INFLAMMATION

 

Inflammation

Inflammation is a nonspecific cellular response to tissue injury. The body has physiological responses that are designed to eliminate invading organisms and protect against infection.

Inflammation is always present with infection, but infection is not always present with inflammation

The inflammatory response is a physiological process that attacks, confines, and kills invading organisms.

It also allows for tissue repair after damage from an invading organism or from tissue injury and death.

It is the local response of living tissues injury due to injury due to any agencies and that attempts to self-protection to remove harmful stimuli including damage cells, pathogens and being the healing process.

  

Etiology / Causes for inflammation

1.     Infective Agents: Viruses, Bacteria, Fungi etc

2.     Physical Agents: heat cold radiation trauma

3.     Chemical agents: Acid, base, organic solvents, poison

4.     Immunological Agents: Cell mediated and antigen antibody reaction

5.     Inert materials: foreign body.

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The inflammatory process involves a vascular phase and a cellular phase.

            1. The vascular phase consists of the following processes, which occur almost  simultaneously:

§  Temporary vasoconstriction to avoid blood loss after injury

§  Vasodilation to increase blood supply to the area, leading to redness and increased warmth of the area

§  Increased hydrostatic pressure related to the increase in blood flow

§  Increased permeability of blood vessel walls caused by chemical mediators

§  Leakage of fluid and cells out of capillaries into interstitial spaces so that toxins are diluted. This leakage of fluid and eventually protein leads to increased osmotic pressure in the interstitial spaces and edema.

 

2.   The cellular phase involves the response of white blood cells (WBCs) to the cellular  injury. It begins as chemotactic substances are released from the tissues by cellular injury and complement is activated. Neutrophils are the first WBCs to arrive at the site and are the main phagocytic cell.

The processes involved in the cellular phase are as follows:

§  An increased number of WBCs are attracted to the site of injury by chemotactic factors.

§  WBCs adhere to the vessel wall during a process called margination.

§  WBCs migrate through the vessel wall into the interstitial tissue during a process called diapedesis or emigration.

§  WBCs are attracted to the inflamed site by chemotactic factors.

§  Neutrophils ingest the bacteria and dead cells through a process of coating microorganisms called opsonization.

§  This coating allows the bacteria and dead cells to be easily engulfed and killed by WBCs.

§  Neutrophils then die, releasing proteolytic enzymes that liquefy the dead cells and bacteria, resulting in the formation of pus.

§  Fibrin is secreted by fibroblasts and serves to wall off the area to prevent the spread of bacteria and lay the groundwork for tissue rebuilding

Inflammotory  Mediators:

Clinical Manifestations:

The signs and symptoms related to inflammation can be local and/or systemic depending on the location and severity of the inflammatory response.

There are five cardinal local symptoms of inflammation:

·       Redness (rubor) – hyperaemia from vasodilation,

·       Heat (calor) due to increased metabolism at inflammatory site,

·       Swelling (tumor) due to the fluid exudates that form in the interstitial tissue,

·       Pain (dolor) caused by the pressure of the exudates and release of chemicals that irritate nerve endings, and

·       Loss of function (functio laesa) related to the pain and swelling.

Systemic manifestations of inflammation include an increased WBC count (Leukocytosis) with a shift to the left, malaise, nausea and anorexia, increased pulse and respiratory rate, and fever

Types of Inflammation

The basic types of inflammation are acute, subacute, and chronic.

v  In acute inflammation, the healing occurs in 2 to 3 weeks and usually leaves no residual damage. Neutrophils are the predominant cell type at the site of inflammation.

v  A subacute inflammation has the features of the acute process but lasts longer. For example, infective endocarditis is a acute inflammation, but it persists for weeks or months.

v  Chronic inflammation lasts for weeks, months, or even years. The injurious agent persists or repeatedly injures tissue. The predominant cell types present at the site of inflammation are lymphocytes and macrophages. Examples of chronic inflammation include rheumatoid arthritis and osteomyelitis.

Management:

The best management of inflammation is the prevention of infection, trauma, surgery, and contact with potentially harmful agents.

v  Vital signs are important to note with any inflammation, especially when an infectious process is present.

v  Adequate nutrition is essential so that the body has the necessary factors to promote healing when injury occurs.

v  Sponge baths increase evaporative heat loss, they may not decrease the body temperature.

v  Antipyretics should be given to reduce temperature.

v  Acetaminophen acts on the heat-regulating center in the hypothalamus.

v  Antihistamine drugs may also be used to inhibit the action of histamine.

Drug Therapy:

Drug	Mechanism of Action
Antipyretic Drug:     §  Salicylates(asprin)     §  Acetomenophen     §  NSAID	Inhibit synthesis of PGs
Anti inflammatory  Drug:     §  Salicylates(asprin)     §  Corticosteroids     §  NSAID	Inhibit synthesis of PGs Interfere with tissue granulation   Inhibit synthesis of PGs

RICE. Rest, ice, compression, and elevation (RICE) is a key concept in treating soft tissue injuries and related inflammation.

Rest: Rest helps the body use its nutrients and 0 2 for the healing process.

Cold: Cold application is usually appropriate at the time of the initial trauma to promote vasoconstriction and decrease swelling, pain, and congestion from increased metabolism in the area of inflammation.

Compression and immobilization. Compression counters the vasodilation effects and development of edema. Compression by direct pressure over a laceration occludes blood vessels and stops bleeding.

Immobilization of the inflamed or injured area promotes healing by decreasing the tissues' metabolic needs.

Elevation. Elevating the injured extremity above the level of the heart reduces the edema at the inflammatory site by increasing venous and lymphatic return. Elevation also helps reduce pain associated with blood engorgement at the injury site. Elevation may be contraindicated in patients with significantly reduced arterial circulation.