Inflammation

and Wound Healing

Inflammation

* Is a sequential reaction to cell injury * Is not

synonymous with infection. Inflammation is
always present with infection, but infection is not
always present with inflammation. * Infection is
caused by invasion of tissues or cells by microorganisms
such as bacteria, fungi, and viruses. * Inflammation is
caused by nonliving agents such as heat, radiation,
trauma, and allergens.

Mechanism of inflammation:

* Vascular response
* Cellular response
* Formation of exudates
* Healing
Mechanism of inflammation:
* Vascular response
* After cell injury, arterioles undergo transient
vasoconstriction.
* injured cells produce histamine, which
causes vasodilatation
Mechanism of inflammation:

* Vascular response
 * Hyperemia = increased blood flow *
Plasma proteins seep into the cell,
particularly albumin, which exerts oncotic
pressure that further draws fluid from blood
vessels, leading to edematous formation. *
Fibrin strengthens a blood clot formed by
platelets.
Mechanism of inflammation:

* Cellular Response
* The blood flow through capillaries in the
area slows as fluid is lost and viscosity
 increases.
* Neutrophils and monocytes move into the
injured site through margination,
diapedesis and chemotaxis.
Mechanism of inflammation:

* Margination = movement going to the inner

surface of the capillaries
* Diapedesis = a process in which the cells
adapt their shape to fit through the pores in the
capillary walls and slide through one area of
the cell at a time.
 Mechanism of inflammation:

* Chemotaxis = is the mechanism for ensuring

accumulation of neutrophils and monocytes at
the focus of injury.
Mechanism of inflammation:

* Neutrophils
* The first leukocytes to arrive (usually within 6 to 12
hours).
* They phagocytize (engulf) bacteria, other foreign
materials, and damaged cells.
* With their short life span (24 to 48 hours), dead
neutrophils soon accumulate. In time a mixture of dead
neutrophils, digested bacteria, and other cell debris
accumulates as a creamy substance termed pus.
* Bone marrow releases more neutrophils into the
circulation, resulting in leukocytosis (elevated
WBC).
Mechanism of inflammation:

* Monocytes
 * Are phagocytic cells that migrate to the site
of injury.
* They are attracted to the site by chemotactic
factors and usually arrive at the site within 3
to 7 days after the onset of inflammation.
* They transform into “macrophages’’ that
assist in phagocytosis of the inflammatory
debris.
Mechanism of inflammation:

* Lymphocytes
* Arrive later at the injury site.
 * Their primary role is related to humoral and
cell-mediated immunity.
Mechanism of inflammation:

* Eosinophils
* Are released in large quantities during an allergic
reaction.
* They release chemicals that act to control the
effects of histamine and serotonin.
* They are also involved in phagocytosis of the
allergen-antibody complex.
* They contain highly caustic chemicals that are
 capable of destroying a parasite’s cell surface.
Mechanism of inflammation:

* Basophils
* Release histamine and heparin from their
granules during inflammation.
Chemical Mediators:

* Complement system:
 * Is a major mediator of the inflammatory
response.
* Major functions are:
* Enhance phagocytosis
* Increased vascular
permeability * Chemotaxis
* Cellular lysis
Chemical Mediators:
* Complement system
activation increase
phagocytosis through
opsonization and
chemotaxis.
* Opsonization = occurs
when the antigen, in
combination with
complement factor C3b
and immunoglobulin,
sticks to the surface of
phagocytic cells. This
leads to more rapid
phagocytosis.

Chemical Mediators:

* Histamines
* Are released by mast cells, injured cells, and
basophils.
 * It causes smooth muscle contraction,
vasodilation, and an increase in vascular
permeability.
Chemical Mediators:

* Prostaglandin
* Is a potent vasodilator and inhibits platelet
and neutrophil aggregation.
* It can also sensitize pain receptors to arousal
by stimuli that would normally be painless. * Is
also a potent pyrogen, acting on the
temperature-regulating area of the
 hypothalamus.
Chemical Mediators:

* Leukotrienes
* A potent chemotactic factor.
* It causes constriction of smooth muscles of
bronchi and increases capillary
permeability.
Mechanism of inflammation:
 Exudate Formation
* Consists of fluid and leukocytes that move from
the circulation to the site of injury.
Types of Inflammatory Exudates:
Type
Description Examples
Serous Results from Skin blisters,
outpouring of fluid pleural effusion
that has low cell and
protein content;
seen in early
stages of
inflammation or
when injury is mild.

Catarrhal
Found in tissues where
cells produce mucus. associated with
Mucus production is upper respiratory
accelerated by tract infection
Runny nose
inflammatory
response
 .
Types of Inflammatory Exudates:
Type
Description Examples
Fibrinous Occurs with increasing Adhesions
vascular permeability and
fibrinogen leakage into
the interstitial spaces.
Excessive amounts
of fibrin coating
tissue
surfaces may cause
them to adhere.
Purulent Consists of WBC, Furuncle,
(pus) microorganisms (dead abscess, cellulitis
and alive), liquefied dead
cells, and other debris.

Types of Inflammatory Exudates:

Type
Description Examples
Hemorrha Results from rupture or Hematoma
gi c necrosis of blood vessel
walls; it consists of
RBCs that escape into
tissue.
 Clinical Manifestations of
Inflammation:

* Systemic manifestations:
* Increased WBC
* Malaise
* Nausea and anorexia
* Increased pulse and respiratory rate
Clinical Manifestations of
Inflammation:
 * Fever
* Cytokines (e.g., inteleukin-1, interleukin-6,
tumor necrosis factor, interferon) are
important in causing the systemic
manifestations of inflammation, as well as
the production of fever.
Clinical Manifestations of
Inflammation:

* Fever
 * Cytokines trigger the onset of fever.
* Prostaglandin = is the most critical metabolic
change that acts directly to increase the
thermostat set point.
* The hypothalamus then activates the autonomic
nervous system to stimulate increased muscle
tone and shivering and decreased perspiration
and blood flow to the periphery.
Clinical Manifestations of
Inflammation:

* Beneficial aspects of fever:

* Increases killing of microorganisms *
 Increases phagocytosis by neutrophils
* Increases proliferation of T cells.
* Enhances the activity of interferon (body’s
natural virus-fighting substance)
Local Manifestations of Inflammation:
Manifestations Cause
Redness (rubor) Hyperemia from vasodilation
Heat (calor) Increased metabolism at inflammatory site
Pain (dolor) Change in pH; change in local ionic
concentration; nerve stimulation
by chemicals (e.g., histamine, prostaglandins); pressure
from fluid exudates.
Swelling (tumor) Fluid shift to interstitial spaces; fluid
exudate accumulation.
Loss of function Swelling and pain

Types of Inflammation:
* 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
* Subacute inflammation = has the features of the acute process
but lasts longer.
* Ex: infective endocarditis, acute inflammation but persists for
weeks or months.
* Chronic inflammation = lasts for weeks, months, or even years.
* Cause may be an alteration in the immune response (e.g.,
autoimmune disease).
* Lymphocytes and macrophages are the predominant cell type
at the site of inflammation
 * Ex: rheumatoid arthritis, and tuberculosis

Healing Process

* The final phase of the inflammatory response.

* Two major components:
* Regeneration and repair
Healing Process

* Regeneration:
* Is the replacement of lost cells and tissues with cells of
the same type.
* Labile cells = divide constantly
* Ex: cells of the skin, lymphoid organs, bone marrow,
* Mucous membranes of gastrointestinal, urinary, and reproductive
tracts.
* Stable cells = retain their ability to regenerate but do so
only if the organ is injured.
* Ex: liver, pancreas, kidney, and bone cells.
* Permanent cells = have left the cell cycle and do not
divide.
* Ex: neurons of the CNS, skeletal, and cardiac muscles

Healing Process

* Repair
 * Is healing as a result of lost cells being
replaced by connective tissue.
* Repair healing occurs by primary, secondary,
or tertiary intention.
Repair

* Primary intention
* healing takes place when wound margins are
neatly approximated, such as in a surgical
incision.
 Phases in Primary Intention
Healing

* Initial phase:
* An acute site has the presence of
inflammatory fibrin clots, erythrocytes,
reaction occurs. * Injured neutrophils,
 macrophages, and debris. epithelial cells; clot
Phase Activity serving as meshwork
Initial phase for starting
Approximation of (3 to 5 capillary growth.
days) incision edges;

migration of
Phases in Primary Intention
Healing
* Granulation phase:
* Fibroblastic, proliferative,
 or reconstructive phase *
Angioblasts
(angiogenesis)=
proliferating capillary sprouts
* Fibroblasts = are immature
connective tissue cells that
secrete collagen.
* Wound is pink and vascular
* Wound is friable, and at
Phases in Primary Intention
Healing
* Maturation phase
* Fibroblasts disappear
as the wound
Phase Activity
Granulation Migration of
phase (5 days fibroblasts; to
4 weeks) secretion of
collagen; abundance of
capillary buds; fragility of
wound
becomes stronger.
* A mature scar is
virtually avascular Maturation Remodeling of
and pale. phase collagen; (scar
* The scar may be strengthening of
more painful at this formation) scar
phase than in the (7 days to
granulation phase several months)
Phase Activity
Repair

* Secondary intention:
* Occurs in wound from trauma, ulceration, and
infection that have large amounts of exudates
and wide, irregular wound margins with
extensive tissue loss.
 Repair

* The inflammatory reaction may be greater than

the primary intention of healing.
* Healing is the same as primary intention, but
major differences are:
 * Greater defect and gaping wound edges
* Granulation takes place from the edges
inward and from the bottom of the wound
upward until the defect is filled.
* More granulation tissue, result is much larger
scar.
Repair
* Tertiary intention “delayed primary intention”
* Occurs with delayed suturing of a wound in which two layers of
granulation tissue are sutured together.
* Ex: a contaminated wound is left open and sutured closed after
the infection is controlled.
* Usually results in larger and deeper scar than primary or
secondary intention.
 Complications of Healing:

* Hypertrophic scar and keloid

formation: * Occur when the body
produces excess collagen tissue
Complications of Healing:

* Hypertrophic scar = is inappropriately large,

 red, raised, and hard. It remains confined to
the wound edges and regresses in time.

Complications of Healing:

* Keloid = is an even greater

protrusion of scar tissue and
 extends beyond the wound edges,
and may form tumorlike mass.
* Predisposing factors:
* Hereditary, dark-skinned
people
* Complaints associated with
keloid:
* Tenderness, pain,
hyperesthesia
Complications of Healing:

* Contracture:
* Shortening of the
muscle or scar tissue
 resulting from
excessive fibrous
tissue formation,
especially if the
wound is near a joint.
* Frequently occurs in
an area that has been
burned.
Complications of Healing:

* Dehiscence:
* Is the separation and disruption of previously joined
wound edges. This occurs when a primary healing
site bursts out.
* Contributing factors:
* An infection may cause an inflammatory process
* Granulation tissue may not be strong
enough to withstand the forces imposed on the
wound.
* Obesity = adipose tissue interferes with healin
Complications of Healing:

* Evisceration = occurs when wound edges

separate to the extent that intestines protrude
through the wound.
 Complications of Healing:

* Adhesion
* abnormal union or connection of separate
tissue surfaces by new fibrous tissue
Nursing interventions during
acute inflammatory
response:
* Rest = helps the body better use its nutrients
and oxygen for the healing process. Prevents
disruption of fibrin formation
* Immobilization = assists the healing process
by decreasing body’s metabolic needs. * the
use of cast, splint, or bandage
Nursing interventions during
acute inflammatory
response:
 * Compress
* Cold application = is appropriate at the time of
the initial trauma to cause vasoconstriction and
decrease swelling, pain, and congestion on the
area of inflammation.
* Heat application = should be used 24 to 48
hours after the injury to promote vasodilation,
increasing the circulation to the inflamed site.
* Elevation = will reduce the edema at the
inflammatory site and increase venous
return.
Drugs Used for Inflammation and
Drug
Healing Mechanism of Action
Antipyretic Lower temperature by
Salicylates (Aspirin) action on heat-regulating
centre in hypothalamus,
resulting in peripheral
dilatation and heat loss;
interfere with formation and
release of prostaglandin
Acetaminophen (Tylenol) Lower temperature by
action on heat-regulating
centre in hypothalamus
NSAIDs (e.g., Inhibit synthesis of
Ibuprofen [Advil]) prostaglandin

Drugs Used for Inflammation and

 Drug
Healing Mechanism of Action

Anti-inflammatory Inhibit synthesis of

Salicylates prostaglandin, reduce
capillary permeability
Interfere with tissue
Corticosteroids granulation, induce
immunosuppressive
effects (decreased
synthesis of lymphocytes)
Inhibit synthesis of
NSAIDs (e.g., prostaglandin
Ibuprofen [Advil])

Nutrition therapy
* Protein = necessary for synthesis of immune
factors, leukocytes, fibroblasts, and collagen *
Carbohydrate = needed for the increased
metabolic energy required in inflammation and
healing
* Vit. C = needed for capillary synthesis and
collagen
* Vit. A = accelerates epithelialization