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Carol Calianno MSN CRNP, CWOCN11/3/17

If specific brands are mentioned or shown in photographs it is done because: There are unique characteristics of the product It is the only product in the category Within product categories, examples of multiple

dressings are shown to demonstrate product type/properties

I have no vested interest, financial or otherwise in any product discussed

Review of different types of wounds Discuss how mechanism of injury and systemic

disease affects treatment choices Review common and advanced wound care

treatment options for acute and chronic wounds

Mechanism of repair depends upon the tissue layers damaged

Partial Thickness - Epidermis and superficial dermal layer heal by regeneration. Does not form granulation tissue. No scarring.

Full Thickness - Deep dermis, appendages, hypodermis, muscle, tendons, ligaments, & bone heal by scar formation. If healing by second intention, granulation tissue is formed.

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Hemostasis Small vessels contact Platelets are activated and aggregate at damaged

vessels Coagulation cascade begins

Inflammation Neutrophils and monocytes begin clean up phase Macrophages are released to stimulate proliferative

phase Prolonged inflammation caused by Increased bacterial levels Repetitive trauma Contributes to hyper-proliferative scaring

(hypertrophic and keloid type scars)

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Only pressure injuries are ‘Staged’

Not all wounds on a diabetic are ‘diabetic ulcers’

If unsure of etiology use terms partial or full thickness to describe wound

Chronic Wound Definitions Wounds, which have failed to proceed through an orderly and timely reparative

process to produce anatomic and functional integrity over a period of 3 months

A wound that does not decrease in size by 30% in 3 weeks or by 50% in 4-5 weeks. If a wound does not decrease in size by 50% in 4 weeks there is a 91% chance it will not be healed within 12 weeks

Terms Stalled Wound Maintenance Wound Non-healable Wound

Widergrow,A.D.(2012) Deconstructing the stalled wound. Wounds (24)3, 58-66

Surgical

Trauma

Cutaneous manifestations of systemic disease

Move rapidly and predictably through the repair process

Most surgical wounds are closed by sutures, staples, adhesive tapes or glue

Surgical Wound Classifications Class I – clean, uninfected. Close with primary closure Class II – clean/contaminated, GI or GU or respiratory tracts were

entered during the surgery. No evidence of infection. Close with primary closure

Class III – open wounds or surgeries with spillage from GI tract. Delayed primary closure ( tertiary intention)

Class IV – Dirty Infected, older wounds, contaminated. Heal by secondary intention

SSI account for 22% of all hospital acquired infections

Poor statistics on outpatient SSI rates Most statistics are for ambulatory care surgical centers Estimated rate for ‘low risk’ procedures 0.74% to 2.42%

Principles for management of surgical site infections: Open and drain the incision Debride necrotic tissue Remove foreign bodies Manage the open wound Fill dead space and allow for wicking of drainage Do not over pack Maintain a moist wound bed Perform serial debridement s as needed. Wet to dry dressings are not an

acceptable method of debridement

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Infectious Diseases Society of America (IDSA) Guidelines for Treatment of Surgical Site Infections*

Fever 1st 48hrs & up to 4 days Evaluate, culture, consider other causes, open wound, start penicillin

and clindamycin

Fever > 4 days Evaluate, check WBC, monitor temp, culture Clean wound trunk, head, neck – cefazolin or vancomycin until

MRSA is ruled out Perineal/GI tract wound –cephalosporin + metronidazole or

levofloxacin + metronidazole or carbapenem

*Stevens, D. L., Bisno, A. L., Chambers, H. F., Dellinger, E. P., Goldstein, E. C., Gorbach, S. L., & ... Wade, J. C. (2014). Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the infectious diseases society of America. Clinical Infectious Diseases: An Official Publication Of The Infectious Diseases Society Of America, 59(2), 147-159. doi:10.1093/cid/ciu296

There are very few controlled trials assessing the effect of topical agents or dressings on healing rates of surgical wounds left to heal by second intention

Foam dressing are the best studied and are preferred over gauze: less pain with dressing changes, better absorption and less frequent dressing changes

Silver impregnated dressings are being used more used often after sternotomy and joint replacement surgery

Classification of burns (1st - 3rd degree system replaced)

Superficial Superficial partial-thickness Deep partial-thickness Full-thickness

Types of burns Thermal – heat or cold Chemical – Alkali, Acid, Vesicant Electrical – Voltage injuries, Arc injuries Radiation Inhalation

Electrical burns are associated with compartment syndrome, neurologic symptoms, and delayed complications

Silver sulfadiazine (SSD) – is quickly deactivated in wounds, requires frequent dressing changes to maintain antibacterial property

A Cochrane review found “some evidence that a particular antibiotic (silver sulfadiazine) applied directly to the burn actually increases the rates of infections by 8% to 80%” *

Air bag burns are caused by sodium hydroxide in aerosol from deployment. SSD and silver dressings can cause semi-permanent staining. For face injuries consider mupirocin

Pruritis associated with burns caused by release of histamine & dry skin Oral antihistamines Cool or tepid baths Moisturizer

* Barajas-Nava LA, López-Alcalde J, Roqué i Figuls M, Solà I, Bonfill Cosp X. Antibiotic prophylaxis for preventing burn wound infection. Cochrane Database of Systematic Reviews 2013, Issue 6. Art. No.: CD008738. DOI: 10.1002/14651858.CD008738.pub2

Partial thickness> 10% BSA

Burns of face, hands, genitals, feet or major joints

All chemical, electrical and inhalation burns

Persons with additional co-morbidities or injuries

Children

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70-80% of all leg ulcers are venous but there are many atypical lesions that can be misdiagnosed. The following are just some of the atypical ulcers that are seen

1. martorell's ulcer2. cutaneous vasculitis3. antiphospholipid syndrome leg ulcer4. necrobiosis lipoidica diabeticorum5. porphyria cutanea tarda leg ulcers6. calciphylaxis7. pyoderma gangrenosum8. kaposi's sarcoma9. squamous cell ca10. basal cell ca

Poor circulation at site of wound Limited arterial

vascularization Edema

Lymphedema

Non-reversal of etiology Recurrent trauma Foreign body retention Elimination/reduction

pressure Edema management

Co-Morbidities

Non-compliance

Poor Nutritional state

Poor wound care choices

Infection/Biofilms

Most common chronic wounds are: Pressure ulcers Venous ulcers Neuropathic ulcers Ischemic ulcers

Reported Rates of Recurrence Pressure ulcers 23%- 40% Venous ulcers 24%- 57% Neuropathic ulcers ~60%

Evidence-based Management Strategies for Treatment of Chronic Wounds Eplasty. . 2009 Jun 4;9:e19. 9e19http://www.pubmedcentral.nih.gov/tocrender.fcgi?journal=527&action=archive

Acute Infection Pain Purulent drainage Odor Edema Erythema Induration Systemic S/S Fever Lethargy Elevated white count Tachycardia Changes in blood pressure Confusion

Chronic Wounds Delayed healing Discolored granulation

tissue Friable granulation tissue Pocketing Foul odor Wound breakdown Increasing pain

Increasing pain and wound breakdown demonstrated 100% specificity as indicator for infection in chronic wounds

Dominant organisms in chronic wounds are Staph Aureus and Pseudomonas

Pooled research showed Staph present 80-100% and Pseudomonas present 43-100%

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Mild erythema around a new wound is normal

Generally, erythema ≥ 3cm = infection

Diabetic full thickness wounds ≥ 4 months old suspect osteomyelitis

Any chronic wound ≥ 6 months old - Consider biopsy

Biofilm development is common in older wounds

60 year old wound

75 year old wound

90 year old wound

Pedestal Formation - Bacteria attach to and move on host cells connecting the bacteria to the cytoskeleton

Tele-sensing Actively probe for information by

releasing proteins to assess conditions beyond the cell surface

Changes in the probes enable the bacteria to mount a specific response.

Smart Parasite Tempering of virulence to avoid

massive host tissue death Recruits other organisms Cause of 80% of all infections

Resist Antibiotics Secrete enzymes to modify

the ABX to an inactive form

Use efflux pumps to expel antimicrobials

Use mutants to render target proteins resistant to ABX

Persister Cells - Specialized survivor cells that become dormant and temporarily tolerant of ABX and metal ions. Then re-awaken and re-seed the host again.

BioFilms

Treatment:Surgically remove the colonized surface

Mechanical injuries Skin tears Pressure ulcers

Arterial ulcers

Venous ulcers

Diabetic ulcers

International Skin Tear Advisory Panel [ISTAP] Classification System

Category 1 Linear tear or flap. Skin edges can be approximated

to within 1mm

Category 2 Partial flap loss that can not

cover the wound bed

Category 3 Complete skin loss, no

epidermal flap

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Cleanse the wound

Realign the flap

Classify, measure

Low adhesive dressing

Maintain moist ( not wet ) surface

Lift dressings gently when changing

For wounds with flaps, draw arrow indicating direction to remove dressing to avoid lifting off flap

National Pressure Ulcer Advisory Panel’s Guidelines for staging

Blanching – Reactive hyperemiaStage I:Intact skin with non-blanchableredness of a localized area usually over a bony prominence. Darkly pigmented skin may not have visible blanching; its color may differ from the surrounding area.

Further description:The area may be painful, firm, soft, warmer or cooler as compared to adjacent tissue. Stage I may be difficult to detect in individuals with dark skin tones. May indicate "at risk" persons

Stage II:Partial thickness loss of dermis presenting as a shallow open ulcer with a red pink wound bed, without slough. May also present as an intact or open/ruptured serum-filled blister.

Further description:Presents as a shiny or dry shallow ulcer without slough or bruising.* This stage should not be used to describe skin tears, tape burns, perineal dermatitis, maceration or excoriation. *Bruising indicates suspected deep tissue injury

Stage III: Full thickness tissue loss. Subcutaneous fat may be visible but

bone, tendon or muscle are not exposed.

Slough may be present but does not obscure the depth of tissue loss.

May include undermining and tunneling.

Further description: The depth of a stage III pressure ulcer

varies by anatomical location. The bridge of the nose, ear, occiput

and malleolus do not have subcutaneous tissue and stage III ulcers can be shallow.

Bone/tendon is not visible or directly palpable.

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Stage IV: Full thickness tissue loss with

exposed bone, tendon or muscle. Slough or eschar may be present on some parts of the wound bed. Often include undermining and tunneling.

Further description: The depth of a stage IV pressure

ulcer varies by anatomical location.

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

Stage IV ulcers can extend into muscle and/or supporting structures (e.g., fascia, tendon or joint capsule) making osteomyelitis

Suspected Deep Tissue Injury: Purple or maroon localized area of

discolored intact skin or blood-filled blister due to damage of underlying soft tissue from pressure and/or shear.

The area may be preceded by tissue that is painful, firm, mushy, boggy, warmer or cooler as compared to adjacent tissue.

Further description: Deep tissue injury may be difficult to

detect in individuals with dark skin tones.

Evolution may include a thin blister over a dark wound bed.

The wound may further evolve and become covered by thin eschar.

Evolution may be rapid exposing additional layers of tissue even with optimal treatment.

Unstageable presence of slough or

eschar obscures depth of wound

Treatment Reduce/Relieve Pressure Bed – mattress overlay Chair – consult to Rehab/PT for

seating evaluation and pressure reducing seat cushion

Refer to Wound Center or Specialist

Until seen consider non-occlusive low adhesive dressing

Maintain moist ( not wet ) surface

Change dressings daily until seen by specialist

It is estimated that 7 million people in the United States have LEVD .

Venous insufficiency is a long-term debilitating disease that accounts for approximately 70 - 90% of all leg ulcers.

Each case of LEVD can cost up to $40,000 in health care resources

The annual cost for the treatment of venous leg ulcers in the U.S. is estimated to be between $570 million and $1.4 billion.

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Typically on lower half of legs at gaiter area or medial malleolus

Wounds are large and shallow with diffuse edges

Throbbing pain with generalized edema

Slough is present with heavy exudate

Hemosiderosis and lipodermatosclerosis usually present

Usually have relief of throbbing pain with elevation

Leg pain and edema that are relieved with elevation

Ankle flaring

Dry flaky itchy skin

Complaints of heaviness and dull ache in the legs

The presence of varicosities

Firm brawny edema [lipodermatosclerosis]

Dull aching or severe leg pain and leg heaviness.

Hemosiderosis

Dry flaky itchy skin

Stasis dermatitis Eczematous changes Erythema Scaling

Weeping dermatitis

May develop as a result of:

Malnutrition

Immobility

Leg trauma – most common cause Mechanical – scratching, abrasion Thermal – use of heating pad Chemical injury – OTC or Rx topicals, household cleaning

agents, plants ( poison ivy)

Peak age 60 -80 years

Venous Ulcers account for 80-90% of all leg ulcers

Estimated 7 million have venous insufficiency world wide and 3 million will progress to ulceration

Recurrence rates range from 57% to 97%

Healing: Most within 40-120 days, 25% remain unhealed at 1 year

LEVD vs. Lymphedema

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Chronic disease - impaired flow of lymph fluid caused by damage to the transport system (common)

lymph node excision Radiation fibrosis long standing venous disease

The end result - compromised lymphatic return with progressive accumulation of protein rich fluid in the interstitial space leading to fibrosis in the soft tissue & greater lymphatic obstruction.

Frequently under treated

Long term management is critical

Primary: rare, caused by congenital defects Secondary:

Commonly caused malignancy and treatment Filariasis: most common cause worldwide parasitic

infection of lymph vessels and nodes. Transmitted by mosquitoes

Stage 0-1 Reversible pitting edema beginning at the foot Negative or borderline Stemmer sign No palpable fibrosis

Stage 2 Nonpitting edema not improved with elevation Positive Stemmer sign Pronounced fibrosis Hyperkeratosis Papillomatosis

Stage 3 Lymphostatic elephantiasis Progressive fibrosis, hyperkeratosis Ulcerations

LYMPHEDEMA VENOUS INSUFFICIENCY

Non-pitting edema Not limited to the lower

leg Can involve genitals Stemmer sign No response to diuretics

Pitting edema Limited to the lower leg Does not involve

genitals No Stemmer sign Can respond to diuretics

“Painful fat syndrome” Negative Stemmer sign Tissue is painful and

bruises easily Palpate hard nodules

under the skin Abnormal distribution of

fat in lower extremities Bilateral heavy hips, thighs Non pitting edema Swelling ends at the

ankles

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First priority in treating venous ulcerations is management of edema COMPRESSION

Multi or single layer wraps are used acutely to manage edema.

Therapeutic support stockings are used for maintenance therapy.

Pneumatic pump devices may be used in the acute and in the maintenance treatment phases.

Dermatitis, scaling and pruritus are common on the periwoundarea, local wound care management must include considerations reduce irritant dermatitis and itching.

Treatment of edema and ulcers require local wound care and compression therapy

Ace wraps and antiembolism hose provide sub-therapeutic levels of compression and are not considered compression therapy

Compression stockings are generally for maintenance therapy after edema and ulcer have resolved

Compression therapy is contraindicated in patients with: Arterial insufficiency Uncompensated congestive heart failure Active untreated cellulitis Untreated infected leg ulcers Active thrombus

Types of Compression

Paste Wraps

Multilayer wraps

Short-Stretch (Single Layer)

Disposable

Reusable

Levels of Compression

Therapeutic level: 30 mmHg ABI >0.8 to 1.3

Low Level: 23 mmHgABI >0.5 to less than 0.8

No compressionABI ≤0.5

Would You compress this leg?

Would you un-roof the bullae?

Would You compress this leg?

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Unstable heart failure/CHF Venous thrombosis ABI<0.6

Subfascial Ligation of Incompetent Perforator Veins

Subfascial Endoscopic Perforating Vein Surgery (SEPS)

Skin grafts

Bioengineered skin equivalents

NPWT

Electrical Stimulation

Limb Elevation

Weight Control

Sodium intake reduction

Exercise

Establish maintenance plan Follow-up Care Patient Education Prevention Exercise

Skin Changes Shiny, Taut, Thin Dry Skin Hair Loss Atrophy of Subcutaneous Tissue Dystrophic Nails Skin Temperature

Ischemic pain: Intermittent claudication: 70 % occlusion Nocturnal pain : 70 – 90% occlusion Rest pain: 90 % occlusion

Ankle-Brachial Index > 1.0 - 1.3 Normal < 0.9 LEAD 0.6 – 0.8 Borderline perfusion <0.5 Severe Ischemia < 0.4 Critical ischemia

Toe Brachial Index <0.64 indicates LEAD

Transcutaneous Oxygen Pressure <40mmHg indicates hypoxic limb, < 30 critical ischemia (predicts failure to heal)

Pulse Volume Recording (PVR) indicated if ABI is >1.3

Can occur on any part of the leg, commonly at or below the ankle at lateral malleolus or on the toes.

Usually small, with even or ‘cliff ’ wound edges

Often appear with dry necrotic wound bed

Deep, painful wounds with minimal or localized edema

Often pain increases with elevation Cramping, aching, fatigue/weakness Tingling, burning type pain Rest pain: constant deep aching pain

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Local wound care is determined by the perfusion state of the extremity.

Use dry dressing for dry stable eschar on non-infected arterial wounds

For moist or draining wounds, choose dressings that are changed daily

Generally, avoid dressings that are changed every 3-5 days such as hydrocolloid dressings

Limit use of debriding agents to selected situations & carefully monitor

Frequently monitor the wound if moist dressings are ordered, such as hydrogels

Monitor regularly for subtle signs of infection

Surgical Options to Improve perfusion Bypass Grafts Endovascular Procedure

Pharmacologic Therapy ACE Inhibitors – increase walking distances Cilostazol – antiplatelete agent, reduce walking pain Aspirin Pentoxifylline – second line, inconsistent results

Hyperbaric Oxygen Therapy Life style Changes

Causes of Neuropathy: Metabolic diseases - diabetes mellitus Autoimmune diseases - lupus erthematosis Organ failure Endocrine diseases - hypothyroidism Infections - Lyme disease, HIV, & Hanson’s disease Trauma - Spinal cord injury, frostbite Idiopathic – genetic or undetermined etiology

Types of Neuropathy Sensory - loss of protective sensation and altered

perception to temperature, pain and touch Autonomic Motor – foot deformities, abnormal weight bearing Automomic - decreased sweating, altered blood vessel

tone

83% of lower limb amputations occur in Diabetics

5 year survival rate after amputation ranges from 41-70%

85% of Diabetic Amputations are Preventable

Three major causes of neuropatic ulcers Poorly Fitted Shoes Repetitive Pressure Penetrating Injuries

Frostbite

Identify perfusion status – at lease 25% of those with neuropathic ulcers have LEAD as well

R/O osteomyelitis

Off load to reduce or eliminate pressure and shear stress

Debride avascular tissue if adequate perfusion.

Chose local wound care to optimize off-loading, absorb/provide moist healing environment, limit contamination opportunities

Consider need for HBO or skin grafting for stalled, non-infected wounds

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Primary and Adjunct Therapies Poor nutrition results in: Decreased wound tensile strength Decreased phagocytic activity Decreased T-cell function Increased morbidity & mortality in surgical and medical

patients

Injury Increases metabolic rate due to release of catecholamine at the

time of tissue damage. Caloric & protein needs increase If no additional insult occurs, metabolic needs return to

baseline within 10-14 days For a chronic wound metabolic needs remain high

Hepatic Proteins Serum albumin 3.5 - 5.0 g/dl Transferrin 230-390 mg/dl Pre-albumin 19.5-35.8 mg/dl

Correlate with overall prognosis, less indicative of actual nutritional status

Reflect conditions causing inflammation Trauma Infection Injury

Creatinine Indirect measurement of skeletal muscle mass Measure of long term protein status Requires normal renal function & urinary output

Hemoglobin Hematocrit B12 Folate Serum Iron Total Iron Binding Capacity [TOBC]

Protein Angiogenesis

Collagen remodeling

Wound contraction

Fat Responsible for development & stability of cell membranes

They participate actively in inflammatory response to injury

Carbohydrates Energy source, turns to glucose

Excessive levels result in impaired healing

Vitamin A - fat soluble; important in deposition of collagen, reverses effects of corticosteroids

Vitamin C - water soluble; cofactor in collagen formation; important to fibroblasts

Zinc - enzyme systems, immune competency & collagen formation

Iron - important in hemoglobin for transport of oxygen

Copper - deficiency results in weaker scar formation, decreased tensile strength

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Amino Acids

Arginine

Glutamine

Cystine

These are indispensible (essential) in conditions of intense stress – trauma, chronic disease, & wounds

Removal of necrotic tissue/foreign bodies Elimination and/or prevention of infection Eliminate dead space Absorption of exudate Maintenance of moist wound environment Thermal insulation Protecting the wound from trauma Protecting the surrounding tissue Adequate nutrition

Avoid use of cleansing agents/solutions that are intended for use on intact skin such as : Chlorhexadine gluconate 4%, povidone iodine

The following are not recommended for routine use: povidone iodine sodium hypochlorite solution (Dakin’s Solution) hydrogen peroxide acetic acid

2008 Cochrane Review concluded that tap water was as effective as saline in cleansing wounds

Hypochlorus Acid HOCI affects microbial cell permeability & kills by binding to critical cell membrane

components Ph 5.4 Reduces odor Breaks down surface debris in wound bed Stable 72 hours at room temperature and 14 days if refrigerated

• Controlled trials found no difference in incidence of post procedure infections for superficial surgical wounds with use of topical antibiotics or a petrolatum based ointment

• Contact dermatitis to neomycin and bacitracin ranges from 1.5% to 13.1% in patch testing

• Mupuricin 2% is effective against methicillin-resistant Staphylococcus [MRSA]. Avoid overuse for non-MRSA

• Hydrogen peroxide interferes with tissue migration and proliferation of fibroblasts, in surgical wounds irrigation with H2O2 has been associated with crepitus, subcutaneous tissue destruction and wound dehiscence

• Povidone-iodine interferes with tissue migration and proliferation of fibroblasts . Can lead to systemic allergic reactions if used on a full thickness wound. S/S include – flu like symptoms, renal failure and anaphylaxis

Tissue Debridement is key factor in the management of non-healing wounds.

All necrotic tissue should be debrided unless it is contraindicated No arterial blood flow to affected area

When only palliative care measures are desired by the patient/family

The patient can not tolerate anesthesia for extensive surgical debridement.

Mechanical - sharp/surgical Irrigation Autolytic - occlusive or semiocclusive dressing

(Transparent films, hydrocolloids, hydrogels, & dextranomers)

Enzymatic - proteolytic substances that breakdown necrotic tissue: collagenase

Biologic - Maggot Therapy Wet-to dry dressings – not recommended Whirlpool – not recommended

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Change dressings as frequently as needed to prevent strike through of drainage to outer dressing and maceration of periwound tissues.

Relieve causative factors if possible: Pressure reduction Remove allergens Edema reduction

Do not mix topical treatments unless the manufacturer stands behind the combination Could be a safety hazard for patient Could nullify the effectiveness Could have a negative interaction between dressing ingredients

Alginate* Antimicrobial* Collagen Composites* Contact layers* Copolymer

Foam* Gauze* Hydrocolloid Hydrogel* Hydrofiber/ Fiber Gelling Transparent Film*

* These are the most helpful to have in your clinic or office

Contact LayersTo reduce trauma to granular wound or exposed structures/organs

There are varying degrees of permeability.

Have little or no ability to absorb

Use occlusive dressings with caution

Vaseline gauze Telfa

MepitelAdaptic

Indications superficial wounds

(skin tears) cover IV sites protect intact skin

Contraindications moderate to heavily

draining wounds wounds with friable

surrounding skin cavity wounds wounds with sinus

tracts full thickness wounds

Designed to absorb small to moderate amounts of drainage

Occlusive or semiocclusive dressing composed of gelatin, pectin & carboxymethylcellulose

Indication – Primary or secondary dressing for Partial and full thickness wounds, light to moderate exudating ulcers

Autolytic debridement

Use with caution in wounds with limited perfusion

Contraindication – known sensitivity to carboxymethylcellulose, infected wounds and heavily exudating wounds

Dressings designed to absorb moderate to large amounts of drainage include: alginates, foams and sodium impregnated gauze Alginates Foams Sodium impregnated

gauze

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Derived from brown seaweed, absorbent and conform to wound shape

Interaction with wound fluid creates gelatinous appearance

Can absorb up to 20x in weight

Indications – Moderate to heavy exudatingwounds

Contraindication – dry wound

Absorbent, non-adherent layer that provides non-traumatic removal

Indication Moderate to heavily exudating wounds Primary dressing for absorption Secondary dressing for wounds with packing Protection of fragile skin

Absorbs drainage around tube

Contraindication - Eschar

Hydrofiber Composed of fibers of

carboxymethylcellulose, non-woven, white cotton like product

Quickly turns to gel when in contact with wound fluid Holds it shape for ease with

removal Absorbs 33% more than

alginate

Indication - Moderate to heavily exudating wounds

Contraindication - Known sensitivity to carboxymethylcellulose

Collagen

• Fibrous insoluble protein produced by fibroblasts

• Indication - Minimal to moderate exudatingulcers; non-infected wounds

• Contraindication - Necrotic ulcers, allergic to biomaterial source (bovine, porcine, sheep)

Combination of 2 or more products manufactured as a single dressing and performs multiple functions

Indication - Minimal to heavy exudate, healthy granulation tissue, necrotic tissue, or mixed ulcers

Contraindication - No border of intact skin for anchoring the dressing

Moisture retentive dressings helpful in maintaining a moist wound environment for wounds with little or no drainage.

Water or glycerin based hydrating dressings

Contraindication - Heavily exudating wounds

Three forms:1. Amorphous2. Impregnated gauze3. Sheet

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Iodine is a well know antimicrobial agent

0.9% iodine is carried in polysaccharide beads

Provides a slow sustained release of iodine in non-cytotoxic concentrations

High rate of absorption from exudating ulcers.

No documented cases of bacterial resistance.

Contraindicated in known iodine allergy, dyes or seafood

Reduces the activity of collagenase, should not be used together

Can break down biofilms

Broad spectrum including MRSA and VRE

Non-toxic, active and readily available

Antimicrobial and mild anti-inflammatory

Silver sulfadiazine Effective for gram positive & negative bacteria as well as anaerobes and yeast Prolonged use may delay re-epithealization Do not use on sulfa sensitive patients

Precautions/Contraindications Should not be used with collagenase Use with caution in children [silver toxicity] Should not be used within 24hours of MRI Should not be used during pregnancy or lactation Should not be used in persons with silver allergy

Effective for gram positive & negative bacteria, anaerobes, fungi, yeast, and viruses

Low incidence of sensitivity

In a moist environment, dressings impregnated with silver can release silver ions over several days

Available in many forms Elemental Organic Inorganic

Some silver dressings require the use of sterile water for wound cleansing, normal saline may inactivate silver ions

Contains active Leptospermum Honey

Indications: Debridement, lowers wound pH, can breakdown biofilm

Available: Gel, alginate, hydrocolloid

Contraindications – allergy to honey, no evidence that sensitivity to bee venom is a contraindication

Indications: malodorous wounds, fistulas

Absorbs drainage and toxins

Typically used in Palliative/Hospice Care

Topical debriding agent may be ordered for eschar or slough on the wound bed

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Preserve lifeSave limb or functionPrevent or control infectionEliminate or minimize pain and stressHeal the woundStabilize the wound if healing is not a realistic

goalPalliative management of symptoms for terminalpatients

Pressure Injuries – reduce/prevent further pressure

LEVD – manage edema Compression

LEAD – improve circulation Revascularize

LEND - prevent further pressure Offload