MSK Flashcards
Describe the causes and common sites of compartment syndrome
Interstitial pressure within a closed fascial compartment resulting in microvascular compromise
Common sites – leg, forearm, thigh
Causes
> Increased internal pressure
> Trauma - fractures, entrapment, bleeding
> Muscle oedema / myositis
> Reperfusion - vascular surgery
> Intracompartmental administration of fluids / drugs
> Increased external compression
> Casts/bandages, full thickness burns
> Impaired consciousness / protective reflexes
» Drug / alcohol misuse
» Iatrogenic
» Positioning in theatre – lithotomy
> Combination
What is the consequence of an untreated compartment syndrome in the arm?
Volkmann’s ischaemic contracture
Describe the pathogenesis of compartment syndrome
External compression
> Swelling after injury + external compression
> Pressure increases and venous flow reduced but arterial inflow continues
> Pressure increases
> External compression removed leads to restoration of venous flow and pressure normalises
Non-expansile compartment
> Bleeding into compartment
> Increased compartment content
> Venous flow reduced but arterial inflow continues so pressure increases
> Ischaemia and permanent damage result
Describe the pathophysiology of compartment syndrome, including later stages
Pressure within compartment exceeds pressure within capillaries – reduced blood flow
Muscles become ischaemic and develop oedema through increased endothelial permeability – vicious cycle
Autoregulatory mechanisms overwhelmed
Necrosis begins in the ischaemic muscles after 4 hours
Damaged muscles release myoglobin
Ischaemic nerves become neuropraxic
May recover if relieved early, permanent damage after 4 hours
Irreversible damage – loss of function, limb or life
Compromise of the arterial supply – late
Describe the time scale associated with damage in compartment syndrome
1 hour
> Nerve conduction normal, muscle viable
4 hours
> Neuropraxis in nerves – reversible
> Reversible muscle ischaemia
8 hours
> Nerve axonotmesis and irreversible change
> Irreversible muscle ischaemia and necrosis
End stage limb changes
> Stiff fibrotic muscle compartments
> Impaired nerve function
> Clawing of limbs
> Loss of function
Describe the clinical presentation of compartment syndrome
Pain out of proportion to that expected from the injury
Pain on passive stretching of the compartment
Pallor
Paraesthesia
Paralysis
Pulselessness
Describe compartment pressure measurements used to determine whether compartment syndrome is present
Normal pressure: 0-4 mmHg, 10 mmHg with exercise
DBP-CP <30 mmHg
Where a patient may be hypotensive, e.g. after trauma, relating the compartment pressure to the diastolic blood pressure (DBP) is more accurate
CP > 30 mmHg
Abnormal with normal BP
Describe the treatment for compartment syndrome
Open any dressings / bandages
> Reassess
> Observation (see if symptoms settle)
> Surgical release if no improvement or deterioration
> > > Fasciotomy
> > > > Full length decompression of all compartments - releases pressure
> > > > Excise any dead muscle
> > > > Leave wounds open
> > > > Repeat debridement every 48h until pressure down and all dead muscle excised
> > > > Outflow restored and pressure normalises
> > > > 48h delayed wound closure +/- plastic surgery or skin grafting
Late presentation
> Irreversible damage already present
> Fasciotomy will predispose to infection
> Non-operative treatment
> Splint in position of function
> Does not restore function but prevents clawing
List the causes of acute monoarthritis
Infection
> Crystal-induced
> Gout
> Calcium pyrophosphate
Reactive (may be oligo-)
Haemarthrosis
Systemic rheumatic condition
Trauma
Describe the pathogenesis of septic arthritis
Acute monoarthritis is septic until proven otherwise
> Usually involves knee
> Can involve any other joint or be polyarticular
Pathogenesis
> Bacteria enter joint and deposit in synovial lining
» Haematogenous spread
» Local invasion / inoculation
> Rapid entry into synovial fluid
> No basement membrane
> Close relationship to blood vessels
List risk factors for septic arthritis
- Previous arthritis
- Trauma
- Diabetes
- Immunosuppression
- Bacteraemia
- Sickle cell anaemia
- Prosthetic joint
Describe the findings of synovial fluid analysis in septic arthritis
Cell count > 50,000 wbcs/mm3
Differential >75% PMNs (polymorph neurophils)
Glucose: low
Gram stain: relatively insensitive test
Culture: positive
> Consider unusual pathogens in immunocompromised
Describe the management of septic arthritis
Joint aspiration
> Daily or more frequently as needed
Antibiotics
Surgical intervention
> Only necessary if patient is not responding after 48h of appropriate therapy
Describe polyarticular septic arthritis
More likely to be over 60 years
Average of 4 jonts
> Knee, elbow, shoulder and hip predominate
High prevalence of RA
Often without fever and leukocytosis
> Blood cultures are positive in 75%
Synovial fluid culture positive in 90%
Staph and strep most common
Poor prognosis
List risk factors for gout
Modifiable
- Obesity
- Alcohol consumption
- High purine diet
- HFCS (high fructose corn syrup)
- Medications
> Aspirin: reduces uric acid excretion
> Diuretics
> Cyclosporin
> Pyrazinamide and ethambutol
> Nicotinic acid
Non-modifiable
- Age
- Male gender
- Race
- Genetic factors
- Impaired renal function
How is gout diagnosed?
Aspirate of synovial fluid
> Birefringent rods (needle-shaped) under polarising microscope being phagocytosed
Describe the clinical presentation of gout
Podagra – gout of first metatarsophalangeal joint, acutely painful, even bedding is painful
History of gout flares or hyperuricaemia
Raised serum uric acid (sUA) between attacks
Can drop acutely as uric acid is mobilised
Describe the differential diagnosis for gout
Septic arthritis
CPPD – calcium pyrophosphate crystal deposition (pseudogout)
> Less commonly first MTP
> Most commonly seen in knee, wrist and shoulder
> Crystals are rhomboid shaped
Describe the treatment of gout
Acute attacks: relieve pain and reduce inflammation
> Non-pharmacological: cold packs
> NSAIDs / Coxibs / Colchicine / Corticosteroids
Long-term: prevent further acute attacks, prevent joint damage, eliminate tophi
> Lifestyle modifications
> > Diet
> Reduce purine intake
> Reduce fructose-containing drinks
> Include skimmed milk, low fat yogurts, vegetable protein and cherries every day
> > Weight loss
> 1kg/month - avoid crash diets
> Avoid high protein diets
> > Moderate exercise
> > Reduce alcohol intake
Urate lowering therapies
> Allopurinol
> Xanthine oxidase inhibitor
> Start 100mg increase in 100mg steps every 4 weeks til target or max 900mg daily
> Febuxostat
> 80mg with option to increase to 120mg after 4 weeks if not at target urate
> More potent xanthine oxidase inhibitor
> Not nephrotoxic
What are the indications for treatment of gout?
Recurring attacks - >2/12
Tophi
Chronic gouty arthritis
Renal impairment (eGFR <60ml/min)
History of urolithiasis
Diuretic therapy use
Primary gout starting at a young age (under 40)
Very high serum urate >500 micromol/L
Describe the pathogenesis of reactive arthritis
Seronegative spondyloarthropathy
> Seronegative for rheumatoid factor
> Strong association with HLA-B27
» Increased likelihood of developing ReA and persistence
ReA develops soon after infection occurs elsewhere in the body
> Viable organism cannot be recovered from a joint – not a true septic arthritis
May involve cross-reactivity between bacterial antigen and joint tissues leading to a perpetuating Th2 cell-mediated response
Persistence of antigenic material (heat shock proteins) due to failed clearance possibly due to polymorphism of toll-like receptors
Describe the groups of bacteria which can cause reactive arthritis
SARA (sexually acquired reactive arthritis)
> Following infection with Chlamydia trachomatis
> Other GU organisms have been implicated
> Neisseria gonorrhoea
> Mycoplasma genitalium
> Ureplasma urealyticum
> Lymecycline may be used
> 70% self-limiting, most disease mild and short-lived
Enteric infections
> Salmonella
> Shigella
> Yersinia
> Campylobacter
> Clostridium
Describe the clinical features of a reactive arthritis
Acute onset usually 2-6 weeks post-infection
Warm, swollen, tender joints, usually lower limb
Systemically unwell
Elevated inflammatory markers and malaise
Triad of arthritis, conjunctivitis and urethritis
70% will resolve in 3-12 months, 50% will recur
Lower limb asymmetric oligoarthritis
Dactylitis – sausage digits
Enthesopathy – Achilles tendonitis, plantar fasciitis
Inflammatory back pain
Extra-articular features
> Conjunctivitis, iritis, keratitis, episcleritis
> Keratoderma blennorrhagica and nail dystrophy
> Urethritis, prostatitis, cystitis, cervicitis
> Circinate balanitis
> Stomatitis, diarrhoea
> Rarely cardiac involvement with aortitis
Describe the investigations and management of reactive arthritis
Investigations
> Joint aspiration to exclude sepsis
> Swabs – urethral, cervical
> Screen for other related infections
> Inflammatory markers – ESR, CRP
> Chlamydia serology
> HLA-B27 for prognostic not diagnostic reasons
Management
> Mild – NSAID and simple analgesia
> Moderate – NSAID, joint aspiration and corticosteroid injection
> Severe or prolonged – refer rheumatology for consideration of DMARD
» Sulphasalazine, methotrexate, anti-TNF alpha
Referrals
> Joint effusions should be aspirated to exclude sepsis
> Ophthalmology if uveitis
> Rheumatology referral indicated if symptoms unrelieved by NSAIDs or joint effusions evident
Describe the factors influencing fracture healing
Type of bone
> Long bones take longer to heal
Mechanism of injury
> High energy injuries
> Take longer as energy is transferred to bone and soft tissue destruction ensues
Closed or open fracture
> Open fractures are prone to infection, can impair healing
Describe indirect fracture healing
Callus formation
> Fracture haematoma and inflammation
> Blood from broken vessels forms a clot
> 6-8h after injury
> Swelling and inflammation with removal of dead bone/tissue cells at fracture site
Fibrocartilagenous (soft) callus
> 3 weeks
> New capillaries organise fracture haematoma into granulation tissue – procallus
> Fibroblasts and osteogenic cells invade procallus
> Make collagen fibres which connect ends together
> Chondrocytes begin to produce fibrocartilage
Bony (hard) callus
> After 3 weeks and lasts 3-4 months
> Osteoblasts make woven bone
Bone remodelling
> Osteoclasts and osteoblasts remodel woven bone into compact bone and trabecular bone
Management
> A degree of movement is desirable to promote tissue differentiation
> Excessive movement disrupts the healing tissue and affects all cellular differentiation
Describe direct fracture healing
Unique artificial surgical situation
Relies upon reduction and compression of bone ends – anatomical reduction
Fracture stable – absolute stability – no movement under physiological load
Mechanism
> No callus
> Cutting cones across fracture site
> Direct formation of bone via osteoclastic resorption and osteoblastic formation
Describe the general blood supply to a bone
Skeleton receives 5-10% cardiac output
Endosteal supply
> Inner 2/3
> Nutrient artery
> High pressure
Periosteal supply
> Outer 1/3
> Capillaries from muscle attachments
> Low pressure
Metaphyseal-epiphyseal vessels
> Ends of long bone
> Separate in children, connected in adults
Describe the blood supply to the femoral neck
Metaphyseal-epiphyseal system
> Medial + lateral circumflex arteries
» Branches of profunda femoris
» Form an extracapsular arterial ring at the base of the femoral neck
Ascending cervical vessels (aka retinacular vessels) pass up the femoral neck and form a subsynovial ring at the base of the femoral head
> Epiphyseal branches from this ring supply the femoral head itself
Other vessels (less extensive)
> Branch of obturator artery (via ligamentum teres); more predominant in children
> Branches from nutrient artery through diaphysis
Describe femoral fractures
Certain types of fracture can cause disruption, particularly to cervical retinacular vessels e.g. displaced intracapsular neck of femur fractures
> Problems with bone healing and avascular necrosis
Describe fractures that cause problems with blood supply
Fractures
> Femoral neck fractures
Surgery
> Surgical fixation of fractures
e.g. intramedullary nail used to fix a long bone fracture – temporary damage to endosteal blood supply
Certain fractures are prone to problems with union because of potential problems with blood supply
> Proximal pole of scaphoid fractures
> Talar neck fractures
> Intracapsular hip fractures
> Surgical neck of humerus fractures
List factors that may inhibit fracture healing
Patient factors
> Increasing age
> Diabetes
> Anaemia
> Malnutrition
> Peripheral vascular disease
> Hypothyroidism
> Smoking
> Alcohol
Medication
> NSAIDs (especially COX-2 inhibitors)
> Reduce local vascularity at fracture site
> Additional reduction in healing effect independent of blood flow
> Steroids (inhibit osteoblasts)
> Bisphosphonates
> Inhibit osteoclastic activity – inhibit bone remodelling
> Recognised bisphosphonate associated fractures (subtrochanteric femoral fractures)
> Delay fracture healing as a result
> Long half-life
Describe avascular necrosis and its consequences
AVN / osteonecrosis
> Bone infarction – tissue death caused by an interruption of the blood supply – near a joint
Can cause
> Infarction of sub-chondral bone
> Collapse of the joint and end stage arthritis
Osteonecrosis is most common in the hip
Pathophysiology
- Interruption to blood flow
- Extraosseous e.g. trauma
- Intraosseous e.g. microcirculation from sickle cell
- Increased extravascular pressure e.g. steroid-induced fat cell hypertrophy
Early stages
> Necrosis always involves the medullary bone first
> Cortex – collateral blood supply
> Articular cartilage spared – receives nutrition from synovial fluid
Later stages
> If bone does not remodel, microdamage does not get repaired and the mechanical properties of the bone are impaired
> Subchondral bone weakens and collapses
> Joint surface becomes irregular and no longer smooth
> Further damage to surrounding articular cartilage – arthrosis
List risk factors for avascular necrosis
Risk factors: AS IT GRIPS Collapse Happens
> Alcohol abuse
> Steroids / sickle cell disease
> Idiopathic
> Trauma (especially joint dislocation)
> Gaucher’s disease / Gout
> Rheumatoid / radiation
> Infection / inflammatory arthritis
> Pancreatitis / pregnancy
> SLE / smoking
> Chronic renal failure / chemotherapy / Caisson disease (decompression sickness)
> Hyperlipidaemia
Describe the clinical presentation and examination of avascular necrosis
Asymptomatic
Pain – infarction or arthritis
Hip (AVN femoral head)
> Groin pain
> Worsens with weight bearing and motion
> Less commonly thigh and buttock pain
Rest pain
Night pain
Clinical examination
> Physical exam findings
> Pain on joint movement
> Limp
> Restricted motion
> Hip (AVN femoral head)
> Limitation in internal rotation and abduction
Describe the changes seen on X-ray in avascular necrosis
Early
> Mild density changes followed by sclerosis / cystic areas
Later
> Subchondral radiolucency
> “Crescent sign” precedes subchondral collapse
> Loss of sphericity and collapse of the femoral head
> Joint-space narrowing and degenerative changes
> AVN is bilateral in 55% of cases
Describe the treatment of avascular necrosis
Depends on stage of disease at presentation
Reduce risk
> Use minimum effective dose of systemic corticosteroids
Early symptoms
> Partial weight bearing
> Bisphosphonates?
Intervention
> Aimed at trying to reperfuse and heal infarcted region
» Core decompression +/- bone graft
» Vascularised bone graft
» Stem cell therapy
> Healing phase
> Creeping substitution – dead bone is replaced by new bone
> If subchondral collapse or arthrosis
> Total joint replacement – hip replacement surgery
What is Kienbock’s disease?
AVN of the lunate bone
Describe the composition of bone matrix
Organic (40%)
> Type I collagen (90%)
> Also type V, XI collagen
> Mucopolysaccharides
> Bone-specific proteoglycans
> Non- collagenous matrix proteins – osteonectin, osteopontin
> Responsible for tensile strength
Inorganic (60%)
> Calcium hydroxyapatite: calcium + phosphorus (also sodium & potassium)
> Responsible for compressive strength
Describe the different types of cells found in bone
Osteoprogenitor - stem cells
Osteoblasts – bone-forming cells
> Derived from mesenchymal stem cells through osteoprogenitor cells
> Produce new bone matrix
> Contain abundant ER and mitochondria
> After laying down new bone, 3 main fates
> Osteocyte – 90% of bone population
> Bone lining cell
> Apoptosis
Osteocytes – mature bone cells
Osteoclasts – bone-resorbing cells
> Large multinucleated cells
> Ruffled border
> Abundant mitochondria and lysosomes (contain acid phosphatase)
Describe the structure of compact bone
Compact e.g. outer shaft of femur
> Aka cortical bone
> Mainly found in diaphysis of long bones
> Lamellae (sheets) of bone matrix arranged concentrically around central neurovascular bundles forming Haversian systems/osteons
> Between each layer of lamellae there are osteocytes, which lie in lacunae
> Canaliculi are small channels derived from lacunae and allow communication between osteocytes
> Larger perforating channels lie perpendicular to vessels – Volkmann’s canals
> Allow perforating vessels to supply each osteon
> Slow turnover rate and metabolic activity
> Stronger and greater resistance to torsion and bending than cancellous bone
