WM510 Lecture 6: Musculoskeletal Conditions and Sports Medicine PDF

Western Internal Medicine I WM510 Taran Kermani MD, L.Ac 1 Musculoskeletal Conditions and Sports Medicine Taran Kermani MD. 2 Degenerative Joint Disease (Osteoarthritis) c A L. , D M i The target tissue in OA is articular n cartilage. a cartilage along with secondary There is destructionrofm e remod...

Western Internal Medicine I WM510 Taran Kermani MD, L.Ac 1 Musculoskeletal Conditions and Sports Medicine Taran Kermani MD. 2 Degenerative Joint Disease (Osteoarthritis) c A L. , D M i The target tissue in OA is articular n cartilage. a cartilage along with secondary There is destructionrofm e remodeling and hypertrophy of the bone. K nis not an in ammatory disease. RA, OA, unlikera a KneeTOA is the leading cause of chronic disability in the Osteoarthritis (OA) is the most common joint disease in humans. elderly. Taran Kermani MD. L.Ac 3 Osteoarthritis Major risk factors for OA include: Age Female sex Genetic factors m r e Repetitive stress K n Obesity a r Ta Major joint trauma , D M i an c A L. Taran Kermani MD. L.Ac 4 fl Classi cation Idiopathic The most common form and where no predisposing factor is evident Secondary c A L. , D M i an Attributable to an underlying cause other arthropathies (gout) endocrine diseases (diabetes mellitus, acromegaly) deposition diseases (hemochromatosis) mechanical factors (valgus or varus deformity, unequal lower extremity length) rm e K nthat will cause stress or trauma to a joint may a Any disease r eventually Ta cause secondary OA. ✓ The most common joint to be a ected is the knee ✓ The 2nd most common joint a ected is the base of the thumb (1st MCP). Taran Kermani MD. L.Ac 5 Presentation The major joints involved in OA are the weight-bearing joints (hip and knee) and the small joints of the ngers (PIPs and DIPs). c A. asymmetric L These joints are a ected in an oligo-articular , or mono-articular pattern. D M progressive, and The joint involvement is very slow, i n irreversible. a m rfails and there is increased pressure Because the cartilage e Kjoint pain increases with exercise and is on articular bone, n relieved bya rest. r Tasti ness is always 6.8 mg/dL). Gout is a metabolic disease of a heterogeneous nature, often familial Hyperuricemia is due to overproduction or under-excretion of uric acid or both Taran Kermani MD. L.Ac 11 *Origin of hyperuricemia Primary gout has a heritable component, several genes whose products regulate urate handling by the kidney. Secondary gout, is related to acquired causes of hyperuricemia rm e K patients About 90% ofn with primaryagout are ar over 30 men, usually T years of age. , D M i an c A L. In women, the onset is typically postmenopausal Taran Kermani MD. L.Ac 12 The characteristic lesion is the tophus: A nodular deposit of monosodium urate monohydrate crystals with an associated foreign body reaction. , D M i n a Tophi are found in cartilage, subcutaneous and periarticular tissues, tendon, bone, the kidneys, etc c A L. rm e K n a r a in ammation of gout is acute TheT believed to be initiated by the Urates have been demonstrated in the synovial tissues and uid during acute arthritis ingestion of urate crystals by monocytes and synoviocytes. Taran Kermani MD. L.Ac 13 Clinical ndings Acute gouty arthritis is sudden in onset and frequently nocturnal. It may develop without apparent precipitating cause or may follow rapid increases or decreases in serum urate levels. Common precipitants are , D M i an c A L. rm e changes in medications K that a ect urate metabolism n a fastingrbefore medical procedures. a T joint of the great toe is the most susceptible The MTP alcohol excess (particularly beer) joint, although others, especially those of the feet, ankles, and knees, are commonly a ected. Taran Kermani MD. L.Ac ff ff fl fl fi 14 Clinical ndings Hips and shoulders are rarely a ected. c A L. If more than one joint is a ected, distribution is usually asymmetrical. , D M i exquisitely tender and The involved joints are swollennand the overlying skin tense, warm, a and dusky red. m r e K n a r Ta As the attack progresses, the pain becomes intense. Taran Kermani MD. L.Ac 15 Clinical ndings Fever is common and may reach 39°C. Tophi may be found in the external ears, feet, olecranon and pre-patellar bursae, and hands. They usually develop years after the initial attack of gout. Local desquamation and pruritus during recovery from the acute arthritis are characteristic, but are not always present. , D M i an c A L. rm e K n of recurrent severe a After years r a attacks, gout can mono-arthritis T evolve into a chronic, deforming Asymptomatic periods of months or years commonly follow the initial acute attack. polyarthritis of upper and lower extremities that mimics RA Taran Kermani MD. L.Ac ff ff fi fi 16 Lab ndings Serial measurements of the serum uric acid detect hyperuricemia in 95% of patients, A single uric acid determination during an acute are of gout is normal in up to 25% of cases. c A L. , D ➡ A normal serum uric acid level, does not exclude gout M ni blood white cell peripheral During an acute attack, the a count is frequently elevated. rm e urate Identi cation of sodium K n uid or material crystals in a joint r aspirated a from a tophus T establishes the diagnosis. The crystals, are needle-like and negatively birefringent when examined by polarized light microscopy. Taran Kermani MD. L.Ac 17 Imaging Early in the disease, radiographs show no changes. Later, punched-out erosions with an overhanging rim of cortical bone (“rat bite”) develop. , D M i a soft n of When these are adjacent to a tissue tophus, they are diagnostic rm gout. e K is increasingly used Ultrasonography n a rthe diagnosis of gout. Small to con rm a tophi T and smaller deposits of urate c A L. crystals can frequently be imaged by ultrasonography. Taran Kermani MD. L.Ac fl fi fi fi 18 Di erential diagnosis Acute gout is often confused with cellulitis. Bacteriologic studies usually exclude acute pyogenic arthritis. , D Pseudo-gout is distinguished by the M i identi cation of calcium n a pyrophosphate crystals (positive m r uid, birefringence) in thee joint usually normal serum uric acid, and K n appearance of the radiographic a r chondrocalcinosis. Ta c A L. Chronic tophaceous arthritis may resemble chronic rheumatoid arthritis. Biopsy may be necessary to distinguish tophi from rheumatoid nodules Taran Kermani MD. L.Ac 19 Treatment Asymptomatic hyperuricemia should not be treated. c A L. Treatment of the acute attack focuses on reducing in ammation, not lowering serum uric acid. , D IL1 Inhibitors NSAID, Colchicine, Corticosteroids, M iperiods is intended to n Treatment during symptom-free a minimize urate deposition in tissues. m r e causes of hyperuricemia are a Potentially reversible K high-purine diet, obesity, alcohol consumption, and use n a r medications. of certain a T All patients with tophaceous gout should receive uratelowering therapy. Taran Kermani MD. L.Ac fl fi ff fl 20 Treatment m r e K n a r Ta , D M i an c A L. Taran Kermani MD. L.Ac 21 Shoulder Taran Kermani MD. L.Ac 22 Subacromial Impingement Syndrome c A is very The shoulder is a ball and socket joint. The socket. L shallow, which enables this joint to have the most motion , of any joint. D M i surrounding muscles The shoulder, relies heavily onnthe a and ligaments to provide stability. m er impingement syndrome describes a The subacromialK collection of diagnoses that cause mechanical nin the subacromial space. a in ammation r aof impingement syndrome can be related to T Causes muscle strength imbalances, poor scapula control, rotator cu tears, subacromial bursitis, and bone spurs. Taran Kermani MD. L.Ac 23 Subacromial Impingement Syndrome c A. establish the With any shoulder problem, it is important ,toL patient’s hand dominance, occupation,D and recreational activities because shoulder injuriesM may present i di erently depending on the demands placed on the n a shoulder joint. m r e with impingement syndrome may Baseball pitchers K complain of pain while throwing. n a r a adults with full-thickness rotator cu tears may Older T not complain of any pain because the demands on the joint are low. Taran Kermani MD. L.Ac ff ff fl ff 24 Clinical ndings Subacromial impingement syndrome classically presents with one or more of the following: pain with overhead activities c A L. , D nocturnal pain with sleeping on the shoulder M i on a jacket or bra). pain on internal rotation (eg, putting n a be appreciable atrophy in the m On inspection, there may r e supraspinatus or infraspinatus fossa. K n impingement syndrome can have mild with The patient a r scapulaawinging. T The patient often has a rolled-forward shoulder posture or head-forward posture. Taran Kermani MD. L.Ac 25 Clinical ndings On palpation, the patient can have tenderness over the anterolateral shoulder at the edge of the greater tuberosity. c A have The patient may lack full active ROM but should. L preserved passive ROM. , D with the Neer and Impingement symptoms can be elicited M i Hawkins impingement signs n a m r e K n a r Ta Taran Kermani MD. L.Ac fi fi 26 rm e K n a r Ta , D M i n a c A L. Taran Kermani MD. L.Ac 27 Imaging The following four radiographic views should be ordered to evaluate subacromial impingement syndrome: the anteroposterior (AP) scapula rule out glenohumeral joint arthritis c A L. , D Mjoint for inferior spurs evaluates the acromioclavicular i nY) the lateral scapula (scapular a rm shape evaluates the acromial e K the axillarynlateral a the glenohumeral joint visualizes r a of the shoulder may demonstrate full- or partial MRI T the AP acromioclavicular joint thickness tears or tendinosis. Ultrasound evaluation may demonstrate thickening of the rotator cu tendons and tendinosis. Taran Kermani MD. L.Ac ff 28 rm e K n a r Ta , D M i an c A L. Taran Kermani MD. L.Ac 29 Treatment The rst-line treatment for impingement syndrome is usually a conservative approach with education, activity modi cation, and physical therapy exercises. Impingement syndrome can be caused by muscle weakness or tear. Physical therapy is directed at rotator cu muscle strengthening, scapula stabilization, and postural exercises. Procedures include arthroscopic acromioplasty with coracoacromial ligament release, bursectomy, or debridement or repair of rotator cu tears. c A L. , D M i n a There is no strong evidence supporting the e ectiveness m of ice and NSAIDs as r a prolonged therapy. e K well to conservative treatment. Most patientsnrespond a Surgical ar T Taran Kermani MD. L.Ac ff fi fi ff 30 Rotator cuff Taran Kermani MD. L.Ac 31 Rotator cuff Tear c A. related Rotator cu tears can be caused by acute injuries L to falls on an outstretched arm or to pulling, on the D shoulder. M i repetitive injuries with It can also be related to chronic n a overhead movement and lifting. m r e Partial rotator cuKtears are one of the most common reasons for impingement syndrome. n a r rotator cu tears are usually more a Full-thickness T symptomatic and may require surgical treatment. The most commonly torn tendon is the supraspinatus. Taran Kermani MD. L.Ac ff ff 32 ff c A L. Most patients complain of weakness or pain with overhead movement. , D M The clinical ndings with rotator cu tears include those i of the impingement syndromen except that with fullathere may be more obvious thickness rotator cu tears m r resistance testing of speci c weakness noted with light e K rotator cu muscles. ntendon strength is tested with resisted a r Supraspinatus Ta abduction at 90 degrees with slight forward shoulder Night pain is also a common complaint. exion to around 45 degrees (“open can” test). Taran Kermani MD. L.Ac 33 Clinical ndings Infraspinatus/teres minor strength is tested with resisted shoulder external rotation with shoulder at 0 degrees abduction, elbow by side. c A.” or Subscapularis strength is tested with the “lift-o L , “belly-press” tests. D Mpositive Neer and The a ected patient usually alsoihas Hawkins impingement tests n a m r e K n a r Ta Taran Kermani MD. L.Ac ff ff fi ff fi fi 34 ff fl Clinical ndings rm e K n a r Ta , D M i an c A L. Taran Kermani MD. L.Ac 35 Imaging Recommended radiographs are similar to impingement syndrome c A. cu L The MR arthrogram can show partial or small rotator , tears. Ultrasonography can be helpful forD patients who cannot undergo MRI testing. M i n Treatment a rm may heal with scarring. Most Partial rotator cu tears e partial rotator cu K tears can be treated with physical therapy n and scapular and rotator cu muscle strengthening. a r a strengthen the remaining muscles to compensate can PTT for loss of strength and can have high rate of success for MRI is the best method for visualizing rotator cu tears. Taran Kermani MD. L.Ac ff 36 ff chronic tears. PT is also an option for older sedentary patients. ff Taran Kermani MD. L.Ac 37 Treatment Full-thickness rotator cu tears do not heal well and also have a tendency to increase in size with time. c A L. 49% of the full-thickness tears get bigger on an average of 2.8 years. Larger tears are associated with worsening pain. Most young active patients with acute, full- thickness tears should be treated with operative xation , D M where muscle is Fatty in ltration is a degenerative process i ninjury to the rotator cu being replaced by fat following a tendons. m r e factor for successful surgical A negative prognostic K treatmentn a r Ana irreversible process, operative interventions are T usually performed when the degree of in ltration is low Taran Kermani MD. L.Ac fi fi ff fi 38 Adhesive Capsulitis Taran Kermani MD. L.Ac 39 Adhesive Capsulitis c A L. Frozen shoulder is seen commonly in patients 40 to 65 years old. It is more commonly seen in women than men, especially in perimenopausal women or in patients with endocrine disorders, such as diabetes mellitus or thyroid disease. , D M i an m r e Patients usually present with a painful shoulder that has a limited K ROM with bothn passive and active movements. a r clinical sign is limitation of movement of external a A useful Twith the elbow by the side of the trunk. rotation Adhesive capsulitis is a self-limiting but very debilitating disease. Strength is usually normal but it can appear diminished when the patient is in pain. Taran Kermani MD. L.Ac 40 There are 3 phases: the in ammatory phase, the freezing phase, and the thawing phase. c A L. During the in ammatory phase, which usually lasts 4–6 months, patients complain of a very painful shoulder without obvious clinical ndings to suggest trauma, fracture, or rotator cu tear. , D Malso usually lasts 4– i During the “freezing” phase,nwhich 6 months, the shoulder becomes sti er and sti er even a though the pain is improving. rm e K phase can take up to a year as the The “thawing” n shoulderaslowly regains its motion. r a T duration of an idiopathic frozen shoulder is The total usually about 24 months, it can be much longer for patients who have trauma or an endocrinopathy. Taran Kermani MD. L.Ac 41 Imaging Standard AP, axillary, and lateral glenohumeral radiographs are useful to rule out glenohumeral arthritis, which can also present with limited active and passive range of motion. rm e K n a r Ta , D M i an c A L. Imaging can also rule out calci c tendinitis, which is an acute in ammatory process in which calci cations are visible in the soft tissue. However, adhesive capsulitis is usually a clinical diagnosis, and it does not need an extensive diagnostic workup. Taran Kermani MD. L.Ac ff fi fl fi ff fl fi fl 42 Treatment Adhesive capsulitis is caused by acute in ammation of the capsule followed by scarring and remodeling. During the acute phase, NSAIDs and physical therapy are recommended to maintain motion. Surgical treatments, which are rarely indicated, include manipulation under anesthesia and arthroscopic release. c A L. , Dt from intrabene There is also evidence of short-termM articular corticosteroid injection or i oral prednisone. n athe shoulder is less painful but During the “freezing” phase, m r remains sti. e K Anti-in ammatory medication is not as helpful during the n a “thawing”rphase as it is during the “freezing” phase, and Ta symptoms usually resolve with time. the shoulder Taran Kermani MD. L.Ac 43 Low Back Pain Taran Kermani MD. L.Ac fi fl ff fl 44 Low Back Pain c A of. Low back pain remains the most common cause L disability for patients under the age of 45 and is the , Dcare visits. second most common cause for primary M i pain is 15–45%. back The annual prevalence of low n a Low back pain is the condition associated with the m r e highest years lived with disability. K n of the low back pain is often di cult to The exactrcause a diagnose; a its cause is often multifactorial, although there T are usually degenerative changes in the lumbar spine. Taran Kermani MD. L.Ac 45 Alarming symptoms for back pain caused by cancer include unexplained weight loss, failure to improve with treatment, pain for more than 6 weeks, and pain at night or rest. Alarming symptoms for infection include fever, rest pain, recent infection (urinary tract infection, cellulitis, pneumonia), or history of immunocompromise or injection drug use. c A L. , D by urinary retention The cauda equina syndrome is suggested M or incontinence, saddle anesthesia,idecreased anal sphincter n lower extremity weakness, tone or fecal incontinence, bilateral a and progressive neurologic rmde cits. e pain due to vertebral fracture include use Risk factors for back K n of corticosteroids, age over 70 years, history of osteoporosis, a r severe trauma, and presence of a contusion or abrasion. a T Back pain may also be the presenting symptom in other serious medical problems, including abdominal aortic aneurysm, peptic ulcer disease, kidney stones, or pancreatitis. Taran Kermani MD. L.Ac fi 46 Physical Examination The physical examination can be conducted with the patient in the standing, sitting, supine, and prone positions: c A Standing: posture can be observed → spinal. L asymmetries include scoliosis, thoracic kyphosis, and , lumbar hyper-lordosis. Active ROM ofD lumbar spine M i and sensation can be Sitting: motor strength, re exes, n a tested m er be evaluated for ROM, should Supine: the hipK particularlyn internal rotation. The straight leg raise test a puts traction and compression forces on the lower r a lumbar T nerve roots Prone: palpate each vertebral level of the spine and sacroiliac joints for tenderness. Taran Kermani MD. L.Ac 47 Neurologic testing of lumbosacral nerve disorders Taran Kermani MD. L.Ac 48 fl Imaging and other tests In the absence of alarming “red ag” symptoms suggesting infection, malignancy, or cauda equina syndrome, most patients do not need diagnostic imaging, including radiographs, in the rst 6 weeks. Most clinicians obtain radiographs for new back pain in patients older than 50 years. If done, radiographs of the lumbar spine should include AP and lateral views. , D M i an c A L. rm e K n a r or nerve conduction studies may be useful Electromyography a T in assessing patients with possible nerve root symptoms MRI is the method of choice in the evaluation of symptoms not responding to conservative treatment or in the presence of red ags of serious conditions. lasting longer than 6 weeks. These tests are usually not necessary if the diagnosis of radiculopathy is clear. Taran Kermani MD. L.Ac 49 Treatment Non-pharmacologic treatments are key in the management of low back pain. Education alone improves patient satisfaction with recovery and recurrence. Patient education and information including safe and e ective methods of symptom control as well as how to decrease the risk of recurrence with proper lifting techniques, abdominal wall/core strengthening, weight loss, and smoking cessation. , D M i an c A L. rm e K stress reduction, and yoga Tai chi, mindfulness-based n a have shown r bene t for chronic low back pain patients. a T PT exercise programs can be tailored to the patient’s symptoms and pathology. Taran Kermani MD. L.Ac fl fi fi fl ff 50 Treatment NSAIDs are e ective in the early treatment of acute LBP c A L. Acetaminophen and oral corticosteroids are relatively ine ective for chronic low back. , D M i nterm, but have the usual a Opioids alleviate pain in the short side e ects and concerns of long-term opioid use rm e chronic neuropathic pain with alpha-2-delta Treatment of moreK n ligands (eg, gabapentin), SSRIs (eg, duloxetine), or TCAs (eg, a r nortriptyline) a may be helpful. T Epidural injections may reduce pain in the short term, and There is limited evidence that muscle relaxants provide shortterm relief; since these medications have addictive potential, they should be used with care. appear to reduce the need for surgery in some patients within a 1-year period but not longer. Taran Kermani MD. L.Ac 51 Spinal Stenosis c A L. OA in the lumbar spine can cause narrowing of the spinal canal. , D stenosis and A large disk herniation can also cause M i compression of neural structures or the spinal artery n with ambulation. a resulting in “claudication” symptoms m r The condition usually a ects patients aged 50 years or e K older. n a r pain that worsens with extension. They report Patients a T reproducible single or bilateral leg symptoms describe that are worse after walking several minutes and that are relieved by sitting (“neurogenic claudication”). Taran Kermani MD. L.Ac ff ff ff ff 52 Spinal Stenosis c A L. On examination, patients often exhibit limited extension of the lumbar spine, which may reproduce the symptoms radiating down the legs. , D M by a Exercises, usually exion-based asidemonstrated n physical therapist, can help relieve symptoms a m injections can also reduce pain r Facet joint corticosteroid e symptoms. K n for spinal stenosis include spinal a Surgical treatments r a (widening the spinal canal or laminectomy), decompression T nerve root decompression (freeing a single nerve), and spinal fusion (joining the vertebra to eliminate motion and diminish pain from the arthritic joints) Taran Kermani MD. L.Ac 53 Lumbar disk herniation Taran Kermani MD. L.Ac fl 54 Lumbar disk herniation c A. or heavy Lumbar disk herniation is usually due to bending L loading (eg, lifting) with the back in exion,,causing D herniation or extrusion of disk contents (nucleus M i However, there may pulposus) into the spinal cord area. n not be an inciting incident. a m r Disk herniations usually occur from degenerative disk e K disease in patients between 30 and 50 years old. n a r The L5–S1 a disk is a ected in 90% of cases. T Compression of neural structures, such as the sciatic nerve, causes radicular pain. Taran Kermani MD. L.Ac 55 Lumbar disk herniation c A L. Discogenic pain typically is localized in the low back at the level of the a ected disk and is worse with activity. MRI is the best method to assess the level and morphology of the herniation and is recommended if surgery is planned , D pain radiating down the “Sciatica” causes electric shock-likeM posterior aspect of the leg often toibelow the knee. nback exion such as bending a Symptoms usually worsen with rm or sitting for long periods. e K herniation can cause numbness and A signi cant disk n a weakness,rincluding weakness with plantar exion of the foot (L5/S1) Taor dorsi exion of the toes (L4/L5). Taran Kermani MD. L.Ac fl fl fl ff fl ff fi 56 Knee Pain Taran Kermani MD. L.Ac 57 Knee Pain c A L. The knee is the largest joint in the body and is susceptible to injury from trauma, in ammation, infection, and degenerative changes. , D years of age and can OA of the knees is common after 50 M i develop due to previous trauma, aging, activities, alignment n a issues, and genetic predisposition. m rshould begin with general questions e Evaluation of knee pain regarding durationK and rapidity of symptom onset and the n mechanisma of injury or aggravating symptoms. r Taor degenerative problems can occur with stress or Overuse compression from sports, hobbies, or occupation. A history of trauma, previous orthopedic problems with, or surgery to, the a ected knee should also be speci cally queried. Taran Kermani MD. L.Ac fi fl ff 58 c c A.A. L ,L , D D M M i i n an a m rm e r e K K n a n r a ar a T T Location of common causes of knee pain 59 ACL injuries c A. The anterior cruciate ligament (ACL) connectsLthe , to the posterior aspect of the lateral femoral condyle D anterior aspect of the tibia. Its main function is to control Mfemur. It also anterior translation of the tibia on the i nthe tibia on the femur. provides rotationally stability of a rm with sporting injuries. They can ACL tears are common e result from both K contact (blow to the knee) and nonn contact (jumping, pivoting) activities. a r Ta usually falls down following the injury, has The patient acute swelling and di culty with weight bearing and complains of instability. Taran Kermani MD. L.Ac ffi 60 Clinical ndings Patients describe symptoms of instability while performing side-to-side maneuvers or descending stairs. c A. The Lachman test (84– 87% sensitivity and 93% L , the tibia speci city). Excessive anterior translation of D compared with the other side indicates injury to the ACL. M i sensitivity and 87% The anterior drawer test (48% n a speci city) A positive test nds ACL laxity compared with m the una ected side.er K Plain radiographs are usually negative in ACL tears but n a are usefulrto rule out fractures. a T MRI is the best tool to diagnose ACL tears and associated articular and meniscal cartilage issues. It has greater than 95% sensitivity and speci city for ACL tears. Taran Kermani MD. L.Ac 61 , D M i an c A L. rm e K n a and active patients will require surgical r Most young a reconstruction T of the ACL. Nonoperative treatments are usually reserved for older patients or those with a very sedentary lifestyle. Physical therapy can focus on hamstring strengthening and core stability. An ACL brace can help stability. Taran Kermani MD. L.Ac fi fi fi ff fi fi 62 Meniscus Injuries Taran Kermani MD. L.Ac 63 Meniscus Injuries c A The menisci act as shock absorbers within,the L.knee. D clicking, and Injuries to a meniscus can lead to pain, M locking sensation. i n a with acute injuries (usually occur Most meniscus injuries m in younger patients)e orrrepeated micro trauma, such as squatting or twisting K (usually in older patients). n a may have an antalgic (painful) gait and r The patient a di culty with squatting. They may complain of catching T or locking of the meniscal fragment Taran Kermani MD. L.Ac ffi 64 Clinical ndings Physical ndings can include e usion or joint line tenderness. McMurray test, the modi ed McMurray test, and the Thessaly test, can be performed to con rm the diagnosis c A. Patients can usually point out the area of maximal L tenderness along the joint line. , D M swelling that Meniscus tears rarely lead to theiimmediate is commonly seen with fractures and ligament tears. n a Swelling usually occurs during the rst 24 hours after the rm injury or later. e K are commonly seen in arthritic knees, it is Meniscus tears n a often unclear r whether the pain is coming from the a T tear or the arthritis. meniscus Taran Kermani MD. L.Ac 65 fi fi ff fi fi fi 66 67 Imaging MRI of the knee is the best diagnostic tool for meniscal injuries (93% sensitivity and 95% speci city). c A. tears in Conservative treatment can be used for degenerative L , older patients. D mild knee OA, M The treatment is similar for patientsiwith including analgesics and PT for strengthening and core stability. n a to arthroscopic partial m A RCT showed that PT compared r e meniscectomy had similar outcomes at 6 months. However, Kwho were assigned to PT alone underwent 30% of the patients n surgery within 6 months. a r a is growing evidence that untreated meniscus tears can ThereT lead to accelerated OA changes. Surgical treatment before Treatment cartilage breakdown is recommended for acute meniscus injuries. Taran Kermani MD. L.Ac fi 68 Carpal Tunnel Syndrome c A. is a An entrapment neuropathy, carpal tunnel syndrome L painful disorder caused by compression of ,the median nerve between the carpal ligament and D other structures M within the carpal tunnel. i n a be compressed by synovitis can The contents of the tunnel m ror carpal joints, recent or malhealed of the tendon sheaths e fractures, tumors,K tissue in ltration, and occasionally n congenital a syndromes (eg, mucopolysaccharidoses). r Ta may occur in uid retention of pregnancy, in The disorder individuals with a history of repetitive use of the hands, or following injuries of the wrists. Taran Kermani MD. L.Ac 69 Carpal Tunnel Syndrome Carpal tunnel syndrome can also be a feature of many systemic diseases, such as RA and other rheumatic disorders (in ammatory tenosynovitis), myxedema, amyloidosis, sarcoidosis, leukemia, acromegaly, and hyperparathyroidism. , D M i an c A L. rm e K n a r a ThereTis a familial type of carpal tunnel syndrome in which no etiologic factor can be identi ed. Taran Kermani MD. L.Ac fi fl fi fl 70 Clinical ndings The initial symptoms are pain, burning, and tingling in the distribution of the median nerve (the palmar surfaces of the thumb, the index and long ngers, and the radial half of the ring nger). c A L. , D into the forearm and M Aching pain may radiate proximally i occasionally proximally to then shoulder and over the neck a and chest. m r e by manual activity, particularly by Pain is exacerbated K extremes of volar exion or dorsi exion of the wrist. n a rbothersome at night. a It is most T Impairment of sensation in the median nerve distribution may or may not be demonstrable. Taran Kermani MD. L.Ac 71 Taran Kermani MD. L.Ac fl fi fl fi fi 72 Clinical ndings A Tinel or Phalen sign may be positive. c A L. A Tinel sign is tingling or shock-like pain on volar wrist percussion. The Phalen sign is pain or paresthesia in the distribution of the median nerve when the patient exes both wrists to 90 degrees for 60 seconds. , D M i an rm e K n a r a T Muscle weakness or atrophy, especially of the thenar The carpal compression test, in which numbness and tingling are induced by the direct application of pressure over the carpal tunnel, may be more sensitive and speci c than the Tinel and Phalen tests. eminence, can appear later than sensory disturbances as compression of the nerve worsens. Taran Kermani MD. L.Ac 73 fi 74 Imaging Ultrasound can demonstrate attening of the median nerve. Sensitivity of ultrasound for carpal tunnel syndrome is variable but estimated between 54% and 98%. EMG and NCV show evidence of sensory conduction delay before motor delay, which can occur in severe cases. c A L. , D M Treatment is directed toward reliefnofi pressure on the median nerve. a m discovered, it should be treated rispatients When a causative lesion e appropriately. Otherwise, in whom carpal tunnel K syndrome is suspected should modify their hand activities n a r or NSAIDs can also be tried. Oral corticosteroids a T Methylprednisolone injections were found to have more e ect at Treatment 10 weeks than placebo, but the bene ts diminished by 1 year. Carpal tunnel release surgery can be bene cial if the patient has a positive EMG Taran Kermani MD. L.Ac fi fi 75 fl