Download An Acute Case of Gout

An Acute Case of Gout
Janina Cervera, R2
1/2/2006
Case
Mr. V is an 81 year old Cambodian gentleman admitted from the Harborview ER
one evening, with a diagnosis of debilitating left foot cellulitis. No interpreter is
available to assist in interviewing the patient. The excellent intern notes in his chart
review that the patient’s PMH is positive for gout, in addition to onychomycosis, high
blood pressure, hyperlipidemia and COPD. He’s not certain what information led to a
diagnosis of gout. Patient medications include aspirin, amlodipine, losartan, lipid and
COPD meds, including prednisone 5 mg PO Qday. Upon admit he is febrile to 38.2, his
left foot is erythematous, swollen and warm from the ankle to the toes, with tenderness at
the great toe MTP. Active flexion is limited at the MTP due to pain. Admit labs show a
WBC of 13, creatinine of 2.8 (previously 1.4). Pointing toward onychomycosis as a
portal of entry for cellulitis, the ED physicians write for Ancef 1 g in the ED prior to
transfer to the floor. After your intern has evaluated the patient, he approaches you with
doubts about the diagnosis of cellulitis in this patient, wondering if this could be acute
gout instead.
This is not an uncommon case on the medicine wards, and one that prompts
several questions. How can you determine whether this is cellulitis or gout? Which of
his other medical problems and medications contribute to gout? How do his lab values
affect his acute treatment? Upon discharge from the hospital, should you consider
prophylactic treatment?
Diagnosis
You and your intern discuss how gout and cellultitis can be differentiated. You’ll
ask the interpreter to question Mr. V about predisposing factors for a gout flare-local
trauma, eating a protein rich meal, drinking beer or spirits. Description of rapid
progression to maximal symptoms over just a few hours would point toward gout as well,
as would the history of previous, similar attacks. His hypertension hyperlipidemia are
often associated with gout, as are obesity, diabetes and atherosclerosis. On physical
exam, you note that Mr. V’s MTP is red, hot and swollen, but so is the rest of his foot.
Although 80% of initial gout flares are monoarticular, especially involving the MTP
(podagra) or knee, often signs of inflammation spread beyond the primary affected joint
toward neighboring joints, which can mimic the presentation of cellulitis. Also, flares
later in the course of gout can be polyarticular, which may be the case of Mr. V (1). The
pt’s fever and elevated WBC can be present in both an infectious process like cellulitis
and an inflammatory process like gout. This is becoming a bit confusing and you begin
to wonder if gout can be diagnosed by history and exam alone, if labs or XRays are
needed. The American College of Rheumatology has established 12 clinical criteria, 6 of
which a patient must have for diagnosis. However this method is to be used only after an
attempt has been made to establish the diagnosis by the gold standard, arthrocentesis.
The ACOR criteria are as follows:
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Maximum joint inflammation within 1 day
More than one attack over time
Monoarticular arthritis (although gout can be polyarticular)
Redness of joint
Great metatarsophalangeal pain or swelling
Unilateral great metatarsophalangeal involvement
Unilateral tarsal involvement
Suspected tophus
Hyperuricemia
Asymmetrical swelling within the joint on x-ray
Subcortical cysts without erosion on x-ray
Joint fluid culture negative for organisms during attack
What is the evidence behind these criteria? Six or more of these symptoms/signs were
present in 88% of patients with acute primary gout, 3% of those with septic arthritis or
rheumatoid arthritis, and 11% of those with pseudogout (2). Considering the usefulness
of serum uric acid alone, a level above 7 has a sensitivity of only 55%, and a specificity
of 93% (3). Plain films of affected joints are suggestive of gout; findings to look for
include bony erosions with overhanging osteophytes, calcification within a suspected
tophus, subcortical cysts, and focal joint-space narrowing (4). What is the evidence
behind joint aspiration? The sensitivity in showing crystals in PMNs is 85%, and the
specificity for gout is 100% (2).
So it seems you’ll need to perform arthrocentesis of his great MTP. To do this
you’ll of course need to get informed consent. Taking time to identify the patient’s
anatomy is important. The needle will be entering the joint space between the distal
metatarsal head and the proximal phalanx, from a medial approach, with traction applied
and the toe flexed 15 to 20 degrees to open up the joint space. In this patient’s case there
was some concern for infection with cellulitis, and the needle should not enter the joint
space through any obvious areas of infection. The area should be cleaned with povidone
iodine and allowed to dry. Sterile gloves may be used, as well as a sterile drape.
Although anesthesia may be obtained with a small gauge needle and a small amount of
1% lidocaine, often it is preferred to enter such an inflamed joint only once, to obtain
fluid. A 22 g needle should be used to enter the space, with at least a 3 cc syringe.
Aspirate fluid should be sent for polarized microscopy, WBC count, Gram stain and
culture. If analyzing the fluid through the polarized microscope yourself, crystals will
appear needle shaped; yellow when parallel to the axis of the polarizer, blue when
perpendicular to the axis. They may be intra- or extra-cellular. The aspirate WBC count
should be about 20,000/uL, greater than 50% PMNs (5). Your arthrocentesis is
successful, and these findings are confirmed in the aspirate from your patient’s great toe
MTP.
Joint space should be entered between the distal metatarsal head and the proximal phalanx, from a medial approach.
Roberts: Clinical Procedures in Emergency Medicine, 4 th Edition, Copyright 2004, Saunders
Treatment of Acute Gout
Acute gout flares will often resolve spontaneously within days to a few weeks.
To speed recovery, several drugs may be used, including NSAIDS, colchicine, systemic
and local steroids. Despite a lack of randomized, placebo controlled trials, NSAIDs are
first line treatment. Several NSAIDs have been compared to one another, including
etodolac, naproxen, flurbiprofen and ketoprofen in randomized contolled trials, with little
differences in efficacy. ASA and other salicylates at low doses (less than 3 g per day),
can cause uric acid retention; Mr. V is on low dose ASA. Indomethacin is a potent
NSAID that has been traditionally used, starting at 50 mg PO TID, tapered by half when
relief is noted, and tapered off completely within 7-10 days. If NSAIDs are
contraindicated due to renal insufficiency (as in Mr. V’s case), PUD, or drug allergy, an
alternative is colchicine, however it has several side effects than can limit its use. In a
1987 study comparing colchicine to placebo in acute gout, 2/3 of patients given
colchicine received relief within 2 days, compared with 1/3 of a placebo group.
However, they developed vomiting and/or diarrhea within the first day (6). The dose is
0.6 mg PO per hour until relief, until 10 doses, or GI side effects limit further dosage. If
a gout flare is limited to 1-2 joints, intra-articular steroids are an option. If all three of
the above are contraindicated, systemic steroids may be considered. Doses are typically
up to 50 mg PO Qday for 3 days, tapered off over 7 to 10 days. Because your patient has
renal failure and his flare seems to involve several of the joints of his foot, systemic
steroids will likely be the treatment of choice.
Treatment of Chronic Gout
It doesn’t appear that Mr. V is on prophylactic therapy. If he has 3 or more attacks
per year, clinical or radiographic joint changes, tophi, or chronic renal insufficiency, you
may need to consider chronic therapy (7). Lifestyle changes include diet modificationlow purine diet, weight loss if obesity is an issue, decrease in alcohol intake (including
beer and spirits). Certain medications such as thiazide and loop diuretics inhibit renal
excretion of uric acid, and niacin and low doses of aspirin (< 3 g daily) increase
hyperuricemia. In our patient’s case, ASA is included in his regimen. Colchicine can be
useful in situations such as this, when medications like diuretics or ASA need to be
continued in patients with gout. It can also be used when allopurinol or uricosurics are
initiated to prevent flares that can occur with changes in UA levels. It may be started at
0.6 mg PO either Qday or BID, Qday for patients with renal insufficiency or heart failure
(the higher dose can precipitate peripheral neuromyopathy). Another consideration is
that of uric acid lowering drugs, indicated when colchicine prophylaxis is not effective,
tophaceous deposits are present, or there is gout related renal damage. These meds
should achieve a UA level below 6 mg/dL. Results of a 24 hour urine UA level
determine which drug to use. UA level less than 800 mg/d is consistent with
undersecretion of uric acid, and indicates uricosuric agents (such as Probenecid) if renal
function is preserved. A value greater than 800 mg indicates overproduction, these
patients will require allopurinol. Uricosurics include Probenecid and sulfinpyrazone;
both block the tubular reabsorption of filtered urate. Contraindications include creatinine
of more than 2 mg/dL. Probenecid may be started at 0.5 g Qday, titrated to 2 g daily.
Sulfinpyrazone may be started at 50-100 mg BID, titrated to 200-400 mg BID. With
either drug, adequate fluid intake to maintain daily urine output of 2 liters is important to
avoid precipitation of uric acid in the urinary tract. Allopurinol is a xanthine oxidase
inhibitor that also lowers plasma urate, indicated in UA overproduction, tophaceous gout,
in patients unresponsive to the uricosuric regimen, and in patients with uric acid
nephrolithiasis. It should be used in low doses in patients with renal insufficiency. The
most frequent adverse effect is the precipitation of an acute gouty attack. The starting
dose of allopurinol 100 mg per day is given for 1 week; the dose is titrated to 300 mg if
the serum uric acid is still high. Allopurinol interacts with other drugs, including
Probenecid. Patients taking both drugs may need to use slightly higher than usual doses
of allopurinol and lower doses of probenecid (8). In speaking with Mr. V, you discover
that this is his third similar episode this year. After his acute flare is controlled, Mr. V
will undergo a 24 hour urine uric acid measurement, and begin a prophylactic therapy
based on these results, as well as lifestyle modification.
References
1. Becker, Michael. “Clinical Manifestations and Diagnosis of Gout.” Up to Date
Online
2. Wallace SL, Robinson H, Masi AT, Decker JL, McCarty DJ, Yu TF. Preliminary
criteria for the classification of the acute arthritis of primary gout. Arthritis
Rheum. 1977;20:895-900.
3. Rigby AS, Wood PH. Serum uric acid levels and gout: what does this herald for
the population? Clin Exp Rheumatol. 1994;12:395-400.
4. Teal et al. “Gout.” ACP-PIER Online
5. Roberts: Clinical Procedures in Emergency Medicine, 4th Edition, Copyright
2004, Saunders)
6. Ahern, MJ, Reid, C, Gordon, TP, et al. Does colchicine work? The results of the
first controlled study in acute gout. Aust N Z J Med 1987; 17:301.
7. Becker, Michael. “Treatment and Prevention of Recurrent Gout.” Up To Date
Online
8. Hellman, et al. “Arthritis and Musculoskeletal Disorders.” Current Medical
Diagnosis and Treatment, 45th Edition, Online