Gout and pseudogout Flashcards
What is gout?
Gout can be defined as arthritis due to deposition of monosodium urate (MSU) crystals within joints causing acute inflammation and eventual tissue damage
The duration and magnitude of hyperuricaemia is directly correlated with the likelihood of developing gouty arthritis and developing uric acid kidney stones.
What is the pathophysiology of gout?
Hyperuricaemia is usually due to impaired renal excretion of urate.
About 90% of people with hyperuricaemia are under-excretors of urate and about 10% are over-producers of urate.
What are the risk factors for gout?
Male gender. Meat. Seafood. Marmite. Alcohol (10 or more grams per day). Diuretics. Obesity. Hypertension. Coronary heart disease. Diabetes mellitus. Chronic kidney disease. High triglycerides. Heart failure. Psoriasis. Chemotherapy.
What is the presentation of gout?
The European League Against Rheumatism (EULAR) guidelines for diagnosis suggest that the development of acute pain in a joint which becomes swollen, tender and erythematous and which reaches its crescendo over a 6- to 12-hour period is highly suggestive of crystal arthropathy, although not specifically of gout.
The inflammation reaches its peak within 24 hours, often with fever and malaise.
Some patients may only present with connective tissue tophi
There is florid synovitis and swelling and extreme tenderness with overlying erythema. Untreated, the attack resolves spontaneously over 5-15 days, usually with itching and desquamation of overlying skin.
Atypical attacks can occur with tenosynovitis, bursitis and cellulitis, with mild discomfort without swelling lasting a day or two.
What are the sites often affected with gout?
50% of all attacks and 70% of first attacks affect the first MTP.
Other sites often affected are:
- Knee
- Midtarsal joints
- Wrists
- Ankles
- Small hand joints
- Elbows
What is tophi?
Chronic tophaceous gout - in this condition large crystal deposits produce irregular firm nodules mainly around extensor surfaces of the fingers, hands, forearms, elbows, Achilles tendons and ears.
Typically, tophi are asymmetrical with a chalky appearance beneath the skin. Damage is usually found in the first MTP joints, midfoot, small finger joint and wrist, with restricted movement, crepitus and deformity.
What are the differentials for gout?
Acute attacks- sepsis and other forms of crystal-related synovitis.
Chronic tophaceous- RA, generalised nodal osteoarthritis, xanthomatosis with arthropathy.
What are the investigations for gout?
For typical presentations such as inflammation of the first MTP joint (also known as podagra) with hyperuricaemia, a clinical diagnosis can be made with reasonable accuracy but is not definitive unless the presence of uric acid crystals can be demonstrated.
Demonstration of MSU crystals in synovial fluid or tophi confirms the diagnosis of gout.
Since gout can present atypically, an opportunity should be taken to examine all samples of synovial fluid aspirated from joints for MSU crystals, even if not inflamed at the time.
Gram staining and culture of synovial fluid should be arranged, even if MSU crystals are found, since gout and sepsis can co-exist.
Renal uric acid secretion
Uric acid level
X-rays for diagnosis of chronic gout. USS, CT and MRI may also be useful.
What is the management of gout?
An ice pack may be useful, as may rest. The joint should be elevated and trauma avoided.
Pharmacological therapeutic options include:
-Non-steroidal anti-inflammatory drugs (NSAIDs).
-Colchicine (500 mcg 2-4 times a day- maximum of 6mg per course)
Useful when NSAIDs are poorly tolerated, in patients with heart failure and in those who are on anticoagulants.
-Corticosteroids.
-Other primarily analgesic compounds.
- EULAR guidelines recommend colchicine and/or NSAIDs as the first-line option for acute gout.
- The opportunity should be taken to discuss lifestyle issues such as weight loss, exercise, diet, alcohol consumption and fluid intake.
What is the next line treatment if there is no improvement after 2-3 days of treatment?
If there is no improvement after 2-3 days:
Review the diagnosis (differentials include septic arthritis, non-urate arthropathy, other arthritides and haemochromatosis).
Check medicine compliance.
Increase doses to the maximum.
Canakinumab.
If the patient still fails to improve, consider combining treatments, or seek specialist advice.
What is canakinumab?
Canakinumab is a recombinant monoclonal antibody active as an inhibitor of proinflammatory cytokine IL-1.
It is licensed for use in patients whose condition has not responded adequately to treatment with NSAIDs or colchicine, or who are intolerant of them.
It can be used for the symptomatic treatment of frequent gouty arthritis attacks (at least three in the previous 12 months)
What is the prevention strategy for gout?
Lifestyle changes
Manage risk factors
ULT drugs
Which lifestyle changes are involved in the prevention of gout?
Drink alcohol sensibly
Avoid dehydration
Dietary intervention - reduction of purine-based foods.
-Meat or seafood significantly increases the incidence of gout.
-Highest purine levels are found in heart, herring, sardines and mussels.
-Other foods which are very rich in purines include liver, kidneys, yeast extracts and oatmeal.
-Soya foods are also high in purines but are less likely than meat or seafood to lead to gout.
Weight reduction
Regular exercise
Smoking cessation
When should ULT drugs be offered to patients?
ULT should be discussed and offered to all patients who have a diagnosis of gout. ULT should particularly be advised in patients with the following:
- recurring attacks (>2 attacks in 12 months);
- tophi;
- chronic gouty arthritis;
- joint damage;
- renal impairment (estimated glomerular filtration rate (eGFR) <60 ml/min);
- a history of urolithiasis;
- diuretic therapy use;
- primary gout starting at a young age
Aim of therapy: To maintain a lower the serum uric acid (sUA) < 300 micromoles /L. This is called treat to target. The lower the sUA the more chances of dissolution of tophi.
Which ULT drugs are used in the prevention of gout?
Allopurinol, febuxostat and sulfinpyrazone.
It is important to explain that medication is normally lifelong and regular monitoring is needed.
Advise the person that allopurinol may cause acute attacks of gout just after initiating treatment and for some weeks afterwards. Explain that they should start their anti-inflammatory treatment as soon as possible and not stop their allopurinol during acute attacks.
For long-term control of gout the formation of uric acid from purines may be reduced with the xanthine-oxidase inhibitors allopurinol or febuxostat. Alternatively, uricosuric drugs may be used to increase the excretion of uric acid in the urine. The uricosuric drug sulfinpyrazone may be used to increase the excretion of uric acid in the urine.
Allopurinol should never be started during an acute attack. Wait for 1-2 weeks after the attack resolves.
Co-prescribe colchicine or a low dose NSAID to prevent an attack of gout whilst initiating therapy, and continue until after hyperuricaemia has settled (usually a total of three months).
