Botten Flashcards
Tendinitis
acute inflammation or irritation of a tendon
Tendinosis
chronic tendon injury
characterized by swelling and pain of a tendon
Tenosynovitis
problems involving tendon and overlying synovial covering
Location tendon problems
Insertional – problems at the point of insertion at the bone
Non-insertional – problems with the tendon itself
Tendinopathy
umbrella term for tendon disorders
What is the function of tendons?
Transmit forces generated from the muscle to the bone to elicit movement.
Absorb external forces to prevent injury to the muscle.
Pathophysiology of tendinopathy
Tendinopathy results from loss of balance between micro damage from overuse and reparative mechanisms
Tendon becomes damaged and the healing process cannot keep up = failed healing response
Chronic Tendon Injury or over use – repetitive loading- causes degeneration/disorganisation of collagen fibres
– May decrease in number
– May have an increase in surrounding matrix
– Invasion of blood vessels to try and stimulate healing
Increased cellularity, but little inflammation
Risk factors for tendinopathy
Age – peak is middle age, because older population tend to be less active
Chronic Disease - Diabetes, RA - affect soft tissues and ability to heal
Adverse Biomechanics – e.g. a very tight calf always places the Achilles tendon under an increased load even during normal activities
Repetitive Exercise – recreational or occupational
Recent increase in activity
Quinolone Antibiotics – targets the tendons
• e.g. Ciprofloxacin
Clinical Features of tendinopathy
- Pain
- Swelling
- Thickening
- Tenderness on palpation
Can be clarified with provocative tests – ask patient to contract muscle group against resistance -> pain
diagnosis of tendinopathy
Ultrasound – can see the shape of tendon, determine vascularization using doppler
MRI – Tendinopathy best seen on T1.
• Helps exclude any other pathology
Non-operative Treatment of tendinopathy
Most give a success rate of about 80% in two years
- NSAIDs
- Activity modification
- Physiotherapy – stretching, eccentric exercises
- GTN patches
- PRP (platelet rich plasma) injection
- Extracorporeal Shockwave Therapy
- Steroid injection (controversial)
GTN patches for tendinopathy
Vasodilator
Increases local perfusion in an attempt to stimulate a healing response
Takes up to 12 weeks to see effects
Adherence may be poor
Side effects - headaches
Extra Corporeal Shockwave Therapy for tendinopathy
Same mechanism as used to break up kidney stones
Breaks down calcification and causes local trauma to stimulate healing
Operative treatment for tendinopathy
Considered if non-operative treatments fail
Debridement - excision of diseased tissue
(Tendon transfers) – in patients if the tendon is too diseased
Compartment Syndrome
Elevated interstitial pressure within a closed fascial compartment resulting in microvascular compromise
Common sites
• Lower leg – most common site
• Forearm
• Thigh
These muscle groups are enclosed by fascial compartments -> no flexibility for swelling
Lack of perfusion causes tissue death within 4-6 hours
Causes of Compartment Syndrome
1) Increased internal pressure
• Bleeding
• swelling
• iatrogenic infiltration – e.g. incorrect cannula insertion
2) Increased external compression
• Casts / bandages
• full thickness burns
3) Combination
Pathophysiology of Compartment Syndrome
Pressure within the compartment exceeds pressure within the capillaries -> microcirculation collapses
Decreased perfusion causes muscle ischaemia. This results in
• muscle swelling
• Increased permeability – fluid leaks into interstitial space
These cause further increased pressure
Autoregulatory mechanisms are overwhelmed
Muscle necrosis/myoglobin release (due to damage)
• Myoglobin is toxic to the kidneys
• Loss of function of limb or loss of life due to renal failure
Neurapraxia
temporary loss of motor and sensory function due to blockage of nerve conduction
Initially reversible if relieved early
permanent damage may result after as little as 4 hours
End stage compartment syndrome
Stiff fibrotic muscle compartments
Impaired nerve function – if any muscle survives it will not be useable because the nerve supply is damaged
Clawing of limbs – contracture of the muscles
Loss of function
Clinical Features of compartment syndrome
6 P’s
Pain – disproportionate to that expected from the injury
Pain on passive stretching of the compartment
• E.g. wiggling of toes, stretching of fingers
Pallor – compromised vascular supply
Parathesia – loss of nerve function
Paralysis
Pulselessness – very late sign
- Swelling
- Shiny Skin
- Autonomic Responses– sweating, tachycardia,
Which body part (and nerve) will be impacted first with compartment syndrome of the lower leg?
1st Dorsal webspace affected first
deep peroneal nerve
indicates a problem in the deeper compartments
Treatment of compartment syndrome
Urgent
Open any constricting dressings / bandages
Reassess
Surgical Release
• Full length decompression of all compartments
• Excise any dead muscle
• Leave wounds open
• Repeat debridement until pressure decreases and all dead muscle is excised
Amputate if there is already irreversible damage
Acute hot joint Differential diagnosis
- Septic arthritis
- Crystal arthropathy
- Trauma/haemarthrosis
- Early presentation of polyarthorpathy e.g. RA
Investigation of an acute hot joint
Short history of acute, hot, swollen and tender joint(s) should be regarded as having septic arthritis until proven otherwise
Aspirate synovial fluid
o Gram stain and culture before antibiotics
o NB: may be negative!
o Microscopy
Blood culture should always be taken
FBC
X-ray of no value in this context
Septic arthritis - clinical presentation
- Pain
- Fever
- red, hot, swollen and agonisingly painful joint
- loss of function
- Effusion
most common Causative organisms or septic arthritis
Staphylococcus aureus – most common
Gram negative organisms in 5-20% - commonly children, elderly, immunocompromised/ IVDU
o Neisseria gonorrhoea
o Haemophilus influenzae (children)
NB: culture is negative in over 20%
risk factors for septic arthritis
- RA/OA/other inflammatory arthitides
- Biologic DMARD therapy
- Joint prosthesis/surgery
- Low SE status
- IVDU
- Alcoholic liver disease
- Diabetes
- Cutaneous infection/ulcers
Routes by which bacteria can reach a joint
1) Haematogenous route
2) Dissemination from osteomyelitis (bone infection)
3) Spread from an adjacent soft tissue infection
4) Diagnostic or therapeutic measures
5) Penetrating damage by puncture or trauma
Which conditions may cause septic arthritis?
- Lyme disease – borrelia burgdoferi
- Brucellosis
- Syphilitic arthritis – congenital and acquired
What are the types of Crystal arthropathy?
gout
pseudogout
Gout
Most common inflammatory arthritis
characterised by recurrent attacks of a red, hot, tender and swollen joint
Caused by excess levels of uric acid
Leads to deposition of urate crystals in/near joints or soft tissue (tophi)
Causes of gout
Primary – hyperuricaemia due to genetic predisposition
Secondary – high uric acid due to: o myeloproliferative disorder (PRV) o leukaemia treated by chemo o thiazides o chronic renal disease
which factors can cause higher levels of uric acid?
o older ages o Obesity o high alcohol consumption o high protein diet o diabetes mellitus
Diagnosis of gout
Can be clinical diagnosis alone if obvious factors (hyperuricaemia and recurrent podagra)
Definitive diagnosis = MSU crystals
Diagnosed by aspirate
negatively birefringent needle shaped crystals seen on polarized microscopy
Serum urate levels and U&Es
Presentation of gout
typically presents with an acute monoarthropathy
• mainly (> 50%) occurs in the joint of the big toe (metatarsophalangeal joint)
• However it can be polyarticular.
- Hyperacute - Maximum intensity within 6-12 hours
- Rapid onset swelling and tenderness
Pathophysiology of gout
Chronic elevation of uric acid levels above the saturation point
Deposited preferentially in peripheral joints and subcutaneously as tophi
Asymptomatic period - crystal levels build
Acute attack can be precipitated by: o Trauma o Surgery o Starvation o Infection o diuretics
If untreated -> further attacks/irreversible joint damage
Management of gout
Acute
o NSAIDs – high doses reduce pain and swelling
o Alternatives – colchicine, corticosteroids
o NB: stop statins as co-prescrition with colchinine increased the risk of myopathy
If attacks are repeated - urate lowering therapy
o Allopurinol – xanthine oxidase inhibitor
ULT should be offered to all patients who have a diagnosis of gout
Gout differential diagnosis
- Septic arthritis (in acute monoarthropathy)
- Reactive arthritis
- Haemarthosis
- Pseudogout
Pseudogout
Calcium pyrophosphate crystal deposition
crystals form in the synovial fluid, cartilage and extra-articular tissues (chondrocalcinosis)
acute monoathropathy typically of larger joints
usually spontaneous and self-limiting, but can be provoked by:
o Surgery
o Illness
o trauma
Can be secondary to hyperparathyroidism or haemochromatosis
Pseudogout diagnosis
Positively birefringent rhomboid shaped crystals on aspiration
Management of pseudogout
- Aspiration helps reduce the pain and swelling
- NSAIDs
- colchicine
Reactive arthritis
Sterile synovitis which occurs following a distant mucosal infection (classically GU or GI)
Occurs as an autoimmune response to infection elsewhere in the body
Triad (unusual) of:
o Post infectious arthritis
o Non-gonoccoccal urethritis
o Conjunctivitis
Preceding illness usually a urethritis or diarrhoeal
Trigger organisms for reactive arthritis
o Salmonella
o Shigella
o Yersinia
o chlamydia trachomatis
Clinical features of reactive arthritis
- Acute, asymmetrical lower limb arthritis
- Larger joints of lower limbs
- More common in men
- Days – weeks post infection
Enteropathic arthritis
reactive synovitis seen with UC and Crohn’s disease
An asymmetrical lower limb arthritis
Treatment of the bowel disease and NSAIDs
X-ray findings in osteoarthritis
LOSS: • Loss of joint space • Osteophytes • Subarticular sclerosis • Subchondral cysts
Osteoarthritis
- Degenerative joint disease
- disorder of articular cartilage
- Commonest form of arthritis
- Middle aged/elderly
- Affects weightbearing joints – hip, knee
- Pain and crepitus on movement
- Worse with prolonged activity
- Joint instability
- Stiffness after rest
functions of bone
Structural
o Support
o Protection
o Movement
Mineral Storage
o Calcium
o Phosphate
Indirect healing
Secondary healing via callus formation
‘Formation of bone via a process of differential tissue formation until skeletal continuity is restored’
INFLAMMATION, REPAIR AND REMODELLING
Steps of indirect healing
- Fracture haematoma and inflammation
- Fibrocartilage (SOFT) callus - lasts 3 weeks
- Bony (HARD) callus - lasts 3 months
- Bone Remodeling
Direct Fracture Healing
Unique ‘artificial’ surgical situation
‘Direct formation of bone, without the process of callus formation, to restore skeletal continuity’
Relies upon compression of the bone ends
Pattern of blood supply to bones
- Endosteal: Inner 2/3rds
* Periosteal: Outer 1/3rd
Compromise of blood supply to bones
1) Anatomical factors:
Certain fractures are prone to problems with union or necrosis (bone death) because of potential problems with blood supply
Blood supply with an end artery (no collateral blood supply)
2) Surgical factors (iatrogenic) - e.g. stripping of periosteum
What type of fractures require surgical intervention because they compromise blood supply with an end artery?
- Proximal pole of scaphoid fractures
- Talar neck fractures
- Intracapsular hip fractures
- Surgical neck of humerus fractures
Which factors impair Fracture healing?
Patient factors • Increasing age • Diabetes • Anaemia • Malnutrition • Peripheral vascular disease • Hypothyroidism • Smoking • Alcohol
Medication
– NSAIDs - inhibit osteoblasts and osteoclasts, reduce vascularity
– Steroids - decrease bone metabolism
– Bisphosphonates - inhibit osteoclasts and induce apoptosis in osteoblasts
Osteonecrosis
also called AVascular Necrosis (“AVN”)
refers to bone infarction (tissue death caused by an interruption of the blood supply) near a joint
most common in the hip and shoulder
bilateral in majority
AVN Clinical Presentation
Osteonecrosis can be asymptomatic and found incidentally on imaging
Most patients present because of pain, either from the infarction itself or from secondary arthritis due to subchondral collapse
Rest pain occurs in about 2/3 of patients
o unlike OA patients – because it is an infarction process, not just related to movement
night pain occurs in about 1/3 of patients
Which movements of the hip are most limited with AVN of the femoral head?
osteonecrosis causes particular limitation in internal rotation and abduction
Pathophysiology of AVN
Always involves the medullary bone first
Blood flow disruption causes a period of ischaemia, followed by infarction. Areas of bone necrosis develop. Osteoclasts resorb the necrotic bone and try to replace it with new bone (creeping substitution).
If this is too slow, the necrotic cancellous bone collapses. Results in secondary damage –> subchondral collapse leads to end stage arthritis
Causes of AVN
may be unclear
o sickle cell anaemia
o Vascular damage - trauma
o Increased intraosseous pressure (oedema)
o mechanical stresses
Bone remodeling
process by which osteoclasts secrete acid and proteolytic enzymes to digest the bone matrix and osteoblasts synthesize new organic matrix leading to the deposition of newer, better bone
How does AVN cause arthritis?
If bone dies, it does not remodel
micro-damage does not get repaired
If enough damage accumulates, sub-chondral bone can be weakened to the point of collapse
sub-chondral bone collapse causes the joint surface to become irregular
If one side of the joint surface is not smooth, it will damage the other surface
What is the classical sign of AVN of x-ray?
crescent sign (subchondral radiolucency)
seen just before collapse
other:
o Subchondral collapse
o Bone remodelling
Risk factors for AVN
- History of trauma, especially a joint dislocation
- Corticosteroid use or Cushing’s disease
- Alcohol abuse
- Sickle cell disease/haemoglobinopathies
How can you prevent AVN?
minimum effective dose of systemic corticosteroids should be used. If possible, steroid-sparing agents should be used
Patients at high risk of AVN should be educated about AVN and advised to report symptoms as soon as possible
What effect does the position of a femoral neck fracture have on the blood supply to the femoral head?
Vessels reflect along retinaculae
a subcapital (intracapsular) fracture will risk damaging vessels to femoral head
This can lead to avascular necrosis
different treatment:
• Hemiarthroplasty for displaced subcapital fracture to replace head with loss of blood supply
• Sliding hip screw for intertrochanteric fracture as blood supply is intact and therefore fracture will heal
PAGET’S DISEASE OF BONE
- increased bone turnover
- osteoclastic and osteoblastic activity
- raised alkaline phosphatase
complications include fracture deformity and rarely sarcoma
CHARACTERISTIC X-RAY FINDING OF PAGET’S DISEASE OF BONE
blade of grass sign
lucent leading edge in a long bone seen during the lytic phase
Chondrosarcoma
malignant cartilaginous tumour
What are the three main classes of bone disorders and their characteristic findings?
Degenerative - Bone production (sclerosis, osteophytes)
Inflammatory - Periarticular erosions
Depositional - Periarticular soft tissue masses
What would you see on imaging of an inflammatory bone disorder?
erosions
soft tissue swelling
symmetrical joint space narrowing
monoarthopathy = infection; polyarthropathy = RA/spondyloarthropathy
What would you see on imaging of a degenerative bone disorder?
asymmetrical joint space narrowing
osteophytes
sclerosis
How do Subchondral Cysts form?
Synovial fluid is forced into the subchondral bone, causing a cystic collection of joint fluid
How can you recognise Secondary Degenerative Arthritis?
– Atypical locations
– Atypical appearance
– Atypical age
Name 4 seronegative arthropathies. Which gene are they associated with?
(tend to have HLA-B27 association)
– Psoriatic arthritis
– Reactive arthritis
– Ankylosing spondylitis
– Inflammatory bowel disease
Discitis
inflammation that develops between the intervertebral discs of the spine
Ankylosis
abnormal stiffening and immobility of a joint due to fusion of the bones
