History

Fact Explanation
Joint pain Gout is characterized by recurrent attacks of acute inflammatory arthritis. Gout has become more common in recent decades. It affects more commonly in men aged 20 -40 years and in women older than 50 years. Abrupt onset of severe excruciating joint pain most commonly affects the metatarsal-phalangeal joint of the great toe is the classical feature of acute gouty arthritis. The big toe is not the only joint that can be affected by gout symptoms. Pain can appear in many joints, including fingers, wrists, elbows, knees, ankles and feet. Acute attack of gout usually affect one joint. [1,2] Pain comes often overnight, and then reduces in few days. It is so severe that even the weight of a bed sheet or slightest movement can cause pain. Pain may relieve when the foot is hung outside of the bed. there may be a history of more than one acute arthritis attack. [1,2,3]
Restricted movements of the joint Due to severe pain [1]
Joint swelling Due to the inflammation triggered by the monosodium urate crystal deposition in joints. [1,2]
Redness over the joint Due to the inflammation triggered by the monosodium urate crystal deposition in joints. [1,2,3]
Fever Apart from the common symptoms attributed to the inflammation, systemic symptoms such as fever can sometimes occur as a result from a severe form inflammation. Chills and rigors may accompany. [1,2,3]
Skin itching Edema caused by the inflammation stretches the skin leading to some itching over the affected site. [1]
Joint deformity Recurrent acute attacks can cause chronic tophaceous gout. Tophi are hard and painless deposits of monosodium urate crystals in soft tissue that may occur in the helix of the ear, over olecranon processes, and over interphalangeal joints. These tophi cause joint erosion and destruction. [1]
Risk factors and triggering factors Any factor that causes hyperuricemia can increase the risk of gout. Modifiable risk factors include a high-purine diet, alcohol use, obesity, diuretic therapy, red meat and seafood consumption where as consumption of dairy products is said to be protective. [1] Studies show that many patients with gout have the metabolic syndrome, hypertension, diabetes, hyperlipidemia or chronic kidney disease. Common triggers for acute gout are infections, intravenous contrast media, acidosis and rapid fluctuations in serum uric acid concentrations such as with trauma, surgery, psoriasis flare-ups, initiation of chemotherapy, diuretic therapy, and stopping or starting allopurinol.[1,2,4]
Asssociations Long term hyperuricemia results in uric acid crystals in the renal collecting system or urate crystals deposition in the renal medulla, which may lead to nephrolithiasis or urate nephropathy. [1] There is a known observational associations between plasma uric acid and hyperuricaemia with risk of ischaemic heart disease and blood pressure. [5]
References
  1. EGGEBEEN,A.T. Gout: An Update. Am Fam Physician[online], 2007,76,801-8, 811-2. [viewed 14 May 2014] Available from: http://www.aafp.org/afp/2007/0915/p801.html
  2. RIDER T. G., JORDAN K. M.. The modern management of gout. Rheumatology [online] December, 49(1):5-14 [viewed 14 May 2014] Available from: doi:10.1093/rheumatology/kep306
  3. PITTMAN,J.R, M.H. BROSS, Diagnosis and Management of Gout, Am Fam Physician [online] . 1999 Apr, 1,59(7),1799-1806. [viewed 14 May 2014] Available from: http://www.aafp.org/afp/1999/0401/p1799.html
  4. SO ALEXANDER. Gout in the spotlight. Array [online] 2008 December [viewed 14 May 2014] Available from: doi:10.1186/ar2396
  5. PALMER T. M., NORDESTGAARD B. G., BENN M., TYBJAERG-HANSEN A., DAVEY SMITH G., LAWLOR D. A., TIMPSON N. J.. Association of plasma uric acid with ischaemic heart disease and blood pressure: mendelian randomisation analysis of two large cohorts. BMJ [online] December, 347(jul18 1):f4262-f4262 [viewed 15 May 2014] Available from: doi:10.1136/bmj.f4262

Examination

Fact Explanation
Joint tenderness Tenderness occurs over the affected joint, classically over metatarsal-phalangeal joint of the great toe. The pain threshold is very low that even the weight of a bed sheet or slightest movement can be tender. [1,2,3]
Redness over the joint Due to the inflammatory reaction. [1]
Extra articular manifestation Occasionally, polyarticular tophaceous gout presents as subcutaneous nodules that can mimic rheumatoid arthritis. These nodules are formed from monosodium urate crystal deposition as a result of recurrent gouty arthritis attacks. [1,2,3] Extra articular tophi are most commonly found in bursae (the most common site is olecranon processes). Other sites are helix of the ear and over interphalangeal joints. [1]
References
  1. EGGEBEEN,A.T. Gout: An Update. Am Fam Physician[online], 2007,76,801-8, 811-2. [viewed 14 May 2014] Available from: http://www.aafp.org/afp/2007/0915/p801.html
  2. RIDER T. G., JORDAN K. M.. The modern management of gout. Rheumatology [online] December, 49(1):5-14 [viewed 14 May 2014] Available from: doi:10.1093/rheumatology/kep306
  3. PITTMAN,J.R, M.H. BROSS, Diagnosis and Management of Gout, Am Fam Physician [online] . 1999 Apr, 1,59(7),1799-1806. [viewed 14 May 2014] Available from: http://www.aafp.org/afp/1999/0401/p1799.html

Differential Diagnoses

Fact Explanation
Septic arthritis Septic arthritis has a classical triad of symptoms, namely low grade fever, pain and impaired range of motion. It presents as a monoarthritis. The symptoms may evolve over a few days to weeks. [1]
Pseudogout (Chondrocalcinosis) This is caused by deposition of calcium pyrophosphate dihydrate crystals in the connective tissues. The knee joint is the most commonly affected. Chondrocalcinosis is more common in older adults. It can present as an acute or chronic inflammatory arthritis that causes pain in one or more joints. [2]
Rheumatoid arthritis. Chronic symmetrical inflammatory polyarthritis affecting small and large joints including hand, knee, wrist, ankle and neck. Deformity may vary depending on the joint affected in hand. These include ulnar deviation, boutonniere deformity, swan neck deformity and Z-thumb (hyperextension of the interphalangeal joint, fixed flexion and subluxation of the metacarpophalangeal joint). There are extra articular manifestations such as subcutaneous nodules and carpal tunnel syndrome. More common in females. [3]
Bursitis Bursitis is the inflammation of bursae of synovial fluid in the body. It commonly affects superficial bursae. Symptoms vary from localized warmth and erythema to joint pain and stiffness. [4]
Cellulitis It is a bacterial infection of the dermis and subcutaneous tissue. The typical signs and symptoms of cellulitis is an area which is red, hot, and painful. The borders of the area of redness are generally not sharp. [5]
References
  1. CARPENTER CHRISTOPHER R., SCHUUR JEREMIAH D., EVERETT WORTH W., PINES JESSE M.. Evidence-based Diagnostics: Adult Septic Arthritis. [online] December, 18(8):781-796 [viewed 14 May 2014] Available from: doi:10.1111/j.1553-2712.2011.01121.x
  2. MACMULLAN P, MCCARTHY G. Treatment and management of pseudogout: insights for the clinician Ther Adv Musculoskelet Dis [online] 2012 Apr, 4(2):121-131 [viewed 14 May 2014] Available from: doi:10.1177/1759720X11432559
  3. RICHIE, A.M, M.L.FRANCIS,Diagnostic Approach to Polyarticular Joint Pain, Am Fam Physician[online]. 2003 Sep, 15,68(6),1151-1160. [viewed 2 May 2014]. Available from: http://www.aafp.org/afp/2003/0915/p1151.html
  4. STELL IM. Management of acute bursitis: outcome study of a structured approach. J R Soc Med [online] 1999 Oct, 92(10):516-521 [viewed 14 May 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1297391
  5. COX NH, COLVER GB, PATERSON WD. Management and morbidity of cellulitis of the leg. J R Soc Med [online] 1998 Dec, 91(12):634-637 [viewed 14 May 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1296982

Investigations - for Diagnosis

Fact Explanation
White blood cell count Even in the absence of n infection, white blood cell count can be as high as 40 × 10*9/L and may be difficult to distinguish from acute septic arthritis. [1,2]
Erythrocyte sedimentation rate (ESR) ESR is high due to inflammation. [1,2]
Synovial Fluid Analysis Examination of synovial fluid is the most accurate method for diagnosing gout. The aspirated sample is examined through a microscope under polarized light. This reveals the presence of monosodium urate crystals, which will nearly always confirm a diagnosis of gout. Examination of aspirated joint fluid can rule out other disorders that mimic gout, such as septic arthritis and pseudogout. Occasionally, patients with gout may present without uric acid crystals in the synovial fluid aspirate. However, aspiration repeated later usually shows crystals in the synovial fluid of most of these patients. White blood cell count is usually 2,000 to 50,000 per mm3. [1,2]
Serum Uric Acid A low level of uric acid in the blood makes a diagnosis of gout much less probable, and a very high level increases the likelihood of gout. Uric acid levels in the blood during an attack of gout can lie within or below the normal range or hyperuricemia may be prevalent in population and doesn’t necessarily indicate gout. Therefore serum uric acid measurements are not sufficient for confirming or ruling out gout. [1,2,3]
Radiography Radiography is not very useful in diagnosing initial attacks of acute gouty arthritis. The radiographic findings are generally nonspecific and consisting of soft tissue swelling around a joint. Radiographic findings will not occur within the first year of disease onset. These are punched-out erosions or lytic areas with overhanging edges. Tophi can be seen in late gout. [4]
Ultrasonography Ultrasonography shows tophaceous deposits in soft tissues, joints, cartilage, as well as erosions, synovitis, and increased vascularity. The characteristic appearance of a tophus includes an anechoic halo and hyperechoic heterogeneous center. Urate deposition over the superficial layer of hyaline cartilage as an irregular echogenic line producing the “double contour sign”. A joint effusion is an early but nonspecific finding in gout patients. Ultrasound is also the primary imaging modality used for needle guidance during diagnostic and therapeutic interventions, including aspirating fluid for crystals. [4]
Computed Tomography Conventional CT is extremely sensitive in identifying characteristic gout erosions and tophus. A tophus can be intra- (Figure 15) or extra-articular, as well as located in tendons and subcutaneous tissues, showing preponderance to the pressure points. [4]
Magnetic Resonance Imaging (MRI) MRI is helpful in the localization of gout deposit in the deeper tissues like the spine. MRI helps in diagnosing the extent of disease involvement of the bursae and tendons. [4]
References
  1. EGGEBEEN,A.T. Gout: An Update. Am Fam Physician[online], 2007,76,801-8, 811-2. [viewed 14 May 2014] Available from: http://www.aafp.org/afp/2007/0915/p801.html
  2. PITTMAN,J.R, M.H. BROSS, Diagnosis and Management of Gout, Am Fam Physician [online] . 1999 Apr, 1,59(7),1799-1806. [viewed 14 May 2014] Available from: http://www.aafp.org/afp/1999/0401/p1799.html
  3. RIDER T. G., JORDAN K. M.. The modern management of gout. Rheumatology [online] December, 49(1):5-14 [viewed 14 May 2014] Available from: doi:10.1093/rheumatology/kep306
  4. GIRISH GANDIKOTA, MELVILLE DAVID M., KAELEY GURJIT S., BRANDON CATHERINE J., GOYAL JANAK R., JACOBSON JON A., JAMADAR DAVID A.. Imaging Appearances in Gout. Arthritis [online] 2013 December, 2013:1-10 [viewed 14 May 2014] Available from: doi:10.1155/2013/673401

Investigations - Fitness for Management

Fact Explanation
Renal function tests Some medications used in the management of the acute and chronic gouty arthritis affects renal function. eg - NSAIDs, Colchicine, Allopurinol. So, before starting therapy, a baseline eGFR, Blood urea and serum electrolyte are necessary. [1,2]
Liver function tests Some medications used in the management of the acute and chronic gouty arthritis affects renal function. eg - Colchicine So, before starting therapy, baseline liver function tests are necessary. [1,2]
References
  1. RIDER T. G., JORDAN K. M.. The modern management of gout. Rheumatology [online] December, 49(1):5-14 [viewed 14 May 2014] Available from: doi:10.1093/rheumatology/kep306
  2. EGGEBEEN,A.T. Gout: An Update. Am Fam Physician[online], 2007,76,801-8, 811-2. [viewed 14 May 2014] Available from: http://www.aafp.org/afp/2007/0915/p801.html

Investigations - Followup

Fact Explanation
Serum uric acid Follow up with serum uric acid should be done after an acute episode preferably after one month. If the patient is on uric acid lowering drugs, uric acid levels should be evaluated more frequently. [1]
Renal function tests The medication used for the treatment of chronic gouty arthritis affects renal function. eg - NSAIDs, Colchicine, Allopurinol. So, it is necessary to evaluate renal function with eGFR, Blood urea and serum electrolyte are necessary. [2,3]
Liver function tests The medication used for the treatment of chronic gouty arthritis are hepato toxic. eg - Colchicine. So, it is necessary to evaluate liver function tests. [2,3]
References
  1. SILVA L, MIGUEL ED, PEITEADO D, VILLALBA A, MOLA M, PINTO J, VENTURA FS. Compliance in gout patients. Acta Reumatol Port [online] 2010 Oct-Dec, 35(5):466-74 [viewed 15 May 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/21245815
  2. RIDER T. G., JORDAN K. M.. The modern management of gout. Rheumatology [online] December, 49(1):5-14 [viewed 14 May 2014] Available from: doi:10.1093/rheumatology/kep306
  3. EGGEBEEN,A.T. Gout: An Update. Am Fam Physician[online], 2007,76,801-8, 811-2. [viewed 14 May 2014] Available from: http://www.aafp.org/afp/2007/0915/p801.html

Management - General Measures

Fact Explanation
Dietary management Dietary changes can help reduce the amount of uric acid in the blood. Purine rich food should be avoided such as shellfish and organ meats such as liver, brains and kidneys. [1]
Maintaining good hydration Maintaining adequate hydration (about 2 L per day) is important for minimizing attacks and decreasing the formation of kidney stones. [1]
Limiting alcohol consumption Reduce the consumption of alcohol as alcohol is known to have a diuretic effects and can contribute to dehydration which ultimately can precipitate the acute gout attack. [1,2]
Reducing weight Can improve hyperuricemia in obese patients. [1,2]
Ice packs Has a good analgesic effect. [1]
Acetaminophen Acetaminophens such as paracetamol relieve pain by elevating the pain threshold.[1,2]
Non steroidal anti-inflammatory Drugs (NSAIDs) Drugs of choice in most cases of acute gout. Indomethacin 50 mg three times daily for four to 10 days or Naproxen 500 mg twice daily for four to 10 days is the usual regimen. NSAIDs have many adverse effects such as gastrointestinal ulcer disease, bleeding or perforation. These are increased in the elderly and a proton pump inhibitor should be co administered. However they should be used cautiously with presence of renal insufficiency. [1,2,3,4]
Colchicine Colchicine suppresses the inflammation. It is thought to impairs the motility of granulocytes and hence prevents the inflammation that initiate an attack or it may involve reduction in uric acid deposition. Usual dose is 0.6 mg orally two or three times daily. It should generally be avoided if glomerular filtration rate (GFR) is less than 10 mL/min due to narrow therapeutic window and risk of toxicity, It should also be avoided in patients with severe renal or hepatic impairment because it can lead to bone marrow suppression and neuromyopathy. [1,2,3,4
Corticosteroids Corticosteroids are potent anti-inflammatory effectors. Prednisone, 20 to 40 mg daily for two or three days, then taper over 10 to 14 days is the usual regimen. Alternatively intra-articular or intramuscular methylprednisolone may be beneficial. Intra-articular therapy may be the treatment of choice if only one or two accessible joints are involved. Steroids should be avoided in patients with joint sepsis and used cautiously in patients with diabetes. [1,2,3,4]
References
  1. EGGEBEEN,A.T. Gout: An Update. Am Fam Physician[online], 2007,76,801-8, 811-2. [viewed 14 May 2014] Available from: http://www.aafp.org/afp/2007/0915/p801.html
  2. RIDER T. G., JORDAN K. M.. The modern management of gout. Rheumatology [online] December, 49(1):5-14 [viewed 14 May 2014] Available from: doi:10.1093/rheumatology/kep306
  3. PITTMAN,J.R, M.H. BROSS, Diagnosis and Management of Gout, Am Fam Physician [online] . 1999 Apr, 1,59(7),1799-1806. [viewed 14 May 2014] Available from: http://www.aafp.org/afp/1999/0401/p1799.html
  4. JORDAN K. M., CAMERON J. S., SNAITH M., ZHANG W., DOHERTY M., SECKL J., HINGORANI A., JAQUES R., NUKI G.. British Society for Rheumatology and British Health Professionals in Rheumatology Guideline for the Management of Gout. Rheumatology [online] 2007 May, 46(8):1372-1374 [viewed 14 May 2014] Available from: doi:10.1093/rheumatology/kem056a

Management - Specific Treatments

Fact Explanation
Allopurinol Allopurinol lowers the blood uric acid level by preventing uric acid production. It affects the metabolic conversion of purines by inhibiting xanthine oxidase, the enzyme responsible for the conversion of xanthine to uric acid. Allopurinol is the mainstay of chronic treatment. Adverse effects are rash, vasculitis, eosinophilia, life-threatening hypersensitivity reaction, hepatitis, decreased renal function and bone-marrow suppression. So the dose should be reduced in renal impairment. [1,2,3,4]
Probenecid Probenecid is commonly used to decrease uric acid blood levels by increasing the excretion of uric acid into the urine. It acts by preventing the reabsorption of uric acid by the kidney and hence increasing its excretion from the body in the urine.[1,2,3]
Sulfinpyrazone The mechanism is same as in probenecid.[1,2,5]
Febuxostat It is a new agent which selectively inhibits Xanthine oxidase independent of the redox state and does not affect other enzymatic pathways in purine/pyrimidine metabolism. This can be used in patients with renal impairment without adjustment of the doses.[1,2,3,4]
References
  1. JORDAN K. M., CAMERON J. S., SNAITH M., ZHANG W., DOHERTY M., SECKL J., HINGORANI A., JAQUES R., NUKI G.. British Society for Rheumatology and British Health Professionals in Rheumatology Guideline for the Management of Gout. Rheumatology [online] 2007 May, 46(8):1372-1374 [viewed 14 May 2014] Available from: doi:10.1093/rheumatology/kem056a
  2. EGGEBEEN,A.T. Gout: An Update. Am Fam Physician[online], 2007,76,801-8, 811-2. [viewed 14 May 2014] Available from: http://www.aafp.org/afp/2007/0915/p801.html
  3. RIDER T. G., JORDAN K. M.. The modern management of gout. Rheumatology [online] December, 49(1):5-14 [viewed 14 May 2014] Available from: doi:10.1093/rheumatology/kep306
  4. PITTMAN,J.R, M.H. BROSS, Diagnosis and Management of Gout, Am Fam Physician [online] . 1999 Apr, 1,59(7),1799-1806. [viewed 14 May 2014] Available from: http://www.aafp.org/afp/1999/0401/p1799.html
  5. SO ALEXANDER. Gout in the spotlight. Array [online] 2008 December [viewed 14 May 2014] Available from: doi:10.1186/ar2396