---
title: Gout Acute Flare Management
description: A clinical reference on the diagnosis and management of acute gout flares.
keywords: [gout, arthritis, flare, uric acid, colchicine, NSAIDs]
category: clinical
---

## Introduction

Gout is a common form of inflammatory arthritis caused by the deposition of monosodium urate (MSU) crystals in the joints and surrounding tissues. Acute gout flares are characterized by a rapid onset of severe joint pain, swelling, erythema, and tenderness, often affecting the first metatarsophalangeal joint (podagra). Prompt recognition and management of acute gout flares is essential to alleviate patient discomfort and prevent long-term joint damage.

## Diagnostic Criteria

The diagnosis of an acute gout flare is based on a combination of clinical presentation and laboratory findings. The 2015 American College of Rheumatology (ACR) and European League Against Rheumatism (EULAR) classification criteria for gout include the following:

1. Presence of MSU crystals in the synovial fluid or tophus
2. Joint/bursa aspiration with negative birefringence under polarized light microscopy
3. Acute onset of a typical acute arthritis episode
4. Erythema, tenderness, or swelling in the first metatarsophalangeal joint
5. Tophus (a deposit of MSU crystals) confirmed by clinical examination or imaging
6. Serum uric acid level > 6.8 mg/dL (404 μmol/L)

The presence of MSU crystals in the synovial fluid is the gold standard for diagnosis, but joint aspiration may not always be feasible, especially during the acute phase. In such cases, a combination of clinical features and laboratory findings can help establish the diagnosis.

## Acute Flare Management

The primary goals of acute gout flare management are to rapidly alleviate symptoms, reduce inflammation, and prevent long-term joint damage. The management approach typically involves a combination of pharmacological and non-pharmacological interventions.

### Pharmacological Interventions

1. Colchicine:
   - Mechanism of action: Inhibits microtubule assembly and neutrophil migration, reducing inflammation.
   - Dosing: Oral colchicine 0.5-1 mg, followed by 0.5 mg every 1-2 hours until symptom relief or maximum dose of 1.2 mg is reached.
   - Contraindications: Severe renal or hepatic impairment, concomitant use of strong CYP3A4 inhibitors.

2. Nonsteroidal Anti-Inflammatory Drugs (NSAIDs):
   - Mechanism of action: Inhibit prostaglandin synthesis, reducing inflammation.
   - Dosing: Oral indomethacin 50-75 mg three times daily or naproxen 500-750 mg twice daily.
   - Contraindications: History of peptic ulcer disease, cardiovascular disease, renal impairment.

3. Glucocorticoids:
   - Mechanism of action: Suppress inflammation by inhibiting the production of inflammatory mediators.
   - Dosing: Oral prednisone 30-40 mg daily or intramuscular triamcinolone acetonide 40 mg.
   - Contraindications: Uncontrolled diabetes, active infection, osteoporosis, peptic ulcer disease.

The choice of pharmacological intervention depends on the patient's comorbidities, contraindications, and previous response to treatment. Combination therapy with colchicine and an NSAID or glucocorticoid may be considered for severe or refractory cases.

### Non-Pharmacological Interventions

1. Joint/limb rest and elevation: Reduce mechanical stress and promote resolution of inflammation.
2. Ice therapy: Apply ice packs to the affected joint for 15-20 minutes several times per day to reduce pain and swelling.
3. Dietary modifications: Limit purine-rich foods (e.g., red meat, seafood, alcohol) to reduce uric acid production.

### Monitoring and Follow-up

During the acute flare management, it is essential to monitor the patient's response to treatment and any potential adverse effects. Clinicians should assess the following parameters:

1. Pain and swelling: Evaluate the severity and progression of joint symptoms using a numeric rating scale or the Gout Assessment Questionnaire.
2. Inflammatory markers: Monitor serum C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) to assess the degree of inflammation.
3. Renal function: Assess serum creatinine and estimated glomerular filtration rate (eGFR) to ensure appropriate medication dosing and to monitor for any renal complications.
4. Adverse effects: Monitor for gastrointestinal, cardiovascular, or musculoskeletal adverse effects related to the medications used.

Patients should be followed up within 2-4 weeks to evaluate the resolution of the acute flare and to initiate long-term urate-lowering therapy, if indicated.

## Prophylaxis and Long-Term Management

After the resolution of the acute flare, it is essential to address the underlying hyperuricemia and prevent future gout attacks. This is typically achieved through the use of urate-lowering therapies, such as xanthine oxidase inhibitors (e.g., allopurinol, febuxostat) or uricosuric agents (e.g., probenecid).

The 2020 American College of Rheumatology (ACR) Guideline for the Management of Gout recommends initiating urate-lowering therapy in patients with:

1. Tophaceous gout
2. Recurrent gout flares (≥2 flares per year)
3. Chronic kidney disease stage 2 or higher (eGFR <90 mL/min/1.73m²)

When initiating urate-lowering therapy, it is important to provide prophylactic treatment with colchicine or low-dose NSAIDs to prevent acute gout flares, which can be triggered by the rapid lowering of uric acid levels.

## Conclusion

Effective management of acute gout flares is essential to alleviate patient discomfort and prevent long-term joint damage. A combination of pharmacological interventions, including colchicine, NSAIDs, and glucocorticoids, along with non-pharmacological measures, can help quickly resolve the acute symptoms. Ongoing monitoring and follow-up, as well as the initiation of long-term urate-lowering therapy, are crucial for preventing future gout attacks and managing the underlying hyperuricemia.