"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]

The table below reproduces the lecture's descriptive ranges, not diagnostic cut-offs. The categories overlap substantially: a lower WBC count does not exclude infection, and crystal arthritis may produce a very high neutrophil count. Culture and the whole clinical picture are decisive. ^[8]

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.

Slide microscopy images demonstrate: "Perpendicular blue" — a negatively birefringent (MSU) crystal appears blue when perpendicular to the compensator axis; "Parallel blue" — a positively birefringent (CPPD) crystal appears blue when parallel to the compensator axis. ^[1]

Why does birefringence occur? A birefringent crystal has different refractive indices along different axes. It splits plane-polarised light into fast and slow components, creating a phase delay; some light therefore emerges through the crossed analyser. The first-order red compensator adds a known retardation, producing orientation-dependent blue or yellow colours. Identify the crystal from shape + sign + orientation, not colour alone: CPP crystals may be only weakly birefringent and can be missed.

Optical Pathway of Polarised Microscopy [1]

The lecture diagram (slide 14) is a simplified optical model:

1. Unpolarised light passes through the polariser, selecting one vibration plane.
2. An anisotropic crystal resolves that light into two components travelling at different velocities.
3. With the polariser and analyser crossed, the unchanged background is dark, while the phase-shifted components from the crystal can pass.
4. A first-order red compensator makes the sign of birefringence visible from the colour change relative to its marked slow axis.

This is more precise than saying a crystal simply “twists” all light into a horizontal plane. Also remember the diagnostic safety point: seeing crystals establishes crystal deposition, but it does not exclude a simultaneous infection. ^[8]

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. In a clinically stable patient, obtain joint fluid and blood cultures before antibiotics; in sepsis, shock or rapidly progressive illness, obtain cultures if immediately possible but do not delay empirical therapy for aspiration. ^[8][10]
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
• Before antibiotics when the patient is clinically stable — this improves pathogen yield; instability changes the priority to immediate sepsis treatment ^[8]
• Anticoagulation is not an automatic contraindication — assess INR/anticoagulant exposure, platelet count, site, concomitant antiplatelets and local procedural policy. The bleeding risk of aspiration on therapeutic warfarin is low, and anticoagulation should not become a reason to abandon an urgent septic-joint evaluation. ^[12]
• 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]

1. Aspirate promptly and send microbiology before antibiotics if the patient is stable.
2. Start empirical antibiotics after sampling, or immediately in sepsis/shock; cover S. aureus and tailor additional coverage to age, exposure, local resistance, Gram stain and host risks. ^[8][10]
3. Discuss urgent drainage with orthopaedics. Arthroscopic lavage is commonly preferred for accessible large native joints; open revision is considered when there are adhesions, advanced synovial disease, cartilage/bone damage, difficult anatomy or failed arthroscopy. A fixed “acute = scope, chronic = open” rule is too rigid. ^[8]
4. Reassess source control if pain, fever, drainage or CRP fail to improve; repeat aspiration/debridement is for an unfavourable course rather than an automatic sequence. Evaluate for adjacent osteomyelitis or abscess with MRI when indicated. ^[8][10]
5. Individualise antibiotic route and duration. Adult SANJO guidance suggests culture-directed treatment, often 1–2 weeks IV followed by 2–4 weeks oral when clinical signs and CRP are improving, but acknowledges the absence of adult trials; children may need shorter courses when uncomplicated and responding. Follow local microbiology/infectious-disease guidance rather than a blanket “4–6 weeks IV.” ^[8][10]

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 — a uniformly bloody aspirate supports haemarthrosis, but distinguish it from a traumatic tap (blood may diminish across sequential tubes; a traumatic sample may clot). Send cell count and culture if infection remains plausible.

• Treat the "treatable" underlying causes
  • Trauma: surgical repair if indicated
  • Haemophilia: factor replacement
  • Anticoagulant-associated bleeding: assess severity, drug level/INR, indication and thrombotic risk; hold or reverse only when clinically appropriate rather than automatically
  • 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" → Patient-specific first-line options are an NSAID, low-dose colchicine, or a glucocorticoid (oral, IM or intra-articular after excluding infection). Reserve IL-1 blockade for failure, intolerance or contraindication to conventional agents. Do not use aspirin as flare treatment, but do not stop correctly indicated low-dose antiplatelet aspirin. ^[9]

"When should you start urate-lowering therapy?" → First establish an indication (tophi, gout-related radiographic damage or frequent flares; selected higher-risk first-flare patients). If indicated, it can be started during a flare with anti-inflammatory treatment; start low, titrate to serum urate < 6 mg/dL and give 3–6 months of prophylaxis. ^[9]

"What drug interaction must you know with xanthine-oxidase inhibitors?" → Azathioprine/mercaptopurine: febuxostat is contraindicated; allopurinol requires specialist thiopurine dose reduction and close blood-count monitoring. ^[13][14]

"Who needs HLA-B*58:01 testing before allopurinol?" → Higher-risk groups (including Han Chinese, Korean, Thai and African American ancestry) and those covered by local policy; testing is not universally recommended for every ancestry. ^[9]