Surg Med - Wound Care - Exam 2

Inflammatory Wound Healing

Days 1-6

Chemoattractant release

Phagocytosis

Removal of foreign bodies and bacteria

Proliferative Wound Healing

Days 4-21

Fibroblast proliferation

Provisional ECM synthesis

Granulation tissue formation

Re-epithelialization

Remodeling Wound Healing

3 weeks to 2 years

Type I collagen accumulation

Crosslinking of collagen

Scar tissue formation

Increase in tensile strength

Optimizing Scar Quality

Tension reduction

Layered closure

Moist wound environment

Avoid infection and ischemia

Use appropriate dressings and sun protection

Optimize nutrition and systemic health

Massage after healing (remodeling phase)

Optimal Healing - Necessities

Well vascularized wound bed

Free of devitalized tissue

Minimal bacterial burden

Controlled exudate, moist environment

Healthy granulation tissue

Wound Dressings

Eliminate dead space

Control exudate

Prevent bacterial growth

Ensure proper fluid balance

Demonstrate cost-efficiency

Manageable for the patient/support staff

Partial Thickness Wound

Loss of epidermis +/- some dermis

Stage 2 pressure ulcer, blister, skin tear

No slough – heal through epithelialization rather than granulation tissue

Less scarring

Full Thickness Wound

Loss of epidermis, dermis, and subcutaneous tissue and/or deeper

Requires granulation/contraction

Higher infection risk

Often needs advanced closure/grafting

Local Factors - Impaired Wound Healing

Infection/Debris/Foreign Body

Tension

Mechanical stress/pressure

Ischemia

Necrotic tissue

Systemic Factors - Impaired Wound Healing

Diabetes

Smoking/nicotine

Malnutrition

Steroids/Immunosuppression

Obesity

Vascular Disease

Renal failure

PostOp Wound Care - Assessment

Is the wound intact?

Drainage?

Erythema?

Pain out of proportion?

Fever?

Fluctuance?

Necrosis?

PostOp Wound Care - Dressing

Keep clean

Moist, but not macerated

Avoid unnecessary dressing changes

24-48 hours

Immediate postop dressing often left intact _______

Wound Dehiscence

Partial or complete disruption of any or all layers of the operative wound

Wound Dehiscence Local Factors

Inadequate closure - easiest modifiable factor

Fascial layers are strength layers!

Increased pressure

Deficient wound healing

Anything that disrupts healing - i.e., seromas, hematomas,

5-8d

wound dehiscence most commonly occurs _______ post-op (when the strength of the healing tissue is at a minimum)

Venous Stasis Ulcer

Caused by chronic venous hypertension and inflammation

Appearance: shallow, irregular ulcer with moderate to heavy exudate, warm, painful, pruritic

Venous Stasis Ulcer - Associations

hemosiderin staining

stasis dermatitis

"champagne leg"

lipodermatosclerosis

Venous Stasis Pathophys

Valve failure → venous reflex → tissue congestion + hypoxia

Leads to inflammation and ulceration

Worsened by protein-rich fluid buildup and trauma

Venous Stasis Ulcer Tx

Control Edema

Use dressings that wick moisture away from the wound and break down wound debris

Pneumatic (lymphedema) compression pumps

Investigate for infection

Optimize comorbid conditions

weight-bearing

diabetic ulcers are most common on _________ surfaces

Diabetic Ulcers

may be small at the surface but have large subcutaneous dead space and possible bone involvement

Higher risk for osteomyelitis, thus, amputation

X-ray – not positive in early disease

Follow up with MRI or CT if wound has been present >4 weeks

WG1

superficial ulcer

WG2

deep structure involvement WITHOUT infection

WG3

deep structure involvement with infection: abscess, osteomyelitis

WG3/4

deep structure invovlement/abscess/osteomyelitis and eschar

Diabetic Ulcer Tx

Blood sugar control is essential (120-140 mg/dL)

Debride callus

Often complicated by small vessels disease

First 4 weeks are critical

Actively reassess during this time – don’t delay care

Consider hyperbaric O2 therapy for Wagner grade 3-4

Total Contact Cast → Gold Standard for offloading DFUs

Stage 1 Decubitus Ulcer

Non-blanching erythema of intact skin

Edema

Lightly Pigmented

Deeply Pigmented

Transparent film for protection

Stage 2 Decubitus Ulcer

Partial-thickness skin loss exposing the dermis

Semi-occlusive (transparent film) or occlusive dressing (hydrocolloid or hydrogel) so that any necrotic tissue that is present is digested by enzymes normally present in wound base

Stage 3 Decubitus Ulcer

Full-thickness skin loss

Wet-to-Dry dressings for light debridement; generally require debridement and possibly treatment of infection; necrotic tissue promotes bacterial growth and impairs wound healing

Stage 4 Decubitus Ulcer

Full-thickness skin loss w/ exposed or palpable fascia, muscle, tendon, ligament, cartilage, or bone

Wet-to-Dry dressings for light debridement; generally require debridement and possibly treatment of infection; necrotic tissue promotes bacterial growth and impairs wound healing

Deep Tissue Injury

Intact or Non-Intact skin with persistent non-blanchable deep red or purple discoloration or bruising

Unstageable Decubitus Ulcer

Full-thickness skin and tissue loss, but damage cannot be confirmed due to slough or eschar

Decubitus Ulcer Tx

Reduce Pressure, but prevent new injury

Control infection

Improve nutritional status

General principles - debridement and dressings/wound packing

PM&R referral

Film Dressings

Dry to minimally exudative wounds

Allows oxygen in, moisture out, and visual inspection of wound

Tegaderm

Hydrocolloids

For low to moderate exudate

Occlusive, retains moisture, promotes autolytic debridement

Hydrogels

Used on dry/dessicated wound to add moisture to wound bed

Options: No additives, Silver impregnated, Collagen impregnated

Alginates

Reacts with wound exudate and forms a hydrophilic gel → can cause maceration due to heavy drainage

Stimulate macrophage activity +/- silver for antimicrobial properties

Can be a very soft dressing choice for tender wounds

minimal exudate

do not use alginates with wounds that have what?

Foams

For moderate to high exudate

Gentle on surrounding skin

Absorptive dressings/powders

For heavy to copious drainage/significant exudate

Also, when dressing change frequency must be reduced

Nonadherent Gauze

Minimize trauma during removal

Lightly exudative wound

topical abx

Not universally recommended for all wounds – overuse can be harmful

Can be used for:

Mild local wound infxns (superficial abrasions, minor lacs)

Prevention of infection in clean, superficial wounds

Colonized wounds at risk for infection, especially in high-risk patients (e.g., diabetics)

Contaminated surgical wounds or wounds healing by secondary intention

Bacitracin

Gram positive (especially staph)

Sufficient for most minor wounds

Neomycin

Gram negative

Common allergen - delayed hypersensitivity reactions

Polymyxin B

Gram negative

Often combined with bacitracin/neomycin

Mupirocin

MRSA, Gram positive

Good for infected/colonized wounds

Silver Sulfadiazine

Broad spectrum (esp burns)

Use limited to burns and high-risk wounds

enzyme debriding agents

Topical medications that chemically break down necrotic or devitalized tissue to help clean a wound bed

enzyme debriding agents - purpose

Remove nonviable tissue

Reduce bacterial burden

Promote granulation tissue formation

Support progression toward healing

Collagenase

Breaks down collagen in necrotic tissue

Selectively digests devitalized tissue

Preserved more healthy tissue than sharp debridement

Enzyme Debriding Agents - Indications

Chronic wounds with necrotic tissue

Pressure injuries

Diabetic ulcers

Patients who are poor surgical candidates

Patients unable to tolerate sharp debridement

maggot therapy

Form of biodebridement using live, sterile larvae to clean, non-healing wounds

Helps when sharp debridement is CI

CI with exposed blood vessels/bleeding risk or pyoderma gangrenosum

Growth Factors

Biologically active proteins that stimulate cell migration, proliferation, and tissue regeneration

Helps "jump start" healing cascade in a stalled wound

Clean, non-infected wounds (infxn inhibits effectiveness)

Patients with good offloading, perfusion, and glucose control

Regranex

Platelet Derived Growth Factor (PDGF)

Used for diabetic foot ulcers, full thickness, lower extremity

Apply daily, requires moist wound bed

Apligraf, Dermagraft

Contain multiple growth factors via bioengineered skin substitutes

Used for chronic venous ulcers, diabetic foot ulcers

Costly, used in refractory cases

Platelet-Rich Plasma (PRP)

Autologous platelets

Off-label use in wound and surgical healing

Still being studied; mixed results

Bioengineered Skin Substitutes

Bottom layer (dermal) is made of a fibrous protein material (collagen) from cows and a substance made from shark cartilage

Top layer (epidermal) is made of silicone

Allows blood vessels and other cells to grow a new layer of skin while the collagen is absorbed into the body

Silicone layer helps close the wound and prevent fluid loss

Negative Pressure Wound Therapy

Applies continuous negative pressure (commonly ~125 mmHg) to the wound bed

Promotes granulation tissue formation and angiogenesis

Removes exudate and decreases wound/periwound edema

Assists with wound contraction and may decrease wound healing time

Hyperbaric Oxygen Therapy

Patient lies in hyperbaric chamber set at 2.0-2.4 ATMS and 100% O2 concentration for approx 2 hours

First 20 minutes spent bringing the patient to desired pressure (2x atmospheric pressure)

Two 5 min normal air breaks

Usually requires daily treatment for at least 20 treatments

Electrical Stimulation

Mimics natural bio-electric system of healing

Chronic wounds with stalled healing despite standards of care

CI in malignancy, osteomyelitis, presence of electrical implants, over carotid sinus, or pregnant uterus

Electrical Stimulation - MOA

Increased blood flow and tissue perfusion

Stimulation of fibroblast and epithelial cell migration

Promotion of angiogenesis

Inhibition of bacterial growth

Enhanced collagen synthesis and granulation tissue formation