Imaging may be helpful. Plain radiographs are often normal, but it may show soft tissue swe lling that can be radiodense with hemosiderin deposition. Calci \201 cation, however, is n ot a feature of PVNS and would suggest a malignant lesion or perhaps chondromatosis (see be low). \200 Erosions and subchondral cysts (also on nonweight-bearing surfaces) can be see n. Loss of joint space can occur late in the condition. Typically, this is not associated w ith juxta-articular osteoporosis or osteophyte formation. MRI can be highly suggestive of P VNS if there is suf \201 cient hemosiderin and fat deposition in the lesion. Treatment of PVNS \200 Localized forms of PVNS are treated by marginal excision of the le sion. \200 The prognosis is good. \200 Diffuse forms of PVNS tend to be progressive and recurrent. Treatment techniques have included synovectomy, radiation therapy, arthrodesis, and arthrop lasty. No one technique has particularly good results; however, there is only limited exper ience and little long-term follow-up. The most commonly reported treatment is surgical synovectomy. MISCELLANEOUS DISORDERS OF SYNOVIUM 519 Synovial chondromatosis \200 This condition is characterized by chondrometaplasia of the subsynovial connective tissues. The joint is \201 lled with a thickened white/blue nodula r synovium. The cause is unknown, the disorder uncommon, and the process nonmalignant. It tends to occur more often in middle-aged men and has never been reported i n prepubertal childhood. Clinically the condition resembles PVNS (above) but tends to be slowly progressive and sometimes self-limiting with regression. Plain radiographs may show punctate calci \201 cation outlining the joint margin. The diagnosis should be con \201 rmed on synovial biopsy. In rare cases there may be transformation to a chondrosarcoma. Treatment is surgical and usually managed with arthroscopy, removing loose bodies and/or the synovial membrane. CHAPTER 18 Miscellaneous conditions 520 Amyloidosis \200 A number of disorders and clinical settings are associated with the extracellular deposition of amyloid, a proteinaceous, \201 brillar material. The low solu bility of amyloid and its relative resistance to proteolytic enzymes contributes to the irr eversible and often progressive course of amyloidosis. Despite morphological similarities (including the formation of a beta pleated sheet), amylo id is a heterogeneous group of proteins. All types of amyloid \201 brils have a carbohydr ate moiety in the form of glycosaminoglycans and proteoglycans. Most forms of amyloid also contain the extra \201 brillar protein, amyloid-P (protein AP). The different amyloid proteins are often related to distinct clinical forms of amyloidosis. At present, at least 17 proteins have been characterized. The detail of these proteins is beyond the scope of this book. However, two types are important as manifestations of a resp onse to chronic systemic in \202 ammation; amyloid-L (AL) and amyloid-A (AA). Protein AL consists of monoclonal immunoglobulin light chains and is seen in idiopathic and myeloma-associated amyloidosis. The clinical features of AL and A A are shown in Table 18.8. Protein AA (derived from serum amyloid A (SSA), an acute phase apolipoprotein), is associat ed with conditions such as secondary reactive amyloidosis and FMF (see Table 18.9). The mechanisms by which the various precursor proteins are converted to insoluble amyloid \201 brils, the reasons for the predilection of certain pr oteins for particular organs and tissues, and the reasons why not all cases of a particular chronic in \202 ammatory disorder develop amyloid are not clear. The most studied mechani sms are those associated with the reactive AA type amyloidosis. Clinically, amyloidosis may be associated with nephrotic syndrome, cardiomyopathy, hepatomegaly, peripheral neuropathy, malabsorption, and orthostatic hypoten sion. Reactive AA amyloidosis is mainly associated with long-standing infectious or noninfectious in \202 ammation, and less frequently with cancer. In the context of rheumatic disorders AA amyloidosis is mainly seen in: \200 Adult RA \200 JIA \200 AS There are several rheumatic conditions that are rarely associated with AA amyloidosis. In t hese conditions there is a relatively low level of the acute-phase protein SAA. These condi tions include: \200 SLE \200 systemic sclerosis \200 Sj gren \200\231s syndrome AMYLOIDOSIS 521 Table 18.8 The clinical features of AL and AA amyloidosis Organ/condition Comment AL amyloidosis Heart Death occurs in 50% of cases from: restrictive cardiomyopathy, congestive heart failure, co nduction disturbances Lungs 90% develop cough and dyspnea Skin 40% of cases: papules, nodules, tumors Neuropathy 10% of cases get carpal tunnel syndrome Macroglossia Vasculopathy Amyloid arthropathy Autonomic disturbance Common to AL and AA Weakness Fatigue Weight loss Renal Nephrotic syndrome/renal failure \200\224major cause of death in AA*, cause of death in one -third of AL patients Gastrointestinal tract Malabsorption, obstruction, diarrhea, hepatosplenomegaly* In AA amyloid the spleen, liver, and kidneys are often involved \201 rst. CHAPTER 18 Miscellaneous conditions 522 Diagnostic procedures \200 The diagnosis of amyloidosis is made by tissue biopsy (usually abdominal subcutaneous fat), and alkaline Congo red stain showing the amyloid deposits as a pple green/yellow under the polarizing microscope. The strong calcium-dependent af \201 nity of protein AP for amyloid \201 brils is also u sed diagnostically in radiolabeled serum amyloid protein (SAP) scintigraphy. This technique may localize amyloid and could be of value in assessing degrees of response to treatment. Other laboratory tests include DNA analysis to detect the genetic variants of proteins know n to make up the hereditary amyloidoses. Treatment of amyloidosis \200 The condition is progressive and there is no cure. Marked heterogeneity of the hereditary amyloidoses makes counseling dif \201 cult as well. The pr ocesses by which the disorder may be controlled include liver transplantation for lysosomal amyloidosis and bone marrow transplantation. For patients with AL amyloidosis, treatment with melphalan and prednisone prolongs survival. In the rheumatic diseases, cytotoxic drugs such as cyclophosphamide (often in combination with corticosteroids) have improved the prognosis in RA and JIA patie nts. Familial Mediterranean fever \200 This condition has been in the literature since the ear ly 1900s and was more recently characterized in the 1960s. Most cases (80%) present before the age of 20 and it is very rare to present with a \201 rst attack after the age of 40. Abnormalities of the gene coding for the protein pyrin (on chromosome 16) have been identi \201 ed and constitute the only test speci \201 c for the diagnosis of FMF. FMF is an autosomal recessive disorder. It most frequently affects peopl e of eastern Mediterranean descent, especially Armenians, Arabs, and Sephardic and Ashkenaz i Jews. The most common symptoms of abdominal pain and pleurisy are related to serositis, present i n up to 95% of cases. 75% of cases develop an arthritis that may be erosive and is most oft en isolated to a single joint. A rash with dermal neutrophil in \201 ltration (rather than a vasculitis) is common and looks not unlike erysipelas. Amyloidosis can occur in up to 40% of cases and does not appear to be associated with sever ity or frequency of attacks of FMF. Patients may develop renal failure, proteinuria, or mal absorption. Treatment includes NSAIDs for pain and continuous colchicine 0.6 mg po bid-tid. Up to 65% o f cases can achieve complete remission with this regimen. A further 30% can achieve partial remission. All remaining cases should stay on daily colchicine to help prevent amyloidosis . Concern over long-term use of prophylactic colchicine in FMF has not been borne out and t he bene \201 ts of controlling the condition outweighing any potential complication. It is , however, recommended AMYLOIDOSIS 523 that amniocentesis be a routine part of antenatal treatment to exclude colchicine-related c hromosomal aberrations. Newer agents such as anakinra, etanercept, and in \202 iximab may play a role in the manag ement of patients who are refractory to colchicine. Tumor necrosis factor-associated periodic syndrome (TRAPs) \200 This term covers a group of conditions similar to FMF but occurring in non-Mediterranean areas and associated with mutations in the TNF receptor superfamily ty pe 1A. The onset is in the second decade and presents with rash, fever, abdominal pain, disabling arthralgias, and myalgias. 20% of patients develop amyloid AA. \200 Colchicine is not ef \201 cacious. Corticostero ids may reduce the length and severity of attacks. Etanercept has been used successfully in some patients. Anakinra, an IL-1 receptor antagonist, is now the treatment of choice for these disorders. Table 18.9 The clinical features of Familial Mediterranean fever Clinical feature Comments Short attacks of high fever (39 \200\22340 C) Repeated and unpredictable Painful in \202 ammation Abdomen \200\22490% of cases (may develop adhesions) Chest \200\22445% of cases. Often febrile pleurisy Joints \200\224most often monoarthropathy, especially the knee with acute onset pain and sw elling with resolution over 1 \200\2234 weeks. Aseptic necrosis Skin \200\224erysipelas-like erythema, often below the knee to the dorsum of the foot Other \200\224orchitis, mild splenomegaly AA amyloidosis Renal \200\224early, terminal renal failure Cardiac, hepatic, GI \200\224see Table 18.8 Autosomal-recessive inheritance Virtual ethnic restriction: Sephardi Jews, Ashkenazi Jews, Armenians, Anatolian Turks, Arab s CHAPTER 18 Miscellaneous conditions 524 Fibromyalgia and chronic widespread pain \200 Chronic widespread pain (CWP) is a common \201 nding present in 5 \200\22310% of the general population. In the absence of diffuse degenerative or in \202 ammatory rheumatic disease the two most common conditions found in association with CWP ar e \201 bromyalgia (FM) and joint hypermobility syndrome (JHS) (see Chapter 16). CWP affects women more than men with a ratio of 1.5:1, and is de \201 ned as pain for >6 months in two or more sites both above and below the pelvis. Treatment of CWP is similar to that for FM and JHS. \200 Fibromyalgia is a subtype of CWP that is characterized by fatigue, somatic, and cognitive symptoms (see Table 18.10 and Cha pter 2). \200 American College of Rheumatology Classi \201 cation Criteria (1990) requir e tenderness on pressure in at least 11 of 18 speci \201 ed areas ( \200\234tender points \200\235) and the presence of widespread pain, but research indicates that in clinical prac tice, the tender point count often is performed incorrectly, or not at all. Using the classi \201 cation criteria for FM (see Table 18.10), prevalence rates range from 0.5 \200\2234% with a female: male ratio of 10:1. \200 American College of Rheumatology Diagnostic Criteria (2010) establish a diagnosis of \201 bromyalgia based on a combination of two factors: a Widespr ead Pain Index (WPI) and a Symptom Severity scale (SS). These criteria de \201 ne \201 bromyalgia as WPI (cid:4)(cid:3)7 and SS (cid:4) 5, or WP I 3 \200\2236 and SS (cid:4) 9 (Table 18.11). These diagnostic criteria correctly classify 88.1% of cases classi \201 ed by the ACR Classi \201 cation Criteria, and are better able to capture patients who no longer have tender points because they have responded to treatment. FM cases tend to aggregate within families. \200 FM is also found in up to 25% of patient s with RA (see Chapter 5), AS (see Chapter 8), and SLE (see Chapter 10). It is also commonl y found in the hypermobility syndrome (see Chapter 16) and overlaps symptomatically with th is condition and chronic fatigue syndrome in many ways. Care must be taken to avoid misdiag nosing CWP/FM as the only cause for pain when there is autoimmune rheumatic disease present . FM is a controversial condition and its existence as a distinct entity remains uncertain. I ts etiology is multifactorial, with neurological, psychological, and behavioral factors imp ortant in its development. Psychological stresses may precede the onset of FM and CWP. \200 Both FM and CWP are ofte n associated with other somatic symptoms such as chronic fatigue, irritable bowel syndrome, multiple chemical sensitivities, and headache syndromes. Other causes of fatigue should al ways be excluded e.g., hypothyroidism, hypoadrenalism, and anemia. FIBROMYALGIA AND CHRONIC WIDESPREAD PAIN 525 Alterations in hypothalamic \200\223pituitary axis function in response to stress have been explored, but no differences between FM and controls have been found. Both CWP and FM are associated with alterations in peripheral and central pain processing. Painful stimuli are detected at lower levels in affected patients. Allodynia (pain in respo nse to nonpainful stimuli) found in these conditions is thought to be due to central sensit ization and an \200\234ampli \201 cation \200\235 phenomenon. CSF levels of noradrenaline and serotonin metabolites are decreased in FM. These transmitte rs are involved in descending spinal cord pain inhibitory pathways, and the observed reduct ion may be responsible in part for central sensitization. Treatment \200 It is of paramount importance to consider carefully the way in which an explanation is given as to the nature of the condition. Many patients have suffered disa ppointment and blows to self-esteem and con \201 dence. It may take some time and may be b est approached over several visits. Many will be seeking a physical cause for the pain and may misinterpret discussion about pain ampli \201 cation and its treatment as labeling the ir condition as psychological. The label \200\234psychological \200\235 is in itself also legitimate medically, but to the layperson it often stirs ideas of \200\234crazy, \200\235 \200\234all in the head, \200\235 or \200\234malingerer. \200\235 Table 18.10 ACR 1990 criteria for diagnosis of \201 bromyalgia (FM) History of widespread pain: Pain is considered when all of the following are present: Pain in the left and right side o f the body, pain above and below the waist, axial skeletal pain, pain present for 3 months The diagnosis is made when there is pain in at least 11/18 tender point sites on digital pa lpation with 4 kg pressure*. There are 9 tender point sites, which are present bilaterally: 1. Occiput: at the suboccipital muscle insertions 2. Low cervical: at the anterior aspects of the intertransverse spaces at C5 \200\223C7 3. Trapezius: at the midpoint of the upper border 4. Supraspinatus: at origins above scapula spine near medial border 5. 2nd rib: at 2nd costochondral junction 6. Lateral humeral epicondyles: 2 cm distal from epicondyles 7. Gluteal: in upper outer quadrants 8. Greater trochanter: posterior to trochanter 9. Knees: at medial fat pad proximal to joint line Fibromyalgia said to be present when both criteria are satis \201 ed. FM is not excluded b y the presence of another disorder. CHAPTER 18 Miscellaneous conditions 526 It is important to assess the effect of symptoms on the patient \200\231s life, and to deve lop a good rapport so that psychosocial issues can be discussed. Chronic fatigue can be ver y disabling. The emphasis in the explanation should be reassurance that there is no serious underlying i n \202 ammatory/systemic condition or damage to the joints and muscles. Reassure that othe r conditions are absent and that no further investigations are needed. Although exercise may cause a short-term increase in pain, a prolonged exercise program has been shown to be bene \201 cial. Low impact activities such as Tai Chi and pilates may be especially helpful. Pacing of activities is also important, avoiding patterns of periods of overactivity when f eeling well, followed by periods of inactivity due to pain and fatigue afterwards. Pacing i s one key component of Cognitive Behavioral Therapy, a chronic pain program that, alongside aerobic rehabilitation, may be of signi \201 cant bene \201 t to patients with FM, CWP, and JHS. This multidisciplinary approach (psychologists, physical therapists, occupational therapists, doctors) has been tried with some success but remains incompletely studied. Education of family and partners is invariably helpful and often essential. NSAIDs and corticosteroids are not effective as the pain is not due to in \202 ammation or tissue damage, and may cause increased morbidity due to side effects. Narcotics should be avoided. Many patients will have tried analgesics with little effect. This in itself can fu el anxiety about the cause and severity of their underlying condition as well as frustratio n and lack of con \201 dence in their doctor. Tricyclic antidepressants such as amitriptyline (10 \200\22350 mg qhs) are often helpful in improving quality of sleep, decreasing morning stiffness and alleviating p ain. Patients should be warned of side-effects such as dry mouth and that they may take 3 \200\2234 weeks to take effect. Patients are often also wary of being given an antidepressa nt. An explanation that it is being used as an analgesic is important to improve adherence. Amitriptyline is one of a group of drugs that increase 5-hydroxytryptamine. Amitriptyline may be combined with tramadol successfully. \200 The ef \201 cacy of selec tive serotonin reuptake inhibitors (SSRI) is controversial. The use of \202 uoxetine, sertraline, or citalopram improves mood, but are less effective than tricyclics in treating pain, fatigue and sleep disturbance. Venlafaxine (serotonin and noradrenaline reuptake inhibitor) in high doses is effective in treating multiple symptoms in FM. Low dose treatment is generally ineffective. Sedative hypnotics may be used to improve sleep. \200 Both CWP/FM are conditions with rel apses and remissions. Most patients will have ongoing symptoms. Patients with appropriate coping strategies, improveme nts in psychosocial stressors, and good social support networks are more likely to have a b etter outcome. FIBROMYALGIA AND CHRONIC WIDESPREAD PAIN 527 Table 18.11 ACR diagnostic criteria for diagnosis of \201 bromyalgia (FM) Diagnostic criteria require the presence of the following: 1. WPI (cid:2) 7 and SS (cid:2) 5, or WPI 3 \200\2236 and SS (cid:2) 9 2. Symptoms must be present for at least 3 months 3. An alternate diagnosis is not present. Widespread Pain Index (0 \200\22319 points): the total number of areas in which the patient has had pain over the past week. Areas counted include the chest, abdomen, upper back, low er back, neck, and bilateral shoulder girdle, upper arm, lower arm, hip, upper leg, lower l eg, and jaw. Symptoms Severity scale score (0 \200\22312 points): the sum of the severity of three sympt oms (fatigue, waking unrefreshed, cognitive symptoms) and severity of somatic symptoms in g eneral, when each is rated on a scale from 0 to 3: 0 points: no problem/symptoms 1 point: mild problems/few symptoms 2 points: moderate problems/symptoms 3 points: severe problems/many symptoms Wolfe F et al. The American College of Rheumatology Preliminary Diagnostic Criteria for Fib romyalgia and Measurement of Symptom Severity. Arthritis Care and Research 2010; 62(5): 600 \200\223610. This page intentionally left blank 529 Chapter 19 Common upper limb musculoskeletal lesions Shoulder (subacromial) impingement syndrome 530 Adhesive capsulitis (AC) 533 Lateral epicon dylitis (tennis elbow) 534 For a detailed view on the differential diagnosis of the entire range of upper limb lesions , see Chapter 2 CHAPTER 19 Common upper limb musculoskeletal lesions 530 Shoulder (subacromial) impingement syndrome Shoulder impingement syndrome is caused by comp ression of the rota- tor cuff by the acromion. This results in shoulder pain, particularly when the patient reaches overhead, or rolls over the shoulder at night. Weakness and loss o f range of motion at the shoulder are also commonly reported. For diagnostic work-up and st eroid injection of the shoulder, see Chapter 2. \200 Shoulder impingement syndrome is the most common cause of shoulder pain in adults. Pain is often referred to the upper arm. \200 The causes include acute rotator cuff tendo nitis (which may be calci \201 c), subacromial bursitis, rotator cuff tear with cuff instability and impingeme nt, and glenohumeral instability owing to a number of different lesions (e.g., labral tear, synovitis due to crystalline arthritis). Inferior acromial osteophytes/AC joint OA can accompany any subacromial lesion, and are risk factors for recurrent rotator cuff disease. Long-term rotator cuff disease can lead to \200\230cuff arthropathy \200\231, with OA of the glenohumeral joint and signi \201 cant chronic morbidity. In children or young adults with shoulder impingement syndrome, consideration of an underly ing glenohumeral (instability) lesion is mandatory. Steps important in making a diagnosis \200 Exclude alternate causes of shoulder pain, inc luding rotator cuff tear, adhesive capsulitis, and referred pain from the neck or abdomen ( e.g., cholecystitis with pain referred to the shoulder). Elicit evidence of shoulder impingement by testing passive range of motion at the shoulder while applying 5 \200\22310 lb of pressure down on the acromion (see Table 19.1). An AP X-ray can show speci \201 c changes (see Plate 2) that identify underlying glenohumeral or bony pathology. Plain radiographs are also useful for identifyin g calci \201 c tendonitis. Consider requesting an AP view with 30 external rotation at t he arm, an outlet Y view, and an axillary view. MR may be necessary to rule out subtle glenohumeral pathology. MR characterizes sites of cu ff in \202 ammation and is more sensitive than US in identifying cuff tears. SHOULDER (SUBACROMIAL) IMPINGEMENT SYNDROME 531 Conservative management of cuff/SA bursal in \202 ammation (see Figure 19.1) \200 Avoid overhead arm activities. \200 Trial a full-dose regular NSAID for 2 weeks. \200 If the rotator cuff is intact, consider steroid injection (e.g., triamcinolone acetonide 40 mg; see Plate 13) and local anesthetic injection (e.g., 5 ml 1% lidocaine). Approach laterally or posteriorly. \200 Consider physical therapy 1 \200\2232 weeks later if the cuff muscles are weak. \200 Consider a second injection after 6 weeks . Table 19.1 The range of disorders presenting with a subacromial impingement pattern of pain . Clinical testing, though it can be elaborate, has been shown repeatedly in studies not to be as speci \201 c as the original literature appeared to suggest. Condition Diagnosis made by Supraspinatus/cuff tendonitis MR or US Subacromial bursitis (e.g. trauma, RA, gout, CPPD) US/MR Rotator cuff tear (partial or full) MR Long head of biceps tendonitis Clinical, US/MR OA ACJ (impingement of osteophytes on cuff) Clinical, X-rays, MR Glenohumeral instability due to labral trauma (e.g., SLAP lesion), arthritis GH joint MR Enthesitis (e.g. deltoid origin at acromion) in SPAs Clinical, US Lesion at suprascapular notch (e.g., cyst, tophus) MR CHAPTER 19 Common upper limb musculoskeletal lesions 532 Subacromial impingement highly likely on clinical grounds ?Glenohumeral joint pathology X-ray and MR or CT-arthrogram Yes No No Yes Good strength and bulk in supraspinatus, infraspinatus, and LH of biceps tendon? Has had 2 injections? No Yes Assume no major cuff tear No Either: Regular NSAID or Inject long acting steroid* mixed with 0.5 \200\2231.0 cc of 1% li docaine under acromion and start physical therapy 2 weeks later Review in 6 weeks ?Better Yes or Discharge Use 20 \200\22340 mg triaminolone acetonide (e.g., Kenolog) or methylprednisolone acetate. Fig. 19.1 Pragmatic algorithm for managing subacromial impingement pain. ADHESIVE CAPSULITIS (AC) 533 Adhesive capsulitis (AC) Pain and diminished active and passive range of motion (in the abs ence of an intrinsic joint disorder) is highly suggestive of AC. The etiology is unknown, b ut it involves capsular and coracohumeral ligament contrac- tures. The condition is more co mmon in women than men (typically affecting women age 40 \200\22360 years), and is four tim es more common in diabetics. AC occurs bilaterally in 15% of patients. Recurrence is unusua l. If left alone, pain usually resolves within 2 years, but the patient may be left with lo ng-term restriction of shoulder movement. Making the diagnosis \200 Do not confuse AC with shoulder impingement syndrome. With impingement, passive range of motion remains intact, and is less painful than active moveme nts. With AC, both passive and active ranges of motion are equally impaired. Clues to the diagnosis from examination include marked restriction of external rotation; al so, with abduction, the scapula moves very early \200\224 normally it doesn \200\231t move until 30 of abduction has been completed. If the presentation is delayed (e.g., >6 months), a secondary impingement syndrome may have evolved as some range of motion begins to return. Principles of management \200 Rule out associated conditions: diabetes, hypothyroidism, l ung carcinoma, myocardial infarction, stroke, and protease inhibitor use for HIV infection. Control pain during the initial painful \200\223stiff phase of the condition. Consider NSAI Ds, intra-articular steroid injections (e.g. 40 mg triamcinolone acetonide + 5 \200\22310 m l 1% lidocaine), suprascapular nerve block, or a short course of prednisone (starting with 30 mg/d) for 3 weeks. 1 Mobilize with physical therapy early, but be aware this may be limited by poor pain control. Consider surgery if conservative management fails after 6 months. Surgical procedures focus on releasing contracted/ \201 brotic tissue of the anteroinferio r capsular structures. Procedures associated with good results include arthroscopic or open release with manipulation under anesthesia (MUA) or arthroscopic release alone. The latter may be combined with steroid injections. 1 Buchbinder R, Hoving JL, Green S et al . Short course prednisolone for adhesive capsuliti s: a ran- domised, double blind, placebo controlled trial. Ann Rheum Dis 2004; 63 :1460 \200\2239. CHAPTER 19 Common upper limb musculoskeletal lesions 534 Lateral epicondylitis (tennis elbow) This condition is common, affecting 1 \200\2233% of th e adult population, typically in the age group 40 \200\22360 years. The dominant arm is mos t affected. It is rare in elite tennis players, but up to 40% of social players get it at s ome time. About 90% of all patients seen in clinical practice do not get this from playing tennis! It is thought to be due to cumulative trauma overuse disorder from mechanical overloading. If chronic, it can lead to tendon degeneration and osseous changes. Poor prognosis is assoc iated with manual work, high level physical strain at work, and high baseline pain and dist ress. Diagnostic procedures \200 The main differential diagnoses are: elbow joint lesions, refe rred neck pain and enthesopathies (e.g., DISH or enthesitis linked to spondyloarthropathies \200\224see Chapter 8). Pain is elicited by resisted force in pronation (e.g., handshakes, turning doorknobs, carrying bags). There is tenderness at the lateral humeral condyle with pain elicited by resisted \201 ng er and wrist extension. Pain often extends down the extensor side of the forearm. Enthesopathies, tendon tears, and joint lesions may be diagnosed by an experienced musculoskeletal ultrasonographer. MR may miss mild epicondylitis/enthesitis and appearances are not speci \201 c. MR is more useful for ruling out tendon tears and joint lesions. Do not use MR of the elbow to discri minate elbow lesions from referred neck pain. Principles of management \200 During the acute phase, lateral epicondylitis should be tre ated with activity restriction, pain control, and immobilization. Injection around the epicondyle with triamcinolone should be considered if conservative therapy is insuf \201 cient. \200 Isometric grip exercises ma y also help with recovery. \200 Surgery is rarely indicated, and should be considered onl y in patients with persistent symptoms despite several months of therapy (see Figure 19.2). LATERAL EPICONDYLITIS (TENNIS ELBOW) 535 Establish diagnosis accurately clinically (see text) Inform and educate about triggering factors e.g. at work. Remove or reduce triggers Long-standing or previous treatment New New or long-standing/ previously treated? Hydrocortisone injection 25 mg and NSAID. Review in 4 weeks Consider 2nd injection with triamcinolone actonide 20 mg or methyl prednidolone acetate or acupuncture, physical therapy therapeutic US and review in 4 weeks Better? No Yes Review in 4 weeks and discharge if better Yes No MR or US Better? Yes LE confirmed or tendon tear Refer to orthopedic surgeon Yes Other elbow lesion? Manage accordingly Yes Consider other diagnoses: ?referred neck pain ?chronic pain syndrome Normal imaging Fig. 19.2 Pragmatic algorithm for managing lateral epicondylitis (LE). This page intentionally left blank 537 Chapter 20 Back pain Conditions causing acute or subacute back pain in adults 538 Management of chronic back pai n 544 Management of back pain in children and adolescents 546 CHAPTER 20 Back pain 538 Conditions causing acute or subacute back pain in adults Acute mechanical back pain \200 Most cases in a primary care setting are due to lumbar muscle strain or sprain; this presents with diffuse pain in the lower back to buttocks, and resolv es spontaneously. If pain is related to posture or movement, especially of the thoracic cag e, and local tenderness is felt at the lumbosacral junction, then the pain is highly likely to be musculoskeletal. The clinician should be aware of \200\234red \202 ags \200\235 that may mandate more thorough investigation, such as cauda equina syndrome, saddle anesthesia, leg weakness, bil ateral sciatica, and bladder dysfunction (see Table 20.1). Herniated disks account for 4% of lower back pain. Disc herniation presents with leg pain radiating past the knee, and is most common in patients between 20 a nd 50 years old. Degenerative causes of back pain, including degenerative disc disease, facet joint hypertro phy and spinal stenosis, are more common in older patients (see Facet Hypertrophy/Facet Joi nt Syndromes, later in this chapter). The immediate management is adequate and regular analgesia (not \200\234as needed \200\235 ), advising only minimal bed rest, encouraging mobilization and normalization of activities . Short courses of muscle relaxants such as cyclobenzaparine (10 mg po qhs, up to tid) should be considered; these agents decrease muscle spasm and aid sleep. The clinician should explore patient fears and, when appropriate, reassure that serious illness is unlikely, tests are not usually needed, severe pain is oft en short-lived but milder pain may be present for longer, and that recurrences are common. Radiographs are likely to be unhelpful for planning management in most cases and radiologists often advise against getting them. MR of the lumbar spine, for example, frequently demonstrates abnormal \201 ndings in asymptomatic patients; the relat ionship between such \201 ndings and clinical symptoms is not always clear. A rehabilitation approach should be considered (see Table 20.2). The strength of evidence f or therapies is variable. Adherence may be a problem with rehabilitation programs but adher ence may be augmented by providing patient education literature. A study by the U.S. Preventative Services Task Force (USPSTF) concluded that there was insuf \201 cient evidence to recommend the use of exercise to pre vent back pain, although this may still be worth considering. CONDITIONS CAUSING ACUTE/SUBACUTE BACK PAIN IN ADULTS 539 Table 20.1 Warning signs for sinister pathology in back pain 1 Red- \202 ag signs: 1. First pain age <20 or >55 years 6. Immunosuppression/steroids 2. Pain at rest 7. Malaise/weight loss 3. Trauma 8. Osteoporosis 4. Progressive neurologic de \201 cit 9. Intravenous drug use 5. History of cancer 10. Failure to improve in 6 weeks Table 20.2 Therapies used in facilitating rehabilitation after acute mechanical low back pa in Manipulation Either done by an osteopath, chiropractor, or physical therapist. Some controversy about th e size of bene \201 t due to poor methodological studies. Avoid using in cases of intracta ble back pain (see Chronic back pain). McKenzie exercises Passive extension exercises designed to improve pain and stiffness associated with disc and anterior spinal structure pathology. May aggravate pain from posterior spine structures, e .g., facet joints, spinous processes. Hydrotherapy or balneotherapy Poorly studied but warmth can ease movement and augment land-based exercises. Might be cons idered after initial painful phase to regain normal movements and mobility. Obviously will only suit a few patients and resources may be limited. Graded activity programs Useful for patients who require guidance and would be unable to gain optimally from home ex ercise regime. A plan for rehabilitation with milestones is useful for some patients. Behavioral programs Focuses on psychological aspects of pain, involves moderate supervision and planned withdra wal of treatment. Differs from some other approaches in that the therapist takes on the \200\234control \200\235 of the back pain. Limited resources may restrict provision of this approach. Choice of patients for program important, although data are limited. CHAPTER 20 Back pain 540 Back pain and nerve root lesions (see also Chapter 2) \200 Root compression occurs most o ften because of acute or subacute disc prolapse or foraminal stenosis. The peak incidence i s age 30 \200\22350 years. About 70% resolve within 3 months and 90% within 6 months. \200 Root compression should be suspected if acute or subacute back pain is associated with segmental nerve or sciatic leg pain. Acute sciatic pain (affecting the outer and posterior leg) is often sharp or burning in nature, and most frequently arises from acute disc prolapse of either L 4/5 or L5/S1 (>90% cases). Sciatica is characterized by leg pain projecting past the knee, which may be more severe than the associated back pain. A patient with a herniated disc may present with complaints of sciatica; evidence of disc herniation may be elicited through physical examination by strai ght leg raise or crossed straight leg raise (i.e., elevation of unaffected leg). These test s are positive if pain is felt in the buttock or back at a leg angle of 30 \200\22360 . Pain elicited at a leg angle <10 is consistent with musculoskeletal back pain. A neurologic examination is essential: L5 root lesions give decreased strength of the foot and great toe dorsi \202 exion, standing on heel, and decreased ankle re \202 ex and sens ation over great toe. S1 root lesions give decreased strength in plantar foot \202 exion, dif \201 culty weight-bearing on toes, and decreased ankle re \202 ex and sensation on t he sole or outer part of foot. Principles of management \200 In general, 30 \200\22360% of patients recover in 1 week. \200 NSAIDs, acetaminophen, and muscle relaxants should be considered \201 rst. Some pat ients will require narcotics for pain control. Bed rest should be limited; prolonged bed re st leads to worse outcomes. \200 An epidural steroid injection can improve pain in the sh ort term, but its impact on long-term outcomes is less clear. A meta-analysis showed that 1 in 7 patients who receive a steroid epidural experience >75% improvement in pain in the short term and 1 in 13 get >50% symptom improvement in the long term. Physical therapy and supervised rehabilitation using lumbar extensor exercise regimes may be of bene \201 t. MR can characterize lesions, but 25% of asymptomatic people have frank disc protrusions; th us MR gives poor speci \201 city. MR should be used only to con \201 rm a diagnosis. The absolute indications for surgery (see Table 20.3) are cauda equina, progressive muscle weakness, and neuropathy causing functional disability. Facet hypertrophy/facet joint (FJ) syndromes \200 FJ OA of the lumbar spine is common in middle-aged/elderly adults, can be part of in \202 ammatory generalized OA, and is associa ted with spondylolytic spondylolisthesis (i.e., forward slippage of a vertebra, usually L5, in relationship to the vertebrae below). Psoriatic arthritis (see Chapter 8) can also affect FJs and is under- recognized as a cause of low back pain. CPPD arthritis (see Chapter 16) may also affect FJs. CONDITIONS CAUSING ACUTE/SUBACUTE BACK PAIN IN ADULTS 541 Table 20.3 Surgical approaches for lumbar disc prolapse Discectomy Essential for disks causing cauda equina syndrome and progressive neurological de \201 cit s. Excluding aforementioned indications, compared to conservative therapy, in a RCT 66% vs. 33% patients were satis \201 ed following surgery at 1 year, 66% vs. 51% were satis \201 ed at 4 years; thus bene \201 t of surgery in the long term is small. Adverse events with surgery include: mortality (<0.2%), dural tears (4%), permanent nerve root injuries (<1%). 70% success rate in short term. Risk of failure from surgery relates to hysteria or hypoch ondriasis scores on MMPI* and presence of litigation claims. Smaller surgical \201 eld re sults in earlier mobilization and less postoperative disability. Outcomes similar to those of conventional discectomy. Suctioning of central disc material causing disc decompression and relieving nerve root pressure. Associated with low complication rate and rapid rehabili tation. Non-RCT data suggest similar ef \201 cacy to discectomy. Injection of proteolytic enzyme into disc. RCTs suggest standard discectomy is superior. Rare but devastating neurol ogical complications and risk of anaphylaxis (0.3%). Vaporizing of part of disc by laser in troduced through a needle probe. Ef \201 cacy possible similar to discectomy. No RCT data. Microdiscectomy Percutaneous discectomy Chemonucleolysis Laser lumbar discectomy Prosthetic intervertebral disc replacement Also indicated for degenerative disc disease, post- laminectomy syndrome and nonspeci \201 c persistent low back pain. Arti \201 cial disks consist of 2 endplates separated by plia ble inner core. Anterior approach needed. Good results reported in open series for pooled p atient groups. Complication rate may be high (up to 45%). MMPI = Minnesota Multiphasic Personality Inventory. Typical symptoms include pain on hyperextension or rotation of the lower back; pain is refe rred to the upper buttocks, is worse while standing still, and eased by forward lumbar \202 exion. Facet hypertrophy itself cannot be felt, but FJ syndrome is accompanied by muscle spasm and super \201 cial soft-tissue tenderness. Arthritic FJs may be seen on oblique spinal radiographs; however, imaging in general cannot reliably identify symptomatic FJ joints. Facet joint injection wi th anesthetic may con \201 rm the diagnosis if this results in signi \201 cant pain relie f.