Complication of Fractures Complications of fractures tend to be classified according to whether they are local or systemic and as well as the

general complication. The following are the complication of fractures according to their types: General Complications: 1. Shock 2. Diffuse coagulopathy (DIC) 3. Crush syndrome 4. Venous thrombosis & Pulmonary embolism 5. Fat embolism 6. Gas Gangrene a.) Shock Commonest cause of death in fractures of major bones like pelvis or femur External or internal haemorrhage. External: compound fractures injuring major vessels of the LIMB Internal: injury to body cavities- chest or pelvis Internal is more difficult to diagnose. Shock results from the loss of blood when there is fracture. The bleeding could either be external or not visible. Also, shock results from the loss of extracellular fluid into the damaged tissues that occurs when there is fracture. Large quantities of blood are lost in fracture as bone is a vascular structure especially those in femur and pelvis. What to observe: Thirst, rapid shallow breathing, the lips and skin are pale and the extremities feel cold, impaired renal function test and decreased urinary output. Management: 1. Restoration of blood volume 2. Relieving patients pain 3. Providing adequate splinting 4. Protecting the client from further injury b.) Diffuse Coagulopathy (DIC)-

A bleeding disorder characterized by reduction in the elements involved in blood clotting due to their use in widespread clotting within the vessels. In the late stages, it is marked by profuse hemorrhaging.

Management:

Stop the bleeding Fresh Frozen Plasma (FFP) Cryoprecipitate Platelet transfusion Heparin

c.) Crush Syndrome Serious medical condition characterized by major shock & renal failure following a crushing injury to skeletal muscles or tourniquet left too long. It is renal failure following extensive crushing injury of muscles.

Pathogenesis: Crushing of muscles causes entry of myoglobin into circulation. Myoglobin precipitates in renal tubules causing acute tubular necrosis, metabolic acidosis & hyperkalemia

Clinical features (appear within 2-3 days of injury) Signs of deficient renal function: Oliguria (Scanty urine) Apathy Restlessness Delirium Cardiac arrhythmia & failure

Hypothermia Shock

Management:

PREVENTION Strict tourniquet timing

Amputation limb crushed severely tourniquet left on > 6 hrs above site of compression & before compression released

Monitor intake & output Dialysis Correct electrolytes & acidosis Antibiotics

d.) Deep vein thrombosis and Pulmonary Embolisms

Deep vein thrombosis and pulmonary embolism are major complications that can occur after ankle injuries. It is a common complication originating from altered hemodynamics in lower limb and spinal injuries.

Virchow's triad decreased flow rate of the blood damage to the blood vessel wall hypercoagulability

Virchows triad factor Clot formation in large vein thrombus breaks off Emboli Site: leg, thigh and pelvic vein. Risk factors:

Management: Correct hypovolemia Calf muscle exercise Proper positioning Well fitting bandages & cast Limb elevation Graduated compression stockings Calf muscle stimulation Anticoagulation Ambulate patient Limb elevation Heparinization Thrombolysis Oxygenation or ventilation

e.) Fat Embolism Fat globules from marrow pushed into circulation by the force of trauma that causing embolic phenomena It is a life threatening complication of fracture where fat globules occlude the small blood vessels. Embolism is the process of occlusion of blood vessel by any material which is brought to the site from elsewhere by bloodstream.

Pathogenesis Injury to large bones (e.g. femur) release fat globule from bone marrow to blood stream. Alternatively fat can also be released from the adipose tissue. The fat globules obstruct capillary vasculature of the lungs.

Also, fat is converted to free fatty acid, which induces toxic vasculitis followed by thrombosis which obstruct the microvasculature.

Watch out for: Brain: mental confusion Lung: breathlessness, ARDS Skin: Petechia

Management: Prevent hypoxemia oxygenation or ventilation

Rule out head injury CT Scan of brain

Monitor fluid & electrolyte balance CVP, urinary catheter

f.) Gas Gangrene Rapid and extensive necrosis of the muscle accompanied by gas formation and systemic toxicity due to clostridium perfringens infection

Clinical Manifestations: sudden onset of pain localized to the infected area. swelling , edema +/- pyrexia profuse serous discharge with sweetish and mousy odor . Gas production Management: early diagnosis . surgical intervention and debridement are the mainstay of treatment. IV antibiotics fluid replacement. hyperbaric Oxygen

Early Complications: 1. Visceral Injury 2. Vascular Injury 3. Compartment Syndrome 4. Haemarthrosis 5. Infection a.) 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 b.) 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 X-ray: suggest high-risk fracture. Angiogram should be performed to confirm diagnosis.

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 C.) 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. An increased pressure within enclosed osteofascial space that reduces capillary perfusion below level necessary for tissue viability; the underlying mechanism is: - increased volume within space - decreased space for contents - combination of both Trauma with bleeding/swelling

Bleeding disorders Burns Tight wraps Traction Surgical positioning Pneumatic antishock garment Reprefusion swelling Casting & Wraps

Pathophysiology: Increased compartment pressure leads to increased venous pressure which decreases A-V gradient resulting in muscle and nerve ischemia. Clinical Manifestations : The six Ps: Pressure: palpation of compartment and its tension or firmness

Pain: Exaggerated with passive stretch of the involved muscles in compartment Earliest symptom but inconsistent Paresthesia:Peripheral nerve tissue is more sensitive than muscle to ischemia Will progress to anesthesia if pressure not relieved Paralysis: late finding Pallor Pulselessness Management: Lower leg to level of the heart Remove cast Split all dressings down to skin Fasciotomy if continued clinical findings and/or elevated compartment pressure 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. 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 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

D.) Hemarthrosis 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. E.) Infection Closed fractures hardly ever Open fractures may become infected Post traumatic wound may lead to chronic osteomyelitis Manifestations wound is inflammed draining seropurulent fluid Management

antibiotic excise the devitalised tissue tissues opened & drained the pus

Late complications: 1. Delayed Union 2. Non-union 3. Mal-union 4. Avascular Necrosis 5. Osteoarthritis 6. Joint Stiffness a.) 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 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 Mechanical Over-rigid fixation-fixation devise Imperfect splintage Excessive traction creates a gap#(delay ossification in the callus) 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)

Management: 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) B.) 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

C.) Malunion fragments that are joined in an unsatisfactory position

Factors: failure to reduce the fracture failure to hold the reduction while healing proceed gradual collapse of comminuted / osteoporotic bone

d.) 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 Management : 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 e. ) Osteo Arthritis 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 f. ) 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

Prepared by Nikki Arapol