Setting: emergency department
CC: “My toe hurts real bad!”
VS: BP: 144/94 mm Hg; P: 96 beats/minute; T: 102°F; R: 18 breaths/minute
Pain can cause hypertension and tachycardia.
HPI: A 34-year-old Asian man arrives at the emergency department with the acute onset of severe pain in the great toe of his right foot that developed over a few hours. He had one episode like this before a few months ago but never went to the hospital because of being uninsured at that time. He took an over-the-counter NSAID and it got better in a day or two. Today the pain came on very suddenly, and his toe is clearly red and warm.
PMHx/Medications: none
PE:
General: uncomfortable man, in pain trying to stay immobile
Extremities: Great toe of right foot is warm, red, and extremely tender. Overlying skin is tense (Figure 8-3).
HEENT: no tophi
Skin: no tophi
Tophi = Gout
Figure 8-3. Podagra denotes gouty inflammation of the first metatarsophalangeal (MTP) joint. Note the swelling and erythema. (Reproduced with permission from Kevin J. Knoop, MD, MS.)
Tophi
• Deposits of monosodium urate crystals
• Foreign body reaction
Initial Orders:
Arthrocentesis
Ibuprofen
Basic metabolic panel (CHEM-7)
Uric acid level
Acute gout and septic joints can look very similar.
Men have higher uric acid levels.
Gout is more common in men than in women.
Reports:
Synovial fluid cell count: WBCs 44,000/μL; 80% neutrophils; Gram-stain negative
CHEM-7: blood urea nitrogen (BUN) 21 g/dL (elevated); creatinine 1.8 mg/dL (elevated)
Uric acid level: 7.2 mg/dL (The normal level for men is 2.4–7.4 mg/dL.)
• Uric acid levels are normal in 25% of acute gout attacks.
• Uric acid level decreases from precipitation as crystals in an acute attack.
The cell count is 39,000/μL, predominantly neutrophils, and the uric acid level is normal. What is the appropriate approach for this patient?
a. Treat the gout.
b. Treat the infectious arthritis.
c. Treat both the gout and infectious arthritis.
d. Wait for definitive tests to treat.
e. Give intraarticular antibiotics only.
Answer c. Treat both the gout and infectious arthritis.
The patient’s cell count is in a range equivocal for gout and infectious arthritis, the Gram stain shows no organisms, and the uric acid level is normal.
Infectious arthritis:
• Cell count: usually >50,000 to 100,000/μL
• Stain: 50% to 70% sensitive
• Culture: 90% sensitive, but takes 2 to 3 days
Gout:
• Cell count: 20,000 to 50,000/μL
• Uric acid level: normal in 25% of patients
Gout attacks are extremely painful. When the diagnosis is unclear, it is best to order treatment for both infectious arthritis and gout until the crystal analysis is done. Intraarticular antibiotics are never needed for septic arthritis. All antibiotics will pass into the joint fluid.
Synovial lining has no basement membrane.
All antibiotics pass into the synovial fluid.
Orders:
Crystal analysis by polarized light microscopy
Ceftriaxone and vancomycin IV
Rheumatology evaluation
Intraarticular triamcinolone
Do not use NSAIDs in patients with renal insufficiency.
• Prostaglandins dilate the afferent arteriole.
• NSAIDs cause vasoconstriction of the afferent arteriole.
• NSAIDs cause papillary necrosis.
Report:
Crystal analysis: positive for negatively birefringent needle-shaped crystals
Acute Gout
• Monocytes and synoviocytes ingest uric acid crystals.
• They get inflamed.
The patient continues to have extremely severe pain for the next 4 to 6 hours. As you move the clock forward reexamine the patient and do an “Interval History.” If steroids work, they will do so after about 6 hours, the same as they do in an acute asthma exacerbation. If there is a contraindication to NSAID use such as renal insufficiency or active ulcer disease, use steroids.
Steroids and Acute Gout
• Single joint: inject
• Multiple joints: IV or oral
As the clock moves to 12 to 24 hours after the injection of triamcinolone, there is marked improvement in symptoms. The toe is less red, less warm, and less febrile.
Acute gout causes fever.
When is colchicine the answer for gout?
a. Never
b. As an alternative to NSAIDs for acute gout
c. As first-line preventive therapy
d. As an alternative to xanthine oxidase inhibitors in prevention
Answer d. As an alternative to xanthine oxidase inhibitors in prevention
Colchicine is no longer used to treat acute gout. Acute gout is treated with NSAIDs, and if there is renal insufficiency or ulcer disease, with steroids. Colchicine is an alternative to xanthine oxidase inhibitors such as allopurinol or febuxostat in preventing gout attacks.
Colchicine inhibits microtubule formation.
Orders:
CHEM-7
Uric acid level
Never start allopurinol during an acute gout attack!
In questioning the patient about the food he’s eaten, what is most likely to have caused the acute attack?
a. Milk and cheese
b. Steak and beer
c. Butter and eggs
d. Gluten (wheat)-containing foods
Answer b. Steak and beer
Red meat, beer, and seafood have the highest purine content. Dairy products decrease the risk of gouty attack. Milk, butter, and eggs are low-purine foods.
Vegetables with rapid growth have high purine content:
• Asparagus
• Spinach
• Peas, lentils
Alcohol increases uric acid production.
Report:
CHEM-7: BUN 25 g/dL (elevated); creatinine 2.1 mg/dL (elevated)
Uric acid level: 7.8 mg/dL (The normal level for men is 2.4–7.4 mg/dL.)
What is the mechanism of renal dysfunction in gout?
a. Vasoconstriction of the afferent arteriole
b. Urate crystal deposition in the medulla and pyramids
c. Obstructive renal stones
d. Inhibition of filtration at the glomerulus
e. Excess filtration at the glomerulus
Answer b. Urate crystal deposition in the medulla and pyramids
Renal insufficiency is directly proportional to the height of a person’s uric acid levels. The higher the uric acid level, the more uric acid will deposit in the kidney and form stones. Uric acid has no effect on filtration or on the vasculature.
Drugs That Cause Gout Attacks
• Thiazides
• Niacin
Move the clock forward. Once pain has improved, you can send the patient home and have him come back for an office visit. In several weeks, recheck the uric acid level and start uric acid–lowering medications.
Order:
Allopurinol orally
Uric acid level
Move the clock forward 1 week and recheck uric acid levels. Seeing the patient right after the start of allopurinol is the correct approach because
Allopurinol hypersensitivity (rash, renal failure) is common.
Xanthine oxidase inhibitors can precipitate acute gout attacks.
Colchicine to prevent an attack on starting allopurinol is an acceptable use of colchicine.
If the uric acid level is not controlled on allopurinol, then switch allopurinol to febuxostat. If febuxostat is not controlling the patient, add an uricase medication. Pegloticase metabolizes uric acid to allantoin.
Pegloticase
• It is an uricase.
• It metabolizes uric acid to allantoin.
• Allantoin is easily excreted by the kidneys.
Probenecid
• Increases urinary excretion of uric acid
• Not effective with low urine flow or renal insufficiency
If on moving the case forward, kidney stones are described, the treatment is to alkalinize the urine. Calcium oxalate stones form in an alkaline urine, but uric acid stones dissolve in alkaline urine.
Urine acid solubility increases with urine pH >6.0.