697 Clinical features of osteomyelitis Patterns of infection Cancellous bone is typically aff e cted in adults \200\224commonly in vertebrae (IV drug use) and feet (diabetics); in childre n, vascular bone is most aff ected (eg in long-bone metaphyses \200\224esp. distal femur, u pper tibia). Infection leads to cortex erosion, with holes (cloacae). Exudation of pus lift s up the periosteum interrupting blood supply to underly- ing bone and necrotic fragments o f bone may form (sequestrum). The presence of sequestra is typical of chronic infection. Ne w bone formation created by the elevated periosteum forms an involucrum. Pus may discharge into joint spaces or via sinuses to the skin. The patient Pain of gradual onset over the co urse of a few days \200\224with ten- derness, warmth, and erythema at the aff ected part; u nwillingness to move; slight eff usion in neighboring joints; signs of systemic infection. All signs are less marked in adults. Risk factors \200 Diabetes \200 Vascular disease \200 Impaired immunity \200 Sickle cell disease \200 Surgical prostheses \200 Open fractures \200 Impaired immunity a m u a r t d n a s c i d e a p o h t r O Fig 2. Axial T1-weighted MRI of the foot through the metatarsals, showing reduced signal wi thin the \201 rst metatarsal (from replacement of the marrow fat with pus) consistent wit h osteomyelitis. Fig 1. Osteomyelitis causing destruction of the 5th metatarsal head and the base of the 5th proximal phalanx. Note also the vascular calci \201 cation in this patient, who had diabe tes. Fig 3. Axial T1-weighted MRI of the same patient as \201 g 2, this time with FAT SAT (fat saturation) and IV gadolinium contrast. The eff ect of this technique is to suppress the m arrow fat and enhance the infection. Images courtesy of Norfolk and Norwich Uni- versity Hospital (NNUH) Radiology Department. Bone tumors: malignant Tumors present with pain, swelling or pathological fracture. Bone is a common site for secondaries (eg from breast, bronchus, prostate, kidney). Primary bone n eoplasia is rare: incidence of 9 per million population/ year.132 Delays in diagnosis are c ommon. Metastases are blood-borne and usually arise in the lungs or other bones. Staging is done with MRI or combination techniques such as PET-CT.133 Treatment of these rare and hig hly aggressive primary tumors is best carried out in multidisciplinary specialist treatment centers. Osteosarcoma is the most common malignant primary bone tumor.1 Pri- mary osteosar coma typically aff ects adolescents and arises in the metaphyses of long bone, especially a round the knee. Secondary osteosarcoma may arise in bone aff ected by Paget \200\231s disea se or after irradiation. Radiography: Bone destruction and new bone formation, often with m arked periosteal elevation (sunray spiculation and Codman \200\231s triangle, respectively) . Treatment: Resection + chemotherapy, eg doxorubicin, cisplatin and methotrexate.134 A cur e rate of 60 \200\22370% is achievable.134 Giant cell tumor Rare tumor \200\224characteriz ed by multinucleated giant (osteoclast like) cells \200\224hence also called osteoclastoma. This histologically \200\230benign \200\231, primary skeletal neoplasm, with unpredictabl e biological aggressive- ness, is commonest in 20 \200\22344-yr-olds.135 It occurs around e piphyses (esp. knee). The tumor is osteolytic and often slowly progressive, sometimes resul ting in pathological fracture. Treatment is by detailed and thorough curettage result- ing in 75% cure. Recurrences are usually treated by wide excision. Ewing \200\231s sarcoma This malignant round-cell tumor of long bones (typically diaphysis) and limb girdles, usually p resents in adolescents. Radiographs show bone destruction, concentric layers of new bone fo rmation ( \200\230onion-ring \200\231 sign) and a soft tissue mass. MRI is helpful. Typical ly those with Ewing \200\231s sarcoma have a t11 : 22 chromosomal translocation. Treatment: Chemotherapy, surgery and radiotherapy are required. The key adverse prognostic factor is metasta- ses at diagnosis (5-year recurrence-free survival is 22% \200\224vs 55% if no meta s- tases at diagnosis).136 n=975 Chondrosarcoma may arise de novo or from malignant transfo rmation of chondromas. It is usually associated with pain or a lump and presents in the axi al skeleton of the middle-aged. \200\230Popcorn calci \201 cation \200\231 is typical on radiog- raphy. MRI/CT will better de \201 ne tumor extent. Treatment: It doesn \200\231t r espond to chemotherapy or radiotherapy, so treatment is by excision. Inadequate surgery is accompanied by local recurrence, often of a higher grade of ma- lignancy. The cure rate dep ends on the type and grade of chondrosarcoma at diagnosis. Malignant \201 brous histiocyt oma is the rarest primary bone tumor. It arises in middle age, often at the site of a previ ous bone abnormality (eg bone in- farcts). Treatment is as for osteosarcoma. Chordomas aris e from notochord remnants in the spine and are typically sa- cral, and quite big before a d iagnosis is made. Bladder & bowel sphincter prob- lems may occur. Radical surgery + pre-op radiotherapy cure <20%. The others may have a slow and diffi cult death.137 Surgical recons truction (after excising a bone tumor) may involve replac- ing aff ected bone with a metal and polyethylene endoprosthesis \200\224as an alter- native to amputation. Excellent and du rable reconstruction is possible using massive endoprostheses or bone allografts. 85% of pa tients now have limb salvage following chemotherapy for primary bone tumors. 698 \200 Radiological features \200 Bone destruction \200 New bone formation \200 Soft tissue swelling \200 Periosteal elevation a m u a r t d n a s c i d e a p o h t r O 1 There are many diff erent subtypes, including intramedullary, periosteal, parosteal & tel angiectatic. 699 Bone tumors: benign Osteochondroma is the commonest benign bone tumor, usually occurring ab out the knee, proximal femur, or proximal humerus. Presents as a painful mass associated wi th trauma. Seen on x-ray as a bony spur arising from the cortex and usually pointing away f rom the joint.Treatment: Remove if causing symptoms, eg pressure on adjacent structures. An y osteochondroma continu- ing to grow after skeletal maturity must be removed because of ri sk of malig- nancy (arises rarely in solitary osteochondromas but in up to 10% of patients with hereditary multiple exostoses \200\224an autosomal dominant inherited condi- tion). Os teoid osteoma is a painful benign bone lesion that occurs most commonly in long bones of ma les 10 \200\22325yrs old (and also often in the spine). It appears as local cortical sclero sis on radiographs with a central radiolucent nidus. Within the nidus there may be a small nucleus of calci \201 cation The nidus produces prostaglandins leading to pain unrelated t o activity, and relieved by aspirin (and other prostaglandin inhibitors) Treatment: CT guid ed biopsy and radio- frequency ablation.138 NB: in young adults, any bone pain responding t o aspirin within 15min could be caused by an osteoid osteoma. Plain radiographs may miss th ese tumors. CT is the best imaging modality.139 Chondroma These benign cartilaginous tumors may arise from bone sur- faces or within the medulla (=enchondromata). They may cause loca l swelling or fracture. Treatment is rarely needed, except to exclude malignancy (chon- dro sarcoma \200\224see OPPOSITE). NB: Carney \200\231s syndrome is gastric leiomyosarcoma, plu s pulmonary chondroma plus a non-adrenal paraganglioma.140 Fibrous dysplasia of bone is a d evelopmental abnormality where bone is not properly formed. May lead to pain and increased risk of fracture. Surgical stabilization is sometimes needed. In the polyostotic form bisph osphonates may help relieve symptoms. a m u a r t d n a s c i d e a p o h t r O Soft tissue sarcomas (STS)1 STS are uncommon ( 1500/yr in UK) but can arise in any mesenchy mal tissue, originating from fat, muscle etc, presenting as a painless enlarging mass. Risk factors include neuro \201 bromatosis type 1 (OHCM, p518) and previous radiotherapy. Diag nosis: Any lump that has any feature from the MINIBOX is to be considered malignant until p roved otherwise. Imaging with MRI followed by needle biopsy at a specialist sarcoma unit is recom- mended. Pathological diagnoses include rhabdo-myosarcoma (most common in children), liposarcoma, leiomyosarcoma, \201 brosarcoma etc. Gene expression pro \201 ling is help ing to improve diagnosis and indicate tumors which may respond to chemotherapy. Treatment i s by excision with wide margins fol- lowed by radiotherapy for most. Alkalylating agents: t rabectedin has a role.1 Most adult STS are not sensitive to other chemotherapy but it may b e used for metastatic disease. Prognosis is related to histological grade, size and depth o f the tumor. High-grade, large, deep tumors have <50% 5yr survival. STS in children often r espond well to chemotherapy; survival is better. Consider STS malignant if \200 Bigger than 5cm \200 Increasing in size \200 Deep to t he deep fascia \200 Painful Gastrointestinal stromal tumors (GIST) GIST is an easy-to-misdiagnose submucosal sarcoma ar ising chie \202 y in the upper GI tract. It is the commonest GI mesenchymal neoplasm. Trea tment: Surgery. 50% recur and spread to liver. Imatinib can help.141 1 NICE have advised on care of soft tissue sarcoma: www.nice.org.uk/page.aspx?o=csgsarcoma. \200 142 Congenital disorders of bone and cartilage1 Osteogenesis imperfecta (OI) is an inherited di sorder of type I collagen that results in fragile, low density bones. It aff ects 1 in 20,0 00. OI has historically been classi \201 ed into four forms (although type IV, the most di verse, has re- cently been expanded into types IV \200\223VII). 700 I The mildest and most common form. It is autosomal dominant. Associated with blue sclerae (due to increased corneal translucency) and 50% have hearing loss. Fractures typically occu r before puberty. There is a normal life expectancy. II Lethal perinatal form with many fractures and dwar \201 sm; it is recessive. III Severe form \200\224occurs in about 20%. Recessive. Fractures at birth + progressive spinal and l imb deformity, with resultant short stature; blue or white sclera; dentinogenesis imperfect a common (enamel separates from defective dentine, leaving teeth transparent or discolored) ; Life expectancy is decreased. a m u a r t d n a IV Moderate form, autosomal dominant. Fragile bones, white sclerae after infancy. Radiographs: Many fractures, osteoporotic bones with thin cortex, and bow- ing deformity of long bones. Histology: Immature unorganized bone with abnormal cortex. Treatment: Prevent injury. Physio, rehab and occupational therapy are key. Osteotomies may correct deformity. Intramedullary rods are sometimes used in long bones. Medical treatments include bisphospho nates Current research is looking at the possibility of gene therapy.143 Achondroplasia is the most common form of disproportionate short stature.It occurs due to reduced growth of c artilaginous bone It is autosomal dominant, but 80% are from spontaneous mutation. 95% are caused by mutation in the gene encoding \201 broblast growth factor receptor type 3 (FGF R3).144 Aff ected ba- bies have large heads (>97th centile) with ventriculomegaly and front al bossing, normal trunk length, short limbs, and \201 ngers all the same length. Gross m otor skills develop later \200\224only 50% sit unsupported at 9 months, and only 50% walk a lone at 18 months.144 Condition speci \201 c growth charts are available to monitor develo pment.145,146 Adults are short with \200\200lumbar lordosis, bow legs, and short proximal arms & legs. Lifespan, mental & sexual development are normal. Com- plications include tibi al bowing, joint hypermobility, hydrocephalus, foramen magnum compression (5 \200\22310%), recurrent otitis media and hearing loss, sleep ap- noea (75%) and \200\200BMI Radiographs: Short proximal long bones (rhizomelic short- ening) & wide epiphyses. Treatment: Involves monitoring for potential complica- tions. Growth hormone has been tried.147 Hereditary mult iple exostoses (HME \211\210 diaphyseal aclasia) is an autosomal dominant disorder in whic h certain proteins accumulate in the Golgi appara- tus leading to cartilage-capped tumors ( exostoses/osteochondromata) de- veloping from aff ected cartilage at the end of long bones. These point away from the nearby joint. If severe, bones are broad and badly modeled, caus ing short stature as well as forearm, knee, and ankle deformity. Beware of ma- lignant tran sformation to chondrosarcomas2 or osteosarcomas. HME is usu- ally caused by defects in vari ous EXT genes which encode enzymes catalyzing synthesis of heparan sulfate, an important co mponent of the extracellular ma- trix. Treatment: Removal of symptom-producing exostoses.14 8 Osteopetrosis Lack of diff erentiation between cortex and medulla of bone (from underlyin g failure of osteoclastic bone resorption) results in very hard dense \200\230marble \200 \231 bones that are brittle. Anemia and thrombocytopenia may result from decreased marrow s pace. Deafness and optic atrophy can result from compression of cranial nerves. Lack of rem odeling preserves variations of ossi \201 c density causing the characteristic \200\230bo ne within a bone \200\231 appearance. s c i d e a p o h t r O 1 See Neuro \201 bromatosis (OHCM p518), Marfan \200\231s (OHCM p720), Ehlers \200\223Danl os & Morquio \200\231s, p143. 2 Cartilage tumor classi \201 cation: Is the lesion benign o r malignant? Is the lesion a pure or impure cartilaginous tumor? Is the epicenter of the le sion intraosseous, juxtacortical, or in the soft tissues? The most common benign tumors are enchondroma, osteochondroma, chondroblastoma, and chondromyxoid \201 broma. Chondrosarco ma is malignant.149 701 Developmental bone biology Because bone is ossi \201 ed, we tend to think of it as the arc hitectural rock around which our living tissues are constructed. But bone maintenance and d evelopment is a highly dynamic and regulated process sensitive to a wide variety of hormone s, in \202 ammatory mediators, growth factors, and genetic in \202 uences which become ab errant whenever there are deletions, insertions, and missense mutations.150 The concept of a master gene is useful to indicate how genes relate and interact. Master genes encode prot eins that can control other genes by directly binding to their DNA, for example, transcript ion factor OSF2 (osteoblast speci \201 c transcription factor 2) gene is thought to serve as a master gene regulating expression of other genes, allowing mesenchymal stem cells to d iff erentiate into osteoblasts. OSF 2 maps close to a chromosomal locus on chromosome 6P21 (thought to be important eg in craniocleidodysos- tosis). NB: master genes make a mockery o f genes vs environment questions. One gene is an environment for another, and the eff ects of each may be cata- strophic in some environments or negligible in others. a m u a r t d n a s c i d e a p o h t r O Remain in light \200 the diff erent types of bone \200 Cancellous Trabeculations form a n et- work of parallel lamellae, the spaces be- ing \201 lled with connective tissue or bon e. This type of bone does not make callus when healing; also called \200\230spongy \200 \231 bone. Cartilagenous Formed from growth plates (p683). Compact Non-cancellous bone that is formed from Haversian canals and con- centric lamellae. Cortical The super \201 cial thin layer of com- pact bone. Fig 1. Lamellar bone architecture. Endochondral Develops in cartilage that has been destroyed by calci \201 cation and subsequent resorption. Heterotopic Forms outside the normal skeleton either from a pathological process (eg in the heart) or as a reaction to local trauma/surgery. Lamellar The overall normal type of adult bone (subdivided into cancellous and compact), ch aracterized by repeating architectural patterns \200\224 \201 g 1. \200 Membranous Forme d from intramembranous ossi \201 cation (eg clavicle). \200 Sesamoid Bone formed in a te ndon where it passes over a joint (eg the pisiform bone in \202 exor carpi ulnaris, and the patella). Woven Embryonic bone in which the connective tissue \201 bres are arranged and interlaced irregularly. Remain in light \200 The diff erent types of joint \200 Cartilagenous, primary Hyaline ca rtilage between the bone ends. Only types are the costochondral and sternochondral (1st rib) joints. Cartilagenous, secondary As above, but with a layer of \201 brocartilage be- tween the la yers of hyaline cartilage. Only types (that all lie in the midline) are the manubriosternal , intervertebral, pubic symphysis, xiphisternal and sacrococcygeal joints. Fibrous Fibrous tissue between bones; eg radio-ulnar interosseous membrane. \200 Synovial Joint cavity containing synovial \202 uid, with hyaline cartilage on the bone surface; eg acetabulofemoral, glenohumeral. Synovial, atypical Joint cavity containing synovial \202 uid, with \201 brocartilage on the bone surface a \201 brocartilage disc; eg acromioclavicular and ster- noclavicula r joints (with disks). NB: \201 brocartilage is found on the articulat- ing surface of an y bone that undergoes intramembranous ossi \201 cation. Osteochondroses I The osteochondroses are a group of conditions characterized by the abnorm al endochondral ossi \201 cation of epiphyseal growth during childhood. Osteochon- drosis (also called osteochondritis) occurs in the wrist, elbow, hip, knee, an- kle, \201 ngers, toes and spine. The underlying cause of most osteochondroses is unknown, although inherita nce, overuse/trauma, rapid growth and anatomic con \201 guration may be predisposing facto rs. All osteochondroses undergo an interuption of blood supply to the epiphysis, followed b y bone and cartilage necrosis, revascularization and regrowth of bone Scheuermann \200\231s disease The commonest cause of kyphosis in 13 \200\22316-yr-olds. It is an autosomal domin ant. The normal ossi \201 cation of ring epiphyses of sev- eral thoracic vertebrae are aff ected. Deforming forces are greatest at their anterior border, so vertebrae are narrower h ere, causing kyphosis. During the active phase, vertebrae may be tender. Patients appear ro und shouldered and hunched \200\224they tend to present for deformity rather than pain. R adiographs: Irregular vertebral endplates, Schmorl \200\231s nodes and \200\201disc space anterior wedging. 3 adjacent vertebral bodies of at least 5 of wedging is pathogno- mo nic. Schmorl \200\231s nodes are herniations of the intervertebral disc through the vertebr al endplate. Treatment: If posture control (eg standing during lessons rather than sitting) and exercise (eg swimming) fails, physiotherapy spinal braces can help, though curvatur e may recur over time after discontinuation of bracing. Surgery may be tried for severe kyp hosis (>75 ) with curve pro- gression, refractory pain, or neurological de \201 cit.151 C alv \200\231s vertebra Presents with symptoms similar to Scheuermann \200\231s disease bu t in a younger age group (typical age is 2 \200\22310yrs). Unlike Scheuermann \200\231s dis ease is not due to ischaemic necrosis but to eosinophilic granulomata (de- tected via CT gu ided biopsy) \200\224thus it is not a true osteochondrosis. Typical site is a thoracic vert ebra; if cervical/atlas, torticollis may result. Symptoms: Pain tenderness over the aff ected vertebra; slight kyphosis. Imaging: Radiographs/ CT/MRI can show dense, \202 attene d vertebral body with disc space preserved; bone scans can show a hyperactive spot. \202 \202 \202\202 : Sarcoma; osteomyelitis. Treat- ment: Bed rest plaster cast immobilizatio n. Kienb ck \200\231s disease Aff ects male adults 20 \200\22340 years. Pain is felt over the lu- nate (esp. during active wrist movement). Grip is impaired due to pain. As- sociate d with negative ulnar variance. Radiographs: Dense lunate with a little depth reduction ear ly; more marked \202 attening later, leading later to osteoar- thritis. Treatment: Early: manage symptomatically with splinting and analge- sia; early + suffi ciently symptomatic: ulnar lengthening or radial shortening, capitates shortening; late + symptomatic: proximal row carpectomy, intercar- pal arthrodesis, total wrist arthrodesis.1 Once arthritis is esta blished, lunate excision does not help. Wrist arthrodesis is the last resort. Panner \200 \231s disease/Osteochondritis dissecans (OCD) of the elbow represent a continuum of disease of the capitellum. Panner \200\231s disease is the avascular necrosis of the ossi \201 c nucleus of the capitellum. Mostly presents in boys un- der 10yrs, causing lateral elbow pai n and swelling. Conservative managment is usually all that is required. OCD of the elbow af f ects the surface below the car- tilage of the anterior capitellum. A loose body is formed (1 \200\2233cm across) from a convex joint surface when a segment of subchondral bone and cartilage be- comes avascular and separates from underlying bone. Adolescents experience ea rly aching and eff usions after use, and sudden painful locking of joints once pieces have separated to make loose bodies. Radiographs: Lucent areas in a piece about to separate, the defect from which the piece has separated, and loose bodies after separation. Treatment: S table lesions are managed conserv- atively in a hinged brace. Unstable lesions may need \201 xation removal of loose bodies. Closed wedge resection may lead to revascularizatio n.152 702 a m u a r t d n a s c i d e a p o h t r O The navicula is the bone at the top of the foot and is separated from the meta- tarsals by the 3 cuneiform bones with which it articulates. Moving proximally, it articulates with the talus. Navicula is Latin for a small ship. K hler \200\231s disease Children aff ected ar e 3 \200\2235-yr-olds. Pain is felt in the mid-tarsal region and they limp. There may be na vicular tenderness. Radiographs: Dense, deformed bone ( \201 g 1). Treatment: Symptomatic: resting the foot or wearing a walking plaster. Prognosis: Excellent, with very few longter m problems.138 Freiberg \200\231s disease (infraction) This may be classed as an osteochond ritis dis- secans of the lesser metatarsal heads, most commonly the 2nd. It presents as for efoot pain, that worsens with pressure, usually starting around the time of puberty. There may be microfractures at the junction of the metaphysis and the growth plate \200\224precis e etiology is unknown. Radiographs: Epiphysis of a metatarsal head becomes granular, fragme nted and \202 attened. Treatment: Good shoes metatarsal pad. Limit activity for 4 \200 \2236 weeks. If severe, consider removal of aff ected bone with bone grafting or interposit ional arthroplasty and use of a walking plaster. 703 a m u a r t d n a s c i d e a p o h t r O Eponyms of osteochondroses Eponym Friedrich disease Froelich disease Panner \200\231s disease (p702) Kienb ck \200 \231s disease (p702) Scheuermann s disease (p702) Perthes disease (p682) Blount disease Os good \200\223Schlatter disease (p704) Sinding \200\223Larsen disease (p704) K hler s disea se (above) Sever s disease (p704) Freiberg s disease (above) Site aff ected Clavicle Humeral condyles Capitellum of humerus Lunate bone (in adults) Vert ebral ring epiphyses Hip Proximal tibial epiphysis Tuberosity of the tibia Secondary patell ar center Navicular bone Calcaneal apophysis Head of 2nd or 3rd metatarsal Fig 1. Oblique radiograph of the left foot, showing sclerosis and deformity of the navicula , secondary to K hler \200\231s disease.1 Images courtesy of Norfolk and Norwich University Hospital (NNUH) Radiology Department. 1 Patients with Kienb k \200\231s disease who avoid surgery tend to change profession, whe reas surgery often results in being unable to return to the previous occupation. Osteochondroses 2 Osgood \200\223Schlatter \200\231s syndrome (OSS) is tibial tuberosity ap ophysitis that af- fects children 10 \200\22315yrs old. \200 : \200 \211\210 3 : 1. The \200\230accepted theory \200\231 suggests that re- peated traction causes in \202 ammatio n and chronic avulsion of the secondary ossi \201 cation center of the tibial tuberosity, leading to in \202 ammation, hence its association with physical overuse. The pain below t he knee is worse on strenuous activ- ity and quadriceps contraction (lift straight leg agai nst resistance). The tuberosity looks enlarged and is tender. OSS is self-limiting in >90% of cases. Radiographs: Tibial tuberosity enlargement ( fragmentation). Note the appearanc e of a normal immature tibial tuberosity, \201 g 1. MRI shows the tendonitis. NB: diagnos is is clinical, not simply radi- ological. Treatment: Standard treatment is limita- tion of activity, ice, oral anti-in \202 ammatories, knee padding and physiotherapy. Plaster cast immo- bilization is now uncommonly used as it leads to quadriceps wasting \200\224short-te rm immobilization Courtesy of Norfolk and in a brace is occasionally used.153 Tibial tuberc le Norwich University Hospital excision may be recommended if the above fail.154 (NNUH) Rad iology Department. Sinding Larsen \200\231s disease (jumper \200\231s knee) Traction tendin opathy with calci \201 - cation in the proximal attachment of the patellar tendon, which m ay be partially avulsed. Symptoms, treatment are similar to Osgood \200\223Schlatter \200 \231s disease (above), but the onset tends to be 1 \200\2232yrs earlier.155 Sever \200\231s disease This common calcaneal apophysitis is probably from strained attachment of the Achi lles tendon. It is usually self-limiting. Typical age: 8 \200\22313yrs. There is pain behin d the heel (bilateral in 60%) limping, and tender- ness over the lower posterior calcane al tuberosity. Radiographs: Often nor- mal. Treatment: Physiotherapy and heel raise. If nee ded, a below-knee walking plaster may give pain relief. Most are well after 5 weeks.156 Ava scular necrosis (osteonecrosis) Sites of infarction: Hip (commonest), knee, shoulder. Imagi ng: MRI is best; sclerotic or porotic bone due to infarc- tion; joint surface odd, osteocho ndral fragments.157 Local causes: Trauma (eg fractured neck of femur); secondary to rheumat oid, severe osteoarthritis, pso- riatic arthropathy, or neuropathic joints. Systemic: Thala ssaemia, sickle-cell (+ any cause of microthrombi, eg platelets \200\200 in leukemia), NSAI Ds/steroids (eg post-transplant), SLE, scleroderma, SBE, dyslipidaemia, alcoholism, pancrea ti- tis, diabetes, big burns, radiation, divers (p813), Cushing \200\231s & Gaucher \200 \231s diseases. Treatment: Immobilization; analgesia; for hips, arthroplasty.158 704 a m u a r t d n a Fig 1. Normal appear- ance of an immature tib- ial tuberosity on X-ray. s c i d e a p o h t r O 705 Sport and exercise medicine Sport and exercise medicine is a relatively new medical special ty that, in its broadest sense, encompasses performance in sport and the care of injury. Sp ecialties involved: \200 Clinical medicine \200 General practice \200 Orthopedics \200 Radiology \200 Physiology \200 Anatomy \200 Biomechanics \200 Kinetics \200 Physiotherapy \200 Podiatry \200 Nutrition \200 Pharmacology \200 Epidemiology \200 Psychology The ever-increasing standards and demands in professional sport have driven competitors to new heights and lengths (the consequences of which for some are justi \201 ably punishing) , but by far the larg- est group of those undertaking sport do so for pure enjoyment. The i mportance of health and exercise running in partnership cannot be understated, and helping all those who enjoy sport to be healthy and safe has become a multidisciplinary \201 eld with sub- stantial breadth of expertise (see MINIBOX). There are also other facets to this specialty, including per- formance in extreme environments and supporting those with medica l illness in sporting activity. a m u a r t d n a s c i d e a p o h t r O Overuse injuries are a major cause of morbid- ity \200\224see p715 for overuse phenomena ou tside sport.159,160 Repetitive activity, a mainstay of sport (eg as in baseball pitching, c ycling, golf, running), causes tissue damage over time, with rate of injury ex- ceeding rat e of recovery. There are many theories on the role of stress, me- chanical fatigue, and in \202 ammatory factors in causation. Symptoms depend on the site and type of tissue involve d (eg nerve, muscle, bone, tendon, liga- ment) but usually equate to local pain exacerbated by use. Problems com- monly seen include shin splints (shin soreness, common in un \201 t runners on hard surfaces and due to muscle tears, mild anterior compartment syndrome or st ress fracture) and tennis elbow, p666.1 84 Treatment This usually involves rest, physiother apy, technique evaluation, NSAIDs, local corticosteroid injection ( \200\207beware the comp lication of tendon rupture), or surgery on specialist advice. The threshold for treatment ( espe- cially surgery) may be diff erent for professional sports players. For soft tissue in juries, the treatment in the \201 rst 24h is \200\230RICE \200\231: Rest: Ice: A splint or plaster cast may help Cold is anesthetic and a vasoconstrictor. Apply ice packs (eg a packet of frozen peas wrapped in a cloth) or cold compresses intermittently for <10m in at a time, to avoid cold injury Compression: Strapping restricts swelling and further bleeding Elevation: Ideally elevate the aff ected part above the heart to improve drainage from the aff ected p art and to reduce pain \200\207Correct management reduces pain, recovery time and later disability. Rehabilitatio n Passive stretching to maintain joint mobility and muscle length, then progressive active exercise until the full range and strength of movement is restored, eg wobbleboards for ank les. Sportsmen must then retrain to full \201 tness. Also consider NSAIDs, rubefacients, and ultrasound. Prevention and safety are a vital part of good training and performance. \200 Is the patient preparing the body for activity with a proper warm-up? In- adequate warm-up increases the risk of injury. Cooling-down is also important in reducing muscle soreness. \200 Is (correct) protective equipment being worn? \200 Many acute and chronic injuries are caused by unsuitable equip ment, faulty technique, or unwise training schedules. \200\207Get advice from a coach. 1 Other relevant pages: Golfer \200\231s elbow, p666; tennis elbow, p666; iliotibial tract syndrome, p688; march fracture, p694; plantar fasciitis, p694; soft tissue injuries, p715; fractures in general, p734; injuries to the hand, p746; knee ligament injury, p754; ankle s train, p756; head injury, p758; heat exhaustion/injury, p788. Joint replacement Joint replacement has been used for at least 70yrs.1 Each year 80,000 hi ps and >80,000 knees are replaced in England and Wales.161 Hip replacement This is carried out to relieve pain and disability caused by arthropathies of the hip \200\22485% are to re place osteoarthritic hips. Other condi- tions which may result in replacement are: rheumato id arthritis, avascular necrosis of head of femur; congeni- tally dislocated hip; fractured neck of femur. Women outnumber men by 2 : 1; and the over 65-yr-olds ac- count for 2 in e very 3 procedures.163 Many prostheses are available; most consist of a metal femoral compo- nent with an intramedullary stem sometimes held in place by bone cement, and a plastic ace tabular compo- nent \200\224 \201 g 2. Early success of operation occurs in 90%. Later pro blems of loosening or infection are heralded by return of pain. If plain radiographs are in conclusive in the case of loosening, strontium or technetium scans may reveal increased bon e activity. Suspected sepsis should be investigated by WCC, ESR, and ultrasound-guided aspi ration. Revision arthroplasty is more successful for loosening than for infection. Joint su rvival: By 9 \200\22310yrs post-op 11% of implants have been revised. Be cautious in recomm ending replacement to those in their 60s who are likely to cause ex- cessive wear of the pr osthesis. Earlier replacement is used for rheumatoid ar- thritis as joints tend to be gross ly aff ected younger \200\224and excessive delay may result in surgery upon very rare \201 ed osteoporotic bone. Central migration of the prosthesis via perforation of the medial ac etabular wall is a rare cause of exter- nal iliac artery and bladder injury.165 Hip resurfa cing is an evolving method to consider for active people \200\20565yrs with endstage arthr opathy ( \201 g 3). It is experi- mental as long-term data are sparse. \200 166 In a 2008 trial, 93% had good/excellent results at 2 \200\2238yrs, and no loosening; revision rate: 4%.167 Knee replacement consists of resection of ar- ticular surfaces of the knee, then res urfacing with metal and polyethylene components. Replace- ment may be total or partial (uni compartmental). Indications for knee replacement: pain at rest, or disturbing sleep, or mak ing housebound. Pain correlates poorly with radiological signs. Success rate: 95%. Joint su rvival: 90% last 15yrs (better than hips). Revision rates are similar. Quality of life can be transformed, even if >80yrs old. Other joints Joint spacers are used in \201 nger join ts for rheumatoid, with success. Elbow re- placements are beginning to show some success. S houlder replacement ( \201 g 1) success rates are approaching those of knees. Preventing p ulmonary emboli (PE) Follow local evidence-based proto- cols. DVT occurs in \205\224 of m ajor orthopedic events, but fatal PE in only 0.1 \200\223 0.2%.168 n=130,000 Low-molecular weight heparin (LMWH) halves DVT rate and lowers risk of fatal PE by 75%.169 In major orth opedic surgery, low-molecular weight heparin (LMWH) is preferable to ordinary heparin. CI: uncontrolled bleeding/risk of bleeding (eg peptic ulcer); endocarditis; children. Dose exam ple: Dalteparin 2500U 2h pre-op and at 12h post-op, then 5000U once/day for 1 week. In knee s, fondaparinux 2.5mg/day may be better than enoxaparin.170 n=1049 The oral agents dabigatr an and rivaroxaban may be easier to take. DVT/PE prophylaxis may need continuing for 28 \200\22325 days post-hip surgery and 10 \200\22314 days post-knee sur- gery.2 NB: if rate o f fatal PE is always <<0.1%, in some centers prophylaxis may not be warranted.171 706 \200 Early complications \200 VTE 4% \200 Dislocation 3% \200 Deep infection 2% \200 Fra cture 1% \200 Nerve palsy 1% \200 Limb-length a m u a r t d n a discrepancy 1% \200 Death 0.4 \200\2230.7%164 s c i d e a p o h t r O Fig 1. AP image shoulder hemi- arthroplasty. Courtesy of Norfolk and Norwich University Hos pital (NNUH) Radiology Department. 707 Infected hip and knee prostheses This may be a disastrous complication of joint replacement \200\224presenting with pain, loss of function, fever, or wound in \202 ammation. Periope rative wound complications, obesity, increased age, diabetes mellitus, steroid use and rheu - matoid arthritis increase risk. Staphyloccal skin commensals are the most common infectiv e organisms Investigations: CRP/ESR, blood culture and aspi- ration of joint. Plain radiogr aphs may show peri-prosthetic loosening. CT/MRI may be of limited use due to artifact. Gall ium/labeled leukocyte imaging may be useful in hard to diagnose cases Treatment: Early on, debridement + anti- biotics may be enough. Later, with loosening of components, radical deb ride- ment must include removal of all prosthetic material, as well as any involved bone an d soft tissue. Sometimes reconstruction by exchange arthroplasty works, eg for less virulen t infections. Antibiotics may be needed for months. Patient selection is vital, eg those wi thout draining sinuses, without immuno- compromise, and with adequate bone quality after de bridement.172 The Mayo Clinic reports a 13% failure rate with a 2-stage reconstruction. a m u a r t d n a s c i d e a p o h t r O Another alternative may be the removal of all foreign material and allowing ankylosis to occur, ie a Girdlestone pseudarthrosis, for the hip. SBE \200\223style antibio tic prophylaxis antibiotic-impregnated cement? \200 Dentistry-associated prosthesis in fection with oral bacteria is very rare and risks of antibiotics are palpable (>500 penicil lin-caused deaths/yr, in the USA), and SBE-style prophylaxis is not recommended. Colonoscopy + polypectomy may be more risky than dentistry; some rec- ommend prophylaxis, if <6 months since replacement. The best prophylaxis might be achieved with a combination of gentamicin-im- pregnated cemen t, systemic antibiotics for >24h, and surgery performed in ultra- clean environments (lamin ar air \202 ow theaters/surgeons in space suits , although the additional cost of this m ay be prohibitive or prove to be ineff ective). Reim- plantation need not require use of ce ment: hydroxyapatite coated total prosthe- ses are an alternative.173 See \201 g 2 for th e usual constituents found in bone cement. Other systemic long-term complications of joint replacements174 Fine frag- mentation may lead to metal poisoning (eg cobalt) targeting mito chondria: suspect if visual/hearing loss and 24h urine cobalt excretion >1.5 g/L. Fig 2. AP radiograph of a cemented total hip arthroplasty. Bone cement usually contains: me thylmethacrylate (forms the polymer); a starter, initiator + inhibitor chemicals; an antibi otic (eg gentamicin clindamycin); a coloring agent (eg chlorophyll, hence green color); and a radiopaci \201 er (eg ZrO2 or BaSO4).1 1 The \201 rst hip replacement was done by Philip Wiles at the Middlesex Hospital in 1938. The Charnley low friction arthroplasty was \201 rst used in the 1960s. 2 For DVT/PE prophylaxis, NICE recommends using either LMWH, fondaparinux, dabigatran or rivaroxaban for 10 \200\22335 days post-op depending on the typ e of surgery, and agent chosen. Fig 3. AP radiograph of the left hip after Bir- mingham hip resurfacing.2 Images courtesy of Norfolk and Norwich Uni- versity Hospital (NNUH) Radiology Department. Joint injection and aspiration Joint aspirations Diagnostic role: Any blood, crystals, or p us?175 Therapeutic role: For tense eff usions, septic eff usions, and haemarthroses. Approa ches for speci \201 c joints are given below and on p710. \200\207Remember that aspiratio n of a joint with a prosthesis should only be done under the strictest sterile condi- tions (ie in the operating theater) to minimize risk of introducing infection. Steroid injection s to in \202 amed joints, bursae, or tendon sheaths aim to \200\201in \202 ammation and relieve pain, perhaps by \200\201prostaglandin synthesis, stabiliz- ing mast cells, or \200\201tissue calci \201 cation, or increasing vascularization and per- meability of syno vium. Side effects: Skin atrophy (hydrocortisone acetate is safer than triamcinolone), haem arthrosis, facial \202 ushing, urticaria, Charcot \200\231s arthropathy, post-injection \202 are syndrome (synovitis with fever), paresis, and septic arthritis ( \211 1 in 14,000 injections). \200\207It is essential that steroids are not used in septic conditions and, if any doubt at all exists, results of syno- vial \202 uid culture should be awaited. Re member the possibility of tuberculous synovitis \200\224especially in immigrant populations . Repeated injections are more dangerous: beware ligamentous laxity, joint instability, cal ci \201 cation, or tendon rupture. 708 a m u a r t d n a