High Yield Overview

GOUT AND CRYSTAL ARTHROPATHY

Monosodium Urate | Negatively Birefringent | Needle-Shaped Crystals

MSUMonosodium urate crystals

NegativeBirefringence under polarized light

1st MTPPodagra - classic location

6.8Serum urate saturation (mg/dL)

STAGES OF GOUT

Asymptomatic Hyperuricemia

PatternElevated urate, no symptoms

TreatmentLifestyle modification

Acute Gouty Arthritis

PatternSudden monoarticular attack

TreatmentNSAIDs, colchicine, steroids

Intercritical Period

PatternAsymptomatic between attacks

TreatmentUrate-lowering therapy

Chronic Tophaceous Gout

PatternTophi, chronic arthropathy

TreatmentULT, consider surgery

Critical Must-Knows

MSU crystals are needle-shaped and negatively birefringent (yellow parallel to polarizer)
Podagra (1st MTP involvement) is the classic presentation
Joint aspiration is gold standard for diagnosis - even during acute attack
Urate-lowering therapy target is serum urate less than 6 mg/dL (360 micromol/L)
Surgical indications: mechanical symptoms, ulceration, infection, nerve compression

Examiner's Pearls

"
Negatively birefringent = yellow when parallel to polarizer axis
"
Acute attack: do NOT start allopurinol - may prolong attack
"
Dual-energy CT can identify urate deposits non-invasively
"
Tophi surgery: avoid primary closure over large defects

Critical Gout Exam Points

Crystal Identification

MSU crystals: Needle-shaped, negatively birefringent (yellow parallel, blue perpendicular). CPPD crystals: Rhomboid, positively birefringent (blue parallel, yellow perpendicular). This distinction is fundamental to diagnosis.

Acute Attack Management

Do NOT start urate-lowering therapy during acute attack - may prolong symptoms. Treat with NSAIDs, colchicine (within 12 hours), or corticosteroids. Continue existing ULT if already established.

Surgical Indications

Orthopaedic involvement for: mechanical symptoms from tophi, skin ulceration over tophi, secondary infection, nerve compression (carpal tunnel), joint destruction requiring arthroplasty.

Imaging Features

Radiographic signs: Punched-out erosions with overhanging edges ("rat bite"), preserved joint space until late, soft tissue tophi with calcification. Dual-energy CT shows urate deposits as green.

Crystal Arthropathy Comparison

Feature	Gout (MSU)	Pseudogout (CPPD)
Crystal shape	Needle-shaped	Rhomboid/rod-shaped
Birefringence	Negative (yellow parallel)	Positive (blue parallel)
Classic joint	1st MTP (podagra)	Knee, wrist
Radiographic sign	Punched-out erosions	Chondrocalcinosis
Risk factors	Purine-rich diet, alcohol, obesity	Age, OA, metabolic disease
Urate-lowering therapy	Yes - allopurinol, febuxostat	No specific therapy

Mnemonic

NEEDLEGout Crystal Features

Needle-shaped crystals

Long, thin morphology

Erosions with overhanging edges

Rat bite appearance on X-ray

Elevated uric acid

Serum urate greater than 6.8 mg/dL

Definitely negatively birefringent

Yellow when parallel to polarizer

Locations: 1st MTP classic

Podagra is pathognomonic

Early morning attacks common

Nocturnal crystal precipitation

Memory Hook:NEEDLE crystals cause NEEDLE-sharp pain in gout!

Mnemonic

COINSAcute Gout Treatment

Colchicine

Within 12 hours of onset most effective

Oral NSAIDs

Indomethacin, naproxen - first line

Intra-articular steroids

If monoarticular and NSAIDs contraindicated

No allopurinol initiation

Do not start ULT during acute attack

Systemic steroids

If polyarticular or contraindications

Memory Hook:Spend your COINS wisely on acute gout treatment!

Mnemonic

MUSICSurgical Indications for Tophi

Mechanical symptoms

Limited ROM, tendon dysfunction

Ulceration of overlying skin

Risk of secondary infection

Secondary infection

Requires debridement

Impingement on nerves

Carpal tunnel, ulnar neuropathy

Cosmetic concerns

Large visible tophi

Memory Hook:When tophi cause problems, it's time to make MUSIC with surgery!

Overview and Epidemiology

Gout is the most common inflammatory arthritis in adults, caused by deposition of monosodium urate (MSU) crystals in joints and soft tissues. It results from prolonged hyperuricemia leading to crystal formation when serum urate exceeds its saturation point of 6.8 mg/dL (404 micromol/L).

Epidemiology:

Prevalence: 1-4% of adults in developed countries
Male to female ratio: 4:1 (equalizes after menopause)
Peak incidence: Males 40-50 years, females post-menopause
Increasing prevalence due to obesity, metabolic syndrome, aging population

Risk Factors:

Dietary: Purine-rich foods (red meat, seafood), alcohol (especially beer), fructose-sweetened beverages
Medications: Thiazide diuretics, low-dose aspirin, cyclosporine
Comorbidities: Chronic kidney disease, metabolic syndrome, hypertension, obesity
Genetic: Variants in urate transporters (URAT1, GLUT9)

Pathophysiology Pearl

MSU crystals trigger the innate immune system via the NLRP3 inflammasome, leading to IL-1beta release. This explains why IL-1 inhibitors (anakinra, canakinumab) are effective in refractory cases.

Pathophysiology

Understanding the pathophysiology of gout is essential for both diagnosis and management. The disease results from a complex interplay of uric acid metabolism, crystal formation, and inflammatory responses.

Uric Acid Metabolism

Production:

Uric acid is the end product of purine metabolism in humans
Purines derived from dietary intake (exogenous) and cellular turnover (endogenous)
Key enzyme: Xanthine oxidase converts hypoxanthine to xanthine to uric acid
Humans lack uricase enzyme (present in most mammals) - cannot break down uric acid further

Excretion:

70% renal excretion via complex tubular handling
30% gastrointestinal excretion
Key transporters: URAT1 (reabsorption), ABCG2 (secretion), GLUT9

Crystal Formation

Saturation point:

Monosodium urate (MSU) saturates at 6.8 mg/dL (404 micromol/L)
Below this level, crystals gradually dissolve
Above this level, crystals can precipitate in tissues

Factors promoting crystallization:

Lower temperature (explains predilection for peripheral joints)
Lower pH (trauma, exercise-induced acidosis)
Presence of nucleating agents
Connective tissue matrix components

Inflammatory Response

NLRP3 Inflammasome activation:

MSU crystals are phagocytosed by macrophages
Crystals destabilize lysosomal membranes
Cathepsin B released into cytoplasm
NLRP3 inflammasome assembly triggered
Caspase-1 activation
Pro-IL-1beta cleaved to active IL-1beta
Massive inflammatory cascade initiated

Inflammasome Mechanism

The NLRP3 inflammasome pathway explains why IL-1 inhibitors (anakinra, canakinumab) are effective in refractory gout. This is increasingly tested in fellowship exams as it bridges basic science with clinical application.

Resolution:

Acute attacks are self-limiting (7-14 days)
Aggregated neutrophil extracellular traps (NETs) help resolve inflammation
Coating of crystals by proteins reduces immunogenicity
Anti-inflammatory macrophage phenotype emerges

Clinical Presentation

Acute Gouty Arthritis

Classic presentation:

Rapid onset over 6-12 hours, often waking patient from sleep
Exquisitely painful - unable to tolerate bedsheet contact
Monoarticular in 85-90% of initial attacks
Podagra (1st MTP) is the classic location - 50% of first attacks
Signs of inflammation: Erythema, warmth, swelling mimicking cellulitis

Common joint involvement:

First metatarsophalangeal joint (podagra) - 50%
Ankle and midfoot - 25%
Knee - 15%
Wrist, fingers, elbow - 10%

Chronic Tophaceous Gout

Features:

Tophi: Chalky deposits of MSU crystals in soft tissues
Common locations: Fingers, olecranon bursa, Achilles tendon, ears
Joint destruction: Erosive arthropathy with preserved joint space initially
Tendon involvement: Can cause rupture (Achilles, patellar, extensor tendons)

Physical Examination

Inspection:

Swelling and erythema over affected joint
Tophi visible as subcutaneous nodules (white-yellow through skin)
Skin ulceration over tophi in advanced cases

Palpation:

Extreme tenderness - even light touch is painful
Warmth over affected joint
Tophi are firm, irregular nodules

Investigations

Laboratory Studies

Synovial fluid analysis (Gold Standard):

MSU crystal identification under polarized microscopy
Needle-shaped, negatively birefringent crystals
WBC count: 10,000-70,000/microL (predominantly neutrophils)

MSU crystals under polarized light microscopy — Polarized light microscopy demonstrating the GOLD STANDARD for gout diagnosis - monosodium urate (MSU) crystal identification. Numerous needle-shaped crystals appear bright yellow/orange against a dark background, scattered throughout the synovial fluid field. Key diagnostic features: (1) NEEDLE-SHAPED MORPHOLOGY - MSU crystals are long, thin, and needle-like (distinguishes from CPPD which are rhomboid), (2) NEGATIVE BIREFRINGENCE - the bright yellow/orange appearance when the crystal long axis is PARALLEL to the polarizer axis indicates negative birefringence (MSU are yellow when parallel, blue when perpendicular; CPPD is opposite), (3) INTRACELLULAR LOCATION - crystals visible both free in fluid and phagocytosed within neutrophils (confirms active inflammation). The identification of needle-shaped, negatively birefringent crystals in synovial fluid is DIAGNOSTIC of gout - even if serum urate is normal (serum urate can be normal during acute attacks in 30-40% of cases). Joint aspiration should be performed DURING acute attacks, and crystal identification takes precedence over serum urate levels for diagnosis.Credit: Jegapragasan M et al. via Evid Based Spine Care J via Open-i (NIH) (Open Access (CC BY))

Birefringence principles for crystal identification — Educational grid demonstrating the fundamental PHYSICS OF CRYSTAL BIREFRINGENCE underlying gout diagnosis. This 12-panel display (3 rows × 4 columns) shows how needle-shaped crystals appear under different polarized light conditions. Columns represent: (1) Negatively birefringent transparent (MSU-like), (2) Positively birefringent transparent (CPPD-like), (3) Non-birefringent transparent, (4) Non-birefringent absorptive. The critical distinction between gout (MSU = negative) and pseudogout (CPPD = positive) depends on the COLOR when crystal long axis is parallel to polarizer: MSU is YELLOW parallel (negative birefringence), CPPD is BLUE parallel (positive birefringence). Rotating the slide 90 degrees inverts the colors (MSU goes yellow to blue, CPPD goes blue to yellow), confirming true birefringence. This demonstrates why compensated polarized light microscopy (with red compensator plate) is essential - crystals with negative birefringence subtract from baseline retardation (appear yellow), while positive birefringence adds to it (appear blue). Essential for teaching trainees the microscopy technique they must master for crystal arthropathy diagnosis.Credit: Zhang Y et al. via Sci Rep via Open-i (NIH) (Open Access (CC BY))

Tophus histopathology — Two-panel histopathology demonstrating the PATHOLOGICAL APPEARANCE of chronic tophaceous gout. Panel (a): H&E staining showing tissue with purple/violet inflammatory infiltrate surrounding areas of crystal deposition. Panel (b): Higher magnification showing pink/eosinophilic tissue with needle-shaped CLEFTS or spaces representing where urate crystals dissolved during standard histological processing (MSU crystals are water-soluble and dissolve in formalin fixation). Key features: (1) Needle-shaped clefts in stellate or radial pattern - the characteristic 'ghosts' of dissolved MSU crystals, (2) Granulomatous foreign body reaction - surrounding crystal deposits are histiocytes, multinucleated giant cells, and chronic inflammatory cells, (3) Fibrous capsule - mature tophi develop fibrous encapsulation. Tophi represent END-STAGE poorly controlled gout - develop when serum urate elevated above saturation (6.8 mg/dL) for years. SURGICAL INDICATIONS for tophus excision: mechanical symptoms, skin ulceration (infection risk), nerve compression, cosmetic concerns. This reinforces that gout is not just acute inflammatory arthritis but can progress to destructive chronic arthropathy requiring orthopaedic intervention.Credit: Gupta A et al. via J Cytol via Open-i (NIH) (Open Access (CC BY))

Advanced holographic microscopy for automated crystal detection — Multi-panel comparing EMERGING LENS-FREE HOLOGRAPHIC MICROSCOPY with conventional compensated polarized light microscopy (CPLM) for automated crystal detection. Left: Large hologram image with yellow boxes marking regions of interest. Right panels: top row shows grayscale 'Lens-free differential', 'Lens-free', and 'CPLM 40-h 25μm' images; bottom row shows purple/magenta false-color images with white arrows pointing to needle-shaped MSU crystals. Traditional CPLM requires experienced operator, time-consuming manual review, and subjective interpretation. Lens-free holographic microscopy offers potential advantages: wide field-of-view (image entire sample without moving stage), digital automated crystal detection, quantification of crystal burden, and potential point-of-care testing. However, CPLM remains CLINICAL GOLD STANDARD with color birefringence information (distinguishes MSU from CPPD), universal availability, and decades of validation. This demonstrates the FUTURE DIRECTION toward automated point-of-care testing in emergency departments without requiring rheumatology expertise, but candidates must know CPLM is current standard.Credit: Zhang Y et al. via Sci Rep via Open-i (NIH) (Open Access (CC BY))

Multi-region crystal analysis demonstrating thorough specimen examination — Multi-panel demonstrating the principle of MULTIPLE SAMPLING and thorough synovial fluid examination across three regions of interest (ROI 1, ROI 2, ROI 3). Each ROI shown with: top panels - grayscale 'Lens-free differential' and 'Lens-free sub-region' images; bottom panels - purple/magenta false-color 'Lens-free pseudo-color' and 'CPLM lens 40-0.75NA' images. White arrows point to individual needle-shaped MSU crystals in each region. Key clinical lessons: (1) HETEROGENEOUS CRYSTAL DISTRIBUTION - MSU crystals not uniformly distributed in synovial fluid; examining only one field may miss crystals (false negative), requiring systematic review of entire slide, (2) CRYSTAL QUANTIFICATION - the three ROIs show varying crystal densities; burden correlates with inflammation severity and can be semi-quantified (rare, moderate, abundant), (3) VALIDATION - same crystals identified by both lens-free microscopy and CPLM across multiple ROIs validates new technique's sensitivity/specificity. Practical implications: PROPER SPECIMEN COLLECTION requires removing maximum fluid (crystals settle by gravity; bottom fluid has higher yield), analyzing fresh if possible (crystals can dissolve over time), using heparin or no anticoagulant (EDTA causes dissolution), and examining thick wet mount (not thin smears). NEGATIVE ASPIRATE does NOT exclude gout - sensitivity only 80-90%; if clinical suspicion high, treat empirically and consider repeat aspiration or ultrasound.Credit: Zhang Y et al. via Sci Rep via Open-i (NIH) (Open Access (CC BY))

Serum uric acid:

May be normal during acute attack (paradoxical decrease)
Elevated greater than 6.8 mg/dL (360 micromol/L) supports diagnosis
Target for ULT: less than 6 mg/dL (360 micromol/L)

Additional labs:

Renal function (CKD common comorbidity)
Lipid profile and glucose (metabolic syndrome)
CBC (elevated WBC during acute attack)

Imaging

Plain Radiographs:

Early: Soft tissue swelling, normal bone
Established: Punched-out erosions with overhanging edges ("rat bite" or "mouse ear")
Preserved joint space (unlike OA)
Soft tissue tophi may calcify

Bilateral hand radiographs showing severe chronic tophaceous gout — Advanced tophaceous gout: Bilateral PA hand radiographs demonstrating extensive destructive changes of chronic gout. Note multiple punched-out erosions with characteristic overhanging edges throughout the metacarpals and phalanges, large soft tissue tophi (non-calcified), and relative preservation of joint spaces in early-stage affected joints. This Pacific Islander patient had longstanding poorly controlled gout.Credit: McQueen FM et al., Arthritis Res Ther - CC BY 4.0

Plain radiographs demonstrating characteristic gouty erosions in hand and foot — Classic gouty erosions on plain radiography: (a) Oblique hand view demonstrating bone erosions at MCP and interphalangeal joints with characteristic punched-out appearance (arrowheads), (b) Hand radiograph showing more advanced erosive changes with severe joint destruction (arrows), (c) First metatarsophalangeal joint with well-defined erosions and overhanging edges (arrows). These 'overhanging edge' or 'rat bite' erosions are pathognomonic for gout.Credit: Perez-Ruiz F et al., Arthritis Res Ther - PMC2714107 (CC-BY)

Ultrasound:

Double contour sign: Hyperechoic line on hyaline cartilage surface
Aggregates and tophi visible
Useful for guided aspiration

Dual-Energy CT (DECT):

Color-codes urate deposits (typically green)
Sensitivity 90%, specificity 83%
Useful when aspiration not possible
Can detect occult tophi

Management

Acute Attack Management

Do NOT Initiate ULT During Acute Attack

Starting allopurinol or febuxostat during an acute gout flare can prolong the attack by mobilizing urate crystals. Treat the acute attack first, then initiate ULT 2-4 weeks after resolution. However, continue ULT if already established.

First-line options:

NSAIDs: Indomethacin 50mg TDS, naproxen 500mg BD - continue until attack resolves
Colchicine: Most effective within 12 hours of onset. Loading dose 1mg, then 0.5mg 1 hour later. Low-dose regimen preferred.
Corticosteroids: Prednisolone 30-40mg daily for 5-7 days, or intra-articular injection

Refractory cases:

IL-1 inhibitors (anakinra) for patients with contraindications to all above
Joint aspiration alone provides significant relief

Urate-Lowering Therapy (ULT)

Indications for ULT:

Recurrent acute attacks (2 or more per year)
Presence of tophi
Radiographic changes
Chronic kidney disease stage 2 or greater
Urolithiasis

Agents:

Allopurinol: First-line. Start low (50-100mg), titrate to target. PBS listed in Australia.
Febuxostat: Alternative if allopurinol intolerant. More potent urate lowering.
Probenecid: Uricosuric. Requires good renal function. Not commonly used.

Target:

Serum urate less than 6 mg/dL (360 micromol/L)
Less than 5 mg/dL if tophi present for faster dissolution

Surgical Management

Indications for Surgery

Mechanical symptoms: Large tophi limiting joint motion or tendon function
Skin ulceration: Over tophi with risk of secondary infection
Secondary infection: Debridement of infected tophi
Nerve compression: Carpal tunnel, ulnar neuropathy from tophi
Joint destruction: Arthroplasty for end-stage arthropathy
Tendon rupture: Repair or reconstruction

Surgical Principles

Tophus Excision

Preoperative:

Optimize medical management (ULT established)
Assess skin viability and plan closure
Consider staged procedures for large tophi

Technique:

Incision planned to allow adequate exposure and closure
Identify and protect neurovascular structures
Debulk tophaceous material - chalky white deposits
Curette affected bone if involved
Assess tendon integrity
Irrigate thoroughly

Closure considerations:

Primary closure if possible
Negative pressure wound therapy for large defects
Skin grafting or flap coverage may be required
Avoid tension on skin closure

Postoperative:

Continue ULT to prevent recurrence
Wound care and monitoring for healing
Physiotherapy for ROM

This completes the tophus excision approach.

Complications

Disease Complications

Chronic erosive arthropathy: Joint destruction, subluxation
Tendon rupture: Achilles, patellar, extensor tendons
Carpal tunnel syndrome: From tophaceous deposits
Renal complications: Uric acid stones, urate nephropathy
Cardiovascular disease: Independent risk factor

Surgical Complications

Wound healing problems: Skin necrosis, delayed healing over tophi
Infection: Risk increased with ulcerated tophi
Recurrence: If ULT not optimized
Tendon injury: During tophus excision

Evidence Base

Colchicine Dosing in Acute Gout

Terkeltaub RA et al. • Arthritis Rheum (2010)

Key Findings:

Low-dose colchicine as effective as high-dose for acute gout
Significantly fewer GI side effects with low-dose regimen
Optimal timing within 12 hours of attack onset

CARES Trial - Febuxostat vs Allopurinol

White WB et al. • N Engl J Med (2018)

Key Findings:

Higher all-cause mortality with febuxostat vs allopurinol
Cardiovascular death significantly higher with febuxostat
FDA added black box warning to febuxostat

Dual-Energy CT for Gout Diagnosis

Choi HK et al. • Ann Rheum Dis (2012)

Key Findings:

DECT has 90% sensitivity for urate crystal detection
Specificity of 83% makes it useful diagnostic adjunct
Can detect occult tophi not visible clinically

Treat-to-Target Strategy in Gout

Doherty M et al. • Lancet (2018)

Key Findings:

95% achieved urate target with structured care vs 30% usual care
Significant reduction in gout flares with treat-to-target
Tophus resolution achieved in majority of patients

Exam Viva Scenarios

Practice these scenarios to excel in your viva examination

VIVA SCENARIOStandard

Scenario 1: Acute Gouty Arthritis

EXAMINER

"A 52-year-old obese man presents with sudden onset severe pain and swelling of his right first MTP joint. He woke at 3am unable to tolerate the bedsheet touching his foot. He drinks beer regularly. Examination shows an exquisitely tender, erythematous, swollen 1st MTP joint."

EXCEPTIONAL ANSWER

Thank you. This presentation is classic for acute gouty arthritis affecting the first MTP joint - podagra. I would confirm the diagnosis with joint aspiration for crystal analysis, expecting to find negatively birefringent needle-shaped MSU crystals under polarized microscopy. For acute management, I would prescribe NSAIDs such as naproxen 500mg twice daily or indomethacin 50mg three times daily, with gastroprotection. I would NOT start urate-lowering therapy during the acute attack. I would advise rest, ice, and elevation. Once the acute attack resolves in 1-2 weeks, I would discuss long-term urate-lowering therapy with allopurinol, lifestyle modifications including weight loss, reduced alcohol intake, and dietary changes.

KEY POINTS TO SCORE

Identify podagra as classic gout presentation

Joint aspiration is gold standard for diagnosis

NSAIDs first-line for acute attack

Do NOT start allopurinol during acute attack

COMMON TRAPS

✗Starting allopurinol during acute attack

✗Treating as cellulitis without aspiration

✗Missing metabolic syndrome workup

LIKELY FOLLOW-UPS

"What if the patient has CKD stage 3?"

"How would you differentiate from septic arthritis?"

"What are the targets for urate-lowering therapy?"

VIVA SCENARIOStandard

Scenario 2: Chronic Tophaceous Gout

EXAMINER

"A 65-year-old man with a 15-year history of gout presents with a large tophus over his left olecranon causing skin breakdown. He has limited elbow flexion. Serum urate is 9.2 mg/dL despite allopurinol 300mg daily."

EXCEPTIONAL ANSWER

Thank you. This patient has chronic tophaceous gout with a large olecranon tophus causing mechanical symptoms and skin ulceration. My management would involve optimizing his medical therapy first - his serum urate target should be less than 5 mg/dL given the tophi. I would increase his allopurinol dose with appropriate monitoring, aiming for maximum tolerated dose or switch to febuxostat if inadequate response. Surgically, given the skin breakdown and mechanical symptoms, I would recommend elective excision of the tophus. Preoperatively, I would ensure his gout is controlled. Intraoperatively, I would plan for adequate exposure, careful debridement of tophaceous material, assess underlying bone and bursa, and plan closure carefully - potentially with negative pressure wound therapy if primary closure is not possible. Postoperatively, I would continue optimized ULT and provide wound care.

KEY POINTS TO SCORE

Optimize ULT before elective surgery - target less than 5 mg/dL with tophi

Skin ulceration is a surgical indication

Plan for potential wound healing challenges

Continue ULT postoperatively to prevent recurrence

COMMON TRAPS

✗Operating without optimizing medical management

✗Underestimating wound closure challenges

✗Stopping ULT perioperatively

LIKELY FOLLOW-UPS

"What if the wound cannot be closed primarily?"

"How would you manage if the tophus is infected?"

"What perioperative prophylaxis would you use for gout flare?"

VIVA SCENARIOStandard

Scenario 3: Crystal Identification

EXAMINER

"You are shown a polarized microscopy image of synovial fluid showing needle-shaped crystals that appear yellow when aligned parallel to the polarizer. What is your diagnosis?"

EXCEPTIONAL ANSWER

Thank you. These are monosodium urate crystals diagnostic of gout. The key features are the needle-shaped morphology and negative birefringence - appearing yellow when parallel to the polarizer axis. This is in contrast to CPPD crystals which are rhomboid or rod-shaped and positively birefringent, appearing blue when parallel. The mnemonic I use is 'Yellow Parallel in Gout' or 'Blue Parallel in Pseudogout.' This finding in synovial fluid is diagnostic for gout, even in the absence of elevated serum urate levels, which can paradoxically be normal during an acute attack.

KEY POINTS TO SCORE

MSU crystals: needle-shaped, negatively birefringent

Yellow when parallel to polarizer = negative birefringence

CPPD: rhomboid, positively birefringent (blue parallel)

Crystal analysis is diagnostic even with normal serum urate

COMMON TRAPS

✗Confusing positive and negative birefringence

✗Assuming normal urate excludes gout

✗Missing CPPD as differential

LIKELY FOLLOW-UPS

"What if you see both crystal types?"

"How do you perform polarized microscopy?"

"What other conditions can cause crystal arthropathy?"

Australian Context

In Australia, gout prevalence is increasing and parallels rising rates of obesity and metabolic syndrome. Indigenous Australians have particularly high rates of gout, with prevalence up to 10% in some communities, related to genetic factors and high rates of chronic kidney disease.

PBS-listed medications:

Allopurinol: First-line ULT, PBS listed without restriction
Colchicine: PBS listed for acute gout and prophylaxis
Febuxostat: PBS listed as Authority Required for patients intolerant of or unresponsive to allopurinol

Management should include screening for and addressing cardiovascular risk factors given the strong association between gout and cardiovascular disease. The Australian Rheumatology Association endorses treat-to-target strategies with serum urate goals of less than 6 mg/dL (360 micromol/L) or less than 5 mg/dL (300 micromol/L) in tophaceous disease.