The Integumentary SystemRepair and Management: An Overview

Joseph McCulloch, PT, PhD, FAPTA Objectives

After reading this article, you should be able to:

begin to subside, the wound enters the phase of maturation, which may continue for months or years. (See Illustration.)

Explain the physiological events related to wound repair (inflammation, proliferation, maturation). Discuss the varying etiologies of wounds. Describe the selection of tests and measures in the examination of patients with wounds. List the basic principles of an intervention program for patients with wounds of varying etiologies.

Physiological Events
Inflammatory Phase of Repair
Physical disruption of soft tissues results in damage to the blood and lymphatic vessels. Immediate vasoconstriction is the response to this event and is mediated by such local factors as serotonin and by the autonomic nervous system.3 These vessel-occluding events are not related to the coagulation process that follows. Instead, they are transient in nature, allowing blood flow to be slowed as the hemostatic process is activated.4 Concurrent with transient vasoconstriction, other hemostatic mechanisms are called into play. Damage to the endothelial cells and blood vessels causes collagen to be exposed. In conjunction with locally generated thrombin, exposed fibrillar collagen stimulates platelet aggregation at the wound site.5 Leukocytes also begin adhering to the vessel wall, particularly at the venule level.6 Active vasodilationtriggered by histamine, plasmaactivated substances, and platelet-derived vasoactive substancesfollows the initial vasoconstrictive phase. This process begins the clinical manifestation of inflammation. Although histamine is a potent vasodilator, its action is short-lived. The longer-term vascular permeability appears to be caused by other factors, with prostaglandins as one of the biggest factors.7 Increased vascular permeability is a key factor in continuation of the inflammatory process. As the acute inflammatory process progresses, neutrophils begin migrating through the more permeable endothelial lining of the blood vessels. This migration occurs in an amoeboid fashion, caused by chemotactic attraction and an active movement of the cells known as diapedesis. Neutrophils are the predominant cell type in the early stages of repair. As repair progresses, neutrophil counts decrease, and macrophages prevail. Macrophages become actively phagocytic and produce enzymes such as collagenase that assist in autolysis. Autolysis is a selective form of debridement that is facilitated by dressings that maintain a moist wound environment and sequester the bodys endogenous debriding agents. More important,

This article is the updated version of Wound Healing and Management (PT Magazine, December 1996), written by Joseph McCulloch, PT, PhD, FAPTA, Executive Associate Dean, School of Allied Health Professions, Louisiana State University Sciences Center, Shreveport, La.

Introduction/Physiological Events
The role of physical therapy in the management of individuals with chronic wounds continues to expand. The practice of managing hospitalized patients who have wounds solely with whirlpool baths and wet-to-dry dressing changes has given way to the development of wound care centers within physical therapy departments whose therapists specialize in wound management.1 In addition, there are private practice physical therapy outpatient clinics that have wound care as a primary offering.2 A solid understanding of the physiological events in integumentary repair is necessary to manage patients with dermal wounds. Although the environment necessary to promote repair varies according to the state of the underlying tissue, wounds generally heal through the same sequence of events. The sequence begins with an acute inflammatory response, which consists of a series of overlapping eventsincluding a vascular response and a cellular reactionand the chemical mediators that trigger and control these events. The inflammatory response is followed by the proliferative phase of repair. This phase involves neovascularization and production of a collagen network that helps restore structural integrity to the wound. As proliferative events

macrophages have been found to trigger and direct many aspects of the inflammatory reaction and tissue healing.8 They are essential to wound healing and assist in decontaminating the wound and creating an environment conducive to granulation tissue development.6 One of the primary objectives during integumentary repair is the reestablishment of skin as a functional barrier. Within hours of injury, keratinocytes respond to the epidermal defect. Keratinocytes are the major cells of the epidermis and are responsible for the production of keratin, the tough, flexible protein found in the stratum corneum. Although often discussed separately from the vascular response, epidermal repair occurs concurrently during the inflammatory phase. Repair begins as epidermal and adnexal basal cells start to flatten, lose their intracellular tonofilaments, and develop actin filaments at the cytoplasmic edges of the cell. Keratinocytes undergo mitosis and then begin to roll and slide over the intact cells. While they are migrating, the proliferative potential of the keratinocyte is inhibited.9 Cells continue migrating until their movement is halted by contact with other approaching keratinocytes. This is called contact inhibition. In a shallow wound, as contact inhibition signals the arrival of cells from the approaching edges of the wound, the process of thickening this thin layer begins. Continuing mitosis results in the development of successive layers of cells.

According to Nedlec et al,17 contraction generally proceeds at about 0.5 to 0.75 mm per day and continues for 12 to 14 days. Contact inhibition, or the edges of the wound approximating, will stop the process. If the force resisting closure is greater than the myofibroblasts closing force, contraction will cease. This is of clinical importance because the practice of firmly packing a wound with gauze or other dressings has the potential to impede wound contraction.17 One way to determine whether a wound has the potential to close by contraction is to try to approximate the wound edges. If the edges cannot be approximated, then epithelialization and scarring will have to play a major role in repair. Once the contraction process is completed, it is the myofibroblasts that appear to have a role to play in the production of hypertrophic scars.17 As fibroblasts and myofibroblasts advance through the dermis, they synthesize and secrete hyaluronic acid and a glycoprotein substance called fibronectin. This gel-like material lays down an extracellular matrix to which fibroblasts will bind. In addition, approximately 5 days after migration into the wound, fibroblasts begin to synthesize proteoglycans that stimulate the formation of collagen.18,19 As collagen is deposited, resilience and tensile strength of the tissue begin to increase. Collagen synthesis increases over the first 2 or 3 weeks after injury.20 Although collagen is not necessary for contraction to occur, a healed wound lacking in collagen will have less tensile strength. Conversely, as collagen content increases in a wound, the likelihood of further contraction decreases.21 As fibroplasia occurs, there is a concurrent angiogenesis that serves to reestablish the circulatory network within the wound.11 Several factors have been shown to stimulate angiogenesis. These include chemotatic factors supplied by neighboring cells and matrix, fibronectin, heparin, and platelet factors. In addition, factors such as low oxygen tension, lactic acid, and biogenic amines may facilitate the process.11,22-24 The clinical result of this angiogenic event is the development of granulation tissue that may be seen in the wound as red, roughened tissue.11

Proliferative Phase of Repair

As epidermal cell migration continues, wounds progress beyond the acute inflammatory phase and begin to exhibit characteristics that herald the second phase of repair, proliferation. This phase is associated with fibroplasia and development of the vascular network of granulation tissue. Proliferation begins shortly after injury as some fibroblasts reproduce and migrate into the wound, likely stimulated by a number of serum factors such as platelet-derived growth factor (PDGF), epidermal growth factor (EGF), and fibroblast growth factor (FGF).10,11 The exact mechanism of action of the activating factors is not fully understood. Some fibroblasts change shape and function to become myofibroblasts and become the predominant cell type found in granulation tissue of wounds undergoing contraction.12,13 Contraction, the process by which a fullthickness wound closes by the centripetal movement of surrounding tissue, is one of the major mechanisms by which deep incisional wounds heal if not sutured initially.14 Fibroblasts and myofibroblasts both have contractile proteins within them that, with appropriate stimulation, will pull on the extracellular matrix and draw the wound edges closer together.11,15 Most contraction, however, is believed to be the result of the actin-rich myofibroblasts.16 2

Maturation, or Remodeling, Phase

During the maturation phase, collagen continues to be deposited and the wounds resilience and tensile strength continue to increase. As previously mentioned, collagen synthesis increases early in the repair process and reaches a maximum level 2 or 3 weeks postinjury.20 As maturation continues, changes occur in the type of collagen synthesized. Type III collagen is the major type synthesized by fibroblasts during repair. It tends to be highly disorganized and gel-like in nature and contributes minimally to tensile strength.8 With maturation, type I collagen becomes the more predominant type. The exchange of type III and type I collagen is brought about

through a well-controlled process of new collagen synthesis and old collagen lysis and appears to be stimulated by stress across the closed wound.6,13 Tensile strength of the wound continues to increase for as long as a year after injury. After complete healing, the wound will have approximately 80% of the strength of uninjured skin.6 This strength difference has particular importance in healed pressure ulcers because subsequent pressure over the scar could result in failure of the weaker tissue. During examination, maturation may be recognized by a paling of the scar tissue and a cessation of scar contraction.

people with peripheral vascular disease or congestive heart failure. 3. Allergies to medication or to physical agents. Just as physical therapists need to know about adverse reactions to oral medications, they need to ascertain whether patients have had any undesirable reactions to topical agents such as moisturizers or wraps (eg, the Unna boot, an impregnated gauze wrap that has been used in the management of venous insufficiency ulcers26). Care should be taken to avoid the use of any topical ointments with similar components. 4. Previous interventions and any changes in patient status following these interventions. Why repeat history? If the patient has been treated unsuccessfully in the past for a given wound condition, the physical therapist can save time by determining why the intervention may have failed. Perhaps the previous treatment was performed inappropriately or at the wrong stage of healing. If so, the patient should be educated as to why and how the intervention should be tried again. 5. Use of tobacco products. Use of these products constricts arteries and can compromise blood flow to ischemic areas. 6. Use of blood-thinning agents. Prior to considering use of sharp debridement, the physical therapist should question the patient about use of blood-thinning agents. Debriding a wound on a patient who is taking such agents could result in serious, perhaps even life-threatening, complications. During the history, information is gathered concerning the patients current complaints or symptoms. Specifically, the physical therapist should query how current symptoms are altered by varying situations. For instance, if the patient complains of leg pain associated with a lower-extremity ulcer, it would be important to know if walking increases or decreases the pain. An increase in pain with walking could indicate an ischemic problem, whereas a decrease in pain could suggest a problem of venous origin. It therefore is important to first localize symptoms to determine whether the patient is having problems related to the wound itself or to another area. Depending on the nature of the process that caused the wound, the patient may report areas of anesthesia from a neuropathic process, rest pain secondary to ischemia, or swelling secondary to venous insufficiency.

Examination of the Patient With a Wound

History
The history provides the physical therapist with information that is critical in determining the diagnosis and prognosis and in developing the plan of care. The American Physical Therapy Associations (APTAs) Guide to Physical Therapist Practice25 (Guide) provides a documentation template that delineates the type of information that should be gathered from all patients, including, but not limited to: living environment, general health status, social/ health habits, medical/surgical history, current condition and chief complaint, functional status and activity level, and medications. A patient with a wound should be questioned specifically about how the wound developed. Was the wound a result of trauma, was it secondary to another problem such as swelling, or did it develop insidiously? Questions should be asked relative to mechanism of injury and the events that caused the patient to seek care. The following information gathered in taking the history may be especially important to patients with wounds due not only to the consequences of the disease process but due to the possible consequences of the interventions that may be used: 1. Presence of diabetes. People with diabetes may have numerous complications in wound healing secondary to high blood sugar levels and neuropathies that affect sensory and motor function in the extremities. These individuals may not be able to detect pressure on the plantar surface of their feet and therefore may be at risk for wound development or for healing complications. 2. History of peripheral vascular disease or congestive heart failure. Any conditions that affect delivery of oxygenated blood and removal of venous blood can complicate wound healing. In addition, compression therapy that might be indicated for swelling could cause severe complications in 3

Systems Review
As with any patient, the physical therapist must review the cardiovascular, pulmonary, integumentary, musculoskeletal, and neuromuscular systems in addition to communication, affect, cognition, and learning style. Impairments in any of these systems could have an impact

on the management of the patient and the outcome of wound healing. For example, in a patient with a neuropathic foot ulcer secondary to diabetes, a reduction in ankle range of motion might lead to increased plantar pressure that could delay healing. Likewise, in individuals with venous insufficiency ulcers, a gait analysis might reveal a disturbance in stride length. These individuals might have a shuffling gait that does not effectively use the calf muscle pump. Strategies to improve gait could have a major impact on lower-extremity edema. In reviewing the integumentary system, the physical therapist should note not only the integumentary disruption and the location of the wound but also pliability (texture), presence of scar formation, skin color, and skin integrity.25(p34)

All of the above information would be of value not only in identifying the cause of the integumentary disruption but in planning a course of management and documenting progress and healing.

Signs of infection. A sudden increase in drainage can be a

sign of a worsening problem or of an abscess that has spontaneously begun to drain. Most wounds have surface colonization of bacteria. Clinical infection in acute wounds has been correlated with the presence of greater than 105 pathogenic organisms per gram of tissue.28 There is poor specificity and predictive value in this correlation, however, and quantitative cultures are not readily available clinically.26 The physical therapist must frequently rely on many of the clinical signs identified by Linholm,29 which include: increasing pain, erythema, edema, heat, purulence, delayed healing, discolored and friable granulation tissue, pocketing at the base of the wound, foul odor, and wound breakdown.

Tests and Measures: Integumentary Integrity

Numerous tests are available to assist in examining patients, but the physical therapist does not use all of the available tests with any one patient. As stated in the Guide, Physical therapists individualize the selection of tests and measures based on the history they take and systems review they perform, rather than basing their selection on a previously determined medical diagnosis.25(pS43) Depending on the patient, the physical therapist might select tests from any number of test-and-measure categories that are described in the Guide.25 For patients with wounds, one of those selected categories would certainly be integumentary integrity. In examining the wound, the physical therapist might focus on characterizing or quantifying the following25:

If several of the above signs are present, a culture should be taken. If a quantitative culture is not available, a swab culture should be performed.30 The wound bed should be thoroughly prepared before taking the culture. This involves cleansing with saline and superficial debridement to permit access to the deeper compartments of the wound.30 A widely accepted practice in wound care is to use a zig-zag technique of 10-point coverage when performing a swab culture.31 This technique has never been validated, however, and is thought to possibly increase the yield of nonsignificant superficial colonizers.30 An alternative technique might be to sample from the area of the wound that demonstrated the most significant clinical signs.

Activities, positioning, and postures that aggravate the wound or scar or that produce or relieve trauma (eg, using observations, pressure-sensing maps). Burn (eg, using body charting, planimetry). Signs of infection (eg, using cultures, observations, palpation). Wound characteristics, including bleeding, contraction, depth, drainage, exposed anatomical structures, location, odor, pigment, shape, size, staging and progression, tunneling, and undermining (eg, using digital and grid measurement, grading of sores and ulcers, observations, palpation, photographic assessments, wound tracing). Wound scar tissue characteristics, including banding, pliability, sensation, and texture (eg, using observations, scar rating scales).

Wound characteristics: size and depth. Various simplified techniques exist for measuring the size and depth of wounds. One of the easiest ways to document wound diameter is to trace the margins using a piece of clear acetate film and a fine-point indelible-ink marker.
Various simplified techniques exist for measuring the size and depth of ulcers.32 The greatest length and width of the wound are determined, and the values are multiplied to yield an estimate of the surface area. Although this measurement technique generally converts an elliptical object into a rectangle, it has been shown to be a fairly reliable and easy-to-obtain measurement to document healing.33 If the clinician has access to a computer and appropriate software, the tracing can be digitized, and the area can be computed electronically for a more accurate measurement.34 Many wounds are not superficial but instead are deep and often may track or tunnel. Monitoring depth of a wound is important to ensure that the wound is not closing prematurely. A cotton-tipped applicator can be used for 4

this purpose (Fig. 1). The applicator is placed to the depth of the wound and then withdrawn and measured with a tape measure. A cotton-tipped applicator also can be used to gauge the degree of undermining present in a wound.32,35 Another simple technique of wound volume measurement is to fill a syringe with a known quantity of saline. With the extremity positioned so that the wound cavity is parallel to the floor, saline is injected into the cavity until it is filled. Subtracting the volume of liquid remaining in the syringe from the original amount gives some indication of volume (Fig. 2). Irregular wound borders and an inability to position the patient to prevent spillage can compromise the accuracy of this measurement.32,36 Ulcer Advisory Panel (NPUAP)37 and the Agency for Health Care Policy and Research (AHCPR)38 (now the Agency for Healthcare Research and Quality [AHRQ]) both recommended the use of a 4-stage classification system for pressure ulcers. This system, originally developed by Shea,39 describes levels of destruction from the epidermis inward: Stage IDestruction is limited to the epidermis. Edema and an ill-defined area of nonblanchable erythema may be present (Fig. 3). This staging is consistent with the pressure ulcer stage listed under Inclusion in Guide Preferred Practice Pattern 7B, Impaired Integumentary Integrity Associated With Superficial Skin Involvement.25(p601) Stage IIThere is discontinuity of the skin, with loss of the epidermis and, to varying degrees, the dermis (Fig. 4).This staging is consistent with the pressure ulcer stage listed under Inclusion in Preferred Practice Pattern 7C, Impaired Integumentary Integrity Associated With Partial-Thickness Skin Involvement and Scar Formation.25(p619) Stage IIIA full thickness of dermis is involved. Often there is undermining of deeper tissues (Fig. 5).This staging is consistent with the pressure ulcer stage listed under Inclusion in Preferred Practice Pattern 7D, Impaired Integumentary Integrity Associated With Full-Thickness Skin Involvement and Scar Formation.25(p637) Stage IVThe full-thickness involvement penetrates into the fascia. Frequently, muscle and bone are involved (Fig. 6). This staging is consistent with the pressure ulcer stage listed under Inclusion in Preferred Practice Pattern 7E, Impaired Integumentary Integrity Associated With Skin Involvement Extending into Fascia, Muscle, or Bone and Scar Formation.25(p655) 5

Wounds other than pressure ulcers are typically broadly defined as having partial-thickness (equivalent to a Stage I/II pressure ulcer) or full-thickness (equivalent to a Stage III/IV pressure ulcer) depth. Regardless of how a wound is classified, healing should not be described by reverse staging.40,41 Wounds heal by various degrees of epithelialization and scarring. This is to say that a Stage IV wound does not become a Stage III, then a Stage II, then a Stage I wound; rather, a Stage IV wound becomes a healing Stage IV wound. In a similar manner, wounds that are healing but that are not secondary to pressure would be classified as healing fullor partial-thickness wounds.

Wound characteristics: staging. The National Pressure

Wound characteristics: location. Many ulcers have characteristic locations. Ulcers secondary to venous insufficiency, for example, frequently occur over the area surrounding the medial malleolus,42 whereas ulcers secondary to arterial insufficiency frequently occur over the toes.43 In patients with diabetes, ulcers secondary to pressure and insensitivity classically are noted over weightbearing surfaces on the plantar aspect of the foot.44 These locations are by no means absolute, and patients may have ulcers secondary to mixed etiologies. Wound characteristics: drainage. In addition to size and
depth of an ulcer, any drainage that might be present should be noted. The amount, color, odor, and consistency of drainage from the wound should be documented, and notations should be made as to whether any of these characteristics have changed significantly since the previous examination. For instance, a sudden increase in drainage can be a sign of a worsening problem or of an abscess that has spontaneously begun to drain. Likewise, a wound that has an odor that was not previously present could indicate increased bacterial colonization or even infection. In examining the tissues adjacent to the wound, the physical therapist might focus on characterizing or quantifying the following25:

Activities, positioning, and postures that produce or relieve trauma to the skin (eg, using observations, pressure-sensing maps, scales). Assistive, adaptive, orthotic, protective, supportive, or prosthetic devices and equipment that may produce or relieve trauma to the skin (eg, using observations, pressure-sensing maps, risk assessment scales). Skin characteristics, including blistering, continuity of skin color, dermatitis, hair growth, mobility, nail growth, sensation, temperature, texture, and turgor (eg, using observations, palpation, photographic assessments, thermography).

Associated signs and symptoms. Trophic changes (eg, dry skin, brittle nails, hair loss) may indicate poor arterial nutrition to the area. The importance assigned to these changes should be weighed with respect to the patient's age and the body part being examined. Sun-exposed areas of the body may exhibit dryer skin than more protected areas. In addition, nails tend to become more brittle with age.
Skin color can provide information about the functional status of the circulatory system. In the presence of ischemia, a cyanotic appearance or pallor may be noted in light-skinned individuals. The color of the lips, mucous membrane, and nail beds can provide even more information regarding oxyhemoglobin concentration. In chronic venous insufficiency, skin discoloration occurs because of deposition of hemosiderin, a pigment attached to hemoglobin that stains tissues when red blood cells undergo lysis extravascularly. The result is a brownish discoloration of the skin in light-skinned individuals or a hyperpigmentation in darker-skinned individuals.45 With aging, some skin atrophy may occur, causing the skin to be thinner than normal and shiny in appearance. Monitoring skin temperature in the area surrounding a wound allows assessment of the relative severity of an inflammatory response. Sudden and dramatic changes in skin temperature, frequently associated with erythema, can be indicative of developing cellulitis or an infection that may require medical attention. Many methods are available for monitoring skin temperature, ranging from a surface probe, known as a thermistor, to a radiometer, which measures infrared radiation from the skin. The radiometer allows the clinician to quickly scan an area and has been shown in preliminary studies to be a reliable means of assessing temperature that provides readings comparable to surface thermistors.46 One benefit that infrared radiometers provide over surface probes is the ability to measure temperature directly over the wound.

4+=Depression lasts for greater than 30 seconds. Another means of quantifying edema is to perform a circumferential measurement of the extremity. Circumferential measurements may be taken with a tape measure using anatomical landmarks that will allow measurement reproducibility.32 Volumetric measurements can be of benefit when assessing size of irregularly shaped areas and are probably the most accurate assessment of edema available to the therapist because variations in limb contour do not complicate measurement. Volumetric tests use water displacement as a means of quantifying extremity volume.47-49 These tests are performed by slowly lowering the body part into a filled volumeter (Fig. 7). The water overflow is collected and measured in a graduated cylinder.

Sensory integrity. Individuals with disordered cutaneous sensibility are at an increased risk for development of wounds secondary to pressure and extremes of temperature. If a sensory deficit is suspected, the physical therapist should determine the extent of the involvement. Temperature and pain signals travel by small afferent fibers and can be tested with the pinprick technique.50 This test is performed by alternately pressing the sharp and dull ends of a safety pin or paper clip to a patients skin and asking the patient to report whether he or she feels a sharp or dull sensation. Great care should be exercised in performing this test on elderly people or anyone with fragile skin.
Pinprick and light touch give some indication of the degree of cutaneous sensibility. Another method to test sensation is monofilament testing. Semmes-Weinstein monofilaments are graded by manufacturers on a scale of 1.65 to 6.65 for the force required to cause the filament to bow when pressed against the skin.51,52 The higher the monofilament number, the more force required for bending. In patients with neuropathy secondary to diabetes, monofilament testing has become a standard of examination.32 The 5.07 monofilament, which, on bowing, exerts 10 g of force against the skin, is typically used. If a patient cannot sense this level of force over the plantar bony prominences of the foot (metatarsal head and digits), the patient has lost protective sensation and is at risk for ulcer development.

Other Tests and Measures

Anthropometric characteristics. If edema is present in an extremity or in the area about the wound, it can be documented in a variety of ways. One of the simplest techniques is to quantify the pitting that occurs from the pressure of the examiners digit. Pitting can be recorded as 1+ to 4+ according to the following scale32:
1+=Barely perceptible depression. 2+=Easily identified depression takes about 15 seconds to resolve. 3+=Depression takes between 15 and 30 seconds to resolve. 6

Circulation (arterial, venous, lymphatic). If the findings of the tests previously discussed suggest that the wound may be of venous or arterial origin, a thorough examination of the peripheral vascular system is warranted. Such an examination is beyond the scope of this article but is discussed in depth by Lampe.32
As noted earlier, in addition to assessment of the vascular system, physical therapists should be acutely aware of the need to examine the neuromuscular and musculoskeletal systems of all patients with chronic wounds. The

immediate goal of intervention may be to heal the wound, but the overall goal of physical therapy is to return the individual to as high a level of physical functioning as possible. For this reason, the physical therapist should examine such areas as muscle performance (especially muscle strength), range of motion, and reflex integrity.

To adequately accomplish these goals, the physical therapist must take care to ensure that prescribed interventions do not impede wound healing.

Debridement
Epithelialization is a requirement for wound healing. Because epithelial cells grow best in a warm, moist environment and will not migrate across necrotic tissue, it may be necessary to perform substantial debridement of existing necrotic tissue from a wound bed.53 Such debridement may require that the wound initially be enlarged to expose healthy tissue. When debridement is indicated, several options are available. In order to determine which option is best, the physical therapist must consider whether or not the patient can tolerate sharp debridement. If extensive debridement is necessary and requires anesthesia, the surgeon most appropriately handles this. When selective debridement of necrotic tissue is performed without the need for anesthesia, the physical therapist can provide this intervention, using mechanical or chemical means. Sharp debridement is a mechanical method available to the physical therapist, but care should be taken to use proper sterile, sharp instrumentation and to avoid the temptation to use disposable suture-removal or dressing kits. Instruments in such kits may be of poor quality and may not be sharp enough for the task at hand. If there is extensive necrotic tissue that cannot be completely removed in a single therapy session, autolytic debridement (debridement by the bodys endogenous enzymes) can be facilitated by the application of moisture-retentive dressing, which will be discussed later. Another debridement option is the use of enzymatic debriding agents such as Accuzyme* or Collagenase Santyl Ointment. If the therapist believes that sharp debridement is not advised due to anticoagulation therapy or an inability of the patient to tolerate the procedure, enzymatic debridement may be indicated. A discussion should be held with the referring practitioner and a prescription obtained for the enzyme. Care should be taken to follow the product insert when applying the agent.53-55 Whirlpool baths historically have been advocated as a debriding tool. In their review of adjunct physical agents and mechanical modalities, Hess et al56 concluded that although whirlpool is used frequently, it has not been proven to be beneficial in wound healing. In the opinion of McCulloch and Kloth,57 the use of whirlpool baths is of value only in removing loosely adherent devitalized tissue from a wound, as is often seen in large surface area burns. Whirlpool baths have no ability to remove densely adherent necrotic debris from a wound, and, in conditions such as venous insufficiency, they are contraindicated because of adverse effects of the dependent position.58,59 7

Intervention: Integumentary Repair and Protection Techniques

The Guide25(p117) lists the following anticipated goals and expected outcomes for integumentary repair and protection techniques: Impact on pathology/pathophysiology:

Debridement of nonviable tissue is achieved. Joint swelling, inflammation, or restriction is reduced. Nutrient delivery to tissue is increased. Pain is decreased. Physiological response to increased oxygen demand is improved. Soft tissue or wound healing is enhanced. Soft tissue swelling, inflammation, or restriction is reduced. Tissue perfusion and oxygenation are enhance. Wound size is reduced.

Impact on impairments:

Gait, locomotion, and balance are improved. Integumentary integrity is improved. Joint integrity and mobility are improved. Muscle performance (strength, power, and endurance) is increased. Postural control is improved. Sensory awareness is increased. Weight-bearing status is improved.

Impact on functional limitations:

Ability to perform physical actions, tasks, or activities related to self-care, home management, work (job/ school/play), community, and leisure is improved. Level of supervision required for task performance is decreased. Performance of and independence in activities of daily living (ADL) and instrumental activities of daily living (IADL) with or without devices and equipment are increased. Tolerance of positions and activities is increased.

Dressings
Following debridement, the physical therapist usually must make a decision about the best means of dressing the wound. The sheer number of dressing products available today makes this a formidable task. Prior to deciding on any dressing product, the physical therapist should take into consideration the factors that were addressed during the examination. Specifically, what are the location and stage of the wound? Is it a cavity wound that needs filling, or a necrotic wound that requires more debridement? How much drainage is present? Is infection present, or is the wound clean and granulating? With answers to these questions, the physical therapist can make a much more logical selection of the appropriate dressing. Current dressings generally promote a moist environment to facilitate cellular proliferation and migration as the wound advances through the 3 stages of healing. Although dressings are generally classified by structural components into one of the categories listed below, the physical therapist should think more about the function of the dressing. Dressings are designed to absorb excessive exudate from a wound, maintain the level of moisture that is present, or, in the case of desiccated wounds, provide needed moisture. Understanding these different functions facilitates clinical decision making. The following list is not intended to be all-inclusive but to provide a general classification for the major dressing types. Readers are encouraged to refer to more comprehensive sources for detailed information, such as the discussion of dressings by Myer.60

Hydrocolloids. Hydrocolloid dressings provide the most

occlusive environment of synthetic dressings. For this reason, they are beneficial in trapping endogenous agents that can facilitate autolytic debridement. They also can be left in place for several days to a week, depending on the degree of exudate present. Because of the highly occlusive nature of hydrocolloid dressings, there is an increased risk of tissue maceration associated with their use. This can be minimized by the use of a barrier film or ointment that can protect the periwound skin. Some hydrocolloids develop an odor as melting of the dressing occurs. This odor may be mistaken as a sign of infection. If the dressing is indeed the source of the odor, the odor should disappear once the wound is irrigated.

have been noted for their absorptive powers.67 Both types require some form of secondary dressing to hold them in place. Alginates are made from either sodium alginate or sodium/calcium alginate obtained from seaweed and kelp. Fiber dressings generally are made of carboxymethylcellulose fiber and are highly absorptive.68 Dressings that are used to assist mechanical debridement should be used judiciously. Wet-to-dry gauze is one type of dressing that has been used because it can collect tissue exudate and aid in removal of necrotic debris. The debriding power of gauze is nonselective, however, and can result in tissue desiccation, pain, and damage to fragile granulating tissue.60 If gauze dressings are used in conjunction with chemical debridement agents and topical antimicrobials, the agents may need to be discontinued as the wound begins to granulate so as not to interfere with fibroblast growth.69,70 If gauze dressings are the only option available to patients at this point, however, the gauze should be applied wet-towet, with saline as the wetting agent.60 Because the objective is to keep the wound bed moist, more frequent dressing changes are required. The frequency of the dressing change is dictated by the state of the dressing at the time of removal. That is, if the dressing has dried, more frequent changes are indicated. Once the wound base is debrided and granulating, as would be indicated by a beefy red appearance, it should be protected from further trauma that can be caused by frequent dressing changes, dry dressings, and overzealous use of topical agents. Occlusive films or hydroactive dressings can be used at this point.51

Alginate and fiber dressings. These types of dressings

Transparent films. As the name implies, these are thin,

clear dressings that permit visualization of the wound. They have no absorptive properties and are therefore used in minimally exudative wounds in which epithelialization is desired. Film dressings provide a good interface with the environment that protects the fragile wound bed and maintains desired moisture.61 impermeable form. They also vary in the thickness of the foam. Thin foam dressings provide mild absorption and allow for some evaporation of exudate. Thicker foam dressings are more absorptive and therefore less permeable. They tend to work well on wounds that produce a great deal of exudate.62,63

Foams. Foam dressings come in both semipermeable and

and sheet form. The gels have high water content and are useful in introducing moisture to a desiccated wound and maintaining wound moisture in arid climates.64 These dressings also soften necrotic tissue and aid in autolytic debridement. Amorphous hydrogels also can be used as a lining for cavity wounds along with a secondary filler of a saline-moistened gauze.65,66

Hydrogels. Hydrogel dressings come in both amorphous

Physical Agents and Mechanical Modalities

Physical therapists have many modalities at their disposal, some of which have documented evidence of accelerating wound repair. Other modalities, however, have only the 8

manufacturers claims of accelerated healing, with no strong scientific evidence to substantiate the claims.

Hydrotherapy. Once a wound has been debrided, it should be carefully cleansed as often as necessary, but also should be protected from harsh topical agents. Whirlpool baths provide a means of gently cleansing a wounded area, but may be overkill because the entire patient or body part must be immersed in the water. This immersion requires a large amount of water and a great deal of effort to keep equipment decontaminated. In addition, the pressure exerted by the whirlpool turbines may be excessive.45,71
A more direct and controlled approach for localized wounds is to use pulsatile lavage with suction.45,72 Lavage devices on the market today allow for the delivery of an irrigant at a preset pressure.73 Some, such as the Simpulse VariCare System (Fig. 8), provide lavage tips with a diversion system to help prevent suctioned debris from cycling back through the irrigation gun. This permits a disposable gun to be used several times on the same patient. There also is some preliminary research that suggests that the negative pressure created by the suction may stimulate development of granulation tissue.74

Evidence exists to support the use of IPC 2 or 3 times per week at a pressure of 40 to 50 mm Hg.82,83 The compression-rest ratio generally is set to about 3:1, allowing upward to 45 seconds for the veins to refill during the rest phase.84 Intermittent pneumatic compression should be used with caution in individuals with lymphatic disease. The lymphatics are a low-pressure system and can be further damaged by aggressive compression.85,86 Vacuum-assisted closure (VAC) uses negative pressure to enhance closure of recalcitrant wounds. The technique involves application of subatmospheric (negative) pressure, at controlled levels of 50 to 125 mm Hg below ambient pressure, to a wound via an open-celled polyurethane foam dressing sealed in place with an occlusive film cover (Fig. 9).87,88 The dressing is then connected to a computercontrolled vacuum pump that controls the cycling of negative pressure at a prescribed rate. Developed from the initial work of Argenta and Morykwas,88 the VAC has radically changed how large cavity wounds are managed. At least two randomized clinical trials have been published that support the use of VAC, one on patients with fullthickness decubitus ulcers89 and another on patients with chronic, nonhealing wounds,90 and more than 50 published case studies have described this intervention in the management of a variety of chronic wounds. Patients with diabetes frequently develop ulcers on the plantar aspect of the foot secondary to pressure and insensitivity. Such ulcers are indolent because patients, insensitive to pain, continue to walk on the affected extremities. One of the major approaches to management of these patients is to off-load the extremity. Physical therapists may initially need to assist repair by placing the patients affected extremity in a total-contact walking cast (Fig. 10).91 When the patients status is such that the physical therapist is reluctant to use a total-contact cast for instance, when there is excessive drainage from a wound or fluctuating edemathe use of a posterior walking splint is another option (Fig. 11). Although Birke92 indicated that such a device does not provide pressure relief as effectively as a total-contact cast, the walking splint does have the advantage of allowing daily wound care and dressing changes. Birke and Patout93 suggested that total-contact casts could be bifurcated in order to allow for wound care. Total-contact casts and posterior walking splints can assist in relieving pressure from the ulcer, thereby helping it to heal. When ulcers are located on the distal aspects of the foot, wedge shoes such as the OrthoWedge# may be of benefit (Fig. 12).94 After healing, corrective measures must be taken to modify the patients shoes; otherwise, breakdown is likely to recur. Orthotic modification should be aimed at redirecting foot pressure from bony prominences.95 9

Thermotherapy. Chronic wounds tend to be hypothermic because they are associated primarily with diabetes and other conditions that reduce blood flow.75 Limited evidence suggests that providing gentle warmth to chronic wounds, particularly pressure and venous insufficiency ulcers, can increase the rate of wound healing.76-78
extremity dependent edema in individuals with venous insufficiency may result in wounds not healing or even in wounds enlarging.79,80 Various extremity wraps have been designed to control edema. The least effective of these wraps seems to be the standard elastic wrap.81 This wrap has a tendency to lose elasticity with repeated use and is also difficult to apply with uniform pressure. In recent years, various controlled tension wraps such as SurePress High Compression Bandage have been introduced. These bandages have rectangular guides that convert to squares when stretched to the appropriate length, thereby helping to ensure proper pressure with each application. A 4-layer bandage system, Profore||, provides several forms of compression. The first layer is an absorptive cotton wrap. Layers 2 and 3 are short and long stretch bandages, respectively. The fourth layer is a cohesive wrap. The manufacturer claims that, when applied according to manufacturers instructions, the system provides a pressure of 40 mm Hg at the ankle. Intermittent pneumatic compression (IPC) may provide much needed assistance to the damaged muscle pump.

Compression therapies. Failure to address lower-

Individuals with arterial ulcers offer great challenges to the wound care clinician, especially if problems lie within smaller vessels. Attempts to promote vasodilation via reflex heating and warm whirlpool baths were reported in the literature several decades ago,96 but current support for this form of heating is lacking. In many of these patients, vascular reconstruction is an option.97,98 If reconstruction is not possible, wounds may never heal but instead may worsen to the point of gangrene. At such a time, amputation may be the only option.

Electrotherapeutic Modalities
One of the most popular and successful agents used to accelerate repair is high-voltage pulsed current (HVPC).99 Studies suggest that HVPC used at a frequency of 100 pulses per second for 60 minutes, 5 days a week, will promote improved healing of dermal ulcers.99-104 Intervention typically involves application of an electrode over the wound via a sterile saline-moistened gauze interface, with the other electrode placed some distance from the wound to improve current penetration.105 When debridement or epithelialization is the goal, the positive electrode should be placed over the wound. For all other instances, the negative electrode is used.99 Although there is an abundance of research supporting the beneficial effects of electrical stimulation in wound repair, the Centers for Medicare and Medicaid Services (CMS) have limited reimbursement for this device for Medicare recipients. Current reimbursement guidelines indicate that in order for electrical stimulation to be considered for reimbursement in wound care, the wound must have been present for at least 30 days and not have responded to standard care.106 (For an in-depth discussion of electrical stimulation and wound healing, refer to Beginning My Way Back: Neuropathic Plantar Ulcer in a Patient With Diabetes Who Is Homeless, by Bottomley.) Ultrasound has been shown to be of benefit in all three phases of wound repair (inflammation, proliferation, remodeling). For many years, ultrasound was promoted as an anti-inflammatory modality. Work by Goddard and colleagues107 demonstrated that not only was ultrasound not an anti-inflammatory agent, it was actually proinflammatory. Ultrasound caused the degranulation of mast cells, which accelerated the inflammatory process. During the proliferative phase, ultrasound in vitro has been shown to cause fibroblasts to secrete collagen.108 Both in vivo research109 and in vitro research110 have demonstrated acceleration in the wound contraction process. Quantitative data also are available to support the hypothesis that, when injured skin is treated with therapeutic ultrasound during the inflammatory and early proliferative phases of repair, skin repair can be accelerated.111,112 10

Older research showed that therapeutic ultrasound administered during the maturation/remodeling phase of repair has moderate success in improving the mechanical properties of mature scar tissue.113,114 It has been suggestedbut not demonstrated in the peer-reviewed literaturethat much greater success may be obtained when intervention is initiated immediately after injury.115 In recent reviews, Hess et al56 noted that ultrasound has shown benefit but that further controlled trials are needed to establish effectiveness, whereas Cullum et al116 and the Centre for Evidence Based Nursing117 concluded that although there was not a statistical difference in healing rates with ultrasound therapy, the direction of the treatment effect was consistently in favor of ultrasound. According to Kloth,12 ultrasonic generators capable of producing a 1- or 3-MHz signal are best for treating dermal tissue, with treatment typically delivered at less than 0.5 W/cm2, pulsed 2 milliseconds on, 8 milliseconds off. The appropriate frequency depends on the depth of the tissue to be treated, because penetration of ultrasound is frequency dependent. Kloth indicated that, for more superficial tissues, 3 MHz ultrasound is preferred.12

Compression Therapies: Use of VacuumAssisted Closure (VAC)

As previously described, physical therapists have a wide variety of interventions from which to choose in the management of patients with wounds. Vacuum-assisted closure, which has had a major impact on wound management, is one of those interventions. Consider the following case example, for which the patient/client management elements of examination, evaluation, diagnosis, prognosis, and intervention have been abbreviated for the purpose of illustration. Mr B was a 39-year-old man with a history of type 2 diabetes. He was admitted to the hospital on October 26 with a diagnosis of infection in the left foot following an amputation of the great toe several weeks earlier (Fig. 13). He reported that he did not use any tobacco products (which can constrict arteries and compromise blood flow27) or alcohol. Mr B lived at home with his wife, who prepared his meals and assisted in wound care consisting of dressing changes with saline-moistened gauze 3 times per day. He was able to take care of all other activities of daily living. He performed limited ambulation with the assistance of a wedge shoe and a cane. Mr B was unemployed but reported that, when Im able to, he worked in manual labor jobs. Prior to the amputation, Mr B had not been hospitalized for any surgical procedures. He was under medical management for hypertension and hyperlipidemia, both of

which, according to the medical record, were being successfully control through the use of medications. Following hospital admission in October, Mr B was placed on intravenous antibiotic therapy. On November 18, he was taken to the surgical department for debridement. Following the procedure, the surgeon dressed the wound with an alginate dressing covered by gauze. On the first postoperative day, Mr B was referred for physical therapy for wound management. During the history and systems review, the physical therapist determined that Mr B was alert, oriented to person, place, and time, and not in acute distress. The wound dressing was intact and dry. The test-and-measure categories on which the physical therapist decided to focus during the examination included anthropometric characteristics, circulation, sensory integrity, and integumentary integrity.

granulation tissue was not flush with the skin surface, and the wound needed assistance with contraction. Based on evidence reported in the peer-reviewed literature,88-90 the physical therapist expected that, in this patient with a type 2 diabetic ulcer, VAC therapy would promote wound contraction and perfusion and prepare the wound bed for acceptance of a graft. If the patient had had a more shallow wound that needed to be kept moist to promote epithelialization, the use of alginates, hydrocolloids, or foams would have provided the proper environment at less cost and greater ease of use. The physical therapist concluded that the prognosis for full healing of the wound was great due to the patients relatively young age and good arterial supply to the extremity. The physical therapist had some experience in providing VAC therapy and felt confident in using it. The VAC sponge was cut to size for the wound taking care to avoid overlap on intact skin, as maceration could result. The occlusive film was draped over the sponge, and the dressing was attached to the VAC unit. Negative pressure was set at 125 mm Hg, per manufacturer recommendation for this type of wound. The VAC therapy continued uninterrupted for 48 hours. At the first dressing change, the physical therapist noted that there was 100% beefy-red granulation tissue present and that the wound had decreased in size to 2.5 4 cm and had 1 cm of depth. The physical therapist noted no periwound maceration. Had there been periwound maceration, the physical therapist would have used a skin preparation, such as zinc oxide, to protect the area. A hydrocolloid dressing also could be used to border the wound. This protects the periwound tissue and allows a place for the VAC film dressing to be attached. If the wound had shown no sign of decreasing in size, the therapist would have referred the patient to the physician for further vascular workup. The physical therapist decided to apply another VAC dressing and to continue the intervention for 48 hours on and intermittent cycle at 75 mm Hg of negative pressure as suggested by the manufacturer. This protocol continued for a total of 12 days, with steady progress noted at each dressing change. Following 14 days of VAC therapy, the physical therapist and the plastic surgeon evaluated the patient jointly and deemed the wound ready for acceptance of a graft (Fig. 14). On December 5, the patient underwent placement of a mesh graft. He was followed in the hospital for 1 week and then discharged to home. At follow-up on December 22 and January 5, the wound was fully epithelialized (Fig. 15). The patient was then referred for custom-made orthoses and extra-depth shoes to prevent wound recurrence. 11

Anthropometric characteristics. Using the scale described by Lampe,32 the physical therapist determined that there was 1+ pitting edema (barely perceptible depression) over the dorsum of the left foot. Circulation (arterial, venous, lymphatic). Posterior tibial and dorsalis pedis pulses were palpable bilaterally, and there was a good capillary refill to the remaining digits. Sensory integrity. The physical therapist assessed protective sensation using Semmes-Weinstein monofilaments and found protective sensation to be absent below the level of the ankle bilaterally. This was not a new finding, as Mr B had had loss of protective sensation for several years, as reported in the medical record. Integumentary integrity. Mr B had a clean postoperative
wound secondary to debridement of a previously infected great toe amputation. The post-operative wound measured 3 by 5 cm and consisted of 95% beefy-red granulation tissue. There was 5% necrotic connective tissue evident at the medial margin of the wound. The periwound tissue was mildly macerated. The wound was 1.5 cm in depth, and no sinus tracks were noted. Based on evaluation of these and other examination data, the physical therapist classified this patient as belonging to both Practice Pattern 4J, Impaired Motor Function, Muscle Performance, Range of Motion, Gait, Locomotion, and Balance Associated With Amputation (the primary pattern for this patient) and to Practice Pattern 7E, Impaired Integumentary Integrity Associated With Skin Involvement Extending Into Fascia, Muscle, or Bone and and Scar Formation (the focus of this case example). The therapist concluded that this patient would benefit from VAC therapy because the wound was clean, the

Footnotes
* Healthpoint Ltd, 3903 Hulen St, Ft Worth, TX 76107.

9 Roenigk RK, Roenigk HH. Surgical Dermatology: Advances in Practice. St Louis, Mo: CV Mosby Co; 1993. 10 Bennett NT, Schultz GS. Growth factors and wound healing: biochemical properties of growth factors and their receptors. Am J Surg. 1993;165:728-737. 11 Davidson JM. Growth factors, extracellular matrix, and wound healing. In: Kloth LC, McCulloch JM, eds. Wound Healing: Alternatives in Management. 3rd ed. Philadelphia, Pa: FA Davis Co; 2002:129-149. 12 Kloth LC. Adjunctive interventions for wound healing. In: Kloth LC, McCulloch JM, eds. Wound Healing: Alternatives in Management. 3rd ed. Philadelphia, Pa: FA Davis Co; 2002:360361. 13 Tomasek J, Gabbiani G, Hinz B, et al. Myofibroblasts and mechano-regulation of connective tissue remodelling. Nat Rev Molecular Cell Biol. 2002;3:349-363. 14 Gabbiani G, Ryan G, Majne G. Presence of modified fibroblasts in granulation tissue and their possible role in wound contraction. Experientia. 1971;27:549-550. 15 Grinnell F. Fibroblasts, myofibroblasts, and wound contraction. J Cell Biol. 1994;124:401-404. 16 Skali O, Gabbiana G. The biology of the myofibroblast relationship in wound contraction and fibrocontractive diseases. In: Clark R, Henson P, eds. Molecular and Cellular Biology of Wound Repair. New York, NY: Plenum Press; 1988:373. 17 Nedlec B, Ghahary A, Scott P, Tredget E. Control of wound contraction: basic and clinical features. Hand Clinics. 2000;16:289302. 18 Singer I. The fibronexus: a transmembrane association of fibronectin-containing fibers and bundles of 5 mm filaments in hamster and human fibroblasts. Cell. 1979;16:675-685. 19 Ruoslahti E, Yamaguchi Y. Proteoglycans as modulators of growth factor activities. Cell. 1991;64:867-869. 20 Kanzler M, Gorsulowsky D, Swanson N. Basic mechanisms in the healing cutaneous wound. J Dermatol Surg Oncol. 1986;12:1156-1164. 21 Bell E, Invarsson B, Merrill C. Production of a tissue-like structure by contraction of collagen lattices by human fibroblasts of different proliferative potential in vitro. Pro Natl Acad Sci USA. 1979;76:1274-1278. 22 Raju K, Alessandri G, Gullino P. Characterization of a chemoattractant for endothelium induced by angiogenesis effectors. Cancer Res. 1984;44:1579-1584. 23 Azizkhan R, Azizkhan J, Zetter B, Folkman J. Mast cell heparin stimulates migration of capillary endothelial cells in vitro. Exp Med. 1980;152:931-944.

Abbott Laboratories, 100 Abbott Park Rd, Abbott Park, IL 600064.

Davol Inc, 100 Sockanossett Crossroad, PO Box 8500, Cranston, RI 02920. ConvaTec, Bristol-Myers-Squibb, 100 Headquarters Park Dr, Skillman, NJ 08558.

||

Smith & Nephew Inc, Wound Management Division, 11775 Starkey Rd, Largo, FL 33799-1970.

Kinetic Concepts Inc, 8023 Vantage Dr, PO Box 659508, San Antonio, TX 78265-9508. Darco International Inc, 1327 7th Ave, Huntington, WV 25701.

Summary
This article has provided a review of mechanisms by which wound healing occurs in humans, with an emphasis on the role of physical therapists in clinical decision making. A series of tests and measures were suggested that could be incorporated into examination. The intervention section gave an overview of methods of management, including characteristics of various dressings and their indications for use. A brief synopsis of adjunctive physical therapy modalities also was presented.

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85 McCulloch JM. Management of wounds secondary to vascular disease. In: Kloth LC, McCulloch JM, eds. Wound Healing: Alternatives in Management. 3rd ed. Philadelphia, Pa: FA Davis Co; 2002:409-428. 86 Weissleder H, Schuchhardt C. Lymphedema Diagnosis and Therapy. Bonn, Germany: Kagerer Kommunikation; 1997:1-270. 87 McCallon S, Knight C, Valiulis J, et al. Vacuum-assisted closure versus saline-moistened gauze in the healing of postoperative diabetic foot wounds. Ostomy Wound Manage. 2000;46:26-34. 88 Argenta LC, Morykwas MJ. Vacuum-assisted closure: a new method for wound control and treatmentclinical experience. Ann Plast Surg. 1997;38:563-576.

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