4. CAUSES Sudden trauma direct(fracture of the ulna caused by blow on the arm) indirect(spiral fractures of the tibia and fibula due to torsion of the leg, vertebral compression fractures, avulsion fractures) Stress or fatigue-repetitive stress(athletes, dancers, army recruits) Pathological(osteoporosis, Paget’s disease, bone tumour)
14. FRACTURES DISPLACEMENT After a complete fracture the fragments usually displaced: partly by the force of injury partly by gravity partly by the pull of muscles attached to them. 4 types: Translation/Shift Alignment/Angulation Rotation/Twist Altered length
17. Healing by callus Callus is the response to movement at the fracture site to stabilize the fragments as rapidly as possible. Steps:
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20. Healing without callus For fracture that is absolutely immobile: impacted fracture in cancellous bone. fracture rigidly immobilized by internal fixation New bone formation occurs directly between fragments. Gaps between the fracture surfaces are invaded by new capillaries & bone forming cells growing in from edges. For very narrow crevices(<200um), osteogenesis produces lamellar bone(mature). For wider gaps, osteogenesis begins with woven bone (immature) first which is then remodelled to lamellar bone (mature bone).
25. First aid management Airway, Breathing and Circulation Splint the fracture Look for other associated injuries Check distal circulation – is distal circulation satisfactory? Check neurology – are the nerve intact? AMPLE history- Allergies, Medications, Past medical history, Last meal, Events Radiographs – 2 views, 2sides, 2 joints, 2 times.
30. Reduce Aim for adequate apposition and normal alignment of the bone fragments The greater contact surface area between fragments, the more likely is healing to occur
31. However, there are some situations in which reduction is unnecessary: When there is little or no displacement When displacement does not matter (e.g. in some fractures of the clavicle) When reduction is unlikely to succeed (e.g. with compression fracture of the vertebrae)
33. Closed Reduction Suitable for Minimally displaced fractures Most fractures in children Fractures that are likely to be stable after reduction
34. Most effective when the periosteum and muscles on one side of fracture remain intact Under anaesthesia and muscle relaxation, a threefold manoeuvre applied: Distal part of the limb is pulled in line of the bone Disengaged, repositioned Alignment is adjusted
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36. Mechanical Traction Some fractures (example fracture of femoral shaft) are difficult to reduce by manipulation because of powerful muscle pull However, they can be reduced by sustained muscle mechanical traction; also serves to hold the fracture until it starts to unite
37. Open Reduction Operative reduction under direct vision Indications: When closed reduction fails When there is a large articular fragment that needs accurate positioning For avulsion fractures in which the fragments are held apart by muscle pull When an operation is needed for associated injuries When a fracture needs an internal fixation
43. Disadvantage and complications Patient kept on bed for long time Pressure ulcer General weakness Pulmonary infection Contracture Pin tract infection Thromboembolic event Methods Traction by gravity Balanced traction Fixed traction
48. Fixed Traction Principle = balanced traction Useful for when patient has to be transported Thomas’s splint
49. Cast Splintage Methods: Plaster of Paris Fibreglass Especially for distal limb # and for most children # Disadvantage: joint encased in plaster cannot move and liable to stiffen Can be minimized: Delayed splintage (traction initially) Replace cast by functional brace after few weeks
78. Exercise Prevention of edema active exercise and elevation Active exercise also stimulates the circulation. Prevents soft-tissue adhesion and promotes fracture healing. Preserve the joint movement Restore muscle power Functional activity
79. Management of Open Fractures Abreakin skin and underlying soft tissues leading directly to communicating with the fracture
93. Surgical Debridement Type II and type III require surgical debridement. Important aspect of wound management. Reduce bacteria, remove foreign bodies, remove devitalized tissue. Removal of dead tissue reduces bacterial burden and accelerate healing. 89
95. Wound Closure Uncontaminated I & II can be sutured – provided without tension All other wounds left open, packed with moist sterile gauze, to be inspected 24-48 hours – primary delayed closure If wound cannot be closed without tension – skin grafting
97. Stabilization of the fracture To reduce infection and assist recovery of soft tissue Depends on: degree of contamination length of time from injury to operation amount of soft tissue damage If <8 hours: up to IIIA treated as closed fractures: Splintage Intramedullary nailing Plating External fixation Others: External fixation
101. General Complications Shock Diffuse coagulopathy Respiratory dysfunction Crush syndrome Venous thrombosis & Pulmonary embolism Fat embolism Gas Gangrene Tetanus
102. General 1: Shock Altered physiologic status with generalized inadequate tissue perfusion relative to metabolic requirements. irreversible damage to vital organs
107. General 4: Crush Syndrome[traumatic rhabdomyolitis] Serious medical condition characterized by major shock & renal failure following a crushing injury to skeletal muscles or tourniquet left too long Bywaters’ Syndrome
109. General 5: Deep vein thrombosis and pulmonary embolism. Virchow’s triad factor Clot formation in large vein thrombus breaks off Emboli Site: leg, thigh and pelvic vein. Risk factors:
110. General 5: Management Deep vein thrombosis and pulmonary embolism. Anticoagulation Ambulate patient Established thrombosis/embolism Limb elevation Heparinization Thrombolysis Oxygenation or ventilation PREVENTION Correct hypovolemia Calf muscle exercise Proper positioning Well fitting bandages & cast Limb elevation Graduated compression stockings Calf muscle stimulation
111. General 6: Fat Embolism Fat globules from marrow pushed into circulation by the force of trauma that causing embolic phenomena
114. General 7: Gas Gangrene Rapid and extensive necrosis of the muscle accompanied by gas formation and systemic toxicity due to clostridium perfringens infection
115. General 7: Gas Gangrene Prevention: ALL DEAD TISSUE [4C] SHOULD BE COMPLETELY EXCISED,
116. General 8: Tetanus A condition after clostridium tetani infection that passes to anterior horn cells where it fixed and cant be neutralized later produces hyper-excitability and reflex muscle spasm
118. Early 1: Visceral injury Fractures around the trunk are often complicated by visceral injury. E.g. Rib fractures pneumothorax / spleen trauma / liver injuries. E.g. Pelvic injuries bladder or urethral rupture / severe hematoma in the retro-peritoneum . Rx: Surgery of visceral injuries
119. Early 2: Vascular injury Commonly associated with high-energy open fractures. They are rare but well-recognized. Mechanism of injuries: The artery may be cut or torn. Compressed by the fragment of bone. normal appearance, with intimal detachment that lead to thrombus formation. segment of artery may be in spasm. It may cause Transient diminution of blood flow Profound ischaemia Tissue death and gangrene
120. Early 2: Vascular injury X-ray: suggest high-risk fracture.Angiogram should be performed to confirm diagnosis.
121. Early 2: Vascular injury muscle ischaemic is irrevesible after 6 hours. Remove all bandages and splint & assess circulation Skeletal stabilization – temporary external fixation. Definitive vascular repair. Vessel sutured endarterectomy
122. Early 3: Compartment Syndrome A condition in which increase in pressure within a closed fascial compartment leads to decreased tissue perfusion. Untreated, progresses to tissue ischaemia and eventual necrosis
123. Early 3: Compartment Syndrome Most common sites (in ↓ freq): leg (after tibial fracture) -> forearm -> thigh -> upper arm. Other sites: hand, foot, abdomen, gluteal and cervical regions. High risk injuries: # of elbow, forearm bones, and proximal 3rd of tibia (30-70% after tibial #) multiple fracture of the foot or hand crush injuries circumferential burns
125. Early 3: Compartment Syndrome Vicious cycle ↑ fluid content Constriction of compartment ↑ INTRACOMPARTMENTAL PRESSURE Capillary basement membranes become leaky -> oedema Obstruct venous return Vascular congestion Muscle and nerve ischaemia Further ↑ intracompartmental pressure ↓ capillary perfusion Compromise arterial circulation -> PROGRESSIVE NECROSIS OF MUSCLES AND NERVES !!
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127. A vicious circle that ends after 12 hours or less Necrosis of the nerve and muscle within the compartment Nerve -capable to regenerate Muscle -infarcted Never recover Replaced by inelastic fibrous tissue ( Volkmann’s ischaemic contracture)
128. Investigations of compartment sydromes Intra-compartment Pressure Measurement (ICP) Use of slit catheter; quick and easy Indications: Unconscious patient Those who are difficult to assess Concomitant neurovascular injury Equivocal symptoms Especially long bone # in lower limb Perform as soon as dx considered > 40mmHg – urgent Rx! (normal 0 – 10 mmHg)
129. Investigations of compartment syndromes Other Ix – limited value; +ve only when CS is advanced Plasma creatinine and CPK Urinanalysis – myoglobinuria Nerve conduction studies Ix to establish underlying cause or exclude differentials X-ray of affected extremity Doppler US/arteriograms – determine presence of pulses; exclude vascular injuries and DVT PT/APTT – exclude bleeding disorder
130. Management Prompt DECOMPRESSION of affected compartment Remove all bandages, casts and dressings Examination of whole limb Limb should be maintained at heart level Elevation may ↓ arterio-venous pressure gradient on which perfusion depends Ensure patient is normotensive. Hypotension ↓ tissue perfusion, aggravate the tissue injury.
131. Management Measure intra-compartment pressure If > 40mmHg Immediate open fasciotomy If < 40mmHg Close observation and re-examine over next hour If condition improve, repeated clinical evaluation until danger has passed Don’t wait for the obvious sings of ischemia to appear. If you suspect An impending compartment syndrome, start treatment straightaway
132. Fasciotomy Opening all 4 compartments Divide skin and deep fascia for the whole length of compartment Wound left open Inspect 5 days later If muscle necrosis, do debridement If healthy tissue, for delayed closure or skin grafting
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134. Complications Volkmann’s ischaemiccontracture Motor/sensory deficits Kidney failure from rhabdomyolysis (if very severe) Infection – fasciotomy converts closed # to open # Loss of limb Delay in bone union Prognosis excellent to poor, depending on how quickly CS is treated and whether complications develop
135. Early 4: Nerve Injury It’s more common than arterial injuries. The most commonly injured nerve is the radial nerve [in its groove or in the lower third of the upper arm especially in oblique fracture of the humerus] Common with humerus, elbow and knee fractures Most nerve injuries are due to tension neuropraxia.
136. Early 4: Nerve Injury Damaged by laceration, traction, pressure or prolonged ischaemia
137. Early 4: Nerve Injury Investigations Electromyography Nerve conduction study May help to establish level and severity of lesion Clinical features Numbness and weakness Skin smooth and shiny but feels dry Muscle wasting and weakness Sensation blunted Tinel’s sign +ve
139. Early 5: Haemarthrosis Bleeding into a joint spaces. Occurs if a joint is involved in the fracture. Presentation: swollen tense joint; the patient resists any attempt to moving it treatment: blood aspiration before dealing with the fracture; to prevent the development of synovial adhesions.
140. Early 6: INFECTION Closed fractures – hardly ever Open fractures – may become infected Post traumatic wound – may lead to chronic osteomyelitis
142. Late 1: DELAYED UNION Union of the upper limbs - 4-6 weeks Union of the lower limbs - 8-12 weeks(rough guide) Any prolong time taken is considered delayed
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144. Late 1: DELAYED UNION Factors are either biological or biomechanical Biological : Poor blood supply Tear of periosteum, interruption of intramedullary circulation Necrosis of surface# and healing process will take longer Severe soft tissue damage Most important factor Longer time for bone healing due less inflammatory cell supply Infection: bone lysis, tissue necrosis and pus Periosteal stripping Less blood circulation to bone
145. Mechanical Over-rigid fixation-fixation devise Imperfect splintage Excessive traction creates a gap#(delay ossification in the callus) Late 1: DELAYED UNION
146. Clinical features: Tenderness persist Acute pain if bone is subjected to stress* ( * ask pt to walk, move affected limb) X RAYS -visible line# and very little callus formation/periosteal reaction - bone ends are not sclerosed/ atrophic (it will eventually unite) Late1: DELAYED UNION
147. Tx: conservative and operative Eliminate possible causes of delay Promote healing Immobilization should be sufficient to prevent movement at # site(cast / internal fixation) Not to neglect # loading so, encourage muscle exercise and weight bearing in the cast/brace Operation > 6 mths & no signs of callus formation Internal fixation and bone graffting (operation-least possible damage to the soft tissue) Late 1: DELAYED UNION
148. Late 2 : NON-UNION In a minority of cases, delayed union--non-union Factors contributing to non-union:- inadequate treatment of delayed union too large gap interposition of soft tissues between the fragments The growth has stopped and pain diminished- replaced by fibrous tissue - pseudoarthrosis Treatment :- conservative / operative atrophic non-union – fixation and grafting hypertrophic non-union – rigid fixation
149. Late 2: NON UNION bone ends are rounded off or exuberant Hypertrophic non union Bone ends are enlarged, osteogenesis is still active but not capable of bridging the gap ‘elephant feet’ on X ray Atrophic non union Cessation of osteogenesis No suggestion of new bone formation
150. Non-union X- ray A – Atrophic non- union B – Hypertrophic non- union A B
151. Late 2: Non union Tx: Mostly symptomless Conservative Removable splint For hypertrophic non-union, functional bracing-induce union Pulsed electromagnetic fields and low frequency pulsed u/s can also be used to stimulate union. Operative Hypertrophic--Rigid fixation (internal or external) Atrophic--Excision of fibrous tissue ,sclerotic tissue at bone end, bone grafts packed around the fracture
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154. Late 3: MALUNION Factors:- failure to reduce the fracture failure to hold the reduction while healing proceed gradual collapse of comminuted / osteoporotic bone
156. Late 3: Mal-union X-ray are essential to check the position of the fracture while uniting. important- the first 3 weeks so it can be easily corrected Clinical features: Deformity usually obvious , but sometimes the true extent of malunion is apparent only on x-ray Rotational deformity can be missed in the femur, tibia, humerus or forearm unless is compared with it’s opposite fellow
158. Late 4: AVASCULAR NECROSIS Certain region-known for their propensity to develop ischaemia and bone necrosis Head of femur Proximal part of scaphoid Lunate Body of talus (Actually this is an early complication however the clinical and radiological effects are not seen until weeks or even months) No clinical feature of avascular necrosis but if there is a failure to unite or bone collapse-pain
159. A B The cardinal X-ray feature – increased bone density in the weight-bearing part of the joint(new bone ingrowth in necrotic segment)
160. Treatment:- Avascular necrosis can be prevented by early reduction of susceptible fractures and dislocations. Arthroplasty - Old people with necrosis of the femoral head. Realignment osteotomy or arthrodesis - for younger people with necrosis of the femoral head Symptomatic treatment for scaphoid or talus
161. Late 5: OSTEOARTHRITIS A fracture-joint may damage the articular cartilage and give rise to post traumatic osteoarthritis within a period of months. Even if the cartilage heals, irregularity of the joint surface may cause localized stress and so predispose to secondary osteoarthritis years later
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163. Late 6: JOINT STIFFNESS Commonly occur at the joints close to malunion or bone loss eg: knee, elbow, shoulder Causes of joint stiffness haemarthrosis -> lead to synovial adhesion oedema and fibrosis adhesion of the soft tissues Worsen by prolong immobilization Treatment prevented with exercise physiotherapy
Type I open fracture can be managed with non-operative approach and closed reduction.
may lead to irreversible damage of the life supporting organs.Thirst, rapid shallow breathing, the lips and skin are pale and the extremities feel cold,if the compansation fails….. impaired renal function test and decreased urinary output.
It’s a re-perfusion injury seen after the release of crushing pressure, there will be release of muscular breakdown products(myoglobin,k+,p) which have nephrotoxic effect on the kidneyFirst describe by Eric Bywaters
It’s a re-perfusion injury seen after the release of crushing pressure, there will be release of muscular breakdown products(myoglobin,k+,p) which have nephrotoxic effect on the kidneyFirst describe by Eric Bywaters
Petechial haemorrhage
4C – Colour – blue-black purpleConsistency – MushyContractibility – unableCut – not capable to bleedDeep, penetrating wound in muscular tissue should be explored, ALL DEAD TISSUE SHOULD BE COMPLETELY EXCISED, if there is doubt about tissue viability, the wound should be left opened
