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Arthropathies

Arthropathies is a general term that describes any disease of the joints. A group of arthropathic disorders can afflict the joints, such as sacroiliitis which causes inflammation in the sacroiliac joint. There is Charcot’s, which is degeneration of a weight bearing join and arthrogryposis which means, “curving of joints.” Doctors use arthropathy interchangeably with arthritis, which means “joint inflammation.” Forms of arthropathy that are distinct from arthritis are Neuropathic arthropathy that is nerve damage from diabetes or other nerve condition which results 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.  Finger tips 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 problem in people with hemophilia. For Answers to any questions you may have please call Dr. Jimenez at 915-850-0900


Rheumatoid Arthritis RA and Chiropractic Medicine El Paso, Texas

Rheumatoid Arthritis RA and Chiropractic Medicine El Paso, Texas

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.


11860 Vista Del Sol Dr #128, Rheumatoid Arthritis RA and Chiropractic Medicine El Paso, Texas

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.

Your Chiropractic Source

Our chiropractic team has experience helping patients with RA, and we are interested in doing the same for you. We understand how hard it can be to have RA. Let us help you get the relief you deserve.

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.

11860 Vista Del Sol Dr #128, Rheumatoid Arthritis RA and Chiropractic Medicine El Paso, Texas


11860 Vista Del Sol Dr #128, Rheumatoid Arthritis RA and Chiropractic Medicine El Paso, Texas

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.

Take2_PB_Healthcare
Take2_PB_Healthcare

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.

Diagnosis and Management of Rheumatoid Arthritis

Diagnosis and Management of Rheumatoid Arthritis

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   image-16.png

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  
Dr Jimenez White Coat
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 Green Call Now Button H .png  

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.  
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EXTRA EXTRA | IMPORTANT TOPIC: El Paso, TX Chiropractor Recommended

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References

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, Cabezón 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. http://www.effectivehealthcare.ahrq.gov/ ehc/products/14/85/RheumArthritisClinicianGuide.pdf. Accessed June 23, 2011.
24. Choy EH, Smith C, Doré 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.

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Ankle & Foot Diagnostic Imaging Arthritis & Trauma II| El Paso, TX.

Ankle & Foot Diagnostic Imaging Arthritis & Trauma II| El Paso, TX.

Lisfranc Fracture-Dislocation

ankle foot arthritis and trauma el paso tx.
  • 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)

ankle foot arthritis and trauma el paso tx.
  • 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.
  • Management: non-operative: short-leg cast/immonbilization-4-6 wk. operative: arthrocsopic removal.
  • Complications: premature 2nd DJD

Metatarsal Injuries

ankle foot arthritis and trauma el paso tx.
  • Acute & Stress fractures are common: m/c 5th MT & 2nd, 3rd MT.
  • 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

ankle foot arthritis and trauma el paso tx.
  • 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

ankle foot arthritis and trauma el paso tx.
  • (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.

Ankle & Foot Imaging

 

How Arthritis Can Affect the Knee

How Arthritis Can Affect the Knee

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.

 

Dr Jimenez White Coat
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

 

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.

 

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EXTRA EXTRA | IMPORTANT TOPIC: El Paso, TX Chiropractor Recommended

 
Knee Arthritis: Diagnostic Imaging Approaches II | El Paso, TX.

Knee Arthritis: Diagnostic Imaging Approaches II | El Paso, TX.

Sagittal Fluid Sensitivity

knee arthritis chiropractic care el paso tx.
  • 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

Septic Arthritis (SA)

  • 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

knee arthritis chiropractic care el paso tx.

 

  • 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
knee arthritis chiropractic care el paso tx.

Radiography

knee arthritis chiropractic care el paso tx.

 

  • 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

knee arthritis chiropractic care el paso tx.

 

  • 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

knee arthritis chiropractic care el paso tx.

 

  • 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
  • Articles: https://www.aafp.org/afp/2011/0915/p653.html
  • https://www.aafp.org/afp/2016/1115/p810.html

Crystal-Induced Knee Arthritis

  • Crystalline arthritis: a group of arthropathies resulting from crystal deposition in and around the joint.
  • 2-m/c: Monosodium urate crystals (MSU)  and Calcium Pyrophosphate Dehydrate crystals (CPPD) arthropathy
  • 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
knee arthritis chiropractic care el paso tx.

 

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

knee arthritis chiropractic care el paso tx.

 

  • 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
knee arthritis chiropractic care el paso tx.

 

Large S.T.

knee arthritis chiropractic care el paso tx.

 

  • 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

knee arthritis chiropractic care el paso tx.

 

  • 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

Additional Articles

Knee Arthritis

 

Evaluation of Patients Presenting with Knee Pain: Part II. Differential Diagnosis

Evaluation of Patients Presenting with Knee Pain: Part II. Differential Diagnosis

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).  

 

Table 1 Common Causes of Knee Pain

 

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.  

 

Table 2 Differential Diagnosis of Knee Pain

 

Figure 1 Anterior View of the Structures of the Knee

 

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  

 

Dr Jimenez White Coat

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.  

 

 

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.

The authors indicate that they do not have any conflicts of interest. Sources of funding: none reported.

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

 

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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EXTRA EXTRA | IMPORTANT TOPIC: El Paso, TX Chiropractor Recommended

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References
1. Calmbach WL, Hutchens M. Evaluation of patients presenting with knee pain: part I. History, physical examination, radiographs, and laboratory tests. Am Fam Physician 2003;68:907-12.
2. Walsh WM. Knee injuries. In: Mellion MB, Walsh WM, Shelton GL, eds. The team physician’s hand- book. 2d ed. St. Louis: Mosby, 1990:554-78.
3. Dunn JF. Osgood-Schlatter disease. Am Fam Physi- cian 1990;41:173-6.
4. Stanitski CL. Anterior knee pain syndromes in the adolescent. Instr Course Lect 1994;43:211-20.
5. Tandeter HB, Shvartzman P, Stevens MA. Acute knee injuries: use of decision rules for selective radiograph ordering. Am Fam Physician 1999;60: 2599-608.
6. Waters PM, Millis MB. Hip and pelvic injuries in the young athlete. In: DeLee J, Drez D, Stanitski CL, eds. Orthopaedic sports medicine: principles and practice. Vol. III. Pediatric and adolescent sports medicine. Philadelphia: Saunders, 1994:279-93.
7. Schenck RC Jr, Goodnight JM. Osteochondritis dis- secans. J Bone Joint Surg [Am] 1996;78:439-56.
8. Ruffin MT 5th, Kiningham RB. Anterior knee pain: the challenge of patellofemoral syndrome. Am Fam Physician 1993;47:185-94.
9. Cox JS, Blanda JB. Peripatellar pathologies. In: DeLee J, Drez D, Stanitski CL, eds. Orthopaedic sports medicine: principles and practice. Vol. III. Pediatric and adolescent sports medicine. Philadel- phia: Saunders, 1994:1249-60.
10. Petsche TS, Selesnick FH. Popliteus tendinitis: tips for diagnosis and management. Phys Sportsmed 2002;30(8):27-31.
11. Micheli LJ, Foster TE. Acute knee injuries in the immature athlete. Instr Course Lect 1993;42:473- 80.
12. Smith BW, Green GA. Acute knee injuries: part II. Diagnosis and management. Am Fam Physician 1995;51:799-806.
13. McCune WJ, Golbus J. Monarticular arthritis. In: Kelley WN, ed. Textbook of rheumatology. 5th ed. Philadelphia: Saunders, 1997:371-80.
14. Franks AG Jr. Rheumatologic aspects of knee dis- orders. In: Scott WN, ed. The knee. St. Louis: Mosby, 1994:315-29.
15. Brandt KD. Management of osteoarthritis. In: Kel- ley WN, ed. Textbook of rheumatology. 5th ed. Philadelphia: Saunders, 1997:1394-403.
16. Kelley WN, Wortmann RL. Crystal-associated syn- ovitis. In: Kelley WN, ed. Textbook of rheumatol- ogy. 5th ed. Philadelphia: Saunders, 1997:1313- 51. 1
7. Reginato AJ, Reginato AM. Diseases associated with deposition of calcium pyrophosphate or hy- droxyapatite. In: Kelley WN, ed. Textbook of rheumatology. 5th ed. Philadelphia: Saunders, 1997:1352-67.
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Knee Arthritis: Diagnostic Imaging Approaches I | El Paso, TX.

Knee Arthritis: Diagnostic Imaging Approaches I | El Paso, TX.

Degenerative Knee Arthritis

  • Knee Arthritis
  • Knee OA (arthrosis) is the m/c symptomatic OA with 240 cases per 100,000, 12.5% of people >45 y.o.
  • Modifiable risk factors: trauma, obesity, lack of fitness, muscle weakness
  • Non-modifiable: women>men, aging, genetics, race/ethnicity
  • 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

OA: L.O.S.S. Radiologic Presentation

knee arthritis chiropractic care el paso tx.

 

  • Typical radiologic-pathologic presentation of  OA: L.O.S.S.
  • Loss of joint space (non-uniform/asymmetrical)
  • Osteophytes
  • Subchondral sclerosis
  • Subchondral cysts
  • Bone deformity: Genu Varum- is the m/c deformity d/t medial knee compartment affected more severely
  • In addition: a weakening of periarticular soft tissues, instability and other changes

Imaging

knee arthritis chiropractic care el paso tx.

 

  • Radiography is the modality of choice
  • Views should include b/l weight bearing
  • Evaluation of joint space is crucial. Normal joint space -3-mm
  • Grading is based on the degree of joint space narrowing (JSN), osteophytes, bone deformation, etc.
  • Grade 1: minimal JSN, suspicious osteophytes
  • Grade 2: appreciable osteophytes and JSN on AP weight-bearing view
  • Grade 3: multiple osteophytes, definite JSN, subchondral sclerosis
  • 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

knee arthritis chiropractic care el paso tx.

 

  • 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

knee arthritis chiropractic care el paso tx.

 

  • 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)
  • Additional features: PF OA, intra-articular osteophytes, secondary osteocartilaginous loose bodies and subchondral cysts (above arrows)

Secondary Osteochondromatosis

knee arthritis chiropractic care el paso tx.

 

  • Intra-articular osteocartilaginous loose bodies known as secondary osteochondromatosis
  • Typical in DJD especially of the large joints
  • It may accelerate further cartilage destruction and progression of OA
  • May worsen signs of synovitis
  • Intra-articular locking, catching etc.

Management of Severe Knee OA

knee arthritis chiropractic care el paso tx.

 

  • Conservative care: NSAID, exercise, weight loss etc.
  • Operative care should be used if conservative care failed or symptoms progress despite conservative efforts in severe OA cases
  • Review article
  • https://www.aafp.org/afp/2018/0415/p523.html

Calcium Pyrophosphate Dehydrate Deposition Disease

knee arthritis chiropractic care el paso tx.

 

  • CPPD arthropathy common in the knee
  • 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.
  • Lab tests: RF, CRP, anti-cyclic citrulline peptide antibodies (anti-CCP Ab). CBC
  • 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

knee arthritis chiropractic care el paso tx.

 

  • 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

knee arthritis chiropractic care el paso tx.

 

  • 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

knee arthritis chiropractic care el paso tx.

 

  • 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

knee arthritis chiropractic care el paso tx.

 

  • 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

Knee Arthritis

 

Evaluation of Patients Presenting with Knee Pain: Part I. History, Physical Examination, Radiographs, and Laboratory Tests

Evaluation of Patients Presenting with Knee Pain: Part I. History, Physical Examination, Radiographs, and Laboratory Tests

Knee pain is a common health issue among athletes and the general population alike. Although symptoms of knee pain can be debilitating and frustrating, knee pain is often a very treatable health issue. The knee is a complex structure made up of three bones: the lower section of the thighbone, the upper region of the shinbone, and the kneecap.

Powerful soft tissues, such as the tendons and ligaments of the knee as well as the cartilage beneath the kneecap and between the bones, hold these structures together in order to stabilize and support the knee. However, a variety of injuries and/or conditions can ultimately lead to knee pain. The purpose of the article below is to evaluate patients with knee pain.

Abstract

Family physicians frequently encounter patients with knee pain. Accurate diagnosis requires a knowledge of knee anatomy, common pain patterns in knee injuries, and features of frequently encountered causes of knee pain, as well as specific physical examination skills. The history should include characteristics of the patient’s pain, mechanical symptoms (locking, popping, giving way), joint effusion (timing, amount, recurrence), and mechanism of injury. The physical examination should include careful inspection of the knee, palpation for point tenderness, assessment of joint effusion, range-of-motion testing, evaluation of ligaments for injury or laxity, and assessment of the menisci. Radiographs should be obtained in patients with isolated patellar tenderness or tenderness at the head of the fibula, inability to bear weight or flex the knee to 90 degrees, or age greater than 55 years. (Am Fam Physician 2003; 68:907-12. Copyright© 2003 American Academy of Family Physicians.)

Introduction

Knee pain accounts for approximately one-third of musculoskeletal problems seen in primary care settings. This complaint is most prevalent in physically active patients, with as many as 54 percent of athletes having some degree of knee pain each year.1 Knee pain can be a source of significant disability, restricting the ability to work or perform activities of daily living.

The knee is a complex structure (Figure 1),2 and its evaluation can present a challenge to the family physician. The differential diagnosis of knee pain is extensive but can be narrowed with a detailed history, a focused physical examination and, when indicated, the selective use of appropriate imaging and laboratory studies. Part I of this two-part article provides a systematic approach to evaluating the knee, and part II3 discusses the differential diagnosis of knee pain.

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History

Pain Characteristics

The patient’s description of knee pain is helpful in focusing the differential diagnosis.4 It is important to clarify the characteristics of the pain, including its onset (rapid or insidious), location (anterior, medial, lateral, or posterior knee), duration, severity, and quality (e.g., dull, sharp, achy). Aggravating and alleviating factors also need to be identified. If knee pain is caused by an acute injury, the physician needs to know whether the patient was able to continue activity or bear weight after the injury or was forced to cease activities immediately.

 

Mechanical Symptoms

The patient should be asked about mechan- ical symptoms, such as locking, popping, or giving way of the knee. A history of locking episodes suggests a meniscal tear. A sensation of popping at the time of injury suggests liga- mentous injury, probably complete rupture of a ligament (third-degree tear). Episodes of giving way are consistent with some degree of knee instability and may indicate patellar sub- luxation or ligamentous rupture.

Effusion

The timing and amount of joint effusion are important clues to the diagnosis. Rapid onset (within two hours) of a large, tense effusion suggests rupture of the anterior cru- ciate ligament or fracture of the tibial plateau with resultant hemarthrosis, whereas slower onset (24 to 36 hours) of a mild to moderate effusion is consistent with meniscal injury or ligamentous sprain. Recurrent knee effusion after activity is consistent with meniscal injury.

Mechanism of Injury

The patient should be questioned about specific details of the injury. It is important to know if the patient sustained a direct blow to the knee, if the foot was planted at the time of injury, if the patient was decelerating or stopping suddenly, if the patient was landing from a jump, if there was a twisting component to the injury, and if hyperextension occurred.

A direct blow to the knee can cause serious injury. The anterior force applied to the proximal tibia with the knee in flexion (e.g., when the knee hits the dashboard in an automobile accident) can cause injury to the posterior cruciate ligament. The medial collateral ligament is most commonly injured as a result of direct lateral force to the knee (e.g., clipping in football); this force creates a val- gus load on the knee joint and can result in rupture of the medial collateral ligament. Conversely, a medial blow that creates a varus load can injure the lateral collateral ligament.

Noncontact forces also are an important cause of knee injury. Quick stops and sharp cuts or turns create significant deceleration forces that can sprain or rupture the anterior cruciate ligament. Hyperextension can result in injury to the anterior cruciate ligament or posterior cruciate ligament. Sudden twisting or pivoting motions create shear forces that can injure the meniscus. A combination of forces can occur simultaneously, causing injury to multiple structures.

 

Medical History

A history of knee injury or surgery is important. The patient should be asked about previous attempts to treat knee pain, including the use of medications, supporting devices, and physical therapy. The physician also should ask if the patient has a history of gout, pseudogout, rheumatoid arthritis, or other degenerative joint diseases.

Dr Jimenez White Coat

Knee pain is a common health issue which can be caused by sports injuries, automobile accident injuries, or by an underlying health issue, such as arthritis. The most common symptoms of knee injury include pain and discomfort, swelling, inflammation and stiffness. Because treatment for knee pain varies according to the cause, it’s essential for the individual to receive proper diagnosis for their symptoms. Chiropractic care is a safe and effective, alternative treatment approach which can help treat knee pain, among other health issues.

Dr. Alex Jimenez D.C., C.C.S.T. Insight

Physical Examination

Inspection and Palpation

The physician begins by comparing the painful knee with the asymptomatic knee and inspecting the injured knee for erythema, swelling, bruising, and discoloration. The mus- culature should be symmetric bilaterally. In particular, the vastus medialis obliquus of the quadriceps should be evaluated to determine if it appears normal or shows signs of atrophy.

The knee is then palpated and checked for pain, warmth, and effusion. Point tenderness should be sought, particularly at the patella, tibial tubercle, patellar tendon, quadriceps tendon, anterolateral and anteromedial joint line, medial joint line, and lateral joint line. Moving the patient’s knee through a short arc of motion helps identify the joint lines. Range of motion should be assessed by extending and flexing the knee as far as possible (normal range of motion: extension, zero degrees; flex- ion, 135 degrees).5

Patellofemoral Assessment

An evaluation for effusion should be conducted with the patient supine and the injured knee in extension. The suprapatellar pouch should be milked to determine whether an effusion is present.

Patellofemoral tracking is assessed by observing the patella for smooth motion while the patient contracts the quadriceps muscle. The presence of crepitus should be noted during palpation of the patella.

The quadriceps angle (Q angle) is determined by drawing one line from the anterior superior iliac spine through the center of the patella and a second line from the center of the patella through the tibial tuberosity (Figure 2).6 A Q angle greater than 15 degrees is a predisposing factor for patellar subluxation (i.e., if the Q angle is increased, forceful contraction of the quadriceps muscle can cause the patella to sublux laterally).

A patellar apprehension test is then performed. With fingers placed at the medial aspect of the patella, the physician attempts to sublux the patella laterally. If this maneuver reproduces the patient’s pain or a giving-way sensation, patellar subluxation is the likely cause of the patient’s symptoms.7 Both the superior and inferior patellar facets should be palpated, with the patella subluxed first medially and then laterally.

 

Cruciate Ligaments

Anterior Cruciate Ligament. For the anterior drawer test, the patient assumes a supine position with the injured knee flexed to 90 degrees. The physician fixes the patient’s foot in slight external rotation (by sitting on the foot) and then places thumbs at the tibial tubercle and fingers at the posterior calf. With the patient’s hamstring muscles relaxed, the physician pulls anteriorly and assesses anterior displacement of the tibia (anterior drawer sign).

The Lachman test is another means of assessing the integrity of the anterior cruciate ligament (Figure 3).7 The test is performed with the patient in a supine position and the injured knee flexed to 30 degrees. The physician stabilizes the distal femur with one hand, grasps the proximal tibia in the other hand, and then attempts to sublux the tibia anteriorly. Lack of a clear end point indicates a positive Lachman test.

Posterior Cruciate Ligament. For the posterior drawer test, the patient assumes a supine position with knees flexed to 90 degrees. While standing at the side of the examination table, the physician looks for posterior displacement of the tibia (posterior sag sign).7,8 Next, the physician fixes the patient’s foot in neutral rotation (by sitting on the foot), positions thumbs at the tibial tubercle, and places fingers at the posterior calf. The physician then pushes posteriorly and assesses for posterior displacement of the tibia.

 

Collateral Ligaments

Medial Collateral Ligament. The valgus stress test is performed with the patient’s leg slightly abducted. The physician places one hand at the lateral aspect of the knee joint and the other hand at the medial aspect of the distal tibia. Next, valgus stress is applied to the knee at both zero degrees (full extension) and 30 degrees of flexion (Figure 4)7. With the knee at zero degrees (i.e., in full extension), the posterior cruciate ligament and the articulation of the femoral condyles with the tibial plateau should stabilize the knee; with the knee at 30 degrees of flexion, application of valgus stress assesses the laxity or integrity of the medial collateral ligament.

Lateral Collateral Ligament. To perform the varus stress test, the physician places one hand at the medial aspect of the patient’s knee and the other hand at the lateral aspect of the distal fibula. Next, varus stress is applied to the knee, first at full extension (i.e., zero degrees), then with the knee flexed to 30 degrees (Figure 4).7 A firm end point indicates that the collateral ligament is intact, whereas a soft or absent end point indicates complete rupture (third-degree tear) of the ligament.

Menisci

Patients with injury to the menisci usually demonstrate tenderness at the joint line. The McMurray test is performed with the patient lying supine9 (Figure 5). The test has been described variously in the literature, but the author suggests the following technique.

The physician grasps the patient’s heel with one hand and the knee with the other hand. The physician’s thumb is at the lateral joint line, and fingers are at the medial joint line. The physician then flexes the patient’s knee maximally. To test the lateral meniscus, the tibia is rotated internally, and the knee is extended from maximal flexion to about 90 degrees; added compression to the lateral meniscus can be produced by applying valgus stress across the knee joint while the knee is being extended. To test the medial meniscus, the tibia is rotated externally, and the knee is extended from maximal flexion to about 90 degrees; added compression to the medial meniscus can be produced by placing varus stress across the knee joint while the knee is degrees of flexion. A positive test produces a thud or a click, or causes pain in a reproducible portion of the range of motion.

Because most patients with knee pain have soft tissue injuries, plain-film radiographs generally are not indicated. The Ottawa knee rules are a useful guide for ordering radiographs of the knee10,11.

If radiographs are required, three views are usually sufficient: anteroposterior view, lateral view, and Merchant’s view (for the patellofemoral joint).7,12 Teenage patients who report chronic knee pain and recurrent knee effusion require a notch or tunnel view (posteroanterior view with the knee flexed to 40 to 50 degrees). This view is necessary to detect radiolucencies of the femoral condyles (most commonly the medial femoral condyle), which indicate the presence of osteochondritis dissecans.13

Radiographs should be closely inspected for signs of fracture, particularly involving the patella, tibial plateau, tibial spines, proximal fibula, and femoral condyles. If osteoarthritis is suspected, standing weight-bearing radiographs should be obtained.

 

Laboratory Studies

The presence of warmth, exquisite tenderness, painful effusion, and marked pain with even slight range of motion of the knee joint is consistent with septic arthritis or acute inflammatory arthropathy. In addition to obtaining a complete blood count with differential and an erythrocyte sedimentation rate (ESR), arthro- centesis should be performed. The joint fluid should be sent to a laboratory for a cell count with differential, glucose and protein measure- ments, bacterial culture and sensitivity, and polarized light microscopy for crystals.

Because a tense, painful, swollen knee may present an unclear clinical picture, arthrocentesis may be required to differentiate simple effusion from hemarthrosis or occult osteochondral fracture.4 A simple joint effusion produces clear, straw-colored transudative fluid, as in a knee sprain or chronic meniscal injury. Hemarthrosis is caused by a tear of the anterior cruciate ligament, a fracture or, less commonly, an acute tear of the outer portion of the meniscus. An osteochondral fracture causes hemarthrosis, with fat globules noted in the aspirate.

Rheumatoid arthritis may involve the knee joint. Hence, serum ESR and rheumatoid factor testing are indicated in selected patients.

The authors indicate that they do not have any conflicts of interest. Sources of funding: none reported.

In conclusion, knee pain is a common health issue which occurs due to a variety of injuries and/or conditions, such as sports injuries, automobile accidents, and arthritis, among other problems. Treatment of knee pain depends largely on the source of the symptoms. Therefore, it is essential for the individual to seek immediate medical attention to receive a diagnosis.

Chiropractic care is an alternative treatment option which focuses on the treatment of a variety of injuries and/or conditions associated with the musculoskeletal and nervous system. 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.

 

blog picture of cartoon paper boy

EXTRA EXTRA | IMPORTANT TOPIC: El Paso, TX Chiropractor Recommended

 

 

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References

1. Rosenblatt RA, Cherkin DC, Schneeweiss R, Hart LG. The content of ambulatory medical care in the United States. An interspecialty comparison. N Engl J Med 1983;309:892-7.

2. Tandeter HB, Shvartzman P, Stevens MA. Acute knee injuries: use of decision rules for selective radiograph ordering. Am Fam Physician 1999;60: 2599-608.

3. Calmbach WL, Hutchens M. Evaluation of patients presenting with knee pain: part II. Differential diag- nosis. Am Fam Physician 2003;68:917-22

4. Bergfeld J, Ireland ML, Wojtys EM, Glaser V. Pin- pointing the cause of acute knee pain. Patient Care 1997;31(18):100-7.

5. Magee DJ. Knee. In: Orthopedic physical assessment. 4th ed. Philadelphia: Saunders, 2002:661-763.

6. Juhn MS. Patellofemoral pain syndrome: a review and guidelines for treatment. Am Fam Physician 1999;60:2012-22.

7. Smith BW, Green GA. Acute knee injuries: part I. History and physical examination. Am Fam Physi- cian 1995;51:615-21.

8. Walsh WM. Knee injuries. In: Mellion MB, Walsh WM, Shelton GL, eds. The team physician’s hand- book. 2d ed. St. Louis: Mosby, 1997:554-78.

9. McMurray TP. The semilunar cartilage. Br J Surg 1942;29:407-14.

10. Stiell IG, Wells GA, Hoag RH, Sivilotti ML, Cacciotti TF, Verbeek PR, et al. Implementation of the Ottawa knee rule for the use of radiography in acute knee injuries. JAMA 1997;278:2075-9.

11. Stiell IG, Greenberg GH, Wells GA, McKnight RD, Cwinn AA, Caciotti T, et al. Derivation of a decision rule for the use of radiography in acute knee injuries. Ann Emerg Med 1995;26:405-13.

12. Sartoris DJ, Resnick D. Plain film radiography: rou- tine and specialized techniques and projections. In: Resnick D, ed. Diagnosis of bone and joint disor- ders. 3d ed. Philadelphia: Saunders:1-40.

13. Schenck RC Jr, Goodnight JM. Osteochondritis dis- secans. J Bone Joint Surg [Am] 1996;78:439-56.

Close Accordion

Diagnosis of Hip Complaints: Arthritis & Neoplasms Part II | El Paso, TX.

Diagnosis of Hip Complaints: Arthritis & Neoplasms Part II | El Paso, TX.

Ischemic Osteonecrosis

diagnosis hip arthritis and neoplasms el paso, tx.

 

  • Ischemic Osteonecrosis (More accurate term) aka avascular necrosis AVN: this term describes subarticular (subchondral) bone death
  • Intramedullary bone infarct: depicts osteonecrosis within the medullary cavity of the bone (above x-ray image)
  • Causes: m/c: trauma, systemic corticosteroids, diabetes, vasculitis in SLE. The list is long. Other vital causes: Sickle cell disease, Gaucher disease, alcohol, caisson disease, SCFE, LCP, etc.
  • Pathology: ischemia and bone infarct with resultant devitalized center surrounded by ischemia and edema with normal bone on the outer periphery (MRI double line sign)
  • Sub-articular necrotic bone eventually collapses and fragments leading to progressive bone and cartilage destruction and rapidly progressing DJD
  • Early Dx often missed but crucial to prevent severe DJD

M/C Sites

diagnosis hip arthritis and neoplasms el paso, tx.

 

  • Hips, shoulders, talus, scaphoid bone. Many peripheral idiopathic AVN sites are known by their eponyms (e.g., Kienbock aka AVN of the lunate bone, Preisier aka scaphoid AVN)
  • Radiography is insensitive to early AVN and may only present as subtle osteopenia
  • Some of the early appreciable rad features are increased patchy bone sclerosis followed by sub-articular bone collapse or “crescent sign” signifying stage-3 on Ficat classification (above)
  • Earliest detection and early intervention can be achieved by MRI (most sensitive modality)
  • If MRI contraindicated or unavailable, 2nd most sensitive modality is radionuclide bone scan (scintigraphy)
  • X-ray and CT scanning are of equal value

Coronal MRI Slice

diagnosis hip arthritis and neoplasms el paso, tx.

 

  • Fluid sensitive, sensitive coronal MRI slice revealing bill ischemic osteonecrosis of the femoral head
  • MRI findings: l

Tc99-MMDP Radionuclide Bone

diagnosis hip arthritis and neoplasms el paso, tx.

 

  • Bone scan reveals a central area of photopenia (cold spot) d/t necrotic fragment surrounded by increased osteoblastic activity as increased uptake of Tc-99 MDP in the right hip
  • The patient is a 30-year-old female with breast cancer and chemotherapy treatment who suddenly presented with right hip pain

Radiographic Progression of AVN

diagnosis hip arthritis and neoplasms el paso, tx.

 

  • Later stages present with articular collapse, subarticular cysts, increased patchy sclerosis and complete flattening of the femoral head with resultant severe DJD. Rx: THA

Management

diagnosis hip arthritis and neoplasms el paso, tx.

 

  • Early imaging Dx with MRI or bone scintigraphy is essential
  • Referral to the Orthopedic surgeon
  • Core decompression (above) can be used to revascularize the affected bone during earlier stages but produces mixed results
  • Delayed changes of AVN: THA as IN severe DJD cases

B/L THA

diagnosis hip arthritis and neoplasms el paso, tx.

 

  • B/L THA in the patient with ischemic osteonecrosis of the right and later left hip
  • When B/L hip AVN is present, typically consider systemic causes (corticosteroids, diabetes)

Inflammatory Arthritis Affecting the Hip

diagnosis hip arthritis and neoplasms el paso, tx.

 

  • Consider common systemic inflammatory condition such as RA and AS/EnA
  • Hip RA may develop in 30% of patients with RA
  • Key features to DDx inflammatory arthritis vs. DJD is symmetrical/uniform aka concentric joint loss often leading to axial migration and Protrusion Acetabule in advanced cases
  • Key element between RA vs. AS: the presence of RA bone erosion w/o productive bone changes or enthesitis in AS d/t inflammatory subperiosteal bone proliferation, whiskering/fluffy periostitis (collar-type enthesitis circumferentially affecting head-neck junction)
  • Dx: Hx, PE, labs: CRP, RH, anti-CCP Ab (RA)
  • CRP, HLA-B27, RF- (AS)

Septic Arthritis

diagnosis hip arthritis and neoplasms el paso, tx.

 

  • Gonococcal infections, iatrogenic causes, I.V. drug use, and some others
  • Routes: hematogenous, adjacent spread, direct inoculation (e.g., iatrogenic)
  • Clinically: pain and reduced ROM presented as monoarthritis, generalized signs/symptoms. CBC, ESR, CRP changes. ARthrocentesis and culture are crucial
  • M/C pathogen Staph. Aureus & Neisseria Gonorrhea
  • 1st step: radiography, often unrewarding in the early stage. Later (4-10 days) indistinctness of the white cortical line at the femoral articular epiphysis, loss of joint space, effusion as a widening of the medial joint area (Waldenstrom sign)
  • MRI – best at early DX: T1, T2, STIR, T1+C may help with early. Early I.V. antibiotics crucial to prevent rapid joint destruction

Slipped Capital Femoral Epiphysis (SCFE)

diagnosis hip arthritis and neoplasms el paso, tx.

 

  • Important to diagnose but easily missed potentially leading to Ischemic Osteonecrosis of the femoral head aka AVN
  • Presents typically in overweight children (more often boys), age over eight years. Greater incidence in African-American boys
  • 1st step: radiography, especially look for a widened physeal growth plate (so-called pre-slip). Later, slip and disturbed Klein’s line (above image). MRI – best modality for early Dx and early intervention
  • The frog lateral view often demonstrates the medial slip better than the AP view

Clinically Limping Child or Adolescent

diagnosis hip arthritis and neoplasms el paso, tx.

 

  • M>F (10-18 years). African-Americans are at greater risk. 20% of cases of SCFE are B/L. Complications: AVN >>DJD
  • Radiography: AP pelvis, spot, and frog leg may reveal slippage as Klein line failed to cross through the lateral aspect of the femoral head
  • Additional features: physis may appear widened
  • MRI w/o gad, is required for the earliest Dx and prevention of complications (AVN)

Normal and Abnormal Klein Line

diagnosis hip arthritis and neoplasms el paso, tx.

 

  • Consistent with SCFE. The physis is also widened. Dx: SCFE
  • Urgent referral to the Pediatric Orthopedic surgeon

Subtle Changes in Left Hip

diagnosis hip arthritis and neoplasms el paso, tx.

 

  • Note suspected subtle changes in the left hip that may require MR examination to confirm the Dx
  • Delay in care may result in major complications

Perthes’ Disease

diagnosis hip arthritis and neoplasms el paso, tx.

 

  • aka Legg-Calves-Perthes Disease (LCP)
  • Refers to Osteochondritis of the femoral head with osteonecrosis likely d/t disturbed vascularization of the femoral head
  • Presents typically in children (more often boys) aged under eight years as atraumatic “limping child.” 15% may have B/L Perthe’s
  • Imaging steps: 1st step x-radiography, followed by MRI especially in stage 1 (early) w/o x-ray abnormalities
  • Unspecific signs: joint effusion with Waldenstrome sign+ (>2-mm increase in medial joint space compared to the opposite side). Past approach: Fluoroscopic Arthrography (replaced by MRI)
  • Pathologic-Radiologic Correlation: in well-established cases, the femoral head characteristically becomes sclerotic, flattened and fragmented due to avascular necrosis (AVN). Later on, an occasional Coxa Magna changes may develop (>10% femoral head enlargement)
  • Management: symptoms control, bracing. Boys at younger ate show better prognosis d/t more immaturity and better chances of bone/cartilage repair mechanisms. In advanced cases, operative care: osteotomy, hip arthroplasty in adulthood if advanced DJD develops

Common Neoplasms & Other Conditions Affecting Hip/Pelvis

diagnosis hip arthritis and neoplasms el paso, tx.

 

  • M/C hip & pelvis neoplasms in adults: bone metastasis ( above far left), 2nd m/c Multiple Myeloma (M/C primary bone malignancy in adults). Tips: remember Red Marrow distribution. Less frequent: Chondrosarcoma
  • Paget’s disease of bone (above-bottom left image) is m/c detected in the pelvis and Femurs
  • Children and young adults ‘limping child’ benign neoplasms: Fibrous Dysplasia (above middle image), Solitary Bone Cyst (21%), Osteoid Osteoma, Chondroblastoma. Malignant pediatric neoplasms: m/c Ewing Sarcoma (above middle right and bottom images) vs. Osteosarcoma. >2y.o-consider Neuroblastoma
  • Imaging: 1st step: radiography followed by MRI are most appropriate.
  • If Mets are suspected: Tc99 bone scintigraphy is most sensitive

Multiple Myeloma

diagnosis hip arthritis and neoplasms el paso, tx.

 

  • Multiple Myeloma in a 75-y.o male (AP pelvis view)
  • Chondrosarcoma in a 60-y.o male (axial and coronal reconstructed CT+C slices in the bone window)

 

Hip Pelvis Arthritis & Neoplasms

Diagnosis of Hip Complaints: Arthritis & Neoplasms Part I | El Paso, TX.

Diagnosis of Hip Complaints: Arthritis & Neoplasms Part I | El Paso, TX.

Degenerative Joint Disease (DJD)

diagnosis hip arthritis and neoplasms el paso tx.

Macroscopic & Microscopic Appearance of Normal vs. Damaged Articular Hyaline Cartilage by DJD

diagnosis hip arthritis and neoplasms el paso tx.

Hip Osteoarthritis (OA) aka Osteoarthrosis

diagnosis hip arthritis and neoplasms el paso tx.
  • Symptomatic and potentially disabling DJD
  • Progressive damage and loss of the articular cartilage causing denudation and eburnation of articular bone
  • Cystic changes, osteophytes, and gradual joint destruction
  • Develops d/t repeated joint loading and microtrauma
  • Obesity, metabolic/genetic factors
  • Secondary Causes: trauma, FAI syndrome, osteonecrosis, pyrophosphate crystal deposition, previous inflammatory arthritis, Slipped Capital Femoral Epiphysis, Leg-Calves-Perthes disease in children, etc.
  • Hip OA, 2nd m/c after knee OA. Women>men
  • 88-100 symptomatic cases per 100000

Radiography is the Modality of Choice for the Dx and Grading of DJD

diagnosis hip arthritis and neoplasms el paso tx.
  • Special imaging is not required unless other complicating factors exist
  • The acetabular-femoral joint is divided into superior, axial and medial compartments/spaces
  • Normal joint space at the superior compartment should be 3-4-mm on the AP hip/pelvis view
  • Understanding the pattern of hip joint narrowing/migration helps with the DDx of DJD vs. Inflammatory arthritis
  • In DJD, m/c hip narrowing is superior-lateral (non-uniform) vs. inflammatory axial (uniform)

AP Hip Radiograph Demonstrates DJD

diagnosis hip arthritis and neoplasms el paso tx.
  • With a non-uniform loss of joint space (superior migration), large subcortical cysts and subchondral sclerosis
  • Radiographic features:
  • Like with any DJD changes: radiography will reveal L.O.S.S.
  • L: loss of joint space (non-uniform or asymmetrical)
  • O: osteophytes aka bony proliferation/spurs
  • S: Subchondral sclerosis/thickening
  • S: Subcortical aka subchondral cysts “geodes.”
  • Hip migration is m/c superior resulting in a “tilt deformity.”

Radiographic Presentation of Hip OA May Vary Depending On Severity

diagnosis hip arthritis and neoplasms el paso tx.
  • Mild OA: mild reduction of joint space often w/o marked osteophytes and cystic changes
  • During further changes, collar osteophytes may affect femoral head-neck junction with more significant joint space loss and subchondral bone sclerosis (eburnation)
  • Cyst formation will often occur along the acetabular and femoral head subarticular/subchondral bone “geodes” and usually filled with joint fluid and some intra-articular gas
  • Subchondral cysts may occasionally be very large and DDx from neoplasms or infection or other pathology

Coronal Reconstructed CT Slices in Bone Window

diagnosis hip arthritis and neoplasms el paso tx.
  • Note moderate joint narrowing that appears non-uniform
  • Sub-chondral cysts formation (geodes) are noted along the acetabular and femoral head subchondral bone
  • Other features include collar osteophytes along head-neck junction
  • Dx: DJD of moderate intensity
  • Referral to the Orthopedic surgeon will be helpful for this patient

AP Pelvis (below the first image), AP Hip Spot (below the second image) CT Coronal Slice

diagnosis hip arthritis and neoplasms el paso tx.
  • Note multiple subchondral cysts, severe non-uniform joint narrowing (superior-lateral) and subchondral sclerosis with osteophytes
  • Advanced hip arthrosis

Severe DJD, Left Hip

diagnosis hip arthritis and neoplasms el paso tx.
  • When reading radiological reports pay particular attention to the grading of hip OA
  • Most severe (advanced) OA cases require total hip arthroplasty (THA)
  • Refer your patients to the Orthopedic surgeon for a consultation
  • Most mild cases are a good candidate for conservative care

Hip Arthroplasty aka Hip Replacement

diagnosis hip arthritis and neoplasms el paso tx.
  • Can be total or hemiarthroplasty
  • THA can be metal on metal, metal on polyethylene and ceramic on ceramic
  • A hybrid acetabular component with polyethylene and metal backing is also used (above right image)
  • THA can be cemented (above right image) and non-cemented (above-left image)
  • Non-cemented arthroplasty is used on younger patients utilizing porous metallic parts allowing good fusion and bone ingrowth into the prosthesis

Failed THA May Develop

diagnosis hip arthritis and neoplasms el paso tx.
  • Most develop within the first year and require revision
  • Femoral stem may fracture (above left)
  • Postsurgical infection (above right)
  • Fracture adjacent to the prosthesis (stress riser)
  • Particle disease

Femoroacetabular Impingement Syndrome

diagnosis hip arthritis and neoplasms el paso tx.
  • (FAI): abnormality of normal morphology of the hip leading to eventual  cartilage damage and premature DJD
  • Clinically: hip/groin pain aggravated by sitting (e.g., hip flexed & externally rotated). Activity related pain on axial loading esp. with hip flexion (e.g., walking uphill)
  • Pincer-type acetabulum: > in middle age women potentially  many causes
  • CAM-type deformity: > in men in 20-50 m/c 30s
  • Mixed type (pincer-CAM) is most frequent
  • Up until the 90s, FAI was not well-recognized

FAI Syndrome

diagnosis hip arthritis and neoplasms el paso tx.
  • CAM-type FAI syndrome
  • Radiography can be a reliable Dx tool
  • X-radiography findings: osseous bump on the lateral aspect of femoral head-neck junction. Pistol-grip deformity. Loss of normal head sphericity. Associated features: os acetabule, synovial herniation pit (Pit’s pit). Evidence of DJD in advanced cases
  • MRI and MR arthrography (most accurate Dx of labral tear) can aid the diagnosis of labral tear and other changes of FAI
  • Referral to the Orthopedic surgeon is necessary to prevent DJD progression and repair labral abnormalities. Late Dx may lead to irreversible changes of DJD

AP Pelvis: B/L CAM-type FAI syndrome

diagnosis hip arthritis and neoplasms el paso tx.

Pincer-Type FAI with Acetabula Over-Coverage

diagnosis hip arthritis and neoplasms el paso tx.
  • Key radiographic signs: “Cross-over sign” and abnormal center-edge and Alfa-angle evaluation methods

Dx of FAI

diagnosis hip arthritis and neoplasms el paso tx.
  • Center-edge angle (above the first image) and Alfa-angle (above the second image)
  • B/L CAM-type FAI with os acetabule (above right image)

MR Arthrography

diagnosis hip arthritis and neoplasms el paso tx.

Hip Pelvis Arthritis & Neoplasms

Ankylosing Spondylitis Sufferers Find Relief With Chiropractic. El Paso, TX.

Ankylosing Spondylitis Sufferers Find Relief With Chiropractic. El Paso, TX.

Ankylosing Spondylitis is a type of arthritis that typically begins during adolescence or in a person’s early twenties and occurs more often in men than in women. However, once experiences onset, they are affected for the rest of their lives. It is estimated that between 0.2% and 0.5% of individuals in the United States suffers from ankylosing spondylitis.  It can cause significant pain, discomfort, and immobility. While there is no cure for the condition, the symptoms can be treated, bringing some degree of comfort and mobility.

What is Ankylosing Spondylitis?

Ankylosing Spondylitis, or AS, is a type of arthritis that causes inflammation in the spine. While the vertebrae are primarily involved, it can also affect other joints as well, including the hips, shoulders, heels, ribs, and the small joints of the feet and hands.

In some cases, the heart, lungs, and even eyes can be involved. If left untreated, the condition can progress, causing chronic pain that can be severe as the spinal inflammation increases. More advanced cases can cause the spine to grow new bone formations so that it is immobile, or fixed, sometimes resulting in kyphosis, which is a bowed or forward-stooped posture.

What Causes Ankylosing Spondylitis?

While genetics is believed to be a key player in the development of Ankylosing Spondylitis, the exact cause has not yet been determined. The majority of people who have AS also carry a specific gene that has been linked to the condition.

This gene produces HLA-B27, a protein or genetic marker, that more than 95% of Caucasians with ankylosing spondylitis have. However, some people don’t have this protein who develop AS and many people do carry this marker yet never develop the condition.

Researchers theorize that there may be other genes that may be involved, as well as environmental factors that trigger the gene activation, such as a bacterial infection, causing people who are susceptible to AS to activate it. Scientists have identified more than 60 genes that are believed to be associated with AS with only about 30% that are linked to HLA-B27 regarding overall risk. Other genes that have been identified as key to AS include IL-23, IL-17, IL-12, and ERAP.

It is also believed that AS can be triggered when the intestinal defenses break down, allowing certain bacteria into the bloodstream. This can, in turn, cause an immune response.

 Ankylosing Spondylitis chiropractic treatment el paso tx.

How is Ankylosing Spondylitis Treated?

AS cannot be cured, but the symptoms can be treated to relieve stiffness and pain as well as delay or prevent spinal deformity and other complications. The damage that it does to the joints is irreversible, so it is best if treatment is started before that occurs. There are several ways that AS is treated:

  • Medication – Nonsteroidal anti-inflammatory drugs (NSAIDs) like indomethacin (Indocin) and naproxen (Naprosyn) are commonly used to treat the symptoms of AS. They can be useful in relieving pain, inflammation, and stiffness but may cause some side effects, including gastrointestinal bleeding. This makes long-term use impractical and even unsafe. If NSAIDs do not help, other medications may be prescribed, including:
    • Golimumab (Simponi; Simponi Aria)
    • Certolizumab pegol (Cimzia)
    • Adalimumab (Humira)
    • Etanercept (Enbrel)
    • Infliximab (Remicade)
  • Physical therapy – PT is often recommended to help with flexibility, strength, and pain relief. It can help with posture and prevent some of the more debilitating symptoms.
  • Surgery – Most people with AS do not require surgery, but it may be recommended if there is severe joint damage or pain. In some cases, it can cause significant damage to hip joints, and they will need to be replaced.
  • Chiropractic – Many patients with AS have with outstanding results with chiropractic treatment. It is non-invasive and does not have the unpleasant side effects that many medications have.

Chiropractic Treatment for Ankylosing Spondylitis

Chiropractors strongly recommend chiropractic treatment for the non-acute inflammatory stage of AS. Once the condition has progressed to acute joint disease, there is a very high risk of injury or damage to the connective tissue. Adjustments and exercise are used to relieve symptoms, but some of the traditional spinal manipulation treatments are not performed.

A chiropractor will also make recommendations to the patient regarding lifestyle changes that can help with symptoms, such as stopping smoking. Tobacco use can increase inflammation and damage connective tissue. They may also advise increasing their intake of omega three fatty acids in their diet. Regular chiropractic care can help patients manage symptoms and prevent disease progression, improving their quality of life.

Cerebral Palsy Chiropractic Treatment

Spinal Arthritis Diagnostic Imaging Approach Part II

Spinal Arthritis Diagnostic Imaging Approach Part II

 

spinal arthritis el paso tx.

 

  • Spinal Arthritis
  • Ossification of Posterior Longitudinal Ligament (OPLL). Less frequent than DISH.
  • Greater clinical importance d/t spinal canal stenosis and cervical myelopathy
  • Asian patients are at higher risk
  • Both OPLL & DISH may co-exist and increase the risk of Fx
  • Imaging: x-rad: linear radioopacity consistent with OPLL
  • Imaging modality of choice: CT scanning w/o contrast
  • MRI may help  to evaluate myelopathy
  • Care: surgical with laminoplasty (above right image) that has been pioneered and advanced in the Far East

 

M/C Inflammatory Arthritis In Spine

 

spinal arthritis el paso tx.

 

  • Rheumatoid spondylitis (Rheumatoid arthritis) d/t inflammatory synovial proliferation pannus rich in lymphocytes, macrophages, and plasma cells
  • C/S RA may affect 70-90% of patients
  • Variable severity from mild to destructive disabling arthropathy
  • RA IN C/S m/c affects C1-C2 due to an abundance of rich synovial tissue
  • Typically infrequent in the thoracic/lumbar region
  • Sub-axial C/spine may be affected later due to facets, erosions, ligament laxity and instability showing “Stepladder” appearance
  • Clinically: HA, neck pain, myelopathy, etc. inc. Risk of Fx/subluxation. Any spinal manipulation HVLT ARE STRICTLY CONTRAINDICATED.
  • Rx: DMARD, anti-TNF-alfa, operative for subluxations, etc.

 

Rheumatoid Spondylitis C1-C2. Perform X-radiography initially with flexed-extended views. Note Dens erosion, C1-2 subluxation (2.5 mm) that changes on mobility

 

spinal arthritis el paso tx.

 

spinal arthritis el paso tx.

 

  • RA spondylitis: an erosion of the odontoid with the destruction of C1-C2 ligaments and instability
  • Stepladder aka Step-step sub-axial deformity d/t facets erosions and ligamentous destruction/laxity
  • MRI required to evaluate cord compression/myelopathy

 

spinal arthritis el paso tx.

 

  • Sagittal T2 WI MRI of pt with RA. Rheumatoid pannus formation is present at C1-2 (arrow) causing mild cord compression
  • RA pannus may develop early before frank x-radiography changes noted
  • Clinically: HA, neck pain, tingling in UE, positive Lhermitte phenomenon d/t cervical myelopathy

 

Operative Care of Rheumatoid Spondylitis and Its Complications

 

spinal arthritis el paso tx.

 

Seronegative Spondyloarthropathies

 

  • Ankylosing Spondylitis (AS)
  • Enteropathic Arthritis (EnA) (d/t IBD: Crohn’s & UC) identical to AS on imaging
  • Psoriatic Arthritis (PsA)
  • Reactive Arthritis (ReA)
  • All share the following features: m/c HLA-B27 marker, RF-, Sacroiliitis, Enthesitis, Ocular Involvement (i.e., conjunctivitis, uveitis, episcleritis, etc.)
  • AS & EnA are radiographically virtually indistinguishable, but EnA typically presents with less severe spinal changes than AS
  • Both PsA & ReA present with virtually identical spinal changes, but ReA typically affects the lower extremity compared to PsA affecting hands and feet

 

spinal arthritis el paso tx.

 

spinal arthritis el paso tx.

 

  • AS: likely autoimmune systemic inflammatory disease that targets SIJ, spinal facet joints annuls of the disc, rib joints and all spinal ligaments.
  • Key path feature: enthesitis.
  • Extraspinal features: uveitis, aortitis, pulmonary fibrosis, amyloidosis, cardiovascular disease.
  • M:F 4:1, age: 20-40 m/c. Clinic LBP/stiffness, reduced rib expansion <2 cm is > specific than HLA-B27, progressive kyphosis, risk of Fx’s.
  • Imaging steps: 1st step-x-rays to id. Sacroiliitis/spondylitis. MRI & CT may help if x-rays are unrewarding.
  • Labs: HLA-B27, CRP/ESR, RF-
  • Dx: clinical+labs+imaging.
  • Rx: NSAID, DMARD, anti-TNF factor therapy
  • Key Imaging Dx: always presents initially as b/l symmetrical sacroiliitis that will progress to complete ankylosis. Spondylitis presents with continuous ascending discovertebral osteitis (i.e., marginal syndesmophytes, Romanus lesion, Anderson lesion), facets and all spinal ligament inflammation and fusion with a late feature of “bamboo spine, trolley track, dagger sign,” all indicating complete spinal ossification/fusion. Increasing risk of Fx’s.

 

spinal arthritis el paso tx.

 

Key Dx of Sacroiliitis

 

  • Blurring, cortical indistinctness/irregularity with adjacent reactive subchondral sclerosis initially identified primarily on the iliac side of  SIJs.
  • Normal SIJ should maintain a well defined white cortical line. Dimension 2-4 mm. May look incongruous d/t 3D anatomy masked by 2D x-rays.

 

spinal arthritis el paso tx.

 

Key Imaging Dx In Spine

 

  • Marginal syndesmophytes and inflammation at the annulus-disc (above arrows) at the earliest dx; by MRI as marrow signal changes on T1 and fluid sensitive imaging (above top images).
  • These represent enthesitis-inflammation that will ossify into bamboo spine.
  • Lig ossification: trolley track/dagger sign

 

spinal arthritis el paso tx.

 

  • AS in extraspinal joints: root joints, hips, and shoulders
  • Symphysis pubis
  • Less frequent in peripheral joints (hands/feet)
  • All seronegatives may present with heel pain d/t enthesitis

 

spinal arthritis el paso tx.

 

  • Complication: Above Carrot-stick/chaulk-stick Fx

 

spinal arthritis el paso tx.

 

  • PsA & ReA (formerly Reiter’s) present with b/l sacroiliitis that virtually identical to AS
  • In the spine PsA & ReA DDx from AS by the formation of non-marginal syndesmophytes aka bulky paravertebral ossifications (indicate vertebral enthesitis)
  • For a clinical discussion of Spondyloarthropathies refer to:
  • https://www.aafp.org/afp/2004/0615/p2853.html

 

Spinal Arthritis

Spinal Arthritis Diagnostic Imaging Approach Part I

Spinal Arthritis Diagnostic Imaging Approach Part I

Degenerative Arthritis

  • Spinal Arthritis:
  • Spondylosis aka Degenerative disease of the spine represents an evolution of changes affecting most mobile spinal segments beginning with:
  • Intervertebral disc (IVD) dehydration (desiccation) and degeneration aka Degenerative Disc Disease (DDD) with an abnormal increase in mechanical stress and degeneration of posterior elements affecting 4-mobile synovial articulations ( true osteoarthritis)
  • 2-Facets in the L/S & 2-Facets & 2-Uncovertebral joints in the C/S
  • Imaging plays a significant role in the diagnosis, grading, and evaluation of neurological complications (e.g., spondylotic myelopathy/radiculopathy)
  • X-radiography with AP, Lateral & Oblique spinal views provides Dx and classification of Spondylosis
  • MR imaging may help to evaluate the degree of neurological changes associated with degenerative spinal canal and neural foraminal stenosis
spinal arthritis el paso tx.
  • Spinal motion segment:
  • 2-adjacent vertebrae
  • IVD (fibrocartilage)
  • 2-facets (synovial)
  • Pathology: loss of disc height increases mechanical stress on mobile elements
  • Ligamentous laxity/local instability
  • Spinal osteophytes aka spondylophytes & bony facet/uncinate proliferation
  • Disc herniation and often disc-osteophyte complex
  • Ligamentum flavum “hypertrophy” or thickening due to buckling
  • Loss of normal lordosis with or w/o reversal or kyphosis
  • Vertebral canal & neural foraminal stenosis

Neutral lateral cervical radiograph: note mild to moderate disc narrowing and spondylophyte formation at C5-6 & C6-C7 (most common levels affected by cervical spondylosis). Straightening or flattening with mild reversal of cervical lordosis. Some mild facet proliferation is noted at the above levels

spinal arthritis el paso tx.
  • On radiographs: evaluate for disc height (mild, moderate or severe) loss
  • End-plate sclerosis & spondylophytes; mild, moderate or severe
  • Facet and uncinate irregularity, hypertrophy/degeneration; mild, moderate or severe
  • Note degenerative instability aka degenerative spondylolisthesis/retrolisthesis
  • Normal or lost lordosis vs. degenerative kyphosis
  • Key Dx: correlate with a clinical presentation: neck/back pain with or w/o neurological disturbance ( myelopathy vs. radiculopathy or both)
spinal arthritis el paso tx.
  • Uncinate processes undergo degeneration/proliferation resulting in uncovertebral arthrosis
  • Early findings present with mild bone proliferation along the cortical margin (white and black arrows) if compared to normal uncinate (orange arrow)
  • Later, more extensive bone proliferation extending into and narrowing vertebral canal and neural osseous foramina (IVF’s) may be noted. The latter may contribute to spinal/IVF stenosis and potential neurological changes
  • Posterior oblique views may help further
spinal arthritis el paso tx.
  • AP lower cervical (a) and posterior oblique (b) views
  • Note mild uncinated process proliferation with neural foraminal narrowing (arrows)
  • Typically if less than a third of IVF becomes narrowed, patients may present w/o significant neurological signs
spinal arthritis el paso tx.
  • Lumbar spondylosis is evaluated with AP and lateral views with additional AP L5-S1 spot view to examine lumbosacral junction
  • Typical features include disc height loss/degeneration
  • Intra-discal gas (vacuum) phenomenon (blue arrow) along with spondylophytes
  • Degenerative spondylolisthesis and/or retrolisthesis (green arrow) may follow disc and facet degeneration and can be graded by the Meyerding classification
  • In most cases, degenerative spondylolisthesis rarely progresses beyond Grade 2
  • Lumbar facet degeneration seen as bone proliferation/sclerosis and IVF narrowing
spinal arthritis el paso tx.
spinal arthritis el paso tx.
  • MR imaging w/o gad C is an effective modality to evaluate clinical signs of spondylosis & associated neurological complications with pre-surgical evaluation
  • Case: 50-y.o Fe with neck pain. Case b-45-y.o.M (top a b images). MRI reveals: loss of disc hydration or desiccation, spondylophytes and disc herniation w/o neurological changes
  • (Bottom images) Left: preoperative and right postoperative MRI slices of the patient presented with clinical signs of cervical spondylotic myelopathy. Note disc herniation, ligam flavum hypertrophy and canal stenosis (left)
spinal arthritis el paso tx.
  • Sagittal MRI slice of lumbar DDD manifested with disc desiccation and posterior herniation effacing thecal sac
  • Correlating sagittal and axial slices will be more informative to evaluate canal stenosis and potential degree of neurological involvement (above-bottom images)
spinal arthritis el paso tx.
spinal arthritis el paso tx.

Diffuse Idiopathic Skeletal Hyperostosis (DISH) aka Forestier disease

  • Flowing degenerative ossification of ALL
  • M/c Thoracic spine. 2nd m/c-cervical spine
  • Dx by imaging only. X-radiography is sufficient
  • CT w/o contrast helps with Dx of Fx
  • Men>women. Pts>60-y.o. Extensive DISH shows 49% association with type 2DM
  • Complications: Chalk (carrot) stick Fx. Unstable 3-column Fx requiring surgical fusion
  • Sagittal reconstructed CT scan slice in bone window
  • Chalk stick Fx at C5-C6 in the patient with DISH and OPLL

Spinal Arthritis

Imaging the Spine in Arthritis: a Pictorial Review

Imaging the Spine in Arthritis: a Pictorial Review

Many types of arthritis can affect the structure and function of the muscles, bones and/or joints, causing symptoms such as, pain, stiffness and swelling. While arthritis can commonly affect the hands, wrists, elbows, hips, knees and feet, it can also affect the facet joints found along the length of the spine. One of the most well-known types of arthritis, known as rheumatoid arthritis or RA, is a chronic inflammatory disease of the joints which occurs when the human body’s own immune system attacks the synovium, the thin membrane that lines the joints. According to the article below, imaging the spine in arthritis is fundamental towards its proper treatment.

 

Abstract

 

Spinal involvement is frequent in rheumatoid arthritis (RA) and seronegative spondyloarthritides (SpA), and its diagnosis is important. Thus, MRI and CT are increasingly used, although radiography is the recommended initial examination. The purpose of this review is to present the typical radiographic features of spinal changes in RA and SpA in addition to the advantages of MRI and CT, respectively. RA changes are usually located in the cervical spine and can result in serious joint instability. Subluxation is diagnosed by radiography, but supplementary MRI and/or CT is always indicated to visualize the spinal cord and canal in patients with vertical subluxation, neck pain and/or neurological symptoms. SpA may involve all parts of the spine. Ankylosing spondylitis is the most frequent form of SpA and has rather characteristic radiographic features. In early stages, it is characterized by vertebral squaring and condensation of vertebral corners, in later stages by slim ossifications between vertebral bodies, vertebral fusion, arthritis/ankylosis of apophyseal joints and ligamentous ossification causing spinal stiffness. The imaging features of the other forms of SpA can vary, but voluminous paravertebral ossifications often occur in psoriatic SpA. MRI can detect signs of active inflammation as well as chronic structural changes; CT is valuable for detecting a fracture.

 

Keywords: Spine, Arthritis, Rheumatoid Arthritis, Spondyloarthropathies

 

Introduction

 

The spine can be involved in most inflammatory disorders encompassing rheumatoid arthritis (RA), seronegative spondyloarthritides (SpA), juvenile arthritides and less frequent disorders such as, arthro-osteitis and SAPHO (synovitis, acne, pustulosis, hyperostosis, osteitis) syndrome.

 

During the last decade, the diagnostic use of magnetic resonance imaging (MRI) and computed tomography (CT) has increased considerably, although radiography is still the recommended initial examination. It is therefore important to know the characteristic radiographic findings in arthritides in addition to the advantages of supplementary MRI and CT. This review will focus on the different imaging features and be concentrated on the most frequent inflammatory spinal changes seen in RA and SpA, respectively. These two entities display somewhat different imaging features, which are important to recognize.

 

Dr-Jimenez_White-Coat_01.png

Rheumatoid arthritis is an autoimmune disease which causes the human body’s own immune system to attack and often destroy the lining of the joints. Although it commonly affects the small joints of the hands and feet, rheumatoid arthritis, or RA, can affect any joint in the human body. The neck, or cervical spine, can be affected more often than the lower back if rheumatoid arthritis affects the joints in the spine. 

Dr. Alex Jimenez D.C., C.C.S.T.

 

Rheumatoid Arthritis

 

Involvement in RA is usually located in the cervical spine where erosive changes are predominantly seen in the atlanto-axial region. Inflamed and thickened synovium (pannus) can occur around the odontoid process (dens) and cause bone erosion and destruction of surrounding ligaments, most seriously if the posterior transverse ligament is involved. Laxity or rupture of the transverse ligament causes instability with a potential risk of spinal cord injury. Cervical RA involvement is a progressive, serious condition with reduced lifetime expectancy [1], and its diagnosis is therefore important [2, 3].

 

Fig. 1 Standard radiography of the cervical spine in rheumatoid arthritis (RA). (a) Lateral radiographs in neutral position and (b) during flexion in addition to (c) lateral and (d) anterior-posterior (AP) open-mouth view of the atlanto-axial region (45-year-old woman). The flexion view (b) shows abnormal distance (>3 mm) between the posterior aspect of the anterior arc of the atlas and the anterior aspect of the dens (black line). Note that the spino-laminar line of the atlas (arrow) does not align with that of the other vertebrae, confirming the presence of anterior subluxation, but there is no stenosis of the atlanto- axial canal; the posterior atlanto-dental interval (white line) is >14 mm. The open-mouth view (d) shows erosion at the base of the dens (arrow). (a) and (b) show concomitant disc degenerative changes at the C4–C6 level.

Fig. 2 Lateral and rotatory atlanto-axial subluxation. AP open- mouth view in a 53-year-old man with RA. There is narrowing of the atlanto-axial joints with superficial erosions (black arrow) and lateral displacement of the axis with respect to the lateral masses of the atlas (white arrow); in addition signs indicating rotatory displacement with asymmetry of the distance between the dens and the lateral masses of the atlas.

 

Radiography of the cervical spine is mandatory in RA patients with neck pain [3]. It should always include a lateral view in a flexed position compared with a neutral position in addition to special views of the dens area to detect any lesions and/or instability (Fig. 1). A supplementary lateral view during extension can be useful to assess reducibility of atlanto-axial subluxation possibly limited by pannus tissue between the anterior arc of the atlas and dens.

 

Anterior atlanto-axial subluxation is the most frequent form of RA instability in the occipito-atlanto-axial region, but lateral, rotatory and vertical subluxation can also occur. The definition of the different forms of instability by radiography is as follows [3].

 

Anterior atlanto-axial subluxation. Distance between the posterior aspect of the anterior arc of the atlas and the anterior aspect of the dens exceeding 3 mm in a neutral position and/or during flexion (Fig. 1). It may cause stenosis of the atlanto-axial canal presenting as a posterior atlanto-dental interval<14 mm (Fig. 1).

 

Lateral and rotatory atlanto-axial subluxation. Displacement of the lateral masses of the atlas more than 2 mm in relation to that of the axis and asymmetry of the lateral masses relative to the dens, respectively (Fig. 2). Rotatory and lateral subluxation is diagnosed on open-mouth anterior-posterior (AP) radiographs. Anterior subluxation often coexists because of the close anatomical relation between the atlas and the axis.

 

Posterior atlanto-axial subluxation. The anterior arc of the atlas moves over the odontoid process. This is rarely seen, but may coexist with fracture of the dens.

 

Vertical atlanto-axial subluxation is also referred to as atlanto-axial impaction, basilar invagination or cranial setting, and is defined as migration of the odontoid tip proximal to McRae’s line corresponding to the occipital foramen. This line can be difficult to define on radiographs, and vertical subluxation has therefore also been defined by several other methods. Migration of the tip of the odontoid process >4.5 mm above McGregor’s line (between the postero-superior aspect of the hard palate and the most caudal point of the occipital curve) indicates vertical subluxation (Fig. 3).

 

Fig. 3 Vertical atlanto-axial subluxation, measurement methods. (a) Lateral normal radiograph in neutral position showing the location of McGregor’s line (black) between the postero-superior aspect of the hard palate and the most caudal point of the occipital curve. Migration of the tip of the dens >4.5 mm above McGregor’s line indicates vertical subluxation. The distance indicated by the white line between McGregor’s line and the midpoint of the inferior margin of the body of axis is used to evaluate vertical subluxation according to Redlund-Johnell and Pettersson’s method. A distance less than 34 mm in men and 29 mm in women indicates vertical subluxation. (b) Sagittal CT reconstruction of a normal cervical spine showing the location of McRae’s line corresponding to the occipital foramen and the division of the axis into three equal portions used by Clark’s method for diagnosing vertical subluxation. If the anterior arc of the atlas is in level with the middle or caudal third of the axis there is slight and pronounced vertical subluxation, respectively. (c) Ranawat’s method includes determination of the distance between the centre of the second cervical pedicle and the transverse axis of the atlas. A distance less than 15 mm in males and 13 mm in females indicates vertical subluxation [4].

Fig. 4 Vertical subluxation. (a) Lateral radiograph with McGregor’s line (black line; 61-year-old man with RA). The tip of the dens is difficult to define, but measurement according to Redlund-Johnell’s method (white line) results in a distance of 27 mm, which is below the normal limit. In accordance with this, the anterior arc of the atlas is level with the middle third of the axis. (b) Ranawat’s method, the distance between the centre of the second cervical pedicle and the transverse axis of the atlas is below the normal limit (9 mm). Thus, all measurements indicate vertical subluxation. Supplementary MRI, (c) sagittal STIR and (d) T1-weighted images show erosion of the dens and protrusion of the tip into the occipital foramen causing narrowing of the spinal canal to 9 mm, but persistence of cerebrospinal fluid around the cord. There is a 9-mm-thick mass of pannus tissue between the dens and anterior arc (black line) exhibiting small areas with high signal intensity on the STIR image (arrow) compatible with slight activity, but signal void fibrous pannus tissue predominates.

The occurrence of dens erosion can, however, make this measurement difficult to obtain. The Redlund-Johnell method is therefore based on the minimum distance between McGregor’s line and the midpoint of the inferior margin of the body of the axis on a lateral radiograph in a neutral position (Fig. 3) [4]. Visualisation of the palate may not always be obtained. Methods without dens and/or the palate as landmarks have therefore been introduced [4]. The method described by Clark et al. (described in [4]) includes assessment of the location of the atlas by dividing the axis into three equal portions on a lateral radiograph. Location of the anterior arc of the atlas in level with the middle or caudal third of the axis indicates vertical subluxation (Fig. 3). Ranawat et al. have proposed using the distance between the centre of the second cervical pedicle and the transverse axis of the atlas at the odontoid process (Fig. 3) [4]. To obtain the diagnosis of vertical subluxation a combination of the Redlund-Johnell, Clark and Ranawat methods has been recommended (described in [4]). If any of these methods suggests vertical subluxation MRI should be performed to visualize the spinal cord (Fig. 4). Using this combination of methods vertical subluxation will be missed in only 6% of patients [4]. It is mandatory to diagnose vertical subluxation; this can be fatal because of the proximity of the dens to the medulla oblongata and the proximal portion of the spinal cord. Risk of cord compression/injury occurs, especially in patients with flexion instability accompanied by erosive changes in the atlanto- axial and/or atlanto-occipital joints, causing the vertical subluxation with protrusion of the dens into the occipital foramen (Figs. 4, 5).

 

Subaxial RA changes also occur in the form of arthritis of the apophyseal and/or uncovertebral joints, appearing as narrowing and superficial erosions by radiography. It can cause instability in the C2-Th1 region, which is mainly seen in patients with severe chronic peripheral arthritis. Anterior subluxation is far more frequent than posterior subluxation. It is defined as at least 3 mm forward slippage of a vertebra relative to the underlying vertebra by radiography including a flexion view (Fig. 6). Changes are particularly characteristic at the C3–4 and C4–5 level, but multiple levels may be involved, producing a typical “stepladder” appearance on lateral radiographs. The condition is serious if the subaxial sagittal spinal canal diameter is <14 mm, implying a possibility of spinal cord compression [2]. The instability may progress over time, especially if the C1–C2 region is stabilized surgically (Fig. 6) [5].

 

Fig. 5 Vertical subluxation with spinal cord compression. MRI of the cervical spine in a 69- year-old woman with advanced peripheral RA, neck pain and clinical signs of myelopathy. (a) Sagittal STIR, (b) sagittal T1 and (c) axial T2 fat-saturated (FS) images show erosion of the dens and protrusion of the tip into the occipital foramen causing compression of the spinal cord, which exhibits irregular signal intensity (white arrows). The osseous spinal canal has a width of approximately 7 mm (black line). There is heterogeneous signal intensity pannus surrounding the dens compatible with a mixture of fibrotic and oedematous pannus tissue (black arrows) in the widened space between the dens and the anterior arc of the atlas.

 

Discitis-like changes and spinous process erosion may also be detected by radiography in RA, but are relatively rare, whereas concomitant degenerative changes occur occasionally (Fig. 1).

 

Cross-sectional imaging in the form of CT and MRI eliminates overprojecting structures and can improve the detection of RA changes. Osseous changes (erosions, etc.) can be clearly delineated by CT [6]. Additionally, MRI visualizes soft tissue structures (pannus; spinal cord, etc.), signs of disease activity and sequelae of inflammation in the form of fibrous pannus. These advantages of CT and MRI in patients with atlanto-axial involvement are illustrated in Figs. 7 and 8, including the possibility of detecting signs of arthritis by MRI before the occurrence of erosive changes (Fig. 8) [3].

 

Fig. 6 Subaxial instability. (a) Flexion view in a 64-year-old woman with advanced peripheral RA showing anterior atlanto-axial instability as well as subaxial instability at multiple levels. (b) Flexion view 2 years later after surgical stabilization of the atlanto-axial region demonstrates progression of the subaxial instability, especially between C3 and C4 (white arrow). There is a characteristic “stepladder” appearance, which also occurred on the initial radio- graphs (a), but is less pronounced.

Fig. 7 Advantages of CT and MRI. (a) Supplementary CT and (b-f) MRI of the patient shown in Fig. 1. CT demonstrates erosion not only at the base of the dens, but also at the tip and at the atlanto-axial and atlanto-occipital joints, which are difficult to visualize by radiography. MRI, (b) sagittal STIR and (c) sagittal T1 of the entire cervical spine and post-contrast T1FS images of the atlanto-axial region, (d) sagittal, (e) coronal and (f) axial. Oedematous voluminous pannus surrounding the dens is seen on the STIR and T1 images (black arrows) in addition to C4/5 and C5/6 disc degeneration with posterior protrusion of the disc at C4/5. The post-contrast T1FS images confirm the presence of vascularized enhancing pannus around the dens (white arrows) and demonstrate improved anatomical delineation compared with the STIR image. There is no sign of spinal cord compression.

Fig. 8 Non-radiographic MR findings. MRI in a 41-year-old woman with peripheral erosive RA and neck pain, but normal cervical radiography. (a) Post-contrast axial and (b) coronal TIFS images show signs of active arthritis with synovial contrast enhancement at the left atlanto-axial joint in addition to enhancing pannus tissue at the left side of the dens (white arrows). There is also a subchondral enhancing area in the axis (black arrow) compatible with a pre-erosive lesion.

 

A diagnostic strategy according to Younes et al. [3] is recommended (Fig. 9). This includes an indication for radiography in all RA patients with disease duration >2 years as cervical involvement may occur in over 70% of patients and has been reported to be asymptomatic in 17% of RA patients. It is recommended to monitor patients with manifest peripheral erosions accompanied by RF (rheumatoid factor) and antiCCP (antibodies to cyclic citrullinated peptide) positivity every second year and patients with few peripheral erosions and RF negativity at 5-year intervals. MRI is indicated in patients with neurological deficit, radiographic instability, vertical subluxation and subaxial stenosis [2, 3]. Visualisation of the spinal cord is especially important to detect cord injury or risk of injury. MRI should therefore always be performed in RA patients with neck pain and/or neurological symptoms [3, 7].

 

Seronegative Spondyloarthritides

 

According to European classification criteria [8, 9], SpA is divided into: (1) ankylosing spondylitis (AS), (2) psoriatic arthritis, (3) reactive arthritis, (4) arthritis associated with inflammatory bowel disorders (enteropathic arthritis) and (5) undifferentiated SpA. Inflammatory changes at the sacroiliac joints always occur in AS and are part of most other forms of SpA. Spinal changes are also a feature of SpA, especially in the late stages of AS.

 

Ankylosing Spondylitis

 

Ankylosing spondylitis is the most frequent and usually the most disabling form of SpA. It has a genetic predisposition in the form of a frequent association with the human leukocyte antigen (HLA) B27 [10]. AS often starts in early adulthood and has a chronic progressive course. It is therefore important to diagnose this disorder. According to the modified New York Criteria [11], the diagnosis of definite AS requires the following: manifest sacroiliitis by radiography (grade ≥2 bilateral or unilateral grade 3–4 sacroiliitis; Fig. 10) and at least one of the following clinical criteria: (1) low back pain and stiffness for more than 3 months improving with activity, (2) limited movement of the lumbar spine and (3) reduced chest expansion. These criteria are still used in the diagnosis of AS despite the increasing use of MRI to detect the disease early. It is therefore important to know both the characteristic radiographic features and the MR features of AS.

 

Early radiographic spinal changes encompass erosion of vertebral corners (Romanus lesions) causing vertebral squaring and eliciting reactive sclerosis appearing as condensation of vertebral corners (shiny corners; Fig. 10). These changes are caused by inflammation at the insertion of the annulus fibrosus (enthesitis) at vertebral corners provoking reactive bone formation [12]. Later on slim ossifications appear in the annulus fibrosus (syndesmo- phytes) (Fig. 11) [13]. With disease progression the spine gradually fuses because of syndesmophytes crossing the intervertebral spaces in addition to fusion of apophyseal joints, resulting in complete spinal fusion (bamboo spine; Fig. 12). In advanced disease the supra- and interspinous ligaments may ossify and be visible on frontal radiographs as a slim ossified streak (Fig. 12). The occurrence of a single central radiodense streak has, the “dagger sign”. When the ligamentous ossification occurs together with ossification of apophyseal joint capsules, there are three vertical radiodense lines on frontal radiography (trolley-track sign).

 

Fig. 9 Diagnostic strategy. According to Younes et al. [3] radiography of the cervical spine is indicated in all RA patients with disease duration >2 years. It should at least include open-mouth and lateral views in neutral and flexed positions. Because of the occurrence of asymptomatic cervical involvement in 17% of RA patients, it is recommended to monitor patients with intervals of 2–5 years depending on positivity for the rheumatoid factor. MRI is indicated in patients with neurological deficit, radiographic instability, atlanto-axial impaction and subaxial stenosis. CT may add information in rotatory and lateral subluxation because of the possibility of secondary reconstruction in arbitrary planes and a clear visualisation of the atlanto-occipital joints [6].

Erosive changes within intervertebral spaces (Andersson lesions) have been detected by radiography in approximately 5% of patients with AS [14], but more frequently by MRI (Fig. 11) [15].

 

Persistent movement at single intervertebral spaces may occur in an otherwise ankylosed spine, sometimes caused by non-diagnosed fractures. This can result in pseudo- arthrosis-like changes with the formation of surrounding reactive osteophytes due to excessive mechanical load at single movable intervertebral spaces [14]. The diagnosis of such changes may require a CT examination to obtain adequate visualization (Fig. 13).

 

One of the life-threatening complications of AS is spinal fracture. Non-fatal fractures have been reported to occur in up to 6% of AS patients, especially in patients with long disease duration [16]. Fractures may occur after minor trauma because of the spinal stiffness and frequently accompanying osteoporosis. Fractures often occur at intervertebral spaces, but usually involve the ankylosed posterior structures and are thereby unstable (Fig. 14). Obvious fractures can visualize by radiography, but fractures may be obscured. It is therefore mandatory to supplement a negative radiography with CT if fracture is suspected (in the case of trauma history or a change in spinal symptoms). The occurrence of cervico-thoracic fractures may cause spinal cord injury and be lethal even following minor trauma [17].

 

Cross-sectional CT or MR imaging can be advantageous in the diagnosis of AS changes. CT providing a clear delineation of osseous structures is the preferred technique for visualizing pseudo-arthrosis and detecting fractures (Figs. 13, 14). CT is superior to MRI in detecting minor osseous lesions such as erosion and ankylosis of the apophyseal, costo-vertebral and costo-transversal joints (Fig. 15). MRI can visualize signs of active inflammation in the form of bone marrow and soft tissue oedema and/or contrast enhancement. It has therefore gained a central role in the evaluation of disease activity [15]. MRI can, however, also detect sequelae of inflammation consisting of fatty deposition in the bone marrow and chronic structural changes such as erosion and fusion of vertebral bodies [15].

 

Characteristic MR findings early in the disease are activity changes mainly consisting of oedema at vertebral corners and/or costo-vertebral joints (Fig. 16) [13]. The inflammatory changes at vertebral corners are characteristic of AS. Based on the occurrence of severe or multiple (≥3) lesions in young patients, AS changes can be distinguished from degenerative changes with a high reliability [18].

 

Fig. 10 Relatively early changes in ankylosing spondylitis (AS). (a) AP radiograph of the sacroiliac joints in a 28-year-old man presenting with typical definite bilateral AS sacroiliitis (grade 3) in the form of bilateral joint erosion accompanied by subchondral sclerosis. (b) Initial spinal changes consisting of erosion of vertebral corners (Romanus lesion) with vertebral squaring corresponding to Th11, Th12, L4 and L5 accompanied by condensation of the vertebral corners—shiny corners (arrows).

During the disease course signs of activity can also occur at syndesmophytes, apophyseal joints and interspinous ligaments (Fig. 16). Detection of inflammation at apophyseal joints by MRI, however, demands pronounced involvement histopathologically [19]. The inflammation at vertebral corners is the most valid feature and has been observed related to the development of syndesmophytes by radiography [12], establishing a link between signs of disease activity and chronic structural changes.

 

Chronic AS changes detectable by MRI mainly consist of fatty marrow deposition at vertebral corners (Fig. 17), erosion (Fig. 11) and vertebral fusion in advanced disease (Fig. 12). Fatty marrow deposition seems to be an a sign of chronicity being significantly correlated with radiographic changes, in particular, vertebral squaring [15]. Erosions are more frequently detected by MRI than by radiography (Fig. 11) [15] and can present with signs of active inflammation and/or surrounding fatty marrow deposition compatible with sequels of osseous inflammation. Syndesmophytes, however, may not always be visible by MRI because they may be difficult to distinguish from fibrous tissue unless there is concomitant active inflammation or fatty deposition (Figs. 11, 16) [15, 20].

 

The possibility of visualizing disease activity by MRI has increased its use to monitor AS, especially during anti-TNF (anti-tumour necrosis factor) therapy [21, 22]. Several studies have shown that MR changes are frequent in the thoracic spine (Fig. 16) [15, 23]. It is therefore important to examine the entire spine using sagittal STIR or T2 fat-saturated (FS) and T1-weighted sequences. Supplementary axial slices can be necessary for visualising involvement of apophyseal, costo-vertebral and costo-transversal joints (Fig. 16) [24, 25]. Post-contrast T1FS sequences can sometimes be advantageous as they provide better anatomical delineation [26]. Additionally, dynamic contrast-enhanced MRI may be superior to static MRI in monitoring disease activity during anti-TNF therapy [27]. Whole-body MRI gives the possibility of detecting involvement in other areas without losing important information about spinal and sacroiliac joint involvement [28, 29].

 

Other Forms of SpA

 

Radiographic changes in reactive and psoriatic arthritis are often characterized by voluminous non-marginal syndesmophytes (parasyndesmophytes) or coalescing ossification of the paravertebral ligaments in addition to asymmetrical sacroiliitis (Fig. 18) [30].

 

Reactive arthritis is self-limiting in most patients. However, in patients with chronic reactive arthritis and HLA B27 the axial changes may progress to changes somewhat similar to those seen in AS and can then be regarded as AS elicited by infection [10].

 

Fig. 11 Syndesmophytes and erosions in AS. (a) Lateral radiograph in a 29-year-old man with the characteristic slim ossification (syndesmophytes) at the periphery of the annulus fibrosus (black arrows) in addition to erosion of the endplates at the intervertebral (iv) space between L3 and L4 (white arrow). Supplementary MRI, (b) sagittal STIR and (c) T1-weighted images show small oedematous areas in the erosion at iv L3/4 on the STIR image and surrounding fatty marrow deposition on T1 as a sign of previous osseous inflammation. There are additional erosive changes (black arrows, c) not clearly delineated by radiography and slight oedema at the vertebral corners (white arrows, b). Note that the syndesmophytes demonstrated by radiogra- phy are not visible on MRI.

Fig. 12 Advanced AS. (a) AP and (b) lateral radiograph in a 55-year-old man showing vertebral fusion due to syndesmophytes crossing the intervertebral spaces in addition to fusion of the apophyseal joints (bamboo spine). The interspinous ligaments are ossified, presenting as a slim ossified streak on the frontal radiograph (dagger sign; arrows). MRI, sagittal T1- weighted images of (c) the cervico-thoracic and (d) lumbar region, respectively, shows a general narrowing of the intervertebral discs with partial osseous fusion of the vertebral bodies, especially in the lumbar region (arrows). In addition a characteristic AS deformity with reduced lumbar lordosis and thoracic kyphosis.

Fig. 13 Pseudo-arthrosis-like changes in AS. (a) AP and (b) lateral radiograph showing vertebral fusion except at iv Th10/11. There is surrounding osteophyte formation at this iv space (arrows). Supplementary CT, (c) sagittal and (d) coronal 2D reconstruction, demonstrates lack of fusion of the vertebral bodies and apophyseal joints at this level (arrows). (e) 3D reconstruction clearly demonstrates the exuberant surrounding reactive osteophytes.

Fig. 14 Spinal fracture in AS. (a) AP and (b) lateral radiograph of the thoracic spine in a 64-year-old man with advanced AS and increasing back pain over 4 weeks. The lateral view demonstrates a slight malalignment at the anterior aspects of the vertebral bodies of Th9 and Th10, and the iv is irregularly narrowed on the AP view, all suggesting fracture (arrows). CT, (c) sagittal and (d) coronal reconstruction, shows fracture through the iv space and the posterior structures (arrows). There is widening of the intervertebral space anteriorly in the supine position used for CT compared with the upright position used during radiography.

Axial psoriatic arthritis (PsA) occurs in approximately 50% of patients with peripheral PsA [31]. It differs radiographically from AS by the voluminous paravertebral ossifications and the occurrence of spinal changes without concomitant sacroiliitis in 10% of patients [32]. Axial PsA may be clinically silent [33], and involvement of the cervical spine is frequent (atlanto-axial or apophyseal joint changes). The cervical recognize may include atlanto-axial instability as seen in RA (Fig. 19), but the pathogenesis and thereby imaging findings are different. In PsA radiography and CT usually visualize new bone formation in the region of the dens. This is elicited by osseous inflammation (osteitis) and/or inflammation at ligament/ tendon attachments (enthesitis) detectable by MRI (Fig. 19). Osteitis is often a feature of spinal PsA and can occur together with paravertebral ossification/para- syndesmophytes and erosion of vertebral plates (Fig. 20). , and illustrated MR findings in PsA are based on personal observations and seem to reflect the radiographic changes encompassing a mixture of osteitis, enthesitis and erosion. Unfortunately, there is a lack of systematic description of spinal changes in PsA by MRI. Some of the patients described under the term SAPHO (synovitis, acne, pustulosis, hyperostosis, osteitis) syndrome may have PsA. SAPHO is a collective term often used for inflammatory disorders primarily presenting with osseous hyperostosis and sclerosis, and they are frequently associated with skin disorders. The most commonly affected site in SAPHO is the anterior chest followed by the spine [34]. The PsA changes shown in Fig. 20 are characterized by hyperostosis and sclerosis, both main features of SAPHO. However, this patient did not have anterior chest involvement.

 

Fig. 15 CT detection of costo-vertebral changes in AS. Axial CT slices showing erosive changes (a) and ankylosis of costo-vertebral joints (b), respectively (arrows).

Fig. 16 Activity changes in AS by MRI. Sagittal STIR of (a) the cervico-thoracic and (b) the lumbar spine of the patients shown in Fig. 10 obtained 3 years before the radiography. There are multiple high signal intensity areas corresponding to vertebral corners (white arrows). Additionally, osseous oedema of the costo-vertebral joints (a, black arrows) seen on the lateral sagittal slice of the thoracic spine. (c) Axial post-contrast T1FS of an inflamed costo-vertebral joint confirmed the presence of joint inflammation in the form of osseous enhancement in both the vertebra and the rib (arrows) in addition to joint erosion. (d) Midline sagittal post-contrast T1FS shows an enhancing syndesmophyte. (e) Inflammatory changes at the apophy- seal joint in a 27-year-old man; sagittal STIR image of the lumbar region showing subchondral osseous oedema in the lower thoracic region (white arrows), and both osseous and soft tissue oedema corresponding to the lumbar apophyseal joints (black arrows). Note that the osseous oedema in the pedicle of Th12 extends to the region of the costo-vertebral joint. (f) Coronal post-contrast T1FS of the lumbar spine shows additional enhancement corresponding to the interspinous ligament between L2 and L3 (arrows).

Fig. 17 Chronic changes in AS by MRI. Sagittal T1 (a) the cervico-thoracic and (b) the lumbar spine of the patients shown in Fig. 10. There are multiple fatty marrow depositions at vertebral corners and also posteriorly in thoracic vertebral bodies (b, arrows). This was observed to have developed since the MRI performed 3 years previously (shown in Fig. 16 a-d) and corresponds to areas of previous inflammation.

In patients with enteropathic arthritis associated with Crohn’s disease or ulcerative colitis, the spine is often osteoporotic with various accompanying SpA features by radiography, mostly AS-like changes. However, by MRI there may be more pronounced inflammation in the posterior ligaments than seen in the other forms of SpA (Fig. 21).

 

Fig. 18 Psoriatic arthritis (PsA), paravertebral ossifications. (a) AP and (b) lateral radiograph of the lumbar spine in a 48-year-old man with PsA showing voluminous paravertebral new bone forma- tion (arrows) in addition to fusion of the second and third vertebral bodies. There was no concomitant sacroiliitis. (c) AP radiograph of the thoraco- lumbar junction in a female patient with axial PsA demon- strating coalescing paravertebral ossifications (arrows).

Fig. 19 Cervical PsA. (a) Lateral radiographs in the neutral position and (b) during flexion in a 61-year-old woman show atlanto-axial instability with a 4-mm distance between the anterior arc and the dens (white line). Additionally, ankylosis of the apophyseal joints (black arrows) and new bone formation anterior to the C4-7 vertebral bodies (white arrows). CT, (c) axial slice and coronal reconstruction of the dens area, demonstrates new bone formation in the atlanto-axial region (arrows); (d) coronal reconstruction of the lower cervical region shows voluminous new bone formation on the right side of the vertebral bodies (arrows). MRI, (e) sagittal STIR and (f) T1-weighted images, shows homogeneous osseous inflammation corresponding to the dens (arrows) with surrounding irregular oedema compatible with a mixture of osteitis and enthesitis. Note that the anterior new bone formation visualised by radiography is difficult to detect on MRI.

Fig. 20 Lumbar PsA. (a) AP and (b) lateral radiograph in a 50-year- old man show voluminous paravertebral ossifications anteriorly and at the right side of the third lumbar vertebra and adjacent iv spaces. MRI, (c) sagittal STIR, (d) T1 and (e) post-contrast T1-weighted images, demonstrates manifest osseous inflammation (osteitis) in the form of oedema and enhancement of the vertebral body, slight enhancement in the paravertebral new bone formation and erosion of the upper vertebral plate compatible with a mixture of osteitis, enthesitis and erosive changes.

Fig. 21 Enteropathic SpA. Sagittal STIR image of the lumbar spine in a 27-year-old man with ulcerative colitis demonstrates oedema corresponding to the interspinous ligaments (arrows) and spinous processes as signs of inflammation. There are only minimal activity changes corresponding to the vertebral bodies, located to the anterior vertebral corners.
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Rheumatoid arthritis of the spine can cause neck pain, back pain, and/or radiating pain in the upper and lower extremities. In severe cases, RA can also lead to the degeneration of the spine, resulting in the compression or impingement of the spinal cord and/or the spinal nerve roots. As a chiropractor, we offer diagnostic imaging to help determine a patient’s health issue, in order to develop the best treatment program.

Dr. Alex Jimenez D.C., C.C.S.T.

 

Conclusion

 

Radiography is still valuable in the diagnosis of spinal inflammatory disorders. It is necessary for visualizing instability and is superior to MRI for detecting syndesmophytes. However, MRI and CT can detect signs of spinal involvement before they can be visualized by radiography. MRI adds information about potential involvement of the spinal cord and nervous roots in addition to signs of disease activity and chronic changes such as fibrous pannus in RA and fatty marrow deposition, erosion and vertebral fusion in SpA. MRI is therefore widely used to monitor inflammatory spinal diseases, especially during anti-TNF therapy.

 

Computed tomography is particularly valuable in the detection of fracture and minor osseous lesions as well as in the evaluation of pseudo-arthrosis. In conclusion, rheumatoid arthritis most commonly affects the structure and function of your hands, wrists, elbows, hips, knees, ankles and feet, however, people with this chronic inflammatory disease can experience back pain. Imaging the spine in arthritis is fundamental to determine treatment. The scope of our information is limited to chiropractic as well as to spinal injuries and conditions. 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 Topics: Acute Back Pain

 

Back pain is one of the most prevalent causes of disability and missed days at work worldwide. Back pain attributes to the second most common reason for doctor office visits, outnumbered only by upper-respiratory infections. Approximately 80 percent of the population will experience back pain at least once throughout their life. The spine is a complex structure made up of bones, joints, ligaments, and muscles, among other soft tissues. Because of this, injuries and/or aggravated conditions, such as herniated discs, can eventually lead to symptoms of back pain. Sports injuries or automobile accident injuries are often the most frequent cause of back pain, however, sometimes the simplest of movements can have painful results. Fortunately, alternative treatment options, such as chiropractic care, can help ease back pain through the use of spinal adjustments and manual manipulations, ultimately improving pain relief.

 

 
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EXTRA IMPORTANT TOPIC: Sciatica Pain Chiropractic Therapy

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References

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Hypermobility Syndrome

Hypermobility Syndrome

Hypermobility Syndrome is a condition of the joints. Characterized by the ability of the joint to move beyond its normal range of motion and is sometimes called “loose joints” or “double jointed.” It is typically a genetic disorder and often identified in children. The gene passes from parent to child, so the condition tends to run in families. Estimated that 10 to 15 percent of children who are otherwise considered to be normal have joints that are hypermobile. However, it can be found in all ages and does not seem to be confined to a particular age group, ethnic group, or population although there are more cases of girls being hypermobile than boys.

Hypermobility Signs and Symptoms

The signs and symptoms of hypermobility can vary widely from person to person. Some people may not experience any symptoms while others have muscle and joint pain along with mild swelling. Usually noted in the evening or later afternoon as well as after moderate physical activity or exercise. The most common areas for pain and achiness are the elbows, knees, thigh muscle, and calf muscle. Often rest will provide relief.

A person who is hypermobile is usually more prone to soft tissue injuries and sprains. Additionally, the affected joints may be more inclined to become dislocated. It can also cause back pain, impaired joint position sense, and even flat feet, osteoarthritis, and nerve compression disorders. Other symptoms include increased bruising, chronic pain, loose skin, and thin scars. Children and young people who are hypermobile often experience growing pains more often than other children.

Most children will grow out of hypermobility; their joints will lose some of their flexibility as they get older along with the symptoms of rarely persist beyond childhood although some adults do find that they get dislocations and sprains much easier.

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Causes of Hypermobility

The exact cause of hypermobility is not known, although it does seem to run in families. Genes play a large part in the process, particularly those involved in collagen production which is a vital protein for tendon, joint, and ligament development and function. There are also several associated conditions. Genetic disorders like Ehlers-Danlos and Marfan have hypermobility as a component as does Down Syndrome.

Hypermobility Treatment

Treatment for hypermobility depends on the patient. It depends on the symptoms that they are experiencing as well as the severity and how much of an impact the condition has on their quality of life. Mild symptoms may not require any treatment while more moderate to severe symptoms may warrant medication like naproxen, ibuprofen, or acetaminophen for pain. All of which, can be bought over the counter.

Patients can ward off many of the symptoms or eliminate them by engaging in regular exercise, protecting the joints, practicing good posture, muscle strengthening exercises, and balancing techniques. Orthotics to correct flat feet can also be beneficial.

Chiropractic for Hypermobility

Many people use chiropractic for hypermobility pain and discomfort. The doctor will use adjustments to bring the joints into the appropriate movement pattern and the body into proper alignment, allowing the body to function as it should and relieves stress from joints that were compensating due to misalignment.

The patient may also be advised to do specific exercises at home, and get counseling on improving their posture. Because chiropractic treats the entire body, the patient will find that they learn how to best live with the condition without medication and manage pain naturally. Patients report dramatic improvement in their distress and mobility after regular, consistent chiropractic visits.

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