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8. septic arthritis 30th dec 14
- 1. Septic Arthritis By: Pawan KBAgrawal, Resident MDGP, Year II, IOM, 30th December 2014, Tuesday.
- 2. OUTLINE • Introduction • Pathophysiology •Clinical features • Diagnosis • Differentials • Treatment • Complications • Prognosis • References 30-Dec-14 2Pawan KB Agrawal
- 3. INTRODUCTION • Infection ofjoint space. • often bacterial but could be fungal or viral. • rheumatologic emergency as joint destruction occurs rapidly and can lead to significant morbidity and mortality. 30-Dec-14 3Pawan KB Agrawal
- 4. INTRODUCTION • Prevalence:range from8 to 27 % • a 2007 systematic review that included a total of 6242 patients with acutely painful joints showed 653 (10 percent) had septic arthritis1. 30-Dec-14 4Pawan KB Agrawal
- 5. INTRODUCTION Predisposing factors: Elderly >60years Diabetes mellitus Rheumatoid arthritis Prosthetic joint Recent joint surgery Skin infection, cutaneous ulcers IV drug abuse, alcoholism Previous intra-articular injection 30-Dec-14 5Pawan KB Agrawal
- 6. PATHOPHYSIOLOGY • S aureusis 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. 30-Dec-14 6Pawan KB Agrawal
- 7. PATHOPHYSIOLOGY • In theelderly, 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. 30-Dec-14 7Pawan KB Agrawal
- 8.
- 9.
- 10. CLINICAL FEATURES Usually presentwith 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. 30-Dec-14 10Pawan KB Agrawal
- 11. CLINICAL FEATURES 20 %of septic joint infections are polyarticular3. 30-Dec-14 11Pawan KB Agrawal
- 12. CLINICAL FEATURES Joint affectedAttitude 1.Knee Flexion 2. Hip Flexion, abduction & internal rotation. 3. Shoulder Adduction & internal rotation. 4. Elbow Flexion & mid pronation 5. Wrist Flexion 6. Ankle Planter flexion30-Dec-14 12Pawan KB Agrawal
- 13. DIAGNOSIS Arthrocentesis usually purulent with increasedcount (50,000 to 150,000 cells/mm3) The synovial fluid glucose is often depressed and lactic acid concentration is elevated. 30-Dec-14 13Pawan KB Agrawal
- 14. DIAGNOSIS Arthrocentesis usually purulent with increasedcount (50,000 to 150,000 cells/mm3) The synovial fluid glucose is often depressed and lactic acid concentration is elevated. Synovial fluid culture 30-Dec-14 14Pawan KB Agrawal
- 15.
- 16. DIAGNOSIS X-ray: The earliest findingsare 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. 30-Dec-14 16Pawan KB Agrawal
- 17.
- 18. DIAGNOSIS Later, joint-space narrowing couldbe 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. 30-Dec-14 18Pawan KB Agrawal
- 19. DIAGNOSIS Blood cultures arepositive 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. 30-Dec-14 19Pawan KB Agrawal
- 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. 30-Dec-14 20Pawan KB Agrawal
- 21. DIAGNOSIS Radionuclide bone scans: technetium-99m methyldiphosphonate increasein isotope accumulation in areas of osteoblasts and increased vascularity 30-Dec-14 21Pawan KB Agrawal
- 22. DIFFERENTIALS Gout Pseudogout Transient synovitis Rheumatoid arthritis Viralarthritis Lyme disease 30-Dec-14 22Pawan KB Agrawal
- 23. TREATMENT Principle: Antibiotics Joint drainage & Jointrest. 30-Dec-14 23Pawan KB Agrawal
- 24. TREATMENT General support: analgesics, antipyreticsand joint splintage for first few days. Definitive care: IV antibiotics for initial 1-2 wks followed by oral antibiotics for 3-4 wks. 30-Dec-14 24Pawan KB Agrawal
- 25.
- 26. TREATMENT Concurrent systemic corticosteroids arealso supposed to shorten duration of illness with less residual joint damage and dysfunction7. 30-Dec-14 26Pawan KB Agrawal
- 27. TREATMENT Joint drainage: needle aspirationor 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. 30-Dec-14 27Pawan KB Agrawal
- 28. TREATMENT 30-Dec-14 Pawan KBAgrawal 28
- 29. TREATMENT 30-Dec-14 Pawan KBAgrawal 29
- 30. TREATMENT 30-Dec-14 Pawan KBAgrawal 30
- 31. TREATMENT 30-Dec-14 Pawan KBAgrawal 31
- 32. TREATMENT 30-Dec-14 Pawan KBAgrawal 32
- 33. FOLLOW UP • Oncegeneral 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. 30-Dec-14 Pawan KB Agrawal 33
- 34. FOLLOW UP • Ifdeformity is present, subsequent osteotomy should be planned to correct it. 30-Dec-14 Pawan KB Agrawal 34
- 35. COMPLICATIONS Partial or completedestruction of epiphysis. Retarded growth Ankylosis Osteomyelitis Sepsis 30-Dec-14 35Pawan KB Agrawal
- 36. PROGNOSIS Poor outcome predictors: Ageolder than 60 years Infection of hip or shoulder Underlying RA Persistent positive findings. Delay in therapy. 30-Dec-14 36Pawan KB Agrawal
- 37. PROGNOSIS Irreversible loss ofjoint function in 25-50% Mortality ranges from 5-15%6. 30-Dec-14 37Pawan KB Agrawal
- 38. TOM SMITH ARTHRITIS Septicarthritis 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. 30-Dec-14 38Pawan KB Agrawal
- 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. 30-Dec-14 39Pawan KB Agrawal
- 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 . 30-Dec-14 40Pawan KB Agrawal
- 41. • THANK YOU… 30-Dec-14 41Pawan KB Agrawal
Editor's Notes
- #7 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
- #8 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
- #9 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
- #10 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.
- #11 Positive findings on synovial fluid cultures after 7 days of appropriate therapy Delay of 7 days or longer in instituting therapy
- #12 Positive findings on synovial fluid cultures after 7 days of appropriate therapy Delay of 7 days or longer in instituting therapy
- #13 Positive findings on synovial fluid cultures after 7 days of appropriate therapy Delay of 7 days or longer in instituting therapy
- #14 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).
- #15 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).
- #16 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).
- #17 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.
- #18 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.
- #19 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.
- #20 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.
- #21 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.
- #22 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.
- #33 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.
- #37 Positive findings on synovial fluid cultures after 7 days of appropriate therapy Delay of 7 days or longer in instituting therapy
- #38 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.
- #39 Positive findings on synovial fluid cultures after 7 days of appropriate therapy Delay of 7 days or longer in instituting therapy