MSK Flashcards
Osteochondroma
bony outgrowth on the external surface with a cartilaginous cap.
very small (1%) risk of malignant transformation
These do not usually case any problems but can produce local pain. Knee common
Mx: Any lesion growing in size or producing pain may require excisional biopsy.
Enchondroma
Intramedullary and usually metaphyseal cartilaginous tumour caused by failure of normal enchondral ossification at the growth plate.
Usually lucent and can cause pathological fractures
Mx: Once a fracture has healed or if there is a risk of impending fracture they may be scraped out (curettage) and filled with bone graft to strengthen the bone.
Simple bone cyst (aka unicameral bone cyst)
- Single cavity benign fluid filled cyst in a bone
- They are probably a growth defect from the physis (growth plate) and are therefore metaphyseal in long bones
- Can cause weakness leading to pathological fracture.
Mx: curettage and bone grafting
Aneurysmal bone cyst
Contains lots of chambers which are filled with blood or serum. Due to small arteriovenous malformation.
• The lesion is locally aggressive causing cortical expansion and destruction
- painful and pathological fracture
Mx: Curettage and grafting or the use of bone cement.
Giant cell tumour of bone
Locally aggressive: metaphyseal region but tend to involve the epiphysis and can extend to the subchondral bone adjacent to the joint.
consist of multi-nucleate giant cells
Painful & pathological facture
Ix: soap bubble
Mx
intralesional excision with use of phenol, bone cement or liquid nitrogen to destroy remaining tumour material and
• Very aggressive lesions with cortical destruction may need joint replacement.
Fibrous dysplasia
Fibrous dysplasia
- Disease of a bone usually occurring in adolescence where a genetic mutation results in lesions of fibrous tissue and immature bone. One bone (monostotic) or more (polyostotic).
- Defective mineralization may result in angular deformities and the affected bone is wider with thinned cortices.
- stress fractures and shepherds crook deformity
Fibrous dysplasia Mx
• Bisphosphonates may reduce pain
Pathologic fractures should be stabilized with internal fixation and cortical bone grafts used to improve strength
Osteoid osteoma
Small nidus of immature bone surrounded by an intense sclerotic halo
Intense constant pain, worse at night due to the intense inflammatory response.
• The lesion may be seen on x-ray however bone scan (intense local uptake) and CT can confirm the diagnosis.
Mx: NSAIDs and CT guided radiofrequency ablation or en bloc exision
Brodies abscess
subacute osetomyelitis
Brown tumours
Hyperparathyroidism
Osteosarcoma
most common form of primary bone tumour
malignant tumour producing
younger age groups
secondary Paget’s disease, infarcts, radiation
Osteosarcoma signs/symptoms
- Around the knee (60%), proximal femur, proximal humerus and pelvis.
- Present as painful mass, sudden fracture
- Destructive, lifts periosteum (Codman’s triangle)
- Metastatic spread is usually haematogenous but can be lymphatic (lungs, bone & brain)
Osteosarcoma Mx
Surgery
Adjuvant chemotherapy after primary treatment
Chrondosarcoma
- Cartilage producing primary bone tumour
- It tends to occur in an older age group (mean age 45) apart from clear cell and mesenchymal that affect younger patients
Chondrosarcoma signs/symptoms and classification
pelvis or proximal femur
Locally invasive in bone and into muscle and fat
o Conventional (90%); intramedullary (central) or juxtacortical (peripheral).
o Clear cell – Malignant chondrocytes have abundant clear cytoplasm
o Mesenchymal - Sheets of well differentiated hyaline appearing cartilage with surrounding small round cells
o Dedifferentiated - Low grade chondrosarcoma with a separate high grade component that does not produce cartilage
Chondrosarcoma Mx
- They are not radiosensitive and unresponsive to adjuvant chemotherapy thus far.
- Surgery
Fibrosarcoma and Malignant Fibrous Histiocytoma
tend to occur in abnormal bone (bone infarct, fibrous dysplasia, post irradiation, Paget’s disease).
• Fibrosarcona tends to affect adolescents or young adults.
Mx: Surgery
Ewing’s sarcoma with signs/symptoms
Malignant tumour of primitive cells in the marrow
Most cases occur between the ages of 10 and 20.
associated with fever, raised inflammatory markers and a warm swelling, and may be misdiagnosed as osteomyelitis.
• Usually affect diaphysis of long bones (femur) and pelvic bones
• Painful enlarging masses
• Radiology shows destructive lesion
o Involves surrounding tissue
o Reactive bone gives onion skin appearance
Ewings sarcoma Mx
Radio and chemo sensitive
Giant cell tumour of tendon sheath
- Small firm swelling usually found on the flexor tendon sheath of a finger
- They may or may not be painful and can erode bone if large enough.
- When in a joint the lesion is known as Pigmented Villonodular Synovitis (PVNS).
Mx: Excision
Angiosarcoma Fibrosarcoma Liposarcoma Rhabdomyosarcoma Synovial sarcoma Leiomyosarcoma
• Angiosarcoma is a malignant tumour from blood vessels
• Fibrosarcoma and Malignant Fibrous Histiocytoma arise from fibrous tissue
• Liposarcoma arises from fat.
• Rhabdomyosarcoma is a malignant tumour of skeletal muscle.
• Synovial sarcoma originates in the synovial lining of joints or tendons.
Leiomyosarcoma
: malignant tumour from smooth muscle
Bursitis
- small fluid filled sac lined by synovium around a joint which prevents friction between tendons, bones, muscle and skin.
- Commonly inflamed bursae which usually occur after repeated pressure or trauma
- Bacterial infection can cause a bursal abscess (usually from a small wound on the limb) and gout may cause a bursitis.
- With inflammatory bursitis the fluid component of the swelling usually subsides but a thickened bursal sac may be left
Osteochondritis
painful type of osteochondrosis where the cartilage or bone in a joint is inflamed. It often refers to osteochondritis dissecans (OCD).
Impact or traction injuries cause bleeding and oedema within the bone, resulting in capillary compression.
• Bone necrosis ensues resulting in compression, fragmentation or separation of bone (and overlying cartilage if intra‐articular) which may cause flattening and incongruence of a joint or a pothole on the surface.
Common sites affected by compression in osteochondritis
2nd metatarsal head (known as Freiburg’s disease), the navicular bone (known as Kohler’s disease), the lunate of the carpus (known as Kienbock’s disease and the capitellum of the elbow (known as Panner’s disease).
Paget’s disease
chronic disorder which results in thickened, brittle and mis‐shapen bones
• Viral infection (paramyxoviruses) and genetic defects have been implicated in the aetiology.
• Increased osteoclast activity (possibly due to an exaggerated response to vitamin D) results in increased bone turnover.
• Osteoblasts become more active to try to correct excessive bone resorption.
• The osteoblasts form new bone however the new bone fails to remodel sufficiently and the resulting bone despite its increased thickness and bone density is brittle and can fracture easily.
• This excessive turnover is not coordinated, leading to patchy areas of high density (sclerosis) and low density (lysis). This results in enlarged and misshapen bones with structural problems that increase the risk of pathological fractures. It particularly affects the axial skeleton (the bones of the head and spine).
Paget’s signs/symptoms
- Bones commonly affected include the pelvis, femur, skull, tibia and sometimes the ear ossicles (resulting in conductive deafness).
- Paget’s disease of the bone can be asymptomatic and present as an incidental finding on X-ray.
- It can also cause arthritis (if close to the joint), pathologic fractures, deformity, pain and high output cardiac failure (due to increased blood flow through pagetic bone).
Paget’s Ix
• Serum ALK raised, Ca and P normal
• X- ray Findings
o Bone enlargement and deformity
o “Osteoporosis circumscripta” describes well defined osteolytic lesions that appear less dense compared with normal bone
o “Cotton wool appearance” of the skull describes poorly defined patchy areas of increased density (sclerosis) and decreased density (lysis)
o “V-shaped defects” in the long bones are V shaped osteolytic bone lesions within the healthy bone
• Bone scans – increased uptake
Paget’s Mx
• Bisphosphonates (inhibit osteoclasts) or calcitonin (reduce calcium levels in blood) if extensive lytic disease
• NSAIDs for bone pain
• Calcium and vitamin D supplementation, particularly whilst on bisphosphonates
• Surgery is rarely required for fractures, severe deformity or arthritis
o Joint replacement, long intramedullary nails or plates for femoral fractures
Monitor ALP, osteosarcoma and spinal stenosis
Osteogenesis imperfecta
Brittle bone disease, osteogenesis imperfect is a defect of the maturation and organization of type 1 collagen
Osteogenesis imperfecta signs/symptoms
- Multiple fractures of childhood, short stature with multiple deformities, blue sclerae and loss of hearing.
- Bones tend to be thin (gracile) with thin cortices and osteopenic
- Mild = normally x rays with history of low energy fractures
Generalised (Familial) Joint Laxity
- Double jointed and voluntary dislocation
- More prone to soft tissue injuries e.g. ankle sprains and recurrent dislocations of joints e.g. shoulder and patella – painful
Marfans syndrome
- AD or sporadic mutation of the fibrillin gene
- Tall stature with disproportionately long limbs and ligamentous laxity
- High arched palate, scoliosis, pectus excavtum, lens dislocation, retinal detachment, aortic aneurysm and cardiac valve incompetence (premature death)
Mx: surgery for scoliosis and joint instability e.g. fusions
Ehlers-Danlos Syndrome (type III)
autosomal dominantly inherited with abnormal elastin and collagen formation
- Profound joint hypermobility
- Vascular fragility with ease of bruising, joint instability and scoliosis
Duchenne muscular dystrophy
- Defect in the dystrophin gene involved in calcium transport
- Absence of the gene product dystrophin
- Dystrophin is essential for cell membrane stability
Duchenne muscular dystrophy signs/symptoms
• ages of 2 and 5 years.
• results in muscle weakness which may only be noticed when the boy starts to walk with difficulty standing (Gower’s) and going up stairs.
• Progressive proximal muscle weakness, aged of 10 can no longer walk, by 20 progressive cardiac and respiratory failure develop
o Death early 20s
• Initial proximal muscle weakness with calf pseudohypertrophy.
• Myocardium is also affected
Duchenne muscular dystrophy Ix
- Raised serum CK (100 times more)
- Abnormal muscle biopsy: variation in muscle fibre size, necrosis, regeneration and replacement of fat.
- Absence of dystrophin on immunochemical staining
Duchenne muscular dystrophy Mx
- Physiotherapy, splintage and deformity correction – prolong mobility
- Spinal scoliosis – spinal surgery correction
- Portable respiratory support improves life expectancy
- Prednisolone slows the decline in muscle strength and function in the short term. Gene therapy
Cerebral Palsy
- Neuromuscular disorder with onset before 2‐3 years of age due to an insult to the immature brain before, during or after birth
- Causes: genetic problems, brain malformation, intrauterine infection in early pregnancy, prematurity, intra‐cranial haemorrhage, hypoxia during birth and meningitis
CP types
Spastic CP
• 80% of cases with injury to motor cortex upper motor neurons or corticospinal tract resulting in weakness and spasticity which may worsen as the child grows
Ataxic CP
• Ataxic (which affects the cerebellum) which reduces co‐ordination and balance
Athetoid CP
• Affecting the extrapyramidal motor system, the pyramidal tract and basal ganglia which results in an uncontrolled writhing motion, sudden changes in tone and difficulties controlling speech.
CP limbs affected
- Affects one limb (monoplegic)
- one ipsilateral upper and lower limb (hemiplegic – the most common)
- both legs only (diplegic)
- all 4 limbs usually with learning difficulties (total body involvement).
CP UMN and LMN signs/symptoms
weakness, fatigue, poor balance and sensory deficits
spascitiy
hyperreflexia
clonus
cocontraction
CP Mx
- Physiotherapy, splintage (orthotics) to prevent contractures
- Baclofen (injection- intrathecally) – subarachnoid space – lower dose and fewer SE – spasticity
- Boxtox also for spasticity
Surgical:
o Hip excision or replacement to treat painful hip dislocation
• contracture joint release
• correction of severe scoliosis (cobb angle >45 degrees)
o protect respiratory function and help careers – seating and comfort
• joint fusions and tend/on transfers
Spinda bifid: how and types
Congenital disorder where the two halves of the posterior vertebral arch fail to fuse, probably in the first six weeks of gestation.
- Mild: Spina Bifida Occulta: No associated problems apart from tethering of spinal cord and roots – high arched foot (Pes cavus) and clawing of toes
- Severe: Spina Bifida Cystica: contents of the vertebral canal herniate through the defect with either herniation of the meninges alone (a meningocele) or with the spinal cord or cauda equina (myelomeningocle)
Meningocele vs myelomeningocele
o A meningocele is not usually associated with neurological sequelae
o myelomeningocele usually has a neurological deficit (motor and sensory) below the lesion and most will never function independently.
o associated with hydrocephalus (excess CSF around the brain raising intracranial pressure) and the degree of disability depends on the spinal level affected.
Polio and Mx
viral infection which affects motor anterior horn cells in the spinal cord or brainstem resulting in a lower motor neurone deficit.
Mx
Vaccination
• residual paralysis can be treated with splintage (caliper, orthotics) and shortening of a leg can be helped with a shoe raise
Tendon transfers may improve function whilst some deformities especially of the foot or ankle can be treated with fusion (arthrodesis)
• Flail joints may also be treated with arthrodesis in a position of maximal function and shortening can be treated with lengthening of the short side or shortening of the long side
Syndactyly
Polydactyly
Syndactyly: two digits are fused together
Polydactyly: extra digit
Erbs palsy
injury to the upper (C5 & C6) nerve roots resulting in loss of motor innervation of the deltoid, supraspinatus, infraspinatus, biceps and brachilais muscles.
Erbs palsy signs/symptoms and Mx
Internal rotation of humerus: waiters tip
Mx:
Physio and surgery: release contractures and tendon transfers
Klumpke’s Palsy with signs/symptoms and Mx
lower brachial plexus injury (C8 &T1 roots) caused by forceful adduction
•paralysis of the intrinsic hand muscles +/‐ finger and wrist flexors and possible Horner’s syndrome (due to disruption of the first sympathetic ganglion from T1).
Mx
• no specific treatment
• Total brachial plexus palsy after birth carries the poorest prognosis
Normal lower limb development (knee)
• Children at birth normally have varus knees (bow legs) which become neutrally aligned at around 14 months, progressing to 10 to 15° valgus (knock knees) at age 3 and then gradually regress to the physiologic valgus of 6° by around the age of 7‐9.
Valgus vs varus deformity
- A valgus deformity at the knee will result in a more of a knock knee appearance with a larger gap than normal between the feet/ankles.
- A varus deformity will result in a larger gap between the knees
Most resolved at 10
Excess genu varum causes
Growth disorder of the medial proximal tibial physis known as Blount’s disease resulting in marked and persisting (beyond 4‐5 years) varus deformity
Other causes of genu varum include: rickets, tumour (osteochondroma), traumatic physeal injury and skeletal dysplasia.
Excess genu valgum
rickets, tumours (osteochondroma and endochondroma), trauma and neurofibromatosis whilst some cases are idiopathic.
o Refer if asymmetric, painful or severe (over 2sd)
o >8cam intermalleolar distance at age of 11 - refer
Genu Varum (Bow legs) and Genu Valgus (Knock knees) Mx
• Surgical Osteotomy or growth plate manipulation surgery
o External fixator
o 8 plate
In toeing causes
Femoral neck anterversion the femoral neck is slightly anteverted (pointing forwards).
Internal tibial torsion – the bone can be rotated inward about its vertical axis but as this is a normal variation, it should ignored.
Forefoot adduction – can cause the apparent in‐toeing. There remains debate about whether surgery is useful in cases which persist after 7 or 8 years of age. Certainly surgery should not be considered before this age as the majority resolve in time.
Flat feet
- Flat feet are part of normal variation and usually do not reflect underlying pathology
- We are born with flat feet but most develop medial arch once walking as tibialis posterior strengthens
- Flat feet usually asymptomatic and some people will have it in adulthood
- Usually by age of 3
- Need to determine if flexible (fine) or fixed (usually bone reason for it to be flat)
Flexible flat feet
• Mobile/flexible flat feet are those where the flattened medial arch forms with dorsiflexion of the great toe (Jack test) o Related to ligamentous laxity (familial or idiopathic) o Dynamic (present weight bearing only) o Normal variant
Fixed flat feet
- Arch remain flat regardless of load or great toe dorsiflexion – underlying bony abnormality
- tarsal coalition where the bones of the hindfoot have an abnormal bony or cartilaginous connection
- underlying inflammatory or neurological disorder
Mx: surgery
Curly toes and Mx
Minor overlapping of the toes and curling of toes is common with the fifth toe is most frequently affected.
Mx: most will correct without intervention but they can occasionally cause discomfort in shoes and persistent cases in adolescence may require surgical correction
Cavus feet with signs/symptoms and Mx
very high arch. This causes an excessive amount of weight is placed on the ball and heel of the foot when walking or standing
- can lead pain and instability
Mx: refer if getting progressive
Developmental Dysplasia of the Hip (DDH)
dislocation or subluxation of the femoral head during the perinatal period which affects the subsequent development of the hip joint.
Untreated = shallow acetabulum, false one occurs proximal to the original one with a shortened limb
Severe OA – reduced contact area, gait affected
DDH risk factors
- positive family history of DDH, breech presentation, first born babies, Down’s syndrome and the presence of other congenital disorders (talipes, arthrogryposis).
- Over 4kg
DDH signs/symptoms
shortening, asymmetric groin/thigh skin creases and a click or clunk on the Ortolani or Barlow manoeuvres.
DDH Dx
- Barlow test (dislocatable hip with flexion and posterior displacement)
- Unstable hips with a positive Ortolani test (reducing a dislocated hip with abduction and anterior displacement)
- Require further evaluation with ultrasound which should detect a dislocated hip, an unstable hip or a shallow acetabulum.
- X-rays cannot be used for the early diagnosis of DDH as the femoral head epiphysis is unossified until around 4‐6 months but x-rays are the investigation of choice after this age.
DDH Mx
Dislocated or unstable hips – Pavlik harness (hips in flexion and abduction – maintains reduction)
• 23-24 hours a day for up to 12 weeks until USS is normal (6 weeks full time and 6 weeks part time). Be wary of AVN. 4-6 months in age
18 months and older:
o CR spica (close reduction)
o OR spica (open surgery)
o pelvic osteotomy to deepen and re-orientate acetabulum
Transient synovitis
- Inflammation of synovium often secondary to viral illness (self-limiting) - URTI
- 2-10 ages and boys more
Transient synovitis signs/symptoms and Mx
- History of URTI
- Limp, reluctance to weight bear, ROM may be restricted
- May present with referred pain to knee (but less common)
- Hip lying flexed/externally rotated
- Radiographs – exclude perthes disease, normal or near normal CRP. If in doubt, aspiration
NSAIDs and rest
Perthes disease
• idiopathic osteochondritis of the femoral head
• ages of 4 to 9, common in boys, particularly very active boys of short stature.
• The femoral head transiently loses its blood supply resulting in necrosis with subsequent abnormal growth.
• The femoral head may collapse of fracture.
• Subsequent remodelling occurs however the shape of the femoral head and congruence of the joint is determined by age of onset and the amount of collapse
- older children fare worse
- lead to hip arthritis and hip replacement
Perthes disease signs/symptoms
- Pain and limp – unliteral
- Loss of internal rotation is usually first clinical sign followed by loss of abduction and later on a positive Trendellenburg test from gluteal weakness.
Perthes Mx
- None
- Regular x-ray and avoidance of PA
- Some cases the femoral head becomes aspherical, flattened and widened.
- The lever arm of the abductor muscles is altered resulting in weakness (Trendelenburg positive).
- Occasionally the femoral head may sublux (partially dislocate) requiring an osteotomy of the femur or acetabulum.
SUFE – Slipped Upper Femoral Epiphysis
condition mainly affecting overweight pre‐pubertal adolescent boys where the femoral head epiphysis slips inferiorly in relation to the femoral neck.
• Girls are less commonly affected and hypothyroidism or renal disease may predispose to SUFE.
• The growth plate (physis) is not strong enough to support body weight and the femoral epiphysis slips due to the strain (1/3 are bilateral)
SUFE signs/symptoms
The pain may be felt in the groin (like other hip pathology) and purely in knee (obturator nerve)
Loss of internal rotation (hip is in external rotation)
shortened and loss of flexion and abduction
SUFE Ix and Mx
X ray
Mx
• Internal fixation (pin femoral head) to stabilise any slippage and physeal closure
o AVN is an complication (femoral head)
• Bolt in (pin) or hip replacement – going to keep revising the hip replacement if done
Inflammation of the tibial tubercle apophysis
Osgood‐Schlatter’s disease
• Inflammation of the inferior pole of patella
Sinding‐Larsen‐Johanssen disease.
Apophysitis Mx
self‐limiting conditions requiring rest +/‐ physiotherapy.
• Patients may be left with a bony prominence which does not require surgery
Patellofemoral dysfunction and Mx
- The aetiology is unclear and may be due to muscle imbalance, ligamentous laxity and subtle skeletal predisposition (genu valgum, wide hips, femoral neck anteversion).
- There may be softening of the hyaline cartilage of the patella (chondromalacia patellae).
Mx: rest and physiotherapy
Surgery for resistance cases to shift forces on patella (tibial tubercle transfer)
Osteochondritis dissecans (OCD)
• fragment of hyaline cartilage with variable amount of bone fragments and breaks off the surface of the joint e.g. medial femoral condyle of knee
Talipes Equinovarus (Club Foot)
congenital deformity of the foot
• Utero abnormal alignment of the joints between the talus, calcaneus and navicular (50% bilateral)
• The abnormal alignment of these joints results in contractures of the soft tissues (ligaments, capsule & tendons) resulting in a deformity consisting of ankle equinus (plantarflexion), supination of the forefoot and varus alignment of the forefoot which are not immediately correctable.
Late diagnosis: Fixed deformity – child walks on outside of their foot – very difficult to correct and extensive surgery (soft tissue +/- bony procedures) with less satisfactory results
Talipes Equinovarus (Club Foot) Mx
Ponseti technique
• commenced as soon as possible after birth and the deformities are corrected progressively in stages and held in plaster casts with 5 or 6 weekly cast changes
• Tenotomy of the Achilles tendon – maintains full correction
• Once full correction is achieved the child is then placed in a brace consisting of boots attached to a bar which is worn 23 hours a day for 3 months and used during sleep until the age of 3 to 4 to try to prevent recurrence.
Tarsal coalition
abnormal bridge (bony, fibrous or cartilaginous) between the calcaneus and navicular or between the talus and calcaneus. • painful fixed flat foot deformity in older children.
Tarsal coalition Mx
- Symptoms may improve with splintage / orthotics
* Resistant pain may require surgery to reTarsal move the abnormal connection
Scoliosis
lateral curvature of the spine (and also rotational deformity) which can be idiopathic (most common) or secondary to neuromuscular disease, tumour (e.g. osteoid osteoma), skeletal dysplasia or infection
• Younger children with scoliosis usually have an underlying cause and may progress more readily to a severe curve.
• Any painful scoliosis warrants urgent investigation (MRI for tumour or infection).
Scoliosis Mx
- Mild, non-progressive scoliosis does not require surgery
- Larger curves may require surgery for cosmesis or to improve wheelchair posture (neuromuscular disease such as cerebral palsy)
- Severe curves – restrictive lung defect and surgery to prevent breathing difficulties
- Correction of larger curves carries a risk of spinal cord injury (intraoperative monitoring may be used).
Spondylolisthesis
• slippage of one vertebra over another and usually occurs at the L4/L5 or L5/S1 level.
• It can be due to a developmental defect or a recurrent stress fracture (Spondylolysis) of the posterior elements which fails to heal.
o pars interarticularis of the vertebral arch
Spondylolisthesis signs/symptoms and Mx
low back pain
• may have a radiculopathy with severe slippage.
• They may have a paradoxical “flat back” due to muscle spasm and can present acutely with a characteristic waddling gait.
Mx:
• Minor: Rest and physiotherapy
• Severe: stabilisation and possibly reduction – risk of neurological injury
Mechanical back pain
recurrent relapsing and remitting back pain with no neurological symptoms. Worse with movement and relived with rest
Causes
• Obesity, poor posture, poor lifting, poor PA, depression, degenerative disc prolapse, facet joint OA and spondylosis
• Spondylosis is where the intervertebral discs lose water content with age resulting in less cushioning and increased pressure on the facet joints leading to secondary OA.
Mechanical back pain Mx
analgesia, rest and physio
• Spinal stabilisation for single level (2 adjacent vertebrae) OA or instability or patient has not improved despite physio/conservative management
Acute disc tear / Discogenic back pain
- An acute tear can occur in the outer annulus fibrosis of an intervertebral disc which classically happens after lifting a heavy object (e.g. lawnmower).
- The periphery of the disc is richly innervated and pain can be severe
- Pain is characteristically worse on coughing (which increases disc pressure).
- Symptoms usually resolve but can take 2‐3 months to settle.
- Analgesia and physiotherapy
Sciatica/Lumbar Radiculopathy signs/symptoms
radicular pain is felt as a neuralgic burning or severe tingling pain, often like severe toothache radiating down the back of the thigh to below the knee.
o L3/4 prolapse > L4 root entrapment > pain down to medial ankle (L4), loss of quadriceps power, reduced knee jerk
o L4/5 prolapse > L5 root entrapment > pain down dorsum of foot, reduced power Extensor Hallucis Longus and tibialis anterior
o L5/S1 prolapse > S1 root entrapment > pain to sole of foot, reduced power plantarflexion, reduced ankle jerks
acute disc tear Mx
- Analgesia, maintaining mobility and physiotherapy
- Gabapentin if severe leg pain
- Can resolve in 3 months
- Surgery (discectomy
Spinal Stenosis and claudication causes
• Spondylosis and combination of bulging discs, bulging ligamentum flavum and osteophytosis results in the cauda equina of the lumbar having less space
Spinal stenosis signs/symptoms and Mx
• 60 years and over and claudication in legs when walking
o the claudication distance is inconsistent
o the pain is burning (rather than cramping)
o pain is less walking uphill (spine flexion creates more space for the cauda equina) or cycling
o pedal pulses are preserved
Mx
• conservative: analgesia, physiotherapy and weight loss
• Surgery: MRI evidence and no improvement from above – decompression surgery to increase space for cauda equina
Cauda Equina syndrome
very large central disc prolapse can compress all the nerve roots of the cauda equina
• Surgical emergency as affected nerve roots include the sacral nerve roots (mainly S4 & S5 but variable and others contribute) controlling defaecation and urination
• Prolonged compression can potentially cause permanent nerve damage requiring colostomy and urinary diversion and urgent discectomy way prevent this catastrophe
Cauda equina signs/symptoms
bilateral leg pain, paraesthesiae or numbness and complain of “saddle anaesthesia” – numbness around the sitting area and perineum.
• Altered urinary function is typically urinary retention but incontinence can also occur.
• Faecal incontinence and constipation can also occur.
• A rectal examination (PR) is mandatory and it is considered negligent not to perform this is a cauda equine syndrome is missed.
Mx:
MRI and urgent discectomy
Osteoporotic crush fractures and Mx
severe osteoporosis, spontaneous crush fractures of the vertebral body can occur leading to acute pain and kyphosis
Mx
• Conservative: analgesia, physiotherapy
• Surgical: balloon vertebroplasty
Cervical spondylosis
Spondylosis can occur with disc degeneration leading to increased loading and accelerated OA of the facet joints.
slow onset stiffness and pain in the neck which can radiate locally to shoulders and the occiput.
Mx: physio and analgesia
Cervical spine instability causes
RA (atlanto-axial subluxation - destruction of synovial joint) and down syndrome (atlanto‐axial (C1/C2) instability with subluxation)
Screen with flexion/extension X rays
Red flags for back pain
Back pain in <20 years and >60 years
Nature of pain: constant, severe and worse at night
Systemic upset
Hip replacement for which diseases…
primary OA or arthritis due to RA, seronegative inflammatory arthropathy, AVN, dysplasia, Perthes or SUFE
Hip replacement pseudotumour
local reaction to metal debris resulting in an inflammatory “pseudotumour” which can cause necrosis of muscle and bone
Decision to undergo THA
- Level of pain and disability
- Conservative: simple analgesics, physiotherapy, use of a stick (which reduces the joint force by 15%), weight reduction and modification of activities
Avascular necrosis (AVN)
hip joint is one of the commonest sites of AVN which as previously discussed may be primary / idiopathic or secondary to alcohol abuse, steroids, hyperlipidaemia or thrombophilia.
necrosis because of failure of the blood supply to the femoral head
• idiopathic (most common) or associated with trauma (injury to femoral head blood supply (medial femoral circumflex)
AVN risk factors and signs/symptoms
- Irradiation
- Trauma
- Haemolytic diseases
- Dysbaric disorders: nitrogen embolism from diving
- Diabetes
- Alcoholism
- Steroid use
Insidious onset of groin pain – exacerbated by impact or stairs
• Normal examination (unless disease has advanced to collapse/OA)
