- Greenstick fractures usually occur in immature bone (i.e. children)
- Pathological fractures are normally a result of cancer and/or osteoporosis etc
- When looking for problems with non-contractile elements, you'll get pain on passive, isotonic, active etc just NOT with isometric! Why? Because isometric is straining the soft tissues structures (i.e. muscle) and not stressing the joint!
- Remember during gait there is a lot of eccentric muscle activity occuring so don't get stuck in the concentric mind frame!
Saturday, 23 January 2010
Some things I learnt from PAM1 Summative Assessment
Sunday, 17 January 2010
Passive Movements
"Movements produced on a person by an external force (i.e. no voluntary muscle contractions by patient) provided either by a person or a machine (CPM)"
Sub-divided into:
- Physiological passive movements (mobilisations)
- Accessory movements (mobilisations) - Glides,Rolls,Distractions,Compressions,Rotations (cannot be performed actively)
- Passive stretching (mobilisations)
- Adverse Neural Tensioning (ANT)
- Manipulations
Structures Involved:
- INTRA-ARTICULAR: subchondral bone; articular cartilage, synovial fluid, synovial membrane, menisci and fat pads
- PERI-ARTICULAR: joint capsule, supporting ligaments, tendons, muscles, fascia, skin, blood & lymphatic vessels, nerves
Normal Restrictions to Joint ROM:
- Joint capsule
- Ligaments
- Muscles & their tendonous attachements (active/passive insufficiency)
- Bone/cartilage approximation i.e. shape and joint surface (loose packed,closed packed)
Abnormal Restrictions to Joint ROM:
- Increased synovial fluid volume/pressure
- Muscle imbalance
- Mal-tracking
- Trauma
- Abnormal physiological changes in connective tissue due to immobilisation
- Decrease in water in tissue matrix = abnormal points of collagen cross-linking - 'adhesions'
- Atrophy of ligaments
- Tendons degrade
- Muscle contractures
- Nerve tensioning
- Synovial tissue atrophy
- Pain/guarding mechanism (muscle spasm)
Beneficial Physiological Effects:
- Maintains ROM/Increases ROM
- Cartiliage healing/nutrition (hydrokinetic transport)
- Smearing of synovial fluid reducing friction
- Appropriate alignment
- Increases lymphatic drainage/helps reduce oedema
Indications
- Assessment of passive ROM
- Diagnostic testing
- Maintaining joint ROM in a paralysed or unconscious patient
- Reducing joint pain
- Reducing muscle spasm / guarding
- Restoration of range (correction of 'mal-tracking and/or passive stretching)
- Facilitates healing process
Limitations
- CANNOT CHANGE DISEASE PROCESS
- WILL NOT prevent muscle atrophy
- WILL NOT increase strength or endurance
Contractions
- Excessive pain
- Joints adjacent to unstable fractures
- DVT in area
- Infection
- Active inflammatory (R.A)
Range of Motion
- Direction of movement will depend on the desired efffect
- Amplitude of the passive movement can be graded to indicate where in the available range the technique is being performed
- Helpful in matching the induced range of P.M. to the desired mobilising effect depending on the irritiability of the lesioned structure
Maitland Grading Scale
- 1 - SMALL amplitude movement performed at the beginning of range (within resistance free zone)
- 2 - LARGE amplitude movement performed within a resistance free part of the range
- 3 - LARGE amplitude movement performed into resistance or up to the limit of resistance
- 4 - SMALL amplitude movement performed into resistance or up to the limit of resistance
- 5 - High velocity, short amplitude thrust often near or at the limit of abnormal movement, at speed outside of patient's control
Friday, 15 January 2010
Rationale For Proprioceptive Exercises
Is the exercise...
- Weight bearing appropriate?
- Reactive (external stimuli or not and are these varied in weight,size,shape if objects, speed, is the trainer or therapist the stimuli?)
- Goal driven?
- Functional? (e.g. sports specific)
- Base of support (wide, narrow, stable, unstable)
- Visual Stimuli or no visual stimuli (eyes closed or open?)
- Pace (slow or quick? Does it hit the slowly adapting and rapidly adapting proprioceptors?)
- Pertubation/Complexity?
- Multiplane/multiaxial?
Rationale For Strength Exercises
IS THE EXERCISE...
- Weight bearing appropriate? (NWB/PWB/FWB)
- With or against gravity? (e.g. gravity counter balanced or additional resistance - Oxford Scale)
- Functional?
- OVERLOAD (is the target muscle or muscle group being stressed enough to elicit an adaption?)
- SPECIFICITY (SAID - Specific Adaptions to Imposed Demands)
- Single plane or multi-plane? (is the muscle being loaded in all 3 planes?)
- Open or closed chain?
- Ranges? (through full ROM? Inner/Mid/Outer - appropriate to rehab level?)
- Isometric/eccentric/concentric (appropriate to stage of injury?)
- Motivational?
- Fun?
- Fibre recruitment (is it recruiting the fibres required for their function e.g. Type I, Type IIa/IIb slow and fast twitch)
- Intensity (high/med/low?)
- Reps & Sets? (endurance,hypertrophy,strength) avoid atrophy
- Isolated or intergrated? (compound/mutli-joint exercise or isolated muscle?)
Thursday, 7 January 2010
Joint Classification (Smart Arse way of describing joints!)
KNEE - Modified bicondylar synovial joint
- 2 degrees freedom of movement (flexion/extension & ext/interal rotation)
- Conjunt rotation (external rotation) occurs during the last 30 degrees of extension to
achieve closed packed position (automatic/accessory movement)
- Adjunct rotation (physiological/voluntary) movement in flexion
ANKLE - Uniaxial hinge type synovial joint
- Between tibia/fibula and trochlea of talus
- Reinforced by fibrous capsule, medial deltoid ligament (4 parts), lateral ligament
(3 parts)
- 1 degree freedom of movement (dorsi/plantar flexion)
HIP - Multi axial ball & socket synovial joint
- Between acetabulum and head of femur
- Acetabular labrum deepens the acetabular cavity creating more stability
- Fibrous joint capsule reinforced by 3 ligaments
- 3 degrees freedom of movement (flexion/extension, ab/adduction, med/lateral rotation)
MTP - Multiaxial condyloid synovial joint
- Surrounded & strengthened by articular capsules and collateral ligaments
- 2 degrees freedom of movement (flexion & extension & ab/adduction)
- 2 degrees freedom of movement (flexion/extension & ext/interal rotation)
- Conjunt rotation (external rotation) occurs during the last 30 degrees of extension to
achieve closed packed position (automatic/accessory movement)
- Adjunct rotation (physiological/voluntary) movement in flexion
ANKLE - Uniaxial hinge type synovial joint
- Between tibia/fibula and trochlea of talus
- Reinforced by fibrous capsule, medial deltoid ligament (4 parts), lateral ligament
(3 parts)
- 1 degree freedom of movement (dorsi/plantar flexion)
HIP - Multi axial ball & socket synovial joint
- Between acetabulum and head of femur
- Acetabular labrum deepens the acetabular cavity creating more stability
- Fibrous joint capsule reinforced by 3 ligaments
- 3 degrees freedom of movement (flexion/extension, ab/adduction, med/lateral rotation)
MTP - Multiaxial condyloid synovial joint
- Surrounded & strengthened by articular capsules and collateral ligaments
- 2 degrees freedom of movement (flexion & extension & ab/adduction)
Tuesday, 5 January 2010
Acute/inflammatory stage 0-72hrs
1) Damage to local blood vessels (capillaries), bleeding and cell death (trigger inflammation)
2) Local initial vasoconstriction (to limit fluid loss - but results in more cell death due to increased lack of oxygenated blood available at injury site)
3) Release of chemical mediators (histamine/serotonin etc) from dying cells causing VASODILATION or surrounding undamaged vessels, increasing their permeability, which can be seens as REDNESS (erythema) and felt as HEAT (calor) - permeability allows leukocytes to emigrate into site of injury guided by chemotaxis.
4) Damaged nerve endings give rise to pain (dolor), chemical irritation from mediators and increasing pressure from excess fluid and inflammatory exudate in the area (more responsible for pain in the later stages)
5) 'Walling Off' - Local vasodilation is not enought to prevent fluid loss so we get platelets activated by cell death (necrosis) become very sticky and release chemicals to activate the enzyme thrombin which converts fibrinogen (element of blood plasma) into FIBRIN which creates a sticky matrix to trap cellular debris and platelets to form a blood clot (temporary solution to fluid loss)
6) Leukocytes (neutrophils 6-24 hrs / monocytes & lymphocytes 24-48hrs) or white blood cells clear debris that wasn't caught by the sticky matrix and fight off an infection present.
7) Histamine causes local vasodilation within hours to introduce new plasma* rich blood for next stage of repair (each phase is laying the ground work for the next)
*Plasma = liquid portion of blood (90% water)
2) Local initial vasoconstriction (to limit fluid loss - but results in more cell death due to increased lack of oxygenated blood available at injury site)
3) Release of chemical mediators (histamine/serotonin etc) from dying cells causing VASODILATION or surrounding undamaged vessels, increasing their permeability, which can be seens as REDNESS (erythema) and felt as HEAT (calor) - permeability allows leukocytes to emigrate into site of injury guided by chemotaxis.
4) Damaged nerve endings give rise to pain (dolor), chemical irritation from mediators and increasing pressure from excess fluid and inflammatory exudate in the area (more responsible for pain in the later stages)
5) 'Walling Off' - Local vasodilation is not enought to prevent fluid loss so we get platelets activated by cell death (necrosis) become very sticky and release chemicals to activate the enzyme thrombin which converts fibrinogen (element of blood plasma) into FIBRIN which creates a sticky matrix to trap cellular debris and platelets to form a blood clot (temporary solution to fluid loss)
6) Leukocytes (neutrophils 6-24 hrs / monocytes & lymphocytes 24-48hrs) or white blood cells clear debris that wasn't caught by the sticky matrix and fight off an infection present.
7) Histamine causes local vasodilation within hours to introduce new plasma* rich blood for next stage of repair (each phase is laying the ground work for the next)
*Plasma = liquid portion of blood (90% water)
Internal anatomy of muscle fibres
- Sarcomere - The portion of a myofibril between two Z-discs
- Sarcoplasmic reticulum (SR) - Loose network of flattened tubules that surrounds the myofibrils in the muscle cell
- Transverse 'T' tubules - Invaginations of the sarcolemma that allow muscle action potentials (electrical chemical impulses) to pass into the centre of the cells causing depoloraization and release of calcium ions from the SR (run over and around the sarcoplasmic reticulum)
- Terminal Cisternae (lateral sacs) - Expanded regions of the SR, found on both sides of T tubules
- Calcium ions - concentrated in the SR when muscle fibre is at rest (flood out when muscle contracts)
- Triad - A T tubule and two terminal cisternae
General anatomy of muscle fibres
- Sarcolemma - the plasma membrane in muscle fibre
- Muscle fibres are multinucleotide - Being exceptionally wide and long, muscle fibres (0r cells) need many nuclei to regulate the metabolic demands of contractile proteins (e.g. actin and myosin)
- Sarcoplasm - The protein filled cytoplasm of muscle fibres
Sunday, 3 January 2010
Tissue Proliferation (fibrous repair) 1-10 days + post injury - Pathophysiology
- Ongoing phagocytosis
- Angiogenesis
- Production of collagen fibres (initially produced in random fashion)
- Absorption of inflammatory exudate
Factors influencing the rate of healing in the stages of proliferation and remodelling
- Severity of initial trauma: A severe second degree ligament sprain of the lateral ligament complex of the ankle will have a more prolonged proliferation and remodelling period than a first degree ligament sprain affecting the same structure.
- Early Management: When the necessary foundations have been set in place (e.g. protection, rest of tissues etc) for proliferation and repair can potentially reduce onset of chronic inflammation.
- Tissue Vascularity: e.g. skeletal muscle = highly vascular = more potential for repair than a a ligament = avascular
- Age: Younger people are quicker to heal than older
- Nutrition: e.g. protein deficiency, adequate nutrition that is also related to bloodflow is required for healing to take place
- Medication: Use of NSAIDS and steroidal drugs slow down proliferation and remodelling processes.
- Temperature: Colder it is = slower rate of healing
- Appropriate loading of healing tissue during rehab
EXUDATE - a definition
Material such as fluid, cells, cellular debris
(serous fluid, red blood cells, fibrinogen, tissue debris, white blood cell break down products)
which have escaped blood vessels and been deposited into tissues or on tissue surfaces, usually as a result of inflammation
EXUDATE (in contrast to transudate) characterised by high content of protein, cells or solid material
Intersitial Fluid / Hydrostatic Pressure
Interstitial Fluid
The fluid that bathes and surrounds the cells (intercellular spaces)
Composed of: water, sugar, salt, hormones, co-enzymes, fatty acids, amino acids, neurotransmitters, cellular products
Provides a means of delivering materials to the cells (intercellular communication), and removal of metabolic waste products.
Hydrostatic Pressure
The pressure exerted by fluid (e.g. water) at rest
Increases in direct proportion to the density and depth of the fluid
General physiotherapy aims of early-phase management (Bleeding & Inflammation)
Acute Phases 1 & 2 : Bleeding (0-10hrs) & Inflammation (72hrs)
The aims are:
- To reduce pain
- To limit and reduce inflammatory exudates
- To reduce metabolic demands of tissue
- To protect the newly forming tissue from disruption
- To promote new tissue growth and fibre alignment
- To maintain general levels of cardiovascular and musculoskeletal fitness / activity
'REDUCE, REDUCE, PROTECT, PROMOTE, LIMIT, MAINTAIN'
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