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Chapter 14 445 Musculoskeletal problems Symptoms of musculoskeletal disease 446 Neck pain 448 Low back pain 450 Shoulder problems 454 Elbow problems 456 Wrist and hand problems 458 Hip and pelvis problems 462 Knee problems 466 Ankle and foot problems 470 Sports med...

Chapter 14 445 Musculoskeletal problems Symptoms of musculoskeletal disease 446 Neck pain 448 Low back pain 450 Shoulder problems 454 Elbow problems 456 Wrist and hand problems 458 Hip and pelvis problems 462 Knee problems 466 Ankle and foot problems 470 Sports medicine 474 Management of sporting injuries 476 Bone disorders 478 Rickets and osteomalacia 480 Osteoporosis 482 Treatment options for osteoporosis 484 Osteoarthritis 486 Rheumatoid arthritis 488 The spondyloarthropathies 492 Crystal-induced arthritis 494 Connective tissue diseases 496 Polymyalgia and giant cell arteritis 498 Vasculitis 500 Tiredness and chronic fatigue syndrome 502 Miscellaneous conditions 504 0 5 4 450 CHAPTER 14 Musculoskeletal problems Low back pain Definitions Acute low back pain New episode of low back pain of 3mo Causes of back pain Table 14.2 History Ask about: Circumstances of pain—history of injury; duration Nature/severity of pain—pain/stiffness mainly at rest/at night, easing with movement suggests inflammation (e.g. discitis, spondyloarthropathy) Associated symptoms—numbness, weakness, bowel/bladder symptoms PMH—past illnesses (e.g. cancer), previous back problems Exclude pain not coming from the back (e.g. GI/GU pain; AAA) Examination Deformity, e.g. kyphosis (typical of ankylosing spondylitis), loss of lumbar lordosis (common in acute mechanical back pain), scoliosis Palpate for tenderness, step deformity, and muscle spasm Assess flexion, extension, lateral flexion, and rotation while standing Ask to lie down—this gives a good indication of severity of symptoms In lower limbs look for muscle wasting and check power, sensory loss, and reflexes (knee jerk and ankle jerk)—Table 14.3. Assess straight leg raise (SLR)—sciatica is present if SLR on one side elicits back/buttock pain (usually ipsilateral) compared to SLR on the other side ! Red flags 55y Past history of cancer Unwell Non-mechanical pain AAA Weight d Pain that worsens HIV Widespread when supine Immune suppression neurology Night-time pain IV drug use Structural Thoracic pain Taking steroids deformity Management of acute back pain in the community Triage ac- cording to history and examination—Figure 14.1, E p. 452 For patients who do not require immediate referral Consider analgesia, e.g. NSAIDs (for short time + consider gastroprotection); weak opioids (± paracetamol). Use Keele STarT Back screening tool (Box 14.1): If total score ≤3, explain likely natural history of the pain and advise to avoid bed rest and maintain normal activities as far as possible (d chance of chronic pain). Suggest self-help exercises If total score is ≥4, check question 5–9 sub-score: If ≤3—if not resolved in 4wk, refer for physical therapy. Options include: back exercise classes, physiotherapy, chiropractic, osteopathy or acupuncture, if available If ≥4—if not resolved in 4wk, refer directly for specialist intervention—sooner if worsening or severe pain In all cases, challenge any ‘yellow flag’ factors (Figure 14.1, E p. 452) that may inhibit recovery and delay return to normal functioning  LOW BACK PAIN 451 Table 14.2 Causes of back pain: age suggests the most likely cause Age (y) Causes 15–30 Postural Trauma Spondylolisthesis Mechanical Fracture Pregnancy Prolapsed disc Ankylosing spondylosis 30–50 Postural Spondyloarthropathies Degenerative Prolapsed disc Discitis joint disease >50 Postural Malignancy (lung, breast, Osteoporotic Degenerative prostate, thyroid, kidney) collapse Paget’s disease Myeloma Other Spinal stenosis Abdominal aortic Spinal infection causes Cauda equina tumour aneurysm Referred pain Table 14.3 Neurology with lumbosacral nerve root entrapment Root Sensory changes Motor weakness Reflex changes L2 Front of thigh Hip flexion/adduction None L3 Inner thigh Knee extension Knee L4 Inner shin Knee extension Knee Foot dorsiflexion L5 Outer shin Knee flexion None Dorsum of foot Foot inversion Big toe dorsiflexion S1 Lateral side of foot/sole Knee flexion Ankle Foot plantarflexion Box 14.1 Keele STarT Back Pain Scoring Tool Ask patients to consider the following statements and state whether they agree or disagree with them. Thinking about the past 2wk: 1. My back pain has spread down my leg(s) at some time in the last 2wk 2. I have had pain in the shoulder or neck at some time in the last 2wk 3. I have only walked short distances because of my back pain 4. In the last 2wk, I have dressed more slowly than usual because of back pain 5. It’s not really safe for a person with a condition like mine to be physically active 6. Worrying thoughts have been going through my mind a lot of the time 7. I feel that my back pain is terrible and it’s never going to get any better 8. In general I have not enjoyed all the things I used to enjoy If the patient agrees with a statement, score 1; if disagrees, score 0. 9. Overall, how bothersome has your back pain been in the last 2wk? Not at all, slightly or moderately—score 0 Very much or extremely—score 1 2 5 4 452 CHAPTER 14 Musculoskeletal problems Figure 14.1 Triage of acute back pain 0 Do not X-ray routinely X-rays require a high radiation dose and clinically meaningful findings are rare. Exceptions: Young (2.5 standard deviations (SD) below the young adult mean (i.e. T score of 3mo or frequent courses of steroids, in addition: Add bone protection agent (e.g. bisphosphonate) for patients >65y or with history of fragility fracture or Refer patients 19kg/m2 and adequate intake of calcium and vitamin D (Tables 14.6 and 14.7, E p. 481) Give Ca2+ and/or vitamin D supplements to postmenopausal women with dietary deficiency; also consider if on long-term steroids, >80y, housebound, or institutionalized Regular exercise Weight-bearing activity >30min/d d fracture rate Stop smoking Women who stop smoking pre-menopause have a 25% d fracture rate post-menopause d alcohol consumption to po preparations). Causes non-healing gum lesions. Treatment is with sur- gical excision of the affected bone. Risk of osteonecrosis i after dental work—advise patients to have a dental check-up and any necessary dental work done before starting bisphosphonate treatment, and report any oral symptoms when on treatment to their dentist. Atypical femoral fracture Prolonged bisphosphonate treatment >5yl oversuppression of bone turnover and i bone fragility. Acute sub-trochanteric or mid-shaft femoral fractures are most common.  A ‘drug holiday’ of 1–5y has been proposed for low-risk patients after 5y use—follow local guidance. Denosumab 60mg sc every 6mo. Monoclonal antibody that d osteoclast activation and d bone resorption. For postmenopausal osteoporosis when bisphosphonates are contraindicated/not tolerated and severe osteoporosisN Can be used for women with severe CKD; correct hypocalcaemia before starting treatment. May cause osteonecrosis of the jaw Raloxifene 60mg od. Selective oestrogen receptor modulator (SERM). Use if previous fragility fracture, bisphosphonates are not tolerated or contraindicated, or there is an unsatisfactory response with bisphosphonates (further fracture and/or d in BMD after ≤1y treatment). Not recommended for primary prevention of osteoporotic fractureN Avoid if past history of DVT/PE, cholestasis, endometrial cancer, or undiagnosed vaginal bleeding HRT (E p. 688). Postpones postmenopausal bone loss and d fractures. Optimum duration of use is uncertain (>5–7y) but benefit disappears 51y HRT should not be considered first-line therapy for long-term prevention of osteoporosis. HRT remains an option where other therapies are contraindicated, cannot be tolerated, or if there is a lack of response; risks and benefits should be carefully assessed Teriparatide Third line for postmenopausal women and second line for men with past history of fragility fracture if other treatments are not tol- erated/ineffective and specific T-score and clinical criteria are met. Given by daily injection. Maximum duration of use is 18mo. Consider referral for consultant initiation if other treatment options are exhausted. Osteoporosis in men Currently only bisphosphonates and teriparatide are recommended for treatment of osteoporosis in men. Monitoring There is no consensus about duration of treatment for osteoporosis or monitoring of BMD during treatment. Circumstances in which repeat DXA scanning might be necessary include: Fragility fracture on treatment If considering a change in treatment When considering restarting therapy after a drug holiday Referral Consider referral to an appropriate specialist if (U = urgent re- ferral; R = routine referral): Another cause for fragility fracture is suspected (e.g. metastasis)—U Fragility fracture on treatment—R Unusual presentation of osteoporosis, e.g. premenopausal woman—R For consideration of treatment with IV bisphosphonate, denosumab, or teriparatide—R Further information National Osteoporosis Guideline Group Clinical guideline for the preven- tion and treatment of osteoporosis. M www.shef.ac.uk/NOGG NICE (2008, updated 2018) Alendronate, etidronate, risedronate, raloxifene, strontium ranelate and teriparatide for the primary and sec- ondary prevention of osteoporotic fragility fractures in postmenopausal women. M www.nice.org.uk/guidance/ta161 NICE (2010) Osteoporotic fractures—denosumab. M www.nice.org.uk/ guidance/ta204 NICE (2015) Menopause: diagnosis and management. M www.nice.org. uk/guidance/ng23 6 8 4 486 CHAPTER 14 Musculoskeletal problems Osteoarthritis Osteoarthritis (OA) is the most important cause of locomotor disability. It used to be considered ‘wear and tear’ of the bone/cartilage of synovial joints but is now recognized as a metabolically active process involving the whole joint—i.e. cartilage, bone, synovium, capsule, and muscle. The main reason for patients seeking medical help is pain. Level of pain and disability are greatly influenced by the patient’s personality, anxiety, depres- sion, and activity, and often do not correlate well with clinical signs. Risk factors i age (uncommon ♂; i in black and Asian populations; genetic predisposition; obesity; abnormal mechanical loading of joint, e.g. instability; poor muscle function; post-meniscectomy; certain occupations, e.g. farming. Symptoms and signs Joint pain ± stiffness, synovial thickening, de- formity, effusion, crepitus, muscle weakness/wasting, and d function. Most commonly affects hip, knee, and base of thumb. Typically exacerbations last weeks to months. Nodal OA, with swelling of the distal interphalangeal joints (Heberden’s nodes) has a familial tendency. Investigations X-rays may show d joint space, cysts and sclerosis in subchondral bone, and osteophytes. OA is common and may be a coinci- dental finding. Exclude other causes of pain, e.g. check FBC and ESR if inflam- matory arthritis is suspected (normal or mildly i in OA—ESR >30mm/h suggests RA or psoriatic arthritis). Management of osteoarthritis in primary care Employ a holistic approach. Assess effect of OA on the patient’s functioning, quality of life, occupation, mood, relationships, and leisure activities. Formulate a manage- ment plan with the patient that includes self-management strategies, effects of co-morbidities and regular review. Information and advice Give information and advice on all relevant aspects of osteoarthritis and its management. Arthritis Research UK produces a range of leaflets for patients. Use the whole multidisciplinary team, e.g. refer to: Physiotherapist for advice on exercises, strapping, and splints OT for aids Chiropodist for foot care and insoles Social worker for advice on disability benefits and housing Orthopaedics for surgery if significant disability/night pain d load on the joint Weight reduction can d symptoms and may d progres- sion in knee OA. Using a walking stick in the opposite hand to the affected hip and cushioned insoles/shoes (e.g. trainers) can also help. Exercise and improving muscle strength d pain and disability, e.g. walking (for OA knee), swimming (for OA back and hip but may make neck worse), cyc- ling (for OA hip and OA knee—but may worsen patellofemoral OA). Refer to physiotherapy for advice on exercises especially isometric exercises for the less mobile. Pain control Use non-pharmacological methods first (activity, exercise, weight d, footwear modification, walking stick, TENS, local heat/cold treatments)  OSTEOARTHRITIS 487 Regular paracetamol (1g qds) is first-line drug treatment for all OA and/ or topical NSAIDs for knee/hand OA only. Topical NSAIDs have less side effects than oral NSAIDs and are more acceptable to patients Use opioids, oral NSAIDs, or COX2 inhibitors as second-line agents in addition to, or instead of paracetamol. Use the lowest effective dose for the shortest possible time. Co-prescribe a proton pump inhibitor (e.g. omeprazole 20mg od) with NSAIDs if taking for >1wk Low-dose antidepressants, e.g. amitriptyline 10–75mg nocte (unlicensed) are a useful adjunct especially for pain causing sleep disturbance Capsaicin cream can also be helpful for knee/hand OAN Aspiration of joint effusions and joint injections Can help in exacerbations. Some patients respond well to long-acting steroid injections—it may be worth considering a trial of a single treatment. Hyaluronic acid knee injec- tions are not recommended by NICE. Complementary therapies 760% of sufferers from OA are thought to use CAM, e.g. copper bracelets, acupuncture, food supplements, dietary ma- nipulation. There is good evidence chiropractic/osteopathy can be helpful for back pain, but otherwise evidence of effectiveness is scanty. Advise patients to find a reputable practitioner with accredited training who is a member of a recognized professional body and carries professional indem- nity insurance.  Other drugs/supplements Glucosamine It is controversial whether glucosamine modifies OA progression. It is available OTC but not recommended by NICE Strontium ranelate d progression of OA, d pain, and i mobilityR. Place in OA management is yet to be determined Psychological factors Have a major impact on the disability from OA. Education about the disease, and emphasis that it is not progressive in most people, is important. Seek depression and anxiety with screening tools—E p. 173. Treat as needed. Refer To rheumatology To confirm diagnosis if coexistent psoriasis (psoriatic arthritis mimics OA and can be missed by radiologists); rule out 2° causes of OA (e.g. pseudogout, haemochromatosis) if young OA or odd distribution; if joint injection is thought worthwhile but you lack expertise or confidence to do it To orthopaedics If symptoms are severe for joint replacement. Refer as an emergency if you suspect joint sepsis Further information NICE Osteoarthritis: care and management. M www.nice.org.uk/guid- ance/cg177 Information and support for patients Arthritis Care F 0808 800 4050 M www.arthritiscare.org.uk Arthritis Research UK F 0800 5200 520 M www.arthritisresearchuk.org 8 4 488 CHAPTER 14 Musculoskeletal problems Rheumatoid arthritis Rheumatoid arthritis (RA) is the most common disorder of connective tissue affecting 71% of the UK population. It is an immunological disease, triggered by environmental factors, in patients with genetic predisposition. Disease course is variable with exacerbations and remissions. ! Refer all suspected cases of rheumatoid arthritis to rheumatology— early treatment with disease-modifying drugs can significantly alter disease progression. Refer urgentlyN if: Small joints of the hands/feet are affected >1 joint is affected There has been a delay of ≥3mo between onset of symptoms and seeking medical advice Presentation Can present at any age—most common in middle age. ♀:♂ 83:1 Variable onset—often gradual but may be acute Usually starts with symmetrical small joint involvement—i.e. pain, stiffness, swelling, and functional loss (especially in the hands)—joint damage and deformity occur later Irreversible damage occurs early if untreated and can l deformity and joint instability Other presentations—monoarthritis; migratory (palindromic) arthritis; PMR-like illness; systemic illness of malaise, pain, and stiffness Symptoms and signs Predominantly peripheral joints are affected— symmetrical joint pain, effusions, soft tissue swelling, early morning stiff- ness. Progression to joint destruction and deformity. Tendons may rupture. Specific features—Table 14.8. Differential diagnosis Diagnosis may not be easy—consider: Psoriatic arthritis Bilateral carpal tunnel syndrome Nodal OA Other connective tissue disorders SLE (especially in ♀ 50y Investigations Check FBC (normochromic normocytic or hypochromic, microcytic anaemia), ESR, and/or CRP (i). May have i platelets, d WCC Rheumatoid factor and anti-CCP antibodies are +ve in the majority. A minority have a +ve ANA titre X-rays—normal, periarticular osteoporosis or soft tissue swelling in the early stages; later—loss of joint space, erosions, and joint destruction Management A multidisciplinary team approach is ideal, e.g. GP, medical and surgical teams, physiotherapist, podiatrist, OT, nurse specialist, and social worker. Screening for depression E p. 173 General support Provision of information about the disease, treatments, and support available (including equipment and help with everyday activities, self- help and carers groups, disabled parking badges, financial support—E p. 108). Physical therapy Exercises, splints, appliances, and strapping help to keep joints mobile, d pain, and preserve function.  RHEUMATOID ARTHRITIS 489 Table 14.8 Specific features of rheumatoid arthritis Hands Ulnar deviation of the fingers ‘z’ deformity of the thumb Swan neck (hyperextended PIP and flexed DIP joints) and boutonnière (flexed PIP and extended MCP joints, hyperextended DIP joint) deformities of the fingers (Figure 14.7) d grip strength and d hand function causes disability Legs and feet Subluxation of the metatarsal heads in feet and claw toes l pain on walking Baker’s cyst (E p. 468) at the knee may rupture mimicking DVT Spine Especially cervical spine—causing neck pain, cervical subluxation, and atlanto-axial instability leading to a risk of cord compression. X-rays are required prior to general anaesthesia Non-articular Common. Weight d, fever, malaise. features Rheumatoid nodules (especially extensor surfaces of forearms) Vasculitis—digital infarction, skin ulcers, mononeuritis Eye—Sjögren’s syndrome, episcleritis, scleritis Lungs—pleural effusions, fibrosing alveolitis, nodules Heart—pericarditis, mitral valve disease, conduction defects Skin—palmar erythema, vasculitis, rashes Neurological—nerve entrapment, e.g. carpal tunnel syndrome, mononeuritis, and peripheral neuropathy Felty’s syndrome—combination of RA, splenomegaly, and leucopenia. Occurs in patients with long-standing RA. Recurrent infections are common. Hypersplenism l anaemia and thrombocytopenia. Associated with lymphadenopathy, pigmentation, and persistent skin ulcers. Splenectomy may improve the neutropenia C-reactive protein (CRP) Acute phase protein that i ≤6h after an acute event. Follows clinical state more rapidly than ESR (E p. 636). Not i by SLE, leukaemia, UC, pregnancy, OA, anaemia, polycythaemia, or heart failure. Highest levels are seen in bacterial infections (>10mg/L). Boutonnière deformity Swan neck deformity Figure 14.7 Boutonnière and swan neck deformities of the fingers Information and support for patients Arthritis Care F 0808 800 4050 M www.arthritiscare.org.uk Arthritis Research UK F 0800 5200 520 M www.arthritisresearchuk.org 0 9 4 490 CHAPTER 14 Musculoskeletal problems Medication NSAIDs and simple analgesics e.g. regular paracetamol. Provide symptom- atic relief but do not alter the course of disease. Patients’ response to NSAIDs is individual—start with the least gastric toxic, e.g. ibuprofen 200– 400mg tds and alter as necessary, e.g. to naproxen 500mg bd. If the patient has a history of indigestion/gastric problems, consider adding gastric pro- tection, e.g. PPI, or, if there is no history of CVD, using a COX2 inhibitor, e.g. celecoxib 100mg bd. Corticosteroids Intra-articular injections of steroids (e.g. triamcinolone) can settle localized flares (e.g. knee or shoulder) and can be used up to 3×/y in any particular joint. Depot IM injections or IV infusions (pulses) can also help settle an acute flare but offer short-term benefits with the risk of sys- temic side effects. Daily low-dose oral steroids help symptoms and there is some evidence that they can modify disease progression, but concerns about adverse side effects have limited use. Disease-modifying drugs (DMARDs) Methotrexate Gold Hydroxychloroquine Sulfasalazine Azathioprine Ciclosporin Penicillamine Leflunomide Cyclophosphamide Biologic therapies, e.g. rituximab, infliximab, etanercept, adalimumab Use only under consultant supervision. d disease progression by modifying the immune response and inflammation. Used individually or in combin- ation, they are now started very early in the disease (i.e. first 3–6 mo)— hence the need for early referral. DMARDs can take several months to show any effect. Before starting check baseline U&E, Cr, eGFR, LFTs, FBC and urinalysis. Side effects and monitoring—Table 14.9. ! Results requiring action Total WBC 105fL check vitamin specialist B12/folate Intramuscular gold FBC and urinalysis at the time Ask patients to report: (Myocrisin®) of each injection Symptoms/signs of 50mg monthly CXR within 1y of start of infection—especially treatment sore throat Bleeding/bruising Breathlessness/cough Mouth ulcers/metallic taste or rashes Penicillamine FBC, urinalysis 2-weekly for Altered taste (can be 500–750mg/d 3mo and 1wk after any i dose. ignored), rash maintenance Then monthly Azathioprine FBC and LFT weekly for 6wk, GI side effects, rash, bone 1.5–2.5mg/kg/d then every 2wk until dose/ marrow suppression maintenance monitoring stable for 6wk. Avoid live vaccines Then monthly ! If allopurinol is co-prescribed, d dose to 25% of the original Ciclosporin FBC and LFT monthly until Rash, gum soreness, 1.25mg/kg bd dose/monitoring stable for hirsutism, renal failure/i Cr maintenance 3mo, then every 3mo (if i by >30% from baseline, U&E, Cr/eGFR every 2wk withhold and discuss with until dose stable for 3mo, then rheumatologist), i BP monthly Monitor BP Lipids 6-monthly Hydroxychloroquine Baseline eye check and annual Rash, GI effects, ocular side 200–400mg/d check of visual symptoms and effects (rare) maintenance visual acuity Leflunomide FBC and LFT monthly for 6mo Rash, GI, i BP, i ALT 10–20mg/d then, if stable every 2mo Check weight and BP at each maintenance review ! Before starting check baseline U&E, Cr, eGFR, LFTs, FBC, and urinalysis. 9 4 494 CHAPTER 14 Musculoskeletal problems Crystal-induced arthritis Hyperuricaemia i serum uric acid. Causes: Drugs Cytotoxics; diuretics; ethambutol i cell turnover e.g. lymphoma; leukaemia; psoriasis; haemolysis d excretion Primary gout; CKD; hyperparathyroidism Disorders of purine synthesis e.g. Lesch–Nyhan syndrome GoutG Intermittent attacks of acute joint pain due to deposition of uric acid crystals. Prevalence: 3–8/1000. i with age; ♂:♀ 85:1. Risk factors: FH Acute infection Polycythaemia Obesity Surgery Leukaemia Excess alcohol CKD Diuretics High-purine diet (Table 14.10) Plaque psoriasis Cytotoxics 0 Untreated gout is associated with i risk of death, CVD, and CKD. Presentation Acute gout Painful swollen joint (distal joints, e.g. big toe, feet, and ankles, most commonly); red skin which may peel ± fever. Can be poly- articular—especially in elderly ♀. May mimic septic arthritis Chronic gout Recurrent acute attacks, tophi (urate deposits) in pinna, tendons, and joints ± joint damage Investigation Usually a clinical diagnosis. If investigations are required, con- sider: blood (i WCC; i ESR; normal or i uric acid); microscopy of synovial fluid (sodium monourate crystals on polarized light microscopy); X-ray (soft tissue swelling unless severe disease when erosive pattern). Management Figure 14.8. Refer to rheumatology if serum urate cannot be controlled with drugs available in primary care or if symptoms are not set- tling despite treatment. Calcium pyrophosphate deposition disease (CPPD) Also known as pseudogout. Inflammatory arthritis due to deposition of pyro- phosphate crystals. Associated with OA, hyperparathyroidism, and haemo- chromatosis. Attacks are less severe than gout and may be difficult to differentiate from other types of arthritis. Knee, wrist, and shoulder are most commonly affected. Acute attacks can be triggered by intercurrent illness. Chondrocalcinosis may be seen on X-ray (calcification of articular cartilage). Presence of joint crystals confirms diagnosis. Management Treat acute attacks like acute gout. A chronic form also occurs—frequently erosive. Refer to rheumatology for confirmation of diagnosis and advice on management and disease-modifying drugs. ! Septic arthritis The most important differential diagnosis for acute gout. It is most common in children