12.2 Ankylosing Spondylitis, Psoriatic Arthritis, Gout & Pseudogout (CPPD)
Key Takeaways
- Seronegative Spondyloarthropathies share a strong genetic association with HLA-B27, enthesitis (inflammation at tendon/ligament insertions to bone), negative RF and anti-CCP serologies, and prominent axial or asymmetric peripheral skeletal involvement.
- Ankylosing Spondylitis (AS) is characterized by bilateral sacroiliitis, ascending syndesmophyte formation leading to complete spinal fusion ('bamboo spine'), restricted spinal mobility (<5 cm expansion on the Schober test), and severe vulnerability to unstable 'chalk-stick' fractures from minor trauma.
- Psoriatic Arthritis (PsA) presents with dactylitis ('sausage digits'), distal interphalangeal (DIP) joint destruction, nail dystrophy (pitting and onycholysis), and characteristic 'pencil-in-cup' deformities on plain radiographs.
- Gout is diagnosed by needle-shaped, strongly negatively birefringent monosodium urate (MSU) crystals under polarized light microscopy, whereas Pseudogout (CPPD) exhibits rhomboid-shaped, weakly positively birefringent calcium pyrophosphate crystals and radiographic chondrocalcinosis.
- Acute gout flares are managed with NSAIDs, colchicine, or corticosteroids (never alter urate-lowering therapy during an acute flare); chronic hyperuricemia requires xanthine oxidase inhibitors (Allopurinol titrated to target serum urate <6.0 mg/dL with HLA-B*5801 screening).
Ankylosing Spondylitis, Psoriatic Arthritis, Gout & Pseudogout (CPPD)
Core Clinical Principle: Seronegative Spondyloarthropathies (SpA) and crystal-induced arthropathies comprise distinct clinical entities characterized by robust inflammatory cascades. Spondyloarthropathies are unified by HLA-B27 expression, enthesitis, and negative autoantibodies, while crystal arthropathies result from intra-articular precipitation of microcrystals that trigger the NLRP3 inflammasome. Rapid differentiation ensures targeted pharmacotherapy and prevents catastrophic orthopaedic complications.
1. The Seronegative Spondyloarthropathy Family
The seronegative spondyloarthropathies are a group of interrelated inflammatory rheumatic diseases that share several core clinical, genetic, and pathophysiological features:
CORE CHARACTERISTICS OF SERONEGATIVE SPONDYLOARTHROPATHIES
┌──────────────────────────────────────┬──────────────────────────────────────┐
│ 1. Strong HLA-B27 Genetic Link │ 2. Pathognomonic Enthesitis │
│ • Present in 90–95% of AS cases │ • Primary inflammation at tendon, │
│ • Present in 50–70% of PsA cases │ ligament, and capsule insertions│
├──────────────────────────────────────┼──────────────────────────────────────┤
│ 3. Absence of Autoantibodies │ 4. Distinct Articular Patterns │
│ • Negative Rheumatoid Factor (RF) │ • Axial skeleton (Sacroiliitis) │
│ • Negative Anti-CCP antibodies │ • Asymmetric oligoarthritis │
├──────────────────────────────────────┼──────────────────────────────────────┤
│ 5. Common Extra-Articular Features │ 6. Overlapping Disease Entities │
│ • Acute anterior uveitis (iritis) │ • Ankylosing Spondylitis (AS) │
│ • Aortitis / aortic regurgitation │ • Psoriatic Arthritis (PsA) │
│ • Inflammatory bowel disease (IBD)│ • Reactive Arthritis & Enteropathic│
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The Pathophysiology of Enthesitis
Unlike RA, where inflammation begins in the vascular synovial lining, SpA begins at the enthesis—the anatomical interface where tendons, ligaments, joint capsules, or fascial planes insert into bone (e.g., Achilles tendon insertion at the calcaneus, plantar fascia insertion, patellar tendon, costosternal junctions). Stress and microtrauma at enthesial sites trigger local IL-23 / IL-17 cytokine axis activation, resulting in local bone resorption followed by exuberant, disordered reactive new bone formation (osteoproliferation) and syndesmophyte bridging.
2. Ankylosing Spondylitis (AS): Pathophysiology & Spinal Ankylosis
Ankylosing Spondylitis is a chronic, progressive, systemic inflammatory disease of the axial skeleton, predominantly affecting young adults (onset typically between 20 and 40 years of age; male-to-female ratio ~2:1).
ASCENDING STRUCTURAL PROGRESSION OF AS
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│ 1. Bilateral Sacroiliitis (Earliest Hallmark) │
│ (Erosion and subchondral sclerosis of the sacroiliac joint margins) │
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│ 2. Romanus Lesions & Marginal Squaring of Vertebral Bodies │
│ (Osteitis at anterior corners of vertebral bodies; loss of lordosis)│
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│ 3. Ascending Syndesmophyte Formation │
│ (Vertical, thin, marginal bony bridges across intervertebral discs) │
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│ 4. Complete Spinal Ankylosis & Calcification ('Bamboo Spine') │
│ (Ossification of anterior longitudinal ligament & facet fusions) │
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Clinical Presentation: Inflammatory Back Pain
Inflammatory back pain in AS exhibits distinct characteristics that differentiate it from common mechanical back pain:
| Clinical Parameter | Inflammatory Back Pain (AS) | Mechanical Back Pain (Lumbar Strain / Disc) |
|---|---|---|
| Age of Onset | < 40–45 years (insidious onset) | Any age (often acute onset after lifting/strain) |
| Duration | Chronic (> 3 months) | Acute (< 4–6 weeks) or episodic |
| Morning Stiffness | Severe (> 30–60 minutes) | Brief (< 15–30 minutes) |
| Effect of Exercise | IMPROVES with movement / physical activity | WORSENS with physical activity / loading |
| Effect of Rest | WORSENS with rest / inactivity (nocturnal waking) | IMPROVES with recumbency / rest |
| Buttock Pain | Alternating, deep gluteal pain (sacroiliitis) | Unilateral radiating dermatomal pain (radiculopathy) |
3. Objective Clinical Assessment & Mobility Testing in AS
Certified orthopaedic nurses evaluate axial mobility and disease progression utilizing three validated physical examination measurements:
CLINICAL MOBILITY ASSESSMENT IN AS
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│ 1. Modified Schober Test (Lumbar Spine Flexion) │
│ • Patient stands erect; mark the lumbosacral junction (L5–S1 line). │
│ • Place a second mark 10 cm superiorly and a third mark 5 cm inferiorly. │
│ • Patient bends fully forward with knees straight; measure new distance: │
│ - NORMAL: Expands by > 5 cm (total distance increases from 15 to ≥ 20 cm)│
│ - AS ABNORMAL: Restricted expansion < 5 cm indicates spinal ankylosis. │
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│ 2. Thoracic Chest Expansion Measurement │
│ • Place tape measure circumferentially around 4th intercostal space. │
│ • Measure difference between maximal forced expiration and inspiration: │
│ - NORMAL: ≥ 5 cm chest expansion. │
│ - AS ABNORMAL: Reduced to < 2.5 cm due to costovertebral joint fusion; │
│ causes severe restrictive pulmonary defect (vital capacity drops). │
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│ 3. Occiput-to-Wall Distance (Tragus-to-Wall) │
│ • Patient stands with heels and buttocks touching a vertical wall. │
│ • In advanced fixed kyphosis ('question-mark' posture), occiput cannot │
│ touch the wall; measure distance between occipital protuberance & wall. │
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4. Orthopaedic Trauma Emergency: 'Chalk-Stick' Spinal Fractures
An ankylosed, fused spine functions biomechanically as a single, rigid, long bone with a long lever arm. Concurrently, severe secondary trabecular osteoporosis develops within the shielded vertebral bodies.
CHALK-STICK (CARROT-STICK) SPINAL FRACTURE
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│ Pathophysiology: │
│ • Minor low-energy trauma (e.g., ground-level fall, bumping head on car) │
│ • Fracture shears completely through the fused anterior & posterior columns │
│ • Highly unstable, three-column sheer injury (most common at C5–C7 & T11–L2)│
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│ Clinical Consequences & High Mortality: │
│ • Extremely high risk of complete spinal cord transection & epidural hematoma│
│ • Neurological deficits occur in up to 50–70% of displaced fractures. │
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│ CRITICAL NURSING ACTIONS & IMMOBILIZATION RULES: │
│ • Maintain STRICT spinal precautions in the patient's BASELINE KYPHOTIC │
│ POSTURE! NEVER force the patient's head or neck flat onto a standard flat │
│ spine board (forcing extension will displace the fracture and crush cord).│
│ • Place customized padding, pillows, or folded blankets beneath the head │
│ and thoracic spine to preserve the patient's chronic flexed alignment. │
│ • STAT non-contrast CT / MRI of the entire spine. │
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Long-Term Nursing Care & Physical Therapy in AS
- Postural Training: Instruct patients to sleep on a firm mattress without a head pillow (or with a thin cervical roll) and encourage daily prone lying for 15 to 30 minutes to promote hip and thoracic extension, combating the progressive flexion contracture tendency.
- Extension Exercises & Breathing: Daily spinal extension stretching, swimming, and deep breathing chest expansion exercises.
- Pharmacotherapy: First-line: scheduled nonsteroidal anti-inflammatory drugs (NSAIDs at full anti-inflammatory doses); if inadequate, escalate to TNF-α inhibitors (adalimumab, etanercept, infliximab) or IL-17A inhibitors (Secukinumab, Ixekizumab). Conventional DMARDs (methotrexate) are ineffective for axial AS.
5. Psoriatic Arthritis (PsA): Clinical Phenotypes & Hallmarks
Psoriatic Arthritis is a heterogeneous, chronic inflammatory musculoskeletal disease occurring in up to 30% of patients with cutaneous psoriasis. Cutaneous lesions precede joint manifestations in ~70% of cases.
HALLMARK CLINICAL FEATURES OF PsA
┌─────────────────────────┬─────────────────────────┬─────────────────────────┐
│ Dactylitis │ DIP Joint & Nail │ Radiographic │
│ ('Sausage Digit') │ Involvement │ 'Pencil-in-Cup' │
├─────────────────────────┼─────────────────────────┼─────────────────────────┤
│ • Uniform, diffuse, │ • Prominent involvement │ • Marked osseous erosion│
│ painful swelling of an│ of Distal Inter- │ of proximal phalanx │
│ entire finger or toe │ phalangeal (DIP) │ head into a tapered │
│ • Concomitant flexor │ joints (spared in RA) │ point ('pencil') │
│ tenosynovitis & joint │ • Psoriatic Nail │ • Adjacent distal base │
│ synovitis │ Pitting, onycholysis, │ expands & cups │
│ • Strongly linked to SpA│ subungual keratosis │ • Arthritis Mutilans │
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Clinical Distinctions in PsA
- Articular Patterns: PsA exhibits five classic clinical subtypes: 1) Asymmetric oligoarthritis (<5 joints), 2) Symmetric polyarthritis (mimicking RA but involving DIPs), 3) Distal interphalangeal (DIP) predominant disease, 4) Spondylitis (axial disease with asymmetric sacroiliitis), and 5) Arthritis Mutilans (severe destructive osteolysis causing telescoping 'opera-glass' fingers [main-en-lorgnette]).
- Nail Dystrophy: Psoriatic nail pitting (>20 discrete pits), onycholysis (separation of the nail plate from the bed), subungual hyperkeratosis, and 'oil drop' discoloration strongly correlate with adjacent DIP joint arthritis due to the direct anatomical extension of the enthesial extensor tendon fibers into the nail root.
6. Crystal-Induced Arthropathies: Gout vs. Pseudogout (CPPD)
Crystal arthropathies are severe inflammatory joint disorders driven by the precipitation of microcrystals into synovial fluid and articular cartilage, activating the NLRP3 inflammasome and releasing massive surges of Interleukin-1β (IL-1β).
POLARIZED MICROSCOPY & CLINICAL DIFFERENTIATION MATRIX
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│ Diagnostic Feature │ Gout (Monosodium Urate - MSU) │ Pseudogout / CPPD Disease │
├─────────────────────┼─────────────────────────────────┼─────────────────────────────────┤
│ Crystal Morphology │ Needle-shaped, elongated, │ Rhomboid-shaped, rectangular, │
│ │ sharp-ended intracellular shards│ blunt-ended crystals │
├─────────────────────┼─────────────────────────────────┼─────────────────────────────────┤
│ Polarized Light │ **STRONGLY NEGATIVE** │ **WEAKLY POSITIVE** │
│ Birefringence │ **BIREFRINGENCE** │ **BIREFRINGENCE** │
│ │ • Yellow when PARALLEL to axis │ • Blue when PARALLEL to axis │
│ │ • Blue when PERPENDICULAR │ • Yellow when PERPENDICULAR │
├─────────────────────┼─────────────────────────────────┼─────────────────────────────────┤
│ Primary Predilection│ **1st Metatarsophalangeal** │ **Knee joint** (>50% of cases), │
│ │ **(MTP) joint (Podagra >50%)**; │ Wrist (TFCC), Pubic Symphysis, │
│ │ Ankle, Instep, Olecranon bursa │ Shoulder, Metacarpophalangeal │
├─────────────────────┼─────────────────────────────────┼─────────────────────────────────┤
│ Radiographic Signs │ 'Punched-out' / 'rat-bite' bone │ **Chondrocalcinosis** (punctate,│
│ │ erosions with overhanging scler-│ linear calcifications within │
│ │ otic edges; soft tissue tophi │ hyaline/fibrocartilage menisci) │
├─────────────────────┼─────────────────────────────────┼─────────────────────────────────┤
│ Underlying Patho- │ Hyperuricemia (serum urate │ Local inorganic pyrophosphate │
│ physiology │ >6.8 mg/dL; underexcretion 90%) │ overproduction (ANKH mutations) │
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7. Gout: Clinical Phases & Pharmacotherapy
Gout progresses through four clinical phases: 1) Asymptomatic hyperuricemia, 2) Acute gouty arthritis, 3) Intercritical period (asymptomatic intervals between flares), and 4) Chronic tophaceous gout.
PHARMACOTHERAPY OF GOUT: ACUTE VS. CHRONIC
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│ 1. ACUTE GOUT FLARE MANAGEMENT (Target: Rapid Inflammatory Control) │
│ • First-Line Options (Initiate within 24 hours of flare onset): │
│ a) NSAIDs: Indomethacin (50 mg TID) or Naproxen (500 mg BID) at full anti-│
│ inflammatory doses (avoid in renal insufficiency / peptic ulcer disease)│
│ b) Colchicine: 1.2 mg loading dose PO, followed by 0.6 mg 1 hour later │
│ (total 1.8 mg in first 24h); inhibits neutrophil chemotaxis/tubulin. │
│ c) Systemic Corticosteroids: Oral Prednisone (0.5 mg/kg/day tapered over │
│ 7–10 days) or Intra-articular Triamcinolone (ideal in monoarthritis). │
│ • CRITICAL RULE: NEVER START OR ABRUPTLY STOP Urate-Lowering Therapy (ULT) │
│ during an acute flare (abrupt serum urate shifts prolong/intensify flare).│
│ If patient is ALREADY on ULT, maintain the established dose without change│
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│
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│ 2. CHRONIC URATE-LOWERING THERAPY (Target: Serum Urate < 6.0 mg/dL) │
│ • Indications: ≥2 flares/year, tophi, radiographic damage, urate nephrolith │
│ • First-Line Xanthine Oxidase Inhibitors (XOIs): │
│ a) Allopurinol: Titrate up from 100 mg/day (target: serum urate <6.0 mg/dL│
│ or <5.0 mg/dL for severe tophi). Adjust dose in renal impairment. │
│ - MANDATORY GENETIC SCREENING: Screen for **HLA-B*5801 allele** in │
│ patients of Han Chinese, Korean, Thai, or African descent prior to │
│ initiation to prevent fatal **Allopurinol Hypersensitivity Syndrome**│
│ (SCAR / DRESS / Toxic Epidermal Necrolysis). │
│ b) Febuxostat: Potent non-purine XOI; preferred in allopurinol allergy/CKD│
│ • Mandatory Concomitant Anti-Inflammatory Prophylaxis: │
│ - Co-prescribe low-dose **Colchicine (0.6 mg daily or BID)** or low-dose │
│ NSAID for **3 to 6 months** when initiating ULT to prevent mobilization │
│ flares caused by submicroscopic crystal dissolution. │
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Dietary & Lifestyle Nursing Education in Gout
- Purine Restriction: Strictly limit organ meats (liver, kidneys, sweetbreads), red meats (beef, lamb, venison), and high-purine seafood (anchovies, sardines, mussels, scallops).
- Alcohol Elimination: Avoid all beer (brewer's yeast contains concentrated purine guanosine; alcohol metabolism degrades ATP to AMP, elevating urate while competing with urate for renal excretion) and hard distilled spirits.
- Eliminate High-Fructose Corn Syrup (HFCS): Fructose is the only carbohydrate that directly accelerates purine nucleotide degradation in hepatocytes, driving rapid serum uric acid spikes; eliminate sugar-sweetened sodas and processed juices.
- Hydration: Maintain vigorous oral fluid intake (>2.5 to 3 L/day) to optimize renal urate clearance and prevent intraluminal uric acid crystal precipitation and nephrolithiasis.
A 28-year-old male with a 6-year history of ankylosing spondylitis presents to the emergency department after a low-energy ground-level fall. He complains of sharp mid-thoracic back pain and lower extremity paresthesias. Radiographs reveal a complete transvertebral fracture through the T10–T11 fused spinal segment. Which nursing action is mandatory during initial trauma stabilization?
During a rheumatology clinic visit, the orthopaedic nurse performs a Modified Schober Test on a patient being evaluated for ankylosing spondylitis. The nurse marks the lumbosacral junction (L5–S1 line), places a second mark 10 cm superiorly and a third mark 5 cm inferiorly (initial span = 15 cm). When the patient bends fully forward, the measured span increases to 17.5 cm (a 2.5 cm expansion). How should the nurse interpret this objective finding?
An adult patient presents with excruciating, warm, erythematous swelling of the first metatarsophalangeal (MTP) joint that began abruptly overnight. Diagnostic arthrocentesis yields cloudy synovial fluid. Under compensated polarized light microscopy, which microscopic finding confirms the definitive diagnosis of acute gouty arthritis?
A 56-year-old male with recurrent gouty arthritis and chronic tophi is initiated on allopurinol for long-term urate-lowering therapy. Which clinical instruction and prescribing principle must the orthopaedic nurse reinforce?