Complex Regional Pain Syndrome (reflex sympathetic dystrophy): soft tissue complication of musculoskeletal injury Manifestations o severe pain – aching, burning o Increases with stimulation, movement of limb
o cause unclear – believed to have sympathetic nervous system component autonomic nervous system dysfunction o increased swelling o vasomotor instability – flushed and warm, or cold and pale muscle wasting thin, shiny skin abnormalities of nails and bone may occur decreased muscle strength and disuse can lead to contractures and osteoporosis Management o pain management o prevention of disability Thromboemboli: people with a lower extremity fracture are at increased risk of developing thromboembolic disorders such as pulmonary embolism and deep vein thrombosis due to inactivity and reduced weight bearing exercise prophylactic management o anticoagulant prophylaxis (heparin) o graduated compression stockings o use of intermittent pneumatic compression devices Fat Embolism Syndrome: a group of clinical manifestations resulting from the presence of fat droplets in small blood vessels, the lungs or other organs after a long bone fracture or other major trauma. fat emboli are released from bone marrow or fat tissue at the fracture site and enter the venous system through torn veins. clinical manifestations begin within a few hours to 3 – 4 days after injury Clinical features: substernal chest pain dyspnoea low grade fever cyanosis tachycardia diaphoresis pallor cerebral dysfunction from fat emboli in cerebral circulation o disorientation, seizures, focal neurological deficits skin and mucosal petechiae – chest, neck, axillae, shoulders Management: support respiration and oxygenation maintain adequate fluid balance reduce inflammation (corticosteroids)
early stabilization of the fracture Phases of bone healing Phase 1. Haematoma formation Break in bone → disruption of periosteum and blood vessels in the cortex, marrow and surrounding soft tissues → bleeding from damaged ends of bone cells and soft tissues o – blood loss may vary from 200mL – 1500mL o →Haematoma forms within the medullary canal, between the fractured ends of the bone and beneath the periosteum blood flow to the injured area is disrupted o → bone tissue immediately adjacent to the fracture dies o - dead cells and other debris from the fracture site o → intense inflammatory response Inflammatory response → o vasodilatation → redness, warmth o ↑ cell permeability → exudation of plasma into surrounding tissues → swelling o Infiltration by inflammatory leukocytes, growth factors and mast cells that simultaneously decalcify the fractured bone ends • within 48 hours after injury – angiogenesis (growth of new blood vessels) occurs o → ↑blood flow to the entire bone Phase 2. Fibrocartilagenous callus formation:
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- One '19
- Bone fracture, comminuted fractures