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Septic arthritis &post arthroplasty infections

Septic arthritis &post arthroplasty infections. Presenter R N MBUVA Moderator Mr MWANGI. scope. Septic arthritis Prosthetic infections. Part 1. Septic arthritis. Definition. Inflammation of a synovial membrane with purulent effusion into the joint capsule, often due to bacterial infection.

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Septic arthritis &post arthroplasty infections

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  1. Septic arthritis &post arthroplasty infections Presenter R N MBUVA Moderator Mr MWANGI

  2. scope • Septic arthritis • Prosthetic infections

  3. Part 1

  4. Septic arthritis

  5. Definition • Inflammation of a synovial membrane with purulent effusion into the joint capsule, often due to bacterial infection

  6. Synonyms • Bacterial, suppurative, purulent or infectious arthritis, gonococcal or nongonococcal

  7. septic arthritis • 0.2%-0.7% of hospital admissions • Peak incidence in the first years of 1st decade and >50 years • Males>Females

  8. Risk Factors for Septic Arthritis • Previous arthritis • Trauma • Diabetes Mellitus • Immunosupression • Bacteremia • Sickle cell anemia • Prosthetic joint

  9. Infection Sources • Trauma: direct • Hematogenous: IV drug injection • Osteomyelitis adjacent to joint capsule • Soft tissue infections: cellulitis, abscess, bursitis, tenosynovitis

  10. Pathogenesis • Systemic bacteremia-invades synovial cartilage • Postulation-collagen receptors in staph aureus -lack of basement membrane in capillaries of synovium -synovial fibroblasts inhibit phagocytosis

  11. pathogenesis • Features of acute Infiltration • Lymphocytes 3/52 • Destruction of cartilage after ground substance degradation4-6/7 • Depletion of ground substance-activation of bacteria enzymes and T lymphocytes • Ground substance degradation-collagen exposed

  12. Up-to-Date 2004

  13. clinical presentation • Painful ROM, swelling, erythema, not bearing weight, recent illnesses • Children: • pseudoparalysis or disuse of limb, not septic • antalgic limp • Fevers not consistent • Have parent examine the child

  14. Labs • Leukocyte count not reliable early stages • 25% of children had elevated counts and 65% the diff was abnormal • ESR • Nonspecific test of inflammation • Affected by cell size, shape and protein content • i.e. sickle cell, anemia, steroids • Not reliable in neonates • Elevated in 48-72 hrs returns to baseline 2-4 weeks Mayo series, Morey et al: only 5 of 76 had ESR below 20mm/hr, elevated in 90% of patients w/ septic arthritis

  15. ESR • No change w/ antibiotic therapy • Continues to rise 3-5 days – after this may consider change in tx • Not good for early evaluation of tx

  16. CRP • Rises within 6 hrs and peaks 30-50hrs • Half life 47hrs • Makes this marker of greater value for early diagnosis and resolution of inflammation • CRP is elevated in trauma, in otitis media(22%bacterial 65% viral)

  17. Cultures • Blood cultures • yield organisms 30-50% of cases • Decreases w/ previous antibiotic therapy • Aspiration of joint fluid • Gram stain, leukocyte cell count, PMNs • Cell counts 80,000 – 100,000/ml likely septic arthritis • Frank and Nelson: 126 positive culture • Counts of 50,000/ml or less in 55%, 34% had <25,000/ml, only 44% had >=100,000/ml • Other inflammatory processes can give you >80,000/ml • Gram stain can give you a presumptive early diagnosis • 1/3 are positive

  18. Imaging • Plain x rays • Ultrasound • Used frequently in pediatrics assessing the hip for effusion/dislocations • Cannot differentiate between TSH and septic arthritis by positive effusion alone • If extracapsular effusion may distinguish between osteomyelitis around hip/pelvis • CT,MRI&Bone scans not necessary • Bone scan – Tc99-good osteoblastic activity indium111 and gallium citrate more sensitive and specific for infection i • CT scans-good anat,distinguishes soft tissue and bone infection • MRI sensitivity 97% and specificity 92%

  19. Kocher et al. 1999 • Hx of fever • Nonweightbearing • ESR >40mm/hr • WBC >12,000/mm3

  20. Kochers criteria • The likelihood of septic arthritis was • 0.2% if no criteria were present, • 3% if one • 40% if two • 93% if three • 99% if four • Unfortunately not reproducible • Caird et al-crp&esr –more likely • Luhmann-visit another facility more likely

  21. Management • Nade • Principles-1joint adequately drained 2ABX given to diminish effects of sepsis 3joint rested in a stable position

  22. Indications for Surgery • Aspiration vs. debridement • Joint does not respond to serial aspirations • No improvement in 48hrs of tx • Frank pus is aspirated • Loculations noted on MRI or U/S • Documented Hip and SI septic arthritis should be debrided surgically • No change in morbidity between arthroscopic vs. arthrotomy of knee

  23. Abx Treatment • IV abx 4-7 days • Check CRP,WBC every 2 days • Once labs normalize and clinically improving consider discharge • Continue tx 2-3 weeks with oral or IV abx (PICC line) • No true standardization of tx • Get ID involved

  24. Rehabilitation • Splinting for 48 hrs • Salter 1981 • Rabbit knees septic S. aureus • Had arthrotomy and abx tx • Casting vs. ROM w/ CPM vs. cage activity • CPM fared sig. better on pathology of cartilage w/ decreased ground substance • WBAT once rom and pain subsided

  25. Prognosis and complications • Poor prognosis factors • Immunodeficiency, RA, prematurity, osteomyelitis, hip, prosthetic infections, + blood cultures, symptoms >1 week, >4 joints, + cultures after aspiration after 7 days of abx tx • Complications: • Mortality 8%-15% in three series • arthritis stiffness, dislocation, subluxation, AVN, local growth distrubance, osteomyelitis, postinfection synovitis • Favorable outcome in 50%-80% of cases

  26. Lyme Arthritis • Caused by infection with the spirochete Borrelia Burgdorferi • Early stage disease • Localized - Erythema chronicum migrans, fever, arthralgia and myalgia, sore throat, • Disseminated- disseminated skin lesions, facial palsy, meningitis, radiculoneuropathy, and rarely heart block • Early disease may remit spontaneously • 50% of untreated cases develop late features • Late • Arthritis is a manifestation of late disease-months or years after exposure • Intermittent migratory asymmetric mono- or oligo-arthritis • 10% develop chronic large joint inflammatory arthritis

  27. Lyme Arthritis • Treatment • Early localized • Doxy 100 mg po BID or Amox 500 TID (kids) for 2-4 weeks • Early disseminated or late disease • Oral or parenteral abx depending on the severity of the disease • Neuro or cardiac disease usually treated with IV ceftriaxone 2 g daily for 3-4 weeks. • Lyme arthritis may be treated with oral abx for 4 weeks.

  28. Disseminated gonococcal infection • Occurs in 1-3% on patients infected with GC • Most patients have arthritis or arthralgia as a principal manifestation • Common cause of acute non-traumatic mono- or oligo-arthritis in the healthy host

  29. Gonococcal arthritisHost factors • Women > men • Recent menstruation • Pregnancy or immediate postpartum state • Complement deficiency (C5-C9) • SLE

  30. Gonococcal arthritis • Consider screening/treating for chlamydia • HIV testing • Syphillis testing • Screen sexual partners

  31. Gonococcal arthritis • Ceftriaxone 1gm IV or IM q24 hours • Spectinomycin 2 gm IV or IM q12 hours for ceph allergic patients • May use fluoroquinolones if susceptible

  32. Parvovirus B19 Arthritis • Small non-enveloped DNA virus • Erythrovirus genus • Replicates only in erythrocyte precursors • Transmission • Respiratory, parenteral, vertical • 25-68% of infections are asymptomatic

  33. Erythema Infectiosum • “5th disease” • 10% of children and 50% of adults have joint symptoms

  34. Parvovirus B19 Arthritis • Begins about 2 weeks after infection • Symmetrical involvement of the small joints of the hands and wrists and the knees • Usually resolves in about a month without joint damage • 20% may have persistent disease**

  35. Parvovirus B19 • Clinical features may mimic an early autoimmune disease • High prevalence of autoantibodies • RF, ANA, ACA, ANCA, anti-ds DNA • May persist for some time after infection is cleared • Has been implicated in the pathogenesis in both RA and SLE

  36. Diagnosis and Therapy • Parvovirus B19 IgM + • Parvovirus B19 IgG indicates past infection. • highly prevalent in the general population since asymptomatic infxn is very common. • PCR can be used • Immuncompromised people may not mount an antibody response • Therapy is supportive • NSAIDs • Steroids are rarely necessary

  37. Tuberculous arthritis • History of exposure is helpful • PPD may be negative • Synovial fluid stain usually negative • Culture may take 6-8 weeks to grow • Best yield is probably synovial biopsy

  38. PART 2

  39. POST ARTHROPLASTY INFECTIONS

  40. INCIDENCE • For knee generally low 0.1-2% • For hip 1-2%

  41. MECHANISM • Intraoperative seeding-low virulent • Blood spread • Fretting-micromotion between implants -DM -sepsis -steroid use -Long hospital stay -long theatre time>3hrs -blood loss > 1500cc -smoking

  42. Methods of prevention • Treatment of superficial and deep infection • I.V prophylactic antibiotics • Others-laminar flow -closed body exhaust suits -careful tissue handling -antibiotic cement -minimize theatre traffic

  43. BIOFILM • There are five stages of biofilm development 1Initial attachment-van der waals forces 2Irreversible attachment-cell adhesion structures, hydrophobicity,quorum sensing 3Maturation I: 4Maturation II: 5Dispersion:

  44. BIOFILM

  45. Biofilm • Pathophysiology has been greatly improved by the biofilm model • Conditions for biofilm formation: necrotic tissue and bone, which have a foreign-body effect and are colonized by bacteria. • Pathogens 1st form surface colonies, multiply.

  46. Biofilm • Matrix offers protection from mechanical influences and makes it harder for AB, body’s own defense cells, and Ig to penetrate, functioning as a diffusion barrier. • Pathogens pass from a high metabolic rate and rapid multiplication into greatly reduced metabolism and slowed biological Rx. • This can reduce their sensitivity to antibiotics by a factor of 10(3)

  47. Biofilm • Neutrophilic granulocytes penetrate the biofilm poorly and in the process lose their ability to phagocytose. • Apoptosis occurs with excessive complement activation and release of radicals and proteases, resulting in a local immune deficiency.

  48. Biofilm • In lower layers of the biofilm, conditions are anaerobic, reducing growth rate and metabolic activity of pathogens. • Insensitive to antibiotics. • After Tx has ended, return --->active mode, show resistance to the originally administered AB

  49. Biofilm • return from sessile to planktonic phase is possible, and clinically triggers local or systemic recurrence of Ix. • Biofilm population = permanent source of virulent pathogens • Safest Tx= surgical removal of sequestrum bearing biofilm

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