Rheumatology + Orthopaedics Flashcards
Clinical presentation of septic arthritis
Signs + symptoms
- Painful, hot, red, swollen joint - usually single joint
- Restricted movement/stiffness
- Rapid onset
- Systemic symptoms (not always) - fever, malaise, sweats, rigors
Which joints are most commonly affected by septic arthritis?
Hip and knee
What percentage of septic arthritis is polyarticular?
20%
List risk factors for septic arthritis
- Disease of joint e.g. osteoarthritis
- Prosthetic joint
- Recent joint surgery
- Leg ulceration
- Trauma to joint/skin
- IVDU
- Immunosuppression
Describe the possible routes of infection in septic arthritis and give examples of each
- Direct inoculation e.g. joint surgery
- Contigious spread from adjacent bone e.g. osteomyelitis
- Haematogenous seeding from a distant site e.g. bacteraemia due to meningitis
What is the most common causative organism of septic arthritis? List other common causes of septic arthritis
- Staphylococcus aureus most common
- Neisseria gonorrhoea in sexually active
- Group A strep - strep pyogenes most common
- Haemophilus influenza
- E. Coli
Differential diagnosis of acute monoarthritis
- Septic arthritis
- Crystal arthritis - gout or pseudogout
- Reactive arthritis
- Seronegative arthritis
- Haemarthrosis
- Specific to site e.g. knee - bursitis
How can differential diagnosis for acute monoarthritis be narrowed down using a patient’s history?
- Septic arthritis - usually rapid onset, Hx orthopaedic interventions, primary joint disease, IVDU, immunosuppression, sexual history (gonococcal)
- Reactive arthritis - asymmetrical and polyarticular, symptoms of urethritis, conjunctivitis, diarrhoea, rash, travel history (traveller’s diarrhoea)
- Crystal deposition - rapid onset, previous episodes acute attack in same or other joint with spontaneous resolution, use of diuretics, history of renal calculi, alcoholism, presence of tophi, foot joints involved (gout)
- Ankylosing spondylitis - eye inflammation, low back pain
- Psoriatic arthritis - polyarticular, skin/nail symptoms - patches, pitting
- Haemarthrosis - coagulopathy, anticoagulant medications, trauma
Important points in clinical examination of acute monoarthritis
- Affected joint and joints above and below - ROM, soft tissue around joint, effusion
- Skin
- Eyes
- Systemic symptoms - observations, relevant systems e.g. eyes, skin
Which investigations should be used in acute monoarthritis?
+ interpretation
**Joint arthrocentesis for synovial fluid aspiration in any hot, swollen, tender joint with restricted movement. **
(Considered septic arthritis until proven otherwise)
* Send for - WCC, crystal analysis, gram staining, culture
Bloods
* FBC - WCC (infection), Hb (haemarthrosis)
* ESR, CRP - infection, inflammatory/autoimmune
* Blood culture - infection, done even if apyrexial
* Serum urate - gout
* ANA and RF - rheumatoid arthritis, other inflammatory causes
* U&Es - baseline (e.g. prior to antibiotics), may be deranged in sepsis
* LFTs - baseline
Imaging
* Plain X-ray films of affected joint as baseline
* US for diagnosis/guiding aspiration
* MRI if osteomyelitis suspected or deep joint
Bedside
* MSSU, urinalysis
* Wound swab
* Sputum
How should joint arthrocentesis be carried out in acute monoarthritis?
- Refer to orthopaedics if joint prosthesis or hip joint (will require US guidance)
- Should be carried out in sterile environment
- Use smallest needle possible
- Can be done in patients on anticoagulants e.g. warfarin
- Withdraw as much fluid as possible for symptomatic relief, may need to massage joint to encourage drainage
- Cellulitis of skin over joint is relative contraindication
Features of synovial fluid analysis which suggest septic arthritis
- Colour - yellow/green
- Clarity - cloudy/opaque
- Increased viscosity
- WCC > 50,000 cells/mm3
- > 75% neutrophils
- Gram stain positive
- Negative crystals
Features of synovial fluid analysis which suggest a non-inflammatory pathology
- Colour - straw/yellow
- Clarity - translucent
- High viscosity
- WCC - 200-2000 cells/mm3
- <25% neutrophils
- Gram stain negative
- Negative crystals
Features of synovial fluid analysis which suggest inflammatory cause of arthritis
- Colour - yellow
- Clarity - cloudy
- Viscosity - decreased
- WCC - 2000-50000 cells/mm3
- > 50% neutrophils
- Gram stain negative
- Crystals positive
Features of synovial fluid analysis which suggest haemarthrosis
- Colour - red/xanthochromic
- Bloody
- WCC - 200-2000mm3
- 50-75% neutrophils
- Gram stain negative
- Crystals negative
Classification system for septic arthritis
Newman’s class
A - isolation of pathogenic organism from joint
B - isolation of pathogenic organism from another source
C - typical clinical features and turbid joint fluid in presence of previous antibiotic use
D - suggestive pathology or post-mortem features of septic arthritis
Risk factors for gout
- Male gender
- Obesity
- High purine diet - meat and seafood
- Alcohol
- Diuretics
- CVD or CKD
- Family history
Which joints are typically affected by gout?
- Metarsophalangeal joint (base of big toe)
- Carpal joints
- Carpometacarpal joints (base of thumb)
Describe the crystals seen in gout
Negatively birefringent of polarised light
Monosodium urate crystals
Needle shaped
X-ray findings in gout
- Joint space maintained usually
- Lytic lesions in bone
- Punched out erosions - sclerotic borders, overhanging edges
Management of acute gout flare
- NSAIDs first line (+ PPI)
- Colchicine second line if NSAIDs contraindicated e.g. renal impairment, significant heart disease
- Steroids considered third line
Common side effects of colchicine and how to prevent
GI upset - diarrhoea
Lower dose
Describe long-term management of gout
Lifestyle - healthy diet, avoid alcohol, maintain healthy weight
Urate-lowering therapy - started 2-4 weeks after acute flare has settled
* Offerred if multiple/troublesome flares, CKD 3-5, diuretic therapy, tophi, chronic gouty arthritis
* Monitor serum urate levels - aim for <360 micromol/L or lower if tophi/arthritis, frequent flares despite urate below target
* Allopurinol or febuxostat first line (allopurinol in CVD)
Mechanism of action of allopurinol in gout treatment
Xanthine oxidase inhibitor - reduces production of uric acid (product of purine metabolism)
Crystals seen in pseudogout
Positive birefringement of polarised light
Calcium pyrophosphate crystals
Rhomboid shaped
X-ray findings in pseudogout
Chondrocalcinosis - thin white line in middle of joint space caused by calcium deposition (pathognomonic)
Other changes - LOSS
L - loss of joint space
O - osteophytes
S - subarticular sclerosis
S - subchondral cysts
How is pseudogout managed?
- Symptomatic management - NSAIDs, colchicine, joint aspiration, steroid injections, oral steroids
- Arthrocentesis in severe cases
Define gouty tophi. Where are they most commonly found?
- Subcutaneous deposits of uric acid
- Small joints and connective tissue of hands, elbows, ears
- DIP joints in hands most commonly affected
Management of septic arthritis
Joint aspiration to remove purulent material + for symptomatic relief - closed aspiration or arthroscopic drainage, aspirate to dryness, may need serial aspiration
Empirical IV antibiotics until organism/sensitivities known -
* Native joint - IV flucloxacillin
* Penicillin allergy or MRSA suspected - IV vancomycin
* High risk for gram negative - add IV gentamicin
* Prosthetic joint - IV vancomycin (+/- IV gentamicin)
* Gonococcal infection suspected - cephalosporin
Native joint - 2 weeks IV, 4 weeks oral
Prosthetic joint - 6 weeks IV
What do crystals in synovial fluid indicate?
Gout, pseudogout or septic arthritis - can be co-existent
Describe the pattern of joint involvement in RA
Symmetrical
Polyarticular
Distal small joints - hands + feet
* Hands - MCP, PIP
* Wrist
* Ankle
* Can be larger joints e.g. knees, shoulders, elbows
Symptoms of inflammatory arthritis
- Pain - worse after rest, improves with activity (opposite to OA)
- Swelling
- Warmth
- Redness
- Tenderness
- Stiffness - early morning stiffness >1 hour
- Persistent - generally accumulates joints over time
- Systemic symptoms - fatigue, weight loss, flu-like illness, muscle aches and weakness
Signs of RA
Synovitis - boggy on palpation
Positive squeeze test - pain when squeezing metacarpal/tarsal joints
Deformity
* Swan neck - MCP flexion, PIP hyperextension, DIP flexion
* Boutonniere’s - PIP flexion, DIP hypertextension
* Z-thumb - CMC flexion, MCP hypertextension, PIP flexion
* Ulnar deviation - deformity of MCP joints, fingers deviate towards ulnar side
Rheumatoid nodules - firm, hard swellings over extensor surfaces
Extra-articular features
* Ocular - scleritis, episcleritis, Sicca syndrome (secondary Sjogren’s)
* Cardiorespiratory - pleural effusions, pulmonary nodules, pulmonary fibrosis, pericarditis, serositis
* Splenomegaly
* Peripheral neuropathy
* Anaemia of chronic disease
* Amyloidosis
* Lymphadenopathy
* Carpal tunnel syndrome
* Felty’s syndrome - RA, neutropaenia, splenomegaly
Differential diagnosis for RA
How to differentiate between differentials and RA
- Psoriatic arthritis - small joints of hand and feet but less symmetrical, DIP involved, skin/nail symptoms
- Polyarticular gout - tophi, risk factors for gout
- Osteoarthritis - worse with movement, better with rest, <1 hour early morning stiffness, less symmetrical, larger joints
- SLE - polyarthritis in small joints of hands and feet but usually non-deforming, additional signs e.g. rash, mouth ulcers, alopecia, Raynaud’s, Sicca syndrome
- Polymyalgia rheumatica - shoulder pain and stiffness primarily, older woman
- Reactive arthritis - recent infection, can cause symmetric hand and feet arthritis
- Sarcoidosis - CXR
- Septic arthritis - acutely painful, hot, swollen joint, signs of sepsis e.g. fever
- Seronegative spondyloarthritis - history of psoriasis, back pain, bowel problems
Define palindromic rheumatism
Self-limiting short episodes of inflammatory arthritis with joint pain, stiffness, swelling typically affecting only a few joints.
Last 1-2 days, then completely resolve.
Positive antibodies (RF, anti-CCP) with palindromic rheumatism –> progression to full RA more likely
RA consequences in the cervical spine
Atlantoaxial subluxation
* C2 (axis) and odontoid peg shift within C1 (atlas)
* Due to local synovitis and damage to ligaments and bursa around odontoid peg
* Can cause spinal cord compression and is an emergency
* Important if having GA requiring intubation - MRI pre-op to assess
Investigations used in RA diagnosis
- CRP and ESR - usually elevated in RA (40% normal)
- Rheumatoid factor - present in 60-70% RA
- Anti-CCP if negative for RF - present in 80% RA
- Imaging - US (synovitis), X-ray (hands and feet), MRI
Describe the early and late X-ray changes seen in RA
Early
* Peri-articular osteopaenia
* Soft tissue swelling
* Loss of joint space
Late
* Peri-articular joint erosion
* Joint destruction
* Subluxation
Compare the antibodies used in diagnosis of RA
- Rheumatoid factor vs anti-CCP
- Similar sensitivity but anti-CCP higher specificity (90-95%)
- Test for anti-CCP in patients with suspected RA who are RF negative
What is rheumatoid factor?
How is it detected?
What does it indicate in RA?
Circulating antibody (usually IgM) that reacts with the Fc portion of own IgG
Detected by either:
Rose-Waaler test - sheep red cell agglutination
Latex agglutination test (less specific)
Positive in 70-80% of RA, high titre associated with severe progressive disease (not a marker of disease activity)
Conditions associated with rheumatoid factor
- Rheumatoid arthritis
- Felty’s syndrome (RA, splenomegaly, neutropaenia) - 100%
- Sjogren’s syndrome - 50%
- Infective endocarditis - 50%
- SLE - 20-30%
- Systemic sclerosis - 30%
- General population - 5%
- Rarely - TB, HBV, EBV, leprosy
When should a patient with suspected RA have a routine/urgent referral?
- Refer for appointment within 3 weeks for persistent synovitis of unknown cause
- Urgent referral (within 3 working days) if small joints of hand or feet affected, more than one joint affected, delay of 3 months or longer from onset of symptoms to presentation
Even if CRP/ESR, negative anti-CCP or RF
Diagnostic criteria used in RA
American College of Rheumatology/European League Against Rheumatism (ELAR)
Score based on
* Joints involved - more and smaller joints score higher
* Serology - rheumatoid factor and anti-CCP
* Inflammatory markers - ESR, CRP
* Duration of symptoms - more or less than 6 weeks (longer scores)
Score of 6 or more - diagnostic for RA
Functional assessments/disease monitoring scores used in RA
DAS28 - disease activity score
* Assessment of 28 joints
* Points given for swollen joints, tender joints, ESR/CRP result
* Used to monitor disease activity and response to treatment
HAQ-II - health assessment questionnaire disability index
* Patient reported - difficulty with ADLs
SF-36 - short form 36
* Patient reported
* Health-related quality of life
Risk factors for worse prognosis in RA
- Younger onset
- Male
- More joints and organs affected
- Presence of RF and anti-CCP
- Erosions seen on X-ray
Describe approach to management of RA
Induction/initiation therapy
* Step-up approach - introduce and escalate single drug to maximum tolerated dose, if ongoing disease activity add a further drug
* Step-down approach - several drugs started at once then gradually withdrawn
* Parallel - combination introduced at same time and maintained
Monitor response to treatment with CRP and disease activity score (e.g. DAS28)
Treat acute flare-ups
How are acute RA flares treated?
Oral NSAIDs for pain/stiffness - ibuprofen, naproxen, diclofenac (+ PPI)
COX-2 inhibitors e.g. etoricoxib
Glucocorticoids - oral prednisolone, IM/intra-articular methylprednisolone or triamcinolone acetonide
What is the first line long-term treatment for RA?
CsDMARDs - offer first line and within 3 months of symptom onset
* Methotrexate
* Leflunomide
* Sulfalazine
* Hydroxychloroquine if mild or palindromic disease
Methotrexate
* Mechanism of action
* Dose frequency
* Side effects
* Monitoring requirements
* Pregnancy considerations
* Interactions
- Folate metabolism antagonist - inhibits dihydrofolate reductase
- Injection or tablet once a week, also folic acid 5mg once a week on a different day
- Side effects - mouth ulcers, mucositis, liver toxicity, bone marrow suppression and leukopaenia, ?pulmonary fibrosis
- Monitoring - FBC, LFTs
- Contraindicated in pregnancy - teratogenic
- Interactions - trimethoprim/co-trimoxazole increases risk of marrow aplasa, high dose aspirin increased risk of methotrexate toxicity as reduced excretion
Advise for methotrexate and pregnancy
Avoid pregnancy for at least 6 months after treatment stopped
Men using methotrexate need to use effective contraception for 6 months after treatment
Leflunomide
* Mechanism of action
* Side effects
* Pregnancy considerations
- Interferes with pyrimidine production - component of RNA and DNA
- Side effects - mouth ulcers, mucositis, hypertension, rashes, peripheral neuropathy, liver toxicity, bone marrow suppression and leukopaenia
- Contraindicated - pregnancy (teratogenic), women and men
Sulfalazine
* Mechanism of action
* Dosing regimen
* Side effects
* Monitoring requirements
* Pregnancy considerations
- Immunomodulatory - immunosuppressive and anti-inflammatory, against folate, T and B cells
- Daily dosing
- Side effects - GI, headache, rash, temporary male infertility (reduced sperm count), bone marrow suppression
- Monitoring requirements - FBC, U+Es, LFTs
- Safe in pregnancy - folic acid 10mg daily, started 3 months pre-conception
Hydroxychloroquine
* Mechanism of action
* Dosing regimen
* Side effects
* Monitoring
* Pregnancy considerations
- Immunosuppression via interaction with toll-like receptors, disrupting antigen presentation and increasing pH in lysosomes of immune cells
- Daily dose
- Side effects - nightmares, reduced visual acuity (macular toxicity), liver toxicity, skin pigmentation, headache, nausea, muscle pain, rash
- Monitoring requirements - ocular after 5 years
- Safe in pregnancy
Second, third and fourth line management RA
- Second line - combination of two conventional DMARDs
- Third - methotrexate plus biological therapy, usually TNF inhibitor
- Fourth - methotrexate plus rituximab
Options of biological DMARDs for RA and examples of each
- Anti-TNF - adalimumab, inflixumab, etanercept, golimumab, certolizumab pegol
- Anti-CD20 - rituximab
- Anti-IL6 - sarilumab
- Anti-IL6 receptor - tocilizumab
- JAK inhibitors - tofacitinib, baricitinib
Criteria for commencing biologic therapy in RA
British society rheumatology/NICE guidelines
* Failed on at least two conventional DMARDs, one of which must be methotrexate unless contraindicated
* Severe disease - DAS28 >5.1 on at least two occasions one months apart
* Continue only if adequate response within first six months, defined as reducting in DAS-28 of >1.2
Screening required before commencing bDMARDs
- Viral hepatitis and HIV (including anti-core Ab)
- Varicella
- CXR and IGRA (TB)
- Vaccination - influenza, pneumococcal
Contraindications to bDMARDs
- Active infection
- Active or latent TB
- Pregnancy
- Malignancy
- Diverticular disease (IL-6)
Monitoring required for bDMARDs
- Infections
- Malignancy
- Bloods (FBC, LFTs)
- Awareness with vaccination
Side effects of anti-TNF drugs
- Vulnerability to severe infections and sepsis
- Reactivation of TB and hepatitis B
Side effects of rituximab
- Vulnerability to severe infections and sepsis
- Night sweats
- Thrombocytopaenia (low platelets)
- Peripheral neuropathy
- Live and lung toxicity
Describe the types of tissues which make up bones
Cortical (compact/tubular) bone
* Shafts of long bones
* Slow turnover rate
* Stiffer, more resistant to torsion and bending
Cancellous (spongey/trabecular) bone
* Ends of long bones, cuboidal/flat bones
* Higher turnover rate, more remodelling
* More elastic
Matrix - organic (collagen, proteins) and inorganic (calcium, phosphorus)
Cells - osteoprogenitor, osteocytes, osteoblasts, osteoclasts
Describe the sections of bones and how these differ in adults vs children
- Epiphysis - end of bone
- Diaphysis - shaft, where nutrient artery enters bone
- Metaphysis - transitional flared area between diaphysis and epiphysis
- Physis (growth plate) - in children only, between metaphysis and epiphysis
List the types of fracture healing and when these occur
- Indirect healing (secondary) - more common, no anatomical reduction or rigid stabilisation, more similar to endochondral bone formation with fibrocartilaginous soft callus –> bony hard callus then osteoclastic remodelling
- Direct healing (primary)- when bone fragments are ‘artificially’ fixed together (surgically) with compression, no callus formation just new bone formation through osteoblastic formation and osteoclastic resorption
List the stages of indirect fracture healing
Inflammation –> repair –> remodelling
1. Fracture haematoma and inflammation (6-8 hours post-injury) - blood from broken vessels form clot, swelling and inflammation at fracture site
2. Fibrocartilage (SOFT) callus (3 weeks post-injury) - granulation tissue formed, fibroblasts and osteogenic cells produce collagen, chondrocytes begin to produce fibrocartilage which gives stability
3. Bony (HARD) callus (3-4 months post-injury) - osteoblasts make woven bone
4. Bone remodelling - osteoclasts remodel woven bone –> compact and trabecular bone
Describe the role of movement in fracture healing
- Movement and weight bearing are important in healing - bone laid down in relation to stress put across it
- A degree of movement desirable but excessive movement disrupts healing tissue and affects cellular differentiation (stabilisation useful)
Describe the process of direct fracture healing
- Direct formation of bone without callus formation
- Inflammation –> formation of bone via osteoclastic absorption and obsteoblastic formation via cutting cones at fracture site
- Initially randomly laid down then remodelled
Describe the stages of X-ray findings seen during normal fracture healing
- Widened fracture line (10-14 days) - blurring of fracture ends, finding in both normal and abnormal healing (should narrow in normal healing)
- Callus formation (2 weeks) - initially immature, fluffy, indistinct –> dense, organised, bridges, ossified, endosteal callus obliterates the fracture line
- Radiologic union - mature external bridge callus across fracture, very variable time depending on fracture site
What factors influence callus size during fracture healing?
Increased
* Larger bones
* Diaphyseal fracture
* More motion - cast vs surgical fixation
* Comminution
* Infection
* Steroids
Decreased
* Smaller bones
* Metaphyseal fracture
* Impaction
* Rigid fixation
When is a fracture ‘healed’?
Fracture union - clinical diagnosis
* No tenderness at fracture site
* No motion at fracture site
* Stable - weightbearing without support
(Identifiable before radiologic union - too little bridging bone to see on X-ray)
Radiologic union - much later
* Continuous external bridge mature callus
* Re-established medullary space
List the factors which influence the rate of fracture healing
- Local soft tissue trauma
- Fragment vascularity
- Patient age
- Method of treatment - rigid fixation heal faster
- Fracture gap
- Motion - longer if moving
- Infection
- Underlying bone disease
- Intra-articular fracture slower (synovial fluid slows new bone formation)
- Steroids
Define disuse atrophy in fracture healing
- Acute osteoporosis which occurs as a result of normal fracture healing
- At and distal to fracture site
- Occurs 5-7 weeks after immobilisation
- Reversal takes 4+ weeks
- Risk of fragility fractures esp. in elderly
Define compound fracture and describe the mechanisms of compound fractures
Open fracture - skin overlying fracture is broken, allowing communication between the fracture and external environment
Compound from within (inside-out)
* Broken end of bone breaks through or pierces the skin
Compound from without (outside-in)
* External violence causes laceration or tissue trauma
* Higher likelihood of contamination
Classification system for open fractures
Gustillo-Anderson classification
* Type 1 - <1cm
* Type 2 - 1-10cm, >1cm wound with moderate soft tissue damage
* Type 3 - >10cm or high energy, extensive soft tissue damage (or segmental fractures, extensive contamination, high velocity injuries)
* 3A - adequate tissue for coverage
* 3B - extensive periosteal stripping, requires flap (inadequate soft tissue coverage)
* 3C - vascular injury requiring vascular repair
Scoring system for type 3C open fractures
Mangled extremity severity system (MESS)
* Limb ischaemia - time (>6 hours) and clinical signs (pulse, temperature, sensation)
* Patient age (<30, 30-50, >50)
* Shock - hypotension
* Injury mechanism - low - very high energy
Complications of open fractures
- Soft tissue infection
- Osteomyelitis
- Tetanus
- Crush syndrome - traumatic rhabdomyolysis (shock and kidney failure after crushing of skeletal muscle)
- Skin loss
- Non-union
- Amputation
Describe the emergency management of open fractures
BOAST guideline
* Control bleeding
* Remove gross debris
* Cover with sterile dressing - photograph before so dressing can stay on until definitive management in theatre
* Realignment and splinting
* IV antibiotics
* Tetanus prophylaxis
* Assessment of vascular and neurological status - repeat systematically, especially after reduction/splinting
* Imaging - may require trauma CT, angiography
Describe the definitive management of open fractures
- Debridement using fasciotomy lines for wound extension - timing dependant on level of contamination of wound (e.g. immediately if agricultural, sewage)
- Irrigation - 6L saline
- ?Delayed primary amputation
- Stabilisation - often requires external fixator
- Multidisciplinary approach - orthropaedic, plastics, rehabilitation
How do clavicle fractures usually occur?
What is the most common location of clavicle fracture? Why?
- Fall onto outstretched hand
- Direct blow to shoulder
- Middle third/midshaft is most easily fractured - thinnest with no ligamentous/muscle attachments
- Middle 1/3 - 80%
- Lateral 1/3 - 15%
- Medial 1/3 - 5%
Describe the management of clavicle fractures
- Usually conservative - depends on location, shortening, displacement, patient fractures
- Conservative management - immobilisation with simple triangular sling, analgesia
- If more than 2cm of shortening, lateral, comminuted/Z pattern - may need open reduction with internal fixation (ORIF)
What are the potential complications of clavicle fractures?
- Delayed union
- Malunion
- Non-union
- Palpable bump
- Stiffness
- Infection
- Palpable metalwork
Which X-ray views should be used for suspected clavicular fractures?
- Frontal (AP)
- Cephalic tilt (15-45 degree)
How should clavicle fractures be described radiologically?
Fracture
* Location of fracture along shaft
* Angulation and fracture end displacement (including direction)
* Comminution
* Degree of overlap - measure
Associated findings and relevant negatives
* Acromioclavicular joint and sternoclavicular joint alignment
* Coracoclavicular distance
* Glenohumeral joint
Associated traumatic injuries
* Rib fractures
* Vertebral fractures
* Scapular fractures - floating shoulder
* Pneumothorax
Describe the types of shoulder dislocation, the mechanisms of injury which cause them and their prevalence
- Anterior (>90%) - head of humerus moves anteriorly in relation to glenoid cavity
- Occurs when arm if forced posteriorly while abducted and extended at the shoulder, trauma e.g. fall on an outstretched arm, sports injuries
- Posterior (2-4%) - associated with uncoordinated muscle contraction e.g. seizure or electric shock
- Inferior (luxatio erecta, <1%) - high-energy, hyperabduction force to arm
Describe the clinical presentation of shoulder dislocations
- Present acutely after injury - usually aware of dislocation
- Severe pain and restriction of movement of shoulder
- Prominent acromion, shoulder flattened (loss of symmetrical roundness), prominent humeral head, arm slighly abducted, elbow flexed, forearm internally rotated and supported by other hand
- Empty glenoid fossa - palpable dent where head of humerus should be
- Inferior dislocation - arm fixed, abducted, overhead position
What is the most commonly dislocated large joint?
Shoulder - approximately 50%
Injuries associated with shoulder dislocations
Damage to the glenoid labrum - rim of cartilage around glenoid cavity which creates deeper socket for head of humerus
* Bankart lesions - tears to anterior labrum, occurs with repeated anterior subluxations or dislocations
- Hill-Sachs lesions - compression fractures of posterolateral part of head of humerus when shoulder dislocates anteriorly, makes shoulder less stable and at risk of further dislocations
- Axillary nerve damage - loss of sensation in ‘regimental badge’ area over lateral deltoid, motor weakness in deltoid and teres minor muscles
Fractures
* Humeral head
* Greater tuberosity of humerus
* Acromion of scapula
* Clavicle
- Rotator cuff tears - especially in older patients
- Brachial plexus injuries
Which imaging techniques are used in shoulder dislocation?
Xray - may not be required before reduction
* Frontal (AP)
* Y-view (lateral)
* Axillary film, arm abducted at 70-90 degrees, taken from angle of 45 degrees through axilla - for posterior dislocation
MRI arthrogram
* MRI with contrast injected into shoulder joint
* To assess soft tissue damage e.g. Bankart and Hill-Sachs lesions
Arthroscopy - camera into joint to visualise structures
Special test used to assess for shoulder instability
Apprehension test - shoulder instability, often positive after previous anterior dislocation or subluxation
Shoulder abducted to 90 degress, elbow flexed to 90 degrees, shoulder externally rotated while watching patient
Patient will be anxious/apprehensive if unstable shoulder
Define subluxation
Partial dislocation of joint
Shoulder dislocation appearance on X-ray
Anterior
* AP view - humeral head lies medial and inferior to glenoid fossa
* Lateral view - humeral head anterior and inferior to glenoid fossa
* Humeral head also inferior to coracoid process
Posterior
* AP view - glenohumeral joint widened and humeral head has ‘light bulb’ appearance due to forced internal rotation of humerus
* Lateral view - humeral head posterior to glenoid fossa
What are the roots of the brachial plexus?
Anterior rami of spinal nerves C5, 6, 7, 8 and T1
Describe the path of the brachial plexus and its divisions
- Roots leave spinal cord via intervertebral foramina of vertebral column
- Pass between anterior and medial scalene muscles to enter the base of the neck
- Roots converge at base of neck to form trunks - superior (C5 + 6), middle (C7), inferior (C8 + T1)
- Trunks cross posterior triangle of neck
- Trunks divide into anterior and posterior divisions, leave the posterior triangle and pass into axilla
- Anterior and posterior divisions combine to form three cords named by position relative to axillary artery
- Lateral cord - anterior division of superior trunk, anterior division of middle trunk
- Posterior cord - posterior divisions of superior, middle and inferior trunk
- Medial cord - anterior division of inferior trunk
- Major branches - musculocutaneous nerve, axillary nerve, median nerve, radial nerve, ulnar nerve
Roots, motor functions, sensory functions of musculocutaneous nerve
- Roots - C5, 6, 7 –> superior + middle trunks –> lateral cord
- Motor functions - brachialis, biceps brachii, coracobracialis (elbow/shoulder flexion)
- Sensory functions - gives off lateral cutaneous branch of forearm, innervates lateral half of anterior forearm and small lateral portion of posterior forearm
Axillary nerve roots, motor function, sensory function
- Roots - C5 + 6 –> superior trunk –> posterior cord
- Motor function - teres minor and deltoid muscles, abduction (15-90 degrees), flexion, extension and rotation of shoulder
- Sensory function - gives off superior lateral cutaneous nerve, innervates inferior deltoid region (regimental badge area)
Median nerve - roots, motor functions, sensory functions
- Roots - C6, 7, 8 and T1 –> superior, middle and inferior trunks, lateral and medial cords
- Motor functions - most flexor muscles of forearm, thenar muscles, lateral lumbricals associated with index and middle fingers (wrist and 2rd and 3rd digit flexion, thumb opposition and flexion, pronation)
- Sensory functions - gives off palmar cutaneous branch which innervates lateral palm and digital cutaneous branch which innervates the lateral three and a half fingers on the palmar surface of the hand
Radial nerve - roots, motor functions, sensory functions
- Roots - C5, 6, 7, 8, T1 –> superior, middle and inferior trunks –> posterior cord
- Motor functions - triceps brachii, muscles in posterior compartment of forearm (extension of elbow and wrist)
- Sensory functions - posterior of arm and forearm, posterolateral aspect of hand, proximal half of posterior thumb, index finger and lateral half of middle finger
Ulnar nerve - roots, motor functions, sensory functions
- Roots - C8 + T1 –> inferior trunk –> medial cord
- Motor function - muscles of hand (except thenar muscles and two lateral lumbricals), flexor carpi ulnaris and medial half of flexor digitorum profundus (abduction of fingers, flexion of medial digits, adduction of thumb)
- Sensory function - anterior and posterior surfaces of medial one and a half fingers and associated palm area
Describe the clinical assessment of shoulder dislocations
Assess for
* Fractures
* Vascular damage - pulses, CRT, pallor
* Nerve damage - loss of sensation in regimental patch area (axillary nerve damage)
Describe the emergency management of shoulder dislocations
- Relocate/reduce shoulder as soon as safely possible - muscle spasm which occurs over time makes it harder to relocate and increases risk of neurovascular injury during relocation
- Various methods of closed reduction
- Relocation usually done in ED
- Exclude fractures before reduction
- Analgesia, muscle relaxants and sedation used during relocation as appropriate, gas and air may be used
- Broad arm sling used to support arm after relocation
- X-ray performed post-reduction to ensure success
- Immobilisation after reduction
- May require surgical management
Indications for surgical management of shoulder dislocation
- Unsuccessful closed reduction
- Displaced Bankart lesion
- Recurrent shoulder dislocations
- If young and active early surgery may be required to prevent recurrent dislocations in the future
Follow-up required for shoulder dislocations
- High risk of recurrent dislocations, especially in young patients
- Physiotherapy to reduce risk of further dislocations
- May require shoulder stabilisation surgery - prolonged recovery peroid (3+ months)
Risk factors for proximal humerus fractures
- Elderly - >65
- F>M
- Osteoporosis
- High energy trauma
Classification of proximal humerus fractures
Neer classification - describes the number of fracture parts and their displacement
Parts:
* Articular surface (humeral head)
* Greater tuberosity
* Lesser tuberosity
* Humeral shaft
Displacement for each part if
* >1cm
* 45 degree angulation
What is the anatomical vs surgical neck of the humerus? What are their significances in proximal humeral fractures?
- Anatomical - residual epiphyseal plate, oblique angle, divides the head of the humerus from the greater and lesser tubercles
- Rare to have fractures through anatomical neck, if displaced by >1cm risk of avascular necrosis to the humeral head
- Surgical - distal to greater tubercle and lesser tubercle, proximal to deltoid tuberosity
- Most proximal humerus fractures through surgical neck (in children most common is greensick fracture through surgical neck)
Mechanism of injury of proximal humerus fractures
- Older patients - fall on an outstretched hand
- Younger patients - high-energy trauma
Proximal humeral fractures presentation
- Pain and swelling
- Decreased motion
- Ecchymosis of chest, arm and forearm
How are proximal humeral fractures assessed?
Neurovascular examination
* Axillary nerve injury most common - determine deltoid muscle function and lateral shoulder sensation
* Arterial injury may be masked by extensive collateral circulation preserving distal pulses
Examine for concomitant chest wall injuries
X-rays - AP of scapula and glenohumeral joint (Grashey), axillary view, lateral Y view of scapula
Sometimes requires CT, rarely MRI for soft tissue injury
Management of proximal humeral fractures
Conservative - sling immobilisation followed by progressive rehabilitation:
* Minimally displaced
* <2 parts
* Not a surgical candidate
* Severely comminuted, 4 parts
Open reduction, internal fixation
* 2 parts, displaced
* Greater tuberosity displaced >5mm
* 3/4 parts in young patient
Arthroplasty
* Hemiarthroplasty - young patient with fracture not suitable for fixation (poor outcomes)
* Reverse shoulder replacement - unable to fix and rotator cuff defunctioned due to tuberosity involvement
Complications of proximal humerus fractures
- Decreased ROM
- Pain
- Non-union
- Axillary nerve palsy
Describe the mechanism of injury of humeral shaft fractures
Bimodal distribution
* Young - high energy trauma
* Elderly - osteopaenic, low energy
Describe the classification of humeral shaft fractures
Location
* Proximal
* Middle
* Distal 1/3
Pattern
* Spiral
* Transverse
* Comminuted
Holstein-Lewis
* Spiral fracture of the distal 1/3 of shaft associated with radial nerve palsy
Assessment of humeral shaft fractures
- Examine limb alignment - shortening and varus deformity
- Pre-operative/reduction neurovascular exam is critical - examine and document status of radial nerve pre- and post-reduction
- X-ray - AP and lateral
Management of humeral shaft fracture
- Usually conservative with humeral brace
- Open reduction, internal fixation - open, vascular injury, plexus injury, forearm fracture (floating elbow), polytrauma
- Radial nerve palsy - only an indication for surgery if palsy occurs after an intervention or manipulation of the fracture
Which fracture is associated with radial nerve palsy?
Humeral shaft - especially middle and middle-distal parts
Transverse and spiral fractures more likely to be associated with radial nerve palsy than oblique and comminuted patterns of fracture
Radial head fracture mechanism of injury
Fall onto outstretched hand with pronated forearm
Injuries associated with radial head fracture
- Lateral collateral ligament injury (up to 80%)
- Medial collateral ligament injury
- Essex-Lopresti injury - radial head fracture, distal radioulnar joint injury, interosseus membrane injury
- Coronoid fracture
- Olecranon fracture
- Monteggia fracture/dislocation
- Scaphoid fracture
Classification of radial head fracture
Mason types 1-4
* Type 1 - non-displaced or minimally displaced (<2mm), no mechanical block to rotation
* Type II - displaced >2mm or angulated, possible mechanical block to forearm rotation
* Type III - comminuted and displaced, mechanical block to motion
* Type IV - radial head fracture with associated elbow dislocation
Things to look for in hand + wrist examination
- Scars - traumatic, carpal tunnel
- Swelling e.g. ganglions
- Skin colour - erythema, rashes
- Nails - pitting, onycholysis, nail fold infarction
- Muscle wasting - thenar, hypothenar and interosseous
- Skin thinning or bruising - steroids
- Psoriatic plaques
- Deformity - Z-thumb, swan neck, Boutonnieres, mallet finger, ulnar drift, clawed hand
- Elbows - psoriatic plaques, rheumatoid nodules
Hand and wrist examination - things to feel
- Temperature
- Radial and ulnar pulses
- Capillary refill time
- Thenar and hypothenar eminence muscle bulk
- Palmar thickening - Dupuytren’s
- Joint palpation - distal radio-ulnar joint, radio-carpal joint, thumb CMC, MCP, IPJ
- MCP joint squeeze
- Anatomical snuffbox - scaphoid fracture
- Radial nerve sensation - first dorsal webspace
- Median nerve sensation - thenar eminence
- Ulnar nerve sensation - hypothenar eminence
Movements for hand and wrist examination
Active
* Finger extension and flexion
* Finger abduction and adduction
* Wrist extension and flexion
* Pronation and supination
* Thumb flexion and extension
* Thumb abduction and adduction
* Pronation and supination
Passive if active reduced
Screening test for radial, ulnar and median nerve
* Wrist and finger extension against resistance - radial
* Index finger abduction against resistance - ulnar
* Thumb abduction against resistance - median
Special and function tests hand and wrist examination
- Power grip
- Pincer grip
- Pick up a small object
- Tinel’s test - tap over carpal tunnel, tingling/pain in distributation of median nerve = carpal tunnel syndrome
- Phalen’s test - wrist in forced flexion, tingling or pain in median nerve distribution = carpal tunnel syndrome
- Tinel’s test at elbow - tap over ulnar nerve behind medial epicondyle, tingling and pain over ulnar distribution = ulnar compression
Things to look for in elbow examination
- Cubitus valgus/varus
- Scars - operative or traumatic
- Bruising
- Swelling - effusion, inflammatory arthropathy, dislocation
- Muscle wasting
- Rheumatoid nodules
- Psoriatic plaques
- Popeye sign - ruptured biceps tendon
Feel - elbow examination
- Temperature
- Palpate joints - proximal radio-ulnar joint, ulno-trochlear joint, radial head, radiocapitellar joint, lateral (Tennis) and medial (Golfer) epicondyle of humerus, olcecranon
- Biceps tendon
- Bend to 90 degrees to look for effusion
Move - elbow examination
Active and passive
* Elbow flexion/extension
* Pronation/supination
* Feel for crepitus
Elbow examination special tests
- Medial epicondylitis (Golfer’s elbow) - active wrist flexion against resistance, palpate medial epicondyle
- Lateral epicondylitis (Tennis elbow) - active wrist extension against resistance, palpate lateral epicondyle
- Can hand reach mouth
Articulations of the scapula
- Glenohumeral joint - glenoid fossa of scapula and head of humerus
- Acromioclavicular joint - acromion of scapula and clavicle
Articulations of the humerus
- Glenohumeral joint - head of of the humerus with glenoid fossa of the scapula
- Elbow joint - capitulum articulates with head of the radius and trochlea articulates with the trochlear notch of the ulna
Articulations of the ulna
- Trochlear notch of ulna articulates with trochlea of humerus
- Proximal radio-ulnar joint - radial head and radial notch of ulna
- Distal radio-ulnar joint - distally the ulnar head articulates with the ulnar notch of the radius
Articulations of the radius
- Elbow joint - head of radius articulates with capitulum of the humerus
- Proximal radioulnar joint - radial head and radial notch of ulna
- Wrist joint - distal radius and carpal bones (scaphoid and lunate
- Distal radioulnar joint - articulation between ulnar notch and head of the ulna
List the bones of the hand
- Carpal bones (proximal) - 8
- Metacarpals - 5 (one per digit)
- Phalanges (distal) - three per finger (proximal, middle, distal), two per thumb (proximal and distal)
Describe the arrangement of the carpal bones
Proximal bones (lateral to medial)
* Scaphoid
* Lunate
* Triquetrum
* Pisiform
Distal bones (lateral to medial)
* Trapezium
* Trapezioid
* Capitate
* Hamate
List the rotator cuff muscles
- Supraspinatus
- Infraspinatus
- Teres minor
- Subscapularis
Describe the attachments of the rotator cuff muscles
- Supraspinatus - supraspinous fossa of the scapula to greater tubercle of the humerus
- Infraspinatus - infraspinous fossa of scapula to greater tubercle of humerus
- Subscapularis - subscapular fossa of scapula to lesser tubercle of humerus
- Teres minor - posterior surface of scapula to greater tubercle of humerus
Deltoid muscle attachments
Lateral third of the clavicle, acromion and spine of the scapula –> deltoid tuberosity on the lateral aspect of the humerus
Innervations of the deltoid muscle
Axillary nerve
Main actions of the deltoid muscle
Shoulder abduction - >15 degres
Shoulder flexion and extension
Shoulder medial and lateral rotation
Teres minor attachments
Posterior surface of the inferior angle of the scapula –> medial lip of the intertubercular groove of the humerus
Teres major actions
- Medial rotation
- Adduction
- Extension of flexed arm
Teres major innervation
Lower subscapular nerve
Supraspinatus actions
Abducts arm 0-15 degrees, assists deltoid beyond 15 to 90
Supraspinatus innervation
Subprascapular nerve
Infraspinatus actions
Lateral rotation
Infraspinatus innervation
Suprascapular nerve
Subscapularis actions
Medial rotation
Subscapularis innervation
Upper and lower subscapular nerves
Teres minor actions
Laterally rotates arm
Teres minor innervation
Axillary nerve
Pectoralis major attachments
- Clavicular head - anterior medial clavicle
- Sternocostal head - anterior surface of the sternum, superior six costal cartilages, aponeurosis of the external oblique muscle
- Distally - intertubercular sulcus of the humerus
Pectorialis major actions
Adducts and medially rotates arm
Draws scapula anteroinferiorly
Clavicular head - arm flexion
Innervation of the pectoralis major
Lateral and medial pectoral nerves
Pectoralis minor attachments
3rd-5th ribs, inserts into coracoid process of scapula
Pectoralis minor action
Stabilises scapula, draws it anteroinferiorly against thoracic wall
Pectoralis minor innervation
Medial pectoral nerve
Serratus anterior attachments
- Lateral aspects of ribs 1-8
- Attach to costal surface of the medial border of the scapula
Serratus anterior actions
Rotates scapula to allow arm to be raised above 90 degrees
Holds scapula against ribcage
Serratus anterior innervation
Long thoracic nerve
Subclavius muscle attachments
- Junction of 1st rib and its costal cartilage, inserts onto inferior surface and middle third of clavicle
Subclavius action
Anchors and depresses the clavicle
Subclavius innervation
Nerve to subclavius
What is the clinical impact of long thoracic nerve damage? What kind inuries can cause this?
Winged scapula - loss of serratus anterior muscle anchoring
Usually from traction injuries - upper limb stretched violently
Axillary lymph node clearance (e.g. breast cancer) can also cause
Borders of the axilla
- Apex - lateral border of 1st rib, superior border of scapula, posterior border of clavicle
- Lateral - intertubercular groove of the humerus
- Medial - serratus anterior and thoracic wall (ribs and intercostals)
- Anterior - pectoralis major, underlying pectoralis minor and subclavius muscles
- Posterior - subscapularis, teres major, latissimus dorsi
Contents of the axilla
- Axillary artery
- Axillary vein - cephalic and basilic veins drain into
- Brachial plexus
- Axillary lymph nodes
- Biceps brachii (short head) and coracobrachialis
List the extrinsic muscles of the shoulder/superficial back muscles
Superficial
* Trapezius
* Latissimus dorsi
Deep
* Levator scapulae
* Rhomboid major
* Rhomboid minor
Trapezius attachments, actions, innervation
- Attachments - skull, nuchal ligament, spinous processes of C7-T12 –> clavicle, acromion, scapula spine
- Actions - upper fibres elevate and rotate scapula during abduction of arm, middle fibres retract scapula, lower fibres pull scapula inferiorly
- Innervation - accesory nerve, proprioception from C3/4
Latissimus dorsi attachments, actions, innervation
- Atachments - spinous processes of T7-T12, iliac crest, thoracolumbar fasci and inferior three ribs –> intertubercular sulcas of humerus
- Actions - extends, adducts and medially rotates arms
- Innervation - thoracodorsal nerve
Levator scapulae attachments, actions, innervation
- Attachments - transverse processes of C1-4 –> medial border of scapula
- Actions - elevates scapula
- Innervation - dorsal scapular nerve
Rhomboid major attachments, actions, innervation
- Attachments - spinous processes T2-5 –> medial border of scapula
- Actions - retracts and rotates scapula
- Innervation - dorsal scapular nerve
Rhomboid minor attachments, actions, innervation
- Attachments - spinous processes C7-T1, attaches to medial border of scapula at level of spine of scapula
- Actions - retracts and rotates the scapula
- Innervation - dorsal scapular nerve
List the muscles of the upper arm and describe their innervation and blood supply
Anterior compartment
* Muscles - biceps brachii, brachialis, coracobrachialis
* Innervation - musculocutaneous nerve
* Blood supply - brachial artery
Posterior compartment - triceps brachii
* Innervation - radial nerve
* Blood supply - profunda brachii artery
Biceps brachii attachments and function
- Attachments - long head from supraglenoid tubercule of scapula, short head from coracoid process of the scapula –> radial tuberosity and fascia of forearm via bicipital aponeurosis
- Function - supination, flexion at elbow and shoulder
Which spinal nerve does the biceps tendon reflex test?
C6
Coracobrachialis attachments and function
- Coracoid process of scapula –> medial humerus shaft
- Function - flexion of arm at shoulder, weak adduction
Brachialis attachments and function
- Medial/lateral humeral shaft –> ulnar tuberosity
- Function - flexion at elbow
Triceps brachii attachments and function
- Long head from infraglenoid tubercle
- Lateral head from humerus, superior to radial groove
- Medial head from humerus, inferior to radial groove
- Converge and insert into olecranon of ulna
Which spinal nerve is tested by the triceps reflex?
C7
List the muscles of the anterior compartment of the forearm and describe their action and innervation
- Superficial - flexor carpi ulnaris, palmaris longus, flexor carpi radialis, pronator teres
- Intermediate - flexor digitorum superficialis
- Deep - flexor pollicis longus, flexor digitorum profundus, pronator quadratus
Pronation, flexion of wrist and fingers
Innervated by median nerve except flexor carpi ulnaris, medial half of flexor digitorum profundus (ulnar nerve)
List the muscles of the posterior compartment of the forearm, describe their action and innervation
- Superficial - brachioradialis, extensor carpi radialis longus and brevis, extensor digitorum communis, extensor digiti minimi, extensor carpi ulnaris, anconeus
- Deep - supinator, abductor pollicis longus, extensor pollicis brevis, extenor pollicis longus, extensor indicis
Generally - extension of wist and fingers
* Brachioradialis - flexion at elbow
* Abduction/adduction of wrist/thumb
* Supination
All innervated by the radial nerve
What causes wrist drop?
Damage to the radial nerve proximal to the elbow - loss of extensor muscle innervation
* Axilla - humeral dislocations or fractures of the proximal humeus
* Radial groove of humerus - humeral shaft fracture
What is the origin point of the muscles of the posterior compartment of the forearm vs anterior compartment of the forearm?
Posterior compartment - lateral epicondyle of the humerus
Anterior compartment - medial epicondyle of the humerus
List the instrinsic muscles of the hands and describe their innervation and actions
(Action of those whose names don’t describe them)
- Thenar muscles - opponens pollicis, abductor pollicis brevis, flexor pollicis brevis (median nerve)
- Hypothenar muscles - opponens digiti minimi, abductor digiti minimi, flexor digiti minimi brevis (ulnar nerve)
- Lumbricals - flexion at MCP, extension at IP joints, lateral two lumricals innervated by median nerve, medial two lumbricals innervated by ulnar nerve
- Interossei - dosal and palmar (dorsal do abduction, palmar do adduction), both innervated by ulnar nerve
- Palmaris brevis - grip (ulnar nerve)
- Adductor pollicis - adducts thumb (ulnar nerve)
Describe the blood supply to the arm
- Subclavian artery –> axillary artery –> brachial artery –> radial and ulnar arteries –> superficial and deep palmar arches
- Superficial veins - cephalic vein + basilic vein (connected by median cubital vein) –> axillary vein –> subclavian vein
- Deep veins - ulnar veins + radial veins –> brachial vein –> axillary vein –> subclavian vein
Shoulder examination - look
- Scars - operative / traumatic
- Asymmetry
- Swelling
- Muscle wasting - deltoid, trapezius, supraspinatus, infraspinatus
- Winged scapula - push hands against wall
Shoulder examination - feel
- Temperature
- Palpate joints - sternoclavicular joint, clavicle, acromioclavicular joint, acromion, coracoid process, head of humerus, greater and lesser tubercle of humerus, spine of scapula
Shoulder examination - move
Compound movements (screening)
* Arms behind head - external rotation and abduction
* Arms behind back, reach up - internal rotation an adduction
Active movement
* Shoulder flexion/extension
* Shoulder abduction/adduction
* Internal rotation
* External rotation
* Abduct and palpate scapula for smoothness of scapular movement
Passive movement - feel for crepitus
Shoulder examination - special tests
Supraspinatus
* Supraspinatus assessment (empty can test/Jobe’s test) - abduct to 90 degrees, angle forwards at 30 degrees, point thumb to floor, push down on arm (abduction against resistance)
* Impingement - painful arc, pasively move to maximum abduction, pain from 60-120 degrees
Infraspinatus/teres minor
* External rotation against resistance
* External rotation in abduction - 90 degree abduction, bend elbow to 90 degress, passively externally rotate shoulder (inability to maintain = Hornblower’s sign)
Subscapularis
* Internal rotation against resistance - hand behind back, press against hand while lifting off back
Acromioclavicular joint
* Scarf test - flex shoulder to 90, place hand on contralateral shoulder, apply resistance to elbow in contralateral direction
Hip examination - look
- Scars
- Swelling
- Asymmetry
- Quadriceps, gluteal wasting
- Leg length discrepancy
- Pelvic tilt
- Flexion abnormalities
- Gait - ROM, limping, leg length, turning, waddling, Trendelenburg’s gait
Hip examination - feel
- Temperature
- Palpate joint - greater trochanter
- Leg length assessment - apparent (umbilicus to medial malleolus), true (ASIS to medial malleolus)
Hip examination - move
Active
* Flexion
* Extension
Passive
* Flexion
* Internal rotation
* External rotation
* Abduction
* Adduction
* Extension
Hip examination - special tests
- Thomas’s test - for fixed flexion deformity, lie flat with hand under lumbar spine, passively flex other hip and observe contralateral hip
DON’T DO IF HAVE HIP REPLACEMENT - DISLOCATION RISK) - Trendelenburg’s test - for hip abductor weakness, stand with hands on shoulders, fingers on iliac crests, stand on one leg and observe for lateral pelvic tilt
Knee examination - look
- Scars
- Swelling
- Psoriasis plaques
- Valgus (apex medial) or varus (apex lateral)
- Quadriceps wasting
- Hyperextension or fixed flexion deformity
- Popliteal swellings
- Patellar position
- Gait - ROM, limping, leg length, turning, high stepping
Knee examination - feel
- Temperature
- Measure quadriceps bulk
- Palpation of extended knee - patella, patellar ligament, medial and lateral joint lines
- Assess for effusion - patellar tap, sweep test
- Palpation of flexed knee - patella, patellar ligament, medial and lateral joint lines, tibial tuberosity, popliteal fossa
Knee examination - move
Active
* Flexion
* Extension
Passive
* Flexion
* Extension
Knee examination - special tests
Cruciate ligament assessment
* Posterior sag sign - PCL
* Anterior drawer test - ACL
* Posterior drawer test - PCL
* Lachman’s test - ACL
Collateral ligament assessment
* Varus stress test - LCL
* Valgus stress test - MCL
* Can repeat if stable with knee flexed to 30 degrees
Mensci assessment
* McMurray’s test - medial meniscus, lateral meniscus
Foot and ankle examination - look
- Gait - ROM, limping, leg length, turning, height of steps
- Scars
- Swelling
- Psoriasis plaques
- Fixed flexion deformity of toes
- Big toe misalignment
- Calluses
- Foot arch
- Heel - valgus or varus
- Muscle wasting
- Achilles tendon
Ankle and foot examination - feel
- Temperature
- Pulses - posterior tibial, dorsalis pedis
- MCP joint squeeze
- Ankle and foot palpation - metatarsal and tarsal bones, tasral joint, ankle joint, subtalar joint, calcaneum, medial/lateral malleoli, distal fibula
- Achilles tendon and gastrocnemius
Ankle and foot examination - move
Active + passive
* Plantarflexion
* Dorsiflexion
* Toe flexion
* Toe extension
* Ankle/foot inversion
* Ankle/foot eversion
Passive only
* Subtalar joint
* Midtarsal joint
Ankle and foot examination - special tests
- Simmonds’ test - achilles tendon rupture
Spine examination - look
- Scars
- Muscle wasting
- Scoliosis
- Asymmetry
- Pelvic tilt
- Gait - ROM, limping, leg length, turning, Trendeleburg’s gait, waddling gait
Spine examination - feel
- Spinal processes and sacroiliac joints
- Paraspinal muscles
Spine examination - move
- Cervical spine - flexion, extension, lateral flexion, rotation
- Lumbar spine - flexion, extension, lateral flexion
- Thoracic spine - rotation
Spine examination - special tests
- Schober’s test - 5cm below PSIS, 10cm above, should increase to >20cm
- Sciatic stretch test - straight leg raise
- Femoral nerve stretch test
Complications of septic arthritis
- Osteoarthritis
- Osteomyelitis
- Osteonecrosis
- Sepsis
Define neuropraxia
- Mildest form of traumatic peripheral nerve injury
- Focal segmental demyelination at site of injury without disruption of axon continuity
What causes neuropraxia?
Usually due to blunt injury - external blow, causes:
* Compression
* Ischaemia
* Inflammation
What signs/symptoms does neuropraxia cause?
- Motor/sensation deficit
- Numbness/tingling/burning
- Flaccid paralysis of muscles innervated by injured nerves/nerve
- Transient symptoms - usualy resolve days-weeks after injury
Define axonotmesis
- More severe than neuropraxia, less than neurotmesis
- Damage to axons and myelin sheath, endoneurium, perineurium and epineurium intact
What causes axonotmesis?
- More severe injury than neuropraxia - crush or sretch usually
Classification of peripheral nerve injuries
Seddon’s/Sunderland’s classification
First degree (class I)
* Neurapraxia - temporary interruption of conduction without loss of axonal continuity
* No Wallerian degeneration
* Full recovery within days to weeks
Second degree (class II)
* Axonotmesis - loss of relative continuity of axon and myelin, preservation of connective tissue framework of nerve
* Wallerian degeneration distal to site of injury
* Recovery possible without surgical treatment, although sometimes required
Third degree (class III)
* Neurotmesis - endoneurium lesion, epineurium and perineurium intact
* Wallerian degeneration distal to injury
* Surgical intervention often necessary
Fourth degree (class III)
* Same as third degree but only epineurium remain intact
* Surgical intervention necessary
Fifth-degree (class III)
* Same as third degree but complete transection of nerve
* No recovery without surgical treatment
Define Wallerian degeneration
Degeneration of the axon distal to an injury when nerve fibre is cut or crushed
Define neurotmesis
Nerve and nerve sheath severed
Signs and symptoms of neurotmesis
- Pain
- Dysesthesias
- Complete loss of sensory and motor function of the affected nerve
Describe a hemiplegic gait and list causes
- Hemiplegia = spastic flexion of the upper limb and extension of the lower limb, extended leg is elongated so patients have to circumduct leg to prevent foot from dragging on ground
- Caused by lesion in the CNS, resulting in unilateral weakness and spasticity
Causes
* Unilateral cerebral lesion - stroke, space-occupying lesion, trauma, multiple sclerosis
* Hemisection of the spinal cord - trauma
Clinical features associated with hemiplegic gait
- Increased tone ith clasp knife spasitcity
- Hyperreflexia withor without clonus
- Upgoing plantars i.e. positive Babinski
- Reduced power
- Sensory deficit - pattern of sensory loss depends on the site of the lesion in the nervous system
Define diplegic gait
- Similar to hemiplegic gait but bilateral in nature
- Spasticity worse in lower limbs compared with upper limb
- Hips and knees flexed and abducted and ankles are extended and internally rotated
- Knees forced together due to spasticity in adductor muscles resulting in leg overlap when walking (scissoring)
- Circumduction of both legs during swing phase
- Upper limb may have flexor posturing of the elbows and wrist with shoulders and fingers in adduction
- Lack swinging movements present in normal gait
Clinical features associated with biplegic gait
- Increased tone with clasp-knife spasticity
- Hyperreflexia with or without clonus
- Upgoing plantars (i.e. positive Babinski)
- Reduced power
- Sensory deficit – if a diplegic gait is caused by spinal cord pathology, the ‘sensory level’ (ie. the lowest dermatome level with normal sensation) correlates with the level of spinal cord pathology
- Wasting and fasciculations (consider motor neuron disease)
Causes of biplegic gait
Spinal cord lesion (sensation usually affected):
* Prolapsed intervertebral disc
* Spinal spondylosis
* Spinal tumour
* Transverse myelitis
* Spinal infarct
* Syringomyelia
* Hereditary spastic paraparesis
Bilateral brain lesion:
* Cerebral palsy
* Multiple sclerosis
* Bilateral brain infarcts
* Midline tumour (e.g. paraspinal meningioma)
* Motor neuron disease: associated with lower motor neuron findings
Describe the features of a Parkinsonian gait
- Initiation: typically slow to start walking due to failure of gait ignition and hesitancy.
- Step length: reduced stride length with short steps is common (shuffling gait). Each step may get progressively smaller as the patient attempts to retain balance (known as festinant gait).
- Arm swing: reduced arm swing on one or both sides (often an early feature of Parkinson’s disease).
- Posture: flexed trunk and neck causing a stooped appearance.
- Tremor: resting tremor can be observed when the patient is distracted by walking.
- Turning: impaired balance on turning or hesitancy is common due to postural instability.Initiation: typically slow to start walking due to failure of gait ignition and hesitancy.
Clinical features associated with Parkinsonian gait
Tremor
Rigidity
Bradykinesia
Hypomimia
Causes of Parkinsonian gait
- Idiopathic Parkinson’s disease
- Vascular Parkinson’s disease
- Dementia with Lewy bodies
- Parkinson’s plus syndromes (e.g. multisystem atrophy and progressive supranuclear palsy)
- Drug-induced Parkinsonism (e.g. antipsychotics, antiemetics)
- Dementia pugilistica
Describe an ataxic gait
- Stance: a broad-based ataxic gait is typically associated with midline cerebellar pathology (e.g. a lesion in multiple sclerosis or degeneration of the cerebellar vermis secondary to chronic alcohol excess).
- Stability: a staggering, slow and unsteady gait is typical of cerebellar pathology. In unilateral cerebellar disease, patients will veer towards the side of the lesion.
- Turning: patients with cerebellar disease will find the turning manoeuvre particularly difficult.
Clinical features associated with ataxic gait
Clinical features associated with cerebellar ataxia:
* Nystagmus
* Ataxic dysarthria
* Dysmetria
* Intention tremor
* Dysdiadokokinesia
Clinical features associated with sensory ataxia:
* Positive Romberg’s sign
* Impaired proprioception
* Impaired vibration sensation
* Absence of other cerebellar signs (e.g. dysmetria, nystagmus, dysarthria)
Clinical features associated with vestibular ataxia:
* Vertigo
* Nausea
* Vomiting
Causes of ataxic gait
Cerebellar ataxia:
* Cerebellar stroke (ischaemic or haemorrhagic)
* Space-occupying lesion
* Multiple sclerosis
* Alcoholism
* B12 deficiency
* Drugs (e.g. phenytoin, carbamazepine, barbiturates, lithium)
* Genetic disease (e.g. Frederich’s ataxia, spinocerebellar ataxia)
* Paraneoplastic disease
Sensory ataxia:
* Peripheral neuropathy (e.g. diabetes mellitus)
*
Vestibular ataxia:
* Labyrinthitis
* Meniere’s disease
* Acoustic neuroma
Describe a neuropathic gait
- Weakness of the dorsiflexors of the foot
- Causes foot drop and dragging of the toes during the swing stage
- To prevent toes dragging on the floor, knee and hip flex excessively, creating a ‘high stepping’ gait
Clinical features associated with neuropathic gait
Peripheral vascular disease
Peripheral sensory impairment
Distal muscle weakness
Reduced or absent reflexes
Causes of foot drop
- Isolated common peroneal nerve palsy (e.g. secondary to trauma or compression)
- L5 radiculopathy (e.g. disc prolapse)
- Generalized polyneuropathy involving multiple nerves (e.g. diabetic neuropathy, motor neurone disease, Charcot-Marie Tooth disease)
Describe a myopathic gait
Hip abductor weakness results in an inability to stabilize the pelvis during the stance phase. As a result, the pelvis tilts downwards towards the unsupported side during the swing phase of the gait cycle.
The body compensates to prevent the swinging foot from dragging by:
* Laterally flexing the torso away from the leg in swing phase; this draws the pelvis and leg up off the floor (causing the characteristic ‘waddling’ appearance)
* Circumducting the leg
Clinical features associated with myopathic gait
- Difficulty standing from a seated position without the use of the arms
- Difficulty standing from a squat or sitting up from a lying position
- Positive Trendelenburg’s sign; when the patient stands on one leg, the pelvis drops towards the contralateral side
Causes of myopathic gait
Systemic disease:
* Hyperthyroidism
* Hypothyroidism
* Cushing’s syndrome
* Acromegaly
* Polymyalgia rheumatica
* Polymyositis
* Dermatomyositis
Muscular dystrophies:
* Duchenne’s muscular dystrophy
* Becker’s muscular dystrophy
* Myotonic dystrophy
Describe a choreiform gait
Involuntary movements such as:
* Oro-facial dyskinesia (grimacing or lip-smacking)
* Choreic movements of the upper and lower limbs (writhing, dance like semi-purposeful movements)
The involuntary movements are usually present at rest, however, walking can accentuate the movements.
Causes of choreiform gait
Basal ganglia disease:
* Huntington’s disease
* Sydenham’s chorea
* Cerebral palsy (choreiform type)
* Wilson’s disease
* Dopaminergic medications (e.g. Parkinson’s medications)
Describe an antalgic gait
- Abnormal gait pattern which develops as a result of pain
- Typically the stance phase is reduced on the affected leg resulting in a limping appearance
Causes of antalgic gait
Any cause of lower limb pain such as:
* Osteoarthritis
* Inflammatory joint disease
* Lower limb fracture
* Nerve entrapment (e.g. sciatica)
List the common causes of an abnormal gait
- Lower limb pain - osteoarthrtitis, inflammatory joint disease etc.
- Neurological disease - Parkinson’s, peripheral neuropathy, stroke etc.
Define compartment syndrome
Critical pressure increase within a confined compartmental space, intra-compartmental pressure in a fascial compartment becomes elevated beyond the capillary perfusion pressure
Most common sites of compartment syndrome
Can be any but most commonly leg, thigh, forearm, foot, hand and buttock
Describe the aetiology/pathophysiology of compartment syndrome
- Typically occurs follwing high energy trauma, crush injuries or fractures that cause vascular injury
- Other causes - iatrogenic vascular injury, tight casts//splints, DVT, post-reperfusion swelling
- Fascial compartments are enclosed by a tough fascia which is resistant to expansion, any swelling or fluid accumulated will increase the intra-compartmental pressure
- As pressure increases, veins are compressed, increasing hydrostatic pressure which pushes fluid out of veins and into the compartment, increasing the pressure further
- Traversing nerves are compressed, causing a sensory +/- motor deficit in the distal distribution (paraesthesia)
- As intra-compartmental pressure reaches the diastolic pressure, the arterial inflow will be compromised and the limb will become ischaemic
Risk factors for compartment syndrome
- Major surgical procedures (e.g. orthopaedic repair, post-embolectomy, post-laparotomy)
- Blunt trauma
- Burns
- Reperfusion injury
- Crush injury
- Fractures: closed or open
- Tight casts
- Ongoing intra-abdominal bleeding
- Penetrating trauma (e.g. vascular injury)
- Malignancy
Describe the clinical features of compartment syndrome
- Syptoms usually within hours but can present up to 48 hours post-insult
- Most reliable symptom is severe pain, disproportionate to injury, not relieved by initial measures
- Pain worse with passively stretching of muscle across fascial compartment
- Compartment feels tense (but not generally swollen - not able to extend)
- Paraesthesia - evolving neurology
- Can progress to acute limb ischaemia - pain, pallor, perishingly cold, paralysis, pulselessness (pulse can be present even at late stages)
What initial measures can be used to identify if pain is due to compartment syndrome?
Analgesia e.g. IV morphine
Elevation of limb to level of heart
Removal of any tight bangaes/dressings/casts
If pain persists after 30 minutes - highly suggestive of compartment syndrome
How is compartment syndrome diagnosed?
- Usually diagnosed clinically
- Can use intra-compartmental pressure monitoring - especialluy useful in nconscious patients/those with nerve blocks
- <30mmHg difference between diastolic BP and compartment pressure - increased risk of compartment syndrome
- Intra-compartment pressure of >40mmHg with clinical signs is diagnostic of acute compartment syndrome
- Creatinine kinase trending upwards may aid diagnosis
How is compartment sydrome managed?
- Initial management - remove external dressings/bandages/casts, IV analgesia, maintain blood pressure (IV fluids)
- Urgent fasciotomy is definitive management
- Leave incisions open for 24-48 hours, then debride any dead tissue and close wounds (leave subtending fascia open)
- Monitor renal function closely due to potential rhabdomyolysis or reperfusion injury - IV fluids
List the complications associated with acute compartment syndrome
- Irreversible neuroascular damage to affected limb
- Rhabdomyolysis, reperfusion injury - renal impairment
- Muscle/joint contracture e.g. Volkmann’s contracture
- Infection
- Amputation
- Long term disability
Describe chronic compartment syndrome
- Associated with exertion, during which pressure in compartment rises, blood flow to compartment is restricted and symptoms start
- Resolves during rest
- Symptoms - pain, numbness, paraesthesia
- Needle manometry can be used to measure pressure increase during exertion
- May require faciotomy to treat
List the compartments of the lower leg
- Anterior
- Lateral
- Superficial posterior
- Deep posterior
List the compartmets of the thigh
- Anterior
- Medial
- Posterior
List the compartments of the forearm
Superficial volar compartment
Deep volar compartment
Dorsal compartment
Mobile wad compartment
List the regions of the vertebral column and the number of vertebrae in each region
- Cervical - 7
- Thoracic - 12
- Lumbar - 5
- Sacrum 5 (fused)
- Coccyx - 4 (fused)
At what level does the spinal cord terminate? What lies in the inferior part of the spinal column?
- Terminates at level of L2, region called conus medillaris, continues as filum terminale which anchors the spinal cord to the coccyx
- Cauda equina is a collection of nerves inferior to the conus medillaris that continue to travel through the vertebral collum to the coccyx
Where is the cauda equina located?
Occupies the lumbar cistern, a subarachnoid space inferior to the conus medullaris
Surrounded by CSF
Begins at vertebral level of L1
Which nerves make up the cauda equina? What do they innervate?
- L2-L5
- S1-S5
- Coccygeal nerve
- Innervation of pelvic organs, motor innervation of hips, knees, ankles, feet, internal and externalanal sphincter, sensory innervation of the perineum, parasympatheitc innervation of the bladder
What is the most common cause of cauda equina syndrome?
List the other causes.
- Central disc prolapse/herniation - L5/S1 and L4/5 most common
- Trauma - vertebral fractures or subluxation
- Malignancy - primary or metastatic
- Spinal infection - abscess, meningitis, tuberculosis/Pott’s disease, discitis
- Inflammation - ankylosing spondylitis
- Iatrogenic - spinal anaesthesia, post-operative haematoma, manipulation
Describe the presentation of cauda equina syndrome
- Lower motor neurone signs and symptoms
- Reduced lower limb sensation (often bilateral) - including saddle anaesthesia
- Bladder/bowel dysfunction - retention, incontinence, reduced anal tone
- Lower limb motor weakness
- Lower limb hyporeflexia
- Severe back pain
- Impotence
Investigations for suspected cauda equina syndrome
Urgent lumbar-sacral MRI spine
Pre- and post-voiding bladder scan looking for retention and incomplete bladder empyting
Classification of cauda equina syndrome
- Cauda equina syndrome with retention - back pain with unilateral or bilateral sciatica, lower limb motor weakness, sensory disturbance in the saddle region, loss of anal tone and loss of urinary control
- Incomplete cauda equina syndrome - as above, only altered urinary sensation (e.g. loss of desire to void, diminshed sensation, poor stream, need to strain), painful retention may precede painless retention in some cases
- Suspected cauda equina syndrome - severe back and leg pains with neurological symptoms and signs and a suggestion of sphincter disturbance
Most will progress to complete compression if untreated
What is the differential diagnosis of cauda equina syndrome?
Radiculopathy – presents with radiating back pain, however there will be no faecal, urinary, or sexual dysfunction in these patients
Cord compression – a surgical emergency with a similar pathophysiology to CES, however is characterised by upper motor neurone signs
Muscloskeletal pain – relating to strain of paraspinal muscles, with severe pain that may lead to limited movement, but no other focal neurological signs
How is cauda equina syndrome managed?
- Adequate analgesia, catheter if urinary retention
- Urgent surgical decompression within 24 hours of symptom onset - laminectomy +/- discectomy
- Radiotherapy/chemotherapy may be used if malignant cause
Complications of cauda equina syndrome
Paraplegia
Lower limb numbness
Chronic urinary retention or incontinence
Chronic sexual dysfunction
How should a patient involved in major trauma be assessed?
(C)ABCDE
Catastrophic haemorrhage
Airway (with c-spine protection)
Breathing
Circulation
Disability
Exposure
How should the cervical spine be assessed in major trauma?
High risk criteria - requires imaging and immobilisation
* Age 65 or older
* Dangerous mechanism of injury (fall from over one metre or down five or more steps, or an axial loading injury)
* Paraesthesia in any limb(s)
Low risk - none of the high risk criteria, one or more of
* Involved in a minor rear-end motor vehicle collision
* Comfortable sitting
* Ambulatory since the injury
* No midline cervical spine tenderness
* Delayed onset of neck pain
Low risk doesn’t require imaging/immobilsation unless can’t rotate head 45 degrees to left and right
List the life-threatening chest injuries
TOM CAT
Tension pneumothorax
Open pneumothorax
Massive haemothorax
Cardiac tamponade
Airway injury
Tracheobronchial injury
Where can blood be lost from?
- On the floor - external wound
- Chest cavity
- Abdominal cavity
- Pelvis
- Long bones
What is the lethal triad in major haemorrhage? How can this be avoided?
Hypothermia: keep warm with blankets, warmed air, use a blood warmer to give blood, and when examining the patient, limit their exposure to the minimum necessary
Acidosis: maximise oxygenation and treat/prevent hypoventilation to prevent respiratory acidosis. Avoid giving crystalloids as this can exacerbate acidosis.
Coagulopathy: avoid crystalloids or unbalanced blood products as they can cause dilutional coagulopathy. Permissive hypotension (aiming for a target systolic of 80-100mmHg) can be used to avoid excessive fluid administration and prevent dilutional coagulopathy.
What symptoms are suggestive of cardiac tamponade?
Beck’s triad
* Jugular venous distension
* Quiet heart sounds
* Hypotension
How is a secondary survey performed?
- After all life-threatening injuries have been identified and addressed
- History (AMPLE) - allergies, medication, PMH including tetanus status, last meal, events leading to injury
- Head-to-toe examination - head and face, neck, chest, abdomen, limbs, back , buttocks and perineum, genitalia
Describe the immediate resuscitation of a trauma patient
C - catastrophic haemorrhage
* Direct pressure, haemostatic dressing, touniquets
A - airway
* Definitive airway if patient cannot support own airway or will not be able to - rapid sequence induction of anaesthesia and intubation
* May require surgical airway via surgical cricothyroidotomy
* While awaiting definitive airway can due jaw thrust to support airway (avoid head-tilt chin-lift due to risk of c-spine injury or nasopharyngeal airway due to risk of basal skull fracture)
C-spine
* Immobilise with hard collar or head blocks
B - breathing
* Oxygen
* Treat e.g. tension pneumothorax, haemothorax
C - circulation
* Pharmacological - tranexamic acid, reverse antigcoagulation
* Cannulation
* Blood tests - FBC, U&Es, LFTs, coagulation screen, group + save, toxicology screen, lactate
* Blood product transfusion - 1:1:1 packed red cells, fresh frozen plasma, platelets
* ECG
D - disability
* CT head
* Raised ICP - IV mannitol, hypertonic saline
* Surgical intervention?
E - exposure
* Analgesia
* Wound care
* Fractures
List the types of shock and causes of each
- Septic shock - bacterial infections e.g. appendicitis, pneumonia, necrotising fasciitis
- Haemorrhagic shock - blood loss
- Neurogenic shock - high level spinal cord transection
- Cardiogenic shock - ischaemic heart disease, myocardial trauma/contusion
- Anaphylactic shock
Stages of haemorrhagic shock
Describe the pathophysiology of the formation of fat emboli
Mechanical theory – Fatty tissue is directly released into the vascular circulation as a result of trauma
Biochemical theory – Inflammatory response to the trauma causes release of free fatty acids into the venous system from the bone marrow
Causes
* Acute long bone fractures
* Intramedullary instrumentation - intramedullary nailing, hip/knee arthroplasty
Define fat embolism syndrome
Systemic manifestations of fat emboli within the microcirculation
Describe the clinical presentation of fat embolism syndrome
- Usually following trauma
- Worsening shortness of breath
- Confusion
- Drowsiness
- Petechial rash
- Signs - tachypnoea, tachycardia, hypoxia, confusion, low-grade pyrexia
Describe the diagnostic criteria for fat embolism syndrome
Gurd’s criteria can be used for the diagnostic aid for fat embolism syndrome. The presence of 2 Major or 1 Major + 4 Minor criteria is deemed diagnostic
Major criteria = Petechial Rash, Respiratory Insufficiency, Cerebral Involvement
Minor criteria = Tachycardia, Pyrexial, Retinal Changes, Jaundice Thrombocytopaenia, Anaemia, Raised ESR, Fat macroglobulinaemia
Which investigations should be done in suspected fat embolism syndrome. What findings are suggestive of FES?
- Routine bloods, including FBC, CRP, U&Es, LFTs, and a clotting screen
- ABG - type 1 respiratory failure
- Blood film may show the presence of fat globules
- CXR will classically show diffuse bilateral pulmonary infiltrates
- CTPA scan - ground-glass changes with a global distribution
How is fat embolism syndrome managed?
- Supportive
- Often requires mechanical ventilation
How can fat embolism syndrome be prevented?
- Early fracture stabilisation (within 24 hours) of long bone fracture
- Close monitoring - pulse oximetry
How should the c-spine be immobilised during intubation?
Manual in-line stabilisation
Describe this X-ray
Transverse fracture through the proximal humerus (surgical neck of humerus) with displacement of the distal component
Describe this X-ray
A transverse, comminuted fracture of the surgical neck of humerus is accompanied by a fracture line separating the greater tubercle from the rest of the humeral head
Describe this X-ray
- Dislocation of the right acromioclavicular joint, with the clavicle displaced superiorly
- Widening of the coracoclavicular distance - 23mm
Describe this X-ray
AP view of the shoulder
Humeral head is dislocated from the glenoid of the scapula and is now inferior to the coracoid of the scapula - anterior dislocation
Describe this X-ray
Shoulder AP
The glenohumeral joint is widened and the humeral head has taken on a more rounded ‘light bulb’ shape
= posterior glenohumeral dislocation
Classification system used for ACJ joints
Rockwood classification
* Type 1 - clavicle not elevated above acromion
* Type II - clavicle elevated but not above superior border of acromion
* Type III - clavicle elevated above superior border of acromion but coracoclavicular distance less than twice normal (<25)
* Type IV - clavicle displaced posterior into trapezius
* Type V - clavicle markedly elevated and coracoclavicular distance more than double normal (>25mm)
* Type VI- clavicle inferiorly displaced behind coracobrachialis and biceps tendons - rare
Describe the stabilisers of the elbow
- Primary static stsabilisers - humeroulnar joint and medial and collateral ligaments
- Secondary static stabilisers - radiocapitellar joint, joint capsule, common flexor and extensor origin tendons
- Dynamic stabilisers - anconeus, brachialis, triceps brachii muscles
Clinical presentation of elbow dislocations
- Typically present following a high-energy fall
- The joint will be painful and deformed, with associated swelling and decreased function (usually near immobile in near full extension with disruption of the equilateral triangle of the elbow)
Which nerve is commonly injured due to elbow dislocation? What symptoms does this cause?
Ulnar nerve
* Pain/numbness/tingling on ulnar side of arm/hand
* Claw-like deformity - hyperextension at MCP and flexion at proximal and distal IP of 4th and 5th fingers
* Reduced finger abduction
Which muscles, joints and nerves are involved in:
* Claw hand deformity
* Hand of Benediction deformity
* Wrist drop?
When is the deformity seen?
- Medial lumbricals, DIP and PIP flexion, MCP extension, ulnar nerve
- Flexor digitorum profundus and superficialis, flexor pollicis longus and brevis, MCP, DIP and PIP extension, median nerve
- Extensor muscles (extensor carpi ulnaris, extensor digiti minimi, extensor digitorum, extensor indicis, extensor carpi radialis brevis, extensor carpi radialis longus), wrist joint, radial nerve
Claw hand - when extending fingers
Hand of Benediction - when flexing fingers
Wrist drop - when extending wrist
What is the most common type of elbow dislocation?
Posterolateral
Which age group are elbow dislocations most commonly seen in?
10-20 years old
Describe the mechanism of injury of elbow dislocations
Typically - axial loading, supination and valgus force
How should a vascular examination be carried out in patients with an elbow dislocation?
Capillary refill - good capillary refill can be found even in those with an arterial injury, due to the elbow having a rich collateral circulation
Pulse - any concern over the pulse of the limb will warrant a Doppler ultrasound for further assessment
How are elbow dislocations classified?
- Anatomical location of olecranon in relation to the humerus
- Simple vs complex - simple has no associated fracture, complex has associated fracture
What is a terrible triad injury? Why is it terrible?
- Elbow dislocation associated with a LUCL tear, radial head fracture, and coronoid tip fracture
- Causes very unstable elbow and is associated with a poor outcome
- Likely to have recurrent problems with instability, stiffness, and arthrosis
Investigations for elbow dislocation
X-rays - AP and lateral (loss of the radiocapitellar and ulnotrochlea congruence)
CT only if associated fractures
Management of elbow dislocation
Closed vs open reduction +/- ORIF and soft tissue repair (if fracture)
Closed reduction
* Requires sufficient analgesia/sedation
* In-line traction or manipulation of the olecranon (in distal and anterior direction)
* Elbow then flexed to 90 degrees with back slab
* X-ray to confirm reduction
* Neurovascular status re-assessed and documented
* If the lateral collateral ligament is damaged the elbow will be more stable in pronation, if the medial collateral ligament is disrupted the elbow will be more stable in supination
Initially immobilisation then rehabilitation
Which complications are associated with elbow dislocations?
- Early stiffness with loss of terminal extension
- Ulnar nerve stretch injury
- Recurrent instability - reuccrence rate low (<2%)
- Heterotophic ossification
What is the most common mechanism of injury of a radial head fracture?
Fall on an outstretched hand
What soft tissue injuries are associated with radial head fractures?
Ligament injury
* Lateral collateral ligament (LCL) injury most common (up to 80% on MRI)
* Medial collateral ligament (MCL) injury
Essex-Lopresti injury
* Radial head fracture
* Distal radioulnar joint (DRUJ) injury
* Interosseus membrane injury
Classification of radial head fractures
Mason classification
Type 1 - non-displaced or minimally displaced, no mechanical block to rotation
Type 2 - Displaced >2mm or angulated, possible mechanical block to forearm rotation
Type 3 - comminuted and displaced, mechanical block to motion
Type 4 - radial head fracture with associated dislocation
Describe the clinical presentation of radial head fractures
- Pain
- Tenderness along lateral aspect of elbow
- Limited elbow or forearm motion - supination/pronation
- Ecchymosis
- Swelling
How should patients presenting after a fall on an outstretched hand be assessed?
Fully examine the wrist, elbow and shoulder - can have bone or soft tissue injuries of any of these
* Inspection
* Palpation
* Movement
* Stability testing - ligaments, drawer tests, interosseous mebrane
* Neurovascular examination
May require imaging (plain films) - AP and lateral elbow, forearm/wrist, shoulder
CT for more complex injuries and to determine degree of comminution
MRI for soft tissue injuries
What findings on X-ray suggest a radial head fracture?
Radial head fractures can be easily missed on plain radiographs and occasionally only an elbow effusion may be seen
Elbow effusions on a lateral projection is termed a “Sail sign”, shown as an elevation of the anterior fat pad, in keeping with an occult fracture
How are fractures of the radial head managed?
Mason type 1 injuries – treated non-operatively, with a short period of immobilization with sling (less than 1 week) followed by early mobilisation
Mason Type 2 injuries – if no mechanical block then can be treated as per a type 1 injury, whilst if a mechanical block is present then these may need surgery (typically ORIF)
Mason Type 3 injuries – will nearly always warrant surgical intervention, either via ORIF or radial head excision or replacement (especially in highly comminuted fractures)
What complications are associated with radial head fractures?
Elbow stiffness and loss of forearm rotation
Radiocapitellar joint arthritis
Heterotopic ossification
What is a nightstick injury? How do they occur?
- An isolated fracture of the ulnar shaft
- Direct blow to forearm, often when putting forearm in front of face to defend against weapon e.g. police nightstick, bat, fist
- Can also occur due to fall
What complications are associated with forearm fractures and fracture-dislocations?
- Infection - ORIF, open fractures
- Compartment syndrome - high risk in these injuries, especially if open, crush injjuries, vascular injuries
- Non-union
- Malunion
Describe the fracture-dislocation syndromes of the forearm
A Monteggia fracture is defined as a proximal 1/3 ulna fracture with an associated radial head dislocation.
A galeazzi fracture is a distal 1/3 radial shaft fracture with an associated distal radioulnar joint (DRUJ) injury.
What is the typical mechanism of injury of forearm fracture-dislocations?
- Monteggia - direct blow to posterior elbow
- Galeazzi - direct dorsolateral wrist trauma
- Fall on an outstretched hand, arm pronated
Which age group are forearm fracture-dislocations most common in?
Children - 4-13 years
Classification of Monteggia fractures
Bado classification
Type 1 - fracture of proximal or middle ulna with anterior dislocation of radial head (60%)
Type 2 - fracture of proximal or muddle ulna with posterior dislocation of the radial head (more common in adults, 15% overall)
Type 3 - fracture of ulnar metaphysis with lateral dislocation of radial head
Type 4 - fracture of proximal or middle third of ulna and radius with dislocation of radial head in any direction (rare)
Describe the presentation of forearm fracture-dislocations
Symptoms - pain, swelling
Monteggia - may be obvious dislocation at radiocapitellar joint, loss of ROM at elbow, PIN neuropathy
Galeazzi - point tenderness over fracture site, instability with pronation/supination, wrist/midline forearm pain with DRUJ stress
What kind of nerve injury is associated with a Monteggia fracture? What symptoms does this cause? How is this managed?
PIN neuropathy - posterior interosseous nerve (deep branch of the radial nerve in the forearm)
Symptoms:
Radial deviation of hand with wrist extension
Weakness of thumb extension
Weakness of MCP extension
Usually spontaneously resolves within 2-3 months, nerve conduction studies if not
What imaging should be done in forearm fractures/fracture dislocations?
X-ray - AP and lateral views of the forearm, elbow and wrist
What findings on X-ray are suggestive of a distal radioulnar joint injury?
Ulnar styloid fx
Widening of joint on AP view
Dorsal or volar displacement on lateral view
Radial shortening (≥5mm)
How are Monteggia fractures managed?
Closed reduction - more common and successful in children, if greenstick, complete transverse/short oblique fracture
ORIF of ulnar fracture - most adults, children if open, long oblique, comminuted
After ORIF of ulnar injury radial head dislocation can usually have closed reduction, may require open if closed unsuccessful
Classification of Galeazzi fractures
Classified according to direction of radial displacement
Type I - dorsal displacement
Type II - volar displacement
How are Galeazzi fractures managed?
All require ORIF of radius with reduction and stabilisation of DRUJ (unstable injury)
Stabilisation of DRUJ can be with immobilisation in supination (6 weeks, if stable after radius ORIF), percutaneous pin fixation (if reducible but unstable after radius ORIF), open surgical reduction (if reduction is blocked), ORIF (if large ulnar styloid fragment)
How are adult both bone forearm fractures managed?
Non-operative - cast/brace, rarely done in completely non-displaced fractures in patients who are not surgical candidates
External fixation if severe soft tissue injury
ORIF - most common
ORIF with bone grafting - significant bone loss
IM nailing - if very poor soft tissue integrity, high rate of non-union
What does this X-ray show?
Lateral view of elbow/forearm
Monteggia fracture/dislocation - proximal 1/3 ulnar fracture and anterior radial head dislocation (type 1)
What does this X-ray show?
Lateral view of forearm/wrist
Galeazzi fracture/dislocation - distal 1/3 radial fracture and dorsal dislocation of distal ulna (type I)
What does this X-ray show?
Transverse fracture through the proximal humerus with displacement of the distal component - surgical neck fracture
What does this X-ray show?
A transverse fracture of the surgical neck of humerus is accompanied by a fracture line separating the greater tubercle from the rest of the humeral head. Comminuted fracture.
What does this X-ray show?
Oblique fracture of the humerus shaft
Distal component is markedly displaced
What is the most common kind of wrist fracture?
Colles fracture
Describe the typical mechanism of injury of distal radius fractures
Fall on an outstretched hand - especially in older, osteoporotic patients
High energy in younger patients
Describe the common eponymous distal radius fractures
Colles’ fracture - extra-articular distal radius fracture with dorsal comminution, dorsal angulation, dorsal displacement, radial shortening, and an associated avulsion fracture of the ulnar styloid (not always seen in fractures described as Colles), occurs due to low energy, typically a ‘fragility fracture’ in osteoporotic bone
Smith’s fracture - extra-articular distal radius fracture with volar angulation, with or without volar displacement, usually due to falling backwards causing forced pronation, low energy
Barton’s fracture - intra-articular distal radius fracture with associated radio-carpal dislocation, either dorsal or volar depending on which lip of the radius is involved
Chauffer’s fracture - radial styloid fracture
Die-punch fracture - depressed fracture of the lunate fossa of the articular surface of the distal radius
What risk factors are associated with distal radius fractures?
The main risk factors for distal radius fractures are related to osteoporosis:
Increasing age
Female gender
Early menopause
Smoking or alcohol excess
Prolonged steroid use
Describe the clinical presentation of a distal radius fracture
History of trauma
Immediate pain +/- deformity
Swelling
Reduced ROM due to pain
Neurological involvement - paraesthesia or weakness
How should a patient with a suspected distal radius fracture be assessed?
Examine hand, wrist, elbow +/- shoulder
Neurovascular examination of arm -
CRT and pulses
Median, radial and ulnar nerve motor and sensory function
If DIPJ of 2nd digit and IPJ of thumb extend when doing an okay sign - AIN involvement
X-ray - AP, lateral, oblique
CT if intra-articular, for surgical planning
MRI - soft tissue injury
What measurements are used to diagnose a distal radius fracture on X-ray?
Radial height - normal 11mm, <11
Radial inclination - normal 22 degrees, <22 degrees
Radial (volar) tilt - normal 11 degrees, <11
How are distal radius fractures managed?
All require closed reduction - traction and manipulation under anaesthetic
Non-operative - closed reduction and splint/cast immobilisation with below-elbow back slab cast
Indications - extra-articular, <5mm radial shortening, dorsal angulation <5 degrees
Operative
Closed reduction, percutaneous pinning - extra-articular fracture with stable volar cortex
ORIF
External fixation - open, highly comminuted, medically unstable
What are the indications for ORIF in distal radius fractures?
Radiographic instability
Dorsal angulation >5 degrees
Vorsal or dorsal comminution
Displaced intra-articular fractures >2mm
Radial shortening >5mm
Associated ulnar fracture - other than ulnar styloid fracture
Severe osteoporosis
Articular margin fractures
Comminuted and displaced extra-articular fractures
Die-punch fractures
Progressive loss of volar tilt and radial length following closed reduction and casting
What are the complications associated with distal radius fractures?
Malunion - poor realignment leads to shortened radius compared to ulnar, leads to reduced wrist motion, wrist pain and reduced forearm rotation
Median nerve compression - especially if malunion
Osteoarthritis - especially if intra-articular
What is the most common neurologic complication of distal radius fractures? How is this managed?
Median nerve neuropathy
Acute carpal tunnel release performed if progressive paresthesia, weakness in thumb opposition, paresthesias that do not respond to reduction and last >24-48 hours
How is manipulation of a distal radius fracture performed?
Local or systemic analgesia and/or anaesthetic
Sedation - nitrous oxide +/- fentanyl, propofol + fentanyl, ketamine
Bier’s block
Haematoma block
US guided block
Reduction - prolonged traction on distal fragment, hyperextend the distal fragment, flex back into position
Plaster to maintain position
What does this X-ray show?
Trasverse fracture of the distal radius
Dorsal angulation and displacement
Shortening creating a very narrowed ulnocarpal space
= Colle’s fracture
What does this X-ray show?
Oblique fracture of the distal radius
Volar displacement and angulation
Shortened radius
= Smith’s fracture
What does this X-ray show?
Comminuted intra-articular distal radius fracture and displaced fracture of the ulnar styloid
= Barton’s fracture
What does this X-ray show?
Radial head fracture - fracture line not visible
Effusion indicated by raised fat pads is only sign of fracture
What does this X-ray show?
Radial head fracture - fracture line extends into articular surface of radial head
What does this X-ray show?
Effusion - raised fat pads
Subtle buckling of the radial head cortex anteriorly
= radial head fracture
What does this X-ray show?
Ulna dislocated posteriorly from the trochlea of the humerus
Radius has dislocated from the capitulum of the humerus
What does this X-ray show?
Elbow dislocation - ulna and radius dislocated from humerus
Describe the blood supply of the scaphoid. What are the clinical implications of this?
Blood supply from the radial artery
Dorsal branch 80% of blood supply, enters in the distal pole and travels. ina retrograde fashion towards the proximal pole
Volar branch supplies the other 20%
The scaphoid is at risk of avascular necrosis after fracture because of its ‘retrograde blood supply’ which enters at its distal end, and moves proximally. This means that a fracture to the middle (or ‘waist’) of the scaphoid may interrupt the blood supply to the proximal part of the scaphoid bone rendering it avascular.
The more proximal the scaphoid fracture, the higher the risk of AVN
List the parts of the scaphoid. How commonly is each part fractured?
Proximal pole - 25%
Waist - 65%
Distal pole - 10%
What is the typical mechanism of injury of scaphoid fractures?
Fall onto an outstretched hand - axial load across a hyperdorsiflexed, pronated and ulnarly deviated wrist
Describe the typical clinical presentation of scaphoid fractures
History of trauma
Sudden onset wrist pain
+/- bruising, swelling
Pain and restricted pronation
Tenderness in floor of anatomical snuffbox, pain on palpation of scaphoid tubercle, pain on telescoping of thumb
Describe the structure of the anatomical snuffbox and its contents
Triangular depression on the lateral aspect of the dorsum of the hand
Defined laterally by the abductor pollicis longus and extensor pollicis brevis tendons (the 1st extensor compartment), and medially by the extensor pollicis longus tendon (the 3rd extensor compartment)
Contents - radial artery, superficial radial nerve, cephalic vein
Floor made of the scaphoid, along with the trapezium (distally) and the radial styloid (proximally)
What is the differential diagnosis for a scaphoid fracture?
Distal radial fracture
Alternative carpal bone fracture
Fracture of the base of the 1st metacarpal
Ulnar collateral ligament injury
Wrist sprain
De Quervains tenosynovitis
How is a suspected scaphoid fracture investigated?
Can be difficult to detect, up to 40% missed initially
X-ray - scaphoid series (PA, lateral, oblique, PA angled), if negative but still sufficient clinical suspicion should have wrist immobilised and repeat X-ray in 10-14 days
If still negative but scaphoid fracture suspected - MRI of wrist
Which other injuries are associated with scaphoid fractures?
Scapholunate ligament rupture
Perilunate dislocation
How are scaphoid fractures managed?
Non-operative - cast immobilisation
Majority of fractures
If stable, non-displaced fracture
If normal X-ray but suspicion of scaphoid fracture
Operative
Percutaneous screw fixation - proximal pole fracture displacement >1mm, non-displaced waist fractures
ORIF - significantly displaced, associated perilunate dislocation, comminuted, unstable vertical or oblique
What complications are associated with scaphoid fractures?
Scaphoid non-union (5-10%, higher rates for proximal pole fractures), treatment is with vascularised or non-vascularised bone grafting
Avascular necrosis - 13-50%, higher risk with more proximal fractures
Malunion
Scaphoid non-union advanced collapse - progressive arthritis of wrist due to chronic scaphoid nonunion
What do these X-rays show?
Scaphoid fracture visible on only PA and PA + ulnar deviation views
What does this X-ray show?
Transverse scaphoid waist fracture
What does this X-ray show?
Triquetrum fracture - comminution of the dorsal cortex of the triquetrum
Soft tissue swelling over the dorsum of the wrist
What does this X-ray show?
Fracture through the hamate
What does this X-ray show?
Perilunate dislocation
Dorsal dislocation of the capitate
Which X-ray view is best for assessment of perilunate/lunate dislocations? What signs indicate these injuries on X-ray?
Lateral view
Perilunate - capitate not sitting in distal articular ‘cup’ of lunate, line drawn through radius and lunate does not intersect capitate, lunate in articulation with distal radius, abnormal scapholunate and capitolunate angles, scaphoid fracture present in 60%
Lunate - lunate displaced and angulated volarly, ‘spilled teacup’ appearance, lunate does not articulate with capitate or radius
How are perilunate/lunate dislocations managed?
All require operative management for definitive management
May have initial closed reduction and splinting
Then open reduction, ligament repair, fixation, possible carpal tunnel release
Which nerve is most commonly affected in perilunate/lunate dislocations?
Median nerve
Describe the parts of the metacarpals. Which part is most commonly fractured? Which metacarpal is most commonly fractured?
Head, neck or shaft
Neck most commonly fractured
Fifth metacarpal most commonly injured
Which conditions are commonly associated with metacarpal fractures?
Open fractures - common over dorsal MCP joints
Tendon laceration
Neurovascular injury
Compartment syndrome - multiple fractures/dislocations, crush injuries
Describe the common fracture patterns seen in metacarpal injuries and how they are managed
Boxer’s Fracture – a fracture of the 5th metacarpal neck, which typically occurs from a clenched fist striking a hard surface (such as a wall); these are typically very stable fractures and can be managed with a period of buddy taping and then full mobilisation
Bennett’s Fracture – an intra-articular fracture of the 1st metacarpal base with a palmar and ulnar fragment, usually with some degree of subluxation or dislocation of CMC joint, typically requires reduction and surgical fixation.
Rolando Fracture – an intra-articular fracture of the 1st metacarpal base, with a Y or T configuration. This fracture pattern typically requires reduction and surgical fixation.
Describe the clinical presentation of metacarpal fractures/dislocations
History of trauma
Pain and swelling overlying injuries
Reduced ROM at affected joint
May have rotational deformity - make a fist, finger rotated internally or externally (no longer pointing towards scaphoid tubercle), may have overlying fingers (scissoring)
How are metacarpal injuries investigated?
X-ray hand - PA, oblique, lateral
CT if complex, fracture-dislocations, pre-op planning
How are metacarpal fractures managed?
Remove jewellery
Analgesia
Elevate in high-arm sling to reduce swelling
Mainly non-operative management - immobilisation with buddy taping, ulnar gutter or volar resting splint, repeat X-ray to assess for displacement
Surgical management
Indications - rotational deformity, intra-articular involvement, significant volar angulation, significant shortening, unstable fracture pattern
Techniques - closed reduction and percutaneous fixing with K-wires, ORIF
How are metacarpal dislocations managed?
Closed reduction then immobilisation - simple dislocations
Open reduction - complex dislocations/delayed presentation
Describe the clinical presentation of 5th metacarpal fracture-dislocations
Typical mechanism - punching
Pain
Swelling
Ulnar deviation of 5th digit
How are 5th metacarpal fracture-dislocations managed?
Reduction closed/open
K-wire fixation as usually unstable
What does this X-ray show?
4th and 5th MCP joint dislocation
What does this X-ray show?
Boxer’s fracture
Fracture of 4th and 5th metacarpal
What does this X-ray show?
Intra-articular fracture of the ring finger middle phalanx
What does this X-ray show?
Comminuted fracture of the little finger distal phalanx due to a crush injury
Transverse fracture of the ring finger middle phalanx
What does this X-ray show?
Boxer’s fracture
What does this X-ray show?
Bennett’s fracture - intra-articular fracture of the 1st metacarpal base, subluxation
What does this X-ray show?
Rolando fracture - Y shaped fracture of base of 1st metacarpal
What is the ‘position of safety’ for hand immobilisation?
Wrist at 30 degrees of flexion
MCP joint at 80-90 degrees of flexion
PIP and DIP joints fully extended at 0 degrees
Clinical presentation of phalanx dislocations
Pain and deformity of affected digit
Skin puckering - interposition of soft tissues within joint
May have collateral ligament injury - check with lateral stressing while in flexion
Hyperextension - incompetency of volar plate
May have traction neuropraxia due to stretched of adjacent digital nerves
How should phalanx fractures/dislocations be investigated?
X-ray - AP, lateral, oblique
Views of individual fingers
V-sign - dorsal joint widening, indicates subtle subluxation
How are PIP fracture dislocations managed?
Non-operative - closed reduction and splinting, if <40% joint involved and stable
Operative - closed reduction and percutaneous pinning or ORIF, if >40% of joint involved and unstable
How are DIP dislocations and fracture-dislocations managed?
Non-operative - closed reduction +/- splinting, 1st line
Operative - open reduction +/- flexor digitorum profundus repair, if two reduction attempts fail
Other operative - volar plate arthroplasty, arthodesis, amputation
Complications associated with phalanx fracture-dislocations
DIPJ stiffnes
Mallet finger deformity - seen with volar dislocations
What does this X-ray show?
Shenton’s line disrupted
Increased density of femoral neck due to overlapping impacted bone
Lesser trochanter more prominent than usually due to external rotation of the femur
= subcapital intracapsular fracture
What does this X-ray show?
Complete fracture of the full diameter of the femoral neck
Total displacement of the 2 fracture components
Loss of Shenton’s line
What does this X-ray show?
Intertrochanteric femur fracture
Comminution with separation of the lesser trochanter
What does this X-ray show?
Subtrochanteric femur fracture
Describe the articular surfaces of the hip
Acetabulum = cup on inferolateral pelvis
Deepened by fibocartilaginous collar - acetabular labrum
Head of femur = hemisphere, fits into acetabulum
Both covered in articular cartilage
Describe the attachments of the hip joint capsule
Proximally - edge of acetabulum
Distally - intertrochanteric line anteriorly, femoral neck posteriorly
Describe the ligaments of the hip
Intracapsular
Ligament of head of femur - from acetabular fossa to fovea of femur, encloses a branch of the obturator artery (artery to head of femur), minor source of arterial supply to hip
Extracapsular
Iliofemoral ligament - from anterior inferior iliac spine, bifurcates and inserts into intertrochanteric line of the femur, Y shaped, prevents hyperextension, strongest extracapsular ligament
Pubofemoral ligament - from superior pubic rami to intertrochanteric line of femur, triangular, prevents excessive abduction and extension
Ischiofemoral - from body of ischium to greater trochanter of femur, spiral orientation, prevents hyperextension and holds femoral head in acetabulum
Describe the arterial supply of the hip joint. Why is this clinically important?
Complex blood supply including:
Branches of profunda femoris artery - medial and lateral femoral circumflex
Branches of internal iliac artery - superior and inferior gluteal artery, obturator artery
Obturator artery gives off artery of ligamentum teres which travels inside the ligament of the head of the femur to supply the femoral head - significant source of blood supply in children, not sufficient in adults (after growth plate closes, >15) to prevent AVN if other blood supply disrupted
Tochanteric anastomosis - circumferential connection involving superior gluteal artery, medial femoral circumflex and lateral femoral circumflex arteries around the femoral neck, supplies the femoral head
The supply to the femoral head is retrograde, meaning it moves from distal to proximal. If there is a displaced intracapsular NOF the blood supply will be cut off and the head can undergo avascular necrosis.
Describe the innervation of the hip. What is the clinical significance of this?
Sciatic, femoral and obturator nerves
Same as knee - can have referred pain in either joint
What is the typical mechanism of injury of neck of femur fractures?
Mostly low energy in older patients, e.g. fall
Also high energy in younger patients e.g. RTA, fall from height, associated with other significant injuries
Where can neck of femur fractures occur? How are they classified by location?
NOF = anywhere from subcapital region of the femoral head to 5cm distal to the lesser trochanter
Intracapsular - subcapital region of femoral head to basocervical region of femoral neck, immediately proximal to the trochanters
Extra-capsular - outside the capsules
Inter-trochanteric - between greater and lesser trochanter
Sub-trochanteric - from lesser trochanter to 5cm distal
What kind of NOF fractures are at risk of avascular necrosis?
Displaced intra-capsular fractures
How are intra-capsular NOF fractures classified?
Garden classification
Grade I - incomplete fracture, valgus impaction (non-displaced)
Grade II - complete fracture, non-displaced
Grade III - complete fracture, partially displaced (trabeculae at an angle)
Grade IV - complete fracture, fully displaced (trabeculae are parallel)
Describe the clinical presentation of a neck of femur fracture
History of trauma, often low-energy
Pain - groin, thigh or referred to knee
Inability to weight bear
Leg shortened, abducted and externally rotated - classically displaced fractures
Pain on pin-rolling and axial loading
Distal neurovascular deficits rare
What causes the characteristic leg deformity seen in NOF fractures?
Unapposed pull of external rotators (e.g. iliopsoas - attached to lesser trochanter)
What are the risk factors for neck of femur fractures?
Age - >65 in women >75 in men
Risk factors for osteoporosis. -menopause, amenorrhoea, smoking, excessive alcohol intake, physical inactivity, steroids
History of falls
Poor nutrition
Low BMI
Visual impairment (risk of falls)
History of tumours - primary or secondary bone tumours, breast, bowel, prostate, kidney, lung, thyroid tumours
Differential diagnosis for neck of femur fractures
Other fractures e.g. pubic ramus, acetabulum, femoral head, femoral shaft
Dislocated hip
Femoral head avascular necrosis
Slipped capital femoral epiphysis (intermittent pain for months, pain worse on activity)
Tendonitis of any muscles of the hip
Hip bursitits
Osteomyelitis (fever, chills, swelling, redness)
How should suspected neck of femur fractures be investigated?
Plain film radiographs - AP, lateral, AP pelvis (assess contralateral hip)
Full length femoral X-ray if suspicion of pathological fracture
Investigate cause of fall - FBC, U&Es, urine dip, CXR, ECG
CT - determine displacement/comminution
MRI - if negative X-ray but still clinical suspicion, gold standard for exclusion
Describe the initial management of a neck of femur fracture
A-E - often concurrent injuries
Analgesia - paracetamol, opioids, iliofascial/femoral nerve block
Avoid NSAIDs - increased risk of second NOF fracture
IV access - fluid resuscitations, ?blood transfusion, administration of medications
Assess + managed complications e.g. correct anaemia, ?reverse anticoagulation and ?VTE prophylaxis, volume depletion, infection
Describe the stratification of surgical management of neck of femur fractures
Intra-capsular:
Non-displaced (blood supply to femoral head intact) - internal fixation (cannulated hip screw)
Displaced (risk of AVN) - total or hemiarthroplasty (total if well, good mobility pre-injury, indepedent)
Extra-capsular:
Intertrochanteric/basocervical fracture - dynamic hip screw (sliding screw) or short IM nail
Sub-trochanteric - intramedullary nail
Describe hip total and hemiarthroplasty
Total - replace head of femur and acetabulum
Hemiarthroplasty - replace femoral head and neck via femoral component fixed in proximal femur
Describe a dynamic hip screw
Lag screw into the neck, a sideplate, and bicortical screws
The lag screw is able to slide through the sideplate, allowing for compression with weight bearing and primary healing of the bone
Describe cannulated hip screws
Three parallel screws in an inverted triangle formation, driven into femoral head across fracture to stabilise fracture
Describe the use of an intramedullary nail for NOF fractures
The titanium rod is placed through the medullary cavity of the femur for stabilisation
What does this X-ray show?
Cannulated hip screws
What does this X-ray show?
Dynamic hip screw
What does this X-ray show?
Total hip arthroplasty
What does this X-ray show?
Hip hemiarthroplasty
What does this X-ray show?
Intramedullary nail
What post-operative complications are associated with neck of femur fractures?
Surgical site infection
VTE
Bleeding
Fat embolism
Post-operative delirium
Nerve/vessel injury
Muscle/ligament damage
Leg-length discrepancies
Describe the post-operative management of neck of femur fractures
Analgesia
Rehabilitation - early mobilisation and weight bearing
Falls risk assessment
Dietetic assessment - avoid protein-caloric malnutrition
Axial bone densitometry - assess for osteoporosis, offer anti-resorptive therapy to reduce risk of future fragility fractures
Antibiotic prophylaxis
Thromboembolism prophylaxis
When is non-operative management appropriate in neck of femur fractures? How is this done?
Patients not fit for surgery
Short life expectancy
Delayed presentation with signs of healing
Immobile patients
Patient choice
Casts/splints/traction - period X-rays required
Poor outcomes - high mortality
Describe the long term complications of NOF fractures
30% mortality in 1 year
50% do not return to functional baseline
Non-union
Femoral head AVN
Peri-prosthetic fracture
Aseptic prosthetic loosening
Dislocation of prosthesis
Deep infection/prosthetic joint infection
Define osteoporosis and osteopaenia. What is the clinical implication of these conditions?
Both describe loss of bone mineral density - osteopaenia less severe than osteoporosis
Increases bone fragility and susceptibility to fragility fractures
List the risk factors for osteoporosis
Endocrine disease including Diabetes mellitus, Hyperthyroidism, and hyperparathyroidism
GI conditions that cause malabsorption such as Crohn’s disease, Ulcerative colitis, Coeliac disease, and Chronic pancreatitis
CKD
Chronic liver disease
COPD
Menopause
Immobility
BMI of less than 18.5 kg/m²
Age
Oral corticosteroids (dependent on the dose and duration of treatment, >7.5mg per day for >3 months significantly increases risk)
Smoking.
Alcohol (3 or more units daily).
Previous fragility fracture (risk increases with increasing number of fractures)
Risk is highest for previous hip fractures and lowest for previous vertebral fractures
Rheumatological conditions, such as Rheumatoid arthritis, and other inflammatory arthropathies
Parental history of hip fracture
Drugs - SSRIs, PPIs, anticonvulsants e.g. carbamazepine
Define osteoporotic and fragility fractures. Where do these mot commonly occur?
A fragility fracture is defined as a fracture following a fall from standing height or less. May occur without fall (e.g. vertebral fracture).
An osteoporotic fracture is a fragility fracture occurring as a consequence of osteoporosis.
Characteristically occur in the wrist, spine, and hip, but can also occur in the arm, pelvis, ribs, and other bones.
How is the risk of fragility fractures assessed? Who should be assessed? How is it interpreted?
FRAX tool - predicts absolute risk of hip fracture and major osteoporotic fractures (spine, wrist, shoulder) over the next 10 years (QFracture score also used)
Should be used in all women >65, men >75
Also used in women 50-64 and men 50-74 with risk factors
Younger than 50 if high-dose steroids, previous fragility fracture, untreated premature menopause
Low risk <10% risk score
Intermediate risk - close to 10%
High risk >10%
What investigation is done to assess bone mineral density? How is this done and how is it interpreted?
Dual-energy X-ray absorptiometry (DEXA)
Measures bone density at hip and produces Z and T score
Z score - number of SDs the patients bone density is below the mean for their age
T score - number of SDs below the mean for a healthy young adult
T score is used for WHO classification
How are FRAX scores and BMD measurement used to guide management of osteoporosis?
FRAX outcome without a BMD result will suggest one of three outcomes:
Low risk – reassure
Intermediate risk – offer DEXA scan and recalculate the risk with the results
High risk – offer treatment
FRAX outcome with a BMD result will suggest one of two outcomes:
Treat - -2.5 or lower
Lifestyle advice and reassure
What lifestyle changes are recommended in management of osteoporosis?
Activity and exercise
Maintain a healthy weight
Adequate calcium intake
Adequate vitamin D
Avoiding falls
Stop smoking
Reduce alcohol consumption
Describe Vitamine D and calcium supplementation in management of osteoporosis
If adequate calcium intake (700mg/day) - Vitamin D only (400 units)
If inadequate calcium - 400 or 800 units Vitamin D and 100mg calcium
Describe bone-sparing therapy in management of osteoporosis
If T-score 2.5 or less, consider if on high dose steroids
Bisphosphonate - alendronate 10mg OD or 70mg once weekly, risedronate 5mg OD or 35mg once weekly
Other options - denosumab, strontium ranelate, raloxifene, HRT
What are the side effects of bisphosphonates?
Gastrointestinal (most common) — nausea, dyspepsia, mild gastritis, and abdominal pain. More likely in the first month of treatment. Take on an empty stomach sitting upright for 30 minutes before moving or eating. NSAIDs may increase risk.
Bone, joint, and/or muscle pain (common)
Oesophageal reactions (uncommon) — oesophagitis, oesophageal ulcers, oesophageal strictures, and oesophageal erosions.
Osteonecrosis of the jaw (rare)
Osteonecrosis of the external auditory canal (very rare).
Atypical stress fractures
How should patients with osteoporosis be followed up?
Low-risk - lifestyle advice, follow-up in 5 years for repeat assessment
On bisphosphonates - FRAX and DEXA scan after 3-5 years, treatment holiday considered if BMD improved and no fragility fractures
Which bones make up the pelvis? List the articulations of the pelvis
Two hip bones (innominate/pelvic bones) - ilium, ischium and pubis
Sacrum and coccyx
Articulations -
Two sarcoiliac joints - between ilium and sacrum
Sarcoccygeal symphysis - sarcum and coccyx
Pubic symphysis - between pubic bodies
Describe the major foramina of the pelvis and their contents
Greater sciatic foramen -
Divided into suprapiriform and infraspiriform foramen by piriformis muscle
Suprapiriform - superior gluteal artery, vein and nerve
Infrapiriform - sciatic nerve, pudendal nerve, inferior gluteal artery, vein and nerve, posterior femoral cutaneous nerve, nerve to obturator internus, nerve to quadratus femoris
Lesser sciatic foramen
Internal pudendal artery, vein and nerve, obturator internus tendon, nerve to obturator internus
Obturator foramen - obturator artery, vein and nerve
Anterior and posterior sacral foramina - anterior and posterior divisions of the sacral nerves
Describe the mechanism of injury of pelvic fractures
Low energy - fall from standing height in osteoporotic patient, most commonly pubic ramus fracture
High energy - direct or transmitted trauma e.g. RTA, more extensive fractures, can include acetabulum and sacroiliac joint (if involving pelvis ring will usually have fractures in two places)
Can be unstable injuries requiring emergency surgery, associated with soft tissue and vascular injury (bladder and urethra at high risk of damage), can result in life-threatening haemorrhage
Describe the clinical presentation of high-energy pelvic ring fractures
History of high-energy trauma - usually blunt
Pain and inability to weight bear
Swelling
Deformity
Injury to sacral nerve roots - bladder/bowel incontinence, loss of sensation
Signs of bleeding - ecchymosis, haematoma formation (perineal, scrotal, labial)
Abdominal injuries, urethral injuries (gross haematuria)
Open fractures - including internal open fracture into rectum or vaginal vault
How should patients with suspected pelvic fractures be initially assessed and managed?
Follow ATLS protocol - primary survey to identify life-threatening injuries
Hypotension can indicate pelvic fracture with life-threatening haemorrhage - pelvic binder should be applied
Imaging - AP, inlet view and outlet view X-rays requires to assess pelvic ring
Usually a trauma CT is performed so X-rays not required
What is the purpose of a pelvic binder in suspected pelvic fractures? Where should it be applied?
Provides skeletal stability which allows for clot formation - prevents ongoing haemorrhage and development of coagulopathy
Centered over greater trochanter
How does haemorrhage occur in pelvic fractures?
Venous injury (80%) - shearing injury of posterior venous plexus, leads to retroperitoneal haemorrhage (can hold up to 8L of blood)
Bleeding cancellous bone
Arterial injury (less common, 10-20%) - superior gluteal most common
Describe the classification of pelvic ring fractures
Young and Burgess classification – based on the vector of the disrupting force and the resulting degree of displacement
Antero-posterior compression (APC)
Lateral compression (LC)
Vertical shear (VS)
Tile classification - based on the stability of the pelvic ring
A-type - rotationally and vertically stable
B-type - horizontally unstable but vertically stable
C-type - both horizontally and vertically unstable
Denis classification - for fractures of the sacrum, describes the line of the fracture in relation to the sacral foramina
Type 1 - lateral to the foramina
Type 2 - transforaminal
Type 3 - medial to the foramina
Describe the injuries produced by each type of force in the Young and Burgess classification of pelvic ring fractures
Antero-posterior compression - pubic symphysis disruption, more severe has disruption of posterior ligamentous structures of the pelvis
Lateral compression - pubic ramus fracture –> fracture of iliac blade (creates floating fragment) on side of compression, more severe than have contralateral iliac wing fracture
Vertical shear - detachment of sacrum from rest of pelvis, bilateral in more severe
What does this X-ray show?
Fracture through superior and inferior pubic rami - obturator ring is incomplete on the right
What does this X-ray show?
Step in cortical edge of pelvic ring - acetabular fracture, passes to obturator ring and through inferior pubic ramus
What does this X-ray show?
Pubic symphysis and right sacroiliac joint are widened - APC 3
What does this X-ray show?
ASIS avulsion fracture - small fragment of bone detached, pulled off by sartorius tendon
Normal appearance of unfused iliac crest apophysis - teenager
What does this X-ray show?
Loss of smooth arcuate lines
Sacral fracture
How are pelvic ring fractures definitively managed?
If haemodynamically unstable may require interventional radiology or trauma laparotomy +/- retroperitoneal packing
Indications for operative management - life-threatening haemorrhage, unstable fracture, open fracture, associated urological injury
Operative management involves a combination of anterior and posterior stabilisation
What does this X-ray show?
Lateral malleolus tip fractured distal to the ankle joint - Weber A
What does this X-ray show?
Fracture through distal fibula at level of ankle joint - Weber B
What does this X-ray show?
Distal fibula fracture, at level of ankle joint - Weber B
What does this X-ray show?
Distal fibula fracture, above level of ankle joint - Weber C
Transverse medial malleolus fracture
Distal tibiofibular joint also widened
What does this X-ray show?
Fractures of both the lateral malleolus (Weber C) and medial malleolus
What does this X-ray show?
Trimalleolar fracture - fracture of medial, lateral and posterior malleolus
What does this X-ray show? What should be done next?
Subtle widening of the ankle medially indicates instability at the distal tibiofibular joint
A Maisonneuve fracture should be suspected and images of the proximal fibula obtained
What does this X-ray show?
Pilon fracture - fracture of the distal tibia involving the articular surface of the tibia
What does this X-ray show?
Osteochondral fracture of the talar dome
What does this X-ray show?
Trimalleolar fracture - lateral malleolus fracture (Weber C), posterior malleolus fracture, medial malleolus fracture
The joint is unstable and widened anteriorly and at the distal tibiofibular syndesmosis
The talus is displaced posteriorly and laterally along with the medial and lateral malleolus bone fragments
What does this X-ray show? What should be done next?
Complete dislocation of the talus from the tibia and fibula
Get proximal views of the tibia/fibula - fibula fracture common if widening of tibiofibular joint distally
What does this X-ray show?
Complete dislocation of the talus from the tibia and fibula
Describe the bones and articular surfaces of the ankle
Bones of leg - tibia, fibula
Bones of ankle - talus, calcaneus
Tibia and fibula are bound together by tibiofibular ligaments, forms a socket covered in hyaline cartilage = mortise
Body of talus fits into mortise
Describe the ligaments of the ankle - their attachments and purpose
Medial (deltoid) ligament - medial malleolus –> talus, calcaneus, navicular bones (resists over-eversion)
Lateral ligament - lateral malleolus –> lateral talus, posterior talus, calcaneus
Syndesmosis - anterior inferior tibiofibular ligament, posterior inferior tibiofibular ligament, intraosseous ligament, intraosseous membrane, inferior transverse ligament
Describe the neurovascular supply of the ankle
The arterial supply to the ankle joint is derived from the malleolar branches of the anterior tibial, posterior tibial and fibular arteries.
Innervation is provided by tibial, superficial fibular and deep fibular nerves.
What is an ankle fracture?
A fracture of any malleolus (lateral, medial, or posterior), with or without disruption to the syndesmosis
What is a Pilon fracture?
Fracture involving the tibial articular surface of the ankle joint
How are ankle fractures classified?
Anatomically:
Isolated lateral malleolar fracture
Isolated medial malleolar fracture
Bimalleolar fracture (medial + lateral malleolar fracture)
Trimalleolar fracture (medial, lateral, posterior malleolar fracture)
Weber classification for lateral malleolus fractures
Type A = below the syndesmosis
Type B = at the level syndesomosis
Type C = above the level of the syndesmosis
Lauge-Hansen classification - based on ankle position at time of injury and deforming force used
Describe the presentation of ankle fractures
Ankle pain following traumatic injury
Inability to weight bear
Reduced ROM
Associated deformity if fracture dislocation
Ecchymosis, fracture blisters, open fracture
Which patients with ankle injuries should have an X-ray?
Ottowa rules
In the presence of any of the below features, plain radiographs must be undertaken:
Bone tenderness at the posterior edge or tip of the lateral malleolus, OR
Bone tenderness at the posterior edge or tip of the medial malleolus, OR
An inability to bear weight both immediately and in the emergency department for four steps
They cannot be used in cases if the patient is intoxicated or uncooperative, has other distracting painful injuries, has diminished sensation in their legs, or has gross swelling.
How should suspected ankle fractures be investigated?
Plain radiograph - AP and lateral (with ankle in full dorsiflexion)
CT scan for complex, especially displaced posterior malleolus fragment
How are ankle fractures managed?
Conservative - stable lateral/medial malleolus fracture, posterior with <25% joint involvement or <2mm step, Weber A or B, unfit for surgery
Immediate reduction under sedation to realign, below knee back slab
Surgical management - displaced bi/trimalleolar, Weber C, Weber B with talar shift, open fracture
ORIF
What complications are associated with ankle fractures?
Post-traumatic arthritis
ORIF - surgical site infection, DVT or PE, neurovascular injury, non-union, metalwork prominence
What does this Xray show?
Hip dislocation - femoral head lies superior and lateral to the acetabulum
What does this X-ray show?
Hip dislocation - total hip replacement Ball of the femoral component is displaced from the cup of the acetabular component
Describe the mechanism of injury of hip dislocations
High-energy trauma - RTA, significant fall from height
Often associated with other injuries
Describe the types of hip dislocation and their clinical features
Posterior dislocation: Accounts for 90% of hip dislocations, mainly due to axial load on femur. The affected leg is shortened, adducted, and internally rotated.
Anterior dislocation: The affected leg is usually abducted and externally rotated. No leg shortening.
Central dislocation
How do hip dislocations present?
Acute pain
Inability to weight bear
Deformity
How are hip dislocations investigated?
X-ray - AP
CT - determine direction of dislocation, loose bodies and associated fractures (should always be done after reduction)
How are hip dislocations managed?
ABCDE approach
Analgesia
Closed reduction first line (unless associated femoral neck fracture)
If irreducible or delayed presentation - open reduction
Reduction should be within 4 hours to prevent avascular necrosis/nerve injury
What are the complications of hip dislocations?
Sciatic or femoral nerve injury
Avascular necrosis
Osteoarthritis: more common in older patients.
Recurrent dislocation: due to damage of supporting ligaments
Describe the mechanism of injury of knee dislocations
High-energy - RTA, crush injury, fall from height
Low-energy - athletic injury, walking (typically obese)
Hyperextension leads to anterior dislocation
Posterior force across proximal tibia leads to posterior dislocations (dashboard injuries)
What injuries are associated with knee dislocations?
Vascular injury
Nerve injury - common peroneal injury (25%), tibial nerve injury less common
Fractures in 60%
Soft tissue injuries - patellar tendon rupture, periarticular avulsion, displaced menisci
Describe the types of knee dislocations, the forces that cause them and associated injuries
Anterior (30-50%) - hyperextension injury, usually PCL tear
Posterior (30-40%) - axial load on a flexed knee, highest incidence vascular injury (popliteal artery tear)
Lateral - varus or valgus force, usually PCL and ACL tear
Medial - varus or valgus force, usually disruption of PCL
Rotational - usually irreducible
Describe the clinical presentation of knee dislocation
History of trauma
Knee pain and instability
Deformity of knee
50% spontaneously reduce
Swelling, effusions, abrasions, ecchymosis
Pulses absent/diminished - vascular injury (may still be vascular injury with normal pulses)
Sensory/motor deficit - peroneal or tibial nerve injury
How are knee dislocations imaged?
X-ray - pre- and post-reduction AP and lateral
CT - fractures
MRI - soft tissue injuries, after acute reduction
How are knee dislocations managed?
Emergent closed reduction followed by vascular assessment
Immobilisation as definitive management
Open reduction - irreducible, posterolateral dislocation, open fracture-dislocation, vascular injury
Delayed ligamentous reconstruction/repair if required
What complications are associated with knee dislocations?
Vascular compromise
Stiffness - arthrofibrosis
Laxity and instability
Peroneal nerve injury
What does this X-ray show?
Total dislocation of the knee
Tibia and fibula rotated
What does this X-ray show?
Lateral dislocation of the patella
What does this X-ray show?
Patellar fracture - wide separation of the upper and lower poles of the patella
Define Lisfranc injuries
Severe injuries to the tarsometatarsal (Lisfranc) joint between the medial cuneiform and the base of the 2nd metatarsal. They can be either solely ligamentous injuries or involving the bony structures of the midfoot (fracture-dislocation)
Describe the mechanism of injury and clinical presentation of Lisfranc injuries
Most commonly due to severe torsional or translational forces applied through a plantar flexed foot - usually RTA, athletic injuries
Severe midfoot pain
Difficulty weight bearing
Swelling and tenderness over midfoot
Plantar bruising is highly suggestive
Tarsometatarsal injuries - features of compartment syndrome
Piano key sign - prominence of metatarsal bones - reduce down with pressure
How should suspected Lisfranc injuries be imaged?
X-ray - AP, oblique, lateral foot view while weight bearing
CT scan for pre-op panning of comminuted fracture
MRI for ligamentous injury
What features on X-ray suggest a Lisfranc injury?
Widening of the interval between the base of the 1st and 2nd metatarsal
Bony fragment (“fleck sign”) in the space between the 1st and 2nd metatarsal, indicates avulsion of the Lisfranc ligament from the base of the second metatarsal
Disruption of a line drawn from the medial base of the 2nd metatarsal to the medial side of the middle cuneiform (on AP view)
Malalignment of the medial border of the lateral cuneiform and the medial edge of the 3rd metatarsal, or medial border of the cuboid and the medial edge of the 4th metatarsal (on oblique view)
Dorsal displacement of the proximal bases of the 1st or 2nd metatarsals (on lateral view)
How are Lisfranc injuries classified?
Hardcastle and Myerson classification can be used to classify Lisfranc injuries:
Type A – complete homolateral dislocation
Type B1 – partial injury, medial column dislocation
Type B2 – partial injury, lateral column dislocation
Type C1 – partial divergent dislocation
Type C2 – complete divergent dislocation
How are Lisfranc injuries managed?
Significantly displaced - closed reduction in A&E to correct gross deformity and protect soft tissue - gentle traction to midfoot and corrective pressure to metatarsal base, then placed in backslab
If no significant diaplcement - manage conservatively with cast immobilisation and non-weight bearing mobilsation for 6-12 weeks
Displaced - operative management
Temporary external fixation then definitive screw fixation
List the complications of Lisfranc injuries
Post-traumatic arthritis - 25%
Midfoot compartment syndrome important
Define mechanical back pain
Back pain that arises from the spine, intervertebral disks or surrounding soft tissue
Often a specific cause is not identified
Describe the interpretation of T-scores
Describes bone mineral density as number standard deviations from normal for healthy young adult
>-1 is normal
<-1 but >-2.5 represents osteopaenia
<-2.5 osteoporosis (can be +/- fracture, fracture alone can diagnose osteoporosis)
Describe the clinical presentation of mechanical back pain?
Often have identifiable injury - bending or lifting
Pain and stiffness
Few clinical features
No red flag symptoms
Describe the differential diagnosis of mechanical back pain
Muscle or ligament sprain
Facet joint dysfunction
Sacroiliac joint dysfunction
Herniated disc
Spondylolisthesis (anterior displacement of a vertebra out of line with the one below)
Scoliosis (curved spine)
Degenerative changes (arthritis) affecting the discs and facet joints
How should mechanical back pain be investigated?
No investigation required unless another diagnosis suspected
Patients with a short history (< 6 weeks) do NOT need routine investigation
Prolonged symptoms or patients with RED flags should be investigated
– FBC with differential WCC
– ESR
– LFT’s
– Bone profile
– Myeloma screen
– CRP
How is mechanical back pain managed?
Promote patient education
Good early symptomatic control using simple analgesia - NSAIDs first line, codeine, benzodiazepines for muscle spasm (only up to 5 days)
Early return to normal activities (including work)
Self referral to physiotherapists
Safety netting advice for red flag symptoms
List the common causes of spinal nerve root impingement
Herniated disc
Spondylolithesis
Facet joint hypertrophy
Bone spurs
Fracture - trauma or pathological
Malignancy - usually metastatic
Infection - extradural abscesses, osteomyelitis (Pott’s disease, Herpes Zoster)
Describe the pathogenesis of nerve root compression in intervertebral disc herniation
Nucleus pulpous prolapses out via a defect in the degenerative annulus fibrous
Compresses the adjacent nerve root or the exiting nerve root, depending on location of disc herniation
What is the most common location of intervertebral disc herniation?
95% are L4/5 or L5/S1
Describe the clinical presentation of nerve root impingement
Radicular pain - leg pain usually worse than back, dermatomal distribution
Pain worse when sitting usually
Associated neurological deficit - numbness, tingling, weakness
L3 - sensory loss over anterior thigh, weak quadriceps, reduced knee reflex, positive femoral stretch test
L4 - sensory loss anterior aspect of knee, weak quadriceps, reduced knee reflex, positive femoral stretch test
L5 - sensory loss dorsum of foot, weakness in foot and big toe dorsiflexion, reflexes intact, positive sciatic nerve stretch test
S1 - sensory loss posterolateral aspect of leg and lateral aspect of foot, weakness in plantar flexion of foot, reduced ankle reflex, positive sciatic nerve stretch test
Describe the special tests used to test for nerve root impingement
Straight leg raising (SLR)
* Pain = increased nerve root tension and lack of the normal excursion of the root at the herniation site.
Laségue sign - flexion of knee in straight leg raise
* Should cause pain in the ipsilateral leg distal to the knee
* If contralateral leg pain can be elicited this is thought as a pathognomonic sign of disc herniation (Crossover sign)
How is nerve root impingement diagnosed? What are the indications for investigation?
MRI
Indications:
>6 weeks radicular pain failed conservative measures
Neurological deficit
Bilateral lower limb deficit or peroneal symptoms - urgent referral to on-call orthopaedic service for emergency MRI to rule out CES
What is the most important thing to consider when assessing a fracture?
Soft tissue injury - neurovascular injury, damage to the soft tissue envelope around the fracture
Which investigation is best for assessing intra-articular fractures?
CT
What are the principles of fracture management?
Reduce
Retain - immobilise
Rehabilitate
How to describe a fracture
Location - which bone or joints, where in the bone (epiphysis, metaphysis, diaphysis, proximal, middle or distal shaft)
Configuration - transverse, oblique, spiral etc.
Displacement - undisplaced, angulated, translated, shortened, rotated
Stability
Open?
How is the configuration of a fracture described? What kind of forces cause each type of fracture?
Transverse - direct blow
Oblique - bending force
Spiral - rotational force
Comminuted - high energy
Segmental - high energy
Avulsion - musculo-tendinous pull off
Compression - axial force
Torus - child, low energy
Greenstick - child, bending force
What are the the types of fracture displacement? How are these described?
Undisplaced - no loss of fracture position
Angulated - describe the angulation of the distal portion of the fracture with respect to the proximal portion
Translated - medio-lateral or anteroposterior drift of the fracture, describe in percentages
Shortened
Rotated - internal or external, usually best assessed clinically
Describe the options for fracture immobilisation
Conservative - casts, slings, splints, traction
Surgical - smooth wires, plates and screws, intramedullary nail, external fixation
Compare the surgical methods of fracture immobilisation in terms of invasiveness, stability etc.
Smooth wires - minimally invasive, poor stability, quick
Intramedullary nail - moderately invasive, very stable, longer procedure
Plates and screws - more invasive, very stable, longer procedure
External fixation - can be applied quickly in patients who are unstable/have other injuries, minimal soft tissue stripping
Describe the types of fracture non-union and their causes
Atrophic - failure of biology, smoking, malnutrition, immunocompromised
Hypertrophic - failure of immobilisation
How is fracture non-union treated?
Bone graft
Bone accelerant
Internal fixation
Which nerve is compressed in carpal tunnel syndrome?
Median nerve
Which nerve is compressed in cubital tunnel syndrome?
Ulnar nerve
What is the distribution is pain/paraesthesia classically in carpal tunnel syndrome?
Thumb, index, middle and radial half of ring finger
Which structures pass through the carpal tunnel?
Flexor pollicis longus, the four flexor digitorum superficialis, the four flexor digitorum profundus as well as the median nerve
How is the motor function of the median nerve tested?
Thumb abduction
What structure does the ulnar nerve pass between the 2 heads of?
Flexor carpi ulnaris
Describe the classical distribution of pain/paraesthesia in cubital tunnel syndrome
Little finger and ulnar half of ring finger
Which pulley becomes thickened and constricted in trigger finger?
A1
What is the most sensitive imaging technique for diagnosing a scaphoid fracture?
MRI
Which nerve supplies sensation to the sole of the foot?
Tibial nerve terminal branches
What movement occurs at the subtalar joint?
Inversion/eversion
Which foot and ankle joint has the greatest range of movement?
1st metatarsal joint
How is spinal nerve root impingement managed?
Majority non-surgical
Physiotherapy
Analgesia - simple analgesia and NSAIDs
Spasm - benzodiazepines (short course initially)
Unless CES and progressive neurological deficit surgery not considered earlier than 6 weeks from onset of symptoms
If symptoms >6 weeks - MRI, referral to orthopaedic surgeon
List the red flag signs of back pain and conditions they are associated with
Cauda equina syndrome - faecal incontinence, urinary retention (painless, with secondary overflow incontinence), saddle anaesthesia
Infection - immunosuppression, IVDU, fever
Fracture or infection - chronic steroid use
Fracture - significant trauma, osteoporosis or metabolic disease
Malignancy/metastatic disease - >50, history of malignancy, weight loss, night pain
Describe the clinical signs of spinal cord compression
Impaired sensation in dermatomal levels below level of cord compression
Pain
Bi/uni-lateral weakness
Upper motor neurone signs - hypertonia, hyperreflexia (absent reflexes at level of compression), Babinski’s sign, clonus
Autonomic involvement late stage - bowel incontinence, constipation, urinary retention
Describe the key presenting feature of central spinal stenosis
Intermittent neurogenic claudication = pain from intermittent compression and/or ischaemia of single or multiple nerve roots within the intervertebral foramen or central spinal canal
Symptoms when standing/walking, bending forward relieves symptoms
Lower back pain, buttock and leg pain, leg weakness, tingling, numbness
Mild symptoms may be only heaviness of legs, severe can have impaired motor function and bowel/bladder dysfunction
How can spinal cord compression be distinguished from cauda equina syndrome?
Spinal cord compression - UMN signs
Cauda equina - LMN signs
How should suspected malignant cord compression be investigated and managed?
Urgent MRI - whole MRI spine within 24 hours of presentation
Management
High dose oral dexamethasone
Urgent oncological assessment for consideration of radiotherapy or surgery
Define scoliosis and kyphosis
Scoliosis = abnormal lateral curvature of the spine
Kyphosis = excessive convex curvature of the spine (forward curvature along the sagittal plane)
Describe the types of scolisosis in terms of direction of curve
Dextroscoliosis - primary curve towards right
Levoscoliosis - primary curve towards left
Describe the presentation of scoliosis
Sideways curvature of the spine/body posture
Shoulders/hips uneven
Muscular back pain
Local ligament pain
Impaired pulmonary function - progressive severe scoliosis
Describe the presentation of kyphosis
Visible deformity of spine - excessive forward curvature
Increased forwards posture of head
Uneven shoulder height
Back pain - worse with movement
More severe - chest pain, SOB, loss of sensation, bowel/bladder incontinence
What does this X-ray show?
Thoracic scoliosis (dextroscoliosis)
What does this X-ray show?
Kyphosis
Describe the anatomic course of the ulnar nerve at the elbow
Passes posterior to elbow through ulnar (cubital) tunnel
Travels between two heads of the flexor carpi ulnaris and continues into the forearm and hand
Describe the borders of the ulnar tunnel
Medial wall - medial epicondyle of humerus
Lateral wall - olecranon of ulna
Floor - elbow joint capsule and medial collateral ligament of elbow
Roof - cubital tunnel retinaculum (arcuate ligament of Osbourne)
What sign indicates ulnar nerve palsy?
Froment’s sign - paralysis of adductor pollicis
Hold paper between thumb and index finger, paper pulled away, cannot hold onto paper without flexing thumb at interphalangeal joint
Describe causes of cubital tunnel syndrome and associated conditions
Prior fracture/dislocation of the elbow
Bone spurs/osteoarthritis of elbow
Repetitive/prolonged activities with flexed elbow
Cubitus varus or valgus deformities
Medial epicondylitis
Burns
Tumours and ganglion cysts
Heterotopic ossification
Describe the clinical features of cubital tunnel syndrome
Paresthesias of small finger, ulnar half of ring finger and ulnar dorsal hand
Initially intermittent then constant
Chronic - weakness and muscle wasting
Night symptoms - sleeping with arm in flexion, relieved by hanging arm out of bed/running under water
Examination - 4th and 5th digit clawing, ulnar nerve subluxation over medial epicondyle as elbow moves through flexion-extension, sensory deficit in ulnar digits, Froment’s sign, Tinel’s sign positive over cubital tunnel, elbow flexion for >60 seconds reproduces symptoms
How is cubital tunnel syndrome managed?
Conservative - avoid aggravating activity, physiotherapy, NSAIDs, night elbow splinting (NOT steroids - risk of injuring nerve)
Operative - cubital tunnel decompression surgery
What are the indications for surgical management of nerve root impingement?
Absolute:
Cauda equina syndrome
Progressive neurologic deficit
Relative:
Intractable radicular pain
Neurologic deficit that does not improve with conservative measures
Recurrent sciatica following successful trial of conservative measures
Describe the initial investigations and management of cauda equina syndrome
PR exam - sensation and anal tone
Bladder scan pre and post void to assess for bladder emptying
If suspicion of CES then urgent MRI
Refer to neurosurgeons if MRI not immediately available out of hours for transfer
If proven needs emergency surgical decompression
Define and compare tennis elbow and golfer’s elbow and their clinical presentation
Overuse injuries which cause elbow pain
Golfer’s elbow = medial epicondylitis (extensor carpi radialis brevis tendon)
Tennis elbow = lateral epicondylitis (flexor-pronator tendon)
Lateral epicondylitis much more common
Lateral epicondylitis - pain and tenderness over lateral epicondyle, worse on resisted wrist extension with elbow extended or supination of forearm with elbow extended
Medial epicondylitis - pain and tenderness over medial epicondyle, worse on wrist flexion and pronation, may have ulnar nerve involvement
Describe the management of Tennis elbow
Non-operative - NSAIDs, physiotherapy, steroid injections, effective in 95%
Operative - release and debridement of ECRB origin
Describe the management of Golfer’s elbow
Non-operative - NSAIDs, physiotherapy, bracing, steroid injections, effective in 95%
Operative - debridement and reattachment of flexor-pronator origin
Describe the presentation of olecranon bursitis
Swelling, pain, redness and warmth over posterior aspect of elbow. Fever and malaise if infective.
What causes olecraonon bursitis?
Trauma
Prolonged pressure
Infection
Rheumatoid arthritis
Gout
How is olecranon bursitis diagnosed?
Uric acid level
CRP
Aseptic needle aspiration of bursa (Gold standard for diagnosis of infection) - urgent gram stain, culture and sensitivity, pathology for crystals
How is olecranon bursitis managed?
Non-infective - ice, elevation, NSAIDS, treat cause (e.g. gout)
Infective - after aspiration start broad-spectrum antibiotics, oral or IV depending on severity
Recurrent - ?bursectomy
How can olecranon bursitis and septic arthritis of the elbow be distinguished?
Bursitis - ROM usually preserved, only mild discomfort unless at extremes of movement
Septic arthritis - any movement produces large amounts of pain
List causes of shoulder osteoarthritis
Primary osteoarthritis
Secondary osteoarthritis
Post-traumatic - fracture or dislocation
Inflammatory/crystalline arthritis (RA, gout etc.)
Osteonecrosis (AVN)
Rotator cuff arthropathy - massive RC tear leading to arthritis
What does this X-ray show?
Rheumatoid arthritis of the shoulder - large peri-articular erosions around humeral head, erosion of distal clavicle
Widening of acromioclavicular joint
What does this X-ray show?
Sclerosis of humeral head and glenoid fossa
Narrowed joint space
Osteophyte lower border of humeral head
= shoulder OA
Describe the clinical presentation of shoulder osteoarthritis
Shoulder pain
Reduced ROM - especially external rotation due to anterior capsule contraction
Night pain
Crepitus
How is shoulder OA managed?
Non-operative - NSAIDs, physiotherapy, steroid injections
Operative - joint replacement
List the structures which contribute to stability of the shoulder joint
Rotator cuff muscles
Glenoid labrum
Ligaments
Biceps tendon
Describe the presentation of subacromial impingement
Progressive pain in anterior superior shoulder
Pain exacerbated by abduction, relieved by rest
Associated with weakness and stiffness
Examination
Painful arm of abduction between 60-120 degrees
Neer impingement test = arm internally rotated and passively flexed, positive if pain in anterolateral shoulder
Hawkin’s test - shoulder and elbow flexed to 90 degrees, humerus stabilised, passively internally rotate arm, positive if pain in anterolateral shoulder
Describe the presentation of rotator cuff tears
Can be acute onset with injury or gradual onset
Shoulder pain
Weakness and pain with movements relating to site of tear e.g. abduction with supraspinatus tear
Night pain
Describe the special tests used for each rotator cuff muscle
Supraspinatous - Jobe’s test (empty can test)
Infraspinatous - external rotation lag
Teres minor - Hornblower sign
Subscapularis - lift-off test, Belly-press test
How are rotator cuff tears managed?
Non-operative - physiotherapy, NSAIDS, steroid injection
Operative - rotator cuff repair (young, fit), rotator cuff debridement (elderly irreparable tear), tendon transfer (young, fit, irreparable tear), reverse total shoulde arthroplasty (if massive tear with advanced arthritis)
List the conditions associated with carpal tunnel syndrome
Diabetes Mellitus
Hypothyroidism
Rheumatoid Arthritis
Acromegaly
Wrist fractures
Pregnancy
Use of heavy vibrating machinery
Describe the signs and symptoms of carpal tunnel syndrome
Nocturnal waking with tingling - relieved by shaking hands/running under water
Altered/reduced sensation in the median nerve distribution - thumb, index, middle and half of ring finger
Difficulty manipulating small objects
Clumsiness - dropping cups/mugs/loose change
Reduced power thumb abduction
Thenar muscle wasting (late sign)
+ve Tinel’s sign and Phalen’s test
Describe the management of carpal tunnel syndrome
Wrist splints - especially for nocturnal symptoms
Steroid injections - especially during pregnancy
Carpal tunnel decompression surgery - local anaesthetic with tourniquet, divide flexor retinaculum longitudinally
Describe the key X-ray changes seen in osteoarthritis
L – Loss of joint space
O – Osteophytes (bone spurs)
S – Subarticular sclerosis (increased density of the bone along the joint line)
S – Subchondral cysts (fluid-filled holes in the bone)
Describe the signs of osteoarthritis in the hands
Heberden’s nodes (in the DIP joints)
Bouchard’s nodes (in the PIP joints)
Squaring at the base of the thumb at the carpometacarpal joint
Weak grip
Reduced range of motion
How is OA of the hand managed?
Physiotherapy/exercise
Orthoses e.g. splints
Topical NSAIDs - diclofenac gel
Oral analgesics - NSAIDs
Intra-articular steroid injections - used for painful interphalangeal joints
Surgery for structural hand abnormalities if other treatments have failed - trapziectomy for thumb base OA, arthodesis/arthroplasty for interphalangeal OA
Describe the cause of flexor tendon synovitis (trigger finger) and associated conditions
Constriction and thickening of A1 pulley, nodules on tendon
Risk factors:
Activities involving prolonged gripping and use of the hand
RA
Diabetes
Female
Age
How does trigger finger present?
Initially painless clicking/locking/catching when trying to extend finger
Most commonly middle or ring finger
More than one finger can be involved, may be bilateral
Can become painful over time
What is the differential diagnosis for sticking fingers?
Trigger finger
Extensor tendon subluxation
Dupuytren’s disease
Radial nerve or PIN palsy
What is the differential diagnosis of tingling fingers?
Peripheral nerve entrapment (Carpal Tunnel Syndrome and Cubital Tunnel Syndrome)
Central nerve entrapment
Peripheral Neuropathy
How is trigger finger managed?
Non-operative - splintage, steroid injections
Operative - surgical release/widening of A1 pulley
Describe the risk factors and associated conditions of Dupuytren’s disease
M>F
Family history - autosomal dominant, variable penetrance
Caucasian Northern European
Diabetes
Epilepsy
Anti-convulsants
Alcohol/liver disease
Describe the presentation of Duputren’s contracture
Fixed flexion deformities of MCP and PIP joints, most commonly ring and little fingers
Difficulty with ADLs (can’t put hand in pocket, poke themselves in the eye when washing their face)
If young patient then ectopic manifestations are indicative of aggressive disease (= Dupuytren’s diathesis)
How is Dupuytren’s disease managed?
Needle aponeurectomy - under LA a hypodermic needle is used to cut the cords
Collagenase injections - injection of an enzyme into the cords that digests the collagen and weakens the cord allowing it to be ‘snapped’ by firm extension of finger 24-72hrs later
Fasciectomy - surgical excision of the cords
Dermofasciectomy - surgical excision of cords and overlying skin then application of a full thickness skin graft
List the most common locations of ganglion cysts
Most commonly hands and feet
Dorsal carpal
Volar carpal
Volar retinacular (tendon sheath)
Dorsal DIP joint
How are ganglion cysts managed?
Leave alone (many will spontaneously regress)
Aspirate (~50-70% successful)
Excise (~90% successful)
How should a finger amputation/partial amputation be assessed?
Level - tip, distal to flexor digitorum superficialis, proximal to FDS, hand, forearm, arm
Vascularity and time from injury
Bone, tendon and nerve injury - bone loss, nail loss, skin loss
How are distal finger tip amputations managed?
Trim bone if too long
Dressing only
Terminalisation and primary closure
Local advancement/transposition flap
How are proximal finger amputations managed?
Dependent on extent of amputation:
Distal to FDS but proximal to DIPJ - ideal for replant because PIPJ is undamaged and likely to be flexible
Proximal to FDS - if a single digit then terminalise rather than replant as PIPJ likely to be very stiff leading to a single stiff extended finger
Hand and more proximal - replant
How should hand lacerations be assessed?
Vascular assessment - capillary refill, pulses, if vascular compromise but potential for replantation/revascularisation then it is a surgical emergency
Neurological assessment - assess if there is injury to nerves of hand
Tendon assessment - if finger laceration need to differentiate between tendons of FDS (PIP flexion) and FDP (DIP, PIP and MCP flexion)
Describe the management of hand lacerations in the ED
Local anaesthetic (neurological assessment first) and irrigation
Tetanus/IV Abx
Dressing and back slab
Low threshold for surgical exploration - any suspicion of tendon/nerve injury refer to orthopaedics/plastics
Describe the presentation of hip osteoarthritis
Pain - in groin, thigh, buttock or knee
Aggravated by weight bearing and improved with rest
Worse at end of day and better in the mornings
Stiffness - improves with mobility, with grinding or crunching
Antalgic gait
Pain on passive movement, reduced ROM
Severe - fixed flexion deformity, Trendelenburg gait
How is hip OA managed?
Initial management
Analgesia - WHO analgesic ladder
Weight loss
Exercise
Smoking cessation
Physiotherapy
Steroid joint injections
Definitive management - total or hemiarthroplasty
List the complications associated with total hip replacement
Thromboembolic disease
Bleeding
Dislocation - during extremes of hip flexion, present with clunk, pain and inability to weight bear
Infection
Nerve injury
Loosening of the prosthetic
Leg length discrepancy
Describe the pathological process which causes avascular necrosis of the hip
Trauma - vascular injury to vessels supplying femoral head results in ischaemia
Non-traumatic AVN:
Intra-vascular coagulation of the intra-osseous microcirculation results in venous thrombosis
Subsequent retrograde arterial occlusion, causes intra-osseous hypertension
Decreased blood flow to osteocytes in femoral head
Disruption of vascular supply/ischaemia causes osteocyte necrosis
Process of bone resorption and incomplete repair, loss of structural integrity from demineralisation and trabecular thinning
Ultimately causes subchondral bone fracture and femoral head collapse
List common causes of avascular necrosis of the femoral head
Traumatic - femoral head/neck fracture, hip dislocation, slipped upper femoral epiphysis
Non-traumatic
Alcohol abuse
Steroids
Irradiation
Haematological disease e.g. leukaemia, lymphoma, sickle cell
Dysbaric disorders e.g. decompression sickness from deep sea diving
Hyper-coagulable states e.g. pregnancy
Connective tissue disorder e.g. SLE, vasculitis
Viral e.g. hepatitis, HIV
Idiopathic
Describe the typical presentation of slipped upper femoral epiphysis
Adolescents aged 10-16, during rapid growth
Male
Some ethnicities higher risk e.g. black
Obesity is most significant risk factor - increased forces through physis
Presentation can be acute, after injury, subacute (<3 weeks) or chronic and more insidious (>3 weeks)
May have limp
Groin pain, often referred to thigh or knee
Leg externally rotated and shortened
Localised tenderness around hip joint
Pain on attempts to rotate hip with decreased range of motion, especially internal rotation
Describe the X-ray appearance of slipped upper femoral epiphysis
Disruption of Shenton’s line
Steel sign - shadow behind superior femoral neck
Widening of physis, reciprocal decrease in height of epiphysis
Prominent lesser trochanter due to external rotation of hip joint
Klein’s line - line drawn along superior edge of the femoral neck fails to intersect the lateral part of the superior femoral epiphysis
What are the X-ray views used to identify slipped upper femoral epiphysis?
AP pelvis, frog-leg lateral
Check opposite hip joint as bilateral SUFE not uncommon
List the risk factors for developmental dysplasia of the hip
Female
First born
Left hip (60%, due to common intra-uterine position)
Breech position in utero or delivery
Family history in parent or first degree sibling
Other MSK abnormalities e.g. foot deformity
Oligohydramnios
Large birthweight for gestational age
Define developmental dysplasia of the hip
Abnormal development of the hip joint resulting in dysplasia (shallow underdeveloped acetabulum), possible subluxation of the joint (partial displacement) and potential hip dislocation (complete displacement)
Describe the clinical presentation of developmental dysplasia of the hip at each stage of development
Neonate to <3 months:
Asymmetry e.g. extra or deeper thigh creases
Positive Ortolani and Barlow tests (palpable hip subluxation on exam), reduced abduction
> 3 months to 18 months:
Asymmetry, leg length discrepancy
Limitation in hip abduction
> 1 year to walking child:
Difficulty walking or unusual gait
Lumbar lordosis, Trendelenburg gait (abductor weakness), toe-walking (to accommodate for leg length discrepancy)
Pelvic obliquity (misalignment)
Delayed presentation into childhood and adolescence:
Groin, thigh, trochanter hip pain
Leg length discrepancy
Unexpectedly large ROM
Describe the imaging which can be used in diagnosis of developmental dysplasia of the hip at each stage and the findings
Neonate to <3 - hip joint US
>6 months - femoral head begins to ossify so X-rays can be used
Delayed presentation - X-ray may show early onset osteoarthritis
Describe the clinical tests used to diagnose developmental dysplasia of the hip
Barlow test - attempts to dislocate an articulated femoral head
Ortolani test - attempts to relocate a dislocated femoral head
How is developmental dysplasia of the hip managed at each stage?
Neonate to <3 months - splintage of joints in abduction and flexion with hips in a reduced position (Pavlik harness) can result in remodelling of acetabulum
> 3 months to 18 months - closed or open reduction of hip joint under anaesthesia with immobilisation in hip spica cast for minimum of 3 months
> 1 year to walking child - closed or open reduction under anaestheisa with immobilisation in hip spica cast for minimum 3 months +/- femoral or acetabular osteotomy if significant dysplasia
Delayed presentation - femoral or acetabular osteotomy, if OA already started to develop will likely require total hip replacement
Describe the typical history of a patient presenting with a quadriceps tendon rupture
Usually elderly men with pre-existing tendinopathy from fall or eccentric loading of tendon - complain of pain in area before rupture (indicates tendinopathy)
In younger patient usually direct trauma
Describe the clinical presentation of quadriceps tendon rupture
Site of rupture typically at insertion of tendon into patella
Can be complete or partial
Bruising and swelling around quadriceps tendon
Tenderness at site of rupture
May have palpable defect
Unable to extend knee against resistance
If complete tendon rupture present may be unable to perform straight leg raise
Describe the typical history of a patient presenting with a patellar tendon rupture
Affects younger age group than quadricep rupture, commonly male and aged 20 – 40
Infra-patellar pain after sudden quadriceps contraction with knee in flexed position e.g. jumping during sport
May have popping sensation
Describe the clinical presentation of patellar tendon rupture
Elevated patella with large haemarthrosis
Tenderness at site of rupture
May have palpable defect around inferior pole of patella
If complete tear will be unable to straight leg raise or maintain extension of knee
Reduced ROM at knee joint with difficulty weight bearing
List the risk factors for quadricep and patella tendon ruptures
Previous tendon injury
Existing tendinopathy
Previous corticosteroid injection
Steroid use
Co-morbidities e.g. SLE, rheumatoid arthritis, chronic renal disease, diabetes
Increasing age (for quadricep rupture)
Describe the findings on X-ray in quadriceps/patellar tendon rupture and the views needed to visualise changes
Quadriceps - AP and lateral X-rays of knee will show effusion and possible ‘patella baja’ (abnormally low lying patella)
Patella - AP and lateral X-rays of knee show proximal migration of the patella, ‘patella alta’
How are quadriceps and patella tendon ruptures managed?
Quadriceps - open repair followed by protection in extension cast or splint
Patella
Non-operative (for partial tears with intact extensor mechanism) - immobilisation in full extension with progressive exercise programme
Operative (for complete rupture) - open repair of tendon
Describe the typical mechanism of a meniscal tear
Traumatic tear - young patients, twisted knee while flexed and weight-bearing, onset of symptoms soon after
Degenerative disease - older patients, more minor twisting
How does a meniscal tear present?
Typical mechanism of injury
Pain, may localise periarticularly
Instability, more notable when flexed
Swelling and effusion around knee, develops gradually following injury
Localised joint line tenderness on palpation, medial side more commonly injury than lateral
ROM limited by swelling and effusion
Locking - block to full extension, indicates torn meniscus is becoming trapped between joint
Positive McMurray’s test
Describe the typical mechanisms associated with knee ligament injuries
ACL - forced flexion or hyperflexion of the knee, twisting injury or direct blow behind upper tibia, often sporting injury
PCL - hyperextension or forced displacement of upper tibia with respect to femur, can occur when falling onto an object, less common than ACL
MCL - twisting injury, possible to have pure valgus force but uncommon
LCL - varus force, less common than MCL
Describe the presentation of knee ligament injuries
ACL - haemarthrosis which develops rapidly after injury, generalised tenderness, positive anterior drawer and Lachman’s test
PCL - haemarthrosis, generalised tenderness, posterior sag
MCL - bruising and swelling over medial knee, tenderness over ligament and medial joint, laxity on valgus stress
LCL - bruising and swelling over lateral knee, tenderness over ligament and lateral joint, laxity on varus stress
Describe the clinical presentation of hallux valgus
Painful medial prominence, aggravated by walking, weight bearing, wearing narrow-toed shoes
Hallux in valgus, pronated position at rest
May have inflammation or skin breakdown over prominence at base of hallux
Excessive ROM in transverse plane
Contracture of extensor hallucis longus with longstanding joint subluxation
Describe the radiological features of hallux valgus
Lateral deviation and joint subluxation
Measure angle between first metatarsal and first proximal phalanx - diagnosed if angle >15 degrees (mild 15-20, moderate 21-39, severe >40)
List the risk factors for development of hallux valgus
Female
Connective tissue disorders
Hypermobility syndromes
Anatomical variants - long first metatarsal bone, malalignment of the first MTP joint, and flat feet
How is hallux valgus managed?
Analgesia
Adjusting footwear
Orthosis if flat feet
Physiotherapy
Surgical management - if QOL significant impacted
Chevron procedure - osteotomy of first metatarsal, shifted laterally to normal alignment, fixed by pins and screws (mild deformity)
Scarf procedure - osteotomy of shaft of first metatarsal, distal portion moved laterally and fixed with screws (moderate to severe)
Lapidus procedure - base of first metatarsal and medial cuneiform fused (if tarsometatarsal joint hypermobility)
Keller procedure - MTP joint capsule opened, joint surfaces removed, stabilised by suturing surrounding tissues (if MTP arthritis)
Describe the attachments of the Achilles tendon and its function
Gastrocnemius (originates on the posterior femur) and soleus (originates on the posterior fibula and medial tibia, deep to gastrocnemius) join together to form the Achilles tendon, which inserts on the posterior calcaneus
Contraction of these muscles causes plantarflexion of the foot to allow for walking, running and jumping
Describe the presentation of Achilles tendonitis
Pain/aching in heel, worse with activity, stiffness, tenderness, swelling, nodules on palpation
Simmonds’ test negative
List the risk factors for Achilles tendon rupture
Sports – ‘weekend warrior’
Increasing age
M>F
Achilles tendinopathy
Steroid injections, systemic steroids
Fluoroquinolone antibiotics e.g. ciprofloxacin, levofloxacin
Describe the typical mechanism of Achilles tendon rupture
Usually traumatic during a sporting event
Can occur with:
Sudden forced plantarflexion
Violent dorsiflexion in a plantarflexed foot
Describe the clinical presentation of Achilles tendon rupture
Symptoms:
Suggestive history with pop
Sudden onset pain in Achilles/calf
Feeling of something hitting them in the back of the leg
Difficulty walking, unable to stand on tiptoes
Signs:
Increased resting ankle dorsiflexion
Loss of power on plantar flexion (still possible due to peroneal tendons)
Increased passive dorsiflexion
Positive Simmonds’ test
Palpable ‘step’ or gap in Achilles tendon
How is an acute Achilles tendon rupture managed?
Same-day orthopaedics review
Immediate management:
Analgesia
Immobilisation – splinted in plaster in full equinus (toes pointed)
Non-weight bearing
VTE prophylaxis while immobilised
Conservative
Boot to immobilise ankle, initially with foot in full plantarflexion, over 6-12 weeks ankle gradually moved to neutral position, higher rate of rerupture than surgery
Operative
Open end-to-end achilles tendon repair or percutaneous repair
After repair, same process of immobilisation in plantarflexion –> neutral position
Describe the clinical features of pes planus
Adults - frequently rolling ankle/ankle sprains
Children - asymptomatic usually
Pain across medial longitudinal arch and ankle, can also affect midfoot, heel, knee, hip or back
Standing - medial arch dropped, calcaneal valgus
Altered gait pattern
Contracted Achilles tendon
Describe the clinical features of pes cavus
Pain under first metatarsal
Calcaneal varus
Plantar fasciitis
Ankle arthritis
Achilles tendonitis
Back pain
Tripping
Lateral ankle instability and foot pain
List the common causes and associated conditions of pes cavus
Often underlying neurological condition - Charcot-Marie-Tooth idsease, spinal dysraphism, polyneutritis, intraspinal tumours, poliomyelitis, syringomyelia, Friedreich ataxia, cerebral palsy, spinal cord tumours
Congenital clubfoot
Post-traumatic bone malformation
Contracture of plantar fascia
Shortening of Achilles tendon
List the common causes and associated conditions of pes planus
Congenital:
Hypermobility syndromes - Ehlers-Danlos syndrome, Down syndrome, Marfan’s syndrome
Cerebral palsy
High BMI
Acquired:
Diabetes
Foot and ankle injury - rupture or dysfunction of posterior tibial tendon
Pregnancy
List the factors which contribute to development of diabetic foot disease
Neuropathy - peripheral neuropathy and loss of proprioceptive sensation
Peripheral arterial disease - macro and microvascular ischaemia
List complications of diabetic foot disease
Calluses
Ulceration
Charcot’s arthropathy
Cellulitis
Osteomyelitis
Gangrene
Describe the pathophysiology of osteoporosis
Imbalance between bone formation and bone resorption - resorption by osteoclasts takes weeks, formation by osteoblasts takes months
Increased activity of osteoclasts and osteoblasts
Loss of trabecular bone, both mineralised and collagen components
Describe the pathophysiology of osteomalacia
Qualitative bone disorder secondary to low vitamin D levels that lead to decreased bone mineral content
Causes low calcium and phosphate levels - secondary hyperparathyroidism leads to increased reabsorption of bone
Causes:
Vitamin D deficiency - malabsorption (coeliac, IBD), lack of sunlight, diet
CKD
Drug induced e.g. anticonvulsants
Inherited - hypophosphataemic rickets
Liver disease e.g. cirrhosis
Describe the types of osteomalacia and examples of causes of each
Vitamin D dependent:
Low UV exposure
Low oral intake
Low intestinal absorption (cyastic fibrosis, chronic pancreatitis, coeliac disease, gastrectomy)
Drugs - anticonvulsants
Hepatobiliary disease
Rare hereditary forms
Alcoholism
Tumours
Hypophosphataemia
Vitamin D independent (decreased mineralisation due to phosphate deficiency):
Defects in renal tubular functioning - renal tubular acidosis, Fanconi syndrome
Drugs - bisphosphonates, fluoride, excessive use of phosphate-binding antacids
Rickets - defective mineralisation during growth in childhood
Vitamin D resistant Rickets (hypophosphataemic, X-linked dominant)
Vitamin D deficiency Rickets (nutritional)
Type I and II Vitamin D dependent (autosomal recessive)
Renal osteodystrophy
Hyperparathyroidism
Describe the clinical presentation of Ricket’s
Most prominent at large physes - knee, wrist
Fraying and widening of metaphysis - cupping
Increased physeal width and cortical thinning and bowing
Bowing of long bones
Rachitis rosary - widening of anterior rib at costal cartilages leads to lines of prominences (like beads)
Kyphosis
Flattening of skull
May have pain at deformities
Describe the biochemical features of osteomalacia
Low serum calcium
Low serum phosphate
High serum Alk phos
High serum PTH
Low Vit D - 25-(OH) and 1,25-(OH)
Low urinary calcium
Describe the clinical features of osteomalacia
Pain in bones and muscles
Proximal muscle weakness - waddling gait
Fractures - insufficiency fractures (Looser zones - wide, transverse lucencies with sclerotic borders traversing partway through a bone)
Trefoil pelvis - loss of pelvic volume
Biconcave vertebral fracture
How is osteomalacia managed?
Vitamin D supplementation - may require loading dose
Calcium supplementation if dietary intake insufficient
Describe the clinical features of Paget’s disease
Localised pain and tenderness
Increased focal temperature due to hyperaemia - vasculariy
Increased bone size
Bowing deformities
Kyphosis
Decreased ROM
Often asymptomatic at time of diagnosis
Describe the pathophysiology of Paget’s disease
?Viral aetiology - paramyxovirus + genetic susceptibility
Increased uncoordinated osteoclast and osteoblast activity - lytic –> sclerotic
Patchy areas of high density (sclerotic) and low density (lytic) bone - enlarged, misshaped bones with structural problems, increased risk of pathological fractures
Usually polyosteotic - femur, tibia, pelvis, skull, spine affected commonly
Describe the biochemical features of Paget’s disease
Calcium and phosphate normal Alkaline phosphate raised
Urinary hydroxyproline raised
Describe the radiological features of Paget’s disease
Skull
Osteoporosis circumscripta - large, well-defined lytic lesion
Cotton wool appearance - mixed lytic and sclerotic
Diploic widening - expansion of cancellous bone between innner and outer tables of calvaria
Tam O’Shanter sign - skull hanging over facial bones
Pelvis
Cortical thickening and sclerosis of iliopectineal and ischiopubic lines
Acetabular protrusion
Enlargement of pubic rami and ischium
Long bones
Blade of grass/candle flame sign - subchondral area of lucency with advancing tip of V-shaped osteolysis, extending towards diaphysis
Lateral curvature of femur
Anterior curvature of tibia
Spine
Picture frame sign - cortical thickening and sclerosis encasing the vertebral margins
Squaring - flattening of normal concavity of anterior margin of vertebral body
Vertical trabecular thickening
List common complications associated with Paget’s disease
Deafness - cranial nerve entrapment
Osteogenic sarcoma
Fractures
Skull thickening
High-output cardiac failure
Spinal stenosis and spinal cord compression
Hyperparathyroidism
How is Paget’s disease managed?
Expectant if symptoms minimal
Bisphosphonates first line
Calcitonin
Arthroplasty/fracture fixation if necessary - likely to bleed excessively
Describe the pathophysiology of avascular necrosis
Mechanisms which lead to ischaemic - vascular interruption, intravascular occlusion, intraosseous extravascular compression
Reduced subchondral blood supply induces hypxoia, leading to loss of integrity of cell membranes and necrosis of cells
Invasion of neutrophils and macrophages
Causes subchondral collapse and subsequent joint degeneration
List risk factors for avascular necrosis
Direct cellular toxicity - chemotherapy, radiotherapy, thermal injury, smoking
Intravascular occlusion - coagulation disorders, sickle cell crises
Repetitive trauma
Steroids - high doses for prolonged periods
Alcohol misuse
Autoimmune disease e.g. lupus
Bisphosphonate use
Decompression illness
List the most common sites of avascular necrosis
Sites with retrograde blood supply or low collateral capabilities
Femoral head
Knee
Talus
Humeral head
Mandible
Wrist - lunate, scaphoid
Describe the aetiology of and risk factors for ankylosing spondylitis
90% are HLA-B27 positive
Affected first degree relative
Typically presents in young men - affects men and women equally ?
Describe the clinical features of ankylosing spondylitis
Typically young man in teens - 30s
Symptoms develop gradually over >3 months
Lower back pain and stiffness and sacroiliac pain
Worse with rest, improves with movement
Pain worse at night and in the morning - takes at least 30 minutes for stiffness to improve
Reduced lateral flexion, reduced forward flexion (Schober’s test), reduced chest expansion
Systemic associations (As)
Achilles tendonitis (+ plantar fasciitis - enthesitis)
Anaemia
Anterior uveitis
Aortitis, aortic regurgitation
Apical fibrosis (pulmonary fibrosis)
AV node block - heart block
+
Inflammatory bowel disease
Weight loss, fatigue
Chest pain
Dactylitis
Restrictive lung disease
List common benign bone tumours and describe their features (origin, site, demographic, X-ray appearance)
Osteoid osteoma - arises from osteoblasts, tend to be small, most common in long bones (femur, tibia), <25 y/o, X-ray sclerotic margin and radiolucent nidus
Osteochondroma - derived from cartilage/bone, most common benign bone tumours, usually males <20 y/o, X-ray catilage-capped ony projection on external surface of bone, metastatic transformation rare
Giant cell tumour - tumour of multinucleated giant cells within a fibrous stroma, 20-40 years, usually in epiphysis of long bone, X-ray shows double bubble or soup bubble
Enchondroma - cartilage tumour, usually in hands, 20-50, well-defined lucent, central medullary lesion on X-ray
Lipoma - tumours of mature fat, 40-60, common in upper back, thighs, buttocks, shoulders, arms. may see radiolucent lesion on X-ray, seen on CT/MRI
Which cancers commonly metastasise to bone?
Breast
Prostate
Thyroid
Renal
Lung
Which cancers can present with bone pain?
Bone tumours - primary or mets
Myeloma
Lymphoma
What are the most common sites for bone metastases?
spine
pelvis
ribs
skull
long bones
How do bone metastases present?
Bone pain
Pathological fractures
Hypercalcaemia
Raised ALP
List the most common primary bone malignancies and their tissue of origin
Osteosarcoma - bone
Ewing’s sarcoma - marrow
Chondrosarcoma - cartilage
Describe the presentation of primary bone malignancies
Bone pain - worse at night, constant or intermittent, resistant to analgesia
Atypical bony or soft tissue swelling/masses
Pathological fractures
Easy bruising
Mobility issues - unexplained limp, joint stiffness, reduced ROM
Inflammation and tenderness over bone
Systemic symptoms - weight loss, fatigue, night sweats
Describe the typical demographics for primary bone malignancies (age, sex, genetic associations, location)
Osteosarcoma - mostly in teens - 20s (growth spurt), associated with genetic conditions (Li Fraumeni p53 and familial retinoblastoma RB1) arise from metaphysis of distal femur, proximal tibia or proximal humerus
Chondrosarcoma - males, 30-50, proximal femur, distal femur, pelvis, scapula
Ewing’s sarcoma - children, diaphysis of long bones such as femur, tibia and humerus, also flat bones e.g. pelvis
Describe the investigations for primary bone tumours
X-ray - malignant poorly defined with blurred borders, involve soft tissue, have cortical destruction
MRI - soft tissue involvement
Bone biopsy
Staging - Enneking staging system (based on surgical grade, local extent and presence or absence of metastases)
Describe the X-ray appearance of common primary bone tumours
Osteosarcoma - medullary and cortical destruction, significant periosteal reactions (Codman’s triangle or Sunburst pattern)
Ewing’s sarcoma - lytic lesion with periosteal reactions, layers of reactive bone leading to ‘onion skin’ appearance
Chondrosarcoma - lytic with calcification, cortical remodelling, endosteal scalloping
How are common primary bone tumours managed?
Osteosarcoma - aggressive surgical resection, systemic chemotherapy
Ewing’s sarcoma - neoadjuvant chemo then surgical excision
Chondrosarcoma - surgical resection
List common post-operative complications in orthopaedic patients
Blood loss
Delirium
Nausea
Infection
Pain
AKI
Shock
Compartment syndrome
Thromboembolic disease
Describe the clinical assessment of delirium
History not always possible
Screening tool - abbreviated mental test score (AMTS), more detailed e.g. MMSE, ACE-III
Clinical examination
Confusion screen - FBC, U&Es, LFTs, coag/INR, urinalysis, imaging (CT head, CXR) etc.
List risk factors for delirium
Age >65
Multiple co-morbidities
Underlying cognitive impairment e.g. dementia
Renal/hepatic impairment
Male
Sensory impairment - hearing, visual
Significant injury
Sleep disturbance
Pain
Environmental changes
Drugs - illicit, alcohol
Describe the strategy for management of pain post-operatively
WHO pain ladder
Step 1 - PRN paracetamol
Step 2 - PRN opioid (+ ketamine infusion?)
Step 3 - PRN opioid (nurse controlled or PCA)
Step 4 - opioid infusion
List risk factors for nausea and vomiting in post-op patients
Female
History of motion sickness or previous PONV
Non-smoker
Post-operative opiates
Younger age
Use of volatile anaesthetics
Describe the assessment of pyrexia in post-operative patients
A-E assessment if unstable
History - symptoms which point to symptoms
Examine for signs of resp infection, UTI, IV line infections, wound infections, calf tenderness, specific signs from operation (e.g. peritonism in anastomotic leak)
Septic screen - bloods, urinalysis, cultures, imaging
Scores - qSOFA (RR >22, altered mental state, SBP <100, >2 points)
List causes of hypovolaemia in post-operative patients
Blood loss - intra- or post-operative
GI loss - vomiting/diarrhoea
Being NBM for prolonged period without adequate replacement
Third space losses - sepsis, bowel obstruction, burns
Relative hypovolaemia - anaesthetic drugs
List clinical features of post-operative haemorrhage
Tachypnoea
Tachycardia
Dizziness
Agitation
Reduced urine output
Hypotension
Reduced consciousness level
Describe the classes of blood loss
Class I
<750ml, <15% blood loss
HR, BP, RR normal
Urine output >30ml/hr
Class II
750-1500ml, 15-30% blood loss
HR 100-120, normal BP, RR 20-30
Urine output 20-30ml/hr
Class III
1500-2000ml, 30-40% blood loss
HR 120-140, BP low, RR 30-40
Urine output 5-20ml/hr
Class IV
>2000ml, >40% blood loss
HR >140, BP low, RR >40
Urine output <5 ml/hr
Describe management of post-operative haemorrhage
A-E assessment
Direct pressure to bleeding site if visible
Urgent blood transfusion if moderate to severe - if severe bleeding: packed red cells, platelets, FFP
May need to re-operate for definitive haemostasis
Describe the pathological factors which contribute to development of venous thromboembolism post-operatively
Virchow’s triad:
Blood stasis - immobilisation, tourniquet
Endothelial injury - surgical disruption, position, manipulation of limb
Hypercoagulability - trauma response/blood loss, patient factors e.g. smoking, sepsis, malignancy
Describe the presentation of post-operative patients with VTE
DVT - unilateral leg pain and swelling
PE - sudden onset dyspnoea, pleuritic chest pain, cough, rarely haemoptysis, tachycardia, tachypnoea, pyrexia, raised JVP, pleural rub/effusion
List risk factors for VTE
Increasing age
Previous VTE
Smoking
Pregnancy or recently post-partum
Recent surgery (especially abdominal surgery, pelvic surgery, or hip or knee replacements)
Prolonged immobility (> 3 days)
Hormone replacement therapy or the combined oral contraceptive pill
Current active malignancy
Obesity
Known thrombophilia disorder (e.g. antiphospholipid syndrome or Factor V Leidin)
List initial investigations and management of post-operative patients with suspected DVT
DVT - calculate Well’s score
<1 - measure d-dimer to exclude
>1 - doppler scan (or contrast venography)
Management - DOAC usually (sometimes warfarin or LMWH or both), 3 months in provoked DVT, may require lifelong anticoagulation if persistent risk factor or high risk recurrence
Describe initial investigations and management of post-operative PEs
PE Well’s score
<4 - D-dimer to exclude
>4 - CTPA (or V/Q scan if poor renal function)
ECG - sinus tachycardia typically seen
Management - if stable anticoagulate with DOAC (or LMWH +/- warfarin), if unstable thrombolysis, IVC filter if secondary to recurrent DVTs
Describe thromboprophylaxis for surgical patients
Consider in all patients undergoing lower limb surgery
Al patients undergoing surgery should have mechanical thromboprophylaxis - anti-embolic stocking, intermittent pneumatic compression (intra-operatively), early mobilisation
Pharmacological prophylaxis - aspirin, warfarin, unfractionated heparin (e.g. clexane), DOACs (rivaroxaban, apixaban)
Describe the pathophysiology of fat embolism syndrome
Occurs when fatty tissue enters the systemic circulation
Mechanical theory - fatty tissue directly released into vascular circulation due to trauma (long bone fractures are greatest risk)
Biochemical theory - inflammatory response to trauma causes release of free fatty acids into the venous system from bone marrow
Fat emboli cause severe inflammatory response in local tissues, increases vessel permeability - causes cerebral oedema and ARDS
List the risk factors for fat embolism syndrome
Young age
Long bone fractures
Closed fractures
Multiple fractures
Conservative management for long bone fractures
Hip/knee arthroplasty
Describe the clinical presentation of fat embolism syndrome and the criteria used in diagnosis
Following trauma/surgery, within 24-72 hours
Worsening shortness of breath
Confusion, drowsiness
Petechial rash - classically axilla and conjunctiva
On examination - tachypnoea, tachycardia, hypoxia
Non-specific neurological signs - acute confusion, seizures
Low grade pyrexia
Gurd’s criteria - 2 major or 1 major and 4 minor
Major - petechial rash, respiratory insufficiency, cerevbral involvement
Minor - tachycardia, pyrexia, retinal changes, jaundice, thrombocytopaenia, anaemia, raised ESR, fat macroglobinaemia
Describe the investigations used in diagnosis of fat embolism syndrome and findings which suggest FES
Bloods - FBC, CRP, U&Es, LFTs, clotting screen
ABG - type 1 respiratory failure
Blood film - fat globules
CXR - bilateral diffuse pulmonary infiltrates
CTPA - ground-glass changes with global distribution
Describe management of fat embolism syndrome
Largely supportive - mostly require respiratory support (mechanical ventilation)
Steroids not shown to be effective in treatment
How can fat embolism syndrome be prevented?
Fix long bone fractures as early as possible
Close monitoring of patients with intramedullary nailing - continuous pulse oximetry
List the organisms commonly associated with bone and soft tissue infections
Staph aureus
Streptococci
Pseudomonas
MRSA
Salmonella - sickle cell disease
List the clinical features of a patient presenting with sepsis
Symptoms of infection e.g. urinary symptoms, cough/SOB, erythematous/discharging wound, peritonism
Features of organ dysfunction - hypoxia, oliguria, AKI, thrombocytopaenia, coagulation dysfunction, hypotension, hyperlactaemia (>2), reduced consciousness
How should a patient presenting with sepsis be initially managed?
Sepsis 6:
Measure urine output - catheterise if appropriate
Measure lactate (+ other routine bloods)
Take blood cultures - prior to Abx
Give IV fluids - initial bolus 500-1000ml, ongoing reassessment
Give IV antibiotics - empirical then targeted therapy
Give oxygen - 15L trauma non-rebreather mask, aim for 94-98% (88-92% in chronic CO2 retainers)
Describe management of native and prosthetic joint septic arthritis
Empirical antibiotics started ASAP after blood cultures and joint aspirate taken
Native joint - IV flucloxacillin (IV vancomycin if MRSA or penicillin allergic, + gentamicin if high risk for gram negative)
Prosthetic joint - IV vancomycin + IV gentamicin
Infected native joint - irrigation and debridement (may need multiple)
Prosthetic - washout, revision surgery (acute or staged)
Describe the presentation of limb cellulitis
Erythema
Warm to touch
Tense
Thickened
Oedematous
Bullae - fluid-filled blisters
Golden-yellow crust - staph aureus infection
Systemic upset - fever, confusion, tachycardia, hypotension, tachypnoea
Describe the spectrum of severity of cellulitis
Eron classification
Class I - no signs of systemic toxicity, no uncontrolled co-morbidities
Class II - systemically unwell or systemically well but with co-morbidity (e.g. PAD, chronic venous insufficiency, morbid obesity)
Class III - significant systemic upset e.g. acute confusion, tachycardia, tachypnoea, hypotension, unstable co-morbidities or limb threatening infection due to vascular compromise
Class IV - sepsis syndrome or a severe life-threatening infection e.g. necrotising fasciitis
How is cellulitis managed?
Mild skin/soft tissue infection - oral flucloxacillin
Moderate/severe cellulitis - IV flucloxacillin (IV vancomycin if MRSA/penicillin allergy, IV clindomycin if rapidly progressing)
List the types and causes of necrotising fasciitis
Type I - polymicrobial, mixture of anaerobes (e.g. bacteroides) and aerobes (e.g. staph aureus), more common, especially in elderly/co-morbid
Type II - monomicrobial, primarily caused by strep pyogenes (group A strep, can also be Panton-Valentine leucocidin-positive staph aureus), more common in young patients with history of trauma
Describe the clinical features of necrotising fasciitis
May have precipitating event e.g. bite, trauma, surgery
Rapid progression
Severe pain, out of keeping with clinical signs
Haemodynamic instability - fever, tachycardia, hypotension
Multi-organ dysfunction
Overlying skin can be normal initially, will progress with erythema, oedema, crepitus, vesicles/bullae, obvious skin necrosis
Positive finger sweep test
How is necrotising fasciitis managed?
Suspected necrotising fasciitis - urgent debridement/surgical exploration, antibiotics (flucloxacillin, benzxylpenicillin, metronidazole, clindamycin, gentamicin)
Describe the clinical presentation of a hand or limb abscess
Painful
Tender
Erythematous
Initially swelling is firm, then progresses to fluctuant, may then spontaneously drain
Local cellulitis
Lymphangitis - tracking
Regional lymphadenopathy
Fever
How is a hand or limb abscess managed?
Incision and drainage if significant pain/swelling - usually under LA, may require GA
Antibiotics if signs of systemic infection, cellulitis, immunocompromise
List common causes of a limping child
Toddler:
Transient synovitis
Infection - septic arthritis, osteomyelitis
Developmental dysplasia of the hip
Trauma - any fracture, sprain etc.
Older child:
Transient synovitis
Infection
Trauma
Perthes’ disease
Adolescent
Transient synovitis
Infection
Trauma
Slipped upper femoral epiphysis
Late Perthes’
Overuse syndromes - Osgood Schlatter’s disease, Sever’s disease
Other
Neuromusclar - Duchenne’s muscular dystrophy, cerebral palsy
Bony dysplasia - club foot
Discoid meniscus
Osteochondritis dissecans
Tarsal coalition
Arthritides
How can the diagnosis of the cause of a limping child be determined from history/examination/investigation features?
Trauma - history of injury, X-ray appearance (stress fracture may not be visible initially)
Infection - pyrexial, generally unwell, pain on any movement of joint, local warmth/tenderness, raised WCC, CRP/ESR
Transient synovitis - age 3-8, similar presentation to infection but less severe, often preceded by viral illness, may be recurrent, bloods usually normal
DDH - usually picked up early on routine checks, if missed may present with limp or delayed gait, shortened leg, reduced abduction, painless
Perthes’ disease - boys > girls, age 4-8
SCFE - usually around puberty, groin or knee pain
Osgood-Schlatter’s disease - palpable tender lump at tibial tuberosity, anterior knee pain, exacerbated by physical activity
Meniscal tear - twisting injury, symptoms of locking or catching
Juvenile arthritis - gradual onset, intermittent joint pain and swelling, single joint often affected, general malaise
Describe the differences between fractures in children and fractures in adults
More buckle and greenstick fractures - bone more fibrous with tough periosteum
Epiphyseal growth plate is area of weakness - epiphyseal fractures occur commonly
Less severe growth plate fractures (Salter-Harris I-III) do not cause growth disturbance, more severe (Salter-Harris IV) traverses growth plate and cause growth disturbance if not properly reduced
Fracture healing occurs faster, difficult to correct position if not done quickly
Remodelling ability means less than perfect position can be acceptable (ability decreases with age)
Loss of length is made up by overgrowth (as long as <2cm)
Produce more callus - often palpable
Pathological fractures occur due to bone cysts, osteitis, neoplasm, osteogenesis imperfecta
Describe the classification of growth plate fractures in children and the most common locations of each fracture type
Salter-Harris classification
Salter-Harris I - separation of growth plate without bone involvement (metaphysis or epiphysis), most commonly at distal fibular epiphysis
Salter-Harris II - fracture across growth plate, small fragment of metaphysis attached to epiphysis, most commonly at distal radial epiphysis
Salter-Harris III - fracture across growth plate with extension across epiphysis, most commonly at distal tibial epiphysis, occasionally in epiphyses of proximal and middle phalanges of fingers
Salter-Harris IV - combination of II and III, fracture line traverses epiphysis and part of diaphysis, most commonly in lateral condylar mass of elbow and distal tibial epiphysis
Salter-Harris V - crush injury of part of the epiphysis, nothing seen on X-ray, diagnosis only made as result of deformity occurring at growth plate, most common at distal tibial epiphysis but rare
What are the important points in examination of a supracondylar distal humeral fracture in children?
Neurological examination - evaluate for:
AIN neuropraxia - unable to flex interphalangeal joint of thumb and distal interphalangeal joint of index finger (can’t make OK sign)
Median nerve injury - loss of sensation over volar index finger
Radial nerve neuropraxia - inability to extend wrist, MCP joints, thumb IUP joint
Vascular exam - assess pulse and perfusion
Describe the pathophysiology of deformity in clubfoot
Cavus (high arch) - tight intrinsics, flexor hallucis longus, flexor digitorum longus
Adductus of forefoot - tight tibialis posterior
Varus - tight tendoachilles, tibialis posterior, tibialis anterior
Equinus (limited dorsiflexion) - tight tendoachilles
(CAVE)
List conditions associated with clubfoot
Most commonly idiopathic. Associations include:
Spina bifida
Cerebral palsy
Edward’s syndrome (trisomy 18)
Oligohydramnios
Arthrogryposis
How is clubfoot managed?
Conservative (most common) - Ponseti method
Manipulation and progressive casting, usually corrected in 6-10 weeks, usually requires Achilles tenotomy
Brace at night until 4 years old
List red flags for non-accidental injury in children
Multiple injuries
Bruises shaped like hands or identifiable objects
Bruises, lacerations or abrasions on non-bony parts of body or face/ears
Multiple bruises or clustered bruises
Bruises, lacerations or abrasions in a child who cannot mobilise
Human bites
Thermal injuries in places you would not expect to come into contact with a hot object, in the shape of an object (e.g. cigarette) or sharply delineated (immersion injury)
Fractures of different ages on imaging (especially if no record of seeking medical care)
Occult rib fractures, spiral fractures, metaphyseal corner fractures
Multiple subdural haemorrhages
Retinal haemorrhages
Delayed presentation
List common paediatric lower limb/foot conditions which can be normal variants
Pigeon toeing (persisting femoral anteversion) - normal variant aged 2-4, due to rotational posture of hips and joint laxity, worsened by sitting in W position, resolves with time
Splay feet - opposite to pigeon toed, resolves naturally with time usually
Genu varum and valgum - often bow legs from 6 months - 2 years, above 2 years knock knee is more common, often worse in obese children but resolve spontaneously
Flat feet - most infants have flat feet, arch reappears when standing on toes and will resolve with age
Describe the clinical presentation of psoriatic arthritis
Equally occurs in men and women, most commonly presents ages 30-50
Mostly peripheral polyarticular disease, asymmetric
DIP joint involvement common
Axial involvement 5% at presentation
Pain, morning stiffness, swelling, tenderness of joints
Enthesitis - inflammation at insertion of tendons and ligaments, most commonly Achilles
Dactylitis - inflammation of whole digit, fingers or toes
Severity of arthritis and skin symptoms usually do not correlate
Skin disease - scalp, intergluteal and perianal lesions associated with higher risk of PsA
Nail disease - discoloured (yellow/brown), onycholysis, pitting, ridging, subungal keratosis
List comorbidities commonly associated with psoriatic arthritis
CVD - hypertension, IHD (mitral valve prolapse, aortic root dilation, aortic regurgitation)
Lymphoma/malignancy
Depression
Uveitis
Obesity
Osteoporosis
NAFLD
Renal disease
IBD
Describe the differences between psoriatic and rheumatoid arthritis in terms of presentation
Rheumatoid has autoantibodies
Rheumatoid tends to be more symmetrical whereas PsA is usually asymmetrical
Psoriasis has skin and nail involvement
DIP and axial involvement in PsA, rare in RA
Enthesitis and dactylitis in PsA
Bone proliferation occurs in PsA, more bone erosion in RA
Genetic susceptibility - HLA-B27 in PsA, HLA-DRB1 in RA
Describe the radiological features of psoriatic arthritis
Periostitis - inflammation of periosteum, causes thickened, irregular outline of bone
Ankylosis - bones join together
Osteolysis - destruction of bone
Dactylitis - soft tissue swelling
Pencil-in-cup appearance - central erosions of bone beside joints, one bone looks hollow, other is narrow and sits inside the cup
How is psoriatic arthritis managed?
NSAIDs first line for peripheral arthritis, axial disease, dactylitis and enthesitis
Topical treatment first line for skin/nail disease
Systemic DMARDs (e.g. methotrexate) second line for peripheral arthritis, skin and nail changes
Biologics (anti-TNF, IL-12, 23, 17) option for inadequate response to first line for peripheral arthritis, axial disease, dactyltitis, enthesitis, skin and nail disease
Intra-articular steroid injections option for peripheral arthritis
List assessment tools for psoriasis and psoriatic arthritis
Screening test:
Psoriasis Epidemiology Screening Tool (PEST)
Measurement of response to treatment:
Psoriatic arthritis response criteria (PsARC) for disease improvement
American College of Rheumatology Response (ACR20)
Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) - used for axial disease
Dermatology assessment tool:
Psoriasis Area and Severity Index (PASI)
How does ankylosing spondylitis present clinically?
Typically young man, teens - 20s (actually affects men and women equally)
Gradual onset lower back pain and stiffness
Sacroiliac pain (buttocks)
Pain and stiffness worse with rest, improves with movement
Pain worse at night, may wake from sleep
Morning stiffness - >30 minutes
Reduced lateral flexion and forward flexion (Schober’s test)
95% HLA-B27 positive
List the extra-axial associations of ankylosing spondylitis
Enthesitis - Achilles, planter fasciitis
Dactylitis
Uveitis
Aortitis
Heart block
Restrictive lung disease
Pulmonary fibrosis - apical
Chest pain - costosternal joint inflammation
Anaemia
IBD
Peripheral arthritis
List the radiographical changes seen in ankylosing spondylitis
Squaring of vertebral bodies
Subchondral sclerosis and erosions
Small erosions at corners of vertebral bodies with reactive sclerosis - shiny corner sign
Syndesmophytes - bone overgrowth where ligaments insert into bone
Ossification of ligaments, discs and joints
Fusion of facet, sacroiliac, costovertebral joints
= ‘Bamboo spine’
List radiographic features of sacroiliitis
Sacroiliac joints widen then narrow
Subchondral erosions, sclerosis, proliferation of iliac side
End-stage - SI joint may be seen as a thin line or not visible
What does this MRI show?
Decreased fat signal, increased fluid signal due to bone oedema adjacent to sacroiliac joints = active sacroiliitis (likely to be normal on X-ray)
How is ankylosing spondylitis managed?
NSAIDs first line - manage pain (can try multiple NSAIDs if response not adequate)
Steroids - used during flares to control symptoms (oral, IM or joint injections)
Biologics - anti-TNF, IL-17
Physiotherapy
Bisphosphonates for osteoporosis
Surgery occasionally for deformities of spine/other joints - spinal fractures are complication
Describe the clinical presentation of enteropathic arthritis
Peripheral and axial arthritis (including sacroiliitis with or without spondylitis)
Extra-articular manifestations - enthesitis, dactylitis, tendonitis, periostitis, osteoporosis, uveitis, erythema nodosum, pyoderma gangrenosum
+ inflammatory bowel disease
How is enteropathic arthropathy managed?
Steroids/DMARDs (including anti-TNF) used to treat IBD often help with symptoms of arthritis
Can also use intra-articular steroid injections, NSAIDs (may exacerbate IBD)
Describe the clinical presentation of reactive arthritis
Onset after gastroenteritis or sexually transmitted infection (chlamydia most common) - within 4 weeks
Typically asymmetrical
1-3 joints affected usually
Warm, swollen, painful joint
Extra-articular associations - dactylitis, urethritis, conjunctivitis, uveitis, circinate balanitis, keratoderma blenorrhagica
HLA-B27 positive
How is reactive arthritis managed?
Need to rule out septic arthritis - give antibiotics until this has been done (via joint aspirate, taken before antibiotics started, also send for crystal examination)
NSAIDs
Steroid injections into affected joint
Systemic steroids may be required, especially when multiple joint affected
Most resolve within 6 months and don’t recur, recurrent cases may require DMARDs or anti-TNF medications
Describe the tools used to monitor inflammatory spinal disease activity
BASDAI – Bath Ankylosing Spondylitis Disease Activity Index
BASFI – Bath Ankylosing Spondylitis Functional Index
BASMI – Bath Ankylosing Spondylitis Metrology Index (measures spinal mobility)
Measure CRP
List the key points in a rheumatological history
PRISM:
P - pain - SOCRATES
R - rashes, skin lesions and nail changes
I - immune - systemic sclerosis (CReST), SLE, Sjogren’s
S - stiffness (RA, AS, SLE, reactive arthritis)
M - malignancy - weight loss, night sweats, fatigue, fever, appetite
Extra-articular manifestations - uveitis, dry eyes/mouth, interstitial lung disease, urethritis etc.
Describe the clinical presentation and laboratory findings of polymyalgia rheumatica
> 50, F>M
Bilateral proximal muscle pain and stiffness in neck, shoulder and pelvic girdle for >2 weeks
Worse with movement
Interferes with sleep
Morning stiffness for >45 minutes
Systemic symptoms - fever, weight loss, night sweats, malaise, anorexia
Strong association with giant cell arteritis - may present with symptoms of GCA (jaw claudication, scalp tenderness, visual changes)
CRP/ESR raised
Antibodies negative
How is polymyalgia rheumatica managed?
Steroids - response aids diagnosis
Prednisolone 15mg/day, assess response and step down dose
(give PPI and bone protection)
Describe the presentation and laboratory features of giant cell arteritis
Severe unilateral headache around temple/forehead
Scalp tenderness
Jaw claudication
Blurred or double vision
Irreversible painless complete sight loss can occur rapidly
Systemic symptoms - fatigue, depression, fever, anorexia, night sweats
50% have features of PMR
ESR/CRP high
Temporal artery biopsy - multi-nucleated giant cells
How is GCA managed?
Immediate initiation of steroids (before confirming diagnosis) - if no visual loss high-dose oral prednisolone, if vision loss IV methylprednisolone given first (+ same day ophthalmology review)
PPI and bone protection
Taper steroid dose over months
Aspirin 75mg daily - decreases vision loss and stroke
Describe the types of systemic sclerosis (scleroderma)
Limited cutaneous systemic sclerosis - most common, involves skin or face and skin below elbows and knees (hands and feet)
Diffuse cutaneous systemic sclerosis - same areas affected as limited disease + skin on trunk and proximal limbs and internal organs (lungs, kidneys, heart, GI tract)
Describe the clinical presentation of systemic sclerosis
Limited cutaneous systemic sclerosis - CREST
C - calcinosis, deposits of calcium in soft tissues
R - Raynaud’s, colour change in hands from white –> purple –> pink
E - oesophageal dysmotility - dysphagia
S - sclerodactyly - thickness and tightness of skin of fingers
T - telangiectasia red spots around mouth, nose and sometimes palms
Diffuse systemic sclerosis -
CREST symptoms + proximal limb and trunk skin involvement
GI - oesophagitis, oesophageal strictures, paralytic ileus, constipation, malabsorption
Lungs - interstitial fibrosis, pulmonary hypertension
Cardiac - pericarditis, heart failure, arrhythmias
Kidneys - glomerulosclerosis, intimal hyperplasia
Which antibodies are associated with systemic sclerosis?
ANA - positive in 90%
Anti-SCL 70 - more associated with diffuse
Anti-centromere - more associated with limited
(RF positive in 30%)
How is systemic sclerosis managed?
Immunosuppressants slow disease progression - cyclophosphamide
Analgesia
CCB for Raynaud’s (nifedipine)
Skin emollients
Describe the clinical presentation and laboratory findings in polymyositis and dermatomyositis
Symmetrical, proximal muscle weakness
Mostly affects shoulder and pelvic girdle
Extra-skeletal manifestations - dysphagia, interstitial lung disease, arrhythmias, acute tubular necrosis
Elevated creatinine kinase is key diagnostic feature
Dermatomyositis - same symptoms with skin involvement
Gottron lesions (scaly erythematous patches) on knuckles
Photosensitive erythematous rash on back, shoulders and neck
Purple rash on face and eyelids (heliotrope)
Periorbital oedema
Subcutaneous calcinosis
Can be a paraneoplastic syndrome
Which antibodies are associated with polymyositis and dermatomyositis?
Anti-Jo-1 antibodies - polymyositis (+ dermatomyositis, especially associated with interstitial lung disease)
Anti-Mi-2 antibodies - dermatomyositis
ANA - dermatomyositis
How are polymyositis and dermatomyositis managed?
High-dose steroids - assess response by improvement in muscle strength
Methotrexate, azathioprine, mycophenolate used as steroid sparing agents
IVIG, plasmapheresis, biologics may be used if inadequate response
List the types of vasculitis by vessel size
Large vessel:
Giant cell arthritis
Takayasu’s arteritis
Aortitis
Medium vessel:
Polyarteritis nodosa
Eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome)
Kawasaki disease
Small vessel:
Henoch-Schonlein purpura
Eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome)
Microscopic polyangiitis
Granulomatosis with polyangiitis
Anti-glomerular basement membrane disease
Describe the general presentation of vasculitis
Purpura
Joint and muscle pain
Peripheral neuropathy
Renal impairment
Gastrointestinal disturbance (diarrhoea, abdominal pain and bleeding)
Anterior uveitis and scleritis
Hypertension
Systemic - fatigue, fever, weight loss, anorexia, anaemia
Describe the immune laboratory findings in vasculitis
CRP/ESR usually raised
Autoantibodies:
ANCA positive - most vasculitides
p-ANCA (MPO antibodies) - microscopic polyangiitis and Churg-Strauss syndrome
c-ANCA (PR3 antibodies) - granulomatosis with polyangiitis
Immune complex small vessel vasculitis
Henoch-Schonlein purpura - IgA
Goodpasture’s - anti-GBM
List risk factors for SLE
Female
Ethnicity - Asian, Hispanic, Black
20s-30s
Sunlight exposure
Genetic - family history, HLA-DR2/3
Describe the clinical presentation of SLE
Constitutional symptoms - fatigue, fever, mouth ulcers, lymphadenopathy, weight loss
Musculoskeletal - arthralgia (non-erosive), myalgia
Skin - malar rash, discoid rash, photosensitivity, Raynaud’s, livedo reticularis, non-scarring alopecia
Cardiovascular - pericarditits, myocarditis
Respiratory - pleurisy, fibrosing alveolitis
Renal - proteinuria, glomerulonephritis
Neuropsychiatric - anxiety and depression, psychosis, seizures
Describe the laboratory findings in SLE
Anaemia
Leukopaenia
Thrombocytopaenia
Raised ESR
CRP usually normal unless co-existing infection
Immunology
ANA raised - high sensitivity
Anti-Smith antibodies - high specificity
Anti-dsDNA - high specificity, also used to monitor disease activity
Antiphospholipid antibodies - secondary to SLE, in 40%, associated with increased risk of VTE
List the measures used to monitor disease activity in SLE
ESR
CRP usually normal unless underlying infection
Complement (C3/4) - low during active disease (complex formation leads to consumption of complement)
Anti-dsDNA used for disease monitoring
How is SLE managed?
First line - NSAIDs, steroids, hydroxychloroquine
Sun avoidance and suncream
Other immunosuppresants in resistant/severe disease - methotrexate, ciclosporin, azathioprine etc.
Biologic therapies - rituximab, belimumab
Describe the clinical presentation of Sjogren’s syndrome
Dry eyes - grittiness, foreign body, irritation
Dry mouth - difficulty swallowing food, dental caries, decreased taste
Salivary gland and lacrimal gland enlargement
Vaginal dryness
Associated conditions - cutaneous vasculitis, arthralgia, interstitial lung disease, dysphagia, nausea, interstitial nephritis, renal tubular acidosis, peripheral neuropathy, fibromyalgia
Lymphoma - long term risk
How is Sjogren’s syndrome diagnosed?
Schirmer test - filter paper under lower eyelid, measure level of moistness after 5 minutes (<10mm significant)
Often RF and ANA positive
Anti-Ro - positive in 70%
Anti-La - positive in 30%
How is Sjogren’s syndrome managed?
Artificial saliva and tears
Pilocarpine - stimulate tears/salivary flow
Punctal occlusion
Systemic treatment - hydroxychloroquine, methotrexate
Biologics - rituximab
Describe the presentation of mixed connective tissue disease
Raynaud’s
Arthralgia
Skin inflammation and thickening, hair loss
Muscle weakness
Oesophageal dysfunction
Pulmonary hypertension
Interstitial lung disease
Rarely - cardiac and renal involvement
Lymphadenopathy
Splenomegaly
Which antibodies are associated with mixed connective tissue disease?
ANA
Anti-RNP - specific
Describe the presentation of anti-phospholipid syndrome
Venous/arterial thrombosis - DVT, PE, stroke, MI
Recurrent miscarriages
Livedo reticularis
Thrombocytopaenia
Prolonged APTT
Pre-eclampsia
Pulmonary hypertension
Which antibodies are associated with antiphospholipid syndrome?
Antiphospholipid antibodies:
Lupus anticoagulant
Anticardiolipin antibodies
Anti-beta-2 glycoprotein I antibodies
How is antiphospholipid syndrome managed?
Primary thromboprophylaxis - low-dose aspirin
Secondary thromboprophylaxis -
Initial venous thromboemoblic events - lifelong warfarin with target INR of 2-3
Recurrent VTE - lifelong warfarin (add aspirin), INR 3-4
If pregnant - LMWH + aspirin
List the antibodies tested for in diagnosis of rheumatological diseases and the conditions most strongly associated with each
RF - rheumatoid arthritis
ANA - generally connective tissue disorders
Anti-CCP - RA
Anti-dsDNA - SLE
Anti-Ro - Sjogren’s, neonatal lupus
Anti-La - Sjogren’s
Anti-SM - SLE
Anti-Jo-1 - polymyositis
Anti-centromere - limited cutaneous systemic sclerosis
Anti-Scl-70 - diffuse cutaneous systemic sclerosis
Anti-RNP - mixed connective tissue disease
p-ANCA (MPO) - microscopic polyangiitis and Churg Strauss
c-ANCA (PR3) - granulomatosis with polyangiitis
Describe the patterns of disease seen in ANCA-associated vasculitis
Includes granulomatosis with polyangiitis (Wegner’s), eosinophilic granulomatosis with polyangiitis (Churgh-Strauss syndrome) and microscopic polyangiitis
Highest incidence in >70s
Symptoms:
Constitutional - fever, weight loss, fatigue, night sweats, myalgia
Upper respiratory tract - epistaxis, crusty nasal secretions, hearing loss, sinusitis, saddle shaped nose due to septum perforation
Lower respiratory tract - cough, wheeze, haemopytsis, consolidation on CXR
Kidneys - glomerulonephritis
Skin - purpuric rash
Eye - scleritis
Nerve - peripheral neuropathies (wrist/foot drop)
