Yr4 MSK - Lectures Flashcards
What is OA?
- Which joints are typically affected?
- OA is a group of overlapping genetic and mechanically driven disorders with similar morphologic features and clinical outcomes: end result is joint failure.
- Causation is unclear but genetic factors (heritability estimated at 40 – 70 %), and environmental factors such as occupation and joint injury are likely to be the major aetiologic contributors (e.g. farm workers have a 5 fold increased risk for hip OA).
Role of Ageing in OA?
Role of BMI in OA?
BMI (weight) and OA
* Obesity increases the risk of OA in females.
* Framingham data shows that a Wt. loss of 5 kg reduced the risk of Knee OA by a half and that weight loss (averaging 4kg) reduced knee pain.
* Decreased body mass improves mobility.
List 3 differences between OA and RA?
What is Erosive OA?
- What pattern on radiographs?
Erosive OA
* Probably a separate or unique disease (phenotype), however still a matter of conjecture
* Note the marked cartilage and central bone erosion
List 6 Signs & Symptoms of OA?
2 Classic clinical features?
Symptoms and Signs of OA
1. Joint pain – worse with use or activity
2. Transient post-resting joint stiffness
3. Loss of movement or pain on movement with restricted range
4. Tenderness – articular and peri-articular
5. Bony and soft tissue swelling
6. Crepitus
Why do some patients with OA experience pain and others don’t?
- Pain may arise from stretching of the capsule and/or “inflammation” in the synovium (MRI studies show that change in synovial thickening correlates with change in pain severity (r = 0.3, P <0.005)
- Pain may arise from the bone – there is a correlation between pain and bone marrow oedema lesions on MRI (longitudinal studies show that when pain gets worse, BMLs get larger)
List 5 Current Drug Therapy in OA.
- Proposed Therapy Pyramid in OA?
- Effect size of OA therapies?
- Advantages & Limitations?
Current Drug Therapy in OA
1. Analgesics
2. NSAIDs – topical and oral (parenteral rarely used in chronic disease)
3. Coxibs
4. IA Glucocorticoids
5. IA Hyaluronan
List 5 Possible future therapies for OA?
Possible future therapies for OA
1. CINODs (cyclo-oxygenase inhibiting nitric oxide donors, e.g. Naproxcinod)
2. Topical NSAIDs with improved drug delivery.
3. IL-1 antagonists (Orthokine, Anakinra, Canakinumab for selected disease)
4. Regenerative strategies - autologous chondrocytes (ACI) & autologous stem cells
5. Improved surgical techniques
List the Radiological features of OA (6) vs. RA (4)?
Diagnosis of OA?
- When to consider additional testing?
Diagnosis of OA
Clinical diagnosis - can be made confidently on clinical grounds alone if the following are present:
- persistent activity related pain in one or several joints
- age ≥45 years
- morning stiffness ≤30 minutes
When to consider additional testing
- younger individuals with joint symptoms/signs of OA
- presence of atypical symptoms and signs
- presence of weight loss or constitutional symptoms
Rheumatoid Arthritis - Epidemiology
- Prevalence?
- Median age at diagnosis?
- Gender?
Rheumatoid Arthritis - Epidemiology
- 1% population
- median age at dx = 50yr
- females x 3
What causes RA?
Describe the pathophysiology?
RA - Cause… (unknown)
Multifactorial
- genes + environment
- associated with HLA-DR4
Immune-mediated attack on joints
- Activated T-cells, macrophages, fibroblasts = Produce inflammatory cytokines…
Inflammation of synovium
- Proliferation, fluid secretion
- Invasion of cartilage and bone, joint destruction
- ?over-simplification
Rheumatoid Arthritis
- Presentation?
- Diagnosis?
- Early recognition?
RA - Presenting complaint
- Joint pains = “Inflammatory”
- Improved with activity & NSAIDs
- Worsened by rest
- Morning stiffness >1hr (fluid resorbed)
- Joint swelling
- Polymyalgic symptoms
- Systemic symptoms = fatigue, vasculitis, fever…
JOINT PAIN – Don’t just use SOCRATES!
Rheumatoid Arthritis
- Describe the joint involvement?
- 2 typical features on clinical examination?
- Which 2 conditions are associated & their treatments?
**RA - Joint involvement **
- Symmetrical
- Polyarticular (May be oligoarticular at onset)
- Small and large joints
- MCPs, wrists, MTPs = RA until proven otherwise
- PIPs NOT DIPs
- Knee, shoulder, hip, ankle (most peripheral joints)
- Cervical spine, TMJ - Will not involve the lower back!
- PMR – up to 30% will have - Tx = steroids (15mg) 12months
- Consider GCA - gold standard diagnosis = temporal artery biopsy (can also ultrasound) - Tx = steroids (50mg)
What is the most common cause of joint pain?
= viral
List the investigations you would order for suspected RA? (8)
- What Abs and what %?
List 7 Extra-articular manifestations of RA?
RA – Extra-articular manifestations
1. Nodules (RF+)
2. Ocular – Sicca (dry mucous membranes/eyes), epi/scleritis
3. Pulmonary - Nodules, serositis, alveolitis, fibrosis
4. Neuropathy - Entrapment, mononeuritis, peripheral neuropathy, cervical myelopathy
5. Vasculitis
6. Splenomegaly + Neutropaenia = Felty’s syndrome (extraordinarily rare)
7. Cardiac - Pericarditis, valvular/ conduction abnormalities
- Pay attention to cardiac risk factors
Outline the treatment for RA? (4)
RA - Treatment
1) Disease-modifying medication
- Methotrexate
- Leflunomide, Hydroxychloroquine, Sulfasalazine
2) Anti-inflammatories
- Prednisolone
- NSAIDs
3) Biological agents
4) Monitoring/ treatment of related conditions = Heart disease, osteoporosis
Main tx for RA: Low-dose Methotrexate
- MOA?
- Dosing?
- What must you also prescribe?
- 6 symptoms of methotrexate toxicity?
Other than methotrexate, list 4 other DMARDs you may use in the management of RA?
- MOA?
- Dosing?
- Toxicity/SEs?
What is Tumour Necrosis Factor (TNF)?
- List 6 anti-TNF bDMARDs?
Tumour Necrosis Factor (TNF)
- Key pro-inflammatory cytokine
- Secreted by macrophages, lymphocytes
- Stimulates cell activation, adhesion molecules, enzyme induction, other pro-inflammatory CKs
- Elevated levels in RA serum, synovium
- TNF transgenic mice - erosive arthritis
Discuss the Biological Agents used in RA
- Side effects?
- Monitoring - which 3 blood tests? Treatment efficacy?
Biological Agents in RA
- Well-tolerated
- Increased infection risk
- TB = Need to screen for TB as will cause dissemination of ghon complex
- Upper respiratory tract, soft tissue infections
- ? Increased malignancy risk Skin cancers
- Similar efficacy across the group
List the non-pharmacological treatments of RA?
RA – Other treatment aspects
- Physiotherapy = Improve strength, function (incl. Hydrotherapy)
- Occupational therapy - Wrist splints, Functional aids
- Support groups
- Surgery - Wrist fusion, MCP prosthetics = Becoming less common
What is Pyrophosphate Arthropathy?
Pyrophosphate Arthropathy
- A chronic arthropathy in which the deposition of calcium pyrophosphate in the articular cartilage is considered pathogenic.
- There may be a family history - up to 30% of cases are now thought to be heritable.
- Like gout it may present in an acute form, usually as a monoarthritis (pseudogout), generally affects large joints and is characterized by an intense synovitis, which may be accompanied by systemic symptoms and signs, such as fever, very rarely it may be migratory.
- CPPD is rarely palpable in the soft tissues , unlike urate in gouty tophi
- An example of pseudogout affecting the shoulder is shown in the next slide.
What is Chondrocalcinosis?
- Who gets it?
- What disease should you suspect?
Chondrocalcinosis
- Calcification in the articular cartilage or meniscal cartilage or fibrocartilage ( e.g. triangular ligament in the carpus)
- Increases with age and very common in the elderly (affects approx. 30% of persons over 80 yrs).
- Pseudogout or pyrophosphate arthropathy should be suspected if there is chondrocalcinosis in a symptomatic joint.
What is pseudorheumatoid pyrophosphate arthropathy?
One form of PPA is referred to as pseudorheumatoid pyrophosphate arthropathy
- Multiple affected joints
- Often symmetrical joint involvement
- Due to the pattern of joint involvement and the symmetry, it can be difficult to distinguish from RA
- The presence of chondrocalcinosis in X-rays and CPPD crystals in joint tissue or aspirates is discriminatory.
- An example is shown in the next slide.
Describe the athroscopic appearance & morphology of CPPD deposits?
What is the Treatment of Pyrophosphate Arthropathy and Pseudogout?
Arthroscopic appearance of CPPD deposits
- In some cases, CPPD can be seen in the articular cartilage.
- It can be difficult to distinguish from Urate deposits.
- Sometimes CPPD and Urate co-exist.
- Biopsies of joint tissue should be placed in absolute alcohol (which preserves the crystalline material), NOT formalin.
Morphology of CPPD
- CPPD crystals are rhomboidal and are positively birefringent under polarized light.
- Urate crystals in contrast are needle shaped and negatively birefringent under polarized light
Gout
- Epidemiology?
- Presentation of attacks?
- Pyramid of severity/symptoms?
Gout
- Still the commonest inflammatory disease of the joints in men.
- Affects 1.4% of the adult population in urban Australia and 4% of Aboriginal Australians.
- Acute attacks may be infrequent in the “prodromal phase” of chronic and destructive gout.
- 90% of attacks of gout are monoarticular and the MTP1 joint is most commonly affected.
- Distal joints (e.g. IPs in fingers, IT and MTP joints in the feet) are much more often affected than proximal.
- Prevalence in USA has doubled in the past 20 years – dietary factors may be highly important, especially in men (increased fructose intake).
List the Risk Factors for Gout
- 4 Natural?
- 4 Iatrogenic?
Risk Factors for Gout
Natural
1. Renal disease
2. Alcohol
3. Dietary fructose intake
4. High cell turnover e.g. leukaemia, lymphoma, psoriasis
Iatrogenic
1. Chemotherapy
2. Diuretics
3. Low dose aspirin
4. Other drugs e.g. cyclosporin
Laboratory Findings in Gout?
Laboratory Findings
- Identification of urate (sodium monourate or SMU) crystals either in an inflamed or uninflamed joint is diagnostic.
- Serum urate can be misleading as it may fall during an acute attack and is not always elevated in between attacks.
- An elevated serum urate does not confirm gout and a normal or low serum urate does not exclude it.
Use of Imaging studies to diagnose gout
- Plain xrays?
- US?
- MRI?
- Dual energy CT?
Use of Imaging studies to diagnose gout
- Plain X-rays – have the capacity to identify gouty erosions
- US - has the capacity to identify gouty erosions in multiple joints without use of ionising radiation
- MRI – high sensitivity for gouty erosions and tophaceous deposits, also very useful for assessing the extent of gouty synovitis
- Dual energy CT – capable of detecting urate deposits in joints and soft tissues, high sensitivity and specificty, exposure to moderate ionising radiation, may be pos. when aspirate reveals no crystals. Could be a game changer! A new imaging modality which has a high sensitivity for urate deposition (deposits shown in green). CPPD crystal deposits cannot be imaged with this methodology.
Treatment of Gout
- Acute attack? What should you check for?
- Long-term management?
- 4 New therapies?
Treatment of Gout
- For the acute attack, moderate to high dose short acting NSAIDs are best (eg Indocid 50 mg qid) together with immobilisation of the affected part)
- Following the acute attack consider whether there are reversible factors eg excess alcohol, diuretics, inappropriate diet.
- Check for renal disease
List 5 Spondyloarthropathies.
- 6 Characteristic features?
Spondyloarthropathies
1. Ankylosing spondylitis
2. Psoriatic arthritis
3. Reactive arthritis
4. Enteropathic arthritis
5. Undifferentiated spondyloarthritis
Characteristic features
1. Enthesitis
2. Inflammatory back pain
3. Asymmetrical peripheral oligoarthritis
4. Dactylitis
5. Extra skeletal features
6. Association with HLA-B27
What is Enthesis?
- Which joints are most affected?
What is Dactylitis?
Enthesis
- Site of attachment of ligament/ tendon into bone
- Inflammation (enthesitis) = primary site of pathology in SpA
- Affects the vertebrae, sacroiliac jts, peripheral joints
- Leads to underlying bony reaction
- Also manifest by Achilles tendonitis, plantar fasciitis
Describe the typical features of Inflammatory Back Pain/Ank spond back pain? (9)
Inflammatory Back Pain
1. Morning stiffness >30 min
2. Improvement with exercise, Not with rest
3. Insidious onset
4. Onset <40yo
5. Persistence >3mon
6. Improvement with NSAIDs
7. Alternating buttock pain
8. Awakening in the second half of the night - Due to back/ buttock pain (Family history of SpA)
- Describe the peripheral arthritis in Ankylosing spondylitis?
- What are the 3 extra-skeletal features of Ank-spond?
Peripheral Arthritis
- Asymmetrical
- Oligoarthritis < 4 joints
- Lower limb - Knees, hips, ankles
Ankylosing Spondylitis = The “prototype” SpA
- Epidemiology: prevalence? gender? which HLA association? onset?
- 4 features?
- Clinical findings?
- Imaging? (3)
Ankylosing Spondylitis
Epidemiology
- Prevalence ~ 1%
- M:F 2.5:1
- 90% HLA-B27+
- Onset <45yo
Features
1. Inflammatory back pain
2. Alternating buttock pain
3. Enthesitis, Oligoarthritis, Iritis/Colitis/Rash
4. (Cardiac disease, lung fibrosis)
Clinical Findings: Limitation of spinal mobility
- Modified Schober’s test, Occiput-to-wall, lumbar side flexion, chest expansion
Imaging
- Radiographic sacroiliitis - May lag 5-10 yrs after symptom onset
- Spinal syndesmophytes
- MRI - Enthesitis, bone marrow oedema, erosions, sclerosis
Ankylosing Spondylitis = The “prototype” SpA
- Evolution?
- Management?
Management
- Exercise & NSAIDs - For all! = May be enough
- DMARDs if peripheral arthritis = Methotrexate, sulfasalazine
- TNF inhibitors: Adalimumab, Etanercept, & Infliximab
Psoriatic Arthritis
- How many people with psoriasis will get psoriatic arthritis?
- Joint patterns?
Psoriatic Arthritis
- Up to 30% of patients with psoriasis
Various joint patterns
- Asymmetrical LL oligoarthritis
- Symmetrical polyarthritis
- Spondylarthritis
- 50% HLA-B27+
- DIP arthritis
- Arthritis mutilans
List the clinical features/clue that might suggest psoriatic arthritis?
Management of Psoriatic arthritis?
Clues
- Psoriasis! - Check extensor surfaces, scalp (postauricular), natal cleft, umbilicus
- Family history
- Nail changes - Pitting, ridging, onycholysis, hyperkeratosis
- Dactylitis
- X-ray changes = “Chunky” syndesmophytes & Osteolysis, new bone formation
Reactive Arthritis
- Overview: How does it present in developed countries vs. returned travellers? Which pathologies?
- Pattern?
- 5 Other features?
- Management?
Overview
- Sterile peripheral arthritis
- Within 1/12 of primary infection elsewhere
- Developed countries - Urogenital infection = Chlamydia trachomatis
- Returned travellers - Gastrointestinal infection = Salmonella, Shigella, Yersinia, Campylobacter
Pattern = Usually an asymmetrical LL oligoarthritis - Often florid
Other features
1. Urethritis / diarrhoea
2. Ocular inflammation
3. Enthesitis
4. Dactylitis
5. Mucocutaneous lesions
Enteropathic Arthritis
- Overview: What % of Crohn’s patients? Pattern?
- Which HLA association?
- 3 Other features?
- Management?
Mechanical Back Pain
- Who gets it?
- Clinical presentation?
- 6 Red flags?
- Management? (6)
Mechanical Back Pain
- Older age group
- Gradual onset
- Intermittent exacerbations
- Worse in pm
- Worse with activity
- Can be stiff in am, 5-10 mins
Back Pain - Red Flags
1. Sudden onset
2. Nocturnal pain - Wakes from sleep
3. Weight loss
4. Fevers, sweats
5. Neurological symptoms - Lower limb, sphincters
6. PHx of Cancer - X-ray, bone scan, other Ix (mammogram)
List 5 Connective Tissue Diseases.
Connective Tissue Diseases
1. Systemic Lupus Erythematosus (SLE) - Anti-phospholipid syndrome
2. Scleroderma
3. Sjogren’s Syndrome
4. Inflammatory myopathies
5. Other - Mixed CTD, Vasculitis, Sarcoidosis
Systemic Lupus Erythematous (SLE)
- Epidemiology: Incidence? Prevalence? Gender?
- Risk factors? (4)
SLE – Risk Factors
1. Genetics - Twin studies
o 25-50% concordance for monozygotic twins
o 2-5 % for dizygotic twins
2. Susceptibility alleles - HLA-DR2, DR3
o RR 2-5x
3. Inherited complement deficiencies - C4a deficiency & C1q deficiency
4. Environment
- Hormonal factors No convincing increased risk with OCP
- Smoking
- Infections - eg. EBV
- Stress
List the Organ-specific vs. Systemic autoimmune diseases?
Organ-specific autoimmune disease
1. Thyroid - Hashimoto’s, primary myxedema, thyrotoxicosis
2. Stomach - pernicious anaemia
3. Adrenal - Addison’s disease
4. Pancreas - insulin dependent DM
Systemic autoimmune diseases - SLE
1. CNS Disease
2. Rash
3. Pleuritis
4. Pericarditis
5. Glomerulonephritis
6. Raynaud’s phenomenon
7. Arthritis
What are the 11 ACR SLE criteria (not diagnostic criteria)?
SLE – ACR criteria (not diagnostic criteria)
1. Malar rash
2. Discoid rash
3. Photosensitivity
4. Mouth ulcers
5. Arthritis
6. Serositis
7. Renal
8. CNS
9. Haematological
10. Immunological – DNA, Sm, APAs
11. ANA
List the Clinical features of SLE?
- 5 Mucocutaneous?
- 3 Musculoskeletal?
Musculoskeletal (60-80%)
1 - Arthritis
- Often pain, tenderness > objective signs of inflammation
- Small joints of the hands (MCP, PIP)
o Also wrists, knees – can be any joint
- Non-erosive, usu non-deforming
o Deformities typically reducible
2 - Osteonecrosis
- Hips most common
- Often following steroid treatment
3 - Myalgia - Overt myositis uncommon
Clinical Features of SLE
- Renal? What investigations must you do?
- 4 CVS (usually serous)?
- 5 Respiratory?
- 8 CNS?
CNS Clinical Features of SLE
1. “Anything”
2. Headache
3. Seizures
4. Transverse myelitis
5. Vasculitis
6. Thrombosis
7. Psychiatric
8. Movement disorders – e.g. chorea
SLE – Clinical features
- 3 Other?
- Which syndrome is it associated with (recurrent miscarriage)? Prevention?
- Outline the frequency of lupus manifestations?
SLE – Clinical features - Other
1. Constitutional - Lethargy, fevers, sweats
2. Haematological - Cytopaenias & Haemolytic anaemia
3. Vasculitis
Anti-phospholipid syndrome = EXAM Q!
* Anti-cardiolipin antibody, lupus anticoagulant
- Arterial / venous clots
- Livedo reticularis
- Recurrent miscarriage - due to failure of placenta to develop (early loss) = Prevention – clexane (LWMH)
3 Main Investigations for SLE?
- Which antibody do 95% of people with lupus have?
- What % of the normal population have ANA?
- 2 Types of ANA: Which is associated with SLE? Which with CREST?
- List 6 2) Extractable nuclear antigens (ENA) and the disease they are associated with?
- Which antibody has high specificity for SLE (95%) but lower sensitivity than ANA?
- List 8 autoimmune conditions other than SLE which can be ANA+?
Other Autoimmune diseases with ANA+ other than SLE
1. RA
2. Thyroid disease
3. Autoimmune hepatitis
4. Lyme disease
5. Sjogrens
6. Scleroderma
7. Myositis
8. MCTD
What type of ANA is this?
= Homogenous
Outline the treatment for SLE
- 3 main drugs: when to use?
- Risk of what SE with Hydroxychloroquine ?
- 6 Other immunosuppressive therapies?
SLE – Treatment
1 - Hydroxychloroquine (Plaquenil)
- Anti-malarial
- 200-400mg/d
- < 6.5 mg/kg – minimal ocular toxicity
- Slow-acting = 2-3 months onset/ offset
- Reduces: musculoskeletal, mucocutaneous symptoms, disease flares
2 - NSAIDs - Adjunctive for arthralgia
3 - Prednisolone
- Acute treatment of disease flares
- High-dose may be required for acute renal/ CNS disease, vasculitis
- Rarely required for long-term disease suppression
Scleroderma
- What is it?
- Epidemiology: Incidence? Prevalence? Gender? Onset?
- Cause? (4)
- Pathogenesis?
Scleroderma
- Rare multisystem disorder
- Small blood vessel abnormalities
- Fibrosis of skin and internal organs = “skleros” – hard, “derma” – skin
- Autoimmunity
Epidemiology
- Incidence 20/106 per year
- Prevalence 20-70/105
- F:M ?7-12:1
- Onset: 35-65yo
Scleroderma – Clinical features
- Limited disease: CREST? What ANA centromere pattern?
- Diffuse Disease: Which antibody? Major cause of mortality?
- What is the Roman Breast Plate Sign?
Limited Scleroderma – Clinical features = Skin involvement restricted to the distal limbs + face
- Includes CREST syndrome: Calcinosis, Raynaud’s phenomenon, Esophageal dysmotility, Sclerodactyly, Telangiectasia
- Centromere-pattern ANA characteristic
- Isolated pulmonary hypertension, digital ischaemia more common cf diffuse disease
- Lung, cardiac, renal involvement less common
- What is the treatment for Scleroderma (organ specific)?
- What ANA centromere pattern is this?
= Anti-centromere pattern
Sjogren’s syndrome
- 5 Clinical Features?
- 2 Investigations?
- 4 Treatments?
Sjogren’s Syndrome - Clinical Features
1. Sicca symptoms – eyes and mouth - May be the only manifestations
2. Arthritis
3. Increased lymphoma risk
4. Peripheral neuropathy, respiratory disease
5. May be primary/ secondary to other autoimmune disease
Inflammatory Myopathy
- Old classification? (3)
- New classification?
- Presentation?
- Diagnosis - 1 main thing + 4 others?
Old classification:
1 - Polymyositis (PM) - Proximal muscle weakness
2 - Dermatomyositis (DM)
- Proximal muscle weakness
- Rash – Gottren’s papules, heliotrope rash, shawl sign
3 - Inclusion body myositis (IBM)
- Weakness of quadriceps, forearm flexors
- Often older patients
Presentation = Progressive proximal, symmetrical weakness
Diagnosis
1. Elevated CK = NO 1!
2. Pos ANA, ENA (Anti-Jo1), Myositis Ab
3. Muscle biopsy
4. EMG
5. MRI
Myopathy Classification
- What is IMNM?
- Which antibody is associated with statin myopathy (NOT myalgia)?
Myopathy - Treatment? (3)
- What diagnosis do you need to consider in newly presenting myopathy?
Myopathy - Treatment
1 - Cease trigger (statin)
2 - Immune suppression
- Prednisolone
- IVIG, Rituximab (DM)
- Azathioprine, Methotrexate
3 - Treat related conditions
- Underlying malignancy (DM, PM)
- Interstitial lung disease
Myopathy – can be paraneoplastic - consider cancer diagnosis in newly presenting myopathy!
IMNM Subtypes? (2)
Peripheral Nerve Syndromes - Fibre Size & Presentation
- How do small fibre neuropathies present? (4)
- How do large fibre neuropathies present? (3)
List 7 common drug-induced neuropathies?
5 Features of Trigeminal Neuralgia?
Peripheral Nerve Syndromes - Bells Palsy
- What is it?
- Are the forehead muscles spared?
- Ixs?
- Treatment?
- Prognosis: What % recover?
- 7 Secondary causes?
Guillain-Barre Syndrome
- What it is?
- Clinical presentation?
- Which infection most commonly recognised?
- Key finding on clinical examination?
- 7 Differentials?
- 2 Treatment options? Which is better?
Explain the relationship of nerve roots to vertebrae?
Cervical Spine
- How are cervical nerves numbered?
- What must you be careful of with intubating patients with cervical spine disease?
Cervical Spine
- NOTE: Cervical nerves (C1-C7) are above their numbered vertebra, whereas all others (C8 and below) are below their numbered vertebra
- Patients with long standing rheumatoid arthritis and psoriatic arthritis may develop involvement of the upper cervical spine.
- Be very careful with intubating a patient with atlanto-axial subluxation and avoid damage to the upper cervical cord.
- Prior to surgery, if subluxation is a possibility, check lateral X-rays of the cervical spine in flexion and extension. Usually in patients with long-standing arthritis with erosions at other sites
- Outline the entire body’s dermatomes.
- Outline the dermatomes of the upper limbs?
- Name the 4 tendon reflexes of the upper limbs and their cervical nerve root?
What might a patient with a C7 Radiculopathy do to relieve pain?
Draw the Brachial Plexus.
- What 4 conditions might involve the brachial plexus?
- What palsy of the brachial plexus can occur with traction at birth?
Involvement of brachial plexus is seen in:
1. Microvascular disease (diabetes, radiation, inflammation)
2. Trauma
3. Malignancy (lung and breast, lymphoma)
4. Thoracic outlet syndrome (compressive)
Outline Brachial Plexus Root Injuries
- Upper trunk - which roots? clinical syndromes/features?
- Lower trunk - Name of paralysis?
List 7 peripheral entrapment neuropathies of the upper extremity and thorax and their location/syndrome?
List 10 peripheral entrapment neuropathies of the lower extremity and their location/syndrome?
What is Ulnar Nerve Entrapment in the Cubital Tunnel?
- Presentation?
Ulnar Nerve Entrapment in the Cubital Tunnel
Lesions of the ulnar nerve below the elbow cause greater ulnar nerve clawing due to preservation of the flexor digitorum profundus.
What is Carpal Tunnel Syndrome?
- Which nerve & its course & sensory supply to the hand?
- Relationship between ulnar tunnel (Guyon’s canal) and carpal tunnel?
Median Nerve = Carpal Tunnel Syndrome
Carpal Tunnel Syndrome
- List 3 Clinical tests/features you would examine for?
- Tinel sign = a way to detect irritated nerves. It is performed by lightly tapping over the nerve to elicit a sensation of tingling or “pins and needles” in the distribution of the nerve.
- Phalen’s test = A positive test is defined as the occurrence of pain or paresthesias in at least one finger innervated by the median nerve when the hands are put back to back.
- Opponens pollicis weakness test = opposing the thumb to little finger against resistance.
List 8 Signs/Symptoms of Carpal Tunnel Syndrome?
- Where is pain localised to? Where might it radiate?
List 10 conditions associated with carpal tunnel syndrome.
What is ‘Saturday night’ palsy?
- Introduction?
- Aetiology?
- History?
- Clinical Presentation - Clinical features? (4)
- Evaluation?
- Management?
Saturday Night Palsy = Radial Nerve Palsy in Humeral Groove
- Fracture or direct injury
- Results in both motor and sensory changes.
- A wrist drop occurs if the lesion is above the origin of the posterior interosseous nerve.
- All radial nerve palsies result in inability to extend the MCPs.
- Lesions above the humeral groove also result in triceps weakness.
What is Devil’s grip?
Lower Extremity Nerves & Dermatomes?
What are 2 stretch tests of the lower limb and their diagnosis?
Which nerve might a surgeon cut deliberately during an inguinal hernia repair? Why?
Ilio-inguinal neuralgia
- Nerve injury can occur following repair of inguinal hernia
- Surgeons frequently cut the nerve to avoid pain post-op
What is Meralgia Paraesthetica?
- Which nerve? its course?
- Causes?
- Clinical presentation?
Meralgia Paraesthetica = Lateral Femoral Cutaneous Nerve
Tarsal Tunnel Syndrome
- Outline the tarsal tunnel and the branches of the posterior tibial nerve?
- Clinical presentation?
What is a Morton’s neuroma?
What is Planovalgus?
- Overview? (2)
- Presentation? (4)
- Assessment? (4)
-
Flatfoot = Planovalgus
Overview
- Flattened medial longitudinal arch and Valgus Heel
- Normal alignment hindfoot / heel is 6 deg valgus
Presentation
- Asymptomatic Concerned
- Pain with running, sport, work, certain footwear
- Persistent Pain……..often medial first, lateral later
- “Fallen Arches”
Assessment of Adult Flatfoot
- Painful or Not
- Severity (normal physiologic valgus = 6deg)
- Flexible or Rigid…… Subtalar Complex and Arch
- Treatment so far…….orthotics, injections, analgesia
Flatfoot = Planovalgus
- List 6 Differential Diagnoses?
- When would you image? How? (3)
Differential Diagnosis Flatfoot
1. Mobile Flatfoot usually persisting from childhood
2. Spastic Peroneal Flatfoot…..rigid and painful
3. Accessory Navicular
4. Inflammatory Arthritis
5. Osteoarthritis with arch collapse
6. Neuromuscular including Charcot
7. Post-traumatic
8. Adult Acquired Flatfoot = result of Tib Post Tendon dysfunction
Flatfoot = Planovalgus
- Management?
- Surgical reconstruction?
Treatment Symptomatic Flexible Flatfoot
- Footwear advice
- Orthotics with medial heel wedge
- If more severe (and flexible)…..
1. UCBL heel cup
2. Hinged brace / Caliper
3. Injection: Beware
4. Surgery
Flatfoot Reconstruction
- Calcaneal Osteotomy (medialise heel)
- Medial Cuneiform (open wedge)
- Lateral column lengthening (corrects abductn)
- Achilles lengthening
- FDL tendon transfer
- Much improved comfort and function but long rehab >4mths
Cavovarus Foot
- What is it?
- Presentation? (5)
- Aetiology? (7)
- Management? (5)
Ankle Arthritis
- 4 Clinical features?
- Aetiology? (4)
- Imaging - when & how?
Clinical Features of Ankle OA
1. Pain
2. Stiffness
3. Swelling
4. Loss of Alignment
Aetiology: often Post Traumatic
1. Inflammatory
2. Chronic Instability /Malalignment eg untreated Cavovarus
3. Primary OA
4. Haemochromatosis
Imaging Ankle OA
- Plain Xrays Standing
- CT only if unsure re surrounding joints esp subtalar, talo-navic
- MRI only if ?other diagnosis eg osteochondral defect talus
Ankle Sprain
- Management?
- 3 Differentials?
Overview
* Very common injury
* Incomplete damage to lateral ligament(s)
* Inversion
* RICE, avoid re-injury
* Temporary crutches / boot for relief
* Review if not steadily improving first few weeks
* Complete ATFL rupture still non-Op
Differentials for Ankle Sprain
- Osteochondral fracture Talus?
- Syndesmotic Injury - “high ankle sprain”?
Metatarsalgia
- Overview?
- Diagnosis?
- Treatment? (6)
- Surgery? (5)
Hallux Valgus
- What are they?
- Management?
- Surgery?
Bunions = Hallux Valgus - Proceed with Caution
- Christian Louboutin +ve - “Have to wear these shoes for work”
- Need to get them done before they look like my Grandmother’s feet
- Over-emotional
- Teenagers - ”Gross! …… like, total Goober Feet!”
- Cringe / air quotes if mention “sensible shoes”
- The commonest cause of a disappointing outcome is unrealistic expectations
Paediatric Orthopaedics
- Whats different?
Kids are Different
* Congenital malformations
* Developmental abnormalities
* Dependence
- NAI
- Psychological abuse
- Nutritional deficiencies
Developmental Dysplasia of the Hip (DDH)
- What is it?
- Incidence?
- Risk Factors - 4 Fs?
Developmental Dysplasia of the Hip (DDH)
* Formerly “Congenital” or CDH
* Broad spectrum
- Dysplasia = abnormality of development
- Subluxation = femoral head sits within the acetabulum, but is decentred or able to be displaced within the acetabulum
- Dislocation = femoral head sits outside the acetabulum. Either reducible or irreducible
Incidence:
- 1/1000 dislocated
- 10/1000 subluxed/dysplastic
- Left 60%, Right 20%, Bilateral 20%
Developmental Dysplasia of the Hip (DDH)
- Diagnosis?
- Examination - 5 Clinical Features & 2 tests?
- Management?
Diagnosis of Developmental Hip Dysplasia (DDH)
- In the newborn period DDH is a clinical diagnosis, and a radiographic one (USS not XR!)
- Earlier diagnosis, better outcome
Examination for DDH
1. Asymmetrical crease
2. Decreased abduction
3. Leg length discrepancy – Galeazzi’s sign
4. Limp
5. Beware of bilateral DDH
Congenital Talipes Equinovarus (CTEV)
- What is it?
- Overview?
- Aetiology?
Cerebral Palsy
- Definition?
- Aetiology?
- Classification?
- Management?
Scoliosis
- Overview?
- 5 Red flags?
- Most common form?
- What test?
- Management - 3 options?
Overview
- Lateral curvature of the spine in the coronal plane of >10°
- Can be:
- 1 - Structural
o Passively non-correctible
o Vertebral rotation
- 2 - Non-Structural
o Fully passively correctible
o No rotational component
Red Flags in Scoliosis
1. Male
2. Left sided curves
3. Pain
4. Rapid progression
5. Neurology
Any of these abnormalities requires further investigation (ie MRI)
What is the commonest reason for admission of child?
Outline the Salter-Harris Classification? (5 Types)
Non-Accidental Injury in Children
- Definition?
- Prevalence?
- 5 Risk factors?
- Presentation?
- Management?
Non-Accidental Injury
* Any act or failure to act that results in harm.
* Abuse second most common cause of death in infants 1-6 months.
* Risk factors include:
1. First born
2. Prematurity
3. Step-children
4. Disabled children
5. Lower socioeconomic class
Define a Fracture?
- Approach?
- 5 Physical Signs of Fractures?
- Classification of #s?
= Breaking of a bone or cartilage
Physical Signs Of Fractures
1. Deformity
2. Abnormal Mobility
3. Crepitus
4. Loss Of Function
5. Local Bone Tenderness
Fractures in the Young?
Fractures in the Old?
- 4 Types of pathological fractures?
- What is the Gustilo classification?
YOUNG
- CHILDREN’S FRACTURES:
Greenstick, Salter Harris (1-5)
OLD - OSTEOPOROTIC FRACTURES (insufficiency):
- Neck of femur
- Colles
- Neck of humerus
- Spine
FRACTURE CLASSIFICATION
PATHOLOGICAL:
1. Pagets
2. Osteogenesis Imperfecta
3. Tumour
4. Osteoporosis
How do fractures heal?
PRIMARY FRACTURE HEALING
- “No movement = No Callus”
- Absolute stability
SECONDARY Fracture Healing
- “Movement = Callus”
- Relative Stability
What are the 8 Non-surgical treatments for a fracture?
NON SURGICAL
IMMEDIATE/EARLY
1. First aid
2. Stop bleeding
3. Splint limb
4. Cover open wounds
5. Early-fluid replacement
6. Tetanus prophylaxis
7. Antibiotic cover
8. Pain relief
LATE - Definitive therapy
What is the Surgical treatment for fractures?
Complications of fractures
- 3 Immediate?
- 3 Early?
- 7 Late?
SURGICAL TREATMENT
IMMEDIATE & EARLY
- same as non-operative
LATE
- debridement of tissues
- fixation of bone-internal or external
- tissue repair and grafting
- compromise surgery-late amputation
