CHAPTER 1 MUSCULOSKELETAL SIGNS

1 Anterior drawer test

Anterior drawer test

Mechanism/s The ACL arises from the anterior aspect of the tibial plateau and inserts into the medial aspect of the lateral femoral condyle. It limits anterior movement of the tibia upon the femur. Loss of continuity of the ACL permits 90º inappropriate anterior movement of the tibia and thus knee joint instability. Sign value A literature review of six studies reported variable sensitivity of 27–88%, specificity of 91–99%, FIGURE 1.1 positive LR of 11.5 and negative LR of Anterior drawer test for anterior cruciate 2 ligament injury 0.5. A literature review by Solomon DH et al. of nine studies reported a sensitivity of 9–93% and specificity of 23–100%.1 Description While a positive anterior drawer With the patient lying supine, the knee sign (+LR 11.5)2 has been suggested to at 90° flexion and the foot immobilised be strong evidence of ACL injury, the by the examiner, the proximal third results are not uniform, with another of the tibia is pulled towards the study reporting a +LR 2.0 (sensitivity examiner. In a positive test, there is 83%, specificity 57%, –LR 0.3).3 A anterior (forward) movement of the negative anterior drawer sign cannot tibia without an abrupt stop.1 reliably exclude ACL injury (sensitivity Condition/s 27–88%; –LR 0.5).2 When strong clinical suspicion persists, further associated with diagnostic steps are necessary (e.g. • Anterior cruciate ligament (ACL) interval re-examination, MRI, injury arthroscopy). CLINICAL PEARL

2 Apley’s grind test

Apley’s grind test 1

is increased rotation relative to the unaffected side, this is suggestive of a ligamentous lesion. If rotation plus compression is more painful or there is decreased rotation relative to the unaffected side, this is suggestive of meniscal injury.4 Condition/s associated with • Meniscal injury Mechanism/s FIGURE 1.2 Direct mechanical force upon the Apley’s grind test injured meniscus elicits tenderness. Sign value A review by Hegedus EJ et al. reported Description a pooled sensitivity of 60.7% and With the patient lying prone and the specificity of 70.2% with an odds ratio knee at 90° flexion, the lower leg is of 3.4.5 Significant heterogeneity in passively internally and externally the data limits its accuracy. Overall, rotated while axial pressure is applied Apley’s grind test has limited diagnostic to the lower leg. The test is considered utility, limited supporting data and, positive if tenderness is elicited. in the acute setting, the manoeuvre The process can also be combined produces severe pain.6 with or without distraction. If rotation McMurray’s grind test has more plus distraction is more painful or there robust supporting data.

3 Apley’s scratch test

Apley’s scratch test

Condition/s associated with Common • Rotator cuff muscle injury • Labral tear • Anterior shoulder dislocation • Bicipital tendonitis • Adhesive capsulitis (frozen shoulder) • Acromioclavicular joint injury Mechanism/s The shoulder joint is a complex structure. Its components include the humeral head, glenoid fossa, acromion, clavicle, scapula and surrounding soft FIGURE 1.3 tissue structures. Under normal One of three manoeuvres of Apley’s circumstances the shoulder joint is scratch test capable of a vast range of movement. Based on Woodward T, Best TM. The painful Apley’s scratch test assesses shoulder: part 1, clinical evaluation. Am Fam Phys 2000; 61(10): 3079–3088. glenohumeral abduction, adduction, flexion, extension, internal rotation and external rotation. Tenderness or limited range of movement suggests injury to Description one or more components of the Apley’s scratch test is a general range shoulder joint. of movement assessment of the shoulder joint (i.e. glenohumeral, Sign value acromioclavicular, sternoclavicular and Apley’s scratch test is a useful scapulothoracic joints). The patient is component of the general shoulder instructed to touch the unaffected exam but has limited utility for a shoulder anteriorly and posteriorly specific diagnosis. The position of the (behind their head), and touch the shoulder at which tenderness or limited inferior scapula posteriorly (behind range of movement occurs should be their back). Tenderness and/or limited noted. In the patient with an abnormal range of movement while performing Apley’s scratch test, further diagnostic these movements is considered an manoeuvres should be performed to abnormal test.7 narrow the differential diagnosis.

4 Apparent leg length inequality (functional leg length)

Apparent leg length 1 inequality (functional leg length)

ABC

FIGURE 1.4 Measurement of leg lengths A The apparent leg length is the distance from the umbilicus to the medial malleolus; B pelvic rotation causing an apparent leg length discrepancy; C the true leg length is the distance from the anterior superior iliac spine to the medial malleolus. Based on Firestein GS, Budd RC, Harris ED et al., Kelley’s Textbook of Rheumatology, 8th edn, Philadelphia: WB Saunders, 2008: Fig 42-24. Description Ligamentous laxity A disparity between the relative The ligaments on one side (e.g. in the distance from the umbilicus to the hip joint) may be more flexible or medial malleolus of each leg.8 By longer than their counterparts, making definition it implies asymmetry of the the femur sit lower in the joint capsule. lower extremities in the absence of a Joint contracture bony abnormality. (See ‘True leg A joint contracture impairs full range length inequality’ in this chapter.) of movement. If the knee joint is contracted in a flexed position, the Condition/s length of the affected side will be less associated with than the opposite leg during maximal • Altered foot mechanics attempted extension. • Adaptive shortening of soft tissues Altered foot mechanics • Joint contractures Excessive pronation of the foot eventuates in and/or may be • Ligamentous laxity accompanied by a decreased arch • Axial malalignments height compared to the ‘normal’ foot, resulting in a functionally shorter Mechanism/s limb.8 An apparent or functional leg length inequality may occur at any point from the pelvis to the foot.8

5 Apparent leg length inequality (functional leg length)

Sign value significant effect is controversial.8 The test should be interpreted in relation The distance (anywhere from to the patient’s history and full gait 3–22 mm) at which apparent leg length assessment. inequality results in a clinically

6 Apprehension test

Apprehension test 1

• Rotator cuff muscle injury • Glenoid labrum injury • Glenoid defect (e.g. Bankart’s fracture) • Humeral head defect (e.g. Hill– Sachs fracture) Less common – atraumatic • Connective tissue disorder: Ehlers–Danlos syndrome, Marfan’s syndrome FIGURE 1.5 • Congenital absence of glenoid Apprehension test The arm is abducted and placed in an Mechanism/s externally rotated position. Note the right Glenohumeral joint instability is caused arm of the examiner is providing anterior traction on the humerus, pulling the by dysfunction of the bony and/or soft posterior part of the humeral head forward. tissue structures that maintain joint The same test can be done from the back, stability: glenoid, humeral head, joint with the patient sitting up and the examiner capsule, capsuloligamentous or pushing forward on the posterior head of glenohumeral ligaments, labrum, and the humerus. rotator cuff muscles. The shoulder joint is susceptible to instability due to its inherent mobility and complex soft Description tissue structures responsible for stability. The apprehension test is an assessment In the apprehension test, the joint is of glenohumeral joint instability. With placed into a position vulnerable to the patient sitting or lying supine, the instability. It is the typical position shoulder is placed into 90° abduction, precipitating traumatic anterior 90° external rotation and 90° elbow shoulder dislocation. For this reason, a flexion. The examiner applies pressure significant number of healthy patients to the posterior aspect of the proximal will experience apprehension during humerus and attempts to move the this manoeuvre. humeral head anteriorly (see Figure 1.5). The test is positive if the Sign value patient experiences apprehension due to T’Jonck L et al. reported a sensitivity impending subluxation or dislocation of 88.0%, specificity of 50%, positive of the glenohumeral joint.9 likelihood ratio of 1.8 and negative likelihood ratio of 0.23.10 Condition/s The apprehension test for associated with glenohumeral joint instability is a moderately useful screening test. Based More common on available data, the test has limited – traumatic utility to rule in the diagnosis. It is not • Recurrent glenohumeral joint used in the setting of acute anterior subluxation or dislocation shoulder dislocation. 7 Apprehension–relocation test (Fowler’s sign)

Apprehension–relocation test (Fowler’s sign)

• Glenoid labrum injury • Glenoid defect (e.g. Bankart’s fracture) • Humeral head defect (e.g. Hill– Sachs fracture) Less common – atraumatic • Connective tissue disorder: FIGURE 1.6 Ehlers–Danlos syndrome, Marfan’s Apprehension–relocation (Fowler) test syndrome Note that pressure is applied anteriorly to the proximal humerus. • Congenital absence of glenoid Description Mechanism/s The apprehension–relocation test is an The underlying anatomy and causes of assessment of glenohumeral joint glenohumeral joint instability are instability. The relocation manoeuvre outlined under ‘Apprehension test’ and is typically performed following the apply here. In the apprehension– apprehension test (see ‘Apprehension relocation test, symptomatic relief is test’). With the patient sitting or lying due to restoration of the normal supine, the shoulder is placed into 90° anatomical relationship of the humeral abduction, 90° external rotation and head in the glenohumeral joint. 90° elbow flexion. The examiner applies pressure to the anterior aspect Sign value of the proximal humerus and attempts T’Jonck L et al. reported a sensitivity to move the humeral head posteriorly. of 85%, specificity of 87%, positive The test is positive if the patient likelihood ratio of 6.5 and negative 10 experiences relief of apprehension (i.e. likelihood ratio of 0.18. Lo et al. no longer feels impending shoulder reported sensitivity of 32% and 11 dislocation). specificity of 100%. Speer KP et al. reported a sensitivity of 68% and Condition/s specificity of 100%.12 The apprehension–relocation test is associated with a useful screening manoeuvre for • Recurrent glenohumeral joint anterior glenohumeral joint instability. subluxation or dislocation It appears to be more specific than the • Rotator cuff muscle injury ‘apprehension test’ alone.

8 Bouchard’s and Heberden’s nodes

Bouchard’s and Heberden’s 1 nodes

Mechanism/s A number of studies have implicated bony osteophyte growth as the principal causef o Heberden’s and Bouchard’s nodes.13 Other contributing factors or theories include: • genetic predisposition • endochrondral ossification of hypertrophied cartilage as a result FIGURE 1.7 14 Prominent Heberden’s nodes of chronic osteoarthritic changes Based on Ferri FF, Ferri’s Clinical Advisor, • traction spurs growing in tendons Philadelphia: Elsevier, 2011: Fig 1-223. in response to excessive tension and repetitive strain.15 Description Sign value Bouchard’s nodes are bony outgrowths Bouchard’s or Heberden’s nodes are or nodules found over the proximal a classical sign of interphalangeal interphalangeal joints of the hands. osteoarthritis15,16 and are associated Heberden’s nodes are similar but with generalised osteoarthritis.17,18 located over the distal interphalangeal The presence of Bouchard’s and/or joints. Heberden’s nodes is predictive of the 19 Condition/s radiographic changes of osteoarthritis. associated with • Osteoarthritis • Familial

9 Boutonnière deformity

Boutonnière deformity

Central tendon slip

Lateral band

A Functional tendinous interconnections between two extensor tendons

B

FIGURE 1.8 Digital extensor mechanism A The proximal interphalangeal joint is extended by the central tendon slip (an extension of the hand’s dorsal extensor tendon); B the X is a functional representation of the fibrous interconnections between the two systems. Based on DeLee JC, Drez D, Miller MD, DeLee and Drez’s Orthopaedic Sports Medicine, 3rd edn, Philadelphia: Saunders, 2009: Fig 20B2-27.

Central tendon slip 1 3

2 4 Lateral band

1 Central tendon slip pulls off bone 2 Retracted central tendon slip pulls on lateral band 3 The lateral band, in turn, hyperextends the DIP joint 4 With no central tendon connection the PIP joint flexes, completing the full boutonnière deformity

FIGURE 1.9 Pathoanatomy of boutonnière deformity The sequence is: rupture of the central tendon slip, which then simultaneously pulls on the lateral bands, pulling the DIP joint into hyperextension and the PIP into flexion. Based on DeLee JC, Drez D, Miller MD, DeLee and Drez’s Orthopaedic Sports Medicine, 3rd edn, Philadelphia: Saunders, 2009: Fig 20B2-28.

10 Boutonnière deformity

Description Inflammatory Used to describe a deformity of the arthropathy (e.g. 1 resting finger in which the proximal rheumatoid arthritis) interphalangeal (PIP) joint is flexed and Pannus in the PIP joint (which may be the distal interphalangeal (DIP) joint is present in rheumatoid arthritis) can hyperextended. damage the central slip tendon.20 Chronic inflammation and synovitis of Condition/s the joint may result in persistent PIP associated with flexion and gradual elongation of the central slip tendon. Subsequent volar • Inflammatory arthropathy (e.g. migration of the lateral bands results in rheumatoid arthritis) the characteristic deformity.21–24 • Central slip extensor tendon injury Trauma Mechanism/s Forced flexion of an extended PIP Disruption or avulsion of the central slip joint, crush injury or penetrating injury extensor tendon and volar migration of may result in avulsion of the central the lateral bands of the extensor tendon tendon slip. Typically, the degree of mechanism result in PIP flexion and deformity increases in the days DIP extension. The sign derives its following the injury. Acutely, the name from the appearance of the deformity may be subtle. central tendon slip, which was thought to resemble a buttonhole, or boutonnière Sign value in French, when torn. A boutonnière deformity is classically The central tendon slip attaches to associated with rheumatoid arthritis the dorsal aspect of the middle phalanx. occurring in up to 50% of patients Its main function is to maintain PIP with the disease. extension and stabilise the extensor In a patient with blunt or tendon apparatus. If the central tendon penetrating trauma, the presence of a is disrupted or avulsed (torn off the boutonnière deformity should be base of the middle phalanx), the actions considered evidence of a central slip of the lateral bands and flexor extensor tendon injury. digitorum profundus are unopposed, resulting in resting PIP flexion and DIP hyperextension.

11 Bulge/wipe/stroke test

Bulge/wipe/stroke test

More common • Osteoarthritis • Rheumatoid arthritis • Haemoarthrosis – trauma, coagulopathy • Gout

A • Infection – septic arthritis, gonococcal arthritis, transient synovitis Less common • Pseudogout (calcium pyrophosphate deposition disease) • Tumour

B Mechanism/s Mechanical manipulation of excess FIGURE 1.10 fluid in the synovial joint capsule Demonstration of the bulge test for a small results in visible fluid shift. The wipe synovial knee effusion or bulge test displaces synovial fluid The medial aspect of the knee has been from one part of the synovial joint to stroked to move the synovial fluid from this area (shaded depressed area in A); B shows a another, thus suggesting the presence bulge in the previously depressed area after of a joint effusion as the cause of knee the lateral aspect of the knee has been swelling. tapped. Based on Firestein GS, Budd RC, Harris ED Sign value et al., Kelley’s Textbook of Rheumatology, Limited evidence has been gathered on 8th edn, Philadelphia: WB Saunders, 2008: Figs 35-9A and B. the value of this test as an individual sign. Some authors report that this test Description may pick up on as little as 4–8 mL of The bulge, wipe or stroke test is used to swelling.25 An effusion in the absence assess for knee joint effusion. With the of acute traumatic injury or systemic patient supine and their knee extended, disease is most commonly due to the examiner ‘swipes’ the medial aspect osteoarthritis.26 of the knee joint to displace fluid into Gogust F e al.27 reported the wipe the superolateral aspect of the synovial test as having a sensitivity of 11–33% compartment, and then swipes the and specificity of 66–92% for lateral side looking for a visible fluid identifying the presence of a knee shift. The test is positive if the examiner effusion. Emphasis should be placed sees a wave of fluid. upon identifying a joint effusion in the setting of septic arthritis, an Condition/s orthopaedic emergency. associated with Any condition causing a knee effusion.

12 Butterfly rash (malar rash)

Butterfly rash (malar rash) 1

Mechanism/s The exact mechanism is unclear. However, like the underlying disorder in SLE, it is thought to result from an autoimmune reaction caused by genetic, environmental and immunological factors. Factors shown to be involved include:28 • A genetic predisposition to ineffective or deficient complement, leading to a failure to clear immune complexes of apoptotic cells, which in turn increases the chance of the development of autoimmunity. • Sunlight has been shown to damage and/or induce apoptosis of keratinocyte proteins in the epidermis and can stimulate autoantibody production. Sunlight FIGURE 1.11 may also increase the chance of Malar rash of SLE keratinocytes being destroyed by Reproduced, with permission, from Goldman L, complement and antibody- Ausiello D, Cecil Medicine, 23rd edn, dependent mechanisms. Philadelphia: Saunders, 2007: Fig 287-3. • Altered cellular and humoral immunity reactions have been seen Description in studies reviewing cutaneous A red or purple, macular, mildly scaly manifestations of lupus. rash that is seen over the bridge of the It is likely that a combination of nose and cheeks. The shape of the rash these factors leads to immune can somewhat resemble a butterfly. deposition in the skin, damage, The rash spares the nasolabial folds, oedema and the characteristic malar which helps distinguish it from other rash. rashes (e.g. rosacea). It is also photosensitive. Condition/s associated with Common • Systemic lupus erythematosus (SLE) • Drug-induced lupus erythematosus • Dermatomyositis

13 Butterfly rash (malar rash)

Genetic Altered cellular and Environment predisposition humoral immunity

Deficiency in Sunlight complement Keratinocyte damage/proteins Failure to clear Inflammatory cytokine cells of production and complement autoantigen exposure

Increased Increased auto- chance of auto- antibody immunity production

Autoimmune reaction and complex deposition – damage to collagen and blood vessels

Malar and other cutaneous rashes in SLE

FIGURE 1.12 Mechanism of malar rash

Sign value The malar rash is seen in approximately 40% of patients with SLE.28 It has a sensitivity of 57% and specificity of 96% for SLE.14 Its absence does not exclude the diagnosis.

14 Calcinosis/calcinosis cutis

Calcinosis/calcinosis cutis 1

» Systemic sclerosis » Burns • Metastatic » Due to hypercalcaemia or hyperphosphataemia of any cause » Chronic renal failure – most common » Excess vitamin D » Primary hyperparathyroidism – rare » Paraneoplastic hypercalcaemia » Destructive bone disease (e.g. Paget’s disease) • Iatrogenic » Calcium gluconate injections FIGURE 1.13 » Tumour lysis syndrome Calcinosis • Idiopathic Hard, whitish nodules of the digit representing dystrophic calcinosis in this • Calciphylaxis patient with dermatomyositis. » End-stage renal disease Reproduced, with permission, from James WD, » Altered calcium metabolism Berger T, Elston D, Andrews’ Diseases of the Skin: Clinical Dermatology, 11th edn, Philadelphia: Saunders, 2011: Fig 26-12. Mechanism/s Dystrophic calcinosis Dystrophic calcinosis occurs when Description crystals of calcium phosphate or Calcinosis refers to the formation or hydroxyapatite are deposited in the skin deposition of calcium in soft tissue. secondary to inflammation, tissue damage Calcinosis cutis more specifically refers to and degeneration.30 Calcium and calcium deposits in the skin. phosphate levels are usually normal. Condition/s Proposed mechanisms include: • High local levels of alkaline associated with phosphatase break down a Conditions associated with calcinosis pyrophosphate that normally may be classified as dystrophic, inhibits calcification.31 metastatic, iatrogenic, idiopathic or calciphylaxis. • Tissue breakdown may lead to denatured proteins that bind to • Dystrophic calcinosis phosphate. These phosphate– » Scleroderma protein compounds may react with » Dermatomyositis calcium and thus provide a nidus » SLE for calcification.32

15 Calcinosis/calcinosis cutis

Metastatic calcinosis • Vitamin D deficiency owing to Abnormal calcium or phosphate renal failure worsens initial metabolism with high levels of hypocalcaemia and, therefore, either or both is present. Excess further stimulates secondary calcium and/or phosphate allows for hyperparathyroidism. the formation and precipitation of Iatrogenic calcium salts. Intravenous administration of calcium In chronic renal failure a number of or phosphate may cause local mechanisms lead to altered phosphate extravasation and precipitation of and calcium metabolism: hydroxyapatite in surrounding tissue. • Decreased renal excretion Inflammation of the surrounding tissue of phosphate leads to secondary to the injection may also hyperphosphataemia. cause calcium and protein release, • Hyperphosphataemia results in a contributing to precipitation. compensatory rise in parathyroid Idiopathic hormone (PTH) in an attempt to Occurs in the absence of tissue injury excrete phosphate. The rise in or systemic metabolic disturbance. PTH results in an increase in phosphate absorption from the gut Sign value and also mobilises calcium from the There is very limited evidence on this bones, resulting in more calcium sign and it is rarely seen in isolation. being available to precipitate with If identified, further investigation is phosphate. warranted.

16 Charcot foot

Charcot foot 1

A C

Achilles Achilles

Normal

Calcaneal pitch Loss of B calcaneal pitch

FIGURE 1.14 Charcot foot A, B The classic rocker-bottom Charcot foot, with collapse and then reversal of the longitudinal arch; C loss of the normal calcaneal pitch, or angle relative to the floor, in patients with Charcot collapse of the arch. Reproduced, with permission, from Mann JA, Ross SD, Chou LB, Chapter 9: Foot and ankle surgery. In: Skinner HB, Current Diagnosis & Treatment in Orthopedics, 4th edn, Fig 9-8. Available: http://proxy14.use.hcn.com.au/content.aspx?aID=2321540 [10 Mar 2011].

Description when mobilising. This leads to a A progressive destructive arthropathy of destructive cycle of continued loading 33 on the injured foot and progressive the ankle and foot. In its early stages, 34 it may present as unilateral foot oedema damage. following minor trauma. In advanced Under the inflammatory theory, disease, significant destruction of bones when the same local insult occurs and joints may occur (particularly in (microfracture, subluxation or fracture), the midfoot), resulting in collapse of inflammatory cytokines are released, the plantar arch and development of including TNF-α and interleukin-1β. ‘rocker-bottom foot’. These two cytokines have been shown to increase activation of RANK ligand Condition/s (RANKL), which in turn increases the transcription factor nuclear factor-κB associated with (NF-κB). The net result of this is Conditions resulting in sensory stimulation of the maturation of osteoclasts, neuropathy: which further eat away at bone. This • Diabetes mellitus – most common predisposes the patient to engage in • Syphilis – original description by another vicious cycle of further Charcot fractures, inflammation, abnormal PEARL CLINICAL weight loading and osteolysis.34 Mechanism/s Regardless of underlying In neurotraumatic theory, peripheral contributing factors, the RANKL/ neuropathy caused by diabetes leads to OPG (osteoprotegerin) pathway is decreased pain sensation and impaired thought to be a common denominator. proprioception. Thus, if an acute injury RANKL is a member of the tumour occurs (e.g. microfracture, subluxation necrosis factor (TNF) superfamily, and or fracture), the patient feels little or OPGe is th competitive protein of no pain and does not ‘guard’ the foot RANKL. The process of bone

17 Charcot foot

Trauma Neuropathy osteopenia due to unrestricted RANKL activity.35 Abnormal Other contributing factors include: loading • Sympathetic denervation in distal Increased limbs leads to increased peripheral force blood flow – hyperaemia and more inflammation.36 Dislocation Fracture • Pre-existing osteopaenia has been seen in both type 1 and type 2 diabetes via a number of Osteopenia Pro-inflammatory mechanisms,36 and this predisposes cytokines the diabetic patient to (TNF- , interleukin-1 ) α β microfracture. Osteoclastogenesis • Abnormal loading mechanics. RANKL » Oxidative stress and the NF-κB Inflammation formation of reactive oxidant species (ROS) with local FIGURE 1.15 dysregulation of Simplified inflammatory and neurotraumatic immunoinflammatory mechanisms of Charcot foot processes. Based on Jeffcoate WJ, Game F, Cavanagh PR, » AGE/RAGE pathway − Lancet 2005; 366: 2058–2061. hyperglycaemia generates AGEs. These promote change resorption and formation is controlled in both intra- and bye th level of RANKL and OPG, and extracellular proteins, which many factors contribute to this become defective and lose pathway. functionality. Binding of AGE RANKL has been shown to to receptors for AGE (RAGE) accelerates ROS production, mediate osteolysis in Charcot foot by activating NF-κB. An increase stimulating osteoclastic differentiation in AGE-modified collagen of monocytes/macrophages and has been shown to affect triggering the synthesis of nuclear osteoblastic cell differentiation factor-κβ (NF-κβ), spurring and function in vitro. This may maturation. play a role in the pathogenesis Hyperglycaemia can increase the of osteopaenia, which is level of advanced glycation end present in patients with poorly products (AGEs), reactive oxygen controlled diabetes. species (ROS), and oxidised lipids, » PI3 kinase pathway − PI3 which may all enhance the expression kinase normally impedes of RANKL in diabetes. inflammation via enhanced The pro-inflammatory state nitric oxide (NO) production. NO may cause apoptosis of increases cytokine expression (TNF- , α osteoclast progenitors as well IL-1β and IL-6), which may also as inhibit the resorptive action increase RANKL. Diabetic neuropathy of mature osteoclasts. The PI3 is associated with exhaustion of kinase and NO pathway may calcitonin gene-related peptide be compromised in diabetes. (CGRP) stores from C and Aδ nerve » Altered Wnt/β-catenin fibres. The deficiency of CGRP may pathway (an important bone further accelerate underlying anabolic pathway).

18 Charcot foot

Hyperglycemia 1 AGE/RAGE ↑, PKC ↑, PI3 kinase ↓ Neuropathy

NO ↓ Osteoblast ↓ ROS ↑ Repetitive trauma CGRP ↓ Blood flow ↑

BMD ↓ oxPTM ↑ TNF-α, IL-1β, IL-6 ↑ BMD ↓

Inflammation IL-4 ↓ FLS activated RANKL/OPG ↑ IL-10 ↓ OPG ↓ MMPs↑ Activated osteoclast ↑ NO ↓

Joint destruction Osteolysis Osteoclasts ↑ Monocytes ↑

Acute DNOAP DKK-1, Wnt-1 ↓ sclerostin ↓ Osteolysis/ligaments injury Inflammation

trauma neuropathy persistent hyperglycemia neuropathy Fracture/dislocation Repetitive trauma

Deformity neuropathy stable Chronic DNOAP oxPTM: oxidative post-translational modifications BMD: bone mineral density FLS: fibroblast-like synoviocytes MMPs: matrix metalloproteinases DNOAP: diabetic neuropathic osteoarthropathy

FIGURE 1.16 Detailed mechanism behind the development of Charcot foot From Zhao H-M, Diao J-Y, Liang X-J et al. Pathogenesis and potential relative risk factors of diabetic neuropathic osteoarthropathy. Journal of Orthopaedic Surgery and Research 2017; 12: 142.

» Altered fibroblast-like The presence of foot pain, heat and/ synoviocytes (FLS). or swelling in the diabetic patient needs » OPG genetic polymorphisms.35 immediate attention including referral to diabetic/high-risk foot clinics or Sign value orthopaedic and diabetic specialist Patients with Charcot foot are at higher services. risk of diabetic foot ulcers (affecting up to 50% of patients)37,38 and amputation.36

19 Crepitus

Crepitus

Description the articular cartilage of the joint surfaces occurs, creating erosions and Grating, crunching, popping or irregularity. Two rough surfaces crackling sounds heard and/or felt over moving against each other produce joints during passive range of motion crepitus. examination. In rheumatoid arthritis, the Condition/s autoimmune response and subsequent inflammation, cytokine release and associated with pannus formation cause destruction of • Arthropathy cartilage. » Osteoarthritis In osteoarthritis, repetitive strain » Rheumatoid arthritis with loss of glycosaminoglycans and activation of matrix metalloproteinases • Trauma (MMPs) is principally responsible for » Cartilaginous injury – damage. meniscal injury, labral injury » Ligamentous injury – anterior Sign value cruciate ligament Altman R et al. reported crepitus had a » Fracture sensitivity of 89%, specificity of 58%, positive likelihood ratio of 3.0 and General negative likelihood ratio of 0.2 for mechanism/s predicting osteoarthritis of the knee.39 Crepitus of the joints is caused when Crepitus is common in patients with two rough surfaces grind against one another. osteoarthritis. Crepitus alone has limited diagnostic value, due to its Rheumatoid/osteoarthritis presence in other common disease In both rheumatoid arthritis and states. osteoarthritis arthritis, degeneration of

20 Dropped arm test

Dropped arm test 1

FIGURE 1.17 Dropped arm test Based on Multimedia Group LLC, Occupation Orthopedics. Available: http://www.eorthopod.com/ eorthopodV2/index.php?ID=7244790ddace6ee8ea5da6f0a57f8b45&disp_type=topic_detail&area =6&topic_id=4357b9903d317fcb3ff32f72b24cb6b6 [28 Feb 2011].

Description responsible for the first 15° of motion. The deltoid muscle is responsible for With the patient upright, the examiner movement beyond 15°.40 Therefore, if a passively moves the patient’s arm to rotator cuff tear (e.g. supraspinatus 90° of abduction. Then the patient is muscle tear) or subacromial asked to slowly lower the arm to the impingement is present, the ability of anatomical position. A positive test the arm to maintain abduction is occurs if the patient is unable to impaired. perform the action due to pain or if the arm just ‘drops’ to the side. Sign value Condition/s Murrell GAC et al. and Dinnes J et al. reported a sensitivity of 10% and associated with specificity of 98%, and a calculated • Rotator cuff muscle injury (e.g. positive likelihood ratio greater than 10 supraspinatus muscle) for rotator muscle tear.41,42 Park HB • Subacromial impingement et al. reported a sensitivity of 27%, • Neurogenic weakness specificity of 88%, positive likelihood ratio of 2.3 and negative likelihood • Suprascapular nerve palsy ratio of 0.8 for subacromial • Axillary nerve palsy impingement.43 • C5 radiculopathy When positive, the dropped arm test significantly increases the probability of Mechanism/s rotator cuff muscle tear (supraspinatus Abduction of the arm from 0° to 90° is muscle tear) or subacromial dependent upon the supraspinatus and impingement. A negative test does not deltoid muscles. The supraspinatus is reliably exclude the diagnosis.

21 Eichhoff’s test

Eichhoff’s test

contents of the first extensor synovial compartment: the tendons of abductor pollicis longus and extensor pollicis brevis. Repetitive strain injury or inflammatory disorders cause inflammation, leading to swelling over the radial aspect of the wrist. This narrows the space that the abductor pollicis longus and extensor pollicis brevis pass through on their way to FIGURE 1.18 the hand. Eichhoff’s test This manoeuvre and Finkelstein’s test involve generation of a passive distension and shear stress between the tendons and radius on its blunt styloid Description edge. In essence, the abductor pollicis The patient places their thumb within longus and extensor pollicis brevis the palm of the examiner’s hand, who tendons are moved into the narrowed grasps it tightly. The hand is then compartment and stretched, causing abducted towards the ulna by the pain. examiner (see Figure 1.18). Sign value Condition/s There is limited data on the evidence associated with of Eichhoff’s test’s diagnostic accuracy • De Quervain’s tenosynovitis in diagnosing de Quervain’s tenosynovitis. One small study Mechanism/s suggested Eichhoff’s test was associated De Quervain’s tenosynovitis is with more false positives than an inflammatory condition of the Finkelstein’s test.44

22 Finkelstein’s test

Finkelstein’s test 1

radial aspect of the wrist (at the abductor pollicis longus tendon or extensor pollicis brevis tendon) is considered a positive test result. Condition/s associated with • De Quervain’s tenosynovitis Mechanism/s De Quervain’s tenosynovitis is an inflammatory condition of the contents of the 1st extensor synovial compartment: abductor pollicis longus and extensor pollicis brevis tendons. Repetitive strain injury or inflammatory disorders cause inflammation that, in turn, causes swelling over the radial aspect of the wrist. This narrows the space through FIGURE 1.19 which the abductor pollicis longus and Finkelstein’s test extensor pollicis brevis pass on their With the thumb inside the hand, the wrist is ulnarly deviated. Pain indicates a positive way to the hand. When performing test. this manoeuvre, the abductor pollicis Based on Frontera WR, Silver JK, Rizzo Jr longus and extensor pollicis brevis TD, Essentials of Physical Medicine and tendons are moved into the narrowed Rehabilitation, 2nd edn, Philadelphia: compartment and stretched, causing Saunders, 2008: Fig 24-2. pain.45 Sign value Description There is limited data on the evidence The examiner applies force at the for Finkelstein’s test in diagnosing De patient’s thumb metacarpal, placing Quervain’s tenosynovitis. De the wrist into forced ulnar deviation. Quervain’s tenosynovitis is a clinical Tenderness with the manoeuvre at the diagnosis.

23 Gottron’s papules

Gottron’s papules

Description Violaceous (violet-coloured) papular rash on the dorsal aspect of the interphalangeal joints.46 Condition/s associated with • Dermatomyositis Mechanism/s One histological study47 demonstrated lymphocytic infiltration, epidermal atrophy and vacuoles in the basal layer of the skin, in addition to other findings. The mechanism is unknown. Sign value Gottron’s papules are said to be pathognomonic for dermatomyositis; however, they are not present in all FIGURE 1.20 patients with the disease.48 Gottron’s papules Found over bony prominences: fingers, elbows and knees. The lesions are slightly elevated, violaceous papules with slight scale. Reproduced, with permission, from Habif TP, Clinical Dermatology, 5th edn, Philadelphia: Mosby, 2009: Figs 17-20, 17-21. CLINICAL PEARL

24 Hawkins’ impingement test

Hawkins’ impingement test 1

Clavicle Acromion Bursa Glenoid Rotator cuff Scapula

Humerus

FIGURE 1.21 Hawkins’ test anatomy

FIGURE 1.22 Hawkins’ test

Description Mechanism/s With the patient upright, shoulder and The tendons of the rotator cuff muscles elbow both flexed to 90°, the examiner pass through a narrow space between internally rotates the shoulder joint. the acromion process of the scapula, The sign is positive if tenderness is bursa and the head of the humerus. elicited (see Figure 1.22). Hawkins’ impingement test exacerbates narrowing in the coracoacromial space Condition/s and will worsen pre-existing impingement of the tendons and associated with muscles when present. The position • Rotator cuff muscle impingement advances the greater tuberosity towards – supraspinatus, teres minor, or against the coracoacromial ligament. infraspinatus muscles This manoeuvre will also elicit • Rotator cuff tendonitis tenderness when rotator cuff tendonitis

25 Hawkins’ impingement test

is present, due to mechanical forces or A pooled analysis of 1029 patients compression on the injured tendon or across six studies by Alqunaee M muscle.49 et al.52 reported a sensitivity of 74% and specificity of only 57%. Given Sign value these results, the test is of little value to Calis M et al. reported a sensitivity of the examiner, while a negative test has 92% and a specificity of 26–44% for moderate utility. Further physical identifying rotator cuff tendonitis.50 examination and imaging should be Macdonald PB et al. reported a used to confirm the diagnosis. sensitivity of 83% and a specificity of 51% for NLR of 0.3 for rotator cuff tear.51

26 Heliotrope rash

Heliotrope rash 1

Condition/s associated with • Dermatomyositis • Paraneoplastic syndrome Mechanism/s The mechanism is unknown but thought to be autoimmune in origin. Skin lesions demonstrate perivascular CD4 positive T-cell infiltration in the FIGURE 1.23 dermis.53 Heliotrope eruption seen in dermatomyositis Sign value Reproduced, with permission, from Firestein GS, Occurring in up to 83% of cases Budd RC, Harris ED et al., Kelley’s 54 Textbook of Rheumatology, 8th edn, in a specific European region, the Philadelphia: WB Saunders, 2008: Fig 47-10. heliotrope rash is thought to be pathognomonic of dermatomyositis and should trigger further investigation. Description Skin changes associated with Usually described as a macular, dermatomyositis may precede muscle confluent, purple or violaceous rash weakness, EMG abnormalities and over both eyelids and periorbital tissue. elevations in creatinine phosphokinase It can present with or without oedema. by weeks or months. CLINICAL PEARL CLINICAL

27 Kyphosis

Kyphosis

Normal spine Kyphotic spine Mechanism/s Narrowing of the anterior aspect of the vertebral body is common in most forms of kyphosis. Osteoporosis/degenerative joint disease In degenerative or osteoporotic kyphosis, poor posture, mechanical straining and osteoporosis result in degeneration and/or compression fractures of the vertebrae. There is a relative loss of height of the anterior aspect of the vertebral body, leading to increased thoracic kyphosis. Congenital kyphosis Congenital kyphosis results from either a failure of formation or a failure of FIGURE 1.24 segmentation of the vertebral body The normal and kyphotic spines elements.55 In failure of segmentation, Note the prominent convexity of the the anterior part of the vertebral body kyphotic spine. fails to separate from the vertebral body below, resulting in anterior fusion of the anterior aspect of the vertebrae. Description The posterior aspect continues to grow, Abnormally pronounced convex resulting in kyphosis.55 curvature of the thoracic spine as seen from the side. Kyphosis may be visible Scheuermann kyphosis Scheuermann kyphosis is a form of from any direction when severe. Often adolescent kyphosis. The mechanism referred to in elderly females as the behind Scheuermann kyphosis is ‘dowager’s hump’. multifactorial,56 including: Condition/s • herniation of vertebral disc material associated with into the vertebral body, causing decreased vertebral height and More common increased pressure anteriorly, • Osteoporosis/degenerative joint leading to abnormal growth and disease wedging of the vertebrae • Traumatic – vertebral body fracture • a thickened anterior ligament Less common • abnormal collagen matrix. • Ankylosing spondylitis • Congenital • Scheuermann kyphosis

28 Kyphosis

Sign value untreated. Acute worsening in the degree of kyphosis in an elderly patient Kyphosis in paediatric patients may be should prompt consideration of 1 suggestive of congenital kyphosis, pathological fracture. which can have serious complications and lead to significant disability if left

29 Lachman’s test

Lachman’s test

Mechanism/s The ACL arises from the anterior aspect of the tibial plateau and inserts into the medial aspect of the lateral femoral condyle. It limits anterior movement of the tibia on the femur. If the ACL is intact, the tibia should not have significant forward movement; if it is ruptured, there will be inappropriate anterior movement of the FIGURE 1.25 Lachman’s test of the anterior cruciate tibia and knee joint instability. ligament (ACL) With 20–30° knee flexion, the tibia is Sign value moved forward on the femur to test the A review by McGee of five studies integrity of the ACL. reported a sensitivity of 48–96%, a specificity of 90–99%, a positive likelihood ratio of 17.0 and a negative likelihood ratio of 0.2.2 A positive Lachman’s test is strongly Description 2 predictive of ACL injury (+LR 17.0). The patient lies supine with the knee In a patient with a high clinical at 20–30° flexion. The examiner suspicion of ACL injury despite a immobilises the femur just above the negative Lachman’s test (–LR 0.2),2 knee with one hand and attempts to further evaluation is necessary (e.g. pull the proximal tibia anteriorly with interval re-examination, MRI). In the other hand; the thumb is placed general, Lachman’s test is considered upon the tibial tuberosity. The test is the better examination manoeuvre for positive if there is anterior movement ACL injury when compared with the of the tibia without an abrupt stop. anterior drawer sign and pivot-shift Condition/s test.57 A more recent systematic review of six studies found a sensitivity of associated with 81–89%, specificity of 91–100%, with • Anterior cruciate ligament (ACL) a +LR of up to 42, but with wide injury confidence intervals.58 CLINICAL PEARL

30 Livedo reticularis

Livedo reticularis 1

Less common • Secondary LR Present in numerous disorders including: • Hypercoagulable state » Antiphospholipid syndrome » Cryoglobulinaemia » Multiple myeloma » DVT • Microangiopathy/microangiopathic haemolytic anaemia (MAHA) » Thrombotic/thrombocytopenic purpura (TTP) » Haemolytic uraemic syndrome » Disseminated intravascular coagulation • Vasculitis/arteriopathy » Snedden’s syndrome » Calciphylaxis • Connective tissue disorders (e.g. SLE, dermatomyositis) FIGURE 1.26 • Embolisation (e.g. cholesterol Livedo reticularis – a net-like pattern, often erythematous or violaceous in colour embolisation syndrome) Reproduced, with permission, from Floege J et al., • Drug side effect Comprehensive Clinical Nephrology, 4th » Amantadine edn, Philadelphia: Saunders, 2010: Fig 64-13. » Quinine General Description A macular, bluish/purple discolouration mechanism/s Arterioles arising from the dermis of the skin that has a lacy or net-like divide to form a capillary bed. These appearance.

capillaries then drain into the venules PEARL CLINICAL Condition/s of the venous plexus. Livedo reticularis results from increased visibility of the associated with venules of the skin. Venodilatation of More common superficial venules and deoxygenation of blood in the plexus are two main • Primary or idiopathic livedo factors.59 reticularis (LR) In general, venodilatation is caused • Hypothermia by altered autonomic nervous system • Elderly function, circulating factors that cause

31 Livedo reticularis venodilatation or in response to local Hypothermia (autonomic hypoxia. Venodilatation results in nervous system) engorged venules, making them larger The normal physiological response to and thus easier to see through the skin. hypothermia is arteriolar vasospasm. Deoxygenation is principally caused This decreases arteriolar blood flow, 59 by decreased cutaneous perfusion, local tissue hypoxia and venous plexus which can be the result of decreased dilatation. arteriolar inflow60 or decreased venous outflow. These are caused by: Elderly The previous mechanisms apply to • decreased arteriolar inflow – vasospasm elderly patients, but with the added due to cold, autonomic nervous element of thinning of the skin that system activity, arterial thrombosis occurs with old age. This delicate and or increased blood viscosity relatively translucent skin makes it • decreased venous outflow – venous more likely that the venous plexus will thrombosis, increased blood be visible. viscosity. Anti-phospholipid Primary or idiopathic syndrome livedo reticularis Anti-phospholipid syndrome is LR without the presence of underlying associated with arterial and venous disease or hypothermia is associated thrombosis, resulting in increased with spontaneous arteriolar vasospasm, tissue hypoxia and venule dilatation which decreases oxygenated blood (due to venous stasis). inflow, causing tissue hypoxia and increased deoxygenation of venous blood.61

Underlying condition: e.g. anti-phospholipid syndrome, polycythaemia DVT, infection, ANS dysfunction, cryoglobulinaemia etc.

Arterial thrombosis or vasospasm ANS decreased arteriolar inflow dysfunction Local hypoxia Venous thrombosis Circulating decreased venous outflow venodilators

Venodilatation Deoxygenation of RBCs

Engorged and enlarged venous plexus + discoloured deoxygenated blood

Livedo reticularis

FIGURE 1.27 Mechanism of livedo reticularis

32 Livedo reticularis

Amantadine Sign value This is an antiviral and anti-Parkinson’s Primary or idiopathic LR is a diagnosis 1 medication. Its involvement in LR is of exclusion; a secondary cause should thought to be related to a combination be sought. of catecholamine-induced vasospasm • LR has been shown to have a and the effects of amantadine on significant relationship with N-methyl-D aspartic acid receptors in anti-phospholipid syndrome, with the skin. up to 40% of patients presenting Cryoglobulinaemia with LR as the first sign.62 Cryoglobulins are proteins that become • Livedo reticularis in a patient with insoluble and precipitate when the SLE is associated with the temperature drops. Increasing viscosity development of neuropsychiatric results in stasis and tissue hypoxia. symptoms. In addition, cryoglobulinaemia is associated with microvascular thrombosis.

33 McMurray’s test

McMurray’s test

summary of the value of a number of tests and history is provided in Table 1.1. Condition/s associated with • Meniscal injury Mechanism/s By extending the flexed knee while applying external or internal rotation of the leg, the femoral condyle is moved over the tibia and meniscus. Crepitus will be present when the femur moves FIGURE 1.28 over the torn meniscal fragment. McMurray’s test Sign value Description In a review of two studies McGee This test begins with the patient lying reported a sensitivity of 17–29%, a supine and knee flexed to 90°. The specificity of 96–98%, a positive medial meniscus is palpated with one likelihood ratio of 8.0 and a negative hand on the posteromedial edge of the likelihood ratio of 0.2 for detecting joint, while the other hand holds the meniscal injury.2 In a meta-analysis ankle and performs external rotation. Scholten RJPM et al. reported a The lateral meniscus is assessed with one sensitivity of 10–63% and specificity of hand over the posterolateral aspect of 57–98%.63 the joint while the leg is internally In the setting of acute knee joint rotated. The test is positive if ‘clunking’ injury this manoeuvre is often very is felt as the meniscal fragment is painful. These patients are often moved against the femur. instructed to rest, ice, elevate and Physical examination of knee immobilise the affected knee, and pathology can be challenging, especially return at a later date for repeat in the presence of acute pain. A examination.

34 McMurray’s test

TABLE 1.1 116 Key physical examination tests for knee pathology versus MRI 1 Test Joint line Location Thessaly McMurray’s Apley’s tenderness test test test test Sensitivity 0.62 (0.52 to 0.63 (0.53 to 0.72) 0.43 (0.34 0.83 (0.75 to 0.71) to 0.52) 0.89) Specificity 0.55 (0.44 to 0.63 (0.53 to 0.73) 0.72 (0.61 0.39 (0.29 to 0.66) to 0.80) 0.49) LR+ 1.38 (1.05 to 1.72 (1.26 to 2.33) 1.52 (1.04 1.36 (1.14 to 1.62) 1.81) to 2.21) LR– 0.69 (0.51 to 0.50 (0.44 to 0.78) 0.80 (0.65 0.44 (0.28 to 0.93) to 0.97) 0.69) OR 2.00 (1.14 to 2.93 (1.66 to 5.19) 1.91 (1.08 3.08 (1.67 to 3.50) to 3.38) 5.67) PPV 0.55 (0.46 to 0.57 (0.48 to 0.66) 0.59 (0.48 0.50 (0.43 to 0.64) to 0.69) 0.57) NPV 0.52 (0.41 to 0.57 (0.47 to 0.67) 0.49 (0.41 0.64 (0.51 to 0.62) to 0.58) 0.76) LR– = likelihood ratio for negative test; LR+ = likelihood ratio for positive test; OR = odds ratio. p-values are based on a chi-squared distribution to assess whether or not the sensitivities, specificities, PPV or NPV are equal along the four physical tests and clinical history.

35 Neer’s impingement test

Neer’s impingement test

FIGURE 1.29 Neer’s impingement test Description the proximal humerus. Narrowing of this space due to abnormalities of the The patient’s shoulder is placed into acromion, acquired weakness in the 90° flexion and internal rotation, with posterior rotator cuff muscles the elbow in full extension. The (supraspinatus, infraspinatus, teres examiner then stabilises the scapula minor), or muscle hypertrophy in with one hand and passively moves the overuse, may cause impingement and shoulder joint to 180° flexion with the inflammation. other hand. If tenderness is elicited at In Neer’s test, passive shoulder the anterolateral aspect of the shoulder flexion from 90° to 180° exacerbates joint, the test is positive. underlying narrowing of the passage Condition/s made up by the acromion, coracoacromial ligament and humeral associated with head, resulting in compression of its • Rotator cuff impingement/ contents (i.e. the supraspinatus and tendonitis infraspinatus tendons). » Supraspinatus » Infraspinatus Sign value • Subacromial bursitis Calis M et al. reported a sensitivity of 88.7%, a specificity of 30.5%, a Mechanism/s positive predictive value of 75.9% and The supraspinatus tendon and a negative predictive value of 52.3%.50 infraspinatus tendon transverse a Macdonald PB et al. reported a narrow passage between the acromion, sensitivity of 75%, a specificity of coracoacromial ligament and the 47.5%, a positive predictive value of humeral head before they insert into 36% and a negative predictive value

36 Neer’s impingement test

of 82.9% for the test to identify Neer’s impingement test is patients with subacromial bursitis. somewhat useful to exclude rotator cuff The same study reported a sensitivity tendon impingement with a negative 1 of 83.3%, a specificity of 50.8%, a test. The test has limited potential to positive predictive value of 40.0% and identify patients with rotator cuff a negative predictive value of 88.6% for impingement, because many painful the test to identify patients with rotator shoulder conditions may result in a cuff tendon impingement.51 ‘positive’ test.

37 Patellar apprehension test

Patellar apprehension test

Condition/s associated with • Patellofemoral instability Mechanism/s The patella normally rests in the patellofemoral groove, sliding up and down through this groove during knee flexion and extension. It is kept in place by the quadriceps tendon and patellar ligament, as well as other supporting structures. If these structures are damaged the patella is susceptible to lateral instability. By displacing the patella laterally during attempted active knee extension, the examiner is deliberately attempting to displace the patella out of the groove to assess for patellofemoral instability. FIGURE 1.30 Patellar apprehension test The patient experiences a sensation of the Sign value patella dislocating as a lateral force is applied There is limited evidence supporting to the medial edge of the patella with the the use of this test. One small study knee slightly flexed. reported a sensitivity of 39%.64 This is Reprinted, with permission, from DeLee JC, in contrast to another small study of 51 Drez D, Miller MD, DeLeed an Drez’s patients reporting a sensitivity of Orthopaedic Sports Medicine, 3rd edn, Philadelphia: Saunders, 2009: 100%, specificity of 88%, PPV 89%, Fig 22C1-5. NPV 100%, +LR 8.3 and −LR of 0 for predicting patellar instability.65 Description With the patient supine and knee slightly flexed (20–30°), the examiner applies pressure, attempting to displace the patella laterally, while the patient is instructed to straighten the knee. The test is positive if apprehension is elicited due to impending lateral patella instability/dislocation or tenderness.

38 Patellar tap

Patellar tap 1

• Gout • Infection – septic arthritis, gonococcal arthritis, transient synovitis Less common • Pseudogout (calcium pyrophosphate A deposition disease) • Tumour Mechanism/s In the setting of a moderate-to-large joint effusion, the patella is displaced anteriorly relative to the distal femur at the knee joint. Application of pressure B to the suprapatellar pouch accentuates anterior patellar displacement. When FIGURE 1.31 pushed or ‘tapped’, the patella can be Patellar tap Note that the left hand squeezes the felt to float down through the fluid and suprapatellar pouch (A), while the other collide against the distal femur. In a ‘taps’ the patella (B). normal knee, the patella and femur are in close contact and therefore cannot Description be made to click together. With the patient lying supine with the leg extended, pressure is applied over Sign value Gogust F e al. reported a sensitivity of the suprapatellar pouch, displacing 0–55% with specificity of 46–92%, synovial fluid forward towards the depending on the clinician completing patella. With the other hand the patella the examination.27 A larger study by is pushed or tapped downwards. A Kastelein M et al., looking at effusions palpable click as the patella hits the in traumatic knee injury, reported a underlying bone is a positive test. sensitivity of 83%, a specificity of Occasionally the patella will also 49%, a positive likelihood ratio of 1.6 ‘bounce’ back up to the examiner’s and a negative likelihood ratio of 0.3.66 fingers. The same study indicated that, Condition/s although the bulge test may be able to detect a smaller effusion, the patellar associated with test is more likely to be associated with Any condition causing a knee effusion: a clinically important effusion. More common The available data, limited by heterogeneity, suggests limited utility • Osteoarthritis of the patellar tap. Emphasis should be • Rheumatoid arthritis placed upon the suspected aetiology of • Haemarthrosis – trauma, a joint effusion, such as septic arthritis coagulopathy (an orthopaedic emergency).

39 Patrick’s test (FABER test)

Patrick’s test (FABER test)

Condition/s associated with Any cause of sacroiliitis including, but not limited to: More common • Osteoarthritis/degenerative joint disease • Trauma Less common • HLA-B27 spondyloarthropathy » Ankylosing spondylitis » Psoriatic arthritis » Reactive arthritis FIGURE 1.32 » Enteropathic arthritis FABER test (associated with inflammatory bowel disease) • Infectious sacroiliitis Description Mechanism/s With the patient lying supine, the Manipulation of the hip with flexion, knee is flexed to 90° and the foot abduction and external rotation results placed on the opposite knee. The in distraction of the inflamed sacroiliac flexed knee is then pushed down joint,67 thereby eliciting tenderness. by the examiner to produce external rotation of the affected hip. If Sign value tenderness is elicited in the area of Limited sound methodological studies the buttocks, the test is considered exist e for th FABER test.68 Individual positive for sacroiliitis, whereas studies, however, have reported a tenderness in the groin suggests hip sensitivity of 69–77%68–70 and a joint pathology. specificity of 100%.69 For detecting FABER is a mnemonic for the labrals tear of the hip, the FABER test movements of the hip during the test hasr poo diagnostic accuracy: (i.e. Flexion, Abduction, External sensitivity 65%, specificity 19% and Rotation). positive likelihood ratio 0.80.71

40 Phalen’s sign

Phalen’s sign 1

Description The patient puts their wrists into a position of 90° flexion and presses them into one another for 1 minute. The presence of paraesthesias and/or numbness in the distribution of the median nerve is a positive test. Condition/s associated with • Carpal tunnel syndrome (the most common causes of median nerve palsy)

FIGURE 1.33 Mechanism/s Hand placement in Phalen’s test In carpal tunnel syndrome, crowding within the carpal tunnel or repetitive strain injury results in chronic inflammation of the median nerve. When the wrist is flexed, the flexor retinaculum, which acts as a pulley on the digital flexor tendons, pulls them down onto the median nerve72 and acutely increases pressure on the nerve. This manoeuvre increases pressure within the carpal tunnel, further irritating the nerve, thus worsening neuropathic sensory abnormalities.

FIGURE 1.34 Sign value Median nerve distribution of paraesthesias D’Arcy CA et al. reported a wide in the hand range of a sensitivity of 10–91%, a specificity of 33–76%, a positive likelihood ratio of 1.1–2.1 and a negative likelihood ratio of 0.3–1.0.73 However, a more recent study, also comparing clinical tests with nerve conduction, reported a sensitivity of 74% across all severities of carpal tunnel syndrome, with a specificity of 74%. The sensitivity in identifying mild to moderate severity CTS was 92%.74

41 Posterior drawer test

Posterior drawer test

Condition/s associated with • Posterior cruciate ligament (PCL) tear Mechanism/s The PCL attaches the posterior aspect of the tibia to the lateral medial condyle (see Figure 1.36). It is a short ligament which restricts anterior movement of the femur on the tibia and posterior movement of the tibia. FIGURE 1.35 When the posterior cruciate is Performing the posterior drawer test damaged or deficient, abnormal movement is possible. The posterior drawer test is used to assess the Description integrity of the PCL. With the patient and examiner in the same position as for the anterior drawer Sign value The posterior drawer test is a useful test, the examiner pushes the lower sign, with reported sensitivity of leg posteriorly, gently moving the 90–95%, specificity of 99% and a+ LR proximal tibia backwards. If there is a of 97.8 if present.76 tear in the posterior cruciate ligament, there will be significant abnormal posterior movement with a soft endpoint (see Figure 1.35).

42 Posterior drawer test

1

Femur

Lateral Medial condyle condyle Anterior cruciate ligament Ligament of Humphry Tendon of Popliteus Ligament of Wrisberg Lateral meniscus Medial meniscus Fibular collateral Tibial collateral ligament ligament

Posterior cruciate ligament

Tibia Fibula

FIGURE 1.36 Anatomy of the knee showing posterior cruciate ligament attachments and relationships

43 Proximal weakness/proximal myopathy

Proximal weakness/proximal myopathy

TABLE 1.2 Description Mechanisms of inflammatory myopathies Proximal myopathy is a muscle disorder which results in proximal Disease Mechanism muscle group weakness (e.g. shoulder: Polymyositis T-cell (in particular pectoralis major, deltoid, biceps; CD8) and hip: gluteal, quadriceps, iliopsoas, macrophage adductor). Proximal weakness is rapidly destruction of muscle assessed by asking the patient to rise fibres from a seated position and/or perform Dermatomyositis Complement and the motion of hanging washing on a antibody destruction clothesline. A complete assessment of of microvasculature; power should be performed. the deposition of complement and Condition/s antibody complexes associated with leads to inflammation and destruction of • Inflammatory myopathy muscle fibres and » Polymyositis hence weakness » Dermatomyositis • Endocrine myopathy Mechanism/s » Hyperthyroidism – see Inflammatory myopathies Chapter 7, ‘Endocrinological Inflammatory myopathies result signs’ in immunologically mediated » Hypothyroidism – see Chapter inflammation and destruction of 7, ‘Endocrinological signs’ skeletal muscle, causing weakness » Hyperparathyroidism – see (see Table 1.2). Chapter 7, ‘Endocrinological signs’ Systemic disorders Proximal myopathy may present in a • Systemic disorders number of systemic rheumatological » Systemic lupus erythematosus disorders such as SLE and RA. It is (SLE) thought that circulating antibody » Rheumatoid arthritis complexes, deposited in tissues and/or • Genetic targeted at muscles, damage muscle » Myotonic dystrophy fibres, resulting in weakness. » Spinal muscular atrophy Sign value • Other Patients with gradual-onset progressive » Myasthenia gravis symmetric proximal muscle weakness » Polymyalgia rheumatica should be evaluated for a myopathy.

44 Psoriatic nails/psoriatic nail dystrophy

Psoriatic nails/psoriatic nail 1 dystrophy

A B

C

FIGURE 1.37 Nail dystrophic changes A Nail pitting; B onycholysis; C severe destructive change with nail loss and pustule formation. Reproduced, with permission, from Firestein GS, Budd RC, Harris ED et al., Kelley’s Textbook of Rheumatology, 8th edn, Philadelphia: WB Saunders, 2008: Fig 72-3.

Description Psoriatic nail changes refer to a number of different abnormalities seen in the nails rather than just one sign. Changes include:76 • Pittingf o the nail plate • Subungual hyperkeratosis under the nail plate • Onycholysis (nail lifting) and changes in nail shape • ‘Oil drops’ and ‘salmon patches’ • Splinter haemorrhages Condition/s associated with • Psoriasis FIGURE 1.38 ‘Oil drops’ under the nail • Psoriatic arthritis Reproduced, with permission, from Habif TP, Clinical Dermatology, 5th edn, Philadelphia: Mechanism/s Mosby, 2009: Fig 8-23. The mechanism is poorly understood. It is likely that a combination of

45 Psoriatic nails/psoriatic nail dystrophy

genetic, immunological and chronic grows, leaving a depression in the nail inflammatory changes lead to psoriatic plate.76,78 nail changes. Subungual keratosis Psoriasis is thought to be a disease Excessive proliferation of keratinocytes of abnormal immunology in which an under the nail plate leads to the atypical T-cell response occurs, part of accumulation of keratotic cells. This which results in an aberrant often leads to a raised and thickened proliferation of T cells which migrate nail plate.77 to the skin and activate and release various cytokines (e.g. IFN-γ, TNF-α Oil drops and IL-2). These cytokines induce Thought to be caused by the changes in keratinocytes and are also accumulation of neutrophils that associated with the development of the become visible through the nail plate. 77 characteristic psoriatic skin lesions. Salmon patches Focal hyperkeratosis of the nail bed and Nail pitting 76 Nail pitting is the result of multifocal altered vascularisation. abnormal nail growth. The nail matrix Splinter haemorrhages is made up of keratinocytes, which See Chapter 3, ‘Cardiovascular signs’. generate the keratin that results in production of the nail plate. As new Sign value cells are produced, the older cells are Studies report psoriatic nail changes pushed forwards and ‘grow’ the nail. may be present in up to 15–50% of In psoriatic nails, there are cases of psoriasis and have a lifetime parakeratotic cells that disrupt normal prevalence of 80–90%.79,80 Several keratinisation and nail production. studies report a higher incidence of These abnormal cells group together psoriatic nail changes (75–86%) in and then get sloughed off as the nail patients with psoriatic arthritis.81–84

46 Raynaud’s syndrome/phenomenon

Raynaud’s syndrome/ 1 phenomenon

A B

Cold exposure/stress response

Altered local Impaired Increased Other factors vascular habituation sympathetic e.g. hormonal, sensitivity function of CV and increased blood response to activation viscosity, stress endothelial damage

Imbalance of vasoconstrictors vs vasodilators

Vasoconstriction

Raynaud’s syndrome/phenomenon

FIGURE 1.39 Raynaud’s phenomenon A Sharply demarcated pallor of the distal fingers resulting from the closure of the digital arteries; B cyanosis of the fingertips. Reproduced, with permission, from Kumar V, Abbas AK, Fausto N, Aster J, Robbins and Cotran

Pathologic Basis of Disease, Professional Edition, 8th edn, Philadelphia: Saunders, 2009: PEARL CLINICAL Fig 11-28.

Description 1 white – blanching associated with Raynaud’s syndrome/phenomenon vasoconstriction of the blood occurs in the digits from various vessels stimuli, resulting in peripheral 2 blue – cyanosis hypoperfusion followed by hyperaemia. 3 red – when blood flow is restored It has three ‘colour’ phases: and hyperaemia results.

47 Raynaud’s syndrome/phenomenon

Condition/s cell membrane and interact with its ligand.89 associated with 2 Impaired habituation of the Common cardiovascular response to stress is also • Raynaud’s phenomenon thought to contribute. Habituation is the gradual Less common extinction of a response to a • Vasculitis stimulus over time. In normal » Buerger’s disease individuals, ongoing exposure to a stress results in habituation, and • Autoimmune/connective tissue decreasing incidence and duration disorders of the response.85,86 » Scleroderma (systemis 3 Local vascular factors – an imbalance sclerosis) between local vasoconstrictive » Systemic lupus erythematosus factors (endothelin, 5-HT, » CREST syndrome thromboxane [TXA] and other » Sjögren’s syndrome cyclo-oxygenase [COX] pathway » Dermatomyositis products) and vasodilatory factors 85,86 » Polymyositis (nitric oxide [NO]) may also exist in Raynaud’s syndrome. » Rheumatoid arthritis » Local endothelin may not • Drugs produce enough NO for » Beta blockers vasodilatation.86 » Repeated vasospasm causes Mechanism/s oxidative stress and reduced NO production, thus Raynaud’s syndrome occurs due to an decreasing vasodilatation.85 exaggerated vasoconstrictive response causing transient cessation of blood » Inappropriately greater production of endothelin and flow to the digits.85–88 thromboxane (TXA2) in The cause of this abnormal response to cold also occurs, vasoconstrictive response is leading to marked multifactorial: vasoconstriction.85,86 1 Increased sympathetic nerve activation » In some studies, a higher than (centrally and peripherally mediated) normal endothelin-1, a potent – in response to cold temperatures vasoconstrictor, was seen in or stressful situations, enhanced patients with primary sympathetic nerve activation Raynaud’s syndrome.86 leads to vasoconstriction of 4 Other factors. fSome o these include: the arterioles in the digits. » oestrogen – causing Larger numbers of alpha-2- sensitisation of vessels to adrenoreceptors may result vasoconstriction85,86 in more pronounced » increased blood viscosity86 85–88 vasoconstriction. The increase » decreased amounts of in alpha-2-adrenoreceptors calcitonin gene-related involves reactive oxygen species, peptide (CGRP) neurons Rho/Rho kinase and the actin – impairing normal nerve cytoskeleton. Cold can induce sensitivity, activation and Rho/Rho kinase, causing more vasodilatation86 adrenoreceptors to move to the » endothelial damage.

48 Raynaud’s syndrome/phenomenon

Secondary Raynaud’s • raised levels of angiotensin II – a syndrome vasoconstrictor 1 Structural vascular abnormalities (in • lackf o compensatory angiogenesis addition to the factors outlined above) to meet the demands of proliferated are thought to play a role in Raynaud’s intima – leading to ischaemia. phenomenon occurring secondary to an underlying disease process. Sign value In scleroderma (systemic sclerosis), Although not always associated with abnormal proliferation of intimal cells other rheumatological complaints, a results in endothelial cell damage. thorough history and examination of a Abnormal endothelial cells then patient presenting with Raynaud’s exacerbate vasospasm by:86,88 syndrome needs to be undertaken to assess for other underlying causes. It is • perturbing smooth muscle cells, said that the majority of patients with causing them to proliferate and scleroderma recall these symptoms contract many years before the onset of skin • enhancing pro-coagulant activity induration. Further, Raynaud’s and inhibitors of fibrinolysis, thus phenomenon is present in 90–99% of promoting microthrombi patients with diffuse or limited • promoting inflammation through scleroderma.90 release of adhesion factors. Other factors thought to contribute in systemic sclerosis include:86

49 Saddle nose deformity

Saddle nose deformity

• Cocaine use, complication • Congenital syphilis – rare Mechanism/s Destruction of the nasal septum or support cartilage results in the deformity. Direct trauma or prior surgery is the most common aetiology. Wegener’s granulomatosis Wegener’s granulomatosis is an autoimmune vasculitic disorder characterised by necrotising granulomas affecting the small blood vessels of the upper and lower airways. It is thought that immune complex deposition or an autoimmune response results in inflammation and damage/ destruction of the vessels and their surrounding structures. In immune disease, the cartilaginous structures of the outer nose and septum are generally FIGURE 1.40 Saddle nose deformity more severely involved than the bony Reproduced, with permission, from Firestein GS, nasal dorsum. Severe disease may cause Budd RC, Harris ED et al., Kelley’s progressive loss of septal support, Textbook of Rheumatology, 8th edn, leading to enlarged anterior septal Philadelphia: WB Saunders, 2008: Fig 82-5. perforations, resulting in significant collapse of nasal cartilage.91 Relapsing polychondritis Description Relapsing polychondritis is an Collapse of the middle section of the autoimmune chronic inflammatory nose relative to the tip and dorsum, disorder resulting in the destruction of like a saddle. cartilage – in particular auricular and Condition/s nasal cartilage.25 associated with Sign value More common Saddle nose deformity occurs in up to 65% of relapsing polychondritis, and • Trauma 9–29% of patients with Wegener’s • Iatrogenic – nasal surgery granulomatosis.25 Less common • Wegener’s granulomatosis • Relapsing polychondritis

50 Sausage-shaped digits (dactylitis)

Sausage-shaped digits 1 (dactylitis)

Uncommon • Tuberculosis • Gout • Sarcoidosis • Disseminated gonorrhoea Mechanism/s Spondyloarthropathies Irritation of the flexor tendons, flexor tendon sheath and surrounding soft FIGURE 1.41 tissues due to pro-inflammatory Sausage-shaped digits (dactylitis) in a patient cytokines results in pronounced diffuse with psoriatic arthritis inflammation of the digits.93,94 Recent Reproduced, with permission, from Tyring SK, high-resolution MRI studies in Lupi O, Hengge UR, Tropical Dermatology, psoriatic arthritis reported flexor 1st edn, London: Churchill Livingstone, 2005: tendon pulley and sheath-related Fig 11-16. enthesitis as the more specific cause.95 Tuberculosis dactylitis Description A variant of tuberculous osteomyelitis Fusiform swelling of multiple digits whereby TB granulomas invade the such that it is difficult to visualise the short tubular bones of the hands and 92 individual joints (e.g. PIP, DIP). Or, feet and then the surrounding tissues, more simply, fingers or toes that are causing inflammation and swelling.93 so swollen they look like sausages. Dactylitis typically affects multiple Syphilitic dactylitis digits, whereas flexor tenosynovitis is a A manifestation of congenital syphilis distinct entity usually only present in where the syphilitic spirochetes invade one digit. perichondrium, bone, periosteum and marrow and thus inhibit osteogenesis. Condition/s Inflammation from the invasion is another contributing factor to pain and associated with swelling of the digits.93 More common Sarcoid dactylitis • HLA-B27 spondyloarthropathy Sarcoid non-caseating granulomas » Psoriatic arthritis invade bone and soft tissue, causing » Ankylosing spondylitis swelling and inflammation.93 » Reactive arthritis Sickle cell dactylitis » Enteropathic arthritis In sickle cell anaemia, a haemoglobin (associated with inflammatory S-gene mutation results in rigid and bowel disease) ‘sickle’-shaped red blood cells under • Sickle cell anaemia – paediatric hypoxic conditions. Acute sickling in

51 Sausage-shaped digits (dactylitis)

the peripheral circulation results in arthritis,97 being present in 16–24%97 digital ischaemia and painful fusiform of reported cases, with lifetime digital swelling. It typically occurs in incidence and prevalence of 48% and the paediatric population. 33%, respectively.98 It is seen in only 4% of tuberculosis93 cases. Sign value Identification of sausage-shaped In regards to patients with seronegative digits or dactylitis in an adult should spondyloarthropathy, sausage-shaped prompt an evaluation for a seronegative digits have a sensitivity of 17.9% spondyloarthropathy. Development and a specificity of 96.4%.96 The of dactylitis in a child of African or development of dactylitis may be a Mediterranean descent should prompt marker for progression of psoriatic evaluation for sickle cell disease.

52 Sclerodactyly

Sclerodactyly 1

Condition/s associated with • Scleroderma (systemic sclerosis) • CREST syndrome (i.e. Calcinosis, Raynaud’s phenomenon, Oesophageal dysmotility, Sclerodactyly, Telangiectasia) Mechanism/s In scleroderma, T cells infiltrate the FIGURE 1.42 skin and set in motion a cascade of Sclerodactyly with flexion contractures events including abnormal fibroblast and Reproduced, with permission, from Firestein GS, Budd RC, Harris ED et al., Kelley’s growth factor stimulation. This in turn Textbook of Rheumatology, 8th edn, leads to increased production of Philadelphia: WB Saunders, 2008: Fig 47-12. extracellular matrix, fibrillin and type 1 collagen and other factors. Ultimately this results in fibrosis and thickening of the skin. Sign value Description Skin thickening is seen more often in Thickening and tightening of the skin diffuse scleroderma (27%) than in covering the digits. limited disease (5%).99

Genetic factors Environmental Other factors

Immunological reaction – mononuclear cells and cytokines infiltrate layers of skin

Vascular inflammation, fibroblasts stimulated, TGF-β released, growth factors, other factors released

Collagen, fibrillin, fibronectin, extracellular matrix synthesis and deposition

Fibrosis, skin thickening and tightening

Sclerodactyly

FIGURE 1.43 Proposed mechanism of sclerodactyly

53 Shawl sign

Shawl sign

thinned epidermis, and increased dermal mucin deposition.101 Factors contributing to these changes include: • Dysregulated cytokine production and cell-mediated processes. Histopathology of dermatomyositic lesions have shown the principal infiltrating cell in the skin is the CD4+ T lymphocyte, distributed mainly in the perivascular upper FIGURE 1.44 dermis. Shawl sign • In skin biopsies, a significantly Note discolouration over the posterior shoulder and neck. increased number of both CD-40+ Reproduced, with permission, from Hochberg MC cells (including keratinocytes and et al., Rheumatology, 5th edn, Philadelphia: mononuclear cells in the dermis), as Mosby, 2010: Fig 144-7. well as infiltrating CD4+ CD-40L+ T-lymphocytes, are found. Activation of the CD-40/CD-40L Description system may cause upregulation A confluent, violaceous, macular rash of several pro-inflammatory over the posterior shoulders and neck. molecules, including IL-6, IL-15, IL-8 and MCP-1. Condition/s • Dysregulated apoptosis of associated with keratinocytes. The exact mechanism for keratinocyte • Dermatomyositis apoptosis is unclear, but includes UVB light, Fas-FasL, TNFα, and Mechanism/s CD8+ T-cell-mediated activation Complement and antibody mediated of the apoptosis pathway. microvascular injury likely results in the development of the rash.100 • Photosensitivity is an important Dermatomyositis is a systemic clinical feature. Exposure to inflammatory disorder primarily of sunlightd an specifically UVA and muscle and skin characterised by UVB radiation may serve a central microvascular damage due to antibody role in disease onset and complex and complement deposition. persistence. Exposure to UVB Genetic predisposition, viruses and radiation has also been shown to UV e light ar all thought to play upregulate the pro-inflammatory a role.100 cytoking TNF-α. The cutaneous changes in • Excess mucin deposition has been dermatomyositis include: hypothesised to occur secondary hyperkeratosis, epidermal basal cell to increased hyaluronic acid vacuolar degeneration, pathological production by dermal fibroblasts apoptosis of epidermal basal and following immunological suprabasal cells, dyskeratosis, a focally stimulation.

54 Shawl sign

Sign value of dermatomyositis, skin manifestations occur. However, skin manifestations Although not pathognomonic, the may occur without the onset of muscle 1 shawl sign is strongly associated with symptoms.102 dermatomyositis. In up to 30% of cases

55 Simmonds–Thompson test

Simmonds–Thompson test

(absence of plantarflexion) can be elicited. Condition/s associated with • Achilles tendon rupture Mechanism/s Normally, squeezing the gastrocnemius and soleus muscles results in shortening of the distance between the Achilles tendon insertion site and distal femur, FIGURE 1.45 103 Simmonds–Thompson test causing plantarflexion. If the Achilles The calf muscles are squeezed, and the test tendon is ruptured, no movement is positive if there is no ankle plantarflexion. occurs. Sign value With a sensitivity of 96%, specificity Description of 93%, +LR 13.5 and −LR of 0.05,104 With the patient lying prone on the it is a worthwhile test to perform if an exam table with their ankles hanging Achilles rupture if suspected. A positive overe th end, the examiner squeezes test almost certainly suggests significant the calf muscle. The test is considered damage to the tendon, but does not positive if no movement in the ankle always indicate complete rupture.105

56 Speed’s test

Speed’s test 1

against resistance from the examiner. The test is positive if tenderness is elicited. Condition/s associated with • Biceps tendonitis • SLAP lesion (Superior Labral tear from Anterior to Posterior) – an injury of the glenoid labrum Mechanism/s FIGURE 1.46 Traction on an inflamed biceps tendon Speed’s test or pressure on a labral tear will result in The examiner actively resists the patient tenderness. lifting the extended arm. Sign value Holtby R et al., in predicting biceps Description pathology and SLAP lesions, reported The patient sits or stands with the a sensitivity of 32%, a specificity of shoulder in 90° flexion, elbow extended 75%, a positive likelihood ratio of 1.28 and the palm facing up (supinated). and a negative likelihood ratio of The patient attempts to lift the arm up 0.91.106 This test has limited value.

57 Subcutaneous nodules (rheumatoid nodules)

Subcutaneous nodules (rheumatoid nodules)

Repeated trauma

Local vascular damage

Neoangiogenesis and Endothelial injury + IgM RF immune granulation tissue formation complex/complement deposited in vessel walls

Direct activation of monocytes Complement-mediated activated monocytes

TGF-β, TGF-α, fibronectin, proteases, other cytokines, cells

Pallisading granuloma – rheumatoid nodule

FIGURE 1.47 Mechanism of rheumatoid nodule formation

Description Visibled an palpable subcutaneous nodules typically occur over bony prominences and/or extensor surfaces. Condition/s associated with • Rheumatoid arthritis FIGURE 1.48 Large rheumatoid nodules are seen in a Mechanism/s classic location along the extensor surface of the forearm and in the olecranon bursa Thought to be mediated via Th-1 inflammatory response.107 Trauma over Reproduced, with permission, from Goldman L, Ausiello D, Cecil Medicine, 23rd edn, bony prominences causes local vessel Philadelphia: Saunders, 2007: Fig 285-9. damage that leads to new blood vessel growth and granulomatous tissue formation. Endothelial injury results in Sign value accumulation of immune complexes Seen in 20–25% of seropositive and stimulates monocytes to secrete rheumatoid arthritis. They are the IL-1,, TNF TGF-β, prostaglandins most common extra-articular and other factors, including proteases, manifestation of the disease. Frequency collagenases and fibronectin. This of development of nodules is associated ultimately leads to angiogenesis, with elevated rheumatoid factor fibrin deposition and formation titres.108 The presence of nodules is of the characteristic rheumatoid associated with a more severe disease nodule.107,108 phenotype.109

58 Sulcus sign

Sulcus sign 1

Mechanism/s In the setting of anterior shoulder dislocation, the head of the humerus moves inferiorly relative to the glenohumeral joint. This causes traction of the skin overlying the glenohumeral joint, and a dimple over the space between the acromion and the humeral head may be seen. Sign value FIGURE 1.49 Anterior shoulder dislocation is often Sulcus sign apparent on inspection with the arm Note the slight dimple under the acromion. held anteriorly and internally rotated. Reproduced, with permission, from DeLee JC, Radiographs should be obtained to Drez D, Miller MD, DeLeed an Drez’s confirm the diagnosis. Testing for Orthopaedic Sports Medicine, 3rd edn, Philadelphia: Saunders, 2009: Fig 17H2-16. glenohumeral head instability, Tzannes and Murrell110 found a sulcus sign of 2 cm or more to have a specificity of Description 97% for multidirectional instability; With the patient’s arm relaxed and however, the corresponding sensitivity hanging by the side, the examiner was only 28%. If positive, the sign looks at the shoulder area. If chronic supports glenohumeral head instability subluxation is suspected, the examiner and/or a subluxation, but should be may apply traction to the arm to elicit confirmed with imaging. the sign. Dimpling of the skin between the acromion and humeral head is a positive test. Condition/s associated with • Anterior shoulder dislocation • Anterior shoulder subluxation • Glenohumeral joint instability

59 Supraspinatus test (empty-can test)

Supraspinatus test (empty-can test)

Mechanism/s The supraspinatus muscle works in concert with the deltoid muscle during shoulder abduction and stabilises the humeral head in the glenoid fossa. Mechanical strain upon an injured supraspinatus muscle or tendon will result in tenderness and/or weakness during this manoeuvre.

FIGURE 1.50 Sign value Supraspinatus or empty-can test McGee, in a review of two studies in patients with rotator cuff muscle tears with painful supraspinatus tests, Description reported a sensitivity of 63–85%, a The patient sits or stands with the specificity of 52–60% and a positive shoulder in 90° flexion, 30° abduction, likelihood ratio of 1.7.75 A review of with the elbow extended and the five studies of patients with rotator cuff thumbs pointing towards the ground, muscle tears with weakness during as if emptying two cans. The examiner testing, reported a sensitivity of applies downward pressure as the 41–84%, a specificity of 58–70%, a patient attempts to lift the arms up. positive likelihood ratio of 2.0 and a The test is positive if the patient negative likelihood ratio of 0.5.2 experiences tenderness or is unable to The supraspinatus test has limited hold up their arm. utility and may be positive in several other shoulder conditions. Detection of Condition/s weakness has more diagnostic utility associated with than tenderness alone. • Supraspinatus tear • Supraspinatus tendonitis • Supraspinatus impingement

60 Swan-neck deformity

Swan-neck deformity 1

Attenuated or ruptured extensor tendon

A

Contracted Dorsal subluxation triangular ligament of lateral band

Attenuated transverse retinacular ligament B

FIGURE 1.51 Swan-neck deformity pathoanatomy A Terminal tendon rupture may be associated with synovitis of DIP joint, leading to DIP joint flexion and subsequent PIP joint hyperextension. Rupture of flexor digitorum superficialis tendon can be caused by infiltrative synovitis, which can lead to decreased volar support of PIP joint and subsequent hyperextension deformity; B lateral-band subluxation dorsal to axis of rotation of PIP joint. Contraction of triangular ligament and attenuation of transverse retinacular ligament are depicted. Based on Jupiter JB, Chapter 70: Arthritic hand. In: Canale TS, Beaty JH, Campbell’s Operative Orthopaedics, 11th edn, Philadelphia: Elsevier, 2007: Fig 70-13.

Description Mechanism/s A deformity characterised by distal A relative imbalance of flexor and interphalangeal (DIP) joint flexion and extensor tendons of the digit due to proximal interphalangeal (PIP) joint chronic synovial inflammation.111 A hyperextension in the resting digit, to variety of changes may result in this some extent resembling a swan’s neck. deformity, whose basis is inflammatory disruption of the collateral ligaments, Condition/s volar plates, joint capsule or invasion of associated with the flexor tendons.112 The resulting changes may be: Common • Rheumatoid arthritis

61 Swan-neck deformity

• attenuation or disruption of the extensor tendon on the distal phalanx, leading to unopposed flexion – and thus the flexed DIP joint • disruption of the retinacular ligament (which helps hold the finger in flexion), leading to unopposed extensor forces at the PIP joint and PIP joint hyperextension. Sign value Swan-neck deformity is classically associated with rheumatoid arthritis. In FIGURE 1.52 patients with acute trauma with forced Swan-neck deformity DIP flexion during active extension, Reproduced, with permission, from Jupiter JB, Chapter 70: Arthritic hand. In: Canale TS, mallet finger (i.e. extensor tendon Beaty JH, Campbell’s Operative avulsion distal to DIP joint) should be Orthopaedics, 11th edn, Philadelphia: Elsevier, considered. 2007: Fig 70-14.

62 Telangiectasia

Telangiectasia 1

TABLE 1.3 Telangiectasia-associated conditions Systemic diseases Carcinoid syndrome Ataxia–telangiectasia Mastocytosis Dermatomyositis Scleroderma – especially periungual telangiectasia Systemic lupus erythematosus Hereditary haemorrhagic telangiectasia Liver cirrhosis

General mechanism/s Telangiectasias are predominantly persistently dilated small capillaries and venules. The exception to this is FIGURE 1.53 Telangiectasia associated with systemic hereditary haemorrhagic telangiectasia, sclerosis (scleroderma) as these lesions are arteriovenous (AV) Note the skin tightening around the lips. malformations. Reproduced, with permission, from Habif TP, Clinical Dermatology, 5th edn, Philadelphia: Hereditary haemorrhagic Mosby, 2009: Fig 17-30. telangiectasia (HHT) HHT is an autosomal dominant disorder causing development of AV malformations, due to a genetic Description abnormality of the TGF-β receptor. Permanent dilatation of superficial The TGF-β pathway is known to peripheral vessels resulting in blanching modulate vascular architecture, matrix red lesions on the skin. Telangiectasia formation and basement membrane 113 may present as a fine red line or a development. punctum (dot) with radiating lines.46 Scleroderma The underlying mechanism for Condition/s telangiectasia in scleroderma is associated with unknown. It is presumed that there is There are numerous conditions endothelial injury, leading to aberrant associated with telangiectasia, including angiogenesis and the development of but not limited to those listed in new vessels. It has been suggested that Table 1.3. the TGF-β pathway may be involved.113

63 Telangiectasia

Spider naevus • Telangiectasias in adulthood that See ‘Spider naevus’ in Chapter 6, are located around the mucous ‘Gastroenterological signs’. membranes, extremities and under the nails are associated with Sign value hereditary haemorrhagic Location and characteristics of telangiectasia. telangiectasia can assist in diagnosis. • The presence of increased numbers • Periungual telangiectasia of telangiectasias may indicate (telangiectasia next to the nails) is the development of pulmonary said to be highly suggestive of SLE, vascular disease in scleroderma. scleroderma or dermatomyositis.114 Telangiectasia may be a clinical • Broad macules with a polygonal marker of more widespread mat microvascular disease in or oval shape, known as 115 telangiectasias, are associated with scleroderma. CREST syndrome.114

64 Thessaly test

Thessaly test 1

FIGURE 1.54 Thessaly test

Description Mechanism/s The test is performed with the knee at The knee meniscus (lateral and medial) 5° and 20 of flexion. The examiner is fibrocartilaginous tissue that separates supports the patient by the hands as the femur from the tibia. The menisci they stand flatfooted. The patient then provide rotational stability and act as rotates their knee and body, internally shock absorbers, among other and externally, three times, keeping the functions. The Thessaly test creates knee in slight flexion (5°). The same loading conditions on the meniscus and movement is repeated with the knee a rotational stress that may result in flexed to 20°. The test is always reproduction of pain, catching or other performed first on the normal knee so reported symptoms. that the patient is comfortable with performing the manoeuvre (i.e. how to Sign value keep the knee in 5° and then 20° of Blytht M e al.116 compared the accuracy flexion). See Figure 1.54. of physical tests for meniscal tears to MRI-based diagnosis (see Table 1.1 on Condition/s page 35). The Thessaly test had only associated with moderate value in assessment when compared to MRI. The tests may be • Meniscal tears useful initially, but realistically, definitive imaging is required.

65 Thomas’ test

Thomas’ test

1

2

3 FIGURE 1.55 Performance of Thomas’ test

Description Mechanism/s With the patient lying supine, the knee Drawing up the knee and flexing one and hip on the ‘normal’ side are flexed, side of the hip rotates the pelvis. In with the knee held against the chest. A order to keep the alternate leg flat on positive test occurs if the opposite leg the bed, the hip flexors and rectus rises off the table. femoris must stretch enough to allow the leg to lie flat. In other words, if the Condition/s hip flexors are contracted, the affected associated with leg will rise as the pelvis rotates. • Hip flexion contracture – fixed Sign value flexion deformity A systematic review of diagnostic tests • Iliotibial band syndrome for hip pathology found minimal • Normal ageing/stiffness scientific evidence for Thomas’ test due to methodological flaws.117 There is limited value in this sign.

66 Tinel’s sign

Tinel’s sign 1

Increased carpal tunnel pressure and damage to median nerve

Altered membrane excitability

Increased mechanosensitivity

Easier discharge on tapping

Paraesthesias in median nerve distribution

FIGURE 1.57 Mechanism of Tinel’s test

FIGURE 1.56 Completing Tinel’s test and resulting damage to the median Tapping over the wrist causes pins and nerve. It is thought that this damage needles in the fingers. results in altered mechanosensitivity118 of the median nerve, possibly due to an abnormally excitable membrane. So, Description when lightly struck through the skin, Paraesthesias in a median nerve the inflamed nerve functions distribution occur when the examiner abnormally. taps with a finger at the distal wrist over the median nerve. It should be Sign value noted that Tinel’s original description D’Arcy CA et al. reported Tinel’s was not specific for the median nerve sign had limited or no value in but rather for the sensation of ‘pins and distinguishing people with carpal 73 needles’ arising from any injured nerve tunnel syndrome from those without. tested in this way. A review of several studies reported a sensitivity of 25–60%, a specificity of Condition/s 64–80%, a positive likelihood ratio of associated with 0.7–2.7 and a negative likelihood ratio of 0.5–1.1. Neither Tinel’s sign nor • Carpal tunnel syndrome Phalen’s sign reliably rule in or rule out 118 Mechanism/s carpal tunnel syndrome. In carpal tunnel syndrome, there is increased pressure in the carpal tunnel

67 Trendelenburg’s sign

Trendelenburg’s sign

Condition/s associated with • Gluteus medius muscle weakness » Superior gluteal nerve palsy – iatrogenic » Lumbar radiculopathy » Sequelae of hip joint pathology • Osteoarthritis • Slipped femoral capital epiphysis (SCFE) – paediatrics • Legg–Calve–Perthes disease Negative Positive – paediatrics

FIGURE 1.58 Trendelenburg test Mechanism/s Note that the positive test on the right The gluteus medius muscle originates indicates a problem with the left hip from the iliac crest and inserts into abductors – remember ‘the sound side sags’. the greater trochanter of the femur. Based on Goldstein B, Chavez F, Phys Med Normally when we stand on one leg, Rehabil State Art Rev 1996; 10: 601–630. the gluteus medius muscle abducts the hip joint to maintain normal alignment Description of the pelvis. With gluteal medius The patient is asked to stand on one weakness, the sound side (the side leg while bending the other knee so opposite to the stance leg) sags, or tilts the foot is held off the ground. For the downwards. sign to be present, the pelvis must be seen to ‘drop’ on the unsupported side. Sign value Confusingly, the pathology is not Given the number of potential causes, a located on the ‘dropped’ side, but in positive Trendelenburg sign is fairly the opposite leg, hence the saying ‘the non-specific; however, it is never sound side sags’. normal and should be investigated.

68 True leg length inequality (anatomic leg length inequality)

True leg length inequality 1 (anatomic leg length inequality)

Description Mechanism/s The leg length is measured from the True, or anatomic, leg length equality anterior iliac spine to the medial relates to the actual length of the bones malleolus. There is no clear definition and anatomical structures making up as to what constitutes a significant the hip and the lower limb. Therefore, discrepancy. Some authors suggest that any problem in the anatomy that it is not clinically relevant until there is constitutes the leg length (from the head more than 20 mm difference between of the femur down to the ankle) may legs.119 cause a discrepancy. For example, abnormalities in growth plates during development may lead to one leg being Condition/s longer than the other. Aberrant healed associated with fractures can also lead to a shortened leg. • Fracture – hip, femur, tibia • Dislocation – hip, knee Sign value A leg length discrepancy is a non- • Post-surgical shortening specific sign. It should be interpreted in • Congenital disorders the context of the patient’s history.

69 Ulnar deviation

Ulnar deviation

stable than interphalangeal joints. Progressive inflammatory changes from rheumatoid arthritis result in stretching of the joint capsule and ligaments, causing instability. Extrinsic forces on the joints tend to pull in a direction of ulnar deviation. Possible factors include:108,111 • the normal tendency of fingers to move towards the ulnar side on flexion • inflammation of the FIGURE 1.59 carpometacarpal (CMC) joints in Ulnar deviation and subluxation the 4th and 5th fingers causes The hand shows typical manifestations of further spread of the metacarpals in end-stage erosive changes around the metacarpophalangeal joints, with volar and flexion, producing an ‘ulnarly’ ulnar drift of the fingers. directed force on the extensor Reproduced, with permission, from Firestein GS, tendons Budd RC, Harris ED et al., Kelley’s • stretching of the collateral ligaments Textbook of Rheumatology, 8th edn, of the MCP joints, accessory Philadelphia: WB Saunders, 2008: Fig 66-5. collateral ligaments or flexor tunnels that permits volar displacement of the proximal Description phalanges. Displacement of the metacarpo­ Radiocarpal ulnar phalangeal and/or radiocarpal joint deviation towards the ulnar aspect of the wrist. Progressive inflammatory changes lead to progressive synovitis of the wrist Condition/s joint and carpal bones, including the associated with scaphoid. Abnormal wrist mechanics • Rheumatoid arthritis develop due to translocation of the • Pigmented villonodular synovitis carpal bones relative to the radius, and imbalance of mechanical forces.108 Mechanism/s Sign value Metacarpophalangeal Ulnar deviation of the MCP joints is (MCP) joint classically associated with rheumatoid MCP joints are condylar and are able arthritis, although other causes should to move in two planes. They are less be considered.

70 V- sign

V- sign 1

Condition/s associated with • Dermatomyositis Mechanism/s Complement- and antibody-mediated microvascular injury likely results in the development of the rash.120 Dermatomyositis is an inflammatory myopathy characterised by microvascular damage and destruction of muscle by antibody complex and complement deposition. Genetic FIGURE 1.60 predisposition, viruses and UV light are Irregular patchy erythema with associated 100 prominent telangiectasias in a woman with all thought to play a role. See dermatomyositis Heliotrope rash and Shawl sign. Reproduced, with permission, from Shields HM et al., Clin Gastroenterol Hepatol 2007; Sign value 5(9): 1010–1017. Although not pathognomonic, the V-sign is highly suggestive of dermatomyositis. In up to 30% of Description cases, skin manifestations including the A confluent, macular, violet/red rash V-sign may occur before development seen over the anterior neck and upper of the characteristic muscle weakness. chest. Often found in a V-shape similar to the neck of a shirt.

71 Valgus deformity

Valgus deformity

Valgus Varus

FIGURE 1.61 Examples of valgus and varus deformities of the knees

Description • Limited soft tissue stabilising the 1st MTP joint results in forces Angulation of the distal bone of a joint pushing the toe laterally being away from the midline of the body. relatively unrestrained. Condition/s • Owingo t the anatomy of the associated with metatarsocuneiform joint, increased pressure under the first metatarsal Associated conditions are given in (e.g. from excessive pronation) will Table 1.4. tend to displace the first metatarsal. Mechanism/s • Inflammatory joint disease may Hallux valgus precipitate the formation of hallux valgus by damaging ligaments and Anatomical, biomechanical and altering normal joint alignment. pathological factors contribute to the formation of hallux valgus. Some of those identified include:121

72 Valgus deformity

TABLE 1.4 Valgus deformity-associated conditions 1 Hip Knee Ankle Toe Osteochrondrosis Cerebral palsy Paralytic Biomechanical Idiopathic Osteochrondrosis Congenital Blount’s disease Osteochrondrosis Rickets Psoriatic arthritis Paralytic Multiple sclerosis Osteochrondrosis Cerebral palsy Rheumatoid Rheumatoid arthritis arthritis Osteoarthritis Intra-articular damage Connective tissue disorders

Anatomical absence of Inflammatory disease – muscle stabiliser – from Excessive destruction of ligaments metatarsal to proximal pronation and normal joint integrity great toe

Medial displacement of proximal toe, lateral displacement of distal toe

Chronic stress on medial ligaments – eventual disruption of medial ligaments

Unopposed adductor ligament action

Chronic stress – eventual hallux valgus deformity

FIGURE 1.62 Factors involved in the mechanism of hallux valgus

Knee valgus (genu Sign value valgum) Valgus deformity has limited utility. Genu valgum may be caused by a Aetiologies differ largely depending numberf o disorders. Basic mechanisms upon the site of the deformity. for a number of these conditions are shown in Table 1.5.

73 Valgus deformity

TABLE 1.5 Genu valgum mechanism/s Condition Basic mechanism Vitamin D deficiency A lack of vitamin D leads to abnormal bone mineralisation, softer-than-normal bones, abnormal bone regrowth and bowing of the legs. Mechanical forces play a role in bone regrowth Paget’s disease Invasion with paramyxovirus leads to abnormal activation of osteoclasts and aberrant osteoblast activity. Deformation of the bone and knee can lead to anatomical changes and valgus deformity Osteochrondrosis Interrupted blood supply, especially to the epiphysis, leads to necrosis and then later bone regrowth – resulting in abnormal formation of femur and knee joint – and eventually a valgus deformity Neuromuscular disorders Weak quadriceps, gastrocnemius and hip abductors may cause knees to enter valgus position56

74 Varus deformity

Varus deformity 1

Description Angulation of the distal bone of a joint towards the midline. Condition/s associated with Associated conditions are given in Table 1.6. Mechanism/s Coxa vara Present if the angle between the femoral neck and shaft is less than 120°. Congenital Congenital coxa vara may present in infancy or later in childhood. It is often bilateral and characterised by progressive bowing of the femur and a defect in the medial part of the neck of FIGURE 1.63 the femur.56 Bowingf o both legs in infantile Blount’s disease Rickets Reproduced, with permission, from Harish HS, Pressure placed on the femoral neck of Purushottam GA, Wells L, Chapter 674: abnormally mineralised bone distorts Torsional and angular deformities. In: Kliegman RM et al., Nelson Textbook of Pediatrics, its normal architecture. 18th edn, Philadelphia: Saunders, 2007: Fig 674-8.

75 Varus deformity

Perthes’ disease Although the underlying cause of Perthes’ disease is unknown, there is a loss of blood supply to the femoral head. Avascular necrosis of the femoral head results in distortion of the normal bony alignment of the femur. Genu varum Genu varum or ‘bow-leggedness’ is normal in many children up to 2 years.122,123 It should be differentiated from Blount’s disease. Blount’s disease The underlying mechanism of genu varum in Blount’s disease is unknown. Abnormal growth of the medial tibial epiphyseal growth plate causes FIGURE 1.64 progressive varus deformity at the knee Metaphyseal chondrodysplasia, type Schmid joint.123 There is bilateral coxa vara, the metaphyses are splayed and irregular, and there is lateral Hallux varus bowing of the femora. Hallux varus is comprised of Reproduced, with permission, from Adam A, medial deviation of the first Dixon AK (eds), Grainger & Allison’s metatarsophalangeal (MTP) joint, Diagnostic Radiology, 5th edn, New York: Churchill Livingstone, 2008: Fig 67.13. supination of phalanx and interphalangeal flexion or claw toe. It results from an imbalance between Sign value osseous, tendon and capsuloligamentous Aetiologies differ largely depending structures at the first MTP joint.124 upon the site of the deformity.

TABLE 1.6 Varus deformity-associated conditions Hip Knee Ankle Toe Congenital disorders (e.g. Physiological Trauma Complication from cleidocranial dysplasia, – common bunion surgery Gaucher’s disease) Perthes’ disease Blount’s disease Iatrogenic Trauma Development dysplasia of Rickets Congenital Burn injury with hip contracture Slipped capital femoral Trauma Rheumatoid arthritis epiphysis (SCFE) Rickets Infection Psoriatic arthritis Osteomyelitis Tumour Charcot–Marie–Tooth (CMT) disease Paget’s disease Skeletal dysplasia Avascular necrosis Trauma

76 Yergason’s sign

Yergason’s sign 1

LBT Subscapularis Lesser tuberosity Humerus Scapula A

B

FIGURE 1.65 Yergason’s sign

Description C The examiner stands in front of the patient, who has their arms flexed to FIGURE 1.66 90° at the elbow and the palms facing Yergason’s sign pathoanatomy Overhead view of the subscapularis muscle, downwards (pronated). The patient long f head o the biceps tendon (LBT) and then tries to supinate the forearm bicipital groove. A Intact structure depicting against resistance from the examiner. normal anatomy; B partial tear of the subscapularis tendon from the attachment one th lesser tubercle, with the LBT Condition/s subluxed over the lesser tubercle into the associated with subscapularis muscle; C complete tear of the subscapularis tendon from the attachment • Biceps tendonitis one th lesser tubercle, with the LBT • SLAP lesion (Superior Labral tear subluxed over the lesser tuberosity and the from Anterior to Posterior) – an subscapularis tendon. injury of the glenoid labrum Based on Pettit RW et al., Athletic Training Edu J 2008; 3(4): 143–147. • Rotator cuff injuries

Mechanism/s originates on the lip of the glenoid The long head of biceps is the main labrum. The fibrous extension of the supinator of the arm. With resistance subscapularis muscle covers the long against supination, the muscle head of the biceps tendon and holds and tendon are stressed and any it in place.125 If this fibrous extension inflammation or damage is is ruptured, the biceps tendon is exacerbated, resulting in tenderness. susceptible to subluxation. Continuous The long head of biceps travels in subacromial impingement can wear the bicipital groove of the humerus and away the capsule above the long head

77 Yergason’s sign

of the biceps tendon. This causes ratio of 0.72.106 A more recent ongoing injury.75 meta-analysis and systematic review reported a specificity of 95%, with Sign value significant heterogeneity between Holtby R et al., in predicting biceps studies.126 tendon pathology and SLAP lesions, In detecting rotator cuff tendonitis, reported a sensitivity of 43%, a the reported sensitivity was 37% and specificity of 79%, a positive likelihood specificity 87%, with a+ LR of 2.8 and ratio of 2.05 and a negative likelihood −LR of 0.7.127

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