"Joint aspiration with synovial fluid analysis for leucocyte count, Gram's stain, culture, and crystal, is the most important test." ^[2]

Indications for joint aspiration: ^[1]

1. Suspicion of infection
2. Suspicion of crystal-induced arthritis
3. Suspicion of haemarthrosis
4. Differentiating inflammatory from non-inflammatory arthritis

What to examine: ^[1]

This table is one of the highest-yield exam tables in the entire lecture. Commit the WBC thresholds and PMN percentages to memory.

Why viscosity matters: Hyaluronic acid is the main contributor to synovial fluid viscosity. In inflammation, hyaluronic acid is degraded by enzymes from inflammatory cells, so viscosity drops. That is why non-inflammatory fluid has high viscosity (intact hyaluronic acid) while inflammatory fluid has low viscosity.

Haemarthrosis synovial fluid: ^[1]

This is a classic exam question. The principle: when you look at synovial fluid under compensated polarised light using a first-order red compensator, birefringent crystals change colour depending on their orientation relative to the compensator's optical axis.

Birefringence can be detected by a colour shift to blue (positive) or yellow (negative) when the long axis of the crystal is aligned with the optical axis of a first order red compensator. ^[1]

How to remember the colour convention:

• Think of the mnemonic: "Parallel blue = positive birefringence" → This means when the crystal's long axis is parallel to the compensator axis, a positively birefringent crystal (CPPD) appears blue. ^[1]
• Conversely, a negatively birefringent crystal (MSU/gout) appears yellow when parallel to the axis.

Why does birefringence occur? A birefringent material has different refractive indices along different axes. When plane-polarised light passes through, the crystal splits the light into two rays that travel at different speeds. The compensator plate converts these differences into visible colour changes. This is a purely physical property of the crystal structure — MSU crystals have a different molecular lattice than CPPD crystals, hence the opposite birefringence.

Complete list from the lecture — any of these can appear as "name 3 investigations" in an SAQ:

• CBC — leukocytosis in sepsis
• ESR — non-specific inflammatory marker
• Biochemistry including serum uric acid level — elevated in gout but NOT diagnostic alone
• PT and aPTT — coagulopathy screen for haemarthrosis
• Cultures of blood, urine, or other possible primary infection sites
• Serological tests: ANA & RF/ACPA — if suspecting RA or SLE
• Radiograph of the joint AND contralateral joint — baseline comparison
• Synovial fluid analysis or synovial biopsy
• Other imaging: Ultrasound, CT, or MRI

Bacterial infections, especially those due to Gram-positive organisms, can destroy the joint cartilage within a few days. ^[1] Proteolytic enzymes released by bacteria and inflammatory cells (PMNs) break down collagen and proteoglycans in cartilage. The avascular nature of cartilage means once destroyed, it cannot regenerate. Prompt and proper treatment will usually leave the joint without permanent structural damage. ^[1]

1. Haematogenous — most common; bacteria seed the joint via bloodstream
2. From osteomyelitis — contiguous spread, especially in infants (epiphyseal vessels cross growth plate)
3. Adjacent soft tissue infection
4. Diagnostic/therapeutic procedures — iatrogenic (arthrocentesis, intra-articular injection)
5. Penetrating damage — puncture or cutting

Risk factors:

This table is extremely high-yield for EMQs and SAQs.

Classically abrupt onset, usually monoarticular involving large weight-bearing joints. The classic presentation:

• Hot, swollen, tender joint
• Restriction of movement (any movement is excruciating)
• Systemic upset: fever, malaise

1. High level of suspicion — this is the most important point
2. Look for: Acute history of a hot, swollen, and tender joint with restriction of movement
3. If suspicion is high, treat even in the absence of fever — but only after joint aspiration
4. Negative Gram smear or culture does NOT exclude sepsis — sensitivity of Gram stain is ~50–75%; always correlate clinically
5. Involve orthopaedic surgeons — surgical drainage is often needed

Synovial fluid aspiration is key:

• Fluid to be sent fresh for relevant stains and culture
• Prior to commencement of antibiotic therapy — you need the organism!
• Warfarin does NOT contraindicate needle aspiration — the risk of missing septic arthritis far outweighs bleeding risk
• Suspected hip sepsis requires ultrasound guidance — hip joint is deep; blind aspiration is unreliable

Additional investigations:

• Blood cultures should ALWAYS be taken — bacteraemia is the usual route
• CBC, ESR, CRP — inflammatory markers
• Electrolytes, renal and liver function — detect end-organ damage and guide antibiotic choice (dose adjustment in renal impairment)
• Plain X-ray — may show soft tissue swelling, joint effusion, periarticular osteopenia; normal early on
• MRI is the most appropriate imaging where required — also sensitive in detecting osteomyelitis ^[1]

These are the steps examiners expect you to know:

1. Confirm diagnosis by examination of joint aspirate
2. Urgent joint irrigation and debridement
3. Acute phase → arthroscopy
4. Delayed or chronic cases → open arthrotomy
5. Repeated surgical debridement until infection under control
6. Be prepared for co-existing osteomyelitis

Why arthroscopy for acute and arthrotomy for chronic? In the acute phase, arthroscopy allows joint washout with minimal tissue damage and quicker recovery. In chronic or delayed cases, there may be organised pus, fibrous adhesions, or necrotic tissue that require direct visualization and more aggressive debridement — hence open arthrotomy.

Medical management (from supporting material): IV antibiotics for 4–6 weeks. Empirical: IV flucloxacillin/cloxacillin (covers S. aureus). If Gram-negative suspected: add a third-generation cephalosporin. If gonococcal: IV ceftriaxone. Adjust based on culture and sensitivity. ^[5]

The lecture provides a comprehensive categorisation:

• Trauma — most common overall
• Haemophilia (congenital Factor VIII and IX deficiency)
• Acquired haemophilia (autoantibodies against clotting factors)
• Drugs (warfarin or heparin)

• Pain, swelling, stiffness

• Arthrocentesis — bloody synovial fluid confirms diagnosis

• Treat the "treatable" underlying causes
  • Trauma: surgical repair if indicated
  • Haemophilia: factor replacement
  • Warfarin: reverse anticoagulation if appropriate, adjust INR
  • Acquired haemophilia: immunosuppression

Recurrent haemarthrosis (especially in haemophilia) leads to haemophilic arthropathy: iron from blood degradation deposits in the synovium → chronic synovitis → cartilage destruction → secondary OA. Prophylactic factor replacement in haemophilia patients aims to prevent this.

"Name the indications for joint aspiration" → State all four from the lecture: suspicion of infection, crystal arthritis, haemarthrosis, differentiating inflammatory vs non-inflammatory.

"What is the most important investigation for acute monoarthritis?" → Joint aspiration with synovial fluid analysis (cell count, Gram stain, culture, crystal under polarised microscopy).

"A 35-year-old man with acute painful swollen 1st MTP joint. Name the most likely diagnosis and gold standard investigation." → Gout; demonstration of negatively birefringent needle-shaped MSU crystals under compensated polarised light microscopy of joint aspirate.

"List drugs used in acute gout" → First line: NSAIDs (indomethacin), COX-2 inhibitors (etoricoxib), colchicine. Second line: steroids, anti-IL-1 (anakinra, canakinumab). Avoid aspirin.

"When should you start urate-lowering therapy?" → ASAP. No need to wait until the acute attack has completely subsided.

"What drug interaction must you know with allopurinol?" → Avoid with azathioprine (risk of severe myelosuppression).

"What screening test before starting allopurinol?" → HLA-B5801* (risk of SCAR/TEN).