Also called gouty arthritis, gout is a painful form of arthritis caused by too much uric acid in the body. Painful outbreaks can be concentrated on the big toe, as well as swelling and pain in the ankles, knees, feet, wrists, or elbows. Left untreated, gout can cause permanent damage to the joints and kidneys. Gout is most often seen in men, especially those between the ages of 40 and 50. This is a widespread disease. In this article, we will consider how to treat gout during an exacerbation.

How to treat gout during an exacerbation

The goal of treating outbreaks of gouty arthritis is to quickly and safely reduce pain, inflammation, and disability. The decision about which medicine to use is based on several factors, including the risk of bleeding, kidney health, and past history of ulcers in the stomach or small intestine. Anti-inflammatory drugs are the best treatment for acute gout attacks and start best at the start of an attack.

People with a history of gout should keep their medications on hand to treat the attack because early treatment is an important factor in determining how long it takes to reduce the pain, severity, and duration of the attack.

Nonsteroidal anti-inflammatory drugs (NSAIDs) work to reduce joint swelling, such as ibuprofen, naproxen, indomethacin. Among NSAIDs, naproxen is considered one of the safer drugs for cardiovascular side effects and has documented effectiveness in acute gout. NSAIDs are generally recommended for people who have no history of kidney or liver disease. And who do not have bleeding problems, do not use anticoagulant drugs such as warfarin, and who have no history of stomach ulcers or duodenal ulcers. They are most effective in treating an attack of gout.

Although aspirin is an NSAID, it is usually not recommended for the treatment of gout because it can, depending on the dose used, increase or decrease the level of urate in the blood.

Colchicine – Colchicine may be prescribed instead of NSAIDs. Colchicine does not increase the risk of ulcers, does not know the interaction with anticoagulants and does not affect kidney function in the proper doses. However, colchicine can have unpleasant side effects, including diarrhea, nausea, vomiting, and stomach cramps. It has been shown that lower doses of colchicine than previously used were just as effective in acute gout as the higher doses recommended in the past and the side effects of the gastrointestinal tract were much less problematic. Colchicine appears to be most effective in the first symptoms of an acute attack. It should be taken only as a pill. Doses should be reduced in people with impaired renal function. Intravenous colchicine should be avoided due to potentially serious side effects.

Corticosteroids. Anti-inflammatory steroids, also better known as glucocorticoids, are effective in treating acute gout attacks. Commonly used oral corticosteroids include prednisone, prednisolone, and methylprednisolone.

Corticosteroids may be used if NSAIDs and colchicine cannot be used. They can be injected directly into the affected joint (called intra-articular injection), or they can be prescribed as tablets or by intramuscular injection. People who have multiple affected joints or cannot take NSAIDs or colchicine can be given oral steroids. There may be an increased risk of a re-attack of gout in people taking oral corticosteroids in severe attacks, where the dose is reduced too quickly. For this reason, the dose of corticosteroids should be slowly reduced over a period of 10 to 14 days.

Long-term urate-lowering therapy

Therapy to prevent the progression of gout may include medications and lifestyle changes that can be used in the long run to reduce urate levels and thus prevent or reverse urate crystals that cause gout deterioration. Progressive gout can cause severe gouty arthropathy, disability, kidney stones, and possibly kidney damage. People who have one or more complications are especially encouraged to use methods of treating gout during an exacerbation of urate reduction.

Medications – lowering the level of (hyperuricemic drugs) drugs reduce the level of urate in one of three ways: they increase the removal of uric acid by the kidneys, reduce the production of urate, or turn urate into a more easily excreted allantoin. Drug therapy, as a rule, begins after the elimination of gout. People who regularly take medications and maintain urate levels below the target range of 6 mg/dl for several months to several years will end up with fewer attacks. It is currently recommended that preventive therapy be continued indefinitely since there is no benefit in stopping the medication.

What are the causes of gout

Uric acid is a waste product generated during the normal breakdown of purines, naturally occurring substances found in foods such as liver, mushrooms, anchovies, mackerel, dried beans, etc.

uric acid is usually excreted from the blood by the kidneys and leaves the body with urine. However, high levels of uric acid can build up in the body, either when the kidneys release too little uric acid or when the body produces too much uric acid. This condition is known as hyperuricemia.

A high concentration of uric acid in the blood will eventually turn the acid into urate crystals, which can then accumulate around joints and soft tissues. Deposits of needle-shaped urate crystals are responsible for inflammation and painful symptoms in gout.

There are several factors that can make a person more susceptible to gout:

  • Close relatives had cases of the disease.
  • Overweight.
  • Kidney problems.
  • Exposure to lead.
  • Drinking plenty of alcohol.
  • Taking certain medications like diuretics.

What are the symptoms of gout

Common symptoms of gout:

  • Severe joint pain, most pronounced in the first 12-24 hours.
  • Joint pain that lasts from a few days to several weeks and covers more and more joints over time.
  • Redness, soreness, and swelling of the joints.

The first attack of gout often occurs on the thumb. Historically, it was called Gout and was considered the “king of the diseases and diseases of the kings.” The onset is usually rapid, with the development of pain, redness, swelling, and soreness of the affected joint, often within a matter of hours. Sometimes an initiating factor can be identified, such as a recent binge with alcohol or purine foods, local trauma, or the start of certain medications. How to treat gout during an exacerbation – without treatment, gout usually settles within seven to ten days.

As uric acid levels continue to increase, attacks become more frequent, with each attack lasting longer and more joints involved.

In the end, uric acid crystals accumulate in large visible nodes under the skin called tofi, in addition to their presence inside the joints. The ignition caused by the accumulation of these crystals ultimately causes erosion of the affected bones. This leads to permanent deformation of the joints, and sometimes to rupture of the skin covering the tofu (which then risks becoming infected).

Gout and pseudogout

Gout and pseudogout are very similar to each other, but each of them has different characteristics. The amount of pain experienced by a patient with pseudogout is usually less than that of a patient with gout. The main difference between gout and pseudogout is the types of crystals that are deposited in the joints and cause inflammation. Monosodium salt crystals cause gout, while pseudogout causes calcium pyrophosphate crystals.

Testing and diagnostics.

Although gout has painful and distinctive symptoms during outbreaks, its symptoms may be vague at other times. The doctor can remove a sample of fluid from the joint so that it can be examined under a microscope for the presence of urate crystals.

Some joint infections can cause gout-like symptoms. If there is a suspicion of infection, the doctor can check the fluid from the joint for bacteria, see above for how to treat gout during an exacerbation.

Categories: Gout


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