PRESSURE ULCER PREVENTION &

TREATMENT

Prepared byLinda Kennedy-Mull

All SCI individuals are at risk for developing pressure ulcers (PU).

Pressure Ulcers occur more frequently in people

with:

More extensive paralysis & completeness of SCI

Longer duration of SCI Less functional independence (para’s vs. quad’s)

Irresponsible behavior – smoking/ETOH/drug abuse

Poor nutrition Those who won’t assume

responsibility for skin care

Incidence:

32-40% of individuals admitted to SCI units in the USA develop pressure ulcers during initial hospitalization:

37% of ulcers were sacral ulcers & of those, 50% were Stage III or IV.

Recurrence

’97 study – 176 veterans with SCI had 35% recurrence rate; smoking, diabetes & coronary / vascular disease all associated with highest risk of recurrence.

Costs:

’94 study – total cost of treatment was ~ $1,335 Billion / year. 69% of this provided in hospitals

’92 study – cost was: ~ $70,000 to treat full thickness

ulcer ~ $20-30,000 to treat less serious

ulcers

RISK FACTORSStandard Risk Factors:

Malnutrition

Moisture

Loss of Sensation

Friction

Incontinence

Shearing

Immobility

RISK FACTORSAssess Degree of Risk

Use Braden Scale:

Admission Every time patient’s condition

changes Monthly in NHCU

* Use clinical judgment as well

RISK FACTORSAssess Demographic &

Psych/social Risk Factors Age

Sex

Marital Status

Education

Ethnicity, Cultural Values Cognition

Substance Abuse

Psychological Health

RISK FACTORSNormal Skin

Largest single organ of the body Main function is to isolate &

protect the body from environment Skin insulates the body & helps

maintain core body temp Skin consists of 2 layers:

Epidermis, Dermis

RISK FACTORSNeurologically Impaired Skin

SCIs have altered autonomic nervous system

Degree of alteration varies with level of injury

SCI above T6 changes functional properties of the skin-sweating reflex is lost

SCIs are unable to maintain constant body temp in early stages following injury

RISK FACTORSNeurologically Impaired Skin

Changes that occur in skin: Increase in collagen catabolism Decrease in amino-acid metabolites in

skin Decrease in Type I & II collagen, which

robs the skin of elasticity & strength Skin is more fragile below injury Decrease blood flow & supply below

injury, which affects delivery of nutrients, etc.

* Takes 3-5 years for changes to

stabilize

RISK FACTORSMuscle Atrophy Caused by

Paralysis

Produces loss of muscle bulk: Less cushioning

Less protection

Less absorption of mechanical forces

PHYSIOLOGY of WOUND HEALING

Two Mechanisms of Repair

Regeneration: replacement of lost tissue with more of the same tissue

Connective Tissue Repair: lost tissue is replaced by scar formation

Type of Repair: determined by the tissue layer involved

PHYSIOLOGY of WOUND HEALING

Partial Thickness Wounds:

Epidermal Repair: Inflammatory response

Epithelial proliferation

Migration (resurfacing)

Re-establishment of epidermal layers

Dermal Repair: Concurrent with epithelialization

Angiogenesis Fibroblasts

become plentiful– 7 days

Collagen fibers are visible – 10 days

PHYSIOLOGY of WOUND HEALING

Full Thickness Wounds:(3 Phases)

Inflammatory Phase (1-4 days) Hemostasis Characterized by:

– Edema– Erythema– Heat– Pain

Macrophages arrive: destroy bacteria & clean wound

Produces chemo attractants & growth factors

PHYSIOLOGY of WOUND HEALING

Full Thickness Wounds (continued)

Proliferative Phase (3-20 days) Granulation tissue develops Wound contracts Collagen is produced to give strength

& elasticity

Maturation Phase (up to 2 years) Begins when the wound has closed Tensile strength of scar tissue =/<80%

PRESSURE ULCERS

Most pressure ulcers can be prevented, but sometimes even VIGILANT nursing care will not prevent the development or worsening of ulcers in some high-risk individuals.

Improving Nutrition Managing Incontinence Activating Prevention Measures

Frequent turning Use of overlays, low air loss, etc.

PRESSURE ULCERS(CONTINUED)

Four Goals for Protection Identify at risk individuals & factors

placing them at risk Maintaining & improving tissue

tolerance to pressure Protecting against adverse effects of

external mechanical forces Reducing incidence through

education

Severe Pressure Ulcer with Bone Loss

PRESSURE ULCERSStaging of Pressure Ulcers: WOCN

Staging Stage I: non-blanching

erythema of intact skin

Stage II: partial thickness skin loss involving epidermis &/or dermis. Ulcer is superficial & presents as an abrasion, blister, or shallow crater

* Staging Limitations: Echar/slough prevents

staging Identifying Stage I is difficult

in dark skin No reverse staging as

wound heals

Stage III: full thickness skin loss involving damage or necrosis of subcutaneous tissue that may extend down to, but not through, the fascia. Presents as a deep crater with or without undermining.

Stage IV: full thickness skin loss with extensive damage, destruction,or necrosis of muscle, bone or supporting structures. Undermining & sinus tracts may be present

Stage I Pressure Ulcer

Stage II Pressure Ulcer

Stage III Pressure Ulcer

Stage IV Pressure Ulcer

PRESSURE ULCERSUlcer Assessment

Stage the Ulcer

Location

Size – measure weekly or more often,if dramatic change

Drainage: exudate, transudate (serosanguinous), amount

Undermining, Tunneling, Sinus Tract

PRESSURE ULCERSUlcer Assessment (continued)

Tissue Type: viable/non-viable, describe as red, yellow, tan, black, etc.

Surrounding Skin: Pain/sensation or lack of in SCI Edema Induration Color Maceration Fungus Hair present

ULCER TREATMENT

Goals Evolve as the

patient’s wound progresses

Dressings change from absorbent, to debriding, to maintaining moist wound environment

Patient & family education

Treatment / Intervention

Pressure Relief REPOSTIONING Overlays, mattress

replacement, static or dynamic, low air loss, air fluidized

SCI Pressure Relief

Assisted Repositioning

Types of Overlay Mattresses

ULCER TREATMENTDebridement

Enzymatic

Mechanical = whirlpool, wet-to-dry, irrigation <30psi

Sharp

Autolytic

Biosurgery = maggots

Maggot Treatments

ULCER TREATMENT Electrical

Stimulation Increases oxygen & nutrient

transport Decreases edema Increases fibroblastosis Increases collagen

development• Indication: chronic wounds

not responding to conservative tx

• Contraindicated: in osteo, malignancy, pacemakers, over pregnant uteruses, over heart or carotid sinuses, or over laryngeal musculature

Surgical Flap Repair Skin Graft

Appropriate Dressing Choice is based on 3

aspects: Color of wound Depth of wound Exudates

Other considerations: Infection Tissue surrounding wound Fragility of skin Medical conditions

impacting healing Change Tx if wound has

not improved after 2-4 wks or Immediately, if negative outcome

Flap Repair

Skin Grafting

FACTORS IMPACTING WOUND HEALING

Tissue Perfusion & Oxygenation – impaired in SCI

Intrinsic Factors Steroid

dependence Immuno-

suppression Age Disease Malnutrition:

albumin <3.5

Extrinsic Factors Pressure Sheering Friction Moisture Medications

(antineoplastics,etc.)

FACTORS IMPACTING WOUND HEALING

Infection Infection vs. Contamination

All chronic wounds are contaminated, but can still heal

Infection prolongs the Inflammation Phase & delays healing

Obtain appropriate cultures: superficial swab, needle aspiration, tissue biopsy.

Culture Technique: 10 point method

FACTORS IMPACTING WOUND HEALING

Treatment Systemic antibiotics Topical antiseptics, antimicrobial,

antibiotic agents NPUAP – do not use topical antiseptics to

reduce Bacterial load. If used, limit to 2-3 days

Cytotoxic topical agents: Betadine Dakins (bleach) Acetic Acid (vinegar) Hydrogen Peroxide

PREVENTION MEASURES Reposition at lease q2 hrs.

using pillows or foam wedges

Keep bony prominences from direct contact from one another

Provide total heel pressure relief for patients who are immobile

Side-to-side turning of no more than 30 degrees rotation

Keep head of bed at lowest degree of elevation consistent with condition

Limit amount of time HOB is elevated to prevent shearing

Prevent moisture accumulation

Use lifting devices to move patient; friction injuries can be prevented by using linen to move patient, using lotion & films

At risk patient should be automatically placed on a pressure reducing device: Zone-Aire Beds RIK Gel Flotation Mattresses Alternating Pressure Mattress Water Mattress

PREVENTION MEASURES

Chair bound patients need pressure relieving cushions – consult O.T.

Chair bound patients need repositioning q 1 hr or taught to shift weight q 15 minutes

Positioning of chair bound patients should include consideration of postural alignment, distribution of weight, balance, stability, & pressure relief

Conduct DAILY comprehensive skin inspections

Education of patient, family / significant other

Roho Wheelchair Cushion