Slipped Upper Femoral Epiphysis

Background

• One of the most common adolescent hip problems (around 10/100,000 children per year)
  • The epiphysis usually slips posteriorly relative to the diaphysis of the femur
• Most common in boys and occurs usually around the growth spurt in adolescence (mean age 13)
  • More common in overweight children; left hip slightly more prevalent
  • Whilst weight and mechanical factors (as well as others e.g. hypothyroidism; hypopituitarism; radiation treatment) may play a role, SUFE represents an underlying instability of the proximal growth plate- the exact cause of which is unknown

Classification

• The most important classification is whether the joint is
  • Stable (90%) i.e. the patient is still able to weight bear (function relatively unimpaired)
  • Unstable (10%) the patient is unable to weight bear- requires urgent management
• Other classifications include
  • time-based i.e. acute (symptoms for < 3 weeks); chronic and acute on chronic
  • Southwick angle classification (measurement of the difference between both hips in the femoral head-shaft angle on the frog radiograph)
    • Mild <30°; Moderate 30-50° and severe >50°
  • Grading by degree of slippage
    • I (Up to a third); II (up to a half); III (more than half)

Presentation

• Most commonly presents with hip and/or groin pain
  • Often an acute event but may present but can have had mild symptoms preceding this
  • Can present as radiated knee pain
  • Worse on movement/weight bearing
  • May cause antalgic gait
  • May limit hip movement- particularly internal rotation and abduction (indeed the leg may rest in external rotation/adduction)
• Differential
  • Perthes disease
  • Septic arthritis
  • Developmental dysplasia
  • Synovitis

Investigation

• X-rays
  • An x-ray of the pelvis will usually detect a SUFE
    • Trethowan’s sign
      • Klein’s line (the line drawn up the lateral edge of the neck of the femur) should intersect the femoral head. It fails to do so in SUFE due to slip.
    • You may also see widening of the growth plate (epiphysiolysis) and blurring of the proximal femoral metaphysis (overlapping of the metaphysis and displaced epiphysis)
• Occasionally, where diagnosis is in doubt, a CT or MRI may help confirm the diagnosis

Management

• Surgical management of the affected side
  • Percutaneous fixation with cannulated screw(s)
• There is some controversy as to whether to fix the other side also (bilateral in up to 20% of cases)- currently not recommended
• Without fixation, particularly in unstable cases, there is a risk of osteoarthritis; chondrolysis (breakdown of cartilage and subsequent bony degeration/damage) and avascular necrosis of the femoral head

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Scoliosis

Abnormal curvature of the spine in the coronal plane (>10°).

Background/epidemiology

• Scoliosis <10° is not abnormal (considered a normal variation)
  • Around half of patients with AIS (adolescent idiopathic scoliosis- most common form) develop a curvature >70°
• It is estimated to affect 2-3% of the population; 80% is idiopathic
• The most common type is adolescent idiopathic scoliosis (affects between 0.5 and 3% of people, most commonly between the ages 12-14, and, in IAS, is much more common in females (90%)
  • Other common types include
    • Juvenile idiopathic scoliosis (aged between 3 and 10; more common in females; likely to progress/require surgery due to curvature presenting prior to growth spurt at puberty)
    • Infantile idiopathic scoliosis (< age 3; more common in males)
    • Congenital idiopathic scoliosis
    • Neuromuscular and Pathologic Scoliosis (Secondary conditions)
• In older children, curvature is usually to the right.  In infants, left sided curvature is more common.
• As curvature progresses, vertebral bodies rotate towards convexity and spinous processes away from convexity.  In severe cases, this can impair cardiorespiratory function.

Presentation

• May be asymptomatic and detected by chance- note that screening is not routinely offered in the UK (some patients also have a family history)
• Usually present with back (thoracic) pain
• On examination (see back examination)
  • Shoulders/waistline may not be level and/or ribs/scapulae may be more prominent in certain areas
  • Note that the hip usually protrudes on the concave side
  • Adam’s Test
    • Ask the patient to bend forward- a fixed scoliosis becomes more prominent
  • It is important also to look for leg length inequality; any focal neurology (change in reflexes) or any signs of congenital/hereditary conditions e.g. midline skin defects, cafe au lait spots.

Investigations

• XR spine
  • Calculating the Cobb angle (between the uppermost and lowermost vertebra of the primary curvature seen on erect AP XR) is important in deciding management/prognosis

Management

• Exercises
  • Back exercises have very little effect on curvature but can maintain mobility/range of movement and may improve pain
• Bracing
  • Used mainly for curvatures between 20° and 40°, which are well balanced (i.e. have a compensatory secondary curve), and in patients who are growing (in puberty) in which a brace may halt the progression and occasionally improve the deformity
  • Usually not definitive- used mainly to maintain curvature stability in younger patients until adolescence when operative management may be more suitable
• Surgery
  • Spinal fixation (posterior spinal fusion most common) can be used in patients with a curvature of >40°
    • rare but carries risk of neurological complications

Kyphosis and Scheuermann’s disease

Kyphosis is the apical-dorsal curvature of the spine in the sagittal plane (i.e. curves away from the body).  There is normal thoracic kyphosis of around 20-40°.  Abnormal kyphosis is a curvature (measured as Cobb’s angle (between T2-T12)) of >45°.

Background/Aetiology

• Pathological kyphosis most commonly occurs in the thoracic spine although rarely can occur elsewhere in the spine.
• It is not uncommon amongst the elderly population (occurs in around 20-30% of patients >65) and is more common in women
• Risk factors include
  • Osteoporosis; vertebral (wedge) fractures and degenerative disc disease
  • Problems with proprioception; poor posture; spinal muscle weakness/attenuation
  • Other causes include trauma; ankylosing spondylysis and other arthritides; and rarely neoplasms and infections
• Kyphosis can impair physical functioning; quality of life and mortality directly and indirectly
  • Increased risk of vertebral fracture
  • May affect balance and likelihood of falls
  • Decline in gait speed/mobility
  • In some cases, can impair pulmonary, GI and gynaecological function

Presentation

• Most patients are asymptomatic and kyphosis is purely aesthetic
• Some may present with back pain
• On examination, there is usually a thoracic kyphosis and there may also be compensatory lumber hyperlordosis
  • Tight hamstrings/difficulty with straight leg raise may also be present
• Rare but important features include those of myelopathy i.e. neurological problems (including pain/altered sensation, weakness, altered tone/reflexes, problems with gait etc)
• Indications for surgical management (note not absolute)
  • Neurological deficits
  • Kyphosis >70° (no pain) or >65° with pain
  • Loss of anterior vertebral height >50%

Management

• For purely postural related kyphosis, exercises and education about posture may benefit patient symptoms (may not entirely relieve kyphosis)
• Surgical management is reserved only for severe cases
  • Smith-Peterson osteotomy, pedicle subtraction and vertebral column resection can all be options for corrections
  • Anterior release spinal fusion may also be used in Scheuermann’s disease/severe cases

Scheuermann’s disease

• In children and adolescents, abnormal kyphosis can occur as what is thought to be the result of a genetic defect causing collapse of the vertebrae
  • A family history is common
  • Patients
• Classically defined as anterior wedging of >5° across three consecutive vertebrae, and is different from postural kyphosis by the rigidity of the kyphosis (not corrected by hyperextension)

Hip Examination

Intro

• Wash hands, Introduce self, Check patient name and DOB/CHI, Explain procedure and gain consent

Look

• General: age, mobility, mobility aids, trauma etc
• Standing:
  • Posture, asymmetry, muscle wasting, scars, deformity (also look at the back for scoliosis and the gluteal muscles
  • Trendelenburg’s test
    • Look at the patient’s ASIS and ask them to stand on one leg (you may want to be ready to support them)
    • Normally the gluteals will contract so that the contralateral (unsupported) leg rises to balance.  If the contralateral side dips, the abductor muscles are weak on the side they are standing.
• Gait:
  • Speed, limp, arm swing, abnormal gaits e.g. Trendelenburg (wide-based waddle); antalgic
• Lying
  • Look at leg length, comparing symmetry and rotation, scars, sinuses, skin changes etc
  • Measure apparent (xiphisternum/umbilicus to medial malleolus: if unequal, spinal or pelvic problem) and true leg length (from ASIS to medial malleolus: if unequal, true limb shortening e.g. fracture)

Palpate/Feel

• Start on normal side
• Bony landmarks (where possible) e.g. greater trochanter, ASIS, pubic rami
• Temperature and skin etc

Move

• Do all movements actively (except rotation) then passively
• Test leg movement roughly by rolling the legs gently on the bed
• Flexion (130°); (NB Extension is not routinely tested on the couch);
• Test Abduction (45°) and adduction (30°)
  • NB Abduction/adduction is not always tested actively
• Test Internal rotation passively by flexing the hip and knee to 90° and rotating the leg so that the knee points inwards (vice verse for external rotation)
  • Internal rotation lost early in osteoarthritis

NB Some practitioner’s will still perform Thomas’ test for fixed flexion deformity.  However, in Tayside, at least, it is becoming less routine and is no longer part of the hip examination.

Knee Examination

Intro

• Wash hands, Introduce self, Check patient name and DOB/CHI, Explain procedure and gain consent

Inspection

• General: patient; mobility aids
• Gait: any antalgic gait, limp, locking knee
• Standing: alignment, varus/valgus deformity, swelling, redness, asymmetry
• Lying: skin (scars, swelling, bruising); joints (effusion, nodules, psoriasis/skin changes); alignment and position
• Measure quadriceps bulk (hand’s breadth above the patella) (NB not always performed)

Feel

• Skin- temperature
• Joint
  • with the knee at 90° flexion, feel the patella, along the joint line
  • note any tenderness, synovial thickening etc
  • also feel for any abscesses/popliteal bursitis
• Effusion
  • Patellar tap
    • Empty the suprapatellar pouch with one hand and push down on the patella with one/two finger(s) of the other hand (positive if the patella sinks before hitting the femur)
  • Cross fluctuation may be performed if there is a large effusion
    • Empty the suprapatellar pouch with the other hand below the patella.  Positive if the pressure/ripple is felt with either hand with alternating compressions
  • For smaller effusions (more common) the bulge test is performed
    • ‘Sweep’ the fluid out of the patella bursa, beginning infero-medially and moving superiorly (superomedial aspect); the repeat laterally beginning superiorly and ending inferiorly.  Positive it there is a ‘bulge’ on the medial side after emptying when the lateral side is swept.

Move

• NB Good to compare with the non-affected knee- test active and passive movements (palpating the joint with passive movement)
  • Flexion (normal 140°) and Extension (normal 0°) (also lift the foot off the bed and look for any hyperextension (normal up to 10°))
• Special tests
  • Collateral ligament stress tests
    • Hold the ankle/lower leg in one arm, and, with the knee at 0 and 30° flexion, apply varus (LCL) and valgus (MCL) stresses
    • Excessive movement suggests tear
  • Cruciate ligaments
    • Drawer test
      • With the knee flexed at 90° and the foot on the bed (often useful to sit on the patient’s foot to support it), with your fingers in the popliteal fossa and thumbs on the tibial tuberosity, apply anterior (ACL) and posterior (PCL) forces on the tibia
    • Lachman’s test
      • with the knee slightly flexed, one hand supporting the thigh, pull the calf anterior (ACL laxity)
  • Menisci
    • McMurray’s test
      • Flex the knee as much as possible, externally rotate the foot, apply a lateral force to the knee and extend the leg (med meniscal stress)
      • Flex the knee, internally rotate and apply a medial force and extend the leg (lat meniscal stress)
    • Apley’s manoeuvre (rarely done in practice)
      • With the patient prone (on front); apply downwards force to knee whilst flexed at 90°, and rotate the foot.
  • Patellofemoral apprehension
    • Flex the knee whilst pushing on the patella laterally

Finish

• Thank patient, wash hands,
• Document/explain findings and suggests further investigations/management

Talipes Equinovarus (Club foot)

Background

• Inverted and plater flexed deformity of the foot/ankle, usually diagnosed at the newborn exam
• Occurs in around 1 in 1000 and twice as common in males
  • Around 50% are bilateral

Causes

• Usually idiopathic
• Associated with
  • Spina bifida; cerebral palsy; Edward’s syndrome (trisomy 18); oligohydramnios; arthrogryposis (multiple joint contractures at birth)

Diagnosis/Investigation

• Often clinical (rarely investigated further)

Management

• Ponseti method
  • Manipulation/progressive casting starting as soon as possible once the diagnosis has been made (within weeks of birth)
  • Usually successful after 6-10 weeks
• Patients may require Achilles tenotomy following this
• Night time braces can also be used up until the child is of school age

Adhesive capsulitis (Frozen Shoulder)

Background

• Poorly understood condition that can be disabling
• Features include thickening of the synovial capsule, adhesions within the subacromial or subdeltoid bursa, adhesions to the biceps tendon
• Thought to have an incidence of 3-5% in the general population (one of the most common orthopaedic problems)
  • More common in patients with diabetes and thyroid disease; more common in women, average age 40-65 years
  • Usually unilateral

Classification/Aetiology

• Primary (idiopathic)
  • Insidious onset and progression
• Secondary (trauma- usually not directly but due to subsequent immobilisation)

Clinical Phases

1. Freezing/painful stage
   • In general, patients don’t present in this phase as they think it will resolve spontaneously.  However, pain tends to progress and ROM becomes limited
   • Typically 3-9 months
   • Characterised by acute synovitis of the glenohumoral joint
2. Frozen/Transitional stage
   • Shoulder pain may improve such that there is no pain but ROM tends to remain limiting but not worsening
   • Usually external rotation most limited, then flexion and internal rotation
• Typically 4-12 months
3. Thawing stage
   • ROM can improve and shoulder gradually returns to normal
   • Lasts anywhere from 12-42 months

Presentation

• Ask about symptom onset (any incidents/injury/trauma etc)
  • Often non-dominant hand (as there can be a tendency not to use this at all after injury)
• Ask if symptoms are worse at night (often are) and ask about activities of daily living
• On examination, there is often reduced ROM in all directions.  Pain may be a limiting factor.
  • The shoulder may be tender to palpate

Investigations

• Although diagnosis is clinical, X-rays and other imaging modalities (namely MRI) may exclude other pathology)

Management

• Pain relief (Paracetamol and NSAIDs) with physiotherapy are usually most beneficial
  • Steroid injection may be helpful and a quick relief prior to physiotherapy
• Surgery is rarely performed

Shoulder Examination

Introduction

• Wash hands, introduce yourself, check patient ID, explain procedure and gain consent
• You may, at this point, want to ask if they have difficulty reaching for things, brushing hair, dressing themselves (screen for function).

NB In an osce, you often won’t need to ask if the patient has any pain at the moment but this may be good to do now also.

Look

• Adequately expose the shoulder
• Look from the front, side and back and with the patient leaning against a wall
• Look for symmetry, wasting, scars, obvious bony deformity, any winging of the scapula

Feel

• Feel over the joint for temperature
• Starting at the sternoclavicular joint, palpate along the clavicle to the acromioclavicular joint, palpate the acromion and then around the spine of the scapula round the back
  • also palpate the dorsal spine and interscapular area
• Feel the anterior and posterior lines of the glenohumeral joint
• Feel the muscles around the joint and bones
• Note any prominences/breaks in continuity, any tenderness

Move

• Begin with active (patient alone) movement
  • Flexion (‘arm up’)
  • Extension (‘bend arm and push backwards’)
  • Abduction (‘arm out to the side’)
  • Adduction (‘bring your arm across your body’)
  • External rotation (‘bend your elbow into your side and move your hand out the way’)
  • Internal rotation (‘can you put your arm behind your back’)
• Perform movements passively (assisted), feeling the joint for any crepitus, locking
• Note range of movement and reason for limitation (pain or resistance)

Special Tests

Note that the first section (Isolation) is most important to perform.

• Isolating the specific rotator cuff muscles
  • ‘Lift-off’ test (for subscapularis)
    • Ask the patient to put their hand behind their back and push against your hand
    • Pain indicates a problem (e.g. tear) of the subscapularis
    • Alternatively, if the patient can’t reach behind the back
      • Ask the patient to abduct the shoulder (~60°) and flex the elbow (you may want to support them their with your other hand) and pull with their hand towards their stomach (‘in to your tummy’) against resistance from you
  • External rotators (supra- and infra-spinatus; teres minor)
    • With the patients elbows flexed, resist external rotation of the shoulder
    • Pain/weakness suggests problems with these muscles
  • Supraspinatus (most commonly affected)
    • Painful arc- the patient will normally have pain on abduction (usually between 60° and 120°)
    • ’empty can’ test’
      • With the patient’s arm in 90° flexion, 30° abduction and internally rotated (thumb towards the floor as if emptying a can)
      • Resist upward movement of the arm (flexion)
• Impingement
  • Neer’s impingement test
    • With the patients arm in slight abduction, passively flex the shoulder up so that the patient’s arm is next to their ear
    • If you stabilise the shoulder, and, if possible, press under the acromion (trapping the arm as it flexes), this can be more sensitive
  • Hawkins test (impingement)
    • With the patient’s shoulder and elbow flexed at 90° and the shoulder in slight abduction, internally rotate the shoulder as far as possible (i.e. curve the arm towards the body)
• Bicep’s tendinitis
  • Speed’s test (biceps tendon)
    • With the patient’s shoulder in 90°, elbow extended and arm supinated, apply a downward force to the forearm
  • Yergason’s test (biceps tendon)
    • Shoulder in neutral position, elbow flexed to 90° and arm pronated
    • Grasp the patient’s forearm and ask them to flex and supinate against resistance
• Instability
  • Apprehension testing
    • Shoulder in 90° abduction and slight extension with the elbow flexed.  Passive external rotation.  (If you press forward on the glenohumeral joint too)
    • If the patient becomes nervous, or you dislocate the shoulder, this is a positive test
    • If you repeat the test but with posterior force applied anteriorly, the patient’s apprehension is lifted.  A ‘surprise’ test is the sudden removal of the force and recurrence of apprehension.
  • Sulcus sign
    • Pull down on the humerus
    • The acromion should become more prominent.  A sulcus (/dip) suggests laxity/instability
  • Load/shift test (or Drawer test)
    • Stabilise the scapula and grasp the humeral head, pulling it anteriorly and posterioly
    • Normally there is some degree of laxity
    • This can be performed supine with the shoulder over the side of the bed also

Functional Tests

• Finally, ask the patient if they can reach behind their back and up behind their head

End

• Thank the patient, let them re-dress, present/record any findings
• Wash hands

Developmental Dysplasia of the Hip

Refers to a wide range of pathology- from mild acetabular dysplasia with a stable hip to more severe dysplasia with instability, to established dysplasia with or without subluxation or dislocation.  Usually detected in the neonate.

• It affects 1-3% of newborns.
• Early (post-natal) diagnosis and treatment can reduce the risk of progression and the development of complications
  • When the femoral head is aligned with the centre of the acetabulum, the dysplastic acetabulum often normalises within the first few months of life.  If the hip remains dislocated, soft tissue contractures develop rapidly and surgery may be required
• Left hip is more commonly affected than the right.  Up to 20% are bilateral.
• More common in females (4:1)

Risk factors/Aetiology

• Exact cause is unknown but genetic factors and environmental influences may contribute.
  • Having an affected sibling increases risk by 5%
  • Breech presentation (17-fold; 7-fold if C-section)
  • Large for gestational age
  • Multiple pregnancy
  • Oligohydramnios

Screening and Diagnosis

• Screening takes place within 24 hours of birth, before discharge from hospital, 6 weeks, between 6-9 months, and at walking age.

Barlow test (left) and Ortolani test (right). In the Barlow test (baby’s right hip), the hip is adducted and flexed to 90°; the examiner holds the distal thigh and pushes posteriorly on the hip joint. The test is positive when the femoral head is felt to slide posteriorly as it dislocates. In the Ortolani test (baby’s left hip), the pelvis is stabilised by the examiner and each hip examined separately. In a baby with limited hip abduction in flexion, the hip is flexed to 90° and gently abducted while the examiner’s finger lifts the greater trochanter. In a positive test the femoral head is felt to relocate into the acetabulum. The dislocated femoral head (pictured on the opposite hip) has now been reduced back into joint

• Barlow and Ortilani tests are used post-natally and at 6 weeks to screen for DDH.
  • asymmetry of leg folds
• Late diagnosis
  • Limited hip abduction at 90° flexion; differences in knee height- ‘short thigh’- Galleazzi test (when lying supine at 90/90 flexion); leg length discrepency
  • Problems with walking (NB not usually delayed walking, but trendelenburg gait), painless limp, walking on toes

Investigations

• Ultrasound scans are useful in assessing DDH up until the age of 4-5 months whilst the hips are still cartilagenous.  After this age, radiography is used to assess DDH.
  • There may be a small ossific nucleus of the femoral head (the femoral head densifies in the newborn period- this may not occur in DDH)
  • The joint may have subluxed (disruption of Shenton’s line)
  • A high acetabular index (the angle of the acetabulum to the horizontal line between two hips)

Management

• For children under 4.5-6 months who are Ortolani positive i.e. have a reducible hip, a Pavlik harness is most commonly used
  • Secures the hips in 100° flexion and marked abduction.  It allows the soft tissues of the capsule to strengthen and the tight hip adductors to stretch
• Surgery is usually required for children presenting late (>6 months) and in those who have failed harness treatment (e.g. Ortolani negative)
  • If under 18 months, usually just reduction surgery
  • If >18 months, additional osteotomy may be required

Osteoarthritis

A degenerative disorder of synovial joints, characterised by

1. Focal areas of damage to the articular cartilage
2. Remodelling of underlying bone and the formation of osteophytes (new bone at joint margins)
3. Mild synovitis

Any joint can be affected but most commonly the larger weight-bearing joints (hip, knee) are affected.  Hands can also be affected, as can the spine.

Epidemiology

• It is the most common cause of joint pain- affecting around 8.5 million people in the UK
  • 20% of adults aged 45-64 have osteoarthritic pain in the knee and around 12% of people >65 have osteoarthritic hip pain
• Prevalence increases with age; and affects females slightly moreso than males (1.7:1)

Aetiology/Risk factors

• Age
• Obesity/overweight
• Previous trauma
• Genes
  • Osteoarthritis carries significant hereditability, often moreso than rheumatoid arthritis
  • Bone morphogenic protein (BMP) and wingless type (WNT) genes have been implicated, as well as MTPs
• Reduced muscle strength / joint laxity or malalignment
• Bone density
  • High bone density increases the likelihood of development
  • Low bone density increases the likelihood of progression
• Occupation
  • Athletic, labour i.e. over-using joints

Pathophysiology

• Biomechanical factors e.g. trauma, ligament laxity, joint instability are drivers for the development in OA.  It is thought that microtrauma around the joint activates an immune response, causing inflammation.  It is this that degenerates the cartilage and initiates new bone formation (and possibly pain too- although this is more likely to be mechanical).
• It can be described as the far end of the spectrum of normal healing.

Presentation

• Joint pain develops over years.  As a result, some patients will present at a stage where the pain is severe enough to warrant management
  • Pain is often better in the mornings/at rest and worse on exertion
    • If affecting the lower limb- ask about walking distance and stairs
    • Note that pain in the knee may be referred from the hip
• Reduced range of joint movement (usually due to pain but can be due to stiffness/progression of the disease)
  • In joints like the knee and shoulder, there may be a ‘catch’ on movement (pseudo-locking)
    • the knee may also ‘give-way’ (important to ask)
    • advanced disease of the knee may produce a varus deformity
  • In the hip- painful restriction of internal rotation is usually the first sign
    • A fixed flexion deformity (Thomas’s test positive) is also commonly seen
• This may result in an abnormal gait (usually antalgic)
• There may also be swelling of the joint- not usually grossly erythematous, but more fluid in the joint space (check for effusion of the knee).  The joint can be tender (less common cf rheumatoid).  Bony swelling is more commonly seen later on (these are often asymptomatic)
  • e.g. DIP joints- Heberden’s nodes); PIP (Bouchard’s nodes)
• There may be joint crepitus
• Muscle wasting of the effected area may also be seen.  This can be due to the patient not wanting to use the joint due to pain but can also worsen the progress of OA.

Investigations

• Management is largely determined by the history (pain is a greater indicator for management than investigation findings)
• X-ray
  • Osteophytes
  • Loss of joint space/ cartilage loss
  • Bone cysts
  • Subarticular sclerosis
• Other tests e.g. FBC/LFTs/bone biochemistry are usually normal
• MRI may be useful if another cause of pain is suspected e.g. ligament injury
• Aspiration of effusion should only be done if there is suspicion of infection/septic arthritis

Management

• Varies with the severity of symptoms, x-ray findings, patient preference etc
• Drugs for pain are commonly NSAIDs and paracetamol (take before pain starts if possible)
  • Paracetamol and topical NSAIDs are recommended first line
  • use the analgesic ladder for pain control
  • If pain is not controlled and there are reasons not to go for surgery, intraarticular steroids are often very useful
• Physiotherapy/exercises may be useful if the patient has problems with muscle wasting
• Weight loss
• Surgery
  • Indicated if there is OA evidence on x-ray and if the disease is significantly affecting the patient’s daily lifestyle
  • Joint arthroplasties tend to last around 10-15 years