MSK Flashcards
What are the clinical findings of ankylosing spondylitis?
reduced chest expansion, reduced lateral flexion and reduced forward flexion (Schober’s test)
Sulfasalazine can cause what?
Reduced sperm count -> usually returns to normal upon stopping the medication
What would joint aspiration of rheumatoid arthritis show?
- High WBC
- Polymorph neutrophils
- Cloudy/Yellow appearance
What is previous chemo a big risk factor for?
Avascular necrosis
Methotrexate plus trimethoprim can cause what?
Bone marrow suppression and panycytopenia
DIP swelling and dactylitis with arthritis suggests what?
Psoriatic arthritis
Which antibody is specific for anti-phospholipid syndrome?
Anticardiolipin antibody
What are the smoking cessation drugs?
- Nicotine replacement (causes N+V, headaches, flu symptoms)
- Varenicline (causes nausea and C/I in pregnancy/BF)
- Bupropion (reduces seizure threshold)
What type of shock does tension pneumothorax cause?
Obstructive
Which lung cancer is gynaecomastia associated with?
Adenocarcinoma of the lung
What does an isolated rise in ALP suggest?
Pagets disease of the bones
What is Paget’s disease of the bone?
Increased but uncontrolled bone turnover- XS osteoclast resorption and increased osteoblastic activity
What is most commonly affected in Paget’s
Skull, spine/pelvis, long bones of lower extremities
Paget’s predisposing factors?
Age, male, northern latitude, FHx
Paget’s CP
- 5% symptomatic
- older male with bone pain and raised ALP
- bone pain: pelvis, lumbar, femur
- bowing of tibia, bossing of skull
Paget’s Ix
- bloods
- other markers of bone turnover
- x-ray= osteolysis in early disease; mixed lytic/sclerotic lesions later. Skull= thickened vault, osteoporosis circumscripta
- Bone scintigraphy (increased uptake at sites of active bone lesions)
Bloods in Paget’s?
- Raised ALP
- Ca and phosphate normal (sometimes hypercalcaemia with prolonged immobilisation)
Other markers of bone turnover in Paget’s?
- procollagen type I N-terminal propeptide (PINP)
- serum C-telopeptide (CTx)
- urinary N-telopeptide (NTx)
- urinary hydroxyproline
Paget’s Mx?
- Bisphosphonate (oral risedronate or IV zoledronate)
- calcitonin less common
Paget’s indications for Mx
Bone pain, skull or long bone deformity, fracture, periarticular Paget’s
Paget’s Cx
Deafness, bone sarcoma, fractures, skull thickening, high-output cardiac failure
subchondral erosions, sclerosis
and squaring of lumbar vertebrae
Anklyosing spondylitis
What is the most common site of metatarsal stress fractures?
2nd metatarsal
hyperpigmentation of the palmar creases indicates what?
Addisons
How should proximal scaphoid pole fracture be managed?
Refer to orthopaedics for surgical fixation
Features of a acetabular labral tear?
- Following trauma
- Hip/groin pain
- Snapping sensation
Features of a femoroacetabular impingement?
- More chronic history
Long term steroid use/chemo therapy + someone with hip pain suggests?
Avascular necrosis of the hip
Pain following tibial surgery?
Compartment syndrome
What is the management of AVN?
If displaced: total hip replacement for anyone who is mobile, no co-morbidities etc otherwise hemiarthroplasty
If not displaced: internal fixation
Rheumatic vs psoriatic arthritis?
Psoriatic will be asymmetrical
When should uric acid levels be measured again with gout?
2 weeks after the flare has settled
X-ray findings for rheumatoid arthritis
L – loss of joint space
E – erosions
S – soft tissue swelling
S – soft bones (periarticular osteopenia)
+ juxta-articular osteoporosis
subluxation
Extra-articular manifestations of RA?
Nodules, scleritis, episcleritis, pleural effusion, Felty, anaemia, Raynaud’s, carpal tunnel
RA, Splenomegaly and neutropenia?
Felty
Antibody of choice for RA
Anti-ccp
Hand signs for RA
- Ulnar deviation
- Swan neck deformity
- Z neck thumb
- Muscle wasting
- Wrist subluxation
What organism can cause septic arthritis with metal joint?
Early stages after surgery - staph aureus
Later onset - staph epidermidis
What are risk factors for septic arthritis?
RA, DM, Immunosuppression, Penetrating injury, infection elsewhere
What are the rotator cuff muscles?
Supraspinatus
Infraspinatus
Teres minor
Subscapularis
What muscles are responsible for shoulder abduction?
0-15 degrees: supraspinatus
15 - 90 degrees: deltoid
90 degrees+: Trapezius and serratus anterior
Which muscles does the accessory nerve innervate?
Deltoid and teres minor
Investigations to assess for supraspinatus impingement?
US and MRI
Proximal muscle weakness + raised CK + no rash
Polymyositis
Dermatomyositis vs polymyositis
Dermatomyositis would have a rash
What would be seen on X-ray to support a diagnosis of ankylosing spondylitis?
Sacro-ilitis
What should be given to women >75 with a fragility fracture?
Bisphosphonates
When should a referral for sciatica be considered?
4-6 weeks after analgesia + physio treatment
What are the features of ankylosing spondylitis?
Apical fibrosis
Anterior uveitis
Aortic regurgitation
Achilles tendonitis
AV node block
Amyloidosis
and cauda equina syndrome
Pain worse on walking on tip toes?
Plantar fasciitis
Fever + back pain + IVDU
Iliopsoas abscess
What is the treatment for psoas abscess?
Abx + percutaneous drainage
muscle wasting of the hands, numbness and tingling and possibly autonomic symptoms
Neurogenic thoracic outlet syndrome
What is osteomalacia?
Softening of the bones secondary to vit D deficiency
How does osteomalacia present?
- Bone pain/tenderness
- Fractures e.g NOF
- Proximal myopathy: waddling gait
How would osteomalavcia present on investigations?
- Low Vit D
- Low calcium and phosphate
- Raised ALP
- Translucent bands over the X-ray
Management of NOF fractures
Non-displaced + intracapsular: cannulated screw fixation
Stable + extra capsular: dynamic hip screw
Displaced + Intacapsular if not very mobile older patient: Hemiarthroplaty
Displaced + intracapsular if young/mobile older patient: Total hip arthroplasty
flexion deformities of his 4th and 5th digit which cannot be passively corrected
Duputrynes contracture
What is often the earliest sign of Dupuytrens?
Firm, thickened palmar nodule over the metacarpal head
What are risk factors for Dupuytrens?
- Diabetes
- Alcohol
- FH
- AIDS
Limited vs diffuse cutaneous systemic sclerosis
Diffuse will have widespread skin and organ involvement (lungs and kidneys)
What is fat embolism?
A syndrome secondary to trauma/fractures/orthopaedic surgery
How does fat embolism present?
Pulmonary: PE like symptoms
Neuro: altered mental status, seizures, coma
Derm: petechial rash on upper body
Managed with supportive treatment/prophylaxis
What are common precipitants of gout?
- Surgery
- Dehydration
- Alcohol
- Trauma
- Infection
- Foods rich in purines
What are x-ray findings of gout?
- Normal joint space
- Soft tissue swelling
- Periarticular erosions
What can be some examination findings of osteoarthritis?
- Antalgic gait
- Joint swelling
- Joint tenderness
- Pain on movement
- Crepitus
- Reduced ROM
purple discolouration of eyelids in dermatomyositis?
Heliotrope
What are Gottron’s papules?
Rough, red papules over the knuckles -> dermatomyositis
What antibodies are associated with dermatomyositis?
Anti-Jo, Anti-MI, RF, ANA
What is Raynauds phenomenon?
Peripheral digital ischaemic caused by vasospasm which is precipitated by cold/emotion
What are some causes of Raynauds phenomenon?
- SLE
- Raynaud’s disease
- RA
- Ehler-Danlos
- Beta blockers
- Atherosclerosis
What are the features of CREST?
Calcinosis
Raynaud’s
Oesophageal dysmotility
Sclerodactyly
Telangiectasia
What respiratory condition is associated with AS?
Pulmonary fibrosis
What is mononeuritis multiplex?
Damage to 2+ peripheral nerves
What are causes of mononeuritis multiplex?
- HIV/AIDS
- Diabetes
- RA
- Sarcoidosis
What is the definitive investigation for Sjogrens?
Salivary gland biopsy
What is the most common cause of cauda equina syndrome?
Lumbar disc herniation at L4/L5/ or L5/S1
Pseudogout is strongly associated with what?
Haemochromatosis
What are the most specific markers for SLE?
anti-dsDNA and anti-SM
ANA - most sensitive
Erb’s palsy has injury to which myotomes?
C5 and C6 (11 erbs and spices)
How does Erb’s palsy present?
Imparied wrist extension and elbow flexion - waiters tip
Carbamazepine increases risk of what?
Osteoporosis
Back pain red flags?
- Thoracic or cervical spine pain
- Progressive pain not relieved by rest
- Fevers, chills, weight loss
- Early morning stiffness > 30 mins
- Bowel/bladder/neuro dysfunction
What should be given for cord compression secondary to bone metastases?
Dexamethasone
Osteoporosis risk factors?
Steroids
Hyperthyroidism/Hyperparathyroidism
Alcohol/Smoking
Thin
Testosterone deficiency
Early menopause
Renal failure
Erosive bone disease
Diabetes
What is a Colles fracture?
Fracture of the distal radium with dorsal angulation of the distal fracture fragments
Septic Arthritis in a prosthetic joint?
Admit patient and arrange ortho review
pain and swelling at the base of the thumb and along the radial aspect of the wrist, often worsened by thumb movement or grasping in a YOUNG person
De Quervain;s tenosynovitis
What should take place before starting anyone on biologics?
Quantiferon test - assess for TB as biologics can reactivate latent TB
Abx regiment for septic arthritis?
2 weeks of IV plus 4 weeks of orals
Which antibodies are specific for anti phospholipid
Anti-beta-2-glycoprotein I antibody
What is a common early finding in professional players who have had trauma?
Osteoarthritis
What cover should be given to those receiving allopurinol?
NSAIDs cover for 3 months as allopurinol can acutely raise urate levels
‘rain-drop skull’
Myeloma
‘pepper pot skull’
Hyperparathyroidism
What are the most common side effects of colchicine?
Diarrhoea, nausea + vomiting
What scoring system can be for RA and what does it indicate?
Disease-activity score
<2.6 - remission
>5.1 - high disease activity
What is the dose for steroids in GCA?
60mg of prednisolone
How would lumbar spondylosis present?
- Arthritis like pain which gets worse throughout the day in older patients
What is recommended in patients with GCA with CVD risk factors/IHD?
Aspirin 75mg as prophylaxis
What is the inheritance of Marfans?
Autosomal dominant
How should methotrexate be monitored?
FBC, Renal function and LFTs weekly until established then every 2-3 months
What can patients with limited systemic sclerosis develop as a late manifestation?
Interstitial lung disease
What investigation should be done for women with polymyalgia due to steroid use?
DEXA
What are the 4 features of antiphospholipid syndrome?
Clots - VTE/PE
Livedo reticularis
Obstetric loss
Thrombocytopenia
c-ANCA positive?
Granulomatosis with polyangiitis
What are features of granulomatosis with polyangiitis?
- Resp involvement
- Kidney involvement: glomerulonephritis
- Systemic symptoms
- Ocular manifestations e.g. scleritis
How is granulomatosis with polyangiitis managed?
- Cyclophosphamide/rituximab in acute
- Azathioprine/Methotrexate during remission
asthma, nasal polyps and a mononeuritis multiplex
Eosinophilic granulomatosis with polyangiitis
Recurrent oral and genital ulcers with uveitis and erythema nodosum?
Behcet’s disease- HLA B51
Common sites where osteoporotic fragility fractures occur?
- Pubic ramus
- Hip
- Distal radium
- Proximal humerus
What are side effects of bisphosphonates?
- Abdominal pain
- Dyspepsia
- Nausea
- Abdominal distension
- Oesophageal ulceration
What is the first line imaging in myeloma?
MRI
Acute back pain in a patient with osteoporosis?
Think osteoporotic verterbral fracture -> X-ray needed
What is the Z score adjusted for in patients with DEXA scans?
Age, gender and ethnic factors
What antibodies are found in CREST syndrome?
Anti-centromere
What is Behcet’s syndrome?
- Common in young Turkish men
- Oral ulcers, genital ulcers and anterior uveitis
- Erythema nodosum also present
Which DMARD is associated with retinopathy?
Hydroxychloroquine
What is Caplan syndrome?
Massive fibrosis in patients with RA and pneumoconiosis
What is polyarteritis nodosa?
Medium vessel vasculitis common in middle aged men with Hep B
Can cause testicular pain, weight loss, HTN, renal failure
PANCA positive
Ejection systolic murmur with SLE?
Libman-Sacks endocarditis
What are some skin changes with dermatomyositis?
- Heliotrope rash of eyelids
- Periorbital oedema
- Dilated capillary loops under the fingernails
What are some symptoms of dermatomyositis?
- Muscle swelling
- Muscle tenderness
- Arthralgia
- Fatigue
- Weakness
What are some symptoms of fibromyalgia?
- Pain
- Sleep disturbance
- Paraesthesia
- Memory disturbance
- Headaches
- Dizziness
What are some skin changes with Reiters?
- Mouth ulcers
- Erythema nodosum
- Keratoderma blennorrhagica (yellow/brown papules on soles of feet)
What are some cardiac complications of Reiters?
- Pericarditis
- Aortic regurg
- Aortitis
What is there not in someone with polymyalgia?
True weakness of muscles -> normal power
Management of a prolapsed disc?
Analgesia + Physio
Painful click on McMurrays test?
Think twisted knee injury - meniscal tear
What is a Galeazzi fracture?
Dislocation of the distal radioulnar joint with an associated fracture of the radius
tenderness in the anatomic snuffbox dorsally
Scaphoid fracture
What should be corrected before giving bisphosphonates?
Calcium level / Vit D deficiency
Pain on the radial side of the wrist/tenderness over the radial styloid process in a young women?
De Quervain’s tenosynovitis
What does co-trimoxazole contain?
Trimethoprim -> think about methotrexate
Most likely places for bone mets?
Women - breast
Men - prostate
What are major risk factors for osteoporosis?
- Steroid use
- RA
- Alcohol excess
- Low BMI
- Smoking
What will the blood test values be with osteoporosis?
Everything normal
Imaging of choice for osteomyelitis?
MRI
lead pipe appearance of the colon
Ulcerative colitis
popping sensation, immediate swelling and immediate unable to weight-bear
ACL injury - Lachmans test
Knee locking and giving-way
Meniscal lesions
What is the management of newly diagnosed RA?
Methotrexate and oral steroids
Z score is helpful for what?
Diagnosing secondary osteoporosis
Compartment syndrome produces what?
Pain on passive stretch
What is the management of flares of rheumatoid arthritis?
Steroids oral or IM
When can reactive arthritis present and how long do symptoms last?
- Can develop upto 4 weeks after initial infection
- Symptoms last around 4-6 months
dull shoulder pain, that often disturbs sleep, followed by
stiffness and loss of shoulder mobility
Frozen shoulder - Adhesive capsulitis
Management of undisplaced scaphoid fractures?
Cast for 6-8 weeks
What are some hand signs of psoriatic arthritis?
- Dactylitis
- Nail pitting
- Onchylosis
- Nail discolouration
What are some X-ray findings of psoriatic arthritis?
- Soft tissue swelling
- Bony erosions
- Pencil in cup deformity
- Loss of joint space
What is the most severe form of psoriatic arthritis?
Arthritis mutilans
What is the treatment of psoriatic arthritis?
- NSAIDs if mild
- Methotrexate
- anti-TNF biologics
Chalky nodules in someone with gout?
Gouty tophi
What HLA type is rheumatoid?
HLA-DR4 / HLA-DR1
Risk factors for pseudogout?
- Steroid use
- Hyperparathyroidism
- Haemochromatosis
- Wilson’s
- Acromegaly
What is the prognosis of pseudogout?
Resolves within 10 days
What are some complications of eosinophilic granulomatosis with polyangiitis?
- HF
- Myocarditis
- HTN
- Stroke
- Bowel ischaemia
- Pancreatitis
Prophylactic bisphosphonates should be offered to who?
Those with T score <1.5 if they are on steroids for more than 3 months
What should alendronate be changed to if patients are experiencing bad GI side effects?
Risedronate
SGLT-2 inhibitors can increase the risk of what?
Ulcers or infection -> increased risk of amputation
Which organism causes osteomyelitis in sickle cell?
Salmonella
anti-histone antibodies can be a sign of what?
Drug induced lupus - common causes include isoniazid, phenytoin
Lace like rash on shins is a sign of what?
Livedo reticularis -> associated with anti-phospholipid syndrome
raised CRP in a patient with known SLE
Can suggest underlying infection
What is an early x ray finding of rheumatoid arthritis?
Juxta-articular osteopenia
What is a fragility fracture?
A fracture from a fall from standing height or less
What are examples of fragility fracture?
- Vertebral compression fractures
- Hip
- Distal radium
- Proximal humerus fracture
Nerve and which fracture they are associated with?
Radial - fracture of shaft of humerus (wrist drop)
Ulnar - supracondylar fracture of humerus
Axillary - fracture of proximal humerus
Bilateral carpal tunnel?
Rheumatoid
Lateral knee pain in a runner?
Iliotibial band syndrome -> treat with stretches
Lateral epicondylitis causes what?
- Pain worse on supination of the wrist
- Pain worse on wrist extension against resistance
What is the main structure which is damaged in scaphoid fractures?
dorsal carpal branch of the radial artery
dislocation of the proximal radioulnar joint in association with an ulnar fracture
Monteggia fracture
Most common sites of osteomyelitis in children and adults?
Children - Metaphysis
Adults - Epiphysis
What are different management options for carpal tunnel?
- Night splints
- Intraarticular steroid injections
- Carpal tunnel decompression
Bruised, swollen, deformed and painful elbow?
Think supracondylar fracture
What would Perthes disease x-ray show?
- Widening of joint space
- Decreased femoral head size
- Flattening
What are surgical management options for osteoarthritis?
- Osteotomies
- Arthroplasty
What is duputryens?
Thickening of the palmar fascia which eventually causes a fixed flexion deformity
What is the most common type of shoulder dislocation?
Anterior dislocation
What is the weight bearing status after NOF surgeries?
Cannulated screws - less than full initially
Everything else - full weight bearing
Radiculopathy vs myelopathy
Radiculopathy - compression of a single nerve root which has exited the spinal cord
Myelopathy - pain due to compression of the spinal cord
Which nerve roots correspond to reflexes?
Ankle - S1/2
Knee - L3/L4
Bicep - C5/C6
Tricep - C7/C8
Simmonds test - calf squeeze
Achilles tendon rupture
Which knee compartment is most commonly affected in osteoarthritis?
Medial
Open tibial fractures should be covered with what?
Sterile saline gauze
Which muscle is responsible for the weakness in thumb abduction in carpal tunnel?
Abductor pollicis brevis
Haematogenous vs direct contamination?
Haematogenous - infection reaches bone through bloodstream
Direct contamination - infection spreads directly from adjacent tissues/structures to the bone
Bakers cysts occur secondary to what?
Degeneration
Imaging for achilles tendon rupture?
US
What is the test of choice for Duputryen’s?
Table top test
Which arteries are at risk in NOF?
Circumflex arteries
Soft, non-tender swelling near joints or tendons, containing clear,
viscous fluid
Ganglionic cyst
Sciatic nerve originates from?
L4-S3
What is RICE mnemonic for soft tissue injuries?
Rest, ice, compression, elevation
Synovial fluid aspiration in someone with reactive arthritis?
No organisms will be recovered + cloudy/yellow colour
What is the most common mechanism of ankle sprains?
Inversion
Any MSK pain/Osteoarthritis first line treatment?
Topical NSAIDs/Oral NSAIDs
What is spondylolisthesis?
One vertebra slips out of line with one above it, usually in the lumbar spine
Pain on painful arc with normal X ray?
Painful arc syndrome / subacromial bursitis / impingement syndrome
Trigger finger management?
- Rest and splint
- NSAIDs
- Steroid injections
What are examination findings of NOF?
Affected side shortened
Externally rotated
Abducted
S/E of bisphosphonates
- Oesophageal erosions
- Osteonecrosis of jaw
- Atypical fractures
CREST antibodies?
- Anti-centromere
- Anti-Scl70
What are pulmonary complications of CREST?
- Pulmonary fibrosis
- Pulmonary HTN
What are causes of sciatica?
- Spinal stenosis
- Disc herniation
- Pelvic tumours
Greenstick fractures are unique to who?
Children - usually under 10s
3rd line management for acute gout in renal disease?
Steroids
What is the investigation of choice for Takayasu’s arteritis?
CT angio
What is Caplan syndrome?
RA plus pulmonary nodules
What is the diagnostic test for Behcet’s disease?
Pathergy test
Diabetics are susceptible to what infections?
Staphylococcal
diffuse thickening of the pancreatic body and tail
Sausage pancreas sign -> autoimmune pancreatitis
Antiphospholipid causes prolonged what?
APTT
What drug makes Raynaud’s worse?
Propranolol
RA spares which joint?
DIP
Progressive shoulder pain with reduced ROM in middle aged?
Frozen shoulder
Management of achilles tendonitis?
Rest, NSAIDs and physio if symptoms persistent beyond 7 days
What is Simmonds triad?
- palpation
- examining the angle of declination at rest
- squeeze test
Investigation for suspected hip fracture if X-ray is normal?
MRI
What can be done for NOF fractures?
Iliofascial nerve block
What is the most common reason for revising a total hip replacement?
Asceptic loosening of the implant
Joint aspirate with high WBC count, mainly neutrophils with well patient?
Rheumatoid
Gold standard diagnostic investigation for Ankylosing spondyliitis?
MRI of sacroiliac joints
Methotrexate can cause what when not given folate alongside?
Macrocytic anaemia due to folate deficiency
What is the treatment for reactive arthritis?
NSAIDs
Management of patients who do not respond to steroids in poly myalgia?
Refer to specialist
Compartment syndrome can cause what?
Rhabdomyolysis
Management of undisplaced patella fracture with intact extensors?
Conservative with knee immobilisation
Management of renal hypertensive crises in systemic sclerosis?
ACE inhibitors
What are S/E of leflunomide?
Raised BP and peripheral neuropathy
What is the anticoagulant of choice in antiphospholipid?
Warfarin
Kids born to mums with SLE/Sjogrens can get what?
Congenital heart block -> neonatal lupus syndrome
Axial spondyloarthritis?
group of clinically heteriogeneous chronic inflam rheumatologic conditions that may cause MSK and extra MSK manifestations
features of axial (saroiliac joints and spine) and peripheral spondyloarthritis can overlap and coexist
eg. alkylosing spondylitits
Radiographic axial spondyloarthritis is characterised by?
signs of sacroilitis and structural changes on x-ray (aka ankylosing spondylitis)
Non-radiographic axial spondyloarthritis?
no x-ray changes but possible sarcoilitis on MRI
Extra-MSK manifestations of axial spondyloarthritis?
acute anterior uveitis, IBD, psoriasis
Ankylosing spondylitis?
HLA-B27 associated sponyloarthropathy
When does ankylosing spondylitis typically present?
20-30yrs
men>women
Spondyloarthropathy?
group of chronic inflam diseases that affects the joints
Features of ankylosing spondylitis?
- typically young man with lower back pain and stiffness of insidious onset
- stiffness worse in morning and improves with exercise
- may be pain at night which improves on getting up
- extra-MSK manifestations
Stiffness in ankylosing spondylitis?
worse in morning and improves with exercise
Clinical exam in ankylosing spondylitis?
- reduced lateral flexion
- reduced forward flexion (Schober’s test)
- reduced chest expansion
What test is used in ankylosing spondylitis?
Schober’s= reduced forward flexion
line is drawn 10 cm above and 5 cm below the back dimples (dimples of Venus). The distance between the two lines should increase by more than 5 cm when the patient bends as far forward as possible
Extra-MSK features of ankylosing spondylitis?
Apical fibrosis
Anterior uveitis
Aortic regurgitation
Achilles tendonitis
AV node block
Amyloidosis
cauda equina syndrome
peripheral arthritis (25%, more common if female)
When to suspect and refer for ankylosing spondylitis?
- low back pain, spinal stiffness, <45yrs and >3m with:
- 4+ of: started before 35yrs, waking at night with pain, buttock pain, improves with movement and within 48hrs of NSAIDs, FHx, current/past arthritis or/+ psoriasis
or
- with 3 criteria and +ve HLA-B27 blood test
or
- suspected dactylitis
Ix for ankylosing spondylitis?
- Bloods= inflam markers raised; HLA-B27 +ve (positive in 90%)
- Plain x-ray of sacroiliac joints= diagnosis (may be normal in early disease)
- If X-ray -ve then MRI
- spirometry= restrictive defect
Later changes of ankylosing spondylitis on plain x-ray of sacroiliac joints?
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
What would MRI in ankylosing spondylitis show?
signs of early inflam invl. sacroiliac joints (bone marrow oedema)
Why in ankylosing spondylitis does spirometry show a restrictive defect?
combination of pulmonary fibrosis, kyphosis and ankylosis of costoverebral joints
Mx of ankylosing spondylitis?
- regular exercise eg. swimming
- 1st= NSAIDs
- physio
- if peripheral joint invl. may consider DMARDs eg. sulphasalazine
- Anti-TNF therapy if persistent high disease despite other Tx eg. entanercept and adalimumab
Follow up for pt with ankylosing spondylitis?
- risk of osteoporosis and screening every 2yrs
- same day referral to opthal if acute anterior uveitis suspected
Compartment sydrome?
raised pressure within a closed anatomical space; will eventually compromise tissue perfusion resulting in necrosis
Compartment syndrome is a Cx that may occur following what?
fractures
or ischaemia reperfusion injury in vascular pts
2 fractures that may cause compartment syndrome?
supracondylar fractures and tibial shaft injuries
Sacroiliac joints?
joints that connect the sacrum (the base of the spine) to the ilium (the pelvis)
Features of compartment syndrome?
- Pain= esp on movement (even passive), XS use of breakthrough analgesia
- paraesthesia
- pallor
- paralysis of muscle group may occur
- arterial pulse may still be felt
Why may arterial pulsation still be felt in compartment syndrome?
as the necrosis occurs as a result of microvascular compromise
What does NOT rule out compartment syndrome?
presence of a pulse
Pt has fracture, has pain on movement (even passive) and is using excessive use of breakthrough analgesia?
think compartment syndrome
Diagnosis of compartment syndrome?
- measure intracompartmental pressure; >20mmHg pressure is abnormal and >40 is diagnostic
- typically no pathology on x-ray
fasciotomy?
surgical procedure that involves cutting the fascia, or connective tissue, around a muscle to relieve pressure and increase blood flow
limb saving procedure
Mx of compartment syndrome?
- prompt and extensive fasciotomies
- aggressive IV fluids
Compartment syndrome: why do pts require aggressive IV fluids?
Myoglobinuria may occur following fasciotomy and result in renal failure.
What may happen in fasciotomy for compartment syndrome?
if operator is inexperienced, smaller incisions may be performed and in the lower limb the deep muscles may be inadequately be decompressed
Compartment syndrome: what if muscle groups are frankly necrotic at fasiotomy?
should be debrided and amputation may be considered
How quick does death of muscle groups occur in compartment syndrome?
within 4-6hrs
Gout?
type of arthritis caused by monosodium urate crystals forming inside and around joints, causing sudden flares of severe pain, heat and swelling
Joints affected in gout?
any joint but most commonly= distal joints eg. toes, knees, ankles, finger joints
Most important RF for the development of gout?
hyperuricaemia
RFs for gout?
- hyperuricaemia
- increasing age
- FHx
- genetics
- obesity
- male
- diet
- postmenopausal
- medications
- CKD, HTN, DM
What type of diet is a RF for gout?
XS alcohol, sugary drinks, red meat, seafood
What drugs are RFs for gout?
diuretics (thiazides, furosemide), low-dose aspirin, ciclosporin, alcohol, cytotoxic agents, pyrazinamide
Cx of gout?
- CVD
- chronic arthritis
- CKD
- joint damage
- reduced QOL
- renal stones
- tophi
Tophi?
hard, stone-like deposits of monosodium urate crystals that form in the soft tissues, cartilage, tendons, or bones near joints
usually painless
eg. in gout
Presentation of gout?
rapid onset severe pain, redness and swelling in one or both first metatarsophalangeal joints. May be midfoot, ankle, knee, hand, wrist or elbow.
tophi
Ix for gout?
- clinical exam
- serum urate 6mg/dL (360micromol/L) or more confirms diagnosis
Mx for gout?
acute= NSAIDs or colchicine (until 1-2d after flare resolved) or short course oral corticosteroid (pred 30-35mg od 3-5d)
long term= urate-lowering therapy eg. allopurinol or febuxostat
Who should urate-lowering therapy eg. allopurinol be offered to pts with gout?
multiple/troublesome flares
CKD stage 3-5
on diuretic therapy
have tophi
or have chronic gout
Where can tophi in gout appear?
extensor surfaces of affected joints, Achilles tendons, dorsal aspect of hands and feet and in the helix of the ears. They suggest longstanding, untreated gout.
Most common joint affected in gout?
1st metatarsophalangeal joint (big toe)
Is gout monoarticular?
usually bit can be oligoarticular or rarely polyarticular
When does flare severity reach max intensity in gout?
within 24hrs
When to measure serum urate level for gout diagnosis?
diagnosis= 360micromol/L or more
- if lower but suspect gout repeat serum urate in 2-4w after flare settled
Diagnosis of gout?
- serum urate level 2-4w after flare has settled
if uncertain then:
- joint aspiration and microscopy of synovial fluid
- still uncertain the x-ray
Gout differential diagnosis?
- bursitis, tenosynovititis, cellulitis
- haemochromatosis
- psuedogout
- osteoarthritis
- psoriatic arthritis
- reactive arthritis
- RA
- septic arthritis
- trauma
What must be considered in any person who is systemically unwell (with or without a temperature) and an acutely painful, hot, swollen joint?
septic arthritis
Self-care advice for gout?
- rest and elevate limb
- keep joint exposed and in cool environment
- consider ice pack
Follow up following acute flare of gout?
4-6w after settled:
- serum urate
- review meds
form of microcrystal synovitis caused by the deposition of monosodium urate monohydrate in the synovium
gout
What causes gout?
chronic hyperuricaemia (uric acid >0.45mmol/l)
Gout episodes?
typically flares that can last several days then often symptom free episodes in between
Name 4 commonly affected joints in gout?
1st MTP joint= big toe
knee
ankle
wrist
Synovial fluid analysis in gout?
needle shaped negatively bifringent monosodium urate crystals under polarised light
X-ray findings in gout?
- joint effusion (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
MOA of colchicine used for acute flares of gout?
inhibits microtubule polymerization by binding to tubulin, interfering with mitosis. Also inhibits neutrophil motility and activity
Slow onset of action
Main side effect of colchicine?
diarrhoea
When should colchicine for acute gout be used with caution?
in renal impairment: reduce dose if GFR 10-50 and avoid if <10ml/min
Acute flare of gout, if pt is on allopurinol should this be continued alongside other drugs for acute flares?
yes continue allopurinol
if havent started it before, start once acute flare settled
Urate lowering therapy is particularly recommended for pts with gout when?
Now offer to all pts after 1st attack.
Esp:
- >= 2 attacks in 12 months
- tophi
- renal disease
- uric acid renal stones
- prophylaxis if on cytotoxics or diuretics
Allopurinol dose for gout?
initial dose of 100 mg od, with the dose titrated every few weeks to aim for a serum uric acid of < 360 µmol/l
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 if pt has a reduced eGFR
colchicine cover should be considered when starting allopurinol. NSAIDs can be used if colchicine cannot be tolerated.
Avoid what foods in gout?
food high in purines eg. liver, kidneys, seafood, oily fish (mackerel, sardines), red meat, yeast products
Other considerations in the Mx of gout?
- high vit C may lower serum uric acid
- maybe stop precipitating drugs eg. thiazides
Lesch-Nyhan syndrome?
hypoxanthine-guanine phosphoribosyl transferase (HGPRTase) deficiency
x-linked recessive therefore only seen in boys
features: gout, renal failure, neurological deficits, learning difficulties, self-mutilation
What may cause hyperuricaemia (increased levels of uric acid)?
secondary to increased cell turnover or reduced renal excretion of uric acid
may be associated with hyperlipidaemia and HTN and metabolic syndrome
Hyperuricaemia caused by increased synthesis examples?
Lesch-Nyhan disease
myeloproliferative disorders
diet rich in purines
exercise
psoriasis
cytotoxics
Hyperuricaemia caused by decreased excretion examples?
drugs: low-dose aspirin, diuretics, pyrazinamide
pre-eclampsia
alcohol
renal failure
lead
Pseudogout?
form of microcrystal synovitis caused by the deposition of calcium pyrophosphate dihydrate crystals in the synovium.
aka acute calcium pyrophosphate crystal deposition disease
Pseudogout RFs?
- increasing age
- haemochromatosis
- hyperparathyroidism
- low magnesium, low phosphate
- acromegaly
- Wilsons
Features of pseudogout?
knee, wrist and shoulders most commonly affected like gout just different cause
Gout vs pseudogout?
Gout is caused by monosodium urate monohydrate crystals; pseudogout is caused by calcium pyrophosphate (CPP) crystals
Joint aspiration findings in psuedogout?
weakly-positively birefringent rhomboid-shaped crystals
X-ray findings in pseudogout?
chondrocalcinosis
- in the knee this can be seen as linear calcifications of the meniscus and articular cartilage
Mx of psuedogout?
aspiration of joint fluid, to exclude septic arthritis
NSAIDs or colchicine intra-articular, intra-muscular or oral steroids as for gout
can use long term low dose colchicine in chronic to reduce flares
TUC eg. magnesium supplement if hypomagnesaemia
Ix for pseudogout?
- joint aspiration for microscopy diagnostic
- x-ray affected joints
can screen for RFs= ferritin (haemochromatosis), magnesium, thyroid function (hypothyroidism), inflam markers +ve, Ca and PTH (hyperparathyroidism)
Correct name now used instead of pseudogout?
calcium pyrophosphate deposition disease
Greater trochanteric pain syndrome?
regional pain syndrome where chronic intermittent pain is felt around the greater trochanter
What is the greater trochanter?
bony prominence on lateral aspect of the hip
tronchanteric bursitis?
inflam of a bursa adjacent to greater trochanter
Greater trochanteric pain syndrome is caused by what?
inflam or physical trauma in muscles, tendons, fascia or bursae
Common population affected by greater trochanteric pain syndrome?
women>men
40-60yrs
What other conditions is greater trochanteric pain syndrome typically seen with?
low back pain, osteoarthritis of knee, RA and fibromyalgia
Mx of greater trochanteric pain syndrome?
> 90% recover fully with conservative Tx eg. rest, pain relief, physio or corticosteroid injection
RFs for a poorer outcome of greater trochanteric pain syndrome?
higher initial pain intensity, longer duration of pain, greater movement restriction, higher functional impairment, older age
Diagnosis of greater trochanteric pain syndrome?
clinical
CP of greater trochanteric pain syndrome?
- lateral hip pain, worse with exercise
- point tenderness adjacent to greater trochanter
- when tendons & muscles attached to greater trochanter are put under tension on exam= point tenderness and pain
What should be excluded when diagnosing greater trochanteric pain syndrome?
sports hernia, osteoarthritis, lumbar nerve root compression, infection of bursa
Advice for greater trochanteric pain syndrome?
- usually self-limiting
- avoid activity that may worsen pain
- ice pack applied 10-20mins several times a day
- analgesia= paracetamol, NSAIDs
- weight loss
if initial Mx doesnt help then= peri-trochanteric corticosteroid injection and physio
Emergency referral in greater trochanteric pain syndrome?
- hip pain with systemic symptoms
- infection s&s
- known primary malignancy
- suspicion of pathological fracture
- sudden inability to bear weight
- Hx of fall
Urgent referral to ortho in greater trochanteric pain syndrome?
severe pain unresponsive to analgesia and persistent loss of function
Referral to ortho for greater trochanteric pain syndrome?
<40, persistent, affects ADLs, not responded to 3m physio
painful irritable and stiff hip affecting ADLs
Features of greater trochanteric pain syndrome?
- chronic lateral hip/thigh/buttock pain
- intermittent or persistent
- gradual
- worsen over time
- may radiate down lateral aspect of thigh but rarely below knee
- aggravated by physical activity eg. walking and with pressure on that side of body eg. lying down
- pain on palpation of greater trochanter
Tests to examine for greater trochanteric pain syndrome?
- Trendelenburg’s
- Single leg stance
- Hip flexion, abduction, external rotation (FABER)
- Hip flexion, adduction, external rotation (FADER)
- resisted active abduction
- resisted internal rotation
- resisted external rotation
Gait in greater trochanteric pain syndrome?
Antalgic gait — there is a shortened stance on the affected leg, and when walking, less time is spent bearing weight on the affected side than on the other.
Trendelenburg gait — there is a lateral trunk lean towards the supported limb during the stance phase.
On palpation of the greater trochanter in greater trochanteric pain syndrome, where is tenderness elicited?
at a point over the gluteus medius tendon or its insertion into the greater trochanter.
Pain on greater trochanter palpation?
greater trochanteric pain syndrome
Trendelenburgs test
With the person standing, they are observed from behind while lifting each foot off the ground in turn.
A positive test is the pelvis dipping (rather than staying horizontal or rising slightly) on lifting the unaffected leg.
Single leg stance test?
The person is asked to remain standing on their affected leg with their contralateral knee flexed to 90 degrees for 30 seconds using a finger on the unaffected side on a wall for balance.
The test is positive if there is lateral hip pain within the 30 seconds.
Hip flexion, abduction, external rotation (FABER test)
The lateral malleolus of the test leg is placed above the patella of the contralateral leg, the pelvis stabilized via the opposite anterior superior iliac spine and the knee passively lowered so the hip moves into abduction and external rotation. If there is lateral hip pain, the test is positive.
Hip flexion, adduction, external rotation (FADER test)
With the person lying supine, the hip is passively flexed to 90°, adducted, and externally rotated to end of range. If there is lateral hip pain, the test is positive.
Resisted active abduction
With the person lying supine their hip joints are placed in the neutral position (legs together and straight out). The affected hip joint is abducted by 45 degrees while the person resists the movement. If there is lateral hip pain, the test is positive.
Resisted internal rotation
With the person lying supine, the affected hip joint is positioned at 45 degrees flexion and maximal external rotation. The hip joint is internally rotated while the person resists the movement. If there is lateral hip pain, the test is positive.
Resisted external rotation
With the person lying supine, the affected hip joint is positioned at 45 degrees flexion and maximal internal rotation. The hip joint is externally rotated while the person resists the movement. If there is lateral hip pain, the test is positive.
What may greater trochanteric pain syndrome be referred to as?
trochanteric bursitis
What is greater trochanteric pain syndrome due to?
repeated movement of the fibroelastic iliotibial band and is most common in women aged 50-70 years.
2 features of greater trochanteric pain syndrome?
1) pain over the lateral side of hip/thigh
2) tenderness on palpation of the greater trochanter
Juvenile idiopathic arthritis (JIA)?
arthritis occurring in pt <16yrs and lasts for >6m
3 types of Juvenile idiopathic arthritis (JIA)?
- systemic onset= aka Still’s disease
- polyarticular= more than 4 joints
- pauciarticular= 4 or less joints
Pauciarticular JIA?
4 or less joints are affected
60% of cases of JIA
Features of pauciarticular JIA?
joint pain and swelling: usually medium sized joints e.g. knees, ankles, elbows
limp
ANA may be positive in JIA - associated with anterior uveitis
Another name for systemic onset JIA?
Still’s disease
Features of systemic onset JIA?
pyrexia
salmon-pink rash
lymphadenopathy
arthritis
uveitis
anorexia and weight loss
Ix for systemic onset JIA?
ANA may be positive, especially in oligoarticular JIA
rheumatoid factor is usually negative
What is used to rule out clinically significant foot and ankle fractures to reduce the use of x-ray imaging?
Ottawa Ankle Rule:
1) location of pain= malleolar or midfoot
2) bone tenderness location
2) inability to weight bear both immediately after injury AND in ED
When is an ankle x-ray only required in ?ankle fracture?
if any pain in malleolar zone and any one of:
- bony tenderness at the lateral malleolar zone (from the tip of the lateral malleolus to include the lower 6 cm of posterior border of the fibular)
- bony tenderness at the medial malleolar zone (from the tip of the medial malleolus to the lower 6 cm of the posterior border of the tibia)
- inability to walk four weight bearing steps immediately after the injury and in the emergency department
In what pts is the hip a common site of fracture?
esp in osteoporotic elderly females
What is a risk in displaced hip fractures?
avascular necrosis as the blood supply to the femoral head runs up the neck
Features of hip fracture?
- shortened and externally rotated leg
- pain
- may be able to weight bear if non-displaced or incomplete neck of femur fracture
Pts with non-displaced or incomplete neck of femur fractures may be able to do what?
weight bear
Classification of hip fractures based on location?
intracapsular (subcapital) or extracapsular
Intracepsular (subcapital) hip fractures?
from the edge of the femoral head to the insertion of the capsule of the hip joint
Extracapsular hip fracture?
can either be trochanteric or subtrochanteric (lesser trochanter is the dividing line)
Classification of hip fractures?
Garden system
Garden system classification for hip fractures?
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
What type of hip fracture according to the Garden system classification is blood supply disruption most common?
types III and IV
2 types of intracapsular hip fracture?
- undisplaced fracture
- displaced fracture
Mx of intracapsular undisplaced hip fracture?
internal fixation
or hemiarthroplasty if unfit
Mx of intracapsular displaced hip fracture?
replacement arthroplasty (total hip replacement or hemiarthroplasty) to all pts
total hip replacement favoured over hemiarthoplasty if pt= able to walk idependently outdoors with no more than use of a stick; not cognitively impaired and med fit for anaesthesia and the procedure
Mx of extracapsular hip fracture?
if stable intertrochantic fractures= dynamic hip screw
if reverse oblique, transverse or subtrochanteric fractures= intramedullary device
Most common site of stress fracture?
metatarsals
Stress fracture?
when fracture occurs due to repeated mechanical stress
Metatarsal fractures>
quite common; can be limited to 1 metatarsal or multiple eg. by direct trauma or crush injuries
Most common metatarsal affected in fracture?
proximal 5th (also most common site of midfoot fractures)
1st is least commonly fractured
5th metatarsal fractures?
Proximal avulsion fractures (pseudo-Jones fractures)= most common type. Occurs at the proximal tuberosity. Usually associated with a lateral ankle sprain and often follow inversion injuries of the ankle.
Jones fractures= much less common. This is a transverse fracture at the metaphyseal-diaphyseal junction.
Metatarsal stress fractures?
occurs in otherwise healthy athletes eg. runners
most common site of met stress fractures is 2nd metatarsal shaft
5th metatarsal fractures usually associated with what?
lateral ankle sprain and often follow inversion injuries of the ankle
Features of metatarsal fracture?
pain and bony tenderness
swelling
antalgic gait
Ix for metatarsal fractures?
- x-rays
- isotope scan or MRI= in case of stress fractures as x-ray often normal.
When may isotope scan or MRI be preferred to x-ray in metatarsal fractures?
help establish stress fractures, may appear normal on x-ray
x-ray for metatarsal fractures?
distinguish between displaced and non-displaced fractures to help guide Mx
stress fractures normally appear normal but sometimes there is a periosteal reaction seen 2-3w later
Patella
sesamoid bone that develops within the the quadriceps tendon (dividing it into the quadriceps tendon superiorly and the patella ligament inferiorly).
Protects the knee from physical trauma and plays important role in the extensor mechanism of the knee.
How does the patella increase efficieny of quadriceps movement (extensor mechanism of knee)?
The quadriceps apply force around a centre of rotation (the knee joint). The patella increases the distance of the quadriceps tendon from this centre of rotation thereby increasing its efficiency (if you imagine it is easier to open a door by pushing or pulling near the handle as opposed to near the door hinge).
Patella anatomy?
roughly triangular in coronal and axial planes. The anterior surface is flat and the posterior surface is composed of a medial and lateral facet and articulates with the femur at the patellofemoral joint.
How can the patella be injured?
- direct or indirect means
- consider in the context of the entire extensor mechanism of the knee
- consider posterior surface of the patella as any disruption of the patellofemoral joint may lead to secondary osteoarthritis down the line.
On the posterior surface of the patella, any disruption of the patellofemoral joint may lead to what?
secondary osteoarthritis down the line
Direct injury causing patella fracture?
direct blow or trauma to front of knee eg. fall or dashboard injury
usually an undisplaced crack or comminuted fracture, but with an intact extensor mechanism
Indirect injury causing patella fracture?
when quads forcefully contract against a block to knee extension
eg. when someone catches their foot against a solid obstacle and in order to prevent themselves from falling the quads contract forcefully
results in transverse patella fracture with possible disruption of the extensor mechanism
Direct injury to patella may result in what?
undisplaced crack or comminuted fracture, but with an intact extensor mechanism
indirect injury to patella may result in what?
transverse patella fracture with possible disruption of the extensor mechanism.
Clinical features of patella fracture?
- swelling and bruising
- open wound= ? open fracture (more urgent Mx)
- pain and tenderness around knee, localised to patella and palpable gap may be appreciable
- if able to straight leg raise= extensor mechanism is grossly intact; may be difficult due to pain so have pt lie on side to eliminate gravity
Ix for patella fractures?
plain films, min of 2 views required (AP and lateral)
if diagnosis still in doubt, skyline views can be taken but is uncomfortable and difficult to obtain
Mx of undisplaced patella fractures, particularly vertical fractures with an intact extensor mechanism?
can be managed non-operatively in a hinged knee brace for 6w and pt allowed to fully weight bear
Mx of displaced patella fractures and those with loss of extensor mechanisms?
consider operative Mx with either tension band wire, inter-fragmentary screws or cerclage wires
then pt placed in hinged knee brace for 4-6w and allowed to fully weight bear
Tendinopathy?
term describing pain, swelling and impaired function of the tendon
Achilles tendon?
thickest and strongest tendon in the body; made up of fibres from the gastrocneumius and soleus muscles
Achilles tendon pathology is common in who?
active people
Cx of achilles tendon injury?
tendon rupture, negative impact on a pts ability to work and carry out ADLs, limitation in sports activity
Signs and symptoms of Achilles tendinopathy?
- aching (or sharp) pain in heel, aggravated by activity or pressure to the area
- stiffness in the tendon, may occur in morning or after period of prolonged sitting
- tenderness, swelling, crepitus along the tendon
Suspected achilles tendon rupture?
same day assessment by ortho specialist
Mx of achilles tendinopathy?
- Mx of underlying cause
- cold packs/ice after acute injury
- analgesia for pain relief eg. paracetamol
- rest, exercise when pain allows
What if symptoms of Achilles tendinopathy fails to improve within 7-10d?
refer to physio
Chronic achilles tendinopathy or fails to respond to Mx?
refer to sports physician or ortho
Pain in achilles tendinopathy?
ache or sharp pain in heel
- worse with activity or pressure to area
- Gradual onset of pain 2–6 cm proximal to the Achilles tendon insertion that limits activity suggests mid-portion Achilles tendinopathy.
- Pain and swelling at the insertion to the posterior calcaneus with impairment of function suggests insertional tendinopathy.
- some symptoms at both the insertion and mid-portion.
Stiffness in achilles tendinopathy?
may occur in morning or after period of prolonged sitting
What can be used to assess pain and severity with activity win people with achilles tendinopathy?
Victorian Institute of Sports Assessment-Achilles (VISA-A) questionnaire
RFs for achilles tendinopathy?
DM, dyslipidaemia, fluoroquinolone use
Diagnosis of achilles tendinopathy?
- clinical: examine if no rupture
- imaging not usually recommended
- Ix for ULC= lipid profile, HbA1c, ?fluoroquinolone use
Examination findings for achilles tendinopathy (do not examine if achilles tendon rupture)?
redness, swelling, and asymmetry
Palpate along the length of the tendon for tenderness, heat, crepitus, thickening, and nodularity.
Tenderness on palpation of the mid-portion of the tendon is indicative of mid-portion Achilles tendinopathy.
Tenderness on palpation around the distal 2 cm of the tendon is usually found in insertional Achilles tendinopathy.
Evaluate the range of motion of the ankle. Pain worsens with passive dorsiflexion of the ankle.
Hop and heel-raise endurance tests, as appropriate.
CP of achilles tendinopathy?
- sudden pain back of leg, may be audible snap
- may occur with running or exercise, may be like being kicked or hit by a racket
- 1/3 with complete rupture say no pain
- aching of calf, swelling, mild bruising, weakness when pushing off with affected foot
- difficulty weight bearing
In some cases, why may pt with achilles tendinopathy be able to walk?
other plantar flexors may mask the tendon injury
How to exclude achilles tendon rupture?
Simmonds triad (angle of declination, palpation, and the calf squeeze test)
Simmonds triad examination to exclude achilles tendon rupture?
(angle of declination, palpation, and the calf squeeze test)
- abnormal angle of declination= rupture may lead to greater dorsiflexion of the injured ankle and foot compared with the uninjured limb.
- Feel for a gap in the tendon. No gap may be felt because of local swelling or bleeding. Bruising may be seen.
- Gently and sequentially squeeze the calf muscles= in acute rupture of the Achilles tendon the injured foot will typically remain in the neutral position when the calf is squeezed.
Why may the diagnosis of chronic achilles tendon rupture be difficult?
- pain and swelling often subsided and the gap may have filled with fibrous tissue.
- Calf muscles may be wasted.
- Other muscles may facilitate plantar flexion.
Differential diagnosis for achilles tendoninopathy?
True tendon pain (from rupture or tendinopathy) is usually confined to the tendon itself.
Retrocalcaneal bursitis.
Plantaris tendinopathy.
Dislocation of the peroneal or other plantar flexor tendons.
Posterior ankle impingement.
Haglund’s deformity.
Os trigonum syndrome.
Fascial tears.
Calcaneal fracture.
Irritation or neuroma of the sural nerve.
Fat pad irritation.
Systemic inflammatory disease.
Tx for achilles tendinopathy in secondary care (if conservative measures fail)?
non-surgical= Eccentric exercise, or a heavy-load, slow-speed (concentric/eccentric) exercise programme (if not already tried); Extracorporeal shock-wave therapy (ESWT) — acoustic shockwaves are passed through the skin to the affected tissue.
Surgery= if chronic or not responsive to Tx; debridement and removal of diseased areas of tendon
Most common cause of posterior heel pain?
achilles tendon disorders
Examples of achilles tendon disorders?
tendinopathy (tendinitis), partial tear, complete rupture
What are associated with achilles tendon disorders?
floroquinolone use eg. ciprofloxacin
hypercholesterolaemia (predisposes to tendon xanthomata)
DM
Gradual onset of posterior heel pain that is worse following activity; morning pain and stiffness common?
achilles tendinopathy (tendiniti)
3 supportive Mx for achilles tendinopathy?
- simple analgesia
- reduction in activities
- calf muscle eccentric exercies
playing a sport or running; an audible ‘pop’ in the ankle, sudden onset significant pain in the calf or ankle or the inability to walk or continue the sport
achilles tendon rupture
How is Simmond’s triad examination be conducted to exclude achilles tendon rupture?
ask pt to lie prone with their feet over the edge of the bed. Look for an abnormal angle of declination; Achilles tendon rupture may lead to greater dorsiflexion of the injured foot compared to the uninjured limb.
Feel for a gap in the tendon and gently squeeze the calf muscles if there is an acute rupture of the Achilles tendon the injured foot will stay in the neutral position when the calf is squeezed.
Imaging of choice for suspected achilles tendon rupture?
USS
Suspected achilles tendon rupture?
acute referral to ortho and USS
Bony components of ankle joint include what
distal tibia and fibula and the superior aspect of the talus
- form a mortise with the body of the talus acting as the tendon
- arrangement is secured by ligamentous structures
Ligaments in the ankle?
1) syndesmosis binds the distal tibia and fibula together (another example of a syndesmosis is the distal radio-ulnar joint). It is composed of the anterior inferior tibiofibular ligament (AITFL), posterior inferior tibiofibular ligament (PITFL), interosseous ligament (IOL) and the interosseous membrane.
2) Distal fibular= secured to the to the talus by the anterior and posterior talofibular ligaments (ATFL and PTFL) and to the calcaneus by the calcaneofibular ligament.
Sometimes referred to collectively as the lateral collateral ligaments.
3) Distal tibia= secured to the talus by the deltoid ligament, in view of its triangular shape.
Sprain?
stretching, partial or complete tear of a ligament
Types of ankle sprains?
- high ankle sprain= invl syndesmosis
- low ankle sprain= invl lateral collateral ligaments
Presentation of low ankle sprain?
- injury to ATFL most common
- inversion injury common mechanism
- pain, swelling, tenderness over affected ligaments and sometimes bruising
- able to weight bear unless severe
Most common type of ankle sprain?
low sprain
Inversion injury to the ankle can cause what?
low ankle sprain
Grades of low ankle sprain?
Grade I (mild)= stretch or micro tear to ligament; minimal bruising/swelling; weight bearing normal
Grade II= partial tear; moderate bruising/swelling; minimal pain on weight bearing
Grade III (severe)= complete tear; severe swelling and bruising; severe pain on weight bearing
Ix for low ankle sprain?
- 15% associated with fracture so x-ray according to Ottawa ankle rules
- MRI if persistent pain= can evaluate perineal tendons
Tx for low ankle sprain?
- RICE= rest, ice, compression, elevation
- occasionally= removable orthosis, cast and/or crutches may be needed short term
- fails or signif joint instability= MRI and surgery but rare
Presentation of high ankle sprain?
- injury to syndesmosis
- rare and severe
- caused by external rotation of food causing talus to push fibula laterally
- weight bearing painful
- pain when tibia and fibula squeezed together at mid calf (Hopkin’s squeeze test)
Hopkin’s squeeze test?
high ankle sprain
Pain when the tibia and fibula are squeezed together at the level of the mid-calf
Injury to ankle caused by external rotation of foot causing talus to push fibula laterally?
high ankle sprain
Ix for high ankle sprain?
- x-ray= may show widening of tibiofibular joint (diastasis) or ankle mortise
- MRI= if high suspicion but normally just plain films
Tx of high ankle sprain?
- if no diastasis= non weight bearing orthosis or cast until pain stops
- diastasis or failed non-op Mx= operative fixation
What are isolated injuries to the deltoid ligament in ankle associated with?
they are rare
fracture so look for Maisonneuve fracture of the proximal fibula.
Ankle mortise anatomically reduced= same Tx as low ankle sprain
- if not then reduction and fixation
Common cause of lateral knee pain in runners?
iliotibial band syndrome
iliotibial band syndrome?
common cause of lateral knee pain in runners (1 in 10 regular runners)
tenderness 2-3cm above lateral joint line
Mx of iliotibial band syndrome?
- activity modification and iliotibial band stretches
- no improvement then physio
Causes of knee pain?
osteoarthritis, injuries (muscle strain, ligament damage, fractures); inflam conditions; infection; tumours; referred pain from hip or lumbosacral spine; bursitis
RFs for knee pain?
- increasing age
- obesity
- knee-straining work
- participation in sport
Red flags for knee pain?
- infection (septic arthritis or osteomyelitis)
- tumours
- inflam polyarthritis
- signif bony or soft tissue injury eg. fractures, dislocation and tendon/ligament rupture
When is admission or referral for immediate hospital assessment indicated in knee pain?
septic arthritis, slipped capital femoral epiphysis, fracture, neurovascular damage, quadriceps or patellar tendon rupture, severe soft tissue injury with gross instability, first-time traumatic patellar dislocation, or a recurrent dislocation associated with moderate or severe swelling.
When is admission or referral for immediate hospital assessment indicated in knee pain in a child?
limp or suspected Henoch-Schönlein purpura.
infection (such as fever, erythema, swelling) or severe pain, swelling, instability or inability to weight bear in association with an acute injury.
What if signif soft tissue injury is suspected in pt with acute knee pain following trauma?
acute knee clinic (admission or immediate assessment)
Ottawa knee rule?
determine whether an X-ray is needed in people over 2 years with a suspected knee fracture.
Only required after a knee injury for people with any of these findings:
1) Inability to weight bear both immediately and during the consultation for four steps (inability to transfer weight twice onto each lower limb regardless of limping).
2) Inability to flex the knee to 90 degrees.
3) Tenderness of the head of the fibula.
4) Isolated tenderness of the patella (no bone tenderness of the knee other than the patella).
5) Age 55 years or older.
Direct blow to the knee can cause what?
anterior knee= patellar fracture or if knee in flexion can cause PCL injury; hyperextended knee can cause ACL injury
lateral knee= medial collateral ligament injury or patellar dislocation
medial knee= lateral collateral ligament injury (uncommon) or patellar dislocation
Knee injury: what can sudden decleration or stopping cause?
ACL injury
Twisting or pivoting can injury the knee how?
can injure the menisci or cause ACL injury. If twisted when the knee is extended, patellar subluxation or dislocation can occur.
Hyperextension of the knee can cause what?
ACL and PCL injury
Anterior knee pain may be caused by what?
Patellar subluxation or dislocation.
Osgood-Schlatter disease.
Patellar tendonitis.
Patellofemoral pain syndrome.
Patellar or quadriceps tendon rupture.
Patellofemoral joint arthritis.
Medial knee pain may be caused by what?
Medial collateral ligament sprain.
Medial meniscal tear.
Pes anserine bursitis.
Medial plica syndrome.
Medial compartment arthritis.
Lateral knee pain may be caused by what?
Lateral collateral ligament sprain.
Lateral meniscal tear.
Iliotibial band tendonitis.
Lateral compartment arthritis.
Posterior knee pain may be caused by what?
Baker’s cyst.
Posterior cruciate ligament injury.
Posterior horn meniscal tears.
What does Lachman’s test test for?
ACL tear
What does the anterior drawer/draw test test for?
ACL tear
What does the pivot shift test test for?
ACL tear
What does the posterior drawer/draw test test for?
PCL tear
What does the posterior sag test test for?
PCL tear
What does the valgus stress test test for?
Medial collateral ligament injury
(Joint line tenderness may also indicate meniscal tear)
What does the varus stress test test for?
Lateral collateral ligament injury
(Joint line tenderness may also indicate meniscal tear)
What does the patellar apprehension test test for?
Subluxing or dislocating patella
What does the McMurray test test for?
meniscal tear
What does the Thessaly test test for?
meniscal tear
Testing for effusion in knee?
- patellar tap test
- stroke test
- cross fluctuance test for larger effusions
Most commonly injured knee ligament?
ACL
Common mechanisms of injury to the ACL?
- lateral blow to knee
- skiing
- non-contact= sudden twisting or awkward landing (most common) eg. hyperextension
Features of ACL injury?
- sudden popping sound
- knee swelling
- instability
- feeling that knee will give way
2 tests to test for ACL injury?
anterior draw test and Lachman’s test
Anterior draw test to test for ACL injury?
the patient lies supine with the knee at 90 degrees
the examiner should place one hand behind the tibia and the other grasping the patient’s thigh. It is important that the examiner’s thumb be on the tibial tuberosity
the tibia is pulled forward to assess the amount of anterior motion of the tibia in comparison to the femur
an intact ACL should prevent forward translational movement
Lachman’s test to test for ACL injury?
variant of anterior draw test, but the knee is at 20-30 degrees
evaluate the anterior translation of the tibia in relation to the femur and is considered a variant
more reliable than anterior draw test
Knee pain= meniscal tear typically results from what?
twisting injuries
Knee pain= meniscal tear features?
pain worse on straightening the knee
knee may ‘give way’
displaced meniscal tears may cause knee locking
tenderness along the joint line
Test to test for meniscal tear (knee pain)?
Thessaly’s test - weight bearing at 20 degrees of knee flexion, patient supported by doctor, postive if pain on twisting knee
Thessaly’s test - weight bearing at 20 degrees of knee flexion, patient supported by doctor, postive if pain on twisting knee
Condition?
meniscal tear
Common knee problems in children and young adults?
- Chondromalacia patellae
- Osgood-Schlatter disease
(tibial apophysitis) - Osteochondritis dissecans
- Patellar subluxation
- Patellar tendonitis
Referred knee pain may come from where?
hip problems such as slipped upper femoral epiphysis
Key features of chondromalacia patellae?
Softening of the cartilage of the patella
Common in teenage girls
Characteristically anterior knee pain on walking up and down stairs and rising from prolonged sitting
Usually responds to physiotherapy
Key features of Osgood-Schlatter disease
(tibial apophysitis)?
seen in sporty teens
pain, tenderness and swelling over tibial tubercle
Key features of osteochondritis dissecans?
Knee pain after exercise
Intermittent swelling and locking
In children and young adults
Key features of Patellar subluxation?
Medial knee pain due to lateral subluxation of the patella
Knee may give way
in children and young adults
Key features of Patellar tendonitis?
More common in athletic teenage boys
Chronic anterior knee pain that worsens after running
Tender below the patella on examination
Osgood-Schlatter disease?
apophysitis of the tibial tuberosity that causes anterior knee pain during adolescence and is usually self-limiting
Osgood-Schlatter disease is thought to occur as a result of what?
repetitive strain from the patella tendon at its insertion on the ossification centre (apophysis) of the tibial tuberosity
Apophysis?
a normal developmental outgrowth of a bone which arises from a separate ossification centre, and fuses to the bone later in development; usually where muscle, tendon or ligament inserts
apophysitis= inflam of this
ossification= process of making new bone
ossification centre= area this happens
RFs for Osgood-Schlatter disease?
age= during growth spurts in adolescence
sports eg. running, jumping, repetitive bending of knee
biomechanical factors= quad muscle tightness, reduced flexibility of hamstrings
Type of knee pain in Osgood-Schlatter disease?
- unilateral (70%)
- during growth spurts (8-12yrs girls, 12-15yrs boys)
- develops slowly, mild and intermittent but can progress to continuous and severe
- fluctuates
- exacerbated by activity eg. running, jumping, kneeling
- improves with rest and skeletal maturity
- settles over w to m but can take 1-2yrs to resolve
- 10% persist into adulthood= chronic pain, decreased lower body strength
Exam findings in Osgood-Schlatter disease?
tenderness over tibial tuberosity that is provoked by knee extension against resistance, swelling or bony enlargement of the tibial tuberosity
normal passive ROM and absence of effusion
tenderness over tibial tuberosity that is provoked by knee extension against resistance, swelling or bony enlargement of the tibial tuberosity
Osgood-Schlatter disease
Ix for Osgood-Schlatter disease?
- clinical unless features of other causes of knee pain eg. persists at night or after rest, systemic symptoms, sudden after trauma, bone/joint pain at other sites
- routine x-ray not recommended to confirm diagnosis
Mx of Osgood-Schlatter disease?
- paracetamol +/or NSAIDs
- protective knee pads when kneeling
- intermittent ice packs over tibial tuberosity (10-15mins up to 3x d)
- exercise modification & muscle stretching exercises= swimming, cycling, straight leg raises
Osgood-Schlatter disease: what if pain does not improve or it worsens despite Mx?
- reassess cause: refer to paeds or ortho surgon
- physio referral
- persist into adulthood= ortho surgeon is symptoms affecting functioning
Differential diagnosis for Osgood-Schlatter disease (knee pain)?
- tumour
- juvenile idiopathic arthritis
- referred pain from hip= SUFE, transient synovitis; perthes
- trauma
- infection= septic arthritis or osteomyelitis
- osteochondritis dissecans, patellofemoral pain syndrome, chondromalacia patellae, and patellar dislocation or subluxation.
Preventative strategies for Osgood-Schlatter disease?
regular quadriceps and hamstring stretching and cross-training (swimming, cycling)
Most common cause of heel pain seen in adults?
plantar fasciitis
Pain in plantar fasciitis?
heel pain usually worse around the medial calcaneal tuberosity
Mx of plantar fasciitis?
rest feet where possible
wear shoes with good arch support and cushioned heels
insoles and heel pads may help
- analgesia and ice pack; consider short term USS guided corticosteroid injections
- if no better= refer to ortho or podiatrist or physio
Plantar fasciitis?
persistent pain associated with degeneration of plantar fascia as result of repetitive microtears in the contracted fascia
common 40-60yrs
Characteristic symptoms of plantar fasciitis?
- insidious onset
- intense pain during 1st steps after waking or period of inactivity
- pain reduces with moderate activity but worsens later during day or after long periods of standing/walking
Signs of plantar fasciitis?
Tenderness on palpation of the plantar heel area (esp localized around the medial calcaneal tuberosity).
Limited ankle dorsiflexion range (with the knee in extension).
Positive ‘Windlass test’ (reproduction of pain by extension of the first metatarsophalangeal joint).
Tightness of the Achilles tendon.
An antalgic gait (abnormal walking to avoid pain) or limping.
Differential diagnosis of plantar fasciitis?
Achilles tendonitis.
Calcaneal stress fractures.
Fat pad atrophy.
Sub-calcaneal bursitis.
Other less common neuro and MSK causes, such as nerve entrapment, peripheral neuropathy, plantar fibromatosis, and plantar fascia rupture.
Neoplasm and vascular insufficiency (very rare).
Diagnosis of plantar fasciitis?
clinical
Most people with plantar fasciitis will make full recovery within how long?
1yr
Osteoarthritis (OA)?
long term disorder of synovial joints which occurs when damage triggers repair processes leading to structural changes within a joint, with features of localised cartilage loss, remodelling of adjacent bone and formation of osteophytes, and mild synovitis
3 symptoms of osteoarthritis?
pain, stiffness and loss of function
What joints can be involved in osteoarthritis?
any synovial joint= knees, hips, small joints of hand most common
Flare of osteoarthritis?
sudden, sustained increase in symptoms for at least 24hrs, worse than usual patterns and lasts 3-8d
Causes of osteoarthritis?
multifactorial: genetics, biological (age, obesity), biomechanical (joint injury and damage)
Flares of osteoarthritis?
acute-on-chronic flares
may fluctuate
Cx of osteoarthritis?
joint deformity and chronic pain
Features of osteoarthritis?
- activity related joint pain= 1 or few joints at any one time; develops over m-yrs
- no morning stiffness or for <30mins
- functional limitation
Signs:
- bony swelling
- joint deformity
- restricted and painful ROM
- mild synovitis/joint effusion
- crepitus
- joint instability
Diagnosis of osteoarthritis?
- clinical= typical features, posture, gait, BMI, atypical features, other sources of pain
- if uncertain= joint x-ray
Mx of osteoarthritis?
- self care
- simple analgesia= topical NSAIDs (ibuprofen 5% gel 3x d); or oral 2nd line
- refer to MSK MDT= intra-articular corticosteroid injections (work for 2-10w); assistive aids; therapeutic exercise with education (‘structured Tx package’)
- ineffective after 3m= ortho surgeon (?joint replacement)
Hand OA?
typically affects 1st carpometacarpal joint (CMC) at base of thumb, distal interphalangeal (DIP) joint and the proximal interpahalngeal (PIP) joint
- wasting of thenar muscles at base of thumb
- CMC= fixed flexion deformity with hyperextension of distal joints
- advanced= squaring at joint; ulnar or radial deviation
- mucoid cysts
- Heberden’s and Bouchard’s nodes
Why in advaced hand OA may you get ‘squaring’ at the joint?
caused by subluxation (partial dislocation), formation of osteophytes and remodelling of bone
Mucoid cysts in OA of hand?
(painful mucus-filled cysts) adjacent to the joint on the dorsum of the finger, which may cause longitudinal ridging of the nail.
Nodes in OA of the hand?
Heberden’s= bony nodules on the dorsum of the finger next to the DIP joints
Bouchard’s nodes= next to the PIP joints
Hip OA may present with what?
deep pain in anterior groin on walking or climbing stairs
possible referred pain to lateral thigh, buttock, anterior thigh, knee and ankle
painful restriction of internal rotation with hip flexed
painful restriction of internal rotation with hip flexed
OA of the hip
What may be present in hip OA when the disease is advanced?
Trendelenburg gait
A fixed flexion external rotation deformity, with compensatory increased lumbar lordosis and pelvic tilt. The lower limb can be significantly shortened.
Trendelenburg gait?
in advanced hip OA
a lurch towards the affected hip with less time spent weight-bearing on that side and the pelvis tilting down on the unaffected side, caused by wasting and weakness of the gluteal and anterior thigh muscles
Knee OA?
typically bilateral and symmetrical
medial tibiofemoral (causes anteromedial pain on walking), lateral tibiofemoral (anterolateral pain on walking) or patellofemoral compartments (anterior knee pain worsened on incline or going down stairs; aching on prolonged sitting relieved my standing)
pain localsied to affected compartment
Associated features in knee OA?
Giving way — due to altered patella tracking, weak quadriceps muscles, severe patellofemoral involvement, and altered load-bearing mechanics.
Locking (inability to straighten the knee) — suggests loose meniscal cartilage in the joint.
Crepitus and tenderness along the joint line or with pressure on the patella.
Restricted flexion and extension.
weakness of the quadriceps is suggested if…
passive extension of the knee joint is greater than active extension
What may be present in advanced knee OA?
Bony swelling of the femoral condyles and lateral tibial plateau.
Varus (bow-legged), or less commonly valgus (knock-knee), deformity.
An antalgic gait.
X-ray findings in OA (done if uncertain or atypical features)?
subchondral bone thickening and/or cysts
osteophyte formation (new bone formation at joint margins)
loss or narrowing of the joint space (provides an estimate of the severity of cartilage damage).
Self care advice for pt with OA?
- self-care= info, weight loss, good footwear
- exercise= aerobic and muscle strengthening
- physiological support
Common joints affected in osteoarthritis?
DIPs
CMC joint (base of thumb)
Knees
Hips
L spine
C spine (c spondylosis)
DIPS or PIPS in osteoarthritis?
DIPS
Mneumonic for X-ray changes in osteoarthritis?
L.oss of joint space
O.steophytes
S.ubarticular scleorsis
S.ubchondral cysts
Signs in the hands in osteoarthritis?
- Heberden’s nodes (DIPs)
- Bouchard’s nodes (PIPs)
- Squaring at base of thumb (CMC joint)
- weak grip and reduced ROM
When can osteoarthritis be diagnosed clinically?
> 45yrs, typical pain and no morning stiffness (or <30mins)
What should be co-prescribed alongside oral NSAIDs (eg. in osteoarthritis when topical NSAIDs don’t work)?
PPI for gastroprotection
NSAIDs should be used in caution with pts with high BP, why?
they cause HTN by blocking prostaglandins (prostaglandins cause vasodilation)
Why should NSAIDs (ibuprofen and naproxen) be used cautiously in older pts and those on anticoags (aspirin, DOAC) eg. for osteoarthritis?
use short term for flares as:
- GI Cx= peptic ulcers, gastritis
- Renal= AKI (eg. acute tubular necrosis) and CKD
- CVD= HTN, HF, MI, stroke
- exacerbate asthma
Most common presentation of OA (joint)?
knee
then hip
RFs for OA of the hip?
- increasing age
- female
- obesity
- developmental dysplasia of hip
chronic history of groin ache following exercise and relieved by rest
osteoarthritis of hip
Red flags that may suggest an alternative cause in OA of the hip?
rest pain
night pain
morning stiffness >2hrs
What can be used to assess severity of OA of the hip?
Oxford Hip Score
Ix for OA of hip?
clinical
if atypical features= plain x-rays
Definitive Tx for OA of the hip?
total hip replacement
Cx of total hip replacement?
perioperative= VTE,
intraoperative fracture, nerve injury, surgical site infection
leg length discrepancy
posterior dislocation= may occur during extremes of hip flexion; typically presents acutely with a ‘clunk’, pain and inability to weight bear
on examination there is internal rotation and shortening of the affected leg
Most common reason for revision of total hip replacement?
aseptic loosening
- prosthetic joint infection
Summary of osteoarthritis Mx?
1) weight loss; local muscle strenthening exercises & aerobic fitness
1) topical NSAIDs
2) oral NSAIDs + PPI
3rd line) intra-articular steroid injections (2-10w relief)
4) fail= joint replacement
+ walking aids
can use paracetamol short term for flares (only if infrequent) but DO NOT use opioids
Osteomalacia?
softening of bones secondary to low vit D that in turn lead to decreased bone mineral density
Osteomalacia in children vs adults?
children= called rickets
adults= osteomalacia
Causes of osteomalacia?
- vit D def= malabsorption, lack of sunlight, diet
- CKD
- drug induced eg. anticonvulsants
- liver disease eg. cirrhosis
- coeliac
- inherited
inherited cause of osteomalacia?
hypophosphatemic rickets (aka vit D-resistant rickets)
Features of osteomalacia?
- bone pain
- bone/muscle tenderness
- fractures: esp femoral neck
- proximal myopathy= waddling gait
What fracture is common in osteomalacia?
femoral neck
Ix for osteomalacia?
- bloods= low vit D; low Ca and phosphate (30%) and raised ALP
- x-ray= translucent bands (Looser’s zones or pseudofractures)
Tx for osteomalacia?
- vit D supplementation= loading dose initially needed
- Ca supplementation if dietary inadequate
Osteomyeleitis?
infection of the bone
Osteomyelitis may be classified into what?
Haematogenous osteomyelitis and non-haematogenous osteomyelitis
Haematogenous osteomyelitis?
results from bacteraemia
is usually monomicrobial
most common form in children
vertebral osteomyelitis is the most common form of haematogenous osteomyelitis in adults
Most common form of osteomyelitis in children?
Haematogenous osteomyelitis
Haematogenous osteomyelitis RFs?
sickle cell anaemia, intravenous drug user, immunosuppression due to either medication or HIV, infective endocarditis
Non-haematogenous osteomyelitis?
results from the contiguous spread of infection from adjacent soft tissues to the bone or from direct
injury/trauma to bone
is often polymicrobial
most common form in adults
Most common form osteomyelitis in adults?
Non-haematogenous osteomyelitis
Non-haematogenous osteomyelitis RFs?
diabetic foot ulcers/pressure sores, diabetes mellitus, peripheral arterial disease
Most common cause of osteomyelitis (microbio)?
staph.aureus
(except if pt has sickle cell anaemia)
Most common cause of osteomyelitis in sickle cell anaemia pts?
Salmonella species
Ix for osteomyelitis?
MRI
Mx for osteomyelitis?
flucloxacillin for 6 weeks
clindamycin if penicillin-allergic
Mneumonic for ankylosing spondylitis?
S.ausage digitis
P.soriasis
I.nflam back pain
N.SAID responsive
E.nethesis (heel pain)
A.rthritis
C.rohns/UC
H.LA-B27
E.yes (uveitis)
Osteoporosis?
disease characterised by low bone mass and structural deterioration of bone tissue, causing increase in bone fragility and susceptibility to fracture
Does pt know they have osteoporosis?
it is asymptomatic so remains undiagnosed normally until a fragility fracture occurs
Osteoporotic fracture occurs as a consequence of…
increased bone fragility
Characteristic fractures occur where in pt with osteoporosis?
wrist, spine, hip
Fragility fracture?
fracture following a fall from standing height or less
Vertebral fractures in pt with osteoporosis?
may occur spontaneously or as a result of routine activities
RFs for osteoporosis?
Female sex.
Increasing age.
Menopause.
Oral corticosteroids.
Smoking.
Alcohol.
Previous fragility fracture.
Rheumatological conditions, eg. RA and other inflammatory arthropathies.
Parental history of hip fracture.
BMI less than 18.5 kg/m2.
What should be done in pt with fragility fracture prior to calculating fracture risk (osteoporosis)?
Ix to check for non-osteoporotic causes eg. metastatic bone ca and undiagnosed secondary causes eg. hyperthyroidism
Pt presents with fragility fracture, what Ix do you do?
1) rule out non-osteop causes and undiagnosed 2 causes eg. hyperthroidism
2) 10yr fragility fracture risk score PRIOR to arranging DXA scan to measure BMD or starting bisphosphonate except in certain pts (if ‘high risk eg. due to age or RFs then just straight to DXA)
What pts with suspected osteoporosis do you not bother calculating 10-yr fragility fracture risk score for (‘high risk’)? In these pts you just do DXA scan straight away without calculating risk.
> 50yrs with Hx of fragility fracture= offer DXA scan
<40yrs with major RF for fragility fracture= DXA scan then refer to specialist in Tx of osteop depending on BMD T-score
What is the BMD T-score?
the number of standard deviations below the mean BMD of young adults at their peak bone mass.
How to calculate 10 yr fragility fracture risk in pt with suspected osteoporosis? What do you do with the results?
- QFracture or FRAX
High risk= DXA scan to confirm osteop
Intermediate risk= close to threshold and have RFs (eg. taking high dose oral corticosteroids)= DXA scan
Low risk= lifestyle advice and NO scan
What RF for osteoporosis may not be included in FRAX?
pt taking high dose oral corticosteroids
Who should be offered bisphosphonates in suspected osteoporosis?
with BMD T-score of -2.5 or lower
Mx of osteoporosis?
1) 10yr fragility fracture risk score unless ‘high risk’
2) DXA scan for BMD if high risk score/intermediate
3) BMD T-score -2.5 or lower= bisphosphonates
- consider HRT in younger postmen women to reduce risk of fracture
4) manage RFs= smoking, alcohol, Ca & vit D def; falls risk
Why is follow up needed following starting Tx for osteoporosis?
- adverse effects of bone-sparing Tx
- adherence
- need for continuing bisphosphonate after 5yrs
Consider assessing fragility fracture risk in who?
- all women 65yrs+ and all men 75yrs+
- < them ages if RF= previous frag fracture; Hx of falls; current/freq use of oral corticosteroids; FHx hip fracture; BMI <18.5; smoking; alcohol >14units; have secondary causes for osteoporosis
- Do not assess if <50yrs or <40yrs unless major RF
Do not routinely assess fracture risk in pt <50yrs unless they have what major RFs?
Current or frequent use of oral corticosteroids.
Untreated premature menopause.
A previous fragility fracture.
Do not routinely assess fracture risk in pt <40yrs unless they have what major RFs?
Current or recent use of high-dose oral corticosteroids equivalent to, or more than, 7.5 mg prednisolone daily for 3 months or more.
A previous major osteoporotic fracture.
History of multiple fragility fractures.
Consider assessing fracture risk in pt taking what meds, esp in presence of other RFs?
- SSRI
- anti-epileptic= carbamazepine
- aromatase inhib eg. exemastane, anastrozole
- gonadotropin-releasing hormone agonists eg. goserelin
- PPI
- thiazolidinediones eg. pioglitazone
- glitazones
Non-osteoporotic causes for fragility fracture?
- met bone ca
- multiple myeloma
- osteomalacia
- Pagets
Secondary causes of osteoporosis (eg. pt with fragility fracture despite being low risk)?
- endocrine= untreated premature menopause; DM; hyperthyroidism; hypogonadism in men
- RA
- GI that cause malabsorption= crohns; UC; coeliac; chronic pancreatitis
- chronic liver disease= hep B, hep C, NAFLD
- COPD
Osteoporosis: offer a dual-energy X-ray absorptiometry (DXA) scan to measure bone mineral density (BMD) without calculating the fragility fracture risk in people….
Over 50 years of age with a history of fragility fracture.
Younger than 40 years of age who have a major risk factor for fragility fracture — depending on the BMD T-score, refer to a specialist experienced in the treatment of osteoporosis.
Osteoporosis: when can drug Tx without a DXA scan be considered?
in pts with vertebral fracture
Osteoporosis: offer oral bisphosphonates to pt taking corticosteroid therapy without waiting for BMD assessment (should follow later) if they have what RFs?
A prior fragility fracture.
Women age 70 years or over.
Postmenopausal women, and men age 50 years or over taking high dose glucocorticoids (7.5 mg or more of prednisolone daily or equivalent over 3 months).
Postmenopausal women, and men age 50 years or over with a FRAX probability of major osteoporotic fracture or of hip fracture exceeding the intervention threshold.
What pts are at risk of Vit D def?
> 65yrs
not exposed to much sunlight (indoors or wear clothes that cover whole body)
Recommended calcium intake for pt at increased risk of fragility fracture (osteoporosis)?
1000mg/day at least
What are the QFracture and FRAX risk assessment toold for osteoporosis?
predict the absolute risk of hip fracture, and major osteoporotic fractures (spine, wrist, or shoulder) over 10 years.
What score is considered high, intermediate and low risk according to the QFracture and FRAX score for a fragility fracture (osteoporosis)?
QFracture:
- High= 10% or more
- I= below 10% but close
to
- Low= below 10%
FRAX:
- high= red zone of risk chart
- i= amber
- low= green
What factors foes the FRAX score underestimate (when calculating fragility fracture risk)?
Regular use of corticosteroids equivalent to or less than 5 mg prednisolone daily.
Use of corticosteroids more than or equivalent to 7.5 mg prednisolone daily for more than 3 months.
A history of multiple fragility fractures.
High alcohol intake.
Heavy smoking.
Osteoporosis: fracture risk above the recommended threshold eg. 10%?
offer DXA scan
DXA scan stands for?
dual-energy x-ray absorptiometry scan
DXA scan in osteoporosis= T score -2.5 or less?
offer bisphosphonates (bone-sparing drug Tx)
DXA scan in osteoporosis= T score greater than -2.5?
modify RFs, treat underlying conditions and repeat DXA at appropriate interval eg. 2yrs
Fragility fracture risk intermediate eg. close to 10% but below, and they have RFs that may be underestimated by FRAX?
DXA scan to measure BMD and offer Tx if T-score -2.5 or less
Drug Tx for osteoporosis?
alendronate 70 mg once weekly, or risedronate 35 mg once weekly first-line
- 2nd line= ibandronate 150mg once monthly
- still not tolerated= specialist referral for eg. zoledronic acid or denosumab
?vit D and Ca supplements depending on current intake
Calcium management in osteoporosis?
If the person’s calcium intake is adequate (700 mg/day)= 10 micrograms (400 international units) of vitamin D (without calcium) for people not exposed to much sunlight.
Inadequate=
- 10 micrograms (400 international units) of vitamin D with at least 1000 mg of calcium daily.
- Prescribe 20 micrograms (800 international units) of vitamin D with at least 1000 mg of calcium daily for elderly people who are housebound or living in a nursing home
Lifestyle advice for pt with osteoporosis?
- regular exercise to improve muscle strenth
- balanced diet
- stop smoking
- cut down alcohol
After starting bone-sparing Tx for osteoporosis, what should you do?
- follow up: check tolerance after 12-16w
- then at 12m
- then at 5yrs
Atypical fracture in osteoporosis?
new onset hip, groin or thigh pain= stop osteop Tx and arrange x-ray of femur
What if pt has osteoporosis but requires oral corticosteoirds?
maintain bone protection
What when pt has been on bisphosphonates for osteoporosis for 5yrs?
follow up
- if still high risk (started Tx at 70yrs+; previous hip/vertebral fracture or 1+ fracture after starting Tx)= continue for at least 10yrs
- in others= DXA scan: continue for another 5yrs if T score -2.5 or less; if greater then pause treatment for 1.5-3yrs then reasssess
When to reassess fracture risk at anytime in pt with osteoporosis?
if re-fracture occurs or clinical RFs change
Pt sustained osteoporotic fracture whilst on bisphosphonates?
check adherence and exclude secondary causes for oestop; refer to specialist for drug Tx advice
Osteoporosis: If bisphosphonate treatment is discontinued and no new fracture occurs?
reassess fracture risk after 18 months for risedronate and ibandronate, 2 years for alendronate, and 3 years for zoledronate to inform whether treatment should be restarted.
Bisphosphonates MOA?
Analogues of pyrophosphate, a molecule that decreases demineralisation in bone. They inhibit osteoclasts by reducing recruitment and promoting apoptosis
Clinical uses for bisphosphonates?
- prevention and Tx of osteoporosis
- hypercalcaemia
- Paget’s disease
- pain from bone mets
Adverse effects of bisphosphonates?
- oesophagitis and oesophageal ulcers
- osteonecrosis of the jaw
- increased risk of atypical stress fractures of proximal femoral shaft
- acute phase response
- hypocalcaemia
Osteonecrosis of the jaw with bisphosphonates?
greater risk for pts having IV in Tx of ca rather than for osteoporosis or Pagets
poor dental hygiene/prior dental procedure also RF
All pts with cancer before bisphosphonate treatment should have what?
if poor dental status then they should have dental check up as it is a RF for osteonecrosis of the jaw
Acute phase response when taking bisphosphonates eg. for osteoporosis?
fever, myalgia and arthralgia may occur following administration
Why is hypocalcaemia an adverse effect of bisphosphonates?
due to reduced calcium efflux from bone; usually clinically unimportant
How should pt take bisphosphonates for osteoporosis?
‘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’
What should be done before starting a pt on bisphosphonates for osteoporosis?
hypocalcaemia/vit D def should be corrected
but for osteoporosis, calcium should only be prescribed if dietary intake is inadequate; Vit D supplements are normally given
Sometimes bisphosphonates are recommended to be stopped at 5yrs in who?
patient is < 75-years-old
femoral neck T-score of > -2.5
low risk according to FRAX/NOGG
Patients who’ve had a fragility fracture and are >= 75 years of age are presumed to have….
underlying osteoporosis and should be started on first-line therapy (an oral bisphosphonate), without the need for a DEXA scan
If a patient is under the age of 75 years a DEXA scan should be arranged. These results can then be entered into a FRAX assessment (along with the fact that they’ve had a fracture) to determine the patients ongoing fracture risk.
79-year-old woman falls over on to an outstretched hand and sustains a Colles’ fracture (fracture of the distal radius).
Given her age she is presumed to have osteoporosis and therefore started on oral alendronate 70mg once weekly. No DEXA scan is arranged.
Osteoporosis: A DEXA scan should be offered without calculating the fragilty risk score in the following situations?
> 50 years of age with a history of fragility fracture
< 40 years of age who have a major risk factor for fragility fracture - these patients should be referred to a specialist depending on the T-score
before starting treatments that may have a rapid adverse effect on bone density (for example, sex hormone deprivation for treatment for breast or prostate cancer)
QFracture
if the 10-year fracture risk is ≥ 10% then
a DEXA scan should be arranged
FRAX
patients in the orange zone should have…
red zone…
patients in the orange zone should have a DEXA scan if not already done to further refine their 10-year risk
patients in the red zone should also have a DEXA scan if not already done to act as a baseline and guide drug treatment
Osteoporosis: NICE recommend that we recalculate a patient’s risk (i.e. repeat the FRAX/QFracture)?
if the original calculated risk was in the region of the intervention threshold for a proposed treatment and only after a minimum of 2 years, or
when there has been a change in the person’s risk factors
Osteoporosis: risk factors that are used by major risk assessment tools such as FRAX…
history of glucocorticoid use
rheumatoid arthritis
alcohol excess
history of parental hip fracture
low body mass index
current smoking
RFs for osteoporosis other than those including in FRAX?
- sedentary lifestyle
- premature menopause
- Caucasians and Asians
- hyperthyroid, hypogonadism (eg. Turners, testosterone def), growth hormone def, hyperparathyroidism, DM
- multiple myeloma, lymphoma
- IBD, malabsorption (coeliac), gastrectomy, liver disease
- CKD
- osteogenesis imperfecta, homocystinuria
What bloods should be done as a minimum in suspected osteoporosis following a fragility fracture (eg. to rule out other causes)?
FBC
U&Es
LFTs
Bone profile
CRP
TFTs
DEXA scan: T score?
based on bone mass of young reference population
T score of -1.0 means bone mass of one standard deviation below that of young reference population
DEXA scan: Z score?
adjusted for age, gender and ethnic factors
DEXA scan: T score values?
> -1.0 = normal
-1.0 to -2.5 = osteopaenia
< -2.5 = osteoporosis
DEXA scan: osteoporosis?
< -2.5
DEXA scan: osteopaenia?
-1.0 to -2.5
DEXA scan: normal?
> -1.0
Most important RF for osteoporosis?
use of corticosteroids
risk rises significantly once a patient is taking the equivalent of prednisolone 7.5mg a day for 3 or more months.
if it likely that the patient will have to take steroids for at least 3 months then we should start what
bone protection straight away rather than waiting until 3m has elapsed
patient with newly diagnosed polymyalgia rheumatica. As it is very likely they will be on a significant dose of prednisolone for greater than 3 months what should be started immediately
bone protection
Management of patients at risk of corticosteroid-induced osteoporosis: patients can be divided into what 2 groups?
- Patients over the age of 65 years or those who’ve previously had a fragility fracture should be offered bone protection.
- Patients under the age of 65 years should be offered a bone density scan, with further management dependent
Management of patients at risk of corticosteroid-induced osteoporosis= ? for pts under 65yrs who had bone density scan and now need Mx?
T >0= reassure
T 0- -1.5= repeat scan in 1-3yrs
T <-1.5= offer bone protection
First line for bone protection eg. corticosteroid-induced osteoporosis?
alendronate
may need Ca and Vit D too
1st line bone protection following hip fracture?
IV zoledronate
Postmenopausal women, and men age ≥50, who are treated with oral glucocorticoids: what should you do?
if starting ≥7.5 mg/day prednisolone or equivalent for the next 3 months, start bone protective treatment at the same time (alendronate or risedronate)
don’t wait for DEXA scan before starting Tx
+ general osteoporosis Mx
How long should you plan to prescribe oral vs IV bisphosphonates?
oral= at least 5yrs
IV= at least 3yrs
How do bisphosphonates work?
bind to hydroxyapatite in bone, inhibiting osteoclast-mediated bone resorption
Denosumab MOA eg. for osteoporosis?
human monoclonal antibody that inhibits RANK ligand, which in turn inhibits the maturation of osteoclasts
also used for cancer patients with bone metastases to reduce skeletal-related events.
given as a single subcutaneous injection every 6 months
Raloxifene eg. for osteoporosis MOA?
selective oestrogen receptor modulator (SERM)
has been shown to prevent bone loss and to reduce the risk of vertebral fractures, but has not yet been shown to reduce the risk of non-vertebral fractures
has been shown to increase bone density in the spine and proximal femur
may worsen menopausal symptoms
increased risk of thromboembolic events
may decrease the risk of breast cancer
Strontium ranelate eg. for osteoporosis MOA?
‘dual action bone agent’ - increases deposition of new bone by osteoblasts (promotes differentiation of pre-osteoblast to osteoblast) and reduces the resorption of bone by inhibiting osteoclasts
concerns regarding the safety profile of strontium have been raised recently. It should only be prescribed by a specialist in secondary care
should only be used by people for whom there are no other treatments for osteoporosis
increased risk of cardiovascular events: any history of cardiovascular disease or significant risk of cardiovascular disease is a contraindication
not used in patients with a history of venous thromboembolism
may cause serious skin reactions such as Stevens Johnson syndrome
Teriparatide MOA eg. for osteoporosis?
recombinant form of parathyroid hormone
very effective at increasing bone mineral density but role in the management of osteoporosis yet to be clearly defined
Romosozumab MOA eg. for osteoporosis?
a monoclonal antibody that inhibits sclerostin, thereby increasing bone formation and decreasing bone resorption
this dual action significantly improves bone density and reduces fracture risk.
Definition of osteoporosis?
presence of bone mineral density (BMD) of less than 2.5 standard deviations (SD) below the young adult mean density.
Around ?% of post-menopausal women will suffer an osteoporotic fracture at some point.
50%
What does the DEXA scan look at?
hip and lumbar spine
Polymyalgia rheumatica (PMR)?
relatively common condition seen in older pts characterised by muscle stiffness and raised inflam markers
Cause of polymyalgia rheumatica?
condition is closely related to temporal arteritis but underlying cause not understood, does not appear to be vasculitic process
Features of polymyalgia rheumatica?
- typically >60yrs
- rapid onset eg. <1m
- aching, morning stiffness in proximal limb muscles
- WEAKNESS NOT CONSIDERED A SYMPTOM
- mild polyarthralgia, lethargy, depression, low grade fever, anorexia, night sweats
Pt with new temporal arteritis with a history of aching and morning stiffness in proximal limb muscles eg. neck and shoulders and pelvic girdle- what is the background condition?
polymyalgia rheumatica
Ix for polymyalgia rheumatica?
raised inflam markers eg. ESR >40
creatine kinase and EMG normal
Tx for polymyalgia rheumatica?
prednisolone eg. 15mg/od
typically respond dramatically, if they don’t then consider alternative diagnosis
Definition of polymyalgia rheumatica?
chronic, systemic, rheumatic inflam disease characterised by pain and morning stiffness in neck, shoulder and pelvic girdle
RFs for polymyalgia rheumatica?
- older age
- female
- northern european
- infection eg. mycoplasma, chlamydia, pneumonia and parovirus B19
One of most common indications for long term corticosteroid Tx?
polymyalgia rheumatica
Cx of polymyalgia rheumatica?
GCA (may be abrupt in early course of PMR)
Cx of long term corticosteroids
Prognosis of polymyalgia rheumatica?
usually resolves after few days of steroid Tx; treatment is often needed for 1-2yrs and some need low dose for several yrs
relapse is common but responds to restarting/increasing steroid dose
Key features of polymyalgia rheumatica?
Bilateral shoulder and/or pelvic girdle pain lasting more than 2 weeks.
Morning stiffness (for more than 45 minutes).
Evidence of an acute phase response.
Other more general symptoms, such as low-grade fever, fatigue, anorexia, weight loss, or depression.
Diagnosis of PMR?
working diagnosis in the combination of:
- core features
- exclusion of differentials
- +ve response to oral corticosteroids within 1w
- normal inflam markers within 4w
Mx of person with working diagnosis of PMR involves what?
Gradually reducing the dose of corticosteroids when symptoms are fully controlled, adjusting the magnitude of each dose reduction and the duration at each dose to avoid relapses.
Assessing for, and managing, symptoms of relapse, GCA, and steroid-related adverse effects.
Assessing and managing the risk of osteoporosis.
Referral to rheumtology in pts with PMR if?
- not possible to reduce steroids at reasonable intervals without causing relapse
- steroids needed for >2yrs
Type of pain in PMR?
unilateral then quickly is bilateral
worsens with movement
interferes with sleep
shoulder pain may radiate to elbows
hip and neck pain; hip pain may radiate to knees
Stiffness in PMR?
at least 45mins after waking or periods of rest
may be difficult to turn over in bed, rise from chair or raise arms above shoulders
Morning stiffness >45mins and difficulty rising from a chair?
?polymyalgia rheumatica
muscle strength not impaired but pain may restrict movement
What additional symptoms may be present in polymyalgia rhuematica?
peripheral MSK signs:
- carpal tunnel
- peripheral arthritis (knees and wrists): asymmetric and self limiting
- swelling with pitting oedema of hands, wrists, feet and ankles
PMR follow up?
after 1w of pred
then 3-4w of Tx: consider reducing dose, recheck ESR/plasma viscosity and/or CRP to assess Tx response
Pt with core symptoms of PMR and is >50yrs what should you do?
- request ESR/plasma viscosity and/or CRP= raised supports diagnosis but can be normal
- Exclude GCA immediately (as may cause vision loss)
- arrange tests in all pts to rule out other conditions before starting steroids= FBC, U&E, LFT, Ca, ALP, protein electrophoresis, TSH, creatine kinase, RF, urine dip; consider= urine sample for Bence Jones protein, ANA and anti-CCP, CXR
- if PMR most likely= trial prednisolone
When can you make a working diagnosis of PMR?
if pt reports improvement of 70%+ within 1w of steroids and normalisation of inflam markers within 4w
if lesser response, consider uping dose to 20mg
Typical course of Tx for PMR?
Typically, treatment is required for between 1–2 years.
Continue prednisolone 15 mg each day until symptoms are fully controlled (usually 3 weeks), then
Reduce the dose to 12.5 mg each day for 3 weeks, then
Reduce the dose to 10 mg each day for 4–6 weeks, then
Reduce the dose by 1 mg every 4–8 weeks until treatment is stopped.
What must pt with PMR be provided with when started on prednisolone?
blue steroid card= don’t stop abruptly; avoid close contacts who have chickenpox, shingles or measles if no immunity
What to measure at 3 monthly reviews for PMR?
FBC, ESR/CRP, U&E, BP and glucose
Differential diagnosis for PMR?
- degenerative disorders= cervical and L spondylosis, osteoarthritis, bilateral adhesive capsulitis (frozen shoulder) and rotator cuff disorders
- thyroid disease and hyperparathyroidsm
- viral illness
- chronic osteomyelitis
- TB
- infective endocarditis
- RA
- spondyloarthropathy
- SLE
- Ca
- myositis or myalgia due to statins
- PMR like syndrome due to quinidine
- osteomalacia
- fibromyalgia
- chronic fatigue syndrome
Reactive arthritis is part of what group of conditions?
HLA-B27 seronegative spondyloarthropathies
What was reactive arthritis previously called?
Reiter’s triad
(Reiter’s) Triad in reactive arthritis?
urethritis, conjunctivitis and arthritis
‘can’t see, pee or climb a tree’
Reactive arthritis?
arthritis that develops following an infection where the organism cannot be recovered from the joint
eg. post-STI or post-dysenteric (GI disease)
Cant see, pee or climb a tree….
Conjunctivitis, urethritis and arthritis
reactive arthritis
Organisms most commonly associated with reactive arthritis?
Post-STI (m>f)= chlamydia trachomatis
Post-dysenteric form (m&f same)= shigella flexneri; salmonella typhimurium; salmonella enteritidis; yersina enterocolitica; campylobacter
Mx of reactive arthritis?
- analgesia, NSAIDs, intra-articular steroids
- persistent= sulfasalazine and methotrexate
- rarely lasts more than 12m
Features of reactive arthritis?
- arthritis= asymmetrical oligoarthritis of lower limbs
- urethritis symptoms
- eye= conjunctivitis (10-30%); anterior uveitis
- dactylitis
- skin= circinate balanitis and keratoderma blenorrhagica
“cant see, wee or climb a tree”
Circinate balanitis in reactive arthritis?
painless vesicles on the coronal margin of the prepuce (foreskin/skin surrounding clitoris)
Keratoderma blenorrhagica in reactive arthritis?
waxy yellow/brown papules on palms and soles
Methotrexate MOA?
antimetabolite that inhibits dihydrofolate reductase, an enzyme essential for synthesis of purines and pyrimidines
Why is careful prescribing and close monitoring of methotrexate important?
very effective in controlling disease but the side-effects can be life threatening
Indications for methotrexate?
- inflam arthritis, esp RA
- psoriasis
- some chemo ALL
Adverse effects of methotrexate?
- mucositis
- myelosuppression
- pneumonitis
- pulmonary fibrosis
- liver fibrosis
Most common pulmonary adverse effect of methotrexate?
pneumonitis
- similar disease pattern to hypersensitivity pneumonitis secondary to inhaled organic antigens
- typically develops within a year of starting treatment, either acutely or subacutely
- presents with non-productive cough, dyspnoea, malaise, fever
Methotrexate in pregnancy?
avoid pregnancy for at least 6m after stopping methotrexate
men using methotrexate need to use effective contraception for at least 6m after Tx
How is methotrexate taken?
7.5mg weekly starting dose (not daily)
- only one strength of methotrexate tablet should be prescribed (2.5mg)
- co-prescribed with 5mg folic acid
What needs to be co-prescribed with methotrextae?
5mg folic acid once weekly, take >24hrs after methotrexate dose
What needs to be monitored in pts taking methotrexate?
FBC, U&E (renal function) and LFTs before starting, then repeated weekly until therapy stabilised and then monitor every 2-3m
Methotrexate interactions?
trimethorpim and
co-trimoxazole = avoid as increases risk of marrow aplasia
high dose aspirin
What increases the risk of methotrexate toxicity?
high dose aspirin increases risk of methotrexate toxicity secondary to reduced excretion
Tx for methotrexate toxicity?
folinic acid
Rheumatoid arthritis (RA)?
chronic systemic inflam disease
How does RA present?
inflam arthritis affecting small joints of hands and feed symmetrically and equally; any synovial joint can be involved
as it progresses, any system can be affected so increased risk of premature death
Cx and cormorbidities of RA?
CVD, osteoporosis, anaemia, infection
What population does RA typically affect?
women > men
peak onset 30-50yrs
Clinical features of synovitis in RA?
pain, swelling heat and stiffness in affected joints
synovitis vs arthritis?
Synovitis is swelling in the synovial membrane that lines some of your joints that leads to arthritis (acute or chronic joint inflammation in the joint)
Ix for RA?
- clinical= if suspected refer urgently within 3d for specialist assessment to confirm within 3w
to speed up diagnosis:
- bloods= rheumatoid factor +ve in 60-70%
- if -ve in RF= test for anti-CCP (80%)
- x-rays of hands and feet= severity
When should you suspect RA and so refer the pt for assessment?
1 or more of…
- small joints of the hands or feet affected
- more than 1 joint affected
- present for 3m+
Mx for RA?
1) NSAIDs + PPI whilst waiting specialist assessment
2) specialist MX:
cDMARD monotherapy eg. oral methotrexate, leflunomide or sulfasalazine. Dose increased depending on tolerance.
2) may give short-term oral/intramuscular/intra-articular corticosteroids whilst waiting for DMARD to start working
3) not responded= combination of DMARDs
4) severe and still not responded= methotrexate + biological DMARDs
Mx of RA flare?
- exclude septic arthritis
- specialist advice
- short term corticosteroids intra-articular= methylprednisolone acetate ; if can’t then intramuscular; if can’t then oral
When to refer pt with RA for surgical opinion?
- no response to Mx
- persistant pain: joint damage or soft tissue cause
- worsening joint function
- progressive deformity
- persistent localised synovitis
- if Cx= imminent or actual tendon rupture, nerve compression, stress fracture
CP of RA?
symmetrical synovitis= pain, swelling, heat and stiffness in affected joints
most common in small joints of small hands and feet, but any synovial joint can be affected
pain worse at rest
swelling= around joint ‘boggy’ on palpation not boney
siffness= early morning >1hr
- may have rheumatoid nodules; systemic features (fever, fatigue, sweats, weight loss); FHx and extra-articular features
Rheumatoid nodules in RA?
hard firm swellings over extensor surfaces
Extra-articular features in RA?
vasculitis or invl of other body systems eg. eye, lungs and heart
Type of presentation in RA?
normally insidious but can be rapid or relapsing and remitting (palindromic presentation)
In RA, persistent synovitis and poor prognosis is more likey when…
- greater number of joints affected
- swelling and tenderness
- PIPs and MCP joints affected and there is symmetry
- +ve MCP squeeze test
What presentation is associated with ability to diagnose RA from other diagnoses?
inability to make a fist or flex fingers in RA
What Ix can be done in RA to speed up diagnosis and act as baseline measure prior to Tx?
- FBC, renal (U&E) and LFTs
- CRP or ESR (normal in 40%)
Clinically suspect RA (have 1 of: small joints of hand or feet affected, more than one joint, been >3m) but normal acute phase response, negative anti-CCP and RF?
still refer urgently within 3d for specialist assessment within 3w as clinically suspect
Can you prescribe glucocorticoids in primary care for RA whilst awaiting for specialist assessment?
no they may mask the clinical features and delay diagnosis, wait until assessment carried out
Target of Tx in RA?
achieve a target of remission of low disease activity if remission cannot be achieved
What does cDMARD stand for?
conventional disease-modifying anti-rheumatic drug
What can be alternative to a DMARD eg. methotrexate in RA if pt has mild or palindromic disease?
hydroxychloroquine
How long until DMARD takes affect in RA?
can take 2-3m
Other causes of worsening joint symptoms in RA other than a flare?
- avascular necrosis= sudden pain in pt taking steroids in absence of synovitis
- nerve root compression
- anaemia, infection
- failure of meds to control symptoms
- failure to take meds regularly
- osteoporotic fracture
- secondary osteoarthritis
- psychological/social problems
Differential diagnosis for RA?
- connective tissue disorders eg. SLE
- fibromyalgia
- infectious arthritis
- osteoarthritis
- polyarticular gout
- PMR
- psoriatic arthritis
- reactive arthritis
- sarcoidosis
- septic arthritis
- seronegative spondyloarthritis= ?psoriais, back pain or bowel problenms
Symmetrical distal polyarthritis
RA
Most common gene associated with RA?
HLA DR4
Rheumatoid factor (RF)?
autoantibody present in around 70% of RA patients. It targets the Fc portion of the immunoglobulin G (IgG). All antibodies (immunoglobulins) have an Fc portion that interacts with other parts of the immune system. Rheumatoid factor causes immune system activation against the patient’s own IgG, resulting in systemic inflammation. Rheumatoid factor is most often IgM but can be other types of immunoglobulin.
what does anti-CCP antibodies stand for (in RA)?
Anti-cyclic citrullinated peptide antibodies
Anti-CCP antibodies?
More sensitive and specific than rheumatoid factor in RA. They are positive in around 80% of patients with rheumatoid arthritis. They often pre-date the development of rheumatoid arthritis and indicate that a patient will develop the condition at some point.
most common joints affected in RA?
MCP joints
PIP joints
wrist
MTP joints in foot
MCP joints
Metacarpophalangeal joints (knuckle)
PIP joints
Proximal interphalangeal
MTP joints
Metatarsophalangeal joints (in foot- between metatarsal bones and proximal phalanges)
Enlarged and painful distal interphalangeal joints
? Heberden’s nodes due to osteoarthritis.
What large joints may be affected in RA?
ankle, knee, hips, shoulders, C spine (not L)
Arthritis worse with rest, improve with activity. Worse in morning.
RA
Morning stiffness >30mins
RA
Arthritis worse with activity and improve with rest
OA
Morning stiffness <30mins
OA
Palindromic rheumatism?
self-limiting episodes of inflammatory arthritis, with pain, stiffness and swelling typically affecting only a few joints.
symptoms last days, then completely resolve
Joints appear normal between episodes.
RF or anti-CCP antibodies may indicate that it will progress to rheumatoid arthritis.
Same 4 hand signs in RA?
Z-shaped deformity
Swan neck deformity
Boutonniere deformity
Ulnar deviation
RA hand signs: Z-shaped deformity?
to the thumb
RA hand signs: swan neck derformity?
hyperextended PIP and flexed DIP
RA hand signs: boutonniere deformity?
hyperextended DIP and flexed PIP
RA hand signs: ulnar deviation?
ulnar deviation of the fingers at the MCP joints
What causes Boutonniere deformity in RA?
Tear in the central slip of the extensor components at the PIP joint. The central slip connects to the middle phalanx at the PIP, and the lateral bands go around the PIP and connect to the distal phalanx. When the patient tries to straighten their finger, the lateral bands pull on the distal phalanx, causing the distal interphalangeal (DIP) joint to hyperextend and the PIP joint to flex.
What causes swan neck deformity in RA?
opposite of Boutonnieres deformity. It is caused by an extensor mechanism imbalance, causing flexion of the DIP joint and extension of the PIP joint.
Atlantoaxial Subluxation in RA?
Occurs in the C spine.
Synovitis and damage to the ligaments around the odontoid peg of the axis (C2) allow it to shift within the atlas (C1). Subluxation can cause spinal cord compression and is an emergency.
Needs to be considered when a patient is having a general anaesthetic and requires intubation.
MRI can be used to visualise changes in these areas as part of a pre-operative assessment.
Name some extra-articular manifestations of RA?
- eye manifestations
- Pulmonary fibrosis
- Felty’s syndrome
- Sjögren’s syndrome (with dry eyes and dry mouth)
- Anaemia of chronic disease
- CVD
- Rheumatoid nodules
- Lymphadenopathy
- Carpel tunnel syndrome
- Amyloidosis
- Bronchiolitis obliterans
- Caplan syndrome
Felty’s syndrome?
extra-articular manifestation of RA
triad= RA, neutropenia and splenomegaly
RA, neutropenia and splenomegaly
Felty’s syndrome
Bronchiolitis obliterans in RA?
small airway destruction and airflow obstruction in the lungs
Caplan syndrome?
pulmonary nodules in patients with rheumatoid arthritis exposed to coal, silica or asbestos dust
Eye manifestations in RA?
Dry eye syndrome (keratoconjunctivitis sicca)
Episcleritis
Scleritis
Keratitis
Cataracts (secondary to steroids)
Retinopathy (secondary to hydroxychloroquine)
X-ray changes in RA?
Periarticular osteopenia
Joint destruction & deformity (advanced)
L.oss of joint space
E.rosions (boney)
S.oft tissue swelling
S.ubluxation
Scoring systems in RA?
Health Assessment Questionnaire (HAQ) measures functional ability= response to Tx
Disease Activity Score 28 Joints (DAS28) score is used in monitoring disease activity and response to treatment. It involves assessing 28 joints and assigning points for=
Swollen joints
Tender joints
The ESR or CRP result
What is considered the safest cDMARD in RA in pregnancy?
Hydroxychloroquine and sulfasalazine
Examples of biological therapies that can be used in RA (interact with immune system to reduce inflam)?
Tumour necrosis factor (TNF) inhibitors (e.g., adalimumab, infliximab, etanercept, golimumab and certolizumab)
Anti-CD20 on B cells (e.g., rituximab)
Anti-interleukin-6 inhibitors (e.g., sarilumab and tocilizumab)
JAK inhibitors (e.g., upadacitinib, tofacitinib and baricitinib)
T-cell co-stimulation inhibitors (e.g., abatacept)
How do TNF inhibitors work in RA?
Tumour necrosis factor is a cytokine involved in stimulating inflammation. Blocking TNF reduces inflammation.
Main biologics to remember for RA?
- TNF inhibitors= adalimumab, infliximab, entanercept
- Rituximab ( monoclonal antibody that targets the CD20 proteins on the surface of B cells)
Adverse effects of biologics in RA?
cause immunosuppression, increasing the risk of infection, certain cancers (e.g., skin) and reactivation of latent TB.
Why does folic acid need to be co-prescribed with methotrexate?
methotrexate interferes with folate metabolism and suppresses the immune system
RA drug side effects= methotrexate?
Bone marrow suppression and leukopenia, and highly teratogenic
RA drug side effects= leflunomide?
Hypertension and peripheral neuropathy
RA drug side effects= sulfasalazine?
Orange urine and male infertility (reduces sperm count)
RA drug side effects= hydroxychloroquine?
Retinal toxicity, blue-grey skin pigmentation and hair bleaching
RA drug side effects= anti-TNF medications?
Reactivation of tuberculosis
RA drug side effects= rituximab?
Night sweats and thrombocytopenia
American College of Rheymatology criteria for RA?
need 6/10 to diagnose
A) joint involvement= 2-10 large joints (1 point); 1-3 small (2); 4-10 small (3); 10 joints (5)
B) serology= negative RF and ACPP (0); low positive RF or ACPP (2); high positive (3)
C) acute phase reactants= abnormal CRP or ESR (1)
D) duration= >6 w (1)
Acute phase reactants in RA?
CRP/ESR
How can RF be detected?
Rose-Waaler test: sheep red cell agglutination
Latex agglutination test (less specific)
Conditions associated with RF other than RA?
Felty’s syndrome (around 100%)
Sjogren’s syndrome (around 50%)
infective endocarditis (around 50%)
SLE (= 20-30%)
systemic sclerosis (= 30%)
general population (= 5%)
rarely: TB, HBV, EBV, leprosy
What pts with suspected RA should be tested for anti-CCP antibodies?
if RF negative
How long can anti-CPP antibodies be detected for in RA?
may be detectable up to 10 years before the development of rheumatoid arthritis
allows early detection of patients suitable for aggressive anti-TNF therapy
What is RF (in RA for example)?
circulating antibody (usually IgM) that reacts with the Fc portion of the patients own IgG.
1st line antibody test in suspected RA
TNF-inhibitors in RA?
indication= inadequate response to at least two DMARDs including methotrexate
etanercept: recombinant human protein, acts as a decoy receptor for TNF-α, subcutaneous administration, 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, subcutaneous administration
Rituximab for RA?
anti-CD20 monoclonal antibody, results in B-cell depletion
two 1g intravenous infusions are given two weeks apart
infusion reactions are common
Iatrogenic ocular manifestations in RA?
steroid-induced cataracts
chloroquine retinopathy
Most common ocular manifestations in RA?
keratoconjunctivitis sicca (most common)
episcleritis (erythema)
scleritis (erythema and pain)
corneal ulceration
keratitis
Mx of RA in pregnancy?
sulfasalazine and hydroxychloroquine
low-dose corticosteroids may be used in pregnancy to control symptoms
NSAIDs may be used until 32 weeks but after this time should be withdrawn due to the risk of early close of the ductus arteriosus
patients should be referred to an obstetric anaesthetist due to the risk of atlanto-axial subluxation
When do pts with RA typically get flares if they are pregnant?
after delivery
positive ‘squeeze test’ - discomfort on squeezing across the metacarpal or metatarsal joints
RA
Are hand joint deformities an early or late sign in RA?
late
Poor prognostic features in RA?
rheumatoid factor positive
anti-CCP antibodies
poor functional status at presentation
X-ray: early erosions (e.g. after < 2 years)
extra articular features e.g. nodules
HLA DR4
insidious onset
Periarticular?
area surrounding the joint
Most common cause of septic arthritis in adults?
staph aureus overall
young adults who are sexually active= N.gonorrhoeae (disseminated gonococcal infection)
Most common cause of septic arthritis in adults (how is it spread)?
hematogenous spread,
may be from distant bacterial infections eg. abscesses
Most common location of septic arthritis in adults?
knee
Features of septic arthritis in adults?
- acute swollen joint= restricted movement, warm to touch
- fever in majority
Ix for septic arthritis?
- synovial fluid sampling under radiographic guidance
- blood cultures
- joint imaging
What does synovial fluid sampling show in septic arthritis?
- leucocytosis with neutrophil predominance
- gram staining is negative in around 30-50% of cases
- fluid culture is positive in patients with non-gonococcal septic arthritis
When is fluid culture positive in septic arthritis (from synovial joint sampling)?
pts with non-gonococcal septic arthritis
Mx of septic arthritis?
IV Abx that cover gram +ve cocci= flucloxacillin or clindamycin if penicillin allergic
- give 4-6w, switched from IV to oral after 2w
- needle aspiration to decompress joint
- may need arthroscopic lavage
Most common joints affected in septic arthritis in children?
hip, knee, ankle
m>f
Symptoms and signs of septic arthritis in children?
symptoms= joint pain, limp, fever, systemically unwell (lethargy)
signs= swollen red joint, typically only able to minimally move affected joint
Ix for septic arthritis in children?
joint aspiration: for culture. Will show a raised WBC
raised inflammatory markers
blood cultures
Criteria to diagnose septic arthritis in children?
Kocher criteria:
1) fever >38.5 degrees C
2) non-weight bearing
3) raised ESR
4) raised WCC
How to pts with osteoporotic vertebral fractures typically present?
- asymptomatic= my be incidental finding on x-ray
- acute back pain
- breathing difficulties= change in shape may compress organs eg. lungs, heart, intestine
- GI problems= compression abdo organs
- minority will have Hx of fall/trauma
Signs of osteoporotic vertebral fracture?
- loss of height= compress spinal vertebrae so reduction in length of spine
- kyphosis (curved spine)
- localised tenderness on palpation of spinous processess at fracture site
Ix for osteoporotic vertebral fracture?
x-ray spine= wedging of vertebrae due to compression of bone, may show old fractures (sclerotic appearance)
2nd line= CT spine (extent of fracture) or MRI (differentiate from those caused by another pathology like tumour)
Epidemiology of SLE?
F:M (9:1)
Afro-Caribbeans and Asian
onset 20-40yrs
What does SLE stand for?
systemic lupus erythematosus
What type of disease is SLE?
autoimmune disease= a type 3 hypersensitivity reaction
What genes is SLE associated with?
HLA B8, DR2, DR3
What is SLE thought to be caused by?
immune system dysregulation leading to immune complex formation; immune complex deposition can affect any organ eg, skin, joints, kidneys and brain
Immune complex deposition (formed by immune system dysregulation) in SLE can affect where?
any organ icl. skin, joints, kidney and brain
Systemic lupus erythematosus (SLE)?
multisystem autoimmune disorder; typically presents in early adulthood and more common in women & Afro-Caribeean
General features of SLE?
- fatigue
- fever
- mouth ulcers
- lymphadenopathy
- skin features= malar rash
- MSK= arthralgia
- CVD= pericarditis
- Resp= pleurisy, fibrosing alveolitis
- Renal= proteinuria, glomerulonephritis
- Neuropsychiatric= anxiety, depression, seizures
Skin features in SLE (6)?
malar (butterfly) rash: spares nasolabial folds
discoid rash
photosensitivity
Raynaud’s phenomenon
livedo reticularis
non-scarring alopecia
2 types of rash in SLE?
malar (butterfly) rash= spares nasolabial folds
discoid rash= scaly, erythematous, well demarcated rash in sun-exposed areas. Lesions may progress to become pigmented and hyperkeratotic before becoming atrophic
MSK features in SLE?
arthralgia
non-erosive arthritis
Cardiovascular features in SLE?
pericarditis (most common)
myocarditis
Resp features in SLE?
pleurisy
fibrosing aleovlitis
Renal features in SLE?
proteinuria
glomerulonephritis (diffuse proliferative glomerulonephritis is the most common type)
Neuropsychiatric features in SLE?
anxiety & depression
psychosis
seizures
Ix in SLE?
- ANA positive (90%)
- RF +ve (20%)
- anti-dsDNA
- anti-Smith
- anti-RO (SS-A), anti-La (SS-B) and anti-U1 RNP
Antibodies in SLE?
- ANA positive (90%), high sensitivity so useful rule out test, low specificity
- RF +ve (20%)
- anti-dsDNA: very specific but low sensitive
- anti-Smith: high specific, low sensitive
- anti-RO (SS-A), anti-La (SS-B) and anti-U1 RNP
Monitoring in SLE?
1) ESR used; during active disease CRP may be normal, if it is raised may mean infection
2) complement levels (C3,C4) low during active disease
3) anti-dsDNA titres can be used but not present in all pts
Why in SLE are complement levels (C3 and C4) low during active disease?
formation of immune complexes leads to consumption of complement
Mx for SLE?
Hydroxychloroquine
+ NSAIDs and sun-block
internal organ involvement (eg. renal, neuro, eye)= consider prednisolone or cyclophosamide
Lupus nephritis?
severe manifestation of SLE that can result in end-stage renal disease
SLE pts should be monitored how to look for renal Cx (eg. lupus nephritis)?
urinalysis to rule out proteinuria
WHO classification of renal Cx (SLE)?
class I: normal kidney
class II: mesangial glomerulonephritis
class III: focal (and segmental) proliferative glomerulonephritis
class IV: diffuse proliferative glomerulonephritis
class V: diffuse membranous glomerulonephritis
class VI: sclerosing glomerulonephritis
Most common form of renal Cx in SLE?
Class IV (diffuse proliferative glomerulonephritis)
What does renal biopsy show in pt with SLE with renal Cx: Class IV (diffuse proliferative glomerulonephritis) ?
glomeruli shows endothelial and mesangial proliferation, ‘wire-loop’ appearance
if severe, the capillary wall may be thickened secondary to immune complex deposition
electron microscopy shows subendothelial immune complex deposits
granular appearance on immunofluorescence
Mx of renal Cx in SLE?
treat HTN
initial therapy for focal (class III) or diffuse (class IV) lupus nephritis=
glucocorticoids with either mycophenolate or cyclophosphamide
subsequent therapy=
mycophenolate is generally preferred to azathioprine to decrease the risk of developing end-stage renal disease
Boxer fracture?
a minimally displaced fracture of the 5th metacarpal (little finger)
typically following pt punching a hard surface eg. wall
Pt punches wall, what fracture?
boxer (5th metacarpal)
Fall onto outstretched hand- what fracture?
Colles’ fracture
Scaphoid fracture
When does a Colles’ fracture occur?
fall onto outstretched hand (known as a FOOSH)
Colles’ fracture?
distal radius fracture with dorsal displacement of fragments
described as a dinner fork type deformity
3 features of Colles’ fracture?
Transverse fracture of the radius
1 inch proximal to the radio-carpal joint
Dorsal displacement and angulation
How to remember Colles’ fracture?
Dorsally Displaced Distal radius → Dinner fork Deformity
Early Cx of Colles’ fracture?
median nerve injury: acute carpal tunnel syndrome presenting with weakness or loss of thumb or index finger flexion
compartment syndrome
vascular compromise
malunion
rupture of the extensor
pollicis longus tendon
acute carpal tunnel syndrome presenting with weakness or loss of thumb or index finger flexion following fall onto outstretched hand
median nerve injury due to colles’ fracture
What nerve injury does Colles’ fracture cause?
median nerve injury: acute carpal tunnel syndrome presenting with weakness or loss of thumb or index finger flexion
Late Cx of Colles’ fracture?
osteoarthritis
complex regional pain syndrome
Smith’s fracture (reverse colles’ fracture)?
Volar angulation of distal radius fragment (Garden spade deformity)
Caused by falling backwards onto the palm of an outstretched hand or falling with wrists flexed
falling backwards onto the palm of an outstretched hand or falling with wrists flexed- what fracture?
Smith’s
Bennetts’ fracture?
Intra-articular fracture of the first carpometacarpal joint
Impact on flexed metacarpal, caused by fist fights
X-ray: triangular fragment at ulnar base of metacarpal
Impact on flexed metacarpal, caused by fist fights- what fracture?
Bennetts
Monteggia’s fracture?
Dislocation of the proximal radioulnar joint in association with an ulna fracture
Fall on outstretched hand with forced pronation
Needs prompt diagnosis to avoid disability
Fall on outstretched hand with forced pronation- what fracture?
Monteggia’s fracture
Galeazzi fracture?
Radial shaft fracture with associated dislocation of the distal radioulnar joint
Direct blow
What fracture can be associated with a direct blow?
Galeazzi fracture
Pott’s fracture?
Bimalleolar ankle fracture
Forced foot eversion
Forced foot eversion- what fracture?
Pott’s
Barton’s fracture?
Distal radius fracture (Colles’/Smith’s) with associated radiocarpal dislocation
Fall onto extended and pronated wrist
Fall onto extended and pronated wrist- what fracture?
Barton’s fracture
Fractures of the humerus can be divided into what?
proximal humeral fractures
humeral shaft fractures
distal humeral fractures
proximal humeral fractures?
typically seen in elderly
distal humeral fractures?
typically seen in children
includes supracondylar fractures
Examples of Eponymous fractures?
Colles’
Smith’s
Bennett’s
Monteggia’s
Galeazzi
Pott’s
Barton’s
Supracondylar fractures?
fractures of the distal humerus just above elbow joint
typically seen in children and most common type of elbow fracture in children
Features of Supracondylar fractures (fractures of the distal humerus just above elbow joint)?
typically result from a fall onto an outstretched hand
pain
swelling over the elbow immediately
the elbow will typically be in a semi-flexed position
complications due to neurovascular involvement:
median nerve
radial nerve
brachial artery
ulnar nerve
child falls onto outstretched hand and the elbow is now in semi-flexed postition?
Supracondylar fracture (fractures of the distal humerus just above elbow joint)
Mx of Supracondylar fractures (fractures of the distal humerus just above elbow joint)?
non-displaced fractures=
collar and cuff
displaced fractures=
manipulation under anaesthesia with fixation
Types of paediatric fractures?
- complete fracture
- toddlers fracture
- plastic deformity
- Greenstick fracture
- Buckle (‘torus’) fracture
- Growth plate fractures
- Pathological fractures
Paediatric fractures: injury pattern in a complete fracture?
both sides of cortex are breached
Paediatric fractures: injury pattern in a toddlers fracture?
oblique tibial fracture in infants
Paediatric fractures: injury pattern in a plastic deformity?
stress on bone resulting in deformity without cortical disruption
Paediatric fractures: injury pattern in a Greenstick fracture?
unilateral cortical breach only
Paediatric fractures: injury pattern in a buckle (‘torus’) fracture?
incomplete cortical disruption resulting in periosteal haematoma only
Paediatric fractures: injury pattern in a growth plate fracture?
fractures that involve growth plates
How are growth plate fractures in paeds classified?
Salter-Harris system:
I= Fracture through the physis only (x-ray often normal)
II= Fracture through the physis and metaphysis
III= Fracture through the physis and epiphysis 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)
What indicates a growth plate fracture in children?
growth plate tenderness even if x-ray is normal
Mx of growth plate fractures in children?
Injuries of Types III, IV and V will usually require surgery. Type V injuries are often associated with disruption to growth.
Signs of non-accidental injury in children?
Delayed presentation
Delay in attaining milestones
Lack of concordance between proposed and actual mechanism of injury
Multiple injuries
Injuries at sites not commonly exposed to trauma
Children on the at risk register
Bruising of different ages
What conditions may cause pathological fractures in children?
genetic:
- osteogenesis imperfecta
- osteopetrosis
Pathological fractures in children: osteogenesis imperfecta?
Defective osteoid formation due to congenital inability to produce adequate intercellular substances like osteoid, collagen and dentine.
Failure of maturation of collagen in all the connective tissues.
Radiology may show translucent bones, multiple fractures, particularly of the long bones, wormian bones (irregular patches of ossification) and a trefoil pelvis.
Pathological fractures in children: subtypes of osteogenesis imperfecta?
Type I - The collagen is normal quality but insufficient quantity.
Type II - Poor collagen quantity and quality.
Type III - Collagen poorly formed. Normal quantity.
Type IV - Sufficient collagen quantity but poor quality.
Pathological fractures in children: osteopetrosis?
Bones become harder and more dense.
Autosomal recessive condition.
It is commonest in young adults.
Radiology reveals a lack of differentiation between the cortex and the medulla described as marble bone.
Scaphoid fracture?
type of wrist fracture
typically arises as a result of a fall onto an outstretched hand (FOOSH); contact sports (rugby, football) or road traffic accident when pt holding wheel
Result of a scaphoid fracture?
axial compression of the scaphoid, with the wrist hyperextended, and radially deviated
axial compression of the scaphoid, with the wrist hyperextended, and radially deviated
scaphoid fracture
What is it important to examine for in anyone presenting with acutely painful wrist for medico-legal reasons?
scaphoid fracture
Blood supply to scaphoid bone?
Around 80% of the blood supply is derived from the dorsal carpal branch (branch of the radial artery), in a retrograde manner.
Why is it so important to recognise scaphoid fractures?
given the unusual blood supply of the scaphoid bone; Interruption of the blood supply risks avascular necrosis of the scaphoid, with this most commonly complicating proximal injuries.
What do pts with scaphoid fracture present with?
Pain along the radial aspect of the wrist, at the base of the thumb
Loss of grip / pinch strength
Name 5 signs of a scaphoid fracture?
- Point of maximal tenderness over the anatomical snuffbox
- Wrist joint effusion`;
Hyperacute injuries (<4hrs old), and delayed presentations (>4days old) may not present with joint effusions. - Pain elicited by telescoping of the thumb (pain on longitudinal compression)
- Tenderness of the scaphoid tubercle (on the volar aspect of the wrist)
- Pain on ulnar deviation of the wrist
Ix for scaphoid fractures?
- clinical: look for signs, esp 1,3 and 4
- Plain film radiographs of the wrist in the anterior-posterior view, and lateral view
- CT if uncertain or planning operative Mx
- MRI definitive to confirm (use 2nd line when x-ray inconclusive)
X-ray in scaphoid fracture?
‘Scaphoid views’: posterioranterior (PA), lateral, oblique (with wrist pronated at 45º) and Ziter view (PA view with the wrist in ulnar deviation and beam angulated at 20º)
The sensitivity in the first week of injury is only 80%
Mx of scaphoid fracture?
- initial= immobilisation with a Futuro splint or standard below-elbow backslab
- referral to orthopaedics
clinical review with further imaging should be arranged for 7-10 days later when initial radiographs are inconclusive - may need ortho Mx
Ortho Mx of scaphoid fracture?
dependent on the patient and type of fracture
undisplaced fractures of the scaphoid waist=
cast for 6-8 weeks;
union is achieved in > 95%;
certain groups e.g. professional sports people may benefit from early surgical intervention
displaced scaphoid waist fractures=
requires surgical fixation
proximal scaphoid pole fractures=
require surgical fixation
Cx of scaphoid fractures?
non-union → pain and early osteoarthritis
avascular necrosis
Commonest carpal fractures?
scaphoid
Why does fracture of scaphoid risk blood supply?
Surface of scaphoid is covered by articular cartilage with small area available for blood vessels
What forms floor of anatomical snuffbox?
scaphoid
Summarise features of scaphoid fracture?
The main physical signs are swelling and tenderness in the anatomical snuff box, and pain on wrist movements and on longitudinal compression of the thumb.
Ulnar deviation AP needed for visualization of scaphoid
Immobilization of scaphoid fractures difficult
Radial head fracture?
Fracture of the radial head is common in young adults.
It is usually caused by a fall on the outstretched hand.
marked local tenderness over the head of the radius, impaired movements at the elbow, and a sharp pain at the lateral side of the elbow at the extremes of rotation (pronation and supination).
marked local tenderness over the head of the radius, impaired movements at the elbow, and a sharp pain at the lateral side of the elbow at the extremes of rotation (pronation and supination)
radial head fracture
De Quervain’s tenosynovitis?
common condition in which the sheath containing the extensor pollicis brevis and abductor pollicis longus tendons is inflamed
De Quervain’s tenosynovitis typically affects who?
females 30-50yrs
Features of De Quervain’s tenosynovitis?
pain on the radial side of the wrist
tenderness over the radial styloid process
abduction of the thumb against resistance is painful
Finkelstein’s test
Finekelstein’s test in De Quervain’s tenosynovitis?
examiner pulls the thumb of the patient in ulnar deviation and longitudinal traction. In a patient with tenosynovitis this action causes pain over the radial styloid process and along the length of extensor pollisis brevis and abductor pollicis longus
Mx for De Quervain’s tenosynovitis?
analgesia
steroid injection
immobilisation with a thumb splint (spica) may be effective
surgical treatment is sometimes required
Lateral epicodylitits aka
tennis elbow
Lateral epicodylitits (tennis elbow) features?
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 and 2 years. Patients tend to have acute pain for 6-12 weeks
Medial epicondylitis aka
golfer’s elbow
Medial epicondylitis (golfer’s elbow) features?
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
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
Medial epicondylitis (golfer’s elbow)
pain worse on resisted wrist extension with the elbow extended or supination of the forearm with the elbow extended
Lateral epicondylitis (tennis elbow)
Radial tunnel syndrome most commonly due to what?
compression of the posterior interosseous branch of the radial nerve. It is thought to be a result of overuse.
Radial tunnel syndrome features?
symptoms are similar to lateral epicondylitis making it difficult to diagnose
however, the pain tends to be around 4-5 cm distal to the lateral epicondyle
symptoms may be worsened by extending the elbow and pronating the forearm
symptoms are similar to lateral epicondylitis making it difficult to diagnose
however, the pain tends to be around 4-5 cm distal to the lateral epicondyle
symptoms may be worsened by extending the elbow and pronating the forearm
radial tunnel syndrome (compression of the posterior interosseous branch of the radial nerve/overuse)
Cubital tunnel syndrome due to?
compression of ulnar nerve
Cubital tunnel syndrome features?
initially intermittent tingling in the 4th and 5th finger
may be worse when the elbow is resting on a firm surface or flexed for extended periods
later numbness in the 4th and 5th finger with associated weakness
initially intermittent tingling in the 4th and 5th finger
may be worse when the elbow is resting on a firm surface or flexed for extended periods
later numbness in the 4th and 5th finger with associated weakness
cubital tunnel syndrome (ulnar nerve compression)
Olecranon bursitis summary?
Swelling over the posterior aspect of the elbow. There may be associated pain, warmth and erythema. It typically affects middle-aged male patients.
Swelling over the posterior aspect of the elbow. There may be associated pain, warmth and erythema. It typically affects middle-aged male patients.
Olecranon bursitis
Olecranon bursa?
verlying the olecranon process of the elbow beneath the skin. It reduces friction on movement between the skin, tendons, ligaments, and bone, and allows them to glide smoothly over one another.
When does bursitis occur?
when the bursa is irritated and inflamed and is generally classified as:
Non-septic (most common) — sterile inflammation resulting from various causes including trauma or overuse.
Septic — infection resulting from seeding of the bursal sac with micro-organisms, usually bacteria.
Who is olecranon bursitis more common in?
Young or middle-aged men.
People in jobs which involve risk of regular elbow trauma or pressure on the bursa.
For example gardeners and mechanics.
Athletes who play sports which involve repetitive overhead throwing or elbow flexion and extension.
Mx of olecranon bursitis?
conservative measures (such as rest, compression bandaging, avoidance of trauma to the elbows, and analgesia) until symptoms improve.
most resolve without complications; however, recurrent episodes may occur especially after recurrent minor trauma.
CP of olecranon bursitis?
- swelling over the elbow that appears over several hours to several days, may be tender or warm (but may be painless), and is fluctuant.
- Movement at the elbow joint is painless except at full flexion when the swollen bursa is compressed.
- Hx of preceding trauma or bursal disease.
- local skin abrasion.
Non-septic bursitis Mx?
reassurance that most people will respond to conservative treatment.
Considering aspiration, particularly if the effusion is large.
Considering corticosteroid injection into the bursa.
Referral if there is no response to available treatments in primary care after 2 months.
Septic bursitis Mx?
Aspiration and Tx empirically with Abx until culture results are known.
Urgent referral or specialist advice sought if there is no response, or an inadequate response to an antibiotic in septic bursitis, or complications are suspected.
Considering repeated aspiration if swelling, tenderness, and erythema recur.
Mx any associated conditions, such as gout, rheumatoid arthritis, or cellulitis.
Admission to hospital with bursitis?
if…
suspected septic joint (which presents with a limited range of movement of the elbow joint, unlike septic bursitis).
Septic bursitis and severe infection or systemic toxicity.
A pointing abscess requiring incision and drainage, if the expertise to perform this procedure is not available.
Extensive cellulitis.
Recurrent septic bursitis?
urgent referral
or consider referral in non-septic bursitis (in whom septic bursitis has been excluded) does not respond after 2 months of conservative measures
Lateral epicondylitis (tennis elbow)?
typically follows unaccustomed activity such as house painting or playing tennis (‘tennis elbow’). It is most common in people aged 45-55 years and typically affects the dominant arm.
Pain in Lateral epicondylitis (tennis elbow)?
pain and tenderness localised to the lateral epicondyle
pain worse on wrist extension against resistance with the elbow extended or supination of the forearm with the elbow extended
Lateral epicondylitis (tennis elbow) episodes?
episodes typically last between 6 months and 2 years. Patients tend to have acute pain for 6-12 weeks
Mx options for Lateral epicondylitis (tennis elbow)?
advice on avoiding muscle overload for 6w but maintain activity
heat and ice
simple analgesia
consider orthosis eg. forearm strap
steroid injection if severe but only short term relief
physiotherapy
if uncertain, refractory pain, severe impairment or persist 6-12m then refer to ortho surgeon
Definition of Lateral epicondylitis (tennis elbow)?
tendinosis (chronic symptomatic degeneration of the tendon) that affects the common attachment of the tendons of the extensor muscles of the forearm to the lateral epicondyle of the humerus.
Pt with Lateral epicondylitis (tennis elbow) may describe what?
pain around lateral epicondyle with radiation down extensor aspect of forearm
difficulty with common activities= raising cup, shaking hands, shaving, lifting bags
exacerbated by XS and repetitive use of extensor muscles of forearm eg. gripping and repetitive wrist movements; occupational activities eg. vibrating tools, typing, playing piano, tennis, construction work
What is Lateral epicondylitis (tennis elbow) also known as?
lateral elbow pain, ‘rowing elbow’, tendonitis of the common extensor origin, and peri-tendinitis of the elbow.
Lateral epicondylitis (tennis elbow) pathophysiology?
Occurs after minor or unrecognized trauma of the forearm extensor muscles.
Repetitive overuse causes micro-tears near the origin of the common extensor tendon at the lateral epicondyle of the humerus, which initiates a degenerative process.
Examination findings in Lateral epicondylitis (tennis elbow)?
Localized point tenderness on palpation over and/or distal to the lateral epicondyle and along the common extensor tendon.
Pain on resisted middle finger extension.
Pain on resisted wrist extension.
Reduced grip strength due to pain.
Preserved full range of active and passive movement at the elbow and wrist joints.
Ottawa ankle rules state that x-rays are only needed to assess for ankle fracture if…
pain in the malleolar zone and:
1. Inability to weight bear for 4 steps
2. Tenderness over the distal tibia
3. Bone tenderness over the distal fibula
Weber classification for ankle fracture?
Related to the level of the fibular fracture.
Type A is below the syndesmosis
Type B fractures start at the level of the tibial plafond and may extend proximally to involve the syndesmosis
Type C is above the syndesmosis which may itself be damaged
Weber classification for ankle fracture- subtype?
Maisonneuve fracture may occur with spiral fibular fracture that leads to disruption of the syndesmosis with widening of the ankle joint, surgery is required.
Mx of ankle injuries?
All ankle fractures should be promptly reduced to remove pressure on the overlying skin and subsequent necrosis
Young patients, with unstable, high velocity or proximal injuries will usually require surgical repair. Often using a compression plate.
Elderly patients, even with potentially unstable injuries usually fare better with attempts at conservative management as their thin bone does not hold metalwork well.
Discitis?
infection of the intervertebral disc space; can lead to serious Cx eg. sepsis or epidural abscess
Features of discitis?
- back pain
- general= pyrexia, rigors, sepsis
- neuro= eg. changes in lower limb neurology, if epidural abscess develops
Causes of discitis?
- bacterial= staph aureus most common cause of discitis
- viral
- TB
- aseptic
Diagnosis of discitis?
MRI
- CT guided biopsy may be needed to guide antimicrobial Tx
Tx for discitis?
6-8w IV Abx
Choice of antibiotic is dependent on a variety of factors. The most important factor is to identify the organism with a positive culture (e.g. blood culture, or CT-guided biopsy)
the patient should be assessed for endocarditis e.g. with transthoracic echo or transesophageal echo. Discitis is usually due to haematogenous seeding of the vertebrae implying that the patient has had a bacteraemia and seeding could have occurred elsewhere
Cx of discitis?
sepsis
epidural abscess
Red flags for lower back pain?
age < 20 years or > 50 years
history of previous malignancy
night pain
history of trauma
systemically unwell e.g. weight loss, fever
name 4 specific causes of lower back pain?
- facet joint
- spinal stenosis
- ankylosing spondylitis
- PAD
Causes of lower back pain (LBP): facet joint?
May be acute or chronic
Pain worse in the morning and on standing
On examination there may be pain over the facets. The pain is typically worse on extension of the back
Causes of lower back pain (LBP): spinal stenosis?
Usually gradual onset
Unilateral or bilateral leg pain (with or without back pain), numbness, and weakness which is worse on walking. Resolves when sits down. Pain may be described as ‘aching’, ‘crawling’.
Relieved by sitting down, leaning forwards and crouching down
Clinical examination is often normal
Requires MRI to confirm diagnosis
Causes of lower back pain (LBP): ankylosing spondylitis?
Typically a young man who presents with lower back pain and stiffness
Stiffness is usually worse in morning and improves with activity
Peripheral arthritis (25%, more common if female)
Causes of lower back pain (LBP): peripheral arterial disease?
Pain on walking, relieved by rest
Absent or weak foot pulses and other signs of limb ischaemia
Past history may include smoking and other vascular diseases
What does low back pain refer to?
pain in the lumbosacral area, from the 12th ribs to the iliac crest, and sometimes the buttocks and gluteal folds.
Non-specific low back pain?
pain not attributable to an underlying cause. It is also referred to as ‘mechanical’, ‘musculoskeletal’, or ‘simple’ low back pain
90-95% cases in primary care
Acute vs chronic low back pain?
A= <3m
C= 3m+
RFs for low back pain?
obesity, physical inactivity, heavy lifting, and stress or depression.
prognosis of low back pain?
self-limiting normally and usually resolves within few w
Cx of low back pain?
impact on daily activities including work, study, leisures, and sleep; depression and anxiety; increased risk of falls and chronic pain.
Assessment for pt with low back pain?
onset, type, site, and pattern of pain; any pain radiation; duration of symptoms; associated symptoms and red flags; impact on daily functioning; drug treatments.
Examine: gait, posture, spine for localized tenderness and range of movement; red flags; and neuro examination.
Using a risk stratification screening tool to assess risk factors for a prolonged or complex recovery if non-specific low back pain is suspected.
Mx of non-specific low back pain?
keep active, normal activities when able, local heat for symptom relief
NSAIDs; 2nd line- short term codeine +/- para
exercise programmes
occy health assessment
review if persist or worsen after 3-4w
?refer to chronic pain
Lumbar spinal stenosis?
central canal is narrowed by tumour, disc prolapse or other similar degenrative changes
Lumbar spinal stenosis presentation?
combination of back pain, neuropathic pain and symptoms mimicking claudication
Sitting is better than standing and patients may find it easier to walk uphill
How to differentiate lumbar spinal stenosis from true claudication?
Sitting is better than standing and patients may find it easier to walk uphill rather than downhill. Makes lumbar spinal stenosis a likely underlying diagnosis, the absence of such symptoms makes it far less likely.
Pathophysiology of lumbar spinal stenosis?
degenerative disease commonest cause
Degeneration begins in intervertebral disk where biochemical changes (cell death and loss of proteoglycan and water content) lead to progressive disk bulging and collapse.
Leads to increased stress transfer to the posterior facet joints, which accelerates cartilaginous degeneration, hypertrophy, and osteophyte formation; this is associated with thickening and distortion of the ligamentum flavum.
The combination of the ventral disk bulging, osteophyte formation at the dorsal facet, and ligamentum flavum hyptertrophy combine to circumferentially narrow the spinal canal and the space available for the neural elements.
The compression of the nerve roots of the cauda equina leads to the characteristic clinical signs and symptoms of lumbar spinal stenosis.
Diagnosis of lumbar spinal stenosis?
MRI= canal narrowing
Historically a bicycle test was used as true vascular claudicants could not complete the test.
Tx for lumbar spinal stenosis?
laminectomy
Paget’s disease of the bone?
disease of increased but uncontrolled bone turnover. It is thought to be primarily a disorder of osteoclasts, with excessive osteoclastic resorption followed by increased osteoblastic activity.
How common is Paget’s?
5% UK but only 1 in 20 have symptoms
What is most commonly affected in Paget’s?
skull, spine/pelvis, and long bones of the lower extremities
Paget’s predisposing factors?
increasing age
male sex
northern latitude
family history
Clinical features of Paget’s?
- only 5% symptomatic
- bone pain (e.g. pelvis, lumbar spine, femur)
-classical, untreated features: bowing of tibia, bossing of skull
- typically: older male with bone pain and an isolated raised ALP
older male with bone pain and an isolated raised ALP
?Paget’s
Bowing of tibia and bossing of the skull?
classic untreated features of Paget’s
Ix for Paget’s?
- Bloods= raised ALP, normal Ca and phosphate; hypercalcaemia may occur with prolonged immobilisation
- other markers of bone turnover= PINP, CTx, NTx, urinary hydroxyproline
- x-rays
- bone scintigraphy
Markers of bone turnover results in Pagets?
raised alkaline phosphatase (ALP)
calcium and phosphate are typically normal.
Hypercalcaemia may occasionally occur with prolonged immobilisation
other markers of bone turnover includeL
procollagen type I N-terminal propeptide (PINP)
serum C-telopeptide (CTx)
urinary N-telopeptide (NTx)
urinary hydroxyproline
X-ray findings in Paget’s?
osteolysis in early disease → mixed lytic/sclerotic lesions later
skull x-ray: thickened vault, osteoporosis circumscripta
Bone scintigraphy in Paget’s?
increased uptake is seen focally at the sites of active bone lesions
Indications for Tx in Paget’s?
bone pain
skull or long bone deformity
fracture
periarticular Paget’s
Mx of Paget’s?
if indicated= bisphosphonate (oral risedronate or IV zoledronate)
Cx of Paget’s?
deafness (cranial nerve entrapment)
bone sarcoma (1% if affected for > 10 years)
fractures
skull thickening
high-output cardiac failure
Polyarthritis?
inflammation of 5+joints simultaneously, within the first 6 weeks of symptom onset.
Features of polyarthritis?
pain, swelling, and stiffness in multiple joints
the pattern of joint involvement may be symmetrical, as seen in rheumatoid arthritis, or asymmetrical, as noted in psoriatic arthritis
systemic symptoms= fever, weight loss, and fatigue may also be present, reflecting the underlying systemic inflammatory process.
Differential diagnosis of polyarthritis?
inflammatory arthritis= RA,
psoriatic arthritis, SLE, seronegative spondyloarthropathies
infective= viral : EBV, HIV, hepatitis, mumps, rubella; TB; disseminated gonococcal infection
pseudogout
Henoch-Schonlein purpura
sarcoidosis
Psoriatic arthropathy (arthritis)?
inflammatory arthritis associated with psoriasis and is classed as one of the seronegative spondyloarthropathies
Link between psoriasis and arthritis in psoriatic arthritis?
often precedes the development of skin lesions
Around 10-20% of patients with skin lesions develop an arthropathy with males and females being equally affected.
Presentation patterns in psoriatic arthritis?
symmetric polyarthritis= very similar to rheumatoid arthritis; most common type
asymmetrical oligoarthritis: typically affects hands and feet (20-30%)
sacroiliitis
DIP joint disease (10%)
arthritis mutilans (severe deformity fingers/hand, ‘telescoping fingers’)
Signs in psoriatic arthritis other than the disease patterns?
psoriatic skin lesions
periarticular disease - tenosynovitis and soft tissue inflammation resulting in:
- enthesitis: inflammation at the site of tendon and ligament insertion e.g. Achilles tendonitis, plantar fascitis
- tenosynovitis: typically of the flexor tendons of the hands
- dactylitis: diffuse swelling of a finger or toe
Nail changes
Nail changes in psoriatic arthritis?
pitting and onycholysis
Ix in psoriatic arthritis?
x-ray= ‘penicl-in-cup’ appearance; periostitis; often unusual combination of coexistence of erosive changes and new bone formation
Mx of psoriatic arthritis?
- Mx by rheumatology
Tx similar to RA but:
- mild= NSAID not DMARD
- moderate/severe= methotrexate
- use of monoclonal antibodies such as ustekinumab (targets both IL-12 and IL-23) and secukinumab (targets IL-17)
- apremilast: phosphodiesterase type-4 (PDE4) inhibitor
better prognosis than RA
apremilast: phosphodiesterase type-4 (PDE4) inhibitor MOA in psoriatic arthritis?
→ suppression of pro-inflammatory mediator synthesis
Causes of limping child?
1) transient synovitis
2) septic arthritis/osteomyelitis
3) Juvenile idiopathic arthritis
4) trauma
5) developmental dysplasia of hip
6) perthes disease
7) slipped upper femoral epiphysis
Cervical spondylosis?
degenerative condition affecting the cervical spine, essentially osteoarthritis of the cervical vertebral bodies.
If spinal canal is narrowed due to cervical sponylosis then that can happen?
C vertebral bodies can press on spinal cord resulting in neuro dysfunction
Link between cervical spondylosis and cervical spondylitic myelopathy?
myelopathy occurs in 5-10% pts with C spondylosis
Features of cervical spondylitic myelopathy?
a variety of motor weakness, sensory loss and
bladder/bowel dysfunction may be seen
neck pain
wide-based, ataxic or spastic gait
UMN weakness in the lower legs - increased reflexes, increased tone and upgoing plantars
bladder dysfunction e.g. urgency, retention
Definition of cervical spondylosis?
degenerative condition affecting the cervical spine, particularly the intervertebral discs, vertebral bodies, and facet joints.
Causes of cervical spondylosis?
primarily an age-related process, often referred to as ‘cervical osteoarthritis,’ and is characterised by the progressive deterioration of the spinal structures in the neck region.
Is cervical spondylosis common?
common, esp in >50yrs
by 60yrs radiographic evidence is present in >85% of individuals, although many remain asymptomatic.
4 stages of the pathogenesis of cervical spondylosis (sequence of degenerative changes)?
1) intervertebral disc degeneration
2) osteophyte formation
3) facet joint arthropathy
4) ligamentous hypertrophy
4 stages of the pathogenesis of cervical spondylosis (sequence of degenerative changes): 1) intervertebral disc degeneration?
process begins with the dehydration and shrinkage of the nucleus pulposus within the intervertebral discs, leading to reduced disc height and loss of elasticity.
4 stages of the pathogenesis of cervical spondylosis (sequence of degenerative changes): 2) osteophyte formation?
In response to disc degeneration, the body attempts to stabilise the spine by forming osteophytes, or bone spurs, at the margins of the vertebral bodies and facet joints. These osteophytes can encroach upon the spinal canal and intervertebral foramina.
4 stages of the pathogenesis of cervical spondylosis (sequence of degenerative changes): 3) facet joint arthropathy?
Degenerative changes in the facet joints contribute to instability, inflammation, and further osteophyte formation. This can result in nerve root compression (radiculopathy) or, less commonly, spinal cord compression (myelopathy).
4 stages of the pathogenesis of cervical spondylosis (sequence of degenerative changes): 4) ligamentous hypertrophy?
The ligamentum flavum and other supporting ligaments may thicken and lose elasticity, contributing to spinal canal stenosis and potential neurological complications.
Clinical features of cervical spondylosis?
- neck pain= chronic, stiffness, limited ROM, may radiate to shoulder & upper back
- radiculopathy= compression C nerve roots- radicular pain, paraesthesia, weakness in upper limbs (follows dermatomal pattern)
- myelopathy= severe manifestation due to spinal cord compression; clumisness in hands, gait disturbance, limb weakness, bowel or bladder dysfunction in advanced
- headaches= occipital due to irritation of C nerve roots or muscles in upper C region
Examination findings in cervical spondylosis?
reduced range of motion in the neck, tenderness over the cervical spine, and signs of radiculopathy or myelopathy (e.g., positive Spurling’s test, hyperreflexia, or gait instability).
Ix (imaging) for cervical spondylosis?
- plain x-rays of C spine= disc space narrowing, osteophytes and facet joint arthropathy
- MRI= GOLD; images soft tissue eg. spinal cord, nerve roots and intervertebral discs
- electrophyisological studies= nerve conduction and electromyography to differentiate C radiculopaty from peripheral neuropathy & other conditions
Mx for cervical spondylosis can be what?
conservative or interventional procedures
Mx for cervical spondylosis: conservative?
- NSAIDs
- physio= improve neck strength, postural training
- cervical collar= temp in acute flares but long term use discouraged due to risk of muscle weakness
Mx for cervical spondylosis: interventional procedures?
- cervical epidural steroid injections= if radicular symptoms, temp relief by reducing inflam around affected nerve root
- facet joint injections or radiofrequency ablation= pts with chronic facet-mediated pain
Radiculopathy
neurological state in which conduction is limited or blocked along a spinal nerve or its roots — it is differentiated from radicular pain, although they commonly occur together.
Radicular pain?
usually caused by compression of the nerve root due to cervical disc herniation or degenerative spondylotic changes, but radicular symptoms can also occur without evident compression (for example, due to inflammation of the nerve).
Cervical radiculopathy?
pain and weakness and/or numbness in one or both of the upper extremities, which corresponds to the dermatome of the involved cervical nerve root.
- neck pain secondary to compression or irritation of nerve roots in C spine
- pain may radiate to shoulders, upper back and chest
The most common causes of cervical radiculopathy are
degenerative changes, including cervical disc herniation and spondylosis.
Prognosis of cervical radiculopathy?
most will improve regardless of Tx
88% of people improve within four weeks with non-operative management.
Tests to identify cervical radiculopathy?
The Spurling test.
Arm squeeze test.
Axial traction — a combination of a positive Spurling’s test, axial traction test, and arm squeeze test increases the likelihood of cervical radiculopathy.
Upper limb neurodynamic tests — a combination of four neurodynamic tests and an arm squeeze test can rule out cervical radiculopathy.
Ix for cervical radiculopathy?
not normally needed, usually clinical
For people who have neck pain for less than 4–6 weeks and no objective neurological signs, management should include:
Providing reassurance, information, and advice.
Offering oral analgesia to relieve symptoms.
Considering offering amitriptyline, duloxetine, pregabalin, or gabapentin.
Considering a referral for physiotherapy.
People with cervical radiculopathy that has been present for 4–6 weeks or more, or objective neurological signs?
refer for MRI and for invasive procedures to be considered. These may include interlaminar cervical epidural injections, transforaminal injections, or spinal surgery.
Cervical radiculopathy: Spurling test?
flex the neck laterally, rotate and then press on top of the person’s head. The test is positive if this pressure causes the typical radicular arm pain.
Note: This test should not be performed in people with rheumatoid arthritis, cancer, infection, or possible neck injury.
Cervical radiculopathy: arm squeeze test?
squeeze the middle third of the upper arm with simultaneous thumb and fingers compression (the thumb from posterior on the triceps muscle and the fingers from anterior on the biceps muscle). The test is positive when the pain score (on a 0-10 visual analogue scale) is 3 points or higher during pressure on the middle third of the upper arm compared with two other areas.
How are fractures classified?
based on…
1) bone alignment
2) fracture line
3) cause
4) bone location
5) stability
6) special types
7) pt age
8) special patterns
Types of fracture: based on bone alignment?
- closed (simple) fracture
- open (compound fracture)
Types of fracture: based on bone alignment= closed (simple) fracture?
bone breaks but does not pierce skin
Types of fracture: based on bone alignment= open (compound) fracture?
bone breaks and pierces skin, increases risk of infection
Types of fracture: based on fracture line?
- transverse fracture
- oblique
- spiral
- longitudinal
- comminuted
- segmental
- greenstick
Types of fracture: based on fracture line= transverse fracture?
straight horizontal break across the bone
Types of fracture: based on fracture line= oblique fracture?
angled break across bone
Types of fracture: based on fracture line= spiral fracture?
twisting break resembling a spiral, often caused by rotational force
Types of fracture: based on fracture line= longitudinal fracture?
break that runs along the bone’s length
Types of fracture: based on fracture line= comminuted fracture?
bone shatters into 3 of more fragments
Types of fracture: based on fracture line= segmental fracture?
2 fractures create an isolated segment of bone
Types of fracture: based on fracture line= greenstick fracture?
incomplete break in which one side of the bone bends, common in children
Types of fracture: based on cause?
- traumatic
- pathologic
- stress
Types of fracture: based on cause= traumatic fracture?
caused by direct trauma or force
Types of fracture: based on cause= pathologic fracture?
occurs in weakend bone due to disease eg. tumours or osteoporosis
Types of fracture: based on cause= stress fracture?
small hairline crack caused by repetitive stress or overuse
Types of fracture: based on bone location?
intra-articular
extra-articular
epiphyseal
diaphyseal
metaphyseal
Types of fracture: based on bone location= intra-articular fracture?
break extends into a joint surface
Types of fracture: based on bone location= extra-articular fracture?
break does not involve a joint surface
Types of fracture: based on bone location= epiphyseal fracture?
break at the growth plate in children
Types of fracture: based on bone location= diaphyseal fracture?
break in shaft of a long bone
Types of fracture: based on bone location= metaphyseal fracture?
break in widened part of the bone near the joint
Types of fracture: based on stability?
stable
unstable
Types of fracture: based on stability= stable fracture?
broken ends of the bone are aligned and minimally displaced
Types of fracture: based on stability= unstable fracture?
broken ends are misaligned or move easily
Types of fracture: special types?
- impacted
- compression
- avulsion
- hairline
- buckle (torus)
Types of fracture: special types= impacted fracture?
broken ends of the bone are driven into eachother
Types of fracture: special types= compression fracture?
bone collapses, often seen in vertebrae
Types of fracture: special types= avulsion fracture?
a fragment of bone is pulled away by a tendon or ligament
Types of fracture: special types= hairline fracture?
very thin crack in bone
Types of fracture: special types= buckle (torus) fracture?
an incomplete fracture where one side of the bone buckles under pressure, common in children
Types of fracture: based on pt age?
paediatric
adult
Types of fracture: based on pt age= paediatric fractures?
greenstick, buckle and epiphyseal fractures more common in children due to softer bones
Types of fracture: based on pt age= adult fractures?
complete and comminuted fractures are more typical in adults due to denser brittle bones
Types of fracture: special types?
Colles’
Smiths’
Pott’s
Le Fort
Types of fracture: special types= Colles’ fracture?
distal radius fracture, typically from falling on outstretched hand
Types of fracture: special types= Smith’s fracture?
distal radius fracture with the broken segment displaced toward the palm
Types of fracture: special types= Pott’s fracture?
fracture affecting one or both malleoli (ankle)
Types of fracture: special types= Le Fort fractures?
fractures of the maxilla (face), classified into 3 types based on severity
Mx of stable vs unstable/open fractures?
stable= may only need immobilisation
unstable or open= often need surgery
epiphyseal vs diaphyseal vs metaphyseal
The epiphysis is the rounded end of a long bone that includes the growth plate (in children) and contributes to joint formation; fractures here can affect growth.
The diaphysis is the long, tubular shaft made of dense compact bone and houses the marrow, commonly fractured by trauma.
The metaphysis is the flared region between the diaphysis and epiphysis, consisting of spongy bone and absorbing stress; fractures here are common in children and adults.
Acetabular labral tear?
may occur following trauma (most commonly in younger adults) or as a result of degenerative change (typically in older adults).
Acetabular labral tear features?
hip/groin pain
snapping sensation around hip
there may occasionally be the sensation of locking
Acromioclavicular joint injury?
Injury to the AC joint is relatively common and typically occurs during collision sports such as rugby following a fall on to the shoulder or a FOOSH (falls on outstretched hand).
How are Acromioclavicular joint injuries graded?
graded I to VI depending on the degree of separation.
Grade I and II injuries are very common and are typically managed conservatively including resting the joint using a sling.
Grade IV, V and VI are rare and require surgical intervention.
Mx of grade III injuries is a matter of debate and often depends on individual circumstances.
Avascular necrosis?
death of bone tissue secondary to loss of the blood supply. This leads to bone destruction and loss of joint function.
Avascular necrosis most commonly affects what?
the epiphysis of long bones such as the femur
Causes of avascular necrosis of the hip?
long term steroid use
chemo
alcohol XS
trauma
Features of avascular necrosis of the hip?
initially asymptomatic
pain in affected joint
Ix for avascular necrosis of the hip?
MRI Ix of choice
plain x-ray may be normal initially:
- osteopenia and microfractures may be seen early on
- collapse of the articular surface may result in the crescent sign
Mx for avascular necrosis of the hip?
May need joint replacement
Baker’s cysts (a popliteal cyst)?
not true cysts but rather a distension of the gastrocnemius-semimembranosus bursa. They may be primary or secondary
Primary vs secondary Baker’s cysts (a popliteal cyst)?
Primary: no underlying pathology, typically seen in children
Secondary: underlying condition such as osteoarthritis, typically seen in adults
CP of Baker’s cysts (a popliteal cyst)?
swellings in the popliteal fossa behind the knee
Rupture of Baker’s cysts (a popliteal cyst)?
may occur resulting in similar symptoms to a deep vein thrombosis, i.e. pain, redness and swelling in the calf. However, the majority of ruptures are asymptomatic.
Mx of Baker’s cysts (a popliteal cyst)?
children= usually resolve and don’t require Tx
adults= treat underlying cause
Biceps muscle tendons?
has 2 tendons:
- long tendon attaches to glenoid
- short attaches to coracoid proceps
It inserts distally via another tendon onto the radial tuberosity.
Biceps rupture?
biceps tendon rupture is when one of the tendons (long or short) separates from its attachment site or is torn across it’s full width. This most frequently occurs at the long tendon (90%), but rarely can occur in the distal tendon (10%).
Epidemiology of biceps tendon rupture?
M>F
Proximal tendon rupture= >60yrs, long tendon, most common (90%)
distal= less common, mean age is 40; mainly men
RFs for biceps rupture?
Heavy overhead activities
Shoulder overuse or underlying shoulder injuries which may stress the biceps tendon
Smoking
Corticosteroids; these weaken tendons
Biceps rupture: mechanism of injury?
Proximal biceps long tendon ruptures: typically occurs when the biceps are lengthened and contracted and a load is applied. e.g. the descent phase of a pull-up.
Distal biceps tendon ruptures: Usually when a flexed elbow is suddenly and forcefully extended whilst the biceps muscle is contracted. already
CP of biceps rupture?
sudden pop or tear at shoulder (long tendon) or anticubital fossa (distal tendon) followed by pain, bruising, swelling
Popeye deformity= buscle bulk results in bulge in middle upper arm
distal tendon rupture= reverse popeye deformity
weakness in shoulder & elbow follows eg. difficulty supination
may have chronic shoulder pain prior to rupture then notice improvement in pain
Popeye deformity
rupture of proximal tendon of biceps muscle
Ix for biceps rupture?
- palpate
- biceps squeeze test= if intact then squeeze will cause supination
- 1st Ix= MSK USS
- long head biceps rupture= conservative Mx
- distal biceps= then do urgent MRI as requires surgical intervention
Blood results in Pagets?
ALP high
others normal
Blood results in osteoporosis?
ALP normal
Ca ect all normal
Blood results in secondary bone tumours?
high Ca
high ALP
Buckle (torus) fractures?
incomplete fractures of the shaft of a long bone that is characterised by bulging of the cortex. They typically occur in children aged 5-10 years.
Mx of Buckle (torus) fractures?
typically self-limiting they do not usually require operative intervention and can sometimes be managed with splinting and immobilisation rather than a cast.
Cauda equina syndrome (CES)?
rare
lumbosacral nerve roots that extend below the spinal cord are compressed
What to always consider in pts who present with new/worsening lower back pain and why?
cauda equina
late diagnosis may lead to permanent nerve damage resulting in long term leg weakness and urinary/bowel incontinence
Causes of cauda equina syndrome?
most common= central disc prolapse
this typically occurs at L4/5 or L5/S1
- tumours: primary or metastatic
- infection: abscess, discitis
- trauma
- haematoma
Central disc prolapse causing cauda equina typically occurs at what spinal level?
L4/5 or L5/S1
Possible features of cauda equina (variety of presentations and not one symptom or sign that can diagnose or exclude CES)?
- low back pain
- bilateral sciatica
- reduced sensation/paraesthesia in perianal area
- decreased anal tone (check in pts with new onset back pain)
- uriniary dysfunction eg. reduced awareness of bladder filling, loss of urge to void; incontinence is late sign
Incontinence in cauda equina?
late sign and may indicate irreversible damage
Bilateral sciatica
think cauda equina as 50% present with this
Ix for cauda equina?
urgent MRI
Mx of cauda equina?
surgical decompression
Charcot joint?
(neuropathic joint)
a joint which has become badly disrupted and damaged secondary to a loss of sensation.
most commonly seen in diabetics or caused by neuropathy secondary to syphilis (tabes dorsalis)
Features of charcot joints?
- lot less painful than would be expected given the degree of joint disruption due to the sensory neuropathy
- swollen red and warm joint
- as progresses= affected joint becomes unstable -> abnormal movements and increased risk of fractures & dislocations
- progressive joint destruction can cause significant deformities
common deformities include a collapsed arch in the foot (commonly referred to as ‘rocker-bottom’ foot) or severe joint misalignment - secondary Cx such as skin ulceration and infection can occur due to repeated trauma and poor wound healing
Dupuytren’s contracture?
an abnormal thickening of the skin in the palm of the hand. The skin may develop into a hard lump. Over time, it can cause one or more fingers to curl (contract) or pull in toward the palm.
the ring finger and little finger are the fingers most commonly affected
Epidemiology of Dupuytren’s contacture?
5% prevalence
older male pts
60-70% FHx
Specific causes of Dupuytren’s contracture?
manual labour
phenytoin Tx
DM
alcoholic liver disease
trauma to hand
Mx of Dupuytren’s contracture?
consider surgical treatment of Dupuytren’s contracture when the metacarpophalangeal joints cannot be straightened and thus the hand cannot be placed flat on the table
Features of fat embolism?
Resp= early persistent tachycardia; tachypnoea, dyspnoea, hypoxia 72hrs following injury; pyrexia
Derm= red/browm impalpable petechial rash (25-50%); subconjunctival and oral haemorrhage/petechiae
CNS= confusion, agitation; Retinal haemorrhages and intra-arterial fat globules on fundoscopy
Fat embolism?
when one or more droplet-like particles of fat enter your bloodstream and block circulation through some of your blood vessels.
caused following trauma eg. long bone and pelvic fractures
Ix for fat embolism?
imaging may be normal
fat emboli tend to lodge distally so CTPA may not show vascular occlusion; may see ground glass appearance at the periphery
Fat embolism Mx?
Prompt fixation of long bone fractures
Some debate regarding benefit Vs. risk of medullary reaming in femoral shaft/ tibial fractures in terms of increasing risk (probably does not).
DVT prophylaxis
General supportive care
Fracture diagnosis?
clinical + x-rays of proximal and distal joints= assess for changes in length of the bone, the angulation of the distal bone, rotational effects, presence of material such as glass
Oblique fracture?
fracture lies obliquely to long axis of bone
Comminuted fracture?
> 2 fragments
Segmental fracture?
more than 1 fracture along a bone
Transverse fracture?
perpendicular to long axis of bone
Spiral fracture?
severe oblique fracture with rotation along long axis of bone
Gustilo and Anderson classification system for open fractures?
1 Low energy wound <1cm
2 Greater than 1cm wound with moderate soft tissue damage
3 High energy wound > 1cm with extensive soft tissue damage
3 A (sub group of 3) Adequate soft tissue coverage
3 B (sub group of 3) Inadequate soft tissue coverage
3 C (sub group of 3) Associated arterial injury
Key points in the Mx of fractures?
Immobilise the fracture including the proximal and distal joints
Carefully monitor and document neurovascular status, particularly following reduction and immobilisation
Manage infection including tetanus prophylaxis
IV broad spectrum antibiotics for open injuries
All open fractures should be thoroughly debrided ( and internal fixation devices avoided or used with extreme caution)
Open fractures constitute an emergency and should be debrided and lavaged within 6 hours of injury
Ganglion?
‘cyst’ arising from a joint or tendon sheath. They are most commonly seen around the dorsal aspect of the wrist
W>M
a firm and well-circumscribed mass that transilluminates
ganglion
Mx of ganglion?
often disappear spontaneously after several months
surgical excision is indicated for cysts associated with severe symptoms or neurovascular manifestations
Osler’s nodes?
Osler’s nodes are painful, red, raised lesions found on the hands and feet. They are the result of the deposition of immune complexes.
Bouchard’s nodes?
Hard, bony outgrowths or gelatinous cysts on the proximal interphalangeal joints (the middle joints of fingers or toes.) They are a sign of osteoarthritis, and are caused by formation of calcific spurs of the articular cartilage.
Herberden’s nodes?
Typically develop in middle age, beginning either with a chronic swelling of the affected joints or the sudden painful onset of redness, numbness, and loss of manual dexterity. This initial inflammation and pain eventually subsides, and the patient is left with a permanent bony outgrowth that often skews the fingertip sideways.
Summary of ganglion?
Swelling in association with a tendon sheath commonly near a joint. They are common lesions in the wrist and hand. Usually they are asymptomatic and cause little in the way of functional compromise. They are fluid filled although the fluid is similar to synovial fluid it is slightly more viscous. When the cysts are troublesome they may be excised.
name 4 types of hand lumps?
- osler’s nodes
- bouchard’s nodea
- heberden’s nodes
- ganglion
Hip dislocation?
extremely painful
mostly caused by direct trauma eg. fall from height or RTA
may be associated with other fractures and life-threatening injuries due to the large force required to cause
What is it important to do if ?hip dislocation?
prompt diagnosis and Mx to reduce morbidity
Types of hip dislocation?
Posterior dislocation: (90%) The affected leg is shortened, adducted, and internally rotated.
Anterior dislocation: The affected leg is usually abducted and externally
rotated. No leg shortening.
Central dislocation
Mx of hip dislocation?
ABCDE approach.
Analgesia
A reduction under general anaesthetic within 4 hours to reduce the risk of avascular necrosis.
Long-term management: Physiotherapy to strengthen the surrounding muscles.
Cx of hip dislocation?
Sciatic or femoral nerve injury
Avascular necrosis
Osteoarthritis: more common in older patients.
Recurrent dislocation: due to damage of supporting ligaments
Prognosis of hip dislocation?
It takes about 2 to 3 months for the hip to heal after a traumatic dislocation
the prognosis is best when the hip is reduced less than 12 hours post-injury and when there is less damage to the joint.
iliopsoas abscess?
collection of pus in iliopsoas compartment (iliopsoas and iliacus).
Causes of primary iliopsoas abscess?
Haematogenous spread of bacteria
Staphylococcus aureus: most common
Causes of secondary iliopsoas abscess?
Crohn’s (commonest cause in this category)
Diverticulitis, colorectal cancer
UTI, GU cancers
Vertebral osteomyelitis
Femoral catheter, lithotripsy
Endocarditis
intravenous drug use
Mortality rate in primary iliopsoas abscess vs secondary?
secondary 20%
primary 2.4%
Features of iliopsoas abscess?
fever
back/flank pain
limp
weight loss
Clinical exam of iliopsoas abscess?
Patient in the supine position with the knee flexed and the hip mildly externally rotated
Specific tests to diagnose iliopsoas inflammation:
- Place hand proximal to the patient’s ipsilateral knee and ask patient to lift thigh against your hand. This will cause pain due to contraction of the psoas muscle.
- Lie the patient on the normal side and hyperextend the affected hip. This should elicit pain as the psoas muscle is stretched.
Ix for iliopsoas abscess?
CT abdo
Mx of iliopsoas abscess?
Antibiotics
Percutaneous drainage is the initial approach and successful in around 90% of cases
Surgery is indicated if:
1. Failure of percutaneous drainage
2. Presence of an another intra-abdominal pathology which requires surgery
What is commonly seen following a lateral blow to the knee?
Unhappy triad (damage to):
1) anterior cruciate ligament
2) medial collateral ligament
3) meniscus (lateral meniscus is more commonly injured)
What knee injury may result from twisting injuries and
Anterior drawer test and Lachman test may be positive if damaged
ACL
What knee injury may occur following dashboard injuries?
posterior cruciate ligament
What knee injury may commonly result from skiing and following valgus stress;
damage typically causes abnormal passive abduction of the knee
medial collateral ligament
Isolated injury to what structure in the knee is uncommon?
lateral collateral ligament
What knee injury may result from twisting injuries;
Locking and giving way are common symptoms?
menisci
Ruptured ACL?
Sport injury
Mechanism: high twisting force applied to a bent knee
Typically presents with: loud crack, pain and RAPID joint swelling (haemoarthrosis)
Poor healing
Management: intense physiotherapy or surgery
Ruptured PCL?
Mechanism: hyperextension injuries
Tibia lies back on the femur
Paradoxical anterior draw test
Rupture of medial collateral ligament?
Mechanism: leg forced into valgus via force outside the leg
Knee unstable when put into valgus position
Menisceal tear?
Rotational sporting injuries
Delayed knee swelling
Joint locking (Patient may develop skills to ‘unlock’ the knee
Recurrent episodes of pain and effusions are common, often following minor trauma
Chondromalacia patellae?
Teenage girls, following an injury to knee e.g. Dislocation patella
Typical history of pain on going downstairs or at rest
Tenderness, quadriceps wasting
Dislocation of the patella?
Most commonly occurs as a traumatic primary event, either through direct trauma or through severe contraction of quadriceps with knee stretched in valgus and external rotation
Genu valgum, tibial torsion and high riding patella are risk factors
Skyline x-ray views of patella are required, although displaced patella may be clinically obvious
An osteochondral fracture is present in 5%
The condition has a 20% recurrence rate
Fractured patella?
2 types:
i. Direct blow to patella causing undisplaced fragments
ii. Avulsion fracture
Tibial plateau fracture?
Occur in the elderly (or following significant trauma in young)
Mechanism: knee forced into valgus or varus, but the knee fractures before the ligaments rupture
Varus injury affects medial plateau and if valgus injury, lateral plateau depressed fracture occurs
Classified using the Schatzker system (see below)
Schatzker Classification system for tibial plateau fractures?
1) Vertical split of lateral condyle
2) Vertical split of the lateral condyle combined with an adjacent load bearing part of the condyle
3) Depression of the articular surface with intact condylar rim
4) Fragment of the medial tibial condyle
5) Fracture of both condyles
6) Combined condylar and subcondylar fractures
Schatzker Classification system for tibial plateau fractures: 1) Vertical split of lateral condyle?
Fracture through dense bone, usually in the young. It may be virtually undisplaced, or the condylar fragment may be pushed inferiorly and tilted
Schatzker Classification system for tibial plateau fractures: 2) Vertical split of the lateral condyle combined with an adjacent load bearing part of the condyle?
The wedge fragment (which may be of variable size), is displaced laterally; the joint is widened. Untreated, a valgus deformity may develop
Schatzker Classification system for tibial plateau fractures: 3) Depression of the articular surface with intact condylar rim?
The split does not extend to the edge of the plateau. Depressed fragments may be firmly embedded in subchondral bone, the joint is stable
Schatzker Classification system for tibial plateau fractures: 4) Fragment of the medial tibial condyle?
Two injuries are seen in this category; (1) a depressed fracture of osteoporotic bone in the elderly. (2) a high energy fracture resulting in a condylar split that runs from the intercondylar eminence to the medial cortex. Associated ligamentous injury may be severe
Schatzker Classification system for tibial plateau fractures: 5) Fracture of both condyles?
Both condyles fractured but the column of the metaphysis remains in continuity with the tibial shaft.
Schatzker Classification system for tibial plateau fractures: 6) Combined condylar and subcondylar fractures?
High energy fracture with marked comminution.
Features of meniscal tear?
pain worse on straightening the knee
knee may ‘give way’
displaced meniscal tears may cause knee locking
tenderness along the joint line
Thessaly’s test - weight bearing at 20 degrees of knee flexion, patient supported by doctor, postive if pain on twisting knee
Anterior draw test (test for ACL injury)?
the patient lies supine with the knee at 90 degrees
the examiner should place one hand behind the tibia and the other grasping the patient’s thigh. It is important that the examiner’s thumb be on the tibial tuberosity
the tibia is pulled forward to assess the amount of anterior motion of the tibia in comparison to the femur
an intact ACL should prevent forward translational movement
Lachman’s test (test for ACL injury)?
variant of anterior draw test, but the knee is at 20-30 degrees
evaluate the anterior translation of the tibia in relation to the femur and is considered a variant
more reliable than anterior draw test
Knee injurys in older pts: Infrapatellar bursitis
(Clergyman’s knee) vs Prepatellar bursitis
(Housemaid’s knee)?
Infrapatellar bursitis
(Clergyman’s knee)= associated with kneeling
Prepatellar bursitis
(Housemaid’s knee)= Associated with more upright kneeling
Leriche syndrome?
Atheromatous disease involving the iliac vessels. Blood flow to the pelvic viscera is compromised. Patients may present with buttock claudication and impotence (in this particular syndrome). Diagnostic work up will include angiography, where feasible, iliac occlusions are usually treated with endovascular angioplasty and stent insertion.
Femoral nerve= motor?
knee extension, thigh flexion
Femoral nerve= sensory?
anterior & medial aspect of thigh and lower leg
Femoral nerve= typical mechanism of injury?
hip and pelvic fractures
stab/gunshot wounds
Obturator nerve= motor?
thigh adduction
Obturator nerve= sensory?
medial thigh
Obturator nerve= typical mechanism of injury?
anterior hip dislocation
Lateral cutaneous nerve of thigh= motor?
none
Lateral cutaneous nerve of thigh= sensory?
lateral and posterior surfaces of thigh
Lateral cutaneous nerve of thigh= typical mechanism of injury?
Compression of the nerve near the ASIS → meralgia paraesthetica, a condition characterised by pain, tingling and numbness in the distribution of the lateral cutaneous nerve
Tibial nerve= motor?
foot plantarflexion and inversion
Tibial nerve= sensory?
sole of foot
Tibial nerve= mechanism of injury?
Not commonly injured as deep and well protected.
Popliteral lacerations, posterior knee dislocation
Common peroneal nerve= motor?
foot dorsiflexion and eversion
extensor hallucis longus
Common peroneal nerve= sensory?
Dorsum of the foot and the lower lateral part of the leg
Common peroneal nerve= mechanism of injury?
often occurs at neck of fibula
tightly applied lower limb plaster cast
injury causes foot drop
Injury to what nerve causes foot drop?
common peroneal nerve
Superior gluteal nerve= motor?
hip abduction
Superior gluteal nerve= sensory?
none
Superior gluteal nerve= mechanism of injury?
Misplaced intramuscular injection
Hip surgery
Pelvic fracture
Posterior hip dislocation
Injury results in a positive Trendelenburg sign
Injury to what nerve results in +ve Trendelenburg sign?
Superior gluteal nerve
Inferior gluteal nerve= motor?
hip extension and lateral rotation
Inferior gluteal nerve= sensory?
none
Inferior gluteal nerve= mechanism of injury?
Generally injured in association with the sciatic nerve
Injury results in difficulty rising from seated position. Can’t jump, can’t climb stairs
Injury to what nerve causes difficulty rising from seated position; can’t jump and can’t climb stairs?
inferior gluteal nerve
What muscles are in the anterior compartment of the lower limb?
tibialis anterior
extensor digitorum longus
peroneus tertius
extensor hallucis longus
What nerve is in the anterior compartment of the lower limb?
deep peroneal (aka fibular) nerve
Muscular compartments of the lower limb? (4)
- anterior
- peroneal
- superficial posterior
- deep posterior
Anterior compartment of lower limb muscles= Tibialis anterior:
- action?
- nerve?
dorsiflexes ankle joint, inverts foot
deep peroneal (aka fibular) nerve
Anterior compartment of lower limb muscles= extensor digitorum longus:
- action?
- nerve?
extends lateral four toes, dorsiflexes ankle joint
deep peroneal (aka fibular) nerve
Anterior compartment of lower limb muscles= peroneus tertius:
- action?
- nerve?
dorsiflexes ankle, everts foot
deep peroneal (aka fibular) nerve
Anterior compartment of lower limb muscles= extensor hallucis longus:
- action?
- nerve?
dorsiflexes ankle joint, extends big toe
deep peroneal (aka fibular) nerve
Muscles in the peroneal compartment of the lower limb?
peroneus longus
peroneus brevis
Nerve in the peroneal compartment of the lower limb?
superficial peroneal (aka fibular) nerve
Peroneal compartment of lower limb muscles= Peroneus longus:
- action?
- nerve?
everts foot, assists in plantar flexion
superficial peroneal (aka fibular) nerve
Peroneal compartment of lower limb muscles= Peroneus brevis:
- action?
- nerve?
plantar flexes the ankle joint
superficial peroneal (fibular) nerve
Muscles in the superficial posterior compartment of the lower limb?
Gastrocnemius
Soleus
Nerve in the superficial posterior compartment of the lower limb?
tibial nerve
2 main terminal branches of the sciatic nerve?
tibial nerve
fibular (peroneal) nerve
Superficial posterior compartment of lower limb muscles= Gastrocnemius:
- action?
- nerve?
plantar flexes the foot, may also flex the knee
tibial nerve
Superficial posterior compartment of lower limb muscles= Soleus:
- action?
- nerve?
plantar flexor
tibial nerve
Muscles in the deep posterior compartment of the lower limb?
flexor digitorum longus
flexor hallucis longus
tibialis posterior
Nerve in the deep posterior compartment in the lower limb?
tibial nerve
Deep posterior compartment of lower limb muscles= Flexor digitorum longus:
- action?
- nerve?
flexes the lateral 4 toes
tibial
Deep posterior compartment of lower limb muscles= Flexor hallucis longus:
- action?
- nerve?
flexes the great toe
tibial
Deep posterior compartment of lower limb muscles= Tibialis posterior:
- action?
- nerve?
plantar flexor, inverts the foot
tibial
Meralgia paraesthetica?
syndrome of paraesthesia or anaesthesia in distribution of lateral femoral cutaneous nerve (LFCN)
meros=high
algos=pain
Cause of Meralgia paraesthetica?
entrapment mononeuropathy of the LFCN, but can also be iatrogenic after a surgical procedure, or result from a neuroma. Although uncommon, meralgia paraesthetica is not rare and is hence probably underdiagnosed.
Anatomy in Meralgia paraesthetica syndrome?
The LFCN is primarily a sensory nerve, carrying no motor fibres.
It most commonly originates from the L2/3 segments.
After passing behind the psoas muscle, it runs beneath the iliac fascia as it crosses the surface of the iliac muscle and eventually exits through or under the lateral aspect of the inguinal ligament.
As the nerve curves medially and inferiorly around the anterior superior iliac spine (ASIS), it may be subject to repetitive trauma or pressure.
Compression of this nerve anywhere along its course can lead to the development of meralgia paraesthetica.
Epidemiology of meralgia paraesthetica?
30-40yrs
In some, both legs may be affected.
It is more common in men than women.
Occurs more commonly in those with diabetes than in the general population.
RFs for meralgia paraesthetica?
Obesity
Pregnancy
Tense ascites
Trauma
Iatrogenic, such as pelvic osteotomy, spinal surgeries, laparoscopic hernia repair and bariatric surgery. In some cases, may result from abduction splints used in the management of Perthe’s disease.
Various sports have been implicated, including gymnastics, football, bodybuilding and strenuous exercise.
Some cases are idiopathic.
Symptoms in meralgia paraesthetica?
Burning, tingling, coldness, or shooting pain
Numbness
Deep muscle ache
Symptoms are usually aggravated by standing, and relieved by sitting
They can be mild and resolve spontaneously or may severely restrict the patient for many years.
Signs in meralgia paraesthetica?
Symptoms may be reproduced by deep palpation just below the ASIS (pelvic compression) and also by extension of the hip.
There is altered sensation over the upper lateral aspect of the thigh.
There is no motor weakness.
Ix for meralgia paraesthetica?
pelvic compression test is highly sensitive, and often, can be diagnosed based on this test alone
Injection of the nerve with local anaesthetic will abolish the pain. Using ultrasound is effective both for diagnosis and guiding injection therapy in meralgia paraesthetica
Nerve conduction studies may be useful.
Mx of meralgia paraesthetica?
Physical therapy to strengthen the muscles of the legs and buttocks, and reduce injury to the hips.
Wearing less restrictive clothing.
Weight loss management.
Corticosteroid injection to reduce swelling.
Froment’s sign?
Assess for ulnar nerve palsy
Adductor pollicis muscle function tested
Hold a piece of paper between their thumb and index finger. The object is then pulled away. If ulnar nerve palsy, unable to hold the paper and will flex the flexor pollicis longus to compensate (flexion of thumb at interphalangeal joint).
Phalen’s test?
Assess carpal tunnel syndrome
More sensitive than Tinel’s sign
Hold wrist in maximum flexion and the test is positive if there is numbness in the median nerve distribution.
Tinel’s sign (test)?
Assess for carpal tunnel syndrome
Tap the median nerve at the wrist and the test is positive if there is tingling/electric-like sensations over the distribution of the median nerve.
open fracture
disruption of the bony cortex associated with a breach in the overlying skin. Any wound that is present in the same limb as a fracture should be suspected as being representative of an open fracture
One of the main problems with open fractures is
associated injuries to the surrounding soft tissues. Whilst the skin is usually relatively resistant to trauma, underlying muscle can be damaged or devitalised, nerves, blood vessels and periosteum may all be disrupted the degree to which this occurs correlates with the severity of the injury and the outcome. These can be graded using the Gustilo and Anderson system
Open fractures: Gustilo and Anderson system?
1 Low energy wound <1cm
2 Greater than 1cm wound with moderate soft tissue damage
3 High energy wound > 1cm with extensive soft tissue damage
3 A (sub group of 3) Adequate soft tissue coverage
3 B (sub group of 3) Inadequate soft tissue coverage
3 C (sub group of 3) Associated arterial injury
Open fractures: In Type IIIc injuries, the mangled extremity scoring system (MESS) can help to predict the need for?
primary amputation
Mx for open fractures?
- check for associated injuries, control haemorrhage and extent of injury
- area should be carefully imaged, distal neurovascular status established the wound covered with a dressing and antibiotics administered.
- Early debridement. The aim of the debridement is to remove foreign material and devitalised tissue. In most cases the wound is left open. The wound should be irrigated, generally, 6 litres of saline is used.
- The fracture should be stabilised and an external fixator is often used in the first instance
Most effective Tx for osteoarthritis in pts who experience signif pain?
joint replacement (arthroplasty)
Selection criteria for Osteoarthritis joint replacement?
25% <60yrs
whilst obesity is often thought to be a barrier to joint replacement there is only a slight increase in short-term complications. There is no difference in long-term joint replacement survival
Surgical techniques for joint replacement in osteoarthritis?
hips= cemented hip replacement: metal femoral component is cemented into the femoral shaft. This is accompanied by a cemented acetabular polyethylene cup
uncementened hip replacements more popular in active and younger pts but more expensive
hip resurfacing sometimes used where a metal cap is attached over the femoral head. Younger pts; femoral neck is preserved which may be useful if conventional arthroplasty is needed later in life
Joint replacement in osteoarthritis: post-op recovery?
physio and home exercises
walking sticks or crutches are usually used for up to 6 weeks after hip or knee replacement surgery
Patients who have had a hip replacement operation (eg. due to osteoarthritis) should receive basic advice to minimise the risk of dislocation:
avoiding flexing the hip > 90 degrees
avoid low chairs
do not cross your legs
sleep on your back for the first 6 weeks
Cx of joint replacement in osteoarthritis?
wound and joint infection
VTE so LMWH for 4w after
dislocation
Osteochondritis dissecans (OCD)?
pathological process affecting the subchondral bone (most often in the knee joint) with secondary effects on the joint cartilage, including pain, oedema, free bodies and mechanical dysfunctions.
children and young adults
OCD may progress to degenerative changes if untreated.
Presentation of Osteochondritis dissecans (OCD)?
subacute onset
Knee pain and swelling, typically after exercise
Knee catching, locking and/or giving way: more constant and severe symptoms are associated with the presence of loose bodies
Feeling a painful ‘clunk’ when flexing or extending the knee - indicating the involvement of the lateral femoral condyle
Signs of Osteochondritis dissecans (OCD)?
Joint effusion
Tenderness on palpation of the articular cartilage of the medial femoral condyle, when the knee is flexed
Wilson’s sign for detecting medial condyle lesion
Wilson’s sign in Osteochondritis dissecans (OCD)?
for detecting medial condyle lesion - with the knee at 90° flexion and tibia internally rotated, the gradual extension of the joint leads to pain at about 30°, external rotation of the tibia at this point relieves the pain
Ix for Osteochondritis dissecans (OCD)?
x-ray (AP, lateral and tunnel views)= subchondral cresent sign or loose bodies
MRI= to evaluate cartilage, visualise loose bodies, stage and assess stability of the lesion
Mx of Osteochondritis dissecans (OCD)?
Early diagnosis is important
Clinical signs may be subtle in the early stages hence there should be a low threshold for imaging and/or orthopaedic opinion.
rest, NSAIDs, avoid intense activity 2-4m, physio, may need brace or crutches
Rib fracture?
break in the bony segment of any rib and is most often the consequence of blunt trauma to the chest wall but can be due to underlying diseases which weaken the bone structure of the ribs.
They can occur singly or in multiple places along the length of a rib and may be associated with soft tissue injuries to the surrounding muscles or the underlying lung.
RFs for rib fractures?
- blunt trauma to chest wall
- polytrauma (chest injuries present in 25% major trauma)
- spontaneous= coughing, sneezing eg. if PMH osteoporosis, steroid use, COPD
- pathological= ca mets eg. prostate in men and breast in women
Features of rib fracture?
- severe, sharp chest wall pain worse with deep breaths or coughing
- chest wall tenderness over site of fracture & bruising
- crackles or reduced breath sounds if lung injury
- reduction in ventilation & so drop in O2 sats due to pain/underlying lung injury
- pneumothorax
Serious Cx of rib fractures?
Pneumothorax= reduced chest expansion, reduced breath sounds and hyper-resonant percussion on the affected side
Serious Cx of multiple rib fractures eg. following trauma?
Flail chest- caused by two or more rib fractures along three or more consecutive ribs, usually anteriorly
Flail chest (follows multiple rib fractures)?
caused by two or more rib fractures along three or more consecutive ribs, usually anteriorly
the flail segment moves paradoxically during respiration and impairs ventilation of the lung on the side of injury
the segment can cause serious contusional injury to the underlying lung if left untreated
often requires treatment with invasive ventilation and surgical fixation to prevent complications
Ix of rib fractures?
CT scan GOLD
CXR= A or P fracrures but suboptimal views and non info on soft tissue injury
Mx of rib fractures?
- most cases= conservative + analgesia to ensure breathing not affected by pain. Pain not controlled= can consider nerve blocks
- Surgical fixation if pain still not managed and fractures failed to heal after 12w
- flail chest segments= urgent consideration for cardiothoracic surgery as they can impair ventilation and result in signif lung trauma
Lung Cx of rib fractures?
pneumothorax or haemothorax
What type of rib fractures need to be discussed urgently with cardiothoracic surgery as they can impair ventilation?
flail chest
Most common cause of shoulder pain?
rotator cuff injuries
Rotator cuff injuries include what?
spectrum of:
1. Subacromial impingement (also known as impingement syndrome, painful arc syndrome)
2. Calcific tendonitis
3. Rotator cuff tears
4. Rotator cuff arthropathy
Shoulder pain worse on abduction?
rotator cuff injuries
Signs of rotator cuff injuries?
painful arc of abduction. With subacromial impingement, this is typically between 60 and 120 degrees. With rotator cuff tears the pain may be in the first 60 degrees.
tenderness over anterior acromion
Scaphoid bone?
concave articular surface for the head of the capitate and at the edge of this is a crescentic surface for the corresponding area on the lunate.
Proximally= wide convex articular surface with the radius. It has a distally sited tubercle that can be palpated. The remaining articular surface is to the lateral side of the tubercle. It faces laterally and is associated with the trapezium and trapezoid bones.
The narrow strip between the radial and trapezial surfaces and the tubercle gives rise to the radial collateral carpal ligament. The tubercle receives part of the flexor retinaculum. This area is the only part of the scaphoid that is available for the entry of blood vessels. It is commonly fractured and avascular necrosis may result.
Shoulder dislocation?
occurs when the humeral head dislodges from the glenoid cavity of the scapula.
The shoulder is the most common joint in the body to dislocate, accounting for approximately 50% of all major joint dislocations.
Most common type of shoulder dislocations?
Anterior shoulder dislocations account for > 95% of cases.
Mx for shoulder dislocation?
reduction
If the dislocation is recent then reduction may be attempted without any analgesia/sedation. However, other patients may require analgesia +/- sedation to ensure the rotator cuff muscles are relaxed.
Common shoulder problems?
Adhesive capsulitis
(frozen shoulder)
Supraspinatus tendonitis
(Subacromial impingement,
painful arc)
Shoulder problems: Adhesive capsulitis
(frozen shoulder)?
Common in middle-age and diabetics
Characterised by painful, stiff movement
Limited movement in all directions, with loss of external rotation and abduction in about 50% of patients
Shoulder problems:
Supraspinatus tendonitis
(Subacromial impingement,
painful arc)?
Rotator cuff injury
Painful arc of abduction between 60 and 120 degrees
Tenderness over anterior acromion
Dorsal column lesion
loss of vibration and proprioception
tabes dorsalis, SACD
Spinothalamic tract lesion?
loss of pain, sensation and temp
Central cord lesion?
flaccid paralysis of the upper limbs
Osteomyelitis of the spine?
Normally progressive
Staph aureus in IVDU, normally cervical region affected
Fungal infections in immunocompromised
Thoracic region affected in TB
Infarction to spinal cord?
dorsal column signs (loss of proprioception and fine discrimination)
Cord compression?
UMN signs
malignancy
haematoma
fracture
Brown-sequard syndrome?
Hemisection of the spinal cord
Ipsilateral paralysis
Ipsilateral loss of proprioception and fine discrimination
Contralateral loss of pain and temperature
Signs/symptoms of Brown-sequard syndrome?
Ipsilateral paralysis
Ipsilateral loss of proprioception and fine discrimination
Contralateral loss of pain and temperature
Ipsilateral paralysis
Ipsilateral loss of proprioception and fine discrimination
Contralateral loss of pain and temperature
Brown-sequard syndrome
Dermatomes C2-C4
C2 dermatome covers the occiput and the top part of the neck. C3 covers the lower part of the neck to the clavicle. C4 covers the area just below the clavicle.
Dermatomes C5 to T1?
Situated in the arms. C5 covers the lateral arm at and above the elbow. C6 covers the forearm and the radial (thumb) side of the hand. C7 is the middle finger, C8 is the medial aspect of the hand, and T1 covers the medial side of the forearm.
Dermatomes T2-T12?
The thoracic covers the axillary and chest region. T3 to T12 covers the chest and back to the hip girdle. The nipples are situated in the middle of T4. T10 is situated at the umbilicus. T12 ends just above the hip girdle.
Dermatomes L1 to L5?
The cutaneous dermatome representing the hip girdle and groin area is innervated by L1 spinal cord. L2 and 3 cover the front part of the thighs. L4 and L5 cover medial and lateral aspects of the lower leg.
Dermatomes S1 to S5?
S1 covers the heel and the middle back of the leg. S2 covers the back of the thighs. S3 cover the medial side of the buttocks and S4-5 covers the perineal region. S5 is of course the lowest dermatome and represents the skin immediately at and adjacent to the anus.
Upper limb myotomes?
C5-T1
Lower limb myotomes?
L1 to S1
Anal sphincter myotomes?
S2-S4
What myotome= elbow flexors/biceps?
C5
What myotome= wrist extensors?
C6
What myotome= elbow extensors/triceps?
C7
What myotome= long finger flexors?
C8
What myotome= small finger abductors?
T1
What myotome= hip flexors (psoas)?
L1 and L2
What myotome= knee extensors (quads)?
L3
What myotome= ankle dorsiflexors (tibialis anterior)?
L4 and L5
What myotome= toe extensors (hallucis longus)?
L5
What myotome= ankle plantar flexors (gastrocnemius)?
S1
What myotome= anal sphinceter?
S2,3,4
Stress fractures?
Repetitive activity and loading of normal bone may result in small hairline fractures. Whilst these may be painful they are seldom displaced. Surrounding soft tissue injury is unusual.
Stress fractures- presentation/magament?
may present late following the injury, in which case callus formation may be identified on radiographs. Such cases may not require formal immobilisation, injuries associated with severe pain and presenting at an earlier stage may benefit from immobilisation tailored to the site of injury.
Most common upper limb injury in children <6yrs?
subluxation of the radial head (pulled elbow)
due to the fact that the distal attachment of the annular ligament covering the radial head is weaker in children at this age group.
Signs of subluxation of the radial head (pulled elbow)?
elbow pain and limited supination and extension of the elbow. The child usually refuses examination on the affected elbow due to the pain
Mx of subluxation of the radial head (pulled elbow)?
analgesia and passively supination of the elbow joint whilst the elbow is flexed to 90 degrees
Subluxation?
partial dislocation
Talipes equinovarus (club foot)?
describes an inverted (inward turning) and plantar flexed foot. It is usually diagnosed on the newborn exam.
M>F
50% bilateral
Talipes equinovarus (club foot) assocaitions?
idiopathic
spina bifida
cerebral palsy
Edward’s syndrome (trisomy 18)
oligohydramnios
arthrogryposis
Diagnosis of talipes equinovarus (club foot)?
clinical (the deformity is not passively correctable) and imaging is not normally needed.
Mx of talipes equinovarus (club foot)?
Ponseti method= manipulation and progressive casting which starts soon after birth. The deformity is usually corrected after 6-10 weeks.
An Achilles tenotomy is required in around 85% of cases but this can usually be done under local anaesthetic
night-time braces should be applied until the child is aged 4 years. The relapse rate is 15%
Trigger finger?
common condition associated with abnormal flexion of the digits. It is thought to be caused by a disparity between the size of the tendon and pulleys through which they pass. In simple terms the tendon becomes ‘stuck’ and cannot pass smoothly through the pulley.
Trigger finger associations?
idiopathic
F>M
RA
DM
Features of trigger finger?
more common in the thumb, middle, or ring finger
initially stiffness and snapping (‘trigger’) when extending a flexed digit
a nodule may be felt at the base of the affected finger
Mx of trigger finger?
- steroid injections + finger splint after
- surgery if not responded
Musculocutaneous nerve (C5-C7)= motor?
elbow flexion (supplies biceps brachii) and supination
Musculocutaneous nerve (C5-C7)= sensory?
lateral part of forearm
Musculocutaneous nerve (C5-C7)= typical mechanism of injury?
Isolated injury rare - usually injured as part of brachial plexus injury
Axillary nerve (C5,C6)= motor?
shoulder abduction (deltoid muscle)
Axillary nerve (C5,C6)= sensory?
inferior region of the deltoid muscle
Axillary nerve (C5,C6)= mechanism of injury?
humeral neck fracture/dislocation
results in flattened deltoid
Humeral neck fracture/dislocation resulting in flattened deltoid- injury to what nerve?
Axillary nerve (C5,C6)
Radial nerve (C5-C8)= motor?
extension (forearm, wrist, fingers, thumb)
Radial nerve (C5-C8)= sensory?
small area between the dorsal aspect of the 1st and 2nd metacarpals
Radial nerve (C5-C8)= mechanism of injury?
humeral midshaft fracture
palsy results in wrist drop
Humeral midshaft fracture resulting in wrist drop- injury to what nerve?
Radial nerve (C5-C8)
Median nerve (C6, C8, T1)= motor?
LOAF muscles
Features depend on the site of the lesion:
wrist: paralysis of thenar muscles, opponens pollicis
elbow: loss of pronation of forearm and weak wrist flexion
Median nerve (C6, C8, T1)= sensory?
Palmar aspect of lateral 3½ fingers
Median nerve (C6, C8, T1)= mechanism of injury?
wrist lesion -> carpal tunnel syndrome
wrist lesion causing carpal tunnel syndrome- injury to what nerve?
Median nerve (C6, C8, T1)
Ulnar nerve (C8, T1)= motor?
intrinsic hand muscles except LOAF
wrist flexion
Ulnar nerve (C8, T1)= sensory?
Medial 1½ fingers
Ulnar nerve (C8, T1)= mechanism of injury?
Medial epicondyle fracture
Damage may result in a ‘claw hand’
Medial epicondyle fracture resulting in ‘claw hand’- injury to what nerve?
Ulnar nerve (C8, T1)
Long thoracic nerve (C5-C7)= motor?
serratus anterior
Long thoracic nerve (C5-C7)= sensory?
N/A
Long thoracic nerve (C5-C7)= mechanism of injury?
Often during sport e.g. following a blow to the ribs. Also possible complication of mastectomy
Damage results in a winged scapula
Often during sport e.g. following a blow to the ribs. Also possible complication of mastectomy
Damage results in a winged scapula
Injury to what nerve?
Long thoracic nerve (C5-C7)
Erb-Duchenne palsy (‘waiter’s tip’)?
due to damage of the upper trunk of the brachial plexus (C5,C6)
may be secondary to shoulder dystocia during birth
the arm hangs by the side and is internally rotated, elbow extended
Klumpke injury?
due to damage of the lower trunk of the brachial plexus (C8, T1)
as above, may be secondary to shoulder dystocia during birth. Also may be caused by a sudden upward jerk of the hand
associated with Horner’s syndrome
LOAF muscles (in hand)?
Lateral two lumbricals
Opponens pollis
Abductor pollis brevis
Flexor pollis brevis
ANCA antibodies stands for what?
Anti-neutrophil cytoplasmic antibodies
ANCA (antibodies) are associated with what?
number of small-vessel vasculitides, including:
granulomatosis with polyangiitis
eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome)
microscopic polyangiitis
ANCA associated vasculitis more common with….
increasing age
ANCA associated vasculitis: whilst each condition has its own distinct features, there are a number of common findings…
renal impairment
caused by immune complex glomerulonephritis → raised creatinine, haematuria and proteinuria
respiratory symptoms:
dyspnoea, haemoptysiis
systemic symptoms: fatigue,
weight loss, fever
vasculitic rash: present only in a minority of patients
ENT symptoms: sinusitis
ANCA associated vasculitis: first line Ix?
urinalysis for haematuria and proteinuria
bloods:
- urea and creatinine for renal impairment
- full blood count: normocytic anaemia and thrombocytosis may be seen
- CRP: raised
- ANCA testing (see below)
chest x-ray: nodular, fibrotic or infiltrative lesions may be seen
ANCA types?
cytoplasmic (cANCA) and perinuclear (pANCA)
ANCA types- cANCA and pANCA= There is considerable overlap between which antibodies are found in which condition, but as a rule of thumb…
cANCA - granulomatosis with polyangiitis
pANCA - eosinophilic granulomatosis with polyangiitis + others
cANCA?
- serine proteinase 3 (PR3)
- Granulomatosis with polyangiitis= 90%
- Eosinophilic granulomatosis with polyangiitis= Low
- Microscopic polyangiitis= 40%
- other associated conditions= N/A
- Use for monitoring= Some correlation between cANCA levels and disease activity
pANCA?
- myeloperoxidase (MPO)
- Granulomatosis with polyangiitis= 25%
- Eosinophilic granulomatosis with polyangiitis= 50%
- Microscopic polyangiitis= 75%
- other associated conditions= Ulcerative colitis (70%); Primary sclerosing cholangitis (70%); Anti-GBM disease (25%); Crohn’s disease (20%)
- Use for monitoring= Cannot use level of pANCA to monitor disease activity
ANCA associated vasculitis: general approach to Mx?
once suspected, should be managed by specialist teams (e.g. renal, rheumatology, respiratory) to allow an exact diagnosis to be made. Kidney or lung biopsies may be taken to aid the diagnosis.
The mainstay of management is immunosuppressive therapy.
Antisynthetase syndrome?
autoimmune condition caused by the presence of autoantibodies against aminoacyl-tRNA synthetase enzymes.
These autoantibodies play a critical role in the pathogenesis of the disease by targeting and interfering with these essential enzymes, which are responsible for protein synthesis in cells.
Antisynthetase syndrome most common autoantibody associated with this condition?
anti-Jo-1
Clinical features of Antisynthetase syndrome?
- myositis= muscle weakness, primarily affecting the proximal muscles so difficulties in performing everyday activities, such as climbing stairs or lifting objects. Elevated muscle enzymes, such as creatine kinase (CK), are often observed.
- interstitial lung disease= chronic dry cough, SOB, reduced exercise tolerance. High-resolution CT for diagnosis
- mechanic’s hands
- Raynaud’s phenomenon= episodic vasospasm of the small blood vessels, usually in response to cold or stress, leading to pallor, cyanosis, and erythema of the fingers and toes
Antisynthetase syndrome= mechanic’s hands?
hyperkeratotic, thickened, and cracked skin on the sides of their fingers and palms, resembling the hands of a manual labourer. This distinctive feature, known as ‘mechanic’s hands,’ is a key clinical sign of the syndrome.
Additional features of Antisynthetase syndrome?
- inflam arthritis
- fever
- fatigue, weight loss, malaise
Diagnosis of Antisynthetase syndrome?
based on clinical features, serological tests for specific autoantibodies (like anti-Jo-1), and imaging studies to assess lung involvement. Muscle biopsies and electromyography (EMG) may be used to confirm myositis.
Mx of Antisynthetase syndrome?
immunosuppressive therapy, such as corticosteroids and other immunomodulatory drugs, to control inflammation and prevent disease progression. Patients with significant lung involvement may require additional treatments, including antifibrotic agents and supplemental oxygen.
Behcet’s syndrome?
complex multisystem disorder associated with presumed autoimmune-mediated inflammation of the arteries and veins.
Cause uncertain.
Behcet’s syndrome triad?
oral ulcers, genital ulcers and anterior uveitis
oral ulcers, genital ulcers and anterior uveitis
Behcet’s syndrome
Epidemiology of Behcet’s syndrome?
M>F (more common & more severe)
more common in eastern Mediterranean eg. Turkey
20-40yrs
associated with HLA B51
30% have +ve FHx
Features of Behcet’s syndrome?
1) oral ulcers 2) genital ulcers 3) anterior uveitis
thrombophlebitis and deep vein thrombosis
arthritis
neurological involvement (e.g. aseptic meningitis)
GI: abdo pain, diarrhoea, colitis
erythema nodosum
Diagnosis of Behcet’s syndrome?
no definitive test
diagnosis based
on clinical findings
positive pathergy test is suggestive (puncture site following needle prick becomes inflamed with small pustule forming)
Ca, Phosphate, ALP and PTH in osteoporosis?
Ca= normal
Phosphate= normal
ALP= normal
PTH= normal
Ca, Phosphate, ALP and PTH in osteomalacia?
Ca= decreased
Phosphate= decreased
ALP= increased
PTH= increased
Ca, Phosphate, ALP and PTH in primary hyperparathyroidism (-> osteitis fibrosa cystica)?
Ca= increased
Phosphate= decreased
ALP= increased
PTH= increased
Ca, Phosphate, ALP and PTH in CKD (-> secondary hyperparathyroidism)?
Ca= decreased
Phosphate= increased
ALP= increased
PTH= increased
Ca, Phosphate, ALP and PTH in Paget’s disease?
Ca= normal
Phosphate= normal
ALP= increased
PTH= normal
Ca, Phosphate, ALP and PTH in osteopetrosis?
Ca= normal
Phosphate= normal
ALP= normal
PTH= normal
Osteopetrosis?
group of a rare disorders that cause bones to grow abnormally and become overly dense
Benign bone tumours?
osteoma
osteochondroma (exotosis)
giant cell tumour
Benign bone tumours: osteoma?
benign ‘overgrowth’ of bone, most typically occuring on the skull
associated with Gardner’s syndrome (a variant of familial adenomatous polyposis, FAP)
Benign bone tumours: osteochondroma (exotosis)?
most common benign bone tumour
more in males, usually diagnosed in patients aged < 20 years
cartilage-capped bony projection on the external surface of a bone
Benign bone tumours: giant cell tumour?
tumour of multinucleated giant cells within a fibrous stroma
peak incidence: 20-40 years
occurs most frequently in the epiphyses of long bones
X-ray shows a ‘double bubble’ or ‘soap bubble’ appearance
Malignant bone tumours?
osteosarcoma
Ewing’s sarcoma
chondrosarcoma
Malignant bone tumours: osteosarcoma?
most common primary malignant bone tumour
seen mainly in children and adolescents
occurs most frequently in the metaphyseal region of long bones prior to epiphyseal closure, with 40% occuring in the femur, 20% in the tibia, and 10% in the humerus
x-ray= Codman triangle (from periosteal elevation) and ‘sunburst’ pattern
mutation of the Rb gene increases risk (hence association with retinoblastoma)
other predisposing factors include Paget’s disease of the bone and radiotherapy
Malignant bone tumours: Ewing’s sarcoma?
small round blue cell tumour
seen mainly in children and adolescents
occurs most frequently in the pelvis and long bones. Tends to cause severe pain
associated with t(11;22) translocation which results in an EWS-FLI1 gene product
x-ray shows ‘onion skin’ appearance
Malignant bone tumours: chondrosarcoma?
malignant tumour of cartilage
most commonly affects the axial skeleton
more common in middle-age
Dactylitis?
inflammation of a digit (finger or toe)
Causes of dactylitis?
spondyloarthritis: e.g. Psoriatic and reactive arthritis
sickle-cell disease
other rare causes include tuberculosis, sarcoidosis and syphilis
Discoid lupus erythematosus?
benign disorder generally seen in younger females. It very rarely progresses to systemic lupus erythematosus (in less than 5% of cases). Discoid lupus erythematosus is characterised by follicular keratin plugs and is thought to be autoimmune in aetiology
Features of Discoid lupus erythematosus?
erythematous, raised rash, sometimes scaly
may be photosensitive
more common on face, neck, ears and scalp
lesions heal with atrophy, scarring (may cause scarring alopecia), and pigmentation
Mx of of Discoid lupus erythematosus?
topical steroid cream
oral antimalarials may be used second-line e.g. hydroxychloroquine
avoid sun exposure
Drug-induced lupus?
not all the typical features of systemic lupus erythematosus are seen, with renal and nervous system involvement being unusual. It usually resolves on stopping the drug.
Features of drug-induced lupus?
arthralgia
myalgia
skin (e.g. malar rash) and pulmonary involvement (e.g. pleurisy) are common
ANA positive in 100%, dsDNA negative
anti-histone antibodies are found in 80-90%
anti-Ro, anti-Smith positive in around 5%
Causes of drug-induced lupus?
Most common causes:
procainamide
hydralazine
Less common causes:
isoniazid
minocycline
phenytoin
Ehler-Danlos syndrome?
autosomal dominant connective tissue disorder that mostly affects type III collagen. This results in the tissue being more elastic than normal leading to joint hypermobility and increased elasticity of the skin.
Features and Cx of Ehler-Danlos syndrome?
elastic, fragile skin
joint hypermobility: recurrent joint dislocation
easy bruising
aortic regurgitation, mitral valve prolapse and aortic dissection
subarachnoid haemorrhage
angioid retinal streaks
Referred lumbar spine pain?
Femoral nerve compression may cause referred pain in the hip
Femoral nerve stretch test may be positive - lie the patient prone. Extend the hip joint with a straight leg then bend the knee. This stretches the femoral nerve and will cause pain if it is trapped
Summary of Meralgia paraesthetica?
Caused by compression of lateral cutaneous nerve of thigh
Typically burning sensation over antero-lateral aspect of thigh
Pubic symphysis dysfunction?
Common in pregnancy
Ligament laxity increases in response to hormonal changes of pregnancy
Pain over the pubic symphysis with radiation to the groins and the medial aspects of the thighs. A waddling gait may be seen
Pregnant pt with pain over the pubic symphysis with radiation to the groins and the medial aspects of the thighs. A waddling gait may be seen
pubic symphysis dysfunction
Transient idiopathic osteoporosis
An uncommon condition sometimes seen in the third trimester of pregnancy
Groin pain associated with a limited range of movement in the hip
Patients may be unable to weight bear
ESR may be elevated
An uncommon condition sometimes seen in the third trimester of pregnancy
Groin pain associated with a limited range of movement in the hip
Patients may be unable to weight bear
ESR may be elevated
transient idiopathic osteoporosis
Causes of hip pain in adults?
OA
inflam arthritis
referred L spine pain
Greater trochanteric pain syndrome
Meralgia paraesthetica
Avascular necrosis
Pubic symphysis dysfunction
Transient idiopathic osteoarthritis
HLA antigens are encoded for by genes on chromosome
6
HLA A, B and C are what? DP, DQ and DR?
class I antigens
class II antigens
HLA associations- what one for:
- haemochromatosis?
HLA-A3
HLA associations- what one for:
- Behcet’s disease?
HLA-B51
HLA associations- what one for:
- ankylosing spondylitis
- reactive arthritis
- acute anterior uveitis
- psoriatic arthritis
HLA-B27
HLA associations- what one for:
- coeliac disease?
HLA-DQ2/DQ8
HLA associations- what one for:
- narcolepsy
- Goodpasture’s
HLA-DR2
HLA associations- what one for:
- dermatitis herpetiformis
- Sjogren’s syndrome
- primary biliary cirrhosis
(sometimes DM but not strongly)
HLA-DR3
HLA associations- what one for:
- DMT1
- RA
HLA-DR4
RA= in particular the DRB1 gene (DRB104:01 and DRB104:04 hence the association with DR4)
Hydroxychloroquine
used in Mx of RA and systemic/discoid lupus erythematosus
pharmacologically similar to chloroquine used to treat malaria
Can hydroxychloroquine be used in pregnancy?
yes
Monitoring of hydroxychloroquine?
‘Ask patient about visual symptoms and monitor visual acuity annually using the standard reading chart’
Adverse effects of hydroxychloroquine?
bull’s eye retinopathy - may result in severe and permanent visual loss
baseline ophthalmological examination and annual screening is generally recommened
colour retinal photography and spectral domain optical coherence tomography scanning of the macula
Langerhans cell histiocytosis?
are disorder characterised by the proliferation of Langerhans cells, which are specialised dendritic cells that normally function to present antigen to T lymphocytes. The disease can affect multiple organs, including the bones, skin, lungs, and endocrine system. It is notable for its variable clinical presentation, ranging from isolated bone lesions to multisystem disease.
Features of Langerhans cell histiocytosis?
bone pain, typically in the skull or proximal femur
cutaneous nodules
pituitary involvement: leads to diabetes insipidus due to pituitary stalk involvement
pulmonary involvement: More common in adults, presenting with dyspnoea, cough, and chest pain
recurrent otitis media/mastoiditis
tennis racket-shaped Birbeck granules on electromicroscopy
Diagnosis of Langerhans cell histiocytosis?
biopsy: confirmation is through biopsy showing Langerhans cells with characteristic grooved nuclei and positive staining for CD1a and S100 protein
imaging: radiographs and MRI for bone lesions; CT may be used for chest and abdominal involvement
Tx of Langerhans cell histiocytosis?
localized disease: surgical resection or limited radiotherapy for isolated lesions.
multisystem disease: systemic therapy including steroids, chemotherapy (e.g., vinblastine, cytarabine), and targeted therapies for refractory cases.
supportive care: management of diabetes insipidus, pain control, and treatment of secondary infections.
Young girl with multiple well defined ‘punched out’ osteolytic lesions with scalloped edges (geographic skull) are seen in the bilateral parietal regions. The lesions have a characteristic bevelled edge.
Langerhans cell histiocytosis
Marfan’s syndrome?
autosomal dominant connective tissue disorder
Cause of Marfan’s syndrome?
defect in the FBN1 gene on chromosome 15 that codes for the protein fibrillin-1.
Features of Marfan’s syndrome?
tall stature with arm span to height ratio > 1.05
high-arched palate
arachnodactyly (long curved slender fingers)
pectus excavatum (caved chest)
pes planus (flat foot)
scoliosis of > 20 degrees
dural ectasia (ballooning of the dural sac at the lumbosacral level)
heart, lung and eye symptoms
tall stature with arm span to height ratio > 1.05
high-arched palate
arachnodactyly (long curved slender fingers)
pectus excavatum (caved chest)
pes planus (flat foot)
scoliosis of > 20 degrees
blue sclera
Marfan’s syndrome
Marfan’s syndrome: heart features?
dilation of the aortic sinuses (seen in 90%) which may lead to aortic aneurysm, aortic dissection, aortic regurgitation
mitral valve prolapse (75%),
Marfan’s syndrome: lung features?
repeated pneumothoraces
Marfan’s syndrome: eye features?
upwards lens dislocation (superotemporal ectopia lentis)
blue sclera
myopia
Life expectancy of Marfan’s syndrome/Mx?
used to be around 40-50 years.
But with 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.
McArdle’s disease?
autosomal recessive type V glycogen storage disease
caused by myophosphorylase deficiency
this causes decreased muscle glycogenolysis
Features of McArdle’s disease?
muscle pain and stiffness following exercise
muscle cramps
second wind phenomenon
rhabdomyolysis & myoglobinuria
low lactate levels during exercise
Second wind phenomenon in McArdle’s disease?
occurs when patients experience an improvement in exercise tolerance after a brief rest or reduction in intensity
due to the body’s switch from glycogen-dependent energy metabolism to increased reliance on circulating glucose and fatty acids
this adaptation allows for better energy utilisation during prolonged activity despite the underlying myophosphorylase deficiency.
Myopathies: features?
symmetrical muscle weakness (proximal > distal)
common problems are rising from chair or getting out of bath
sensation normal, reflexes normal, no fasciculation
Myopathies: causes?
inflammatory: polymyositis
inherited: Duchenne/Becker muscular dystrophy, myotonic dystrophy
endocrine: Cushing’s, thyrotoxicosis
alcohol
OA vs RA: aetiology?
OA=
Mechanical - wear & tear
- localised loss of cartilage
- remodelling of adjacent bone
- associated inflammation
RA=
Autoimmune
OA vs RA: gender?
OA= slightly more in W
RA= signif more in W
OA vs RA: age?
OA= elderly
RA= adults of all ages
OA vs RA: typical joints affected?
OA= Large weight-bearing joints (hip, knee); Carpometacarpal joint; DIP, PIP joints
RA= MCP, PIP joints
OA vs RA: typical symptoms?
OA= Pain following use, no morning stiffness or <30mins; improves with rest; Unilateral symptoms; No systemic upset
RA= Morning stiffness, improves with use; Bilateral symptoms; Systemic upset
OA vs RA: x-ray findings?
OA=
Loss of joint space
Subchondral sclerosis
Subchondral cysts
Osteophytes forming at joint margins
RA=
Loss of joint space
Juxta-articular osteoporosis
Periarticular erosions
Subluxation
Osteogenesis imperfecta (brittle bone disease)?
group of disorders of collagen metabolism resulting in bone fragility and fractures.
The most common, and milder, form of osteogenesis imperfecta is type 1
Osteogenesis imperfecta overview?
autosomal dominant
abnormality in type 1 collagen due to decreased synthesis of pro-alpha 1 or pro-alpha 2 collagen polypeptides
Osteogenesis imperfecta features?
presents in childhood
fractures following minor trauma
blue sclera
deafness secondary to otosclerosis
dental imperfections are common
presents in childhood
fractures following minor trauma
blue sclera
deafness secondary to otosclerosis
dental imperfections are common
Osteogenesis imperfecta
Osteogenesis imperfecta Ix?
adjusted calcium, phosphate, parathyroid hormone and ALP results are
Polymyositis?
inflammatory disorder causing symmetrical, proximal muscle weakness
thought to be a T-cell mediated cytotoxic process directed against muscle fibres
may be idiopathic or associated with connective tissue disorders
associated with malignancy
dermatomyositis is a variant of the disease where skin manifestations are prominent, for example a purple (heliotrope) rash on the cheeks and eyelids
typically affects middle-aged, female:male 3:1
Features of Polymyositis?
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 for polymyositis?
elevated creatine kinase
other muscle enzymes (lactate dehydrogenase (LDH), aldolase, AST and ALT) are also elevated in 85-95% of patients
EMG
muscle biopsy
anti-synthetase antibodies: anti-Jo-1 antibodies are seen in pattern of disease associated with lung involvement, Raynaud’s and fever
Mx for polymyositis?
high-dose corticosteroids tapered as symptoms improve
azathioprine may be used as a steroid-sparing agent
Raynaud’s phenomenon?
an exaggerated vasoconstrictive response of the digital arteries and cutaneous arteriole to the cold or emotional stress. It may be primary (Raynaud’s disease) or secondary (Raynaud’s phenomenon).
How does raynaud’s disease typically present?
young women (e.g. 30 years old) with bilateral symptoms.
Secondary causes of Raynaud’s phenomenon?
connective tissue disorders:
- scleroderma (most common)
- rheumatoid arthritis
- systemic lupus erythematosus
leukaemia
type I cryoglobulinaemia, cold agglutinins
use of vibrating tools
drugs: oral contraceptive pill, ergot
cervical rib
Factors suggesting underlying connective tissue disease in Raynaud’s phenomenon?
onset after 40 years
unilateral symptoms
rashes
presence of autoantibodies
features which may suggest rheumatoid arthritis or SLE, for example arthritis or recurrent miscarriages
digital ulcers, calcinosis
very rarely: chilblains
Mx for Raynaud’s phenomenon?
all patients with suspected secondary Raynaud’s phenomenon should be referred to secondary care
first-line: calcium channel blockers e.g. nifedipine
IV prostacyclin (epoprostenol) infusions: effects may last several weeks/months
Rotator cuff muscles?
SItS
Supraspinatus
Infraspinatus
teres minor
Subscapularis
Rotator cuff muscles: Supraspinatus?
aBDucts arm before deltoid
Most commonly injured
Rotator cuff muscles: Infraspinatus?
Rotates arm laterally
Rotator cuff muscles: teres minor?
aDDucts & rotates arm laterally
Rotator cuff muscles: Suprascapularis?
aDDuct & rotates arm medially
Common features of Seronegative spondyloarthropathies?
associated with HLA-B27
rheumatoid factor negative - hence ‘seronegative’
peripheral arthritis, usually asymmetrical
sacroiliitis
enthesopathy: e.g. Achilles tendonitis, plantar fasciitis
extra-articular
manifestations: uveitis, pulmonary fibrosis (upper zone), amyloidosis, aortic regurgitation
Spondyloarthropathies?
ankylosing spondylitis
psoriatic arthritis
reactive arthritis
enteropathic arthritis (associated with IBD)
Sjogren’s syndrome?
autoimmune disorder affecting exocrine glands resulting in dry mucosal surfaces.
Sjogren’s syndrome can be…
primary (PSS) or secondary to rheumatoid arthritis or other connective tissue disorders, where it usually develops around 10 years after the initial onset.
Sjogren’s syndrome more common in who?
females (9:1)
There is a marked increased risk of what in Sjogren’s syndrome?
lymphoid malignancy (40-60 fold).
Sjogren’s syndrome features?
dry eyes: keratoconjunctivitis sicca
dry mouth
vaginal dryness
arthralgia
Raynaud’s, myalgia
sensory polyneuropathy
recurrent episodes of parotitis
renal tubular acidosis (usually subclinical)
Raynaud’s, myalgia
sensory polyneuropathy
recurrent episodes of parotitis
renal tubular acidosis (usually subclinical)
dry eyes: keratoconjunctivitis sicca
dry mouth
vaginal dryness
arthralgia
Raynaud’s, myalgia
sensory polyneuropathy
recurrent episodes of parotitis
renal tubular acidosis (usually subclinical)
Raynaud’s, myalgia
sensory polyneuropathy
recurrent episodes of parotitis
renal tubular acidosis (usually subclinical)
Sjogren’s syndrome
Sjogren’s syndrome Ix?
rheumatoid factor (RF) positive in nearly 50% of patients
ANA positive in 70%
anti-Ro (SSA) antibodies in 70% of patients with PSS
anti-La (SSB) antibodies in 30% of patients with PSS
Schirmer’s test: filter paper near conjunctival sac to measure tear formation
histology: focal lymphocytic infiltration
also: hypergammaglobulinaemia, low C4
Sjogren’s syndrome histology?
focal lymphocytic infiltration
Clinical test for Sjogren’s syndrome?
Schirmer’s test: filter paper near conjunctival sac to measure tear formation
Mx of Sjogren’s syndrome?
artificial saliva and tears
pilocarpine may be helpful to stimulate saliva production
Still’s disease in adults?
rare type of inflam arthritis
Still’s disease in adults epidemiology?
bimodal age distribution - 15-25 yrs and 35-46 yrs
Still’s disease in adults features?
arthralgia
elevated serum ferritin
rash: salmon-pink, maculopapular
pyrexia= typically rises in the late afternoon/early evening in a daily pattern and accompanies a worsening of joint symptoms and rash
lymphadenopathy
rheumatoid factor (RF) and anti-nuclear antibody (ANA) negative
arthralgia
elevated serum ferritin
rash: salmon-pink, maculopapular
pyrexia= typically rises in the late afternoon/early evening in a daily pattern and accompanies a worsening of joint symptoms and rash
Still’s disease in adults
Diagnosis of Still’s disease in adults?
challenging
The Yamaguchi criteria is the most widely used criteria and has a sensitivity of 93.5%.
Mx of Still’s disease in adults?
NSAIDs= should be used first-line to manage fever, joint pain and serositis; they should be trialled for at least a week before steroids are added.
steroids= may control symptoms but won’t improve prognosis
if symptoms persist, the use of methotrexate, IL-1 or anti-TNF therapy can be considered
Systemic sclerosis?
condition of unknown aetiology characterised by hardened, sclerotic skin and other connective tissues. It is four times more common in females
Systemic sclerosis: 3 patterns of disease?
Limited cutaneous systemic sclerosis
Diffuse cutaneous systemic sclerosis
Scleroderma (without internal organ involvement)
Systemic sclerosis: 3 patterns of disease= Limited cutaneous systemic sclerosis?
Raynaud’s may be the first sign
scleroderma affects face and distal limbs predominately
associated with anti-centromere antibodies
a subtype of limited systemic sclerosis is CREST syndrome: Calcinosis, Raynaud’s phenomenon, oEsophageal dysmotility, Sclerodactyly, Telangiectasia
Systemic sclerosis: 3 patterns of disease= Diffuse cutaneous systemic sclerosis?
scleroderma affects trunk and proximal limbs predominately
associated with anti scl-70 antibodies
the most common cause of death is now respiratory involvement, which is seen in around 80%: interstitial lung disease (ILD) and pulmonary arterial hypertension (PAH)
other complications include renal disease and hypertension= patients with renal disease should be started on an ACE inhibitor
poor prognosis
Systemic sclerosis: 3 patterns of disease= Scleroderma (without internal organ involvement)?
tightening and fibrosis of skin
may be manifest as plaques (morphoea) or linear
Systemic sclerosis antibodies?
ANA positive in 90%
RF positive in 30%
anti-scl-70 antibodies associated with diffuse cutaneous systemic sclerosis
- associated with a higher risk of severe interstitial lung disease
anti-centromere antibodies associated with limited cutaneous systemic sclerosis
The following groups should be advised to take vitamin D supplementation:
all pregnant and breastfeeding women should take a daily supplement containing 10µg of vitamin D
all children aged 6 months - 5 years. Babies fed with formula milk do not need to take a supplement if they are taking more than 500ml of milk a day, as formula milk is fortified with vitamin D
adults > 65 years
‘people who are not exposed to much sun should also take a daily supplement’ e.g. housebound patients
(People who are at higher risk of vitamin D deficiency (see above) should be treated anyway so again testing is not necessary)
When to test for vit D def?
patients with bone diseases that may be improved with vitamin D treatment e.g. known osteomalacia or Paget’s disease
patients with bone diseases, prior to specific treatment where correcting vitamin deficiency is appropriate e,g, prior to intravenous zolendronate or denosumab
patients with musculoskeletal symptoms that could be attributed to vitamin D deficiency e.g. bone pain ?osteomalacia
Why is vit D not tested in pt with osteoporosis?
Patients with osteoporosis should always be given calcium/vitamin D supplements so testing is not considered necessary.