This is a review of an article written for the Journal Bone and Joint Surgery in 2018. Hyperuricemia and Gout in Orthopaedics

Gout is a malfunction of the metabolism of uric acid which results in arthritis or the deposit of monosodium urate crystals in the soft tissues, such as tendons, ligaments, joint cartilage and the lining of joints.  These crystalline deposits are known is tophi.  The definition of hyperuricemia is a serum uric acid level over 6.9 mg/dL.  Gout and hyperuricemia have increased in the past several decades to the point where gout is the most common inflammatory arthritis in the United States affecting approximately 8 million Americans.  Only 20% of patients with elevated uric acid levels demonstrate clinical signs of gout.  There are multiple adverse effects of an elevated uric acid including hypertension, coronary artery disease, renal disease, obesity and metabolic syndrome.  Patients with renal impairment may have an inability to normally eliminate uric acid from their system which results in accumulation of uric acid.

As orthopedic surgeons, we become involved in cases where the inflamed joint becomes warm, swollen, red and there may be a concern for an infected joint.  Orthopedic evaluation may be necessary when collections of gout called a tophus cause compression of the nerve or damaged tendon.  Some patients may develop gout after surgery for other causes.  This is likely the result of being dehydrated while waiting for a surgical procedure and being subjected to a lower room temperature while on the operating room table.

Dietary factors that increase the chances of gouty attacks include alcohol, fructose sweetened drinks, meat and seafood.  Gout can also be the result of treatment for other conditions such as tuberculosis, cancer and high blood pressure.  Even patients as early as late adolescence can develop high levels of uric acid in the blood stream and joint fluid.  This can result in deposits of uric acid crystals in the lining of the joint, called the synovium, and the joint cartilage at the end of the bone which covers the surface of the bone within the joint.

Increases in the amount of uric acid in the joint causes these collections of uric acid crystals to be released into the joint fluid.  These crystals then bind to immune cells and may trigger an inflammatory reaction causing sudden increased pain, redness and swelling.

The causes of increased uric acid in the blood stream may be result of overproduction or inability to eliminated from the body or combination of both.  The inability to eliminate uric acid through the kidney is the cause of gout in about 90% of patients.  Overproduction of uric acid is the cause in less than 10% of patients with gout.  Medical conditions resulting in the overproduction of uric acid include chemotherapy treatment for cancer, hemolytic anemia and abnormalities of hemoglobin in the body.  Hemoglobin is contained within every red blood cell to facilitate carrying oxygen to the cells.

Certain medications may also reduce the kidneys ability to eliminate uric acid from the bloodstream including diuretics (water pills), levodopa for parkinsonism, cyclosporine among other medications.  Over-the-counter medications may also precipitate gout attacks including low-dose aspirin, niacin and ascorbic acid (vitamin C).  Conditions that lead to the reduced clearance of uric acid from the bloodstream include chronic kidney disease, high blood pressure, ketosis and lactic acidosis.

Gout is the most common form of inflammatory arthritis affecting approximately 4% of the US adult population.  90% of patients with gout are male with a peak age of initial diagnosis occurring with men in their 40s.  Women may experience gout following menopause.  It is unusual to see a premenopausal woman with gout.

Gout may also be associated with other medical conditions including hypertension, hyperlipidemia, obesity, diabetes, chronic kidney disease and coronary artery disease.  Environmental factors associated with gouty flareups include seafood, alcohol consumption as well as diuretic (water pills) medications.

Many patients present with what is called a “hot joint”.  This is a joint with swelling, redness and warmth and may be presumed to be infected.  Removing some fluid from the joint and performing a microscopic analysis gives the physician the ability to count the number of red and white blood cells and perform microscopic analysis for bacteria and crystals.  Additional lab studies can be performed including a complete blood count (CBC), an erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP) level.  It is possible but uncommon to have a gouty flareup and infected joint simultaneously.

The diagnosis of gouty arthropathy or flareup is confirmed by examining the fluid for the presence of very specific crystals as they appear under the microscope.  The crystals associated with gout seen under the microscope are very characteristic and, when seen, confirm the diagnosis.

It is worth noting that during an acute flareup up to 14% of patients with gout may have a uric acid level which is normal and up to one third of patients may have a uric acid level that is only slightly elevated.

X-rays are always needed in the evaluation of a painful joint condition.  Early in the course of gout, x-rays may be completely normal.  With repeated episodes of gout, the bones may develop erosions next of the joint or cysts within the bone which reflected damage to the cartilage and underlying bone.  An MRI may show fluid in the joint, erosions to the cartilage and bone as well as deposits or crystals within the tendon.  These MRI findings may be interpreted as a tear of the tendon which can be a result of destruction of the tendon from gout crystal deposits.

Gout, as a result of uric acid deposits, is characterized by acute flareups of joint inflammation that can progress to collections of gout crystals, called tophi, associated with erosions of the bone, destruction of joint cartilage, as well as chronic joint pain and loss of joint function.  Patients present complaining of the sudden acute onset of intense joint pain.  The pain typically begins overnight because of the lower body temperature during these hours which result in crystal formation in the joint.  The joint itself may appear to be warm, swollen, red with limited motion.  The painful inflamed joint is usually extremely sensitive even to light touch of the bed sheet.  Any motion of the joint causes extreme pain.  This inflammatory reaction begins in the big toe and up to 50% of cases.  However, both large and small joints of both upper and lower extremities can be affected.  Patients may also report fatigue and fever.

If left untreated, elevated levels of uric acid may result in hypertension, renal failure and other conditions.  Chronic gout may cause deposits of uric acid in the tendons joint and bursa of the body, kidney stones and urate related nerve damage.

Treatment depends on the patient’s specific medical conditions.  For patients with impaired renal function, medications such as febuxostat (Uloric) may be helpful in lowering the uric acid level in the body.  Probenecid is another recommended alternative treatment for gout.  This medication is not recommended in patients with a history of kidney stones.

For the management of acute gouty arthritis, medications which can be used include nonsteroidal anti-inflammatory medications, colchicine, systemic or injected corticosteroids which should be initiated within 24 hours of the onset of symptoms.  Colchicine is an oral medication which can block the inflammatory response caused by the crystals of uric acid in the joint.  However, it is only recommended for attacks that began within 36 hours of evaluation.  Colchicine is typically used for acute attacks whereas allopurinol is used after an attack for long-term treatment to lower uric acid levels.

Finally, steroids may be taken orally or injected into the joint as treatment for acute inflammation.  The major factor determining which of these options is better is based on the number of joints which may be involved in the acute flareup.  Oral prednisone may start that an initial dose of 0.5 mg/kg for 10 days.  Another option is to maintain the full dose for 2-5 days with subsequent tapering of the medication for 7-10 days.  It is common to combine both oral and injected steroids to treat severe pain and acute inflammation.

The treatment of gout is often multidisciplinary including both orthopedic surgery and primary care.  Treatment needs to address the acute attack as well as the causes and medical conditions associated with this condition.

Helping patients understand that dietary and lifestyle recommendations may influence the occurrence of gouty attacks.  Patients with a history of gout should avoid meats in excess as well as sodas and other foods that contain high fructose corn syrup.  Beer, wine and liquor should be limited in patients with gout and alcohol consumption should be avoided during an acute attack.  Patients should also limit eating seafood with high purine content such as sardines and shellfish.

Surgery may be indicated in some patients with gout.  These patients usually have large tophaceous deposits which require debridement or excision from the affected joints.  These deposits may interfere with the motion of tendons in the hand or elsewhere.  Gouty deposits can occur in the tendons of the body including the Achilles tendon and the triceps tendon.  Uric acid crystals can deposit within the tendons causing extensive damage to the tendon resulting in tearing of the tendon and detachment of the tendon from bone.  If these are not treated early on, large tissue defects and functional impairment may result.  Over the long-term, chronic gouty arthritis can destroy the joint.  Final options and treatment may include joint replacement as well as other reconstructive procedures to repair damaged tendons and soft tissues.

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