Principles II Flashcards
Transverse fracture
Those that run across the axis
Oblique fracture
Fracture which goes at angle to axis
Spiral fracture
Runs around axis of bone
Comminuted fracture
Many relatively small fragments
Avulsion fracture
Piece of bone attached to tendon or ligament is torn away
Displaced
Parts of bone break and move from place and don’t remain correctly aligned
Non-displaced
Crack or break in bone remain in alignment and don’t move from their place
Periosteal injury
Direct blow, bleeding under periosteum
e.g. tibia from kick
Bone remodelling happens when
In response to stress
Wolff law
Bone remodels in direct response to the forces applied
Osteoclasts
Resorption
Osteoblasts
Deposition
Stress fracture process
When bone’s reparative capacity is overwhelmed by chronic overload, damage can begin to accumulate, and if allowed to progress this multifactorial process can lead to stress fracture
Bone overuse
Increased osteoclastic activity at sides of bone stress or strain may cause transient weakening of the bone locally, predisposing to microdamage
Unless given appropriate time for healing and osteoblastic mediated bone deposition, adjusting sites of microdamage are thought to coalesce, giving rise to sites of stress reaction or injury
At this stage may be minimally symptomatic, and if do plain film radiograph may appear normal. If patient does not rest with progressive overload the bone becomes increasingly vulnerable and patient develops symptoms that are thought to reflect extent of underlying bone injury
–> if uninterrupted, may develop into stress fracture
Stress fracture
Microfracture due to repetitive loading that, over time, exceeds the bone’s intrinsic ability to repair itself
2 mechanisms for overload
Impact forces
Muscle pull
Impact forces example
Metatarsal in marching
Muscle pull example
Neck of femur in female marathon runners
Fatigue stress fracture
Normal bone unable to keep up with repair when repeatedly damaged or stressed- normal bone, abnormal stresses
Insufficiency stress fractures
Under normal strain, but structurally abnormal because of metabolic bone disease or osteoporosis
Abnormally or weakened bone but normal stress
Stress fractures can occur in
Sedentary people who suddenly take up exercise, may also occur in athletes completing high volume high impact training e.g. running or jumping sports
Also reported in soldiers who march long distance
Where do stress fractures usually occur
Weight bearing bones
Tibia, metatarsals and navicular
Less common stress fracture areas
Femur
Pelvis
Periostitis definition
Inflammation of periosteum (tendon attachment)
Periostitis examples
Medial tibial stress syndrome
Repetitive jump, run, lift and weights
e.g. shin splints
Articular cartilage function
Shock absorber
Joint lubrication
Articular or hyaline cartilage
Covers joint surfaces
Fibrocartilage
Knee meniscus
Vertebral disk
Elastic cartilage
Outer ear
Osteochondral injury
Damage to articular cartilage +/- subchondral bone
Poor healing capacity because of inadequate blood supply (nutrition via diffusion from synovium, aided by joint loading)
Can osteochondral injury predispose to OA
Yes
e.g. talar dome with inversion injury
Osteochondral lesions contributors
Trauma, repetitive strain and poor supply to area
Severity of osteochondral injury
Varies
Small defect/crack to large piece broken up in knee
Osteochondral injury symptoms
Pain Swelling Catching Point tenderness Loss of motion
Confirming osteochondral injury diagnosis
X Ray
MRI
Osteochondral injury conservative treatment
Rest ICE NSAIDS activity modifications Bracing
Osteochondral injury more severe
Arthroscopy often recommended to repair or remove the fragment, and other surgical options include bone grafting, and stimulating blood flow to damaged area
Meniscal injury
Tear
Intervertebral disc injury
Prolapse
Long periods of stress on cartilage
Overuse can cause damage
Inflammation, breakdown and eventual loss of cartilage in joint
Overuse pathway of cartilage
Microscopic inflammation --> Softening --> Fibrillation --> Fissuring --> Gross Disruption
Osteochondritis Dessicans
Separation of bone and cartilage from normal surrounding bone and cartilage
e.g. medial femoral condyle
Osteochondritis Dessicans process
Focal area of subchondral bone that undergoes necrosis
Overlying cartilage remains intact to variable degrees, receiving nourishment from synovial fluid
When osteonecrotic bone is resorbed, the cartilage loses its supporting structure and subsequently the bony fragment may be displaced into joint space
Osteochondritis Dessicans symptoms
Pain during and after sports
In later stages may cause joint swelling and can lock and catch during movement
Dislocation
Complete disassociation of joint surfaces
Subluxation
Articulating surfaces remain partially in contact
Acute joint damage
Associated soft tissue damage
If large, increased risk of recurrent dislocations
Overuse joint damage
Chronic inflammation secondary to overuse
Sinus Tarsi syndrome
Thought to be related to post traumatic complications to recurrent ankle sprains
Present with localised pain in sinus tarsi location, with feeling of instability and aggravation by weight bearing activities
Patients do poorly on uneven surfaces
Sinus Tarsi causes
Inversion ankle sprain (70-80% of the time)
Pinching/impinging of soft tissues due to very pronated foot (20-30%)
Sinus tarsi physical presentation
Pain on sinus tarsi region with aggravation on foot inversion or eversion
Sinus tarsi treatment
NSAIDs Stable shoes Period of immobilisation Over counter orthosis Ankle sleeve
Sinus tarsi resistant cases
Steroid injection
Physical therapy
Cast ormothosis
Rarely surgery is indicated
OA
Fraying of cartilage (+/- loose fragments), bony cysts, subchondral bone sclerosis, osteophytes, thickening of synovium
OA RFs
o Age, FHx, congenital/developmental joint alterations, alterations of supporting structures, injury, obesity, occupational overuse
o Congenital hip dysplasia, slipped capital femoral disease
o Hypermobility
o Meniscal and cruciate stress increase risk of subsequent development of OA by 5-10 times
o Obesity- increased risk of OA in knee particularly in women
o Sex hormones may play part as OA in knee in women more common in postmenopausal women compared to men at same age
o Manual handling jobs e.g. lifting and climbing tasks at work- increased risk of hip and knee OA
o Hip OA- bending or twisting positions
o Knee OA- kneeling or squatting position
o More OA in male soccer players- increased tibiofemoral joint involvements, in weightlifters patellofemoral involvement, in female elite athletes 3x more OA in knee
What happens in OA
Breakdown of cartilage and underlying bone
Inflammation of synovium and joint capsule can also occur
Other structures within joint can be affected- ligaments can become thickened and fibrotic, and menisci damaged
Osteophytes
New bone outgrowths
Can grow on margins of joints in OA, possible in attempt to improve congruence of articular cartilage surfaces on absence of menisci
Subchondral bone OA
Bone vol. increases and becomes less mineralized
Pain OA
Related to thickened synovium and subchondral bone lesions
Primary cause OA
thought to be damage from mechanical stress with its afficient cell repair by joints
Sources of stress may be misalignment of bones, congenital/pathogenic, mechanical injury, fat, loss of strength in muscle supporting joint, impairment of peripheral nerves leading to sudden or uncoordinated movements
Stress (force) causes
Strain= deformation of tissue
Internal force within ligament tries to resist change in dimension caused by external force
Strain
Resultant change in dimension
Elastic range
When force release, tissue will return to original size
Elastic limit
Deformation becomes permanent beyond this
Plastic range
Permanent deformation range
Failure
Sufficient force to cause rupture of tissue
Acute ligament injury- Grade 1
Stretching of fibres
Minimal tearing
No laxity/normal end feel
No instability
Acute ligament injury- Grade 2
Partial tear
Laxity/normal end feel
Loose
Acute ligament injury- Grade 3
Complete tear
LAxity
No end feel
Instability
Collateral ligaments
Knee can pop
Pain and swelling
Cruciate ligaments
Hear popping sound as injury occurs
Leg may buckle as attempt to get up
Swelling within 24-36 hours
Grade 3 ankle sprain
Can also produce popping sound
Severe pain
Swelling and bruising- ligament no longer does job so v unstable
MCL inflammation breaststroke swimmers
Knee
Repetitive valgus loas across knee
MCL elbow
Repetitive throwing with valgus loading
Plantar fasciitis
Overuse syndrome of foot
Pain in heel and bottom of foot
Plantar fasciitis pain
Pain felt bending foot and toes up to ceiling
Most painful at first steps of day or after rest
Pain typically comes on gradually and affects both feet in about 1/3 of cases
Plantar fasciitis RFs
Excessive running Standing on hard surfaces for long time High arches of foot Presence of length inequality Flat feet Obesity seen in 70% of people that present with PF Achilles tendon tightness Inappropriate footwear
Plantar fasciitis treatment
Most cases time and conservative treatment: Stretching Rest Avoidance of walking on hard surfaces Insoles Cushioned shoes Physio Avoidance of stuff
Concentric contraction
Activity whilst muscle is shortening
Eccentric contraction
Activity whilst muscle is lengthening
Isometric contraction
Activity with no change in muscle length
Isotonic
Movement occurring at equal force throughout range
Isokinetic
Movement occurring at equal speed throughout range
Grade 1 tear- pathology
Small number muscle fibres torn
Fascia intact
Minimal bleeding
Grade 1 tear- signs
Mild pain
FROM
Full strength
Grade 2 tear- pathology
Significant number of muscle fibres torn
Increased bleeding
Grade 2 tear- signs
Increased pain
Swelling
Decreased ROM and strength
Palpable haematoma
Grade 3 tear- pathology
Complete tear (usually at musculotendinous junction)
Grade 3 tear- signs
Bleeding and swelling +++
No active contraction
Can be obvious gap where tear has happened
Cramps
Painful, involuntary contractions
Occur suddenly and are temporarily debilitating
In both skeletal and smooth muscle
Skeletal muscle cramps
Caused by muscle fatigue, or lack of electrolytes
e.g. Na, K and Mg
Smooth muscle cramps
Caused by menstruation or gastroenteritis
Cramp triggers
Dehydration, low level of minerals, or reduced blood flow through muscle may be triggers
Lactic acid build up
Leg cramps are associated with
CV disease Haemodialysis Cirrhosis Pregnancy Lumbar canal stenosis
Contusions (N.B. myositis ossificans)
Direct blow causes bleeding with haematoma formation
e.g. dead leg in footballers
Non-hereditary myositis ossificans
Calcifications occur on the side of the injured muscle, most commonly in arms or quads of thighs
Exact mechanism unclear
Thought to be due to inappropriate response of stem cells in bone against injury or because of inflammation, causing inappropriate differentiation of fibroblasts into osteogenic cells
Focal fibrosis
repetitive microtrauma –> chronic inflammation + adhesions
muscle overuse, resultant fibrosis
Chronic Exertional Compartment Syndrome (CECS)
Exercise –> increases intra-compartment pressure –> tight fascia limits expansion –> impairs blood supply –> pain
CECS symptoms
Pain Tightness Cramps Weakness Diminished sensation Can occur for months or years before diagnosed Usually relieved by rest
DOMS
Aching 24-48 hours post exercise (especially eccentric)
Secondary to inflammatory cell/metabolite build up e.g. downhill running
DOMS symptoms
Pain and stiffness
Unaccustomed or strenuous exercise
DOMS mechanism
Thought to be eccentric lengthening exercises which causes microtrauma to muscle fibres
After exercise muscle adapts rapidly and then there is soreness if repeated
Myofascial pain causes
Can be due to injuries, stress, inflammation and poor posture
Subjective weakness of involved muscle
Referred pain from trigger points
Myofascial pain trigger points
Exquisitely tender point in taut band of muscle
Hardening of muscle upon trigger point palpation- hard knots beneath skin
Chronic pain
Can appear in many body parts- characterized into active or latent
Myofascial pain and fibromyalgia
Shared symptoms with fibromyalgia
BUT fibromyalgia generally more widespread, is a systemic disease (central sensitivity syndrome) and usually associated with fatigue
Active myofascial trigger points
Spontaneous pain or in response to movement
Can lead to locally referred pain
Latent myofascial trigger points
Sensitive point with pain or discomfort only elicited in response to compression
Myofascial pain symptoms
Focal point tenderness
Reproduction of pain on muscle on trigger point palpation
Referred pain
Limited ROM following sustained pressure
Myofascial pain treatment
Massage therapy at trigger points- short term relief
Physical therapy- gentle stretching and exercise- useful for recovery full ROM
Gentle stretching reduces symptoms
Gentle activity
CECS symptoms
Brought on by exercise
Extreme tiredness in muscle and painful burning
After exercise, pressure relieves and pain stops after couple of minutes
Symptoms occur at certain threshold of exercise- varies person to person
Foot drop may be symptom
CECs most commonly in
Lower leg
Anterior most common
CECS diagnosis
Diagnosis of exclusion
Measurement of intra-compartmental pressures during symptom production
Non-invasive methods- NIRS using sensors in skin
Imaging studies to exclude other things
MRI
CECS average duration of symptoms prior to diagnosis
28 months
CECS differential diagnosis
Muscle strain
Medial tibial stress syndrome
Stress fracture
Popliteal artery entratment
CECS treatment
NSAIDs
CECS - should avoid
Splints
Casts
Tight wound dressings
CECS treatment if conservative doesn’t work
Fasciotomy
Tendon tears usually occur at
Site of least blood supply
Musculotendinous junction
complete or partial
Tendinopathy
Chronically painful tendon
Tendinosis
Collagen degeneration
Neovascularisation
e.g. patella + achilles tendon
Tendinitis
Inflammation of tendon
e.g. inflammatory arthritides
Paratenonitis
Inflammation of paratenon/tendon sheath
e.g. de Quearvain’s tenosynovitis
Tendinopathy and tendinitis symptoms
Pain Swelling Impaired function Pain worse with movement Mostly around shoulder and elbow
De Q
Inflammation of APL and EPB (control movement of thumb)
De Q symptoms
Pain in outside part of wrist that increases with gripping or rotating wrist, and thumb may be difficult to move
De Q RFs
Include certain repetitive movements, trauma or rheumatic diseases
Finkelstein’s test
Grasps and ulnar deviated hand when thumb held in fist- sharp pain on radius if test positive
for de Q?
Treatment of tendinopathies
Rest NSAIDs Splinting Physio Steroid injections Therapy
80% of people with tendinopathies get better within
6 months
Bursa
Facilitate movement of tendon over bony surface
Bursa acute
Traumatic bursitis
Due to direct knock causing bleeding into bursa
Bursa Overuse
Bursitis
e.g. subdeltoid bursitis
Parapatellar bursitis
Bursitis
pain and tenderness
bursa sacs may swell, making movement difficult
Bursa in what joints most affected
Shoulder
Elbow
Knee
Foot
Neuropraxia
Acute nerve issue
Due to direct blow
Symptoms (tingling, numbness, pain +/- weakness) in distribution of nerve
e.g. common peroneal nerve at neck of fibula
Nerve entrapment
Acute or chronic
e.g. prolapsed intervertebral disc + nerve root compression
Adverse neural tension
Chronic
Irritation of nerve due to local inflammation causing pain on stretching nerve
e.g. carpal tunnel
Carpal tunnel RF
Obesity Pregnancy Repetitive wrist work Hypothyroid Genetics Rheum arthritis
Carpal tunnel treatment
Surgery to cut transverse carpal ligament for persistent cases
Skin acute
Abrasions/lacerations
Skin overuse
Blisters/callus
