a m u a r t d n a s c i d e a p o h t r O cectomy, though is less invasive. Laser discectomy involves radiographically assisted placement of a deliv- ery device into t he disc, through which a laser can be introduced to remove disc material. Lumbar disc arthoplasty (replacement with an arti \201 cial disc) is a concept that has be en around since the late 1980s, and is becoming more common.53 \200 Interspinous spacers relieve pressure that cause the disc to protrude by causing distraction of the spinous proc esses (= \200\230dynamic stabilization \200\231).54 Longterm eff ectiveness is unknown. Chemonucleolysis, which used to be more common, involves injection of chymopapain (a proteo lytic derived from papaya) into the nucleus pulpo- sus \200\224it has been part of practice since the 1960s. There has been contro- versy surrounding the procedure, with shadows hang ing over the effi cacy of the techniques and side eff ects of the agent (eg possible anaphy laxis). It is less invasive than other techniques though is probably less eff ective than s urgical discectomy.55 Fig 1. Lumbar microdiscectomy. Reproduced with kind permission of Dr Aaron Filler; Do You R eally Need Back Surgery? OUP, 2004. Fig 2. Endoscopic discectomy. Kindly provided by Medtronic Sofamor Danek, Inc. METRx Syst em incorporates technology developed by Gary K. Michelson, MD. Speci \201 c and sometimes sinister back pain 678 \200 Typical causes of back pain according to age: 15 \200\22330yrs Prolapsed disc, trauma, frac tures, ankylosing spondylitis (OHCM, p552), spondylolisthesis, pregnancy Prolapsed disc, cancer (lung, breast, prostate, thyroid, kidne y) Degenerative, osteoporosis, Paget \200\231s disease (OHCM p699), malignancy, myeloma (OH CM p362); lumbar artery atheroma (which may itself cause disc degeneration) >30yrs >50yrs Rarer causes Spinal stenosis; cauda equina tumors; spinal infection (usually staphylococcal , also Proteus, E. coli, Salmonella typhi, TB). Often there are no systemic signs of infect ion. Spinal tumors These may be of spinal cord, meninges, nerves, or bone. They may be prim ary, secondary, lymphoma, or myeloma. They may compress the cord, causing pain, lower motor neuron signs at the level of the lesion, upper motor neuron signs and sensory loss below \200\224or bowel and bladder dysfunc- tion. Peripheral nerve function may be impaired resul ting in pain along the course of the nerve, weakness, hypore \202 exia & \200\201sensatio n (p762). With cauda equina involvement there is often urinary retention saddle anesthes ia (p770). When the deposit is in the spinal canal and there is no bone involve- ment, ther e may be no pain, just long tract signs. When bones of the back are involved there is progr essive, constant pain and local destruction of bone. Metastases tend to aff ect cancellous bone, but focal lesions cannot be seen on radiographs until 50% of bone mass is lost. There may be muscle spasm and local tenderness to percussion. Bone collapse may result in deform ity, or cause cord or nerve compression. Tests: ESR; PSA; electrophoresis (for myeloma); LF T. Plain radiographs; CT; MRI; isotope bone scans; bone biopsy. a m u a r t d n a s c i d e a p o h t r O In those with past cancer and current back pain, it is best to do a bone scan \201 rst ( \201 g 1), with plain radiographs of any hot spots suggesting metastases. Pyo genic spine infections This is a notoriously diffi cult diagnosis as all signs of infection may be absent (eg no fever, tenderness, or WCC \200\200, but the ESR is often \200\200). It may be secondary to other septic foci. Pain occurs, and movement is restricted by spasm. It is usually an infection of the disc space (discitis). Risk factors: Diabetes mellitus, immunosuppression, urinary surgery, or cath- eterization. Half of infections are staphyloco ccal; Streptococcal, Proteus, E. coli, Salmonella typhi and TB also occur. Tests: ESR \200 \200; WCC \200\200; radiographs shows bone rarefaction or erosion, joint space narrowing subligamentous new bone formation. Technetium bone scans and MRI ( \201 g 2) are better. Treatment: As for osteomyelitis (p696), resting the back with bed rest, brace, or plaster j acket. Surgery may be needed. Spinal TB Rare in those born in the West, this tends to aff e ct young adults, giving pain, and stiff ness of all back movements. ESR \200\200. Abscesses and cord compression may occur (Pott \200\231s paraplegia). Radiographs show narrow disc s paces and local osteoporosis early, with bone destruction leading to wedging of vertebrae l ater. In the thoracic spine, paraspinal abscesses may be seen on radiographs, and kyphosis on examination; with lower thoracic or lumbar involvement abscess formation may be related to psoas muscle in the \202 ank, or in the iliac fossa. MRI (not CT) is the ideal way to delineate cord compression. Treatment is anti-TB drugs (eg for 1yr; p160) + abscess drainag e. Fixation + bone grafting, or metal rods, plates, or wires needs highly specialized servi ces. If a syrinx (tubular cavity) develops, complete CNS recovery is not expected.56 Centra l disc protrusion This neurosurgical emergency is suggested by bilat- eral sciatica, perine al or \200\230saddle \200\231 anesthesia and disturbance of gut or blad- der function. \200\207Prompt decompression may prevent permanent incontinence. 679 Diagnostic triage: which grOUP encompasses your patient? Simple lumbar pain: \200 Aged 20 \200\22355 with Nerve root pain: \200 One leg hurting more than the back \200 Radiation to foot/toes \200 Hip \202 exion reproduces the pain in leg; \200 Localized neurological signs \200\230mechanical \200\231 backache, eg caused by twisting and worse on moving a m u a r t d n a s c i d e a p o h t r O Patient well in himself; no fevers; no weight loss \200\207For features of potentially sinister back pain, see MINIBOX, on p676. \200\207Sig ns demanding immediate (same-day) referral: gait or sphincter distur- bance; saddle anesthe sia \200\224these suggest cauda equina compression. Fig 1. Bone scan showing multiple metastases from prostatic cancer, including in \201 ltra tion of the pelvis, ribs, left femur and spinal column. Fig 2. Axial T2-weighted MRI of the lumbar spine showing an epidural abscess in the posteri or portion of the spinal canal causing mild stenosis. University Hospital NNUH NHS Trust. Norfolk & Norwich University Hospital (NNUH) NHS Trust. Why do some people get intractable back pain? 39% of adults have, or have had, an intermitt ent chronic back problem, and much energy is expended on frequently fruitless searches for the causes list- ed opposite. Imaging may be non-speci \201 c (subclinical disc protrusion , facet joint arthritis, or minor spondylosis). Risk factors for chronicity: \200 Smoking \200 Psychological morbidity \200 Low income/social class Be cautious of blaming sitti ng at work for chronic back pain. Meta-analyzes do not \201 nd in favor of this popular a ssociation.57 Coexisting cardio-respiratory disease \200 Poor work conditions \200 Number of children (for women and men). Vascular problems may underlie chronicity (hence associations with smok- ing and heart dise ase), and pain may be maintained by involvement of the sympathetic chain, which may mediate hyperaesthesia, hyperpathia (excess pain from minor noxious stimuli), allodynia (pain from minor skin stimula- tion) \200\224but surgical sympathectomy often only provides temporary relief. This implies central neuromodulation of stimuli producing a complex regional pain syndrome. Dorsal horn receptor \201 elds may expand and have their thresholds changed by peripheral injury, so pain is more intense, and appreciated over a wider area than simple a natomy would predict.58 Hip history and examination For hip prostheses, see p706 The movements examined at the hip are described in \201 g 1.59 Internal rotation is often the \201 rst movement to be res tricted by hip disease. Questions Are activities of daily living aff ected? \200\224walking distance, ability to climb stairs (only one at a time possible?), diffi culty getting out of low chairs. Remember that pain in the knee may be referred from the hip. Examination Fol low the routine for joint examination (p657); then also per- form the following tests. Meas urements Apparent leg length disparity (with the lower limbs parallel and in line with the trunk) is called either \200\230apparent shortening \200\231 (eg due to pelvic tilt or \201 xed adduction deformity \200\224which gives the apparent shorten- ing on that side) or \200\230apparent lengthening \200\231 (eg due to \201 xed hip abduction). In these case s, there is no true disparity, as detected by measuring between the anterior superior iliac spine and medial malleolus on each side with the pelvis held square ( \201 g 2) and the l ower limbs held equally adducted or abducted or by comparing leg length by positioning the lower limbs perpendicular to a line joining the anterior superior iliac spines. Fixed defor mity Joint or muscle contractures prevent limbs from being put in the neutral position. Wit h \201 xed adduction deformity, the angle between the limb and the transverse axis of the pelvis (line between both anterior superior iliac spines) is <90 but with \201 xed abd uction deformity it is >90 . Fixed \202 ex- ion deformity is detected by the Thomas test : With the patient supine on an examination couch, \202 ex the good hip up towards the ch est until the lumbar lordosis is obliterated (check by \201 nding it impossible to pass a hand between the patient and the couch in the small of the back). If there is a \201 xed \202 exion deformity the thigh on the aff ected side will lift off the couch as the lumb ar lordosis is obliterated. NB: to assess the full range of extension, have the pa- tient p rone on the table and then extend the hip. The Trendelenburg test is a test of the function of hip abduction and the abil- ity to support the pelvis when standing on one leg. In this state, it is normal for the pelvis to rise on the side of the lifted leg. A +ve test is wh en the pelvis falls on the side of the lifted leg. Causes: 1 Abductor muscle paralysis (glu teus medius and minimus) 2 Upward displacement of the greater trochanter (se- vere coxa var a, below, or dislocated hip) 3 Absence of a stable fulcrum (eg un-united fractures of the n eck of the femur). Gait If a hip is unstable or painful, a stick is used on the opposite si de (the re- verse is true for knees) so as to off -load the hip abductors on the aff ected side. Antalgic gait: Shortening of the stance phase1 on the painful leg occurs, with quick and short steps. Short-leg gait: Discrepancy in length is compensated for by adduction of t he long leg at the hip and abduction of the short leg creat- ing pelvic drop, or an equinus deformity. Trendelenburg gait: A waddling gait caused by weak hip abductors, in which the trunk tilts over the weakened side (can be bilateral) in the stance phase. See OHCM p459. O ther joints to examine Spine, knee, sacroiliac joints/pelvis. Coxa vara ( \201 g 3) This t erm is used to describe a hip in which the angle between the neck and the shaft of femur is less than the normal 125 . Causes: Congenital; slipped upper femoral epiphysis; fracture (trochanteric with malunion, un-united fractures of neck of femur); due to softening of bon es (rickets, osteomalacia, Paget \200\231s disease). Consequences: True shortening of limb; Trendelenburg \200\230dip \200\231 on walking makes the aff ected person limp. 680 \200 a m u a r t d n a s c i d e a p o h t r O 1 The stance phase of gait starts when the forward foot foot makes contact with the ground. Then there is loading, mid- and terminal stance (+preswing) \200\224before the shorter swi ng phase starts. 681 90 a m u a r t d n a s c i d e a p o h t r O 40 \200\22350 30 \200\22340 30 \200\22340 l l a n r e t x E a n r e t n I 110 \200\223135 20 \200\22330 0 0 0 Fig 1. Ball and socket (eg the hip) joints have 3 axes of movement: \202 exion \200\223ex tension (left); ab- & adduction (middle); and external & internal rotation. External rotati on of the ball in the socket is achieved by movement of the shin across the midline, as in the diagram (40 \200\223 50 ). After trauma, a hip at rest in external rotation is likel y to be fractured; if internally rotated dislocation is more likely. These abnormal positio ns occur because of the change in the fulcrum of the force across the hip joint from the il iopsoas muscle (which inserts on to the lesser trochanter of the femur). Fig 3. Coxa vara (L) and coxa valga (R). Fig 2. Measuring leg length: from the anterior superior iliac spine to the medial malleolus . Painful hips in children \200\207When a child complains of pain in the knee, always examin e the hip. \200\207Is T \200\200? If so, do urgent blood cul- ture ultrasound-guided aspiration. Transient synovitis of the hip (TSOH; irritable hip) is the chief cause of hip pain in children. It is a diagnosis of exclusion (exclude: septic arthritis; Perthes \200 \231 disease; and slipped upper femoral epi- physis). Examine the hip clinically and invest igate with plain \201 lms ( \201 gs 1 & 2), FBC, ESR/CRP. Ultrasound is helpful ( \201 g 3), and can guide needle aspiration when pus is suspected, so obviating need for arthroto my.60 Admission for ob- servation, rest and analgesia (eg ibuprofen) may be needed.61 If ot her joints are involved, consider juvenile idiopathic arthritis (p654). Perthes \200\231 di sease (Legg \200\223Calv \200\223Perthes \200\231 disease: \201 g 5) This is osteochond ritis of the femoral head and aff ects those aged 3 \200\22311yrs (typically 4 \200\2237). It is bilat- eral in 10 \200\22315%. \200 : \200 \211\210 4 : 1.62 The disease process i s likely secondary to avascular necrosis of the developing femoral head.63 It presents with pain in hip or knee and causes a limp. On examination all movements at the hip are limited , es- pecially internal rotation and abduction. Early radiographs MRI show joint space w idening. Later there is a decrease in size of the femoral head with patchy density. Later s till, there may be collapse and deformity of the femoral head with new bone formation. Seve re deformity of the femoral head risks early arthritis \200\22440yrs post diagnosis, 40% w ill have a joint replacement. The younger the patient the better the prognosis (due to incr eased ability to re- model). For those with less severe disease (< the femoral head aff e cted on lateral radiographs, and joint space depth well preserved) treatment is bed rest an d NSAIDs until pain-free, followed by radiographic surveillance. If prog- nosis poorer (> femoral head aff ected, narrowing of total joint space) sur- gery may be indicated.64 Slip ped upper femoral epiphysis (SUFE)1 Aff ects those aged 10 \200\22316yrs. 20% are bilateral . \200 : \200 \211\210 3 : 1. About 50% of patients are obese. There is displacement thr ough the growth plate with the epiphysis always slipping down and back. The exact cause is unknown, though it is likely to be a combination of hormo- nal and bio mechanical factors. It usually presents with limping and pain in the groin, anterior thigh, or knee. Can the pa tient weightbear (stable) or not (unstable?). This is important in predicting the risk of c omplications.65 Flex- ion, abduction, and medial rotation are limited (eg lying with foot e xternally rotated). \200 : anteroposterior ( \201 g 1) + frog-leg lateral radiographs of both hips. Treatment, regardless of severity, is stabilization across the physis. Reduction \201 rst may improve function and reduce likelihood of further surgery, but may increase the risk of avascular necrosis (AVN).66 If untreated, consequences may be avascular necros is of the femoral head or malunion predisposing to arthritis.67 \200\207Symptoms may be mi ld so have a high index of suspicion if in correct age grOUP. If occurring in those <10 or >16yrs, then consider an endocrinopathy, eg hypothyroidism, hypogonadism or growth hormone imbalance. Tubercular arthritis This is rare in the UK, but worldwide there is a resur- gen ce of TB. Children aged 2 \200\2235yrs and the elderly are most commonly aff ected. The sym ptoms are pain and a limp. All hip movements cause pain and muscle spasm. Tests: An early r adiographic sign is rarefaction ( \200\201 bone density). Later there is fuzziness of joint margins and narrowing of the joint space. Later, bony erosion may be seen. Ask about conta cts. Check ESR, CXR, and Mantoux test (OHCM p398). Synovial membrane biopsy con \201 rms t he diagnosis of TB ar- thritis. Treatment (eg of hip): Rest + anti-TB drugs (p160), given b y experienced personnel. Arthrodesis may be needed if much joint destruction has occurred. 1 It may be that unrecognized SUFE can cause later osteoarthritis of the hip. 682 \200 Diff erential diagnosis You must rule out: \200 Septic arthritis Then consider: \200 Tu bercular arthritis2 \200\2235yr \200 Perthes \200\231 disease4 \200\2237yr \200 SUFE10 \200\22316yr \200 In \202 ammatory arthritis And by exclusion: \200 TSOH a m u a r t d n a s c i d e a p o h t r O 683 a m u a r t d n a s c i d e a p o h t r O Fig 1. AP radiograph of the right hip showing a SUFE. The changes are subtle, but note that a line (the line of Klein) drawn along the up- per edge of the femoral neck in \201 g 2 would intersect the femoral head, but would not in \201 g 1. More reliable, though even h arder to appreciate, is the widening of the physis \200\224 most prominent at the lateral e dge. Fig 2. Normal AP radiograph of the right hip. Practice your saccadic eye movements be- twee n the two to appreciate the slip down- wards and medially. Fig 3. Hip us, showing joint eff usion \200\224the low re \202 ectivity (black) area super \201 cial to the femoral neck and head. Fig 4. Bones such as the femur grow from a cartilaginous growth plate called a physis (1); the end of a bone beyond the growth plate is called the epiphysis (2); the shaft of a long bone is called the diaphysis (4); the ossi \201 ed portion of bone in a transitional zone between the epiphysis and diaphysis is called the metaphysis (3) and it should always have a smoothly curved cortex. The diaphysis continues (arrow) to the metaphy- sis at the other end of the bone. The stem, -physis, comes from the Greek for \200\230growth \200\231. An a pophysis is a bony outgrowth independ- ent of a center of ossi \201 cation. Epiphyseal inj uries are covered on p737. Image by Tom Turmezei. Fig 5. Right hip radiograph showing model- ling deformity of the femoral head, consist- ent with prior Perthes \200\231 disease. Figures 1, 2, 3 and 5 Courtesy of Norfolk and Norwich University Hospital (NNUH) Radiology Department. Developmental dysplasia of the hip (DDH) DDH refers to a spectrum of pathology from stable acetabular dysplasia to established hip dislocation. It has replaced the term congenital di slocation of the hip (CDH). A world-wide systematic review (in unscreened populations) esti mated prevalence of di- agnosed DDH at 1.3 per 1000.68 UK incidence: 2 per 1000 live births . \200 : \200 \211\210 6 : 1; left/right hip incidence \211\210 4 : 1; bi- lateral in \205\223. Diagnosis Identify all those infants at risk (see MINI- BOX). If high risk, infan t should have ultrasound at 2 \200\2234 weeks, with treatment instigated by 6 weeks if requ ired. All babies should have their hips examined in the 1st days of life and at 6 weeks.1 D etection of DDH is user dependent, but improves with training and guidance.69 The Ortolani and Barlow maneuvers ( \201 g 1) detect unstable hips, but will both be negative in an irr educible dislocated hip, so use other tests as well (see BOX p685). \200\207Be alert to DD H throughout child surveillance (p150) as a hip may be normal at birth, and become abnormal later. Early diagnosis is important as if appropriately aligned in the \201 rst few mont hs of life, a dysplastic hip may normalize. Ultrasound is the imaging of choice, up to 4.5 months, as it is non-invasive and dynamic. In a large series (Nottingham, UK) 40 : 1000 bab ies had evidence of instability on routine ultrasound screening; only 3 : 1000 required tre atment. However, routine ultrasound screening for DDH remains controversial, on ac- count o f the high rate of spontaneous resolution of dysplasia and instability combined with the la ck of de \201 nitive data on functional outcome of interven- tions.70,71 Treatment If neon atal examination suggests instability arrange ultrasonog- raphy. Hips that remain unstable at 6 weeks require prompt treatment. Typi- cally treatment involves splinting in \202 exi on-abduction in an orthosis known as the Pavlik harness.72 Excess abduction (in splint) may cause avascular necrosis of the head of femur \200\224the worst possible outcome of treatm ent. From 6 \200\22318 months examination-under-anesthetic, arthrography and closed reducti on are performed followed by a period of immobilization in a spica hip bandage (spica refer s to the pattern of bandaging, from the Latin for an \200\230ear of corn \200\231), as the harness is less than 50% successful beyond 6 months of age. Open re- duction is sometimes required if closed techniques fail. After 18 months (de- layed presentation) open reduction is required with corrective femoral/pelvic osteotomies to maintain joint stability.73 684 \200 At-risk babies: \200 Breech birth \200 Caesar for breech \200 Other malformations \200 Positive family history \200 Birth weight \200\200 \200 Oligohydramnios \200 Primip/older mother \200 Postmaturity a m u a r t d n a s c i d e a p o h t r O Club foot Neonatal club foot is also known as talipes equinovarus. \200 : \200 >1 : 1; bi lateral in 50%. The foot deformity consists of: 1 Inversion; 2 Adduction of forefoot rela- tive to hindfoot (which is in varus); 3 Equinus (plantar \202 exion) deformity. The foot c annot be passively everted and dorsi \202 exed through the normal range. The preferred tre atment, starting as early as possible, is now the Ponseti method,74 in which the foot is ma nipulated and placed in a long leg plaster cast (which aims to correct the forefoot adducti on and hindfoot varus deformity) on repeated occasions. It is important that deformity corr ection is gradual. If this does not work, operations on soft tissues and/or bones of the fo ot may be carried out later (from 2 years). Associated with myelomeningocoele, arthro- gryp osis and prune belly syndrome. 1 The importance behind picking up DDH is that for a hip to develop normally the femoral he ad must articulate with the acetabulum. Failure to identify the problem early means that th ere is no development of the acetabulofemoral joint, posing real problems for any prospect of surgical correction. 685 a m u a r t d n a s c i d e a p o h t r O Fig 1. Hip tests: the Ortolani test and the Barlow maneuver. Hip tests for DDH Ortolani maneuver This test relocates a subluxed or partially dislocated hip. With the child \200\231s hips \202 exed and abducted, place your \201 ngers on the greater trochanter and try to lift up the femoral head and relocate it into the acetabu- l um. The test is positive when there is a palpable \200\230clunk \200\231 as the hip reloca tes. The test will be negative if there is an irreducible dislocation. Barlow maneuver This test aims to sublux or dislocate an unstable hip. Start with hip \202 exed and adducted slightly. Gently apply axial load to the fe- mur and try to dislocate the femoral head with the thumb. The test is positive when the femoral head is felt to dislocate; this action ma y be accompanied by a \200\230clunk \200\231. Beware repeated Ortolani and Barlow maneuver s which may induce instability. Galeazzi test Looks for apparent shortening of femur caused by dislocation of femoral head. The child lies supine on an examination table with the hip s \202 exed, the feet \202 at on the table, and the ankles touching the buttocks. The t est is positive when the knees are at diff erent heights. This test will be negative if bot h hips are dislocated as there will be no apparent discrepancy. Other signs Unequal leg len gth and asymmetrical groin creases may also suggest DDH (although not present in bilateral cases). Other signs include a widened perineum and buttock \202 attening on the aff ected side. If child is >3 months old, limited abduction (<60 )of hip whilst in \202 exion ma y be the most sensitive test for DDH.75 In older children signs may be: delay in walking an d abnormal waddling gait (aff ected leg is shorter). With bilateral involvement the lumbar lordosis is increased. Knee history and examination The knee is the largest human joint in terms of volume and sur face area of cartilage and is most susceptible to injury, age related wear, in \202 ammato ry ar- thritis and septic arthritis. It consists of a hinge joint between the femur and tib ia. The patella is a sesamoid bone embedded in the quadriceps tendon. It articulates with t he trochlear groove of the femur and increases the mechani- cal advantage of the quadriceps . History Is non-traumatic pain intrinsic to the knee (localized knee pain/with weakness/li mited range of movement/eff usion) or referred (vague pain ra- diation from hip or back) . If traumatic ask about mechanism of injury, noises (clicks/pops/crunching), swelling (and how rapidly it developed), direct impact to the knee, inability to weight bear, locking (m eniscal injury), and giving way (cruciate injury). Examination Examine supine with legs ful ly exposed. Look for alignment, quadriceps wasting and for swelling. Even 5 \200\22310mL of \202 uid will \200\230 \201 ll in \200\231 the me- dial and lateral peripatellar dimpl es giving the knee a general fullness. Con- \201 rm by placing the palm of one hand above the patella over the suprapatellar pouch, and thumb and fore \201 nger of the other hand below the patella. Fluid can be moved between the two by squeezing one hand, then the other . If >15mL \202 uid is present it may be possible to feel a patellar tap (milk \202 uid towards center of knee then ballott patella against the anterior surface of the femur). Pa lpate the medial and lateral joint lines (for osteoarthritis/meniscal/plateau injuries), th e patella, the popliteal fossa and femoral condyles. 686 \200 a m u a r t d n a s c i d e a p o h t r O Check active and passive movement. Flexion should be enough for the heel to touch the butto ck. Compare extension with the \200\230good \200\231 side. Check to see no evidence of cre pitus or \200\230locking \200\231. Ensure patella tendon is intact by examining active kne e extension/straight leg raise. Examine the medial and lateral collateral ligaments with the knee \202 exed 20 \200\223 30 (to relax the posterior capsule and the cruciate ligaments); one hand lifts the ankle, the other stabilizes the knee. Stress the knee by abducting the ankle while pushing the kn ee medially with the hand behind the knee (tests the medial ligament with a valgus stress f orce). Reverse the pressures to give adducting force to test lateral ligament (ie varus str ess). If these ligaments are torn the knee joint opens more widely when the relevant ligame nt is tested (compare knees against each other, as general laxity may be present). Test the cruciate ligaments ( \201 gs 1 & 3) with the knee 90 \202 exed (anterior/ pos terior drawer tests) and at 20 of \202 exion (Lachman \200\231s test). The anterior cru ciate ligament prevents anterior glide; the posterior prevents posterior glide. Excessive g lide in one direction (compare knees again) suggests damage to the relevant ligament. A mor e sensitive test to determine if symptoms are really due to cruciate ligament damage (which can be asymptomatic) is the \200\230pivot shift test \200\231.1 McMurray \200\231s rotation test is an unreliable way of detecting pedunculated me- niscal tears. With the knee \202 exed, the tibia is laterally rotated, then the knee is extended . This is repeated with varying degrees of knee \202 exion, and then again with the tibia medially rotated on the femur. The test is designed to jam the free end of a pedunculated meniscus in the joint \200\224a click being felt and heard and pain experienced by the pati ent as the jammed tag is released as the knee straightens. This test may not detect bucket- handle tears (p754). NB: normal knees often produce patellar clicks. Simply eliciting joint -line tenderness may be a more valid test when combined with a history of mechanical lockin g. Arthroscopy enables internal structures of the knee to be seen and a de \201 nite diagn osis may be made. It also enables a wide range of operations to be done as day-case surgery . This is routinely preceded by MRI. 1 This is so-called because it was found to be positive in patients (eg American Football p layers) who reported to their surgeon that \200\234When I pivot (on my leg) something shif ts \200\235. Anterior view 687 Femur Posterior cruciate ligament Patella a m u a r t d n a s c i d e a p o h t r O Lateral collateral ligament Articular cartilage Anterior cruciate ligament Lateral meniscus Medial collateral ligament Fibula Tibia Medial meniscus Fig 1. The anatomy of the right knee \200\224as seen from in front. The medial collateral l igament is much broader than the lateral ligament, and its deep \201 bres are \201 rmly at- tached to the medial meniscus. The lateral ligament and the lateral meniscus are inter - posed by the popliteal tendon (see \201 g 2), and hence are not connected. Femur Joint capsule Lateral collateral ligament Popliteus tendon Lateral meniscus Fibula Femur Quadriceps femoris tendon Anterior cruciate ligament Posterior cruciate ligament Patella Lateral meniscus Medial meniscus Lateral collateral ligament Patella ligament Tibia Medial collateral ligament Fibula Tibia Fig 2. The synovium of the right knee joint: lateral (left) and posterior views. Note that the synovium extends up behind the patella (remember for joint aspiration, p708), and that both cruciate ligaments are extrasynovial (but are intracapsular). NB: the joint capsule is distended in these images by infusion of \202 uid. Fig 3. Tibial plateau and ligaments. Note that on the tibial plateau the attachments in the midline from anterior to posterior are: \200 Tranverse ligament \200 Anterior horn of medial meniscus \200 Anterior cruciate ligament \200 Anterior horn of lateral meniscus \200 Posterior horn of lateral meniscus \200 Posterior horn of medial meniscus \200 P osterior cruciate ligament. Pain in the knee The common symptoms are anterior knee pain or pain and swelling. Anterior knee pain can be due to many causes (see below). Patellofemoral pain syndrome (PFPS) Is com mon in young athletes \200\224espe- cially runners \200\224and may be associated with overu se as well as lower limb malalignment and patella tracking abnormalities. Patella aching is felt after prolonged sitting or on climbing stairs. There may have been a recent increase in sporting activity or trauma \200\224especially history of patella subluxation/dis- locat ion. Eff usion is rare. Medial retropatellar tenderness and pain on patel- lofemoral compre ssion occur: +ve Clarke \200\231s test = pain on patellofemoral com- pression with tensed q uadriceps muscles. There may be either decreased or increased patella mobility. Diagnosis i s clinical. Treat by relative rest \200\224if due to increased training, with structured re habilitation. Quadriceps strengthen- ing exercises are the mainstay of treatment, but many will bene \201 t from hip strengthening exercises as well.76 Reasonable results are also r eported with electrical stimulators.77 NSAIDs may only be eff ective in reducing pain for a few months.78 If symptoms last >1yr, arthroscopic lateral retinacular release may be tried . Shaving the posterior surface of the patella gives uncertain results. Bipartite patella ( \201 gs 1 & 2) is a congenital fragmentation of the patella, found in 1%. This is usuall y an incidental radiographic \201 nding (not to be in- terpreted as a fracture pattern), but may give pain if the superolateral frag- ment is mobile with tenderness over the juncti on. Extra fragment excision may relieve pain.79 Recurrent patella subluxation A tight later al retinaculum causes the patella to sublux laterally, giving medial pain. The knee may giv e way. It is commoner in girls and with valgus knees. It may be familial, or associated wit h joint lax- ity, a high-riding patella (patella alta), or a hypotrophic lateral femoral co ndyle. Signs: Increased lateral patellar movement, accompanied by pain and the re- \202 e x contraction of quadriceps (ie a +ve patellar apprehension test). Contralat- eral instabil ity and young age at time of initial subluxation are risk factors for chronic recurrence.80 Treatments vary (RCTs are needed). If vastus medialis exercises fail to help, lateral reti nacular release with medial soft tissue realign- ment may be of bene \201 t.81 Patellar te ndon transfer is rarely needed.82 Patella tendinopathy (jumper \200\231s knee) is usually i nitiated by micro- or macro patella tendon tears, eg associated with sudden sporting loads. It can occur anywhere in the patellar tendon, and settles with rest NSAIDs. If unable t o rest, steroid injection around (not into) the tendon may help. Eccentric con- traction ex ercises (tension whilst lengthening the muscle) may also help.83 Iliotibial tract syndrome Typically presents with lateral knee pain and ten- derness over lateral femoral epicondyle. Thought to be due to overuse and associated with movement of the iliotibial tract (thicken ed lateral edge of the tensor fascia lata) and the lateral femoral epicondyle. Common in ru nners, it usually settles with sport modi \201 cation, rest, ice, and NSAIDs, but may need ster- oid injection84 and hip adductor strengthening.85 Medial shelf syndrome The synovial fold above the medial meniscus is in- \202 amed. Pain is superomedial. There may be brie f locking of the knee (mimick- ing a torn meniscus). Diagnosis: Arthroscopy. Treatment: Res t, NSAIDs, local steroid injection, or division of the synovial fold arthroscopically. Hoff a \200\231s fat pad syndrome This is impingement of the infrapatella fat pad. Think of it in those with meniscus or ligament-type symptoms when imag- ing shows they are intact. MRI may show a hypertrophic Hoff a pad impinging between articular surfaces (which causes pain under the patella). There may be hydrarthrosis or haemarthrosis (from arteriole rupture). E xtending a bent knee while putting pressure on the patellar tendon margins elicits pain and a defensive behavior.86 688 \200 a m u a r t d n a s c i d e a p o h t r O 689 \200\230All these hags \200\231 Once, after a stay in hospital with a fracture, a patient who was not quite as deaf as she was supposed to be, told one of us (JML) how she had overh eard a newly arrived orthopedic surgeon say to the ward nurse \200\234What are we going to do with all these hags? \200\235. As he progressed down the ward, turning \201 rst to th e left and then to the beds on the right, his mood became morose, then black \200\224as if he was getting angry that all these \200\230hags \200\231 were clogging up his beds, preve nting his scienti \201 c endeavors. But what was really happening, my patient suspected, w as that, as he turned to left and right, he was really nodding goodbye to his humanity, and , dimly aware of this, he was angry to see it go. On this view, these rows of hags were lik e buoys in the night, marking his passage out of our world. We all make this trip. Is there any way back? The process of becoming a doctor takes us away from the very people we \201 rst wanted to serve (Captain Pollard syndrome, p652). Must medicine take the brightest and the best and turn us into quasi-monsters? a m u a r t d n a s c i d e a p o h t r O The answer to these questions came unexpectedly in the months that followed: sheer pressure of work drove this patient \200\231s observations out of my mind. It was winter, and there was \200\231 \202 u. In the unnatural twilight of a snowy day I drifted from bed to bed in a stupor of exhaustion with a deepening sense of a collapse that could not be put off \200 It was all I could do to climb into bed: but when I awoke, I found I had somehow climb ed into a patient \200\231s bed, who had kindly moved over to make space for me, and was no w looking at me with concern in her eyes. Herein lay the answer: the hag must make room for the doctor, and the doctor must make room for the hag: we are all in the same bed. Fig 1. Bipartite patella at the usual position of the superolateral edge. Fig 2. The same image as \201 g 1, but \200\230win- dowed \200\231 to make the lesion mo re obvious (the bean-sized fragment is between 1 and 2 o \200\231clock). This has been one of the major ad- vantages of digitized image viewing. Figs 1 & 2 courtesy of Norfolk and Norwich Uni- versity Hospital (NNUH) Radiology Departmen t. Other causes of anterior knee pain Chrondromalacia patellae, where there is softening of th e articular carti- lage of the patella. Loose bodies Variable symptoms, may have locking, e ff usion, intermittent sudden pain associated with movement. Osgood \200\223Schatter diseas e Adolescent patients with tenderness at tibial tu- bercle (see p704). Prepatella bursitis (housemaid \200\231s knee) Swelling anterior to patella, typically occurs following trauma or overuse (see p690).