By

Dr. Tehreem Nasir

MBBS, RMP
Septic Arthritis/Pyogenic Arthritis
 Septic Arthritis/ Pyogenic Arthritis
● Septic arthritis is an infection of the joint due to direct inoculation,
contiguous extension, or hematogenous spread of infectious
organisms into the joint space.
● This process causes an acute, inflammatory, monoarticular arthritis.
● A variety of organisms have been implicated, most
commonly S t a p h y l o c o c c u s a u r e u s .
● Previously damaged joints (e.g., rheumatoid arthritis) are at the
highest risk of infection.
● Patients present with a swollen, warm, and tender joint, most
commonly involving the knee.
 Etiology
● Staphylococci:
○ Staphylococcus aureus
○ (most common)
○ S. epidermidis
● Streptococci:
○ Streptococcus pyogenes
○ S. pneumoniae
○ S. agalactiae
● Gram-negative bacteria
○ Pseudomonas aeruginosa
○ Escherichia coli
○ Neisseria gonorrhoeae
○ Haemophilus influenzae
Risk factors
● Infants and children:
○ Joint disease:
○ Prematurity
■ Rheumatoid arthritis
○ Hemophilia (due to hemarthroses)
■ Osteoarthritis
○ Immunosuppression: ■ Gout
■ Chemotherapy
○ Joint procedures:
■ HIV
■ Surgery
■ Sickle cell anemia
■ Intra-articular
■ Diabetes
injections
● Adults: ■ Joint prosthesis
○ Age > 80 years ○ Skin infections or ulcers
○ Chronic disease/immunosuppressin: ○ IV drug use
■ Diabetes
■ HIV
 Pathophysiology
● Invasion of the joint occurs through:
○ Hematogenous seeding (most common)
○ Direct inoculation of organisms into the
joint
○ Extension from an adjacent infection
(osteomyelitis)
● Previously damaged joints are particularly
susceptible to infection by way of:
○ Neovascularization
○ Dysfunctional cellular defenses
○ Absent basement membrane on
the synovial membrane
 ● Bacterial invasion

● Host immune response

● Joint damage
 Progression of the disease:
○ Bacterial invasion → inflammation → release of cytokines
and proteases
○ This response, plus bacterial toxins → destruction of:
● Articular cartilage
● Synovium
● Subchondral bone
○ Pannus formation occurs.
○ If a large effusion develops → impairment of the blood
supply → aseptic necrosis
 Clinical presentation
● Usually acute in onset
● Joint signs and symptoms:
○ Swelling and effusion
○ Warmth
○ Moderate-to-severe pain
○ Erythema
○ Restricted movement
○ Usually monoarticular, but 20% of cases may be polyarticular
● Constitutional symptoms:
○ Fever
○ Fatigue
○ Tachycardia
 Commonly affected joints:
○ Knee (> 50% of cases)
○ Wrist
○ Ankle
○ Hip
○ Elbow
○ Axial
○ joints (in IV drug users):
■ Sacroiliac
■ Sternoclavicular joint
 Diagnosis
O Ar throcentesis (gold standard)
O The diagnosis of septic arthritis is made with synovial fluid analysis
O A positive Gram stain and/or culture confirms the diagnosis.
O A purulent aspirate gives a presumptive diagnosis:
O WBC count > 50,000 cells/μL
O Neutrophils predominance
O Laborator y evaluation
O ↑ Erythrocyte sedimentation rate (ESR)
O ↑ CRP
O ↑ WBC count
O Blood cultures
O Cervical, urethra, rectal, or oropharyngeal swabs for nucleic acid amplification
test if N. gonorrhoeae is suspected
O X-Rays
O USG
O MRI
 Management

septic arthritis is suspected

blood and synovial fluid sample

parenteral antibiotics based on gram stain

joint drainage

adjust antibiotics based on culture and sensitivity results

 Management
● Antibiotic therapy
○ based on the initial Gram stain
○ Vancomycin
○ 3rd- or 4th-generation cephalosporin
● Surgical interventions
○ Joint drainage:
■ Generally warranted in all patients
■ Often requires repeated drainage
■ Options:
● Needle aspiration
● Arthroscopic drainage
● Arthrotomy (open surgery)
○ Surgical debridement in patients with prosthesis
Tuberculous Arthritis
 Tuberculous Arthritis
➜ Epidemiology:
- Increasing due to HIV infections and increased anti-
tuberculous drug resistance
➜ Pathogenesis:
- Secondary direct invasion from adjacent tuberculous
- Hematogenous dissemination from a primary focus in
the lungs or lymph nodes
➜ Risk Factors:
- Elderly, poor, immunocompromised, prisoners,
alcoholics, reactivation due to surgical and joint trauma
Symptoms:
• Chronic monoarthritis of the large and medium weight-bearing joints
(hip, knees) in men aged >50,

• Generating chronic progressive low grade joint pain and swelling

(without warmth or erythema)

• Progressive loss of ROM.

❑Fever, weight loss, anorexia, night sweats

 Diagnosis:
❖ X - R a y s : phemister triad of
❖ Periarticular osteoprosis (shown on
X-ray as decreased bone density)
❖ Periarticular osseous erosion
❖ Reduced joint space
❖ A c i d - f a s t s t a i n (10-20%) of M.
tuberculosis and culture (80%) of
synovial fluid
❖ Open biopsy technique positive for
typical caseous granulomas (94%)
 Treatment
➜ Tr e a t m e n t prevents complete joint obliteration
with fibrous ankylosis (fusion of bones)
➜ Anti-tuberculous drugs
- Isoniazid
- Rifampicin
- Pyrazinamide
- Ethambutol
- streptomycin
Rheumatoid Arthritis
 RHEUMATOID ARTHRITIS
• Rheumatoid arthritis (RA) is a symmetric, inflammatory
polyarthritis and chronic, progressive, autoimmune disorder.
• Risk Factors
• Genetic predisposition:
• 2–3 times more likely in those with a 1st-degree relative with RA
• Associated with:
• HLA-DR1
• HLA-DR4
• Environmental factors:
• Lifestyle:
• Cigarette smoking
• Obesity
• Hormonal
• Infectious
Pathophysiology
• An external trigger sets off the autoimmune response → creation of antigens
• B cells produce antibodies → bind to fibrinogen and collagen
→ complement activation
• Synovium is infiltrated by immune cells → cytokine and chemokine
production → synovial membrane thickening and villus formation
• Hyperplastic synovial tissue (pannus) releases:
• Collagenase
• Interleukins (IL)
• Tumor necrosis factor (TNF)-alpha
• Leads to:
• Continued synovial inflammation
• Cartilage destruction
• Osteoclasts-mediated bone destruction
Clinical Features
• Joint swelling, pain, and morning stiffness (often in the hands).
• Systemic inflammation can lead to extra-articular manifestations such as rheumatoid
nodules, interstitial lung disease, and pericarditis.
• Prolonged and severe disease can lead to irreversible joint deformities.
• Common Hand Findings:
• Boutonniere deformity
• Swan neck deformity
• Symptoms:
• Joint pain
• Joint swelling
• Early morning stiffness ( > 1 hour)
• Characteristics:
• Gradual onset
• Polyarticular
• Symmetric
• Commonly affected joints:
• Wrists
• 2nd and 3rd metacarpophalangeal (MCP) joints
• Proximal interphalangeal (PIP) joints
• Metatarsophalangeal (MTP) joints
• Shoulders
• Elbows
• Hips
• Knees
• Ankles
Diagnosis
• Laboratory testing
• Complete blood count (CBC)
• ↑ Erythrocyte sedimentation rate (ESR)
• ↑ C-reactive protein (CRP)
• ↑ Ferritin
• Rheumatoid factor (RF)

• Synovial fluid analysis:

• Leukocytosis (5,000–50,000 cells/microliter) with
neutrophil predominance
• ↓ Glucose

• X-ray
• Bony Erosion
• Narrow joint space

• MRI
Management
• Nonpharmacological therapies:
• Physical and occupational therapy
• Smoking cessation
• Acute exacerbation management:
• Nonsteroidal anti-inflammatory drugs (NSAIDs)
• Glucocorticoids
• Long-term pharmacological therapy:
• DMARDs
• TNF-alpha inhibitors
• Surgery:
• Indicated for severe damage and limited function
• Can be considered if pharmacologic therapy is
unsuccessful
• Options:
• Joint replacement
• Joint fusion
• Synovectomy
THANK YOU
