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2/22/2013 1 WOUND CARE 101 A PLETHORA OF TIPS FOR EVERYDAY Regina F. Holmes MSN, RN, FNP-BC, CWOCN WOC SPECIALTY NURSING ADVOCATES FOR QUALITY, SAFETY, EFFICIENCY & EFFECTIVENESS IN PATIENT CARE WOC nursing is a specialty recognized by the American Nurses Association (WOCN®, 2010a). •WOC nurses provide expert clinical care to patients with wounds, pressure ulcers, fistulas, drains, stomas & continence disorders (WOCN®-WOCNCB®, 2008). –Improves healing outcomes –Builds a formulary of products to streamline consistent care for patients with WOC issues (e.g., dressings, supplies, modalities, equipment) –Develops protocols for cost-effective resource utilization –Provides proactive risk management •Designs/participates in initiatives to improve patient care such as: –Pressure ulcer prevention programs. –Catheter associated urinary tract infection (UTI ) prevention programs. –Surgical site infection prevention programs.

The Nuts and Bolts of Wound Care - 2018 Charleston … 2013/Holmes.pdf · •WOC nursing is a specialty recognized by the American Nurses Association ... DM, Cardiac, Respiratory,

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2/22/2013

1

WOUND CARE 101 A PLETHORA OF TIPS FOR EVERYDAY

Regina F. Holmes MSN, RN, FNP-BC, CWOCN

WOC SPECIALTY NURSING ADVOCATES FOR QUALITY, SAFETY, EFFICIENCY & EFFECTIVENESS IN PATIENT CARE

•WOC nursing is a specialty recognized by the American Nurses Association (WOCN®, 2010a).

•WOC nurses provide expert clinical care to patients with wounds, pressure ulcers, fistulas, drains, stomas & continence disorders (WOCN®-WOCNCB®, 2008).

–Improves healing outcomes

–Builds a formulary of products to streamline consistent care for patients with WOC issues (e.g., dressings, supplies, modalities, equipment)

–Develops protocols for cost-effective resource utilization

–Provides proactive risk management

•Designs/participates in initiatives to improve patient care such as:

–Pressure ulcer prevention programs.

–Catheter associated urinary tract infection (UTI ) prevention programs.

–Surgical site infection prevention programs.

2/22/2013

2

Elijah

http://www.bing.com/videos/search?q=ostomy&view=detail&mid=0842E987AB863D297E510842E987AB863D297E51&first=0&FORM=NVPFVR

Objectives for today:

1. Identify Common wounds

2. Identify Common Skin Rashes

3. Pharmacological Interventions

4. Treatment Modalities

Factors Impacting Wound Healing

Infection

Local or systemic

Mobility/pressure

Unable to do pressure relief measures

Devices (splints, cast, etc)

Co-morbid disease processes

DM, Cardiac, Respiratory, Autoimmune, Anemia,SCA

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Etiology of Wounds:

Intentional – surgery

Traumatic

Thermal

Autoimmune

Cancer

Allergic

Chemical

Microbial

Pressure/shear/friction

Wound Healing Cascade

Inflammatory Phase

– Stabilize wound by clot formation Platelets

Cytokines (growth factors)

Neutrophils

Wound looks “red”

Last 1-4 days

Wound Healing Cascade

Proliferative Phase

– Clean up – by macrophages Wound debridement

Migration of fibroblasts – needed for collagen synthesis

Angiogenesis

Formation of granulation tissue

Starts around day 4 and last about 21 to 28 days

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Wound Healing Cascade

Maturation Phase

– Final closure Continued formation of granulation tissue

Progressive epithelialization from margins

Simultaneous synthesis and breakdown of collagen

Collagen becomes organized in bundles to increase tensile strength of new tissue

Last from day 21-28 until about 3 months

NOTE: Scar tissue will never be as strong as normal tissue, about 80% strength at 3 months.

Examples of Wound Types: Cancer Allergic

Chemical Microbial

Types of Wounds:

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Types of Wounds:

Acute or Chronic?

Acute are either traumatic or surgical

Chronic wounds

Classification of Wounds

Partial Thickness

- can go into dermal layer but not through

Full thickness

- can go through all layers, even into bone

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IAD:

Do not use a pressure ulcer classification system to describe wounds other than pressure ulcers. Educate the professional on differentiating pressure ulcers from other types of wounds (e.g.venous ulcers, arterial ulcers, neuropathic ulcers,traumatic

IAD:

venous ulcers, arterial ulcers, neuropathic ulcers,

incontinence-associated dermatitis, skin tears, and

intertrigo).”

Copyright EPUAP/NPUAP Nov 2009 from NPUAP.org

IAD risk factors:

Chronic exposure to moisture

Fecal and urinary incontinence

Use of a containment device

Alkaline pH (soaps, ammonia, moist skin)

Overgrowth or infection with pathogens

Friction

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Zinc Oxide:

(ie Desitin, Creamy Desitin, Calmoseptine, Calazime,

EPC, Sensicare, Baza, Criticaid)

.Slightly drying - great for weepy skin

Remove every few days or so using oil (NO SCRUBBING!!!!!)

Use ARD (anorectal drsg) or telfa

since zinc oxide is so thick

Do NOT tape the buttocks!

IAD:

Balsam of Peru

Spray (Granulex) or ointments (BTC, Xenaderm)

Castor oil- protective vegetable oil with antioxidants

Small amount of trypsin- enzyme

Balsam of Peru- a pro-inflammatory substance

Great for those superficial injuries that won’t heal

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Balsam of Peru

because the person doesn’t have a very active

immune response

(inflammation- first phase of healing)

. Avoid on highly inflamed skin!

Treatment

Friction damage/Skin Tears

May be treated with soft silicone or low tack foam dressings. Hold in place with stocking-like products or cotton gauze wraps. They tended to achieve wound closure within 7 to 10 days. cleaning with normal saline, control of bleeding, and clots removal. Skin flaps should be approximated if possible. Dressing applied depends on wound characteristics.

Pressure Ulcers

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Background and Significance

Pressure ulcers are becoming common. According to Heath Cost and Utilization Project(HCUP) developing before or after hospitalization increased by 80% between 1993- 2006(Russo,Steiner, & Spector, 2008).

Pressure ulcer related cost:

Inpatient stays with diagnosis of Pressure Ulcers totaled 11 billion in 2006.

Average Length of stay is 5 days costing $ 10,000,

Average pressure ulcer related stay is 13-14 days costing $16,755-$20,438

More likey to be discharged to a long term care facility(3 times the rate of other dx)

Overall Principles of Effective Wound management

Identify and Correct exologic(environmental) factors

Systemic support for wound healing

Evidenced based topical Therapy

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Background and Significance

56.5 % are > 65 years

Paralysis and spinal cord injuries were most common in younger adults with the diagnosis of pressure ulcers (Russo et al., 2008).

Background and Significance

Pressure ulcers are areas of localized injury to the skin/or underlying tissue usually over a bony prominance, as a result of pressure , or pressure in combination

with shear.”(NPUAP/EPUAP,2009).

Pressure Ulcers

In 2007 the National Pressure Ulcer Advisory Panel(NPUAP) redefined and updated the definitions of pressure ulcer and the stages of pressure ulcers, including the original 4 stages and added 2 new stages; deep tissue injury and unstagable pressure ulcers (WOCN PU Guidelines ,2008).

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NPUAP Pressure Ulcer Staging

Suspected Deep Tissue Injury:

Purple or maroon localized area of discolored intact skin or blood filled blister due to damage to underlying soft tissue from pressure and/or sheer. The area may be preceded by tissue that is painful, firm, mushy, boggy, warmer or cooler as compared to adjacent tissue. NPUAP 2007

DTI:

Stage I:

Intact skin with nonblanchable redness of a localized usually over a bony prominance. Dark skin My not have visible blanching; its color may differ from surrounding skin.

NPUAP 2007

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Stage I

Stage II:

Partial thickness loss of dermis presenting as a shalloe open ulcer with red pink wound bed, without slough. May also present as an intact or opened/ruptured blister.

NPUAP 2007

Stage II

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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 or tunneling.

NPUAP 2007

Stage III

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 includes undermining or tunneling.

NPUAP 2007

2/22/2013

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Stage IV

Unstagable:

Full thickness tissue loss in which the base of the ulcer is covered by slough (yellow, tan, gray, green or brown) and/or eschar (tan, brown or black) in the wound bed.

Copyright: NPUAP 2007

Unstagable

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LEVD:

An estimated 7 million adults in the US have a venous disorder such as venous insufficiency. These under-recognized vascular problems result in severe skin damage and ulcerations of the lower legs, produce pain, and restrict mobility.

LEVD:

Available data indicate that $3 billion is spent annually on leg ulcer care. Approximately 7 out of every 10 individuals with a previous venous leg ulcer (VLU) will experience a new one each year

LEVD:

Assessment

• Four key areas to assess are the

limb, skin, circulation, and wound.

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LEVD Risk Factors:

• 20 – 50% risk of developing a

venous leg ulcer (VLU) if varicosities left

unattended/untreated.

• Restricted ankle movement and

reduced calf muscle pump power.

• Injection drug use.

Triggers:

• External events or exacerbating factors

associated with ~75% of VLUs

– Cellulitis

– Penetrating injury/trauma

– Contact dermatitis

– Rapidly aggravating leg edema

– Burns, Dry skin with itching

– Insect bites

Factors impeding healing

Factors impeding healing

• Pain

• Co-morbid conditions

– Cardiac, rheumatoid arthritis, lymphedema, obesity,

lower extremity arterial disease

• Ulcer deeper than 2 cm

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Factors Impeding Healing:

History of debridement

• Presence of multiple VLUs

• Below normal hemoglobin counts

• Short walking distance < 200 m

• Smoking

• Higher disease severity including lipodermatosclerosis

Factors Impeding Healing

• Medications: corticosteroids and

immunosuppressive agents

• Older age

• Ulcer chronicity > 4 weeks

• Venous refill time < 20 seconds

Venous Dermatitis

• Eczema

– Elevated homocysteine (Hcy) levels

(hyperhomocysteinemia

• LOE = C

– Associated with increase severity of

disorder and VLUs

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Factors contributing to ulcer: Factors contributing to ulcer

recurrence

Body mass index (BMI) ≤ 20 kg/m2

Malnutrition

Depression

Decreased physical activity

Lack of leg elevation

Not wearing compression, Cardiac disease

Diagnostics:

– Duplex scanning with ultrasound, with or without color,

is the most reliable, noninvasive test to diagnose

Diagnostics:

anatomical and hemodynamic abnormalities and to detect reflux in any venous segment

• Photoplethysmography (PPG), air plethysmography (APG)

– Assess perfusion status to rule out combined disease

• Ankle brachial index

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ABI

http://www.youtube.com/watch?feature=player_detailpage&v=5Wclloi-qjU

Diagnostics:

• Skin temperature (increased temperature associated with

VLUs, infection, non-healing) (LOE = C)

Prevention of VLUs and progression of CVD: • Aggressive treatment of:

– Varicosities

• Weight management, physical activity,

foam sclerotherapy

– Cellulitis and acute dermatitis

– Pain

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Prevention of VLUs and progression of CVD: • Compression:

– Recurrence rates are lower in persons wearing high compression

(e.g., 40–50 mm Hg) hosiery compared

to medium (e.g., 30–40 mm Hg) compression hosiery;

Offer strongest compression tolerable

Prevention of VLUs and progression of CVDs – Adherence rates are significantly higher

with

moderate compression than with high-compression

Adjunctive Therapies

• Subfascial endoscopic perforator

(SEPS) surgery:

– there is some positive evidence about

the effects of surgical interventions

such as SEPS on preventing VLU

recurrence.

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Medicatins:

• Horse chestnut seed oil (Aesculus

hippocastanum L).

oral or topical phlebotonics.

• Micronized purified flavonoid

fraction (MPFF).

Patient Education:

Use compression therapy for the

remainder of their life.

• Use highest compression possible or

tolerated.

• Avoid mechanical trauma to the lower

leg.

• Discuss medication options with PCP

Devitalized tissue:

Devitalized tissue

• No one method of debridement has

been shown to be optimal for LEVD

ulcers.

• There is evidence to support the use

of larval (maggot) therapy to remove

necrotic tissue compared to different

types of debridement techniques.

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Topical dressings • There is insufficient evidence to

determine whether honey dressings

are beneficial in decreasing wound

healing rates compared to usual

care (e.g., compression and nonadherent

dressings).

Infection • The offending organism, through culture,

needs

to be determined for appropriate treatment. It is

important to consider the growing concern

regarding antibiotic resistance

Infection:

• Quantitative swab cultures have been

demonstrated to be a reasonable alternative to tissue biopsy in clinical practice for chronic wounds of which venous ulcers are included, to rule out infection

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Infection:

Antibacterial preparations should only be used in cases of clinical infection and not for bacterial colonization.

No conclusive studies to guide definitive topical antibiotic choice, dose and duration.

Use of newer, relatively nontoxic antimicrobials (e.g.,cadexomer iodine or silver dressings) over topical antibiotics

Nutrition:

Oral zinc sulfate does not appear to aid in the healing of leg ulcers in individuals with normal zinc levels. There is also limited evidence of benefit in people with LEVD who have low serum zinc. Thus, further research is needed to determine the benefits of zinc in patients

Compression:

• Multi-layer systems are more effective than single-layer systems

Examples of compression: Profore,Unna’s Boot

Juxta Lite

Trental (pentoxifylline).

– Dosages of 400 mg orally three times per day can accelerate healing of venous ulcers

2/22/2013

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Example of 4 layer Compression:

Juxta- Lite

<iframe width="640" height="360" src="http:" frameborder="0" allowfullscreen></iframe>

IPC:

(IPC) may be used for patients who are immobile or who need higher levels of compression than that which can be provided with

stockings or wraps, such as those with extremely large

legs or who are intolerant of stockings or wraps.

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Medications:

Trental (pentoxifylline).

– Dosages of 400 mg orally three times per day can accelerate healing of venous ulcers

Granulocyte-macrophage colony stimulating factor (GMCSF).

A cytokine with pleiotropic functions) peri-ulcer injection

Medications:

• Horse chestnut seed extract (Escin/Aescin). Dosages of 300 mg containing 50 mg of the active ingredient

escin, twice daily – short term use

• Sulodexide (a glycosaminoglycan composed of low

Medications:

• Sulodexide (a glycosaminoglycan composed of low

molecular weight heparin (80%) and dermatan sulfate

(20%).

– Available orally and intramuscularly

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Surgical Options:

• Superficial venous surgery consists of

perforator ligation, minimally invasive surgery

(endoscopic) and invasive (open) surgery.

Superficial venous surgery combined with

compression compared to compression alone is as equally effective at increasing healing rates at 24 weeks.

Adjunctive Therapies:

• Biologic skin substitutes (BSSs).

• Whirlpool : insufficient evidence to support the use of whirlpool

• Laser therapy—low level (LLLT).

US

– There is limited evidence to support the use of LLLT.

• Electromagnetic therapy.

Adjunctive Therapies:

Negative pressure wound therapy (NPWT)

• Hyperbaric oxygen therapy (HBOT).

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Patient Education and Follow up:

Educate patients about wearing compression for a lifetime, smoking cessation, physical activity/exercising,

avoiding trauma/leg crossing, and following healthy diet

weight management and nutrition.

assess adherence ,condition of stockings, bandages, and wraps.

Lower Extremity Arterial Disease Lower extremity arterial disease (LEAD)

commonly referred to as PVD,PAD ,POAD, refers to disorders affecting the leg arteries.

CVD is the number one killer in the U.S., with 8-10 million people afflicted with LEAD. A disease often silent until a limb or life-threatening event occurs.

Lower Extremity Arterial Disease Based on ABI <0.9 LEAD is present in 29% of

patients 70 years or older and in 29% of patient 50-69 years who use tobacco or have Diabetes.

Uder diagnosed, under treated due to asymptomatic and atypical symptoms( absence of claudification).

Increased risk of CV and Cerebrovascular morbidity and mortality

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Lower Extremity Arterial Disease Lower Extremity Arterial Disease (LEAD)is

chronic and 90% of patients will have a progression of the disease in 5 years (Notcolff et al., 2002). The most common cause is atherosclerosis which is characterized by plaque formation ,thought to be triggered by vascular injury and inflammation.

Lower Extremity Arterial Disease Stenosis results from plaque formation and

over time results in ischemia. LEAD is associated with degenerative disorders such as collagen abnormalities, vasculitic disorders, systemic disorders such as Lupus, and Rheumatoid arthritis. Lower extremety circulatory problems can occur when other conditions are present: protein C deficientcy and Raynaud’s disease.

Risk Factors:

Advanced age

Smoking

Diabetes

Dyslipidemia

Hpypertension

Hyperhomocysteinemia

CRI, Family HX of CVD, Ethnicity

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Risk Factors

Periodontal Disease

Biomarkers associated with LEAD: CRP, Fibrinogen,D-Dimer,

Assessment:

Functional ability

Pain history:

Intermittent Claudication

Exacerbating Factors: elevation and exercise

Alleviating factors: rest,dependency

ALI (6 Ps)verses CLI

ABI

>1.3 Elevated (non-compressable

>1.0 Normal

<0.9 LEAD

<0.6-0.8 Borderline

<0.5 Severe Ischemia <0.4 Critical limb Ischemia

Toe Pressures <30 (<50 DM) = CLI

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ABI

>1.3 Refer further vascular testing

>1 Blood Flow sufficient to heal

<0.9 LEAD: Conservative therapy

<0.6-0.8 Borderline perfusion : vascular referral if no response in 2-4 weeks

<0.5 Severe Ischemia : Vascular

ABI:

Maintain stable dry black eschar

<0.4 CLI : Urgent Vascular evaluation

Medications:

Statins

Cilostazol 100mg BID

ACE inhibitors

Ramipril

ASA

Thienopyridines

Clopidogrel 75 mg maybe > effective than ASA

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Surgical Options:

Bypass/Angioplasty

Skin Grafting

Amputation

Where do diabetic ulcers occur? Diabetic ulcers tend to occur in the following

areas:

– Areas most subjected to weight bearing, such as the heel, plantar metatarsal head areas, the tips of the most prominent toes (usually the first or second), and the tips of hammer toes (Ulcers also occur over the malleoli because these areas commonly are subjected to trauma.)

– Areas most subjected to stress, such as the dorsal portion of hammer toes

Diabetic or Pressure?

The etiologies of diabetic ulceration include neuropathy,7 arterial disease,8 pressure,9 and foot deformity.10

2/22/2013

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Not just traditional pressure With damage to the nervous system, a

person with diabetes may not be able to feel his or her feet properly. Normal sweat secretion and oil production that lubricates the skin of the foot is impaired. These factors together can lead to abnormal pressure on the skin, bones, and joints of the foot during walking and can lead to breakdown of the skin of the foot.

Diabetic or pressure?

SKIN TEARS

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Skin Tears:

Skin Tear of the Hand

Skin Tears:

2/22/2013

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Skin Tear:

Skin Tears:

Skin Tears:

2/22/2013

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Classification of Skin Tears:

What to do?

Step 1: Predicting Risk

It is critical to predict and identify those at

high risk for skin tears so that an appropriate

prevention program can be implemented before

injury occurs (Bank & Nix, 2006; Carville et

al., 2007; LeBlanc et al., 2008). Older adults are

at high risk for the development of skin tears

Prevention Strategies:

Step 2: Prevention Strategies

Most skin tears occur accidentally during routine

patient care activities. Education and involvement

of family and caregivers in the prevention

of skin tear development is imperative.

2/22/2013

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Treatment:

Step 3: Treatment

Although prevention of skin tears should remain

the primary focus, evidence-based wound

care principles should be used when a skin tear

develops. The same principles used for other

wounds should be employed when treating

skin tears.

Treatment :

Skin tears should be treated in a systematic

way to include cleansing with normal saline,

controlling bleeding, removing a clot, and selecting

an appropriate dressing to address

the wound characteristics.

Initial Treatment: Replace the skin flap, if possible, by gently

rolling the skin flap over the wound. Best

practice supports that a skin flap be approximated

if possible, and a hydrogel,

alginate, foam, soft silicone, or nonadherent

dressings be applied over the

replaced flap, depending on the wound

characteristics (LeBlanc & Christensen,

2005; LeBlanc et al., 2005

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Dressing Selection :

Based on Characteristics:

Transparent

Nonadherent

Foam

Silicone

Hydrogel or sheets

alginate

How to Care for Wound with A Skin Flap? A skin flap

may not cover the entire wound, but

should be positioned to increase the

chance for it to “take” onto the wound

bed. The skin flap can be approximated

by using a moistened cotton tip applicator

and gently “rolling” the skin flap into

place. If the skin flap is not viable, debride

MRSA UPDATE IDSA 2012

For a cutaneous abscess, incision and drainage is the primary treatment (A-II). For simple abscesses or boils, incision and drainage alone is likely to be adequate, but additional data are needed to further define the role of antibiotics, if any, in this setting.

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Finger Abscess

http://www.youtube.com/watch?v=aHA44fYCzCk&feature=player_detailpage

Antibiogram

MRSA UPDATE

Antibiotic therapy is recommended for severe or extensive disease (involving ultiple sites of infection) associated cellulitis, signs and symptoms of systemic illness, associated comorbidities or immunosuppression, extremes of age, abscess in an area difficult to drain (eg, face, hand, and genitalia), associated septic phlebitis, and lack of response to incision and drainage alone (A-III).

For outpatients with purulent cellulitis (eg, cellulitis associated with purulent drainage or exudate in the absence of a drainable abscess), empirical therapy for CA-MRSA is recommended pending culture results. Empirical therapy for infection due to β-hemolytic streptococci is likely to be unnecessary (A-II). Five to 10 days of therapy is recommended but should be individualized on the basis of the patient's clinical response

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MRSA CONT.

For empirical coverage of CA-MRSA in outpatients with SSTI, oral antibiotic options include the following: clindamycin (A-II), trimethoprim-sulfamethoxazole (TMP-SMX) (A-II), a tetracycline (doxycycline or minocycline) (A-II), and linezolid (A-II). If coverage for both β-hemolytic streptococci and CA-MRSA is desired, options include the following: clindamycin alone (A-II) or TMP-SMX or a tetracycline in combination with a β-lactam (eg, amoxicillin) (A-II) or linezolid alone (A-II).

MRSA CONT.

For outpatients with nonpurulent cellulitis (eg, cellulitis with no purulent drainage or exudate and no associated abscess), empirical therapy for infection due to β-hemolytic streptococci is recommended (A-II). The role of CA-MRSA is unknown. Empirical coverage for CA-MRSA is recommended in patients who do not respond to β-lactam therapy and may be considered in those with systemic toxicity. Five to 10 days of therapy is recommended but should be individualized on the basis of the patient's clinical response

The use of rifampin as a single agent or as adjunctive therapy for the treatment of SSTI is not recommended (A-III).

MRSA CONT

For hospitalized patients with complicated SSTI (cSSTI; defined as patients with deeper soft-tissue infections, surgical/traumatic wound infection, major abscesses, cellulitis, and infected ulcers and burns), in addition to surgical debridement and broad-spectrum antibiotics, empirical therapy for MRSA should be considered pending culture data. Options include the following: intravenous (IV) vancomycin (A-I), oral (PO) or IV linezolid 600 mg twice daily (A-I), daptomycin 4 mg/kg/dose IV once daily (A-I), telavancin 10 mg/kg/dose IV once daily (A-I), and clindamycin 600 mg IV or PO 3 times a day (A-III). A β-lactam antibiotic (eg, cefazolin) may be considered in hospitalized patients with nonpurulent cellulitis with modification to MRSA-active therapy if there is no clinical response (A-II). Seven to 14 days of therapy is recommended but should be individualized on the basis of the patient's clinical response.

2/22/2013

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MRSA

Cultures from abscesses and other purulent SSTIs are recommended in patients treated with antibiotic therapy, patients with severe local infection or signs of systemic illness, patients who have not responded adequately to initial treatment, and if there is concern for a cluster or outbreak (A-III).

For children with minor skin infections (such as impetigo) and secondarily infected skin lesions (such as eczema, ulcers, or lacerations), mupirocin 2% topical ointment can be used (A-III). 10. Tetracyclines should not be used in children <8 years of age (A-II).

MRSA

In hospitalized children with cSSTI, vancomycin is recommended (A-II). If the patient is stable without ongoing bacteremia or intravascular infection, empirical therapy with clindamycin 10–13 mg/kg/dose IV every 6–8 h (to administer 40 mg/kg/day) is an option if the clindamycin resistance rate is low (eg, <10%) with transition to oral therapy if the strain is susceptible (A-II). Linezolid 600 mg PO/IV twice daily for children ≥12 years of age and 10 mg/kg/dose PO/IV every 8 h for children <12 years of age is an alternative (A-II).

Recurrent SSTIs Preventive educational messages on personal

hygiene and appropriate wound care are recommended for all patients with SSTI. Instructions should be provided to:

i. Keep draining wounds covered with clean, dry bandages (A-III).

ii. Maintain good personal hygiene with regular bathing and cleaning of hands with soap and water or an alcohol-based hand gel, particularly after touching infected skin or an item that has directly contacted a draining wound (A-III).

2/22/2013

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Recurrent SSTIs CONT.

Avoid reusing or sharing personal items (eg, disposable razors, linens, and towels) that have contacted infected skin (A-III).

13. Environmental hygiene measures should be considered in patients with recurrent SSTI in the household or community setting:

i. Focus cleaning efforts on high-touch surfaces (ie, surfaces that come into frequent contact with people's bare skin each day, such as counters, door knobs, bath tubs, and toilet seats) that may contact bare skin or uncovered infections (C-III).

What is the management of MRSA pneumonia? Pneumonia For hospitalized patients with severe community-acquired

pneumonia defined by any one of the following: (1) a requirement for intensive care unit (ICU) admission, (2) necrotizing or cavitary infiltrates, or (3) empyema, empirical therapy for MRSA is recommended pending sputum and/or blood culture results (A-III).

For health care–associated MRSA (HA-MRSA) or CA-MRSA pneumonia, IV vancomycin (A-II) or linezolid 600 mg PO/IV twice daily (A-II) or clindamycin 600 mg PO/IV 3 times daily (B-III), if the strain is susceptible, is recommended for 7–21 days, depending on the extent of infection.

In patients with MRSA pneumonia complicated by empyema, antimicrobial therapy against MRSA should be used in conjunction with drainage procedures (A-III).

CALCIPHYLAXIS

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Dermatologic Delimas

Steven Johnson’s Syndrome

SJS

SJS

2/22/2013

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SJS:

What id this?

Shingles

2/22/2013

44

Herpes:

Opthalmic :

Psoriasis:

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Finger Abscess

http://www.youtube.com/watch?v=aHA44fYCzCk&feature=player_detailpage

Overall Principles of Effective Wound management Identify and Correct exologic factors

Systemic support for wound healing

Evidenced based topical Therapy

Treat the Whole patient, not the hole in the patient!!!

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Wound Management

3 requirements for wound healing

– Etiology-what “caused” the wound. Try to correct or manage the cause.

– Systemic- is the pt ‘able” to heal? Education to pt to improve healing ability.

– Topical- what dressing or topical treatment is applied to the wound . Based on DIPAMOPI.

Etiology

Determine the cause

Correct or manage the cause

– Pressure-support surfaces, turning, etc

– Venous stasis-compression

– Arterial-vascular consult

– Surgical-NA

– Diabetic-glucose control, offloading

– Atypical-varies, referral to dermatology (?)

– Skin tears-improve skin integrity, pad items

Systemic Support

Nutrition-protein 1.2-1.5g/kg/d & calories 30cc/kg/d

Perfusion-decrease reducible factors

BMI-appropriate wt/ht

Activity-

Glucose management

Hydration-30cc/kg/d typical

Immune system

Manage co-morbidities

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Debridement options

Surgical converts chronic wound to acute

wound

best option for full thickness wounds with abscess, sepsis, etc.

Debridement options

Conservative sharp Using scalpel, scissors and/or

pickups/forceps

Best option for patient with loose avascular tissue who is a not good candidate for surgical debridement

NC nurse practice act governs who can do this

Contraindications: clotting disorder, systemic infection

Debridement options

Chemical (Dakin’s solution) Use of non-enzymatic solutions

to promote breakdown of necrotic tissue

Indicated for wound with necrosis and odor

Some confusion of what “1/4 strength” really means

Note: Dakin’s solution loses potency in 24-48 hrs

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Debridement options

Surgical converts chronic wound to acute

wound

best option for full thickness wounds with abscess, sepsis, etc.

Debridement options

Conservative sharp Using scalpel, scissors and/or

pickups/forceps

Best option for patient with loose avascular tissue who is a not good candidate for surgical debridement

NC nurse practice act governs who can do this

Contraindications: clotting disorder, systemic infection

Debridement options

Hydrotherapy

Whirlpool

Best for burns

Con: possible spread of infection

Pulsatile lavage

8-15 psi to soften and remove necrotic tissue, debris, bacteria

Effective on slough, but not on eschar

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Debridement options

Autolytic

Utilizes WBC and enzymes in wound fluid to digest necrotic tissue

Safe, non-invasive Will usually see significant progress within 72 hours

Debridement options

Mechanical debridement:

NON-SELECTIVE and PAINFUL

Use of saline moistened gauze that is allowed to dry on the wound bed, typically 4-8 hours after application

As gauze dries, necrotic tissue (and unfortunately viable tissue) adheres to the gauze

When gauze dressing is removed, the necrotic tissue (and unfortunately the adherent viable tissue) is removed as well

Identify Infection

Tissue biopsy

Most accurate

Most difficult and invasive

Fluid aspiration

Most effective in sterile cavity infections

Swab culture

Only as effective as the operator

Don’t culture “pus” – only clean tissue

Must express fluid from “clean tissue” in wound bed

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Identify and treat infection

All open wounds are contaminated - but…not all wounds are infected

“Bacterial load or bioburden” – may

be too high to allow healing but not “really” infected

Can treat topically

Infection (colony counts > 100,000)

needs to be promptly detected and properly eliminated

Maintain moist wound surface

Moist wound surface promotes cell migration

Moist wound surface prevents cell death (that occurs when wound dries out)

Protect From Trauma

Healing or newly healed tissue is fragile

50% of normal skin strength at 2 weeks

80% of normal within 3 months

NEVER as strong as original

Infection – delays healing

sudden failure to progress can indicate new infection

Repeated injury - delays healing

Scar tissue does not have normal cell regeneration properties

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Insulate

Maintain normal temperature

Negative effects of sub-normal temperature

vasoconstriction

cellular activity declines

Wound Care Product Selection

Pick the product that meets the most acute need at each level of healing

If no progress is seen within 2 weeks, re-assess and modify approach

Every wound care product is GREAT for SOME WOUNDS, BUT--- no one product is GREAT for EVERY WOUND

Advanced Therapies: Ultrasonic Debridement

Ultrasonic-assisted wound debridement

Low frequency US – cleaves through necrotic tissue and biofilm

“painless”

Types of wounds

Any chronic wound

Pressure ulcers

Diabetic ulcers

Venous ulcers

Burns

Surgical wounds

*Sonoca by Söring

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Advanced Treatments: Vacuum Assisted Closure Systems

Wound VAC Must have “relatively” clean wound

bed

Must have some depth

Must be free of infection or at least under treatment

Can be used at home, in hospital or in extended care facilities

Advanced Therapies: Hyperbaric Oxygen

Medical application Other conditions treated:

Autism

Cerebral palsy

Multiple sclerosis

Attention deficit disorder

Fibromyalgia

Chronic fatigue

Crohn’s disease/colitis

MI

Mitochondrial disorders

Ammonia toxicity

Carbon monoxide inhalation

Advanced Treatments: Bioengineered Altered Tissue: Skin

Equivalents

Graft Jacket.

derived from human dermis and

contain collagen fibers

If the wound is like a “crater”, the

Ulcer Repair Matrix (sheet form)

may be used to graft the wound

and aid in the body’s repair.

If the wound is a “tunneling”

wound, the GRAFTJACKET®

XPRESS Scaffold can be used

by applying the graft by syringe

into the wound and filling the

“tunnel”.

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Vacuum Assisted Closure Systems

Blue Sky Must have “relatively” clean wound

bed

Works well with wounds with depth but little open surface area

Instead of foam, uses a suction tubing

Advanced Treatments: Growth factors

Regranex only FDA-approved prescription

medicine that contains platelet-

derived growth factor

Contraindications:

patients with known skin cancers

at the site of application

wounds that are stitched or stapled

patients sensitive to any

components of this product (e.g.,

parabens)

Advanced Treatments: Growth factors

Autologous Platelet Collection System uses 55 ml of patient’s whole

blood

Centrifuge separates blood – isolating plasma into:

Platelet poor

Platelet rich

Platelet “rich” is put into wound

Cell Factor Technologies, Inc GPS Platelet Concentration System

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Advanced Therapies: Hyperbaric Oxygen

Origin of HBO therapy In US: Mid-to-late 1930s

Treat “bends”

Developed in Milwaukee

Medical application Mid-1960’s gained favor

Typical wound conditions:

Burns

Surgical

Infections

Diabetic ulcers

Crushing injuries

Bone fractures

Advanced Treatments: Bioengineered Altered Tissue: Skin

Equivalents

Non-autologous grafts Neonatal foreskins

Interwoven into some form of matrix that either dissolves or becomes incorporated into body tissue

Most sent frozen

Most common: Apligraft, Dermagraft and Graft Jacket

Advanced Treatments: Bioengineered Altered Tissue: Skin

Equivalents

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Advanced Treatments: Bioengineered Altered Tissue: Skin

Equivalents

Transcyte Nylon mesh fabric which has

human fibroblast

Cryopreserved

High levels of protein and growth factors

Nylon is not biodegradable

Advanced Treatments: Bioengineered Altered Tissue: Skin

Equivalents

Advanced Treatments: Bioengineered Altered Tissue: Skin

Equivalents

OASIS comprised of porcine-derived

acellular small intestine

submucosa

compatible with human tissue

unique because it is a complex

scaffolding

provides an optimal environment

- restoration of tissue structure

and function. indicated for partial and full

thickness wounds and skin loss

injuries as well as superficial and

second-degree burns.

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Advanced Therapy: Anodyne

Anodyne Therapy Use of infrared light emitting

diodes (LED)

Penetrates up to 5 cm of tissue depth

Improves circulation

Reduces pain and stiffness

Reduces muscle spasms

Works well with neuropathic ulcers

Advanced Therapies: Probiotics

Probiotics means "for life"

refers to concentrated supplements of beneficial or good bacteria

Over use of antibiotics have weakened immune systems

Probiotics - the good friendly bacteria, promotes the body's natural immunity

keeps us healthy and helps our digestion

necessary to keep the bad bacteria level lower

There are many “good bacteria” available

Examples of Probiotics

Colloidal silver

Oregano

Aloe vera

Calcium magnesium powder

Omega 3 Fish Oil

Reference list

Available on request

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Questions?? [email protected]