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.

 NURSING CARE PLAN FOR THE PATIENT WTH HEPATIC CIRRHOSIS

Nursing diagnosis	Goal	Interventions	Rationale	Remarks
Fluid volume excess related to compromised regulatory mechanisms secondary to cirrhosis of the liver as manifested by pallor, weak in appearance, jaundice, abdominal distension and edema	Maintaining fluid volume and decreased edema	Assess the hydration status	It will provide a baseline data	Patient demonstrated stabilized fluid volume with maintained Intake and output.
		Assess respiratory status , noting increased respiratory	Indicative of pulmonary congestion or edema
		Assess the degree of peripheral and dependent edema	Fluid shift into tissues as a result of sodium and water retention
		Monitor blood pressure	BP elevations are usually associated with fluid volume excess
		Monitor intake and output chart	It reflects circulating volume status
		Monitor serum albumin and electrolytes, particularly potassium and sodium	Decreased serum albumin affects plasma colloid osmotic pressure, resulting in odema formation
		Encourage bed rest, when ascites is present with leg elevated to mobilize edema and ascites.	Bed rest may promote recumbency - induced diuresis
		Provide frequent mouth care.	Decreases sensation of thirst especially when fluid intake is restricted

Nursing diagnosis	Goal	Interventions	Rationale	Remarks
Imbalanced nutrition: less than body requirements related to loss of appetite and decreased GI motility secondary to ascites as evidenced by refusal to eat, weak in appearance, irritability, poor muscle tone, emaciated and abdominal distension	Improving nutritional status	Assess the dietary intake and nutritional status through diet	It will provide a baseline data	After using above nursing interventions patient's appetite improved and nutritional status maintained
		Provide high protein, high calorie diet supplement by vitamin A, D, E, K and folic acid.	Indicative of pulmonary congestion or edema
		Encourage and provide small, frequent diet	Fluid shift into tissues as a result of sodium and water retention
		Provide adequate oral hygiene before meal	BP elevations are usually associated with fluid volume excess
		Provide assistance with activities as needed	It reflects circulating volume status
		Administer medications for nausea and vomiting as per doctor's orders	Decreased serum albumin affects plasma colloid osmotic pressure, resulting in odema formation

Nursing  diagnosis	Goal	Interventions	Rationale	Remarks
Activity intolerance related to generalized body weakness secondary to progressive disease state as manifested by pallor, body malaise, diaphoresis, inability to concentrate, and inability to perform ADLs, weak in appearance, limited ROM and difficulty initiating movements	Maintenance of rest and comfort	Assess the degree of activity tolerance and degree of fatigue	Provide baseline data for better interventions.	After using above nursing interventions the patient participate willingly in necessary activities, learned how conserve energy and verbalized relief from fatigue
		Provide adequate rest	Rest  reduces metabolic demands on the liver
		Adjust the patient in a comfortable position in bed	Proper positioning helps in maximal respiratory efficiencies and prevents bedsores
		Encourage patient to take high protein and caloric diet frequently	Provide energy and helps in healing of tissues
		Administer Oxygen as ordered	Oxygenate damaged cells and prevent further damage.
		Encourage the patient to exercise gradually.	Regular exercise improves activity intolerance
		Encourage the client to do whatever possible e.g self-care	Provide for sense of control and feeling of accomplishment

 

Nursing diagnosis	Goal	Interventions	Rationale	Remarks
Risk for impaired skin integrity related to altered circulation secondary to accumulation of bile salts as evidenced by pruritis, erythema, dry and scaly skin	Maintaining skin integrity	Assess the degree of discomfort related to edema	Provides baseline data for better interventions	After using above nursing interventions patient maintained skin integrity and identified  individual risk factors and demonstrated behaviour techniques prevents skin breakdown.
		Inspect the skin surface / pressure points routinely	Edematous tissues are most prone to breakdown and to the formation of decubitus ulcers
		Frequently change the position of the patient	Pressure on the edematous tissues to improve circulation
		Avoid irritating soaps and use of adhesive tape.	May cause trauma to the skin
		Provide back massage with emollient lotion every 2 hours	Improves blood circulation and prevent bed sores
		Use alternative pressure mattress or low air liss bed	Prevent pressure ulcers
		Keep patients fingernails short and smooth	Minimize scratching of the skin
		Keep linen dry and free of wrinkles	Moisture aggrevates pruritis and increases risk of skin breakdown

 

 

 

 

 

 

 

 

Nursing diagnosis	Goal	Interventions	Rationale	Remarks
Knowledge deficit related todisease and long term treatment	Providing knowledge	Assess the knowledge level of patient & family members by asking questions about disease	Provides baseline data for better interventions	Patient verbalized understanding of disease process , potential complications, and identified necessary lifestyle changes and participate in care.
		Encourage the patient for adequate rest and nutritious diet	Provide early recovery from disease
		Stress importance of avoiding alcohol	Alcohol is leading cause in the development of cirrhosis
		Encourage the patient to report any complication	Absence of complication helps in early recover