Frozen Shoulder aka Adhesive Capsulitis

Mr. Francis Lam is an upper limb surgeon and shoulder consultant, he gives some really great explanations on frozen shoulder in a simple easy to understand way.

Q. What is frozen shoulder?
A. Essentially a chronic fibrosing condition in which fibroblast cells become overactive and lay down abnormally thick layers of collagen causing marked thickening of the shoulder joint capsule. The capsular lining of the joint subsequently contracts and leads to shoulder joint stiffness and pain.

Q. What are the features of frozen shoulder?
A.

• Slow onset of pain felt near insertion of deltoid
• Trouble sleeping on affected side
• Restriction in both active and passive elevation & external rotation

Q. What's the difference between primary and secondary frozen shoulder?

http://www.shoulderspecialist.org/Frozen_Shoulder.html

See also Bowen technique

ANT - Adverse Neural Tension

Also known as AND (adverse neurodynamics) and AMT (adverse mechanical tension) but all basically mean the same thing.

They all describe the process whereby neural tissue is compromised and looses its ability to fully lengthen leading it to be unable to conform to changes in limb and or trunk position.

The 3 mechanisms nerves conform to positions are:

1) Sliding across mechanical interface (bone, muscle, fascia etc)

2) Unwinding of a nerve

3) Becoming stretched and therefore increasing their internal and external tension

In a nutshell, if mechanism 1 and 2 become compromised, mechanism 3 is greatly increased!

• ANT can be used to both diagnositcally test (assess) and treat neural problem

Aetiologies leading to GH impingement

Well for starters let's remind ourselves that aetiology is 'the study of the causes'!

Aetiologies for glenohumeral impingement can be divided into primary (direct cause) or secondary (indirect cause)

Primary

• Subacromial bursal thickening
• Increased subacromial loading
• Trauma (direct macrotrauma/repetetive microtrauma)
• Excessive overhead activity (too much waving to someone)
• Acromioclavicular arthrosis (osteophytes)

Secondary

• GH laxity/instability (note: laxity may be normal for some people)
• Muscle imbalance
• Scapula dyskinesia (difficulty or distortion in performing voluntary movements)
• Glenoid labrum lesions (joint will be less stable if the socket depth is decreased)

Arthroscopy?

A minimally invasive surgery used to either examine and/or treat the damage the interior of a joint, performed using an arthroscope.

Arthroscopic procedures can be used to evaluate or to treat many orthopaedic conditions such as: floating cartilage, torn surface cartilage, ACL reconstruction, trimming damaged cartilage.

Pseudo & True Winging which causes which?

PSEUDO WINGING = Tight pec minor / weak LF traps

TRUE WINGING = Weak serratus anterior

"Oh and thanks Colonel Sanders...too bad most of it's pigeons with aids"

Grimsby's 3 stage program - instability rehab

Stage 1 - low speed, high reps, minimum resistance, beginning and middle range

- to increase muscle endurance and circulation whilst avoiding overexertion

Stage 2 - increasing resistance, add in isometrics in inner ranges

- designed to increase strength and sensitivity to stretch

Stage 3 - Continue to increase resistance (usually 80% 1RM) and add isometrics through a full but not maximal range

Tenosynovitis

Inflammation of the thin inner lining of the sheath that surrounds a tendon. Tenosynovitis is usually caused by excessive friction due to overuse; it is often brought on by working in an awkward position to do a job that involves repetitive movements. A reare cause is bacterial infection. Tendons in the hand and wrist are most commonly affected.

Symptoms

- Pain

- Tenderness

- Swelling over the tendon

- Occasionally crepitus

- Persistent recurrent tenosynovitis may lead to restricted movement as a result of the formation of adhesions (fibrous bands) between the tendon and its sheath.

Treatment

If infection is the cause, antibiotic drugs. Otherwise, treatment is usually NSAIDS, corticosteroid drug injection around the tendon. The hand and wrist may need to be immobilised in a splint for a few weeks. If the condition does not improve, surgery may be required to release adhesions.

Shoulder Impingement

Impingement in the shoulder is a pathology that occurs when a structure (inert or contractile) becomes trapped between the acromion and the humeral head).

2 main types: SUB ACROMIAL (supraspinatus tendon or subacromial bursa)

CORACO HUMERAL (long head of biceps or subscapularis tendon)

Tests to determine impingement: 'Empty Can' test, Kinetic medial rotation test (KMRT) to differentiate between impingement and instability.

Impingement can result from a number of factors but it's important to remember to not just concentrate on the area of pain the patient presents but to look at the big picture (i.e. kinetic chain) as the pain may be resulting from dysfunction or imbalance elsewhere. It could be a postural habit, a muscle imbalance, trauma or a combination of other pathologies that have led to the impingement syndrome.

REMEBER! at the initial assessment cast your net wide!

Some things I learnt from PAM1 Summative Assessment

1. Greenstick fractures usually occur in immature bone (i.e. children)


2. Pathological fractures are normally a result of cancer and/or osteoporosis etc


3. 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!


4. Remember during gait there is a lot of eccentric muscle activity occuring so don't get stuck in the concentric mind frame!

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

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?)

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)

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)

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

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'

Soft Tissue Wound Healing

"Wound healing refers to the body's replacement of destroyed tissue by living tissue"

2 essential components (REG & REP)

• Specialised tissue is replaced by proliferation of surrounding undamaged specialised cells

• L.T replaced by G.T which matures to form S.T


• Lost tissue is replaced by granulation tissue which matures to form scar tissue