The red, hot, swollen joints that signal acute gout attacks are nothing new to most hospitalists. They have appeared on inpatient wards in increasing numbers as gout has nearly doubled in the last 15 years in the general population, said James O’Dell, MD, FACP, president of the American College of Rheumatology.
“While we used to say [incidence] was 1% to 2%, it's at least double that now,” said Dr. O’Dell, who is also chief of rheumatology at the University of Nebraska Medical Center and the Omaha Veterans Administration.
At the root of gout is hyperuricemia, which may lead to the accumulation of monosodium urate crystals in the joints and nearby tissues. Acute attacks occur frequently among inpatients, triggered by blood volume changes with surgery, fluid shifts, medication changes, or other factors. However, patients also may arrive in the emergency department with an acute attack.
Despite its prevalence, gout often is not identified or treated properly. If it were, a lot of pain and expense could be avoided, Dr. O’Dell said.
“We know exactly how to take care of gout in 99% of patients, and if those fairly simple things are followed, 99% of gout patients will do extremely well and not have lots of morbidity, hospitalizations, and costs associated with their gout,” Dr. O’Dell said.
Making the diagnosis
A patient's history can provide the first clues to diagnosing an acute gout attack. He or she may have a personal or family track record of gout and acute attacks in the hospital. The medication history may signal red flags, as well, such as chronic gout therapy that was discontinued on admission. The disease is linked to obesity, metabolic syndrome, diabetes, heart failure, cardiovascular disease, hyperlipidemia, diuretic use, hypertension, and kidney disease, so any of those can be an indicator.
Synovial fluid aspiration is considered the gold standard for diagnosis, experts said. This analysis—which includes culture, crystal analysis and cell count—determines whether the patient has gout, septic arthritis, pseudogout (calcium pyrophosphate deposition), a combination of those or other conditions, thus enabling prompt treatment.
“Ultrasonography and other techniques show promise, but in the vast majority of clinical situations [they] are not appropriate for diagnosis or available at this time,” Dr. O’Dell said.
Serum urate levels are unreliable in making the diagnosis and they should not be used alone for this purpose, according to Brian F. Mandell, MD, PhD, professor and chairman of the department of medicine at the Cleveland Clinic Lerner College of Medicine.
“The serum urate level can be normal or low at the time of an attack, and it is frequently elevated in hospitalized patients for many reasons, but unrelated to whether a patient is experiencing a gout attack,” Dr. Mandell said.
It's important to distinguish between attacks of gout and pseudogout, which can appear similar on clinical examination. Both are marked by hot swollen joints, fever and malaise, and both are more likely to flare after surgery. Gout is more common in the first toe, ankle, or mid-foot, but either condition can appear in a number of joints. While treated the same in the short term, long-term management is different.
Infection is a major concern in the differential of acute gout. “If somebody comes in with a red hot joint, exquisitely painful, and they don't want to move it, the number one thing on your list of concerns should always be septic joint,” Dr. O’Dell said.
Swift diagnosis with aspiration is essential for septic joint, so the patient can begin antibiotic treatment immediately. Staphylococcus aureus is one of the most common causes of septic joints in otherwise healthy patients and destroys joint cartilage very quickly if not treated right away, he added.
Managing an acute flare
A common reason gout is mismanaged is because physicians confuse treatment of an acute attack with management of hyperuricemia.
“The worst thing you can do with a patient with acute gout is try to address the predisposing hyperuricemia—meaning starting the patient on a uric-acid-lowering agent—while he's still having signs of acute inflammation,” said Tim Bongartz, MD, an assistant professor of rheumatology at Mayo Clinic in Rochester, Minn. “This can result in prolongation of the hospitalization, worsening of the flare and a lot of trouble.”
Acute attacks usually are managed with nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine or steroids (oral or intraarticular), depending on the patient's comorbidities and potential medication interactions, he said.
Patients may be able to provide some treatment guidance. “If they have a history of gout in the past and they have been treated with a certain type of treatment, I usually ask what their response was,” said Seoyoung C. Kim, MD, a rheumatologist at Brigham and Women's Hospital in Boston.
Physicians often prescribe oral NSAIDs for gout patients who don't have kidney problems, congestive heart failure, or gastric ulcers; who are not taking anticoagulants; and who do not have other contraindications. Examples include 500 mg of naproxen twice a day or 50 mg of indomethacin three times per day, Dr. O’Dell said.
“If you want more frequent dosing, you can do ibuprofen 600 mg or 800 mg three to four times a day, if they have a pretty good kidney function and are otherwise not contraindicated for NSAIDs,” said Dr. Kim, who also prescribes naproxen sometimes.
Some physicians, including Dr. Bongartz, try to avoid using NSAIDs, however, because of potential kidney side effects.
If a patient has normal kidney function, no biliary disease, and no potential drug interactions, some clinicians use a short course of colchicine, beginning with 1.2 mg and adding 0.6 mg an hour later. In the results of the AGREE trial, published April 2010 in Arthritis & Rheumatism, this regimen provided significant (but not total) pain relief over 24 hours to patients taking the medication very soon after the onset of gout pain. It may not be enough to completely resolve the attack in all patients, however, and increasing the dose can cause diarrhea—a particular problem for patients with lower-extremity joint pain who cannot move quickly, Dr. Mandell noted.
Colchicine also interferes with two important pharmaco-metabolic pathways, Dr. Bongartz said. “Several drugs are excreted through these pathways, and you have a lot of interaction when you're using colchicine,” he said. Cyclosporine, some antibiotics, and antifungal agents can potentially interact with colchicine, he added.
“Either patients are already on these agents in the hospital or there's always a risk that somebody puts them on them and isn't aware of these potential interactions. So colchicine is also something I'm trying to avoid,” Dr. Bongartz said.
If only one joint is affected and infection has been ruled out with a culture, intraarticular injection of steroids may be used when patients are taking a variety of other medications, he said. “Usually within 24 hours the patient does have significant relief,” Dr. Bongartz said.
Dr. Mandell agreed and cautioned that he would be reluctant to inject steroids if a patient was being treated for pneumonia, for example, until he knew the infection hadn't settled in the joint.
If systemic corticosteroids are used, they're most effective at moderate to high doses, with doses depending on the patient's condition. Although the medication can raise blood sugar levels, inpatients can be monitored for this. When administering corticosteroids, it's essential to treat the patient until the attack is completely resolved so it does not return. After complete resolution, Dr. Mandell begins tapering the drug over approximately five days.
“More recently, data and experience are accumulating that antiinterleukin-1 medications can be very effective, very rapidly in treating and resolving acute attacks of gout,” Dr. Mandell said. A medication like anakinra has no side effects in terms of kidney function or heart function, he added. “We do worry about coincident infection, if that's going on, and that would be my main concern,” he said.
For inpatients who have no symptoms of acute gout currently, but mention a history of frequent gout attacks or attacks during past hospitalizations, clinicians may want to prescribe 0.6 mg of colchicine once or twice a day during the hospital stay to prevent an acute attack, Dr. Kim said.
Hospitalists dealing with this condition also may want to consult a rheumatologist, Dr. Bongartz said. “Apart from the very simple big toe flare of gout in the hospitalized patient, I think hospitalists shouldn't be reluctant to involve a rheumatologist in the treatment of these patients—if one is available—just given the complexity of the different agents and the potential mistakes you can make with using these agents the wrong way,” he said.
Arranging for adequate follow-up after gouty flare should be considered part of inpatient treatment, Dr. Bongartz said.
“You're not done by successfully terminating the flare while the patient is in the hospital,” he said. “A lot of work will need to be done once the patient has left.”
For starters, the hospitalist needs to inform the patient's primary care physician about how gout was diagnosed and treated. He or she also needs to ensure that the patient will receive prophylactic uric acid-lowering therapy after leaving the hospital, with the goal of lowering the level to less than 6 mg/dL over a few weeks, Dr. Bongartz said.
“Then usually prophylactic therapy has to be continued for about six months after the patient reaches this goal of below 6 mg/dL, because we have this paradox, a fact of uric acid-lowering therapy, that initially patients will actually be at a high risk of having flares during that uric acid-lowering phase,” he said.
A patient must continue chronic gout therapy (allopurinol or colchicine) if he or she was taking such medication before admission, unless there is an acute medical issue that precludes use of the medication, Dr. Kim said.
Pseudogout is usually treated with chronic antiinflammatory therapy as needed, and possibly colchicine to decrease the frequency of attacks and to treat attacks when they occur. Uric acid-lowering therapy is not effective for pseudogout, Dr. Mandell said.
Patients are important partners in long-term gout management, experts said. They need to understand the difference between an acute attack and treatment of the underlying problem. If they don't understand the treatment process, they often mistakenly wait to take allopurinol until they have an acute attack.
“That's exactly the wrong thing to do,” Dr. O’Dell said. “They need to be taking [allopurinol] on a very chronic basis. [Then] they wouldn't have those flares.”