Chapter 9 Inflammation & Dysfunctional Wound Healing

Complications of Wound Healing

• Keloid Formation

• Contractures

• Dehiscence

• Evisceration

• Stricture

• Fistula

• Adhesions

Kites Catch Drift Easily, Soaring Far Above

Complications of Wound Healing:

Keloid Formation

Excessive collagen causes thick scar tissue.

Complications of Wound Healing:

Contractures

Excessive tightening of tissue leads to limited movement.

Complications of Wound Healing:

Dehiscence

Wound reopens after partial healing.

Complications of Wound Healing:

Evisceration

Internal organs protrude through a wound.

Complications of Wound Healing:

Stricture

Narrowing of a tubular structure (e.g., esophagus).

Complications of Wound Healing:

Fistula

Abnormal connection between organs or tissues.

Complications of Wound Healing:

Adhesions

Bands of scar tissue form, connecting tissues that shouldn’t be connected.

Pathophysiology of Fever

Releases pyrogens (substances that cause fever, i.e. cytokines, microbial organisms, etc.)

• Causes hypothalamus to raise body’s temperature set point

Risks of Fever

Can lead to febrile seizures in children

Dehydration

Excessive tissue damage in prolonged fever

Medications That Reduce Fever

Aspirin

• NEVER GIVE CHILDREN ASPIRIN FOR FEVER

Ibuprofen (Tylenol)

Acetaminophen (Advil, Motrin)

Primary Intention

Cleanly lacerated, clear wound edges, and easily brought together

• e.g., surgical incision

Minimal scarring; easy healing

Simple epithelialization

• Within 5 days (granulation tissue)

• Within 30 days (CT covered by an intact epidermis)

Secondary Intention

Abundant granulation and fibrotic tissue formation

• To replace and restore structure of tissue

Regeneration takes longer; needs new tissue

• Myofibroblasts

  • CT cells that cause contraction

• Increased risk for scarring

Highly susceptible to

• Infection

• Complications

• Deformity

NOTE:

• Regeneration of same cells to replace lost tissue is NOT possible

Tertiary Intention

Missing large amounts of deep tissue

Delayed closure due to infection or other factors

• Cleaned and left open (4-5 days)

• Pack with sterile gauze

• 5th day

  • Phagocytosis of contaminated tissue

  • Epithelialization

  • Collagen deposition

  • Maturation

• Prominent scarring

  • Skin graft needed

Four Phases of Wounding Healing

1. Hemostasis

2. Inflammatory Phase

3. Proliferation Phase

4. Maturation/Remodling Phase

Hemostasis

Exposed collagen of injury

• Attracts platelets

Platelets aggregate

• To secrete inflammatory mediators

Vasoactive amines

• Cause short-term vasoconstriction

Inflammatory Phase

WBCs clear debris and fight infection

Vasodilation, increased vascular permeability, & chemotaxis

5 Cardinal Signs of Inflammation

• Redness (Rubor)

• Heat (Calor)

• Swelling (Tumor)

• Pain (Dolor)

• Loss of function (Functio laesa)

(Should review acute and chronic inflammation later)

Proliferation Phase

Fibroblasts (a CT tissue)

• Synthesizes collagen

• 24 - 48 hrs, forms granulation tissue for foundation of scar tissue

• Wound contraction (due to shortening of fibroblasts)

Creation of new BV (Angiogenesis)

• Granulation tissue Secretes VEGF (vascular endothelial growth factor)

Epithelial cells (Epithelialization)

• Migrate and proliferate to fill wound gap

Maturation/Remodeling Phase

Scar tissue is structurally refined and reshaped by fibroblasts and myoblasts

• Takes ~3 weeks after injury to start remodeling

Factors That Affect Wound Healing

Nutrition: + nitrogen balance (vitamins also)

Oxygen: Facilitates collagen synthesis and WBC function

Circulation: Helps remove waste

Immune strength: Stronger immune system = better

Infection: Single most significant factor in delayed wound healing

Foreign bodies: Debris in wound

Mechanical factors: Torsion, localized pressure, mechanical stress

• Make sure to reposition every 2 hours

Age: Older adults having slowest healing process

“Never Overlook Clever Ideas If Fun Moments Arise”

What Stimulates Histamine Release

• Physical injury

• Immune reactions

• Cytokines

• Other inflammatory mediators

Histamine is Produced by

• Basophils

• Platelets

• Mast cells (richest source)

Systemic Effects of Histamine

• Arteriolar vasodilation

• Large artery vasoconstriction

• Increased permeability of venules

Ex. Responses if histamine released in upper respiratory tract)

• Sneezing

• Runny nose

• Pharyngeal irritation

COX-1 Prostaglandins Pathway

Breaks down arachidonic acid enzymatically into helpful PGs

• Stimulate gastric mucus production

  • To protect gastric mucosa

• Enhance renal perfusion

• Assist platelets to aggregate and form clots

  • (thrombus formation)

COX-2 Prostaglandin Pathway

Yields harmful PGs

• Perpetuate inflammation

  • Causing

    • Pain

    • Fever

    • Swelling

    • Muscle contractions

  • Potentiate effects of other inflammatory mediators