Week 2 Class 1: N2055

Inflammation & Healing

Class Objectives

Discuss the components of the inflammatory response.

Discuss exudate formation and types of exudate.
Describe the different types of wound healing intention.
Identify and discuss factors affecting healing.
Discuss the manifestations of infection.
Discuss the diagnostic tests used to determine infection.
Discuss the complications of healing.
Discuss the assessment and care of inflammation and infection.
Describe the different types of burns.
Discuss how burns are classified.
Describe local and systemic responses to burns.
Describe pathological responses to burns.
Discuss clinical manifestations and care of burns.
Discuss diagnostic tests used when burns occur.

Definitions (expected to do on our own)

Chemotaxis
Dehiscence
Diapedesis
Eschar
Evisceration
Exudate
Granulation
Hemolysis
Hyperemia
Hyperthermia
Hypothermia
Intention
Myoglobinuria
Paralytic ileus

Review

1. Wound healing is a process. Put the following phases of wound healing in

proper sequence.
o
a. vascular, inflammation, proliferation, maturation
o
b. inflammation, proliferation, vascular, maturation
o
c. proliferation, vascular, inflammation, maturation
o
d. maturation, inflammation, proliferation, vascular
2. WBCs are essential for wound healing. Which of the following WBCs have
phagocytic action?
o
a. monocytes, eosinophils, lymphocytes,
o
b. neutrophils, basophils, platelets
o
c. neutrophils, monocytes
o
d. platelets, lymphocytes
3. Full healing of a wound occurs in:
o
a. 2-14 days b. 15-28 days c. 1-12 months d. >1 year to 2 years
4. Once healed, wounds gain 100% tensile strength.
o
a. True b. False
5. During the proliferation stage, FBs or wound re-injury can delay this stage.
o
a. True b. False

Tissue Injury & Repair

Wound healing is a process

Wounds can be visible or invisible

Inflammatory Response (good thing- different cells are going to the wound to start
the healing process)

Involves a sequential reaction to cell injury (step by step reaction)

Neutralizes and dilutes the inflammatory agent
Removes necrotic tissue (dead tissue- black)
Establishes an environment suitable for healing and repair (beneficial)
Natural tendency to view as undesirable but inflammation is actually beneficial.
Always present with infection however, infection is not always present with
inflammation
Infection involves invasion of tissues or cells by microorganisms

Mechanism of inflammation is generally the same regardless of the injuring agent

The intensity of response depends on:

the extent and severity of the injury

the reactive capacity of the injured person

4 phases to the response: wound healing and repair

o
Vascular
o
Inflammation
o
Proliferative
o
Maturation

1. Vascular or hemostasis response (reduce bleeding and prevent any bacteria from
entering)

Capillary circulation
Vasoconstriction (to control hemorrhage, occurs within seconds)
Occurs at site to stop bleeding and reduce exposure to bacteria
Clotting process begins (platelets aggregate to form a clot and plasma protein
system begins to form a fibrin meshwork catching more platelets. Platelets release
ADP to attract more platelets and prostaglandin (pain) to activate other
platelets/serotonin).

2. Inflammation phase (White blood cells and their function- never let monkeys eat
bananas)

Vasodilation (occurs within 10-30 minutes)

Capillaries dilate due to serotonin released by platelets (venules constrict &
arterioles dilate)
Influx of plasma (dilutes toxins, delivers nutrients, brings phagocytes and more
blood and oxygen)
REDNESS, WARMTH, SWELLING, PAIN

Name the phagocytes that respond to the wound inflammatory phase? Vasodilata
Inflammation phase (contd)

Occurs within 0-4 days and is essential for repair & restoration. Prolonged if
infected or necrotic.
What do neutrophils do? Fight infection- first ones to arrive
When do they arrive at the site?
What are SEGS and what if they are elevated?
What are BANDS and what if they are elevated? (When the body is trying to
produce more white blood cells)
What do monocytes do? Later
When do they arrive at the site?
Name 3 functions of monocytes.

Phagocytosis- engulfs another cell (packman)

Inflammation phase * Picture

Exudate Formation (fluid that serves a purpose)

Types include:
o
Serous clear, amber, thin and watery (blister)
o
Fibrinous - cloudy and thin, with strands of fibrin
o
Serosanguineous clear, pink, thin and watery
o
Sanguineous reddish, thin and watery
o
Seropurulent yellow or tan, cloudy and thick
o
Purulent opaque, milky; sometimes green
o
Hemopurulent reddish, milky and viscous
o
Hemorrhagic red, thick (major femoral artery cut)
Consists of fluid and leukocytes that move from the circulation to the site of injury
(depending on what the actual wound is)
Nature and quantity of exudate depend on the type and severity of injury and the
tissues involved
Walling Off Effect
o
Prevents spread of agents to other areas
o
Fibrinogen clots block lymphatic channels and spaces and decrease fluid
flow

WBC Activity
o
Clean up wound and initiate further healing (eat up the garbage)

Neutrophils

Arrive first (short life span) and line walls of capillaries

(margination)

Histamine stimulates cells that line capillaries to contract

Neutrophils pass through capillary walls (diapedesis) to the

site of injury (chemotaxis) and begin phagocytosis
o
Monocytes
Arrive second
On entering tissue spaces turn into macrophages (long life span,
can multiply and stay in damaged tissues for weeks)
Assist in phagocytosis of inflammatory debris

Margination, Diapedesis & Chemotaxis of WBCs

Lewis et al p. 212 * Picture

Other WBCs (immune system)

Basophils
o
Secrete histamine
Eosinophils (allergic reactions)
o
Control inflammatory response by secreting antihistamine

Lymphocytes
o
Help macrophages become more effective
o
Controlled by the adrenocortical hormones

Mediators of Inflammation
o
Mast Cells

When stimulated release

Histamine and serotonin cause capillary dilation

o
Leukotrienes

Cause capillary dilation lasts longer

o
Prostaglandins appear later

Cause capillary dilation (lasts longer) & chemotaxis

Cause pain

**Role of ASA and NSAIDS

o
Kinins (bradykinin)

Plasma protein that increases vascular permeability (dilation of

blood vessels) and fluid in the wound

Allow leukocytes to enter tissue to help with phagocytosis

Kinins act with prostaglandins to cause pain and smooth muscle

contraction
o
Cytokines

Regulate the mobility, differentiation and growth of leukocytes

Best known are interleukins

Promote growth and function of several cells

Account for many manifestations of both acute and chronic

inflammation

Augment immunity promote B cell maturation and

moderate suppressor T cell function
o
Complement System
A group of plasma proteins that are activated by microorganisms
Promotes inflammation and movement of leukocytes into injured
area
Coat microbes that make them more vulnerable to phagocytosis

3. Proliferative phase

occurs 4-21 days

Proliferation, granulation, and contraction
Fibroblasts
o
Secrete collagen framework
Angiogenesis (making blood vessels- can attach little capillaries together to
help with blood flow, good blood flow= things are going to be better)
o
Pericytes regenerate outer layers of capillaries and endothelial cells
produce the lining
Keratinocytes (skin tissue building up in healing process)
o
Responsible for epitheliazation/contracture

Granulation tissue

Epithelialization (consider wound to be healed) (wound healing- decent

protein) affect wound healing- age, lack of movement, lack of nutrition, age,
diabetic people- poor circulation glucose in blood
o
Migration of epithelial cells across the wound surface the wound is
considered closed or healed
o
The epithelium thickens and begins to mature
o
Superficial wounds take about 3 to 5 days
o
Skin grafts are necessary for large wounds or full thickness wounds
because epidermal migration is limited to 3cm

4. Maturation phase (end of healing process)

Can take up to two years

Fibroblast is responsible for remodeling
Scar remodels (collagen synthesis & lysis)
Capillaries disappear and scar appears thin and white, not red.

Phases of Wound Healing (CAWC) *CHART

Healing

Two types of healing:

o
Primary intention
o
Secondary intention

Also tertiary intention i.e. delayed suturing, dog bites

Wound Healing Intention

Refers to the probable process of healing for any wound

Includes 3 types of intention
o
Primary
o
Secondary
o
Tertiary

Primary Intention (suture strips- clean wound)

o
Use of sutures (or other means) to approximate wound edges of an
incision or a clean laceration
o
Healing occurs through collagen synthesis (granulation tissue formation)
with little scarring or contraction
o
Risk of infection and tissue defects is minimal
o
Residual scar is usually thin and flat
o
Types of wounds include surgical incisions, paper cuts

Secondary Intention (leave the wound open and let it heal from the bottom
up- larger- ulcers) (pressure ulcers- waist down- circulation is less)
o
Wounds are left open and heal by generation of tissue
o
Wounds that require the regeneration of more tissue increase the risk of
infection
o
Wounds have a prolonged inflammation phase more time is required for
phagocytosis
o
Epithelialization may not heal the wound because migration of epithelial
cells is limited (cells can only migrate so far- edges)
o
Phases of proliferation and maturation are also prolonged healing takes
place from edges inward and from bottom of wound upwards until the defect
is filled
o
Healing takes place by contraction and formation of scar tissue
o
Healing may be hastened by skin grafts
o
Types of wounds include pressure ulcers

Tertiary Intention (delayed primary intention) (we do this on purpose- pack

wounds because we dont want healing to occur when there's an ulcer
underneath) (dog bites- try not to suture them) (cyst in tailbone/coccyx area)IND, incision and drainage)- open area just above the tailbone- prone to
infection area- pack wound- sterile gauze/ saline - keep it from closing from
the top- want it to heal from bottom- up) Daily dressing changes
o
Used for contaminated wounds
o
The wound is left open because of an infection or risk of infection and then
closed when it is free of debris

Also occurs if a primary wound becomes infected, the wound is opened

and allowed to granulate, then closed

Factors Affecting Healing (lack of nutrition- protein, blood supply, obesity, anemia
(decrease in hemoglobin- decreased oxygen going to the tissue), age, poor
general health, friction on wound, diabetes)
Hemoglobin- Men 140-180, Female 120-160 (lower because of menstruation)

Wounds usually heal at a normal predictable rate

Some factors delay healing
o
Nutritional deficiencies
o
Vit C delays formation of collagen and capillary development, decreases
WBC function
o
Protein decreases supply of amino acids for tissue repair
o
Zinc impairs epitheliazation
Inadequate blood supply
o
Decreases supply of nutrients
o
Decreases removal of debris
o
Inhibits inflammatory response
Obesity
o
Decreases blood supply in fatty tissue
Anemia
o
Supplies less oxygen at tissue level
Advanced age
o
Slows collagen synthesis by fibroblasts
o
Impairs circulation
o
Requires longer time for epitheliazation of skin
o
Alters phagocytic and immune responses
Poor general health
o
Causes generalized absence of factors required to promote wound
healing
Diabetes Mellitus
o
Decreases collagen synthesis
o
Retards early capillary growth
o
Impairs phagocytosis
o
Reduces oxygen supply and nutrients
Mechanical friction on wound (pants- friction)
o
Destroys granulation tissue
o
Prevents apposition of wound edges

What can go wrong?

Wound fails to progress through a normal, orderly, and timely sequence of repair

Dehiscence/evisceration
Chronic inflammation, not acute
Infection
o
abscess formation
o
septicemia

Complications of Healing

Infection (bad bacteria thats not suppose to be in that area- higher risk of
infection)
Septicemia (when infection has been around for long enough and go into
other parts of the body)
o
Systemic infection of the blood
o
Blood contains pathogens that have spread from any part of the body
o
Manifestations include fever, chills, pain, headache, nausea or diarrhea
o
Diagnosed by blood culture C&S (finding what bacteria is in the bloodlet bacteria grow and identify what it is on a jelly pad?) see if antibiotic
is working (petri dishes/ incubator) usually gram- organism
o
Treated vigorously with antibiotics
Hypertrophic Scars and Keloid Formation
o
o

o
o

Occur when body produces too much collagen tissue

Hypertrophic scar (larger) (abnormal/complication of woundsphysiological impact)
inappropriately large, red, raised, hard scar
Remains confined to wound edges and regeresses in time
Keloid
Protrusion of scar tissue that extends beyond the wound edges and may
form tumour like masses
Permanent
May C/O of tenderness, pain and hyperesthesia
Adhesions
Bands of scar tissue between or around organs
Contracture (bed ridden patient whose not moving) (burns)
Necessary for healing but process may become abnormal
A shortening of muscle or scar tissue results from excessive fibrous
formation
End result is deformity or contracture especially if wound is near a joint
Dehiscence (wound separating)
Involves the separation and disruption of previously joined wound edges
(surgical incision or wound closure)
Three causes
Infection
Granulation tissue is not strong enough
Obesity adipose tissue interferes with healing

Evisceration
The protrusion of an internal organ through a wound or surgical incision

Wound complications (teach patients to keep their hands clean- dirtiest after
touching nose or going to washroom)

Chronic inflammation, not acute (doesnt go through all the stages,

continuously goes through inflammation stage) Little blood- good
Granulation tissue- good tissue (pathogens- bacteria)
o Changes occur at site of injury
o Exudate becomes proliferative
o Cycle of cellular infiltration, necrosis, & fibrosis begins
o Repair and breakdown occur simultaneously
o Considerable scarring might occur resulting in permanent tissue damage

Wound Assessment

What caused this wound?

o
Surgical intervention
o
Pressure
o
Venous hypertension
o
Diabetes
o
Burn
o
Trauma
o
Altered vascular supply to limbs

What patient-related factors will impact wound healing? (risk factors)

o
Intrinsic:

Health status/illness

Age & weight

Nutrition

Infection

Impaired circulation

Diabetes

Smoking

Meds (i.e. steroids)

o
Extrinsic:

Mechanical stress

Debris

Environmental temperature

Maceration

Chemicals

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Wound Assessment

What is the anticipated outcome for the wound? Healing time- eyeball and
inside your mouth heal really fast- good blood flow)
o
Healing
o
Maintenance
o
Palliation
Principles of wound care: *not being tested in this class
o
Assess the wound
o
Cleanse the wound
o
Remove necrotic debris
o
Identify & Rx infection
o
Fill the dead space
o
Manage the exudate (get ride of puss/ drainage)
o
Maintain a moist environment
o
Provide thermal insulation
o
Protect the wound healing

Types of wounds (immune to antibiotics)

Primary:
o
Surgical incisions

Pink

Swollen

Small areas of induration

Healing ridge
o
Rx?

Types of wounds (Contd)

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Secondary:
o
Keep wound moist
o
Sterile/clean technique
o
Wet to moist dressing but keep surrounding tissue dry
o
Saline cleanser
o
Gauze dressing

Drains *boot camp

Jackson-Pratt (vacuum suction- mild suction- everything has to be sterileempty when they are 1/2 or 2/3 full- or surgeon will write a specific order)
more we go into open areas the greater risk for infection) examplemastectomy

Hemovac (very similar to Jackson- Pratt) sutured in- tissue might have
grown over top- lots of resistance- might be difficult to pull out)

Penrose (creating a tertiary intention, leave a little "stab wound" open area
so stuff with drain out- shorten daily)

Principles of Surgical Asepsis *not being tested on but expected to know this

A sterile object remains sterile only when touched by another sterile object.
Only sterile objects may be placed on a sterile field
A sterile object or field outside the range of vision is considered contaminated
An object held below a persons waist is considered contaminated
A sterile object or field becomes contaminated by prolonged exposure to air
When a sterile surface comes in contact with a wet contaminated surface the
object or field becomes contaminated by capillary action
Fluid flows in the direction of gravity
The 1 inch edges of a sterile field or container are considered to be contaminated

The Ideal dressing *not being tested on but expected to know

12

Removes excess exudate and toxins

Maintains high humidity at dressing wound interface
Allows for gaseous exchange
Provides thermal insulation
Protects against secondary infection
Free from particulate and toxic compounds
No trauma to wound with removal

See chart on hand out *

Words of wisdom

If its too wet dry it

If its too dry wet it
If its irritated sooth it
If its chronic irritate it

Dressing changes (always follow order- check C&N report)

Assessment
o
Check Drs order
o
Review culture reports
o
Client allergies?
o
Examine the existing dressing

Size & Location & type of dressing

o
Pain scale analgesic required?
o
Clients knowledge
o
Assistance needed?
o
REEDA Redness, Edema, Echymosis, Discharge, Approximation

Dressing changes cont..

Dry
Hydrocolloid
Foams
Irrigation (squirt saline- mini bottles- large ampule)
Moist Dressing
Securing- tape

Tissue Debridement

What is the key factor that would indicate the use of surgical debridement?
o
Infection
o
Presence of a large amount of necrotic tissue
o
Desire to convert a chronic to an acute wound
o
All of the above

Which of the following dressings most effectively support autolytic debridement? (see
your handout)
o
A. gauze
o
B. films/ membranes
o
C. non adherent

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D. hydrocolloid

Which if the following is an acceptable form of mechanical debridement?

o
Wet to dry dressings
o
Scrubbing of wounds
o
Irrigation
o
All of the above
Gauze sponges/ pads

2 x 2
4 X 4
4 X 8
8 X 10 ABD (Abdominal Pad) (thicker/ more drainage)
Advantages absorption of drainage, low cost $$
Disadvantages
o
drainage can seep through the dressing
o
wound may be come macerated if the dressing isnt changed
o
the fibers of the dressing may stick to the wound

Types of dressings see handout

Films/ Membranes
Non Adherent
Foams
Hydrocolloid

Which of the following types of dressings provides an occlusive barrier?

1. Films/ Membranes
2. Non Adherent
3. Foams
4. Hydrocolloid

Which of the following types of dressings sticks minimally to wounds?

14

1. Films/ Membranes
2. Non Adherent
3. Gauze
4. Hydrocolloid

Which of the following types of dressings can absorb the most drainage?

15

1. Films/ Membranes
2. Non Adherent
3. Foams
4. Hydrocolloid