Good notes for septic arthritis

1. Septic arthritis

2. DEFINITION
 Infection of synovium and synovial fluid
 Seen in every ages affecting the Hip joint in children
and Knee in adults.
 It can also be defined as all joint infections caused by
pyogenic bacterias except mycobacterium
tuberculosis.

3. ETIOLIOGY
 S. aureus → in every ages
 H. influenzae → 6 mo-5 years
 N. gonorrhoeae → >10 years, adults (in Western
populations)
 Gram negative bacilli → Immune deficiency, urinary or
intestinal invasive procedures, elderly people, renal failure,
chronic joint disorders and diabetes
 S. epidermidis → Prosthetic joint
 S. aureus/Pseudomonas → i.v. drug use
 S. pneumoniae →Alcoholism, pneumonia, meningitis
 L. monocytogenes → Immune deficiency
 Atypical mycobacteria → Chronic infection

4. Viruses eg :
 Rubella
 Hepatitis A, B, and C
 Parvovirus B19
 Herpes viruses
 HIV (AIDS virus)
 HTLV-1
 Adenovirus
 Coxsackie viruses.

5. TYPES
 Viral arthritis
 Fungal arthritis
 Bacterial arthritis
 Mycobacterial arthritis

6. RISK FACTORS
 Existing joint problems. Chronic diseases and conditions
that affect your joints such as osteoarthritis, gout,
rheumatoid arthritis or lupus may increase your risk of
septic arthritis.
 An artificial joint, previous joint surgery and joint injury also
increase your risk.
 Taking medications for rheumatoid arthritis. People with
rheumatoid arthritis have a further increase in risk because
of the medications they take.
 Rheumatoid arthritis medications may suppress the immune
system, making infections more likely to occur.
 Also, diagnosing septic arthritis in people with rheumatoid
arthritis is difficult because many of the signs and symptoms
are similar.

7. CONT'N
 Skin fragility. If your skin breaks easily and heals poorly,
bacteria may have constant access to your body.
 Skin conditions such as psoriasis and eczema increase your
risk of septic arthritis, as do infected skin wounds. People
who regularly inject drugs also have a higher risk of infection
at the site of injection.
 Weak immune system. A weak immune system may give
you a higher risk of septic arthritis because your body can't
defend itself against infections.
 People with diabetes, kidney and liver problems, and those
taking drugs that suppress their immune system have an
increased risk of infections.

8. PATHOPHYSIOLOGY
• Organisms may invade the joint by direct inoculation,
by contiguous spread from infected periarticular
tissue, or via the bloodstream (the most common
route).
• The normal joint has several protective components.
Healthy synovial cells possess significant phagocytic
activity, and synovial fluid normally has significant
bactericidal activity.
• Rheumatoid arthritis and systemic lupus
erythematosus hamper the defensive functions of
synovial fluid and decrease chemotaxis and
phagocytic function of polymorphonuclear
leukocytes.
• Patients with deficiencies of the terminal components
of complement are susceptible to neisserial

9. Pathogenic invasion
 Previously damaged joints, especially those damaged by
rheumatoid arthritis, are the most susceptible to infection.
 The synovial membranes of these joints exhibit neovascularization
and increased adhesion factors; both conditions increase the chance
of bacteremia, resulting in a joint infection.
 Some microorganisms have properties that promote their tropism to
the synovium. S aureus readily binds to articular sialoprotein,
fibronectin collage, elastin, hyaluronic acid, and prosthetic material
via specific tissue adhesion factors (microbial surface components
recognizing adhesive matrix molecules [MSCRAMMs]).
 In adults, the arteriolar anastomosis between the epiphysis and the
synovium permits the spread of osteomyelitis into the joint space.

10. Cont'n
 The major consequence of bacterial invasion is damage to
articular cartilage.
 This may be due to the particular organism's pathologic
properties, such as the chondrocyte proteases of S aureus,
as well as to the host's polymorphonuclear leukocytes
response.
 The cells stimulate synthesis of cytokines and other
inflammatory products, resulting in the hydrolysis of
essential collagen and proteoglycans.
 Infection with N gonorrhoeae induces a relatively mild
influx of white blood cells (WBCs) into the joint,
explaining, in part, the minimal joint destruction observed
with infection with this organism relative to destruction

11. Cont'n
 As the destructive process continues, pannus formation
begins, and cartilage erosion occurs at the lateral margins of
the joint.
 Large effusions, which can occur in infections of the hip
joint, impair the blood supply and result in aseptic necrosis
of bone.
 These destructive processes are well advanced as early as
3 days into the course of untreated infection.
 Viral infections may cause direct invasion (rubella) or
production of antigen/antibody complexes.
 Such immunologic mechanisms occur in infections with
hepatitis B, parvovirus B19, and lymphocytic
choriomeningitis viruses.

12. CLINICAL PRESENTATION
 Usually, there is a history of recent
trauma/infection
 Frequently affects hip and knee joints
 Sacroiliac joint is affected in brucellosis
 Interphalangeal joints: human and animal bites
 Patients with an infected joint typically present with
the triad of fever (40-60% of cases), pain (75% of
cases), and impaired range of motion. These
symptoms may evolve over a few days to a few
weeks.
 fatigue, anorexia, nausea
 Local findings of inflammation

15. INVESTIGATION
 Synovial fluid sampling: >50.000 leukocytes/ml
• (crystal arthropathies and RA)
• Leukocytes <50.000/ml (Malignancy, steroid use)
• Gram staining and culture i.e. Gram-positive
bacteria 60%, Gram-negative bacteria 40%

16. LAB
 Blood culture / urethral discharge culture
 Yield rate of microorganism 70%
 Antigen detection (S. pyogenes, S.
pneumoniae, H. influenzae)
 PCR (B. burgdorferi, N. gonorrhoeae)
 Leukocytosis, ESR, and CRP increase

17. RADIOLOGY
• PLAIN X-RAY
-Expansion in joint space
-Edema around the joint
-Late structural findings
• Ultrasound
-Collection of fluid in the joint and aspiration
• CT
- Detection of associated osteomyelitis, joint fluid
• MR
- Pyogenic sacroiliitis and spread of joint infection to surrounding
structures

18. TREATMENT
 <5 year-old: 2nd and 3rd generation cephalosporins
 >5 year-old and adults: cefazolin, 2nd gen.
cephalosporins
 S. aureus →cefazolin /vancomycin
 Adults: ciprofloxacin +rifampcin
 N. gonorrhoeae → cefriaxone,
 Gram-negative bacilli→3rd gen. cephalosporin+
aminoglycoside

19. Cont’n
 Gram-positive Streptococcus, methicillin-
sensitive staphylococcus, give Cefazolin,
Sulbactam /ampicillin 4x2 gram
 Meticillin-resistant staphylococcus, give
Vancomycin
 Gram-negative, give Ceftriaxone 1-2 gram

20. Cont’n
 Parenteral tx: 5-7 days then switch to oral tx (2-4
weeks)
 Gram-negative bacilli and S. aureus→ 3 weeks
 Needle aspiration and irrigation → Septic arthritis
needs intervention (emergency) !
 Hip joint septic arthritis →surgical drainage
(Arthritis may disrupt the blood supply of the hip joint)

21. Viral Arthritis
 Usually begins suddenly
 In developed countries, Parvovirus-B19,
 In children, fever, headache, rash, fatigue
 Polyarthralgia
 Symmetrical joint pain

22. Cont'n
 In adults, rubella can cause viral arthritis
 Its rate decreases due to mass vaccination during
childhood
 Infection itself/ after immunization
 It involves small joints

23. Cont’n
 Diagnosis; clinical/serological and polymerase chain
reaction (PCR)
 It resolves spontaneously within 2 weeks,
 In some (20%) female patients, arthritis may persist
for 2 months
 No erosion was seen on joints

24. Fugal arthritis
 Those with chronic disease/ immune suppression
(Candida sp, Cryptococcus, Aspergillus)
 In otherwise healthy people; direct trauma, penetrating trauma
with foreign substance.
 In patients with immune suppression, trauma and
hematogenous spread.
 Treatment is by giving anti-fungal e.g amphotericin B
 Also surgery can be done

25. Mycobacterial arthritis
 10-11% of extrapulmonary TB is bone
/joint TB
 1-3% of all TB cases
 Incidence ↑( HIV prevalence↑)
 In endemic regions, children and young adults; in other parts
elderly and immunosuppressed ones.
Risk factors
 Low socioeconomical status, alcohol, i.v. drug use,
immunosuppressive therapy, HIV infection, joint disorders…

26. Cont'n
 M. tuberculosis → chronic granulomatous
monoarthritis
 Hematogenous spread after primary infection
 A long latent period without sign&symptom
Knee, hip, ankle
 Fever may not be seen, a draining sinus can be
observed

27. Cont'n
 Synovial fluid analysis:
 Leukocytes 10 000-20 000/ml,
 Acid-fast bacilli (AFB), culture………(80%)
 Synovial biopsy; AFB, culture, histology (90%)
PCR
 Anti-TB therapy (with 4 drugs)
 Surgery; periarthricular abscess, reconstruction
surgery

28. DIFFFERENTIAL DIAGNOSIS
 Rheumatic fever
 Acute juvenile arthritis
 RA, gout, reactive arthritis
 Viral arthritis
 Fungal arthritis
 Tuberculous arthritis
 Osteomyelitis
 Cellulitis
 Bleeding into the joint (hemarthrosis)

29. COMPLICATIONS
 Osteomyelitis
 Bone erosion
 Fibrous ankylosis
 Sepsis
 death