Case Study of diagnosis and treatment of Gout

A 50 year-old male presented for an evaluation of rapid onset of pain and swelling in his right toe. The patient reported that he had two similar previous episodes with the same symptoms lasting four to five days and was treated by emergency physicians.

The patient’s past medical history is significant for hypertension and treated with Hydrochlorothiazide.

The review of systems was negative for headache, fever, chills, rash, earache, sore throat, cough, rhinorrhea, vision changes, weight loss, or change in appetite or disposition. The patient was afebrile, and this blood pressure was slightly elevated.

PHYSICAL EXAMINATION: General: The patient is a pleasant male who appears to be in no apparent distress. Vital Signs: blood pressure 123/48, heart rate 76, Temperature 38.3 and 98% on room air. HEENT: Extraocular muscles are intact. Pupils are equal, round, and reactive to light and accommodation. Neck: Supple. No jugular vein distention noted. No carotid bruits noted. Lungs: Clear to auscultation bilaterally. No wheezes, rubs or rhonchi. Heart: Regular rate and rhythm. Normal S1, S2. A 2/6 to 3/6 systolic ejection murmur at the right upper sternal border. PMI is nondisplaced. Abdomen: Notable for laparoscopy surgical wound. Positive bowel sounds. Extremities: MTP is red, hot and swollen. Neurologic: The patient is alert and oriented x3. No focal neurologic deficits noted.

Pathophysiology

Gout is an inflammatory disease characterized by the deposition of uric acid crystals in and around joints, subcutaneous tissues, and kidneys. Although men and women are equally affected by gout, men are six times more likely to have serum concentrations above 7 mg per dL. Gout typically occurs during middle age and is uncommon before the age 30 years old. Women rarely have gouty arthritis attacks before menopause 1.

Clinical Presentation

Gout attacks are usually associated with precipitated events. Patients usually present with rapid onset of severe pain, swelling, redness, and warmth in one or tow joints. This pain and inflammation are caused by inflammatory response. Acute attack untreated attacks usually last two to 21 days depending on cases. There are four clinical stages of gout according to the National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS). The first stage is known as asymptomatic hyperurecemia. During this stage, the patients can have an elevation of uric acid in the blood but they do not have any symptoms yet. After more and more urate deposits around a joint and if any trauma triggers the release of crystal into the joint space, patients will suffer acute attacks of gout. This second stage is known as acute gouty arthritis. The third stage, known as interval or intercritical gout, involves the interval between acute flare gout attacks with persist crystals in the joints. When crystals deposits continue to accumulate, patients are likely to develop chronically stiff and swollen joints. This stage is called chronic tophceous gout. Some permanent damage to affected joints and sometimes to kidneys can be seen. This advanced stage is relatively uncommon if patients receive proper treatment.

Differential Diagnosis

Gout in the elderly is often polyarticular and involves upper extremity joints (especially proximal interphalangeal joints and distal interphalangeal joints). Women present 70% of the time with polyarticular disease rather than the classic monoarticular arthritis seen in men. Gout can be mistaken for rheumatoid arthritis because tophi may resemble rheumatoid nodules and rheumatoid factors often become weakly positive as people age. It may be difficult to differentiate cellulitis or septic arthritis from gout, particularly when a fever, leukocytosis, redness, or desquamation is present. The term pseudogout, for calcium pyrophosphate deposition disease, belies the difficulty in clinically differentiating it from gout. For definitive diagnosis, joint fluid must be aspirated for culture and a search for urate crystals.

Diagnostic Test

The gold standard diagnostic test for gout is an arthrocentesis. The American College of Rheumatology has established 12 clinical criteria, 6 of which a patient must have for diagnosis.

* 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

Treatment and Management

The gold of treating gout is to minimize or eliminate the urate crystals from the joints and other structures associated with them. Several aspects must be taken into consideration and each treatment regiment is varied from patients to patients. The three main objectives that FNP take into consideration are treatment for the acute attacks, prophylaxis against recurrent attacks, and management of hyperurecemia.

Asymptomatic hyperurecemia: urate-lowering drugs is not recommended to treat patients with asymptomatic hyperurecemia. If hyperurecemia is identified, underlying causes such as obesity, hypercholesterolemia, alcohol consumption, and hypertension should be addressed.

Acute gout: NSAIDs are being used as first-line therapy. Indomethacin (Indocin), ibuprofen (Motrin), naproxen (Naprosyn), sulindac (Clinoril), piroxicam (Feldene) are also effective against gout.

Corticosteroids:

intra-articular, intravenous, intramuscular or oral corticosteroids are effective in acute gout. When one or two joints are involved, intra-articular injection of corticosteroid can be used.

Intramuscular triamcinolone acetonide is as effective as indomethacin in relieving acute gouty arthritis. Triamcinolone acetonide is especially useful in patients with contraindication to NSAIDs.

Oral prednisone: is an option when repeat dosing is anticipate. Prenisone, 0.5 mg per kg on day 1 and tapered by 5 mg each day is effective.

Cochicine is also effective treatment for acute gout. However, majority of patients experience gastrointestinal side effects, including nausea, vomiting, and diarrhea.

Patient Education

If they are obese, they should be advised to begin a concerted program of supervised weight reduction (see Chapter 233), but to avoid starvation or very low calorie diets that may only exacerbate the risk of gout. Drinkers should be warned against binges. Maintenance of good hydration needs to be stressed to those at risk for nephrolithiasis. On the other hand, patients will find it comforting to know that severe dietary restrictions are unnecessary. Fasting should be avoided because it may precipitate an attack. The importance of treating an acute attack at the first sign of illness also needs to be stressed. For the patient with interval gout, a discussion of the risks and benefits of prophylactic therapy and the importance of compliance is indicated. Those taking allopurinol should be warned of the risk of a hypersensitivity reaction and advised to cease intake immediately and call the physician at the first sign of a rash, fever, or other manifestation. Pain management is the primary concern during acute phase of and attack. The patient should be advised to take analgesic medications as schedule. The joint should be rested as much as possible in a position of comfort. Ice, not heat, may help with reducing discomfort.

Conclusion

Gout is one of the most causes of acute monoarticular arthritis. Primary gout runs in families and follows multifactorial inheritance. The expanded use of agents that decrease uric acid excretion has significantly increased the incidence of secondary gout. The Fremingham Study suggested that almost half of new cases were associated with thiazide use.

The FNP should be able to properly diagnose acute gout, treat it, prevent recurrence, and minimize the chances for the development of chronic gouty arthritis. Patients who present with asymptomatic hyperuricemia should be further investigated to prevent complications from this disorder.