Acute gouty arthritis

Last revised by Assoc Prof Craig Hacking on 18 Aug 2021

Acute gouty arthritis, also known as a gout flare, is the acute symptomatic phase of gout due to the deposition of monosodium urate crystals in a synovial joint.

Acute gouty arthritis presents as a tender, erythematous, swollen joint. Involvement is typically monoarticular (a single joint). The onset is sudden, most commonly during the night or early morning. The pain reaches peak intensity after 12-24 hours and gradually subsides.

Classical acute gouty arthritis affects the monoarticular large joint of the lower limb: metatarsophalangeal (podagra), knee, ankle, wrist, interphalangeal joints and less commonly hip, shoulder and vertebral column joints. Polyarticular joint involvement is seen in long term untreated gout and as atypical presentation in post-menopausal women.

A diet rich in purine consisting of alcohol and cooked or processed animal and seafood meat increases the risk of acute gouty flares. Whereas purine-rich vegetables such as asparagus and spinach do not increase the risk of gout. Other reported triggers of gout include injury, excessive activities of the joint and dehydration.

Vitamin C intake is a protective factor for acute gouty flares. Vitamin C facilitates renal excretion of uric acid 1.

Acute gouty arthritis occurs due to the deposition of monosodium urate crystal (MSU) within the synovial joint. The synovial fluid is a poor solvent for MSU in crystallization at low temperatures. MSU crystals are phagocytosed by synovial monocytes resulting in lysosomal enzyme and inflammatory cytokine release. Mast cells and neutrophils are recruited in acute gouty arthritis. A combination of inflammatory factors including interleukins (IL-1, IL-6, and IL-8) and platelet and endothelial cell activators increase local vasodilation and vascular permeability and result in the symptomatic presentation of gout 2.

Most radiological findings of gout are due to repeated inflammation and joint degeneration. No radiological features are specific for the initial presentation of acute gouty arthritis. Joint degenerative changes occur in the chronic stages of gout.

Radiographic imaging can be used to assess the severity and monitor the progression of gout and joint involvement.

Ultrasound scans have a diagnostic role in assessing gouty joints. Joint inflammation, synovitis, hypertrophy and bony erosions can be seen on ultrasound scans. Features specific to gout include double contour cartilage line, visualizing urate crystal deposition and tophaceous material.  

The advantages of using ultrasound scans include no patient exposure to ionizing radiation and accessibility to the modality. Due to these benefits, an ultrasound scan can be used to monitor a patient’s response to gout treatment.

CT scans can be used to assess deep intraarticular and intraosseous gouty erosions which may not be detected on ultrasonography. 

Dual-energy CT is increasingly used due to its clinical advantages offered in the detection of gout. Monosodium urate crystal deposits can be detected using Dual-energy CT without the need for invasive joint aspiration. This allows differentiating gout from other arthropathies. Furthermore, multiple articular surfaces can be assessed for gout. However, Dual-energy CT has limited use in early subclinical gout when the amount of monosodium urate crystals are below the detection amount.

The sensitivity of Dual-energy CT in gout is 78-84% and specificity of 93% 3.

Acute flares of gout are usually self-limiting within days to weeks.

Treatment involves symptomatic relief for acute attacks of gout with non-steroidal anti-inflammatory drugs (NSAIDs), steroids, or colchicine.

Long-term management will involve urate-lowering medications such as xanthine oxidase inhibitors, uricosuric drugs, or uricase agents 4.

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