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© 2008 LWW Chapter 4. Tissue Response to Injury: Inflammation, Swelling, and Edema.

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Presentation on theme: "© 2008 LWW Chapter 4. Tissue Response to Injury: Inflammation, Swelling, and Edema."— Presentation transcript:

1 © 2008 LWW Chapter 4. Tissue Response to Injury: Inflammation, Swelling, and Edema

2 © 2008 LWW Inflammation The local response of the body to an irritant Purpose –Defend the body against alien substances –Dispose of dead and dying tissue so repair can take place

3 © 2008 LWW Cardinal Signs of Inflammation Rubor: redness Calor: heat Edema: swelling Dolor: pain Funca laesa: functional loss Each of these signs will occur to some degree when tissue is injured and the body responds with the inflammatory process.

4 © 2008 LWW Common Misconceptions of Inflammation Do you need to limit or eliminate inflammation? No. Inflammation is necessary. –Repair will not occur without inflammation. You cannot eliminate inflammation. You can only minimize the signs of inflammation.

5 © 2008 LWW Common Misconceptions of Inflammation (cont.) Swelling, edema, and inflammation are synonymous –Swelling and edema occur during inflammation. –Edema and swelling are not the same. –All edema causes swelling, but not all swelling is caused by edema.

6 © 2008 LWW Phases of Inflammation Inflammation consists of sequential and overlapping events. 1.Primary injury 2.Ultrastructural changes 3.Chemical mediation 4.Hemodynamic changes 5.Metabolic changes 6.Permeability changes 7.Leukocyte migration 8.Phagocytosis

7 © 2008 LWW Primary Injury Any occurrence that impairs tissue structure or function Most sports injuries are caused by –Macrotrauma (impact or contact) –Microtrauma (overuse, cyclic loading, or friction) –There are many other types of injury, each of which results in the same basic inflammatory reaction. Other examples?

8 © 2008 LWW Primary Injury (cont.) Other causes of injury include –Physical agents (trauma, burns, radiation) –Metabolic processes (hypoxia) –Biological agents (bacteria, viral, parasitic, infection) –Chemical agents (acids, gasses, organic solvents, endogenous chemicals) – Endogenous chemicals Normal secretions In abnormal locations (gout) In increased quantity in a normal location (stomach ulcers) The magnitude after each phase varies according to the causative agent

9 © 2008 LWW Ultrastructural Changes Cellular membrane is disrupted and eventually breaks down. Contents spill out into the extracellular spaces, thereby killing the damaged cell. Two causes –Direct Trauma (primary injury) –Indirect Hypoxia (oxygen deficiency) Enzymes (chemicals) In cells adjacent to the primary injury

10 © 2008 LWW Ultrastructural Changes (cont.) Occur as a direct result of trauma (primary injury) and indirectly as a result of hypoxia (secondary injury) We will discuss this in more detail later in this chapter (see “Orthopedic Injury Model”).

11 © 2008 LWW Ultrastructural Changes (cont.) Lysosome –Supplies chemicals that digest foreign material within the cell and gets rid of it. –If the membrane of the lysosome ruptures, its contents will attack and digest other material.

12 © 2008 LWW Chemical Mediation Histamine, bradykinin, and other chemicals Modify and regulate the rest of the inflammatory response to: –Neutralize the cause of the injury –Remove cellular debris so repair can take place

13 © 2008 LWW Hemodynamic Changes Arteries dilate, increasing blood flow to the injured area. –However, blood vessels that were previously inactive open, so blood flow through individual vessels decreases. Slowing of blood flow is necessary, so WBCs can move to the margins.

14 © 2008 LWW Hemodynamic Changes (cont.) Leukocytes –Marginate –Tumble along the vessel wall –Adhere to the vessel wall near an opening

15 © 2008 LWW Hemodynamic Changes (cont). Leukocytes begin passing though the vessel wall.

16 © 2008 LWW Metabolic Changes ↓ Energy ↓ Oxygen, causes cell to switch to anaerobic metabolism Membrane functions slow down. Sodium pump maintains the concentration of intracellular sodium at a very low level.

17 © 2008 LWW Metabolic Changes (cont.) ↑ Sodium concentration in cell and organelles ↑ Water in cell Cells swell and burst ↑ Intracellular acidosis (lactic acid) Membrane attacked Lysosome digests cell.

18 © 2008 LWW Permeability Changes Histamine and bradykinin increase the permeability of small blood vessels. The endothelial cells contract, pulling away from each other. Gaps are left, through which the WBCs can move out of the vessel and to the injury site.

19 © 2008 LWW Leukocyte Migration WBCs adhere to the endothelium (vessel wall) and/or to other white blood cells. (Reprinted with permission from McLeod I. Inflammation. Kalamazoo, MI: Upjohn, 1973.)

20 © 2008 LWW Leukocyte Migration (cont.) WBCs move out of the vessel by squeezing through the endothelial gaps. Neutrophils first, then larger macrophages (Reprinted with permission from McLeod I. Inflammation. Kalamazoo, MI: Upjohn, 1973.)

21 © 2008 LWW Leukocyte Migration (cont.) Neutrophils Macrophages

22 © 2008 LWW Leukocyte Migration (cont.) Neutrophils –Travel fast and arrive at the injury site first –Provide the first line of defense –When they die, they release chemical mediators that attract macrophages. Death of neutrophils results in a large concentration of chemical mediators released by the cells.

23 © 2008 LWW Leukocyte Migration (cont.) Macrophages –Live for months –Long-lasting second line of defense –Release potent enzymes that may destroy connective tissue, thus adding to the injury –Release chemical mediators that may prolong inflammation –Release factors that aid in healing –Secrete proteins that are important in defense mechanisms

24 © 2008 LWW Phagocytosis Digestion of cellular debris and other foreign material into pieces small enough to be removed from the injury site

25 © 2008 LWW Chronic Inflammation Results from microtrauma but does not necessarily involve an inflammatory reaction –Example: clinically diagnosed Achilles tendinitis and patellar tendinitis in which there is no evidence of an inflammatory reaction Structural disruption and microvascular damage may occur (causing pain and other symptoms) before the classic inflammatory process is set into action.

26 © 2008 LWW Orthopedic Injury Model What happens when a muscle is pulled or an ankle is sprained? Just put an ice bag on it, right? WRONG. This is overly simplistic. Techniques must be based on sound theory if they are to be developed and improved. It is essential to understand the body’s response to injury.

27 © 2008 LWW Orthopedic Injury Model (cont.) Example: typical tissue undergoing a typical muscular injury Used to illustrate inflammation in relation to orthopedic injuries

28 © 2008 LWW Orthopedic Injury Model (cont.) Normal tissue –Cells –Two blood vessels (A, B) –Two nerves (1, 2)

29 © 2008 LWW Orthopedic Injury Model (cont.) Contusion with injury to: –Three cells –Nerve 1 –Blood vessel B

30 © 2008 LWW Orthopedic Injury Model (cont.) Immediate ultrastructural change –Local nerves and blood vessels may be disrupted or broken. –This damage is called primary traumatic damage.

31 © 2008 LWW Orthopedic Injury Model (cont.) Hemorrhage –Few minutes only (usually) –Clot forms, stopping hemorrhage. Pain, from damaged nerve Hematoma forms.

32 © 2008 LWW Orthopedic Injury Model (cont.) Pain, from damaged nerve –Muscle spasm and more pain –Inhibition of muscular strength, range of motion, etc. –Body attempts to protect itself by splinting the area, thus preventing aggravation of injury.

33 © 2008 LWW Orthopedic Injury Model (cont.) The 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. Injury site

34 © 2008 LWW Orthopedic Injury Model (cont.) Fibrin forms into strands, creating a network somewhat like a fishnet. This net captures circulating platelets. A plug forms to seal the damaged vessel.

35 © 2008 LWW Orthopedic Injury Model (cont.) Chemical mediators released from dying cells cause –Hemodynamic changes –Permeability changes –Leukocyte (white cell) migration

36 © 2008 LWW Orthopedic Injury Model (cont.) Secondary enzymatic injury begins.

37 © 2008 LWW Orthopedic Injury Model (cont.) Hemodynamic changes –Blood flow slows down OR –Blood flow ceases Tissue oxygen decreases –Hypoxia –Metabolic changes Secondary hypoxic injury soon seen No flow

38 © 2008 LWW Orthopedic Injury Model (cont.) Phagocytosis –Free protein –Causes edema

39 © 2008 LWW Orthopedic Injury Model (cont.) Secondary hypoxic injury begins. Secondary enzymatic injury continues.

40 © 2008 LWW Orthopedic Injury Model (cont.) Phagocytosis and secondary injury continue.

41 © 2008 LWW Orthopedic Injury Model (cont.) Pressure on undamaged nearby pain fibers cause additional –Pain –Muscle spasm and inhibition

42 © 2008 LWW Orthopedic Injury Model (cont.) Total injury: –Primary injury (yellow) –Secondary injury

43 © 2008 LWW Secondary Injury Model in Review

44 © 2008 LWW Orthopedic Injury Model (cont.) The inflammatory response is not all positive. Example –Slowed blood flow in the vessels on the periphery of an injury and decreased blood flow from the damaged vasculature result in less oxygen to the cells. If prolonged, secondary hypoxic injury occurs. The total amount of damaged tissue is increased, and more debris is added to the hematoma.

45 © 2008 LWW Secondary Injury Model Body’s response to tissue damaged by trauma (primary injury) leads to further tissue damage, known as secondary injury. Two separate mechanisms result in secondary injury: –Enzymatic –Hypoxia

46 © 2008 LWW Decreased Metabolism Theory O 2 needed O 2 available In normal tissue

47 © 2008 LWW Decreased Metabolism Theory (cont.) O 2 needed O 2 available After injury

48 © 2008 LWW Decreased Metabolism Theory (cont.)

49 © 2008 LWW Decreased Metabolism Theory (cont.) O 2 needed O 2 available After injury and cryotherapy

50 © 2008 LWW Secondary Injury Model in Review

51 © 2008 LWW Swelling, Edema, and Vessel Fluid Pressures

52 © 2008 LWW What Is Edema? Accumulation of fluid in the tissue What causes it? –Must first understand normal fluid dynamics

53 © 2008 LWW Fluid Filtration in Normal Tissue Fluid out Fluid in

54 © 2008 LWW Fluid Filtration in Normal Tissue (cont.) All fluid leaving the capillary is returned –Two-thirds via capillary –One-third via lymphatic system

55 © 2008 LWW Fluid Filtration in Normal Tissue (cont.) Occurs constantly between capillary and tissue Sum of multiple forces In capillary and tissue –Oncotic (osmotic) pulls –Hydrostatic pushes O H

56 © 2008 LWW Hydrostatic Pressure Pressure exerted by a column of water The higher the column of water, the greater the pressure. Example: swimming The deeper you go, the higher the column of water above you and the greater the pressure. The depth of the water, not the amount of water, is important. Hydrostatic pressure is exerted by the water portion of the blood.

57 © 2008 LWW Hydrostatic Pressure (cont.) Hydrostatic pressure pushes water. –Capillary hydrostatic pressure pushes fluid out of the capillary. –Tissue hydrostatic pressure pushes fluid into the capillary. CHP tissue capillary THP

58 © 2008 LWW Oncotic Pressure Also called colloid osmotic pressure Results from the attraction of fluid by free protein –Tissue oncotic pressure pulls fluid out of the capillary. –Capillary oncotic fluid pulls fluid into the capillary. tissue capillary COP TOP

59 © 2008 LWW Fluid Filtration in Normal Tissues, Revisited Sum of all forces

60 © 2008 LWW Capillary Filtration Pressure Components CFP = (CHP + TOP) − (THP + COP + EFP) –CFP: Capillary filtration pressure –CHP: Capillary hydrostatic pressure –TOP: Tissue oncotic pressure –COP: Capillary oncotic pressure –THP: Tissue hydrostatic pressure –EFP: External force pressures

61 © 2008 LWW Normal Capillary Filtration Pressure Forces

62 © 2008 LWW Fluid Filtration in Normal Tissue, Revisited

63 © 2008 LWW What Causes Edema? Imbalance of fluid filtration caused by an injury

64 © 2008 LWW Capillary Filtration Pressure Changes after Injury Hematoma (tissue debris and hemorrhage) dumps large amounts of free protein into tissue spaces. Increased tissue oncotic pressure

65 © 2008 LWW Fluid Filtration in Injured Tissue Injury results in a great increase in the tissue oncotic pressure. TOP

66 © 2008 LWW Fluid Filtration in Injured Tissue (cont.) Fluid out Fluid in > >

67 © 2008 LWW Fluid Filtration in Injured Tissue (cont.) Fluid accumulates in tissue.

68 © 2008 LWW Fluid Filtration in Injured Tissue (cont.) More fluid accumulates in tissue.

69 © 2008 LWW Fluid Filtration in Injured Tissue (cont.) Even more fluid accumulates in tissue.

70 © 2008 LWW What Is Swelling? Hemorrhaging and edema –Can do nothing about hemorrhaging –Can minimize edema

71 © 2008 LWW What Causes Swelling? Capillary Tissue spaces Lymphatic

72 © 2008 LWW How Do You Prevent Swelling? Capillary Tissue spaces Lymphatic

73 © 2008 LWW How Do You Prevent Swelling? (cont.) Capillary Tissue spaces Lymphatic

74 © 2008 LWW How Do You Prevent Swelling? (cont.) Capillary Tissue spaces Lymphatic

75 © 2008 LWW How Does Cold Decrease Swelling? As cold decreases secondary hypoxic injury, the amount of free protein in tissues decreases. This causes less tissue oncotic pressure (the major factor for edema). Cold can prevent edema from occurring only if applied soon after injury. Once edema develops, cold application cannot decrease that edema.

76 © 2008 LWW Decreased Metabolism Theory, Revisited Secondary hypoxic injury Normal tissue Injured tissueInjured and with cryotherapy O 2 needed O 2 available

77 © 2008 LWW Time Course of Swelling Swelling immediately after injury is the result of direct hemorrhaging. Edema begins minutes to hours after injury and continues to develop over many hours. –Accounts for the delayed nature of most swelling.

78 © 2008 LWW Secondary Injury and Edema Secondary injury results in increased edema, and increased edema can contribute to increased secondary injury. Two mechanisms –As edema develops, the distance between blood vessel and tissue cells increases. More difficult for oxygen and other substances to diffuse from the circulatory system to the tissue –Edema can compress the blood vessel, thus decreasing circulation to the area.

79 © 2008 LWW Capillary Filtration Pressure Changes after Injury, Revisited If swelling is the result of edema, why does the area turn black and blue? –Isn't this caused by oxidized blood? Some is, but most discoloration in the muscle is caused by oxidized myoglobin from the damaged musculature.

80 © 2008 LWW Common Misconceptions Concerning Ice and Inflammation Many think the purpose of ice is to decrease inflammation. However, inflammation is necessary to prepare for healing. Healing cannot take place until much of the cellular debris is removed from the area. –So decreasing inflammation is not helpful.

81 © 2008 LWW Common Misconceptions Concerning Ice and Inflammation (cont.) Misconception results from confusing inflammation with swelling. The more the swelling is contained, the quicker the injury can heal.

82 © 2008 LWW Common Misconceptions Concerning Ice and Inflammation (cont.) Another misconception concerning ice is that it should be used until the swelling is gone. Ice is effective for preventing swelling but not for removing swelling. Swelling reduction occurs as free protein is removed from the area.

83 © 2008 LWW SummarySummary Inflammation is the body’s response to any injury. –Protects the body against invasion by foreign bodies and prepares the injured tissue for repair. After understanding inflammation, hemorrhaging, and edema, you will be qualified to educate your athletes and coaching staff, who commonly apply ice to decrease inflammation after an injury. –You can explain that swelling is one of the signs of inflammation but is not the process itself; they are separate but related processes.


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