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Ankle and Foot Overuse Disorders
Disease/ Disorder Definition Overuse injuries are defined as tissue damage due to repetitive microtrauma. 1 Typically overuse injuries develop without an identifiable event associated with symptom onset. Some of the most common overuse injures of the foot and ankle are tendinopathies, […]
Stress Fracture of the Hip
[…] and repetitive strain placed on structurally normal bone (fatigue reaction) or normal stress applied to structurally abnormal bone (insufficiency reaction). 1-5 Locations where femoral and/or “hip” stress fractures occur include femoral shaft, femoral diaphysis, femoral neck, pubic ramus, and sacral […]
Juvenile Idiopathic Arthritis
[…] joint with warmth, pain or tenderness) of unknown etiology that occurs for at least 6 weeks in children younger than 16 years of age.1 Thought to be a multifactorial autoimmune disease with unknown exact cause, it can continue into adulthood, causing significant disability, poor functional outcomes, and decreased quality of life.2 Etiology The definitive cause of JIA remains under investigation; however, current research indicates that genetic, immunogenic and environmental factors influence the development of JIA subtypes. Genetic association varies between the disease subtypes. Non-systemic variations of JIA are more likely to be associated with the human leukocyte antigen (HLA) class.3,4HLA-A2 & HLA-B27 are implicated in certain forms off JIA, especially in subtypes with earlier onset. Developing genetic research is focused on the use of genome-wide association studies and transcriptome-wide association studies to identify genes associated with JIA. Most recently, a study identified several novel genes that may be implicated in the development of disease, ANXA3, GPR146, ANKRD9, and TMEM158. While this has improved our understanding of genetic correlations with disease development, conclusive causation remains under investigation.4 In addition to HLA genetic associations, non-HLA genes also play a role in the inflammatory response in certain JIA subtypes, with involvement of both cell-mediated and humoral-immunity. Multiple genes relating to inflammation and immune regulation are believed to be involved, including those that influence TNF, IL2, IL10, IL6 and other inflammatory regulators.2 There is evidence of autoimmune dysregulation, with positive antinuclear antibody (ANA) in 40% of patients. However, evidence from treatments designed to block the inflammatory cascade indicate that systemic inflammation may play a greater role. While there are studies that strongly indicate a genetic component, studies with monozygotic twins have elucidated that environmental factors, such as infections, also play a role. Concordance rates are closer to 25-40% (as opposed to 100%) in these twins.5 Repeated infections and antibiotics during the first two years of life are associated with JIA in multiple studies.2 The most commonly implicated pathogens include Parvovirus B19, Epstein-Barr virus, enteric bacteria, Chlamydia species, Bartonella henselae, Mycoplasma pneumoniae, and Streptococcus pyogenes. External antigens may provoke multiple antigen-specific pathways, including cytotoxic T-cell responses, proinflammatory cytokine production, and the complement cascade, increasing the risk of immune-mediated arthritis during childhood.2 However, it is unclear whether this is due to pathogenic alterations of the microbiome or changes to our immunologic cells. Epidemiology including risk factors and primary prevention JIA is the most common connective tissue disease in children.1 It is currently estimated that JIA may be highly heritable and associated with multiple autoimmune disorders.6,7 0.07 to 4.01 per 1000 children are affected worldwide. The average yearly incidence is approximately 13.9 cases per 100,000 with a prevalence of 16-150 cases per 100,000 people.1 Child onset accounts for 5% of RA cases. Differences in age and sex can also be seen within subtypes of JIA.1,2 For example, in rheumatoid factor (RF) positive JIA, females may outnumber males 9:1 compared to overall JIA ratios. Systemic features of JIA appear to be more common in pediatric than adult onset arthritis. Children are most likely to experience synovitis whereas adults predominate with earlier joint destruction.1 Recent epidemiologic surveys have shown distinctions in geography and ethnic groups. Oligoarthritis is predominant in western countries but rare in areas such as India, South Africa, and the Middle East, where the polyarticular form of JIA is more common. Greater incidences of enthesitis-related arthritis are present in India, Taiwan, parts of Mexico, and Canada. Black Americans have a higher rate of RF positive polyarthritis whereas European ancestry may predispose children to higher rates of ANA positive JIA.8 A multinational study, named the Epidemiology, Treatment, and Outcome of Childhood Arthritis (EPOCA Study), is currently ongoing to obtain epidemiologic data on JIA subtypes. Preliminary data shows a younger age of onset in Western Europe and a higher prevalence of uveitis in this population. While there may be lower rate of incidence in Asian populations, there may be higher rates of systemic arthritis in these patients. Thus far, children in Africa and Eastern Europe have been found to have higher levels of disease activity as well as a lower frequency of inactive disease.9 Our understanding of the etiology of JIA continues to evolve to this day. Patho-anatomy/physiology JIA is an inflammatory syndrome characterized by chronic synovial inflammation with B-lymphocytes. Macrophage and T-lymphocyte invasion occurs along with cytokine release and further synovial proliferation. There is a major pathogenic role for the overproduction of interleukin-6 and interleukin-1.2,6 Eventually, the thickened synovium (pannus) contributes to joint destruction. Within the synovial fluid itself, interleukin-18 expression has consistently been found to be abnormal. The subtypes of juvenile arthritis can be differentiated from one another based on the number of affected joints, underlying biochemistry, and the presence of associated comorbidities. Subtypes are classified using the International League of Associations for Rheumatology (ILAR); however, there is an ongoing study through the Pediatric Rheumatology Internal Trials Organization (Printo) currently working on new classification criteria.11 JIA Subtypes1,10,11,12 Oligoarticular Persistent oligoarthritis: affecting fewer than four joints throughout the course of the disease Extended oligoarthritis: affecting two to four joints during first six months of disease but greater than five joints after six months of disease ANA + lab result in 70-80% of patients Onset: early childhood, In children under 6 years old, Females > Males Most common subtype, 40-50% of children with JIA,1 best prognosis Larger lower extremity joints often with asymmetric arthritis presentation, especially knees, most commonly affected Asymmetric uveitis often develops within first 4 years Require routine eye examinations Ocular damage is common, 50% develop chronic iridocyclitis Polyarticular Affects five or more joints during the first six months of disease Symmetric involvement of small joints of hands and feet Cervical spine and temporomandibular joint (TMJ) may be affected Two subtypes: Rheumatoid factor (RF) negative polyarthritis: More often, patients complain of stiffness versus pain Typically presents with symmetric small joint involvement and severe inflammation Hip involvement 50% of cases, can lead to late disability with erosion of the femoral head 18-30% of JIA Patients Positive ANA in 20-40% of patients RF positive polyarthritis: Less than 5% of all JIA cases, with 50% developing severe arthritis Variable prognosis, more aggressive disease course May have positive antibodies to cyclic citrullinated peptides (anti-CCP)8 ANA+ in 25%-40% of cases Onset: RF positive in late childhood, RF negative is often younger than six years; Females > Males Systemic Arthritis in one or more joints with or preceded by fever of at least two weeks duration and daily fever (for at least three days), and accompanied by at least one of the following signs: non-fixed erythematous skin rash, generalized lymph node enlargement, hepatomegaly or splenomegaly, serositis 5-8% of children develop macrophage activation syndrome (MAS)1 10% of JIA patients Onset: any age, Female = Males Quotidian pattern of high spiking fevers Rash is evanescent, salmon colored, macular, accompanies fever 10%-20% develop acute iridocyclitis Arthritis occurs later, a month or longer Formerly known as Still’s Disease or systemic juvenile rheumatoid arthritis Psoriatic Arthritis and psoriasis with at least two of the following: dactylitis, nail pitting or onycholysis, psoriasis in a first-degree relative 5-10% of patients Onset: biphasic with early peak younger than six years, late peak after six years of age, females =male Enthesitis-Related Enthesitis at the sites of tendon insertion on to bone with at least two of the following: presence or history of sacroiliac joint tenderness or lumbosacral pain HLA-B27 antigen positive onset of arthritis in male over six years of age acute symptomatic anterior uveitis history of ankylosing spondylitis enthesitis-related arthritis sacroiliitis with inflammatory bowel disease acute anterior uveitis (Reiter’s syndrome) in a first-degree relative Occurs in 15-20% of JIA patients Most common sites: calcaneal insertion of Achilles tendon, plantar fascia, tarsal area Most common age of onset is 10 years of age Complications include In 30-40% of patients with this type of JIA, disease progresses to affect sacroiliac joint Uveitis is common: often symptomatic and unilateral Can also progress to spondyloarthropathy Onset: late childhood, commonly after 6 years old, Males > Females Positive Family Medical History may be present Undifferentiated 5% of JIA subtypes Male = Female May meet none or many criteria of other JIA subtypes Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time) Variable dynamic disease progression is seen in the first six months from onset of JIA.6 Patients may experience a cycle of remission and flare ups of symptoms. In a 30 year longitudinal cohort study, it was noted that 59% of JIA patients were in remission (defined as no disease activity and the absence of medications for at least 6 months) at the 30 year follow up; however, 28% of patients in this cohort were still experiencing a heavy symptom load.13 RF positive JIA appears to have lower levels of remission compared to other subtypes of JIA. As children grow into adulthood, previous studies have noted the presence of severe disability in as many as 42.9% of patients; however, more recent publications have noted significantly lower rates of severe disability (3-8.9%) with the highest disability rating in RF+ polyarticular disease. 14 Currently, the best predictor of long standing high disability ratings depends on level of disability at initial presentation. While modern understanding is improving identification and treatment for JIA patients, there are still concerns for long term complications, including mental health concerns.15 Standardized mortality ratios are higher in both male and female patients with JIA when compared to the general population. Likewise patients with systemic JIA had higher mortality incidence when compared to non-systemic subtypes of JIA.16 New onset/acute: Each JIA subtype has varying symptoms; however, all subtypes share several traits: Persistent joint pain, swelling, warmth, and stiffness Symptoms are worse in the morning or after prolonged rest (nap, sitting still) An early sign is the presence of a limp or altered gait A younger child may not verbalize pain, but demonstrate limping or gait alterations if one or both legs are involved Subacute: For some patients with JIA, the course of disease may have episodic flare ups followed by asymptomatic periods. It is important to recognize that remission is currently recognized as a period of 6 months without evidence of disease and without medications to mitigate the disease. Chronic/stable: Complete remission can be expected in most patients, with current estimations at 67% of patients at eight years in remission given new treatment and early diagnosis.18 Remaining patients continue to have symptoms into adulthood, requiring long term medical management and follow up. Pre-terminal: Only in very severe cases, affecting cervical spine or causing significant debility. Specific secondary or associated conditions and complications Anorexia, weight loss, growth failure Cardiopulmonary involvement (pericarditis, pleural effusions with rare complication of tamponade, if large enough) Anemia Decreased physical activity contributes to weakness, obesity (which increases load on joints) Atlantoaxial instability associated with cervical spine involvement increases risk of spinal cord injury Concerns have been raised about increased rates of cancer (does not seem to be related to treatment with biologic agents as was once thought) Uveitis, specifically iridocyclitis. More common in females affected with oligoarticular arthritis and in patients less than six years of age with a positive ANA. Usually asymptomatic, but if not diagnosed early may result in permanent blindness. Growth disturbances, including growth retardation and accelerated growth, resulting in conditions such as leg length discrepancies Micrognathia if TMJ arthritis disturbs the growth plate (particularly in polyarticular JIA) Suppression of the immune system by disease modifying antirheumatic drugs (DMARDs) increases the risk of infections Osteopenia and osteoarthritis Fractures Hepatomegaly, splenomegaly, lymphadenopathy (particularly in systemic JIA subtype) Rare pulmonary manifestations may include interstitial lung disease or pulmonary hypertension19 Macrophage Activation Syndrome (MAS) resulting from uncontrolled activation and proliferation of T-lymphocytes and macrophages is a complication with systemic JIA. It is a life-threatening condition resulting in persistent fever, pancytopenia, hepatosplenomegaly, and coagulopathy. Other autoimmune conditions, four have been associated with JIA Rheumatoid arthritis, Celiac Disease, Hypothyroidism, Systemic Lupus Erythematosus6 Pain is an incredibly common symptom. JIA patients with symptomatic pain are at higher risk of developing Chronic Amplified Pain Syndrome Essentials of Assessment History Joint pain and swelling, often noted incidentally after trauma Stiffness worse in morning or after naps and lasts more than fifteen minutes Symptoms better later in the day Persistence of symptoms for at least six weeks in a six-month period History of fever without other cause, in absence of joint symptoms; may be three days, with a double spike pattern of high temperatures Child refusing to walk, or using hands to walk Pain with ambulation, “gelling” sensation (stiffness after a joint remains in one position for a prolonged period), joint swelling, and difficulty with buttons or writing Photophobia, pain, redness, headache, and visual changes Isolated musculoskeletal pain is generally not JIA Detailed family medical history1,7 Differential diagnoses include: Perthes disease, slipped capital femoral epiphysis (SCFE), malignancy (osteosarcoma for joint pain, leukemia for fever combined with joint pain, lymphoma), ankylosing spondylitis, inflammatory bowel disease, septic arthritis, Kawasaki disease, malaria Physical examination Musculoskeletal: Painful, swollen joints Tenosynovitis>Bursitis Number of joints 2-4: Oligoarticular 5 or more: Polyarticular Any joint can be affected, including small joints of the […]
Pediatric Fractures in Developing Bone
[…] issues In cases of suspicion of child abuse, the clinician is legally obligated to make a report to Child Protective Services. The abused child should receive adequate supportive measures and counseling, and consideration of foster placement if the home environment […]
Skeletal Muscle Physiology
[…] of protein filaments—known as a sarcomere—appears as alternating dark and light bands. Briefly, each sarcomere is demarcated by two dark lines (Z-lines) which serve as anchor points for actin molecules. The Z-line is in turn flanked by the I-band, which […]
Wheelchair and Power Mobility for Adults
Overview and Description Background: An estimated 5.5 million people, or 2.3% of the United States adult population, uses a wheelch air for mobility. Adults greater than age 65 are four times more likely to use a wheelchair.1,2 Independent mobility allows people […]
Peripheral Polyneuropathy Part 2: Treatment
Disease/ Disorder See Peripheral Polyneuropathy Part 1: Evaluation and Differential Diagnosis Essentials of Assessment See Peripheral Polyneuropathy Part 1: Evaluation and Differential Diagnosis Rehabilitation Management and Treatments Available or current treatment guidelines Pharmacologic treatment of peripheral neuropathy hinges upon treating the underlying etiology, when known. Treatment of reversible causes during the acute stage may aid axonal regeneration and remyelination. Immunotherapy for immune-mediated polyneuropathy is beyond the scope of this review and will not be covered. In subacute and chronic cases, palliative care becomes the primary goal of treatment, focusing on symptomatic control. Medications with labeled indications for neuropathic pain in the Unites States are limited to: carbamazepine (trigeminal neuralgia) lidocaine 5% patch, capsaicin 8% patch (postherpetic neuralgia) pregabalin (diabetic peripheral neuropathic pain (DPNP), postherpetic neuralgia, neuropathic pain due to spinal cord injury) duloxetine (DPNP) gabapentin (postherpetic neuralgia) – including extended formulation and combination gabapentin enacarbil tapentadol extended-release (ER) – neuropathic pain associated with diabetic peripheral neuropathy Antidepressants Longevity of use has afforded tricyclic antidepressants (TCAs) an abundance of studies showing treatment efficacy in a wide variety of neuropathic pain disorders. TCAs modulate voltage-gated sodium channels, inhibiting the reuptake of norepinephrine and serotonin. A 2011 practice guideline affirms the efficacy of amitriptyline, but less robust evidence exists for the use of desipramine, imipramine, fluoxetine, or nortriptyline + fluphenazine.1,2 Where prior studies were unable to support use of nortriptyline, a recent prospective clinical trial demonstrated some effectiveness of nortriptyline in cryptogenic sensory polyneuropathy specifically.28 Tertiary amine TCAs (amitriptyline, imipramine, and clomipramine) are not recommended at doses greater than 75 mg/day in adults 65 years and older, due to major anticholinergic and sedative side-effects and potential fall risk.3 An increased risk of sudden cardiac death has been reported with TCAs at doses >100 mg daily.4 TCAs are contraindicated in patients with cardiac arrhythmia, congestive heart failure, recent myocardial infarction, glaucoma, urinary retention, bladder outlet obstruction or benign prostatic hypertrophy, and prolonged QTc interval. Therefore, these drugs require […]
Differential Diagnosis and Treatment of Visceral Pain in the Pelvis and Abdomen
[…] from the skull to the coccyx along the anterior aspect of the vertebral column and terminate in the only unp aired ganglion of the sympathetic chain, the ganglion impar (ganglion of Walther) on the ventral surface of the coccyx. After […]
Nonsteroidal Anti-Inflammatory Medications
[…] one of the most commonly used medications in adults. NSAIDs are frequently used for their analgesic, anti-inflammatory, and antipyretic properties. 1 For many acute pain conditions, NSAIDs have similar or better efficacy compared to opioids.2 CDC clinical practice guidelines for […]
Upper Limb Prosthetics
[…] activation of the TD). This is accomplished by passing a single cable through two separate sections of cable housings (f air lead cable system). In transradial and transhumeral amputations, biscapular abduction and/or humeral flexion control elbow flexion and/or the TD. […]