Clinical skills - Bone pain Flashcards
Osteoporosis
A systemic skeletal disease characterised by low bone mass and deterioration of bone tissue, w/ consequent increase in bone fragility and susceptibility to fracture
Commons sites of fractures due to OP
Spine
NOF
Wrist
Consequences of hip fractures
20% of pts die within a year
50% of survivors are incapacitated
20% require long-term residential care
High risk of future fracture or mortality
Types of vertebral fractures
Wedge
Bioconcave
Crush
Non-modifiable risk factors of OP
Age (major determinant of hip fracture risk)
Gender
Previos fragility fracture at a characteristic site
Endocrine e.g. early menopause
Parental hx of hip fracture
Modifibale risk factors for OP
Low BMI
Lifestyle: smoking, alcohol intake
Low bone density
Drugs increasing the risk of OP
Glucocorticoids Epileptics Aromatose inhibitors Dept injections Thiazides
Co-existing comorbdiities increasing risk of OP
DM RhA SLE Epilepsy HIV 1' hyperparathyoidim
Key determinants of peak bone mass and bone loss
Genes Skeletal geometry Body weight Sex hormones Diet Exercise Racial factors
FRAX
Method used to calculate risk of fracture
Similar to Qfracture
Radiological measure of bone
Dual-energy X-ray absorptiometry (DEXA)
Low dose of radiation
T score
The diff between mean bone density between the pt and a healthy young woman
Normal T score
T > 1.0
Low fracture risk
Osteopenic T score
T < 1.0 to -2.5
Above avg fracture risk
OP T score
T < -2.5
High fracture risk
What creates a very high fracture risk
Severe osteoporosis: T < -2.5 plus one or more fractures
Z scores
The diff between mean bone density between the pt and a healthy aged-matched woman
Pathophysiology of OP
BMU
Coupling of osteoclastic and osteoblastic activity
Imbalance of this relationship
Investigations for OP
FBC ESR/CRP Serum calcium (albumin) Alkaline phosphatase Liver tests Thyroid Myeloma screen 25-hydroxyvitamin D (25OHD) PTH Endocrine: sex hormones/ diabetes/ cortisol GI: coeliac disease antibodies Markers of bone marrow Urine Ca excretion
Strategies for treatment of OP and prevention of fractures
Diet Exercise Lifestyle Treat underlying diseases Drug treatment Falls intervention (medical, OT, physio)
Types of drug treatment for OP
Anti-resorptive
Anabolic
Both
Anti-resorptive drug treatment for OP
Bisphosphonates (alendronate, ibandronate, risedronate, zoledronic acid) HRT Calcium and Vitamin D Calcitriol Raloxifene Denosumab
Anabolic drug treatment for OP
Intermittent PTH – Teriparatide (injected daily)
Anti-resorptive anabolic drug treatment for OP
Strontium ranelate – withdrawn
Duration of drug treatment for OP
Uncertain, 3-5 for bisphosphonate or up to 10 yrs. w/ denosumab
Drug holidays?
Consider se of treatment
Steroids –> early bone los
Some s/e of OP drug treatment
ONJ (osteonecrosis of jaw)
Atypical no
AF
GI
Issues w/ diagnosing and treating osteoporosis
Men
Finding patients w/ fractures – fracture liaison service
Glucocorticoid-induced bone loss – bisphosphonates, little long-term data
Diagnosing OP in men
BMD data only rather than fracture reduction
DEXA based on female reference ranges
Look for secondary causes
Osteogenesis Imperfecta
Syndrome of bone fragility due to mutations in type 1 collagen gene Most cases (85-90%) are caused by a dominant genetic defect There are 7 types – type 1 is most common and mildest and type 11 most severe
Variable in OI
Freq of fractures Stature Coloured sclera Laxity of joints and muscles Bone deformity Scoliosis Brittle teeth Deafness - otosclerosis Respiratory failure Collagen abnormalities
What is treatment of OI directed towards
Preventing or controlling symptoms
Maximising independent mobility
Developing optimal bone mass and muscle strength
Recommendations for OI incl
Care of fractures
Extensive surgical and dental procedures
Physical therapy
Can also use wheelchairs and other mobility aids
Osteomalacia
‘Soft bones’
State of the skeleton arising from impairment of mineralisation
Majority arise from disturbance of Vitamin D and phosphate metabolism
Osteoid
Bone protein matrix, made-up of mostly type 1 collagen and needs to mineralise.
Forms of vit D
D2/ ergocalciferol which is plant derived and consumed in food
D3/ cholecalciferol which is formed from the effect of UV-B sunlight on 7-dehydrocholesterol in skin
Metabolism of vit D
Hydoxylated to 25OHD in liver
Hydoxylated to 1,25(OH)2D in liver or can be metabolised in other cells to form 24,25(OH)2D
Actions of calcitriol
Facilitates calcium and phosphate absorption from the gut
Triggers osteoblast RANKL –> activates osteoclasts –> releasing calcium into the circulation
Triggers osteoblast production of a number of mediators resulting in laying down bone osteoid
Decreases PTH synthesis and secretion
Where does Ca absorption occur
Duodenal
Where does Phosphate absorption occur
Entire small intestine
Associations between vit D deficiency and osteomalacia
Dark skinned immigrants and their breastfed babies
Elderly and infirm
Partial gastrectomy/ intestinal malabsorption
Chronic liver disease/ chronic renal failure
Anticonvulsant medication
Strict diets e.g. lacto vegetarian
Excessive high factor sunblock
Rare hereditary cases
Clinical features of rickets
Growth plate formation is abnormal and becomes wide and irregular
Clinical features of osteomalacia
Can exist without symptoms
Bone and muscle pains, however, are common, often non-spp, chronic and widespread
Myalgias and weakness in hip and proximal leg musculature is typical
Bowing of bone
Ddx for osteomalacia
FM
Chronic fatigue
Depression
Radiology for osteomalacia
Bone softening/ deformity: hourglass thorax, bowing of long bones
Increased fractures, biconcave vertebral bodies
Psuedofractures
Psuedofractures
Lucent band of decreased cortical density Perpendicular to bone surface Often multiple \+/- symmetrical \+/- callus formation
Where are psuedofractres typically found
Femoral neck
Pelvis
Ribs
Investigations for osteomalacia
Bone biochem
25OHD is usually <30 nmol/L (12mg/L) and PTH increased >6.9 pmol/L
Renal function needs testing because low GFR is associated w. phosphate retention
Rarely need bone biopsy
Bone biochem for osteomalacia
ACa is usually low
Phosphate may be normal or low
ALP may be normal or increased
Urinary calcium excretion is usually low
Investigations to exclude other condns mimicking osteomalacia
Liver function Folate Iron studies Coeliac Autoantibodies Autoimmune serology
Treatment for osteomalacia
Treat underlying condn
Vitamin D supplements
Ensure adequate dietary Ca
Vit D supplements for osteomalacia
Cholecalciferol as a high loading dose (IM) in adults and then lower maintenance dose in adults
Hereditary forms of rickets/ osteomalacia
Hereditary vit D resistant rickets
Hypophosphataemic vit D resistant rickets/ X-linked hypophosphatemia (XLH)
Autosomal dominant Hypophosphataemic rickets (ADHR)
Pseudo vitamin D deficiency ricket
Acquired forms of rickets/ osteomalacia
Tumour-induced osteomalacia/ oncogenic Hypophosphataemic osteomalacia
Drugs available for the treatment of bone disease
HRT Calcium and vit D Bisphosphonates Raloxifene PTH Strontium ranelate Denosumab
Main haematological causes of bone pain
Infiltration/ destruction of bone by tumour e.g. plasma cell myeloma
Bone infarction e.g. sickle cell disease caused by occlusion of blood vessels
Bleeding into joints e.g. haemophilia
Rapidly proliferating bone marrow e.g. acute leukaemia, G-CSF
Paget’s disease
Focal disease of bone remodelling
Predispostion for Paget’s
Genetics – 1st degree relatives of an affected person are 7x more likely
Environment – viral infection e.g. paramyxoviral infection, measles, RSV
Epidemiology of Paget’s
2nd most common metabolic bone disease
More common in males
Often asymptomatic – unusual after presentation to involve other bones
Mostly seen in pts 40+
Pathophysiology of Paget’s
Increased osteoblastic and osteoclastic activity
Normal bone is replaced by abnormal haphazard bone – poor bone architecture, expansion of poor-quality bone (weak)
Marrow is replaced w/ fibrous tissue and blood vessels
What does Paget’s increase risk of
Sarcoma
MSK features of Paget’s
Acetabular protrusion Bone deformity Bone pain Fractures Spinal stenosis OA in neighbouring joints
Spinal stenosis
Bony overgrowth and expansion (not leaving enough space around cord)
Why are fractures a feature of Paget’s
Bowing of bone creates areas of weakness (10-30% - fissure fractures in LL)
Clinical features of MSK
MSK
Bone pain
Degenerative joint disease
Deformity – frontal bossing
Bone pain in Paget’s
Variable in symptoms severity
Long bones, skull, pelvis
Due to periosteum being well innervated
Neurological symptoms of Paget’s
Related to bony symptoms and compression of neurological structures
Cerebellar dysfunction Cranial nerve palsies Spina stenosis/ cauda equina Deafness - narrowing of canals Tinnitus Para or quadriplegia
Cardiovascular features of Paget’s
Increased cardiac output (increased blood flow to bone) Heart failure Aortic stenosis Endocardial calcification Atherosclerosis
Metabolic features of Paget’s
Hypercalcaemia
Hyperuricaemia
Immobilisation hypercalciuria
Nephrolithiasis
Bones typically affected by Paget’s
Femur Spine Skull Sternum Pelvis But can be any bone in. off
Examination for Paget’s
Deformity
Tender – starched periosteum
Warm – good blood supply
Ddx for Paget’s
Vit D deficiency Hyperparathyroidism Hyperthyroidism Renal osteodystrophy Malignancy – e.g. metastatic disease and myeloma
Radiographs for Paget’s
Bones are typically expanded, show cortical, thickening, coarsened trabeculae and a mixture of lytic and sclerotic areas
Use plain radiographs, CT, MRI, PET CT and isotope bone scans
‘Blade of grass lesion’
Complications of Paget’s
Deformity and joint pain
Fracture
Osteosarcoma
Treatment of Paget’s
Analgesia
Treat degenerative bone disease
Bisphosphonates – 5mg zoledronate to reduce osteoclast function
Physiotherapy
Surgery – fractures, joint replacement, spinal stenosis
Bisphosphonates for bone disease
Poorly absorbed orally
High affinity for bone
Activated by osteoblast acid
Taken up into osteoclast causing apoptosis
One dose is enough to treat for a number of years
Benign tumours in bone
Osteoid osteoma - severe pain and v small
Benign tumors in cartilage
Chondroma
Osteochondroma (from growth plate)
Benign tumours in fibrous tissue
Fibroma
Benign tumours in vascular tissue
Haemangioma
Primary bone malignancy
Osteosarcoma
Primary cartilage malignancy
Chondrosarcoma
Primary fibrous tissue malignancy
Fibrosarcoma
Primary bone marrow malignancy
Ewing’s sarcoma
Myeloma
Primary vascular malignancy
Angiosarcoma
Rare bone primaries
Osteosarcoma
Chondrosarcoma
Ewing’s tumour
Osteosarcoma
Most common, usually under 20 yrs.
Affects long bones – growth plate e.g. knee
Radiology – sunburst appearance due to lifting of periosteum and Codman triangle
Chrondrosarcoma
Half as common, usually in 40s
Painful and progressive
May arise from underlying benign lesions
Most commonly affects axial skeleton
Ewing’s tumour
Small round blue cell tumour 2nd commonest in childhood From the medullary (long bones and pelvis) cavity Onion on X -ray May present w/ metastases
Most common bone secondaries
Breast Lung Prostate Kidney Thyroid
Why do bone secondaries occurs
The tumours can lodge in bone
Steps to metastasis - bone secondaries
Endothelial progenitor cells essential to lead to angiogenesis
Have to induce osteoclasts
Osteoblastic response is variable depending on tumour cell
Hx for bone malignancies
Bone pain – red flag symptoms
Symptoms from the primary if diagnosed
Functional impairment
Establish co-morbidities and pt expectations and understanding
Look at social circumstances
Previous DXR (radiotherapy) and chemotherapy
Examination for bone cancers
Consistency w/ history and expected findings
Beware co-existing pathologies
Scarring and skin changes
Neurology and vascularity
May not be any abnormalities – high index of suspicion
Investigations for bone cancers
Serum biochem Plain X-rays - essential Isotope bone scan - highlights areas of metabolic activity CT - good for structure MRI - defines soft tissue involvement Bone biopsy
X-rays for bone caners
Shows bone structure
Lysis/ sclerosis
Must include a whole, long bone
Isotope bone scan for bone cancers
No value in assessing structure
Limited use in myeloma
Beware sacral lesions
Darker areas show glucose uptake - could be malignancy or growth plates in a child (symmetrical)
MRI for bone cancers
Essential in spinal disease
“Skip lesions” in long bones
Evaluation of suspected 1’ bone tumours
Management of 1’ bone tumours
Treat as primary bone tumour until proven otherwise
If primary bone – d/w supra-regional service for biopsy there
Management for metastasis
Pain – analgesia, bisphosphonates, DXT, surgery
Functional loss – related to pain
Skeletal integrity – unlikely to benefit from surgery
Achieving skeletal integrity in bone cancer
Intramedullary nails
Joint replacement
Plate/ screw constructs
Cement augmentation
Presentation of pathological vertebral fracture
Thoracic or lumbar back pain after a minor fall Frequently multiple vertebrae
Loss of height and kyphotic deformity of the spine
No pain but complaints of shrinking or becoming round-shouldered
Drug therapy for pathological vertebral fractures
Bisphosphonates - 1st line Denosumab - 2nd line Teriparatide Raloxifene Calcitonin
Presentation of traumatic spinal fractures
Occur with high energy trauma
Vertebrae can be crushed in healthy adults after a vertical fall from a standing height
Aetiology of traumatic spinal fractures
RTA
Diving into a shallow pool
Falls from above standing height
Investigation of traumatic spinal fractures
Cervical spine CT scan
Thoracolumbar spine imaging
MRI - ligament and spinal cord damage
X-rays
Management of traumatic spinal fractures
Spinal immobilisation devices are left in place
Treatment of traumatic spinal fractures
Stable fractures can be mobilized
Unstable fractures require immobilization, bracing or internal fixation
Prognosis of traumatic spinal fractures
Pt w/ spinal cord damage and neurological symptoms have a poor prognosis and often require extensive rehabilitation on a spinal unit
Spinal shock
Period of altered distal function with loss of spincteric control and reflexes (inadequate tissue perfusion after injury)
Pathological fractures
One that requires minimal force to sustain, as a result of underlying pathology and weakness in the bone
Most common locations for pathological fractures
Vertebral Bodies
Neck of Femur
Wrist (Colle’s Fracture)
Humerus/Shoulder
Condns predisposing pathological fractures
Osteoporosis Osteomyelitis Cancer Osteomalacia Paget’s Disease Non-Cancerous Tumours and Cysts Hyperparathyroidism Osteogenesis Imperfecta
Presentation of pathological fractures
Mild to severe pain near the broken bone.
Bruising, tenderness, and swelling near the broken bone.
Numbness, tingling, or weakness near the broken bone.
Loss of movement.
Several days of pain can precede the fracture
Prevention of pathological fractures
Exercise on a regular basis to keep muscles strong and improve bone health.
Get enough vitamin D and calcium.
Use prosthetics or assistive devices, such as supportive shoes, a walking stick, or a zimmer-frame.
Avoid high-intensity activities.
Prognosis of pathological fractures
Cancer - marker of end-stage
Other condns - suggests worsening or current treatment isn’t effective
Risk of delayed-union, malunion or non-union - further issues
When does Type I osteoporosis develop
Between the ages of 50 and 70 when the protective effects of oestrogen in women begin to fade
Can also occur after gonadal failure in men
Common fractures in Type I osteoporosis
Wrist and spine
When does Type II osteoporosis develop
After 70 years
Sometimes referred to as senile osteoporosis
Common fractures in Type II osteoporosis
Hip and spine
What types of bone does Type II osteoporosis affect
Cortical bone
Technetium bone scan
Sensitive to areas of unusual bone re-building activity
Good for Paget’s
Where does OP typically occur
Metabolically active bony trabeculae
Pagets vs bone malignancy
Both are progressive but pts are generally unwell with malignancies
Lab values for OP
Normal Ca
Normal P
Normal ALP
Normal PTH
Lab values for osteomalacia
Decreased Ca
Decreased P
Increased ALP
Increased PTH
Lab values for Paget’s
Normal Ca
Normal P
Increased ALP
Normal PTH
Changes in diet to improve bone strength
High in calcium rich foods such as milk, cheese, yogurt, white bread, oily fish
High in protein rich food such as meat, fish, milk, cheese and yogurt
High in omega-3 rich food such as oily fish
High in vitamin K rich foods such as green leafy vegetables
