INFLAMMATION

Inflammation is a local and nonspecific defensive response of the tissues to injury or infection. It is an
adaptive mechanism that destroys or dilutes the injurious agent, prevents further spread of the injury, and
promotes the repair of damaged tissue. It is characterized by five signs:

a. pain
b. swelling
c. redness
d. heat
e. impaired function of the part (if the injury is severe)

Commonly, words with the suffix –itis describe an inflammatory process. For example, appendicitis
means inflammation of the appendix; gastritis means inflammation of the stomach.

Injurious stressors (inflammatory agents) to body tissues can be categorized as physical agents, chemical
agents, and microorganisms. Physical agents include mechanical objects causing trauma to tissues,
excessive heat or cold (causing burns or frostbite), and radiation. Chemical agents include external irritants
(eg, strong acids, alkalis, poisons, and irritating gases) and internal irritants (substances manufactured
within the body such as excessive hydrochloric acid in the stomach due to altered function).
Microorganisms include the broad groups of bacteria, viruses, fungi, protozoa, and Rickettsia.

The inflammatory response involves a series of dynamic events commonly referred to as the three stages
of the inflammatory response:

First stage: Vascular and cellular responses

FIRST STAGE

At the start of the first stage, constriction of the blood vessels occurs at the site of injury, lasting only a
few moments. This initial constriction is rapidly followed by dilation of small blood vessels (occurring as a
result of histamine released by the injured tissues). Thus, more blood flows to the injured area. This
marked increase in blood supply is referred to as hyperemia and is responsible for the characteristic signs
of redness and heat.

Vascular permeability is increased at the injured site with the dilation of the vessels in response to tissue
necrosis, the release of chemical mediators (eg, bradykinin, serotonin, and prostaglandin), and the release
of histamine. The result of this altered permeability is an outpouring of fluid, proteins, and leukocytes into
the interstitial spaces, clinically manifested by the characteristic inflammatory signs of swelling (edema)
and pain. The pain is caused by the pressure of accumulating fluid on local nerve endings and the chemical
mediators, which are thought to irritate the nerve endings. Too much fluid pouring into areas such as the
pleural or pericardial cavity can seriously affect organ function. In other areas, such as joints, mobility is
impaired.

During the first stage of the inflammatory response, blood flow slows in the dilated vessels. This altered
rate of flow facilitates the mobilization of the increased number of leukocytes (white blood cells) to the
injured tissues. Mobilization of leukocytes includes the two processes of margination and emigration.
Normally, blood cells (erythrocytes, leukocytes, and platelets) flow along the center of a blood vessel, while
a cell-less stream of plasma flows around them against the walls of the blood vessel. When the blood flow
slows, leukocytes aggregate or line up along this inner surface of the blood vessels. This process is known
as margination. Leukocytes then move through the blood vessel wall into the affected tissue spaces, a
process called emigration.

The actual passage of blood corpuscles through the blood vessel wall is referred to as diapedesis.
Leukocytes are attracted to injured cells by chemotaxis. The action of chemotaxis is not fully understood,
but basically leukocytes are drawn toward the source of chemicals released in the injured cells (positive
chemotaxis), or they are propelled away from released chemicals (negative chemotaxis).

In a compensatory response to the exit of leukocytes from the blood vessels, the bone marrow produces
large numbers of leukocytes and releases them into the bloodstream (leukocytosis). The exact
mechanism stimulating this increase is unknown, but it is another sign associated with inflammation. A
normal leukocyte count of 4,500 to 11,000 per cubic millimeter of blood can rise up to 20,000 or more
when inflammation occurs.

SECOND STAGE

In the second stage of inflammation, fluid that escaped from the blood vessels, dead phagocytic cells, as
well as dead tissue cells and products that they release, produce the inflammatory exudates. A plasma
protein called fibrinogen (which is converted to fibrin when it is released into the tissues), thromboplastin
(a product released by injured tissue cells), and platelets together form an interlacing network to form a
barrier, wall off the area, and prevent its spread. During the second stage, the injurious agent is overcome,
and the exudate is cleared away by lymphatic drainage.

The nature and amount of exudate vary in accordance with the tissue involved and the intensity and
duration of the inflammation. The major types of exudates are serous, purulent, and hemorrhagic
(sanguineous). A serous exudates is composed chiefly of serum (the clear portion of the blood) derived
from the blood and serous membranes of the body, such as the peritoneum, pleura, pericardium, and
meninges. It is water in appearance and has few cells. An example is the fluid in a blister from a burn.

A purulent exudate is thicker than serous exudates due to the presence of pus. It consists of leukocytes,
liquefied dead tissue debris, and dead and living bacteria. The process of pus formation is referred to as
suppuration, and the bacteria that produce pus are called pyogenic bacteria. Not all microorganisms are
pyogenic. Purulent exudates vary in color, some acquiring tinges of blue, green or yellow. The color may
depend on the causative organism.

A sanguineous (hemorrhagic) exudate consists of large amounts of red blood cells, indicating damage
to capillaries that is severe enough to allow the escape of red blood cells from plasma. This type of exudate
is frequently seen in open wounds. Nurses often need to distinguish whether the sanguineous exudates is
dark or bright. A bright sanguineous exudate indicates fresh bleeding, whereas dark sanguineous exudate
denotes older bleeding. Mixed types of exudates are often observed. A serosanguineous exudates
(consisting of clear and blood-tinged drainage) is commonly seen in surgical incisions.

THIRD STAGE
The third stage of the inflammatory response, also referred to as the reparative phase, involves the
repair of injured tissues by regeneration or replacement with fibrous tissue (scar) formation.
Regeneration is the replacement of destroyed tissue cells by cells that are identical or similar in structure
and function. It involves not only replacement of damaged cells one by one but also organization of these
cells so that the architectural pattern of the tissue and function are restored.
The stroma is the tissue that forms the framework (connective tissue) or ground substance of an organ.
The parenchyma comprises the essential functional elements of an organ. Functional cells must have
proper relationships between stroma and parenchyma, and among their blood vessels, lymph vessels,
nerves, and ducts. All must regenerate concurrently. If one component lags behind the others, a normal
product will not be formed.
The ability to reproduce cells varies considerably from one type of tissue to another. For example, epithelial
tissues of the skin and of the digestive and respiratory tracts have a good regeneration capacity, provided
that their underlying support structures are intact. The same holds true for osseous, lymphoid, and bone
marrow tissues. Tissues that have little regenerative capacity include nervous, muscular, and elastic
tissues.
When regeneration is not possible, repair occurs by fibrous tissue formation. Fibrous (scar) tissue has
the capacity to proliferate under the unusual conditions of ischemia and altered pH. The inflammatory
exudate with its interlacing network of fibrin provides the framework for this tissue to develop. Damaged
tissues are replaced with the connective tissue elements of collagen, blood capillaries, lymphatics, and
other tissue-bound substances. In the early stages of this process, the tissue is called granulation
tissues. It is a fragile, gelatinous tissue, appearing pink or red because of the many newly formed
capillaries. Later in the process, the tissue shrinks (the capillaries are constricted, even obliterated) and the
collagen fibers contract, so that a firmer fibrous tissue remains. This is called a cicatrix, or scar.
Although scar tissue has the positive attribute of repairing the injured area, it also can present problems. It
can reduce the functional capacity of the tissue or organ. For example, scar tissue in cardiac muscle
renders that area of the heart weaker. Mechanical obstructions can also arise, for example, in the healing
of a duodenal ulcer. Sometimes the pyloric sphincter becomes stenosed as granulation tissue contracts into
scar tissue.
(Kozier 2000:665-667)