Makindo Medical Notes.com

Related Subjects: |Rheumatoid arthritis |Systemic Sclerosis (Scleroderma) |RA vs OA |Acute and Chronic Gout |Calcium Pyrophosphate Deposition (Pseudogout) |Hyperuricaemia |Allopurinol |Rasburicase |Lesch-Nyhan syndrome

It is very rare for acute gout to occur in a rheumatoid joint. The recommendation is to continue treatment until 1-2 days after the attack has resolved. Ensure followed up. Admit the person if septic arthritis is suspected. NB. Urate levels may be normal in acute attack.

About

• Deposition of crystals of Monosodium urate monohydrate
• May result long term in renal failure
• In elderly always consider drug causes e.g. Thiazides, Aspirin

Aetiology

• Overproduction of uric acid
• Failure to excrete Urate from Purine metabolism
• In over 90% of patients, urate excretion genetically determined
• Monosodium urate crystals: strongly negative birefringent needle-shaped crystals
• Crystals cause inflammation due to physical irregularity and high negative surface charge
• Typically affects the first metatarsophalangeal joint - "Podagra"
• May be caused by thiazides and low dose Aspirin and Ciclosporin

Effects of Hyperuricaemia

• May be asymptomatic
• Acute gout
• Chronic interval gout with acute attacks superimposed on low-grade inflammation and potential joint damage
• Chronic polyarticular tophaceous gout = joint pain, activity limitation, structural joint damage and frequent flares
• Urate renal stone formation

Epidemiology

• Acute joint pain in older male (M:F 10:1)
• Population seen in 1-2 % mostly male and older women

Podagra of 1st MTP joint most common

Chronic tophaceous gout

Urate crystals

Risks

• Men risk x 5-10 female
• In those age < 30 always consider enzyme defect or renal disease
• Obesity, Alcohol intake, Hypertension, Hyperparathyroidism
• Post chaemotherapy and tissue breakdown
• Lead poisoning (saturnine gout)
• Myeloproliferative disorders, Haemolysis
• Extreme exercise, Lesch-Nyhan syndrome

Causes of Excess Urate

• Reduced excretion of uric acid
  • CKD, Thiazide diuretics, low-dose aspirin
  • Hypertension
  • Lead toxicity
  • Primary hyperparathyroidism
  • Hypothyroidism
  • Increased lactic acid: alcohol, exercise, starvation
  • Glycogen storage disease type 1
• Increased production of uric acid
  • HGPRT deficiency (Lesch–Nyhan syndrome)
  • PPS overactivity
  • Increased turnover of purines
  • Myeloproliferative disorders, e.g. polycythaemia vera
  • Lymphoproliferative disorders, e.g. leukaemia
  • Others, e.g. carcinoma, severe psoriasis

Clinical

• Attacks tend to occur in the early morning with severe localised pain, erythema and swelling which comes on over 4-6 hours.
• Pain is extreme and can be associated with cellulitis like changes and erythema and worst ever pain. lasts 5-14 days and then settles
• Fever, malaise, raised CRP

Complications

• Chronic gout leads to formation of tophi and Urate crystal deposits usually on extensor surfaces of fingers, hands and elbows
• 20% have renal colic due to urate stones in preceding years
• Chronic Tophaceous gout can cause urate nephropathy and CKD if untreated

Investigations

• FBC, U&E (renal impairment) ESR/CRP elevated
• Serum Urate levels: may be elevated or normal in an acute attack but then rise afterwards so repeat in several weeks
• Joint aspiration may be needed to exclude septic arthritis
• Microscopy: Urate crystals are long and needle-shaped, and show a strong light intensity and negative birefringence
• Radiology: erosions, osteoporosis

Management

• Acute Attack
  • Rest and elevate the limb. Avoid trauma to the affected joint. Keep the joint exposed and in a cool environment. Consider the use of an ice pack or bed-cage. Encourage weight loss, exercise, diet, alcohol consumption, and fluid intake. See Lifestyle advice for more information. Pain relief, look for contributing factors e.g. medications. Obese patients should lose weight, alcohol consumption should be reduced and drugs such as thiazides and salicylates should be withdrawn.
  • Exclude a septic arthritis. May need aspiration. However, most presentations are often small joint and classical gout. Ensure review if worsening or not settling.
  • NSAIDS: If renal function normal then consider a course that goes 2 days beyond the symptoms settling e.g. Indomethacin 50 mg QDS or Diclofenac 50 mg BD. Consider PPI. No need to stop Allopurinol or febuxostat during an acute attack. Ensure patient is reviewed. Any NSAID may be used provided no contraindications exist.
  • Colchicine: if NSAIDS not effective or contraindicated. Oral Colchicine 1 mg stat then 0.5 mg BD or TDS until the gout settles if symptoms persist for those who cannot take NSAIDs. It may cause diarrhoea. Ensure patient is reviewed. Seek help if fails to improve or worsens. Colchicine 0.5 mg BD cover may be continued for 3-6 months to prevent breakthrough flares.
  • Steroids: ensure infection excluded e.g. Prednisolone 10-15 mg for 1 week (some say 3-5 days) or less with a taper but can rebound.
• Prevention
  • Avoid dehydration, aim for ideal body weight
  • Reduce alcohol intake, stop diuretics and aspirin
• Indication for Urate lowering drugs
  • Recurrent attacks of acute gout
  • Evidence of bone or joint damage
  • Tophi
  • Renal impairment
  • Nephrolithiasis
• Allopurinol a Xanthine oxidase inhibitor 300 mg OD is commenced to lower urate and reduce attacks. Indications above. May be given with colchicine or NSAID cover. Lower dose Allopurinol in older start at 50-100 mg daily increasing dose after several weeks.
• Febuxostat 80-120 mg OD: non-purine inhibitor of Xanthine oxidase when allopurinol fails.
• Pegloticase, a pegylated recombinant uricase is given IV and lowers urate levels dramatically. It is for severe, refractory gout to control urate levels when other drugs have failed.

References

• The British Society for Rheumatology Guideline for the Management of Gout 2017