Musculoskeletal Flashcards
Rheumatoid arthritis (RA)
a chronic systemic inflammatory autoimmune disorder that primarily affect the joints but may also manifest with extra articular features e.g. rheumatoid nodules or pulmonary fibrosis
Epidemiology of rheumatoid arthritis (RA)
affects ~1% of the population
more commonly seen in women (2-4x)
peak age of onset 30-50 yrs
Risk factors for rheumatoid arthritis (RA)
smoking*
genetic predisposition (HLA-DR4, HLA-DR1)
obesity
Family history of RA
Arthritic presentation of rheumatoid arthritis (RA)
Polyarthritis:
symmetrical pain, swelling, heat, stiffness (stiffness worse in morning lasting >30min) of affected joint
usually affects metacarpopahryngeal (MCP) / proximal interphalangeal (PIP) / metatarsopharyngeal (MTP) joints, later progressing to affect larger joints
Joint deformities (later in disease):
swan neck deformity (PIP hyperextension, DIP flexion)
boutonniere ferocity (PIP flexion, DIP hyperextension)
Z deformity of thumb (hyperextension of interphalangeal joint, fixed flexion of MCP)
ulnar deviation of fingers
atlantoaxial subluxation
piano key sign (dorsal subluxation of ulna)
NB Distal interphalangeal joints (DIP) are really affected, DIP involvement usually indicates psoriatic arthritis
extra articular manifestations of rheumatoid arthritis (RA)
Rheumatoid nodules:
skin (non tender firm swellings)
lungs (bilateral & peripheral)
Lungs:
pleuritic chest pain, fibrosis
Eyes:
keratoconjunctivitis sicca (most common)
episcleritis, scleritis
anaemia carpal tunnel syndrome purpura vasculitic ulcers Raynauds phenomenon (recurrent vasospasm of fingers & toes)
Examination findings for rheumatoid arthritis (RA)
compression test (Gaenslen squeeze test) = painful compression of MCP joint
may present as painful handshake
Investigation findings for rheumatoid arthritis (RA)
ESR/CRP (↑)
FBC (normochromic normocytic anaemia + thrombocytosis)
LFTs (↑ALP, ↑ gamma GT)
Rheumatoid factor (+ve in 70% of pts)
Antinuclear antibody - ANA (+ve in 30% of pts)
anti-cyclic citrullinated peptide (anti-CCP) antibody (+ve in 70% of pts)
synovial fluid analysis (cloudy, yellow appearance, leucocytosis (WBC = 5000-50,000) ↑proteins)
X-rays (early = loss of joint space, juxta-articular osteoporosis, soft tissue swelling, late= periarticular erosions, subluxation, bon/cartilage erosion, suchondral cysts)
USS (synovitis)
Imagine findings for rheumatoid arthritis (RA)
X-rays:
early = loss of joint space, juxta-articular osteoporosis, soft tissue swelling
late= periarticular erosions, subluxation, bon/cartilage erosion, suchondral cysts
USS; synovitis
Disease severity score for rheumatoid arthritis (RA)
DAS28
Diagnostic criteria for rheumatoid arthritis (RA)
≥6 points is considered RA
Joint distribution: 1 large joint = 0 points 2-10 large joints = 1 point 1-3 small joints = 2 points 4-10 small joints = 3 points >10 joints (at least 1 small) = 5 points
Serology:
negative RF & anti-CCP = 0 points
low positive RF or anti-CCP = 2 points
high positive RF or anti-CCP = 3 points
Duration:
< 6 weeks = 0 points
> 6 weeks - 1 point
Acute phase reactants:
normal CRP/ESR = 0 points
↑ CRP/ESR = 1 point
Antibodies for rheumatoid arthritis (RA)
Rheumatoid factor (+ve in 70% of pts)
Antinuclear antibody - ANA (+ve in 30% of pts)
anti-cyclic citrullinated peptide (anti-CCP) antibody (+ve in 70% of pts)
anti-CCP is most specific
Non drug management of rheumatoid arthritis (RA)
MDT approach
exercise
pain clinics
Pharmacological management rheumatoid arthritis (RA)
Symptomatic treatment:
NSAIDs (e.g. ibuprofen, naproxen) or COX-2 inhibitors (e.g. celecoxib) + a PPI (e.g. lansoprazole)
Corticosteroids:
for short-term flare up management and short term bridging treatment when starting DMARDs
DMARDs:
1st line: Methotrexate + corticosteroids to bridge treatment
other options: hydroxychloroquine, sulfalazine, leflunomide
Biologicals:
if moderate/severe disease after >3 months of DMARDs
e.g. rituximab, TNF-inhibitors (e.g. adalimumab, etanercept)
Methotrexate
given once a week orally, usually co-precribed with folic acid
monitoring: FBC / LFTs / renal function
Side effects: myelosuppresion, liver cirrhosis, pneumonitis, teratogenic (i.e. do not get pregnant )
NB avoid NSAIDs on day of methotrexate dose
Hydroxychloroquine
no regular blood test required
considered safe in pregnancy
side effects: retinopathy (bullseye retinopathy), corneal deposits
Sulfalazine
safe in pregnancy
monitoring: FBC / LFTs / renal function
side effects: interstitial lung disease, oligospermia, Heinz body anaemia, rash
Leflunomide
monitoring: FBC / LFTs / renal function / BP&weight
side effects: cushingoid features, osteoporosis, impaired glucose tolerance, HTN
Felty’s syndrome
complication of rheumatoid arthritis
triad of RA, splenomegaly, neutropenia
only seen in seropositive RA
treat firstling with methotrexate
Caplan syndrome
complication of rheumatoid arthritis in combination with pneumoconiosis (e.g. asbestosis/silicosis)
rapid development of basilar nodules & obstruction of ventilation
usually seen with coal dust exposure
Occular complications of rheumatoid arthritis
dry eye syndrome (keratoconjunctivitis sicca)
episcleritis
scleritis
steroid induced cataracts
Other complications of rheumatoid arthritis
osteoporosis respiratory (bronchiolitis, pulmonary fibrosis, pleural effusion, pulmonary nodules, bronchiolitis) raynauds phenomenon depression amyloidosis carpal tunnel syndrome vasculitis & vasculitic ulcers atlanta axial subluxation (due to inflammatory destruction of ligaments )
Raynaud phenomenon
characterised by paroxysmal vasospasm & subsequent vasodilatory chain of events affecting peripheral arterioles usually in the hands & feet
typically presents in young women
triggers: cold, emotional stress
Aetiology of raynauds
primary = raynauds disease:
onset usually <30y/o
secondary = raynauds phenomenon
may be related to RA, SLE, scleroderma, meds (COCP)
usually later onset in RA/SLE, >40 y/o
Presentation of Raynauds
usually symmetrical ischaemic phase (white) = vasoconstriction → hypoxic phase (blue) → hyperaemic phase (red) = vasodilation affects fingers & toes lasts 15-30 min after removing trigger no tissue damage / ulceration in primary
Management of Raynauds
avoid triggers
1st line: Nifedipine
2nd line: IV prostacyclin (lasts weeks to months)
Polymyalgia rheumatica (PMR)
inflammatory condition of unknown cause
generally affects people ~70y/o, more common in women
usually seen in pts of northern european descent
associated with HLA-DR4 & giant cell arteritis (10% of PMR pts have GCA)
Presentation of polymyalgia rheumatica (PMR)
usually rapid onset (,1 month)
fatigue, malaise, weight, polyarthralgia
morning stiffness (>45min)
symmetric pain/aches of shoulders/pelvic girdle/neck
no weakness
Investigating polymyalgia rheumatica (PMR)
ESR & CRP (↑) (ESR >50mm/h)
negative Rheumatoid factor
no autoantibodies
USS (bursitis of affected joint)
Management of polymyalgia rheumatica (PMR)
low dose corticosteroids e.g. 15mg prednisolone (typically dramatic response to steroids)
NB if no response to steroid consider alternative diagnosis
Giant cell arteritis (GCA) / temporal arteritis
Type of large vessel vasculitis
granulomatous vasculitis of large & medium sized arteries primarily affecting branches of the external carotid arteries, most commonly the temporal artery
most common form of systemic vasculitis in adults
Epidemiology of giant cell arteritis (GCA)
most commonly seen in northern european populations
typical onset >50y/o
more common in women (2-3x)
commonly associated with polymyalgia rheumatica (up to 50% of GCA pts have PMR)
Presentation of giant cell arteritis (GCA)
usually rapid onset (<1 month) headache (temporal/occipital) scalp tenderness unexplained facial pain jaw claudication vision loss/abnormality, diplopia, amaurosis fugax abnormal temporal artery on palpation
Investigations for giant cell arteritis (GCA)
ESR & CRP (↑)
FBC (normochromic normocytic anaemia)
Temporal artery biopsy (gold standard)
temporal artery USS (halo sign, wall thickening, stenosis)
Management of giant cell arteritis (GCA)
1st line: glucocorticoids e.g, prednisolone (give even if negative biopsy but GCA suspected)
+prophylaxis against side effects of long term steroid use e.g. bone protection
NB if no response to steroids, reconsider diagnosis
urgent ophthalmological review (visual loss often irreversible)
Sjogren syndrome
systemic autoimmune condition with lymphocytic infiltration of exocrine glands
Types:
primary = idiopathic, associated with HLA-DR52
secondary (~60% of cases) = associated with RA, SLE, systemic sclerosis, primary biliary cirrhosis
onset usually age 30-40 yrs
~10x more common in women
↑ risk of lymphocytic malignancy (MALT lymphoma)
Sjogren syndrome presentation
Xerostomia (dry mouth) xerophthalmia (dry eyes) keratoconjunctivitis sicca vaginal dryness & dyspareunia dental carries faitgue arthrlagia recurrent parotitis nasal dryness raynauds
Sjogren syndrome investigations
ESR (↑) Rheumatoid factor - RF (+ve in 50%) Antinuclear antibody - ANA (+ve in 70%) anti La - SSB (+ve in 30%) anti Ro - SSA (+ve in 70%)
Schirmers test (quantitatively measures tears) = +ve (<5mm of paper in 5 min)
salivary gland biopsy (focal lymphocytic infiltration)
USS of parotid glands
Sjogren syndrome antibodies
Rheumatoid factor - RF (+ve in 50%)
Antinuclear antibody - ANA (+ve in 70%)
anti La - SSB (+ve in 30%)
anti Ro - SSA (+ve in 70%)
Sjogren syndrome management
Symptomatic treatment:
artificial tears, artificial saliva, regular dental hygiene
pilocarpine (muscarinic agonist) = ↑ saliva & tear production
Antiphospholipid syndrome
autoimmune disorder with ↑ risk of thrombosis as a result of procoagulatory antibodies causing a hypercoaguable state
may be:
primary = idiopathic, associated with HLA-DR7
secondary = associated with SLE, RA, neoplasms
more common in females, usually seen young, fertile women
Antiphospholipid syndrome presentation
recurrent thrombotic events (DVT/PE/livido reticular/sinus thrombosis/stroke/TIA/MI)
recurrent miscarriages/premature birth/IUGR/pre-eclampsia
pulmonary hypertension
thrombocytopenia
arthralgia
splinter haemorrhages
Antiphospholipid syndrome investigations
antiphospholipid antibodies (aPL) / Lupus anticoagulant / anticardiolipin antibodies (on 2 occasions ≥12 weeks apart)
FBC (thrombocytopenia, haemolytic anemia)
clotting (↑APTT)
USS for DVT
MRI/CT (for CVD & PEG)
Antiphospholipid syndrome management
lifestyle modifications
acute management: LMWH/UFH
thromboprophylaxis: low dose aspirin (primary), or warfarin (secondary)
low dose LMWH in pregnancy if ≥pregnancy losses
Ankylosing spondylitis
a type of seronegative spondyloarthropathy, a chronic inflammatory disease of the axial skeleton leading to partial / complete fusion & rigidity of the spine
Epidemiology of Ankylosing spondylitis
peak onset 20-30yrs
3:1 male:female ratio
NB women tend to have milder, subclinical disease
Genetics of Ankylosing spondylitis
strong family tendency (~90% of disease inherited genetically)
associated with HLA-B27
Presentation of Ankylosing spondylitis
back & neck pain (gradual onset, dull pain, slowly progressive)
morning stiffness (improves with activity)
tender sacroiliac joints & buttock pain
↓ mobility of spine (↓ lateral & forward flexion)
↓ chest expansion
enthesitis (especially of achilles tendon)
unilateral anterior uveitis
fatigue
↓ lumbar lordosis
Investigations for Ankylosing spondylitis
pelvic X-ray (sacroilitis = subchondral erosions, sclerosis)
CRP/ESR (↑)
HLA-B27 (+ve)
Spine X-ray (bamboo spine, single central radio dense line (dagger sign), squared vertebral bodies, bony bridges between adjacent vertebrae, syndesmophytes)
Imaging findings for Ankylosing spondylitis
Spine X-ray (bamboo spine, single central radio dense line (dagger sign), squared vertebral bodies, bony bridges between adjacent vertebrae, syndesmophytes)
pelvic X-ray (sacroilitis = subchondral erosions, sclerosis)
Chest X-ray (apical fibrosis)
MRI/CT
Management of Ankylosing spondylitis
1st line: physiotherapy & NSAIDs
2nd line: TNF-alpha inhibitors or DMARDs e.g. sulfalazine if peripheral arthritis
complications of Ankylosing spondylitis
osteoporosis
cardiac problems e.g. aortic regurg
lung problems e.g. apical fibrosis, restrictive pulmonary disease
Psoriatic arthritis / psoriatic arthropathy
chronic inflammatory joint disease associated with psoriasis, its a seronegative inflammatory arthritis
~80% of its have preceding arthritis
most common in middle age, 35-55 yrs
associated with HLA-B27/B17/DR4/DR7
Presentation of psoriatic arthritis
most common presents as asymmetric oligoarthritis mainly affecting DIP & PIP joint with possible spinal involvement (sacroilitis)
enthesitis (mainly achilles tendon & plantar fascia)
tenosynovitis
dactylics (single digits, inflammation & swelling)
nail changes (pitting, yellowing, onycholysis)
history of scalp/nail problems
psoriasis
NB DIP involvement is indicative of psoriatic arthritis
Investigating psoriatic arthritis
X-rays of hands & feet (asymmetrical bony erosions, DIP/PIP involvement)
ESR/CRP (↑)
synovial fluid aspirate (no crystals, ↑ WCC)
CASPAR criteria (to diagnose psoriatic arhtirits)
Management of psoriatic arthritis
NSAIDs (if mild)
local corticosteroid injection
1st line: DMARDs (consider early in disease e.g. methotrexate (if significant cutaneous psoriasis) or leflunomide, sulfalazine)
2nd line: TNF-alpha inhibitors (inadequate control by DMARDs)
Gout
an inflammatory crystal arthropathy caused by the precipitation & deposition of uric acid crystals (monosodium rate crystals) synovial fluid & tissues
more common in men & older people (especially men aged 30-60yrs)
Risk factors for gout
male gender obesity HTN CHD CKD HF diabetes drugs (e.g. diuretics, chemo, cytotoxic drugs)
Presentation of gout
acute onset joint pain with a swollen/tender/erythematous joint (70% of first attacks/50% of all attacks affect 1st metatarsophalangeal (MTP) joint)
other joints affected include knee, wrist, ankles, elbows, small hand joints
tophi may be present (asymmetrical, chalky nodule under skin)
Investigations for gout
May be clinical diagnosis if typical presentation in 1st MTP
synovial fluid analysis (strongly negatively bifringent needle-shaped crystals under polarised light)
serum uric acid (>420 micro mol/L in men / >360micromol/L in women)
X-ray (periarticular erosions, punched out lesions, no periarticular osteopenia)
Synovial fluid analysis results for gout
strongly negatively bifringent needle-shaped crystals under polarised light
Management of gout
Acute attack:
1st line: colchicine & NSAIDs
2nd line: oral prednisolone (if colchicine & NSAIDs contraindicated e.g. Renal problems)
Chronic:
1st line: allopurinol (xanthine oxidase inhibitor)
2nd: febuxostat
Lifestyle modifications:
limit alcohol intake, lose weight
Indications for offering urate lowering therapy
Indications for urate-lowering therapy (ULT):
Offer urate-lowering therapy to all patients after their first attack of gout
ULT is particularly recommended if: >= 2 attacks in 12 months tophi renal disease uric acid renal stones prophylaxis if on cytotoxics or diuretics
Pseudogout / calcium pyrophosphate deposition disease (CPPD)
a crystalline inflammatory arthritis caused by the deposition of calcium pyrophosphate crystals intro articular & periarticular tissues
common in elderly people aged >60 yrs
Causes of pseudogout in younger people
in people <60y/o
precipitating factors include haemochromatosis, hyperparathyroidism, ↓Mg2+, ↓Phosphate, acromegaly, Wilson’s disease
Presentation of pseudogout
often asymptotic
acute monoarticular/oligoarticular arthritis most often affecting the knees
other joints include wrists, shoulders, ankles, hands, feet
usually older than gout but also painful, swollen, erythematous joints
NB may present as a sudden worsening of osteoarthritis
Investigations for pseudogout
synovial fluid analysis (positively bifringent rhomboid shaped crystals under polarised light)
serum Ca/PTH (normal or ↑)
USS
X-ray (chonedrocalcinosis i.e. joint carriage calcificatioN)
Synovial fluid analysis results for pseudogout
positively bifringent rhomboid shaped crystals under polarised light
Management of pseudogout
1st line: NSAIDs
2nd line: intrarticular steroids
3rd line: systemic steroids / colchicine
NB colchicine used if NSAIDS/Steroid contraindicated
Systemic lupus erythematous (SLE)
chronic multisystem autoimmune disease of unknown cause, Type II hypersensitivity reaction
most common in women of childbearing age
onset usually age 20-40 yrs
more common in afro-caribbeans/asians
associated with HLA-B8/DR2/DR3
Presentation of Systemic lupus erythematous (SLE)
malar (butterfly) rash (over cheeks & bridge of nose)
fever, fatigue, weight loss
arthritis in 90% of cases (mainly PIP/MCP joints, generally symmetrical)
Rayanuds
photosensitive rash (rash after sun exposure)
discoid lupus (discoid rash in sun exposed area, scaly erythematous plaques)
mouth ulcers
non-scarring alopecia
myalgia
Systemic features of Systemic lupus erythematous (SLE)
Cardiac:
pericarditis (most common), endocarditis (Libman-Sacks endocarditis), CAD, aortic valve disease
Pulmonary:
pleurisy, pulmonary fibrosis, interstitial lung disease)
nephritis:
Most dangerous organ complication and a common cause of death in SLE, affects >30% of SLE pts
depression/anxiety
vasculitis
Investigations for Systemic lupus erythematous (SLE)
Anti nuclear (ANA) antibody (+ve)
Rheumatoid factor (usually -ve)
anti-dsDNA (+ve)
anti-smith antibodies (+ve)
ESR (↑)
FBC (normochromic normocytic anaemia)
CRP (normal)
antiphospholipid antibodies (may be +ve)
Antibodies for Systemic lupus erythematous (SLE)
Anti nuclear (ANA) antibody (+ve)
Rheumatoid factor (usually -ve)
anti-dsDNA (+ve)
anti-smith antibodies (+ve)
NB anti-dsDNA & anti-smith antibodies =most specific
Management of Systemic lupus erythematous (SLE)
Simple analgesia & NSAIDs (use with care due to GI/cardiac/renal risks) for pain control
avoid sun exposure
corticosteroids (usually as induction therapy)
1st line: Hydroxychloroquine
2nd line: add methotrexate or azathioprine
Cyclophosphamide (for life threatening disease e..g nephritis)
Exacerbating factors for Systemic lupus erythematous (SLE)
oestrogen hormones can exacerbate SLE
consider hormonal contraception carefully
Associated conditions for Systemic lupus erythematous (SLE)
antiphospholipid syndrome
Drug induced lupus
95% of cases are positive for anti-histone antibodies
implicated drugs include chlorpromazine, methyldopa, hydralazine, isoniazid, d-penicillamine and minocycline
Systemic sclerosis/scleroderma
auto-immune mediated tissue disease characterised by production of auto-antibodies and overproduction of collagen due to ↑fibroblast activity leading to abnormal connective tissue growth & fibrosis of skin/organs & vasculopathy
Types of systemic sclerosis
limited cutaneous systemic sclerosis (lcSSc):
more common mainly affects distal limbs & face
may present with CREST syndrome (Calcinosis, Raynaud’s phenomenon, oEsophageal dysmotility, Sclerodactyly, Telangiectasia)
associated with anti-centromere antibodies
diffuse cutaneous systemic sclerosis (dcSSc):
less common, affects proximal limbs & trunk as well as face & distal limbs
↑ risk of mortality (mainly pulmonary involvement)
associated with anti-scl-70 antibodies / anti topoisomerase
Scleroderma:
no internal organ involvement, tightening & fibrosis of skin only
Epidemiology of systemic sclerosis
5:1 female:male ratio
presentation usually 30-50 yrs
Presentation of limited cutaneous systemic sclerosis
a subtype is CREST syndrome
- Calcinosis
- Raynaud’s phenomenon
- oEsophageal dysmotility
- Sclerodactyly
- Telangiectasia
scleroderma affects face and distal limbs predominately
Presentation of systemic sclerosis
thickening & hardening of skin (skin appears smooth/shiny/puffy)
sclerodactyly (fibrotic thickening & tightening of skin of fingers & hands)
Raynauds
multiple painful ischaemic digital ulcers
joint stiffness & pain
mask like facies
microstomia
salt & pepper appearance of skin (dyspigmentation)
myalgia
Antibodies for systemic sclerosis
Anti-nuclear (ANA) antibody (+ve)
anti-scl-70 antibodies / anti topoisomerase associated with diffuse cutaneous systemic sclerosis
anti-centromere antibodies associated with limited cutaneous systemic sclerosis
Myositis
systemic inflammatory muscle wasting disease characterised by weakness due to chronic inflammation of skeletal muscle
PM & DM = 2x more common in women
Types of myositis
Polymyositis (PM):
inflammatory myopathy affecting proximal skeletal muscle
Dermatomyositis (DM):
similar to polymyositis but with skin involvement
Inclusion body myositis (IBM):
inflammatory myositis affecting proximal & distal skeletal muscle
Polymyositis
usually presents age 30-60
symmetrical proximal muscle weakness e..g of pelvic & shoulder girdle, dysphagia, muscle tenderness
Dermatomyositis
2 peaks: 5-15yrs & 40-60yrs
symmetrical proximal muscle weakness e..g of pelvic & shoulder girdle, dysphagia, muscle tenderness
gottrons papules (prominent erythematous papules)
heliotrope rash (erythematous rash on upper eyelids)
mechanics hands (hyperpigmentation & thickening of skin on hands)
photosensitive poikiloderma
V-sign erythema (upper chest & neck)
Inclusion body myositis
usually presents >60y/o
slowly progressive (over years), weakness of proximal & distal muscles
Investigating myositis
often a clinical diagnosis
CK (↑) ESR/CRP (↑) LDH (↑) adolase (↑) muscle biopsy (gold standard) EMG ANA (+ve) myositis specific antibodies
Management of myositis
corticosteroids e.g. prednisolone
UV light protection for DM
physiotherapy
Osteoarthritis (OA)
disabling join disease characterised by a non-inflammatory degeneration of the joint complex (articular cartilage, subchondral bone, synovium)
one of the most common chronic diseases
generally age related, ↑ incidence with age
more common in females
Osteoarthritis (OA) risk factors
obesity family history female sex ↑ age history of joint injury/trauma
Osteoarthritis (OA) risk factors
obesity family history female sex ↑ age history of joint injury/trauma mechanical loading/recreational stress on joint physically demanding occupation/sports
Osteoarthritis (OA) presentation
generally affects hips, knees, CMC, DIP, PIP joints & spine
pain (usually associated with activity, relieved by rest, pain at rest is unusual) generally unilateral joint stiffness ↓ROM joint swelling crepitus morning stiffness (<30min)
usually asymmetrical joint involvement
NB in hands Painless nodes (bony swellings): Heberden’s nodes at the DIPJs Bouchard’s Nodes at the PIPJs. Squaring of the thumbs: Deformity of the CMC joint = fixed adduction of the thumb.
Osteoarthritis (OA) investigations
X-ray (loss of joint space, subchondral sclerosis, subchondral cysts, osteophytes of joint margins)
Osteoarthritis (OA) X-ray findings
loss of joint space
subchondral sclerosis
subchondral cysts
osteophytes of joint margins
Osteoarthritis (OA) investigations
X-ray (loss of joint space, subchondral sclerosis, subchondral cysts, osteophytes of joint margins)
synovial fluid analysis (non inflammatory, yellow/clear, normal WCC)
Osteoarthritis (OA) management
General:
weight loss
physio
Symptomatic:
1st line: paracetamol & topical NSAIDs
2nd line: COX-2 inhibtors, oral NSAIDs, intra-articular steroids
Surgical:
joint replacement
Reactive arthritis
an inflammatory arthritis that occurs after expiosure to certain gastrointestinal & genitourinary infections, its a type of seronegative spondyloarthritis
strong association with HLA-B27
usually seen in young adults especially men after STI
Used to be know as Reiters syndrome
Causes of reactive arthritis
Post enteric: Campylobacter*, salmonella, shigella
Post-venereal: chlamydia trachomatis*
Presentation of reactive arthritis
usually presents 2-4 weeks post infection
classic triad:
- urethritis (can’t pee)
- conjunctivitis (can’t see)
- arthritis (can’t climb trees)
acute onset nausea, fatigue, fever, diarrhoea, urogenital symptoms (dysuria, pelvic pain)
asymmetrical predominantly lower extremity oligoarthritis lower back pain common
Investigations for reactive arthritis
ESR/CRP (↑) Anti nuclear (ANA) antibody (-ve) Rheumatoid factor (-ve) test for HLA-B27 (often +ve) synovial fluid analysis (↑WCC) stool/urogenital/throat cultures X-rays (normal)
Management of reactive arthritis
Symptomatic:
NSAIDs & intraarticular steroids
treat cause:
Abx (to treat organism identified)
persistent disease:
sulfalazine / methotrexate
Septic arthritis
infection producing inflammation in a native or prosthetic joint, most commonly due to haematogenous spread of infection
Septic arthritis aetiology
stap aureus = most common overall
in young sexual active adults Neisseria gonorrhoea is the most common cause
Risk factors for Septic arthritis
↑ age diabetes prosthetic joint immunosuppression underlying joint disease e.g. RA
Presentation of Septic arthritis
knee = most commonly affected joint in adults knee/hip/ankle = most commonly affected joint in children
acute onset of fever, joint pain, restricted ROM
monarticular swollen, erythematous, warm, tender joint
Investigating Septic arthritis
synovial fluid sampling* (↑ WCC, positive culture, yellowish/green colour, turbid)
CRP/ESR (↑)
FBC (↑ WCC)
USS (effusion)
blood cultures
X-ray (unremarkable)
Management of Septic arthritis
IV Abx:
e.g. flucloxacillin (clindamycin/erythromycin if penicillin allergy)
give for 6-12 weeks
joint drainage & aspiration
arthroscopic lavage
Prosthetic joint septic arthritis
often due to skin pathogens eg. staph epidermis or staph aureus if early, i.e. within 12 weeks of implantation
later onset usually doe to haematogenous spread e.g. E. coli, staph aureus, pseudomonas aeruginosa
often managed surgically with irrigation & debridement or exchange of arthroplasty
Synovial fluid analysis in septic arthritis
↑ WCC
positive culture
yellowish/green colour
turbid
Paget’s disease
slowly progressive disease of ↑ bone turnover causing lamellar bone to be replaced with woven bone, due to disorder of osteoclasts with ↑ osteoclastic bone resorption
onset usually age >55, slight male predominance
Risk factors for Paget’s disease
Family history of pagets
male gender
↑ age
Presentation of Paget’s disease
commonly asymptomatic (only ~5% of pts symptomatic)
bone pain e.g. pelvis/lumbar spine/femur
if untreated leads to bossing of skull, bowed tibia
pathological fractures
↑ skin temp in areas of disease
usually only affects 1 bone
impaired hearing (due to cranial nerve entrapment)
Investigations for Paget’s disease
PTH/phosphate/calcium (normal)
ALP - Alkaline phosphatase (↑↑↑)
X-ray (advancing V-shaped lytic lesions, pathological fractures, cotton wool, osteolysis↑ & bone formation↑)
bone scan (areas of dense uptake in pagetoid bone)
Markers of bone turnover e.g. PINP/CTx/NTx (↑)
Management of Paget’s disease
Symptomatic treatment:
NSAIDs/paracetamol for pain
Vit D & Calcium supplements
1st line: Bisphosphonates e.g. zolendronate
2nd line: Calcitonin
Complications of Paget’s disease
bone sarcoma
high output cardiac failure
Osteoporosis
a complex skeletal disease characterised by low bone density and micro-architectural defects in bone tissue resulting in ↑ bone frailty & ↑ susceptibility to fractures
Osteoporosis
a complex skeletal disease characterised by low bone density and micro-architectural defects in bone tissue resulting in ↑ bone frailty & ↑ susceptibility to fractures
more common in women
age of onset usually 50-70yrs
very common overall (1/3 women & 1/5 men in their lifetime)
T-score
based on bone mass of young reference population
Z-score
bone mass adjusted for age, gender, ethnicity
Bone density measurements
normal:
T-score ≥-1
Osteopenia:
T-score -2.5
Osteoporosis:
T-score ≤-2.5
Severe Osteoporosis:
T-score ≤-2.5 + a fracture
Risk factors for osteoporosis
female sex ↑ age white ethnicity psot menopausal corticosteroid use smoking low BMI family history excessive alcohol intake Chronic disease (CKD, RA, UC, Crohns, coeliac, cushing etc) drugs (e.g. PPIs, anticonvulsants)
Investigating osteoporosis
DEXA scan (T-score ≤-2.5)
Fracture risk assessment tool (FRAX) / QFracture (to asses 10 year risk of frailty fracture)
investigate for underlying cause
Management of osteoporosis
For everyone: Vit D supplementation ± calcium supplementation (depending on dietary intake)
1st line: bisphosphonates e.g. alendronate (1st line) or risendronate
2nd line: denosumab (if bisphosphonates contraindicated / special instructions can’t be adhered to)
3rd line: Raloxifene or Strontium ranelate
Bisphophonates
Bisphosphonates are analogues of pyrophosphate, they inhibit osteoclasts by reducing recruitment and promoting apoptosis.
Examples:
alendronate, risendronate
Side effects:
oesophagitis/oesophageal ulcers
osteonecrosis of the jaw
How to take:
Tablets should be swallowed whole with plenty of water while sitting or standing; to be given on an empty stomach at least 30 minutes before breakfast (or another oral medication); patient should stand or sit upright for at least 30 minutes after taking tablet’
Hypocalcemia/vitamin D deficiency should be corrected before giving bisphosphonates.
Contraindications include inability to follow special instructions for administration & history of peptic ulcers
Stopping Bisphophonates
The duration of bisphosphonate treatment varies according to the level of risk. Some authorities recommend stopping bisphosphonates at 5 years if the following apply:
patient is < 75-years-old
femoral neck T-score of > -2.5
low risk according to FRAX/NOGG
Osteomalacia
is a metabolic bone disease characterised by incomplete mineralisation of the underlying mature bone matrix following growth plate closure in adults
the primary cause is Vit D deficiency
NB if its before growth plate closure = rickets
Risk factors for osteomalacia
dark skin ↑ age obesity pregnancy housebound/institutionalised liver disease e..g cirrhosis CKD limited sun exposure anticonvulsant therapy malabsorption syndromes diet (e.g. vegan)
Presentation of osteomalacia
bone pain & tenderness
pathological fractures
waddling gait & difficulty walking
muscle weakness/spasms/cramps
NB in rickets: knock knees, bow legs, features of hypocalcaemia
Investigations for osteomalacia
serum 25-hydrovitamin D (↓) Ca2+ (↓/normal) Phosphate (↓) urea & creatinine (↑ ratio) alkaline phosphatase (↑) 24h urine calcium (↓) PTH (↑)
X-rays (translucent bands/↓ bone mineral density, pseudo fracture - linear areas of low bone density sourounded by sclerotic borders)
DEXA scan (↓ bone density)
Management of osteomalacia
dietary advice
Vit D & calcium supplementation (nb high dose for 8-12 weeks to replenish stores, then lower dose as maintenance)
Osteomyelitis
an infection of the bone marrow which may spread to the bone cortex & periosteum via haversian canals, generally involving a single bone
Types of Osteomyelitis
Haematogenous:
due to haematological bacterial seeding from a remote site, usually monomicrobial
more common in children & adolescents
Direct (contiguous):
direct contact of infected tissue with bone, usually more localised clinical signs
more common in adults
Aetiology of Osteomyelitis
staph aureus most common
in sickle cell pt most common = salmonella
Presentation of Osteomyelitis
limp reluctance to weight bear non specific pain at site of infection malaise, fatigue, fever local inflammation, tenderness, erythema, swelling
vertebral involvement very common in adults
Investigating Osteomyelitis
may be a clinical diagnosis
CRP/ESR (↑) FBC (↑WCC) blod cultures X-ray of affected area MRI* (Imaging modality of choice)
Management of Osteomyelitis
Abx
e.g. flucloxacillin (or erythromycin/clarithromycin if penicillin allergy)
surgical:
bone debridement, abscess drainage, remove infected prosthesis
Risk factors for Osteomyelitis
trauma prosthetic orthopaedic device diabetes PAD IVDU alcoholism immunosuppression
Compartment syndrome
a condition of ↑ pressure within a muscular compartment leading to impaired tissue perfusion due to the ↑ pressure in a closed anatomical space compromising circulation and leading to temporary/permanent muscle & nerve injury
Types of Compartment syndrome
acute:
usually due to trauma, requires prompt diagnosis & treatment
chronic:
usually caused by exercise, present wit recurrent pains & disability which subsides when exercise is stopped
Sites for Compartment syndrome
upper & lower limb compartments
most commonly anterior & deep posterior compartment of leg & the solar compartment of the forearm
i.e. supracondylar fractures and tibial shaft injuries
Aetiology of Compartment syndrome
Acute:
trauma, burns, casts/constrictive bandages, fractures, haematomas
Chronic:
usually in lower legs, exercise induced
Presentation of Compartment syndrome
pain, pallor, paraesthesia, pulselessness, paralysis, poikilothermia
soft tissue sweeling
cold peripheries
abesnt/weak pulses
pain (often out of proportion of extent of injury
Investigating Compartment syndrome
usually clinical diagnosis
compartment pressure measurement (↑, <40mmHg)
Management for Compartment syndrome
prompt & extensive fasciotomy (surgical emergency)
in burns escharotomy
IV fluid resuscitation (to prevent renal failure from myoglobinuria)
if muscle is necrosed may need debridement or amputation
Developmental dysplasia of the hip (DDH)
refers to hip instability, subluxation/dislocation of the femoral head and/or acetabular dysplasia in the developing hip joint
~20% are bilateral
~80% of all cases are female
Risk factors for Developmental dysplasia of the hip (DDH)
female sex breech presentation family history of DDH first born child oligohydramnios multiple pregnacy
Routine screening for Developmental dysplasia of the hip (DDH)
routine part of NIPE & new-born examination at 6-8 weeks
Barlow test: attempts to dislocate articulated femoral head
Ortolani test: attempts to relocated dislocated femoral head
also look at leg length symmetry, asymmetrical gluteal/thigh folds, Galeazi sign (level of knees with hips & knees flexed)
Presentation of Developmental dysplasia of the hip (DDH)
generally asymptomatic in early life
later:
hip pain abnormal leg positing
delayed crawling/walking
toe walking
Investigating Developmental dysplasia of the hip (DDH)
USS (subluxation on provocation test, abnormal relationship between femoral head & acetabulum)
X-ray (abnormal relationship of femoral head & acetabulum)
NB use X-ray first line if infant >4.5 months
Managing Developmental dysplasia of the hip (DDH)
generally spontaneously stables by 3-6 weeks of age
pavlik harness in children aged <4-5 months
surgery:
if response to splint or harness or if late diagnosis
ultrasound screening for Developmental dysplasia of the hip (DDH)
Performed at 6 weeks
used if first degree family history of hip problems in early life
breech presentation at/after 36 weeks irrespective of mode of birth & presentation at delivery
multiple pregnancy
breech presentation at delivery before 36 weeks
Perthes disease
degenerative self limiting disease of the femoral head compromising of necrosis, collapse, repair & remodelling, due to avascular necrosis of the femoral epiphysis
usually presents age 3-10 yrs
5x more common in boys
Presentation of perthes disease
onset over weeks with no history of trauma
limp
limited ROM of hip
hip pain
stiffness
short statue common
some muscle wasting of gluteals & quadriceps
Investigating perthes disease
Bilateral AP & frog leg lateral hip X-rays (show femoral head collapse & fragmentation, subchondral fractures, joint space widening)
Bone scinitgraphy (technetium bone scan)
Managing perthes disease
children <6y/o
conservative (NSAIDs, physio, restriction of activities)
children >6y/o / extensive damage
surgical management with femoral osteotomy
Catterall staging
For perthes disease
Stage 1 Clinical and histological features only
Stage 2 Sclerosis with or without cystic changes and
preservation of the articular surface
Stage 3 Loss of structural integrity of the femoral head
Stage 4 Loss of acetabular integrity
Slipped upper femoral epiphysis (SUFE)
weakness of the proximal femoral growth plate allows displacement of the capital femoral epiphysis
more common in boys
usually age 10-16yrs
Slipped upper femoral epiphysis (SUFE) risk factors
obesity family history endocrine disorders trauma puberty
Slipped upper femoral epiphysis (SUFE) presentation
often seen in obese boys usually aged 10-16yrs (especially during growth spurts)
20-40% are bilateral
dull pain in medial thigh/knee/groin/hip limping ↓ ROM affected leg is externally rooted loss of internal rotation in flexion
Slipped upper femoral epiphysis (SUFE) investigations
Bilateral AP & frog leg lateral hip X-rays (Klein’s line does not intersect the femoral head, femoral head is displaced posterior-inferioir in relation to femoral neck, widening of growth plate)
Slipped upper femoral epiphysis (SUFE) mangement
immediate orthopaedic referral
surgery: usually single crew placed in centre of epiphysis
Slipped upper femoral epiphysis (SUFE) compilations
early hip OA
chondrolysis of hip (degeneration of articular cartilage)
Osgood-Schlatter disease
Tibial osteochondritis thought to arise from overuse if the quadriceps muscles during periods of growth
one of the most common causes of knee pain in active adolescents who play sport
more common in boys (often age 12-15)
Presentation of Osgood-Schlatter disease
progressive anterior knee pain that is worse with activity & reproducible by extension against resistance proximal tibial swelling pain usually gradual onset pain relived by rest tenderness over tibial tuberosity
Investigating Osgood-Schlatter disease
clinical diagnosis
Knee X-ray (enlarge tibial tuberosity)
Mangament of Osgood-Schlatter disease
usually self limiting so manage conservatively (RICE)
physiotherapy (strengthening & stretching quads)
Transient synovitis
selflimitng inflammatory disorder of a joint, usually preceded by URTI commonly affecting hip joint
most common cause of hip pain in children aged 3-10 yrs
NB must exclude septic arthritis
Presentation of transient synovitis
usually younger children (4-10y/o) with preceding viral infection e.g. URTI
unilateral hip/groin pain (not severe) limp refusal to weight bear ↓ ROM Child systemically well (if high grade fever should raise concern of septic arthritis)
Investigating transient synovitis
X-rays
FBC
ESR/CRP
NB generally all normal
Management of transient synovitis
self limiting
analgesia
congenital talipes equinovarus (CTEV) i.e. club foot
congenital orthopaedic condition describing an inverted (upward turning) & plantar flexed foot (i.e. sole of foot pointing medially), usually diagnosed on NIPE
most often idiopathic, ~50% bilateral
associated with spina bifida, cerebral palsy, trisomy 18, oligohydramnios
Management
1st line: serial progressive casting & manipulation (ponseti method)
2nd line: surgery
Flat foot (pes planus)
flat/convex plantar surface
treated with orthotics, manipulation, surgery
Equinus deformity
presents as toe walking, leg length discrepancy, impaired stability
inability to dorsiflex foot above plantigrade
treated with surgical correction or manipulation surgeyr
Pes cavus (high arch)
high longitudinal arch & hind foot virus
treated with orthotics or surgery
Myeloma / Multiple myeloma
malignant plasma cell dyscrasia characterised by uncontrolled proliferation & diffuse infiltration of monoclonal plasma cells in the bone marrow
arises due to genetic mutation which occur as B-lymphocytes differentiate to mature plasma cells
15-20% of haematological malignancies (2nd most common)
generally affects people aged >70yrs
Myeloma presentation
often asymptomatic bone pain (especially back pain) mild fever night sweats weakness, weight loss symptoms of hypercalcaemia (constipation, nausea, anorexia, constipation, thirst) spontaneous/pathological fractures (due to lytic bone lesions) lethargy (due to anaemia) recurrent infections foamy urine (Bence-Jones proteinuria) renal impairment bruising / bleeding
Investigations for myeloma
serum electrophoresis (↑ monoclonal IgG/IgA protein)
urine electrophoresis (↑ Bence-jones protein = immunoglobulin light chain)
serum free light chain assay (↑ levels)
bone marrow biopsy (monoclonal plasma cell infiltration)
FBC (anaemia)
U&Es (↑, renal impairment)
Ca (↑)
whole body MRI/CT (osteoltyic lesions)
Management of myeloma
If symptomatic + suitable for stem cell transplant:
induction with Bortezomib + Dexamethasone
If symptomatic + not suitable for stem cell transplant:
induction with Thalidomide + an Alkylating agent + Dexamethasone
Relapses:
bortezomib monotherapy
Symptomatic:
VTE prophylaxis
zolendronic acid (to help bone strength)
Classifying myeloma
depending on what antibody is produced
IgG myeloma most common
followed by IgA
Monitoring for myeloma patients
FBC
U&Es
Ca2+
Osteoma
benign overgrowth of bone most typically of skull
associated with gardeners syndrome (variant of familia adenomatous polyposis)
Ostechondroma
most common benign bone tumour*
bony outgrowth (exostosis) with cartilaginous cap usually occurring on surfaces of long bone adjacent to growth plates
usually seen in males <20y/o
x-ray = pedunculated/sessile lession of long bones
Ostechondroma bones affected
bony outgrowth (exostosis) with cartilaginous cap usually occurring on surfaces of long bone adjacent to growth plates
Osteoclastoma (giant cell tumour of bone)
tumours of multinucleate giant cells within a fibrous stroma, usually found on long bone epiphysis
seen in people aged 20-40 yrs
X-ray = asymmetric rarefied area at the end of long bone (soap bubble sign)
Osteosarcoma
most common primary bone malignancy occurring in metaphysic of long bones (most common site = ~75% around knee & proximal humerus)
mainly seen in children & adolescence
presents as relatively painless tumour mainly with swelling
X-Ray = Codman triangle (form periosteal elevation) + sunburst pattern (soft tissue calcification)
Most common primary bone malignancy
osteosarcoma
Osteosarcoma
most common primary bone malignancy occurring in metaphysic of long bones (most common site = ~75% around knee & proximal humerus)
mainly seen in children & adolescence
presents as relatively painless tumour mainly with swelling, usually metastasises to lungs
X-Ray = Codman triangle (form periosteal elevation) + sunburst pattern (soft tissue calcification)
Common site of metastases for osteosarcoma
Lungs
Most common site of osteosarcoma
~75% around knee & proximal humerus
Common site of metastases for osteosarcoma & Ewing’s sarcoma
Lungs
Ewings sarcoma
primitive neuroectodermal tumour arising from mesenchymal stem cells, very aggressive (early metastasises to lungs)
usually presents as mass/swelling, most commonly in long bones of arms & legs / pelivs / chest
usually diagnosed around age 15
X-ray: onion skin appearance (multiple layers of new bone)
Ewings sarcoma X-ray findings
onion skin appearance (multiple layers of new bone)
Chondrosarcoma
malignant tumour of the cartilage, presents as deep & dull pain + local swelling
usually seen in middle age
Fibromyalgia
a neurosensory disorder of unknown aetiology characterised by chronic musculocutaneous pain
5-10x more common in women
presents between 20-50y/o
Presentation of fibromyalgia
chronic widespread pain primarily at point where muscles & tendon attach to bones (tender points) diffuse tenderness on examination fatigue unrelieved by rest unrefreshing sleep headache, morning stiffness, dizziness cognitive impairment (fibro fog)
Investigations for fibromyalgia
clinical diagnosis:
symptoms >3 months
presence of ≥11/18 tender points amongst 9 pairs of specced sites
Management of fibromyalgia
pt education
lifestyle changes
Medication (low dose TCAs/SNRIs)
MDT management
Associated conditions with fibromyalgia
functional somatic syndromes (e.g. IBS, chronic fatigue syndrome)
depression
GAD
sleep disorders
Parts of the bone
Diaphysis = shaft of long bone
Metaphysis = between diaphysis & epiphysis
physis = growth plate between epiphysis & metaphysis
epiphysis = end of long bone
Salter-Harris fracture classification
used for paediatric fractures
I Fracture through the physis only (x-ray often normal)
II Fracture through the physis and metaphysis
III Fracture through the physis and epiphyisis to
include the joint
IV Fracture involving the physis, metaphysis and
epiphysis
V Crush injury involving the physis (x-ray may
resemble type I, and appear normal)
Type I Salter-Harris fracture
transverse fracture through growth plate (physis), i.e. separating epiphysis & metaphysis
Type II Salter-Harris fracture
Most common type
transverse fracture of physis (growth plate) & metaphysis i.e. fracture through growth plate and toward middle of bone
Type III Salter-Harris fracture
transverse fracture of physis (growth plate) & epiphysis (end of bone) which includes the joint
i.e. fracture through growth plate and towards end of bone
Type IV Salter-Harris fracture
fractures of physis (growth plate) + metaphysis + epiphysis
Type V Salter-Harris fracture
fracture with impaction & disruption of physis (growth plate)
i.e. crush fracture of growth plate
may look normal on X-ray or like Type I
Hip fractures (NOF)
any fracture of the femur distal to the femoral head & proximal to the level ~5cm below the lesser trochanter
Types of hip fractures
Intracapsular (subcapital):
involve femoral neck between the edge of the femoral head & insertion of the capsule of the hip joint
~50% of hip fractures
may disrupt blood supply to femoral head leading to avascular necrosis
Extracapsular:
fracture distal to the insertion of the capsule, involving/between the trochanters, can be trochanteric or subtrochanteric
Classification for intracapsular hip fractures
Garden classification:
Type I: Stable fracture with impaction in valgus
Type II: Complete fracture but undisplaced
Type III: Displaced fracture, usually rotated and
angulated, but still has boney contact
Type IV: Complete boney disruption
NB Type III & IV cause disruption to blood supply
Garden classification
used to classify intracapsular hip fractures
Risk factors for hip fractures
↑ age osteoporosis falls low BMI female sex high energy trauma (in younger pts)
Epidemiology of hip fractures
relatively common
usually seen in those aged >65 yrs often after low energy trauma e.g. falls from standing height
more common in females
Presentation of hip fractures
Pain in affected hip/thigh/groin (usually upper outer thigh or groin) inability to weight bear ↓ ROM bruising shortened & externally rotated leg
Investigating hip fractures
AP pelvic & lateral hip X-ray (interruption of shelton’s line, fracture is visible)
MRI (if fracture suspected but not visible on X-ray)
Management of intracapsular hip fractures
undiscplaced = internal fixation e.g. cannulated hip screw or hemiarthroplasty
displaced = arthroplasty (total or hemiarthroplasty)
total hip replacement is favoured to hemiarthroplasty if patients:
were able to walk independently out of doors with no more than the use of a stick and
are not cognitively impaired and
are medically fit for anaesthesia and the procedure.
Management of extracapsular hip fractures
generally dynamic hip screw (i.e. internal fixation) if intratrochanteric
intramedullary nail if subtrochanteric
When to perform total hip replacement or hemiarthroplasty in displaced intracapsular hip fractures
total hip replacement is favoured to hemiarthroplasty if patients:
were able to walk independently out of doors with no more than the use of a stick and
are not cognitively impaired and
are medically fit for anaesthesia and the procedure.
Fractured femur
fractures of the femoral shaft & supracondylar fractures
generally secondary to violent trauma / high energy mechanisms of injury in young adults & adolescence
may be due to low energy trauma in older people for example with bone metastases
Presentation of femoral fractures
painful swollen tense thigh inability to weight bear ↓ ROM deformity % shortening of affected side distal neuromuscular deficits
NB be aware of signs of fat embolism
Investigating femoral fractures
AP & lateral X-rays of femur + ipsilateral hip & knee X-ray (to rule out co-exisitng NOF)
Consider CT
Management of femoral fractures
splint / traction fracture (e.g. Thomas splint, KTD)
Surgery:
open/closed reduction, most commonly intramedullary nail used
4-6 months healing time
Supracondylar femur fractures
fracture of the distal 1/3 of the femur, usually due to direct trauma, often comminuted & intra-articular involvement with associated damage to knee joint
presents with pain of distal femur usually worsened by moving knee & inability to weight bear
Pelvic fractures
fractures of the fused ring of the ischium, ilium, pubis often occurring with polytrauma e.g. from RTC
can lead to life threatening haemorrhage & may be shocked
present with pelvic pain, pelvic instability, unequal leg length, haemutria/rectal bleeding, and bruising of the labia/scrotum/flank
classified by Young-burgess classification
investigate with pelvic X-ray / CT
managed surgically if unstable along with angiography for embolisation
Pubic rami fractures
low energy pelvic fractures seen in old people with osteoporosis
generally stable fractures
Ankle fractures
a fracture of ≥1 of the bones of the ankle joint i.e. the tibia / fibula / talus
most common lower limb fracture
Presentation of ankle fracture
local pain & tenderness swelling & haematoma ↓ ROM inability to weight bear skin abnormalities e.g. lacerations/dislocation/tenting joint deformity
Investigating ankle fractures
Physical examination:
Ottawa ankle rules to see if X-ray indicated
X-rays (AP, lateral, oblique views)
Classifying ankle fractures
Weber classification
Related to the level of the fibular fracture.
Type A is below the syndesmosis, usually stable,
syndesmosis intact
Type B fracture at level of syndesmosis, potentially
involving it
Type C fibula fracture above syndesmosis indicating
syndesmosis rupture, usually unstable
Ottowa ankle rules
To indicate if X-ray is indicated
These state that x-rays are only necessary if there is pain in the malleolar zone and:
- Inability to weight bear
- Tenderness over the distal tibia
- Bone tenderness over the distal fibula
Patella fracture
may be caused by direct blow to patella, sudden forceful knee flexion or contraction of quads
typically presents with considerable swelling & bruising + pain & tenderness around knee / patella
diagnosis with AP & lateral knee X-ray
managed with analgesia, immobilisation (knee brace) if undiscplaced/able to extend knee
managed with tension band wire & knee brace if displace/inability to extend knee
Lisfranc fracture
tarsometatarsal fracture that can involve damaged to cartilage of the mid foot joints leading to fracture dislocation
presents with severe mid foot pain, inability to weight bear, bruising & swelling of mid foot
often easily missed on standard foot X-ray so CT =investigation of choice
generally requires ORIF
Metatarsal fractures
relatively common fracture, most frequently affecting 5th metatarsal
presents with pain, bony tenderness, swelling & antalgic gait
diagnosed on foot X-ray
non-displaced = k wire fixation & plaster support displaced = internal fixation e.g. percutaneous pinning
Metatarsal stress fracture
most common stress fracture often seen in healthy athletes
usually affects shaft of 2nd metatarsal
Clavicle fracture
one of the most common acute shoulder injuries, usually due to fall onto lateral shoulder
most common site = middle 1/3 of clavicle
~2-5% of adult fractures, most common paediatric fracture
Presentation of clavicle fractures
history of fall/trauma
pain / swelling / tenderness around clavicle
tenting of skin due to upward distraction by SCM of medial fracture segment
sagging of shoulder due to downward traction force of weight of arm on lateral fracture segment
Investigating clavicle fractures
AP X-ray of clavicle
CXR ( if lung injury suspected)
if sternoclavicular/acromioclavicular joint injury suspected perform MRI/CT
Classifying clavicle fractures
Allman classification: (according to fracture location)
Type I mid shaft/middle third (most common, ~80%)
Type II lateral third (10-15%)
Type III medial third, rare (5%)
Management of clavicle fractures
generally conservatively managed with simple shoulder sling
if open fractures / excessive shortening / displacement = surgery
Humerus fractures
common fracture, usually trauma related but may also be associated with pathological fractures & osteoporosis in the elderly
proximal humerus fractures are most common
Types of humerus fractures
Proximal humeral fractures: (4-5% of all fractures)
common in elderly, usually FOOSH
Humeral shaft fractures: (3% of all fractures)
usually due to trauma/torsion on upper arm
usually associated with radial nerve injury (wrist drop)
Distal humeral fractures:
supracondylar - more common in children
trans condylar - more common in adults
Presentation of humeral fractures
sever local pain exacerbated during palpation or movement of arm
local swelling, deformity, crepitus
Investigating humeral fractures
AP & lateral X-ray of humerus ± trans thoracic & axillary views of shoulder
Management of humeral fractures
Conservative:
if non displaced / closed fracture
= having arm cast or splint & sling
Surgical:
if displaced / open fracture /neurovascular injury
= ORIF or external fixation
Supracondylar fractures
a fracture of the distal humerus superior to the elbow joint, typically transverse fracture over medial & lateral condyles caused by FOOSH
most common paediatric elbow fracture (age 5-7yrs)
presents with pain & refusal to move arm
seen on lateral & AP X-rays ( anterior fat pad (sail) sign = lucent triangle on lateral projection & posterior fat pad sign)
managed with surgical repair followed by elbow immobilisation at 90°
Olecranon fractures
low energy fractures commonly seen in the elderly
presents with swelling & tenderness over olecranon & ↓ ROM + inability to extend elbow
seen on true lateral elbow X-ray
generally requires ORIF (due to unopposed traction of triceps causing displaced fractures)
Condylar fractures
more commonly lateral than medial
seen on lateral & AP X-ray
Capitellum fracture
rare but require prompt diagnosis & management as it may lead to severe functional impairment due to intraarticular & displaced
usually require CT
Radial head & neck fractures
a type of elbow fracture commonly caused by FOOSH
radial head fracture = most common elbow fracture in adults
radial neck fracture = more common in children
presents with swelling over lateral elbow & ↓ ROM, elbow effusion, bruising, point tenderness of radial head
pain worse on rotation
Seen on AP & lateral elbow X-ray ± oblique view (often findings subtle & easily missed)
managed conservatively if non displaced, otherwise ORIF
FOOSH
fall onto outstretched hand
Colles fracture
distal radial fracture with dorsal displacement of fragment, strongly associated with osteoporosis
most common distal radial fracture
diagnosed on AP & lateral X-ray
Freatures of colles fracture
transverse fracture of radius ± ulna (ulna styloid) involvement
2-3 cm proximal to radio-carpal joint
dorsal displacement & angulation
Colles fracture in the elderly
warrants investigation for osteoporosis due to strong association
Presentation of Colles fracture
dorsally displaced & angulated (dinner fork deformity)
after FOOSH
may have ulnar or median nerve damage
Management of colles fracture
generally closed reduction under anaesthesia (e.g. haematoma block) & cast immobilisation
surgical reduction if unstable or intra-articular
Smiths fracture
distal radial fracture ± ulna involvement that has volar (anterior) displacement of the distal fragment (reverse Colles)
due to falling backward onto outstretched hand , presents with garden spate deformity
AP & lateral X-rays (similar to colles but anterior displacement)
usually managed with closed reduction & casting unless fracture dislocation
Barton fracture
distal radial fracture & dislocation of radial carpal joint i.e. colles/smith fracture with dislocation
usually requires ORIF
Chaufferus fracture
intra-articular fracture of the radial styloid process, usually secondary to direct blow to wrist
tend to be unstable even if undisplaced so fixed with K wires
Greenstick fractures of the wrist
a fracture with unilateral cortical breech i.e. periosteum remain intact (convex surface is fractured but concave surface is intact)
a fracture of childhood (<10y/o) more common in forearm
usually associated with some degree of angulation, but unless majorly angulated can be managed with cast immobilisation
Galaezzi fracture
radial shaft fracture + disruption of the distal radial ulnar joint
more common in children
AP & lateral X-rays show displaced fracture of the radius & prominent ulnar head due to dislocation
uncomplicated in children so can be managed with closed reduction
Monteggias fracture
ulna shaft fracture + concomitant dislocation of radial head
X-rays show ulnar fracture & radial head dislocation
usually uncomplicated in children so can be managed with closed reduction & casting
Ulnar shaft fracture
usually due to direct blow to ulna e.g. when raising arm in defence from an attack
Both bone forearm fracture
usually significant force injury e.g.
usually displaced in adults so requires ORIF
Scaphoid fracture
Most common fractured carpal bone (50-80%), usually secondary to FOOSH
usually seen in men aged 20-30 yrs
Blood supply of scaphoid bone
~80% of bloods supply from dorsal carpal branch of radial artery in a retrograde manner
interruption of blood supply risks avascular necrosis of the scaphoid (most commonly seen in proximal fractures)
avascular necrosis occurs in up to 50% of cases
Presentation of scaphoid fracture
pain when applying pressure to the anatomical snuffbox (tenderness of anatomical snuffbox)
↓ grip strength
painful pincing & grasping
pain in scaphoid area on longitudinal thumb compression
Investigations for scaphoid fracture
X-ray (make clear its suspected scaphoid fracture = PA, sure lateral, semi-pronated oblique & PA with wrist in ulna deviation views)
if X-ray inconclusive = MRI
clinical review with further imaging should be arranged for7-10 days later when initial radiographs are inconclusive
Mangement of scaphoid fracture
initially immobilisation with future splint/below elbow back slab
undisplaced = cast immobilisation
displaced or proximal fracture = surgical fixation
Management of scaphoid fracture
initially immobilisation with futuro splint/below elbow back slab
undisplaced = cast immobilisation
displaced or proximal fracture = surgical fixation
Complications of scaphoid fracture
avascular necrosis
non union = early OA & pain
Bennett’s fracture
interarticular fracture base of the age of the thumb which is often unstable
seen when pt has punched someone/something
presents as acute & severe pain / swelling at base of thumb & ↓ROM
PA, lateral & oblique views on X-ray (shows oblique fracture line at 1st metacarpal with triangular fragment at ulnar base of 1st metacarpal)
generally requires ORIF or K wire fixation
Rolando fracture
3 part fracture at the base of the thumb, uncommon fracture
often requires CT
generally requires surgical fixation
Phalangeal fracture
if distal its often a crush injury with associated nail injury/damage
generally all managed conservatively
Enteropathic arthritis
umbrella term to describe several patterns of inflammatory seronegative spondyloarthropathies associated IBD (Crohns & UC)
associated with HLA-B27
Risk factors for enteropathic arthritis
active bowel disease FH of IBD appendectomy smoking presence of extra-intestinal manifestations of IBD
Presentation of enteropathic arthritis
axial arthritis (spondyliits/sacarilitis) of IBD: gradual onset lower back pain radiation to leg symptoms worse in morning & on prolonged sitting / standing
peripheral arthritis of IBD:
usually associated with presence of GI symptoms, more common in Crohns
asymmetric oligoarthritis affecting lower limbs that tends to be migratory & transient
Entesopathy of IBD:
severe localised heel pain at achilles tendon insertion or other tendon insertions
Investigations for enteropathic arthritis
stool microscopy & culture sigmoidoscopy / colonoscopy ESR/CRP (↑) X-ray of affected joints autoimmune screen
Management of enteropathic arthritis
give NSAIDs with care as may worsen GI symptoms
intraarticular / systemic steroids (better for peripheral arthritis)
TNF antagonists
Behcet disease / syndrome
complex multi system disorder of unknown aetiology associated with systemic vasculitis characterised by deposition of immune complexes in arteries & veins
usually seen in mediterranean, east asian, middle eastern population
peak incidence age 20-40yrs, more common in men
associated with HLA-B51
Behcet disease / syndrome presentation
- recurrent oral ulcers
- recurrent genital ulcers
- eye lesions (anterior/posterior uveitis, retinal vasculitis)
- arthritis (non erosive, non deforming asymmetric mono/oligo arthritis usually affecting knees/ankles/hands/wrists)
- skin lesions (erythema nodosum, acneuform eruptions)
- GI disease (vomiting, diarrhoea, abdo pain, GI tract ulceration)
- neurological (memory impairment, impaired balance/speech/movement)
- cardiac (DVT, superficial thrombophlebitis, aneurysms, material thrombosis)
Behcet disease / syndrome investigations
pathergy test (+ve) (subcutaneous skin prick, observe for induration ± pustule formation of 48h)
autoantibodies (-ve)
ESR/CRP (↑)
Behcet disease / syndrome management
topical steroids (for oral / genital ulcers)
topical lidocaine (for pain relief)
colchicine (for arthritis)
immunosuppression with azathioprine or systemic steroids
Shoulder dislocation
The shoulder is a ball & socket joint but unlike the hip has a relatively shallow socket giving it a greater ROM but also making it less stable, generally traumatic dislocation
one of the most commonly dislocated joint (~50% of all dislocations)
repeated dislocations point to hyper mobility or Ehler-Danlos
Epidemiology of shoulder dislocation
more common in males
peak incidence is 20-50 yrs in men & 61-80yrs in females
95% of dislocations are anterior
4% posterior (seen in epileptics)
<1% inferior
Presentation of anterior shoulder dislocation
severe shoulder pain & inability to moved shoulder
arm slightly abducted & externally rotated
humeral palpable below coracoid process
loss of roundness of shoulder
may lead to axillary nerve injury (check regimental badge area) or rotator cuff injury
NB ~30% have associated fracture (consider X-ray to rule out fracture)
Presentation of posterior shoulder dislocation
severe shoulder pain & inability to moved shoulder
less obvious on examination, arm is adducted & internally rotated
nerve & vascular injury is uncommon
Management of shoulder dislocation
immobilisation & analgesia
reduction (closed)
surgery (if closed reduction fails)
neurovascular monitoring during & after reduction
Takayasu vasculitis
Type of large vessel vasculitis
Takayasu vasculitis
Type of large vessel vasculitis with granulomatous inflammation of the aorta & its major branches leading to thickening & stenosis
more common in females & asian population, presenting age 15-45 yrs
presents with malaise, headache, arthralgia, syncope, angina, carotid bruits, unequal BP in upper limbs, weak/absent limb pulses, intermittent claudication & raynauds
investigations include ESR (↑), angiography = gold standard (stenosis), biopsy of affected vessel
managed with corticosteroids & immunosuppression e.g. azathioprine / methotrexate
Kawasaki disease
medium vessel vasculitis in children
presents with >5 days of high fever, strawberry tongue, cervical lymphadenopathy, conjunctival injections, erythema of soles of feet / palms if hand, cracked red lips
Polyarteritis nodosa
medium vessel vasculitis with necrotising inflammation leading to aneurysm formation associated with Hep B infection
usually seen in middle aged men (45-65 yrs)
Presents with fever, malaise, weight loss, arthralgia, HTN / renal impairment, ↑ MI risk, sensorimotor polyneuropathy, abdo pain, N&V, lived reticular
investigations include ESR/CRP (↑), Hep B/C serology (+ve), tissue biopsy, angiography (multiple small aneurysms)
managed with corticosteroids & cyclophosphamide
Antibody for Granulomatosis with polyangiitis (Wegener’s granulomatosis)
cANCA
Granulomatosis with polyangiitis (Wegener’s granulomatosis
systemic ANCA associated vasculitis of small & medium vessels characterised by necrotising granulomatosis affecting upper respiratory tract & kidneys
Granulomatosis with polyangiitis (Wegener’s granulomatosis presentation
epistaxis nasal crusting saddle nose deformity dyspnea haemoptysis oral ulcers treatment resistant pneumonia rapidly progressing glomerulonephritis vasculitic rash
NB upperrepsiratory tract manifestations are most common
Granulomatosis with polyangiitis (Wegener’s granulomatosis investigations
ESR/CRP (↑)
cANCA (+ve)
CXR (generally abnormal, with variety of presentations)
kidney biopsy (epithelial crescent in Bowmans capsule)
urine dip (haemturia, proteinuria)
tissue biopsy (necrotising granulomas)
Granulomatosis with polyangiitis (Wegener’s granulomatosis mangement
steroids
cyclophosphamide (90% response rate)
plasma exchange
Antibody for Eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome)
pANCA
Eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome)
small vessel ANCA associated vasculitis characterised by granulomatous vasculitis with eosinophilia
more commonly involves skin & lungs
Eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome) presentation
asthma (chief complaint) with severe allergic attacks allergic rhinitis/sinusitis mononeuritis multiplex skin nodules palpable purpura Pauci-immune glomerulonephritis
Eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome) investigations
FBC (eosinophilia i.e. ↑ eosinophils >250/μL)
pANCA (+ve)
IgE (↑)
biopsy (confirmatory test)
Eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome) management
corticosteroids ± cyclophosphamide
Microscopic polyangitis
necrotising ANCA associated small vessel vasculitis affecting skin, pulmonary & renal vessels
manifests similar to granulomatosis with polyangitis but spares nasopharynx i.e. pauci-immune glomerulonephritis, HTN, palpable purport, haemoptysis, cough, dyspnoea
investigations include pANCA/cANCA (either may be +e), biopsy (fibrotic necrosis with neutrophil infiltration and no granulomas)
managed with corticosteroids ± cyclophosphamide
Anti-glomerular basement membrane (GBM) disease (Good-Pastures syndrome)
Non ANCA associated, rare small vessel vasculitis caused by anti-GBM antibodies
presents with pulmonary haemorrhage (cough, dyspnoea, haemoptysis), renal (rapidly progressive glomerulonephritis)
investigated with renal biopsy (linear IgG deposits along basement membrane), abnormal renal function tests, anti-GBM antibodies (+ve)
managed with corticosteroids ± cyclophosphamide
Cryoglobulinaemic vasculitis
non ANCA associated small vessel vasculitis characterised by temperature dependent deposition of immunoglobulins/immmune complexes (IgG/IgM) into the wall of blood vessels
associated with type I/II cryoglobulinaemia often in conjunction with Hep C infection
presents with skin lesions, malaise, fatigue, arthralgia, raynauds, hepatosplenomegaly
investigate include cryoglobulinaemia, Hep C/B serology (often +ve), skin/renal biopsy (cryoglobulin deposits)
managed with corticosteroids & rituximab
Hypersensitivity vasculitis
necrotising vasculitis of cutaneous small vessel caused by formation of immune complexes
most common vasculitis seen in clinical practice
presents 7-10 days post drug exposure (e..g NSAIDs, Abc, phenytoin) with painful, palpable prupura
investigated with skin biopsy (gold standards)
managed by discontinue underlying drug + steroids
Biceps tendon rupture
injury to the biceps muscle leading to complete/partial severing of the tendon from the bone
more common in men
proximal rupture usually in older pts >60yrs
distal rupture usually in middle aged men
Types of Biceps tendon rupture
Proximal
rupture of the origin the short head (coracoid process) or long head (glenoid)
most common type ~95% of all cases are of the longe head
Distal:
rupture at the insertion of the biceps tendon i.e. radial tuberosity
~5% of cases
usually in middle aged men
Presentation of biceps tendon rupture
sudden pop/tear followed by pain/bruising/swelling
popeye deformity (muscle bulk bulges in the middle of upper arm)
limited ROM
Investigating biceps tendon rupture
Clinical diagnosis
USS = investigation of choice
consider X-ray or MRI
Management of biceps tendon rupture
Proximal:
conservative, RICE
Distal:
surgical fixation within 2-3 wks of injury to limit fibrosis of muscle
Biceps tendinitis
tendinitis of the long head of the biceps tendon at the insertion on the glenoid
presents as anterior shoulder pain that worsen with lifting
clinical diagnosis ±USS
managed with RICE, NSAIDs or later steroid injections
NB chronic tendinitis is associated with tendon rupture
Subacromial bursitis
inflammation of the bursa located between the acromion, deltoid muscle & head of humerus, usually caused by repetitive overhead motion
presents with joint swelling, erythema, warmth, stiffness + pain on lateral & anterior aspect of shoulder
managed with RICE & NSAIDs
Adhesive capsules (frozen shoulder)
inflammation & fibrosis of the joint capsule leading to contracture of the shoulder joint, usually seen in 45-65y/o pts, more common in women
presents with restriction of movement of glenohumeral join, gradual onset dull pain, stiffness, inability to sleep on affected side
diagnostic test is inability to externally rotate shoulder
Mangement:
1st line: paracetamol
2nd line: NSAIDs
+physio & corticosteroid injections
Subacromial impingement syndrome / supraspinatus tendonitis / painful arc
most common cause of shoulder pain
clinical syndrome caused by compression of tissues around the glenohumeral joint when shoulder is elevated
presents with shoulder pain worse on overhead activities & tenderness over acromion, ↓ROM, nocturnal exacerbation of pain when lying on affected side
painful arc test = +ve (pain between 60-90° of shoulder abdduction)
‘empty can’ test +ve if supraspinatus tendonitis
Calcifying tendonitis
crystalline calcium phosphate depsited in the rotator cuff tendon causing mild pain & ↓ROM
seen as calcium deposit on X-ray
Lateral epicondylitis (tennis elbow)
reactive tendon pathology of forearm extensor muscle origin (lateral epicondyle) caused by repetitive strain
presents with pain & tenderness over lateral epicondyle / along extensor muscles, pain is worse on wrist extension against resistance with elbow extended & supinated
treated with RICE, NSAIDs/paracetamol, physio, steroid injections
Medial epicondylitis (golfers elbow)
reactive tendon pathology of forearm flexor muscle origin (medial epicondyle) caused by repetitive strain, most common cause of medial elbow pain
presents with pain over medial epicondyle & along flexor muscles, worse on activity, pain worse on wrist flexion against resistance with elbow extended & pronated
may be accompanied by ulnar nerve neuropathy = ↓sensation & tingling in 4th/5th digits
treated with RICE, NSAIDs/paracetamol, physio, steroid injections
Elbow dislocation
second most commonly dislocated joint after shoulder, usually caused FOOSH, posterior dislocations are most common
usually seen in ages 10-20yrs
presents with pain, swelling, ↓ROM (inability to flex/extend elbow) & deformity of the elbow
~10% have associated nerve injury
investigated with lateral & AP X-ray (look at radiocapitellar line)
if simple dislocations = closed reduction & immobilise if complex (i.e. +fracture) = ORIF
Olecranon bursitis (student’s elbow)
inflammation of the bursa of the elbow joint that is often caused by leaning on the elbow for long periods
presents with pain & swelling over posterior elbow, with erythema & warmth ± broken skin
generally managed conservatively (RICE + analgesia), consider surgery if olecranon spur contributes to recurrent bursitis
Acromioclavicular (AC) joint seperation
usually caused by direct injury to acromion during fall onto adducted arm or direct blow to acromion
represents ~50% of all athletic shoulder injuries
presents with local tenderness, swelling, bruising, ↓ROM of shoulder, with a visible/palpable step if clavicular separation present
classified using X-ray
managed surgically or conservatively depending on degree of injury
Cubital tunnel syndrome
compression of the ulnar nerve as it passes through the cubital tunnel at the elbow, 2nd most common compressive neuropathy
presents with tingling/numbness of 4th/5th digits, hypothenar weakness/atrophy, claw hand, positive Tinel’s test (tapping over cubital turner =pain/tingling/shock-like sensation)
investigated with nerve conduction studies / USS
managed with Rest, physio, steroid injections or surgery if conservative management fails
Carpal tunnel syndrome
peripheral neuropathy caused by acute/chronic compression of the median nerve the the transverse carpal ligament
most common entrapment neuropathy of the upper extremity (90%)
risk factors include female sex, ↑BMI, pregnancy, wrist trauma, diabetes, RA
Carpal tunnel syndrome presentation
tingling/numbness/pain in median nerve distribution (palmar aspect of the thumb / index / middle finger & 1/2 of ring finger) NB often worse at night, may cause waking
pain may radiate up arm
weakness in hand grip, opposition/abduction of thumb
wasting of thenar eminence
Phalen test +ve:
flex wrist for 60sec = pain/paraesthesia in median nerve distribution
Tinel test +ve:
tapping over median nerve at wrist = distal paraesthesia
Carpal tunnel compression +ve:
pressure over the proximal edge of the carpal tunnel causes paraesthesia in median nerve distribution
Carpal tunnel syndrome investigations
EMG (focal slowing of conduction velocity in median nerve across carpal tunnel)
USS (confirmatory test)
MRI (alternative to USS)
Carpal tunnel syndrome management
wrist splints at night
local corticosteroid injection
surgical decompression of flexor retinaculum
De Quervain’s tenosynovitis
inflammation of the tendon sheath of extensor polices braves & abductor policies longs of the thumb caused by repetitive strain (e.g. texting a lot/holding baby),
usually seen in females aged 30-50
De Quervain’s tenosynovitis presentation
presents with pain ± swelling of radial styloid which may radiate to thumb & painful abduction of thumb against resistance
Finkelstein test +ve (grasp effected thumb & exerts longitudinal traction across palm of hand to ulnar side causing pain)
De Quervain’s tenosynovitis management
NSAIDs, splinting (immobilisation of thumb)
steroid injections
Dupuytrens contracture
progressive fibroproliferative disorder affecting palmar fascia causing fibrous tissue to shorten & thicken common in men aged >60
~70% of pts have positive FH
Presentation of Dupuytrens contracture
most commonly affects 4th/5th digits
45% are bilateral
pitting / thickening of palmar skin & loss of skin mobility
nodule formation then cord formation(thickening resembles tendon)
flexion contracture affecting finger
Mangement of Dupuytrens contracture
physio, splinting, corticosteroid injections
consider surgical treatment (when functional disability e.g. cannot place hand flat on table)
Trigger finger
common condition associated with abnormal flexion of the digits due to fibrocartilagenous metaplasia of the tendon sheath, usually idiopathic
presents with painless locking of finger in flexed position that releases suddenly with snap/pop ± palpable tender nodule at base of MCP joint
often affects ring finger or thumb
managed with steroid injections ± finger splint
Ganglion cyst
bening mucin filled cyst developing along tendons/joints usually seen in hand/wrist (especially dorsally on wrist)
usually asymptomatic but may be seen as fluctuant transilluminant swelling
usually observed, or excision if symptomatic
osler’s nodes
painful red raised lesion found on hands & feet
due to deposition of immune complexes
seen n infective endocarditis
Bouchard’s nodes
hard bony outgrowths or gelatinous cysts found on proximal interphalangeal joint (PIP) which are a sign of OA
Heberden’s nodes
pain & nodular thickening of the dorsal aspect of the distal interphalangeal joint (DIP)
may skew fingertips sideways
Musculocutaenous nerve injury
nerve roots C5-C7
supplies sensory to lateral part of forearm, and motor to elbow flexion & supination via biceps brachii
MOI:
isolated injury is rare, usually injured with brachial plexus
Axillary nerve injury
nerve roots C6/C6
responsible for shoulder abduction (deltoid) & sensory to inferior region of deltoid (i.e. regimental badge area)
MOI:
humeral head/neck fracture or dislocation
results in flattened deltoid and loss of sensation of regimental badge area
Radial nerve function
nerve roots: C5-T1
runs in spiral groove of humerus the anterior to lateral epicondyle where it divides
Innervation:
Motor: triceps, brachioradialis, forearm extensors
sensory: radial 2/3 of dorsal aspects of hand & dorsal aspect of radial 3 1/2 fingers (excluding the median nerve innervation i.e. the tips) + 1st web space
Radial nerve injury
Presentation:
weak supination & elbow flexion
weak wrist & finger extension
loss of hand extension = wrist drop
sensory loss to hand, especially 1st web space
NB if damaged in axilla = triceps paralysis
MOI:
axilla: improper crutch use
midarm: humeral shaft fracture, saturday night palsy/honeymoon palsy (compression of nerve when sleeping intoxicated on furniture)
radial head fracture
Median nerve function
nerve routes: C5-T1
descends with brachial artery, crosses elbow deep to biceps aponeurosis, then runs deep to flexors digitorum superficialis, enters wrist via carpal tunnel
Innervation:
all forearm flexors (except flexor carpi unlearns & medial 1/2 of flexor digitorum profundus = ulnar nerve),
sensory to palmar aspect of lateral 3 1/2 fingers
Median nerve injury
Presentation: if proximal injury: hand of benediction (loss of thumb opposition & abduction + loss of index & middle finger flexion) thenar muscle atrophy weak wrist pronation & flexion
if distal injury:
inability to pinch small objects
thenar muscle atrophy
ape hand (inability to oppose & abduct thumb)
MOI:
carpal tunnel syndrome, humerus fractures, penetrating injury
Ulnar nerve function
nerve roots: C8-T1
runs along posterioirmedial aspect of arm via biceps sulcus, then passes the medial epicondylar groove at elbow
Innervation:
motor: flexor carpi unlearns & medial 1/2 of flexor digitorum profundus, intrinsic muscles of hand, hypothenar muscles
Sensory: medial 1 1/2 fingers on dorsal and palmar aspects
Ulnar nerve injury
Presentation:
atrophy of hypothenar muscles
claw hand deformity (ulnar paradox = claw hand worse in distal nerve lesions)
wasting of intrinsic muscles of hand
MOI:
medial epicondyle fracture, cubital tunnel syndrome
long thoracic nerve
roots: C5-C7
innervates serrates anterior
damage = winged scapula
Hip dislocation
MOI: usually direct trauma e.g. RTCs & falls
90% = posterior dislocations
10% = anterior dislocations
Presentation:
posterior: shortened internally rotated & adducted leg
pain in hip, may radiate to knee
anterior: hip pain, inability to walk/adduct leg, leg
externally rooted, abducted & extended
investigated with AP & lateral hip X-ray, consider CT/MRI to rule out fractuer
management with analgesia & reduction under GA
Leg positioning in hips dislocation vs hip fracture
Hip dislocation:
posterior:
shortened internally rotated & adducted leg
anterior:
leg externally rotated, abducted & extended
Hip fracture:
shortened & externally rotated leg
Anterior cruciate ligament (ACL) injury
most commonly injured knee ligament
Presentation:
loud crack at point of injury, rapid joint swelling, bruising, pain
anterior draw test (+ve)
Lachmanns test (+ve)
imaged using MRI
managed with surgery & intense physio
Posterior cruciate ligament (PCL) injury
usually due to non contact hyeprflexion of the knee with platarflexed foot
Presentation:
loud crack at point of injury, rapid joint swelling, bruising, minimal posterior pain
posterior draw test (+ve) & posterior saga test (+ve)
take X-rays (posterior sag of tibia, bony avulsion) & MRI
Managed conservatively if isolated injury, but surgery if complex
Medial collateral ligament (MCL) injury
direct blow to lateral knee = forced valgus stress ± external rotation
Presentation:
pain, swelling, ecchymosis, deformity, instability of knee, ↑ medial joint laxity
vagus stress test (gently feel for joint line opening when applying valgus stress)
X-ray & MRI to rule out associated injuries
managed conservatively if isolated injury otherwise surgery
Lateral collateral ligament (LCL) injury
usually due to direct blow to medial knee which is relatively rare due to protected position by other knee
usually associated with ACL/PCL tears
presents with knee swelling, ecchymosis, pain, instability
↑ lateral knee laxity
varus stress test (apply virus stress & feel for joint line opening)
X-rays & MRIs
Management: generally surgery as isolated tears are rare
Meniscal tear/injury
may be degenerative image in older people or traumatic in young people (sports injury with rotational force)
Presentation knee pain (↑ with weight bearing & activity) joint line tenderness, restricted knee movements ± knee instability, knee locking / catching knee swelling with delayed onset over 2-36h
MRI - modality of choice
Management is usually RICE & physio or surgical repair if functional limitations
Chondromalacia patellae
inflammation of posterior patella with cartilage softening
usually seen in teenage girls after knee injury
presents with diffuse dull knee pain that is exacerbated by activity e.g. climbing stairs
patellofemoral pain syndrome (runners knee)
one of the most common causes of anterior knee pain commonly seen in young athletes usually due to overuse
> 50% of cases are bilateral
presents with retro/peripatellar knee pain worse on knee flexion during weight bearing exercise & crepitus
managed with RICE, NSAIDs, Physio
Prepatellar bursitis (housemaids knee)
inflammation of the prepatellar bursa usually secondary to prolonged kneeling/repeated falls onto knees
presents with swollen, erythematous, warm & painful knee + local tenderness & swelling of bursa
difficulty kneeling & walking
consider aspiration of bursa
managed with RICE & NSAIDs + Abx (if septic)
Patellar dislocation
patella slips out of trochlear groove usually laterally, usually seen in pts aged 10-17yrs
may be recurrent & spontaneously reduce
presents as severe knee pain, joint effusion, fixed flexion deformity of knee with laterally displaced patella
generally managed with closed reduction under analgesia (entonox) + physio/immobilisation
Iliotibial band sydnrome
overuse injury due to repeated flexion & extension of knee causing friction between iliotibial band & lateral epicondyle
presents with lateral knee pain ~2-3cm superior to lateral knee joint line, generally sharp pain during activity on foot strike & dull pain at rest
managed with physio, activity modification (change biomechanics) & muscle strengthening
trochanteric bursitis
common cause of lateral hip pain localised to greater trochanter
managed with physio, rest, NSAIDs
Achilles tendinitis
overuse injury of the achilles tendon often seen in athletes with recent ↑ exercise intensity
presents with pain & tenderness ~2-6cm above insertion of achilles tendon, with some stiffness
X-ray (may show insertional spur or erosion)
managed with reduced pressure in the area, NSAIDs, RICE, Physio
Achilles tendon rupture
may rupture during sports where a forceful push off is required most often seen in middle aged (30-50yrs)
presents with popping/snapping sound or sensation at tie of injury, sudden severe pain in achilles tendon, difficulty mobilising, weak/absent plantarflexion call swelling ± palpable interruption of affected achilles tendon Thompson test (squeezing calf with legs extended = absent positive plantar flexion)
USS 1st line imaging or MRI if unclear diagnosis
managed with non-weight bearing ASAP
Surgery if young/athletes
conservative if older/less active
Plantar fasciitis
most common cause of heel pain in adults due to inflammation of plantar fascia
presents with heel/plantar pain usually around medial calcaneal tuberosity, pain worse after periods of inactivity & prolonged weight bearing
point tenderness along plantar aponeurosis
Investigated with USS (fascial thickening) or X-ray (bony spurs)
managed with RICE, foot exercises/stretches (e.g. rolling ball underfoot), orthotic insoles, NSAIDs
if no improvement steroid injections
Morton’s neuroma
benign neuroma of the inter metatarsal plantar nerve most common in females
presents with forefoot pain, the sensation of a pebble in their shoe (between 3rd & 4th metatarsal most commonly), may have loss of sensation distally in the toes
investigated with USS
managed by excision if >5mm or USS guided steroid injections + avoiding tight shoes/high heels
Hallux valgus (bunions)
lateral deviation of the big toe at the MTP joint often with concurrent rotation of the large toe, most common forefoot deformity & common in females
presents with pain & inflammation & prominent metatarsal head ± fluid filled bursa
mamboed with advice on appropriate footwear, analgesia & orthotics
Pes planus (flat feet)
collpase of the medial longitudinal arch = eversion of the calcaneus in relation to the talus so the foot pronates
presents as flat/convex plantar surface of foot, absent medial arch when standing, foot pain
managed by corrective casting if congenital immediately after birth or orthotics if acquired
Thoracic outlet syndrome (TOS)
umbrella term for conditions involving compression of neruvascular structures as they pass the lower neck into the axilla, 90% of acmes = neurogenic
can be caused by neck trauma, collar bone fractures, cervical ribs, tumours (e.g. pan coast tumour)
presents with sensory loss, pain in neck/arm, painless wasting of hand muscles, cold/blanching/swelling hands, claudication, ulcers etc
symptoms more pronounced on overhead activity
investigations include provocation manoeuvres, X-rays, CT, angiography
managed with physio, analgesia, decompression surgery
Red flags for lower back pain
age <20 or >50 yrs previous malignancy night pain / waking up with pain history of trauma systemically unwell thoracic back pain
Facet joint associated back pain
may be acute or chronic
pain worse in morning & on standing, worse on extension of back tenderness
tenderness over facets on examination
Spinal stenosis
usually gradual onset, unilateral/bilateral leg pain ± back pain, numbness, weakness
symptoms worse on walking (relieved on sitting)
often have normal clinical examination
NB MRI required for diagnosis
Ankylosing spondylitis back pain
typically a young man presenting with lower back pain & stiffness (worse in morning & improves with activity)
Peripheral arterial disease
pain on walking, relieved with rest, absent/weak foot pulses, may have signs of limb ischaemia
often PMH of smoking & vascular disease
Prolapsed disc presentation
usually produces clear dermatomal leg pain associated with neurological deficits
leg pain usually worse than back pain
pain worse on sitting
most common site L5/S1 followed by L4-L5
so L5 = loss of sensation on dorsal of foot including big toe
Indications for surgical decompression in back pain
if significant/progressive neurological deficits
Bladder/bowel dysfunction
cauda equina syndrome
Type of hypersensitivity reaction in SLE
Type III hypersensitivity reaction
Type 3 is characterised by antigen-antibody complexes.
Azathioprine
A thiopurine methyltransferase (TPMT) test may be needed to look for individuals prone to azathioprine toxicity.
Adverse effects include bone marrow depression nausea/vomiting pancreatitis increased risk of non-melanoma skin cancer
significant interaction with allopurinol & hence lower doses of azathioprine should be used.
considered safe to use in pregnancy.
The A’s of associated features for Ankylosing spondylitis
Apical fibrosis Anterior uveitis Aortic regurgitation Achilles tendonitis AV node block (heart block) Amyloidosis
Causes of avascular necrosis of the femoral head
long-term steroid use
chemotherapy
alcohol excess
trauma
Juvenile idiopathic arthritis (JIA)
arthritis occurring in someone who is less than 16 years old that lasts for more than 6 weeks. Systemic onset JIA is a type of JIA which is also known as Still’s disease
presentation includes pyrexia, salmon-pink rash, lymphadenopathy, arthritis, uveitis, anorexia and weight loss
ANA may be positive (especially in oligoarticular JIA)
rheumatoid factor is usually negative
NBP pauciarticular JIA refers to cases where 4 or less joints are affected. It accounts for around 60% of cases of JIA
Psoas abscess
usually caused by staph aureus (often seen in IVDU)
presents with fever, back/flank pain, limp, weight loss, Antalgic gait
hip flexed & externally rotated at rest
Passive extension / internal rotation = pain
Hip flexion against resistance = pain
Passive extension and/or internal rotation of the affected hip elicits pain
CT abdomen is gold standard investigation
Managment:
1st line: ABx & percutaneous drainage
2nd line surgery (if drainage fails)