Acute gout

In rheumatology, attacks of acute gouty arthritis, which in 70-75% of cases is localized in the first metatarsophalangeal joints of the toes, are defined as acute gout.

The pathology is classified as a disease of the musculoskeletal system and connective tissue (class XIII), ICD 10 code M10.

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Causes of Acute Gout

Considering the pathogenesis of gout, including acute gout, the disease can be classified as a metabolic syndrome. After all, gout, known since ancient times, was not without reason called the "disease of the rich", who ate more meat than less well-off people and suffered from protein metabolism disorders. And the fact that the key causes of acute gout are associated with an increase in the content of uric acid in the blood (a product of protein metabolism) was discovered back in the mid-19th century thanks to the research of the British doctor Alfred Baring Garrod, who discovered this fact in his patients suffering from this disease.

Today, when listing the causes of acute gout, in addition to hyperuricemia and the deposition of uric acid crystals in the joints, tendons and surrounding tissues, doctors most often name:

• diet with high protein (meat) consumption, alcohol abuse;
• urate nephropathy (formation of stones consisting of uric acid salts);
• hyperuricosuria (uric acid diathesis);
• renal failure;
• abdominal obesity and abnormal lipid levels;
• hypertension;
• hemolytic anemia;
• insulin resistance of the body (diabetes mellitus type II);
• polycythemia (increased level of red blood cells in the blood);
• lead poisoning.

And genetic studies confirm the connection between almost 60% of abnormalities in uric acid levels in the blood and the occurrence of acute and chronic gout with mutations in three genes (SLC2A9, SLC22A12 and ABCG2), which are also involved in familial hyperuricemic nephropathy, medullary cystic kidney disease and a number of congenital enzymopathies that disrupt protein metabolism in the body.

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Symptoms of acute gout

Acute gout can affect not only the metatarsophalangeal joints of the big toes, but also other joints (ankles, knees), as well as the fingers and wrists (in rare cases, the elbow joints).

When the first signs of an acute gout attack appear, a person experiences severe burning pain in the joint in the middle of the night (against the background of a physiological decrease in body temperature), the soft tissues surrounding the joint swell (the edema often spreads throughout the foot); the affected area becomes extremely sensitive to touch, and the skin on it turns red and becomes hot. Joint mobility is blocked. In addition, there may be a subfebrile temperature.

These unmistakable symptoms of acute gout appear within 3-10 days, and then subside for a long time. But the pathology does not disappear, but simply does not reveal itself clearly, acquiring a chronic form and spreading to other joints. And from time to time, another acute attack of gout occurs - a gout attack.

Acute pain in gout is explained by the fact that the presence of uric acid crystals in the synovial (intra-articular) fluid causes a protective reaction from the endothelial cells of the synovial membrane (Synovial membrane), which covers the joint capsule from the inside. One of the main functions of this membrane is to protect the joint, and it does so: macrophage cells activate the enzyme cyclooxygenase (COX-2) and the synthesis of anti-inflammatory mediator molecules, prostaglandins, begins. This is how local immune-mediated inflammation is triggered.

Long-term elevated uric acid levels (hyperuricemia) can cause complications in the form of large crystallized deposits of uric acid known as tophi. These do not cause pain in themselves, but their growth causes chronic arthritis due to bone erosion. In some people, acute gout becomes chronic, with constant inflammation and deformation of the joints by the accumulated crystals. Gout can lead to a serious form of bursitis (inflammation of the joint capsule). Excess uric acid can also cause consequences such as the deposition of uric acid crystals in the kidneys, resulting in urate nephropathy.

Diagnosis of acute gout

At first glance, diagnosing acute gout does not cause difficulties: it is enough to examine the joint and listen to the patient’s complaints.

To confirm the diagnosis, the doctor prescribes tests: a general blood test, a biochemical blood test (for the amount of uric acid in the plasma), a urine test (daily), and an analysis of synovial fluid (taken by intra-articular aspiration).

Instrumental diagnostics include X-ray examination of the affected joints, as well as polarization microscopy of the synovial cavity and intra-articular fluid, which helps to identify and visualize crystals of monosodium uric acid or salt deposits. If necessary, doctors conduct an ultrasound examination of the affected joint.

The most important differential diagnosis is to distinguish between acute gout and such joint pathologies as traumatic or septic arthritis, rheumatoid arthritis, pseudopodagra, osteoarthritis, ankylosing spondylitis, calcifying periarthritis, pyrophosphate arthropathy, sarcoidosis.

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Treatment of acute gout

The first question is how to relieve acute pain in gout? Alternating hot and cold compresses on the joint: cold for half a minute, then hot for three minutes, and so on several times.

Among the drugs used to relieve pain and reduce the duration of a gout attack, non-steroidal anti-inflammatory drugs (NSAIDs) are the most effective: Naproxen, Indomethacin, Diclofenac, Aspirin, Ibuprofen, etc.

These medications relieve pain, swelling and inflammation. For example, Naproxen (Naxen, Anaprox, Inaprol, Methoxypropylocin, Artagen and other trade names) is used to relieve an acute attack of gout with an initial dose of 0.8 g, after which it is recommended to take 0.25 g every 8 hours.

Drug treatment of acute gout – to stop gout attacks – includes corticosteroids: orally – Prednisolone in tablets (20-30 mg per day), for injection into the joint – Methylprednisolone (Depo-medrol), Dexamethasone, etc.

It should be borne in mind that surgical treatment is excluded in case of gout attacks. However, in case of acute gout, it is recommended to try folk treatment, among the recipes of which are:

• lubrication of affected joints with an alcohol solution of iodine;
• rubbing sore joints with fly agaric tincture in vodka;
• compresses from a mixture of alcoholic tincture of valerian with triple cologne;
• ointment made from iodized salt and lard or melted laundry soap with turpentine.

But, as you might guess, these drugs cannot provide the guaranteed pain relief that NSAIDs provide.

Herbal treatments – in the form of foot baths with chamomile or sage decoctions, as well as hot compresses from infusions of chickweed, thyme, horseradish leaves or meadowsweet – are also not designed to quickly relieve pain and stop the inflammatory process in the joints.

Homeopathy also uses medicinal plants, offering the following remedies for gout: Colchicum (based on the extract of the crocus Colchicum autumnale), Ledum Pal (based on wild rosemary), Benzoic Acid (benzoic acid), Aconitum (from the poisonous plant aconite), Nux vomica (produced from the seeds of the Strychnos plant, which contains the alkaloid strychnine).

Prevention and prognosis of acute gout

An important part of gout management is prevention, which can help minimize attacks of the disease. This includes combating obesity and reducing the consumption of foods such as meat and seafood, for more information on proper nutrition, see - Diet for Gout and Diet for Gouty Arthritis.

According to Nature Reviews Rheumatology, a low-calorie diet can reduce uric acid levels in obese patients by up to 100 μmol/L, and consuming 1.5 g of vitamin C per day reduces the risk of gout by 45%.

Early diagnosis and treatment aimed at the causes of the disease help prevent joint damage and allow you to live a normal life, so the prognosis is optimistic.

However, without treatment, acute gout will become chronic with destruction of the articular surfaces and deformation of the joints.