Sprains and DislocationWhat is Sprain?

• A sprain is defined as a partial or complete rupture of the fibers of a ligament or complex of ligaments responsible for the stability of a joint.

• Sometimes when the ligament is strong, a fragment of bone is avulsed from the point of insertion of the ligament.

Causes of sprains & dislocations• Most important cause is trauma.• Other causes include pathological conditions like already damaged or

weakened ligaments or joints.• Other pre-existing conditions like infections, arthritis (particularly rheumatoid

arthritis), neoplasm, etc.• Iatrogenic like forceful manipulation etc.

Types of sprains• 1st degree: The ligaments are stretched but not torn through its substance.• 2nd degree: The ligaments are stretched and there is a partial tear through the

substance of the ligament but discontinuity is not there.• 3rd degree: There is total tear through the substance of the ligament leading to

breach or discontinuity of ligament.Principles of Treatment

• Mainstay for the principles of treatment of sprains is immobilization.• The affected part or joint is immobilized either by strapping, compression

bandage, plaster cast, splint etc.• The affected part or limb is elevated to reduce swelling.• Medications like NSAID’s, analgesics etc.

Dislocation• Is a complete loss of congruity between the articulating surfaces of a joint. The

bones taking part in the articulation are displaced relative to one another.Subluxation

• In a subluxation the articulating surfaces of a joint are no longer congruous, but loss of contact is incomplete.

• The term is often used to describe the early stages in a condition which may proceed to complete dislocation.

Types of dislocations• According to the severity: If incomplete it is called subluxation and if

complete it is called dislocation.• According to Anatomy: Anterior, posterior, superior, inferior, central or

combination likes anteroinferior etc.• According to co-existing conditions: If it is associated with fracture it is called

fracture dislocation.Treatment of dislocations

• As it obvious the mainstay of treating dislocation remains reduction of the dislocation and maintaining the same by either strapping, plaster casts, splints etc. until the surrounding soft tissues like capsules and ligaments have healed.

• Reduction must be checked radio logically immediately after reduction and from time to time as needed.

• A very important point is to achieve a congruous reduction.

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FRACTURES• A loss of continuity in the substance of a bone is termed as fracture.• It covers all bony disruptions ranging from the highly comminuted fracture at

one end of the scale to hairline and even microscopic fractures at the other.Causes of fractures

• Direct violence: Caused by the application of stresses which exceed the limits of strength of a bone. Violence is the commonest.

• It can be either by a moving or falling object striking on the bone or if the bone forcibly strikes a resistant object.

• Indirect violence: A twisting or bending stress is applied to a bone and this result in its fracture at some distance from the application of the causal force. For example a rotational stress applied to the foot may cause a spiral fracture of the tibia.

Types of fractures• According to skin injury :• Simple fracture also known as closed fractures. The skin is either intact, or

if there are any wounds these are superficial or unrelated to the fracture. In these types there is no risk of infection from outside. Any hemorrhage is internal.

• Compound or open fractures where there is a wound in communication with the fracture and there are all chances for organisms to enter the fracture site from outside. All compound fractures therefore carry the risk of becoming infected. In addition blood loss from external hemorrhage may be significant.

• Compound or open fractures where there is a wound in communication with the fracture and there are all chances for organisms to enter the fracture site from outside. All compound fractures therefore carry the risk of becoming infected. In addition blood loss from external hemorrhage may be significant.

• Two types: Compound from outside where the external force has damaged the skin and compound from within where due to the fracture the sharp bony ends have pierced the skin.

• Technically compound #: Skin damage is minimal with a small area of early bruising in the centre of which is a tiny tell-tale bead of blood issuing from a puncture wound.

• Fatigue fractures: Stresses repeated with excessive frequency to a bone. Often compared with fatigue in metals which break after repeated bending beyond their elastic limit. Commonest is 2nd MT the march # (so called because of its frequency in army recruits.

• Pathological #: Occurs in as abnormal or diseased bone. Osseous abnormality reduces the strength of the bone.

• Hair-line #: Results from minimal trauma just enough to produce # but not severe enough to produce displacement. Such # may be complete or incomplete. Requires special views or films repeated after 7 to 10 days as decalcification at #site makes # visible. Stress # are generally hair-line & often not diagnosed until a wisp of subperiosteal callus formation is there or increased density at # site.

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• Greenstick #: Occur in children as less brittle bone of the child tends to buckle on the side opposite the causal force. Tearing of periosteum and of surrounding soft tissues is minimal. Reduction is facilitated by the absence of displacement and by the intact tissues on the concavity of the #. Elastic spring of the periosteum may however lead to recurrence of angulations so some surgeons deliberately over correct the initial deformity; this tears the periosteum on the other side and reduces the risk of secondary angulations.

• Transverse #: Inherent stability of this type of # reduces the risk of shortening and favors union. On the other hand area of bony contact is small requiring very strong union before any external support can be discarded.

• Oblique #: # line runs at an angle less than 90 degree to the long axis of bones.

• Spiral #: Line of # curves in a spiral fashion round the bone. Both these # result form indirect violence. Spiral # in particular is caused by torsional forces. Union can be rapid as there is often large area of bone but unopposed muscle contraction readily lead to shortening and displacement.

• Comminuted #: More than 2 fragments are present. It ranges from slight comminution, comminution at # site with a large butterfly fragment to a highly comminuted #. It indicates severe violence & there is greater risk of damage to surrounding tissues. Comminuted # are unstable.

• Double (Segmental) #: Affected bone is fractured at two distinct levels. Instability and difficulty in reduction and fixation are common.

• Impacted #: One fragment is driven into the other. Cancellous bone is usually involved and union is often rapid but may displace if subjected to deforming forces.

• Compression or crush #: Occur in cancellous bone which is compressed beyond the limits of tolerance. If the deformity is accepted union is invariably rapid.

• Avulsion #: Produced by sudden muscle contraction, the muscle pulling off the portion of the bone to which it is attached.

• Depressed #: When a sharply localized blow depresses a segment of cortical bone below the level of surrounding bone. Common in skull bones. Healing is rapid.

• Intra-articular #: # involves a joint. Any residual articular irregularity leads to secondary OA. There is risk of stiffness from IA adhesions. Early mobilization is essential.

• # Close to a joint: Stiffness is a problem due to tethering of neighboring muscles and tendons by spread of callus from healing #.

• # Dislocation: When a joint has dislocated and there is in addition a # of one of the bony components. These are difficult to reduce and unstable. Stiffness and avascular necrosis are two common complications.

• Complex or complicated #: Accompanying damage to major neighboring structures.

• According to level: Shaft or diaphyseal #, between shaft and ends or metaphyseal # and at the ends of bones which includes intra-articular #.

• Also called as M/3rd, L/3rd, U/3rd, junction of U/3rd & M/3rd , junction of M/3rd & L/3rd.

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• Describing the deformity: If the fracture is not displaced it is said to be in anatomical position. Similarly if a perfect reduction is achieved after manipulation it is described as anatomical reduction.

• Displacement: If the bone ends have shifted relative to one another the direction of displacement is described in terms of movement of the distal fragment. A rough estimate is usually made of the percentage of surfaces in contact. When none of the # surface is in contact it is described as having no bony contact or off ended. These are potentially unstable, liable to progressive shortening, delay or difficult union, hard to reduce sometimes due to soft tissue interposition.

• Angulation: Described in terms of the position of the point of angle.• Axial rotation: One fragment rotates on its long axis with or without

accompanying displacement or angulations. Can be over looked unless precautions are taken and possibility kept in mind.

Symptoms and signs• History: Activity, nature of incident, magnitude of the applied forces, point of

impact, direction of the applied forces, some underlying associated condition, site of pain, severity of pain, loss of functional activity etc.

• Examination : Inspection for asymmetry of contour or posture, bruising of skin, grazing, friction burns, lacerations, skin stretch marks, localized swelling of limb, haematoma, tenderness, palpation of sharp bony edge, abnormal mobility, bony crepts, sound of bone ends rubbing together.

X-Ray• Most important• Must include the bone and a proximal and distal joint.• Must be at least in two different planes.• If necessary a specialized view must be taken.• Additional information is gained from CT or MRI.

Pitfalls• In unconscious patient injuries of cervical spine are frequently overlooked so

always have routine screening films of neck, chest and pelvis in these patients.• Impacted # are often missed when only one view is taken.• In children epiphyseal line is often wrongly mistaken for a #.

Fracture Healing• As a result of injury periosteum may be completely or partially torn,

disruption of Haversian system with death of adjacent bone cells, tearing of muscles and other soft tissues.

• Bleeding occurs from bone ends, marrow vessels and damaged soft tissues, with the formation of fracture haematoma which later on clots.

• Fracture haematoma is rapidly vascularised by the in growth of blood vessels from surrounding tissues and for some weeks there is rapid cellular activity. Fibro vascular tissue replaces the clot, collagen fibers are laid down and mineral salts are deposited.

• Subperiosteal bone: New woven bone is formed beneath 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 it is disturbed by excessive mobility at the fracture site, cartilage may be formed instead and remain until a better blood supply is established.

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• Primary callus response: This remains active for a few weeks only. There is much less vigorous formation of callus from the medullary cavity. Nevertheless the capacity of the medulla to form new bone remains indefinitely throughout the healing of the fracture.

• Bridging external callus: If the periosteum is incompletely torn and there is no significant loss of bony contact, the primary callus response may result in external continuity of the fracture (bridging external callus). Cells lying in the outer layer of the periosteum itself proliferate to reconstitute the periosteum.

• If the gap is more substantial, fibrous tissue formed from the organization 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. This mechanism may be due to a change of electrical potential at the 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. Net result of the three mechanisms just mentioned is that the fracture becomes rigid, function in the limb returns and the situation is rendered favorable for the endosteal bone formation and remodeling.

• Endosteal new bone formation: If there is no gap between the bone ends, osteoclasts can tunnel across the fracture line in advance of in growing blood vessels and osteoblasts which form new Haversian system. Dead bone is revascularised and may provide an invaluable scaffolding and local mineral source. This process cannot occur if the fracture is mobile.

• Formation of new cortical bone, with re-establishment of continuity between the Haversian system 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 in growth of medullary callus which remains active throughout the healing phase.

• Where the bone ends are supported by rigid internal fixation there is no need for external bridging callus, as a result it may not be seen or is minimal. Healing of fracture occurs slowly through the formation of new cortical bone between bone ends. It is therefore essential that the internal fixation devices are retained until this process is complete.

• Remodeling: After clinical union, new Haversian systems are laid down along the line of stress. In areas free from stress bone is removed by osteoclasts. Eventually little trace of external bridging callus will remain. The power to remodel is great in children but not so in adults.

Principles of treatment• Primary aim is sound bony union without deformity and restoration of

function.• In addition it must be as quickly as possible and without risk or any

complications, whether early or late.Priorities of treatment

• Manage any respiratory obstruction or impairment.• Correct hemorrhage and shock.• Estimated blood losses are as follows:-• Closed # shaft femur – ½ to 1 liter.• Open ring # of pelvis – 2 to 3 liters.

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• Intra-abdominal hemorrhage – 2 to 3 liters.• Haemothorax – 1 to 2 liters.• Treatment of other associated injuries like head injury, cardiac tamponade

may be due to intra thoracic rupture of the aorta and other intra abdominal visceral injuries.

Factors affecting union• Type of bone: Cancellous bone (spongy bone) – Is generally well advanced

within 6 weeks.• Cortical bone (compact bone): Endosteal callus may take many months to

become reasonably well established. Uncomplicated long bone # may take 9 – 18 weeks to unite. However external bridging callus may allow an earlier return of function.

• Age of patient: In children union of # is rapid. Speed of union decreases as age increases until skeletal maturity. Also children have remarkable powers of remodeling fractures. But remodeling is poor in axial rotation.

• Mobility at # site: Interfere with vascularisation of # haematoma leading to disruption of early bridging callus and may prevent endosteal new bone growth.

• Separation of bone ends due to interposition of soft tissues, excessive traction or following internal fixation leading to resorption of bone ends interferes with normal mechanism of healing.

• Infection: Delay or prevent union.• Disturbance of blood supply: Healing may be interfered. But in case of

cancellous bone it may not interfere with union. Collapse of necrotic bone beyond the level of union is observed at a later date.

• Properties of bone involved: Clavicle is a spectacular example where non-union is extremely rare.

• Joint involvement: When a # involves a joint union is occasionally delayed may be due to dilution of the fracture haematoma by synovial fluid.

• Bone pathology: Some primary and secondary bone tumors may delay or prevent union.

Complications of fractures• Tissue damage: Hemorrhage, oligaemic shock, infection in compound

fractures, electrolyte shifts, protein breakdown and other metabolic responses of trauma.

• Prolonged recumbency: Hypostatic pneumonia, bed sores, DVT, muscle wasting, skeletal decalcification and formation of urinary calculi, UTI etc.

• Anesthesia and surgery: Atelectasis and pneumonia, blood loss leading to anemia or shock, wound infection, mechanical failure of fixation etc.

• Fracture: Disorders of rate and quality of union, joint stiffness, Sudeck’s atrophy, AVN, myositis ossificans, infections, neurological, vascular and visceral complications.

• Slow union: # takes longer than normal but passes through the stages of healing without any deviation from normal clinically or radio logically.

• Delayed union: Union fails to occur within the expected time. Radiographs may show abnormal bone changes. Typically there is absorption of bone at the level of fracture with gap between the bone ends and EBC restricted to a localized area and of a poor quality. However no sclerosis of bone ends is there.

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• Non-union: Fracture has failed to unite and there are radio logical changes which indicate that this situation will be permanent that is fracture will never unite.

• Two types: Hypertrophic – Bone ends appear sclerotic and flared out so that diameter at level of fracture is increased (elephant’s foot). # Line is clearly visible, gap filled with cartilage and fibrous tissue cells. Atrophic – No evidence of cellular activity, bone ends are narrow, rounded, osteoporotic and frequently avascular.

Treatment of complications• Slow union: # is adequately supported.• Delayed union: Reconsider adequacy of fixation, immobilization continued

and # reassessed in 4-6 weeks.• Hypertrophic non-union: If # can be fixed with absolute rigidity the

cartilaginous and fibrous tissue will mineralize and converted to bone.• Process of induction may be stimulated by small electric currents in the gap

between bone ends by embedding percutaneous electrodes in # gap or by placing field coils round the limb.

• Atrophic non-union: # must be held rigidly, fibrous tissue removed from between bone ends, freshened by a limited local trimming, bone ends should be decorticated from level of # back to healthy bone and area around the # is packed circumferentially with cancellous bone grafts.

Complications of fractures• Mal-union: Any # which has united in less than anatomical position. Slightest

deformity particularly in intra articular # is potential source of trouble and may predispose to early sec OA. Firstly aim at adequate reduction & avoid mal union. If detected before union, correct the deformity. If detected after union, corrective osteotomy of deformity is severe.

• Shortening: Generally a sequel of mal union. in children growth is always accelerated as a result of epiphysis being stimulated by increased blood supply. In adults shortening of 1.5 cm is easily tolerated. Shortening more than this is dealt with alteration in footwear. In UL shortening seldom causes any problem.

• Traumatic epiphyseal arrest: If the whole width of the plate is affected, growth may be arrested at that level, leading to progressive shortening of limb. If plate is affected incompletely growth continues more or less normally at one side leading to some shortening of limb and distortion of joint which can be partly corrected by remodeling.

• Joint stiffness: Common complication due to pathology within the joint, close to the joint and remote from the joint.

• Intra articular causes: Intra articular adhesions due to organization of a hemarthrosis, damage to articulating surface or prolonged immobilization.

• # may disrupt the joint to such an extent that there is mechanical block of movement. Movement may be blocked by formation of loose bodies. Sec OA due to intra articular #, AVN, or mal union of #.

• Peri-articular causes: Joint capsules and musculo-tendinous cuffs may become functionally impaired. Fibrosis resulting from direct injury, passive stretching of disuse, edema etc. Displaced # fragment lying close to joint leads to a mechanical block to movement. Myositis ossificans acts as a mechanical block.

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• Causes remote from joints: Tethering or entrapment of muscle by adhesions between # and overlying muscle. Muscle ischemia followed by replacement fibrosis and contractures when there is vascular injury associated (VIC).

• Sudeck’s atrophy: Common after Colles’s #. Not recognized until plaster is removed. Swelling of hand & fingers, skin is warm pink and glazed. Movements are restricted and diffuse tenderness. X-ray shows diffuse osteoporotic mottling of the carpals. It is supposed to be due to atypical sympathetic response to trauma, splintage which is too tight. Usually it is self limiting resolving slowly over 4-12 months. Nevertheless restriction of movements may be permanent. Analgesics and local anesthetics may help.

• AVN: Death of bone due to interference of blood supply. If fragments are small healing is usually uneventful. If fragments are large healing may be delayed. Affected bone becomes soft and distorted in shape, leading to pain, stiffness and secondary OA. AVN and non union are quite distinct. In majority of femoral neck and scaphoid # with AVN, the # has united.

• Myositis ossificans: Calcified mass appears in the tissue near a joint leading to considerable restriction of movements because of mechanical block. It can follow passive stretching of joints. Therefore passive stretching is best avoided especially around elbow. Treatment includes late excision of mass around 6-12 months as early excision may result in massive recurrence.

• Osteitis: Infection is rare in closed # but common in open #. Recurrent pyrexia, pain, tenderness, swelling and raised ESR should arouse suspicion because once fairly established it becomes virtually incurable. Pus C/S, antibiotics, drainage, local dressings etc continued. Implant removal delayed till # healing is seen. If infection is well established and unresponsive saucerisation of area, radical excision of all infected bone and open packing of wound is done. Local antibiotics in forms of beads and irrigation tubes may be used. Rarely amputation has to be considered in profound toxemia and poor GC of patient.

• Acute arterial arrest: Loss of distal pulse, pallor, coldness of skin, loss of capillary response, severe pain in the limb and paraesthesia are found. Most common cause is kinking of vessels. Circulation is immediately restored by correction of the deformity. Occasionally a sharp bone edge may cause arterial rupture, profound arterial spasm, aneurysm or intimal stripping. Treatment includes end to end anastomosis in cleanly cut artery and in case of deficit an in-line reversed vein graft is often used. In case of spasm preliminary irrigation with papaverine is tried.

• Immediate neurological disturbance: Nerve may be stretched over a bone edge over a # or dislocation. If prolonged will lead to local ischemia and interruption of nerve conduction. If stretching is more severe there may be rupture of axons or neural tubes, acute nerve division is rare, mainly seen with compound # due to sharp objects.

• Dislocation of shoulder – Axillary N & rarely other brachial plexus lesions.• # Humerus – Radial N• Dislocation of elbow – Ulnar N, Median N• # around elbow – Median, Ulnar, PIN.• Dislocation of hip – Sciatic• Dislocation of knee or rupture of lat ligaments – Common peroneal N

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• Majority of nerve lesions are in continuity. Assuming that the # or dislocation is reduced, recovery begins after 6 weeks, progressing quite rapidly thereafter.

• If a # is treated surgically, inspect the affected nerve and treat accordingly.• When expected recovery does not occur EMG and NCV is done F/B

exploration.• In clean injury primary repair is must.• Otherwise elective repair delayed until sound wound healing is obtained.• Delayed neurological disturbance: Sometimes nerve palsy develops after a #

has healed. For e.g. Tardy Ulnar N palsy after SC # or Monteggia # dislocation has occurred after up to 60 years. Treated by early anterior transposition of the nerve. Median N palsy developing a few months after Colles’s # is treated by carpal tunnel decompression.

• Delayed tendon ruptures: Seen most frequently at wrist after a Colles’s # as rupture of EPL from gradual fraying of tendon as it rubs against healing # or by traumatic or fibrotic interference with its arterial blood supply resulting in local sloughing of tendon. Best results are obtained by transposition and suture of EI to the distal segment of EPL.

• Other associated complications like visceral complications, fat embolism, OA, and pathological # are to be treated accordingly.

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