THE INFLAMMATORY RESPONSE

Inflammatory response can be acute or chronic.

1. Acute inflammation

• has a short onset and a short duration
• consists of hemodynamic changes, production of an exudate, and the presence of granular leukocytes.

2. Chronic inflammation

• has a long onset and a long duration
• displays a presence of non-granular leukocytes and a more extensive formation of scar tissue.

Cardinal signs of inflammation

1. redness
2. swelling
3. heat
4. pain

Phase I: Acute Phase

1. The acute phase of inflammation is the initial reaction of body tissue to an irritant or injury and is characteristic of the first 3 or 4 days after injury.
2. Acute inflammation is the fundamental reaction designed to protect, localize, and rid the body of some injurious agent in preparation for healing and repair.
3. The main causes of inflammation are trauma, chemical agents, thermal extremes, and pathogenic organisms. 

Tissue and Cell Death

• In an acute phase, tissue death occurs from the actual trauma.

• After trauma, cellular death may continue as a result of a lack of oxygen in the area.

• Continued death also occurs when the digestive enzymes of engulfing phagocytes spillover and kill normal cells.

 This fact points to the major importance of proper immediate care using rest, ice, compression, and elevation (RICE).

Vascular response

First hour

1. At the time of trauma, before the usual signs of inflammation appear, a transitory vasoconstriction occurs, causing decreased blood flow.
2. At the moment of vasoconstriction, coagulation begins to seal broken blood vessels, followed by the activation of chemical influences.
3. Vasoconstriction is replaced by the dilation of venules, arterioles, and capillaries in the immediate area of the injury.

Second hour

1. Vasodilation brings with it a slowing of blood flow, increased blood viscosity, and stasis, which leads to swelling (edema).
2. With dilation also comes exudation of plasma and concentration of red blood cells Much of the plasma exudate results from fluid seepage through the intact vessel lining, which becomes more permeable, and from higher pressure within the vessel.
3. Permeability is relatively transient in mild injuries, lasting only a few minutes, with restoration to a pre-injury state in 15 to 30 minutes. In slightly more severe situations there may be a delayed response with a late onset of permeability. In such cases, permeability may not appear for many hours and then appears with some additional irritation and a display of rapid swelling lasting for an extended period.

Leukocytes pass through the wall of the blood vessel by ameboid action, known as diapedesis, and are directed to the injury site by a process known as chemotaxis (a chemical attraction to the injury).

Cellular response

Mast cells and leukocytes are in abundance.

1. Mast cells are connective tissue cells that contain heparin (a blood anticoagulant) and histamine.

2. Basophils, monocytes, and neutrophils are the major leukocytes.

Basophils are believed to bring anticoagulant substances to tissues that are inflamed and are present during both acute and chronic inflammatory healing phases.

The neutrophils representing about 60% to 70% of the leukocytes arrive at the injury site first, emigrating from the bloodstream through the process of diapedesis and ingest smaller debris through phagocytosis.  Phagocytosisis the process of ingesting material such as bacteria, dead cells, and other debris associated with disease, infection, or injury.  Neutrophils also have chemotactic properties, attracting other leukocytes to the injured area. 

The monocyte, which is a non-granular leukocyte, arrives on the scene after the neutrophils, about 5 hours after injury. Monocytes transform themselves into large macrophages that have the ability to ingest large particles of bacteria or cellular debris.

Chemical mediators Chemical mediators for the inflammatory process are stored and given off by various cells.

1. Histamine

• the first chemical to appear in inflammation, is given off by blood platelets, basophils, and mast cells

• a major producer of arterial dilation, venule, and capillary permeability.

2. Serotonin

• is a powerful vasoconstrictor found in platelets and mast cells.

3. Bradykinin

• which increases permeability and causes pain.

4. Heparin

• is also given off by mast cells and basophils and temporarily prevents blood coagulation.

Bleeding and exudate

The extent of fluid in the injured area is highly dependent on the extent of damaged vessels and the permeability of the intact vessel.

Blood coagulation

1. In the initial stage thromboplastin is formed.

2. In the second stage prothrombin is converted into thrombin under the influence of thromboplastin with calcium.
3. In the third stage thrombin changes from soluble fibrinogen into insoluble fibrin. The plasma exudate then coagulates into a network of fibrin and localizes the injured area