MSK Flashcards
Epidemiology and risk factors for RA
Increased in women (2-4x)
Peak age is 40s
RFs Smoking Genetics - HLA DR4 and 1 Winter Others - increased birth weight, silica exposure, alcohol abstention, obesity, diabetes,
Presentation of RA
ARTHRITIS
Insidious symmetrical polyarthritis
Small joints of hands or feet
Morning stiffness >30 minutes
PIP, MCP, wrist, MTP, ankle, knee, cervical spine (SPARES DIP)
Hand deformities - ulnar deviation, swan neck, Boutonnieres, Z deformity of thumb, piano key deformity of wrist
SYSTEMIC SIGNS
- Eyes: scleritis, episcleritis
- Skin: leg ulcers, rashes, raynauds
- Rheumatoid nodules
- Neuro: carpal tunnel, polyneuropathy
- Resp: pleuritic, pulmonary fibrosis
- CV: pericardial involvement, vasculitis, increased MI
- Kidneys: RARE
- Liver: mild hepatomegaly, raised transaminases
Thyroid disorders, osteoporosis, depression, splenomegaly, lymphadenopathy
Pain, fatigue, myalgia, weight loss
Investigations for RA
- ESR, CRP, plasma viscosity - usually raised (can be normal)
- FBC - normochromic normocytic anaemia, thrombocytosis, raised ferritin
- LFTs - mildly raised ALP and GGT
- Antinuclear antibody in 30% +
Rheumatoid factor - positive in 60-70% (and 10% normal population)
Anti-CCP
X-ray - soft tissue swelling, periarticular osteopaenia, decreased joint space, erosions, deformity
Management of RA
Start within 3 months
Simple analgesia + NSAIDs
DAS28 - number of joints and ESR. For active disease >5.1, remission <2.6
- Methotrexate + alt DMARD + short course steroid (min 6 months)
- different mono/combined DMARD therapy (min 6 month)
- TNF alpha inhibitors (adalimumab, etancercept, infliximab)
- Rituximab (anti CD20) + methotrexate
- Toclizumab (anti IL6)
Surgery if persistent pain, worsening joint function, progressive deformity, nerve entrapment, stress fracture
Complications of RA
Decrease mobility, restricted ADLs
Inability to work
Depression
Vasculitis
Systemic effects - pleuracy, heart complications, lymphadenopathy, neuropathy, anaemia, dry eye syndrome, anaemia, carpal tunnel, tendon rupture
Osteoporosis
Felty’s syndrome - enlarged spleen, decreased WCC + RA
Prognosis of RA
40% disabled in 10 years
Worse prognosis if: <30, male, insidious onset, persistent anaemia, increased number of joints, raised anti-CCP, early Xray changes
Pregnancy beneficial for RA
Criteria for RA
4 or more of:
- morning stiffness >1 hour >6 weeks
- at least 3 joints
- hand joints
- symmetrical
- rheumatoid nodules
- positive for rheumatoid factor
- radiological changes
Epidemiology and risk factors for osteoarthritis
24% adults - knee, 11% hips
RFs Genetic Female Obesity High or low bone density joint injury decrease muscle strength joint laxity or misalignment
Presentation of OA
Clinical without investigation if over 45, pain activity related and no morning stiffness
- Pain exacerbated by exercise, relieved by rest
- Stiffness after rest
- Decreased function and range of movement
- Swelling, tenderness
- Crepitus
- No systemic features
- Heberdens DIP, Bouchards PIP
Investigations for OA
X-ray: osteophytes, decreased joint space, bone cysts, subarticular sclerosis
- MRI for other causes of joint pain
- Blood tests will be normal, should do baseline prior to starting NSAIDs
Management of OA
- Promote function, physio, OT
- Annual review if pain, multiple joints or regular meds
- Encourage exercise
- Encourage weight loss
- Paracetamol +/- topical NSAIDs
- Oral NSAIDs or COX2 inhibitors + PPI
- Intra-articular corticosteroids
NO glucosamine, no arthroscopic lavage or debridement
- Surgery if there is substantial limits on life
Xray changes in OA
Joint space narrowing Subarticular sclerosis Subchondral cysts Bone collapse Osseous loose bodies
Epidemiology and RFs for septic arthritis
1-2% of prosthetic joint replacements
20% of joint surgery revisions
Most commonly staph aureus
RFs Increasing age Prior joint damage Diabetes Joint surgery - hip or knee Immunodeficiency Recent Steroid injection
Presentation of septic arthritis
Single/few joints - acute, very painful Fever Bacteraemia Swollen, warm, tender Effusion
TRIAD - fever, pain, impaired range of motion
Causes of septic arthritis
Staph aureus
Gonococcal
Group B Strep
Lyme disease
Investigations for septic arthritis
FBC - raised WCC, CRP
Synovial fluid examination - raised leukocytes, culture (also exclude crystal arthropathy)
Blood cultures
Imaging - US or MRI/CT
Have a higher index of suspicion if prosthetic joint
Treatment for septic arthritis
Surgical drainage + Lavage + High dose IV antibiotics
Antibiotics
- Start empirically before cultures, cover staph and strep as minimum, for minimum of 2-3 weeks
Flucloxacillin (if staph) - allergy to penicillin = clindamycin
Vancomycin = if MRSA
Cefotaxime - gonococcal
Corticosteroids may decrease extent of cartilage destruction
Splint in position of function
Prognosis of septic arthritis
10-20% mortality
Worse prognosis - over 65, shoulder, elbow or multiple sites
Staph - 50% get back to baseline
Referral for joint replacement
Should have tried all basic treatments (weight loss, pain relief)
If New Zealand score
<39 - primary care
40-69 - non-surgical
70+ then refer for surgery
Patient age, sex, smoking status or BMI should not be a barrier for referral
Complications for joint replacement
Joint infection DVT/PE Stiffness Implant loosening/failure Hip dislocation Time span - need replacement after 10-15 years Bleeding Haemotoma
Classifications of gout
Deposition of monosodium urate monohydrate crystals
- asymptomatic
- hyperuricaemia
- acute gout
- chronic tophaceous gout
PRIMARY - in men 30-60 with acute attacks
SECONDARY - due to chronic diuretic therapy and associated with OA
Epidemiology and RF for gout
Increased in men 9:1
Increased in Asians and South Pacific
High meat diet Diabetes Seafood Alcohol Chronic renal failure Diuretic therapy Obesity High cholesterol HTN CHD Psoriasis
Presentation of gout
First MTP joint (knee, tarsals, wrists, ankles, hands)
Acute pain in swollen joint that reaches crescendo in 6-12 hours
Florid synovitis
Will resolve in 5-15 days
If tophaceous gout - irregular firm nodules with chalky appearance beneath skin
Investigations for gout
Synovial fluid - MSU crystals
Gram staining and culture as infection and gout can co-exist
Serum uric acid - can be raised
Testing fasting lipids and glucose for hyperglycaemia
Management of gout
ACUTE
- NSAIDs and pain relief
- Colchicine
- Systemic corticosteroids
- (continue allopurinol)
ADVICE
- stop alcohol, red meat, reduce protein
- avoid purines - liver, kidney, seafood
- avoid dehydration
- increase exercise, stop smoking
CHRONIC
- Allopurinol
- Canakinumab - if more than 3 attacks per year
Complications of gout
Renal disease from deposition of crystals Severe degenerative arthritis secondary infections carpal tunnel Nerve impingment
Prevention of gout
Manage RFs - HTN, diet, medications
Start treatment if tophi, renal insufficiency, uric acid stones or diuretics.
- Allopurinol - wait 1-2 weeks after attack to start
- Febuxostat
Epidemiology of psoriatic arthritis
5-25% of people with arthritis In 80% psoriasis precedes arthritis Increased in Caucasians 35-55 years old Autoimmune mediated - HLA B27 Women have more rheumatoid pattern, men with spondylitic subtype
Presentation of psoriatic arthritis
Joint stiffness, pain, swelling Relapsing and remitting Enthesopathy - Achilles tendon and plantar fascia common Tenosynovitis - affects flexors 20-30% conjunctivitis
Rheumatoid pattern - symmetrical polyarthritis. Hands, wrists, feet DIP not MCP. FEMALES
Spondylytic pattern - morning stiffness, limitation of back movement, asymmetrical vertebral involvement
Asymmetrical oligoarticular arthritis - dactylitis (sausage fingers)
Lone DIP - hammer blow appearance
Juvenile onset - 20% of childhood arthritis
Investigations for psoriatic arthritis
Raised ESR and CRP
Raised IgA
Raised neutrophils in synovial aspirate, no crystals
X-ray changes - mild bony erosion, asymmetric erosive changes of small joints, DIP and PIP, erosion of distal tuft of distal phalanx
Can do MRI or CT
Management of psoriatic arthritis
Refer to rheumatology
- NSAIDs
- Local corticosteroid injections (never oral due to rebound worsening of psoriasis)
- DMARDs
Methotrexate/sulfasalazine/leflunomide
(not hydroxychloroquine) - TNF inhibitors (adalimumab/etanercept/golimumab/infliximab) if not responding to DMARD
- Cytokine modulator (ustekinumab) if others failed
Complications of psoriatic arthritis
joint destruction Deformity Eye disease Aortitis (rare) Decreased QOL Increased risk of CVD ARTHRITIS MUTILANS - severe deformity (telescopic fingers) Radiological damage in 50%
Complementary therapies for MSK pains
Capsacin -5/5
Fishoil, evening primrose oild for RA
Acupuncture for OA
Glucosamine does not work or chondritin or chiropractors
Epidemiology of SLE
Increased in females 5:1
Peak age - 50-54 for women, 70-74 for adults
Increased in Chinese, SE Asian and afro-Caribbean
RFs HLA DRB1 Defective complement C4 gene UV light EBV Drugs - chlorpromazine, hydralazine, methyldopa
Presentation of SLE
Relapsing remitting
Fatigue and malaise
Arthralgia - early morning stiffness, non-erosive, peripheral, symmetrical
Photosensitive rash - malar rash
Discoid (without systemic features)
Pulmonary - pleurisy, fibrosing alveolitis
APLS - PE
CV - pericarditis, HTN, increased CV risk
Renal - nephritis
Anxiety and depression
Any neurological presentation
Diagnostic criteria for SLE
4 or more from list (not at the same time)
Malar rash Discoid lupus Photosensitivity Oral ulcers Non-erosive arthritis in 2+ joints Pleuritis/pericarditis Renal involvement Seizures/psychosis Positive ANA Haematological disorder Immunological disorder
Investigations for SLE
FBC - Raised ESR, normocytic anaemia, normal CRP, leukopaenia, thrombocytopaenia
Antibodies
- ANA (95% sens)
- Anti-dsDNA - 70% sens but more specific - levels reflect disease process
- Anti-Sm - most specific but 30% sens
- Anti0 SSA(Ro), Anti- SSB(La) in 15% and other connective tissue disease
Check for antiphospholipid antibodies for APLS
Management of SLE
- Avoid sun exposure
- Regular exercise
- NSAIDs
- Hydroxychloroquine for skin, arthralgia and myalgia
- Cyclophosphomide - in life threatening disease
- Mycophenolate mofetil
- Azathioprine
- Methotrexate or ciclosporin
- IV gammaglobulin and granulocyte colony stimulating factor (if resistant)
- BELIMUMAB as adjunct if active and antibody positive
Conditions associated with SLE
APLS scleroderma RA Sjorgen's thyroiditis Drug allergies
Epidemiology of ankylosing spondylitis
0.1% of the population Increased in Northern European Peak onset 20-30 Increased in males (3:1) STRONG FHx - HLA B27
Presentation of ankylosing spondylitis
Insidious onset under 30 years old
Can be mild chronic or intermittent flares
Systemic features - weight loss, fever, fatigue
Morning stiffness
Inflammatory back pain
Pain improves with activity
Early morning wakening
Peripheral enthesis - 33% (Achilles tendonitis, plantar fasciitis)
Peripheral arthritis - 33% - asymmetrical - hips, shoulders, chest wall, TMJ
Tenderness of sacroiliac joints
Limited range of spinal motion
Lumbar lordosis, thoracic kyphosis, buttock atrophy
Extra-articular findings in ankylosing spondylitis
Acute anterior uveitis
Aortitis
Restrictive lung disease - pulmonary fibrosis in upper lobes
Amyloidosis (rare) can cause renal dysfunction
Neuro - C1/C2 subluxation leading to cervical myelopathy
Osteoporosis or osteopaenia
Cauda equina
Diagnostic criteria of ankylosing spondylitis
Radiological findings + 1 clinical finding
Radiological - sacroilitis on X-ray
Clinical
- Lower back pain > 3 months, improves with exercise, not relieved by rest
- Limitation of lumbar movement in both planes
- Limit of chest expansion
Investigations for ankylosing spondylitis
FBC and CRP (can have normocytic anaemia)
LFTs - ALP often raised
Xray - may be normal in early disease, “bamboo spine”, sacroilitis, enthesititis. Spinal osteopaenia common
MRI
SEXA scan
US in enthesitis
Management of ankylosing spondylitis
- No DMARDs
- NSAIDs + PPI
- Local corticosteroid injections
- Oral steroids - short term only
- TNF alpha inhibitors e.g. etanercept or adalimumab]
- Surgery: spinal fixation, vertebral osteotomy
- Bisphosphonates for osteoporosis
Prognosis of ankylosing spondylitis
Increased risk of fractures
Frozen thorax
Blindness from recurrent uveitis
70-90% fully independent
Aetiology of lower back pain
Mechanical - hypermobility, arthritis, disc disease, scoliosis, spinal stenosis, sacroilitis
- Bone disease, osteoporosis, osteomalacia, Paget’s
Non-mechanical:
- Inflammation: Ankylosing spondylitis
- Infection: osteomyelitis
- Cancer: bony mets, myeloma
Referred
- Renal disease
- Sickle cell crisis
- Gynae
- Fibromyalgia
- Dissecting aortic aneurysm
- Posterior duodenal ulcer
Epidemiology of back pain
60-80% have back pain at some point
1% have chronic back pain
RFs
- prolonged standing
- awkward lifting
- demanding jobs
- obesity
- stress
- FHx
Red flags for back pain
Cauda equina syndrome - saddle anaesthesia, urinary/faecal symptoms
Spinal fracture - sudden onset severe pain, relieved by lying down
Cancer or infection - unrelenting pain, worse on lying
Spondyloarthropathy
Investigations for back pain
Do not routinely offer imaging, imaging only if red flag symptoms
- Lumbar X-ray if suspected fracture, mets, collapse from osteoporosis, Paget’s
CT or MRI
FBC, ESR and CRP
LFTs - ALP may be raised
Urine - for infection
Appearance of cancer on X-ray
Prostate - sclerotic
Lung, thyroid, kidney = osteolytic
Breast – either (most commonly osteolytic)
Management of back pain
- Information, reassurance, advice
- Be active, no bed rest
- Regular pain relief (NSAIDs, Paracetamol)
- WHO pain ladder
- Short course muscle relaxant if spams
- Massage, MDT approach and exercise
Yellow flags for back pain
Belief that pain and activity are harmful Sickness behaviours - extended bed rest Social withdrawal Low mood, depression, anxiety, stress Problems at work Over protective family, no support Inappropriate expectations of treatment
When to refer for back pain
- Red flags, 2WW or urgent if CES
- Progressive, persistant, or severe neurological deficit when neuro/ortho in 1 week
- Pain/disability problematic >1-2 weeks - physio
- > 6 weeks sciatica - see within 3 weeks
Red flag symptoms: cauda equina syndrome
Severe or progressive bilateral neurological deficit
Recent onset urinary retention or incontinence
Recent onset faecal incontinence
Perianal or perineal sensory loss
Laxity of anal sphincter
Red flag symptoms - spinal fracture
Sudden onset severe central pain Relieved by lying down History of major or minor trauma Strucutral deformity of spine Point tenderness over vertebral body
Red flag symptoms - cancer or infection
>50, <20 Pain remains when supine, aching night pain, disturbs sleep Hx of cancer Fever, chills and weight loss Recent infection IV drug user Immunocompromised
Red flag symptoms - spondyloarthropathy
Early morning stiffness > 45 minutes
Night pain
“gelling”
Improves with movement, worse after rest
Most common location for sciatica due to disc prolapse
L5-S1
Presentation of prolapsed disc
Unilateral leg pain Radiates below the knee, into feet Leg pain > back pain Positive straight less raise Pain relieved by lying down Exacerbated by long walks and prolonged sitting Single dermatome
cauda equina syndrome
Investigation for prolapse disc
None if symptoms settle in < 6 weeks
MRI is very sensitive
X-ray and CT limited
Management of prolapsed disc
- Analgesia
- Paracetamol/NSAIDs
- Add weak opiod/tramadol
- Consider benzo, TCA or gabapentin
- Pain clinic
- Keep active, encourage swimming
- Heat and massage
- Avoid aggravating activities e.g. lifting
- Physiotherapy
- Surgery
- Discectomy or spinal fusion
- Prosthetic disc replacement
Measurement of bone density
Measured with DEXA scan
It is expressed in relation to a reference population
T-score - SD in relation to healthy population
Z-score - comparison of density for normal age. <2 is below normal
Normal T>1
Osteopaenia T between -1 and -2.5
Osteoporosis T < -2.5
Severe osteoporosis T
Epidemiology and RF for osteoporosis
Increase in women (post-menopause)
Increased with age - 25% at 80 years
2 million women in the UK
RFs
- Parental history of RF
- PMH of fragility fracture
- Low BMI/anorexia
- Corticosteroid > 3 months
- Cushing’s
- Smoking
- Alcohol
- Falls = visual or hearing impairment, decreased strength, cognitive impairment, sedatives,
Secondary causes of osteoporosis
RA/inflammatory arthritis Prolonged immobilisation/sedentary lifestyle Primary hypogonadism Primary hyperparathyroidism Hyperthyroidism Post-transplantation CKD Crohn's, UC, Coeliac Untreated premature menopause Type 1 diabetes COPD Chronic liver disease
Drugs that can contribute to osteoporosis
PPIs Anticonvulsants Depot medroxyprogesterone Antidepressants Thiazolidinediones
Who should be assessed for osteoporosis?
Women > 65, Men > 75 Or under that age, if any RF - Previous fragility fracture - Frequent oral corticosteroids - Hx of falls - FHx of hip fracture - Causes of 2y osteoporosis - BMI <18.5 - Alcohol > 14 units per week
How is osteoporosis risk assessed?
FRAX or QFracture - gives 10 year fracture risk
Green - no treatment or DEXA
Amber - DEXA. Use result to determine if treatment required
Red - treat, no necessity for DEXA
Primary prevention for osteoporosis
Bisphosphonates - ALENDRONATE
- Must have adequate calcium and vitamin D
- Do not take with food
- Cause oesophageal ulcers - drink ++ water and sit up
- 2nd line: risedronate, etidronate
- Denosumab (monoclonal antibody that decreased osteoclasts)
- Strontium ranelate - only to be prescribed by specialists
Secondary prevention for osteoporosis
Bisphosphonates +/- vitamin D/calcium supplements
Raloxifene
Denosumab/strontium
Describe osteomyelitis
Infection of the bone marrow which can spread to the bone cortex and periosteum
- Dead bone can detach causing sequestrum
- Most common distal femur, proximal tibia
2 types
- Haematogenous from remote source
- Direct (from contact with infected tissue)
Pathogens responsible for osteomyelitis
S. aureus (most common)
Haemophilus influenza
Streptococcus
E.coli/Proteus/Pseudomonas/mycobacteria/fungi
Epidemiology and risk factors for osteomyelitis
Increasing incidence (due to increased diabetes and peripheral arterial disease) Bimodal age - children or adults
RFs Trauma/open fracture Prosthetic joint Diabetes Peripheral arterial disease Chronic joint disease Alcoholism IV drug abuse Chronic steroid use Immunosuppression TB Sickle cell HIV/AIDS Catheter use
Presentation of osteomyelitis
Acutely febrile Bacteraemic Painful, immobile limb Swelling Extreme tenderness Exacerbated by movement
If vertebral - unremitting pain, worse at rest, night pain
What is Pott’s disease
Osteomyelitis in the spine with TB
Investigations for osteomyelitis
FBC - raised WCC and CRP Blood cultures Expressed fluid should be cultured Urine dipstick Bone cultures - GOLD STANDARD MRI = imaging of choice
Management of osteomyelitis
4-6 weeks minimum antibiotics - Flucloxacillin, clindamycin if penicillin allergy
MRSA - vancomycin
If chronic infection - 12 weeks
Surgical debridement
Spinal fracture - epidemiology and risk factors
50% of white females will have osteoporotic fracture
Increased in females
RFs as osteoporosis Increased age Low BMI Parental history of fracture Corticosteroids > 3 months Cushing syndrome Smoking Alcohol Falls
Classification of spinal fractures
Wedge compression - isolated anterior column failure
Stable burst - anterior and middle column compression failure, posterior intact
Unstable burst - disruption of anterior, middle and posterior
Flexion-distraction - wedge + tensile failure of posterior and centre of rotation is posterior and anterior
Chance fracture = through spinous process, pedicles and vertebral bodies
Translational fractures = disruption of canal alignment in transverse plane
Presentation of spinal fractures
Central spinal pain Non-radiating Disturbing sleep Can give weakness, numbness and tingling Kyphotic deformity Loss of balance Loss of standing height Usually T7-T8, T12-L2
Investigations for spinal fractures
Lateral view, plain X-ray - wedging, spinal process misalignment FBC, CRP ALP, calcium Blood cultures DEXA scan CT/MRI
Management of spinal fractures
Anterior column only
- 24-48 hours bed rest and analgesia
- Pain will gradually improve over 6-12 weeks
- Naproxen or diclofenac with Paracetamol
- early mobilisation and orthosis
- osteoporosis prophylaxis
- Vertebroplasty/kyphoplasty/surgical stabilisation
- if severe unrelenting pain, stabilising joint fracture by infecting cement
- Pain clinic referral
Multiple column involvement
- STRICT bed rest
- Analgesia
- Open surgical reconstruction +/- decompression
- osteoporosis prophy`laxis
Epidemiology and RFs for osteomalacia
50% adults have insufficient vitamin D
Increased in non-Caucasians
Increased in children and over 65s
FHx has a component
RFs Pregnancy Obesity Housebound/institutionalised Routine covering of face and body Poverty Exclusive breast feeding >6 months Vegetarianism Living at high altitude Alcoholism
Aetiology of osteomalacia
GI malabsorption - surgery, short bowel, chronic pancreatitis, CF, Crohn’s, coeliac, biliary disease
Liver disease - cirrhosis
Renal disease - defective 1,25-D3
Drugs - anticonvulsants, rifampicin, HAART,
Severe calcium deficiency
RARE Hypophosphataemia Systemic acidosis Intoxication with fluoride or aluminium Hyperparathyroidism Mesenchymal tumour
Genetic rare causes
- Fanconi’s syndrome
- Vitamin D dependent rickets (failure to convert 25 to 1,25)
Presentation of osteomalacia in children
Hypocalcaemic seizures or tetany Bone deformity - genu varum Anterior bowing of femur Internal rotation at ankle Irritable and reluctant to weight bear Impaired growth Increased susceptibility o infections
Presentation of osteomalacia in adults
Pain in hip, pelvis, thigh Proximal muscle weakness General lack of well being Diffuse muscle aches and weakness Diffuse muscle aches and weakness Lethargy Waddling gait Costochondral swelling Signs of hypocalcaemia
Bilateral symmetrical multiple fractures - femoral neck, scapula, pelvis
Investigations for osteomalacia
BCP - U&Es including calcium and phosphate LFTs - raised ALP PTH - raised FBC - anaemia if malabsorption Urine for CKD Vitamin D <25nmol/L
Radiograph of long bone - cupping, splaying, fraying metaphysis
DEXA scan for decreased bone density
Management of osteomalacia
Calceferol 10,000IU for 8-12 weeks (use IM if problems with absorption)
- Monitor calcium or a few weeks
- Monitor VitD, PTH, calcium after 3-4 months and every 6-12 months
Mechanism of shoulder dislocation
95% are anterior - traumatic.
Generally a fall with combination of abduction and extension - FOOSH
Posterior - fall with arm in internal rotation and adduction e.g. epileptic fit or electricution
Epidemiology of shoulder dislocation
One of the most commonly dislocated joints
Increased in males due to increased contact sports
Peak at 20-30 and again at 60-80
If multiple dislocations - consider Ehlers-Danlos
Presentation of shoulder dislocation
ANTERIOR
- Holds arm in external rotation
- Humeral head palpable anteriorly
- Abduction and internal rotation are resisted
- CHECK RADIAL PULSE, DELTOID SENSATION (AXILLARY NERVE), RADIAL NERVE FUNCTION
Posterior
- Present with arm adducted and internally rotated
- Abduction and external rotation painful-
- May resemble frozen shoulder
- Vascular and nerve problems not associated generally
Complications of shoulder dislocation
Axillary nerve or artery damage Brachial plexus damage Radial nerve damage Recurrent shoulder dislocation Rotator cuff injury
Bankart lesion - rupture of joint capsule and interior glenohumeral ligament
HillSachs lesion - posterolateral head indentation fracture
Investigations for shoulder dislocation
Xray - AP + axillary
Anterior - head under coracoid on AP, humeral head anterior to glenoid
Posterior - may be normal on AP, may have lightbulb sign due to rotation . Head posterior to glenoid on rotation
Management of shoulder dislocation
Opioid
Benzos for muscle spasms
No fracture - closed reduction
If fracture = surgery
Multiple number of reduction methods
Post reduction re-check neurovascular assessment
Post-reduction xray
Immobilise the shoulder for 3-6 weeks
Analgesia and physiotherapy
Fracture healing stages
- Fracture haematoma
- Fibrovascular tissue replaces clot - collagen fibres laid
- Subperiosteal bone formed at ends beneath periosteum
- Primary callus response (few weeks)
- Bridging external callus
- Endosteoal new bone formation
Common wrist fractures
Colles- distal radius with dorsal displacement of fragments
Smiths - distal radius with volar displacement of fragments
Scaphoid
Bartons - fracture dislocation of radiocarpal joint
Chauffeur’s - radial styloid fracture
Greenstick - children
Colles fracture
Fracture through distal metaphysis of radius within 2-3cm of articular surface - dorsal displacement of fractures
Common in elderly with osteoporosis
From FOOSH - forced dorsiflexion of wrist
Dinner fork deformity = backwards and laterally
CHECK MEDIAN NERVE FOR DAMAGE
Manage with anaesthesia, redaction and back slab. Surgical reduction only if intra-articular.
Complication of colles fracture
Median and ulnar nerve damage Compartment syndrome Deformity on healing Chronic pain Mal-union
Scaphoid fracture
Increased in males 20-30 years
Vulnerable blood supply - high risk of avascular necrosis
From FOOSH or RTA from steering wheel impact
Tenderness in anatomical snuffbox
20% not seen on x-ray - need 4 views: PA, true lateral, semi-pronated oblique, PA and ulnar deviation
Presumptive casting - 10 degrees of flexion with thumb and forefinger able to oppose.
Repeat xray after 2 weeks
Smiths fracture
Reverse colles
Fracture of distal radius with anterior displacement of fragments
Caused by falling backwards
Generally closed reduction
Bartons fracture
Distal radius fracture with additional dislocation at radiocarpal joint
Colles or Smiths + dislocation
May be entrapment of tendons of ulnar nerve or artery
Operative reduction required
Nerve distribution in the hand
Ulnar - pinky side little and half of ring finger both sides
Median - palm side of thumb, first, middle and half of ring finer
Radial - back of hand, thumb, first, middle and half of ring finger. Not finger tips
Most common sites for radial nerve damage
Proximal forearm
Humeral fractures
Radial aspects of wrist
Causes of radial nerve damage
Axilla compression - shoulder dislocation OR Saturday night syndrome
Upper arm - triceps and brachioradialis spared - usually due to fracture of humerous
Elbow - tenderness over radial tunnel
Wrist - radial fracture, elbow deformity, finger drop with intact sensation
Superficial - pain and sensory loss, normal motor. Ruptured synovial effusion at elbow OR handcuffs, wristbands, plastercasts
Muscles supplied by radial nerve that needs testing if suspecting damage
Triceps Brachioradialis Externsor carpi radialis longus Supinator Extensor digitorum
Muscles supplied by ulnar nerve
Hypothenar muscles
Adductor pollicis
3rd and 4th lumbricals
Dorsal and palmar interorssei
Causes of ulnar nerve damage
ELBOW
Cubital tunnel syndrome, medical epicondylitis (golfer’s elbow), supracondylar fracture, osteophytic encroachment in OA
Claw hand deformity, unable to flex terminal phalanges or abduct little finger
Wrist - cutaneous sensation usually spared
Positive Tinel’s and Phalen’s sign
RF for carpal tunnel syndrome
Late 50s Female Obesity FHx Post-colles fracture Short stature Injury Thyroid disorders Diabetes Acromegaly Inflammatory arthritis
Presentation of carpal tunnel syndrome
Tingling, numbness, pain Worse at night Causes wakening Handing hand out of the bed Weakness in hand grip
Positive Phalen’s Test
Positive Tinel’s Test
Phalen’s test
60s of flexion at the wrist causes pain or paraesthesia
Tinel’s test
Tapping over median nerve causes pain or paraesthesia
Investigations and management of carpal tunnel
ENG - median nerve stimulation to detect muscle action potential over thenar eminence
US
MRI if ENG ambiguous
Minimise aggravating factors
Local steroid injections are diagnostic and therapeutic
Surgical decompression - return to work in 12-19 days
What runs through the carpal tunnel
Flexor digitorum superficialis and profundus
Flexor pollicis longus
Flexor carpi radialis
Median nerve
Attachment and function of FDP and FDS
FDS - attaches to middle phalanges.
Flexes PIP, MCP and wrist
FDP - attaches to distal phalanges
Flexes DIP, MCP and wrist
Presentation of extensor tendon damage
Mallet dinger - fixed flexion of DIP
Boutonniere deformity - fixed flexion of PIP
Inability to extend finger
Epidemiology of polymyalgia rheumatica
84 per 100,000
Mean age 73. Exclusively over 50s
Increase in females (3:1)
Increased in North European
Presentation of polymyalgia rheumatica
Morning stiffness > 45 minutes Bilateral shoulder or pelvic girdle aching For over 2 weeks in over 50s Symptoms worse on waking Flu like features at onset Sudden onset over 1-2 weeks
No lymphadenopathy
No active infection
No cancer
No temporal arteritis
Investigations for polymyalgia rheumatica
Raised inflammatory markers - CRP (more sensitive than ESR)
CHECK FBCs, U&Es, LFTs Protein electrophoresis Urinalysis Bence Jones protein,
Consider temporal arteritis in all with PMR
Management for polymyalgia rheumatica
Glucocorticoids
Referral to physio or OT
15mg prednisolone for weeks then drop very slowly
Treatment for 1-2 years. Maintenance dose usually 2.5-5mg
DEXA scan
Calcium and vitamin D therapy +/- bisphosphonates
Monitor - 15% get temporal arteritis
Epidemiology of temporal arteritis
2.2 per 10,000
Increased in northern European
increased in females (3:1)
Common after 60
Presentation of temporal artertitis
Recent onset temporal headache Worse at night Myalgia Malaise Fever Scalp tenderness Transient visual symptoms - diplopia, ischaemic optic neuritis, blurred vision, visual loss, amarousis fugax Jaw claudication Anoexia, weight loss, Thoracic aorta often involve
Diagnostic criteria for temporal arteritis
3 out of 5 needs
Over 50 New headache Temporal artery abnormality - tenderness, pulsation Increased ESR Abnormal artery biopsy
Investigations for temporal arteritis
Urgent referral for temporal artery biopsy
Increased ESR or CRP
FBC - normocytic normochromic anaemia, thrombocytosis
LFTs - raised ALP
Biopsy - 87% sensitivity
Colour duplex ultrasonography
Management of temporal arteritis
Urgent referral - should not delay treatment
Steroids - 40g OD prednisolone, 60g if claudication
If visual symptoms then IV prednisolone
Lower once symptoms resolved or test results normal
Start aspirin and PPI
Osteoporosis prophylaxis
Complications and prognosis of temporal arteritis
Permanent visual loss
Aneurysms, dissections, stenotic lesions of aorta
CNS disease - seizures, strokes
Steroid related complications - osteoporosis, myopathy, bruising, diabetes, HTN
Relief with treatment but relapses are common
Often need steroids for 2 years
Describe radial head and neck fractures
Radial head fractures are the most common elbow fractures in adults
In children - radial neck
Swelling over lateral elbow.
Limited motion and point tenderness
Neurovascular assessment
Investigations - AP and lateral. Fat pad sign
Urgent surgical treatment
Describe olecranon fractures
Often low energy fractures causes by sudden pull of triceps or brachioradialis
Swelling and tenderness over olecranon
Inability to extend against gravity
Should be seen clearly on lateral xray
Immobilise in split at 60-90 degrees of flexion
Elbow dislocation
2nd most common dislocation
Terrible triad -
- Elbow dislocation
- Coronoid process fracture
- Radial head fracture
Associated with injury to brachial artery and nerve
Prompt reduction essential
Types of hip fracture / classification
Femoral neck #
Femoral shaft #
Femoral stress #
Intracapsular - between edge of femoral head and insertion of joint capsule into the hip (intertrochanteric line)
Assume vascular compromise
Extracapsular - distal to intertrochanteric line
Can be due to avulsion fractures from gluteus medius
Assume vascular system spared
Can use Garden’s classification if intracapsular
- Garden 1 - inferior cortex intact, no significant displacement
2 = trabeculae in line, fracture visible from superior to inferior cortex
3 = obvious complete #, slight displacement or rotation
4 = gross and often complete displacement
Risk factors for hip fracture
Increased age
Osteoporosis
Family history of hip fracture (maternal)
osteomalacia
Falls = instability, decreased core strength, gait disturbance, sensory impairment
Presentation of hip fracture
Pain in outer upper thigh or groin
Pain may radiate to the knee
Inability to weight bear
Pain aggravated by flexion and rotation of the leg
shortened, adducted and externally rotated leg
Diagnosis of hip fracture
AP and lateral x-ray
Disruption of trabecular, inferior or superior cortices and abnormality of pelvic contours
Broken Shenton’s line
MRI should be performed if suspected but not seen on x-ray
Shenton’s line
Curved line formed by top of obturator foramen and inner side of neck of femur
Line broken in hip #
Management of hip #
Intracapsular
- surgery within 24 hours
- reduction and internal fixation
- if young patient then dynamic hip screw where possible
- if poor prognosis hemi-arthroplasty
- if otherwise fit full hip-replacement
Extra-capsular
- Dynamic hip screw if trochanteric
- Sub trochanteric = screws, nails and pins
Complications of hip #
Mortality high - 10% at 1 month, 33% at 1 year Infection Haemorrhage Avascular necrosis Delayed union, malunion, non-union Pneumonia MI Stroke DVT/PE Pressure ulcers
Femoral saft #
Severe pain, tense, swollen thigh
Inability to weight bear
X-ray AP and lateral - include bilateral hip and knee for comparison
Management - Cross match - Analgesia - Monitor pulses and sensation - Reduce and surgery - nails most common Early mobilisation
4-6 months healing time
Be aware:
- Acute compartment damage
- Vessel or nerve damage
- Large potential blood loss
Blood supply to femoral head
Most comes from upwards extending branch of profunda femoris which forms lateral and medial circumflex which then forms sub synovial ring
Very small from ligamentum teres - branching from obturator artery
Pelvic #
High energy trauma
Tenderness, bruising, swelling, crepitus
Haematuria and rectal bleeding
Neuro and vascular abnormality in legs
Can be due to lateral compression causing sacral # and sacroiliac disruption (side swipe car accidents)
Can be due to AP compression - head on collisions = open book fracture, springs open hinging on sacroiliac joints
CT, PV and PR for bleeding ATLS! Leg length discrepancy Perineal bruising Pelvic binder at greater trochanter to tamponade bleeding
Patella #
2 ways to fracture
- Direct fall onto flexed knee - stellate shape
- Sudden contraction of quadriceps to prevent fall = transverse #
Check extensor mechanism = can patient lift heel from bed (if in tact then they can)
Management
- Undisplaced = conservative cylinder cast
- Displaced or extensor mechanism affected = surgery
- Tension batwing wiring
- repair extensor retinaculum,
Define compartment syndrome
Caused by increased pressure in a closed anatomical space
Compromises circulation and function of tissues within the space.
Can damage muscles and nerves
Can be acute or chronic
Acute is caused by trauma or intense exercise
Chronic is caused by exercise
Common sites for compartment syndrome
What can they damage
FOREARM
- Ventral: median and ulnar nerves. Radial and ulnar artery
- Dorsal: posterior interosseous nerve. No vessels
LOWER LIMB
- Anterior tibial: deep peroneal nerve. Anterior tibial artery.
- Superficial posterior: none
- Deep posterior: posterior tibial nerves and vessels. Peroneal artery
- Peroneal: deep and superficial peroneal nerves
GLUTEAL
- uncommon. often have muscle necrosis and sciatic nerve palsy due to late diagnosis
ABDOMINAL
- in multiple trauma patient in profound shock
- AKI, cardiac dysfunction, raised central venous pressure
- Sudden release can cause ischaemia reperfusion injury, acidosis and cardiac arrest
Aetiology of acute compartment syndrome
Fractures especially distal limbs Crush injury Burns Infection Prolonged limb compression Vascular - ischaemic, haemorrhage, phlegmasia caerulea dolens Iatrogenic - IM injections, vascular puncture (if anti-coagulated) Muscle hypertrophy in adults
Presentation of acute compartment syndrome
Within 48 hours of injury
Increase pain despite immobilisation of fracture
Sensory deficit in nerves passing through compartment
Muscle tenderness and swelling
Excessive pain on movement
May have peripheral pulses until late stages - pallor, pulselessness
Investigations for acute compartment syndrome
CLINCIAL diagnosis
Can measure pressure
- Wick catheter, pressure transducer and site ported needles
- MRI if ambiguous
Management of acute compartment syndrome
Urgent decompression to reduce ischaemia
Remove all dressings
Urgent orthopaedic referral
open FASCIOTOMY
- skin and deep fascia divided along length of compartment, leave would open
- debride any muscle necrosis
Complication- tissue necrosis
RF for chronic compartment syndrome
athletes under 40 repetitive motion exercise - tennis, running, gymnastics, cycling excessive training
Presentation of chronic compartment syndrome
severe pain and tightness triggered by exercise
Resolves with rest
May have tinging and weakness
May have abnormal gait
Management of chronic compartment syndrome
Deep massage
Limit offending activity
Decompressive fasciotomy - used in athletes that refuse to modify activity
Early complications of lower limb #
LOCAL vascular injury visceral injury e.g. bladder, bowel damage to nerves, tissue or skin haemoarthrosis compartment syndrome wound infection fracture blisters
SYSTEMIC fat embolism shock vte, PE, DVT exacerbation of underlying disease e.g. COPD pneumonia
Late complications of lower limb #
LOCAL delayed union malunion joint stiffness non-union contractures myositis ossificans avascular necrosis algodystrophy osteomyelitis growth disturbance/deformity
SYSTEMIC
gangrene, tetanus, septicaemia
fear of mobilising
RF for delayed union
severe soft tissue damage inadequate blood supply infection insufficient splinting excessive traction increased age severe anaemia diabetes low vitamin D hypothyroid NSAIDs steroids complicated fracture osteoporosis
presentation and management of non-union
pain at site, tenderness, swelling non-use of limb movement at the # site palpable gap absence of callus
weight bearing and casting bone stimulation - teriparatide debridement bone grafting internal fixation
Myositis ossificans
calcifications and bony formation in muscles
increased risk after humeral supracondylar fracture
Algodystrophy
"Sudeck's atrophy" Reflex sympathetic dystrophy Hand or foot Continuous burning pain Accompanied initially with swelling, warmth and redness Then pallor and atrophy
Manage with analgesia and physio
Complications of casts
malunion if misplaced
Cast disease - circulatory disturbance, inflammation, bone disease
- Osteoporosis
- Chronic oedema
- Tissue atrophy
- Joint stiffness
thermal ulcers during hardening pressure ulcers thrombophlebitis infection if wet skin decreased bone density
Complciations of traction
pressure ulcers pneumonia/UTI permanent foot drop contractures peroneal nerve palsy pin tract infection Thromboembolism
Complications of external fixation
Pin tract infection Pin loosening or breaking Interference with joint movement Neurovascular damage Misalignment if misplaced Psychological - visible deformity and disability
Rehab post #
Prompt surgery MDT Physio OT Social workers Orthopaedics \+/- geriatrics
EXERCISE ASAP
Decreased motivation = decreased recovery
Exercise is important
Impact of amputation
PHYSICAL decreased mobility and dexterity stump or phantom limb pain infection increased care requirements muscle contractures therefore require regular stretching DVT/PE
EMOTIONAL traumatic/PTSD depression adapting psychologically to the loss body image issues decreased social activities social isolation
Prosthetic limbs require skin desensitisation with compression bandaging
Ankle joint
Involves tibia, fibular and talus
Syndesmosis joint between tibia and fibular
Tibiotalar joint allows dorsi and plantar flexion
Subtalar joint between talus and calcaneous allows inversion and eversion
Presentation of ankle #
immediate severe pain which can extend to foot and knee swelling bruising tenderness joint deformity inability to weight bear
Ottawa rules for ankle #
X-ray is recommended if:
- over 55
- unable to weight bear for 5 steps either at time of accident or evaluation
- bone tenderness at posterior edge or tip of medial malleolus
- bone tenderness at posterior edge or tip of lateral malleolus
- tender 5th metatarsal, cuboid or navicular
Investigations for ankle #
x-ray (Ottawa rules)
AP, lateral and oblique views
If one injury is seen, look for a second
CT or MRI if soft tissue or intra articular joint
Classification for ankle #
Danis-Weber classification
A - fibular # below syndesmosis
B - fibular # at the level syndesmosis
C - fibular # above syndesmosis indicating rupture
Operative if type C or some type B
Pott’s #
and # dislocation of distal tibia and fibular involving 2 elements of ankle ring, very unstable
Pilon #
fracture of distal tibia and disruption of talar dome
Due to falling from a height
Management of ankle #
ABCDE
If neurovascular compromise reduce immediately (before XR)
Analgesia
If not displaced or type A then conservative (or if not fit for surgery)
4-6 weeks in cast
Repeat x-ray regularly to ensure reduction and healing
if displaces then surgery
If type C or some type B then operative
Also if dislocation, bimalleolar #, joint incongruity
Open reduction and internal fixation
Early remobilisation and weight bearing
Epidemiology of burns
0.3 per 1000
300 deaths per year
Increased in under 5s or over 75
50% occur in kitchens
What is the rule of 9s
Body split into different areas that either have 9% SA or 18%SA to estimate area of burns
9% for head and each upper limb
18% for torso front, torso back and each lower limb
Use Lund and Bower chart for children as not equal
Depth of burns
Epidermal/ Superficial partial thickness
Superficial dermal
Deep dermal
Full thickness (3rd degree)
4th degree
Describe an epidermal/ superficial partial dermal burn
Red Glistening Painful Brisk cap refill Heals in 1 week with no scarring
Describe a superficial dermal burn
Pale pink/ mottled skin Swelling Small blisters Hypersensitive Wet/weeping Brisk cap refill Heals in 2-3 weeks Minimal scarring
Describe a deep dermal burn
Blistering Dry Blotchy, cherry red Does not blanch No cap refill Decreased or absent sensation Heals in 3-8 weeks Scarring May require surgery
Describe a full thickness burn
Old 3rd degree burn Dry White / Black No blisters No cap refill Absent sensation Requires surgical repair/grafting
Describe 4th degree burn
Includes subcutaneous tissue, muscle or bone
Requires reconstruction and often amputation
Initial baseline investigation in burns patient
Bloods - FBC, group and save, carboxyhaemoglobin, glucose, U&Es, pregnancy test
ABG(s)
CXR
Cardiac monitoring
Hourly urine outputs / catheter
Management of minor burns
Stop burning
- remove all clothing. any adherent clothing cool with water. remove all jewellery
- rinse with tap water for at least 20 minutes
- NOT ICED WATER as this causes vasoconstriction and can further tissue damage
- brush off any dry chemicals first
Minor
- wash with soap and water
- is blister >1cm then aspirate aseptically, if <1cm then leave
- non-adhesive dressings with gauze padding, change after 3-5 days
- if infection develops: flucloxacillin / erythromycin
Management of major burns
ABCDE
A - check for inhalation injury
- endotracheal intubation if required
B - ABGs and 100% O2, presume CO poisoning
- elevate head and chest by 20-30 degrees to decrease neck and chest oedema
- RARE: escharotomies to release chest tightness
C - fluid replacement - IV line ASAP
If burns >15% then start fluid replacement for minimum 24 hours
4ml Hartmann’s per kg per % affected
Strong opiate
Sedation
Prevent hypothermia
Other
- fasciotomy
- gastric tube insertion
- antibiotics if infection
- grafts (must be within 3 weeks)
When to refer to burns unit
Under 5, over 60
Burns to face, hands, neck, perineum or full thickness to large area
Inhalation injury
Chemical burn / ionising radiation / high pressure steam injury or electrical injury
>10% SA in adults, >5% in child
Pregnancy
Complications of burns
Respiratory distress Fluid loss, hypovolaemia, shock infection raised metabolic rate increased plasma viscosity muscle damage (if electrical) - rhabdomylysis Poisoning Haemoglobinuria and renal damage Scarring
Indications of inhalation injury
Can be subtle and present over 24 hours after incident
- face/neck burns
- singed eyebrows
- carbon deposits in oropharynx/ sputum
- acute inflammation of oropharynx
- explosion in enclosed space
- hoarseness
- carboxyhaemoglobin >10%
- history of impaired awareness
Intubate and mechanical ventilation
Transfer to burns unit
Signs of non-accidental burns
Delayed or avoidance of treatment Incident not witnessed No explanation Implausible mechanism of injury Details change with time Lack of concern from accompanying adult Abnormal demeanour - withdrawn
Sharply demarcated
Glove and stocking injury
Uniform depth of burn
Donut sparing of buttocks on bottom of tub
Epidemiology of chronic pain
23% worldwide
Increases with age, over 45s
Increased in females
Most common locations: back pain, headache, joint pain
Risk factors Pregnancy Hx of trauma or chronic pain Fhx smoking high risk occupation co-morbid personality
Aetiology of chronic pain
MSK - OA, RA, osteomyelitis, osteoporosis, AS, myofascial disease, PMR, fractures, strains
Neurological - diabetic neuropathy, spinal stenosis, brachial plexus traction injury, thoracic outlet syndrome, trigeminal neuralgia, alcoholism, thyroid disease, pernicious anaemia
headache - migraine, temporal arteritis, glaucoma,
Psychological - depression, anxiety, personality disorder, sleep disturbance
Cancer = mets, myeloma, paraneoplastic syndrome
Systemic diseases = SLE, Sjorgen’s, diabetes, hypothyroid, hyperparathyroidism, HIV, Hep C
Management of MSK chronic pain
Physiotherapy
Paracetamol and/or NSAIDs
OT
Pain management psychology = relaxation techniques, stress management, coping skills, CBT
Management of neuropathic pain
Gabapentin/pregabalin/amitryptiline/duloxetine Capsacin/topic lidocaine oxycodone physio/OT Pain management psychology TENS Pain clinic referral
Alternative therapies used for pain management
Capsacin
Acupuncture OA 5/5, LBP 5/5 GREEN
Chiropractor 2/5 for OA and LBP AMBER
Massage 5/5 LBP FM, 2/5 OA
Relaxation therapy
Tai chi
Yoga
Why would people use alternative therapies for pain relief?
Want more natural treatments Want to feel in control Persistent pain Pain not relieved by conventional treatment Concerns about medication side effects
Benefits of CBT for pain
encourages problem solving attitude
patients are pro=active
involves homework
provides coping mechanisms
small improvement in pain and disability
moderate increase on mood
epidemiology of fibromyalgia
Increase in females (x10) 20-50 years most commonly low income being divorced failing to complete education 5% of population
Presentation of fibromyalgia
chronic widespread pain unrefreshing sleep/tiredness fatigue sleep disturbance morning stiffness paraesthesia feeling of swollen joints problems with cognition headaches light headedness anxiety/depression
Management of fibromyalgia
MDT approach EXERCISE - swimming, aerobic exercise, resistance training CBT Relaxation/physio Paracetamol/weak opioids/ tramadol Antidepressants Pregabalin/gabapentin
Take care not to over investigate
What is O’Donohue’s Triad
Knee injury triad
ACL
MCL
Meniscus tear
Most common to least common knee injury mechanisms
Valgus Twist Hyperextension Hyperflexion Varus
Morton’s neuroma
Interdigital neuritis in the feet
Repeated trauma from walking causes irritation leading to neuroma
Causes anaesthesia of interdigital sides of connecting toes
Treated with surgical removal
Pain on squeezing feet
Jone’s fracture
fracture at the base of the 5th metatarsal
avulsion fracture
Achilles tendon rupture
Describe it as if kicked from behind and then fell
Use Thompson’s test
Decrease recurrence with surgery for management
Place wedges inside a boot for 2-4 weeks
Plantar fascitiis
Heel pain worse on a morning Tenderness over calcaneus Gets better with walking Self-limiting Treat with stretching exercises
Risk factors for congential dysplasia of hip
Female
Oligohydramnios
FHx
Multiple pregnancies
management of congenital dysplasia of the hip
Use US for diagnosis as the femur head is cartilage for 3 moinths
Use calipers/splinting to keep hips externally rotated and abducted
At 3months do x-ray.
Hip spiker
Muscle release
Osteotomy if others fail = if need surgery then they will need a hip replacement in their 30s
Perthe’s disease
Increased in 6-9 year olds
Males
Pain, limping, no history of trauma
Due to avascular necrosis of epiphyseal plates
Head develops asymmetrically - mushroom shapes. Increased subluxation
Slipped capital femoral epiphysis
Hypogonadism occurs in puberty Large hips Males passed off as "growing pains" 3 stages depending on angle of slip 1 = 10 degrees, 2 = 30, 3=45 1&2 fixed with pinning 3 = open fixation, but 20% risk of damaging blood supply Most around knees
Osteogenesis imperfecta
Defect in gene for collagen Increased in females Most die in utero/labour If mild form then multiple breaks Blue sclera Heal very quickly Treat as you would normally treat the fracture Number of fractures decreases with age
Congential talipes equinovarus
Club foot 1% Increased in males or FHx Increased in breech and oligohydramnios 5-10% bilateral
Treat with stretching and manipulation
Serial splinting to minimise surgical intervention
No limitations in life with treatment
Epidemiology of DDH
Developmental dysplasia of the hip 1-3% of newborns Left hip more commonly affected Increased in female babies Increased in countries that swaddle babies
RFs Sibling with DDH First born Vaginal delivery for breech (x17) C-section for breech (x7) Oligohydramnios Multiple pregnancy Prematurity Neuromuscular disorders - CP, meningocoele
20% are bilateral
Screening for DDH
Screened at birth and 6-8 week baby check US at 6 weeks ONLY if: - 1st degree FHx of DDH - Breech after 36 weeks - If breech < 36 weeks scan at birth
Examination for DDH
At 3 months or under
- Look for asymmetry of skin folds, leg length
- Orlani and Barlow tests
- Orlani - forward pressure on femoral head
- Barlow - back pressure on femoral head. If movement then dislocating.
Abduction < 60 degrees at 90 degrees of hip flexion
Over 3 months
- Unilateral limitation and symmetry of hip abduction
- Galeazzi sign: unilateral femoral shortening when supine at hip flexed to 90 degrees
Investigations for DDH
Dynamic US for hip stability and acetabular development
US is better under 4 months
After 4 months, pelvic X-ray better as the femoral ossification centre has developed
Arthrography peri-operatively to determine if open or closed reduction
Management of DDH
Early diagnosis gives better outcome
Most self-stabilise by 2-6 weeks
Non-surgical
- Dynamic flexion-abduction orthosis (Pavlik harness) from the time of diagnosis
- adjust as the child grows, remains in place at all times
- Risk of avascular necrosis or temporary femoral nerve palsy
- contraindicated once over 4.5 months
Surgical
- If don’t respond or late diagnosis
- Closed reduction with adductor or psoas tenotomy
- THEN 3-4 months in abduction brace
- If over 18 months then may need osteotomy
Epidemiology of pes planus
20% of adults 45% of children, but generally resolves before 10 years Common in young children Increased in Africans only pathological in 1% Increased in males Increased with obesity
Foot findings in pes planus
Collapse of medial longitudinal arch
Foot PRONATES
VALGUS position of heel and forefoot
Aetiology of pes planus
CHILDREN
- Normal in 3-6 years
- Neurological problems; CP or polio
- Bony abnormalities: tarsal coalition, accessory navicular bone
- Ligament laxity: Ehler’s-Danlos, Marfan’s
ADULTS
- Physiological in 20%
- Decreased arch strength - dysfunction of tibilias posterior tendon, ligament tear, neuropathic foot (diabetes, polio), arthropathy, OA
- Increased load - shoes limiting movement, tight Achilles tendon, obesity, pregnancy
Symptoms of tibialis posterior dysfunction
Pain or swelling behind medial malleolus and along instep
Change in foot shape (pes planus)
Decreased walking ability and balance
Ache on walking long distances
Management of pes planus
CHILDREN
- treatment often unnecessary
- generic foot orthoses
- surgery only if rigid
ADULTS
- exercise and barefoot walking
- heel cord stretching to lengthen Achilles tendon
- orthtics: heel wedge and arch support
- Advice: shows with low heel and wide toes. weight reduction
Surgical - if rigid, progressive or CP with equinovarus foot
- Soft tissue reconstruction e.g. tibialis posterior or Achilles
- Arthoeresis
- Reconstructive osteotomy for realignment
- Arthrodesis
Complications of pes planus
Tibialis posterior dysfunction Hallux valgus Metatarsalgia Plantar fasciitis Knee pain
Causes of in-toeing
Metatarsus varus
- From birth, inward twisting of forefoot
- Observe, 85% resolve
- If persistent, splinting then surgery
- Associated with DDH
Tibial torsion
- Presents at 1-3 years
- Resolves spontaneously
Internal femoral torsion
- 3-10 years
- Abnormal anteversion of femoral neck
- At birth 40 degrees, 15 as adult, Slow transition causes intoeing
- most have spontaneous resolution
- Some require rotational osteotomy
Genu Varum
Lateral bowing
“bow legged)
Normal in children under 2
Associated with out-toeing
Causes of genu varum
Ricket's Scurvy Blout disease Paget's disease OA (in elderly)
Pathological features of genu varum
Inter-malleolar distance >10cm
FHx of skeletal abnormality
Asymmetry of knees
Abnormally short stature
Genu valgum
Knock kneed Common between 2-4 years If symmetrical usually benign Measure intermalleolar gap Associated with intoeing
Causes:
Rickets
Scurvy
RA/OA
Epidemiology of scoliosis
Increased in FEMALES
2-3%
More common to curve to right
RF Trauma Neuromuscular imbalance Congenital Most are idiopathic
Types of scoliosis
Infantile - before 3 years. Increased in boys. Many resolve spontaneously. Some get severe deformity
Juvenile - 3-10 years. increase in girls. high risk of progression. often require surgical intervention
Adolescent idiopathic scoliosis (AIS) - 10 years to maturity. Occurs at onset or during puberty. Increase in females. Need surgery
Presentation of scoliosis
Increasing pain with increasing deformity
Unlevel shoulders
Waistline asymmetry
Rib prominence
Scoliometer to measure
Can place a wedge under one foot to see improvement, if improvement then may be due to a shorter leg.
Aetiology of scoliosis
Idiopathic (80%)
Congenital malformation of vertebrae (10%) - usually have GU deformity
Neuromuscular - CP, spina bifida, polio
Metabolic - Hunter’s
Crush # from trauma, osteoporosis, TB, malignancy
Dysmorphic syndromes - neurofibromatosis, Marfan’s, osteogenesis imperfect
Causes of anterior bowing of legs
ALWAYS insignificant
- Congenital absence of fibula
- Neurfibromatosis type 1
- Osteogensis imperfecta
Investigations for scoliosis
PA and lateral spine x-rays
Cobb’s angle is used to measure degree of scoliosis, needs to be >10
CT/MRI if required
Management of scoliosis
Infantile - generally no surgery
Juvenile - generally require surgery
AIS - surgery depends on size of curve
Bracing - where still growing, trying to prevent worsening
Exercises
Surgery - in 25%, if Cobb’s angle >45, solid fusion
Magnetic expansion control growth rods
Complications of scoliosis
Decreased exercise capacity and weak respiratory muscles
Compression of abdominal contents
Severe = damage to spinal cord
Psychological problems
Cardiopulmonary problems at 60 degrees, myelopathy at 90 degrees
Scheuermann’s disease
thoracic kyphosis > 40 degrees
Painless
Surgery not required
Define cerebral palsy
Group of permanent disorders of the development of movement and posture causing activity limitation that are attributed to disturbances in development of foetal or infant brain
Classification of cerebral palsy
Spastic types = intermittent increase tone and pathological reflexes
Athetoid - hyperkinesia
Ataxic = loss of muscular co-ordination
Mixed
Other classficiations:
- pre-natal, natal or post-natal
- monoplegia, diplegia, hemiplegia
- congenital or acquired
TORCH infections
Toxoplasmosis Other Rubella Cytomegalovirus Herpes Simplex
Epidemiology of cerebral palsy
1 per 1000 live normal weight births 16 per 1000 underweight live births Increasing maternal age Increased in black population Increase in IUGR
In those severely injures, the lighter the birth the longer the life expectancy
Presentation of cerebral palsy
Delayed developmental milestones
Definitive diagnosis is hard under 18 months
Abnormal posture and movement
Most common = bilateral spastic cerebral palsy
commonly associated symptoms:
- Epilepsy
- Failure to thrive
- Bladder incontinence or increased infection
- Constipation for decrerased mobility and intake
- Drooling
- Sleep disturbance
- orthopaedics: joint contractures, hip/foot deformity, shortened muscles, scoliosis, #
Investigations for cerebral palsy
Clinical examination and parental observation
Exclude other causes:
- Thyroid studies
- Chromosomal analysis
- Pyruvate and lactate levels
- Amino acid levels for metabolism errors
- CSF for hypoxia
Imaging - US or MRI may be helpful
Evoked potentials to check vision and hearing
EEG - to detect damage post hypoxia
Diseases associated with cerebral palsy
Intrauterine infections: TORCH, HIV Congenital malformation Toxic or teratogenic agents = alcohol, smoking, cocaine Maternal abdo trauma Maternal thyroid illness Intracranial haemorrhage Trauma Infection Hyperbilirubinaemia Seizures
Management of CP
Physio, OT, speech therapy, recreational therapy, paediatrics, orthopaedics
- Baclofen for muscle spasm
- Alternatives: tizanidine, botulinum A
- Diazepam or gabapentin
- Surgery for fixed contractures
- Mobility aids
- Heat, cold, vibration to decrease spasticity
- Splinting to increase range of movement at a joint
Complications of CP
Moderate to severe learning difficulties Hearing loss Contractures Failure to thrive Osteoporosis Aspiration pneumonia Dental problems
Decreased life expectancy with severe forms
Define Perthe’s disease
Self-limiting hip disorder caused by ischaemia and subsequent necrosis of femoral head
Epidemiology of Perthe’s disease
4-8 years
Increased in males (4:1)
Increased in obesity
Increased in Caucasians
Pathogenesis of Perthe’s disease
Avascular necrosis of femoral epiphysis
Delayed ossific nucleus
Articular cartilage is nourished by synovial fluid and continues to grow
Cartilage columns distort
Do not undergo normal ossification - excess calcified cartilage in bone
Symptoms are due to # and subchondral collapse
Presentation of Perthe’s disease
Pain in hip or knee causing limp 4-8 years old Effusion due to synovitis 10-15% bilateral (but asymmetrical stages) All hip movements limited Antalgic gait Trendelenburg gait in late stages No history of trauma Roll test: roll leg in internal and external rotation when supine will produce guarding
Investigations for Perthe’s disease
FBC, ESR
X-ray
- Early: widening of joint space or normal
- Later: decrease size of femoral head with patchy deformity
- Later: collapse and deformity of femoral head (increased arthritis)
Hip aspiration if ?septic
Arthrogram or MRI
Management of Perthe’s disease
Under 6s respond better
Over 6s tend to need surgery
Physio to increase muscle strength and range of motion
Surgery - proximal varus osteotomy
Define slipped capital femoral epiphysis
Often atraumatic or associated with a minor injury.
Most common adolescent hip disorders
Instability of proximal femur growth plate
- Preslip
- Acute (10-15%)
- Chronic (85%)
Stable in 90%, unstable in 10%
Epidemiology of slipped capital femoral epiphysis
I per 10,000 13 year old boys 11.5 year old girls Most common hip disorder Bilateral in 20% Left>right Increased in males Incidence rising
RF Obesity Local trauma Neglected septic arthritis Short stature Hypothyroid Hypopituitarism Past radiation of pelvis
Presentation of slipped capital femoral epiphysis
Discomfort in hip, groin, medial thigh during walking Pain worsens with running or jumping Acute <3 weeks, chronic > 3 weeks External rotation of leg on walking Hip motion is limited
Drehmann’s sign - supine, passively flex the hip, leg falls into external rotation and abduction
If chronic - atrophy of thigh and shortening of affected leg
Investigations for Perthe’s disease
AP and frog leg lateral x-ray
- widening of epiphyseal line or displacement of femoral head
Management of Perthe’s disease
Analgesia and immediate orthopaedic referral
Avoid moving or rotating leg
Surgery is mainstay of treatment
- Prevents further slops
- Prevent femeroactabular impingement
- Centre to centre screw fixation across plate
- OR open reduction and osteotomy of femoral neck
Define transient synovitis
Irritable hip
Common between 2 and 12
Acute onset of hip pain and a limp that gradually resolves
Child otherwise well
Clinical features of transient synovitis
Acute onset of hip pain or limp Between 2 and 12 Increased in boys (2:1) Inability to weight bear Leg held in flexion, adduction with slight external rotation Extension limited Child otherwise well persists for 1-2 weeks Resolves spontaneously
Investigations for transient synovitis
Exclude other diagnoses FBC, CRP and ESR X-rays US - for effusion Aspirate fluid
ALL are normal
Management for transient synovitis
Rest and analgesia
Pathophysiology
Duchenne’s muscular dystrophy
Most common muscular dystrophy
X linked recessive
Mutations in dystrophin gene - NO DYSTROPHIN PRODUCED
Progressive muscle degeneration
Presentation of Duchenne’s
Progressive proximal muscular dystrophy
Characteristic pseudohypertrophy of calves
All have symptoms by 3 years
Delayed motor milestones
Waddling gait on running
Gower’s sign = climbing up with hands when getting off floor
Failure to thrive
Speech delay
Raised LFTs
Anaesthetic complications - rhabdomyolysis, malignant hyperthermia
Fatigue
** Lose independent mobility by 8-11 years**
Investigations for Duchenne’s
Raised CK (x10-100x normal) from birth
Normal CK rules out Duchenne’s
Muscle biopsy looking for dystrophin
Genetic analysis
Management of Duchenne’s
Physio and orthoses may increase walking time
Corticosteroids can increase walking by 6-24 months
Bone protection
After loss of mobility (8 to 11) then supportive and orthopaedic care
Monitor cardiac and respiratory function
Complications of Duchenne’s
Joint contractures
Resp failure (most common cause of death)
Cardiomyopathy and cardiac failure
learning difficulty (10-20%)
Immobility - constipation, osteoporosis, obesity, HTN
Weight loss
Differences between Duchenne’s and Becker’s
Very similar
Both x-linked recessive
Dystrophin gene - fully gone in Duchenne’s, partially functional in Becker’s
Walking ability lost at 40-60, in Duchennes 8-11
Presentation of Becker’s is the same but slower
- Difficultly climbing stairs and heavy lifting in teenage years
Epidemiology of Osgood-Schlater’s disease
Common cause of knee pain Boys between 12-15 Girls between 8 and 12 Common in athletes Increased in males
Pathogenesis of Osgood-Schlater’s
Possibly caused by small avulsion fractures from contraction of quadriceps muscles at insertion on proximal tibial apophysis
Usually occurs during growth spurt before tibial tuberosity has finished ossification
Strength of quadriceps exceeds force
As avulsed # heal and grow the tibial tuberosity enlarges
Presentation of Osgood-Schlater’s
Gradual onset of pain and swelling below the knee
Relieved by rest
Made worse by extending the knee against resistance
Tenderness and swelling at tibial tuberosity
Management of Osgood-Schlater’s
Rest from painful activities Ice Physio and stretching exercises Simple analgesia - Paracetamol and ibuprofen No corticosteroid injections Surgery rarely required
Most return to normal in 2-3 weeks
Pathophysiology of Sever’s disease
Line of ossification in calcaneal apophysis is thought to develop microfractures due to recurrent heel stresses combined with growth spurt of puberty
Presentation of Sever’s disease
8 and 14 years old Heel pain in physically active individuals Gradual onset, worse on exercise Relieved by rest Often bilateral tenderness on palpation of heel at Achilles tendon insertion pain or dorsiflexion May have swelling at calcaneous
Investigations and management of Sever’s
X-ray to exclude tumour or fracture
It is a clinical diagnosis
Management with stretching, strengthening, heel lift
Correct alignment with orthoses
Antalgic gait
OA/Trauma
- Avoids certain movements due to pain
- limited joint range of motion
- inability to fully weight bear
- limp with slow and short steps
Ataxic gait
Cerebellar disease
- Arrhythmic steps
- wide based
- unsteady
- highly impaired tandem gait
- difficulty walking straight and turning
Festinated gait
Parkinson’s
- Short steps (petit pas)
- Decreased arm swinging
- Stooped posture
- Festination (hasty but short steps)
- Centre of gravity behind or in front of feet
Hemiparetic gait
Stroke
- Limb extended and circumducted
- Spastic quads and gluts
- Extensors are stronger than flexors in legs
- Foot plantar flexed causes dragging
Scissor gait
Cerebral palsy
- legs flexed slightly at hips and knees
- Spastic gait, stiff, foot dragging
- tiptoe walking
- thighs and knees rub together
Trendelenburg gait
Dropping of contralateral hip as ipsilateral adductors can’t stabilise the pelvis.
Body swings to other side to compensate
Clavicle #
Most commonly middle 1/3
Then lateral 1/3
Then medial 1/3
Complications:
- pneumothorax
- brachial plexus damage
- subclavian vessel damage
Place in figure of 8 bandage and sling for 3 weeks
Bankart lesion
Injury of the anterior glenoid labrum of the shoulder due to anterior shoulder dislocation
Hill Sachs lesion
Damage to the posterior humeral head (reciprocal of Bankart lesion)
How would a patient hold their arm in anterior dislocation?
Holds arm externally rotated and slightly abducted
Damage that can occur in anterior dislocation?
Axillary artery
Axillary nerve (37%)
Suprascapular nerve
Radial nerve
Treatment of anterior shoulder dislocation
Disimpaction
External rotation
Abduction
Internal rotation
Salter Harris classification
Classification of fractures through the epiphyseal growth plate of the bone
1 - S Slip (separated or straight across)
2 - A Above fracture lies above the epiphysis or away from the joint
3 - L Lower - # below the physis in the epiphysis
4 - TE Through Everything - # through metaphysis, physis, epiphysis
5 - R Rammed - crushed physis 9rare)
SALTER mneumonic
Upper motor neuron signs
Upgoing plantar Increased tone Weakness Increased reflexes Sustained clonus
Lower motor neuron signs
Decreased tone Weakness Wasting (atrophy) Arreflexia Muscle fasciculation's
Spinal stenosis
Abnormal narrowing of the spinal canal that can occur in any of the regions of the spine
Most commonly cervical spinal stenosis
Lumbar spinal stenosis is next common
Rare in thoracic
Results in neurological deficit
- Standing discomfort
- Bilateral symptoms
- Numbness
- Weakness
Intermittent neurogenic claudication - lower limb numbness, weakness, diffuse or radicular leg pain with paraesthesia
Weakness of heaviness in buttocks radiating into lower extremities
- Will resolve at rest, takes longer than vascular claudication
Causes of spinal stenosis
Herniated intervertebral discs Compression # OA RA - less common Hereditary - too small at birth Spondylolisthesis - vertebra slips forward on one another Trauma Tumours of the spine
Neurofibromatosis
Group of 3 conditions in which tumours grow in the nervous system
NF1 - neurofibromas
NF2 - schwann cells
Schwannomatosis
BENIGN
Symptoms of neurofibromatosis 1
Light brown spots on skin - café au lait
Freckles in arm pit and groin
Small mumps within nerves and scoliosis
Symptoms of neurofibromatosis 2
Hearing loss Cataracts Balance problems Flesh coloured skin flaps Muscle wasting Bilateral acoustic neuromas
