Inflammation, wounds

and the healing process:

JZ Fall 2015

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imprint 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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Inflammatory Response
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
Inflammatory response can be divided into
Vascular response
Cellular response
Formation of exudate
Healing

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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.

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

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Inflammatory Response
Vascular Response
Fluid in tissue spaces
Initially composed of serous fluid
Later contains plasma proteins, primarily albumin
Proteins exert pressure that further draws fluid from
blood vessels.
Tissue becomes edematous.

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

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

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Inflammatory Response
Cellular Response
Chemical mediators
Histamine
Serotonin
Kinins (e.g., bradykinin)

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Inflammatory Response
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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Inflammatory Response
Clinical Manifestations
Local response to inflammation
Redness
Heat
Pain
Swelling
Loss of function

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Inflammatory Response
Clinical Manifestations
Systemic response to inflammation
Increased WBC count
Malaise
Nausea and anorexia
Increased pulse and respiratory rate
Fever

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Inflammatory Response
Clinical Manifestations
Systemic response to inflammation
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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Inflammatory Response
Clinical Manifestations
Systemic response to inflammation
Fever
Beneficial aspects of fever include increased killing of
microorganisms, increased phagocytosis, and increased
proliferation of T lymphocytes.

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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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Inflammatory Response
Types of Inflammation
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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Nursing and Collaborative
Management
Acute Intervention
Observation
Vital signs
Fever management

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Nursing and Collaborative
Management
Nursing Implementation
Health promotion
Prevention of injury
Adequate nutrition
Early recognition of inflammation
Immediate treatment

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Nursing and Collaborative
Management
Drug therapy
Aspirin
Acetaminophen
NSAIDs
Corticosteroids

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Nursing and
Collaborative
Management
RICE
Rest
Ice
Compression
Elevation

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Inflammation
Healing Process
The final phase of the inflammation process is
healing.
Healing includes two major components:
Regeneration
Repair

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Wound Healing
Regeneration
Replacement of lost cells and tissues
with cells of the same type

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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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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 migration.
Acute inflammatory reaction occurs.

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Wound Healing
Repair
Granulation phase
Fibroblasts migrate to site and secrete
collagen.
Wound is pink and vascular.
Surface epithelium begins to regenerate.

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 Before and After
Granulating

A.

B.

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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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Complications of Healing
The shape and location of the wound
determine how well the wound will
heal.
Certain factors can interfere with
wound healing and lead to
complications.

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Complications of Healing

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

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Wound Measurement

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Nursing Implementation
Wound management and type of
dressing depends on
Type, extent, and character of wound
Phase of healing

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Nursing Implementation
Purposes of wound management
Cleaning a wound
Treating infection
Protecting clean wound from trauma

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Nursing Implementation
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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Jackson-Pratt Drainage
Device

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

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Nursing Implementation
Red Wounds
Protect the wound
Gentle cleaning, if needed

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Nursing Implementation
Yellow Wounds
Dressing that absorbs exudate and
cleanses the wound surface
Hydrocolloid dressings
Black Wounds
Debridement of nonviable, eschar tissue

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Nursing Implementation
Negative-pressure wound therapy
(vacuum-assisted wound closure)
Suction removes drainage and speeds
healing.
Monitor serum protein levels, F&E
balance, and coagulation studies.

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Negative-Pressure Wound
Therapy

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Nursing Implementation
Hyperbaric O2 therapy (HBOT)
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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Nursing Implementation
Drug Therapy
Becaplermin (Regranex)
Nutritional Therapy
Diet high in protein, carbohydrates, and
vitamins with moderate fat

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Nursing Implementation
Infection prevention
Do not touch recently injured area.
Keep environment free from possibly
contaminated items.
Antibiotics may be given
prophylactically.

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Nursing Implementation
Infection control
Culture should be done.
Concurrent swab specimens obtained
from
Wound exudate
Z-technique
Levines technique

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Nursing Implementation
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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