Wound Assessment and Decision-making Options

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Wound Care

Wound Assessment and Decision-making Options Patricia R. Boynton, MS, RN, CS, and Carol Paustian, RN , CP

W ounds have always been part of our human existence. Every year more than 1 million Americans develop pressure ulcers and another 25 million persons are afflicted with various acute and chronic wounds in need of intervention. 13 Impairments in skin integrity can negatively impact physical and psychological health and quality of life. Wound care and management burdens a health care system already challenged by increasingly scarce resources. The objective is quality, efficient, and cost-effective wound care that focuses on prevention, timely and accurate assessment, and early treatment of pressure ulcers and other acute and chronic wounds. Little has been written about wound assessment, healing, and treatment in the critical care environment; yet, growing numbers of acutely ill patients receive care in these areas. Critical care nurses are educated to deliver highly technical, specialized health care. Close attention is given to vital signs, hemodynamics, and to information from equipment that monitors various bodily functions. Criti-

From the Department of Internal Medicine, Section of Geriatrics and Gerontology, University of Nebraska Medical Center; Special Geriatrics Program, Omaha Veterans Affairs Medical Center; and St. Joseph Villa Homecare (PRB); and St. Joseph Hospital at Creighton University Medical Center (CP), Omaha, Nebraska

cally ill patients often have multiple acute, traumatic or chronic conditions that contribute to impaired skin integrity. Cardiovascular conditions affecting tissue perfusion are frequently seen, as are increasing numbers of older adults with aging, fragile skin. 28 In the context of life-threatening illness and the demands of emergent situations, wound prevention and/ or treatment may not be an immediate concern, and critical care professionals may lack the expertise to deliver such care. 21 This article addresses risk assessment, evaluation, and treatment decisions for pressure ulcers and wounds in the context of the critical care patient.

The Body's Largest Organ

The skin, our body's largest organ, protects internal organs from the harsh, outside world. Significant damage to the skin can lead to fluid loss, hypothermia, life-threatening infection or sepsis, and scarring with alterations in body image. Because the skin receives nearly one third of the cardiac output, impaired perfusion can have a major deleterious impact. The epidermis, the outermost layer of the skin is avascular, with a dry top layer of keratinized cells. The epidermis is a protective cover that is the body's barrier against injury,

CRITICAL CARE NURSING CLINICS OF NORTH AMERICA I Volume 8 /Number 2 /June 1996

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contamination and light. Epithelial cells are constantly being moved upward until they are sloughed or abraded off. When a break in the epithelial tissue occurs, the body closes that break by epithelialization. Under the epidermis is the dermis, consisting of collagen and elastin, the proteins that give the skin its tensile strength and elastic recoil. The dermis houses blood vessels and nerves and provides structural support for the skin. 35 Beneath the dermis is the subcutaneous tissue, a nutritional storage depot composed of dense fatty and connective tissue. This layer contains major blood vessels, lymph glands and nerves, and provides insulation, support, and protection for other tissues. Below the subcutaneous tissue is the deep fascia, which covers muscles, nerves, and more blood vessels. Because of the large vascular supply to these layers, both are at risk for ischemia from pressure over bony prominences. Aging skin is more fragile than youthful skin, making it easily injured and slower to heal. Aging impacts nearly all components of the healing response.35• 47 The addition of acute or chronic conditions sets the stage for an inadequate healing response.

Pathophysiology of Wounds

Vascular supply is the most important natural resource for attaining and maintaining skin integrity. 52 An impaired local vascular system and/ or inadequate tissue perfusion limits the transport of oxygen and nutrients to cells, leading to tissue hypoxia,33 necrosis, and delayed healing of any open wound. Health problems that interfere with vascular supply and tissue perfusion include cardiovascular conditions, trauma, surgical procedures, and acute exacerbations of chronic diseases such as diabetes mellitus and renal failure . Related conditions of shock, obesity, hypovolemia, anemia (acute or chronic), hypothermia, and dehydration may weaken the patient beyond the primary diagnosis, further predisposing to morbidity and mortality. Growing numbers of critically ill patients are elderly persons with

fragile skin and aging cardiovascular systems. These older adults often experience profound immobility and are susceptible to wide variations in oxygenation and hemodynamics that can impair tissue perfusion. Patients with these serious health problems have increased risk for pressure ulcers and complex surgical, traumatic, or vascular wounds. The development of pressure ulcers is complex. Pressure greater than 32 mm Hg is the primary cause. 5 In debilitated persons, pressures as low as 25 mm Hg can cause injury. No other factor in isolation can cause a pressure ulcer, but unrelieved pressure can do so quite easily. Consideration is given to intensity and duration of pressure as well as the ability of the skin to tolerate pressure without injury. Decreased activity, impaired mobility, and altered sensory perception impact intensity and duration of pressure to bony prominences. Extrinsic factors of moisture, friction, and shear along with intrinsic factors of malnutrition, advanced age, hemodynamic instability, and changes in skin and body temperature all contribute to decreased tissue tolerance to pressure. 6 Most pressure ulcers begin as nonblanchable, inflamed tissue secondary to thrombosed capillaries. Thrombosed vessels are unable to provide oxygen and nutrients to cells. Collateral circulation may be insufficient to promote repair and avoid tissue necrosis. 1 Lacking vessel repair and adequate tissue perfusion, early injury can decline rapidly to larger, deeper, and more complex pressure ulcers. The greatest risk of developing the most complex pressure ulcers is in the first two weeks of hospitalization, when the patient is most acutely ill. 44 Critically ill patients are frequently inactive and immobile because of medical conditions, surgical and diagnostic procedures and the need to maintain various catheter lines and tubes. Pressure from inactivity and immobility may be compounded by decreased sensory perception from neurological deficits. The patient with a severe stroke and aphasia may experience pain from lying or sitting in the same position, but be unable to communicate that discomfort to others. The contrasting situ-

WOUND ASSESSMENT AND DECISION-MAKING OPTIONS

ation is the patient with a spinal cord injury who is alert and able to communicate but is unable to perceive pain on the trunk or extremities and does not change position. Both patients experience decreased sensory perception and increased risk of tissue necrosis from pressure. Head elevation greater than 30 degrees increases pressure on the coccyx, promoting injury from friction or shear. In semi- or highfowler's position, the skin can adhere to bed linens while the deep fascia and skeletal structure slide down. Blood vessels in the sacral area become angulated and tear, creating a deep, longitudinal injury that becomes ischemic, then necrotic. Although normal skin has the ability to resist moisture, the combination of moisture and enzymes found in urine, feces, wound drainage and fistula output can break the skin barrier and allow maceration and chemical irritation to occur. Severely denuded tissue is very susceptible to injury from pressure. Incidence of pressure ulcers in acute care ranges from 9.2% to 29.5%,9• 37 may be as high as 35% in critical care,7 up to 40% in those with cardiovascular surgery, 27 and from 12% to 66% following any surgery.4; Cardiac catheterization, angiography, coronary bypass surgery, orthopedic procedures, and other surgical/diagnostic procedures that require immobility in the supine position decrease tissue perfusion from pressure as well as from the medical conditions being treated. Common sites where these patients develop pressure ulcers are the trunk, the extremities,58 and the back of the head. Pressure ulcers related to surgical or diagnostic procedures may not appear for 1 to 4 days, making it difficult to identify the setting where the injury began. Timely and routine risk assessment promotes effective prevention, pressure relief, skin care, and appropriate postoperative wound care.4; The Braden Scale for Predicting Pressure Sore Risk is useful for identifying those most at risk for ischemic tissue damage due to pressure exerted on a bony prominence or body surface (Table 1).6 Reliability, predictive validity, sensitivity, and specificity for the Braden Scale have been established,

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recognizing it as a valuable, scientificallytested predictor of risk. 17 For patients with preexisting compromised vascular perfusion, postoperative fluid resuscitation may lead to third-spacing of body fluids and massive edema. Surgical wound hypoxia may be present after abdominal and cardiovascular procedures due to increased oxygen demands in other body parts. Tissue perfusion and surgical wound healing may be further impaired by hypovolemia, hypothermia, and vasoconstrictive drugs common to major surgical procedures. 2; When these stressors are present, surgical wounds have a greater risk of infection and wound dehiscence. Trauma and burns differ from surgical wounds in that widespread injuries are common and a number of physiological functions are impaired. There is extensive stress with concomitant catecholamine release and hormone changes. Blood flow to the skin and subcutaneous tissue is diminished in these shock states, while much of the circulating volume is shunted to protect major internal organs. 20 The ensuing hypermetabolism places the body in a catabolic state for at least 96 hours post trauma, 28 and much longer with extensive burns. Skin integrity may be impacted by the actual injury of trauma or burns, by immobility and impaired perfusion, and by nutritional and metabolic demands. Chronic lack of blood flow to the lower extremities can lead to arterial ulcers. The pathology may involve micro-occlusion of the capillaries or the arteriosclerosis of peripheral vascular disease. The involved limb usually has signs of claudication including pain at rest, dry, thin and hairless skin, decreased or absent pulses, dependent rubor, and elevation pallor. Arterial ulcers are typically located on the lateral aspect of the ankle or lower leg. Acute thrombotic events to the legs can lead to rapid deterioration of even minor injuries, necessitating urgent re-vascularization. Venous ulcers generally develop on the medial aspect of the ankle or lower leg and are the result of a disruption in the forward flow of blood to the heart. 23 Conditions that predispose to venous dysfunction are throm-

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Table 1. THE BRADEN SCALE FOR PREDICTING PRESSURE SORE RISK

Patient's Name Sensory perception : Ability to respond meaningfully to pressure-related discomfort

1. Completely limited : Unresponsive (does not moan , flinch , or grasp) to painful stimuli , due to diminished level of consciousness or sedation , or limited ability to feel pain over most of body surface .

Moisture: Degree to which skin is exposed to moisture

1. Constantly moist: Skin is kept moist almost constantly by perspiration , urine, etc. Dampness is detected every time patient is moved or turned . 1. Bedfast: Confined to bed .

Activity : Degree of physical activity

Mobility: Ability to change and control body position

Date of Assessment

Evaluator's Name

1. Completely immobile: Does not make even slight changes in body or extremity position without assistance.

2. Very limited: Responds only to painful stimuli. Cannot communicate discomfort except by moaning or restlessness , or has a sensory impairment which limits the ability to feel pain or discomfort over 1/2 of body. 2. Very moist: Skin is often, but not always moist. Linen must be changed at least once a shift.

2. Chairfast: Ability to walk severely limited or non-existent. Cannot bear own weight and/or must be assisted into chair or wheelchair. 2. Very limited : Makes occasional slight changes in body or extremity position but unable to make frequent or sign ificant changes independently.

3. Slightly limited : Responds to verbal commands , but cannot always communicate discomfort or need to be turned , or has some sensory impairment which limits ability to feel pain or discomfort in 1 or 2 extremities .

4. No impairment: Responds to verbal commands. Has no sensory deficit which would limit ability to feel or voice pain or discomfort.

3. Occasionally moist: Skin is occasionally moist, requiring an extra linen change approximately once a day .

4. Rarely moist: Skin is usually dry, linen only requires changing at routine intervals .

3 . Walks occasionally : Walks occasionally during day, but for very short distances , with or without assistance . Spends majority of each shift in bed or chair. 3. Slightly limited: Makes frequent though slight changes in body or extremity position independently.

4. Walks frequently: Walks outside the room at least twice a day and inside room at least once every 2 hours during waking hours. 4. No limitations: Makes major and frequent changes in position without assistance .

Nutrition: Usual food intake pattern

Friction and shear

1. Very poor: Never eats a complete meal. Rarely eats more than 1/3 of any food offered. Eats 2 servings or less of protein (meat or dairy products) per day. Takes fluids poorly. Does not take a liquid dietary supplement, or is NPO and/or maintained on clear liquids or IV's for more than 5 days. 1. Problem: Requires moderate to maximum assistance in moving. Complete lifting without sliding against sheets is impossible. Frequently slides down in bed or chair, requiring frequent repositioning with maximum assistance. Spasticity, contractures or agitation leads to almost constant friction.

2. Probably inadequate: Rarely eats a complete meal and generally eats only about 1/2 of any food offered. Protein intake includes only 3 servings of meat or dairy products per day. Occasionally will take a dietary supplement, or receives less than optimum amount of liquid diet or tube feeding . 2. Potential problem: Moves feebly or requires minimum assistance. During a move skin probably slides to some extent against sheets, chair, restraints, or other devices. Maintains relatively good position in chair or bed most of the time but occasionally slides down .

3. Adequate: Eats over half of most meals. Eats a total of 4 servings of protein (meat, dairy products) each day. Occasionally will refuse a meal, but will usually take a supplement if offered, or is on a tube feeding or TPN regimen which probably meets most of nutritional needs.

4. Excellent: Eats most of every meal. Never refuses a meal. Usually eats a total of 4 or more servings of meat and dairy products. Occasionally eats between meals. Does not require supplementation.

3. No apparent problem: Moves in bed and in chair independently and has sufficient muscle strength to lift up completely during move. Maintains good position in bed or chair at all times.

Total Score Copyright Barbara Braden, PhD, RN, FAAN, and Nancy Bergstrom, PhD, RN, 1988; reproduced with permission .

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bases of the deep venous system, postphlebitic syndrome, congestive heart failure, and muscle weakness secondary to paralysis. These conditions increase venous pressure, resulting in edema, brownish discoloration in the lower legs, venous ulcers , and stasis dermatitis. Patients with diabetes mellitus are at special risk for development and delayed healing of injuries secondary to diminished or absent sensation in the feet, foot deformities , and impaired perfusion from peripheral vascular disease. These patients experience decreased resistance to infection from impaired, early inflammatory response and vascular abnormalities of small vessels. 18 The addition of chronic renal disease, and/ or serious cardiac dysfunction further complicates maintenance of skin integrity and the healing process. 34 Major surgery, massive trauma and lifethreatening illness or disease states can prevent ingestion of sufficient nutrients for metabolism. Intravenous solutions of dextrose or saline may be the primary, though inadequate source of nutrition for critically ill patients. Persons with pre-existing, chronic conditions may be malnourished before the onset of an acute illness or injury, placing them at greater risk for impaired skin integrity or decline of existing wounds. In multi-system organ dysfunction syndrome, ischemic events and/ or a lack of gastrointestinal feeding can allow bacteria to permeate the gut and lead to sepsis. The gut can lose the ability to absorb nutrients,56 contributing to more severe malnutrition.

The Healing of Wounds

The healing of wounds is a complex process of tissue repair that is often taken for granted. With necessary factors present, wound healing in well-nourished, healthy people begins when the skin injury occurs and progresses along a predictable continuum of overlapping phases. 49· 51 Although the sequence of events is always the same, the rate of healing is determined by the cause of the wound, its location and depth, the wound environment, and a

number of complex, interrelated factors. Most wounds heal by primary intention in two weeks if the edges are approximated, there is no major tissue loss, the wound is free of debris, and there is no dead space where bacteria give rise to infection. 41 Superficial wounds in highly vascular areas, such as the face and scalp, seem to heal most rapidly, whereas those on the extremities heal more slowly. Healing takes longer in deeper wounds because epidermal cells migrate from the edges of the wound. More granulation tissue must be formed before that migration can occur. Chronic wounds are evidence that the normal process of healing has failed or become static. 10· 15 The normal rate of wound healing cannot be accelerated, but it can be delayed.11 Inflammation, the initial phase of healing, is the body's reaction to injury. Without inflammation there is no healing. As soon as tissue is damaged, blood flows , then coagulates. Platelets are released and interact with injured tissue to initiate clot formation. Redness, warmth, edema and tenderness/ pain are the familiar signs of inflammation. This phase cleans the wound of dead cells and bacteria, and promotes the healing process.19 As inflammation continues for about 3 days, epithelial cells migrate across the wound to protect it from both bacterial contamination and loss of moisture. Epithelial tissue is sensitive to and stimulated by oxygen. The process of epithelialization occurs rapidly in healthy tissue but cannot take place when the vascular or oxygen supply is impaired or when the wound contains necrotic tissue. 11 In the proliferative phase, the material for tissue regeneration is produced, creating a healing environment. This phase begins about 48 hours after injury and continues for 2 to 3 weeks. By the fifth or sixth day, fibroblasts join with Vitamin C and other factors to generate collagen, and support is created for tissue development and strength. 49 Beefy, red granulation tissue forms a new dermis, and a thin, silvery layer of epithelial tissue surrounds the granulation tissue as the wound shrinks. As proliferation progresses, the wound continues to granulate and contract, complet-

WOUND ASSESSMENT AND DECISION-MAKING OPTIONS

ing epithelialization, then moving to the remodeling phase. Wound repair strengthens, and the reorganization of scar tissue begins about the twenty-first day post injury. 25 Although remodeling, or maturation, can continue for as long as 2 years, no more than 70% to 80% of the original tensile strength, or the ability of the skin to resist breaking under tension, is ever regained. Because the skin is the body's major defensive barrier, the effect of both local and systemic factors on wound healing cannot be overestimated. 29 Whenever injury impairs the defense mechanism of intact skin, the risk of infection increases. All wounds are colonized, or have bacteria present, but not all wounds are infected. Bacteria at the level of 105 prevent healing by prolonging the inflammatory stage and promoting wound dehiscence, scarring, and hernia formation. 43 Complications such as osteomyelitis can occur when infection is prolonged, causing extended healing time, 38 pain, increased risk of limb loss, and loss of independence. Up to 75% of deaths occurring within a week of traumatic injury involving the skin can generally be attributed to infection and/ or sepsis.43 Nutrition has a profound effect on wound healing. The most important indicator of nutritional status is serum albumin, 16 which has a short half-life, and can indicate rapid changes in visceral protein stores. Insufficient protein intake and reserves impair cell integrity, cell metabolism, collagen production, tissue repair and regeneration. Inadequate intake of carbohydrates, vitamins, and minerals (such as zinc, copper, and magnesium53) limits energy for cell metabolism, whereas insufficient fat intake inhibits development of the cell membrane. Any healing wound that lacks adequate oxygenation and sufficient nutrition from impaired tissue perfusion has faulty cellular metabolism, forms a weak matrix of collagen, and does not gain the tensile strength to prevent dehiscence or separation. Fecal and/ or urinary incontinence, and excessive wound or fistula drainage not only macerate and irritate intact skin, but also delay healing of open wounds. Impaired immunity, coagulation problems, time between injury

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and treatment, the presence of other injuries, localized edema, foreign bodies in the wound environment, and inefficient wound treatment are additional factors known to impede wound healing.54 Commonly administered medications also delay the healing process. Immunosuppressives and corticosteroids suppress the immune system, increasing the risk of sepsis. Steroids and nonsteroidal, antiinflammatory preparations (NSAIDS) also prevent the release of growth factors into the wound, interfering with the inflammatory phase of healing.24 Antineoplastics decrease the tensile strength of healing tissue, and certain antibiotics can be toxic and inhibit wound healing.

Assessment of Wounds Wound assessment considers the patient as a whole. Each person is an individual, and each wound is unique. Systematic assessment and comprehensive evaluation of both patient and wound provide a consistent method for determining the cause and extent of injury and the status of wound healing and tissue repair. 53 Assessment of the patient's baseline past, and current health helps to establish the cause. The history includes prior trauma, illness and disease, as well as the objective parameters of pertinent laboratory data (hemoglobin, hematocrit, serum albumin, BUN, serum transferrin and total lymphocytes). Observation or visualization of the wound bed is necessary to determine the extent of a wound. Wound inspection may also involve use of an assessment tool, such as the Bates-Jensen Pressure Sore Status Tool. 4 This is a 13-item tool that evaluates specific pressure ulcer characteristics. Each item is rated on a fivepoint scale, with higher scores indicating increasing severity. The tool is helpful in tracking pressure ulcer progress or decline, and in determining when complex ulcers are stable enough to benefit from surgical intervention. Several other instruments that evaluate nonpressure ulcer wounds are available in the literature and are of different utility.4· 36 The challenge is to find a tool that adequately de-

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scribes the specific wound and identifies changes that signal healing, decline, or stabilization of the wound. Nurses caring for patients with wounds are expected to accurately assess, describe, and document impaired skin integrity. A size description involves more than comparison to a common object (for example, "pea- or dimesized"). Description of wound size and depth in centimeters must be documented at least weekly. Use of disposable rulers, dressings with attached plastic grids and acetate tracing sheets are available to assist caregivers in accurately and consistently determining size. Wound depth and the presence of tunneling can be assessed with a sterile cotton applicator. Evaluation of the condition of wound borders is somewhat subjective. In addition, wound size and shape change as the patient's position changes. Uniformity and consistency in measurement is the desirable goal despite the fact that caregivers may have varying levels of expertise in wound assessment. Some methods of wound assessment help to compensate for differences in assessment skill level. Photography, using cameras with grid film , provides more consistent measurement parameters. More expensive, computerized image processing can offer state of the art measurement of visible portions of the wound. Any acceptable tool , or method of assessment provides • Baseline and ongoing evaluation of wound size and depth

Table 2.

• Condition of wound edges • Presence of undermining • Amount and type of necrotic tissue • Amount and type of exudate • Skin color/ condition surrounding wound • Peripheral tissue edema or induration • Presence/ absence of granulation tissue • Status of epithelialization. Only pressure ulcers are classed by stage; other wounds are identified by anatomical depth . Many clinicians currently use the staging schema developed by the National Pressure Ulcer Advisory Panel42 and endorsed by the Agency for Health Care Policy and Research (Table 2).5· 44 When the base cannot be visualized due to the presence of necrosis and/ or eschar, pressure ulcers or wounds cannot be staged or classified until the wound is debrided. Wounds are also classified as acute and chronic. Any wound that has not healed or made significant progress toward healing in 2 to 6 weeks is considered a chronic wound.5 These wounds usually result from underlying disease such as vascular insufficiency, whereas acute wounds begin as injury that disrupts vasculature and initiates hemostasis. Because hemostasis initiates the healing cascade, absence of this event may help to explain the static nature of chronic wounds. 12 Vascular wounds common to the critical care population may be arterial, venous, and/

CLASSIFICATION OF PRESSURE ULCERS

Stage I

Stage II

Stage Ill

Stage IV

Nonblanchable erythema of intact skin (the heralding lesion of skin ulceration)

Partial-thickness skin loss involving epidermis and/or dermis. Ulcer is superficial and presents clinically as an abrasion , blister, or shallow crater.

Full-thickness skin loss involving damage or necrosis of subcutaneous tissue that may extend down to but not through underlying fascia. Ulcer presents clinically as a deep crater with or without undermining of adjacent tissue.

Full-thickness skin loss with extensive destruction, tissue necrosis or damage to muscle, bone or supporting structures, such as tendon , joint capsule , etc.

WOUND ASSESSMENT AND DECISION-MAKING OPTIONS

or neuropathic. Diagnostic studies, often invasive, determine the status of the blood supply, and the cause and extent of disease. Methods for determining vascular status include Doppler studies, prothrombin time, arteriogram, and venogram. Measurement of the Ankle-Brachia! Index (ABI) provides a noninvasive estimate of the ability of vascular flow in the extremity to permit wound healing.15· 61 This index is a measurement of the systolic blood pressure in the ankle, divided by the systolic blood pressure in the brachia! artery. The ABI is a quick and handy tool for bedside evaluation but does not replace the need for more thorough vascular studies in appropriate patients. An ABI of 1 is considered normal while a measurement of less than 0.9 indicates occlusive disease and the likelihood of impaired healing. An ABI of less than 0.45 reflects blood flow inconsistent with wound healing, and possibly with limb salvage. Ischemic wounds have increased susceptibility to infection and tend to deteriorate unless the blood supply is restored. Accurate and appropriate documentation of assessment findings guides treatment decisions, notes healing progress, facilitates reimbursement for care, and protects against litigation.39 Assessment parameters are tracked at least weekly, preferably with pictures as well as with words.32 Wound status can change rapidly, either positively or negatively. No appreciable change in 2 to 4 weeks alerts the caregiver to reevaluate the patient, the wound, and wound management. 5 The process for assessing wounds and related conditions in critical care patients is summarized in Table 3.

Wound Care in Critical Care

The International Committee on Wound Management Consensus Statement defines wound management as "the pursuit of permanent, functional, and aesthetic healing of the patient's wound through the promotion of physiological healing and the prevention or elimination of factors- whether local, systemic or

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external- that disturb healing." 52 Nursing has a major role in wound management. 13 The primary goals are accurate diagnosis, treatment of the cause, and support for the person's ability to heal. If a completely healed wound cannot be achieved, the goal moves to attaining the highest possible functional level within the limits of the disability associated with the wound.15 Wound care begins with assessment and evaluation, progresses to accurate diagnosis, and continues with an integrated plan of direct and supportive care. Historically, direct wound care has been dominated by antiseptics, wet-to-dry dressings, or leaving wounds open to air. All kinds of materials have been used to promote wound healing. Over the past 30 years, greater attention to the healing process, the wound environment, and materials to support healing have significantly improved our understanding of wound healing and care. 40 Antiseptics and plain gauze are no longer state of the science. Achieving a healing environment begins with cleansing, includes debridement of necrosis, then moves to choosing an appropriate cover for the wound. Cleansing removes exudate and necrotic tissue. The objective is gentle, thorough cleansing that avoids mechanical or chemical trauma to healthy tissue. Cleansing, initially and with each dressing change, helps control odor, 48 promotes healing and helps prevent infection. Saline is the cleanser of choice. Various commerical cleansers must be chosen carefully to avoid toxicity to healthy tissue. Antiseptics reduce wound colonization only briefly; there is no evidence of clinical benefit, and they can be toxic. 2• 21 "Never put any chemical in a wound that you wouldn't put in your own eye." 46 Debridement can be accomplished by selective or nonselective methods. Selective methods include autolysis achieved with moist wound therapy, chemical treatment with enzymatic debriding agents, or sharp debridement with scalpel or scissors. Nonselective debridement, such as wet-to-dry dress-

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Table 3. ELEMENTS OF WOUND ASSESSMENT IN CRITICAL CARE PATIENTS Target Area

Assessment Parameters

General health (past and present)

History of trauma, illness , disease Pertinent laboratory data Medication regimen Braden Scale Score (see Table 1)

Impaired skin integrity

Location Measurement Observation of wound bed Stage of wound (see Table 2) Tools such as Bates-Jensen Pressure Sore Status Tool Photographs Ongoing evaluation of wound status

Vascular supply/tissue perfusion

Vital signs , hemodynamics, oxygen saturation , SV02 Skin color, temperature , texture Wound bed color Sensation Pertinent laboratory data Ankle-Brachia! Index (ABI) Doppler studies Arteriogram Venogram Nutritional assessment (intake , laboratory data, weight)

Nutritional status

ings, can remove healthy as well as necrotic tissue. Wounds quickly acquire bacteria unless they are protected by some type of covering. 33 It is important to choose the best dressing for the patient, the wound, and its cause. Effective dressings maintain a moist wound surface while allowing surrounding tissue to remain dry. They should also control odor and pain, avoid trauma , and be

Related Findings

Cardiovascular conditions , trauma, hypermetabolism , surgery, diabetes , renal disease BUN , Serum Transferrin Advanced age, fragile skin Vasoconstrictors, steroids, immunosuppressives, antineoplastics , antiinflammatory agents Sensory perception , mobility, activity, moisture , nutrition , friction and shear Relationship of location to cause of wound Length , width , depth (cm) Presense/absence of undermining and/ or tunneling Amount and type of necrotic tissue Amount and type of exudate Presence/absence of infection Presence/absence of granulation tissue Status of epithelialization Condition of surrounding skin and tissue; presence of edema, erythema or maceration Acute or chronic wound (no change in 2-4 weeks) Hemodynamic instability, shock, inadequate oxygenation, hypo/ hyperthermia Pallor or rubor of skin ; dry, thin, hairless skin Pale, shiny wound Pain/absence of pain ABI < 0 .9 Hypovolemia, elevated prothrombin time Impaired blood flow Albumin < 3 .0 Anemia (acute or chronic) Inadequate protein intake or stores Total lymphocyte count < 2000 Inadequate intake (oral or tube) of calories , vitamins, minerals Dehydration

safe, cost-effective and easy to use. 8• 14• 59 Although dressings have an important role in wound care and healing, surgical repair of certain larger, deeper wounds may be indicated. Each wound is treated individually and needs frequent, ongoing reassessment as healing progresses. Supportive wound management focuses on the physical and mental care of the whole patient. 52 Optimal medical and/ or surgical

WOUND ASSESSMENT AND DECISION-MAKING OPTIONS

treatment of concurrent disease, combined with support for a healthy lifestyle, contribute to positive clinical outcomes.61 Attention is given to the known factors that delay healing. Close monitoring of vital functions supports the host and helps to prevent/control infection. Laboratory and hemodynamic parameters contribute to optimal management. In the presence of vascular disease, surgery may be indicated to increase perfusion and allow healing to occur. Compression therapy is the essential component of treatment for edema associated with venous ulcers. Tight control of glucose levels, combined with moist wound care and patient education contribute to healing of neuropathic ulcers in the patient with diabetes. Close observation of incisional wounds supports early identification of complications. Proper positioning, deep breathing, spirometry, activity, and oxygen administration support pulmonary function, tissue oxygenation, and perfusion at incisional sites. An individualized pain control regimen promotes activity and independence, as well as comfort. Providing opportunities for sleep and relaxation, often rare commodities in critical care, can increase epidermal mitosis and cell growth, contributing to optimal healing of wounds. For maintenance of skin integrity, prevention of further breakdown, and for the cascade of healing to occur in any patient, optimal nutritional intake and supplementation combined with a proper balance of fluids and electrolytes is essential. Timely identification of nutritional risk, combined with nutritional supplementation and ongoing assessment consistent with condition changes are important overall aspects of care. Nutritional support is especially important for critically ill patients faced with metabolic demands increased by life-threatening disease or injury. Although the normal gastrointestinal route of intake is most desirable, 60 the need for tube feeding or total parenteral nutrition is best considered early in the clinical course. Vitamin and mineral supplements may be beneficial , but administration of iron should be avoided in the presence of infection because it may increase the virulence of bacteria.

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We know that patients in critical care experience increased risk for pressure ulcers. Their medical conditions place them at risk before they ever experience pressure from immobility, decreased activity, and altered sensory perception. Management of both intensity and duration of pressure is the priority of care. 44 • 55 The patient with a pressure ulcer or other open wound cannot lie or sit on the injured area. Treatment with any of the pressure-reduction mattresses, overlays, or specialty beds targets patients who have wounds and/ or pressure ulcers on one or more sleep or turning surfaces. 57 The more turning surfaces that are involved, the higher the technology and level of nursing care required. While the perfect therapeutic support surface has not been created, 31 there are factors to consider when selecting appropriate equipment. Elements of an effective support surface are listed30• 31• 57 : Minimizes/ redistributes pressure on bony prominences Controls pressure on other exposed body tissues Improves blood flow Prevents trauma Reduces friction Permits position and weight shifts Allows for ease of transfer Controls skin surface moisture and temperature Is cost-effective and easy to use Is durable and easy to clean Meets infection control standards The same requirements apply to chair/wheelchair cushions and can be even more important than the pressure-reducing mattress for patients who sit in the chair more than fifteen minutes at a time. To choose a therapeutic support surface, health care professionals must know the specific features of each product. 22 Protocols for selecting these surfaces focus on assessment and help to match specific equipment with the individualized needs of the patient (Figure 1). Nursing staff should also be knowledgeable in the use and maintenance of the product in use. Equipment is discontinued when

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DERING THERAPEUTIC SUPPORT SURFACES Actual/Potential Impairment of Skin Integrity

Yes

No

Implement Nursing Care Guidelines/Standard of Care for PreventionfTreatment of Pressure Ulcers

Standard Nursing Care

•

Standard Hospital Mattress or Hospital Replacement Mattress (HRM)

Evaluate for Appropriate Therapeutic Support Surface

Evaluate Individual Goals of Therapy

·' iora~'0';;tmci'r~·; ollowing factors

derate Risk Mild Risk: Braden Score 15-16 Limited Mobility 11 Stage I or II pressure ulcer a Ability to keep patient positioned off ulcer 11

11

c

c c CJ

c c

Moderate Risk: Braden Score 12-16 Limited mobility Drainage and/or body fluids are controlled and at least one other major risk factor Stage Ill or IV pressure ulcer on trunk Post-operative myocutaneous flap Inability to keep patient positioned off ulcer

Cl High Risk: Braden Score <12

c

Profound immobility Drainage and/or body fluids not controlled and at least one other major risk factor CJ Stage Ill or IV pressure ulcer on trunk c Post operative myocutaneous flap c Posterior burns Cl Hypothermia/Hyperthermia a Inability to keep patient positioned off ulcer

c

• Refer to AHCPR Guidelines; for prevention and/or treatment

• Notify skin care team • Refer to AH CPR guidelines for treatment

• Notify skin care team • Refer to AH CPR guidelines for treatment

• 4 inch foam overlay • Hospital replacement mattress (HRM)

• Dynamic air overlay (First Step/Orthoderm) • Low airless therapy (Kinair Ill) • Air fluidized bed (Fluidair/Clinitron)

•Dynam ic air overlay (First Step/Orthoderm • Low air loss therapy (Kinair Ill, Q2Plus, Therapulse) • Low airless therapy with kinetic modalities for respiratory patients (Biodyne) • Air fluidized bed (Fluidair/Clinitron)

Figure 1.

Protocol for matching patient risk for pressure ulcers with therapeutic support surfaces .

WOUND ASSESSMENT AND DECISION-MAKING OPTIONS

the maximum benefit has been achieved. Highly technological support surfaces are generally not used for terminally ill persons except in cases where they can significantly contribute to the person's comfort. Equipment, such as the specialty bed, has an important, adjunctive role, but is no substitute for quality nursing care. 26 Any support surface must be connected to nursing care and interventions consistent with the patient's health care status, risk factors, and wound. 57 Patients require very frequent position changes, nutritional support, assistance to increase mobility, and protection from the trauma of friction, and shear. Heels are protected from friction and pressure by suspension of the legs on pillows. Maintaining the head of the bed at the lowest degree of elevation consistent with the medical condition reduces risk as does limiting the amount of time the head of the bed is elevated. Control of skin surface moisture maintains skin integrity. Urinary and fecal incontinence require aggressive control. Intact skin is kept clean with thorough but gentle cleasing. Skin cleansers that maintain skin pH, and avoid drying and irritation are most desirable. Nursing documentation in critical care manages large volumes of patient data ranging from major to discrete alterations in condition. Documentation of wound care records ongoing assessment of the wound, the procedure for cleansing, each part of the dressing, adjunctive equipment, progress toward healing, and overall effectiveness of therapy.39 Documentation at discharge from critical care summarizes the entire episode of illness as well as wound development, assessment, diagnosis, and treatment. Comprehensive documentation promotes continuity of care and effective communication of overall patient status when persons are transferred from one level of care to the next. 55

Planning for Care

An open wound can be devastating to a person. Combine that with a life-threatening ill-

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ness and the challenge to nurses and other health care professionals can be daunting. Nursing's essential role is grounded in the nursing process of assessment, diagnosis, planning and implementation of care, and ongoing evaluation. The care of impaired skin integrity in critical care sets the stage for what follows in the episode of illness. Making decisions for care is preferably a collaborative effort. Given the high risk of critical care patients for complications, teamwork promotes understanding of the complex, multidimensional needs of the patient. Collaboration is built on common values among team members who communicate effectively and minimize turf issues.38 Wound care involves complex and highly technical interventions as well as the need to plan for care of the whole person. 3 Decision-making may require an analytic approach among nursing, medicine, pharmacy, physical and occupational therapy, and various health care support services. The team is supported by assessment tools, published guidelines for prevention and treatment, 5· 47 diagnostic criteria, and protocols for wound care product and equipment selection. 38• 50• 57 Rehabilitation and discharge planning begin at admission and continue throughout hospitalization and recovery. Every wound is part of a person. 8 To the extent possible, each patient has a role as partner in his or her health care. Involvement in the plan of care empowers the patient and promotes self-advocacy. The patient needs to know the type of wound involved, how it occurred, the role of disease or injury, how to assess for complications, be able to describe the wound and eventually, as able, provide for basic care. Family caregivers or significant others should become involved as appropriate. When a wound cannot be healed, management is directed to comfort and pain control, care of the complications that can be corrected and controlled, and promotion of quality of life within the limitations of the disease and impairment. 52

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BOYNTON and PAUSTIAN

SUMMARY

The increasing presence of multiple, chronic disease states among critically ill patients compounds care of their acute or traumatic conditions. These patients may be admitted with existing wounds and they may develop impaired skin integrity due to a variety of factors related to their illness and treatment. Whereas maintenance of vital functions is the priority of care, critical care nurses are more frequently faced with the challenges presented by pressure ulcers and various other surgical, traumatic, and vascular wounds. These wounds increase morbidity and mortality and result in higher costs for health care. Education in assessment of risk, pathophysiology, the healing process, comprehensive assessment, and efficient, effective wound management contribute to optimal patient outcomes and cost-effective delivery of care.

REFERENCES 1. Alterescu V: Prevention and treatment of pressure

2. 3. 4.

5.

6. 7.

8.

9.

10.

11.

12.

sores. In Cooper OM, Watt RC, Alterescu V (eds): Guide to Wound Care. Libertyville, IL, Hollister, 1983, p 56 Andrews LW: The perils of povidone-iodine use. Ostomy/Wound Management 40:68, 1994 Baranoski S: Collaborative roles lead to success in wound healing. Decubitus 5:66, 1992 Bates-Jensen B, Vrederoe D, Brecht M: Validity and reliability of the pressure sore status tool. Decubitus 5:20, 1992 Bergstrom N, Bennett MA , Carlson CE, et al: Treatment of Pressure Ulcers: Clinical Practice Guideline, No. 15. Rockville, MD , US Deparunent of Health and Human Services. Public Health Service, Agency for Health Care Policy and Research. AHCPR Publication No. 95-0652, 1994 Bergstrom N, Braden BJ, Laguzza A, et al: The Braden Scale for predicting pressure sore risk. Nurs Res 36:205, 1987 Bergstrom N, Demuth PJ , Braden BJ: A clinical trial of the Braden Scale for predicting pressure sore risk. Nurs Clin North Am 22:417, 1987 Bolton L, van Rijswijk L: Wound dressings: Meeting clinical and biological needs. Dermatology Nursing 3:146, 1991 Clarke M, Kadhom HM: The nursing prevention of pressure sores in hospital and community patients. J Adv Nurs 13:365, 1988 Cooper D: Wound healing and assessment. I n Bryant R Ced): Acute and Chronic Wounds-Nursing Management. St. Louis, Mosby-Yearbook, 1992, p 69 Cooper DM: The physiology of wound healing: An overview. I n Krasner D (ed): Chronic Wound Care: A Clinical Source for Healthcare Professionals. King of Prussia, Health Management Publications, 1990, p 1 Doughty D: Principles of wound healing and wound management. In Bryant R (ed): Acute and Chronic Wounds-Nursing Management. St. Louis, MosbyYearbook, 1992, p 31

13. Doughty D: The process of wound healing: A nursing perspective. Progressions 2:3, 1990 14. Field CK, Kerstein MD: Overview of wound healing in a moist environment. Am] Surg 167: 2S, 1994 15. Fowler E: Chronic wounds: An overview. In Krasner D (ed): Chronic Wound Care: A Clinical Source for Healthcare Professionals. King of Prussia, Health Management Publications , 1990, p 12 16. Frantz RA, Gardner S: Elderly skin care: Principles of chronic wound care. Journal of Gerontologica l Nursing 20:35, 1994 17. Gawron CL: Risk factors for and prevalence of pressure ulcers among hospitalized patients. Journal of Wound, Ostomy and Continence Nurses 21:232, 1994 18. Glugla M, Mulder GD: The diabetic foot: Medical management of foot ulcers. In Krasner D (ed} Chronic Wound Care: A Clinical Source for Healthcare Professionals. King of Prussia, Health Management Publications, 1990, p 223 19. Gogia PP: The biology of wound healing. Ostomy/ Wound Ma nagement 38:12, 1992 20. Goodson WH: Traumatic injury. In Cohen IK, Diegelman RF, Lindblad HJ (eds): Wound Healing: Biochemical and Clinical Aspects. Philadelphia, WB Saunders, 1992, p 316 21. Harding KG: Wound care: Putting theory into clinical practice. I n Krasner D (ed): Chronic Wound Care: A Clinical Source for Healthcare Professionals. King of Prussia, Health Management Publications, 1990, p 19 22. Hess CT: Specialty beds: Decision making made easy. I n Krasner D (ed): Chronic Wound Care: A Clinical Source for Healthcare Professionals. King of Prussia, Health Management Publications, 1990, p 152 23. Holloway GA: Lower leg ulcers: An overview. In Krasner D (ed): Chronic Wound Care: A Clinica l Source for Healthcare Professionals. King of Prussia, Health Management Publications, 1990, p 206 24. Hunt T: Overview of wound healing for vascular surgeons. I n Kerstein MD (ed): New Trends in Wound Healing for Vascular Surgeons: Highlights of a Symposium. Princeton, NJ, Excerpta Medica, 1990, p 3 25. Jacobson TM: Obesity and the surgical patient: Nu rsing alert. Ostomy/Wound Management 40:56, 1994

WOUND ASSESSMENT AND DECISION-MAKING OPTIONS

26. Johnson G, Daily C, Franciscus V: A clinical study of hospital replacement mattresses. journal of ET Nursing 18:153, 1991 27. Kemp MG, Keithley ]K, Smith DW, et al: Factors that contribute to pressure ulcers. Res Nurs Health 13:293, 1990 28. Keough V, Letizia M, Baldonado A: Where are we headed? Facing the challenge of elderly trauma. journal of Gerontological Nursing: 20:5, 1994 29. Krasner D: Minimizing factors that impair wound healing: A nursing approach. Ostomy/Wound Management 41:22, 1995 30. Krouskop T, van Rijswijk L: Standardizing performance-based criteria for support surfaces. Ostomy/ Wound Management 41:34, 1995 31. Krouskop T: Factors to consider in selecting a support surface. In Krasner D Ced): Chronic Wound Care: A Clinical Source for Healthcare Professionals. King of Prussia, Health Management Publications, 1990, p 142 32. Kutcher J, Arnell I: Documentation of skin using photography. Ostomy/Wound Management 38:23, 1992 33. Lawrence WT: Clinical management of nonhealing wounds. In Cohen IK, Diegelman RF, Lindblad HJ (eds): Wound Healing: Biochemical and Clinical Aspects. Philadelphia, WB Saunders, 1992, p 541 34. Levenson SM, Demetrious AA: Metabolic factors. In Cohen IK, Diegelman RF, Lindblad HJ (eds): Wound Healing: Biochemical and Clinical Aspects. Philadelphia, WB Saunders, 1992, p 248 35. Mast BA: The skin. In Cohen IK, Diegelman RF, Lindblad HJ (eds): Wound Healing: Biochemical and Clinical Aspects. Philadelphia, WB Saunders, 1992, p 344 36. Mather D, Woods L: A form that makes wound assessment easier. RN 50:37, 1987 37. Meehan M: National pressure ulcer prevalence survey. Advances in Wound Care 7:27, 1994 38. Melchior-MacDougall F, Lander ]: Evaluation of a decision tree for management of chronic wounds. Journal of Wound, Ostomy and Continence Nurses 22:81, 1995 39. Motta G: An update on documentation. Continuing Care 7: 15, 1994 40. Mulder GD, Jeter KF, Fairchild PA: Clinicians' Pocket Guide to Chronic Wound Repair. Spartanburg, SC, Wound Healing Publications, 1992 41. Mulder GD: Quantifying wound fluids for the clinician and researcher. Ostomy/Wound Management 40:66, 1994 42. National Pressure Ulcer Advisory Panel: Pressure ulcers: Incidence, economics, risk assessment. In Consensus Development Conference Statement. West Dundee, IL, National Pressure Ulcer Advisory Panel, S-N Publications, 1989 43. Neuberger GB, ReckingJB: Preventing wound complications in an era of DRGs. In Krasner D (ed): Chronic Wound Care: A Clinical Source for Healthcare Professionals. King of Prussia, Health Management Publications, 1990, p 47

139

44. Panel for the Prediction and Prevention of Pressure Ulcers in Adults: Pressure ulcers in adults: Prediction and prevention. In Clinical Practice Guidelines, Number 3. AHCPR Publication o. 92-0047. Rockville, MD, Agency for Health Policy and Research, Public Health Service, US Department of Health and Human Services, 1992 45. Papantanio C, Wallop J, Kolodner K: Sacral ulcers following cardiac surgery: Incidence and risks. Advances in Wound Care 7:24, 1994 46. Peacock EE: Wound healing and wound care. In Schwartz SI, Shires GT, Spencer FC, et al. (eds): Principles of Surgery, ed4. New York, McGraw-Hill, 1983, p 289 47. Phillips T: A clinician's guide to common dermatology problems. Ostomy/Wound Management 40:70, 1994 48. Rodeheaver G, Baharestani MM, Brabec ME, et al: Wound healing and management: Focus on debridement. Advances in Wound Care 7:22, 1994 49. Rudolph R, Shannon ML: The normal healing process. In New Directions in Wound Healing. Princeton, NJ, ER Squibb & Sons, 1990 50. Saint Joseph Hospital Skin Care Committee: Nursing Care Guidelines for Potential/Actual Impaired Skin Integrity. Omaha, NE, Saint Joseph Hospital at Creighton University Medical Center, 1995 51. Sieggreen M: Healing of physical wounds. Nursing Clin North Am 22:439, 1987 52. Song C, Vigano M, Wijetunge D: ICWM consensus statement: Wound management. Ostomy/Wound Management 39:80, 1993 53. Stotts N, Barbour S, Slaughter R, et al: Wound care practices in the United States. Ostomy/Wound Management 39:53, 1993 54. Stotts N: Impaired wound healing. In Carrieri V, Lindsay A, West C (eds): Pathophysiological Phenomena in Nursing: Human Response to Illness. Philadelphia, WB Saunders, 1986, p 457 55. Tallon R: Critical paths for wound care. Advances in Wound Care: 8:26, 1995 56. Thelan LA, Davie JK, Urden LD, et al: Critical Care Nursing: Diagnosis and Management, ed 2. St. Louis, Mosby-Yearbook, 1994 57. Thomason S, Hawley GG, Wurzel]: Specialty support surfaces: A cost containment perspective. Decubitus 6:32, 1993 58. Troyer-Caudle ]: Debridement: Removal of nonviable tissue. Ostomy/Wound Management 39:24, 1993 59. Winter GD: Formation of the scab and the rate of epithelialization of superficial wounds in the skin of the young domestic pig. Nature 193:293, 1962 60. Young M: Malnutrition and wound healing. Heart and Lung: The Journal of Critical Care 17:60, 1988 61. Zink M, Rosseau P, Holloway G: Lower extremity ulcers. In Bryant R (ed): Acute and Chronic Wounds- Nursing Management. St. Louis, MosbyYearbook, 1992 p 164 Address reprint requests to Patricia R. Boynton, MS, RN, CS 202 Bellevue Boulevard South Bellevue, NE 68005