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Gout

With gout, the characteristic joints when we are talking about crystal arthritis, particularly the first MTP is ankle, knee, the dorsum of the foot, the mid-foot. Almost any joint can be involved but certainly the feet are the most commonly involved followed by the ankles and knees. A pertinent point, I think, to remember is sometimes if you are going to aspirate a joint for diagnostics, first MTP are really difficult to get any significant fluid out of. Itís worthwhile to at least take a look at other joints like knees, because most of us here have experienced aspirating knees. If they have fluid in their knees, even if itís not their very hot joint, sometimes you can make your diagnosis from that fluid instead of trying to aspirate this tiny little joint.

Gout is a disease caused by the over-accumulation of uric acid in the body, resulting in deposits in the tissues like the skin and the joints and possibly other tissues. Understand, gout is not just hyperuricemia. There is a big difference. Hyperuricemia does not mean gout. When people have hyperuricemia they have a higher likelihood of having gout, but just because someone has an acute joint and they have a high uric acid does not mean that they have gout. Mostly itís men, particularly starting at younger age. Men typically starting at 30-50 year olds. Iíve seen men as young as 16, 17 have gouty episodes. I donít think Iíve ever seen a woman - Iíve seen one woman, premenopausal - have gout. Itís just very unusual in women, premenopausal. The one case I can think of, she had horrible tophaceous gout but again predominantly you see it in older women, maybe in their 60ís and 70ís.

There are three stages of gout and I think itís important to separate these stages of gout because treatment is different, depending on where we are at. Thereís the acute phase, which is the acute episode, there is what we call inter-critical gout. Itís a period where people are not having an attack, and then they get the more chronic stage of the tophaceous deposits and at this point people can often be having sort of continual attacks. The acute attack is often very abrupt, as we mentioned. You do not treat it. It may last several days, but more typically probably about 10 days. Even untreated. So when someone comes in with a 13th day of this gouty attack and you put them on something, it may be getting better as opposed to your treatment being wonderful. Peak onset is 30-50 years old. The skin may become red. Sometimes even the area over the inflamed tissue can desquamate, so you get this peeling skin on their first MTP or on the dorsum of their foot. They can develop fevers, elevated white counts, the sed rate is often elevated. As time goes by the attacks tend to become more frequent with a shorter period in between. You have a higher likelihood of them becoming polyarticular. Itís interesting that probably 50% of the attacks.

The first attack is classically the first MTP, about 50% of the patients. About 15% of men and about 30% of women have polyarticular attacks in the first episode. Again, I mentioned that the subsequent attacks have an increasing likelihood of being polyarticular; mid-foot, ankle, heel, knee, wrist, fingers, elbows etc. also can be involved. Acute attacks are often precipitated by procedures; surgery, trauma, episodes like a myocardial infarction, or congestive heart failure, a lot of alcohol ingestion, medications such as diuretics, anything that can cause a sudden change in urate concentration.

Many factors can cause acute hyperuricemia if itís not associated with tissue deposition of monosodium urate, it will not lead to gout. So people have to have that total body access of uric acid in order for them to be predisposed to gout.

After people have recovered from this initial gouty attack there is this inter-critical period. Itís a symptom-free period and a study showed that about 62% had a recurrence within one year, and 78% within two years. That brings up an interesting thought. When someone comes into your office and has had their first episode of gout, do they need to be treated long-term? This usually would bring about a discussion with my patients and myself about what their likelihood of recurrent attacks is, how young are they, what are we worried about long term, and we could sort of weigh all these factors together. We will get into it a little later about what makes our decision. Some people have such a horrible experience with it they say, "Do anything to make this not happen again." But again, typically within a couple of years people have started to have recurrent attacks. The time between the attacks becomes briefer. Sometimes it becomes so regular that there is no letting up at all. Thatís when it can be more easily confused with other disorders. When people get into the chronic stage - Iím talking about people having tophaceous deposits - again, there was a study. Someone tried to evaluation how long it took people to develop tophi. They can occur as early as just a couple of years and as long as 42 years later. Five years later, about 30% of people had tophi. About 50% at 10 years and 72% at 20. This again is important when we start talking about long-term treatment.

Risks for tophi: obviously, if you get it earlier you have a lot more years to develop problems and long duration of untreated disease. The bony tophi tend to occur prior to skin deposits. So if you start seeing tophi in the skin, presume itís in the bones. So if you start seeing tophaceous deposits in the skin - and our biggest concern about the tophi is that they can cause joint destruction - presume itís there and that obviously is going to change your thoughts about how soon you need to treat the patient. The most common places in the skin are in the ears - sometimes in people where you donít see it readily, you can actually transilluminate the helix of the ear and see little deposits in there. The olecranon bursa, the prepatellar bursa, are very common. Occasionally you see them at the Achilles tendon, often where the shoe hits the Achilles tendon. The same place where you can see rheumatoid nodules. As the tophi become advanced, patients may not even have that many acute attacks anymore and they just have these huge deposits of tophi that can be quite destructive. This picture of the ear shows the tophaceous deposits. Whatís really nice is if you see this you can stick a little needle in that an pull out the material, and now youíve got your diagnosis and don't have to stick a needle into any other joints. Iíve done that on a number of occasions.

When you are going to evaluate the patient - I talked about the sed rate and white counts could be up - hyperuricemia is usually present during an acute episode, but not necessarily. Therefore, a normal uric acid at the time of the initial evaluation does not rule out gout. Remember, acute gout is a problem with the overload in the body of uric acid and itís not just a serum problem and anything that abruptly increases or decreases uric acid levels can precipitate an attack. Synovial fluid analysis, obviously of prime importance because thatís where you can make your definitive diagnosis by seeing the crystals. The synovial fluid is usually cloudy, yellowish in color, tends to have fairly decreased viscosity, tends to have a high white count - remember, this is a group II fluid which tends to be, the white count typically is 20,000 - 50,000. Occasionally Iíve seen it up to 70,000 or 80,000 in a gouty patient. Remember, if they do have gout it does not necessarily rule out the fact that they joint could also be septic. So just because you see crystals, donít forget to send it off for culture. Again, the diagnosis will be confirmed by seeing the crystals by this nice strongly negatively birefringent needle-shaped crystals. To make the diagnosis real firm you like to see them within the polys. X-rays, you know, early on all you are going to see is swelling because thereís nothing damaging done yet.

Treatment: when you treat gout you have to remember what your goals are. There are two goals. One is, the guy doesnít want to hurt anymore. The second goal is to consider preventing this destructive arthropathy. Now we donít necessarily have to meet both these goals with every individual. Like I said, if the person is 85-years-old Iím not necessarily concerned about preventing the destructive arthropathy. So keep these in mind when you are deciding which treatment you are going to offer this patient. Secondly, remember that your acute treatment is different from chronic treatment. You donít treat acutely with allopurinol. Iíve seen it done plenty of times, but what does that do? It will abruptly lower uric acid levels which will actually exacerbate the attack and people then stop the medicine and say, "This stuff doesnít work." Itís hard enough getting them to take the medication when you are instituting it for chronic management. Acutely you have a lot of different choices. You can treat with NSAIDís. NSAIDís are my first choice in most cases. Almost any NSAID works. People classically have talked about indomethacin but Iíve used Naprosyn with great success, Iíve used Clinoril, Iíve used almost any of the NSAIDís that you can think of.

Colchicine when you treat someone acutely the tablets are 0.6 mg. Thatís one every hour until relief of symptoms or until toxicity. Usually that toxicity is diarrhea. Typically we limit it so a sum number of pills so people donít end up taking 37 pills, 37 hours in a row. I usually tell them four or five tablets. The one downside to colchicine acutely is that it is a real drag when someone has a real hot, swollen, tender, painful foot and you give them diarrhea and they have to hobble to the toilet every five minutes. So colchicine has that one drawback, and if you have ever treated a patient - particularly if they are in the hospital.