Ch 5 - Tissue Response to Injury: Inflammation, Swelling, and Edema

the inflammatory response

the local response of the body to an irritant

inflammatory response purpose (2)

• defend the body against foreign substances

• dispose of dead and dying tissue so repair can take place

5 cardinal signs of inflammation

• rubor: redness

• calor: heat

• edema: swelling

• dolor: pain

• funca laesa: functional loss

SHARP acronym

swelling

heat

achy

redness

pain

repair will NOT occur

w/o inflammation, can’t eliminate but can only minimize the signs of inflammation

common misconceptions of inflammation

• swelling, edema, and inflammation are synonymous

• swelling and edema occur during inflammation

• edema and swelling are not the same

8 phases of inflammation

• injury

• ultrastructural changes

• chemical mediation

• hemodynamic changes

• metabolic changes

• permeability changes

• leukocyte migration

• phagocytosis

primary injury def

any occurence that impairs tissue structure or function

primary injury def

any occurrence that impairs tissue structure or function

primary injury sport injuries are caused by (2)

• macrotrauma (impact or contact)

• microtrauma (overuse, friction)

primary injury other causes of injury (5)

• physical agents

• metabolic processes

• biological agents

• chemical agents

• endogenous chemicals

ultrastructural changes (2)

• cellular membrane is disrupted and eventually breaks down

• contents spill out into the extracellular spaces thereby killing the damaged cell

ultrastructural changes (2)

• direct (trauma → primary injury)

• indirect (hypoxia, enzymes)

lysosome function

supplies chemicals that digest foreign material within the cell and gets rid of it

lysosome info

if the membrane of the lysosome ruptures, its contents will attack and digest other materials

chemical mediation includes

histamine and bradykinin

chemical mediation regulates by (2)

• neutralize the cause of the injury

• remove cellular debris so repair can take place

hemodynamic changes (2)

• arteries dilate, inc blood flow to the injured area

• slowing of blood flow is necessary so WBCs can move to the vessel margins

hemodynamic changes cont. - leukocytes

• marginate

• tumble along the vessel wall

• adhere to the vessel wall near an opening

metabolic changes (4)

• dec energy

• dec oxygen causes cell to switch to anaerobic metabolism

• membrane functions slow down

• sodium pump maintains [] of IC sodium at a low level

  • cells swell and burst and lysosome membrane ruptures

what happens when lysosome contents burst

contents attack and digest the cell membrane, inc the total amount of tissue destruction

permeability changes

• histamine and bradykinin inc the permeability of small blood vessels

• endothelial cells contract pulling away from each other

• gaps are left which WBCs can move out of the vessel and to the injury site

leukocyte migration

WBCs adhere to the endothelium and/or other white blood cells

2 concerns after leukocyte migration

great amounts of protein-rich fluid escapes

• due to dec fluid blood viscocity inc sometimes to the extent that is blocks circulation

• protein molecules are too large to be reabsorbed into circulation = inc TOP

what is the major cause of edema (TOP)

tissue oncotic pressure

leukocyte migration cont (2)

• WBCs move out of the vessel by squeezing through endothelial gaps

• neutrophils first, then larger macrophages

who is the first on scene for WBCs

neutrophils

who is the clean up crew for WBCs

macrophages

neutrophils (2)

• first line of defense

• when die release chemical mediators that attract macrophages

macrophages (5)

• live for months

• long last 2nd line of defense

• release chem mediators that may prolong inflammation

• release factors that aid in healing

• secrete proteins imp in defense mechanisms

phagocytosis

digestion of cellular debris and other foreign material into pieces small enough to be removed from the injury site

chronic inflammation def

results from microtrauma but does not necessarily involve an inflammatory reaction

chronic inflammation good to know

structural disruption and microvascular damage may occur before the classic inflammatory process is set into action

orthopedic injury model

techniques must be based on sound theory, and it is essential to understand the body’s response to injury

OIM - normal tissue (3)

• cells

• 2 blood vessels

• 2 nerves

OIM - contusion w injury (3)

• 3 cells

• 1 nerve

• 1 blood vessel

contusion OIM step 1

• immediate ultrastructural change (local nerves and b.v may be disrupted/broken)

• aka primary traumatic damage

contusion OIM step 2

• hemorrhage (few mins only)

• pain from damaged nerve

• hematoma forms

contusion OIM step 3

• pain from damaged nerve

• muscle spams and more pain

• inhibition of ms strength

• body attempts to protect itself by splinting the area

contusion OIM step 4

• damaged cells release chemical mediators as a signal to the body that an injury has taken place

• extravascular hemorrhage occurs from broken blood vessels

• swelling occurs

contusion OIM step 5

• fibrin forms into strands, creating a network like fishnet

• net captures circulating platelets

• a plug forms to seal the damaged vessel

contusion OIM step 6

• chem mediators release from dying cells

  • hemodynamic changes

  • permeability changes

  • leukocytes migration

contusion OIM step 7

second enzymatic injury begins

second enzymatic injury

where primary injury response of body leads to further tissue damage aka secondary injury

secondary enzymatic injury info

• hemodynamic changes (blood flow slows down OR ceases)

• tissue oxygen dec (hypoxia, metabolic changes)

when to not apply modalities at this time

secondary injury

the inflammatory response is not all positive (3)

• slowed blood flow in the vessels can dec blood flow, dec oxygen to cells

• if prolonged, secondary hypoxic injury occurs

• total # of damaged tissue is inc, more debris is added to the hematoma

secondary injury model can lead to (2)

• enzymatic action

• metabolic deficiency

edema def

accumulation of the fluid portion of blood in the tissues

fluid filtration in normal tissue (2)

all fluid leaving the capillary is returned

• 2/3 via capillary

• 1/3 via lymphatic system

oncotic

pulls

hydrostatic

pushes

hydrostatic pressure

pressure exerted by a column of water

hydrostatic pressure if exerted by

the water portion of the blood

capillary hydrostatic

pushes fluid out of the capillary

tissue hydrostatic pressure

pushes fluid into the capillary

oncotic pressure aka

colloid osmotic pressure

what is oncotic pressure

results from the attraction of fluid by free protein

2 types of oncotic pressure

• tissue oncotic pressure

• capillary oncotic pressure

tissue oncotic pressure

pulls fluid OUT of the capillary

capillary oncotic pressure

pulls fluid INTO the capillary

capillary filtration pressure equation

CFP = (CHP + TOP) - (THP + COP + EFP)

• CFP: capillary filtration pressure

• EFP: external force pressures

normal capillary filtration net overall pressure

-4 to 7 mmHg

what causes edema

imbalance of fluid filtration caused by an injury

what is the primary pressure attributed to edema

tissue oncotic (TOP)

the effect of cold on swelling (3)

• cold application can minimize swelling but can’t dec it once it has occurred

• cold dec secondary metabolic injury → less TOP

• earlier cryotherapy the better

why should cold packs be applied quickly following an injury?

metabolism will slow down sooner → less total tissue damage

edema begins

minutes to hours after injury

swelling immediately after injury is result of

direct hemorrhaging

secondary injury and edema 2 mechanisms

• edema = distance b/w blood vesse; and tissue cells inc = more O2 difficulty

• edema can compress b.v thus dec circulation to the area