
Sepsis
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36. PROGNOSIS
Poor outcome predictors:
Age older than 60 years
Infection of hip or shoulder
Underlying RA
Persistent positive findings.
Delay in therapy.
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38. TOM SMITH ARTHRITIS
Septic arthritis of hip in infancy
Results in complete destruction
of cartilaginous femoral head.
Presentation is a child in his
preschool age with painless limp
Affected limb is shorter
X-ray shows complete absence
of head and neck of femur.
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39. REFERENCES
1. Margaretten ME, Kohlwes J, Moore D,
Bent S. Does this adult patient have
septic arthritis? JAMA 2007; 297:1478.
2. Goldenberg DL. Septic arthritis and other
infections of rheumatologic significance.
Rheum Dis Clin North Am 1991; 17:149.
3. Dubost JJ, Fis I, Denis P, et al.
Polyarticular septic arthritis. Medicine
(Baltimore) 1993; 72:296.
4. Ernst AA, Weiss SJ, Tracy LA, Weiss NR.
Usefulness of CRP and ESR in predicting
septic joints. South Med J 2010;
103:522.
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40. REFERENCES
5. Hariharan P, Kabrhel C. Sensitivity of
erythrocyte sedimentation rate and C-
reactive protein for the exclusion of
septic arthritis in emergency department
patients. J Emerg Med 2011; 40:428.
6. Kaandorp CJ, Krijnen P, Moens HJ, et al.
The outcome of bacterial arthritis: a
prospective community-based study.
Arthritis Rheum 1997; 40:884.
7. Sharff, K. A. (2013). Clinical
Management of Septic Arthritis. Curr
Rheumatol Rep .
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A joint can become infected by: (1) direct invasion through a penetrating wound, intra-articular injection or arthroscopy; (2) direct spread from an adjacent
bone abscess; or (3) blood spread from a distant site.
Bacterial causes of septic arthritis include staphylococci (40 percent), streptococci (28 percent), gram-negative bacilli (19 percent), mycobacteria (8 per-
cent), gram-negative cocci (3 percent), gram-positive bacilli (1 percent), and anaerobes (1 percent).
30
A joint can become infected by: (1) direct invasion through a penetrating wound, intra-articular injection or arthroscopy; (2) direct spread from an adjacent
bone abscess; or (3) blood spread from a distant site.
Bacterial causes of septic arthritis include staphylococci (40 percent), streptococci (28 percent), gram-negative bacilli (19 percent), mycobacteria (8 per-
cent), gram-negative cocci (3 percent), gram-positive bacilli (1 percent), and anaerobes (1 percent).
30
A joint can become infected by: (1) direct invasion through a penetrating wound, intra-articular injection or arthroscopy; (2) direct spread from an adjacent
bone abscess; or (3) blood spread from a distant site.
Bacterial causes of septic arthritis include staphylococci (40 percent), streptococci (28 percent), gram-negative bacilli (19 percent), mycobacteria (8 per-
cent), gram-negative cocci (3 percent), gram-positive bacilli (1 percent), and anaerobes (1 percent).
30
Bacteria entering the joint initially deposit in the synovial membrane and produce an acute inflammatory cell response.
Because synovial tissue has no limiting basement plate, bacterial organisms may quickly gain access to the synovial fluid, characteristically creating acute-onset, purulent joint inflammation.
there is marked hyperplasia of the lining cells in the synovial membrane within seven days.
In addition, inflammatory cells release cytokines and proteases that cause cartilage degradation and inhibit cartilage synthesis.
Pressure necrosis from large synovial effusions may result in further cartilage and bone loss.
Positive findings on synovial fluid cultures after 7 days of appropriate therapy
Delay of 7 days or longer in instituting therapy
Positive findings on synovial fluid cultures after 7 days of appropriate therapy
Delay of 7 days or longer in instituting therapy
Positive findings on synovial fluid cultures after 7 days of appropriate therapy
Delay of 7 days or longer in instituting therapy
The synovial fluid glucose is often depressed and lactic acid concentration is elevated; however, these tests are not sufficiently sensitive to be of widespread diagnostic utility.
Ultrasonography is the most reliable method for revealing a joint effusion in early cases. Both hips should be examined for comparison. Widening of the space between capsule and bone of more than 2 mm s indicative of an effusion, which may be echo-free (perhaps a transient synovitis) or positively echogenic (more likely septic arthritis).
The synovial fluid glucose is often depressed and lactic acid concentration is elevated; however, these tests are not sufficiently sensitive to be of widespread diagnostic utility.
Ultrasonography is the most reliable method for revealing a joint effusion in early cases. Both hips should be examined for comparison. Widening of the space between capsule and bone of more than 2 mm s indicative of an effusion, which may be echo-free (perhaps a transient synovitis) or positively echogenic (more likely septic arthritis).
The synovial fluid glucose is often depressed and lactic acid concentration is elevated; however, these tests are not sufficiently sensitive to be of widespread diagnostic utility.
Ultrasonography is the most reliable method for revealing a joint effusion in early cases. Both hips should be examined for comparison. Widening of the space between capsule and bone of more than 2 mm s indicative of an effusion, which may be echo-free (perhaps a transient synovitis) or positively echogenic (more likely septic arthritis).
The synovial fluid glucose is often depressed and lactic acid concentration is elevated; however, these tests are not sufficiently sensitive to be of widespread diagnostic utility.
The synovial fluid glucose is often depressed and lactic acid concentration is elevated; however, these tests are not sufficiently sensitive to be of widespread diagnostic utility.
The synovial fluid glucose is often depressed and lactic acid concentration is elevated; however, these tests are not sufficiently sensitive to be of widespread diagnostic utility.
The synovial fluid glucose is often depressed and lactic acid concentration is elevated; however, these tests are not sufficiently sensitive to be of widespread diagnostic utility.
The synovial fluid glucose is often depressed and lactic acid concentration is elevated; however, these tests are not sufficiently sensitive to be of widespread diagnostic utility.
The synovial fluid glucose is often depressed and lactic acid concentration is elevated; however, these tests are not sufficiently sensitive to be of widespread diagnostic utility.
Make a vertical incision beginning about 1 cm below the anterior superior iliac spine inferiorly. • Expose the sartorius muscle on the medial side and the tensor fasciae latae and vastus lateralis muscles on the lateral side. Use blunt dissection to separate these muscles. • Identify the lateral border of the rectus femoris, and retract this muscle medially (Fig. 17-12); this exposes the hip joint capsule. • Incise the capsule, evacuate the pus, and irrigate the joint with saline. • Leave the capsule open, but close the skin loosely over drains. • If wider exposure is required, extend the skin incision proximally onto the iliac crest, and subperiosteally detach the origins of the tensor fasciae latae and gluteal muscles from the ilium. • Protect the lateral femoral cutaneous nerve proximally and the branches of the lateral femoral circumflex artery distally, if possible.
Positive findings on synovial fluid cultures after 7 days of appropriate therapy
Delay of 7 days or longer in instituting therapy
A joint can become infected by: (1) direct invasion through a penetrating wound, intra-articular injection or arthroscopy; (2) direct spread from an adjacent
bone abscess; or (3) blood spread from a distant site.
Positive findings on synovial fluid cultures after 7 days of appropriate therapy
Delay of 7 days or longer in instituting therapy
