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.

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

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• 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

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

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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.

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Vascular & Chemical Response
• Vasodilation chemical mediators
– Endothelial cell retraction
– Increased capillary permeability
– Movement of fluid from capillaries into tissue spaces

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Vascular Response
• 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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Vascular Response
• 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.

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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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Cellular Response
• 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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Cellular Response
• 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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Cellular Response
• Neutrophils
– Pus is composed of
• Dead neutrophils accumulated at the site of injury
• Digested bacteria
• Other cell debris

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Cellular Response
• Neutrophils
– Bone marrow releases more neutrophils in response
to infection, resulting in elevated WBC.

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Cellular Response
• 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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Cellular Response
• 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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Cellular Response
• 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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Cellular Response
• Lymphocytes
– Arrive later at the site of injury
– Primary roles of lymphocytes involve
• Cell-mediated immunity
• Humoral immunity

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Cellular Response

• 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.

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

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• Systemic response to inflammation
– Increased WBC count with a shift to the left
– Malaise
– Nausea and anorexia
– Increased pulse and respiratory rate
– Fever

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– 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.

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– 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.

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

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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)

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

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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

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

Wound Healing
• Repair
– Primary intention
• Includes three phases
– Initial phase
– Granulation phase
– Maturation phase and scar contraction

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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.

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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.

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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).
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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.

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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

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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

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Wound Classification
• Classified by
 Cause
• Surgical or nonsurgical
• Acute or chronic
 Depth of tissue affected
• Superficial, partial thickness, full thickness

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Wound Classification
• Classified by
– Color
• Red
• Yellow
• Black
• May have two or more colors

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Delay of Healing
• Nutritional deficiencies
• Inadequate blood supply
• Corticosteroid drugs
• Infection
• Smoking

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

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Complications of Healing
• Adhesions
• Contractures
• Dehiscence
• Evisceration
• Excess granulation tissue
• Fistula formation

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Complications of Healing
• Infection
• Hemorrhage
• Hypertrophic scars
• Keloid formation

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Nursing Assessment
• Assess on admission and on a regular basis.
• Identify factors that may delay healing.

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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.
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Nursing Diagnoses
• Impaired skin integrity
• Impaired tissue integrity
• Risk for infection

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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

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• 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.

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Focus on Pressure Ulcers

(Relates to Chapter 13,
“Inflammation and Wound Healing,”
in the textbook)

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

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

Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 66

Incidence
• Most common sites
 Sacrum
 Heels


Influencing Factors
• Amount of pressure (intensity)
• Length of time pressure is exerted
(duration)
• Ability of tissue to tolerate externally
applied pressure


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


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


Risk Factors
• Immobility
• Impaired circulation
• Incontinence
• Low diastolic blood pressure
(<60 mm Hg)
• Mental deterioration


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


• 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.


Stage I
• Intact skin with non-blanchable redness
• Possible indicators—Skin temperature,
tissue consistency, pain


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


Stage II
• Partial-thickness loss of dermis
• Shallow open ulcer with red pink wound
bed
• Presents as an intact or ruptured serum-
filled blister


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


Stage III
• Presents as a deep crater with possible
undermining of adjacent tissue
• Depth of ulcer varies by anatomic location.


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


Stage IV
• Undermining and tunneling may also
occur.


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


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


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


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


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).


Skin
• Assess skin temperature using your hand.
 An ulceration may feel warm initially, then
become cooler.


Skin
• 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.


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


Prevention – Education
• Prevention is the best treatment.
• Identify risk factors and implement
prevention strategies.


Prevention


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.


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.


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.


Treatment – Ulcer Care
• Document and describe size, stage,
location, exudate, infection, pain, and
tissue appearance.
• Keep ulcer bed moist.
• Cleanse with nontoxic solutions.
• Debride.


Treatment – Ulcer Care
• Use adhesive membrane, ointment, or
wound dressing.
• Verify good nutrition.
• Teach self-care and signs of breakdown.
• Initiate specialty services.


Operative Repair
• Skin grafts
• Skin flaps
• Musculocutaneous flaps
• Free flaps


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