Unit_1_Day_6__Mechanics-Tissue_Response_

Unit_1_Day_6__Mechanics-Tissue_Response_ - KIN 320 -...

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Unformatted text preview: KIN 320 - Classsroom Notes Biomechanics of Trauma Mechanical Principles for Trauma TRAUMA - injury to a living body caused by the loading of an external force that exceeds the tissue’s maximum tolerance Principle of Loading to Injury Biomechanics of Injury & the Injury Cycle Acute – Traumatic Acute – Gradual Sub-Acute – Traumatic Sub-Acute – Gradual Chronic Acute traumatic - instantaneous Acute gradual - over time (practice) *** Biomechanics of Trauma Injury Terminology General Trauma Sprains Acute injury: results from a single or a few tissue overloads Overuse injury: repeated force application application Overuse may lead to acute, e.g., Achilles tendonitis weakens the tissue and the player may rupture the tendon. look for the injury in athletes. (watch them move around) Subluxations dislocations - shoulders Strains Fractures Musculo-skeletal disorders Tumors Weaknesses Inflammatory responses General Trauma - normal (min) injuries Sprain - joints Strains - muscles Importnace offractures based on nature of activity Fall 2011 1 KIN 320 - Classsroom Notes Injury Terminology Injury Recognition History Levels of Dysfunctions what, when, where, how, etc., nature and extent of the injury deformities bleeding skin color, temperature, texture etc., pain descriptions & localization capability other factors to be considered incidence and distribution level of competition sport specific age, sex etc Annoyances Minor Moderate Major Severe Annoyances - general trauma Major - surgery, no societal implications Severe - paralyzed, losing limb Types of Injury Types of Injury Exposed - dangers are bacterial, fungal and viral infections mechanisms are usually associated with a force being distributed of the surface of the body, i.e., friction, shearing, stretch, or impact Unexposed - no break in the skin, therefore little danger of infection Mechanism: direct impact, indirect force, stretch, torsion, shearing overuse, torsion shearing impingement, etc contusions strains sprains (dislocation/subluxation ) fractures abrasions lacerations - tears incisions - cuts punctures avulsions - loosens a flap of skin Exposed also Septic injury Exposed = inflammatory response No danger of infection, Aseptic injuries Fall 2011 2 KIN 320 - Classsroom Notes Biomechanics of Trauma Types of Injury Types of Injury Microtrauma - forces are generally small, but over a large area Primary Injury normal force and abnormal tissue abnormal force and abnormal tissue abnormal force and normal tissue(overuse) microscopic tearing of tissue secondary mechanical changes due to inflammation cause increase in local pressure and decrease in blood supply Macrotrauma Microtrauma Secondary Injury Macrotrauma Microtrauma Macrotrauma - abnormal very large forces Injury Recognition and Evaluation A Asymmetry R Range of Motion T Texture Signs and Symptoms Signs – descriptive of the qualities of the injury that can be observed by the clinician Vomiting, bleeding, deformation, etc. bleeding deformation etc Symptoms – descriptive qualities of the injury that are identified by the person Pain, nausea, lethargy, etc. Asymmetry - not the same Fall 2011 3 KIN 320 - Classsroom Notes Mechanisms of Injury Inflammation Principles of Loading Reaction of the body to injury & a basic defense against disease Acute – Traumatic Acute - Gradual Subacute – Traumatic Subacute – Gradual Chronic Micro v Macro trauma Primary v Secondary injury Last 3 or 4 days Protect, localize & rid the body of localize injuring agents Prepares for healing process Caused by trauma, chemical or thermal agents Inflammation -Natural response to trauma For both Exposed and Unexposed Inflammation Cardinal Signs of Inflammation Acute Inflammation – initial reaction to injury Sub acute Inflammation – time when symptoms begin to decrease (2 weeks to 1 month) Chronic Inflammation – reactions last longer than a month Calor – Heat Rubor – Redness Edema – Swelling Dolar – Pain Loss of Function Fall 2011 4 KIN 320 - Classsroom Notes Inflammation Edema Vascular changes Excessive fluid in interstitial space Blood vessels dilate Capillary blood pressure rises Permeability of venules increases plasma Lymphatic channels blocked for localization Results from changes in inter v external cell pressures pressures Severity of injury Permeability changes Amount of primary and secondary damage Presence of mediators Hemorrhage Ruptured blood vessel – “ecchymosis” Marked increase in permeability Occurs very quickly following injury Dialating blood cells slows down flow Venules - small veins Edema Depends On Edema Results In Vascular hydrostatic pressure Forces fluids out from the capillaries to tissues Plasma colloid osmotic pressure Moves fluids from tissue to capillaries Limb hydrostatic pressure Independent of biology Dependent on position of the limb Edema - swelling Clogs area around cells reducing oxygen flow Slows the healing process Blocks lymphatic return Affects venous flow and the process of waste removal from the injured cells Edema Mediators Gravity helps Muscular contractions Respiratory process Fall 2011 5 KIN 320 - Classsroom Notes Inflammation Inflammation Mediators Cellular changes Heparin – inhibits coagulation Histamines – vasodilation of the arterioles & increase permeability of venules Kinins – dilate arterioles, chemotactics & pain producers Protaglandins – vasodilation and increase permeability (duration & intensity) Serotonin – vasodilation and increase permeability of capillaries Leukocytes concentrate at wound (phagocytosis) Fibroblast synthesize scar Formation of new capillaries Tissue changes Scar forms Scar strengthens !"##$%&'%#()*#%&+)&,*-$./ ,012'3&4'56788 4."9:./&'%#()*#%; +"##$%&<%#+.$=+")*&<".%=+>/& :##)=":+%<&?"+@&+.:$9:+"=&A).=%B&=:*C+&=@:*D%& :9)$*+&)A&"*"+":>&<:9:D% 8%=)*<:./&'%#()*#%; )==$.#&A.)9&=%>>&<%:+@& =:$#%<&E/&:&E>)=F:D%&)A&5G #$((>/B&=:*&:##"#+&+)& F%%(&9"*"9$9&<:9:D%&+)&)+@%.&+"##$%# ,*-$./&'%#()*#%&6/=>%&H&(:"*I#(:#9I(:"*&=/=>% J6@%9"=:>#&#+"9$>:+%&A.%%&*K&%*<"*D#&L&=:$#%&(:"*&?@"=@& =:$#%#&9K&#(:#9&L&+."DD%.#&E)</C#&(.)+%=+"M%& 9%=@:*"#9KN Fall 2011 6 KIN 320 - Classsroom Notes Trauma Primary Injury Response Cell Death Primary Trauma (blood injured tissue) Greater Risk of Injury Ischemia Reduced Risk of Injury Secondary Response (Edema, hypoxia, hematoma, scab) Return to Full Activity Return to Activity Injury Inflammatory Response to Injury Inflammation Spasm Suboptimal Recovery Optimal Recovery Repair Phases (cellular) Adequate Inadequate Edema Atrophy Pain Rehabilitation *** * !@.%%&4@:#%#&)A&O%:>"*D 4@:#%&,;&P=$+%&,*A>:99:+)./&4@:#% 6:.<"*:>&8"D*#&)A&,*A>:99:+")* 8?%>>"*D 4:"* 6:$#%<&E/& <">:+")*&)A& :.+%.")>%#Q "*=.%:#%<& E>))<&A>)? 4@:#%&,,;& 4.)>"A%.:+")*QR"E.)E>:#+"=Q& '%(:".Q'%D%*%.:+")*&4@:#% '%<*%## O%:+ 6:$#%<&E/& :==$9$>:+")*& )A&E>))<&L& <:9:D%<&+"##$%& =%>># 4@:#%&,,,;&'%9)<%>"*DQ&S:+$.:+")*& 4@:#% potentionally up to 2 years ,*=.%:#%<& =@%9"=:>& :=+"M"+/&L& "*=.%:#%<& E>))<&A>)?&+)& #F"*&#$.A:=% T)##&)A& R$*=+")* U".%=+&"*-$./& ,*=.%:#%<& )A&*%.M%& (:"*Q&#?%>>"*D A"E%.#V& (.%##$.%&)A& @%9:+)9:&)*&*K& %*<"*D# 6@%9"=:>& ".."+:*+#&W E.:</F"*"*V& @"#+:9"*%V& (.)#+:D>:*<"* Remodeling = longest step Important because it involves all injuries Fall 2011 7 KIN 320 - Classsroom Notes 4@:#%&,;&P=$+%&,*A>:99:+)./&4@:#% X8$E#+.:+%&4@:#%Y Foundation phase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`Iab&9"*#KNB&(>:+%>%+&(>$D&A).9%<B&E>))<&=):D$>:+")*B& (.)<$=%#&>)=:>&:*%9": _:#)<">:+")* W "*=.%:#%<&E>))<&A>)?B&"*=.%:#%<&@/<.)#+:+"=& (.%##$.%&"*&E>))<&M%##%>#&J =:(">>:./&(%.9%:E">"+/V&(>:#9:& (.)+%"*#&>%:F&)$+B&(.)+%"*#&:++.:=+&OG5&I %<%9:N 6%>>$>:.&6@:*D%# W =@%9"=:>&.%:=+")*#&#+:.+&"99%<":+%>/ 4.)+%"*&(.%#%*=% I =@:*D%#&)#9)+"=&.%>:+")*#@"(&E%+?%%*&E>))<& L&:<-:=%*+&+"##$%#&J4>:#9:&(.)+%"*& ?@">%&"*+%.#+"+":>&A>$"<& (.)+%"*& K&&OG5&A)>>)?#&(>:#9:&(.)+%"*#&)$+&)A&M%##%>&.%#$>+"*D&"*& %<%9:cN 0%$+.:>"^%#Q<%#+.)/#&)AA%*<"*D& :D%*+#V&.%#+."=+#&+"##$%&<:9:D%& +)&+@%&#9:>>%#+&()##"E>%&+"##$%&L&(.%(:.%#&:.%:&A).&@%:>"*D RICE 4@:#%&,,;&4.)>"A%.:+")*QR"E.)E>:#+"=& 4@:#% X'%(:".Q'%D%*%.:+")*&).&R"E.)E>:#+"=&(@:#%Y 4.)>"A%.:+")*&4@:#% \&(.)=%##%#&)A&#)A+&+"##$%&.%(:". 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Need some motion to reduce atrophy. ,9().+:*=%&)A&6)*+.)>>"*D&8?%>>"*D ,9().+:*=%&)A&6)*+.)>>"*D&8?%>>"*D 7>%M:+")* 6)9(.%##")* 8"*D>%&9)#+&"9().+:*+&A:=+).&"*&#?%>>"*D&=)*+.)> S%=@:*"=:>>/&.%<$=%#&#(:=%&:M:">:E>%&A).&#?%>>"*D& :==$9$>:+")* 2#"*D&:*&%>:#+"=&?.:(V&A".9V&%M%*>/&:((>"%<&(.%##$.%& =:*&E%&:=@"%M%< 6)9(.%##")*&#@)$><&E%&9:"*+:"*%<&=)*+"*$)$#>/&A).& mG&@)$.#&W <%(%*<#&)*&#%M%."+/ l"+@&=@.)*"=&"*A>:99:+)./&=)*<"+")*#&=)9(.%##")*& #@)$><&E%&:((>"%<&$*+">&+@%&#?%>>"*D&"#&:>9)#+& %*+".%>/&D)*% Fall 2011 2#%<&+)&%>"9"*:+%&+@%&%AA%=+#&)A&D.:M"+/&)*&E>))<& ())>"*D P##"#+#&M%*)$#&:*<&>/9(@:+"=&<.:"*:D%&)A&E>))<& :*<&)+@%.&A>$"<#&A.)9&+@%&"*-$.%<&:.%: 7>%M:+")*&#@)$><&)==$.&:#&)A+%*&:#&()##"E>%&<$."*D& +@%&A".#+&mG&@)$.#&)A&+@%&:=$+%&"*-$./&W <%(%*<#& )*&#%M%."+/ 10 KIN 320 - Classsroom Notes S:*:D"*D&+@%&O%:>"*D&4.)=%##& +@.)$D@&'%@:E">"+:+")* .:<%#&)A&8(.:"*#Q8+.:"*#.:<%&,&W #)9%&(:"*V&9"*"9:>&>)##&)A& A$*=+")*V&*)&:E*).9:>&A$*=+")*V&L&9"><& ()"*+&+%*<%.*%##.:<%&,,&W (:"*V&9)<%.:+%&>)##&)A& A$*=+")*V&#?%>>"*D&L&"*#+:E">"+/.:<%&,,,&W %[+.%9%>/&(:"*A$>V&"*%M"+:E>%& >)##&)A&A$*=+")*V&#?%>>"*D S:*:D"*D&+@%&O%:>"*D&4.)=%##& +@.)$D@&'%@:E">"+:+")* 4@:#%&,;&P=$+%&,*A>:99:+)./&4@:#% ,*"+":>&#?%>>"*D&9:*:D%9%*+&L&(:"*&=)*+.)>&:.%& =.$=":> 4',67 ,A&/)$&:.%&+))&:DD.%##"M%&"*&+@%&a#+ \d&@)$.#&+@%& "*A>:99:+)./&(.)=%##&9:/&*)+&@:M%&+"9%&+)&:==)9(>"#@& ?@:+&"+&*%%<#&+) Z/&<:/#&e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all 2011 11 KIN 320 - Classsroom Notes 4:"*&S:*:D%9%*+ Acute Traumatic Injury '%<$=%&(:"*c 6)*+.)>&:=$+%&(:"*c 4.)+%=+&+@%&(:+"%*+&A.)9&A$.+@%.&"*-$./& ?@">%&%*=)$.:D"*D&(.)D.%##"M%&%[%.="#% S"*"9"^%&A$.+@%.&+"##$%&<:9:D% 7*=)$.:D%&(#/=@)>)D"=:>&"*+%.:=+")*&J()#"+"M%& +@"*F"*DV&%+=KN S%<"=:+")*# 6)99$*"=:+")*&?"+@&:+@>%+% 2#%&)A&9)<:>"+"%#&+)&.%<$=%&(:"* Vasoconstriction decreases blood flow within 10 minutes During that time, coagulation begins Vasodilation Slows blood flow Increase viscosity & stasis = Edema Exudate of plasma & concentration of RBC = Hemoconcentration Exudate from damaged cells Permeability increases return to normal in 15-30 min Acute Traumatic Injury Bleeding and Exudates Edema depends on extent of cellular damage Coagulation begins” begins Thromboplastin – prothrombin – thrombin & calcium Thrombin forms soluble fibrinogen and then insoluble Fibrin Phagocytosis begins Fall 2011 12 KIN 320 - Classsroom Notes Acute Traumatic Injury Margination/Pavementing Redistribution of leukocytes Move from center of blood to margins and and line up along epithelial cells Diapedesis – leukocytes pass through blood vessel wall Chemotaxis – chemical attraction of leukocytes to the injured area Healing Mechanism Contraction appears in 3-4 days Prominent for 6-7 days. Reduce wound size by 70% Repair Replaces dead or lost tissue Scar formation Less viable than normal Firm, fibrous, inelastic and devoid of capillaries Fall 2011 13 KIN 320 - Classsroom Notes Healing Process Maturation Phase Continues for 3 weeks or more Different tissues have different healing times times Re-injury reduces the efficiency of remodeling Balance between immobilization and mobilization Healing Mechanism Regeneration Replace lost cells with functional new ones Primary healing – clean Secondary healing – gaps in tissue –SCAR Mediating Factors Type, size and location Vascular supply Environment – blood flow, nutrition, movement, etc. Infections Fall 2011 14 ...
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This note was uploaded on 10/17/2011 for the course KINESIOLOG 320 taught by Professor Powell during the Spring '11 term at Michigan State University.

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