Musculoskeletal
This was previously featured in an exam
This was previously featured in an exam
Question 71 of 180
A 53 year old man presents to the Emergency Department complaining of pain and swelling in his knee. He is able to weight bear but is uncomfortable. He has no significant past medical history and denies trauma. On examination you demonstrate an effusion, and the joint is red, hot and tender. He is able to actively flex the knee from 0 to 80 degrees with only mild discomfort. You aspirate the effusion and receive an urgent microscopy result:
- Cloudy synovial fluid
- Few white cells
- Negatively birefringent needle shaped crystals seen
What is the most likely diagnosis?
Answer:
Swollen knees are a very common reason for people to seek medical attention. Septic arthritis needs to be recognised and excluded as soon as possible. Aspiration involves removing some intra-articular synovial fluid from the joint via a needle using an aseptic technique. Samples are then sent for microscopy, culture and crystal analysis. In the absence of significantly raised white cells on haematology and organisms on microscopy or culture, septic arthritis can usually be excluded. A diagnosis of gout can be confirmed by the presence of negatively birefringent, needle-shaped monosodium urate crystals. Weakly positive rhomboid shaped calcium pyrophosphate crystals are found in pseudogout.Gout and Pseudogout
Musculoskeletal
Last Updated: 12th September 2022
Gout is a disorder of purine metabolism characterised by hyperuricaemia and the deposition of urate crystals in joints and other tissues, such as soft connective tissue or the urinary tract.
The natural history of gout can occur in three distinct phases:
- A long period of asymptomatic hyperuricaemia.
- A period during which acute attacks of gouty arthritis are followed by variable intervals (months to years) when there are no symptoms.
- The final period of chronic tophaceous gout, where people have nodules affecting joints.
The most commonly affected joint is the big toe. It is also common in the midfoot, ankle, knee, fingers, wrist and elbow joints although can affect any joint. Gout tends to attack joints in the extremities because temperatures in the feet and hands can be low enough to precipitate urate from plasma. Thus tophi typically form in the helix of the ear, finger tips, olecranon bursae, and other cool anatomical sites.
Risk factors
- Hyperuricaemia is the single most important risk factor for developing gout. Hyperuricaemia is usually due to impaired renal excretion of urate.
- Secondary causes of hyperuricaemia include hypertension, hyperparathyroidism, Down's syndrome, lead nephropathy, sarcoidosis, medication, chronic renal disease, volume depletion, glycogen storage diseases, lymphoproliferative/myeloproliferative disorders, carcinomatosis, polycythaemia and severe psoriasis.
- Other risk factors for gout include age, male gender, menopausal status in women, renal disease, obesity, metabolic syndrome, dyslipidaemia, and use of certain drugs (for example diuretics), trauma, and genetic factors.
Clinical features
- Arthritis
- Swelling, redness, warmth, and pain on passive movement, typically of the first metatarsophalangeal joint, although any joint can be affected.
- Tophi
- Firm, white nodules under translucent skin, usually occurring over extensor joint aspects such as the elbow or knee, or achilles tendon. They can occur in other areas such as the helix of the ears or dorsum of hands or feet.
- It usually takes at least 10 years after the first attack of acute gout for tophi to develop.
- They are usually pain-free but can become inflamed, infected or ulcerated, or discharge white material.
Investigations
- No initial investigations are required when managing people with typical gout-like symptoms if there is no suspicion of other conditions, such as septic arthritis.
- The following tests may be considered as part of ongoing follow-up of people with gout-like symptoms:
- Joint fluid microscopy and culture
- If diagnosis of gout is in doubt, or septic arthritis is suspected.
- Presence of urate crystals (negatively birefringent on polarised microscopy) in synovial fluid or tophi confirms a diagnosis of gout.
- Serum uric acid
- Usually measured 4 – 6 weeks after an acute attack of gout to confirm hyperuricaemia.
- The formation and deposition of monosodium urate crystals occur when urate levels are persistently above 380 micromol/L.
- Hyperuricaemia may be present without gout and gout may be present without hyperuricaemia.
- Joint x-ray
- Plain radiographs are often normal. Non specific soft tissue swelling and subcortical cysts may be present.
Advanced disease may demonstrate bone erosion.
- Plain radiographs are often normal. Non specific soft tissue swelling and subcortical cysts may be present.
- Joint fluid microscopy and culture
- Screen for cardiovascular risk factors and renal disease if a clinical diagnosis of gout is made
Differential diagnosis
- Septic arthritis
- Septic arthritis must be considered in any person who is systemically unwell (with or without a temperature) and an acutely painful, hot, swollen joint. It is important to diagnose septic arthritis promptly, as late recognition can be fatal.
- Bursitis, cellulitis, tenosynovitis
- Non-urate crystal-induced arthropathy, such as pseudogout
- Pseudogout is formally known as calcium pyrophosphate deposition disease or CPPD.
- Osteoarthritis
- Psoriatic arthritis
- Reactive arthritis
- Rheumatoid arthritis
- Haemochromatosis
- Trauma
Management
- Acute attacks
- Acute attacks should be treated as early as possible (as soon as an attack occurs).
- Pharmacological management
- Prescribe either of the following first-line agents, provided that there are no contraindications:
- A nonsteroidal anti-inflammatory drug (NSAIDs) at a maximum dose as early as possible, and continue the treatment until 1-2 days after the attack has resolved. Co-prescribe a proton pump inhibitor (PPI) for gastric protection.
- Oral colchicine.
- Prescribe either of the following first-line agents, provided that there are no contraindications:
- Choice of first-line agent depends on patient preference, renal function and comorbidities.
- Joint aspiration and intra-articular corticosteroids are an option in people with acute monoarticular gout and co-morbidity provided the diagnosis is certain, the person (and joint) are suitable for injecting and the expertise to inject the joint is available.
- A short course of oral corticosteroids or a single intramuscular corticosteroid injection can be considered in people who cannot tolerate NSAIDs or colchicine, and if intra-articular injection is not possible or in oligo-/polyarticular gout.
- Consider paracetamol as an adjunct for pain relief, in addition to other drug treatment, although this is not generally recommended as a primary treatment.
- Do not stop allopurinol or febuxostat during an acute attack of gout if the person is already established on these drugs.
- Self-care advice:
- Rest and elevate limb
- Avoid trauma to affected joint
- Keep the joint exposed and in a cool environment
- Consider the use of an ice pack or bed-cage
- Discuss lifestyle issues such as weight loss, exercise, diet, alcohol consumption, and fluid intake
- Preventing gout attacks
- Urate-lowering therapy (ULT) should be discussed and offered to all people with a diagnosis of gout.
- Start urate-lowering therapy after the acute attack has resolved.
- Allopurinol is the recommended first-line urate-lowering agent. Start at a low dose and titrate upwards (where tolerated) every four weeks until the serum uric acid (SUA) level is below 300 micromol/L.
- Consider febuxostat as an alternative second-line therapy if allopurinol is not tolerated or is contraindicated (for example if renal impairment prevents adequate allopurinol dose increases).
- Consider prescribing colchicine when initiating or increasing the dose of a ULT as prophylaxis against acute attacks secondary to ULT, and continue for up to 6 months. If colchicine cannot be tolerated, consider a low-dose NSAID or coxib with gastroprotection as an alternative provided there are no contraindications.
- Urate-lowering medication is normally lifelong and regular monitoring is needed.
Complications
- Tophi occur in approximately 50% of people with untreated gout after 10 years. Tophi may create problems with activities of daily living, become inflamed, exude tophaceous material, or develop secondary infection, and adversely impact on quality of life.
- Urinary stones are found in around 14% of people with gout.
- Gout is an independent risk factor for chronic kidney disease, myocardial infarction and cardiovascular disease mortality.
- Other comorbidities include hypertension (74%), hyperlipidaemia, osteoarthritis, obesity (53%), diabetes (26%), congestive heart failure (11%) and ischaemic heart disease (14%).
Gout vs Pseudogout (calcium pyrophosphate deposition disease)
- Pathology
- Gout and pseudogout, while both joint problems caused by crystals, are caused by different kinds of crystals. Gout is caused by sodium urate crystals and pseudogout is caused by calcium pyrophosphate crystals.
- Gout attacks can sometimes be caused by eating lots of red meat, particularly organ meats that are high in purines or drinking certain types of alcohol, such as beer and distilled liquor. Pseudogout is not related to diet.
- Clinically
- Gout is most common in middle-aged men and usually starts in the large toe. This is called podagra. The knee is the most common place for pseudogout to start. Pseudogout tends to occur more evenly in men and women and usually occurs in older people.
- Investigations
- Gout and pseudogout crystals can be seen with the microscope and they look different when viewed in a special polarized light under a microscope. Gout crystals are shaped like a needle and are negatively birefringent. Pseudogout crystals are rhomboid shaped and positively birefringent.
- X-rays can also be helpful as they show different changes. Gout eats away at the bones and joints of the hand and wrist. There may be many small cystic erosions in the bones at the joint surfaces. Pseudogout may be seen on x-ray due to the calcium crystals depositing in the soft tissues around the joints.
- Blood levels of urate are often elevated in gout but are normal in pseudogout.
- Management
- Acute attacks of both may be treated with NSAIDs, colchicine and corticosteroids. However, dietary changes and uric-acid lowering drugs can help prevent attacks of gout but not pseudogout.
Report A Problem
Is there something wrong with this question? Let us know and we’ll fix it as soon as possible.
Loading Form...
- Biochemistry
- Blood Gases
- Haematology
| Biochemistry | Normal Value |
|---|---|
| Sodium | 135 – 145 mmol/l |
| Potassium | 3.0 – 4.5 mmol/l |
| Urea | 2.5 – 7.5 mmol/l |
| Glucose | 3.5 – 5.0 mmol/l |
| Creatinine | 35 – 135 μmol/l |
| Alanine Aminotransferase (ALT) | 5 – 35 U/l |
| Gamma-glutamyl Transferase (GGT) | < 65 U/l |
| Alkaline Phosphatase (ALP) | 30 – 135 U/l |
| Aspartate Aminotransferase (AST) | < 40 U/l |
| Total Protein | 60 – 80 g/l |
| Albumin | 35 – 50 g/l |
| Globulin | 2.4 – 3.5 g/dl |
| Amylase | < 70 U/l |
| Total Bilirubin | 3 – 17 μmol/l |
| Calcium | 2.1 – 2.5 mmol/l |
| Chloride | 95 – 105 mmol/l |
| Phosphate | 0.8 – 1.4 mmol/l |
| Haematology | Normal Value |
|---|---|
| Haemoglobin | 11.5 – 16.6 g/dl |
| White Blood Cells | 4.0 – 11.0 x 109/l |
| Platelets | 150 – 450 x 109/l |
| MCV | 80 – 96 fl |
| MCHC | 32 – 36 g/dl |
| Neutrophils | 2.0 – 7.5 x 109/l |
| Lymphocytes | 1.5 – 4.0 x 109/l |
| Monocytes | 0.3 – 1.0 x 109/l |
| Eosinophils | 0.1 – 0.5 x 109/l |
| Basophils | < 0.2 x 109/l |
| Reticulocytes | < 2% |
| Haematocrit | 0.35 – 0.49 |
| Red Cell Distribution Width | 11 – 15% |
| Blood Gases | Normal Value |
|---|---|
| pH | 7.35 – 7.45 |
| pO2 | 11 – 14 kPa |
| pCO2 | 4.5 – 6.0 kPa |
| Base Excess | -2 – +2 mmol/l |
| Bicarbonate | 24 – 30 mmol/l |
| Lactate | < 2 mmol/l |
