revised focus on inflammation

Focus on Inflammation

(Relates to Chapter 13, “Inflammation and Wound

Healing,” in the textbook)

Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.

2

Inflammatory Response

• Sequential response to cell injury– Neutralizes and dilutes inflammatory agent– Removes necrotic materials– Establishes an environment suitable for

healing and repair


3


• Mechanism of inflammation basically the same regardless of injuring agent

• Intensity of the response depends on– Extent and severity of injury– Reactive capacity of injured person


4


• Inflammatory response can be divided into: – Vascular response– Cellular response– Formation of exudate– Healing


6

Inflammatory Response Vascular Response

• After cell injury, arterioles in area briefly undergo transient vasoconstriction.

• After release of histamine and other chemicals by the injured cells, vessels dilate, resulting in hyperemia.


7

Inflammatory Response Vascular & Chemical Response

• Vasodilation chemical mediators – Endothelial cell retraction – Increased capillary permeability– Movement of fluid from capillaries into tissue

spaces


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• Fluid in tissue spaces– Initially composed of serous fluid– Later contains plasma proteins, primarily

albumin• Proteins exert oncotic pressure that further draws

fluid from blood vessels.• Tissue becomes edematous.


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• As plasma protein fibrinogen leaves blood, it is activated to fibrin by products of the injured cells.

• Fibrin strengthens a blood clot formed by platelets.

• In tissue, clots trap bacteria to prevent spread.


10

Inflammatory Response Cellular Response

• Blood flow through capillaries in the area of inflammation slows as fluid is lost and viscosity increases.

• Neutrophils and monocytes move to the inner surface of the capillaries and then migrate through the capillary wall to the site of the injury.


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• Chemotaxis– Directional migration of WBCs along

concentration gradient of chemotactic factors– Mechanism for accumulating neutrophils and

monocytes at site of injury


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• Neutrophils– First leukocytes to arrive at site of injury (6 to

12 hours) – Phagocytize bacteria, other foreign material,

and damaged cells – Short life span (24 to 48 hours)


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• Neutrophils– Pus is composed of

• Dead neutrophils accumulated at the site of injury• Digested bacteria• Other cell debris


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• Neutrophils– Bone marrow releases more neutrophils in

response to infection, resulting in elevated WBC.


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• Monocytes– Second type of phagocytic cells to migrate

to site of injury from circulating blood– Attracted to the site by chemotactic factors– Arrive within 3 to 7 days after the onset of

inflammation


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• Monocytes– On entering tissue spaces, monocytes

transform into macrophages.– Assist in phagocytosis of inflammatory

debris– Macrophages have a long life span and can

multiply.


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• Macrophage– Important in cleaning the area before

healing can occur– May stay in damaged tissues for weeks– Cells may fuse to form a multinucleated

giant cell.


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• Lymphocytes – Arrive later at the site of injury– Primary roles of lymphocytes involve

• Cell-mediated immunity• Humoral immunity


19


• Exudate– Consists of fluid and leukocytes that move

from the circulation to the site of injury– Nature and quantity depend on the type and

severity of the injury and the tissues involved.


20

Inflammatory Response Clinical Manifestations

• Local response to inflammation– Redness– Heat– Pain– Swelling– Loss of function


21


• Systemic response to inflammation– Increased WBC count with a shift to the

left– Malaise– Nausea and anorexia– Increased pulse and respiratory rate– Fever


22


• Systemic response to inflammation– The causes of the systemic response are

poorly understood, but it is probably due to complement activation and the release of cytokines.

– Some of the cytokines are IL-1, IL-6, and tumor necrosis factor.


23


• Systemic response to inflammation – Fever

• Onset is triggered by release of cytokines.• Cytokines cause fever by initiating metabolic

changes in the temperature-regulating center.• Epinephrine released from the adrenal medulla

increases metabolic rate.


24

Fig. 13-3. Production of fever. When monocytes-macrophages are activated, they secrete cytokines such as interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrosis factor (TNF), which reach the hypothalamic temperature-regulating center. These cytokines promote the synthesis and secretion of prostaglandin E2 (PGE2) in the anterior hypothalamus.

PGE2 increases the thermostatic set point, and the

autonomic nervous system is stimulated, resulting in shivering, muscle contraction, and peripheral vasoconstriction.


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• Patient then experiences chills and shivering.• Body is hot, yet person seeks warmth until the

circulating temperature reaches core body temperature.


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• Beneficial aspects of fever include increased killing of microorganisms, increased phagocytosis, and increased proliferation of T lymphocytes.


28

Inflammatory Response Types of Inflammation

• Acute– Healing occurs in 2 to 3 weeks, usually

leaving no residual damage.– Neutrophils are the predominant cell type

at the site of inflammation.


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• Subacute– Has same features as acute inflammation

but persists longer


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• Chronic– May last for years– Injurious agent persists or repeats injury to

site.– Predominant cell types involved are

lymphocytes and macrophages.– May result from changes in immune

system (e.g., autoimmune disease)


31

Wound Healing

• The final phase of the inflammatory response– Healing

• Two major components--regeneration and repair.

• Regeneration– Replacement of lost cells and tissues with cells

of the same type– Ability to regenerate depends on cell type.– Constantly dividing cells that rapidly regenerate

• Skin, bone marrow, lymphoid organs, as well as mucous membrane cells of the urinary, reproductive, and GI tracts


32

Wound Healing• Regeneration

– Replacement of lost cells and tissues with cells of the same type

• Stable cells such as liver, bone, kidney, and pancreas regenerate in response to injury.

• Permanent cells such as neurons and skeletal and cardiac muscle do not divide.

– Neurons are replaced by glial cells or stem cells.

– Skeletal and cardiac muscle will be repaired with scar tissue.


33

Wound Healing

• Repair– Healing as a result of lost cells being

replaced with connective tissue– More common than regeneration– More complex than regeneration– Occurs by primary, secondary, or tertiary

intention


34Fig. 13-4. Types of wound healing. A, Primary intention. B, Secondary intention. C, Tertiary intention.

35

Wound Healing

• Repair – Primary intention

• Includes three phases– Initial phase– Granulation phase– Maturation phase and scar contraction


36

Wound Healing

• Repair– Initial phase

• Lasts 3 to 5 days• Edges of incision are aligned.• Blood fills the incision area, which forms

matrix for WBC formation.• Acute inflammatory reaction occurs.


37

Wound Healing

• Repair– Granulation phase

• Lasts 5 days to 3 weeks• Fibroblasts migrate to site.• Wound is pink and vascular.• Surface epithelium begins to regenerate.


38

Before and After Granulating


Fig. 13-5. A, Wound clean but not granulating (note lack of red cobblestone appearance), suggesting heavy bacterial contamination or other impediments to wound healing. B, Same wound granulating after 1 week of topical antibiotic use (note healthy red cobblestone appearance).

39

Wound Healing

• Repair Maturation phase and scar contraction

• Begins 7 days after injury and continues for several months/years

• Fibroblasts disappear as wound becomes stronger.

• Mature scar forms.


40

Wound Healing

• Repair Secondary intention

• Wounds that occur from trauma, ulceration, and infection have large amounts of exudate and wide, irregular wound margins with extensive tissue loss.

• Edges cannot be approximated.• Results in more debris, cells, and exudate


41

Wound Healing

• Repair Tertiary intention

• Delayed primary intention due to delayed suturing of the wound

• Occurs when a contaminated wound is left open and sutured closed after the infection is controlled


42

Wound Classification

• Classified by Cause

• Surgical or nonsurgical• Acute or chronic

Depth of tissue affected• Superficial, partial thickness, full thickness


43

Wound Classification

• Classified by– Color

• Red• Yellow• Black• May have two or more colors


44

Delay of Healing

• Nutritional deficiencies• Inadequate blood supply• Corticosteroid drugs• Infection • Smoking


45

Delay of Healing

• Mechanical friction on wound• Advanced age• Obesity • Diabetes mellitus• Poor general health • Anemia


46

Complications of Healing

• Adhesions• Contractures• Dehiscence• Evisceration• Excess granulation tissue• Fistula formation


47

Complications of Healing

• Infection• Hemorrhage• Hypertrophic scars• Keloid formation


48

Nursing Assessment

• Assess on admission and on a regular basis.

• Identify factors that may delay healing.


49

Fig. 13-9. Wound measurements are made in centimeters.

The first measurement is oriented from head to toe, the

second is from side to side, and the third is the depth (if

any). If there is any tunneling (when cotton-tipped

applicator is placed in wound,

there is movement) or undermining (when cotton-tipped

applicator is placed in wound, there is a “lip” around the

wound) this is charted in respect to a clock with 12

o’clock being toward the patient’s head. This wound

would be charted as a full-thickness, red wound, 7 cm × 5

cm × 3-cm, with a 3-cm tunnel at 7 o’clock and 2 cm

undermining from 3 o’clock to 5 o’clock.

51

Nursing Diagnoses

• Impaired skin integrity• Impaired tissue integrity• Risk for infection


52

Nursing Implementation

• Care varies depending on– Causative agent– Degree of injury– Patient’s condition


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• Purposes of wound management– Cleaning a wound– Treating infection– Protecting clean wound from trauma


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• Sutures/fibrin sealant help closure.• Primary intention wounds may be

covered with dry dressing.• Drains may be inserted.• Topical antimicrobials/antibacterials

should be used with caution.


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• Secondary intention wound care depends on etiology and type of tissue in the wound.


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• Red Wounds Protect the wound Gentle cleaning, if needed


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• Yellow wounds– Dressing that absorbs exudate and

cleanses the wound surface– Hydrocolloid dressings

• Black Wounds– Debridement of nonviable, eschar tissue


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• Negative-pressure wound therapy– Suction removes drainage and speeds

healing.– Monitor serum protein levels, F&E

balance, and coagulation studies.


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• Hyperbaric O2 – Delivery of O2 at increased atmospheric

pressure– Allows O2 to diffuse into serum– Last 90 to 120 minutes, with 10 to 60

treatments


60


• Drug therapy Becaplermin (Regranex)

• Nutritional therapy Diet high in protein, carbohydrates, and

vitamins with moderate fat


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• Infection prevention Do not touch recently injured area. Keep environment free from possibly

contaminated items. Antibiotics may be given

prophylactically.


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• Infection control Should cultures be done? Are they reliable? When would wound cultures be reliable? When would they be unreliable?


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• Psychologic implications– Fear of scar or disfigurement– Drainage or odor concerns– Be aware of your facial expressions

while changing dressing.


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Patient Teaching

• Teach signs and symptoms of infection.

• Note changes in wound color or amount of drainage.

• Provide medication teaching.


Focus on Pressure Ulcers

(Relates to Chapter 13, “Inflammation and Wound

Healing,” in the textbook)



66

Pressure Ulcer

• A localized injury to the skin and/or underlying tissue due to pressure with or without shear/friction


67

Incidence

• Most common sites Sacrum Heels


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Influencing Factors

• Amount of pressure (intensity)• Length of time pressure is exerted

(duration)• Ability of tissue to tolerate externally

applied pressure


69

Contributing Factors

• Shearing force—Pressure exerted on the skin when it adheres to the bed and the skin layers slide in the direction of body movement

• Friction—Two surfaces rubbing against each other

• Excessive moisture


70

Risk Factors

• Advanced age• Anemia• Contractures• Diabetes mellitus• Elevated body temperature


71

Risk Factors

• Immobility• Impaired circulation• Incontinence • Low diastolic blood pressure

(<60 mm Hg)• Mental deterioration


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Risk Factors

• Neurologic disorders• Obesity • Pain• Prolonged surgery• Vascular disease


73

Clinical Manifestations

• Ulcers are graded or staged according to deepest level of tissue damage:– Stage I (minor) to stage IV (severe)– Slough or eschar may have to be

removed for accurate staging of some ulcers.


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Clinical Manifestations Stage I

• Intact skin with non-blanchable redness

• Possible indicators—Skin temperature, tissue consistency, pain


75

Clinical Manifestations Stage I

• May appear with red, blue, or purple hues in darker skin tones


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Clinical Manifestations Stage II

• Partial-thickness loss of dermis • Shallow open ulcer with red pink

wound bed• Presents as an intact or ruptured

serum-filled blister


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Clinical Manifestations Stage III

• Full-thickness skin loss involving damage or necrosis of subcutaneous tissue that may extend down to, but not through, underlying fascia


78

Clinical Manifestations Stage III

• Presents as a deep crater with possible undermining of adjacent tissue

• Depth of ulcer varies by anatomic location.


79

Clinical Manifestations Stage IV

• Full-thickness loss can extend to muscle, bone, or supporting structures.– Bone, tendon, or muscle may be visible

or palpable.


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Clinical Manifestations Stage IV

• Undermining and tunneling may also occur.


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Clinical Manifestations Infection

• Signs– Leukocytosis– Fever– Increased ulcer size, odor, or drainage– Necrotic tissue– Pain


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Clinical Manifestations Complications

• Most common—Recurrence• Cellulitis• Chronic infection• Osteomyelitis


83

Assessment

• Assess pressure ulcer risk on admission and at periodic intervals based on care setting and patient’s condition.


84

Assessment Tools

• Use risk assessment tools such as the Braden scale for systematic skin inspection.


85

Assessment of Patients With Dark Skin

• Look for areas of skin darker (purplish, brownish, bluish) than surrounding skin.

• Use natural or halogen light for accurate assessment (fluorescent light casts a blue color that can skew results).


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• Assess skin temperature using your hand. An ulceration may feel warm initially,

then become cooler.


87


• Touch the skin to feel its consistency. Boggy or edematous tissue may indicate

a stage I pressure ulcer.• Ask about pain or an itchy sensation.


88

Planning

• Overall goals No deterioration Reduce contributing factors Not develop an infection Have healing Have no recurrence


89

Prevention – Education

• Prevention is the best treatment.• Identify risk factors and implement

prevention strategies.


90

Prevention


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Prevention – Skin Care

• Remove excessive moisture.• Avoid massage over bony

prominences.• Turn every 1 or 2 hours (with care to

avoid shearing).• Use lift sheets.


92

Prevention – Skin Care

• Position with pillows or elbow and heel protectors.

• Use specialty beds.• Cleanse skin if incontinence occurs.

Use pads or briefs that are absorbent.


93

Prevention – Nutrition

• Caloric intake elevated to 30 to 35 cal/kg/day or 1.25 to 1.50 g protein/kg/day– Supplements, enteral, or parenteral

feedings may be necessary.


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Treatment – Ulcer Care

• Document and describe size, stage, location, exudate, infection, pain, and tissue appearance.

• Keep ulcer bed moist.• Cleanse with nontoxic solutions.• Debride.


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Treatment – Ulcer Care

• Use adhesive membrane, ointment, or wound dressing.

• Verify good nutrition.• Teach self-care and signs of

breakdown.• Initiate specialty services.


96

Operative Repair

• Skin grafts• Skin flaps• Musculocutaneous flaps• Free flaps


revised focus on inflammation

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