Back Clinic Arthropathies Chiropractic and Physical Therapy Team. Charcot’s is degeneration of a weight-bearing joint and arthrogryposis which means, “curving of joints.” this is a general term that describes any disease of the joints. A group of disorders can afflict the joints, such as sacroiliitis, which causes inflammation in the sacroiliac joint. Doctors use arthropathy interchangeably with arthritis, which means “joint inflammation.”The forms that are distinct from arthritis are Neuropathic arthropathy, nerve damage from diabetes, or other nerve conditions resulting in slow damage to joints.
In diabetic people, arthropathy usually affects the foot and ankle. Hypertrophic pulmonary osteoarthropathy is where the bone ends of the ankles, knees, wrists, and elbows start to grow abnormally and painfully. Fingertips start to become rounded, called “clubbing.” This form of arthropathy usually happens to people with lung cancer. And Hemarthrosis is when blood leaks into a joint like the knee. This occurs after injuries or medical procedures and is a problem in people with hemophilia.
Rheumatoid arthritis (RA) is a condition that causes considerable discomfort if diagnosed with this autoimmune disease. This is when your immune system starts attacking your joints, instead of foreign invaders, which then causes inflammation.
The worse the RA, the more severe the symptoms become. If things get bad enough you can lose mobility altogether, which is why it is so important to get treatment. Fortunately, chiropractic is excellent for reducing inflammation and improving mobility. Chiropractic treatment can do a lot to ease your pain and get you back to moving the way you are supposed to.
RA and Chiropractic
Chiropractic is an effective RA treatment for a number of reasons. Chiropractic treatment:
Individual Treatment
The image many people have of a chiropractic adjustment is one of popping backs and hard, jerking motions. While adjustments can certainly include these things, they do not have to. According to the Arthritis Foundation, chiropractors have more than 150 techniques they can use to adjust your body.
They strive to give treatments specific to the needs of each patient, which means adjusting the body as gently as necessary to produce the desired result. If your joints are swollen and painful the chiropractor will carefully work to realign the joint�which reduces inflammation and improves movement�while minimizing any pain or discomfort you feel from the adjustment.
Reduced Inflammation
With RA typically the worst symptoms are the result of inflammation. Chiropractic treatment may not be able to change the way your immune system is malfunctioning, but it can do a lot to help the painful areas become less inflamed.
The treatment you get from your chiropractor will ensure that your joints are moving as properly as possible given your condition. By putting the body back in alignment, chiropractic improves the way the nervous system operates and lessens inflammation.
Improved Mobility
One of the most difficult things for many with RA is the loss of mobility that comes when their joints swell. When the pain becomes more substantial it is normal for RA sufferers to avoid movement because it hurts.
But it is important to remember that movement, even when it hurts, is necessary to maintain joint mobility. The longer you avoid moving a joint the more likely it is that you will lose function.
A useful aspect of chiropractic is that you can get help with moving, so you are not all alone with the daunting prospect of moving your joints so they start working better. Your chiropractor is your partner in movement, helping to guide your body so that it moves as well as possible. Results are different for everyone based on their unique situations, but you can be sure that chiropractic will serve as a powerful tool to keep your body working as well as possible.
Hand Deformed From Rheumatoid Arthritis
Drug-Free and Non-invasive
In chiropractic, the focus is to help the body heal itself, which means avoiding surgery and prescription medications as much as possible. Surgery and medication often have unwanted side-effects�sometimes worse than the problem they were intended to solve. With chiropractic negative side-effects are unlikely. You can get a lot of relief from gentle, effective treatments that will not make you feel worse than when you started.
Please contact our office to schedule an appointment. We look forward to speaking with you!
Opioid Addiction Alternative
Opioids (such as hydrocodone, oxycodone, codeine, and morphine) mask symptoms and do nothing to address the cause of pain.
There is an opioid crisis raging.� A sensible and safe alternative to opioids: Custom-made orthotics help relieve low back pain as well as hip and neck pain by removing imbalances in the musculoskeletal system, which originate in the feet.
Before considering taking an opioid for pain control, give Chiropractic care and foot orthotics a try. The combination of Chiropractic and orthotics is proven in clinical studies.
In 2015, about 2 million Americans had substance abuse disorders related to opioid medications.
In 2012, 80 out of 100 Americans were prescribed opioids. That’s about 259 million prescriptions � more than enough to give every American adult their own bottle of pills.
Less Pain & More Comfort
Custom orthotics help more than your feet! Stabilizing orthotics bring health and healing to the whole body by balancing the musculoskeletal system.
El Paso Back Clinic
Here are some videos that discuss how chiropractic care can help with arthritis, fibromyalgia, seniors and whole body wellness.
NCBI Resources
Here are some articles to check out for extended information on arthropathies.
About 1.5 million people in the United States have rheumatoid arthritis. Rheumatoid arthritis, or RA, is a chronic, autoimmune disease characterized by pain and inflammation of the joints. With RA, the immune system, which protects our well-being by attacking foreign substances like bacteria and viruses, mistakenly attacks the joints. Rheumatoid arthritis most commonly affects the joints of the hands, feet, wrists, elbows, knees and ankles. Many healthcare professionals recommend early diagnosis and treatment of RA.
Abstract
Rheumatoid arthritis is the most commonly diagnosed systemic inflammatory arthritis. Women, smokers, and those with a family history of the disease are most often affected. Criteria for diagnosis include having at least one joint with definite swelling that is not explained by another disease. The likelihood of a rheumatoid arthritis diagnosis increases with the number of small joints involved. In a patient with inflammatory arthritis, the presence of a rheumatoid factor or anti-citrullinated protein antibody, or elevated C-reactive protein level or erythrocyte sedimentation rate suggests a diagnosis of rheumatoid arthritis. Initial laboratory evaluation should also include complete blood count with dif- ferential and assessment of renal and hepatic function. Patients taking biologic agents should be tested for hepatitis B, hepatitis C, and tuberculosis. Earlier diagnosis of rheumatoid arthritis allows for earlier treatment with disease-modifying antirheumatic agents. Combinations of medications are often used to control the disease. Methotrexate is typically the first-line drug for rheumatoid arthritis. Biologic agents, such as tumor necrosis factor inhibitors, are generally considered second-line agents or can be added for dual therapy. The goals of treatment include minimiza- tion of joint pain and swelling, prevention of radiographic damage and visible deformity, and continuation of work and personal activities. Joint replacement is indicated for patients with severe joint damage whose symptoms are poorly controlled by medical management. (Am Fam Physician. 2011;84(11):1245-1252. Copyright � 2011 American Academy of Family Physicians.)
Rheumatoid arthritis (RA) is the most common inflammatory arthritis, with a lifetime prevalence of up to 1 percent worldwide.1 Onset can occur at any age, but peaks between 30 and 50 years.2 Disability is common and significant. In a large U.S. cohort, 35 percent of patients with RA had work disability after 10 years.3
Etiology and Pathophysiology
Like many autoimmune diseases, the etiology of RA is multifactorial. Genetic susceptibility is evident in familial clustering and monozygotic twin studies, with 50 percent of RA risk attributable to genetic factors.4 Genetic associations for RA include human leukocyte antigen-DR45 and -DRB1, and a variety of alleles called the shared epitope.6,7 Genome-wide association studies have identified additional genetic signatures that increase the risk of RA and other autoimmune diseases, including STAT4 gene and CD40 locus.5 Smoking is the major environmental trigger for RA, especially in those with a genetic predisposition.8 Although infections may unmask an autoimmune response, no particular pathogen has been proven to cause RA.9
RA is characterized by inflammatory pathways that lead to proliferation of synovial cells in joints. Subsequent pannus formation may lead to underlying cartilage destruction and bony erosions. Overproduction of pro-inflammatory cytokines, including tumor necrosis factor (TNF) and interleukin-6, drives the destructive process.10
Risk Factors
Older age, a family history of the disease, and female sex are associated with increased risk of RA, although the sex differential is less prominent in older patients.1 Both current and prior cigarette smoking increases the risk of RA (relative risk [RR] = 1.4, up to 2.2 for more than 40-pack-year smokers).11
Pregnancy often causes RA remission, likely because of immunologic tolerance.12 Parity may have long-lasting impact; RA is less likely to be diagnosed in parous women than in nulliparous women (RR = 0.61).13,14 Breastfeeding decreases the risk of RA (RR = 0.5 in women who breastfeed for at least 24 months), whereas early menarche�(RR = 1.3 for those with menarche at 10 years of age or younger) and very irregular menstrual periods (RR = 1.5) increase risk.14 Use of oral contraceptive pills or vitamin E does not affect RA risk.15
Diagnosis
Typical Presentation
Patients with RA typically present with pain and stiffness in multiple joints. The wrists, proximal interphalangeal joints, and metacarpophalangeal joints are most commonly involved. Morning stiffness lasting more than one hour suggests an inflammatory etiology. Boggy swelling due to synovitis may be visible (Figure 1), or subtle synovial thickening may be palpable on joint examination. Patients may also present with more indolent arthralgias before the onset of clinically apparent joint swelling. Systemic symptoms of fatigue, weight loss, and low-grade fever may occur with active disease.
Diagnostic Criteria
In 2010, the American College of Rheumatology and European League Against Rheumatism collaborated to create new classification criteria for RA (Table 1).16 The new criteria are an effort to diagnose RA earlier in patients who may not meet the 1987 American College of Rheumatology classification criteria. The 2010 criteria do not include presence of rheumatoid nodules or radiographic erosive changes, both of which are less likely in early RA. Symmetric arthri- tis is also not required in the 2010 criteria, allowing for early asymmetric presentation.
In addition, Dutch researchers have developed and validated a clinical prediction rule for RA (Table 2).17,18 The purpose of this rule is to help identify patients with undifferentiated arthritis that is most likely to progress to RA, and to guide follow-up and referral.
Diagnostic Tests
Autoimmune diseases such as RA are often characterized by the presence of autoanti- bodies. Rheumatoid factor is not specific for RA and may be present in patients with other diseases, such as hepatitis C, and in healthy older persons. Anti-citrullinated protein antibody is more specific for RA and may play a role in disease pathogenesis.6 Approxi- mately 50 to 80 percent of persons with RA have rheumatoid factor, anti-citrullinated protein antibody, or both.10 Patients with RA may have a positive antinuclear antibody test result, and the test is of prognostic impor- tance in juvenile forms of this disease.19 C-reactive protein levels and erythrocyte sedimentation rate are often increased with active RA, and these acute phase reactants are part of the new RA classification criteria.16 C-reactive protein levels and erythrocyte sedimentation rate may also be used to follow disease activity and response to medication.
Baseline complete blood count with differential and assessment of renal and hepatic function are helpful because the results may influence treatment options (e.g., a patient with renal insufficiency or significant thrombocytopenia likely would not be prescribed a nonsteroidal anti-inflammatory drug [NSAID]). Mild anemia of chronic disease occurs in 33 to 60 percent of all patients with RA,20 although gastrointestinal blood loss should also be considered in patients taking corticosteroids or NSAIDs. Methotrexate is contraindicated in patients with hepatic disease, such as hepatitis C, and in patients with significant renal impairment.21 Biologic therapy, such as a TNF inhibitor, requires a negative tuberculin test or treatment for latent tuberculosis. Hepatitis B reactivation can also occur with TNF inhibitor use.22 Radiography of hands and feet should be performed to evaluate for characteristic periarticular erosive changes,�which may be indicative of a more aggressive RA subtype.10
Differential Diagnosis
Skin findings suggest systemic lupus erythematosus, systemic sclerosis, or psoriatic arthritis. Polymyalgia rheumatica should be considered in an older patient with symptoms primarily in the shoulder and hip, and the patient should be asked questions related to associated temporal arteritis.
Chest radiography is helpful to evaluate for sarcoidosis as an etiology of arthritis.�Patients with inflammatory back symptoms, a history of inflammatory bowel disease, or inflammatory eye disease may have spondyloarthropathy. Persons with less than six weeks of symptoms may have a viral process, such as parvovirus. Recurrent self-limited episodes of acute joint swelling suggest crystal arthropathy, and arthrocentesis should be performed to evaluate for monosodium urate monohydrate or calcium pyrophosphate dihydrate crystals. The presence of numerous myofascial trigger points and somatic symptoms may suggest fibromyalgia, which can coexist with RA. To help guide diagnosis and determine treatment strategy, patients with inflammatory arthritis should be promptly referred to a rheumatology subspecialist.16,17
Rheumatoid arthritis, or RA, is the most common type of arthritis. RA is an autoimmune disease, caused when the immune system, the human body’s defense system, attacks its own cells and tissues, particularly the joints. Rheumatoid arthritis is frequently identified by symptoms of pain and inflammation, often affecting the small joints of the hands, wrists and feet. According to many healthcare professionals, early diagnosis and treatment of RA is essential to prevent further joint damage and decrease painful symptoms. Dr. Alex Jimenez D.C., C.C.S.T. Insight
Treatment
After RA has been diagnosed and an initial evaluation performed, treatment should begin. Recent guidelines have addressed the management of RA,21,22 but patient preference also plays an important role. There are special considerations for women of childbearing age because many medications have deleterious effects on pregnancy. Goals of therapy include minimizing joint pain and swelling, preventing deformity (such as ulnar deviation) and radiographic damage (such as erosions), maintaining quality of life (personal and work), and controlling extra-articular manifestations. Disease-modifying antirheumatic drugs (DMARDs) are the mainstay of RA therapy.
DMARDs
DMARDs can be biologic or nonbiologic (Table 3).23 Biologic agents include monoclonal antibodies and recombinant receptors to block cytokines that promote the inflammatory cascade responsible for RA symptoms. Methotrexate is recommended as the first- line treatment in patients with active RA, unless contraindicated or not tolerated.21 Leflunomide (Arava) may be used as an alternative to methotrexate, although gastrointestinal adverse effects are more common. Sulfasalazine (Azulfidine) or hydroxychloroquine (Plaquenil) pro-inflammatory as monotherapy in patients with low disease�activity or without poor prognostic features (e.g., seronegative, non-erosive RA).21,22
Combination therapy with two or more DMARDs is more effective than monotherapy; however, adverse effects may also be greater.24 If RA is not well controlled with a nonbiologic DMARD, a biologic DMARD should be initiated.21,22 TNF inhibitors are the first-line biologic therapy and are the most studied of these agents. If TNF inhibitors are ineffective, additional biologic therapies can be considered. Simultaneous use of more than one biologic therapy (e.g., adalimumab [Humira] with abatacept [Orencia]) is not�recommended because of an unacceptable rate of adverse effects.21
NSAIDs and Corticosteroids
Drug therapy for RA may involve NSAIDs and oral, intramuscular, or intra-articular corticosteroids for controlling pain and inflammation. Ideally, NSAIDs and corticosteroids are used only for short-term management. DMARDs are the preferred therapy.21,22
Complementary Therapies
Dietary interventions, including vegetarian and Mediterranean diets, have been�studied in the treatment of RA without convincing evidence of benefit.25,26 Despite some favorable outcomes, there is a lack of evidence for the effectiveness of acupuncture in placebo-controlled trials of patients with RA.27,28 In addition, thermotherapy and therapeutic ultrasound for RA have not been studied adequately.29,30 A Cochrane review of herbal treatments for RA concluded that gamma-linolenic acid (from evening primrose or black currant seed oil) and Tripterygium wilfordii (thunder god vine) have potential benefits.31 It is important to inform patients that serious adverse effects have been reported with use of herbal therapy.31
Exercise and Physical Therapy
Results of randomized controlled trials sup- port physical exercise to improve quality of life and muscle strength in patients with RA.32,33 Exercise training programs have not been shown to have deleterious effects on RA disease activity, pain scores, or radiographic joint damage.34 Tai chi has been shown to improve ankle range of motion in persons with RA, although randomized trials are limited.35 Randomized controlled trials of Iyengar yoga in young adults with RA are underway.36
Duration of Treatment
Remission is obtainable in 10 to 50 percent of patients with RA, depending on how remission is defined and the intensity of therapy.10 Remission is more likely in males, nonsmokers, persons younger than 40 years, and in those with late-onset disease (patients older than 65 years), with shorter duration of disease, with milder disease activity, without elevated acute phase reactants, and without positive rheumatoid factor or anti-citrullinated protein antibody findings.37
After the disease is controlled, medication dosages may be cautiously decreased to the minimum amount necessary. Patients will require frequent monitoring to ensure stable symptoms, and prompt increase in medication is recommended with disease flare-ups.22
Joint Replacement
Joint replacement is indicated when there is severe joint damage and unsatisfactory control of symptoms with medical management. Long-term outcomes are support, with only 4 to 13 percent of large joint replacements requiring revision within 10 years.38 The hip and knee are the most commonly replaced joints.
Long-Term Monitoring
Although RA is considered a disease of the joints, it is also a systemic disease capable of involving multiple organ systems. Extra-articular manifestations of RA are included in Table 4.1,2,10
Patients with RA have a twofold increased risk of lymphoma, which is thought to be caused by the underlying inflammatory�process, and not a consequence of medical treatment.39 Patients with RA are also at an increased risk of coronary artery disease, and physicians should work with patients to modify risk factors, such as smoking, high blood pressure, and high cholesterol.40,41 Class III or IV congestive heart failure (CHF) is a contraindication for using TNF inhibitors, which can worsen CHF outcomes.21 In patients with RA and malignancy, caution is needed with continued use of DMARDs, especially TNF inhibitors. Biologic DMARDs, methotrexate, and leflunomide should not be initiated in patients with active herpes zoster, significant fungal infection, or bacterial infection requiring antibiotics.21 Complications of RA and its treatments are listed in Table 5.1,2,10
Prognosis
Patients with RA live three to 12 years less than the general population.40 Increased mortality in these patients is mainly due to accelerated cardiovascular disease, especially in those with high disease activity and chronic inflammation. The relatively new biologic therapies may reverse progression of atherosclerosis and extend life in those with RA.41
Data Sources: A PubMed search was completed in Clinical Queries using the key terms rheumatoid arthritis, extra-articular manifestations, and disease-modifying antirheumatic agents. The search included meta-analyses, randomized controlled trials, clinical trials, and reviews. Also searched were the Agency for Healthcare Research and Quality evidence reports, Clinical Evidence, the Cochrane database, Essential Evidence, and UpToDate. Search date: September 20, 2010.
Author disclosure: No relevant financial affiliations to disclose.
In conclusion, rheumatoid arthritis is a chronic, autoimmune disease which causes painful symptoms, such as pain and discomfort, inflammation and swelling of the joints, among others. The joint damage characterized as RA is symmetrical, meaning it generally affects both sides of the body. Early�diagnosis is essential for treatment of RA. The scope of our information is limited to chiropractic and spinal health issues. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at�915-850-0900�.
Curated by Dr. Alex Jimenez
Additional Topic Discussion: Relieving Knee Pain without Surgery
Knee pain is a well-known symptom which can occur due to a variety of knee injuries and/or conditions, including�sports injuries. The knee is one of the most complex joints in the human body as it is made-up of the intersection of four bones, four ligaments, various tendons, two menisci, and cartilage. According to the American Academy of Family Physicians, the most common causes of knee pain include patellar subluxation, patellar tendinitis or jumper’s knee, and Osgood-Schlatter disease. Although knee pain is most likely to occur in people over 60 years old, knee pain can also occur in children and adolescents. Knee pain can be treated at home following the RICE methods, however, severe knee injuries may require immediate medical attention, including chiropractic care.
1. Etiology and pathogenesis of rheumatoid arthritis. In: Firestein GS, Kelley WN, eds. Kelley�s Textbook of Rheu- matology. 8th ed. Philadelphia, Pa.: Saunders/Elsevier; 2009:1035-1086. 2. Bathon J, Tehlirian C. Rheumatoid arthritis clinical and laboratory manifestations. In: Klippel JH, Stone JH, Crofford LJ, et al., eds. Primer on the Rheumatic Dis- eases. 13th ed. New York, NY: Springer; 2008:114-121. 3. Allaire S, Wolfe F, Niu J, et al. Current risk factors for work disability associated with rheumatoid arthritis. Arthritis Rheum. 2009;61(3):321-328. 4. MacGregor AJ, Snieder H, Rigby AS, et al. Characteriz- ing the quantitative genetic contribution to rheumatoid arthritis using data from twins. Arthritis Rheum. 2000; 43(1):30-37. 5. Orozco G, Barton A. Update on the genetic risk fac- tors for rheumatoid arthritis. Expert Rev Clin Immunol. 2010;6(1):61-75. 6. Balsa A, Cabezo?n A, Orozco G, et al. Influence of HLA DRB1 alleles in the susceptibility of rheumatoid arthritis and the regulation of antibodies against citrullinated proteins and rheumatoid factor. Arthritis Res Ther. 2010;12(2):R62. 7. McClure A, Lunt M, Eyre S, et al. Investigating the via- bility of genetic screening/testing for RA susceptibility using combinations of five confirmed risk loci. Rheuma- tology (Oxford). 2009;48(11):1369-1374. 8. Bang SY, Lee KH, Cho SK, et al. Smoking increases rheu- matoid arthritis susceptibility in individuals carrying the HLA-DRB1 shared epitope, regardless of rheumatoid factor or anti-cyclic citrullinated peptide antibody sta- tus. Arthritis Rheum. 2010;62(2):369-377. 9. Wilder RL, Crofford LJ. Do infectious agents cause rheu- matoid arthritis? Clin Orthop Relat Res. 1991;(265): 36-41. 10. Scott DL, Wolfe F, Huizinga TW. Rheumatoid arthritis. Lancet. 2010;376(9746):1094-1108. 11. Costenbader KH, Feskanich D, Mandl LA, et al. Smoking intensity, duration, and cessation, and the risk of rheu- matoid arthritis in women. Am J Med. 2006;119(6): 503.e1-e9. 12. Kaaja RJ, Greer IA. Manifestations of chronic disease during pregnancy. JAMA. 2005;294(21):2751-2757. 13. Guthrie KA, Dugowson CE, Voigt LF, et al. Does preg- nancy provide vaccine-like protection against rheuma- toid arthritis? Arthritis Rheum. 2010;62(7):1842-1848. 14. Karlson EW, Mandl LA, Hankinson SE, et al. Do breast- feeding and other reproductive factors influence future risk of rheumatoid arthritis? Results from the Nurses� Health Study. Arthritis Rheum. 2004;50(11):3458-3467. 15. Karlson EW, Shadick NA, Cook NR, et al. Vitamin E in the primary prevention of rheumatoid arthritis: the Women�s Health Study. Arthritis Rheum. 2008;59(11): 1589-1595. 16. Aletaha D, Neogi T, Silman AJ, et al. 2010 rheumatoid arthritis classification criteria: an American College of Rheumatology/European League Against Rheumatism collaborative initiative [published correction appears in Ann Rheum Dis. 2010;69(10):1892]. Ann Rheum Dis. 2010;69(9):1580-1588. 17. van der Helm-van Mil AH, le Cessie S, van Dongen H, et al. A prediction rule for disease outcome in patients with recent-onset undifferentiated arthritis. Arthritis Rheum. 2007;56(2):433-440. 18. Mochan E, Ebell MH. Predicting rheumatoid arthritis risk in adults with undifferentiated arthritis. Am Fam Physi- cian. 2008;77(10):1451-1453. 19. Ravelli A, Felici E, Magni-Manzoni S, et al. Patients with antinuclear antibody-positive juvenile idiopathic arthri- tis constitute a homogeneous subgroup irrespective of the course of joint disease. Arthritis Rheum. 2005; 52(3):826-832. 20. Wilson A, Yu HT, Goodnough LT, et al. Prevalence and outcomes of anemia in rheumatoid arthritis. Am J Med. 2004;116(suppl 7A):50S-57S. 21. Saag KG, Teng GG, Patkar NM, et al. American College of Rheumatology 2008 recommendations for the use of nonbiologic and biologic disease-modifying antirheu- matic drugs in rheumatoid arthritis. Arthritis Rheum. 2008;59(6):762-784. 22. Deighton C, O�Mahony R, Tosh J, et al.; Guideline Devel- opment Group. Management of rheumatoid arthritis: summary of NICE guidance. BMJ. 2009;338:b702. 23. AHRQ. Choosing medications for rheumatoid arthritis. April 9, 2008. www.effectivehealthcare.ahrq.gov/ ehc/products/14/85/RheumArthritisClinicianGuide.pdf. Accessed June 23, 2011. 24. Choy EH, Smith C, Dore? CJ, et al. A meta-analysis of the efficacy and toxicity of combining disease-modify- ing anti-rheumatic drugs in rheumatoid arthritis based on patient withdrawal. Rheumatology (Oxford). 2005; 4 4 (11) :1414 -1421. 25. Smedslund G, Byfuglien MG, Olsen SU, et al. Effective- ness and safety of dietary interventions for rheumatoid arthritis. J Am Diet Assoc. 2010;110(5):727-735. 26. Hagen KB, Byfuglien MG, Falzon L, et al. Dietary inter- ventions for rheumatoid arthritis. Cochrane Database Syst Rev. 2009;21(1):CD006400. 27. Wang C, de Pablo P, Chen X, et al. Acupuncture for pain relief in patients with rheumatoid arthritis: a systematic review. Arthritis Rheum. 2008;59(9):1249-1256. 28. Kelly RB. Acupuncture for pain. Am Fam Physician. 2009;80(5):481-484. 29. Robinson V, Brosseau L, Casimiro L, et al. Thermother- apy for treating rheumatoid arthritis. Cochrane Data- base Syst Rev. 2002;2(2):CD002826. 30. Casimiro L, Brosseau L, Robinson V, et al. Therapeutic ultrasound for the treatment of rheumatoid arthritis. Cochrane Database Syst Rev. 2002;3(3):CD003787. 31. Cameron M, Gagnier JJ, Chrubasik S. Herbal therapy for treating rheumatoid arthritis. Cochrane Database Syst Rev. 2011;(2):CD002948. 32. Brodin N, Eurenius E, Jensen I, et al. Coaching patients with early rheumatoid arthritis to healthy physical activ- ity. Arthritis Rheum. 2008;59(3):325-331. 33. Baillet A, Payraud E, Niderprim VA, et al. A dynamic exercise programme to improve patients� disability in rheumatoid arthritis: a prospective randomized con- trolled trial. Rheumatology (Oxford). 2009;48(4): 410-415. 34. Hurkmans E, van der Giesen FJ, Vliet Vlieland TP, et al. Dynamic Exercise programs (aerobic capacity and/or mus- cle strength training) in patients with rheumatoid arthri- tis. Cochrane Database Syst Rev. 2009;(4):CD006853. 35. Han A, Robinson V, Judd M, et al. Tai chi for treat- ing rheumatoid arthritis. Cochrane Database Syst Rev. 2004;(3):CD004849. 36. Evans S, Cousins L, Tsao JC, et al. A randomized con- trolled trial examining Iyengar yoga for young adults with rheumatoid arthritis. Trials. 2011;12:19. 37. Katchamart W, Johnson S, Lin HJ, et al. Predictors for remis- sion in rheumatoid arthritis patients: a systematic review. Arthritis Care Res (Hoboken). 2010;62(8):1128-1143. 38. Wolfe F, Zwillich SH. The long-term outcomes of rheu- matoid arthritis: a 23-year prospective, longitudinal study of total joint replacement and its predictors in 1,600 patients with rheumatoid arthritis. Arthritis Rheum. 1998;41(6):1072-1082. 39. Baecklund E, Iliadou A, Askling J, et al. Association of chronic inflammation, not its treatment, with increased lymphoma risk in rheumatoid arthritis. Arthritis Rheum. 2006;54(3):692-701. 40. Friedewald VE, Ganz P, Kremer JM, et al. AJC editor�s consensus: rheumatoid arthritis and atherosclerotic cardiovascular disease. Am J Cardiol. 2010;106(3): 442-447. 41. Atzeni F, Turiel M, Caporali R, et al. The effect of phar- macological therapy on the cardiovascular system of patients with systemic rheumatic diseases. Autoimmun Rev. 2010;9(12):835-839.
M/C dislocation of the foot at tarsal-metatarsal articulation (Lisfranc joint). Direct impact or landing and plantar or dorsal flexing the foot. Lisfranc ligament holding 2nd MT base and 1st Cu is torn. Manifests with or w/o fracture-avulsion.
Imaging: 1st step: foot radiography in most cases sufficient to Dx. MSK US may help: show disrupted Cu1-Cu2. Ligament and widened space > 2.5mm. MRI may help but not essential. Weight-bearing view aids Dx.
2-types: homolateral (1st MTP joint in contact) and divergent (2-5 MT displaced laterally and 1st MT medially)
Management: operative fixation is crucial
N.B. Atraumatic Lisfranc dislocation is a frequent complication of a diabetic Charcot foot
Osteochondral Injury of the Talus (OCD)
Common. Non-traumatic found in superior-medial talar dome. Traumatic may affect supero-lateral dome.
Clinically: pain/effusion/locking. Imaging is crucial.
1st step: radiography may reveal focal radiolucent concavity/halo, fragment.
MRI helpful esp. if OCD is cartilaginous and to demonstrate bone edema.
Jones Fx: extra-articular Fx of proximal metaphysis of the 5th MT. Prone to non-union. Often fixed operatively.
Pseudo-Jones: intra-articular avulsion of 5th MT styloid/base by eccentric contraction of Peroneus Brevis M. Managed conservatively: boot-cast immobilization. Both Jones & Pseudo-Jones Dx by foot series radiography.
Stress Fx. Calcaneus, 2nd, 3rd, 5th MTs. Repeated loading (running) or “March foot” 2nd/3rd MT. Clinically: pain on activity, reduced by rest. Dx: x-rays often unrewarding earlier. MRI or MSK US may help. Managed: Conservatively. Complications; progress into complete Fx
Turf toe: common athletic hyperextension of 1st MTP-sesamoid/plantar plate complex is tearing. 1st MTP unstable/loose. Managed operatively.
Arthritis of the Foot & Ankle
DJD of the ankle: uncommon a primary OA. Typically develops as 2nd to trauma/AVN, RA, CPPD, Hemophilic arthropathy, Juvenile Idiopathic Arthritis, etc. manifests as DJD: osteophytes, JSL, subchondral cysts all seen on x-rays
Inflammatory Arthritis: RA may develop in the ankle or any synovial joint. Will typically presents with symmetrical Hands/feet RA initially (2nd, 3rd MCP, wrists, MTPs in feet) usually with erosion, uniform JSL, juxta-articular osteopenia, and delayed subluxations.
HLA-B27 spondyloarthropathies: commonly affect lower extremity: heel, ankle esp in Reactive (Reiter). Erosive-productive bone proliferation is a crucial Dx.
Gouty Arthritis: common in the lower extremity. Ankle, mid-foot foot esp 1st MTPs. Initial onset: acute gouty arthritis with ST effusion and no erosions/tophi. Chronic tophaceous gout: peri-articular, intra-osseous punched-out erosions with over-hanging edges, no initial JSL/osteopenia, ST. Tophi may be seen.
Miscellaneous arthropathy: PVNS. Not common. Affects 3-4th decades of life. The result of synovial proliferation with Macrophages and multi-nucleated Giant Cells filled with hemosiderin and fatty accumulation may lead to inflammation, cartilage damage, extrinsic bone erosions. Dx: x-rays are insensity, MRI modality of choice. Synovial biopsy. Management: operative, can be difficult.
Neuropathic Osteoarthropathy
(Charcot’s joint) Common and on the rise d/t epidemic in type 2 DM. May present with pain initially (50% of cases) and painless destructive arthropathy as a late manifestation. Early Dx: delayed. Imaging is crucial: x-rays: initially unrewarding, some SF effusion is seen. MRI helps with early Dx and extremity off-loading. Late Dx: irreversible dislocations, collapse, disability. Note: Lisfrance dislocation in Charcot joint
M/C mid-foot (TM joint) in 40% of cases, ankle 15%. Progression: Rocker-bottom foot, ulcerations, infections, increased morbidity, and mortality.
Early Dx: by MRI is crucial. Suspect it in patients with type 2 DM especially if early non-traumatic foot/ankle pain reported.
Arthritis is characterized as the inflammation of one or multiple joints. The most common symptoms of arthritis include pain and discomfort, swelling, inflammation, and stiffness, among others. Arthritis may affect�any joint in the human body, however, it commonly develops in the knee. � Knee arthritis can make everyday�physical activities difficult. The most prevalent types of arthritis are osteoarthritis and rheumatoid arthritis, although there are well over 100 distinct forms of arthritis, affecting children and adults alike. While there is no cure for arthritis, many treatment approaches can help treat the symptoms of knee arthritis.
Anatomy of the Knee
� The knee is the largest and strongest joint in the human body. It is made up of the lower end of the thigh bone,�or femur, the top end of the shin bone, or tibia, and the kneecap, or patella. The ends of the three bones are covered with articular cartilage, a smooth, slippery structure which protects and cushions the bones when bending and straightening the knee.
� Two wedge-shaped parts of cartilage, known as the meniscus, function as shock absorbers between the bones of the knee to help cushion the joint and provide stability. The knee joint is also surrounded by a thin lining known as the synovial membrane. This membrane releases a fluid which lubricates the cartilage and also helps reduce friction in the knee. The significant kinds of arthritis that affect the knee�include osteoarthritis, rheumatoid arthritis, and post-traumatic arthritis.
Osteoarthritis
� Osteoarthritis is the most common type of arthritis which affects the knee joint. This form of arthritis is a degenerative, wear-and-tear health issue which occurs most commonly in people 50 years of age and older, however, it may also develop in younger people.
� In osteoarthritis, the cartilage in the knee joint gradually wears away. As the cartilage wears away, the distance between the bones decreases. This can result in bone rubbing and it can�create painful bone spurs. Osteoarthritis generally develops slowly but the pain may worsen over time.
Rheumatoid Arthritis
� Rheumatoid arthritis is a chronic health issue which affects multiple joints throughout the body, especially the knee joint. RA is also symmetrical, meaning it often affects the same joint on each side of the human body.
� In rheumatoid arthritis, the synovial membrane that covers the knee joint becomes inflamed and swollen, causing knee pain, discomfort, and stiffness. RA is an autoimmune disease, which means that the immune system attacks its own soft tissues. The immune system attacks healthy tissue,�including tendons, ligaments and cartilage, as well as softens the bone.
Post-traumatic Arthritis
� Posttraumatic arthritis is a form of arthritis that develops after damage or injury to the knee. By way of instance, the knee joint may be harmed by a broken bone, or fracture, and result in post-traumatic arthritis years after the initial injury. Meniscal tears and ligament injuries can cause additional wear-and-tear on the knee joint, which over time can lead to arthritis and other problems.
Symptoms of Knee Arthritis
� The most common symptoms of knee arthritis include pain and discomfort, inflammation, swelling, and stiffness. Although sudden onset is probable, the painful symptoms generally�develop gradually over time. Additional symptoms of knee arthritis can be recognized as follows:
The joint may become stiff and swollen, making it difficult to bend and straighten the knee.
Swelling and inflammation may be worse in the morning, or when sitting or resting.
Vigorous activity might cause the pain to flare up.
Loose fragments of cartilage and other soft tissue may interfere with the smooth motion of the joints, causing the knee to lock or stick through motion. It could also creak, click, snap or make a grinding sound, known as crepitus.
Pain can cause a sense of fatigue or buckling from the knee.
Many individuals with arthritis may also describe increased joint pain with rainy weather and climate changes.
Diagnosis for Knee Arthritis
� During the patient’s appointment for diagnosis of knee arthritis, the healthcare professional will talk about the symptoms and medical history, as well as conduct a physical examination. The doctor may also order imaging diagnostic tests, such as X-rays, MRI or blood tests for further diagnosis. During the physical examination, the doctor will search for:
Joint inflammation, swelling, warmth, or redness
Tenderness around the knee joint
Assortment of passive and active movement
Instability of the knee joint
Crepitus, the grating sensation inside the joint, with motion
Pain when weight is placed on the knee
Issues with gait, or manner of walking
Any signs of damage or injury to the muscles, tendons, and ligaments surrounding the knee joint
Involvement of additional joints (an indicator of rheumatoid arthritis)
Imaging Diagnostic Tests
X-rays. These imaging diagnostic tests produce images of compact structures, such as bones. They can help distinguish among various forms of arthritis. X-rays for knee arthritis may demonstrate a portion of the joint distance, changes in the bone as well as the formation of bone spurs, known as osteophytes.
Additional tests. Sometimes, magnetic resonance imaging, or MRI, scans, computed tomography, or CT,�scans, or bone scans are required to ascertain the condition of the bone and soft tissues of the knee.
Blood Tests
� Your doctor may also recommend blood tests to determine which type of arthritis you have. With some kinds of arthritis, such as rheumatoid arthritis, blood tests can help with the proper identification of the disease.
Although the knee joint is one of the strongest and largest joints in the human body, it is often prone to suffering damage or injury, resulting in a variety of conditions. In addition, however, other health issues, such as arthritis, can affect the knee joint. In network for most insurances of El Paso, TX, chiropractic care can help ease painful symptoms associated with knee arthritis, among other health issues. Dr. Alex Jimenez D.C., C.C.S.T. Insight
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Treatment for Knee Arthritis
Non-surgical Treatment
� Non-surgical treatment approaches are often recommended before considering surgical treatment for knee arthritis. Healthcare professionals may recommend a variety of treatment options, including chiropractic care, physical therapy, and lifestyle modifications, among others.
� Lifestyle modifications. Some lifestyle modifications can help protect the knee joint and impede the progress of arthritis. Minimizing physical activities which aggravate the condition, will put less strain on the knee. Losing weight may also help lessen stress and pressure on the knee joint, resulting in less painful symptoms and increased function.
� Chiropractic care and physical therapy.�Chiropractic care utilizes full body chiropractic adjustments to carefully restore any spinal misalignments, or subluxations, which may�be causing symptoms, including arthritis. The doctor may also recommend physical therapy to create an individualized exercise and physical activity program for each patient’s needs.�Specific exercises will help increase range of motion and endurance, as well as help strengthen the muscles in the lower extremities.
� Assistive devices. Using assistive devices, such as a cane, shock-absorbing shoes or inserts, or a brace or knee sleeve, can decrease painful symptoms. A brace helps with function and stability, and may be particularly useful if the arthritis is based on one side of the knee. There are two types of braces that are often used for knee arthritis: A “unloader” brace shifts weight from the affected section of the knee, while a “support” brace helps support the entire knee load.
� Drugs and/or medications. Several types of medications are useful in treating arthritis of the knee. Since individuals respond differently to medications, your doctor will work closely with you to determine the medications and dosages which are safe and effective for you.
Surgical Treatment
� The healthcare professional may recommend surgical treatment if the patient’s knee arthritis causes severe disability and only if the problem isn’t relieved with non-surgical treatment. Like all surgeries, there are a few risks and complications with surgical treatment for knee arthritis. The�doctor will discuss the possible problems with the patient.
� Arthroscopy. During arthroscopy, physicians use instruments and small incisions to diagnose and treat knee joint problems. Arthroscopic surgery isn’t frequently used in the treatment of arthritis of the knee. In cases where osteoarthritis is accompanied with a degenerative meniscal tear, arthroscopic surgery may be wise to treat the torn meniscus.
� Cartilage grafting. Normal cartilage tissue may be taken from a tissue bank or through a different part of the knee to fill out a hole in the articular cartilage. This process is typically considered only for younger patients.
� Synovectomy. The lining damaged by rheumatoid arthritis is eliminated to reduce swelling and pain.
� Osteotomy. In a knee osteotomy, either the tibia (shinbone) or femur (thighbone) is cut then reshaped to relieve stress and pressure on the knee joint. Knee�osteotomy is utilized when early-stage osteoarthritis has damaged one facet of the knee joint. By changing the weight distribution, this can relieve and enhance the function of the knee.
� Total or partial knee replacement (arthroplasty).�The�doctor will remove the damaged bone and cartilage, then place new plastic or metal surfaces to restore the function of the knee�and its surrounding structures.
� Following any type of surgery for knee�arthritis will involve a period of recovery. Recovery time and rehabilitation will depend on the type of surgery performed. It’s essential to talk with your healthcare professional to determine the best treatment option for your�knee arthritis. The scope of our information is limited to chiropractic and spinal health issues. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at�915-850-0900�.
� Curated by Dr. Alex Jimenez �
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Additional Topic Discussion: Relieving Knee Pain without Surgery
� Knee pain is a well-known symptom which can occur due to a variety of knee injuries and/or conditions, including�sports injuries. The knee is one of the most complex joints in the human body as it is made-up of the intersection of four bones, four ligaments, various tendons, two menisci, and cartilage. According to the American Academy of Family Physicians, the most common causes of knee pain include patellar subluxation, patellar tendinitis or jumper’s knee, and Osgood-Schlatter disease. Although knee pain is most likely to occur in people over 60 years old, knee pain can also occur in children and adolescents. Knee pain can be treated at home following the RICE methods, however, severe knee injuries may require immediate medical attention, including chiropractic care.
Sagittal Fluid Sensitive MR slice showing large synovial popliteal (Baker’s) cyst (above top image) and sizeable synovial effusion (above bottom image)
Note multiple patchy dark signal areas on both images, representing fibrinoid inflammatory deposits aka “rice bodies” a characteristic MRI feature of RA
Management Rheumatological Referral & DRM
Conservative management followed by operative care in complicated cases of tendon ruptures and joints dislocations
Supplemental reading:
Diagnosis and Management of Rheumatoid Arthritis – AAFP
Septic arthritis – d/t bacterial or fungal contamination of the joint. SA may cause rapid joint destruction and requires prompt Dx and antibiotic administration
Joints affected: large joints with rich blood supply (knee 50%>hips>shoulders).
Routs of Infection:
1) Hematogenous is m/c
2) Spread from an adjacent site
3) Direct implantation (e.g., trauma, iatrogenically)
Patients at risk: children, diabetics, immunocompromised, pre-existing joint damage/inflammation, e.g., RA, etc.
I.V. drug users are particularly at risk and also may contaminate atypical joints “the S joints” SIJ, SCJ, Symphysis pubis, ACJ, etc.
Clinically: may vary and depends on host immune response and bacterial virulence. May present with rapid onset or exacerbation of pre-existing joint pain, swelling, limitation of ROM. General signs of malaise, fever, fatigue and elevated ESR, CRP, Leucocytosis may be present.
N.B. Diabetics and immunocompromised may present with fewer manifestations and lack of fever d/t declining immune response
Dx: clinical, radiological and laboratory. Arthrocentesis may be necessary for culture, cell count and purulent synovial examination
Management: I.V. antibiotics
Imaging Dx: begins with radiography but in the early stage most likely will be unremarkable. MRI can be sensitive and help with early identification of joint effusion, bone edema, etc. US may be helpful in the superficial joints and children. US helps with needle guidance. Bone scintigraphy may be used occaisonally if MRI is contraindicated
Routes of Joint Contamination
1. Hematogenous (M/C)
2. Spread from the adjacent site
3. Direct inoculation
M/C organism-Staph aureus
N.B Gonococcal infection may be a top differential in some cases
IV drug users: Pseudomonas, candida
Sickle cell: Salmonella
Animal (cats/dogs) bites: Pasteurella
Occasionally fungal contamination may occur
Radiography
Initially non-specific ST/joint effusion, obscuration/distortion of fat planes. Because it takes 30% of compact and 50-75% trabecular bone to be destroyed before seen on x-rays, radiography is insensitive to some of the early changes. MR imaging is the preferred modality
If MRI is not available or contraindicated. Bone scintigraphy with Tc-99 MDT can help
In children, US preferred to avoid ionizing radiation. In children, US can be more sensitive than in adults due to lack of bone maturation
Radiographic Dx
Early findings are unrewarding. Early features may include joint widening d/t effusion. Soft tissue swelling and obscuration/displacement of fat planes
1-2 weeks: periarticular and adjacent osseous changes are manifesting as patchy demineralization, moth-eaten, permeating bone destruction, loss, and indistinctness of the epiphyseal “white cortical line” with an increase in soft tissue swelling. MRI may be helpful with early Dx.
Late features: complete joint destruction and ankyloses
N.B. Septic arthritis may progress rapidly within days and requires early I.V. antibiotic to prevent major joint destruction
T1 & T2 Knee MRI
T1 (above left) and T2 fat-sat sagittal knee MRI slices reveal loss of normal marrow signal on T1 and increase on T2 due to septic edema. Bone sequestrum d/t osteomyelitis progressing into septic arthritis is noted. Marked joint effusion with adjacent soft tissue edema is seen. Dx: OSM and septic arthritis
Imaging may help the Dx of the septic joint. However, the final Dx is based on Hx, physical examination, blood tests and most importantly synovial aspiration (arthrocentesis)
Synovial fluid should be sent for Gram staining, culture, glucose testing, leukocyte count, and differential determination
ESR/CRP may be elevated
Synovial fluid: WBC can be 50,000-60,000/ul, with 80% neutrophils with depleted glucose levels Gram stain: in 75% gram-positive cocci. Gram staining is less sensitive in gonococcal infection with only 25% of cultures +
In 9% of cases, blood cultures are the only source of pathogen identification and should be obtained before antibiotic treatment
Gout: MSU deposition in and around joints and soft tissues. Elevated levels of serum uric acid (UA) (>7mg/dL) caused by overproduction or under-excretion of uric acid
Once UA reached/exceeded 7mg/dL, it will deposit in the peripheral tissues. Primary gout: disturbed metabolism of nucleic acids and purines break down. Secondary gout: increased cell turnover: Psoriasis, leukemia, multiple myeloma, hemolysis, chemotherapy, etc.
Gout presents with 5-characteristic stages:
1)asymptomatic hyperuricemia (years/decades)
acute attacks of gouty arthritis (waxes and wanes and lasts for several years)
Interval phase between attacks
Chronic tophaceous gout
Gouty nephropathy
Clinical Presentation
Depends� on stages
Acute attacks: acute joint pain “first and the worst” even painful to light touch
DDx: septic joint (both may co-exist) bursitis etc.
Gouty arthritis typically presents as monoarthropathy
Chronic tophaceous stage: deposits in joints, ear pinna, ocular structures, and other regions. Nephrolithiasis etc. Men>women. Obesity, diet, and age >50-60.
Radiography: early attacks are unremarkable and may present as non-specific joint effusion
Chronic tophaceous gout radiography: punched out peri-articular, para-articular and intraosseous erosions with overhanging edges. A characteristic rim of sclerosis and internal calcification, soft tissue tophi. Target sites: lower extremity m/c
Rx: allopurinol, colchicine (esp. preventing acute episodes and maintenance)
Synovial Aspiration
Synovial aspiration with polarized microscopy reveal negatively birefringent needle-shaped MSU crystals with large inflammatory PMN presence. DDx: positively birefringent rhomboid-shaped CPPD crystals (above bottom right) seen in Pseudogout and CPPD
Large S.T.
Density and joint effusion punched out osseous erosion with overhanging margins, overall preservation of bone density, internal calcifications Dx: chronic tophaceous gout
MRI Gout Features
Erosions with overhanging margins, a low signal on T1 and high on T2 and fat-suppressed images. Peripheral contrast enhancement of tophaceous deposits d/t granulation tissue
Dx: final Dx; synovial aspiration and polarized microscopy
The knee is the largest joint in the human body, where the complex structures of the lower and upper legs come together. Consisting of three bones, the femur, the tibia, and the patella which are surrounded by a variety of soft tissues, including cartilage, tendons and ligaments, the knee functions as a hinge, allowing you to walk, jump, squat or sit. As a result, however, the knee is considered to be one of the joints that are most prone to suffer injury. A knee injury is the prevalent cause of knee pain.
A knee injury can occur as a result of a direct impact from a slip-and-fall accident or automobile accident, overuse injury from sports injuries, or even due to underlying conditions, such as arthritis. Knee pain is a common symptom which affects people of all ages. It may also start suddenly or develop gradually over time, beginning as a mild or moderate discomfort then slowly worsening as time progresses. Moreover, being overweight can increase the risk of knee problems. The purpose of the following article is to discuss the evaluation of patients presenting with knee pain and demonstrate their differential diagnosis.
Abstract
Knee pain is a common presenting complaint with many possible causes. An awareness of certain patterns can help the family physician identify the underlying cause more efficiently. Teenage girls and young women are more likely to have patellar tracking problems such as patellar subluxation and patellofemoral pain syndrome, whereas teenage boys and young men are more likely to have knee extensor mechanism problems such as tibial apophysitis (Osgood-Schlatter lesion) and patellar tendonitis. Referred pain resulting from hip joint pathology, such as slipped capital femoral epiphysis, also may cause knee pain. Active patients are more likely to have acute ligamentous sprains and overuse injuries such as pes anserine bursitis and medial plica syndrome. Trauma may result in acute ligamentous rupture or fracture, leading to acute knee joint swelling and hemarthrosis. Septic arthritis may develop in patients of any age, but crystal-induced inflammatory arthropathy is more likely in adults. Osteoarthritis of the knee joint is common in older adults. (Am Fam Physician 2003;68:917-22. Copyright� 2003 American Academy of Family Physicians.)
Introduction
Determining the underlying cause of knee pain can be difficult, in part because of the extensive differential diagnosis. As discussed in part I of this two-part article,1 the family physician should be familiar with knee anatomy and common mechanisms of injury, and a detailed history and focused physical examination can narrow possible causes. The patient�s age and the anatomic site of the pain are two factors that can be important in achieving an accurate diagnosis (Tables 1 and 2). �
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Children and Adolescents
Children and adolescents who present with knee pain are likely to have one of three common conditions: patellar subluxation, tibial apophysitis, or patellar tendonitis. Additional diagnoses to consider in children include slipped capital femoral epiphysis and septic arthritis.
Patellar Subluxation
Patellar subluxation is the most likely diagnosis in a teenage girl who presents with giving-way episodes of the knee.2 This injury occurs more often in girls and young women because of an increased quadriceps angle (Q angle), usually greater than 15 degrees.
Patellar apprehension is elicited by subluxing the patella laterally, and a mild effusion is usually present. Moderate to severe knee swelling may indicate hemarthrosis, which suggests patellar dislocation with osteochondral fracture and bleeding.
Tibial Apophysitis
A teenage boy who presents with anterior knee pain localized to the tibial tuberosity is likely to have tibial apophysitis or Osgood- Schlatter lesion3,4 (Figure 1).5 The typical patient is a 13- or 14-year-old boy (or a 10- or 11-year-old girl) who has recently gone through a growth spurt.
The patient with tibial apophysitis generally reports waxing and waning of knee pain for a period of months. The pain worsens with�squatting, walking up or down stairs, or forceful contractions of the quadriceps muscle. This overuse apophysitis is exacerbated by jumping and hurdling because repetitive hard landings place excessive stress on the insertion of the patellar tendon.
On physical examination, the tibial tuberosity is tender and swollen and may feel warm. The knee pain is reproduced with the resisted active extension or passive hyperflexion of the knee. No effusion is present. Radiographs are usually negative; rarely, they show avulsion of the apophysis at the tibial tuberosity. However, the physician must not mistake the normal appearance of the tibial apophysis for an avulsion fracture. �
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Patellar Tendonitis
Jumper�s knee (irritation and inflammation of the patellar tendon) most commonly occurs in teenage boys, particularly during a growth spurt2 (Figure 1).5 The patient reports vague anterior knee pain that has persisted for months and worsens after activities such as walking down stairs or running.
On physical examination, the patellar tendon is tender, and the pain is reproduced by resisted knee extension. There is usually no effusion. Radiographs are not indicated.
Slipped Capital Femoral Epiphysis
A number of pathologic conditions result in referral of pain to the knee. For example, the possibility of slipped capital femoral epiphysis must be considered in children and teenagers who present with knee pain.6 The patient with this condition usually reports poorly localized knee pain and no history of knee trauma.
The typical patient with slipped capital femoral epiphysis is overweight and sits on the examination table with the affected hip slightly flexed and externally rotated. The knee examination is normal, but hip pain is elicited with passive internal rotation or extension of the affected hip.
Radiographs typically show displacement of the epiphysis of the femoral head. However, negative radiographs do not rule out the diagnosis in patients with typical clinical findings. Computed tomographic (CT) scanning is indicated in these patients.
Osteochondritis Dissecans
Osteochondritis dissecans is an intra-articular osteochondrosis of unknown etiology that is characterized by degeneration and recalcification of articular cartilage and underlying bone. In the knee, the medial femoral condyle is most commonly affected.7
The patient reports vague, poorly localized knee pain, as well as morning stiffness or recurrent effusion. If a loose body is present, mechanical symptoms of locking or catching of the knee joint also may be reported. On physical examination, the patient may demonstrate quadriceps atrophy or tenderness along the involved chondral surface. A mild joint effusion may be present.7
Plain-film radiographs may demonstrate the osteochondral lesion or a loose body in the knee joint. If osteochondritis dissecans is suspected, recommended radiographs include anteroposterior, posteroanterior tunnel, lateral, and Merchant�s views. Osteochondral lesions at the lateral aspect of the medial femoral condyle may be visible only on the posteroanterior tunnel view. Magnetic resonance imaging (MRI) is highly sensitive in detecting these abnormalities and is indicated in patients with a suspected osteochondral lesion.7 �
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A knee injury caused by sports injuries, automobile accidents, or an underlying condition, among other causes, can affect the cartilage, tendons and ligaments which form the knee joint itself. The location of the knee pain can differ according to the structure involved, also, the symptoms can vary. The entire knee may become painful and swollen as a result of inflammation or infection, whereas a torn meniscus or fracture may cause symptoms in the affected region. Dr. Alex Jimenez D.C., C.C.S.T. Insight
Adults
Overuse Syndromes
Anterior Knee Pain. Patients with patellofemoral pain syndrome (chondromalacia patellae) typically present with a vague history of mild to moderate anterior knee pain that usually occurs after prolonged periods of sitting (the so-called �theater sign�).8 Patellofemoral pain syndrome is a common cause of anterior knee pain in women.
On physical examination, a slight effusion may be present, along with patellar crepitus on the range of motion. The patient�s pain may be reproduced by applying direct pressure to the anterior aspect of the patella. Patellar tenderness may be elicited by subluxing the patella medially or laterally and palpating the superior and inferior facets of the patella. Radiographs usually are not indicated.
Medial Knee Pain. One frequently overlooked diagnosis is medial plica syndrome. The plica, a redundancy of the joint synovium medially, can become inflamed with repetitive overuse.4,9 The patient presents with acute onset of medial knee pain after a marked increase in usual activities. On physical examination, a tender, mobile nodularity is present at the medial aspect of the knee, just anterior to the joint line. There is no joint effusion, and the remainder of the knee examination is normal. Radiographs are not indicated.
Pes anserine bursitis is another possible cause of medial knee pain. The tendinous insertion of the sartorius, gracilis, and semitendinosus muscles at the anteromedial aspect of the proximal tibia forms the pes anserine bursa.9 The bursa can become inflamed as a result of overuse or a direct contusion. Pes�anserine bursitis can be confused easily with a medial collateral ligament sprain or, less commonly, osteoarthritis of the medial compartment of the knee. �
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The patient with pes anserine bursitis reports pain at the medial aspect of the knee. This pain may be worsened by repetitive flexion and extension. On physical examination, tenderness is present at the medial aspect of the knee, just posterior and distal to the medial joint line. No knee joint effusion is present, but there may be slight swelling at the insertion of the medial hamstring muscles. Valgus stress testing in the supine position or resisted knee flexion in the prone position may reproduce the pain. Radiographs are usually not indicated.
Lateral Knee Pain. Excessive friction between the iliotibial band and the lateral femoral condyle can lead to iliotibial band tendonitis.9 This overuse syndrome commonly occurs in runners and cyclists, although it may develop in any person subsequent to activity involving repetitive knee flexion. The tightness of the iliotibial band, excessive foot pronation, genu varum, and tibial torsion are predisposing factors.
The patient with iliotibial band tendonitis reports pain at the lateral aspect of the knee joint. The pain is aggravated by activity, particularly running downhill and climbing stairs. On physical examination, tenderness is present at the lateral epicondyle of the femur, approximately 3 cm proximal to the joint line. Soft tissue swelling and crepitus also may be present, but there is no joint effusion. Radiographs are not indicated.
Noble�s test is used to reproduce the pain in iliotibial band tendonitis. With the patient in a supine position, the physician places a thumb over the lateral femoral epicondyle as the�patient repeatedly flexes and extends the knee. Pain symptoms are usually most prominent with the knee at 30 degrees of flexion.
Popliteus tendonitis is another possible cause of lateral knee pain. However, this condition is fairly rare.10
Trauma
Anterior Cruciate Ligament Sprain. Injury to the anterior cruciate ligament usually occurs because of noncontact deceleration forces, as when a runner plants one foot and sharply turns in the opposite direction. Resultant valgus stress on the knee leads to anterior displacement of the tibia and sprain or rupture of the ligament.11 The patient usually reports hearing or feeling a �pop� at the time of the injury and must cease activity or competition immediately. Swelling of the knee within two hours after the injury indicates rupture of the ligament and consequent hemarthrosis.
On physical examination, the patient has a moderate to severe joint effusion that limits the range of motion. The anterior drawer test may be positive, but can be negative because of hemarthrosis and guarding by the hamstring muscles. The Lachman test should be positive and is more reliable than the anterior drawer test (see text and Figure 3 in part I of the article1).
Radiographs are indicated to detect possible tibial spine avulsion fracture. MRI of the knee is indicated as part of a presurgical evaluation.
Medial Collateral Ligament Sprain. Injury to the medial collateral ligament is fairly common and is usually the result of acute trauma. The patient reports a misstep or collision that places valgus stress on the knee, followed by the immediate onset of pain and swelling at the medial aspect of the knee.11
On physical examination, the patient with medial collateral ligament injury has point tenderness at the medial joint line. Valgus stress testing of the knee flexed to 30 degrees reproduces the pain (see text and Figure 4 in part I of this article1). A clearly defined endpoint on valgus stress testing indicates a grade 1�or grade 2 sprain, whereas complete medial instability indicates full rupture of the ligament (grade 3 sprain).
Lateral Collateral Ligament Sprain. Injury of the lateral collateral ligament is much less common than the injury of the medial collateral ligament. Lateral collateral ligament sprain usually results from varus stress to the knee, as occurs when a runner plants one foot and then turns toward the ipsilateral knee.2 The patient reports acute onset of lateral knee pain that requires prompt cessation of activity.
On physical examination, point tenderness is present at the lateral joint line. Instability or pain occurs with varus stress testing of the knee flexed to 30 degrees (see text and Figure 4 in part I of this article1). Radiographs are not usually indicated.
Meniscal Tear. The meniscus can be torn acutely with a sudden twisting injury of the knee, such as may occur when a runner suddenly changes direction.11,12 Meniscal tear also may occur in association with a prolonged degenerative process, particularly in a patient with an anterior cruciate ligament-deficient knee. The patient usually reports recurrent knee pain and episodes of catching or locking of the knee joint, especially with squatting or twisting of the knee.
On physical examination, a mild effusion is usually present, and there is tenderness at the medial or lateral joint line. Atrophy of the vastus medialis obliquus portion of the quadriceps muscle also may be noticeable. The McMurray test may be positive (see Figure 5 in part I of this article1), but a negative test does not eliminate the possibility of a meniscal tear.
Plain-film radiographs usually are negative and seldom are indicated. MRI is the radiologic test of choice because it demonstrates most significant meniscal tears.
Infection
Infection of the knee joint may occur in patients of any age but is more common in those whose immune system has been weakened by cancer, diabetes mellitus, alcoholism,�acquired immunodeficiency syndrome, or corticosteroid therapy. The patient with septic arthritis reports abrupt onset of pain and swelling of the knee with no antecedent trauma.13
On physical examination, the knee is warm, swollen, and exquisitely tender. Even slight motion of the knee joint causes intense pain.
Arthrocentesis reveals turbid synovial fluid. Analysis of the fluid yields a white blood cell count (WBC) higher than 50,000 per mm3 (50 ? 109 per L), with more than 75 percent (0.75) polymorphonuclear cells, an elevated protein content (greater than 3 g per dL [30 g per L]), and a low glucose concentration (more than 50 percent lower than the serum glucose concentration).14 Gram stain of the fluid may demonstrate the causative organism. Common pathogens include Staphylococcus aureus, Streptococcus species, Haemophilus influenza, and Neisseria gonorrhoeae.
Hematologic studies show an elevated WBC, an increased number of immature polymorphonuclear cells (i.e., a left shift), and an elevated erythrocyte sedimentation rate (usually greater than 50 mm per hour).
Older Adults
Osteoarthritis
Osteoarthritis of the knee joint is a common problem after 60 years of age. The patient presents with knee pain that is aggravated by weight-bearing activities and relieved by rest.15 The patient has no systemic symptoms but usually awakens with morning stiffness that dissipates somewhat with activity. In addition to chronic joint stiffness and pain, the patient may report episodes of acute synovitis.
Findings on physical examination include decreased range of motion, crepitus, a mild joint effusion, and palpable osteophytic changes at the knee joint.
When osteoarthritis is suspected, recommended radiographs include weight-bearing anteroposterior and posteroanterior tunnel views, as well as non-weight-bearing Merchants and lateral views. Radiographs show�joint-space narrowing, subchondral bony sclerosis, cystic changes, and hypertrophic osteophyte formation.
Crystal-Induced Inflammatory Arthropathy
Acute inflammation, pain, and swelling in the absence of trauma suggest the possibility of a crystal-induced inflammatory arthropathy such as gout or pseudogout.16,17 Gout commonly affects the knee. In this arthropathy, sodium urate crystals precipitate in the knee joint and cause an intense inflammatory response. In pseudogout, calcium pyrophosphate crystals are the causative agents.
On physical examination, the knee joint is erythematous, warm, tender, and swollen. Even minimal range of motion is exquisitely painful.
Arthrocentesis reveals clear or slightly cloudy synovial fluid. Analysis of the fluid yields a WBC count of 2,000 to 75,000 per mm3 (2 to 75 ? 109 per L), a high protein content (greater than 32 g per dL [320 g per L]), and a glucose concentration that is approximately 75 percent of the serum glucose con- centration.14 Polarized-light microscopy of the synovial fluid displays negatively birefringent rods in the patient with gout and positively birefringent rhomboids in the patient with pseudogout.
Popliteal Cyst
The popliteal cyst (Baker�s cyst) is the most common synovial cyst of the knee. It originates from the posteromedial aspect of the knee joint at the level of the gastrocnemio-semimembranous bursa. The patient reports insidious onset of mild to moderate pain in the popliteal area of the knee.
On physical examination, palpable fullness is present at the medial aspect of the popliteal area, at or near the origin of the medial head of the gastrocnemius muscle. The McMurray test may be positive if the medial meniscus is injured. Definitive diagnosis of a popliteal cyst may be made with arthrography, ultrasonography, CT scanning, or, less commonly, MRI.
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In conclusion, although the knee is the largest joint in the human body where the structures of the lower extremities meet, including the femur, the tibia, the patella, and many other soft tissues, the knee can easily suffer damage or injury and result in knee pain. Knee pain is one of the most common complaints among the general population, however, it commonly occurs in athletes. Sports injuries, slip-and-fall accidents, and automobile accidents, among other causes, can lead to knee pain.
As described in the article above, diagnosis is essential towards determining the best treatment approach for each type of knee injury, according to their underlying cause. While the location and the severity of the knee injury may vary depending on the cause of the health issue, knee pain is the most common symptom. Treatment options, such as chiropractic care and physical therapy, can help treat knee pain. The scope of our information is limited to chiropractic and spinal health issues. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at�915-850-0900�.
Curated by Dr. Alex Jimenez �
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Additional Topic Discussion: Relieving Knee Pain without Surgery
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Knee pain is a well-known symptom which can occur due to a variety of knee injuries and/or conditions, including�sports injuries. The knee is one of the most complex joints in the human body as it is made-up of the intersection of four bones, four ligaments, various tendons, two menisci, and cartilage. According to the American Academy of Family Physicians, the most common causes of knee pain include patellar subluxation, patellar tendinitis or jumper’s knee, and Osgood-Schlatter disease. Although knee pain is most likely to occur in people over 60 years old, knee pain can also occur in children and adolescents. Knee pain can be treated at home following the RICE methods, however, severe knee injuries may require immediate medical attention, including chiropractic care.
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Pathology: da disease of the articular cartilage. Continuing mechanical stimulation follows by an initial increase in water and cartilage thickness. Gradual loss of proteoglycans and ground substance. Fissuring/splitting. Chondrocytes are damaged and release enzymes into the joint. Cystic progression and further cartilage loss. Subchondral bone is denuded and exposed to mechanical stresses. It becomes hypervascular forming osteophytes. Subchondral cysts and bone thickening/sclerosis develop.
Imaging plays a crucial role in Dx/grading and management
Clinically: pain on walking/rest, crepitus, swelling d/t synovitis, locking/catching d/t osseocartilaginous fragments and gradual functional loss. Knee OA typically presents as mono and oligoarthritis. DDx: morning pain/stiffness is >30-min DDx from inflammatory arthritis
Treatment: in mild to moderate cases-conservative care. Severe OA-total knee arthroplasty
Grade 4: severe JSN, large osteophytes, marked subchondral sclerosis and definite bony deformity
Typical report language will state:
Minor, mild, moderate or severe aka advanced arthrosis
Technique
Radiography: AP weight-bearing knees: note severe JSN of the medial compartment more severely with lateral knee compartment. Osteophytes and marked genu varum deformity and bone deformation
Typically medial femorotibial compartment is affected early and more severely
The patellofemoral compartment is also affected and best visualized on the lateral and Sunrise views
Impressions: severe tri-compartmental knee arthrosis
Recommendations: referral to the orthopedic surgeon
Moderate JSN
B/L AP weight-bearing view (above top image): Moderate JSN primarily of the medial femorotibial compartment. Osteophytosis, subchondral sclerosis and mild bone deformation (genu varum)
May present as asymptomatic chondrocalcinosis, CPPD arthropathy resembling DJD with pan predominance of large subchondral cysts. Often found as isolated PFJ DJD
Pseudogout with an acute attack of knee pain resembling gouty arthritis
Radiography is the 1st step and often reveals the Dx
Arthrocentesis with polarized microscopy may be helpful to DDx between CPPD and Gouty arthritis
Rheumatoid Arthritis
RA: an autoimmune systemic inflammatory disease that targets soft tissues of joints synovium, tendons/ligaments, bursae and extra-articular sites (e.g., eyes, lungs, cardiovascular system)
RA is the m/c inflammatory arthritis, 3% of women and 1% of men. Age: 30-50 F>M 3:1, but may develop at any age. True RA is uncommon in children and should not be confused with Juvenile Idiopathic Arthritis
RA most often affects small joints of the hands and feet as symmetrical arthritis (2nd 3rd MCP, 3rd PIPs, wrists & MTPs, sparing DIPs of fingers and toes)
Radiographically: RA presents with joint effusion leading to hyperemia and marginal erosions and periarticular osteoporosis. In the knee, the lateral compartment is affected more frequently leading to valgus deformity. Uniform aka concentric/symmetrical JSN affects all compartments and remains a key Dx clue
An absence of subchondral sclerosis and osteophytes. Popliteal cyst�(Baker’s cyst) may represent synovial pannus and inflammatory synovitis extending into the popliteal region that may rapture and extend into posterior leg compartment
N.B. Following initial RA joint destruction, it is not unusual to note superimposed 2nd OA
Radiography is the 1st step but early joint involvement may be undetectable by x-rays and can be helped by US and/or MRI.
Final Dx is based on Hx, clinical exam, labs, and radiology
Clinical pearls: patients with RA may present with a single knee being affected
Most patients are likely to have bilateral symmetrical hands/feet RA.
Cervical spine, particularly C1-2 is affected in 75-90% of cases throughout the course of the disease
N.B. Sudden exacerbation of joint pain in RA should not underestimate septic arthritis because patients with pre-existing RA are at higher risk of infectious arthritis. Joint aspiration may help with Dx.
Radiographic DDx
RA (above left) vs. OA (above right)
RA: concentric (uniform) joint space loss, lack of osteophytes and juxta-articular osteopenia.
Clinical Pearls: patients with RA may present radiographically with subchondral sclerosis d/t superimposed DJD. The latter feature should not be interpreted as OA but instead considered as secondary OA
AP Knee Radiograph
Note marked uniform JSN, juxta-articular osteopenia and subchondral cystic changes
Clinical Pearls: subcortical cysts in RA will characteristically lack sclerotic rim noted in OA-associated subcortical cysts.
MRI Sensitivity
MRI is very sensitive and may aid during early Dx of RA.
T2 fat-sat or STIR and T1 + C gad contrast fat-suppressed sequences may be included
MRI Dx of RA: synovial inflammation/effusion, synovial hyperplasia, and pannus formation decreased cartilage thickness, subchondral cysts, and bone erosions
MRI is very sensitive to reveal juxt-articular bone marrow edema, a precursor to erosions
Intra-articular fibrinoid fragments known as “Rice bodies” are characteristic MR sign of RA
Note: T2 fat-sat sagittal MRI revealing large inflammatory joint effusion and pannus synovial proliferation (above arrowheads). No evidence of radiographic or MRI bone erosions present. Dx: RA
STIR MR Slices
Note: STIR MR slices in the axial (above bottom image) and coronal planes (above top image) demonstrate extensive synovitis/effusion (above arrowheads) and multiple erosions in the medial and lateral tibial plateau (above arrows)
Additionally, scattered patchy areas of bone marrow edema are noted (above asterisks) such marrow edema changes are indicative and predictive of future osseous erosions.
Additional features: note thinning and destruction of joint cartilage
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