CHAPTER 1 - WOUND/S (PART II)

Define Wound Healing

Normal biological process of the body by which skin or other body tissue/s repair itself after a trauma, as it takes place when the body is trying to achieve anatomical integrity of the injured part in order to restore its full function

Enumerate the types of wound healing

1. Primary Intention / Primary Closure / Primary Union

2. Secondary Intention / Secondary Closure / Secondary Union

3. Tertiary Intention / Delayed Primary Closure / Tertiary Union

Give the definition of Primary Intention / Primary Closure / Primary Union

• Fastest type of closure presenting as a small clean defect with minimal tissue damage & no infection

• healing occurs by approximation of tissue edges with sutures, staples, skin glue (dermabond), or even with tapes (Steri-strips)

Indicate the time frame of Primary Intention / Primary Closure / Primary Union

Heals in 2 weeks with a dense scar within 1 month

Provide the example of Primary Intention / Primary Closure / Primary Union

Surgical incisions, paper cuts, and small cutaneous cuts

Give the definition of Secondary Intention / Secondary Closure / Secondary Union

• extensive injury with considerable tissue loss & severe contamination that appears with separated wound edges

• Healing occurs at the wound bed when the tissue edges cannot be approximated for closure

• Skin or tissue is not enough to pull the edges together (without causing stasis to the area) so visible granulation tissue is formed wherein the resultant scar will be bigger than wounds healed by primary intention

Indicate the time frame of Secondary Intention / Secondary Closure / Secondary Union

Healing time is slower with the restoration of the gap because the wound is kept open for longer time which will render it at high risk of infection

Example of Secondary Intention / Secondary Closure / Secondary Union

Pressure ulcers

Give the definition of Tertiary Intention / Delayed Primary Closure / Tertiary Union

Heavily contaminated injury since there is a need for the wound to be open for a prolonged period of time before wound closure as it requires more connective tissue to heal

Time frame of Tertiary Intention / Delayed Primary Closure / Tertiary Union

Wound is left open for approximately 3-5 days, then it can be closed with wound characteristics similar to primary intention

Example of Tertiary Intention / Delayed Primary Closure / Tertiary Union

Wounds that are kept open to allow drainage & closed at a later time, and a wound that is left open to heal by secondary intention but encounters complications that necessitates debridement followed by the approximation of the wound edges

ACAPSIL

A powder that contains of tiny microspheres that can access all the crevices and areas that would not be touched by traditional bandage type of dressing

ACAPSIL

Intended for use in secondary intention & the 1st part of healing during tertiary intention

ADVANTAGES OF ACAPSIL

• Supports autolytic debridement

• disrupts biofilm

• Remove bacterial toxins

• Supports the immune system in re-establishing the right balance of the inflammatory factors, proteases, & leukocytes on the wound surface to allow wound cleaning & progression into the proliferative healing stage

• It helps the regeneration of the tissue from the wound edges

ACAPSIL

Can work on the entire wound surfaces, but it must cover the entire wound bed up to the wound edges so no spot is left uncovered

ACAPSIL

Wound is cleaned with water (or with 3% Hydrogen peroxide) but not using any form of antiseptic

ACAPSIL

as it helps in the regeneration of the tissue from the wound bed —> it also aids in the granulation & epithelialization process

PHASES OF WOUND HEALING

1. inflammatory phase / lag phase / substrate phase

2. Proliferation phase / fibroplasia phase

3. Maturation phase / remodelling phase

PHASES OF WOUND HEALING

refers to a systematic process of overlapping phases wherein the wound can progress forward and regress back through the phases depending upon the intrinsic & extrinsic forces at work within the patient

INFLAMMATORY PHASE / LAG PHASE / SUBSTRATE PHASE

occurs within the 1st 48-72 hours as it refers to the body’s natural response to injury wherein damaged & dead tissues are cleared out, along with bacteria, and other pathogens or debris

2 RESPONSES OF INFLAMMATORY PHASE / LAG PHASE / SUBSTRATE PHASE

• vascular response

• Cellular response

2 PHASES OF VASCULAR RESPONSE

• primary phase

• Secondary phase

PRIMARY PHASE

Characterized by the following processes that occur at this stage:

• hemostasis

• Vasoconstriction

• Platelet aggregation & degranulation

• Fibrinous clot

• Fibrinolysis

SECONDARY PHASE

characterized by the following processes that occur at this stage:

• venous vasodilation

• Increased vascular permeability

• Lymphatic obstruction

CELLULAR RESPONSE

increased vascular permeability during the inflammatory phase facilitates margination, and extravasation & migration of cellular mediators (macrophages and polymorphonuclear neutrophils / PMN)

PROLIFERATION PHASE / FIBROPLASIA PHASE

• associated with the growth of new tissue that occurs from the 2nd day up to 6 weeks wherein the wound is "rebuilt" with new granulation tissue which is comprised of extracellular matrix & collagen, and a new network of blood vessels develop (process of ANGIOGENESIS)

PROLIFERATION PHASE / FIBROPLASIA PHASE

key elements: net collagen synthesis, increase in wound tensile strength, and scar formation

PROLIFERATION PHASE / FIBROPLASIA PHASE

clinical signs: disappearance of inflammation, wound contraction, itching, and reduction of swelling

PROLIFERATION PHASE / FIBROPLASIA PHASE

• collagen deposition

• Wound contraction

• Epithelialization

COLLAGEN DEPOSITION

fibroblasts deposit a “ground substance” composed mainly of glycosaminoglycans which function to create a scaffold where collagen can be deposited

COLLAGEN DEPOSITION

starts on the 3rd - 4th day wherein net collagen increases in a linear fashion (positive) until the 21st day, and reaches its maximum 60 days pos-injury in which it has 80% tensile strength of normal skin

COLLAGEN

is the principal building block of connective tissue by being the main contributing factor in tensile strength, & comprises 1/3 of the total body protein content

WOUND CONTRACTION

wound heals from side to side but contracts from end to end, as edges of the wound move towards the center to close the wound

WOUND CONTRACTION

characterized by a slight tightness or itchiness as the tissue heals which indicates the wound is ready to enter the maturation phase & presents a reduction of wound size or normal movement (average: 0.6 - 0.75 mm/day)

WOUND CONTRACTION

speed of contraction depends on the following:

• laxity of tissues (wounds on the buttocks contract faster than scalp wounds) and

• wound shape (square wounds contract faster than round wounds)

WOUND CONTRACTION

begins approximately on the 4th - 5th day after injury and the highest rate of wound contraction is on the 10th - 21st day (average: 12-15 days & may be longer if the wound remains open)

EPITHELIALIZATION

requires de-differentiation, mitosis, migration, and then re-differentiation by the basal cells of the epidermis

EPITHELIALIZATION

• when proper healing progresses and epithelial cells arise is a process known as epithelialization

SCAB

is a crust that is formed by the coagulation of blood, pus, & serum on the surface of a wound that gradually falls off for epithelialization to occur

MATURATION PHASE / REMODELLING PHASE

final phase that occurs once the wound has closed (3d week & may last up to 1-2 years upon injury with the remodeling of collagen from type III to type I)

MATURATION PHASE / REMODELLING PHASE

duration is dependent on several FACTORS:

• duration of the inflammatory phase

• type of wound

• location of the wound

• race of the patient

• age of the patient

FACTORS THAT INFLUENCE WOUND HEALING

I. LOCAL FACTORS

• Oxygenation

• Infection

• Foreign body

• Venous insufficiency / venous stasis

• Large defect / poor wound closure

• Tissue tension

• Temperature

II. SYSTEMIC FACTORS

• age

• Sex hormones

• Stress

• Ischemia

• Diseases (e.g., Diabetes, hereditary healing disorders, keloids, etc.)

• Obesity

• Medications (e.g., glucocorticoids / glucocorticosteroids, non-steroidal anti-inflammatory drugs or NSAID, chemotherapeutic drugs, etc.)

• Alcoholism & smoking

• Nutrition

• Immunocompromised conditions

LOCAL FACTORS

• extrinsic & intrinsic factors that directly influence the characteristics of the wound itself

FACTORS THAT INFLUENCE WOUND HEALING (LOCAL FACTORS)

1. Oxygenation

2. Infection

3. Foreign Body

4. Venous Insufficiency/Venous Stasis

5. Large Defect/Poor Wound Closure

6. Tissue Tension

7. Temperature

OXYGENATION

Critical for all processes of wound healing

OXYGENATION

Healing is impaired when oxygenation is not restored

OXYGENATION

• temporary hypoxia after the injury —> triggers wound healing

• prolonged or chronic hypoxia —> delays healing

INFECTION

• decontamination & debridement of a wound hastens the healing process

• Absence of decontamination —> inflammation is prolonged due to incomplete microbial clearance

FOREIGN BODY

presence of a foreign body —> hinders the healing process & infection is likely to proliferate

VENOUS INSUFFICIENCY/VENOUS STASIS

inadequate flow of blood in the veins result to edema —> which delays wound healing

LARGE DEFECT/POOR WOUND CLOSURE

• wounds with large surface areas —> will experience prolonged healing

• Failure in proper wound closure —> will also postpone the healing process

TISSUE TENSION

• abnormal tension (i.e., blanching) affects the quality, aggregation, and orientation of the collagen fibers —> resulting in delayed healing

TEMPERATURE

• temperature controls the rate of chemical & enzymatic processes occurring within the wound including metabolism of cells & tissues engaged in the repair process

• Frequent dressing changes & wound cleansing —> promotes wound healing

FACTORS THAT INFLUENCE WOUND HEALING (SYSTEMIC FACTORS)

• refers to the overall health or diseases state of the individual that affects his/her ability to heal

FACTORS THAT INFLUENCE WOUND HEALING (SYSTEMIC FACTORS)

1. Age

2. Sex hormones

3. Stress

4. Ischemia

5. Diseases (e.g., diabetes, hereditary healing disorders, keloids, etc.)

6. Obesity

7. Medications (e.g., glucocorticoids/glucocorticosteroids, non-steroidal anti-inflammatory drugs or NSAID, chemotherapeutic drugs, etc.)

8. Alcoholism & Smoking

9. Nutrition

10. Immunocompromised Conditions

AGE

increases in age (> 60 years old) is a risk factor —> for impaired wound healing

SEX HORMONES

• estrogen has a more positive effect on wound healing compared to androgen

*note: estrogen acts on the cell lysis to modulate all stages of the healing process

STRESS

• stress has a great impact on human health since most disease such as cardiovascular disease, cancer, & diabetes have been associated with stress

• dysregulation of cytokines occur during stress —> disrupting the wound healing process

• Stressors such as anxiety & depression must be avoided for proper healing

ISCHEMIA

sufficient blood flow must be restored for healing to take place

DISEASES (e.g., diabetes, hereditary healing disorders, keloids, etc.)

• diabetic patients exhibited documented impairment in the healing of acute wounds

• keloids can be prevented (through corticosteroid injection & silicone elastomer sheeting) but once keloids are established, it can be difficult to treat due to its high recurrence rate regardless of therapy

OBESITY

obese individuals frequently face wound complications including infection, dehiscence, hematoma, serum formation, and pressure & venous ulcers

MEDICATIONS

Some medication have the capacity to affect wound healing since they may interfere with clot formation, inflammatory responses, and cell proliferation

glucocorticoids or glucocorticosteroids

inhibit wound repair

short-term NSAIDs (e.g., ibuprofen)

have a negative effect on healing and must be discontinued for a time equal to 4-5 times the drug’s half-life (8-10 hrs.) before surgery

chemotherapeutic drugs

hinder cells metabolism, angiogenesis, & rapid cell division which are critical for appropriate wound repair

ALCOHOLISM & SMOKING

• exposure to alcohol impairs wound healing & increase the incidence of infection

• smokers show a delay in wound healing & an increase in a variety of complications that include:

  • infection

  • Rupture

  • Wound/flap necrosis

  • Epidermolysis

  • Anastomotic leakage

  • A decrease in the tensile strength of the wound

NUTRITION

• deficiencies in the following wound impair would healing:

  • proteins

  • Carbohydrates

  • Glutamine (most abundant amino acid in plasma)

  • Arginine (semi-essential amino acid that improves immune function)

  • Polyunsaturated fatty acid

  • Vitamins A, C, E

  • magnesium

  • Copper

  • Zinc

  • Iron

PROTEIN

most important nutrient that affects wound healing

COLLAGEN

is the major protein component of connective tissue

IMMUNOCOMPROMISED CONDITIONS

these patients are prone to varying levels of infection that prevent optimal wound healing

TISSUE TYPE CATEGORIES OF WOUND HEALING

1. Necrotic Tissue

2. Sloughy Tissue

3. Granulation Tissue

4. Epithelializing Tissue / Epithelizing Tissue

NECROTIC TISSUE

• unsalvageable, non-viable, devitalized tissue that is synonymous with dead tissue

• appears black or dark brown in color and is usually dry with thick, firm, leather-like tissue that cast off/shed off/ fall off (known as ESCHAR) from the surface of the wound

• Certain cells in or one part of the wound die off —> either due to infection, diseases, or age

NECROTIC TISSUE

SLOUGHY TISSUE

GRANULATION TISSUE

EPITHELIALIZING TISSUE / EPITHELIZING TISSUE

soft, blood-rich tissue composed of a series of tightly-packed cells and slowly grows over the granulation tissue that provides the protective layer over the entire body

COMPLICATIONS OF WOUND HEALING

1. Infection of the Wound

2. Wound Dehiscence / Flap Dehiscence / Wound Disruption

3. Incision Hernia

4. Abnormal Scar Formation (e.g., keloids, hypertrophic scars, widespread scars, and atrophic scars)

5. Wound Contracture

INFECTION OF THE WOUND

WOUND DEHISCENCE / FLAP DEHISCENCE / WOUND DISRUPTION

INCISIONAL HERNIA

• breakdown of the deeper layers of the wound in which the skin is intact with the protrusion of the underlying structure through the deeper defect

INCISIONAL HERNIA

• Cause/s: could be due to excessive tension on the suture line, suture breakage, and knot slippage

• Treatment: surgery to reapproximate the edges of the wound

ABNORMAL SCAR FORMATION

• proliferation of abnormal scar tissue that forms at the sire of the injury

*SCARS

Are characterized by the accumulation of excess collagen with decreased lysis and are distinguished from each other by their appearance

COMMON TYPES OF ABNORMAL SCAR FORMATION

• keloids

• hypertrophic scars

• Widespread scars

• atrophic scars

KELOIDS

Definition: elevated fibrous scars that grow beyond the borders if the original wound due to an abnormality in collagen metabolism (i.e., over healing)

KELOIDS

Characteristics: does not tend to resolve spontaneously & may either contribute to enlarge after 6 months from the time of injury, or can appear months (or even 1 year) following the injury)

KELOIDS

Causes: exact cause remains unclear, but biological factors have shown to contribute to keloid development such as overproduction of certain growth factors & multiple fibroblast proteins

KELOIDS

Treatment: corticosteroid injections or application of silicone gel sheets on the surface of the scar

KELOIDS

Familial predilection: significant incidence

HYPERTROPHIC SCARS

definition: scars that stay within the limit of the wound borders (raised or elevated borders) and it is generally seen soon after tissue injury, especially with a contracture across a joint surface where the Langer’s lines were crossed by the incision

HYPERTROPHIC SCARS

characteristic/s: tends to regress with time

HYPERTROPHIC SCARS

cause/s: may be attributed to poor suturing techniques where the edges of the wound are overlapping instead of accurately supposed

HYPERTROPHIC SCARS

non-progressive after 6 months, but treatment can only be attempted after 6 months (which involves the excision of the scar tissue & re-suturing of the wound or through corticosteroid injections)

HYPERTROPHIC SCARS

familial predilection: low incidence

WIDESPREAD SCAR

definition: scars with borders that are flat, wide, & depressed

WIDESPREAD SCAR

characteristic/s: may or may not regress over time

WIDESPREAD SCAR

Cause/s: results from the gradual stretching of fine lines which starts to take place a few weeks after surgery

WIDESPREAD SCAR

appear 6 months after the injury and various treatments include microdermabrasion, exfoliation, laser therapy (which stimulates collagen), etc.

WIDESPREAD SCAR

familial predilection: absent/no inheritance pattern

ATROPHIC SCARS

definition: flat, depressed, generally small & round scars, with an indented or inverted center compared to the surrounding area of skin