By V. Yespas. Franklin Pierce University.
The examples are innumerable safe avalide 162.5 mg, palpable mass diagnosed as a hematoma should be including jumper’s knee (patellar tendon) order avalide 162.5 mg with visa, tennis leg followed clinically to maturation or resolution discount avalide 162.5 mg online. If plain films are normal cheap 162.5 mg avalide with amex, MRI will provide the necessary soft CHRONIC SEQUELA TO TRAUMA tissue contrast for diagnosis. The spectrum of findings range from mild edema to hematoma, partial tear, and Areas of prior hemorrhage, hematoma, or inflamma- complete disruption. Ultrasound is gaining popularity tion may undergo transformation into mature bone. The former name is preferred, Bursae are fluid filled structures with synovial linings since this is not an inflammatory process of the mus- that act as cushions at foci of increased motion or fric- cles. They are classically found between bones and role in recognizing this entity. The finding of peripheral tendons or muscles and skin, but can form anywhere calcification around a soft tissue mass is the hallmark 110 SECTION 2 EVALUATION OF THE INJURED ATHLETE of this entity. This is contrary to osteogenic sarcoma, HAND/WRIST where the osteoid is situated centrally. With Posteroanterior, lateral, and oblique views usually con- maturation, the mineralization of heterotopic ossifica- stitute a hand series. The basic wrist series consists of tion will often completely ossify with marrow induc- four projections, those above as well as a navicular tion. An area of heterotopic ossification immediately (scaphoid) view to lay the bone out on its long axis. These calcifications are usually hydroxyapetite bound, and have a pasty appearance. Depending on the location of the symptoms, radiographs, CT or ultra- Anteroposterior and lateral views are the basic series, sound may be utilized for diagnosis. In the cervical spine, the open SITE SPECIFIC PLAIN RADIOGRAPHY: mouth view shows alignment of the first two vertebral STANDARD AND SPECIAL VIEWS segment lateral masses and the odontoid base. The swimmer’s Each institution has its own set of plain film series and view shows the lower cervical and upper thoracic seg- as such, it is useful to know what views are included ments that may be obscured by shoulder soft tissues in a given radiologic examination. A coned lateral physician may then request a specific view that may view of the L5-S1 disc is often useful, and this level is be crucial for the diagnosis of the suspected pathol- subject to distortion from beam angulation on the ogy, or the radiologist may add or vary the study standard lateral lumbar film. In the setting of acute joint trauma, a three view minimum is usually required. Two perpendicular THORACIC SPINE views suffice for the long bone shafts, and two views are usually adequate for fracture follow-up. A swimmer’s view is frequently obtained to evaluate the upper thoracic segments. Axillary or trans-scapular-Y view are common third projections obtained, needed for a perpendicular The most common view of the pelvis is the AP pro- view of the glenoid. Inlet/outlet and bilateral Judet (lateral scapular) and West Point views may be obtained for oblique) views may also be obtained, but these are evaluation of the glenohumeral joint space, anterior usually reserved for significant acute pelvic trauma. The lateral view should be obtained with the elbow in 90° Anteroposterior and frog-leg lateral views are stan- of flexion. While these provide two views of the proximal soft tissue calcification or acute fracture, and an angu- femur, they show the acetabulum in only one projec- lated radial head view may show a nondisplaced frac- tion. CHAPTER 19 ELECTRODIAGNOSTIC TESTING 111 KNEE Farooki S, Seeger LL: Magnetic resonance imaging in the evalu- ation of ligament injuries. Except in the setting of acute trauma where frac- Imhof H, Fuchsja¨ger M: Traumatic injuries: Imaging of spinal ture is of clinical concern, these should be obtained in the injuries. In acute trauma, the lateral view should Lin J, Fessell DP, Jacobson JA, et al: An illustrated tutorial of be positioned in a cross-table manner to allow demon- musculoskeletal sonography: Part I, Introduction and general stration of a lipohemarthrosis, a sign of fracture. The flexed PA view gives insight musculoskeletal sonography: Part II, Upper Extremity. Am J into the intercondylar notch, and is more sensitive than Roentgenol 175:1071–1079, 2000b.
Immunologic—(+)LE cell preparation or Anti-DNA antibody cheap avalide 162.5mg, or Anti-SM buy discount avalide 162.5mg on-line, false positive test for syphilis 11 buy avalide 162.5mg on line. ANA Clinical Fatigue generic avalide 162.5 mg without a prescription, fever, weight loss, GI complaints Alopecia Vasculitis Arthritis Jaccoud’s Arthritis – Small joints of the hands, wrist, Nonerosive deforming arthritis and knees Ulnar deviations of the fingers and sublux- – Symmetric ations which are reversible early – Migratory, chronic, nonerosive May become fixed – Soft tissue swelling – Subcutaneous nodules – Synovial analysis—ANA (+) – Jaccoud’s arthritis Arthralgias Muscle pain and weakness 112 RHEUMATOLOGY Labs Depressed complement—C3 and C4 Ds-DNA Anti-SM Treatment NSAIDs, corticosteroids, antimalarials, methotrexate, cyclophosphamide, azathioprine, cyclosporine A PROGRESSIVE SYSTEMIC SCLEROSIS (SCLERODERMA) Progressive Chronic Multisystem Disease Classified by the degree of skin thickening Fibrosis-like changes in the skin and epithelial tissues of affected organs Subsets: – Diffuse Cutaneous Scleroderma Heart, lung, GI, kidney ANA(+) Anticentromere Antibody (–) Rapid onset after Raynaud’s phenomenon Variable course—poor prognosis – Limited cutaneous Scleroderma—CREST Syndrome Crest Syndrome Progression after Raynaud’s phenomenon Calcinosis Anticentromere Antibody (+) Raynaud’s phenomenon Good prognosis Esophageal dysmotility – Overlap syndromes Sclerodactyly Combinations of connective tissue disease Telangiectasia – Undefined CTD No clinical or laboratory findings – Localized scleroderma Morphea, linear scleroderma Clinical Skin thickening—face, trunk, neck Symmetric arthritis with involvement of the fingers, hands, arm, legs Initial symptoms—Raynaud’s phenomenon with fatigue, and musculoskeletal complaints Raynaud’s Phenomenon Vasospasm of the muscular digital Causes of Raynaud’s arteries can lead to ischemia, Collagen vascular disease—PSS, ulceration of the fingertips SLE, RA, Dematomyositis/ Triggered by cold and emotional stresses Polymyositis Reversal of episode occurs after Arterial occlusive disease stimulus has ended—and digits rewarmed Pulmonary HTN Present in 90% of patients with scleroderma Neurologic—SCI, CVA Treatment Blood dyscrasia – Education against triggers—cold, smoking Trauma – Rewarming Drugs—ergots, beta blockers, – Calcium channel blockers—nifedipine cisplatin – EMG and biofeedback—self-regulation (Braunwald, et al. ANA AND RF ANA RF MCTD + + RA + + SLE + – Scleroderma (PSS) + – Polymyositis + – Sjögren’s + + (+) HLA-B27 A S Reiter’s Psoriatic arthritis Enteropathy arthropathy Pauciarticular JRA RHEUMATOLOGY 115 VASCULITIS POLYARTERITIS NODOSA Systemic necrotizing vasculitis Male:female ratio is 2:1 Also seen in: Small, medium artery involvement R Glomerulonephritis—#1 cause of death SLE Lungs spared Sjögren’s Skin—palpable purpura Mononeuritis multiplex, arthritis GIANT CELL ARTERITIS: ALSO KNOWN AS TEMPORAL ARTERITIS (TA) More common in females > 50 years old Large arteries Tenderness of the scalp and in the muscle of mastication Headaches, abrupt visual loss in 15% of patients Diagnosis: Elevated ESR, temporal artery biopsy Treatment: High dose steroids imperative to prevent permanent visual loss Polymyalgia Rheumatica (PMR) In view of clinical similarities between PMR patients with and without signs of arteritis in a temporal artery biopsy, many authors believe that PMR is an expression of giant cell arteritis Fever, weight loss, malaise Proximal muscles—neck, pelvic Shoulder Morning stiffness—muscle tenderness Abrupt myalgias/arthralgia Diagnosis: ↑ ESR > 50 Treatment: steroids WEGENER’S GRANULOMATOSIS Small artery involvement Male, middle aged Necrotizing granulomatous vasculitis involving – Upper/lower respiratory tract – Focal segmental glomerulonephritis “Saddle-nose” deformity Pulmonary, tracheal, ocular, and cutaneous manifestation 116 RHEUMATOLOGY TAKAYASU Elastic large arteries—Aorta Asian females, 40 years old Erythema nodosum on the legs Pulselessness, arm claudication BEHÇET’S Small vessels Oral and genital skin ulcers 20% experience venous thrombosis GOODPASTURE’S Pulmonary and kidney involvement SJÖGREN’S SYNDROME Autoimmune-mediated disorder of the exocrine glands CLINICAL PRESENTATION: (sicca symptoms) Dry eyes Dry mouth Skin lesions Parotid involvement LABS: ANA (+), RF (+) Classification: Primary and secondary forms Primary—Dry eyes and mouth with ANA (+) , RF (+) Secondary—sicca symptoms – Sjögren’s syndrome plus evidence of SLE, RA, PSS, Polymyositis EXTRAGLANDULAR MANIFESTATIONS Arthralgias Raynaud’s phenomenon RHEUMATOLOGY 117 ARTHRITIS AND INFECTIOUS DISORDERS SEPTIC ARTHRITIS Clinical Picture: Septic Arthritis Rapid onset of moderate to severe joint pain, erythema, and decreased ROM Monoarticular, leukocytosis Knee is the most common joint Risk factors—age, prosthetic joints, comorbidities such as anemia, chronic diseases, hemophilia. Coli) Bone scans 118 RHEUMATOLOGY Treatment Antibiotic coverage Frequent needle aspirations with arthroscopic lavage TABLE 3–7. Joint Fluid Analysis Property Normal Noninflammatory Inflammatory Septic Viscosity High High Low Variable Color Colorless Straw Yellow Turbid-Yellow Clarity Transluscent Transluscent Transluscent Opaque WBC < 200 < 5000 1000–75000 > 100,000 PMN% < 25 < 25 > 50 > 85 Culture Negative Negative Negative Positive Mucin clot Good Good Fair Poor Glucose Equal to blood Equal to blood < 50 mg/dl > 50 mg/dl lower than lower than blood blood OTHER INFECTIOUS CAUSES OF ARTHRITIS Viral Infections—Rubella, infectious hepatitis Fungi—Seen in Immunocompromised adults Mycobacterium—tuberculosis of the spine (Pott’s disease) – Thoracic involvement – TB arthritis—Hips and knees Monoarticular Radiologic findings—Phemister’s triad Juxta-articular osteoporosis Marginal erosions Joint space narrowing Lyme Disease – Tick borne—Borrelia burgdorferi – Classic presentation Erythema migrans—bull’s eye rash Cardiac, neurologic, articular manifestations – Intermittent migratory episodes of polyarthritis – Commonly affects the knee – Synovial fluid—Inflammatory – Diagnosis—ELISA, Western blot analysis – Management—First-line antibiotics: Adults: Doxycycline Children: Amoxicillin – Pattern of Onset: Bite Rash Systemic dz. Neurologic involvement RHEUMATOLOGY 119 DEPOSITION AND STORAGE DISEASE HEMOCHROMATOSIS Organ damage and tissue dysfunction secondary to excessive iron stores and the deposi- tion of hemosiderin Organs → Hepatic cirrhosis, cardiomyopathy, DM, pituitary dysfunction Skin pigmentation Chronic progressive arthritis – Occurs commonly in second and third MCP, PIP joints. It may also affect the hip joints Males ~40–50 years old Treatment: Phlebotomy, NSAIDs ALKAPTONURIA (OCHRONOSIS) Autosomal recessive Deficiency in the enzyme homogentisic acid oxidase leads to its increase Alkalinization and oxidation causes darkening of tissue parts termed ochronosis – Blueish discoloration of the urine, cartilage, skin, sclera secondary to the accumulation of homogentisic acid Progressive degenerative arthropathy – Onset—in the fourth decade – Spinal column involvement – Arthritis of the large joints, chondrocalcinosis, effusions, osteochrondral bodies WILSON’S DISEASE Autosomal recessive Deposition of copper leads to destruction: – Liver leading to cirrhosis – Brain – Kidneys – Ocular—Kayser-Fleischer rings OA—wrists, MCP, knees, spine Osteoporosis Treatment: Copper chelation with penicillamine, dietary restriction GAUCHER’S DISEASE Autosomal recessive—Ashkenazi Jews Glucocerebroside accumulates in the reticuloendothelial cells of the spleen, liver, and bone marrow Monoarticular hip and knee degeneration 120 RHEUMATOLOGY OTHER SYSTEMIC DISEASES SARCOIDOSIS Systemic chronic granulomatous disease—can affect any organ system Pathogenesis: disseminated noncaseating granulomatous Eight times more common in blacks, females > males Clinical features: – Pulmonary – Hilar adenopathy – Fever, weight loss, fatigue – Arthritis: polyarthritis, 4-6 joints Knees, PIP, MCP, wrists – Skin—Lofgren’s Syndrome – Arthritis, Hilar adenopathy, Erythema nodosum AMYLOIDOSIS Homogeneous eosinophilic material seen with Congo red dye Deposition of amyloid in the kidneys, liver and spleen Clinical features: – Renal disease is primary clinical feature – Cardiomyopathy – Median neuropathy – Pseudoarthritis—periarticular joint inflammation – Effusions: Arthrocentesis—“Shoulder-pad” sign HEMOPHILIA ARTHROPATHY X-linked recessive disorder, predominately in males—associated with HIV 2° to transfu- sions of factor and blood Blood coagulation disorder caused by Factor VIII deficiency (classic hemophilia A) and Factor IX deficiency (Christmas disease, hemophilia B) Bleeding into bones and soft tissue causes hemarthrosis, necrosis and compartment syn- drome Elbow, knee, wrist are common Arthritis is caused by the remaining blood in the joint depositing hemosiderin into the synovial lining → proliferation of the synovium and pannus formation Radiologic: Joint space narrowing, subchondral sclerosis and cyst formation Treatment: Conservative care (immobilization, rest, ice), Factor VIII replacement, reha- bilitation, joint aspiration as a last resort SICKLE-CELL DISEASE Biconcave RBC changes to an elongated crescent sickle-shape causing obstruction of the microvasculature Musculoskeletal complications: – Painful crisis—Most common event Abdomen, chest, back Pain in the large joints from juxta-articular bone infarcts with synovial ischemia RHEUMATOLOGY 121 – Dactylitis—“Hand-Foot” Syndrome Painful non-pitting swelling of the hands and feet – Osteonecrosis Local hypoxia with occlusion to the venous system by the sickled cells 1/3 femoral heads and 1/4 humeral heads go on to osteonecrosis – Osteomyelitis—most commonly caused by Salmonella NEUROPATHIC ARTHROPATHY (CHARCOT’S JOINT) DEFINITION Chronic progressive degenerative arthropathy, secondary to a sensory neuropathy with loss of proprioception and pain sensation, leading to instability and joint destruction CAUSES → “STD” “SKA” → SHOULDER, KNEE, ANKLE Syringomyelia → Shoulder Tabes dorsalis # 2 → Syphilis → Knee Diabetic Neuropathy → # 1 cause → Ankle CLINICAL Early findings: Painless swelling, effusion and joint destruction Late findings: Crepitation, destruction of cartilage and bones, intra-articular loose bodies Subtle fractures RADIOLOGIC Joint destruction Hypertrophic osteophytes Loose bodies caused by micro fractures Disorganization of the joint—Subluxation and dislocation TREATMENT Immobilization Restriction of weight bearing Charcot Joint vs. Osteoarthritis May mimic OA early in the disease— Both have: Soft tissue swelling Osteophytes Joint effusion Charcot joints have: Bony fragments Subluxation Periarticular debris 122 RHEUMATOLOGY TABLE 3–8. Hip Pain in Children (Janig and Stanton-Hicks 1996; Kaggs and Tolo 1996; Koop Quanbeck 1996; Jensen et al. Growth arrest— Proximal and lateral epiphysis avascular stage migration of the femoral Grade I: < 33% 2. Subchondral fracture— head from the Grade II: 33–50% “Crescent sign” acetabulum Grade III: > 50% 3. Healed RHEUMATOLOGY 123 TABLE 3-8 (Continued) Congenital Slipped Capital Femoral Legg-Calve-Perthes Hip Dislocation Epiphysis (SCFE) Disease (LCPD) Treatment Goal—return the hip into Bed rest—weight relief 1. Prevent femoral head pathologic changes Surgery is the preferred collapse Closed Reduction— method of treatment— Containment techniques < 6 mo Knowles pinning Permit weight bearing Position devices Nonsurgical—traction, of the femoral head to Triple diapers body casts, hormonal assist healing and Frejka pillows therapy remodeling Splints: Craig, Von Greater than 6 years old Rosen-Pavlik harness: Abduction braces allows hip motion Petrie casts, Toronto within the safe zone brace, Salter stirrup while maintaining Surgical— abduction Epiphysiodesis Traction, casting, surgical Valgus Osteotomy Complication 1. OA Thomas Test: To detect flexion contractures of the hip and evaluate range of hip flexion 1. Have patient hold one leg on chest, lower other leg flat Indicators of fixed flexion contracture/deformity: 1. Emotional stress May be associated with Irritable Bowel Syndrome, RA, Lyme, hyperthyroidism ARA CLASSIFICATION: 1. Widespread pain—pain in the left and right side of the Classification body above and below the waist. Pain in 11–18 tender points (Figure 3-5) months Bilateral involvement Occipital, lower cervical, trapezius, supraspinatus, second rib, lateral epicondyle, gluteal, greater trochanter, knee FMS SHOULD BE DIFFERENTIATED FROM MYOFASCIAL PAIN SYNDROME AND CHRONIC FATIGUE SYNDROME Myofascial Pain Syndrome Local pain and tender points that resolves with local treatment, but may recur Fatigue, morning stiffness uncommon Chronic Fatigue Syndrome Disabling fatigue at least six months Preceded by a viral syndrome TREATMENT OF FMS Patient education and reassurance Nortriptyline—sleep disturbance RHEUMATOLOGY 125 NSAIDs and corticosteroids Combination therapy is effective Biofeedback, tender point injection Acupuncture, aerobic exercise Greater Trochanter FIGURE 3–5. Fibromyalgia: Location of Specific Tender Points COMPLEX REGIONAL PAIN DISORDER (CRPD) OTHER NAMES Sudeck’s atrophy Algodystrophy Shoulder hand syndrome RSD: Reflex Sympathetic Dystrophy 126 RHEUMATOLOGY CHARACTERISTICS Limb pain, swelling, and autonomic dysfunction Most commonly caused by minor or major trauma CLINICAL FEATURE Pain, deep burning exacerbated by movement – Allodynia—pain induced by a nonnoxious stimulus – Hyperalgesia—lower pain threshold and enhanced pain perception Local edema and vasomotor changes – Extremity is warm, red, and dry initially – Later becomes cool, mottled, and cyanotic Muscle weakness Dystrophic changes – Thin, shiny skin, brittle nails CLINICAL STAGES 1. Acute—few weeks–6 months – Pain, hypersensitivity, swelling, and vasomotor changes – Increased blood flow creating temperature and skin-color changes – Hyperhidrosis 2. Dystrophic—3–6 months – Persistent pain, disability, and atrophic skin changes – Decreased blood flow, decreased temperature – Hyperhidrosis 3. Atrophic – Atrophy and contractures – Skin glossy, cool, and dry RADIOGRAPHIC FINDINGS 1. Plain radiographs Sudeck’s atrophy—patchy osteopenia, ground-glass appearance 2. Three-phase bone scan First two phases are nonspecific, osteoporosis Third phase—abnormal, with enhanced uptake in the peri-articular structures TREATMENT 1. Immediate mobilization—Passive and active ROM, massage, contrast baths, TENS 2. Inflammation—Corticosteroids, initial dose 60–80 mg/day qid dosing for two weeks then gradual tapering the next two weeks 4. Cervical sympathetic ganglia block for the upper extremities, lumbar ganglion block for the lower extremities 5. Surgical sympathectomy—if block is beneficial but transient RHEUMATOLOGY 127 TABLE 3–9. Adults (Janig and Stanton Hicks, 1995) Children Adults Site Lower extremity Upper extremity Spontaneous pain Common Common Allodynia Most patients Most patients Sex ratio Female:male 4:1 Mixed Three-phase Mixed results: Used to rule out other Increased uptake in the third bone scan pathology phase of the affected extremity See decreased uptake of the extremity— decreased atrophic changes Occasionally normal Will have increased uptake normally secondary to bone growth Treatment Physical therapy alone Sympathetic blocks Noninvasive—TENS, Biofeedback Meds—Tricyclic antidepressant Blocks more common in the upper extremity Prognosis Good Poor SYMPATHETIC AND NONSYMPATHETIC CRPD Four tests used to determine if pain is sympathetically mediated; the first two are used more commonly. Sympathetic block with local anesthetic: Local anesthetic is injected at the stellate ganglion (upper extremity) or the lumbar par- avertebral ganglion (lower extremity).
Clark MR purchase avalide 162.5 mg without prescription, Swartz KL: A conceptual structure and methodology for the systematic approach to the evaluation and treatment of patients with chronic dizziness discount avalide 162.5mg fast delivery. Compton P order avalide 162.5 mg amex, Darakjian J buy avalide 162.5mg amex, Miotto K: Screening for addiction in patients with chronic pain and ‘problem- atic’ substance use: Evaluation of a pilot assessment tool. Cote P, Hogg-Johnson S, Cassidy JD, et al: The association between neck pain intensity, physical functioning, depressive symptomatology and time-to-claim-closure after whiplash. Crombez G, Eccleston C, Baeyens F, et al: When somatic information threatens, catastrophic thinking enhances attentional interference. Dersh J, Polatin PB, Gatchel RJ: Chronic pain and psychopathology: Research findings and theoretical considerations. Dickens C, Jayson M, Sutton C, et al: The relationship between pain and depression in a trial using paroxetine in sufferers of chronic low back pain. Druss BG, Rosenheck RA, Sledge WH: Health and disability costs of depressive illness in a major U. Dworkin SF, Von Korff M, LeResche L: Multiple pains and psychiatric disturbance: An epidemiologic investigation. Edwards R, Augustson EM, Fillingim R: Sex-specific effects of pain-related anxiety on adjustment to chronic pain. Emanuel EJ, Fairclough DL, Daniels ER, et al: Euthanasia and physician-assisted suicide: Attitudes and experiences of oncology patients, oncologists, and the public. Ericsson M, Poston WS, Linder J, et al: Depression predicts disability in long-term chronic pain patients. Fishbain DA, Cutler RB, Rosomoff HL, et al: Chronic pain-associated depression: Antecedent or con- sequence of chronic pain? Fishbain DA, Cutler RB, Rosomoff HL, et al: Impact of chronic pain patients’ job perception variables on actual return to work. Fishbain DA, Cutler RB, Rosomoff HL, et al: Prediction of ‘intent’, ‘discrepancy with intent’, and ‘discrepancy with nonintent’ for the patient with chronic pain to return to work after treatment at a pain facility. Fishbain DA, Cutler RB, Rosomoff HL, et al: Validity of self-report drug use in chronic pain patients. Fishbain DA, Goldberg M, Rosomoff RS, et al: Completed suicide in chronic pain. Perspectives on Pain and Depression 21 Fishbain DA, Rosomoff HL, Cutler RB, et al: Do chronic pain patients’ perceptions about their preinjury jobs determine their intent to return to the same type of job post-pain facility treatment. Fishbain DA, Rosomoff HL, Rosomoff RS: Drug abuse, dependence: Addiction in chronic pain patients. Fisher BJ, Haythornthwaite JA, Heinberg LJ, et al: Suicidal intent in patients with chronic pain. Folkman S, Lazarus RS, Gruen RJ, et al: Appraisal, coping, health status, and psychological symptoms. Fordyce W, Fowler R, Lehmann J, et al: Operant conditioning in the treatment of chronic pain. Fordyce WE, Lansky D, Calsyn DA, et al: Pain measurement and pain behavior. Forseth KO, Husby G, Gran JT, et al: Prognostic factors for the development of fibromyalgia in women with self-reported musculoskeletal pain. Gardea MA, Gatchel RJ, Mishra KD: Long-term efficacy of biobehavioral treatment of temporo- mandibular disorders. Gaynes BN, Burns BJ, Tweed DL, et al: Depression and health-related quality of life. Geisser ME, Roth RS, Theisen ME, et al: Negative affect, self-report of depressive symptoms, and clinical depression: Relation to the experience of chronic pain. Greenberg J, Burns JW: Pain anxiety among chronic pain patients: Specific phobia or manifestation of anxiety sensitivity?