Musculoskeletal

Fractures

1) As a result of the injury the periosteum maybe completely or partly torn, there is a disruption of the Haversian systems with death of adjacent bone cells, there may be tearing of the muscle especially on the convex side of the fracture and damage to neighbouring nerves and blood vessels. The skin may also be broached in compound injuries, with the risk of ingress bacteria. 2) Fracture Haematoma Bleeding occurs from the bone ends, marrow vessels, and the damaged soft tissue, with the formation of a fracture haematoma which clots. The fracture haematoma is rapidly vascularised by the ingrowth of blood vessels from the surrounding tissues, and for some weeks there is rapid cellular activity. Fibrovascular tissue replaces the clot , collagen fibres are laid down and mineral salts are deposited. 3) Subperiosteal Bone New woven bone is formed from the periosteum at the ends of the bone. The cells responsible are derived from the periosteum, which becomes stretched over these collars of new bone. If the blood supply is poor, or if it is disturbed by excessive mobility at the fracture site, cartilage may be formed instead and remain until a better blood supply is established. 4) Primary callus response This remains active for a few weeks only. There is a much less vigorous formation of callus from the medullary cavity Never the less, the capacity of the medullar to form new bone remains indefinitely throughout the healing of the fracture 5) Bridging external callus If the periosteum is incompletely torn, and there is no significant loss of bony apposition, the primary callus response may result in establishing external continuity of the fracture ('bridging external callus'). Cells lying in the outer of layer of the periosteum itself proliferates to reconstitute the periosteum If the gap is more substantial, fibrous tissue formed from the organisation of the fracture haematoma will lie between the advancing collars of subperiosteal new bone. This fibrous tissue may be stimulated to form bone ('tissue induction'), again resulting in bridging callus. The mechanism may be due to a change of electrical potential at the fracture site or to a (hypothetical) wound hormone. If the bone ends are offset, the primary callus from the subperiosteal region may unite with medullary callus. The net result of the three mechanisms just described, is that the fracture becomes rigid, function in the limb returns and the situation becomes favourable for endosteal bone formation and remodeling. 6) Endosteal new bone formation If there is no gap between the bone ends, osteoclasts can tunnel across the fracture line in advance of ingrowing blood vessels and osteoblasts which form new Haversian systems. Dead bone is revascularised and may provide an invaluable scaffolding and local mineral source. This process cannot occur if the fracture is mobile. The formation of new cortical bone, with re-establishment of continuity between the Haversian systems on either side, cannot occur if fibrous tissue remains occupying the space between the bone ends. If this is present, it must be removed and replaced with woven bone. This is generally achieved by ingrowth of medullary callus which remains active through the healing phase. Where the bone ends are supported by rigid internal fixation, there is no functional requirement for external bridging callus: as a result, external bridging callus may not be seen, or be minimal. Healing of the fracture occurs slowly through the formation of new cortical bone between the bone ends. It is therefore essential that internal fixation devices are retained until this process is complete. After union-remodelling occurs; excess callus is removed and the medullary cavity is reformed. When the process is advanced the fracture is said to be 'consolidated'.

ACL injury/repair

ANTERIOR DRAW TEST: Patient positioned in long sitting, hip flexed to 40 knee to 90 foot resting on plinth ankle in corresponding plantarflexion. Clinician often sits on edge o plinth slighlty on foot to stabilise. Knee joint line identified and superior aspect of tibia grasped keeping thumbs on joint line either side of patella tendon. tiia pulled forward. +ve soft end feel to ant translation or excessive ant translation compared to non affected knee suggests acl ruputre BOTH SIDES Athrometer- joint motion Surgical- reconstruction= extra capsular and intra capsular or both. graft cut from middle of 3 patellar tendon semtinden also used. synthetic also. Intracapsular weakend by recapsulariation take longer 6-12 weeks. Knee stiffness common due to quad contractures/adhesions. Inflammation-->immobility-->quad weakness. full knee extension not possible. Patellar glide restricted pain occasional. PFJ Pain management, ROM , weightbearing, hemoathrisis. ACL reconstruction: Pathology: Graft harvested from patella tendon with bone blocks or semtindenousus and gracillis, hamstring graft attached to anchors, holes drilled in tibia+fibula for bone blocks (anchors) anchors fixed with screws, incision closed SS ROM decreased ,Weakness, pain swelling

AS

AS is one of a group of inflammatory joint diseases that may affect the spine and which are collectively known as spondyloarthropathies. It is a chronic inflammatory disease of the axial skeleton with variable involvement of peripheral joints and nonarticular structures. It mainly affects joints in the spine and the sacroiliac joint and can eventually cause fusion of the spine. All spondyloarthropathies have common features which may affect a patient, including: sacroiliac/pelviaxial disease which causes pain in the back and/or buttocks peripheral inflammatory arthropathy enthesopathy - the inflammation of tendon insertions non msk syndromes such as skin or eye disease. Pathology AS is caused inflammation ('ankylosing' means 'fusing together', 'spondylitis' means 'inflammation of the vertebrae'). The initial inflammatory site is the enthesis (site of insertion of the ligament, tendon or capsule). Sites of enthesopathy (problems with entheses) include the SI joint, ligamentous structures of the intervertebral discs, manubriostrernal joint and symphasis pubis, achilles ensethopathy and plantar fasciitis. As this inflammation subsides, a healing process follows that results in new bone formation/fibrosis. In the axial skeleton, spontaneous inflammation in the iliac portion of the sacroiliac joints occurs and the reactive bone formation causes bridging of the sacroiliac joint, restricting movement at the joint. The repetition of this inflammatory process causes the progressive nature of AS, with more joints becoming affected, as further bone formation can cause vertebrae to become fused together. In the later stages of AS, longitudinal common ligaments of the spine ossificate and the cervical spine may start to fuse. Signs and Symptoms The clinical signs and symptoms associated with AS usually begin with: The insidious onset of a dull low back pain Prolonged morning stiffness lasting longer than 30minutes and often nocturnal stiffness. This stiffness usually improves with movement and exercise and it is not unheard of for patients to pace at night to help relieve the symptoms. Although it typically starts with low back pain some patients complain of alternating buttock pain. In the early stages there may be few objective findings making diagnosis a challenge although the inflammatory behaviour is a good indicator. Physical signs include: Tenderness to palpation of both SI joints Decreased spinal mobility Reduced chest expansion due to involvement of the costovertebral joints 65% of patients report a moderately severe fatigue

Clavicle Fracture

Aetiology- Junction between 2 cross sectional configuration occurs in middle third / constitutes.vulnerable area to fractures, axial loading Causes: Falls on to affected shoulder 87% direct impact, falls on outstrestched hand. Signs and symptoms: patient with splinting arm adducted across chest supported by contralateral nad to unload shoulder proximal end, brachial plexus damage. Local pain, tenderness swelling shoulder displaced anteriorly + inferiorly upto 9% crepitus. Diagnosis: movement analysis, light palpation, xray. Physio: Offers shoulder girdle stability, mobilization gentle isometric exercises. sling 3-4 weeks strengthening until resistance then diagnonal pnf. Humerus Fractures 1) proximal humerus fractures near shoulder joint fracture to the ball, damage to the rotator cuff tenons, due to cancellous (spongy) nature of humerus bone in this part, collapse + deformation along fracture line ostepososis related. 2) Mid shaft humerus frac- occurs away from shoulder+elbow after force on spiral groove, road accident, radial nerve can be injured 3) Distal humerus fracture- either supracondylar humerus fracture or condylar humerus fracture, supracondyler humerus fracture is at joint of condyle and common in children. Signs and symptoms: 1) Proximal presents with upper extemetiy held closely to chest by contralateral hand with pain swelling crepitus.. abnormal sensation on lateral aspect of proximal over deltoid due to axillary nerve. 2)Mid shaft pain swelling, shortening, damage to radial nerve. 3) Distal end- severe bone pain, loss of function, wrist drop, swelling , bruising, Diagnosis Start exercises supine passive forward elevation using opposite hand, suppine passive external rotation, then passive extension adduction pendulum exercises 6-8 weeks- improve passive ROM rotator cuff strengthiening with isometric/theraband scapular strengthening 8-12 should have 80% full passive +good rotator cuff strength.

ACL Injury

Aetiology- caused by pivoting, deceleration, injury with rotation. External rotation whilst foot fixed, decleration with/out rotation and hyper extension. Mechanism of injury is often roation torque, during pivot valgus stress to joint. Signs and symptoms: Feeling or hearing pop/crack within kne, feeling of giving way, unable to ambulate. Immediate swelling of knee due to hemoarhtrosis for 2-4wks Pain, gives out buckles, instability Diagnosis: Ligament test- LACHMANS: Patient is positioned in long sitting on a plinth. Knee in 15 degrees flexion and their foot is resting on the plinth. Clinician stands on the side of the patient to be tested, clinician maintains knee flexion useing their knee. Furthest away hand stabilises femur and other grasps calf below knee joint line. Hamstrings and quads are relaxed otherwise will produce false positive. Clean forward jerk motion of hand on the calf quickly drawing tibia forwards. +ve soft end feel to the anterior translation or excessive ant translation compared to non affected sugests rupture. BOTH SIDES. PIVOT SHIFT TEST: Patient positioned in long sitting or supine on plinth, hip in 50/70 degrees flexion, knee in 45 degrees. limb supported by clinicians who's hands are on plantar surface of foot and inferior to knee joint on lateral side over head of fibula. Vagus force is produced by applying inwards force through upper hand and medial force through lower as leg is extended. +ve slip or jerk or clunk and 10-20

Adhesive capsulitis:

Aetiology- spontaneous predisposed: diabetes, hyperthyroidism, ischeamic heart, inflammatory, athritis, cervical spondylosis, myocardial, hemiplegia, cerebral tumour, cerebral haemorrhage. Pathology: Repeated microtraumaloss of elasticity of connective tissue inflammatory response cases granulations invading damaged area, fibroblasts=adhesions traps cuff between greater tuberosisty acromion coracoacromial ligament resulting in degenration of bursa and capsule gradual inefficiency of rotator cuff+biceps tendon Mechanical entrapment sets off irritation causing granulation oedema+ fibroblast muscles attached involving tendons degen elongation. Signs and symptoms: insidous onset radiates to deltoid insertions down to lateral aspect of arm. pain at end of range loss of both active and passive range especially external rotation when arm is abducted. atrophy of deltoid+supraspinatus- compensation via scapulothoracic movement. 3 stages 1) Freezing- spontaneous in decreased active and passive movements, flextion, abduction, ext shoulder joint capsule volume decreases. 2) Frozen stage- restricted ROm- ext, inter, add reduction pain 4-12 months ahtroscopy 3) Thawing- decreased caspular thickness MM NSSAIDS, steroids, ahtroscopic capsular relase, manipulation under anaesthetic breaks adhesion+ scar tissue. intraarticular steroid injections PM ice + ultrasound stretch abduct, ext, int, flexion, stretching avoided in freezing stage. MOB- inferior glides+distraction scapular stabilser strengthen, heat, deep+superficial ICE ultrasound

Patella fracture

Aetiology: Direct: trauma to patella produce incomplete simple stellate or communated fracture. Indirect: sudden contraction of quads while knees in semiflexed ostion e.g stumble or fallm transverse fracture not commonly seen. Combined direct/indirect mechanicsm, my be caused by trauma in which patient experiences direct or indirect trauma of the knee i.e falling from height. Pathology: stable fractures: type of fracture is nondisplaced, broken ends of bone meets up correctly and are aligned bones stay in place when healing. transverse: patella has been broken horizontly, stellate: comminuted undisplaced Displaced: when bone breaks and is displaced ends seperate and do not mee. comminuted: very unstable shatter into 3 or more pieces. open: skin broken, bone exposed. more damage to muscles, ligs, tendon, longer to heal. signs and symptoms: pain, swelling, bruising, inability to straighten knee, inability to walk, tenderness. MM: RICE, painkillers, Nsaids, cast/splint 6-8 weeks, surgery on transverse

Prolapsed intervertebral disc

Aetiology: Nucleus pulpsus- jelly, hydophillic draws in water, able to be compressed Annulus fibrosus- cartilage Tendency to degn with age, lower lumbar + cervical 1.casusing fragmentation ofnucleus pulposus and softening of annulus fibrosus 2. Portion of nucleus protrudes through tear in softend annulus at its weakest part, posterior lateral impinges on adjacent nerve roots of spinal cord itslef, episodic or interment 3. fibrosis or repiar overlaps, disc replaced by fibrous tissue. Stages- degen, ploapse, extusion, sequestration. Protrusion is classified as diplacement of disc matterial within limits of intervertebral disc, 4 grades of disruption of annulus: G 0 - no disruption G1- extends into inner third of AF G2- disruption extends as far as the inner 2 thirds of AF G3- extends into outer third, lamellae. Mechanism of injury: progressively from repeated loading/ bending heavy axial loading or flexion/side flexion/ rotation can cause spontaneous pain. 1) Herniated parts of disc push against posterior longitudinal ligaments, nerve root, other structures. Abnormal pressure inttiates pain/prssure nociceptors. 2) nucleus pulposa is hydrophillicattracts water, chemiccals are quite reactive. extruded from restriciton of AF act as irritant to surrounding tissue, stimulating chemical nociceptors. Symptoms: loss of muscle power, sensation, reflexes, severe LBP in relation to spinal movement coinciding with tear of AF followed by sciatica. aggravated by coughing sneezing.stiffness followed pain, tingling numbness. severity decreases over 6 months.

Menisci

Aetiology: Due to aging/degeneration or forceful movement whilst weight bearing/twisting on semflexed knee whilst fixed to the floor. Signs and symptoms: Sudden onset of deep pain within, "felt something go" Tenderness felt over joint line, commonly medially Extension blocked by springy end feel as long as there is no muscle spasm. Pain, which is worse when leg is fully straightened. Stiffness + swelling (swelling within a day/2, If a result of degeneration swelling will persist for months. Decreased ROM at the knee- lack of extension, unable to ambulate Diagnosis: MCMURRAY'S-- patient in supine close to edge of plinth, on the side to be tested. Clinician standing on side, support above knee joint line, grab foot above ankle, so lateral rotation of the tibia on the femur can occur, in small sweeping movements to close medial space and grind or catch meniscus. Then medially rotated to test lateral side of joint space. Performed whilst moving the knee from full flexion to extension. COMPARE TO THE OTHER SIDE Findings: +ve audible click or pop with pain

Patella dislocation

Aetiology: extensor mechanism malialignment, trochlear dysphasia, hypermobility syndrome: Family history, poor muscle power/contraction, general ligament laxity, under developed lateral femoral condyle, GENU valgum (quads pull laterally), sharp twisting motion in flexion- pathology: internal rotaion of femur on externally rotated tibia in weight bearing partially flexed knee, quads contract causing medial retinaculum to rupture, patell forced over edge of lateral femoral condyle, or medial force---> lateral. Signs+ symptoms: medial patella tendon torn, lateral hypermobility, tight lateral retinaculum, abnormal patella tracking, VMO atrophy, excessive hind foot pronation. PM early rehab to prevent VMO from weakening, quad strength, passive/active range of movement. taping/straping.

Mechanical Back Pain

Aetiology: presented through pain in lumbopelvic region, when problems occur here back exerts extra pressure. Generally caused by muscle strains more specific pain usually caused by degenrative disc/ herniated disc. Strain results in LBP, if long term pain due to dystrophy after disuse of affected muscle. Herniated disc occurs in conjunction with degenerated disc, weakened area of disc herniates causing refered pain. Mechanism of injury: Abnormal, excess force, muscular/soft tissue instability Assesment- active movements, passive, functional, neurodynamics (slumped sitting, straight leg raise). Treatment: stay active, avoid bed rest, stretching, active movements. Red flags- incontinence, tiredness, buttock pain (AS), swollen joints.

Anterior talofibular ligament sprain

Anterior body of lateral melleous and neck of talus Aetiology- inversion injury 3 levels: G1- some stretching and minor tearing no joint instability G2- moderate tearing, joint instability G3- total rupture, gross instability SS pain, swelling, bruising, stiffness Assess; VAS, ROM, OXFORD, anterior draw test: test designed to test istability of ankle joint assessing integrity of ligaments, posterior to anterior movement of talus on tibia and fibula. Alteration of ankle position can be used to differentiate between ligaments. +ve response increased ROM, alteration of end feel, symptoms replicated. Patient in long sitting, hip at 40 flexion, 90 knee flexion, foot flat on plith , 10-20 plantarflexion, clinican at base of plinth lateral hand on dorsum of foot, other positioned just above superior joint line of ankle, anterior to posterior force through tibia and fibula producing postero-anterior glide of talus on tibia nd fibula, compare with other side. Treatment- reduce swelling with ice, PSWD Increase healing- SWD, U/s, heat ROM- heat MWMs, AM, active/passive, balnce proprioception.

Muscles strains + tears

Classified by degree of disruption of the muscle and tendon on fibres G1- strain from overstretching, heals without treatment G2- moderate more significant tearing of muscle must be treated with care G3- progressed from untreated G2 total rupture gap in middle of muscle may be felt, contration is useless Epidemiology: Hamstrings strains are most cocmmon in activites requiring sudden acceleration and maximal sprinting most commonly treated by therapists. Aetiology - previous muscle injury fatigue are at risk - warm muscles less at risk. over reach change in direction, slowdonw or sudden acceleration, fall, eccentrically contracted generates more force. Collide, trauma, Factors: poor conditioning, poor technique, muscle fatigue, inadequate warm up, tight muscle, decreasing range or joint movement. Prognosis: 4-6 weeks, re-ruptures common if rehab is insufficient 8-12 weeks after surgery. Diagnosis: pain is revisted in injury, muscle contraction, visible bruising Pathology: Distraction pains occurs across muscle which works across 2 joints most common muscle strains, myofibers basal lamina within myofibers running through endomysium and perimysium are torn. 3 stages of healing: 1) Destruction- ruptured myofibers become necrotised, contraction band is formed within first few hours rupture is sealed by new sarcolemma. ruputred myofibrils contract and the gap fills with hematoma causing brisk inflammatation phase which lasts 3-5 days during which chemical and cells such as satalite cells are produced which remove neurotic muscle fibers. 2) Repair phagocytosis via monocytes, myogenic reserves cells and stalitte cells regenerate damge myofibibrils bleeding occurs in gap between torn muscle ends. 3) Remodelling- scar tissue forms from collagen tissue within the muscle makes it more resilient to further stretched damage, injured site is also revascularised by ingrowing capillaries regeneration may take upto 6 weeks. signs and symptoms: pop or pulling sensation followed by tenderness. stiffness, pain and swelling + visible bruising. whether acute or chronic pain may be moderate or severe with movement decreased strength decreased ROM, tenderness, pain in altered , swelling hematoma causing bruisng spasm decreased ROM diagnosis: functional test with without restraints RICE 20mins 3-4 times a day 48 hours gentle stress isometric strength

Fractures intro

Complete break of continuity of substance of a bone, incomplete break or crack due to application of a force or repititve application. Torsional stresses Tangenital stresses- twisting Factors that make susceptible; high speed travel, weakness (Osteoporosis), old age lack of balance, strength Clinical symptoms: Localised pain, sharp localised tenderness, swelling deformity, abnormal movement patterns or loss of function Patient sometimes hears the crack. Pain muscle spasm with small movements, classification according to displacement: undisplaced- bone ends do not meet+reduction is needed to acheive good alignment. Fracture management- Effects of internal fixation- 1. non-rigid fixation- union depends on the eventual formation of woven bone derived from both periosteum and endosteum 2. intramedullary fixation- union depends on woven bone from periosteum 3. rigid compression plating- no periosteal callus seen. Union must depend on endosteal revascularisation of the area of dead bone. A process is described of direct osetoblastic proliferation from lamellar bone- similar to haversian canal remodelling Fractures with internal fixation can be reduced anatomically and often immobilised early. However, the implant must be strong and endurable enough to support the fracture for some months. Children's fractures- unite more easily and rapidly. Remodeling is more complete process. An incomplete reduction is often acceptable. Only rotational deformities are not corrected well. Delayed union- occur when a fracture doesn't unite within expected time. It may unite eventually given persistent immobilisation. Delayed union is a diagnosis which depends on- mobility, pain and tenderness of fracture site. And an x-ray showing incomplete callus with fracture gap still detectable. Due to- poor blood supply/ infection/ wide gap between 2 ends/ poor nutrition/ old age/ vitamin C deficiency. Non-union- a later stage, where a fracture won't unite without bone grafting. Symptoms are obvious mobility at fracture site and large gap between two bone ends. Malunion- is union of fracture with unacceptable deformity. Fracture healing: 1) Frac hematoma (1week) 2) Boney callus (2-3weeks) 3) Hard callus (4-16) 4) Remodelling (17+)

Distal femur fracture

Conservative treatment: Traction - to treat type A2 and A3 supracondylar fractures if the axial alignment, rotation and femoral length can be restored. A pin is placed below the tibial tuberosity and, with the knee in 20° of flexion, a Thomas splint is used with a Pearson attachment at the level of the fracture. The patient is bed-bound in traction for between 2 and 12 weeks. MUA - manipulation under anaesthetic can be used before traction, in order to get the bone fragments appropriately aligned in the most pain free way. Early fracture bracing/cast bracing - to treat impacted supracondylar fractures that do not have an intracondylar extension. The leg is stabilised using a knee immobiliser to begin with, and is eventually replaced with a fracture brace or knee cast once the pain and swelling have decreased. Delayed cast bracing - after 2 to 3 weeks of traction, when the fracture healing has begun, a cast can be applied. This is done with the knee in extension, with a slight valgus angulation and 20° of external rotation. Surgical treatment: Follow up and rehabilitation: Immediate continuous passive motion enhances cartilage healing, prevents quadriceps contractures, decreases swelling and enhances early knee motion. This is done using a continuous passive motion machine immediately post surgery. The use is maintained full time until ambulation is commenced on the third/fourth post operative day. Active assisted exercise of the quadriceps and hamstrings is required from day 2 onwards to maintain strength. If the fracture is poorly fixated, and the patient is still in traction, early active assisted exercise is still necessary during breaks in traction. Gait training should commence from day 3 to 5, using parallel bars, a walker, or crutches, allowing for partial weight bearing. This is continued until radiographic evidence shows that the fracture is healing. 2-3 months post-op, the patient should progressively increase their weight bearing and begin resistance exercises until the fracture is solidly unified at approximately 4-6 months. Prognosis As severity increases, the prognosis of a good outcome decreases.

TKR+THR

Considered for patients with: severe OA, RA, trauma, loss of function. Pathology: longitudinal incision made from tibial tuberosity to junction of proximal end of quads tendon. Menisci, ACL and sometimes PCL excised. TIbia and femur resected, implants cemented. Joint capsule and skin incision close. SS: Decreased ROM, scarring, pain, swelling, THR: Diseased cartilage of bone and bone replaced. Considered for OA, RA, HOF, fractures. Pathology: Lateral apporach- less chance of posterior dislocation Posterior- better access to proximal femur in overweight patients, igores adductors, skin+ mscle incised to reach acetabulum. Proximal femur. Muscles incised: Gluteus max, medius, tensor fascia lata, vastus lateralis, hip discloation allows access to acetabulu,. Cartilage of acetabulum removal+ metal cap put in place, head and neck of femur sawn off , femoral shaft braced and cleaned for insertion of femoral prosthesis, fixed with/without cement. Leg length measured, hip stable before fracture reduced and joint closed. SS reduced ROM, pain, swelling, unable to weight bear. Assess- VAS, ROM, weakness, Gait, Treat- pain, ice, heat, passive, strength.

Radial Nerve injuries.

Cutaneous supply back of wrist and forearm. Radial nerve innervates- brachioradialis (flexor, supinator, pronator), Triceps, anconeus (extensors), supinator (posterior interosseous), all wrist extensors (ECRL, ECRB, ECU, ED, EPL,) Radial deviators ( ECRL, ECRB) Causes: fracture of the humerus, severe soft tissue damage, shoulder or elbow disloscation, traction injury, plexus compresion, arm hanging over chair, triceps compression during excercise, improper intramuscualar, tight cast, tumour, cyst Symptoms: Loss of muscle strength, abnormal sensation, tingling, atrophy ,weakness Assesment: Isometric, myotomes, neurodynamics: Upper limb tension test 2b: Patient supine, clinician facing down patient, closest arm under patients elbow, other at wrist forcing into wrist flexion, shoulder in neutral, elbow flexed at 90 then 1. shoulder girdle depression, with clinicians hip 2. elbow extension 3. medial rotation 4. wrist and finger flexion. Gonio: elbow extension- Wrist extension- patient sitting, resting on table, in pronation, wrist in neutral hand over end of table, axis of gonio is placed at level of ulnar styloid process, stationary- parallel to long axis of ulna, move- parallel to long axis of 5th metacarpal. move hand upwards. Treatments- Neurodynamics, facilitation, splint, strengthen, active movements. Radial nerve tunnel syndrome- compressed just beyond elbo by muscles in forearm (site of compression, radiocapitular joint, tenderness at extensor origin and fibrous thickening within and at distal margins of supinaotr, If symptoms last more than 12 weeks, surgery. Symptoms- pain outside upper forearm below bend of elbow, down to wrist, pan caused by lifting, gripping, writing, twisting. Posterior interosseuous nerve syndrome- compression from radial wrist extensors and radial sensory nerv, compressed before dividing into medial and lateral branches causing complete paralysis of distal extensors and radial deviators: medial- ECU, EDM ED Lat- APL, EPB EPC.

Clavicle

Distal Non operative: Anterior and posterior U-shape plaster with elbow in extension casting or cuff immobilization Operative Treatment: (no later than 2 weeks post injury) fixation with pins or K-wires (children) ORIF, arthroplasty, 1) Immobilisation should not last more than 3 - 4 weeks as it highly increases the chance of stiffness etc. 2) Once the surgeon is happy the fracture is stable (usually 2-3weeks) full ROM activities should be performed. 3) ¾ weeks post injury the fracture will have begun to heal and auto-assisted exercises can be started, where the patient helps the affected arm with the uninjured one. 4) Progress to unassisted exercises, moving the arm 5) The rate of progression is highly varied in elbow fractures, the physiotherapist will start the patient doing more forceful exercises only once a large amount of physiological movements have been attained. 6) Flexion (the maximal achieved) should return within 2 months 7) Extension (the maximal achieved) should return within 4-6months 8) Some patient may not gain full ROM which can usually be helped by surgery and removal of fixators. 9) Pronation and supination are usually unaffected if alignment is good however strengthening for theses movement will normally be required. Shaft Non Operative Treatment: long arm splint needs to be applied from shoulder to wrist to fully immobilize the extremity cast bracing: - can be used for most closed f# - in most cases, cast braces are applied at 10-12 days following injury Operative Treatment: Internal fixation should for fractures with inadequate reduction or patients with multiple trauma; - Inter Mudallary Nailing: - External Fixation - Plate Fixation: - anterior approach to humerus; - posterior approach to humerus 1) The patient may stay in the sling for 2-3 weeks with the physio exercises beginning early if pain is reasonable and the fracture stable. 2) Emphasis is on maintain the range of motion of the shoulder joint while the fracture heals, by performing bent over pendular exercises to counteract gravity. 3) Week 3 - fracture will have begun to heal and auto-assisted exercises can be started, where the patient helps the affected arm with the uninjured one. 4) Progress to unassisted exercises, moving the arm up above the head, behind the back and behind the neck. 5) At the 6th week, bone has effectively healed, the physiotherapist will start the patient doing more forceful exercises involving gentle stretches at the end of range to improve mobility. Mobilisation techniques to the shoulder joint and strengthening exercises using Theraband are progressed to increase muscle power and joint range. For all of the fractures the exercise rate is dependent on severity, stability of reduction and callus formation

Osteoathritis

End point of a pathological process leading to structural failure of the articular surfaces Aetiology: Primary; due to intrinsic alteration of articular tissues, exhibits in a classical pattern, common in post menopausal women who exhibit bony swellings of distal and intermediate interphalangeal joints. Secondary: Arises as a consequence of another condition, repeated microtrauma may lead to microfractures and subsequent OA, joint infection increases risk as does joint deformity (following fracture), joints with lower proteoglycan and synovial fluid (immobile) are also prone. Pathology: Begins with changes to subchondral bone: redistribution of blood supply in the subchondral bone marrow, micro necrosis of tissue, ts in secondary hyaline cartilage degeneration, accumalatio of micro fracutres makes subchondral bone more brittle, greater stress placed upon articular cartilge. Effect on articular cartilage: minute cracks and loss of water content occur, cartilage softens and fragments, collagen fibres split, attracting water into the cartilage matrix and causing futher flaking, flakes break off and float freely in joint causing locking and irritation.

Supraspinatus tear

Extrinsic- trauma intrinsic. Attachments- medial 2 thirds of supraspinatus fossa upper facet of greater tubercle of humerus. Pathology: overuse of glenohumeral joint stabilises casuing microtrauma, more demand on other stabilsers resulting in fatigue, translation of humeral head to impinge supraspinatus tendon. SS: ROM decreased, pain, weakness of scapular stabilsers, altered posture, proprioception. Hawkings-kennedy test/ scarf test (horizontal adduction), empty cns. Treatment: Strengthen- rotator cuff, lateral, medial, abductors. ROM Horizontal adduction (Scarf)- test for AC joint pathology, impingmenet symptoms, involves adduction and flexion of shoulder. Loading joint structure, may load on anterior aspect of subacromial space. Patient in standingm shoulder adducted across body in 90 flexion, clinican standing by patient supoorting limb fully enabling passive horizontal , over pressure on elbow. Hawkins-kennedy impingement test: test pf rotator cuff disease/pathology, flexion+medial rotation, impingement on subacromial space by clinicialn, medial rotational force push head of humerus agains acromion. Patient standing, shoulder flexed to 90, full medial rotaiton elbow in 90 flexion, limb supported at wrist and elbow, medial rotation through full range. Healing- U/s, SWD, pswd, heat, swelling

NOF Fracture

Fall onto side is most common mech of injury- intracapsular within joint capsule, intertrochanteric hip fracture between GT and glut med + Min attachment (visible bruise at back of upper thigh) Malunion- varus and external rotation Subtrochanteric- regin between lesser trochanter and a point distal, consists of cortical bone Gardens classification: G1- trabeculae angulated inferior cortex intact no significant displacement. G2- trabeculae inline, fracture line visible from superior to inferior cortex no significant displacement G3- obvious complete fracture line with slight displacement/rotation of femoral head. G4- gross complete displacment of the femoral head. Aetiology: Direct fall onto greater trochanger or fall from hight. Hormone dependant osteoporosis causesweakness Osteomalacia- soft/ weak bone. Previous fracture above 50 yrs maternal history of hip fracture smoker Low body weight poor eyesight neuro problems, athritis, sedatives. Symptoms: History of fall followed by pain in the hip if displaced limbs in lateral roation and affected leg is shorter inability to weight bear hemoathrosis- blood filled within capsule no bruising. tenderness over femoral neck.

Fracs conclusion

Fracture healing occurs differently between cortical and cancellous bone. Whereas with fractures to cortical bones (in adults) take about three months, fractures of cancellous bones unite in about six weeks. The osteocytes in trabeculae of cancellous bone have more profuse bloody supply and so bone union occurs fairly rapidly as gap is bridged directly, and little callus is formed (this only occurs in areas of direct contact). Healing of fractures in cancellous bone is associated with crushing of the trabeculae and therefore there is often some residual deformity. Most fractures to the shaft of long bones result from low energy injury and therefore likely to have little soft tissue disruption and a greater fracture stbaility. These fractures can be managed by manipulation and casting. In certain circumstances there is a need to have some sort of internal fixation of the fracture site. As mentioned earlier the fracture requires a certain degree of movement. Internal fiixation of the fracture prevent much of this movement, the consequence being that the healing process take a lot longer. There are other complications of internal fixation such as that of recovery form surgery, the anaesthetic and a greater infection risk. Internal fixation must be considered if it allows for ealry mobilisation or if the fracture is pathological and allows for an early return home for elderly patients as this manages the pain effectively. If the fracture is fragmented or displaced and cannot be re-aligned through manipulation then the fracture may be undergo an open reduction and internal fixation (ORIF) described below. These generally result from high energy injuries and this procedure will facilitate the healing of the soft tissue and thus the help the fracture healing in the long term. Fracture classifications: Transverse Spiral- from torsional force Oblique Communated Segmental Avulsion: bony attachment of ligament torn

Whiplash

Inertial response of the body to forces. Causes neck to move beyond normal range so ligament, tendon and muscles are overstretched. Associated with hyperextension-flexion, patholiogy. Zygapophyseal joints: Cervical zygapophyseal joints have been shown to have fractures of the joints themselves or of the supporting articular pillar. Intervertebral discs: Typical lesions are avulsion of the disc from the vertebral end plate and tears of the anterior annulus fibrosis of the disc. Muscles: Muscles have been shown to have partial and complete tears as well as haemorrhage. Ligaments: The anterior longitudinal ligament merges with the anterior annulus of the intervertebral disc indicating that ligamentous injuries may frequently be associated with disc injuries. Injuries to the interspinous ligament have also been identified. In severe cases the anterior longitudinal ligament may be torn and there is bleeding between the ligament and the vertebrae. This may cause enough retropharyngeal swelling to cause dysphagia a few hours after the injury. Atlanoaxial complex: Fractures to the odontoid peg have been identified following whiplash. There is also evidence of bony injury to other parts of c2 including the laminae and superior articular process. Cervical vertebrae: Major fractures below c2 are uncommon in whiplash but more subtle fractures have been detected, however the incidence of these may be underestimated as they are difficult to detect.

RA

Initially, inflammation of the synovial membrane occurs, possibly due to invasion by an antigen, initiating an antibody-antigen reaction and the activation of the complement system, enhancing the immune response. The immune response causes synovial blood vessels to proliferate, dilate and become congested and the presence of chronic inflammatory cells, such as macrophages, T cells, B cells and plasma cells, causes the synovial membrane to thicken. Lymphocytes, interleukins and other inflammatory mediators provoke differentiation into plasma cells, approx 70% of which produce immunoglobin IgG and IgM rheumatoid factors - the presence of rheumatoid factors is a diagnostic indicator that an individual has RA. The increased number of synovial cells increases production of synovial fluid which accumulates due to the thickening of the synovial membrane. This increases pressure within the joint, causing swelling, pain and tenderness. As RA progresses with prolonged inflammation, the thickened synovial membrane forms villi of inflamed synovial tissue and abnormal granulation tissue (granulation tissue is the new connective tissue and blood vessels that form in the healing process) which project into the articular surface of the joint at the articular margins and bone ends. These projections are called pannus, which adhere to the surface of the articular cartilage, eroding the articular cartilage and bone. If the articular cartilage erodes completely, the bone ends become exposed and joined by fibrous tissue. This fibrous tissue can ossify, fusing the articular joint surfaces, greatly reducing/preventing movement at the joint Damage to the joint may also lead to joint deformities, commonly recognised in the hands and fingers of those with RA. SS Pain- inflmmation/irritation of bone stiffness- morning soup dcreased ROM deformities- swan neck, booteners. swelling decreased proprioception, balance due to ligament laxity tenderness synovial thickness tendon weakness Ax Observation- gait VAS Passive, active isometric, BERG, RHOMBERGS Rx Free active excercise, stretching, TENS, pain US, SWD AM Gait re ed balance board. Secondary complications- heart, pleural effusion, anaemic.

Tennis Elbow- lateral epicondylitis

Lesion to common extension origin, lateral epicondyle, commonly effects tendon of extensor carpi radialis brevis or extensor carpi radialis longus at it's attachment on the supracondylar ridge usually at tenoperiostaial junction where tendon attached to bone. Scar tissue can also form on tendon itslef at musculotendinous junctuon (tendon to muscle) Aetiology: can occur from overuse of muscles as a result of single forcefull injury repeated forcefull wrist extension iwth combined supination, squash javelin, hammering, painting, typing. Pathology: Microtrauma caused by wrist extention and supination cause tiny tears on tendon rough granulation of tissue on underside of tendo and at tenoperiostal junction cause swelling. scar forms Signs and symptoms: Resisted elbow test- resistance against wrist extensor, concentric may reproduce sympoms over site of lesion. patient is in sitting or standing shoulder in 90 flexion elbow extension with forearm pronated wrist in full flexion , support elbow resist extension. +ve pain over lateral epicondyle suggest tendinopathy as does weakness of extensor muscles. Also: Pain and tenderss around lat epicondlye worse when supinating pronating forearm or bending and gripping. Progressive stiffness. MM: nsaids, rest, local corticosterioid injections, paracetmol, stretching to increase pliancy of scar tissue. combined flexion and pronation whilst applying over pressure with other hand. Transvers frictions over extensor origin.

Lateral Malleoulus Fracture

Loss of continuity of one of the bones comprising the ankle+ subtalar joint. Low energy fall during abduction, lateral rotation, sheared off. Avulsed during adduction, no displacement of the talus. Fracture of lateral with lateral shift of talus- abduction or lateral rotation, medial ligament torn allowing displacement. SS Swelling, bruising, inabilty to walk 5 steps.

NOF frac

MM: Accurate reduction, secure fixation, early activity, reduce risk of pressure sores, continence, hydration, patients mental state. Operative techniques: Cannulated screws, dynamic hip screws, hemiathroplasty. open reduction of femoral neck fracture. Physio management: Early active hip movements within 24 hours within 1st week they should be walking crutches. Complications; Avascular necrosis- necrosis of femoral head in 30%with displaced fracs and undisplaced. Blood supllied via 3 routes, ligamentum teres, vessels from capsule, branches from nutrient vessls in bone. fractures sever nutrien vessels and retinaculum vessels from capsule torn ligamentum teres vessels insignificant. Bone cells die. Fracture fails to reunite. Non-union- poor blood supply insuficient , shortening of limb, pain. Prognosis: 10% after 30 days 30% after one year, prevention via excercise, calcium and vit d supplements, HRT, biphosphates, subtrochan-Open reduction and internal fixation is the treatment of choice. Intramedually nails with locking screws into the femoral head or else a compression hip screw and plate will provide satisfactory fixation. Patient is allowed partially weight-bearing with crutches until the fracture is united securely.

Menisci

Meniscis Ax cont'd APLEY'S GRIND TEST--- Patient in prone, knee flexed to 90 degrees. Clinician: 1) standing on side to be tested, hand placed over posterior aspect of the thigh close to posterior aspect of knee. Other hand grasps just above malleoli, vertical pull creating distraction. Maintain distraction whilst medially and laterally rotating foor . 2) Apply compression through line of tibia, compressing joint space. +ve pain reported in stage 2 but not 1. Other: Athroscopy, xray to rule out other problems, MRI for soft tissue Types of tear: Longitudinal, transverse, bucket handle, flap, torn horn. Peripheral part has blood supply to repair 10 weeks scar tissue remodelling. MId portion avascular, tears trimmed/ stitched, transplanted. Management: PRICE- protect, ice, compression, elevation. Goals- reduce pain, swelling, air cast kneecuff for ice. Knee brace stability. hydro flots to allow joggin without touching bottom to improve ROM without weight bearing. MAINTAIN QUADS AND HAMSTRINGS. Jump without pain, walk, jog in straight line.

Whiplash cont'd

Other structures: Injuries to various other structures which have been associated following whiplash injury include, avulsion of the occipital bone, fracture of the occipital condyle, prevertebral haematoma compromising the airway, perforation of the oesophagus. Horners syndrome indicating damage to the cervical sympathetic nerves, damage to recurrent laryngeal nerves, spinal cord injury, perilymph fistula, thrombosis and aneurism of the vertebral artery, dissection or strangulation of an internal carotid artery, retinal angiopathy and anterior spinal artery injury syndrome. Trigger points and myofascial pain may also develop after whiplash. The structures most likely to be injured in whiplash are the zygopophyseal joints, the intervertebral discs and the upper cervical ligaments Signs and symptoms: Neck stiffness, headaches, tenderness along back of neck, Reduced movement of neck or loss of movement, dizziness, sensory disturbance, LBP, radiating pain to head, shoulder neck suggest nerve impingement. Generalised hypersensitivity, parasthesia, muscle weakness, Complications: symptoms from temporomandibular joint visual blurring. memory + conc disturbances. Reduced bulbar perception, vertigo, tinnitus Treatment: NSAIDS Muscle relaxants Corticosteroids Physio managment- electro, massage, ice, tens

Golfers Elbow- medial epicondylitis

Pain at common flexor origin. Aetiology: caused by repitive wrist flexion, gripping due to isometric contraction. Pain in wrist flexor + pronator teres muscles, repitive valgus stress of elbow most common cause, training erros increase rsik. improper technique/equipment. poor endurance flexibility. Pathology: pain distally, flexor pronator muscle group act as stabiliser for ulna collateral ligament. Signs and symptoms: Pain during isometric contraction of wrist flexors tenderness on palpation under medial epicondyle and medial elbow pain with recruitment of wrist flexor and pronator teres muscle. stiffness after exerces ROM limited by pain and muscle spasms. grip weakness Treatment: Rest, med, cortico, ROM maintence, stretch, stregthen wrist flexors.

OA

Pathology cont'd Effect on bone: Degree of bony remodelling in subchondral bone, protection from cartilage is lost so bony ends become hard and abnormally dense, cysts may form in subchondral bone due to brittleness of bone, micro fractures. osteophytes form at articular margins and project into joint causing pain and restricting movement. Effect on synoival membrane: synovial membrane is effected by swelling, cartilage flakes act as an irritant and cause repeated effucions of fluid. Effect on joint capsule and ligaments: undergo fibrous degeneration and adaptive shortening in advanced stages, chronic inflammatory changes are often seen, ligaments become contracted or elongated depending on aspect of joint, joint space decreases, ligaments may be too long and are unable to support joint of provide proprioception. SS: ROM- due to adaptive shortening, alteration of congruency, osteocytes/pain muscle atrophy- due to pain joint enlargement- chronic oedema of synovial membrane and joint capsule crepitus- flaked capsuel and bone ends grate each other. Stiffness due to loss of lubrication + oedema pain- stres on ligaments, contact between bone, osteophytes Knee- sweeling, tenderness, decreased ROM DIP joints- boney swellingm flexion, valgus or varus deformities, tenderness.

RA

Signs and Symptoms: Some of the symptoms experienced in tendinitis are often very similar to those of muscle strains. Heat and swelling, although this may not be visible unless the tendon is particularly superficial, for example the Achilles tendon Stiffness and pain, particularly in resisted movements and stretching Crepitus (grating or crackling sounds) in the affected tendon when moved Weakness A lump alongside the tendon Pain that is worse with movement or activity Pain at night Rx Strengthening of muscles surrounding the affected tendon Stretching Massage. In the sub-acute phase massage can help to drain lymph and fluid from the inflamed area. If there is a tear, the area should be left during the acute phase to allow for healing to begin. Ultrasound Eccentric exercise for rehabilitation of tendinitis is also supported by a number of studies. For example Croisier et al (2001) found that following an isokinetic eccentric exercise training programme, 74% of patients, who had not responded to previous other treatment methods, were completely relieved or had a marked decrease in symptoms.

Shoulder dislocations

Synovial ball and socket, articulates between glenoid fossa of scap and HOH. Partial- subluxation, temp, partial dislocation ball of upper arm bone slips out of shoulder, Full- HOH completely out Aetiology: sport trauma, elderly weakened ligamaents+ trauma anterior dislocations e.ge arm held over head with elbow bent, force applied pushes elbow back and leaves humeral head out of glenoid fossa. FOOSH- external rotation of shoulder Posterior- uncommon asscoitaed with elecctrial injuries and seizures. Pathology: Ant, subcoracoid, subglenoid, subclavicular, intrathoracic. Subcoracoidal- most common, typically caused by trauma involving abduction, extension and external rotation, subcroacoidal when humeral sits anterior and medial to glendoid just inferior to coracoid (60%) subglenoid- humeral head sits inferiro and slightly ant to glenoid (30) trauma involving abduction extension external roattaion- humeral head sits anteriro to glenoid and inferior to coracoid. Subclavicular- strong lateral force intrathoracic- head of humerus impaled in thoracic cavity causd by rotator cuff avulsion neurmuscular injuries are common after axilary nerve, radial, musculocutaneous, media, ulnar. Posterior dislocations: relation to trauma but also instability indicated by hollow under acromion anterior deltoid flattening and palable humeral head posterior. complications: Bankarts lesion- avulsion of inferior glenoid labrum at its attachment to anterior inferior glenohumeral complex. rupture of joint capsule and inferior gelnohumeral ligament. Hills/sachs- posterior humeral head indentation fracture occur due to HOH impaling anterior glenoid. Signs and symptoms- visbily deformed, HOH palpable, pain, instability, arm held in sligh abduction external rotation, weakness tingling, numbness. MM-xray relocation, analgeseics relaxants, early treatment minimises soft tissue damage. neurovascular + rotator cuff reassesed. Physio managment-. Ice heat to reudce swelling and healing, ice 4 times daily for 2 days then heat rehab= 90 flexion abduction not external roation, isometric streghtneing of deltoids+ full ROM elbow prognosis 3-6 weeks.

Tendintis

Tendinopathy is a term used to encompass a number of tendon pathologies. One of the main conditions included is tendinitis. This is inflammation of tendinous tissues, most commonly at tenoperiosteal or musculotendinous junctions, due to excessive stress on the tendons. Tendon degeneration (tendinosis) is often also present. Epidemiology: Tendinitis seems to occur more in those with certain systemic diseases, such as diabetes and rheumatoid arthritis, than the rest of the population The older population are more at risk as their tendons lose elasticity with age Aging can also increase the risk of developing calcific tendinitis as the tendons experience degenerative changes. In this type of tendinitis the combination of degeneration and exertion leads to chronic inflammation and calcium deposits. This can occur in athletes from the age of 30- 35. Athletes using particular tendons excessively can increase their risk of having tendinitis. For example a runner may overuse their Achilles tendon. aetiology: Tendinitis can affect tendons anywhere in the body, although commonly affected sites include: elbow, Achilles tendon, shoulder and wrist. It is caused by overuse or injury of a tendon. (NHS, 2011) These injuries can be sustained through: sports, e.g. playing tennis leading to tendinitis in the elbow repeatedly overusing muscles, known as repetitive strain injury. A common example of this is tendinitis in the wrist due to overuse of a computer mouse Reduced circulation and high friction can also lead to inflammation and tendinitis. Other factors that contribute to tendinitis include inappropriate equipment, play or work conditions, and training or standing surfaces; muscle imbalances; loading, technique and execution errors in sports and workouts; and structural abnormalities. All of these factors can cause additional stress on a tendon, leading to overuse and injury. Signs and Symptoms: Some of the symptoms experienced in tendinitis are often very similar to those of muscle strains. Heat and swelling, although this may not be visible unless the tendon is particularly superficial, for example the Achilles tendon Stiffness and pain, particularly in resisted movements and stretching Crepitus (grating or crackling sounds) in the affected tendon when moved Weakness A lump alongside the tendon Pain that is worse with movement or activity Pain at night Rx Strengthening of muscles surrounding the affected tendon Stretching Massage. In the sub-acute phase massage can help to drain lymph and fluid from the inflamed area. If there is a tear, the area should be left during the acute phase to allow for healing to begin. Ultrasound Eccentric exercise for rehabilitation of tendinitis is also supported by a number of studies. For example Croisier et al (2001) found that following an isokinetic eccentric exercise training programme, 74% of patients, who had not responded to previous other treatment methods, were completely relieved or had a marked decrease in symptoms.

Metartarsal fracture

Trauma to 1st/5th metatarsal or continued stress (2nd/3rd) Tpes: Avulsed: 1/5 Jones- 5th- local trauma to lateral side, transverse fracture through metaphysis + shaft. Transvers fractures can affect all. Hair line (stress) 2nd/3rd- stress- pain after activity gone when resting, rapid swell. SS pinpoint pain, swelling, bruising, ROM Weakness Assesment- VAS, ROM, muscle strength Treat: Pain- ice, then heat, swelling ice, ROM .

Distal femur

Type A = extra-articular fractures A1 = simple, 2 part, supracondylar fractures A2 = metaphyseal wedge fractures A3 = comminuted supracondylar fractures Type B = unicondylar fractures B1 = lateral condyle sagittal fractures B2 = medial condyle sagittal fractures B3 = coronal fractures Type C = bicondylar C1 = noncomminuted supracondylar (Y or T) fractures C2 = supracondylar comminuted fractures C3 = supracondylar or intercondylar comminuted fractures Aetiology: In younger people, particularly men under the age of 35, the cause of this type of fracture is usually a high energy impact/trauma. This is often in the form of a direct application of a large amount of force through a flexed knee, such as when the knee hits the dashboard during a vehicle collision, causing a transverse/oblique fracture. Another cause produces a spiral fracture, when the foot is anchored in place during a fall and the femur is twisted. In older people, particularly women, the cause is a low to moderate force/trauma, such as falling on a flexed knee. However, in this age category, two thirds of cases are preceded by age-related fractures, such as hip or pelvis fractures. Another prevalent cause of this fracture in the elderly is pathologies such as osteoporosis. Signs and Symptoms: The most immediately obvious sigh is the swollen and deformed knee/distal thigh. Deformations may be present but less obvious, including femoral shortening, posterior angulation, and bony displacement. Movement is normally too painful to attempt. Diagnosis: The most definite form of diagnosis is via radiographic evidence, in the form of x-rays. AP and lateral x-rays are taken to confirm the presence of a fracture as well as identifying the type and location. Traction can be applied to the fracture to make the picture clearer. The swelling of the knee and supracondylar area is often a prominent factor, alongside obvious deformities. There will be marked tenderness on palpation of the area. If the patient isn't in too much pain, manipulation will show movement and crepitance at the site of fracture; however this should not be done if the patient is in pain. CT scanning can be used to further examine the fracture, helping to determine any surgical approach that may be necessary. MRI scanning allows for clearing the joints above and below the fracture site, as well as checking the integrity of the soft tissue structures that may be affected.

Common Peroneal nerve injury

Vulnerable to compression around neck of fibular. Causes; Habitual leg crossing, external pressure, prolonged squating, leg brace, trauma/injury, cyst/ganglian/tumour, callus from previous fracture. Signs+symptoms: Decreased sensation, numbness/tingling, slapping gait pattern, foot drop, unable to hold food, toes drag, weakness of foot dorsiflexors (TA, EDL,EHL, Peroneus tertius,) invertors- TA evertors- PL, PB, PT). Assesments: Isometric, oxford grading, neurodynamics of sciatic gonio: Dorsiflexion- Patient supine, knee slightly flexed, fooot in neutral, axis of gonio placed 1.5cm below lateral mellelous , stationary arm parrael to longitudinal axis of fibula moveable arm parallel to 5th metatarsal, bend foot as far you can. Inversion: patient supine, roll under knee, ankle neutral, paper under food, book against sole of foot line drawn parallel to book, turn foot in as far as you can, new line should bisect. Treatments: Passive movements to prevent contractures, stretches, nmes to facilate dorsiflexion, balance board stimulate muscle, splint, strengthen.