Ch 5.ppt - Mechanisms of injury How did it happen...

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Mechanisms of injury How did it happen?
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Mechanisms The thing that causes the injury Contributory factors May increase the likelihood or extent of the injury Ex. Driving faster may increase your change of an accident
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Classification of injury mechanisms Contact or impact Dynamic overload Overuse Structural vulnerability Inflexibility Muscle imbalance Rapid growth
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Classification of injury mechanisms Crushing deformation Impulsive impact Skeletal acceleration Energy absorption Extent and rate of tissue deformation Any injury can be considered some type of stress overload regardless of which list/classification you’re looking at
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Principles of mechanical loading Typical loads are within physiological range Chronic vs acute Chronic: loads have cumulative effect, joggers Acute: one time incident, 1 application of stress Combination: overuse, so degrading. One incident where it tears, acute. 7 factors that characterize load
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Magnitude Location Direction Duration Frequency Variability Rate
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Valgus vs Varus Valgus: knock-knee Non contact knee injuries Varus
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Assessment of injury severity Clinical classification schemes Every injury is different
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Few days up to 6 weeks Leg injuries
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Forgetting things before the hit
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Primary vs secondary injury (direct vs indirect) ex. Primary: knocked on the head Secondary: swelling from the knock ex. Primary: broken toe secondary: change pitching to accommodate for broken toe, gets a shoulder injury from compensation Acute vs Overuse acute: from one big event overuse: from repeated submaximal loading Micro vs Macro trauma (not a bad thing necessarily) micro: not always evident; don’t always know they’re there macro: bigger scale
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Contributory factors
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Response to tissue injury Inflammatory response Aulus Cornelius Celsus (30 BC – AD 38) Redness and swelling with heat and pain Part of inflammatory response Galen AD 129-199 Added ‘functional loss’ Associated with inflammatory response
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Redness and heat- blood vessel dilation Swelling – ↑ capillary hydrostatic pressure and enhanced capillary permeability *Pain – swelling related increase in pressure on nerve endings May be related to the tissue or where it is located Ability to expand: swelling may not be as bad Smaller space, more pressure from confined area swelling, more pain
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Injury → vasoconstrictive response → vasodilation During vasodilation, we have an increased permeability of arteries. Allows exudate to enter the area Exudate – fluid, plasma proteins including fibrinogen, helps from the clot Dilutes area, inactivate any toxins Phagocytes (break down materials), T- cells, B cells, NK cells (reduce the chance of infection)
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Compartment and Entrapment Ratio of mass to volume (density) More mass in confined space= more pressure Problems such as : HACE (high altitude cerebral edema), impingement, carpal tunnel, compartment syndrome HACE: may allow fluids to enter compartments where it does not belong
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  • Spring '17
  • DR. MORRIS

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