Foundations of Wound and Skin Care Flashcards
Epidermis Cell Types and Function
- Kertainocytes: protein keratin filaments, most abundant; at surface
- Langerhans: Monocyte (WBC) turn into Macrophages
- Melanocytes: skin pigment
- Merkel Cell: Mechanosensory receptors for pressure; located on epidermis/dermis interface
What layer of the skin do blisters form? Where is this layer located around the body?
- Layer: Stratum Lucidum
- Located in Lips, Palms, Soles
Epidermal Skin Layers
- Straum Cornium: Stratified Outer Layer with flattened cells overlapping
- Stratum Lucidum: Clear/translucent layer that resist shearing
- Stratum granulosum: layer of granules containing a variety lipids, permeability layer between cells
- Strautum Spinosum: layers of keratin, which flatten to form granules
- Stratum basale/germinativum: basal/germinal layer of cells connecting to dermis and pushes cells towards surface forming fingerprints/footprints.
Epidermis
- Rapid regeneration
- Retains moisture
- Functional barrier
Dermis
- Cutaneous vasculature
- Nutrition to epidermis
- Matrix for fibroblasts
- Struture support for skin
Dermis - Cell Types
- Macrophages (eat necrotic tissue)
- Mast cells
- Fibroblasts (make new tissue)
Subcutaneous Fucntion
- Vascularization to skin/body
- Insulation
Subcutaneous Tissue Cell Types
- Vascular plexus
- Lymphatics
- Adipose tissue
Wound definition
An interruption in the continuity of bodily structures
Wound Classification - Intention
- 1st intention: incised - no tissue loss: epithelization
- 2nd intention: incised - tissue loss: regeneration
- 3rd intention: trauma - structural loss: replacement
What are the 3 phases of wound healing?
- Phase 1: Inflammatory Phase (1-4 days)
- Phase 2: Proliferative Phase (4 days to 11 months)
- Phase 3: Matrix Formation - Remodeling phase (30 days - 2 years)
Phase 1,2 and 3 require what type of interventions?
- Phase 1: Debridement and/or cleaning and compression
- Phase 2: ROM to promote circulation
- Phase 3: Stretching tissue
As soon as one phase gets to the middle the ____ begins.
next phase; therefore there is overlap
Cells interact with their environment (extracellular matrix) through cell surface receptor proteins or ____
cell adhesion molecules (CAMs)
CAMs are cells that glob to help seal wounds
Receptors bind extracellular proteins known as…
ligands
Cell Biology Initiates signal transduction to upregulate or down regulate ____
mRNA (transcription)
Cell biology regulated ____ production (translation)
protein
4 types of ligands:
- Cytokines
- Growth Factors
- Hormones
- Chemokines (Chemotaxis = migration)
____ can be put into wounds to help spead up the healing process.
Growth factors
Cardinal Signs
Inflammatory Phase 1
Calor: Increased Temp
Dolor: Pain
Rubor: Erythema (Redness)
Tumor: Swelling
Loss of Function
An infection =
prolonged inflammatory phase
Sign of infection would be an increase in Cardinal Signs
Cellular Reaction - Hemostasis
Inflammatoy Phase 1
Hagemann Factor XII
* Turns Prothrombin -> Thrombin
* Turns Fibrinogen -> Fibrin
Scab Formation (Eschar)
* Platelets are the first cells to arrive to injury site
* Platelets release Serotonin to create Vasoconstriction
* Platelet produces platelet derived growth factor (PDGF) that forms the Fibrin clot (platelet plug)
* Fibrin clot acts as the protection layer for early repairs (leukocytes, endothelial cells, fibroblasts and smooth muscle cells bind)
* Endothelial cells restructure the fibrin matrix producing Matrix Matalloproteases (MMP’s) and plasmin for fibrinolysis (break down fibrin)
Matrix Metalloproteinases (MMPs)
- Normal response to healing
- 26 zinc-dependent proteolytix enzymes produced by neutrophils, macrophages, fibroblasts, endothelial cells
- Degrade proteins (collagen and growth factors)
- High levels in chronic wounds, contribute to “biofilm” causing tissue breakdown and chronic inflammation
- Regulated by Tissue Inhibitors of Metalloproteinases (TIMPs) which can be insufficent in chronic wounds
Vascular Reaction
Inflammatory Phase 1
- Vasocontriction: Platelets release serotonin (Stop Bleeding)
- Vasodialation: Mast Cells release Histamine (Get rid of debre)
- Edema (Transudate and Exudate)
Transudate
- Clear
- Ex: Blister Fluid
Exudate
- Protein (albumin) and leukocytes (viscous)
- Yellow
Cellular Reaction - Phagocytic
- Prerequisite for healing
- Initiated during the first 24-48 hours and lasts up to 2 weeks
- Purpose: Remove foreign bacteria material, damaged cells, dead tissue
PTs do this through debridement
Polymorphonuclear leukocytes - Cellular Reaction
- 48 to 72 hours
- Neutrophils: release enzymes for autolytic debridement
- Eosinophils: phagocytic; WBC
- Mast Cells: release histamine to create VD and produce chemokines for neutrophil migration to site of injury
Autolytic debridement
- Neutrophils do this!
- Funtion: Phagocytosis (Eat debris), lysosome degradation, kill bacteria
Mononuclear Leukocytes
- Associated with chronic edema
- Essential to wound healing
- Tolerate hypoxia (low O2)
- Become macrophages
- Release chemotactic factors
If someone with a long standing wound comes in and it gets biopsied, what on the biopsy would indicate it is still in the inflammatory/acute phase?
- Monocytes!
- Monocytes should change into macrophages; if they don’t likely becomes a chronic wound
Macrophages
- 72 to 84 hours
- Function in low O2, highly acidotic environment
- Phagocytose (eat) matrix and debris
- Transition between inflammatory phase and proliferative phase
- Secrete cytokines, growth factors (GF) and MMPs
- Angiogenessi GF which stimulates endothelial budding from damaged blood vessels
Lymphocytes
- 5-7 days
- Immune System, WBC, defense
- Down regulates excessive inflammation
- Controls prolifration and repair
- Releases cytokines and GFs
- Overlaps inflammatory and proliferative phases.
Chemical Mediators
Inflammatory Phase 1
- Histamine: Vasodialation, increase wall “leakiness”
- Serotonin: Vasoconstriction
- Kinins: Increase small vessel “leakiness”
- Prostaglandins: Increase permeability and attract leukocytes
When someone takes anti inflammatory medications, what does it do?
- Prevents chemical mediators from working.
- Leads to poorer wound healing (medications and autoimmunte conditions can slow Wound Healing)
Patient presents to hospital with a Concussion and road rash would on there calf. How does this effect wound healing?
- Any type of inflammation in the body such as that caused by a concussion will result in slower wound healing
Diseases such as RA, Lupus, Sarcoidosis and AIDS all are affected by….
the inflammatory response due to wound, perpetuating chronic inflammation
Complement System has ____ plasma proteins that binds antibodies
- 11
- CS: leukocytes and extra plasma proteins that fight infection
Chronic Inflammation
Inflammatory Phase 1
- Occurs in sealed wounds
- Not characterized by cardinal signs of inflammation
- Adhesions form
- Draining, wet, hasn’t progressed, no granulation tissue
Intervention: cut layers away to create acute phase again and provide growth factor moisturizer to help with skin growth
Fibroplasia
Proliferative Phase II
- Myofibroblasts migrate into wound space
- Fibroblasts synthesize (Collagen and Glycosaminoglycans)
Angiogensis/Neovascularization/
Vasculogenesis
Proliferative Phase II
Formation of blood vessels
What does collagen synthesis require?
Collagen is the extracellular matrix
Collagen Requires:
* Oxygen (Exercise increases this!)
* Vitamin C
* Amino Acids
* Zinc
* Magnesium
Smoking delays this process
Why is it important to stretch wounds out?
- Allows for the collagen to lay down nicely and is plyable early
- If you don’t move it becomes stuck (nonmovable)
What intervention is used to help reorganize hypertrophic scarring?
- Use of pressure!
- Ex: Pressure dressing
Re-epithalialization
Proliferative Phase II
- Begins within hours in superficial wounds
- Epithelial cells line skin appendages
- Epithelial cells begin at wound edges and migrate to the center
- Contact inhibition stops epithelialization; Ex: ear percings
What 4 things signal that wound repait is needed?
- Electric gradient (charges)
- Pain (stimulates the CNS)
- Infection
– decreases O2 gradient at wound bed needed for metabolic demand
– new tissue synthesis
– collagen remodeling (anaerobic glycolysis) - Hyperlactate environment (Acidic; Ex: Lactic Acid)
These send signals for chemotaxis
Skin Surface Charge
- -23 mV (Weak electric potential)
- “Skin battery”; driven by Na+ pump
Current of Injury - How does it heal?
- Na+ transports the water in epithelium to internal body fluid creating charge potential of 50 mV across epithelium
- Break in the tissue causes ionic flow through the path of lowest resistance
- Dry wound bed eliminates the voltage gradient
What cells are involved in charge related healing?
- Galvanotaxis; cells needed for repair are attracted to the poles
- Wound infection recreates/sustains the inflammatory phase
- Mast cells: release histamine, vasodilate, increase cell wall permeability, the release heparin to increase endothelial migration
- Epithelium: receives a signal to migrate from macrophages, neutrophils and current of injury
Tissue has a ____ charge
+
Skin has a ____ charge
-
Removing ____ allows for migration to occur faster
eschar
Electrical Stimulation to promote different types of healing
- Autolysis: + on the wound; - on skin
- Infection: - on the wound; + on skin
- Granulation: Alternate everyday
Undefined border of redness is a sign of an ____.
infection
Wound Contraction
Pro Phase II
- Myofibroblasts shrink wounds before or after epithelialization
- Bring wound edges together at a rate of 0.6-0.7 mm/day
- Wounds under stress heal faster and more securely
Shrinking wounds too much may lead to an ____. To prevent it we put dressings in the space to promote ____.
- abcess
- epithelialization
Factors Complicating Wound Healing - intrinsic factors
- foreign material or eschar (contact inhibition)
- immunosuppression
- coagulation disorders
- nutritional deficiencies (Ex: Zinc or protein)
- metabolic diseases, i.e., R.A. or diabetes mellitus
Factors Complicating Wound Healing - Environmental
Tx applied to wound
- “Wound cleansing”
– Saline/ surfactants vs. cytotoxic agents (acetic acid, hydrogen peroxide, betadine, Dakin’s solution)
Good Tx:
* Dressings
* Electrical stimulation (bring edges together)
Factors Complicating Wound Healing - Iatrogenic factors
physical management of wound
- removal of dressings (skin in dressing)
- frequency of wound cleansing
- use of clean or sterile technique
Types of abnormal wound repair
- Hypergranulation – granulation above the skin level
- Hypogranulation – granulation below the skin level
- Hyperwound contraction with hypogranulation and re-epithelialization (tunneling); Ex: skin graft put on too soon
Wound Assessment
- Compile information form pt Hx, Subjective and Objective Exam
- Determine cause, extent of the wound and any conditions that may delay/complicate wound repair
Wound Assessment Subjective
- Pt Hx
- PMH
- Family Hx
- Social Hx
- Current Medications
- Last tetanus shot (within last 10 years)
- Wound Sx w/ activity/rest, elevation, dependency
- Pain
- Parathesia, anesthesia
Objective Wound Exam
Assess and Document:
* Location, size & severity
* Dry or draining - note drainage (amount, color, odor) - Any color is an infection
* Wound edges
* Surrounding tissue
* Evidence of skin nutrition (skin atrophy/dryness)
* Swelling
* Skin discoloration
Wound Measurement Sizing
- Length (Anatomical length from top to bottom
- Width (widest part
- Depth
- Undermining (lift skin and is underneath)
- Tunneling (Entry, NO Exit)
- Fistula (Entry and Exit)
Wound Classification - Color Schemes
- Black: Necrosis
- Yellow: Slough
- Red: Beefy Red Granulation Tissue
Motion Exam
- ROM
- Strength
- General activity/mobility
Clinical Signs of Infection vs Inflammation:
Erythema, Fever, Odor
Edema, Drainage, Pain
Fluid - you smell a sweet smell and the liquid is green, what does this mean?
- Sweet-psudemonas
- Infected
Fluid smells like urine, what does this mean?
- Ammonia (Protease)
- Infected!
Serous Fluid
- Clear drainage
- Healthy
Serosanguinous
- Pink
Sangrious Fluid
- Red
- Likely infected
What is performed in a vascular Exam
- Pulses - distal to wound
- Auscultation to detect a briut-caused by:
– constriction
– plaque
– aneurysm - Doppler
- ABI
Causes of Venous Insufficency
- Calf pump failure (don’t have musculature)
- Decrease in insteristial fibrinolysis (deposits become hard)
- Harvest vein graft (saphenous for bypass surgery)
- Trauma
What does the Trendelenburg test do?
Tests integrity of deep veins (DVTs can form here)
What are superficial veins called?
Spider veins
What are some tests for venous insufficency?
- Percussion test - detect dilated saphenous vein
- Trendelenburg test
- Cuff test (40 mm Hg)/ Homan’s sign
- Doppler ultrasound
- ABI >1.0
Tx - Venous Insufficency
- Cleanse & protect with dressings
- Elevate to decrease edema (Heart level or higher)
- Support with compression wrap
- 40 mmHg
- Ankle pump exercise
- Stop smoking
- Dietary management
If someone has a wound why would it be bad to be on a diet?
- They lose out of the oxygen, protein, acetic acid and magnesium in their diet needed for healing
What are some ways to help rid edema?
- Elevate feet above heart
- Avoid prolonged sitting or standing
- Ankle pumps
- Schedule frequenct rest breaks
Tests for Arterial Insufficiency
- ABI < 1.0
- Rubor of dependency
- Venous filling time
- Claudication time
- Foot print measurements
- Sensory testing with monofilament
- (10 g) 5.07 monofilament
Tx - Arterial Insufficency
- Warm whirlpool (max 98°)
- Dressings to maintain moist environment
- VAC
- Bed rest
- Limit leg elevation & activity
- Limb protection
- Preserve ROM and strength
Surgical Tx - Arterial Insufficency
- Arterial reconstruction (bypass artery)
- Endarterectomy (go in and try to open up artery)
- Angioplasty
- Sympathectomy (cut to open things up; Increases blood flow and decreases pain)
- Cold laser
Diabetic/Neuropathic Wounds
- Greater risk with DM > 15 years
- Greater risk with neuropathy (can’t feel pressure)
- Combination of AI and pressure (Charcot joints)
- Wound healing depends on DM control
- Slows wound healing
- Greater risk of osteomyelitis
- >1.0 ABI
Why do pressure ulcers occur?
- In Soft Tissue
- Usually over bony prominences
- Results of unrelieved pressure over time
Causes/Risk Factors of Pressure Ulcers
- Time/pressure relationship
- 2 hour max in one position
- Capillary closing pressure = 32 mm Hg
- Friction (external rubbing on a surface)
- Shear (stretching of one layer over the other)
- Moisture (Can lead to keratin too wet and masticaiton occurs)
Approxmately ____ of decubitis ulcers occur in the pelvic area
75%
Pressure Ulcer Tx
- Eliminate cause of pressure by reducing or redistributing
- Use pressure relieving devices (PRD’s)
- Increase activity, maintain ROM & strength
- Local wound care
What type of pillow is really good in preventing pressure ulcers?
RIK Fluid Pillow
Heel Protection for wounds
- Non-ambulatory
- Ambulatory
What are 4 important nutritional requirements for wound healing?
- Protein
- Vitamin C
- Zinc
- Mg
Trauma wounds have a higher risk of ____
infection
Traumatic Wound Tx
- Protect healthy tissue
– Wound bed and surrounding tissue - Wound debridement/cleansing
– Foreign and necrotic tissue - Anticipate greater risk of infection
– Systemic Abx and bactericidal dressing - Support wound contraction
– Compression wrapping, VAC, limit joint ROM, ankle pump
Silver is a natural ____
antimicrobial
Wounds from infection are often ____
- Indurated - tissue swelling, hard to the touch
Infection Wound Treatment
- Infection management
– Systemic antibiotics
– Reduce bacterial load from wound bed(debride/cleansing)
– Bactericidal topical dressing - Pain management
– Systemic not topical - Improve circulation
– systemic and local - Manage drainage
– daily dressing changes
– avoid maceration
____ and ____ Trauma will delay healing
- Mechanical and Chemical
- Mechanical Ex: Shear, pressure, ripping off adherent dressings
- Chemical Ex: cleansers and carriers
If you can’t put it in your eye…
don’t put it in your wound
What are 4 things to never put in a wound?
- Dakin’s solution
- Acetic Acid
- Hydrogen peroxide
- Iodine solutions
All are toxic to myofibroblasts
Goals of Wound Cleansing/Debridement
- Rid wound of necrotic tissue
- Prevent infection
- Correct abnormal wound repair
