Gout: Difference between revisions

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== Definition/Description:  ==
== Introduction  ==


[[Image:1st mtp gout.jpg|thumb|1st mtp gout.jpg]]  
[[Image:1st mtp gout.jpg|thumb|Gout: slight redness in the MTP joint of the big toe]]


Gout is a metabolic disorder; however, because the clinical presentation closely resembles arthritis, gout is also classified as '''a form of crystal-induced arthritis''' <ref name="Goodman, Fuller">Goodman CC, Fuller KS. Pathology: Implications for the Physical Therapist. 3rd ed. Saint Louis, MO: Saunders; 2009.</ref>&nbsp; <ref name="Beers">Beers MH, et. al. eds. The Merck Manual of Diagnosis and Therapy. 18th ed. Whitehouse Station, NJ: Merck Research Laboratories; 2006.</ref>.There are three main types of gout, all of which usually begin '''monoarticularly''' at the '''first metatarsophalangeal''' joint and are characterized by sudden pain, swelling, and redness.<ref name="Goodman, Fuller" />&nbsp;<ref name="Beers" />&nbsp;<ref name="Goodman, Snyder">Goodman C, Snyder T. Differential Diagnosis for Physical Therapists: Screening for Referral. St. Louis, Missouri: Saunders Elsevier, 2007.</ref>  
Gout is a characteristically intense acute inflammatory reaction that erupts in response to articular deposits of monosodium urate (MSU) crystals<ref>Cronstein BN, Terkeltaub R. The inflammatory process of gout and its treatment. Arthritis Research & Therapy. 2006 Apr;8(1):1-7 Available: .https://arthritis-research.biomedcentral.com/articles/10.1186/ar1908#Abs1 (accessed 15.5.2022)</ref>. It usually presents with intermittent painful attacks followed by long periods of remission<ref name=":3">Drug and Therapeutics Bulletin. Latest guidance on the management of gout. Available: https://www.bmj.com/content/362/bmj.k2893<nowiki/>(accessed 15.5.2022)</ref>. Most patients with gout have other [[Multimorbidity|comorbidities]]. The prevalence of gout is higher among individuals with chronic diseases such as [[hypertension]], [[Chronic Kidney Disease|chronic kidney disease]], [[diabetes]], [[obesity]], [[Congestive Heart Failure|congestive heart failure]], and [[Myocardial Infarction|myocardial infarction]] .<ref name=":1">Radiopedia Gout Available: https://radiopaedia.org/articles/gout<nowiki/>(accessed 14.5.2022)</ref> <ref name=":2">Fenando A, Widrich J. Gout (podagra).Available:https://www.ncbi.nlm.nih.gov/books/NBK546606/ (accessed 14.5.2022)</ref><ref>Joseph Kaplan, MD, MS, FACEP  Attending Physician, Department of Emergency Medicine, Martin Army Community Hospital, Fort Benning, Georgia</ref>
== Epidemiology ==
Gout typically occurs in those above 40 years. There is a strong male bias of 20:1, with this bias more pronounced in younger and middle-aged adults. In the elderly, the gender distribution is more equal. Rarely seen in children (&lt; 10% of all cases)<ref name=":1" />&nbsp; <ref name="Goodman, Fuller">Goodman CC, Fuller KS. Pathology: Implications for the Physical Therapist. 3rd ed. Saint Louis, MO: Saunders; 2009.</ref>
*


Gout is caused by monosodium urate crystal deposition in tissues leading to arthritis, soft tissue masses (i.e., tophi), nephrolithiasis, and urate nephropathy. The biologic precursor to gout is '''elevated serum uric acid levels''' (i.e., hyperuricemia). <ref>Eggebeen AT. University of Pittsburgh Arthritis Institute, Pittsburgh, Pennsylvania 15261, USA</ref><br>
== Risk Factors ==
The single most important risk factor is sustained hyperuricaemia, which can be caused by overproduction or underexcretion of urate. Hyperuricemia  is abnormally high levels of uric acid in the blood. People with higher serum urate levels are not only at an elevated risk for gout flare-ups but will also have more frequent flare-ups over time.  
[[File:Gout olecranon.jpg|thumb|227x227px|Gout Olecranon]]
Other factors implicated for gout and/or hyperuricemia: older age, male sex, obesity, a purine diet, alcohol, medications, comorbid diseases, and genetics. Offending medications include diuretics, low-dose aspirin, ethambutol, pyrazinamide, and cyclosporine. Genome-wide association studies (GWAS) have found several genes that are associated with gout.


'''Gout''' and '''pseudogou'''t are the 2 most common crystal-induced arthropathies. They are debilitating illnesses in which pain and joint inflammation are caused by the formation of crystals within the joint space. <ref>Joseph Kaplan, MD, MS, FACEP  Attending Physician, Department of Emergency Medicine, Martin Army Community Hospital, Fort Benning, Georgia</ref><br>
* Dietary sources that can contribute to hyperuricemia and gout include consumption of animal food such as seafood (e,g., shrimp, lobster), organs (e.g., liver, and kidney), and red meat (pork, beef).
== Prevalence: ==
* Some drinks like alcohol, sweetened beverages, sodas, and high-fructose corn syrup may also contribute to this disease<ref name=":2" />


Effects over 2 million people in the US.<br>
== Pathology ==
* The most common crystalopathy (in the US)
[[Image:Urate crystals.jpg|thumb|Urate Crystals removed from tophi]]The pathology is characterised by monosodium urate crystals deposition in periarticular soft tissues. Synovial fluid is a poor solvent for monosodium urate hence crystallisation occurs at low temperatures.


* Rarely seen in children (&lt; 10% of all cases)&nbsp; <ref name="Goodman, Fuller" />
There are five recognised stages of gout:


* Predominantly seen in men (most common inflammatory disease in men over age 30) , however it could affect female patients<ref>Dirken-Heukensfeldt KJ, Teunissen TA, Van de Lisdonk EH, Lagro-Janssen AL. “Clinical features of women with gout arthritis.” A systematic review. Clinical rheumatology. 2010 Jun 1;29(6):575-82.</ref>.
# Asymptomatic hyperuricaemia
# Acute gouty arthritis
# Intercritical gout (between acute attacks)
# Chronic tophaceous gout
# Gouty nephropathy<ref name=":1" />


* Peak incidence in the 4th - 5th decades of life
== Characteristics/Clinical Presentation ==
[[File:Tophaceous gout.jpeg|thumb|Tophaceous gout: R great toe and finger IP joints. ]]
Acute gouty arthritis presents with a monoarticular red, inflamed, swollen joint, typically in the lower limb, classically affecting the first metatarsophalangeal joint. Often occurs during sleep, and may go on to involve more than one joint, becoming an oligoarthropathy or rarely, a polyarthropathy.


* Frequency increases in postmenopausal women (lack of estrogen) <ref name="Goodman, Fuller" /> <ref name="Goodman, Snyder" />
The acute phase usually last less than 10 days. within 7-10 days.


== Characteristics/Clinical Presentation:  ==
Patients with chronic uncontrolled hyperuricaemia, eg chronic kidney disease, may develop chronic tophaceous gout. In chronic tophaceous gout, there are solid urate crystal collections (tophi) and chronic inflammatory and destructive changes in surrounding connective tissue. Tophi are typically yellow-white in colour, non-tender, and are typically located within the articular structures, bursae, or the ears<ref name=":1" />.&nbsp;


There are four stages of gout, although diagnosis does not require the presence or occurance of each stage. The four stages are:<br>
== '''Management''' ==
[[Image:X-ray gout.jpg|thumb|X-ray gout.jpg]]The acute gout attacks are painful and potentially disabling, needing immediate treatment. The optimal therapy is towards  controlling pain and inflammation.


*'''Asymptomatic hyperuricemia ( serum urate &gt; 7mg/dl)''': is the phase of gout prior to the first attack, when serum urate levels are elevated but no symptoms are present. <ref name="Goodman, Fuller" /><br>
# Acute flare ups: Management aims at decreasing the inflammation and the resulting pain. The physician should start the treatment within the first 24 hours of onset to reduce the severity and duration of the flare-up. Rest with topical application of ice packs can combined with non-steroidal anti-inflammatory drugs, colchicine, or systemic glucocorticoids. The length of the treatments should be at least 7 to 10 days to prevent rebound flare-ups.<ref name=":2" />
*'''Acute gouty arthritis:''' is the most often found (90%) at the first '''metatarsophalangeal joint'''.Symptoms generally begin with a sudden onset of localized, intense pain, often occuring at night.The pain may be great enough to awaken the patient. Redness, extreme tenderness, and swelling around the joint will occur within a few hours of the initial pain. Hypersensitivity, chills, tachycardia, malaise, and fever may also be present.<ref name="Goodman, Fuller" />&nbsp; <ref name="Beers" /> <ref name="Goodman, Snyder" /> The skin may also become red or purplish, shiny, tense, and warm.&nbsp;<ref name="Beers" /><br><br>'''Gouty arthritis is the''' '''most common clincial presentation:''' 
# Patients with recurrent attacks, tophi, urate arthropathy, or renal damage and to symptomatic patients with very high serum uric acid levels should start urate lowering therapy (ULT). In the long-term xanthine oxidase inhibitors (e.g. allopurinol or febuxostat), uricosuric drugs (e.g. probenecid), or uricase agents (e.g. pegloticase) may be used to reduce urate levels and prevent further acute flares<ref name=":3" />.
# Tophaceous gout can also be managed with surgical excision of symptomatic lesions.


Occasionally, acute gouty arthritis can also occur at the '''fingers, wrist, elbow, knee, ankle, and instep.'''&nbsp; Even more '''rarely''', acute gouty arthritis may present at the '''cervical spine, sternoclavicular joint, shoulder, hip''', and '''sacroilliac joint.'''<ref name="Goodman, Fuller" />&nbsp; <ref name="Beers" />&nbsp;<ref name="Goodman, Snyder" /> The initial attack may last a few days to 2 weeks, if left untreated <ref name="Beers" /> <ref name="Goodman, Snyder" />. Attacks will recur; however time periods of months or years may elapse between them. As the attacks recur, they will become more intense and may spread to other joints in the body <ref name="Goodman, Fuller" /> <ref name="Beers" /> <ref name="Goodman, Snyder" />. A patient may eventually exprience several attacks per year <ref name="Goodman, Fuller" /> <ref name="Beers" />&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;<br>
'''Non-pharmacologic''' : Patients with gout are encouraged to modify their lifestyles to prevent future attacks. Diet recommendations include reducing alcohol consumption, limiting purine-rich foods (meat, seafood, high fructose corn syrup, and sweetened soft drinks), and substituting low-fat or non-fat dairy products for their higher fat content counterparts. Weight loss and adequate hydration will also help reduce gout flare-up frequency<ref name=":2" />.<ref name=":0">Primatesta P, Plana E, Rothenbacher D. Gout treatment and comorbidities: a retrospective cohort study in a large US managed care population. BMC musculoskeletal disorders. 2011 Dec;12(1):103.</ref>
 
== Diagnosis ==
{|
Synovial Fluid Analysis''':''' Monosodium urate crystal identification remains the gold standard for gout diagnosis. Gout flare is marked by the presence of MSU crystals in synovial fluid obtained from affected joints of bursas visualized by direct examination of a fluid sample using compensated polarized light microscopy.<ref name=":2" />
|-
== Physical Therapy Management&nbsp;==
| [[Image:Gout pip.jpg|thumb|Presentation of acute gout at the PIP joint]]
The physical therapist should be aware that any patient with a history of gout, hyperuricemia, and/or a septic joint presentation should be referred for medical evaluation prior to treatment.<ref name="Goodman, Fuller" />  
| [[Image:Gout olecranon.jpg|thumb|Presentation of acute gout at the olecranon]]
|}
* '''The intercritical phase:''' occurs after recovery from each episode.&nbsp;This phase is asymtomatic and may last for months to years at a time.It is important to note that although this is an aysmptomatic stage, serum urate levels are often still elevated and urate crystals may still be present.&nbsp; <ref name="Goodman, Fuller" /><br>
 
*As the gout attacks continue, '''tophi''' will develop in the joints, tendons, bursae, subchondral bone, cartilage, ligaments, subcutaneous tissue, and synovium.<ref name="Goodman, Fuller" />&nbsp; '''Tophi are hard nodules of sodium urate deposits''' that may vary in number and location.<ref name="Goodman, Fuller" /> <ref name="Goodman, Snyder" /> <ref name="Beers" /> Although typically a painless structure, the formation of tophi can cause an acute inflammatory response within the tissue.&nbsp;<ref name="Goodman, Snyder" /> <ref name="Beers" /> As the tophi become enlarged they may cause deformities, and there is potential for them to protrude through the skin and exude a white chalky substance (urate crystals). <ref name="Goodman, Fuller" /> <ref name="Goodman, Snyder" /> <ref name="Beers" />&nbsp; Some of the most common sites of enlarged tophi are the forearm, ear, knee and foot.&nbsp;<ref name="Goodman, Fuller" />&nbsp;
 
&nbsp;&nbsp;&nbsp; Note: ''Prior'' to the use of urate-lowering drugs for the treatment of acute gouty arthritis, tophi developed in approximately 30 - 50% of patients. <ref name="Goodman, Snyder" /><br> [[Image:Urate crystals.jpg|thumb|Urate Crystals removed from tophi]]
 
*'''Chronic tophaceous''' gout is characterized by increased pain, deformity (from tophi), decreased ROM, and subsequent functional loss.<ref name="Goodman, Fuller" />&nbsp;<ref name="Beers" />&nbsp; Due to the treatments used for gout today, chronic tophaceous gout is rare. <ref name="Goodman, Snyder" />
 
Great pictures of the presentation of gout at various stages can also be found at:  
 
[http://www.skinsight.com/adult/gout.htm www.skinsight.com/adult/gout.htm] <ref name="Presentation Pics">http://www.skinsight.com/adult/gout.htm</ref> &nbsp;
 
<br>  
 
== Associated Co-morbidities:  ==
 
Comorbidities with the patterns of  gout treatment, the occurrence and the frequency of acute attacks. Cardiometabolic comorbidities, common in this patients' population, were associated with an increased risk of flares<ref name=":0">Primatesta P, Plana E, Rothenbacher D. Gout treatment and comorbidities: a retrospective cohort study in a large US managed care population. BMC musculoskeletal disorders. 2011 Dec;12(1):103.</ref>
 
== '''Management:''' ==
The acute gout attacks are painful and potentially disabling, needing immediate treatment. The optimal therapy is towards  controlling pain and inflammation '''Drug therapy''' for gout has become an important part of the therapeutic approach to the disease, which includes '''lifestyle modifications'''. Current standards for first-line treatment for acute attacks include '''nonsteroidal anti-inflammatory drugs (NSAIDs),''' '''colchicine''' and '''corticosteroids.''' '''Urate-lowering treatment (ULT)''' ('''most commonly allopurinol''') is usually recommended after the acute attack has resolved.<ref name=":0" />
 
== Medications:  ==
*NSAIDS ((selective/non-selective),Corticosteroids (oral or injections)<ref name="Goodman, Fuller" /> <ref name="Beers" />: for pain and inflammation management during an acute attack<ref name=":0" />.
*Allopurinol: to slow the rate of uric acid production and help prevent future attacks
*Cholchicine: occasionally used in the acute phase; however, use is less common due to frequency of side effects and narrow therapeutic range<ref name="Beers" /> <ref name="Goodman, Fuller" />
*Supplementary analgesics
*Probenecid and sulfinpyrazone may be used to lower serum urate levels<ref name="Beers" /><br>
 
[http://www.rxlist.com/script/main/hp.asp www.rxlist.com/script/main/hp.asp] <ref name="rx list">http://www.rxlist.com/script/main/hp.asp</ref>
 
== Diagnostic Tests/Lab Tests/Lab Values:  ==
 
*Arthrocentesis and synovial fluid analysis:should be performed upon initial presentation.<ref name="Beers" /> <ref name="Goodman, Fuller" />.&nbsp;&nbsp;
(Gout and pseudogout can be differentiated by examination of the fluid aspirate contents of a joint viewed under '''polarised red light:Urate crystals –''' are '''negatively birefringent –''' they will appear a needle shaped crystals)
*Gram stain and culture: to rule out infectious arthritis<ref name="Beers" />
*Elevated serum urate levels may support diagnosis but are not sensitive or specific.&nbsp; Levels should be measured on several different occasions and it is possible for levels to be normal during and actute attack.&nbsp; Elevated levels are considered to be greater than 7mg/dL.<ref name="Goodman, Fuller" /> <ref name="Beers" />
*24 hour urate excretion: normal is 600-900 mg.&nbsp; This may help identify hyper production of uric acid or decreased excretion.<ref name="Beers" />&nbsp;
*X-rays: to examine tophi.&nbsp; X-rays are not essential for diagnosis.&nbsp;<ref name="Goodman, Fuller" /> <ref name="Beers" />
 
[[Image:X-ray gout.jpg|thumb|X-ray gout.jpg]]&nbsp;
 
== Causes:  ==
 
There are three types of hyperuricemia based on cause<ref name="Goodman, Fuller" />: <br>
 
#Primary hyperuricemia is an inherited form of the disorder.<br>
#Idiopathic hyperuricemia does not have a known cause.&nbsp; <br>
#Secondary hyperuricemia can result from a variety of causes including:&nbsp; <br>
 
*renal dysfunction or disease (hemodialysis, polycystic kidney disease, renal insufficiency)<ref name="Goodman, Snyder" /> <ref name="Beers" /><br>
*leukemia, lymphomas, psoriasis<ref name="Goodman, Fuller" /> <ref name="Beers" /> <ref name="Goodman, Snyder" /><br>
*hematopoetic disorders (hemolytic anemia, myeloma, polycythemia vera, myeloproliferative disorder)<ref name="Goodman, Snyder" /><br>
*chemotherapy agents <ref name="Goodman, Fuller" /> <ref name="Beers" /> <ref name="Goodman, Snyder" /><br>
*obesity, fasting <ref name="Goodman, Fuller" /> <ref name="Beers" /> <ref name="Goodman, Snyder" /><br>
*medications (diuretics, salicylates, levodopa, cyclosporine, low dose asprin, vitamin B12)<ref name="Goodman, Fuller" /> <ref name="Beers" /> <ref name="Goodman, Snyder" /><br>
*heavy alcohol consumption<ref name="Goodman, Fuller" /> <ref name="Beers" /> <ref name="Goodman, Snyder" /><br>
*hypertension<ref name="Goodman, Fuller" /> <ref name="Goodman, Snyder" /><br>
*endocrine disorders: (hyperparathyroidism, hypoparathyroidism, hyperthyroidism, diabetes mellitus)<ref name="Goodman, Snyder" /><br>
*a diet rich in purines (shellfish, organ meats, beans, spinach, etc.)<ref name="Goodman, Fuller" /> <ref name="Beers" /> <ref name="Goodman, Snyder" /><br>
*medical stressors (surgery, trauma, infection, etc.)<ref name="Beers" /><br>
*fatigue or emotional stress <ref name="Beers" /><br>
*toxemia of pregnancy, hyperlipidemia, chondrocalcinosis <ref name="Goodman, Snyder" />
 
== Systemic Involvement:  ==
 
None
 
== Medical Management (current best evidence):  ==
 
There are three main goals of the medical management of gout: <br>
 
#Terminate acute attacks
#Prevent recurrance
#Correct and prevent further damage from hyperuricemia<ref name="Goodman, Fuller" /><ref name="Beers" />
 
<u>Termination of acute attacks</u> - NSAIDs are the most common and generally effective treatment for acute attacks.<ref name="Goodman, Fuller" /><ref name="Beers" />&nbsp; Cox-2 inhibitors are often the second choice for those who develop GI toxicity; however, they should be used with great caution with any patient with a history of CV complications or co-morbidities.<ref name="Beers" />&nbsp; Intraarticular corticosteroid injection may also be effective for the management of an acute attack. Colchicine may also be used either po or by IV and may produce substantial pain relief if started immediately after onset of symptoms.&nbsp; Supplementary analgesics may also be recommended along with rest, elevation, and joint protection strategies. <ref name="Goodman, Fuller" /><ref name="Beers" />
 
<u>Prevention of recurrance</u> - Daily low doses of NSAIDs or Cholcicine are commonly used to prevent recurrent attacks.<ref name="Beers" />
 
<u>Correction and prevention of hyperuricemia</u> - Uricosuric drugs or allopurinol may be used alone or in conjunction.&nbsp; Hypouricemic therapy may also be used for patients with tophi and a higher recurrance rate.&nbsp; Dietary restriction of high-purine foods is a less effective treatment technique but is still recommended.&nbsp; Carbohydrate restrictions may also be helpful.&nbsp; Other treatment possibilties include hydration greater than 3 liters per day.&nbsp; Alkalinization of urine, extracorporeal shock wave lithotripsy, and surgical excision may also be beneficial.<ref name="Beers" />
 
A list of high-purine foods can be found at: http://www.niams.nih.gov/Health_Info/Gout/default.asp<nowiki/>.&nbsp; <ref name="FDA" />
 
== Physical Therapy Management (current best evidence):  ==
 
Physical therapy management of gout falls under preferred practice pattern 4E: Impaired joint mobility, motor function, muscle performance, and range of motion associated with localized inflammation. <ref name="Goodman, Fuller" />&nbsp;  
 
The physical therapist should be aware that any patient with a history of gout, hyperuricemia, and/or a septic joint presentation should be refered for medical evaluation prior to treatment.<ref name="Goodman, Fuller" />  


During acute exacerbations the physical therapist should focus on reinforcement of management program and splinting, orthotics, or other assistive devices to protect the affected joint(s). <ref name="Goodman, Fuller" />  
During acute exacerbations the physical therapist should focus on reinforcement of management program and splinting, orthotics, or other assistive devices to protect the affected joint(s). <ref name="Goodman, Fuller" />  


A 2002 study in the Journal of Rheumatology found that the use of cryrotherapy to alleviate the pain associated with acute bouts of gout may be effective.&nbsp;<ref name="cryro">Schlesinger N, Detry MA, Holland BK, Baker DG, Beutler AM, Rull M, Hoffman BI, Schumacher HR Jr. Local ice therapy during bouts of acute gouty arthritis. J Rheumatol 2002; 29(2): 331-334</ref>  
A 2002 study in the Journal of Rheumatology found that the use of cryotherapy to alleviate the pain associated with acute bouts of gout may be effective.&nbsp;<ref name="cryro">Schlesinger N, Detry MA, Holland BK, Baker DG, Beutler AM, Rull M, Hoffman BI, Schumacher HR Jr. Local ice therapy during bouts of acute gouty arthritis. J Rheumatol 2002; 29(2): 331-334</ref>  


During intercritical phases physical therapists may offer assistance with maintinance of ROM, strength, and function.&nbsp; The physical therapist can also assist the patient in the creation of a suitable exercise routine and keeping thier weight under control.&nbsp;<ref name="Goodman, Fuller" /><ref name="FDA">Gout. National Institute of Arthritis and Musculoskeletal and Skin Diseases. December 2006. http://www.niams.nih.gov/Health_Info/Gout/default.asp. Accessed March 2010.</ref>  
During intercritical phases physical therapists may offer assistance with maintenance of ROM, strength, and function.&nbsp; The physical therapist can also assist the patient in the creation of a suitable exercise routine and keeping their weight under control.&nbsp;<ref name="Goodman, Fuller" /><ref name="FDA">Gout. National Institute of Arthritis and Musculoskeletal and Skin Diseases. December 2006. http://www.niams.nih.gov/Health_Info/Gout/default.asp. Accessed March 2010.</ref>
== Pseudogout ==
[[Image:Pseuodgout.jpg|thumb|alt=|Pseuodgout]]Pseudogout, also known as pyrophosphate Calcium pyrophosphate dihydrate disease (CPPD), is defined by the co-occurrence of arthritis with evidence of CPPD deposition within the articular cartilage.  it is characterized by sudden, painful swelling in one or more of the joints. These episodes can last for days or weeks. The most commonly affected joint is the knee. It isn't clear why crystals form in the joints and cause pseudogout, but the risk increases with age. Treatments can help relieve pain and reduce inflammation<ref>Mayo clinic Pseudogout Available: https://www.mayoclinic.org/diseases-conditions/pseudogout/symptoms-causes/syc-20376983<nowiki/>(accessed 15.5.2022)</ref>.


There is a Randomized Clinical Trial which suggests that Electroacupuncture in combination with blood letting puncture and cupping has relatively good results as a treatment for Gout. The treatment is effective mostly because the blood uric acid decreased significantly after the treatment was given to the patients. <ref>Zhao QW, Liu J, Qu XD, Li W, Wang S, Gao Y, Zhu LW.Department of Nutrition, Longnan Hospital, Daqing Oilfield General Hospital Group in Daqing City of Heilongjiang Province, Daqing 163453, China</ref><br>
* It is a form of arthritis that occurs 1/8th as often as gout.  
* Symptoms are very similar to gout; however, the knee joint is primarily affected.
* Diagnosis is made by aspiration of synovial fluid.<ref name="Goodman, Snyder">Goodman C, Snyder T. Differential Diagnosis for Physical Therapists: Screening for Referral. St. Louis, Missouri: Saunders Elsevier, 2007.</ref><ref name="Wheeless">Wheeless, C R. Pseudogout and Chondrocalcinosis. Wheeless' Textbook of Orthopaedics. November 2008.  www.wheelessonline.com/image9/cppd2.jpg. Accessed March 2010.</ref>


There is another study about Electroacupuncture combined with local blocking therapy on acute gouty arthritis that shows an improvement in health status of the patients. This treatment is positive and it also decreases blood uric acid levels. <ref>Liu B, Wang HM, Wang FY. The Forth Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, China</ref><br>
The difference between pseudogout and gout is outlined in below video.  


== Differential Diagnosis: ==
{{#ev:youtube| KdyEuYhrjlM}}
*


<u>'''Pseudogout:'''</u> is a form of arthritis that occurs 1/8th as often as gout.Symptoms are very similar to gout; however, the knee joint is primarily affected. Diagnosis is made by aspiration of synovial fluid.<ref name="Goodman, Snyder" /><ref name="Wheeless">Wheeless, C R. Pseudogout and Chondrocalcinosis. Wheeless' Textbook of Orthopaedics. November 2008.  www.wheelessonline.com/image9/cppd2.jpg. Accessed March 2010.</ref>
== Case Reports ==


'''The difference between pseudogout and gout''' :
One [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1001146/ case report] that presents interesting implications for the physical therapist involves an elderly patient with lumbar spondylodiscal pathology secondary to her polyarticular gout.&nbsp; <ref>Lagier R, Gee W M. Spondylodiscal erosions due to gout: anatomicoradiological study of a case. Annals of the Rheumatic Diseases. 1983 June; 42(3): 350-353.</ref><br>Interesting [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2572609/?tool=pmcentrez case report] involving a middle aged man that developed symptoms of gout during a hospitalization.&nbsp; <ref>Dhoble A, Balakrishnan V, Smith R.  Chronic tophaceous gout presenting as acute arthritis during an acute illness: a case report. Cases Journal. 2008; 1: 238.</ref><br>[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2572609/?tool=pmcentrez Case report] of a patient whose tophi were limiting the FDS tendon. <ref>Sano K, et. al. Atypical Triggering at the Wrist due to Intratendinous Infiltration of Tophaceous Gout. Springer Hand. 2009 March; 4(1): 78-80.</ref><br>[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2612045/?tool=pmcentrez Case report] involving presentation and differential diagnosis of acute monoarthritis.  <ref>Ma L, Cranney A, and Holroyd-Leduc J. Acute monoarthritis: What is the cause of my patient's painful swollen joint. CMAJ. 2009 January; 180(1): 59-65.</ref>


https://youtu.be/KdyEuYhrjlM[[Image:Pseuodgout.jpg|thumb]]
A series of [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC286251/?tool=pmcentrez case reports] that examine some of the negative effects of Colchicine as a form of pharmacological management. <ref>Morris I, Varughese G, and Mattingly P. Colchicine in acute gout. BMJ. 2003 November; 327(7426): 1275-1276.</ref>
* Other differential diagnosis include: RA, neoplasm, septic arthritis, infectious arthritis, acute rheumatic fever, juvenile RA, acute fracture, and palindromic rheumatism. <ref name="Goodman, Fuller" /><ref name="Beers" />\gouty arthritis typically presents with rapid development of severe joint pain, swelling, and tenderness that reaches its maximum within just 6-12 h, especially with overlying erythema, most classically in the first metatarsophalangeal joint. Demonstrating the presence of monosodium urate (MSU) crystals in the joint fluid or tophus has been the gold standard for the diagnosis of gout. <ref>Schlesinger N. Department of Medicine, UMDNJ-Robert Wood Johnson Medical School, New Brunswick, NJ 08903</ref>
== References ==
 
== Case Reports:  ==
 
One case report that presents interesting implications for the physical therapist involves an elderly patient with lumbar spondylodiscal pathology secondary to her polyarticular gout.&nbsp; [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1001146/ www.ncbi.nlm.nih.gov/pmc/articles/PMC1001146/] <ref>Lagier R, Gee W M. Spondylodiscal erosions due to gout: anatomicoradiological study of a case. Annals of the Rheumatic Diseases. 1983 June; 42(3): 350-353.</ref><br>
 
Interesting case report involving a middle aged man that developed symptoms of gout during a hospitalization.&nbsp; [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2572609/?tool=pmcentrez www.ncbi.nlm.nih.gov/pmc/articles/PMC2572609/] <ref>Dhoble A, Balakrishnan V, Smith R.  Chronic tophaceous gout presenting as acute arthritis during an acute illness: a case report. Cases Journal. 2008; 1: 238.</ref><br>
 
Case report of a patient whose tophi were limiting the FDS tendon.&nbsp;&nbsp; [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2654956/?tool=pmcentrez www.ncbi.nlm.nih.gov/pmc/articles/PMC2654956/] <ref>Sano K, et. al. Atypical Triggering at the Wrist due to Intratendinous Infiltration of Tophaceous Gout. Springer Hand. 2009 March; 4(1): 78-80.</ref><br>
 
Case report involving presentation and differential diagnosis of acute monoarthritis. [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2612045/?tool=pmcentrez www.ncbi.nlm.nih.gov/pmc/articles/PMC2612045/] <ref>Ma L, Cranney A, and Holroyd-Leduc J. Acute monoarthritis: What is the cause of my patient's painful swollen joint. CMAJ. 2009 January; 180(1): 59-65.</ref>
 
A series of case reports that examine some of the negative effects of Colchicine as a form of pharmacological management. [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC286251/?tool=pmcentrez www.ncbi.nlm.nih.gov/pmc/articles/PMC286251/] <ref>Morris I, Varughese G, and Mattingly P. Colchicine in acute gout. BMJ. 2003 November; 327(7426): 1275-1276.</ref>
== References:  ==


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    [[Category:Rheumatology]]  
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Latest revision as of 14:52, 9 November 2022

Original Editors - Maggie Kraemer from Bellarmine University's Pathophysiology of Complex Patient Problems project.

Top Contributors - Maggie Kraemer, Admin, Lucinda hampton, Shaimaa Eldib, Fitim Cami, Kim Jackson, Elaine Lonnemann, Simisola Ajeyalemi, Wendy Walker and WikiSysop  

Introduction[edit | edit source]

Gout: slight redness in the MTP joint of the big toe

Gout is a characteristically intense acute inflammatory reaction that erupts in response to articular deposits of monosodium urate (MSU) crystals[1]. It usually presents with intermittent painful attacks followed by long periods of remission[2]. Most patients with gout have other comorbidities. The prevalence of gout is higher among individuals with chronic diseases such as hypertension, chronic kidney disease, diabetes, obesity, congestive heart failure, and myocardial infarction .[3] [4][5]

Epidemiology[edit | edit source]

Gout typically occurs in those above 40 years. There is a strong male bias of 20:1, with this bias more pronounced in younger and middle-aged adults. In the elderly, the gender distribution is more equal. Rarely seen in children (< 10% of all cases)[3]  [6]

Risk Factors[edit | edit source]

The single most important risk factor is sustained hyperuricaemia, which can be caused by overproduction or underexcretion of urate. Hyperuricemia is abnormally high levels of uric acid in the blood. People with higher serum urate levels are not only at an elevated risk for gout flare-ups but will also have more frequent flare-ups over time.

Gout Olecranon

Other factors implicated for gout and/or hyperuricemia: older age, male sex, obesity, a purine diet, alcohol, medications, comorbid diseases, and genetics. Offending medications include diuretics, low-dose aspirin, ethambutol, pyrazinamide, and cyclosporine. Genome-wide association studies (GWAS) have found several genes that are associated with gout.

  • Dietary sources that can contribute to hyperuricemia and gout include consumption of animal food such as seafood (e,g., shrimp, lobster), organs (e.g., liver, and kidney), and red meat (pork, beef).
  • Some drinks like alcohol, sweetened beverages, sodas, and high-fructose corn syrup may also contribute to this disease[4]

Pathology[edit | edit source]

Urate Crystals removed from tophi

The pathology is characterised by monosodium urate crystals deposition in periarticular soft tissues. Synovial fluid is a poor solvent for monosodium urate hence crystallisation occurs at low temperatures.

There are five recognised stages of gout:

  1. Asymptomatic hyperuricaemia
  2. Acute gouty arthritis
  3. Intercritical gout (between acute attacks)
  4. Chronic tophaceous gout
  5. Gouty nephropathy[3]

Characteristics/Clinical Presentation[edit | edit source]

Tophaceous gout: R great toe and finger IP joints.

Acute gouty arthritis presents with a monoarticular red, inflamed, swollen joint, typically in the lower limb, classically affecting the first metatarsophalangeal joint. Often occurs during sleep, and may go on to involve more than one joint, becoming an oligoarthropathy or rarely, a polyarthropathy.

The acute phase usually last less than 10 days. within 7-10 days.

Patients with chronic uncontrolled hyperuricaemia, eg chronic kidney disease, may develop chronic tophaceous gout. In chronic tophaceous gout, there are solid urate crystal collections (tophi) and chronic inflammatory and destructive changes in surrounding connective tissue. Tophi are typically yellow-white in colour, non-tender, and are typically located within the articular structures, bursae, or the ears[3]. 

Management[edit | edit source]

X-ray gout.jpg

The acute gout attacks are painful and potentially disabling, needing immediate treatment. The optimal therapy is towards controlling pain and inflammation.

  1. Acute flare ups: Management aims at decreasing the inflammation and the resulting pain. The physician should start the treatment within the first 24 hours of onset to reduce the severity and duration of the flare-up. Rest with topical application of ice packs can combined with non-steroidal anti-inflammatory drugs, colchicine, or systemic glucocorticoids. The length of the treatments should be at least 7 to 10 days to prevent rebound flare-ups.[4]
  2. Patients with recurrent attacks, tophi, urate arthropathy, or renal damage and to symptomatic patients with very high serum uric acid levels should start urate lowering therapy (ULT). In the long-term xanthine oxidase inhibitors (e.g. allopurinol or febuxostat), uricosuric drugs (e.g. probenecid), or uricase agents (e.g. pegloticase) may be used to reduce urate levels and prevent further acute flares[2].
  3. Tophaceous gout can also be managed with surgical excision of symptomatic lesions.

Non-pharmacologic : Patients with gout are encouraged to modify their lifestyles to prevent future attacks. Diet recommendations include reducing alcohol consumption, limiting purine-rich foods (meat, seafood, high fructose corn syrup, and sweetened soft drinks), and substituting low-fat or non-fat dairy products for their higher fat content counterparts. Weight loss and adequate hydration will also help reduce gout flare-up frequency[4].[7]

Diagnosis[edit | edit source]

Synovial Fluid Analysis: Monosodium urate crystal identification remains the gold standard for gout diagnosis. Gout flare is marked by the presence of MSU crystals in synovial fluid obtained from affected joints of bursas visualized by direct examination of a fluid sample using compensated polarized light microscopy.[4]

Physical Therapy Management [edit | edit source]

The physical therapist should be aware that any patient with a history of gout, hyperuricemia, and/or a septic joint presentation should be referred for medical evaluation prior to treatment.[6]

During acute exacerbations the physical therapist should focus on reinforcement of management program and splinting, orthotics, or other assistive devices to protect the affected joint(s). [6]

A 2002 study in the Journal of Rheumatology found that the use of cryotherapy to alleviate the pain associated with acute bouts of gout may be effective. [8]

During intercritical phases physical therapists may offer assistance with maintenance of ROM, strength, and function.  The physical therapist can also assist the patient in the creation of a suitable exercise routine and keeping their weight under control. [6][9]

Pseudogout[edit | edit source]

Pseuodgout

Pseudogout, also known as pyrophosphate Calcium pyrophosphate dihydrate disease (CPPD), is defined by the co-occurrence of arthritis with evidence of CPPD deposition within the articular cartilage. it is characterized by sudden, painful swelling in one or more of the joints. These episodes can last for days or weeks. The most commonly affected joint is the knee. It isn't clear why crystals form in the joints and cause pseudogout, but the risk increases with age. Treatments can help relieve pain and reduce inflammation[10].

  • It is a form of arthritis that occurs 1/8th as often as gout.
  • Symptoms are very similar to gout; however, the knee joint is primarily affected.
  • Diagnosis is made by aspiration of synovial fluid.[11][12]

The difference between pseudogout and gout is outlined in below video.

Case Reports[edit | edit source]

One case report that presents interesting implications for the physical therapist involves an elderly patient with lumbar spondylodiscal pathology secondary to her polyarticular gout.  [13]
Interesting case report involving a middle aged man that developed symptoms of gout during a hospitalization.  [14]
Case report of a patient whose tophi were limiting the FDS tendon. [15]
Case report involving presentation and differential diagnosis of acute monoarthritis. [16]

A series of case reports that examine some of the negative effects of Colchicine as a form of pharmacological management. [17]

References[edit | edit source]

  1. ↑ Cronstein BN, Terkeltaub R. The inflammatory process of gout and its treatment. Arthritis Research & Therapy. 2006 Apr;8(1):1-7 Available: .https://arthritis-research.biomedcentral.com/articles/10.1186/ar1908#Abs1 (accessed 15.5.2022)
  2. ↑ 2.0 2.1 Drug and Therapeutics Bulletin. Latest guidance on the management of gout. Available: https://www.bmj.com/content/362/bmj.k2893(accessed 15.5.2022)
  3. ↑ 3.0 3.1 3.2 3.3 Radiopedia Gout Available: https://radiopaedia.org/articles/gout(accessed 14.5.2022)
  4. ↑ 4.0 4.1 4.2 4.3 4.4 Fenando A, Widrich J. Gout (podagra).Available:https://www.ncbi.nlm.nih.gov/books/NBK546606/ (accessed 14.5.2022)
  5. ↑ Joseph Kaplan, MD, MS, FACEP Attending Physician, Department of Emergency Medicine, Martin Army Community Hospital, Fort Benning, Georgia
  6. ↑ 6.0 6.1 6.2 6.3 Goodman CC, Fuller KS. Pathology: Implications for the Physical Therapist. 3rd ed. Saint Louis, MO: Saunders; 2009.
  7. ↑ Primatesta P, Plana E, Rothenbacher D. Gout treatment and comorbidities: a retrospective cohort study in a large US managed care population. BMC musculoskeletal disorders. 2011 Dec;12(1):103.
  8. ↑ Schlesinger N, Detry MA, Holland BK, Baker DG, Beutler AM, Rull M, Hoffman BI, Schumacher HR Jr. Local ice therapy during bouts of acute gouty arthritis. J Rheumatol 2002; 29(2): 331-334
  9. ↑ Gout. National Institute of Arthritis and Musculoskeletal and Skin Diseases. December 2006. http://www.niams.nih.gov/Health_Info/Gout/default.asp. Accessed March 2010.
  10. ↑ Mayo clinic Pseudogout Available: https://www.mayoclinic.org/diseases-conditions/pseudogout/symptoms-causes/syc-20376983(accessed 15.5.2022)
  11. ↑ Goodman C, Snyder T. Differential Diagnosis for Physical Therapists: Screening for Referral. St. Louis, Missouri: Saunders Elsevier, 2007.
  12. ↑ Wheeless, C R. Pseudogout and Chondrocalcinosis. Wheeless' Textbook of Orthopaedics. November 2008. www.wheelessonline.com/image9/cppd2.jpg. Accessed March 2010.
  13. ↑ Lagier R, Gee W M. Spondylodiscal erosions due to gout: anatomicoradiological study of a case. Annals of the Rheumatic Diseases. 1983 June; 42(3): 350-353.
  14. ↑ Dhoble A, Balakrishnan V, Smith R. Chronic tophaceous gout presenting as acute arthritis during an acute illness: a case report. Cases Journal. 2008; 1: 238.
  15. ↑ Sano K, et. al. Atypical Triggering at the Wrist due to Intratendinous Infiltration of Tophaceous Gout. Springer Hand. 2009 March; 4(1): 78-80.
  16. ↑ Ma L, Cranney A, and Holroyd-Leduc J. Acute monoarthritis: What is the cause of my patient's painful swollen joint. CMAJ. 2009 January; 180(1): 59-65.
  17. ↑ Morris I, Varughese G, and Mattingly P. Colchicine in acute gout. BMJ. 2003 November; 327(7426): 1275-1276.

  

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