2) WOUND HEALING

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

1) PRIMARY INTENTION / PRIMARY CLOSURE / PRIMARY UNION
2) SECONDARY INTENTION / SECONDARY CLOSURE / SECONDARY UNION
3) TERTIARY INTENTION / DELAYED PRIMARY CLOSURE / TERTIARY UNION

TYPES OF WOUND HEALING

PRIMARY INTENTION / PRIMARY CLOSURE / PRIMARY UNION

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

PRIMARY INTENTION / PRIMARY CLOSURE / PRIMARY UNION

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

PRIMARY INTENTION / PRIMARY CLOSURE / PRIMARY UNION

• time frame: heals in 2 weeks with a dense scar within 1 month

• examples: surgical incisions, paper cuts, and small cutaneous cuts

SECONDARY INTENTION / SECONDARY CLOSURE / SECONDARY UNION

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

SECONDARY INTENTION / SECONDARY CLOSURE / SECONDARY UNION

- healing occurs at the wound bed when the tissue edges cannot be approximated for closure

SECONDARY INTENTION / SECONDARY CLOSURE / SECONDARY UNION

- 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

SECONDARY INTENTION / SECONDARY CLOSURE / SECONDARY UNION

- time frame: healing time is slower with the restoration of the gap because the wound is kept open for a longer time which will render it at high risk of infection

- example: pressure ulcers

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

TERTIARY INTENTION / DELAYED PRIMARY CLOSURE / TERTIARY UNION

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

TERTIARY INTENTION / DELAYED PRIMARY CLOSURE / TERTIARY UNION

- examples: 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 consists of tiny microspheres that can access all the crevices and areas that would not be touched by a traditional bandage type of dressing

ACAPSIL

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

ACAPSIL

advantages: supports autolytic debridement; disrupts biofilm; removes 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; and it helps the regeneration of the tissue from the wound edges

ACAPSIL

can work on the entire wound surface, 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

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

I. INFLAMMATORY PHASE / LAG PHASE / SUBSTRATE PHASE
II. PROLIFERATION PHASE / FIBROPLASIA PHASE

III. MATURATION PHASE / REMODELLING PHASE

PHASES OF WOUND HEALING

HEMOSTASIS

excluded from the 3 phases, but others believe that it is the 1st phase of wound healing

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

1) PRIMARY PHASE
2) SECONDARY PHASE
3) CELLULAR RESPONSE

VASCULAR RESPONSE

PRIMARY PHASE

characterized by the following processes that occur at this stage: hemostasis, vasoconstriction, platelet aggregation & degranulation, fibrinous clot, and fibrinolysis

SECONDARY PHASE

characterized by the following processes that occur at this stage: venous vasodilation, increased vascular permeability, and 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

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 post-injury in which it has 80% tensile strength of normal skin

COLLAGEN

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)

laxity of tissues (wounds on the buttocks contract faster than scalp wounds) and wound shape (square wounds contract faster than round wounds)

speed of contraction depends on the following:

WOUND CONTRACTION

- begins approximately on the 4th - 5th day after injury and the highest rate of wound contraction is on the 10th - 21s 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

SCAB

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)

A) duration of the inflammatory phase

B) type of wound

C) location of the wound

D) race of the patient

E) age of the patient

duration is dependent on several FACTORS IN MATURATION PHASE / REMODELLING PHASE

LOCAL FACTORS

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

OXYGENATION

- critical for all processes of wound healing

- healing is impaired when oxygenation is not restored

triggers wound healing

- temporary hypoxia after the injury →

delays healing

- prolonged or chronic hypoxia →

INFECTION

- decontamination & debridement of a wound hastens the healing process

- absence of decontamination → inflammation is prolonged due to incomplete microbial clearance

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

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

SYSTEMIC FACTORS

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

AGE

- increase 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

estrogen

acts on the cell types to modulate all stages of the healing process

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

- diabetic patients exhibit 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 medications 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 cell metabolism, angiogenesis, & rapid cell division which are critical for appropriate wound repair

ALCOHOLISM & SMOKING

exposure to alcohol impairs wound healing & increases the incidence of infection

ALCOHOLISM & SMOKING

smokers show a delay in wound healing & an increase in a variety of complications that include: infection, rupture, wound / flap necrosis, epidermolysis, anastomotic leakage, and a decrease in the tensile strength of the wound

NUTRITION

deficiencies in the following would impair wound healing: proteins, carbohydrates, glutamine (most abundant amino acid in plasma), arginine (semi-essential amino acid that improves immune function), polyunsaturated fatty acids, vitamin A, vitamin C, vitamin E, magnesium, copper, zinc, and iron

PROTEIN

the most important nutrient that affects wound healing

COLLAGEN

the major protein component of connective tissue.

IMMUNOCOMPROMISED CONDITIONS

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

NECROTIC TISSUE

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

NECROTIC 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

NECROTIC TISSUE

- certain cells in or on one part of the wound die off → either due to infection, diseases, or age

scab

forms on top of a wound and is evidence of wound healing.

Eschar

a collection of dead tissue within the wound and indicates full thickness tissue loss.

SLOUGHY TISSUE

- type of necrotic tissue that is often seen as tissue that is loose & stringy as it separates itself from the wound site

SLOUGHY TISSUE

- most (if not all) of the tissue is dead, usually moist, & appears white, cream / tan, yellow, green, or gray

GRANULATION TISSUE

- polar opposite of necrotic tissue wherein new connective tissue is created as the surface area is healing from a wound or injury

GRANULATION TISSUE

- refers to the normal process of healing where new connective tissue & microscopic blood vessels typically start to grow at the base of the wound and it is able to fill wounds of almost any size

GRANULATION TISSUE

- typically presents a shiny & moist surface that is bumpy or granular in appearance

GRANULATION TISSUE

- color & condition of the granulation tissue is an indicator of how the wound is healing: healthy granulation tissue does not bleed easily & appears pink / red in color, while dark granulation tissue is indicative of poor effusion, ischemia, and / or infection

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

INFECTION OF THE WOUND

- invasion or entry of harmful microorganisms (such as pathogens) into a wound resulting in a superficial wound infection, deep wound infection, or mixed wound infection (e.g., gangrene)

INFECTION OF THE WOUND

- cause/s: may be attributed to incorrect aseptic techniques during the three phases of surgery (i.e., preoperative, intraoperative, & postoperative phase); lack of prophylactic antibiotics, improper wound care; and environmental issues - treatment would include incision & drainage, empirical therapy, and antibiotic packs

WOUND DEHISCENCE / FLAP DEHISCENCE / WOUND DISRUPTION

- refers to the separation of the layers of a surgical wound wherein there is total breakdown of the edges of a wound after surgical repair

WOUND DEHISCENCE / FLAP DEHISCENCE / WOUND DISRUPTION

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

- treatment involves surgery to reapproximate the edges of the wound

INCISIONAL HERNIA

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

INCISIONAL HERNIA

- cause/s: infection, improper surgical or suturing techniques, and poor wound care

- treatment options include surgery or the use of a piece of garment that applies constant pressure to the wound (known as TRUSS)

ABNORMAL SCAR FORMATION

- proliferation of abnormal scar tissue that forms at the site of the injury

SCARS

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

KELOIDS

- definition: elevated fibrous scars that grow beyond the borders of the original wound due to an abnormality in collagen metabolism (i.e., overhealing)

KELOIDS

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

KELOIDS

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

- treatment utilizes corticosteroid injections or application of silicone gel sheets on the surface of the scar

- 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 apposed

- 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)

- 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

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

- familial predilection: absent / no inheritance pattem

ATROPHIC SCARS

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