QuestionSBA
QuestionChoice
Acute gout presents with a rapid-onset (<24hrs) hot, exquisitely tender, and swollen joint, caused by crystal inflammation from uric acid crystals depositing within the joint. 50% of all attacks and 70% of first attacks present in the first metatarsophalangeal joint. There may also be systemic upset and skin desquamation over the site. Risk factors for gout include male gender, alcohol excess, obesity, renal impairment, diabetes mellitus, and diuretics. Gout may be diagnosed without further investigations in someone with hyperuricaemia and podagra (classic acute arthritis in first metatarsophalangeal joint). If there is any doubt, then the gold standard is joint aspiration synovial fluid analysis. Diagnosis would be confirmed if monosodium urate crystals are seen on synovial fluid analysis - they show strong negative birefringence with needle-like morphology
33213
a
Gout
QuestionChoice
Septic arthritis should always be on your differentials with an acute hot and swollen joint. It is a medical emergency with 10% mortality and the most serious cause of monoarthritis. If not treated urgently, the patient may develop joint damage, functional impairment, and persistent pain. The most usual sites for septic arthritis are the knee in adults and the hip in children. The patient may be pyrexial and generally unwell, although systemic symptoms occur in fewer than 50% of cases of septic arthritis, so a low clinical suspicion is required. It uncommonly presents in the metatarsophalangeal joint (2% of joints). The patient in this question is systemically well with rapid onset of symptoms and inflammation presenting in the 1st metatarsophalangeal joint. The most likely diagnosis is therefore acute gout. In practice if there were any doubt, you would take a joint aspirate and start antibiotics while awaiting the fluid analysis, microscopy, culture, and sensitivity
33214
b
Septic arthritis
QuestionChoice
Charcot can present with a hot, swollen, and erythematous joint. It is caused by neuropathy in the foot, most commonly as a result of poorly-controlled diabetes. The patient loses the protective sensation mechanisms which compensate for microtrauma within the feet which then leads to the destruction of the foot and ankle joints. Charcot feet are often not as painful as septic arthritis or gout, and are often painless. They don't present with raised inflammatory markers and the erythema will decrease with elevation. Septic arthritis often will present with raised inflammatory markers and the erythema will be unchanged on elevation. In this question, Charcot foot would unlikely present solely in the metatarsophalangeal joint and with such acute pain. Given the rest of the examination was unremarkable, it is unlikely that it is the cause of this patient's symptoms
33215
c
Charcot foot
QuestionChoice
Septic arthritis should always be on your differentials with an acute hot and swollen joint. It is a medical emergency with 10% mortality and the most serious cause of monoarthritis. If not treated urgently, the patient may develop joint damage, functional impairment, and persistent pain. The most usual sites for septic arthritis are the knee in adults and the hip in children. The patient may be pyrexial and generally unwell, although systemic symptoms occur in fewer than 50% of cases of septic arthritis, so a low clinical suspicion is required. It uncommonly presents in the metatarsophalangeal joint (2% of joints). The patient in this question is systemically well with rapid onset of symptoms and inflammation presenting in the 1st metatarsophalangeal joint. The most likely diagnosis is therefore acute gout. In practice if there were any doubt, you would take a joint aspirate and start antibiotics while awaiting the fluid analysis, microscopy, culture, and sensitivity
33216
d
Hallux valgus
QuestionChoice
Acute pseudogout presents similarly to gout, but with less severe pain and less commonly in the 1st metatarsophalangeal joint. It most frequently presents in the knees and wrists with an acutely inflamed, warm, erythematous, painful joint. Patients may also be pyrexial with raised inflammatory markers. Diagnosis is often made after joint aspiration showing positively birefringent rhomboid-shaped crystals
33217
e
Acute pseudogout
QuestionComment
Taste not gout?
6186
User
subscriber
Dorsal WBC
QuestionComment
What are the water tablets?
22444
QuestionComment
Likely a thiazide diuretic as they're known to cause gout 
22478
User
subscriber
Caragh
QuestionComment
loop diuretics can also cause gout
37793
User
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Imran
User
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Monoclonal Gas
Concept
Chapter
# Summary

Gout is a type of arthritis caused by the accumulation of monosodium urate crystals in and around the joints. It presents acutely with rapid onset of severe pain, swelling and redness of affected joints, with the first metatarsophalangeal joints the most commonly affected. Chronic untreated gout may lead to tophi which are hard nodules made up of monosodium urate crystals that deposit in soft tissues. Gout may be diagnosed clinically, with supportive investigations including a serum urate and synovial fluid analysis looking for monosodium urate crystals. Management of acute gout is with NSAIDs, colchicine or a short course of oral steroids. Urate-lowering therapy with allopurinol or febuxostat should be considered to reduce the risk of further gout flares. 

# Definition

Gout is a form of arthritis that occurs when monosodium urate crystals deposit in joints. This causes both acute inflammation (gout flares) and in the longer-term, a chronic gouty arthritis with tophi (hard deposits of monosodium urate crystals in soft tissues).

# Epidemiology

- Gout is the most common inflammatory arthritis and prevalence is increasing with time (currently 2.5%)
- Hyperuricaemia (high urate) is the main risk factor (although most patients with a high urate do not develop gout, and some patients develop gout with a normal urate)
- Factors that contribute to this include:
- Older age - typically patients are above the age of 40
- Male sex (post-menopausal women are also at increased risk)
- Comorbidities including chronic kidney disease (CKD), diabetes, osteoarthritis, hypertension
- Excess alcohol consumption
- Dietary excess of meat, seafood and sugary drinks
- Overweight or obesity
- Medications such as thiazide diuretics and ciclosporin
- Family history of hyperuricaemia and gout
- Genetic disorders associated with hyperuricaemia such as Lesch-Nyhan or glycogen storage disorders
- Organ transplant recipients
- Acute attacks may be triggered by stressors including:
- Trauma and surgery
- Intercurrent illness
- Alcohol excess
- Sudden excess of protein in the diet
- Chemotherapy (due to cell breakdown)
- Urate-lowering medications can cause a flare (as crystals are shed into the joint space)

# Signs and Symptoms

Overlapping clinical syndromes are caused by the deposition of monosodium urate crystals in different tissues:

**Acute gout** 

- Commonly presents with a monoarthritis
- Pain is severe and rapid in onset, reaching a peak within 24 hours 
- Affected joints become swollen, erythematous and tender
- The first metatarsophalangeal (MTP) joint is the most commonly affected (70% of first attacks)
- Other common sites include the knees, ankles, midtarsal joints, wrists, elbows and small joints of the hands
- Systemic features such as fever and malaise may be seen
- Patients may be tachycardic due to pain

**Tophaceous gout**

- Patients will usually have a history of longstanding recurrent acute gout
- However in atypical cases patients may present with tophi without previous flares
- Tophi are firm white nodules of sodium monosulphate crystals under the skin
- They commonly occur on extensor surfaces of joints such as knees or elbows, the Achilles tendons, backs of hands and feet and on the helices of the ears
- Usually they are painless however they can become infected, inflamed or ulcerated
- They may discharge white material onto the skin surface
- Chronic gouty arthritis may present with tender and stiff joints with reduced range of motion

# Differential Diagnosis

- **Septic arthritis** must be ruled out in patients who are systemically unwell with an acute monoarthritis - urgent synovial fluid analysis is needed if this is suspected
- **Pseudogout** typically affects the knee and wrists rather than the MTP joint; synovial fluid analysis shows calcium pyrophosphate crystals
- **Cellulitis** causes erythema, pain and swelling of the skin rather than the joint - patients may be systemically unwell
- **Trauma** should be asked about in the history as this may cause similar symptoms of pain, difficulty mobilising and swelling
- **Other inflammatory arthritides** such as rheumatoid arthritis may mimic chronic gouty arthritis

# Investigations

**Bedside tests:**

- **Joint aspiration** is the gold standard diagnostic investigation 
- Needle-shaped monosodium urate crystals with negative birefringence are seen in gout
- Synovial fluid should also be sent for gram stain and culture to rule out septic arthritis
- Tophi can be biopsied to look for these crystals

**Blood tests:**

- **Serum uric acid** should be measured in all patients with suspected gout
- A serum urate of 360 micromol/L or more confirms the diagnosis
- Levels may be falsely low in an acute attack and so should be repeated 2-4 weeks after the flare has resolved
- Levels are used to guide urate-lowering therapy if this is initiated as prophylaxis
- **Screening for risk factors** should be considered:
- Fasting glucose or HbA1c for diabetes
- Renal function and urine albumin:creatinine ratio for CKD
- Lipids for hypercholesterolaemia
- **Inflammatory markers** with FBC and CRP should be checked if septic arthritis is suspected
- **Liver function tests** are needed prior to starting febuxostat
- Patients from Han Chinese, Thai and Korean backgrounds should be screened for **HLA-B5801** prior to starting allopurinol (as this increases the risk of severe cutaneous adverse reactions if present)

**Imaging tests:**

- These may be useful to assess chronic disease or where the diagnosis of acute gout is uncertain
- X-rays in chronic disease show punched-out periarticular erosions, areas of sclerosis and tophi
- Ultrasound may show joint effusions, tophi, synovial thickening and erosions

# Management 

**Acute gout flares** 

There are three first-line options for treatment of a gout flare:

- NSAIDs e.g. naproxen
- Give at maximum dose
- Continue until 1-2 days after resolution of symptoms
- Consider giving with a PPI for gastric protection
- Avoid in heart failure, patients at high risk of gastrointestinal bleeding and severe renal failure
- Colchicine
- Dosing is 500 mcg 2-4 times per day
- Continue until pain resolves
- Dose-dependent side effects include diarrhoea, nausea and vomiting
- Oral corticosteroids
- e.g. prednisolone 30mg once a day for 3-5 days
- Useful in patients with contraindications to both NSAIDs and colchicine
- An injection of intramuscular, intravenous or intra-articular steroids can also be considered
- Alongside this, consider other analgesia (e.g. paracetamol) and other non-pharmacological pain relief such as ice packs
- A combination of the above may be tried if a single agent is ineffective
- Patients should be advised to keep the affected joint cool and exposed and to rest and elevate the affected limb
- Patients already on urate lowering treatment should continue this throughout the acute flare

## Prevention

Patients should be followed up 4-6 weeks after an acute episode of gout to think about preventative strategies and assess for risk factors (also see Investigations). 

Optimisation of risk factors may include:

- Reducing alcohol consumption
- Maintaining a balanced diet and healthy weight
- Investigate and treat for comorbidities such as hypertension or CKD
- Review medications and consider switching medications such as thiazides that cause hyperuricaemia
- Where possible, switch antihypertensive medications to losartan or amlodipine, which have modest urate-lowering effects 
- Initiating urate-lowering therapy (see below)

Most patients can be managed in primary care, however the following should prompt referral to or discussion with specialist services:

- Patients with complications of gout
- Atypical presentations (e.g. aged under 30) or uncertain diagnosis
- Pregnant patients
- Stage 3b to 5 CKD
- Organ transplant recipients
- Those at risk of adverse effects with standard medical treatment, or if treatment is ineffective or not tolerated

Indications for **urate-lowering therapy** include:

- Multiple or troublesome gout flares
- Chronic gouty arthritis or tophi
- Patients taking diuretics
- CKD stage 3 to 5

**Starting and monitoring urate-lowering therapy (ULT):**

- ULT should be started at least 2-4 weeks after an acute flare if possible as medications can precipitate further attacks
- Colchicine should be given whilst starting ULT to reduce the risk of a flare (NSAIDs or steroids are second-line)
- Doses should be uptitrated with monthly monitoring of serum urate levels, aiming for a target of 360 micromol/L
- A target urate level of 300 micromol/L may be helpful in patients with tophi or chronic arthritis due to gout, or those who continue to have flares despite ULT
- First-line options are either allopurinol or febuxostat which are both xanthine oxidase inhibitors (so reduce uric acid production)
- Allopurinol is preferred in patients with significant cardiovascular disease
- Second line options include uricosuric medications (e.g. probenecid) - these can promote stone formation so should be avoided if there is nephrolithiasis

# Complications

- Chronic gouty arthritis and permanent joint damage
- Tophi, which may become inflamed or infected
- Nephrolithiasis due to uric acid precipitation - these are responsible for 8% of renal calculi and are radiolucent
- Chronic urate nephropathy - urate deposition in the renal interstitium causes inflammation and fibrosis
- Both allopurinol and febuxostat can cause rashes, which in rare cases may be severe (e.g. Stevens Johnson syndrome or toxic epidermal necrolysis)
- Increased risk of cardiovascular disease and mortality

# NICE Guidelines

[NICE CKS - Gout](https://cks.nice.org.uk/topics/gout/)

[NICE - Gout: diagnosis and management](https://www.nice.org.uk/guidance/ng219/)

# References

[Patient UK - Gout](https://patient.info/doctor/gout-pro)

[Radiopaedia - Gout](https://radiopaedia.org/articles/gout?lang=gb)
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Acute gout typically presents as sudden, severe pain and swelling in the first metatarsophalangeal joint, triggered by uric acid crystal deposition.
A 73-year-old man presents with 12 hours of worsening right foot pain (10/10 severity) and inability to weight-bear. He has no history of trauma.


He can never remember the names of his medical problems or his regular medications, but states he takes "water tablets" for his "heart problems".


On examination, observations are normal. The left foot and knee are non-tender, non-erythematous, with full range of motion. The right knee is unremarkable. The right foot has a large, tender, warm, erythematous mass on the 1st metatarsophalangeal joint, with the rest of the foot showing full range of motion and intact neurovascular function.

Which of the following is the most likely diagnosis?
a