Ortho 2 Flashcards
What is osteomyelitis?
Infection of the bone
- In neonates - metaphysis or epiphysis commonly affected
- in children - metaphysis
- in adults - epiphysis and subchondral regions
What increases incidence of osteomyelitis?
Incidence increases as living conditions drop
How can osteomyelitis start?
Can be acute primary or can spread from local infection eg. boils, abscesses, pneumonia or GU instrumentation
Pathology of osteomyelitis
Cancellous bone is typically affected in adults. Infection leads to cortex erosion with holes (cloacae). Exudation of pus lifts up periosteum interrupting blood supply to underlying bone - necrotic bone fragments form (sequestrum)
What areas of bone are most commonly affected by osteomyelitis in IV drug users, diabetics and children
Vertebrae in IV drug users, feet in diabetics, children is most commonly vascular bone (eg long bone metaphyses, distal femur, upper tibia etc)
What is typically present in the bone in chronic osteomyelitis?
Sequestrum (piece of dead of bone separated from the normal bone by necrosis)
What is involucrum in osteomyelitis
New bone formation created by the elevated periosteum
What can happen visually in osteomyelitis?
Pus may discharge into the joint spaces or via sinuses to the skin
Typical hx and symptoms of osteomyelitis
Pain gradual onset over the course of a few days - tenderness, warmth and erythema at affected part
Unwillingness to move
May have slight joint effusion in neighbouring joints and signs of systemic infection
In whom are osteomyelitis signs less marked
In adults - acute invariably happens in children, in adults it is normally IV drug users or immunosuppressed patients or those with other disease/infection elsewhere
Common organisms for osteomyelitis x4
Staph aureus!!!, Pseudomonas, E.coli, Streptococci (sickle cell may be salmonella)
Tests in osteomyelitis
Bone biopsy and culture is gold standard
Inflammatory markers will be raised
Radiograph in osteomyelitis
Changes won’t show for 10-14 days, then slow haziness and loss of density - later sequestrum and involucrum
MRI is specific and sensitive for earlier osteomyelitis
Treatment of osteomyelitis
Drain abscesses and remove sequestra by open surgery (if very severe)
Vancomycin and cefotaxime IVI for 6 weeks (change if specificity known)
Treatment of pseudomonas osteomyelitis
Ciprofloxacin
What is chronic osteomyelitis?
Any acute osteomyelitis can become chronic with poor treatment
Generally considered chronic if longer than a month
Symptoms of chronic osteomyelitis
Pain, fever and sinus suppuration
Xray in chronic osteomyelitis
Only if advanced infection, acutely - will see soft tissue swelling and may see joint effusion in local joint, then periosteal thickening and regional osteopenia with cortical loss
What is Pott’s disease
Bone TB in vertebra
Risk factors for osteomyelitis x6
Diabetes Vascular disease Sickle cell Impaired immunity Surgical prostheses Open fractures
What cancers commonly metastasise to the bone x4
Breast, bronchus, prostate and kidney
What time of bone cancer is rare
Primary (mostly children apart from chondrosarcoma)
Radiological features of bone cancer x4
Bone destruction, new bone formation, soft tissue swelling, periosteal elevation
What is the most common malignant primary tumour of bone
Osteosarcoma
Who is typically affected by primary osteosarcoma and where do they get it?
Adolescents
Arises in the metaphyses of long bones especially around the knee
Typically in sites of bone growth (metaphysis) presumably because proliferation makes osteoblastic cells more prone to mutation
Treatment of osteosarcoma
Resection + chemotherapy - 90% have limb sparing surgery
Cure rate for primary osteosarcoma
60-70%
What is Ewings Sarcoma?
Round-cell tumour of long bones and limb girdles - usually presents in younger adolescents
Typically occurs in femur, tibia and pelvic bones
What do you see on radiograph with Ewings Sarcoma?
Concentric layers of new bone formation = “onion-ring sign”
and a soft tissue mass
Genetic association of Ewings Sarcoma?
Typically have a t11:22 chromosomal translocation
Treamtent of Ewings Sarcoma?
Chemo, surgery and radiotherapy - chemo first to shrink the tumour
5 year recurrence free survival for Ewings Sarcome?
22% if mets at diagnosis, 55% if no mets - 30% overtly metastatic at presentation
What is Chondrosarcoma and who does it affect?
Carcinoma of cartilage producing cells which affects the axial skeleton as well as long bones
In middle-aged people typically (unlike other bone tumours which are more common in children)
Treatment of chondrosarcoma
Doesn’t respond to chemo or radio
Therefore treat with excision
What is the most common benign bone tumour - where does it occur
Osteochondroma
Occurs about the knee, proximal femur or proximal humerus
Usually around growth plates
Grows with the bone and then will usually stop growing when bone stops growing
Presentation of osteochondroma
Painless lump or local mass effects
Pain with exercise - tendon snapping over the growth
Neurological symptoms - tingling or numbness
Decreased blood flow from vascular compression
Osteochondroma on x ray
Bony spur pointing away from the joint
Treatment of osteochondroma
Remove if causing symptoms from pressure on local structures
Or if continuing to grow after skeletal maturity because risk of malignancy
What do you suspect if boney pain responding to aspirin within 15mins in young adult?
Osteoid Osteoma - nocturnal pain is a significant feature
Details of osteoid osteoma
Painful benign bone lesion occurring in long bones of young males 10-25 years old
responds to aspirin (produces prostaglandins which lead to pain unrelated to activity)
Treatment of osteoid osteoma
CT guided biopsy and radiofrequency ablation - treatment is dependant on symptoms, if can be managed with anti-inflammatories then it will be
Features which lead to suspecting mass as being soft tissue sarcoma x4
Bigger than 5cm, increasing in size, deep to deep fascia, painful
Treatment of soft tissue sarcoma
Excision by wide margins - followed by radiotherapy
What is osteogenesis imperfecta?
An inherited disorder of type I collagen that results in fragile, low density bones = brittle bone disease/ Lobstein syndrome
Incidence of osteogenesis imperfecta?
1 in 20,000 affected
Details of type 1 osteogenesis imperfecta? x8
Mildest and most common Autosomal dominant Blue sclerae (increased corneal translucency) 50% have hearing loss Fractures typically before puberty Loose joints and poor muscle tone Normal life expectancy Normal collagen produced but not enough of it
Details of type 2 osteogenesis imperfecta? x3
Lethal perinatal form with many fractures and dwarfism
Recessive
Most die within first year of life from respiratory failure or intracerebral haemorrhage
Details of type 3 osteogenesis imperfecta? x8
Severe form Occurs in 20% Recessive Fractures at birth and progressive (key feature of type 3) limb and spinal deformity with resultant short stature Blue or white sclera Dentinogenesis imperfecta is common Life expectancy decreased Enough collagen is produced but it's defective
Details of type 4 osteogenesis imperfecta? x6
Moderate form Autosomal dominant Fragile bones White sclera after infancy Has been expanded into types 4-7 Not high enough quality collagen is produced but enough is produced
Radiographs in osteogenesis imperfecta? x3
Many fractures
Osteoporotic bones with thin cortex
Bowing deformity of long bones
Treatment of osteogenesis imperfecta? x4
Prevent injury
Physio, rehab and occupational therapy
Intramedullary rods sometimes used in long bones
Bisphosphonates
What is Achondroplasia?
Most common form of dwarfism due to reduced growth of cartilaginous bone
Inheritance of achondroplasia
Autosomal dominant but 80% are from spontaneous mutations - if inherit two forms of gene (one from each parent) likely to die in first few months of life
Gene mutation causing achondroplasia
95% are caused by mutation in the gene encoding fibroblast growth factor receptor type 3 (FGFR3)
Effects of achondroplasia x5
Large heads with ventriculomegaly and frontal bossing Normal trunk length Short limbs Fingers all the same length Delayed gross motor skills development
Appearance of adults with achondroplasia x4
Short, increased lumbar lordosis, bowed legs and short proximal arms and legs
What is the affect of achondroplasia on lifespan?
None - lifespan normal
What is the affect of achondroplasia on mental and sexual development?
None - both normal
Complications of achondroplasia x6
Tibial bowing Joint hypermobility Hydrocephalus, foramen magnum compression Recurrent otitis media and hearing loss Sleep apnoea Increased BMI
Radiographs in achondroplasia
Short proximal long bones and wide ephiphyses
What is hereditary multiple exostoses?
Autosomal dominant disorder in which certain proteins accumulate in the Golgi apparatus leading to cartilage-capped tumours developing from affected cartilage at the end of long bones (point away from joint)- many osteochondromas/extoses
Effects of hereditary multiple exostoses
If severe, bones are broad and badly modelled
Causing short stature as well as forearm, knee and ankle deformity
Boney spurs may have local effects, nerve/vascular compression
What can occur in hereditary multiple exostoses
Malignant transformation from exostoses/osteochondromata to chondrosarcomas or osteosarcomas
Treatment of hereditary multiple exostoses
Removal of symptom producing exostoses, pain management and physiotherapy
What is osteopetrosis
Lack of differentiation between cortex and medulla of bone following from underlying failure of osteoclastic bone resorption - Marble bone disease/Albers-schonberg disease
What are bones like in osteopetrosis?
Very hard, dense ‘marble’ bones that are brittle
What can you get with osteopetrosis
Anaemia and thrombocytopenia from decreased marrow space
Deafness and optic atrophy from CN compression
Despite being hard the bones are still very brittle therefore multiple fractures
Radiograph in osteopetrosis
Lack of remodelling therefore ossific density with bone within a bone appearance
What are osteochondroses? What are they also called?
Group of conditions characterised by abnormal endochondral ossification of epiphyseal growth during childhood
Also called osteochondritis
Bone grows and then stops and then starts again
Underlying of cause of osteochondroses?
Unknown
Inheritance, overuse/trauma, rapid growth and anatomic configuration may be predisposing factors
Pathology of all osteochondroses?
Interruption of blood supply to epiphysis, followed by bone and cartilage necrosis, revascularisation and regrowth of bone
What is Scheuermann’s disease?
Osteochondrosis - Most common cause of kyphosis in 13-16 year olds
Problem with thoracic vertebrae - deforming forces are greatest anteriorly therefore vertebrae narrower here causing kyphosis
Presentation of Scheuermann’s disease?
Usually present for deformity rather than pain
Radiographing features of Scheuermann’s disease? x4
Irregular vertebral end plates
Schmorls nodes (protrusion of IVD through vertebral body end plate and into adjacent vertebra)
Decreased disc space
Anterior wedging
Treatment of Scheuermann’s disease?
Posture control and exercise
Physiotherapy + spinal braces
Surgery if severe
What is Calve’s vertebra
Not true osteochondroses as due to eosinophilic granulomata but produces similar picture to scheuermann’s disease but in younger child 2-10years
Symptoms of Calves vertebra
Pain and tenderness over affected vertebra with slight kyphosis
Radiograph in Calves vertebra
Flattened vertebral body with disc space preserved
What is Kienbocks disease?
Osteochondroses affecting lunate bone in males 20-40 years
Symptoms of Kienbocks disease
Pain over lunate especially during active wrist movement
Grip impaired due to pain
Radiograph in Kienbocks disease
Dense lunate with a depth reduction - leads to OA
Treatment of Kienbocks disease
Splinting and analgesics
Can do surgery if needs be to restore blood flow to lunate (or to realign bones or remove lunate if severe)
What are Panner’s disease and osteochondritis dissecans of the elbow?
Spectrum of conditions affecting the capitellum (radial attachment on humerus)
Who does Panner’s disease affect and what does it cause?
Affects boys under 10
Lateral elbow pain and swelling
Management of panner’s disease
Usually just conservative management
What does osteochondritis dissecans of the elbow cause?
Loose body from cartilage becoming avascular and separating from bone
Causes early aching and effusion after use in adolescents
Sudden painful locking if loose bodies
Treatment of OCD?
Stable lesions managed conservatively in a hinged brace
Unstable lesions may need fixation +/- removal of loose bodies
What is Kohlers disease?
Navicular osteochondroses in children 3-5 years old
What does Kohlers disease cause?
Pain in mid-tarsal region
Limp
Navicular tenderness
Dense deformed bone on radiograph
Treatment of Kohlers disease
Rest the foot or wear walking plaster - symptomatic treatment
Prognosis good
What is Freibergs disease?
Osteochondritis dissecans of the metatarsal heads - most commonly 2nd
Freibergs disease symptoms
Forefoot pain, worsens with pressure, usually starting around the time of puberty
What is Freidrich disease?
Clavicle osteochondroses
What is Froelich disease?
Humeral condyles osteochondroses
What is Perthes disease?
Osteochondroses of hip
What is Blount disease?
Osteochondroses of proximal tibial epiphysis
What is Osgood-Schlatter’s syndrome?
Osteochondroses - Tibial tuberosity apophysitis (secondary ossification centre) that affects children 10-15 years old - association with overuse
Signs and symptoms of Osgood-Schlatters syndrome?
Pain below the knee, worse on strenuous activity and quadriceps contraction
Tuberosity looks enlarged and is tender
Prognosis of Osgood-schlatters syndrome?
Self-limiting in >90% of cases
Radiograph of Osgood-schlatters syndrome?
Tibial tuberosity enlargement with possible fragmentation (as opposed to normal immature tuberosity appearance)
Treatment of Osgood-Schlatters syndrome
Limitation of activity with ice, oral anti-inflamm’s, knee padding and physiotherapy
Tibial tubercle excision may be recommended if above fail
What is Sinding Larsens disease?
Also called jumpers knee - traction tendinopathy with calcification of proximal attachment of patella tendon - may be partially avulsed
Symptoms similar to OSS but earlier presentation 8-13 years
Structure of hip prostheses
Metal femoral component with intramedullary stem sometimes held in place by bone cement
and a plastic acetabular component
Sign of later loosening or infection with hip replacement
Return of pain
Risk factor BMI for osteoporosis
Low BMI
Osteoporosis risk factors
Menopause RA Low BMI Steroids FHx Immobility
Common cause of tibial nerve injury
Posterior hip dislocation
Signs of tibial nerve damage
Loss of inversion of foot and ability to tiptoe
Sensation of plantar aspect lost (S1)
Signs of femoral nerve injury
Unable to extend knee
Absent knee jerk
Loss of sensation over front and medial thigh
Symptoms of osteosarcoma
Pain, may be worse at night and can be intermittent
Typically just below the knee, worse on exercise
Can be present as sudden fracture due to weakened bone
Symptoms of Ewing’s sarcoma
Pain at site, gets worse and can be extremely painful
Can also get intermittent high fevers, weight loss and severe fatigue (anaemia)
Presentation/symptoms of chondrosarcoma
Pain most common feature but may be swelling therefore palpable lump or local mass effect
Chondrosarcoma on x ray
“popcorn calcification” on x-ray with lysis as well
Osteoid osteoma on imaging
Nidus - Xray is a thickened oval area which is a well-circumscribed lucent area with a sclerotic dot in the centre (black with white in middle)
on CT nidus is seen as well
Pathological steps behind septic arthritis
Bacteria get into joint, inflammatory response causes damage to articular cartilage. Increased permeability and fluid secretion causes joint effusion.
What can happen during healing of septic arthritis?
Raw articular surfaces may result in fibrosis and bony ankylosis
Most common organisms causing septic arthritis in under 3 yr olds x3
Staph Aureus, haem influenza and coliforms
Most common organisms causing septic arthritis in adults x2
S.aureus and neisseria gonorrhoea
Risk factors for septic arthritis
Diabetes, IV drug use, immunocompromised, chronic joint disease (rheumatoid)
What can be seen in gonococcal septic arthritis
Skin pustules near the joint
Radiograph in septic arthritis
Increased joint space, soft tissue swelling
In late cases subchondral bone destruction
Surgical management of septic arthritis
Surgical washout of the joint to remove pus and infected material - either arthroscopy or open (arthrotomy)
Medical management of septic arthritis
Antibiotics given IV 1-2 weeks then oral 4-6 weeks
Splint joint for pain reduction
Physio to prevent fibrosis and maintain joint mobility
