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Wound Care ©TCHP Education Consortium, November 2012, Revised March 20191

Types of WoundsLower Extremity Arterial Disease (LEAD)

Peripheral Arterial Disease (PAD)

Lower Extremity Vascular Ulcers

• Lower Extremity Arterial Disease (LEAD) or Peripheral Arterial Disease (PAD)

• Prevalence:• 40‐70 yrs = 19‐32%

• 80 yr old and older = 40%

• 50‐80% of LEAD are underdiagnosed• LEAD have 5.9x greater risk of death Cardiovascular disease

• LEAD have 6.6x greater risk of death by Coronary artery disease

• Lower Extremity Venous Disease (LEVD) or Chronic Venous Insufficiency (CVI) or Venous Stasis Disease

• Mixed Disease which is both of above etiologies.

Lower Extremity Vascular Ulcers Vascular Screening

• ABI: Ankle Brachial Index:• Ankle systolic pressure/ Brachial systolic pressure

• >1.30 = falsely elevated due to non‐compressible calcified vessels

• >1.0 = normal• <0.9 = asymptomatic, minimal arterial disease, LEAD• <0.6‐0.8 = Borderline Perfusion• <0.5 = severe ischemia, some claudication• <0.40 = Ischemic rest pain, severe claudication, tissue necrosis, potential limb loss, severe disease

• Doppler ABIs are 94% sensitive and 99% specific for PAD

Vascular Screening

• Transcutaneous Oximetry = TCO2s• Tissue oxygenation

• Normal oxygenation for wound healing is 40

Arterial Disease (LEAD / PAD)

• Atherosclerosis of the peripheral arteries result in tissue ischemia

• Most common of the diseases

• Plaque formation causes narrowing of the arteries

• Inflammation can result in vessel lining damage and hardening of the arterial wall




• Progressive: • I – asymptomatic

• II – intermittent claudication (50% occluded)• Pain with moderate activity, relieved with rest

• III – nocturnal• Elevation /legs up: causes pain (sleeping at night with legs up)

• Dependency/legs down: relieves the pain

• IV – tissue necrosis / gangrene (90% occluded)• Rest Pain‐ pain even with no activity at all


Risk Factors:

Cigarette smoking

Diabetes

High cholesterol

Hypertension

Obesity

Inactivity

Risk increases with age

Significant overlap with CAD (coronary artery disease) & LEAD.


• Chronic• Ischemic diseases the symptoms that grow worse over time

• Acute• Develop quickly with sudden decrease of perfusion

• S/S: pain, paralysis, paresthesias, pulselessness, pallor, polar (cold extremity)

• Urgent evaluation needed to avoid nerve and muscle damage

• Critical Limb Ischemia• Refers to advanced LEAD

• Chronic rest pain, ulcers, gangrene

• Goal of care is preserve the limb

Arterial Disease (LEAD / PAD):Lower Extremity Characteristics:

• Thinning of epidermis

Loss of hair, dry, taut, shiny skin

Thickened nails

• Cool to touch

• Color changes with elevation

Pallor (light skin) Ashen (darker skin)

• Pulses may be diminished or absent

• Tips of toes or pressure points on foot

• Site of trauma – bumping of the leg

• Pain is common

Arterial Disease (LEAD / PAD):

Arterial Wound Characteristics:

• Extremely painful

• Difficult to heal unless perfusion can be re‐established

• Prone to infection/ gangrene/ amputation

• Pale or necrotic wound bed

• Dry wound with defined edges and usually round‐ appears like wound was made with a “hole puncher”

Arterial Disease ‐Management / Treatment

• Avoid heat and cold (no hot/cold packs to feet)

• Avoid constriction clothing to legs• Supervised walking program, as appropriate

• Smoking cessation

• Good nutrition• Tight glucose control



Arterial Disease ‐Management / Treatment

Medications• anti‐platelet drugs• vasodilating effects• statins – lower blood lipids• analgesics for pain management

Prevent and manage infection• S/S often muted• When identified prompt systemic antibiotic therapy• Debridement as warranted

Arterial Disease – Surgical Management / Treatment

• Invasive Treatments

Revascularization therapies:‐ Balloon angioplasty

‐ Atherectomy (plaques removed from artery)

• Bypass grafting

• Amputation

Arterial Disease Topical Care= prevention

• Daily skin care‐ use emollients: creams add lipids and soften plaques of dead skin (ex‐urea, ammonium lactate, petrolatum, lanolin, mineral oil and Dimethicone are common emollients

• WHY?‐ Protect from drying, cracking, fissure

• Inspect feet often• Professional nail care• Protect from trauma‐ wear shoes or soft boots

• Bumping into things (w/c bumps), punctures, avoid cuts

• Manage edema‐ use LIGHT compression (8‐15mmHGHG) and elevation

Arterial Ulcer Dressings• Moist dressing‐Arterial wounds generally have less exudate, so choose a hydrating dressing

• Antimicrobial dressing‐ control bacterial burden

• Periwound‐ protect wound edges with skin sealant (i.e. No Sting)

• Non‐occlusive dressing‐ avoid hydrocolloids, tegaderms, etc that can harbor bacteria.

• If wound has black eschar, may need to avoid debridement and avoid moist dressings **

**dry intact eschar can be the body’s own biological protection from infection.

Lower Extremity Venous Disease (LEVD / Venous Stasis Ulcers)

• 80‐90% all ulcers are venous

• 57‐97% will recurrence rate• 26‐28% in 12 months

• Monthly Cost = $2200

Lower Extremity Venous Disease (LEVD / Venous Stasis Ulcers)

• Results from impaired return of venous blood from the leg back to the heart.

• Valve dysfunction• No longer close completely

• Leak and unable to move fluid efficiently

• Risk factors –obesity, pregnancy, thrombophlebitis, leg trauma



Venous Disease (LEVD)Calf muscle function‐

• Serves as a natural pump to push blood pack up to the heart

• Function changes with injury, neurologic disease, joint pain

• Impaired calf muscle risk factors:

• sedentary lifestyle

• prolonged standing

• arthritis

• reduced mobility

• shuffling gait (does not engage calf muscle)

• atrophy with age

Venous Disease (LEVD)

• Accounts for 80 – 90% of all leg ulcers• Ulcerations develop due to skin and tissue changes caused by edema and venous hypertension.

Venous Disease AssessmentVaricositiesSwollen twisted veinsBulge, throbOften on the back of the calf or medial leg

EdemaInitially – pitting edema increases with dependency and reduces with elevation

Eventually ‐ Edema skin becomes “brawny” chronic Non‐pitting

Hemosiderin stainingDiscoloration results from red blood cells spilling out of the capillaries

Venous UlcersVenous hypertension makes fluid leak into the subcutaneous tissues and causes skin breakdown

Venous Disease Assessment

Lipodermatosclerosis‐• fibrosis or hardening of the soft tissue in the lower leg (gaiter area). Gives the leg an “apple core” appearance and a firm bumpy texture.

Venous dermatitis• Common inflammation of the epidermis and dermis• Lower extremity

• s/s afebrile, itching, scaling, weeping, crusting, erythema present, bilateral or unilateral, chronic or acute.

• Staph aureus present in labs

* Often confused with Cellulitis!• S/S fever, pain, warm to touch, little weeping, no crusting

• Often unilateral

Venous Stasis Wounds

• Often shallow and wet in gaiter area

• Peri‐wound maceration

• Irregular wound edges

• Red, ruddy wound base

Peri‐ wound crusting and scaling present

Venous Disease: Dressing considerationsDepends on how much Drainage…..

• Absorbent Dressings (alginate, hydro fiber)

• Non‐stick dressings: adaptic or mineral oil‐emulsion gauze with absorbent cover dressings

• ABD pads, non‐bordered mepilex

• Periwound protection‐ skin prep or barrier creams

• Use caution with adhesives on skin; secure dressings with kerlix and Tetranet



Venous Disease‐Treatment• Compression : Gold Standard

• long term compression stockings

• Wear over dressings AND after wounds are healed for prevention

• Limb elevation

• Exercise

• Weight control

• Medical management‐ for acute management with diuretics if needed short term (ex‐CHF flare ups)

Venous Disease Treatment: Compression is standard of care!

Elastic Compression

• Elastic adapts to change in leg volume: High resting pressure

• Better for sedentary or shuffling gait

• Use with Caution:• for patient’s who cannot remove• Patient’s with poor sensation

• Skin checks‐ risk of device related injury

Inelastic compression

• In‐elastic is more rigid: Low resting pressure

• With ambulation, pressure is place on the valves making them more efficient

Venous Disease Treatment: CompressionElastic options

• Long stretch wraps (Ace Wraps)‐ no longer using at the VA d/t risk of injury

• Compression socks (Jobst )

Multi‐layer wraps (Profore wraps)

Venous Disease Treatment: Compressionin‐elastic

• Short stretch wraps • Rodisol wraps

• Juxta‐fit wrap (CircAid)

• Farrow wrap (Jobst)

• Ready Wrap (Solaris)

• Paste Wraps: Zinc oxide wraps that dry and harden Only works on patient’s who ambulate‐ works with the calf pump muscle.

• Unna Boot

• Gelocast

Considerations for Compression

Contraindications

• Acute DVT

• Acute Infection

• Cardiac Edema: uncompensated CHF

• Advanced Arterial Disease (ABI < 0.5)

• Malignancy: unless palliative

• Renal Disease: related to severity

Precautions

• HTN

• Mild arterial disease (ABI 0.5‐0.8)‐

• Limb paralysis

• Diabetes

• Hx of CHF (Physician approval)

• Mild renal disease

References: Wound, Ostomy, and Continence Nurses Society. (2017). Venous, arterial, and neuropathic lower‐extremity wounds: Clinical resource guide. Mt. Laurel, NJ: Author.

Guideline for management of wounds in patients with lower‐extremity arterial disease. (2014). Mount Laurel, NJ: Wound, Ostomy, and Continence Nurses Society.

Guideline for management of wounds in patients with lower‐extremity venous disease. (2011). Mount Laurel, NJ: WOCN.

Ratliff, C. R., Yates, S., Mcnichol, L., & Gray, M. (2016). Compression for Primary Prevention, Treatment, and Prevention of Recurrence of Venous Leg Ulcers. Journal of Wound, Ostomy and Continence Nursing, 43(4), 347‐364. doi:10.1097/won.0000000000000242



Types of Wounds: Diabetic Foot

Diabetic Foot Ulcers

Screening tool screen shot in CPRS

Monofilament test

Orthotics for shoes

Neuropathic Disease (LEND)

• Complex wounds which develop due to peripheral neuropathy, structural foot problems, edema, callous and ischemia.

• Peripheral Neuropathy is involved in about 78% of DFU

• Study: 678 routine exam

• 65.74% male & 32.25% female had DFU

Neuropathic Disease (LEND)• Neuropathy affects

• Sensory nerves (reduced sensation, numbness)

• Motor (musculature changes)

• Autonomic (function – sweating, temperature regulation, blood flow)

• Structural Foot Changes

• Hammer toes

• Charcot foot (disruption of the ankle joint)

• Bunions

• Heel spurs

• Foot ulcers develop from repetitive stress often with large callous

• copyright 2003 AAWC

Neuropathic Disease Ulcer Characteristics

‐ Usually located over plantar surface over metatarsal heads or

‐ Over areas exposed to repetitive trauma.

‐Moderate to large amounts of exudate

‐Well‐defined borders

‐ Frequently associated

with callous

‐ Signs of infection may be muted.

copyright 2003 AAWC Diabetic Foot Ulcers Risk

• Long history of diabetes

• Long time smoker

• Poor glucose control

• Obesity

• Reduced or absent sensation

• Foot deformities and callus

• Autonomic neuropathy present (increased sweating of the feet)




Prevention

• Monitor feet daily

• Don’t walk barefoot

• Lotion feet daily

• See a Podiatry regularly for foot care and toenail care

• Wear proper footwear

• Control Blood Glucose levels

• Pumice stone for callous formation

Monofilament test• Have patient close eyes• Education patient on what it is• Respond “yes” when felt• Apply monofilament perpendicular to skin’s surface

• Apply sufficient force to cause filament to buckle or bend.

• Smooth motion, not jabbing

• Total duration 1‐2 seconds each area• Apply filament along margin of callus, ulcer, scar and necrotic tissue. NOT over lesions

Sediel HM et al ed Mosby’s guide to physical examination, ed 5, St. Louis, 2003. Mosby.

Treatment

• Offloading

• Total Contact Cast

• Glycemic Control

• Early Interventions

• Debridement

• Antimicrobial dressings

• Education

Diabetic Foot Ulcers ‐Management

• It’s all about PREVENTION

• Daily foot assessment

• Good socks and proper fitting shoes

• Proper nail care

• Protection from heat and cold

• Glucose control

Types of Wounds: IAD



Incontinence‐Associated Dermatitis

• IAD specifically refers to skin problems resulting from exposure to urine and/or feces.

• IAD is included in a much larger group of conditions referred to as moisture‐associated skin damage (MASD)…..this includes skin damage from wound drainage, perspiration, etc.

IAD

MASD

• Incontinence‐associated dermatitis (IAD) is a type of inflammation of the skin that results from exposure to urine and/or stool.

What is IAD?

• Occur in patients with poor health (especially nutrition)

• Compromised mobility

• Raise the risk of infection

• IAD and Pressure Ulcer can co‐exist

• Incontinence is a risk factor for pressure ulcer development

• 22% more likely to get a pressure ulcer

What do IAD and Pressure Injuries have in common?

IAD vs Pressure Ulcer

Parameter IAD Pressure Ulcer

History Urinary and/or fecal incontinence Exposure to pressure/shear

Symptoms Pain, burning, itching, tingling Pain

Location Perineum, peri‐genital area; buttocks, gluteal fold, medial/post thighs, lower back, may be over bony prominence

Usually over bony prominence / under medical device

Shape/edges Diffuse, poorly defined edges/blotchy Distinct edges

Presentation/depth Intact with erythema, superficial,partial thickness skin loss.

Intact skin with non‐blanchable erythema to full thickness skin loss. Base may contain non‐viable tissue.

Other Possible secondary superficial skin infection (candidiasis)

Possible secondary soft tissue infection

• Prevention!!!

• Early identification are key

Management of IAD



ACT APPROACH

ASSESS

Identify etiology

Skin daily

After every incontinence episode

Etiology (urine, stool, ostomy)

Color of skin

Condition of skin (closed, intact, fungal, bacteria)

Divert stool or urine

CLEANSE

Ph cleanser

Maintain acid environment

Reduce friction

Non alkaline soaps

TREAT

Silicone‐based barrier, ointments or creams

Petrolatum or zinc oxide ointments or creams

Film‐forming liquid acrylates (sprays or wipes)

Wick away moisture with super absorbents

Avoid tapes that can damage skin

Use fluid‐lock dressings

• Light skin tones – erythema (pink – red)

• Darker skin tones – pale, darker color, purple, deep red, even yellow(?)

• Poorly defined borders

• Can be patchy

• Can cover large areas

• Full peri‐anal area, buttocks, sacrococcygeal area, thighs

Assess

• May present with vesicles or bullae, papules or pustules

• Epidermis deeply damaged or fully eroded, leaving moist or weeping dermis

• Area may be painful, burning, itching

• Affected skin susceptible to secondary skin infections

• Candidiasis most common

Assess

Ph cleansers

Cleanse

This image cannot currently be displayed.This image cannot currently be displayed.

Ph cleansing wipes

Cleanse

• Protecting with a moisture barrier

• Apply the skin protectant at a frequency with its ability to protect the skin.

• Skin protectant should be compatible with other product being used.

• Apply to all skin exposed to urine and/ or stool.

• Many products already combine products that cleanse and protect (and restore) in one.

Treat



• Secondary infection

• Usually candidiasis

• Treated with anti‐fungal

• Powder, cream or ointment

• Intradry

TreatComparative

Principle Ingredient Description Notes

Petrolatum(petroleum jelly)‐Aloe Vesta‐Vaseline‐Aquaphor‐ “soothing ointments”

Derived from petroleum processing.Common base for ointments.

Forms occlusive layer.

May affect absorbency of pads.Transparent when applied thinly.

Good barrier for urine but not stool.

Zinc Oxide‐Criticaid‐Sensicare‐Calmoseptine‐Sooth and Cool by Medline

White powder (Carboxymethylcellulose) mixedwith a barrier (zinc) form an opaque cream, ointment or paste.

Can be difficult to remove.

Challenge for skin inspection

Remove easily with mineral oil or a petrolatum based product.

Dimethicone‐A&D ointment‐Barrier cloths from variety of vendors.

Silicone‐based Non‐occlusive, does not affect absorbency of pads as much.

Usually transparent after application.

Good barrier for urine but not stool.

Building Blocks—IF in doubt

Intact skin – incontinence wipe + (maybe) skin protectant

Red (intact) skin –incontinence wipe + skin protectant (ointment)

Red (denuded) skin –incontinence wipe + skin

protectant (ointment or paste)

Broken skin plus infection –incontinence wipe + skin

protectant ointment with anti‐fungal component.

Improvement should be noticed in 3‐4 days.

• Mcnichol, L. L., Ayello, E. A., Phearman, L. A., Pezzella, P. A., & Culver, E. A. (2018). Incontinence‐Associated Dermatitis. Advances in Skin & Wound Care, 31, 502‐511. doi:10.1097/01.asw.0000546234.12260.61

References:

Types of Wounds: MARSIMARSI

Mechanical Adhesive Related Skin Injury



Securement Devices

EKG pads

PICC Line

Intravenous

Ostomy Pouching

Medical Device Related Injuries



Medical Device Related Pressure injury

• This describes an etiology.

• Medical device related pressure injuries result from the use of devices designed and applied for diagnostic or therapeutic purposes.

• The resultant pressure injury generally conforms to the pattern or shape of the device.

• The injury should be staged using the staging system.


Nasal Cannula tubing


Nasal Cannula tubing


Oxygen Face Mask


Condom Catheters


Foley Catheters




Bed Pans


CPAP/BIPAP Mask


Splint


PneumoBoots/SCD’s


ACE Wraps


ET Tube




WheelChair Footplate


Trach Face Plate

Tubes and Securement Devices

NG TubesSecurement Devices

Foley Tubing NPWT tubing



PEG tube Nasal Cannula

Neph tube Biliary Tube

Reference

• The Joint Commission. Quick Safety 43: Managing medical device‐related pressure injuries, July 2018



Skin Tears

Skin Tear

• Traumatic injury resulting in the separation of the epidermis from dermis (partial thickness) or separation of the dermis from the underlying tissue (full thickness).

• Often thought of as minor, but can increase the risk of infection and other risks.

• Can happen to any location and to anyone• Increased risk to elderly, neonates• Skin is compromised• Tears are very painful


Skin Tear

• Usually defined by Payne‐Martin Classification SystemI. Skin tear without tissue loss

• Linear – Full thickness; epidermis & dermis pulled apart exposing tissue beneath (looks ike an incision)

• Flap – Partial thickness leaving an epidermal flap to cover exposed dermis; no more than 1mm exposed dermis

II.Skin tear w/partial thickness loss

• Scant tissue loss – Partial thickness with 25% or less of epidermal flap is lost & 75% dermis covered

• Moderate/large tissue loss – Partial thickness with more than 25% of epidermal flap is lost & more than 25% of dermis exposed

III.Skin tear with complete tissue loss

• Partial thickness with no epidermal flap

Payne‐Martin Classification of Skin Tears

Skin Tear Risk Factors

• Daily activities ‐ bathing, dressing, transferring• Sensory loss• Dehydration• Malnutrition• Cognitive impairment• Poor locomotion• Edema• Ecchymosis• Long term use of corticosteroids (reduces collagen strength and elasticity)• Long term consequences of radiation therapy



Skin Tear ‐ Prevention is KEY

• Environmentgood lighting, unobstructed pathwaysproper placement of small furniture, pad sharp edges of furnitureproper positioningmechanical lifts to avoid friction and shear

• Bodyproper nutrition and hydrationenough protein (supplements)frequent offering of fluids and snacksinspect and moisturize skingood nail careprotective clothing and footwear

• Skin

proper application and removal of dressingsavoid tapes and non‐skin friendly adhesivesapply tape without tensionavoid pulling tape off the skinalcohol‐free skin sealants under tape

Skin Tears Management• Try to preserve the skin flap

• Protect surrounding tissueRe‐approximate edges with

stretching the flapProtect from further injury

• Control bleedingApply pressure and elevate the limbIrrigate with saline to clean and remove debrisPat dry

•Extensive tears may require surgical or plastics referral.

Skin Tears Wound Care

• Choose dressing easy to apply

• Non‐adherent

• Maintain moisture

• Protect from shear

• One that does not need frequent changes

• Mark the dressing with the direction of removal• To protect the flap

• Examples: Dermagel ,Vaseline gauze or oil emulsion gauze secured with kerlix or netting.

Skin Tears

• References:Stephen‐Haynes J, Carville K. Skin tears Made Easy. Wounds International 2011; 2(4): Available from http://www.woundsinternational.comaccessed April 17, 2016.

•Bryant, Ruth A., Nix, Denise P., Acute & Chronic Wounds, Current Management Concepts, St. Louis, Mosby, 2012, Print

Burns & Frostbite

Burns

Definition:

An injury to tissue usually caused by heat however can also be caused from abnormal cold, chemicals, poison gas, electricity, or lightning.



Burn Depth

• Four categories• First Degree

• Second Degree

• Third Degree

• Fourth Degree

103

• Thermal

• flame (dry heat)

• scalds (wet heat)• contact (with hot objects)

• Sources: house fires, inhalation of hot air (temp >150(C)), matches, tar, fireworks, cooking spills, hot water, oven door, curling iron.

• Appearance: white and/or charred color, damage continues until temperature cools

Burn Type

• Chemical

• Exposure to acids, alkalis, vesicants• Contact, ingestion, inhalation, injection

• Sources: bathroom cleaners, rust removers, oven cleaner, fertilizers, industrial cleaners

• Appearance: brown or gray tissue; damage is deeper than observation would indicate; severe persistent pain present, damage wont stop until agent is diluted or removed

• Emergency care: irrigate, irrigate, irrigate

Burn Type

• Electrical

• Contact with faulty wiring, damaged cords, appliances, high‐voltage power source, lightning strike.

• Source: electrical current passes through the body and is converted to a thermal (internal) injury.

• Appearance: minimal injury at the point of entry with significant internal injury; possible cardiac dysrhythmias.

Burn Type

• Radiation

• Cancer treatment presenting as immediate injury or revealing itself later (years, sometimes)

• Source: healthy cell damage from the radiation

• Appearance: erythema and/or edema, blisters or shallow ulcer with uneven borders; wet or dry, tissue fibrosis, hypo/hyper pigmentation; scarring, pain

Burn Type Burn Severity



• Superficial burn (First Degree)• “Sunburn” type injury

• Involves the Epidermis

• No scarring or disfigurement

• Can appear dry or wet

• May have small blisters

• Treatment: clean with mild soap daily. Apply lotion to areas. May use aloe based cream is preferred. Nothing alcohol‐based or increased drying may occur. Should heal within 7 days.

Burn Severity• Superficial partial‐thickness (Second degree)

• This involves both the epidermis and into the dermis layer

• Usually looks pink and blistered

• Typically most painful type of burn

• Heals within 2‐3 weeks with minimal scarring• May have pigment changes in darker skin people

• Sometime will require skin grafting

• Treatment: clean with mild soap and water. Silvadene or bacitracin & adaptic applied. Secure with kerlix. Change daily.

Burn Severity

• Deep partial‐thickness (Second/Third degree)

• Involvement of the entire epidermis and dermis. May include fat and muscle.

• Can appear moist, white, blistering.

• Also painful.

• This will require skin grafting after the burn has had time to develop.

• Treatment: clean with mild soap and water. Silvadene or bacitracin & adaptic applied. Secure with kerlix. Change daily.

Burn Severity• Full‐thickness (Third/Fourth Degree)

• This is through the dermis and into the fat and/or muscle.

• Appearance can be dry and waxy with varying color (deep red, white, black, brown)

• Nerve endings are damaged so minimal to no pain

• May see coagulated vessels• Surgery is a must! Usually within the first 48 hours if patient is stable

• Treatment: clean with mild soap and water. Silvadene or bacitracin & adaptic applied. Secure with kerlix. Change daily until surgery.

Burn Severity

113

Referral Criteria

• >10% TBSA

• Face, hands, feet, genitals, perineum, major joints

• Third degree

• Electrical, including lightening

• Chemical burns

• Inhalation injury

• Pre‐existing conditions

• Concomitant trauma

• Pediatrics

• Special social, emotional or rehab needs

(American Burn Association recommendations)

Frostbite and Frostnip



Frostnip

• Pain• Pallor• Numbness

• Completely reversible with warming

• No resulting tissue loss

115

• Tissue injury related to prolonged exposure skin to freezing temperatures.

• Heat loss (freezing) is faster with increased wind speeds ‐ wind chill temperature.

• The longer the tissue is frozen, the greater the damage.

• Injury occurs as tissue slowly freezes with extracellular ice crystal formation, circumferential, progress distal to proximal; potentially reversible.

• Injury also occurs when reperfusion begins!

Frostbite

Frostbite

Injury:

• First Degree

• Second Degree

Classification

• superficial, sensation intact, normal color, blanches, no blisters with rewarming, mild burning, throbbing, sloughing w/no tissue loss

• superficial, edema, clear fluid filled blisters within 24hrs

Frostbite

Injury• Third Degree

• Fourth Degree

Classification

• deep partial thickness injury; hemorrhagic blisters proximal to injury; pale to deep violet color upon presentation, non‐blanching

• full thickness injury, purple or black in color; can affect muscle, tendon, bone; edema is proximal, part distal tissue will mummify over time

• Intoxication – inhibits awareness of cold, shivering, cutaneous vasodilation

• Homelessness

• Greater number are male gender than female

• Neuropathy• Inexperience w/cold weather or stranded in cold weather• Inadequate clothing or constricting clothing• Mental health status – impaired ability to understand cold

• Underlying conditions – malnutrition, PVD, arthritis

Frostbite Risk

• Admit to specialized treatment hospital for all levels of injury to salvage digits.

• Minimize heat loss ‐ change wet clothes to dry, soft clothing, wrap to protect affected limb.

• Do not rub affected tissue! This will increase the damage.

• Do not rewarm unless transfer to specialized treatment hospital is within 1 hour of transport time.

Frostbite Management



• When danger of refreezing is past initiate rapid rewarming ‐ decreases irreversible damage

• Usually water or wet compress 40 degree Celsius

• Pain meds, as appropriate• ALL LEVELS OF FROSTBITE HURTS!!!!!

• Topical aloe vera cream to affected areas even if not open

• Bacitracin can be used later when blisters open

• Elevate the limb

• Ambulate after 24 hours

Frostbite Management ReferencesPhillip, R.L. (2017, October 5). Classification of Burn Injury. Accessed on 11/27/2018 from: https://www.uptodate.com/contents/classification‐of‐burn‐injury

NIH(National Institute of General Medical Sciences). (2018) Burns. Accessed 11/27/18 from: https.//www.nigms.nih.gov/education/pages/factsheet_burns.aspx

Handford,C., Buxton, P, Russell,K., Imray, C,. McIntosh,S., Freer,L., Cochran,A., Imray,C. (2014). Frostbite: a practical approach to hospital management. Extreme Physiology and Management, 3,7.

Pressure Injury: Staging and Prevention

Pressure injury Prevention

• Pressure

• Shear

• Friction

• Moisture

Etiology of a Pressure Injury

•Pressure• Localized injury from ischemia that caused tissue death

• Pressure ulcers can develop when a large amount of pressure is applied to an area of skin over a short period of time.

• They can also occur when less pressure is applied over a longer period of time.

• The extra pressure disrupts the flow of blood through the skin.




PressurePressure is the force that is applied vertically or perpendicular to the surface of the skin. Pressure compresses underlying tissue and small blood vessels hindering blood flow and nutrient supply. Tissues become ischemic and are damaged or die.

• Shear• A strain in the structure

produced by pressure, when its layers are laterally shifted in relation to each other.

• Skeleton moves but the skin remains fixed to the surface.

• Diminishes circulation to tissue and damages tissue and blood vessel integrity


Shear ‐ Shear occurs when one layer of tissue slides horizontally over another, deforming adipose and muscle tissue, and disrupting blood flow (e.g. when the head of the bed is raised > 30 degrees).

When the head of the bed is elevated, the effect of gravity on the body pulls it down toward the foot of the bed.

However, the body resists sliding and may stick to the sheet so the skin is held in place and the weight of the skeleton continues to pull the body downward.

Shear causes much of the damage seen with pressure ulcers.

Typically found over bony prominences or around/under devices.

Majority of pressure injury

occur in the pelvis (sacrum/coccyx)

Heels are second most common

location.

• Friction:

• the resistance that one surface or object encounters when moving over another.

Etiology of a Pressure Injury • Friction and moisture also contribute to the development of pressure ulcers.

• In some individuals, pressure ulcers can occur in as little as two hours.

• Skin damage from pressure or shear may not be visible on the skin for 48 hours or more.



• Moisture

• Excessive moisture on the skin surface (perspiration, urinary, fecal incontinence) is thought to increase risk of pressure injury development

Etiology of a Pressure Injury We know that most pressure ulcers are preventable!

In order to prevent pressure injuries, interventions must be applied:• early•diligently, and •consistently.

Prevention is the key!

•Anticipate who will be at risk for skin breakdown.

• Start prevention strategies before skin breakdown occurs.

•Pressure ulcers are a nursing sensitive measure.

Tools to prevent pressure ulcers:• Skin inspection upon admission and on an ongoing basis.

• Daily Braden Risk Assessment Scale to identify patients with the greatest risk of developing pressure ulcers.

• Nurse initiated prevention strategies,

PREVENTION OF PRESSURE INJURIES IN LTC

• Inspect resident’s skin on day of admission or re‐admission and on a weekly basis thereafter.

• Complete Tissue Tolerance testing for repositioning needs upon admission/re‐admission, annually or with a significant change.

• Complete a Braden Risk Assessment for 4 weeks after admission starting on date of admission, then quarterly or with a significant change.

• Care plan appropriate seating/bed pressure relieving surfaces.

• Care plan repositioning needs if resident is unable to reposition self.

Skin Inspection:A comprehensive, head to toe skin inspection must be done to determine whether existing skin breakdown is present and identify hospital acquired skin breakdown in the very early stages.

Pay special attention to bony prominences



Your skin inspection should also include palpation of the skin

Especially helpful in dark skinned individuals

Be sure to inspect under/around any devices that may be removed

such as braces and splints, tubing and boots.

Pressure ulcers frequently occur under tubing, braces, collars, heel suspension boots, tracheotomies and other devices. The skin inspection must include assessment of the skin under these devices.

Chances to look at skin

• Bathing• Bedpan and toileting• Putting on shoes/slippers• Turning/re-positioning• Applying braces/ Teds/ pneumo boots and other devices

• Dressing changes

What to look for?

When a pressure injury starts, it may appear as a bruise, a blister or just an area of redness.

Suspected Deep TissueInjury at sacrum.

Stage I pressure injury on left trochanter.

Blisters and suspected deep tissueinjury on bilateral heels.

It may be difficult to tell whether skin breakdown is a pressure injury or not.

Early pressure ulcers are more difficult to see on dark skin: make sure lighting is good



Staging of Pressure Injuries NPUAP

• In April 2016, the National Pressure Ulcer Advisory Panel (NPUAP) replaced the term “pressure ulcer” with “pressure injury” in the NPUAP Injury Staging System to reflect injuries to both intact and ulcerated skin.

Pressure Injury: Stage 1

● intact skin with non-blanchableerythema over a bony prominence.

● darkly pigmented skin may not have visible blanching; the color

may differ from the surrounding area.● may be painful, firm, soft, warmer or cooler as compared to adjacent tissue.


● partial thickness loss of dermis

● shallow open injury

● red or pink wound bed, without slough

or

● intact or open/ruptured serum-filled blister

● shiny or dry shallow injury without slough

Stage 2 Pressure injury Is NOT

• moisture associated skin damage (MASD) including incontinence associated dermatitis (IAD),

• intertriginous dermatitis (ITD),

• traumatic wounds (skin tears, burns, abrasions).


● full thickness loss of skin ● adipose (subcutaneous) fat may be

visible● granulation tissue may be present● slough and/or eschar may be present● fascia, muscle, ligament, or bone are

not exposed ● may include undermining and

tunneling ● depth varies by anatomical location. ● the bridge of the nose, ear, occiput and malleolus

do not have subcutaneous tissue, Stage 3 ulcers can be shallow.




● Full thickness tissue loss with exposed bone, tendon or muscle.

● Slough or eschar may be present in

some parts of the wound bed.

● May include undermining and tunneling.

● Exposed muscle, bone or tendon is visible or directly palpable.

● Depth varies by anatomical location.

the bridge of the nose, ear, occiput and malleolus do not have subcutaneous tissue so these ulcers can be shallow.

● Because muscle and/or supporting structures are exposed (e.g., fascia, tendon or joint capsule) osteomyelitis may be possible.

Unstageable● full thickness tissue loss

● base of the injury is covered by slough (yellow, tan, gray, green or brown) and/or eschar (tan, brown or black)

● the true depth, and stage cannot be determined until enough slough and/or eschar is removed to expose the base of the wound

● Stable (dry, adherent, intact without erythema or fluctuance) eschar on the heels serves as "the body's natural (biological) cover" and should not be removed.

Deep Tissue Pressure Injury

● purple or maroon localized area of discolored intact skin or

● a blood‐filled blister

● caused by damage to underlying soft tissue from pressure and/or shear.

●may be preceded by tissue that is painful, firm, mushy, boggy, warmer or cooler than adjacent tissue.

●may be difficult to detect in individuals with dark skin tones.

Do Not Reverse Stage

“Pressure ulcers heal to progressively more shallow depth, they do not replace lost muscle, subcutaneous fat, or dermis before they re‐epithelialize.

Instead, the ulcer is filled with granulation (scar) tissue composed primarily of endothelial cells, fibroblasts, collagen and extracellular matrix. A Stage IV pressure ulcer cannot become a Stage III, Stage II, and/or subsequently Stage I. When a Stage IV ulcer has healed it should be classified as a healed Stage IV pressure ulcer not a Stage 0 pressure ulcer. Therefore, reverse staging does not accurately characterize what is physiologically occurring in the ulcer”. NPUAP position statement on reverse staging

Mucosal Membrane Pressure Injury

• Mucosal membrane pressure injury is found on mucous membranes with a history of a medical device in use at the location of the injury. Due to the anatomy of the tissue, these ulcers cannot be staged.

types of wounds - tchpeducation.com · arterial disease (lead / pad): lower extremity...

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