MSK Ix Mx Flashcards
(46 cards)
Ankle and Foot: Bunions
Ankle and Foot: Morton’s neuroma
Ankle and Foot: Plantar fasciitis
Plantar fasciitis = the most common cause of heel pain seen in adults
The pain is usually worse around the medial calcaneal tuberosity
Mx = Rest the feet where possible
wear shoes with good arch support and cushioned heels
insoles and heel pads may be helpful
Ankylosing spondylitis
Ankylosing spondylitis is a HLA-B27 associated spondyloarthropathy
It typically presents in males (sex ratio 3:1) aged 20-30 years old.
back pain worse at night and first thing in the morning
with alternating buttock pain due to SI joint involvement
The pain and stiffness classically improve after exercise.
Ix:
1st = Hip X-Ray + Inflamm markers
2nd = MRI
3rd = Spirometry
Mx: 1st = NSAIDS
2nd = Anti-TNF drugs (etanercept/Adalimumab)
HLA-B27 is of little use in making the diagnosis as it is positive in:
90% of patients with ankylosing spondylitis
10% of normal patients
Radiographs may be normal early in disease, later changes include:
sacroiliitis: subchondral erosions, sclerosis
squaring of lumbar vertebrae
‘bamboo spine’ (late & uncommon)
syndesmophytes: due to ossification of outer fibers of annulus fibrosus
chest x-ray: apical fibrosis
If the x-ray is negative for sacroiliac joint involvement in ankylosing spondylitis but suspicion for AS remains high, the next step in the evaluation should be obtaining an MRI. Signs of early inflammation involving sacroiliac joints (bone marrow oedema) confirm the diagnosis of AS and prompt further treatment.
Spirometry may show a restrictive defect due to a combination of pulmonary fibrosis, kyphosis and ankylosis of the costovertebral joints.
encourage regular exercise such as swimming
physiotherapy
the disease-modifying drugs which are used to treat rheumatoid arthritis (such as sulphasalazine) are only really useful if there is peripheral joint involvement
the 2010 EULAR guidelines suggest: ‘Anti-TNF therapy should be given to patients with persistently high disease activity despite conventional treatments’
research is ongoing to see whether anti-TNF therapies such as etanercept and adalimumab should be used earlier in the course of the disease
Bursitis
Crystal arthropathy: Gout
Gout is a form of microcrystal synovitis caused by the deposition of monosodium urate monohydrate in the synovium. It is caused by chronic hyperuricaemia (uric acid > 450 µmol/l)
Ix = Synovial fluid analysis + Uric Acid + X-Ray
Acute mx: 1st = NSAIDs/Colchicine + PPI
2nd = Oral pred 15mg/day (or IV)
REMEMBER: NSAIDS cannot be taken if the pt has CKD or MM!
Long-term mx:
1st = Allopurinol (ULT) 100mg OD + 6months cochicine cover
2nd = Febuxostat
Refractory = Uricase
Persistent = Pegloticase
Synovial Fluid analysis;
needle shaped negatively birefringent monosodium urate crystals under polarised light
Uric acid
should be checked once the acute episode has settled down (typically 2 weeks later) as may be high, normal or low during the acute attack
Radiological features of gout include:
joint effusion is an early sign
well-defined ‘punched-out’ erosions with sclerotic margins in a juxta-articular distribution, often with overhanging edges
relative preservation of joint space until late disease
eccentric erosions
no periarticular osteopenia (in contrast to rheumatoid arthritis)
soft tissue tophi may be seen
The maximum dose of NSAID should be prescribed until 1-2 days after the symptoms have settled
Colchicine;
Has a slower onset of action
Caution for renal impairment!: Reduce the dose if eGFR is 10-50 ml/min and to avoid if eGFR < 10 ml/min BNF
Main SE = Diarrhoea
If the patient is already taking allopurinol it should be continued
Indications for urate-lowering therapy (ULT)
- After their 1st attack of gout
- > = 2 attacks in 12 months
- Tophi
- Renal disease
- Uric acid renal stones
- Prophylaxis if on cytotoxics or diuretics
Urate-lowering therapy = wait until inlammation is reduced/pt is not in pain to discuss long-term ULT(allopurinol)
initial dose of 100 mg od, with the dose titrated every few weeks to aim for a serum uric acid of < 360 µmol/l
CKS
A lower target uric acid level below 300 µmol/L may be considered for patients who have tophi, chronic gouty arthritis or continue to have ongoing frequent flares despite having a uric acid below 360 µmol/L
A lower initial dose of allopurinol should be given if the patient has a reduced eGFR
Re colchicine cover: NSAIDs can be used if colchicine cannot be tolerated. The BSR guidelines suggest this may need to be continued for 6 months
Lifestyle modifications
reduce alcohol intake and avoid during an acute attack
lose weight if obese
avoid food high in purines e.g. Liver, kidneys, seafood, oily fish (mackerel, sardines) and yeast products
Other points;
- Stop precipitating drugs (such as thiazides)
- Losartan has a specific uricosuric action and may be particularly suitable for the many patients who have coexistent hypertension
- Increased vitamin C intake (either supplements or through normal diet) may also decrease serum uric acid levels
Elbow: Lateral epicondylitis (tennis elbow)
- Lateral epicondylitis (tennis elbow) = pain and tenderness localised to the lateral epicondyle
pain worse on resisted wrist EXTENSION with the elbow extended or supination of the forearm with the elbow extended
Episodes typically last between 6 months - 2 years. Patients tend to have acute pain for 6-12 weeks
Elbow: Medial epicondylitis (golfer’s elbow)
- Medial epicondylitis (golfer’s elbow) = pain and tenderness localised to the medial epicondyle
pain is aggravated by wrist flexion and pronation
symptoms may be accompanied by numbness / tingling in the 4th and 5th finger due to ulnar nerve involvement
Fibromyalgia = stiff muscle pain
Women are around 5 times more likely to be affected
typically presents between 30-50 years old
Chronic pain: at multiple site, sometimes ‘pain all over’
lethargy
Cognitive impairment: ‘fibro fog’
sleep disturbance, headaches, dizziness are common
Ix = Pt is tender all over
Mx = Tailored to the individual patient.
Aerobic exercise: has the strongest evidence base
CBT
Neuropathic drugs = pregabalin, duloxetine, amitriptyline
Giant cell arteritis (visual loss mx?)
Ix = ESR + temporal artery biopsy
Mx = high-dose pred (pre Ix!) + bisphos
(for bone protection from long-term steroids)
visual loss = IV methylpred then oral pred + emergency opthal review
Raised inflammatory markers
ESR > 50 mm/hr (note ESR < 30 in 10% of patients)
CRP may also be elevated
temporal artery biopsy
skip lesions may be present
note creatine kinase and EMG normal
There should be a dramatic response to IV methylpred, if not the diagnosis should be reconsidered
visual damage is often irreversible
Hip: joint dysfunction (sacroiliac, transient synovitis)
Transient synovitis = irritable hip
Viral infection -> Acute hip pain
It is the commonest cause of hip pain in children. The typical age group is 3-8yo’s
Ix: Important to distinguish from septic arth by looking at high fever(red flag)!
Features
limp/refusal to weight bear
groin or hip pain
a low-grade fever is present in a minority of patients
High fever = septic arthritis
children may be monitored in primary care (with a presumptive diagnosis of transient synovitis) ‘If the child is aged 3–9 years, well, afebrile, mobile but limping, and has had the symptoms for less than 72 hours
Mx = Self-limiting, requiring only rest and analgesia
Idiopathic inflammatory myopathies: polymyositis
Features
proximal muscle weakness +/- tenderness
Raynaud’s
respiratory muscle weakness
interstitial lung disease
e.g. fibrosing alveolitis or organising pneumonia
seen in around 20% of patients and indicates a poor prognosis
dysphagia, dysphonia
Ix = Muscle enzymes + EMG + muscle biopsy + anti-synth/jo-1 antibodies
Mx = high-dose corticosteroids + azathioprine
Muscle enzymes (CK, lactate dehydrogenase (LDH), aldolase, AST and ALT) are elevated in 85-95% of patients
corticosteroids are tapered as symptoms improve
Azathioprine = steroid-sparing agent
Inherited disorders of connective tissue: Marfan syndrome (AD)
Autosomal recessive conditions are often thought to be ‘metabolic’ as opposed to autosomal dominant conditions being ‘structural’, notable exceptions:
some ‘metabolic’ conditions such as Hunter’s and G6PD are X-linked recessive whilst others such as hyperlipidaemia type II and hypokalaemic periodic paralysis are autosomal dominant
some ‘structural’ conditions such as ataxia telangiectasia and Friedreich’s ataxia are autosomal recessive
Marfan Features;
tall stature with arm span to height ratio > 1.05
high-arched palate
arachnodactyly
pectus excavatum
pes planus
scoliosis of > 20 degrees
heart:
dilation of the aortic sinuses (seen in 90%) which may lead to aortic aneurysm, aortic dissection, aortic regurgitation
mitral valve prolapse (75%),
lungs: repeated pneumothoraces
eyes:
upwards lens dislocation (superotemporal ectopia lentis)
blue sclera
myopia
dural ectasia (ballooning of the dural sac at the lumbosacral level)
The life expectancy of patients used to be around 40-50 years.
With the advent of regular echocardiography monitoring and beta-blocker/ACE-inhibitor therapy this has improved significantly over recent years.
Aortic dissection and other cardiovascular problems remain the leading cause of death however.
Joint dislocation (incl. acromio-clavicular, elbow, shoulder, patella)
The shoulder is the most common joint in the body to dislocate, accounting for approximately 50% of all major joint dislocations.
Anterior shoulder dislocations account for > 95% of cases.
Shoulder dislocations occur when the humeral head dislodges from the glenoid cavity of the scapula.
Mx:
Recent = Reduction
Otherwise = analgesia/sedation to relax muscles
Knee: Pain syndromes (iliotibial band, patellofemoral syndrome)
Iliotibial band syndrome is a common cause of lateral knee pain in runners, occurring in around 1 in 10 people who run regularly
Ix = tenderness 2-3cm above the lateral joint line
Mx:
1st = Activity modification and iliotibial band stretches
2nd = if not improving then physiotherapy referral
Osteoarthritis
- Typically presents acutely with a ‘clunk’, pain and inability to weight bear
- On examination there is internal rotation and shortening of the affected leg
- aseptic loosening (most common reason for revision )
prosthetic joint infection
Ix = Clinical diagnosis if typical, otherwise X-Ray*
Mx = paracetamol/NSAIDS
OA knee/hand = topical NSAIDS
2nd = Oral NSAIDs/COX-2 inhibitors(+PPI)*, opioids, capsaicin cream and intra-articular corticosteroids. These drugs should be avoided if the patient takes aspirin
3rd = Joint replacement (if conservative measures fail)
Intra-articular injections = short-term benefit
total hip replacement remains the definitive treatment
All patients should be offered help with weight loss, given advice about local muscle strengthening exercises and general aerobic fitness
Non-pharmacological mx = supports and braces, TENS and shock-absorbing insoles or shoes
*WF1 - NSAIDS + COXi are contraindicated in osteoarthritis!!!?
*main findings on X-Ray = reduced joint space, subchondral sclerosis, bone cysts and osteophytes
Can be caused by long-term use of omeprazole
Osteomyelitis
Most common = S.aureus
SCD pt = Salmonella
Ix = MRI
Mx = flucloxacillin for 6 weeks
clindamycin if penicillin-allergic
Peripheral nerve injuries/palsies
pain ladder?
Polymyalgia rheumatica
Features
typically patient > 60 years old
usually rapid onset (e.g. < 1 month)
aching, morning stiffness in proximal limb muscles
weakness is NOT considered a symptom of polymyalgia rheumatica
also mild polyarthralgia, lethargy, depression, low-grade fever, anorexia, night sweats
Muscle pain without weakness in an elderly person is polymyalgia rather than polymyositis
my-A - A-cheing pain!
my-O - O-ld and weak
Same as GCA
Ix = Inflamm markers
Mx = pred 15mg/od
raised inflammatory markers e.g. ESR > 40 mm/hr
note creatine kinase and EMG normal
patients typically respond dramatically to steroids! failure to do so should prompt consideration of an alternative diagnosis
CK is normal
Cutanea tarda Porphyria = photosensitive rash with blistering and skin fragility on the face and dorsal aspect of hands (most common feature)
Features
hypertrichosis (abnormally placed hair growth)
hyperpigmentation
Ix = Urine + serum iron/ferritin
urine = elevated uroporphyrinogen and pink fluorescence of urine under Wood’s lamp
serum iron ferritin level is used to guide therapy
Mx: 1st = chloroquine 2nd = venesection
Venesection is preferred if iron ferritin is above 600 ng/ml
Psoriatic arthritis
Ix: X-Ray (pencil-in-cup appearance at DIP joint)
Mx: NSAIDS -> methotrex/sulphasal/anti-TNF
Reactive arthritis = An arthritis that develops following an infection where the organism cannot be recovered from the joint
Reactive arthritis is one of the HLA-B27 associated seronegative spondyloarthropathies.
Classic triad = ‘Can’t see, pee or climb a tree’
Mx:
Symptomatic:
1st = analgesia, NSAIDS, intra-articular steroids
2nd = Sulfasalazine and methotrexate are sometimes used for persistent disease
symptoms rarely last more than 12 months
*as Reiter was a member of the Nazi party the term is no longer used
Rheumatoid arthritis
How does it present?
Px = pain is particularly
bad first thing in the morning. On examination, the wrists, metacarpophalangeal
joints and proximal interphalyngeal joints are swollen and warm and stiff
Ix = Anti-cyclic citrullinated peptide antibody + X-Ray (hands+feet)
Mx: Pt with evidence of joint inflammation should start a combination of disease-modifying drugs (DMARD) as soon as possible
Initial:
1st = DMARD(methotrex) + pred(short course)
2nd = Try another DMARD
3rd = TNF-inhibitor (sub-cut etanercept or adalimumab / IV infliximab/rituximab)
Monitoring response to treatment = CRP + DAS28 score
Flares = Corticosteroids - oral/IM
Methotrexate monitoring = FBC(myelosupression) & LFTs(cirrhosis). Other important side-effects include;
pneumonitis
sulfasalazine
leflunomide
hydroxychloroquine
ALWAYS GIVE FOLIC ACID WITH METHOTREXATE
Anti-cyclic citrullinated peptide antibody may be detectable up to 10 years before the development of rheumatoid arthritis. It has a key role in the diagnosis of rheumatoid arthritis, allowing early detection of patients suitable for aggressive anti-TNF therapy. It has a sensitivity similar to rheumatoid factor (around 70%) with a much higher specificity of 90-95%.
NICE recommends that patients with suspected rheumatoid arthritis who are rheumatoid factor negative should be tested for anti-CCP antibodies
TNF-inhibitors
etanercept: recombinant human protein, acts as a decoy receptor for TNF-α, can cause demyelination, risks include reactivation of tuberculosis
infliximab: monoclonal antibody, binds to TNF-α and prevents it from binding with TNF receptors, intravenous administration, risks include reactivation of tuberculosis
adalimumab: monoclonal antibody
Rituximab
anti-CD20 monoclonal antibody, results in B-cell depletion
Septic arthritis
acute, swollen joint
restricted movement in 80% of patients
examination findings: warm to touch/fluctuant
fever: present in the majority of patients
Ix = synovial fluid sampling + blood culture + X-Ray/CT?
Joint aspiration is only +ve in 50% of pts with septic arth! so just start fluclox asap if suspected
Blood cultures: the most common cause of septic arthritis is hematogenous spread
Mx: IV fluclox (clinda if pen-allergic) 4-6weeks + joint needle aspiration
Patients are typically switched to oral antibiotics after 2 weeks
arthroscopic lavage may be required
