CRYSTAL ARTHRITIS

Dr. M Kasi Viswanadham

PG in Orthopaedics

GOUT

word Gout is derived from the latin

word ‘gutta’ means drop.

based on the ancient belief that the arthritis is due to

deposition of malevolent humor by evil spirits into the joint,

drop by drop

Gout is a disorder of purine metabolism

characterized by hyperuricaemia,

deposition of monosodium urate

monohydrate crystals in joints and peri-

articular tissues and recurrent attacks of

acute synovitis.

Late changes include cartilage

degeneration, renal dysfunction and uric

acid urolithiasis.

history

• 2640 BC: podagra first identified by the Egyptians

– 5th century BC: Hippocrates referred to gout as “unwalkable disease” and noted links between gout & lifestyle, demographics & other variables

Galen described the tophi.

Crystals in gouty tophi was first demonstrated

by Antony Van Leeuwenhoek in (1679 )

Sir Alfred Garrod demonstrated hyperuricemia as the basic cause of gout(1848)

McCarty and Hollander established the association between gouty arthritis and articular crystal deposition(1961)

Gout is much more common in men

than in women;

rare before menopause and more

common in old age

Male ,female ratio 2.7:1

pathogenesis

The pathogenesis of gout depends on

three vital steps:

(1) the development of

hyperuricaemia;

(2) the formation of monosodium

urate monohydrate (urate) crystals;

(3) the interaction between the urate

crystals and the inflammatory system.

This disorder can be progressive

through four stages if undertreated

1. Asymptomatic hyperuricemia

2. Acute gout

3. Intercritical gout

4. Chronic tophaceous gout

Asymptomatic hyperurecemia

Asymptomatic

Serum uric acid levels-more than

6mg/dl

risk of gout increases with the degree

and

duration of hyperuricaemia.

Acute gout

most common early clinical

manifestation

Usually, only one joint is affected

initially, but polyarticular acute gout

can occur in subsequent episodes

Factors provking manifestations-.

alcohol,

obesity

abrupt change in serum uric acid

concentration

Diuretic use, hypertension, renal insufficiency, and

osteoarthritis

Most acute attacks of gout involve a

single joint in the lower limb,

most commonly the first metatarso

phalangeal joint also referred to as

podagra.

Others-ankle, heel, knee, wrist, fingers, and elbow joints

Symptoms-severe pain,

Swelling

Erythema

Warmth

Tenderness

Low grade fever

Starts during night peak 1-2 days.lastfor 7-10 days◦ Differential diagnosis-septic

arthritis,cellulitis

Acute gout

Intercritical gout

intercritical period is the time between

the acute attacks;

the term prophylactic period has been

preferred because its emphasizes the

value of medication which inhibits or

prevents recurring acute episodes.

Chronic tophius gout

Massive deposition of monosodium

urate crystal(tophi) in the articular

cartilage, subchondral bone, synovial

membrane, capsular, periarticular

tissue and tendon sheaths.

Occurs late (an avg 12 yrs)after intial

attack

Chronic gout

Tophaceous nodule consist of

multicentric deposition of urate crystal

,inter cellular matrix and foreign body

grannulomatous reaction.

Tophi firm yellow in colour

occsionally discharge cheesy or

chalky white material.

+

o

Complications of tophi gout-pain,soft

tissue damage and deformity,joint

destruction, nerve compression

syndromes

Renal manifestation of gout

Nephrolithiasis

Acte gouty nephropathy

Chronic gouty nephropathy

diagnosis

Base line lab tests-urine analysis

renal function tests

Serum urate- normal value is 6-7 mg/dl (6.8mg/dl)

an elevated serum uric acid level does not indicate or predict gout

hyperuricemia in the absence of symptoms is not diagnostic of gout.

diagnosed based on the discovery of uratecrystals in the synovial fluid or soft tissues.

radiography

Early in the disease, radiographs are

often normal or show only soft-tissue

swelling

Radiographic findings characteristic of

gout, which generally do not appear

within the first year of disease onset

Asymmetrical

Punched out erosion

Lytic lesions

Overhanging edges

Scleorotic borders Differ from rhematoid arthrits

Maintenance of the joint space

Absence of periarticular

osteopenia

Location outside the joint capsule

identification of urate crystals the gold standard for conformation of the diagnosis

identification of urate crystals in synovial fuidusing polarized light microscopy is highly specific for gout

.

examined with a polarizing filter, they are yellow when aligned parallel to the slow axis of the red compensator, but they turn bluewhen aligned across the direction of polarization (ie, they exhibit negative birefringence).

Histology

Sample send in 100% alcohol

ultrasound

A "double contour" sign, consisting of a hyperechoic, irregular line of monosodium urate crystals on the surface articular cartilage overlying an adjacent hyperechoic bony contour

"Wet clumps of sugar," representing tophaceous material, described as hyperechoic and hypoechoicheterogeneous material with an anechoic rim

Bony erosions adjacent to tophaceousdeposits

Differential diagnosis acute

gout= infective (septic) arthritis;

traumatic synovitis;

palindromic rheumatism

seronegativspond-arthritides

Rhematic fever

d Differential diagnosis of chronic

gout nodular rheumatoid arthritis;

osteoarthritis with Heberden’s /

Bouchard’snodes;

Management

Treatment The acute attack

Resting the joint

Applying ice packs if pain is severe,

NSAIDs

Colchicine (may cause diarrhoea, nausea and vomiting)

A tense joint effusion may require aspiration and intra-articular injection of corticosteroids.

Oral corticosteroids.

The sooner treatment is started the sooner is the attack likely to end.

Interval therapy

Between attacks, attention should be

given to simple measures such as

losing weight

cutting out alcohol and

Eliminating diuretics.

Chronic gout

Uricosuric drugs (probenecid or

sulfinpyrazone) can be used if renal

function is normal.

Allopurinol a xanthine oxidase inhibitor,

is usually preferred for patients with

renal complications or chronic

tophaceous gout allopurinol is definitely

the drug of choice

Urate-lowering drugs should never be

started before the acute attack has

completely subsided, and they should

always be covered by an anti-

inflammatory preparation or

colchicine, otherwise they may

actually prolong or precipitate an

acute attack.

Surgery

Ulcerating tophi that fail to heal with

conservative treatment can be

evacuated by curettage

the wound is left open and dressings

are applied until it heals.

Calcium pyrophosphate dihydrate

(CPPD) crystal associated

arthropathies

idiopathic

presents as sporadic episodes in the

majority of patient

rare familial forms

The autosomal dominant form of the disease has

been shown to be related to a mutation in the

ANKH gene, which encodes a transmembrane

inorganic pyrophosphate transport channel

association with some metabolic disorders-

hyperparathyroidism,

haemochromatosis,

hypophosphatasia,

Wilson’s disease,

ochronosis,

hypo-calciuric hypercalcaemia

diabetes mellitus

hypomagnasaemia

intra-articular injections of hyaluronic acid preparations (such as Hylan GF-20) may trigger acute attack of pseudogout

o Age is most important risk factor

Osteoarthritis (OA) - threefold increased risk if CPPD present

Previous joint trauma/injury

Joint surgery/lavage promotes crystal shedding

Incidence and prevalence uncertain

Strong association with age prevalence 3.7% in age 55-59 17% in age 80-84%

CPPD associated arthritis is third most common inflammatory arthritis

most common acute mono-articulararthritis in elderly; typically involves the knee

pathogenesis

Not known

Disorder of articular cartilage with

altered chondrocyte

cartilage matrix abnormalities,altered

activity of enzymes that produces

pyrophoshates which combines with

calcium ions to form CPPD crystals

The deposits are often visible as a

fine layer of calcification overlying the

menisci and articular cartilage of the

knee- termed chondrocalcinosis

The crystals may provoke an acute attack of synovitis- referred to as pseudo-gout.

Pseudo gout Clinical syndrome of acutesynovitis with intraarticular (IA) Calcium pyrophosphate dehydrate (CPP) crystal deposition

o Most common joints knee and wrist

Chronic form referred to as calcium

pyrophosphate deposition (CPPD)

Arthropathy

Increases development of

osteoarthritis

Chondrocalcinosis

Asymptomatic

Incidental finding

Pseudogout is the most common form

presents as acute episodes of synovitis at a single joint, most often at the knee.

More common in men, the ‘attack’ typically lasts from a few days to 3-4 weeks

characterised by acute pain, swelling and warmth at the affected joint, often indistinguishable from gout.

Chronic CPPD: predominately affects

women; it is a progressive, often

symmetric, polyarthritis.

Usually affects the knees, wrists, 2nd

and 3rd MCP’s, hips, spine, shoulders,

elbows and ankles.

Chronic CPPD differs from pseudogout

in its chronicity, involvement of the

spine and MCP’s.

Radiograph of involved joint

Chondrocalcinosis (CC) = linear

densities in joints;

best seen on films of pelvis, hand and

knee

Only detects 40% articular CPPD

disease

Subchondral cysts

Aggressive joint degeneration;

osteophyte

Arthrocentesis

Inflammatory Synovial Aspirate: mean leukocyte count of 24,000 cells/μL with neutrophil predominance

Gram stain and culture necessary to rule out infectious arthritis

Screening for metabolic disorders

Gold standard: synovial fluid analysis under polarized light microscopy with rhomboid crystals, absent/weak positive birefringence polarizing filter

CPP crystals change color depending upon their alignment relative to the direction of the red compensator.

They are positively birefringent, appearing blue when aligned parallel with the slow axis of the compensator and yellow when perpendicular.

The sensitivity of a synovial fluid analysis for crystals is 84%, with a specificity of 100%.

Ultrasound –CPPD in peripheral joints appears as punctuate pattern with thin hyperechoic deposits

Specificity 86.7%, Sensitivity 96.4%;

Sensitivity varies with joint

Most accurate in mild cartilage degeneration

MRI - insensitive for articular CPPD

CT – sensitive for CPPD; however not specific

Differential diagnosis o Gout - negative birefringent monosodium urate crystals; elevated

uric

acid; first attack usually in foot

o OA: may be associated with CPPD; chronic symptoms

o RA : positive serology (Rheumatoid factor, Anti-citrullinatedpeptide

antibody) and elevated acute phase reactants;

morning stiffness;

polyarticular;

symmetric arthritis of wrist, hand or finger joints;

rheumatoid nodules; Symptoms >6 weeks

Septic Arthritis: SF analysis with turbidity, >10,000 PMNs

low glucose and elevated lactic acid;

positive Gram stain and culture

o Trauma

treatment-

o Ice

o Rest

o Joint aspiration

o Intraarticular glucocorticosteroids

o Oral Nsaids

o Cyclooxygenase-2 selective agents

o Colchicine

o Parenteral AdrenocorticotropicHormone

Prognosis

1. Acute attacks self-limited, resolve 7-10 days

2. Progressive joint damage; destructive arthropathy resembling neuropathic(Charcot’s) joints

3. Large joint arthropathy may require joint replacement

II. Basic calcium phosphate hydroxy-

apatite (BCP) crystal associated

arthropathies:

The BCP crystals includes-

hydroxy-apatite,

octacalcium

Phosphate and tricalcium phosphate

Manifestations-Periarthritis / tendonitis

Milwaukee shoulder syndrome (MSS)

Osteoarthritis

Erosive arthritis

Milwaki shoulder syndrome

more common in women

affects a single joint- most often the shoulder, or the knee.

there may be a history of preceding trauma or overuse of the joint.

There are marked degenerative changes

on radiology, with the presence of loose bodies and calcification

BCP crystals is difficult and the diagnosis may

eventually depend upon excluding other causes such as gout or septic arthritis.

THANK YOU

The serum urate concentration may

reduce during an acute attack; a

normal urate concentration at this

point does not rule out a diagnosis of

gout

“Eunuchs do not take gout, nor

become

bald. A women does not take gout

unless her menses be stopped,An

young man does not take gout unless

he indulges in coitus. In gouty

affection, inflammation subsides in 40

days”

hippocrates