Presentation on theme: "Soft Tissue Rheumatism Gary Kunkel, M.D. Division of Rheumatology November, 2005."— Presentation transcript:
Soft Tissue Rheumatism Gary Kunkel, M.D. Division of Rheumatology November, 2005
Objectives Recognize key features of the most common types of bursitis and tendonitis. Describe the general approach to management of bursitis and tendonitis. Recognize the clinical presentation and features of polymyalgia rheumatica and distinguish it from temporal arteritis. Identify the key clinical features and approach to management of fibromyalgia.
Soft Tissue Rheumatism A diverse group of disorders related to musculoskeletal symptoms and disturbances which do not involve intraarticular structures. Passive/active range of motion is a useful tool in distinguishing these conditions from joint problems. –Bursitis/Tendinitis –Polymyalgia Rheumatica –Fibromyalgia
Bursitis Bursa –Sac-like structure –Facilitates motion of muscles and tendons over bony prominences Bursitis –“itis” = inflammation –Inflammation and/or degeneration
Etiology of Bursitis Trauma Chronic overuse or irritation Infection –DM, EtOH, Immunosuppression –Skin portal of entry –Inflammatory bursal fluid (>50,000 wbc/µl) Systemic inflammatory diseases –RA, Gout, CPPD
Symptoms of Bursitis Localized tenderness Swelling if near body surface Warmth and Erythema Pain with local pressure Pain with motion in some cases, but normal passive range of motion.
Olecranon Bursitis Swelling over point of elbow Usually minimally painful except with direct pressure Elbow motion is normal (typically) Common site for septic bursitis –Erythema –Warmth
Trochanteric bursitis Located at gluteal insertion into greater trochanter Aching lateral hip and thigh –Lying down –Walking Exam –Tender to deep palpation –Pain with active hip abduction against resistance
Tendinitis Tendon = dense fibrous connective tissue connecting muscle to bone –Tendon sheath – covers tendons in friction areas Synovial and fibrous layer –Paratenon Tendinitis –injury, inflammation, or degeneration of tendon (tendinosis) Tenosynovitis –inflammation of the tendon sheath
Symptoms and Signs of Tendinitis Pain with motion, especially against resistance Night pain Exam –Swelling, warmth, tenderness on palpation –Pain with passive stretching –Pain with active motion against resistance –Normal joint range of motion on passive testing
DeQuervain’s tenosynovitis --Inflammation and narrowing of the tendon sheath of the abductor pollicis longus and the extensor pollicis brevis at the radial styloid Etiology –Repetitive grasping with thumb while radially moving wrist –Pregnancy and especially after the baby is born!
Finkelstein’s test Induces significant pain in DeQuervain’s tenosynovitis Thumb flexed into palm and covered with fingers Wrist is passively moved ulnarly – stretching the involved tendons
Triggering Sudden locking of digit that must be pulled passively to release Due to –Nodular enlargement of tendon –Stenosis of tendon sheath –Both
Treatment of Tendinitis Avoid aggravating activities. Joint protection – strength/stretch/splint Rest Ice/Heat NSAIDs Steroid injections Surgery
Polymyalgia Rheumatica Age > 50 Bilateral aching and stiffness at shoulders/neck and pelvic girdle –Prolonged morning stiffness –Persistent beyond 1 month ESR > 40 Exclusion of other diseases Prompt response to low dose steroids
PMR -- Epidemiology 7/1,000 over age 50 Increased in caucasians of Northern European descent Females 2X more frequently than males.
PMR – Clinical Presentation Often acute onset Marked stiffness and pain –Mornings especially –ADL’s often affected Systemic symptoms –Fatigue –Fever(mild) –Malaise –Anorexia –Weight loss(mild)
PMR – clinical presentation Exam –Typically normal aside from pain limited motion at shoulders and hips –Probable subtle synovitis and effusions at shoulders and hips Labs –Nonspecific –Markers of inflammation ESR Anemia of chronic disease Elevated platelets
PMR -- Treatment Low dose steroids –Prednisone 7.5 to 15 mg daily –Expect prompt and dramatic response Treatment duration –Often times requires a year or more
PMR and Giant Cell Arteritis Giant cell arteritis (GCA) – specific vasculitis involving the cranial branches of the aorta – (also called Temporal Arteritis) –Important complication without treatment can be blindness. 15% of PMR pts will have GCA 50% of GCA pts will have PMR Treatment of GCA is much more aggressive – high dose steroids
Clues to Dx of GCA in PMR patient Headaches Visual changes(especially double vision or sudden visual loss) Asymmetric arm pulses(large vessel variant) Spiking fevers Significant weight loss(>10 #) Jaw claudication Lack of prompt response to low dose steroids
Fibromyalgia Chronic pain disorder Classification criteria –Widespread musculoskeletal pain –Tender to palpation at 11 of 18 specified tender points
Pathogenesis of FM Fibromyalgia is not an inflammatory disorder. Muscles, tendons, and ligaments from sites of pain are pathologically normal. FM is most likely an disorder of pain processing and subsequent inactivity and deconditioning. –Sleep disturbance –Mood disorders
FM – Epidemiology 10X more common in females 2% prevalence in U.S. – increases w/ age Onset – ages 30 to 55 50% of cases occur after specific emotional or physical trauma/illness
FM – Clinical presentation Diffuse musculoskeletal pain –Neck and shoulders often predominate Pain “in the muscles” Subjective joint stiffness and joint swelling (though not seen on exam)