What is an Acute Gouty Arthritis?

March 02 22:39 2019 Print This Article

It is defined as a disorder in which there is an increase in the level of uric acid in the blood. It is also known as the gout. It crystallizes and is deposited in the joint and tendon. It also involves the surrounding tissues also and affects 1 percent of the population of western countries. In this the attacks are recurrent and are acute inflammatory in the nature which can be red, tender, hot and swollen. The treatment is done with the help of NSAIDs and steroids. As the acute attack has subside the levels of uric acid have decreased in the blood. It occurs due to the changes in the life style and the prevention with the help of allopurinal. It was known as the rich man’s disease or the disease of kings.

What are the signs and symptoms of Acute gouty arthritis ?

It includes the attacks which are recurrent and are acute inflammatory in the nature which can be red, tender, hot and swollen. The meta tarsal phalangeal joint is the most common joint affected by this disorder. Around two third of the patient it occurs at the base of big toe. It is also known as the podagra. It involves foot due to the lower temperature. The people with the long standing hyper uricemia can form tophi which are uric acid crystal deposit in the tissues. These are hard and do not cause any pain. It invades the bone and lead to the erosion of bone with arthritis. The increase in the levels of uric acid can form uric acid crystals which deposit in the kidneys and form stones which lead to the urate nephropathy.

What are the causes of Acute gouty arthritis ?

It may occur due to the use of drugs, life style and medical conditions. The main cause of gout is hyper uricemia. Around one tenth of the people with the hyper uricemia develop gout. The 12 percent of the gout is related to the dietary causes which includes the sugar, alcohol, meat and sea food. The gout is not affected by the intake of protein, vegetables and dairy products. The sedentary life style also increases the risk of gout. It may occur as a complication of a metabolic syndrome which is the combination of hyper tension, diabetes, dys lipidemia, truncal obesity and the increased risk of cardio vascular disease. It may also result in the complication of leukemia. It also acts as a co morbidity with the other diseases which include the poly cythaemia, cyto toxics, obesity, diabetes, hyper tension, renal problems and hemolytic anemia. It may also occur due to the renal failure. It may also act as a complication for the solid organ transplants. There are few studies which have established the link between gout and the poisoning of lead. There is a correlation between the levels of lead in the body, urate excretion and gout. The lead sugar was used to sweeten the wine. It is known as the saturnine gout as saturnus is the alchemical term for metallic lead. The attacks of gout are associated with the diuretics and the low doses of the hydro chloro thiazide do not increase the risk of gout.

What is the patho physiology of Acute gouty arthritis ?

It occurs when the crystals of uric acid occur in the form of mono sodium urate. It precipitates in the joint and tendon. It also involves the surrounding tissues. The normal component of the blood serum is uric acid. It is more likely to form crystals when it has a high concentration. The hyper uricemia is 10 times more common than without the clinical gout. Gout can also occur when the serum uric acid is normal or quite low referred as hypo uricemia. The acute attacks of gout occur along with the sudden decrease in the serum uric acid like the usage of drug such as uricosurics, xanthine oxidase inbhitors and total parenteral nutrition. The abrupt formation of crystals can decrease the serum uric acid level. Irrespective of the serum concentration of uric acid the precipitation of uric acid occurs by the low ph of blood known as acidosis. A similar effect is seen in the urine which is contributed by the uric acid nephro lithiasis. The purine metabolism forms a uric acid and in humans it is excreted in the urine. The purines are generated by the body through the breakdown of cells in the normal cellular turnover. It is ingested as a part of normal diet. Two third of the uric acid excretion occurs by kidneys and the rest of it is done by liver.

What is the diagnosis of Acute gouty arthritis ?

The unique diagnosis of the gout is based on the identification of mono sodium urate crystals present in the synovial fluid. Their morphology resembles a needle and has a strong negative birefringence with the polarized light. It is difficult to perform and requires the use of trainer. The common feature of the gout is hyper uricemia and it supports the diagnosis of gout. But it can also occur without the hyper uricemia. It is defined as a plasma urate levels more than 420 umol per litre or 7 mg per Dl in the males and in the females it is 380 umol per litre. The urate is within the normal range up to 66 percent of the cases. If one suspects gout than the serum urate test should be tested after the attack has subsided. The other blood tests are full blood count, electrolytes, renal and thyroid function tests and erythrocytic sedimentation rate referred as ESR. It exclude the other causes of arthritis mostly the septic arthritis and to investigate the under lying cause of the hyper uricemia. The differential diagnosis in the gout is septic arthritis. The diagnosis can be ruled out by the culture and joint aspiration. The gout can be hard to differentiate from the other conditions. It includes the chondro calcinosis. It is a similar disease in which there is a deposition of calcium pyro phosphate and not uric acid. The gouty tophi which are not located in the joint can be misunderstood for the basal cell carcinoma.

What are the preventive strategies of Acute gouty arthritis ?

It includes the changes in the life style and medicine. They can decrease the uric acid levels. The medicines cannot be started until one to two weeks after the acute attack has been resolved as the chances of worsening the attack are more. They are not used until there is a second attack of gout or there are destructive gout changes and occurrence of urate nephro pathy. The medicines have proved to be cost effective and the urate lowering measures must be done to decrease the serum uric acid levels below 360 micro mol per liter. The dietary factors may decrease the chances of gout. One must avoid sea food, meat and take adequate vitamin C. One must prevent alcohol and fructose along with the prevention of obesity. In obese people a low calorie diet is recommended which decreases the uric acid level by 100 umol per litre. The intake of vitamin c 15000 mg may decrease the risk of gout by 45 percent as compared to 250 mg per day. The lower risk of gout is also associated with the coffee. The uric acid production is blocked by the allopurinol and is the most common hypo urecemic agent. The chronic therapy is safe and well tolerated and can be used in people with the renal impairment. It may also lead to the hyper sensitivity in few people. The probenecid is also effective in the treatment of hyper uricemia but is not as effective as allopurinol. There is a non purine inhibitor of xanthine oxidase which is referred as a febuxostat and which can be used as an alternative to the allopurinol. It is as effective as allopurinol. This drug was approved by the FDA in the year 2009 and by the European medical agency in the year 2008. The uric acid excretion has been increased due to the EDTA which is a chelator of lead. Gout can also be secondary to untreat sleep apnea. It occurs via the release of purines which are the byproducts of breakdown of oxygen starved cells. The treatment for apnea can also effect the incidence of attacks of gout.

What is the epidemiology of Acute gouty arthritis ?

It involves around 1 percent of the population of western countries and its prevalence increases with the age. It is quite common among the men above the age of 30 and females above the age of 50. The different populations have different propensities to develop gout and in the America it is twice as common among the afro American population as compared to the European American population. It is also common in the New Zealand and pacific islands. It is rare in Australia. The aborigines have a high concentration of serum uric acid. In the United States and Italy the attacks of gout are more common in the spring season.

What is the history of Acute gouty arthritis ?

The first description on this disorder was written back in the year 2600 BC. The Egyptians noticed it in the first toe. In the 400 BC the Greek physician Hippocrates also wrote on it. In 30 AD A.C Celsus recognized many effects of the features of gout and linked it with urinary solute, late onset in the women, linked with alcohol and avoidance of the diary products. In the 200 AD the roman surgeon Galen called gout as a discharge of the 4 humors of body which are present in the unbalanced amounts in the joints. It was initially used by the Randolphus of Bocking around 1200 AD. The word gout came from the Latin word gutta means a drop. There was a Dutch scientist known as A V Leuwenhoek who described the microscopic appearance of urate crystals in the year 1679. In the year 1848 English physician AB Garrod told about the excess of uric acid in the blood which may cause gout. The tyrannosaurs also suffered from the gout. There were many medicines which were used to treat the disorder but they were not effective. The traditional remedy is the sodium bicarbonate which is known as the baking soda. It worked by lowering the ph levels in the blood. The sodium added may be inappropriate for the some people.

What is the treatment of Acute gouty arthritis ?

The treatment objectives include the management of the symptoms of acute attacks. The attacks must be prevented and the serum uric acid levels must be decreased. The treatment options can be conservative, application of cold, NSAIDs, steroids and colchicines. In the conservative treatment ice is applied for half an hour many times a day which improves the pain. The first line of treatment of gout is provided by the NSAIDs without any noticeable differences between the effectiveness of agents. The improvement occurs within the 4 hours. They are not recommended which have certain health problems. It can be gastro intestinal, heart or related to the kidney. The most commonly used NSAIDs is indomethacin. Due to the side effects and non provably of the benefits it is replaced by the ibuprofen. The proton pump inhibitor can be given to the people who suffer from gastric irritation due to the use of NSAIDs. The gluco corticoids are found to be equally effective in the treatment of gout as NSAIDs. It can be used if the person is contradicted to the use of NSAIDs. The intra articular steroids have been effective in the treatment of gout but the risk of joint infection is always there. An alternative to the use of NSAIDs is also provided by the colchicines. It leads to the problem in the gastro intestinal tract and has caused a decrease in its usage. Its effect on the gastro intestinal tract depends on the dose and the risk can be decreased by the use of smaller doses. It has the ability to react with the other drugs like erythromycin and atorvastatin.

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