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 ESR
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 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 Aspiration of joint fluid
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

19. Imaging Plain x rays Ultrasound CT,MRI&Bone scans not necessary
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%

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

21. 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

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

23. 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

24. 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

25. 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

26. 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

27. 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

28. 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.

29. 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

30. Gonococcal arthritis Host factors
Women > men
Recent menstruation
Pregnancy or immediate postpartum state
Complement deficiency (C5-C9)
SLE

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

32. 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

33. 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

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

35. 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**

36. 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

37. Diagnosis and Therapy Parvovirus B19 IgM + PCR can be used
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

38. 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

39. PART 2

40. POST ARTHROPLASTY INFECTIONS

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

42. 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

43. 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

44. 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:

45. BIOFILM

46. 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.

47. 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)

48. 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.

49. 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

50. 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

51. Culprit bacteria Staph aureus,MRSA,epidermidis-65-70%
Gram –ve(biofilm forming pseudomonas)
Anaerobes
Polymicrobial-wound discharges
Others-gas gangrene

52. diagnosis A combination –clinical -radiological -pathological
n/b –biofilm shields the bacteria hence neg
bone /WBC scans
-bacteria at times in a semi dormant state – neg cultures

53. clinical Pain Loss of ROM Swelling Local warmth
Signs-sinus,effusion,wound erythema

54. investigations X rays-periosteal reaction,subchondral bone resorption
Aspiration
Bone scan-Tc-not sensitive
-indium WBC –more sensitive
-others-marrow scans
-monoclonal ab scans
Intraop frozen scans >5PMN/hpf –mirra
Synovial biopsy-last resort
pcr

55. classification GUSTILLO Early post op infection<4/52
Late chronic>4/52

56. Coventry Stage I within 3 months of surgery Stage II 3-24 months
Usually transmitted at the time of surgery
Staph and other gram positives most common
Pain, wound drainage, erythema, induration
Stage II months
Stage III >2 years post-surgery
Usually caused by hematogenous spread to abnormal joint surfaces
Joint pain predominates

57. Tsukayama and colleagues-1996
1.+ve intraop cultures-iv antibiotics 2.Early post op infection -1/12 3.Late chronic infection 4.Acute haematogenous infection

58. Periprosthetic joint infection musculoskeletal infection society score
category
staging
description
Infection type 1
Early post op infection <4/52 2
Haematogenous infection<4/52 3
Late chronic infection >4/52
Systemic host grade A
UNCOMPROMISSED B
Compromised <2 compromissing factor C
Compromissed >2 compromissing factors
Local extremity grade
uncompromissed
Compromissed <2
Compromissed>2

59. Management Debridement with prosthesis retention
Debridement with prosthesis removal
-one stage
-two stage

60. GOLD STANDARD 2 stage-removal of prosthesis -I.V antibiotics 6/52
-cement spacer or prostalac
-use of cement in re implantation
-stemmed component

61. Salvaging failed re implantation
Options
1 fusion-those who may ambulate
2resection arthroplasty-fibrosis
3.amputation

62. Prognosis Poor if Delayed diagnosis Virulent organisms
Poor debridement
ISS
Host bed scarred and poor

63. end