The purpose of this educational module is to present the reader with wound care basics for most typical chronic wounds. This is not meant to be an extensive or all-inclusive course which details advanced wound therapies for the wound care specialist. Rather, it is to help the clinician/nurse (in any setting) to become more familiar with basic principles of good wound healing. This module also aims to provide a beginning guide to wound dressings, thereby answering the age-old question, “what should I put on the wound?” In addition, this module includes a basic overview of pain management for wounds - an under-addressed clinical problem.
By the end of this course, the learner will be able to:
Worldwide, there are over 100 million surgical wounds, over 70 million traumatic wounds (including 20 million lacerations), 3.5 million burn wounds, and 24.2 million chronic wounds (including 10 million diabetic foot ulcers, 9.7 million venous leg ulcers, and 4.5 million pressure ulcers) that require treatment each year (Wound prevalence and wound management, 2012-2020 Report). These numbers reflect that more people throughout the world have chronic, complex or non-healing wounds than the total US population with cardiovascular disease (approximately 15 million), asthma (18 million), or diabetes (10 million) (“CDC - 2011 National Estimates - 2011 National Diabetes Fact Sheet - Publications - Diabetes DDT,” n.d.). Chronic, complex or non-healing wounds represent a major health problem and a growing economic concern. To improve wound healing outcomes and decrease the number of chronic or non-healing wounds worldwide, evidence-based wound prevention and treatment strategies are necessary.
Wounds occur as a result of a disruption in the skin’s integrity due to injury (such as surgery or trauma), or disease. Acute wounds are those which follow an orderly, expected pathway to healing. The anticipated timeline for the expected pathway to healing is dependent upon intrinsic factors (such as age, body build, and genetic factors), extrinsic factors (such as mechanical stress, temperature, smoking, radiation, debris, chemicals/medications, and infection), and the size of the wound or extent/depth of the tissue disruption. In other words, normal, acute wound healing may not occur in exactly the same number of days or weeks for all individuals. Acute wound healing for most full thickness injuries of human tissue follows an orderly (though sometimes overlapping) 4 step process immediately after wounding: activation of the clotting cascade (hemostasis), inflammation, proliferation, and scar tissue maturation/remodeling (Sussman & Bates-Jensen, 2012; Hess, 2013; Doughty & McNichol, 2016; Bryant & Nix, 2016).
When an alteration in skin integrity occurs, such as when a teenager falls from a skateboard and scrapes his/her knee, it results in a wound. If the wound is superficial and extends only through the epidermis and perhaps involves the uppermost part of the dermis (but does not involve subcutaneous tissue or underlying structures), it is considered a partial thickness wound (Sussman & Bates-Jensen, 2012). We anticipate this type of wound will heal by regeneration of skin cells and re-epithelialization (superficial skin cells will migrate over the injury and “close the wound”). This wound is not likely to scar. If the wound extends through the epidermis and the dermis and includes subcutaneous tissue or underlying structures, it is considered a full thickness wound. We expect this type of wound to heal by the more complex four-step process listed above, ultimately resulting in scar tissue formation. The location of the wound determines the depth of tissue loss required to establish if a wound is a partial or full thickness wound. Some parts of the body (over the anterior shin, the knuckles of the hands, bridge of the nose, eyelids, etc.) have very thin skin and do not have a significant amount of subcutaneous fat/tissue. A shallow wound over these areas would be a full-thickness wound though they may only extend 2mm deep (or less). Alternatively, wounds over the buttocks or fleshy parts of the body may be of a similar depth, yet remain partial thickness wounds because they do not extend through the dermis into subcutaneous tissue. Areas of the body such as the ears and bridge of the nose have cartilage directly covered by dermis and epidermis. Any wound that involves cartilage is a full thickness wound, even if it appears very superficial (Sussman & Bates-Jensen, 2012; Doughty & McNichol, 2016).
Wounds are said to be healing by primary intention if a linear wound (such as a surgical incision) is re-approximated (edges pulled together) and sutured, stapled, glued or taped together (without gaps) as an initial treatment approach. These wounds will typically form a “healing ridge” by post-operative (post-closure) day 5 in healthy individuals (Sussman & Bates-Jensen, 2012). This healing ridge is evidence of collagen deposition “knitting” the two separate wounded edges together resulting in a healed surgical site. In such a case, the skin at the wounded site should have the same tensile strength as surrounding tissue after healing has fully occurred. This point is important to remember as we move on to discuss wounds that heal by secondary intention.
Wounds are described as healing by secondary intention if they are left open to heal or “fill in” with new granulation tissue and finally close by re-epit in full thickness wounds that heal by secondary intention (or scar tissue formation) will continue to mature 12-18 months after complete closure of the wound opening. The tensile strength of the resulting “scar tissue” in the area of a wound healed by secondary intention will never reach more than 80% of the tensile strength of the surrounding tissue. Therefore, this will always be a “weak spot” in the skin integrity, prone to breakdown before the surrounding tissue. Therefore, a full-thickness pressure ulcer in a location likely exposed to repeated pressure such as the ischia secondary intention instead of flap closure, will be at greater risk of recurrence. This is one reason that surgeons prefer to create surgical skin flaps to close certain wounds such as clean, uncomplicated full thickness pressure ulcers in relatively healthy individuals (with the best chance of surgical healing), instead of leaving these wounds open to heal by secondary intention (Bryant & Nix, 2016).
On the other hand, full thickness wounds which are initially sutured closed, then re-opened (or left open at the start) for awhile and finally sutured, stapled, glued or taped closed again, are said to be closed by tertiary closure. These wounds heal by a combination of scar tissue formation and surgical wound healing. Therefore, their suture lines may or may not reach the tensile strength of the surrounding tissue, depending on the amount of scar tissue formation (Sussman Bryant & Nix, 2016).
As discussed above, full-thickness wounds healing by secondary intention actually heal by scar tissue formation. The wounded human body sets into motion a cascade of processes that results in the production of new collagen to fill the open defect of a full thickness wound in the skin/tissue. If the skateboarder is young and healthy, his/her knee will bleed for a few seconds and clotting factors and fibrin will start clotting the blood. Chemical signals (cytokines) will be initiated which will result in localized edema, redness at the area, slight warmth and pain. The localized pain, edema, warmth and redness will typically resolve in 3-7 days (inflammatory phase of wound healing). If the wound bed is not kept moist, the wound will dry out and a scab will form. Next, the body will produce enzymes (matrix metalloproteinases or MMPs) under the scab to help lift it, especially at the edges. The wound bed under the scab will be moist to promote cellular communication, proliferation and movement (Sussman & Bates-Jensen, 2012; Krasner, 2014; Bryant & Nix, 2016). The skateboarder will likely pick the scab off of the wound, especially if it feels tight or “itchy.” However, the scab will form again, smaller this time, as the wound contracts. If all goes as expected, the wound will completely close (re-epithelialize) in a few weeks. As described, this is an acute wound. Interestingly, George Winter (Winter, 1962) demonstrated that open wounds (not sutured surgical wounds), which are kept continuously moist actually heal almost 50% faster than those allowed to dry out and scab over. The skateboarder’s scenario demonstrates uncomplicated acute wound healing. The typical needs of acute wounds versus chronic wounds are described below.
The typical needs of the uncomplicated ACUTE wound are:
In contrast to acute wounds, any wound that does not follow the expected orderly pathway to healing is a chronic wound. Chronic wounds most often get “stuck” in the inflammatory phase of healing, resulting in delayed wound healing, and often, persistent edema, redness and pain (Schultz, et al 2003; Leaper et al., 2012; Baranoski & Ayello, 2015; Bryant & Nix, 2016).
Inflammation in chronic wounds typically starts as it does in acute wounds: wounding → bleeding→ clotting cascade→ release of cytokines→ edema, warmth, redness, pain. However, unlike acute wounds, in a chronic, complex or recalcitrant wound, the expected pathway to healing stops here and never progresses out of a chronic inflammatory state. The presence of biofilm, or overwhelming infection; malnutrition; immune suppression; certain medications and a variety of other factors can contribute to a wound remaining in a chronic inflammatory state. Chronic wounds get ‘stuck’ in the inflammatory phase of wound healing (Schultz et al., 2003; Leaper et al., 2012; Krasner, 2014).
The typical needs of the CHRONIC wound are similar to the acute wound with one exception:
Remember, this course only addresses the basic needs of wounds and provides a general overview of wound dressings and topical wound treatments. More advanced chronic wound treatments and adjunctive therapies will be discussed in a future course.
This section seeks to provide specific basic information to help you approach the wound from a nursing or caregiver perspective, which focuses on the basic cleansing and dressing of wounds.
Ideally, care of a wound should begin with a “game plan.” There is no strict ‘recipe’ that will fit all wounds, but the following are general measures and recommendations (Sussman & Bates-Jensen, 2012; Hess, 2013; Baranoski & Ayello, 2015; Bryant & Nix, 2016; Doughty & McNichol, 2016) that should be considered with all wound care. Typically, the process of wound dressing changes will look something like this:
Now we will attempt to break this down into individual considerations (remember this is a “basics” course, so please forgive the simplicity if you are a seasoned wound care practitioner). Gathering supplies, selecting the appropriate materials, setting up your workspace, and making the patient and caregiver comfortable are self-explanatory.
Do not take hand washing for granted! You have heard it said that the most important infection control practice is hand washing. This is true. Proper hand washing prevents infection: Wash with soap under running water for at least 15 seconds. No short cuts. Wearing gloves when you perform wound care is necessary in most cases, unless it is a close family member or the patient is doing wound care for themselves. However, wearing gloves is no substitute for hand washing! (CDC, 2012) (Visit Site)
Wound care has advanced tremendously with modern technology. This is good news for patients but complicates things for healthcare providers. Forty years ago, there was only a small list of wound care products to choose from and today there are thousands. However, clinicians need not fret about approaching wound care in modern healthcare. Clinicians need only to remember a few basic principles similar to the ABC’s of CPR. Think of this as the “TIME” for wound care. Schultz et al. (2003) wrote a pivotal article on wound bed preparation which describes a systematic approach to addressing specific needs of the wound bed in full thickness open wounds. In their article, they describe the anagram T-I-M-E to assist clinicians in performing evidence-based wound care.
T is for Tissue - the amount of non-viable or necrotic tissue in the wound bed should be noted and attended to (typically by debridement or removal of the necrotic tissue).
I is for Infection - infection should be identified and determined if it may require systemic treatment (critical infection) versus non-critical chronic bacterial colonization that may require only local management (by debridement and topical therapies).
M is for Moisture – moisture in the wound bed should be managed. A balance of moisture is important for wound healing. Topical wound care (especially dressings) should prevent the wound bed from drying out - at the same time as eliminating excessive moisture in the wound bed. When there is excessive moisture in the wound, and it exceeds the capabilities of the dressing, it often causes moisture damage to the skin surrounding the open wound (maceration). Dressing selection is most important for addressing this specific need of the wound bed.
E is for Edge of the wound - attention should be given to the wound edges. Rounded, “rolled” wound edges prevent epidermal cell migration, which may impair wound closure. Tracking or tunneling in the wound bed, as well as undermining (a ‘lip’ or ledge under the wound edge) may also impair wound healing. Undermining is often caused by shearing forces upon the wound area, frequently seen in pressure ulcers around the sacral area typically due to the patient repeatedly sliding down in the bed.
Other publications have supported this T-I-M-E approach (Carville, 2006; Leaper et al., 2012; Schultz & Dowsett, 2012; Krasner, 2014; Sibbald et al., 2014; Doughty & McNichol, 2016). An article by Carville (2005) suggested also addressing the tissue and skin surrounding the wound opening. The surrounding skin and tissue should be examined for the presence of or worsening of: erythema (redness), edema (swelling), warmth, and skin lesions (blistering, rash, irritation, callus, or maceration, etc.).
Many experts agree it is necessary to cleanse wounds at each dressing change to remove wound exudates, cellular waste, debris, bacteria, etc. However, caution is warranted regarding antimicrobial wound cleansers. Several studies report on the cytotoxicity of various common wound cleansers. Cytotoxicity relates to the substance being toxic to human tissue cells. Cytotoxic wound cleansers will not only kill germs but also kill healthy cells such as the fibroblasts (white cells that manufacture collagen/new tissue) or epidermal keratinocytes (important skin cells) (Krasner, Rodeheaver, Sibbald, & Woo, 2012; Krasner, 2014; Doughty & McNichol, 2016). In addition, many of these cleansers are antimitotic (prevent cellular mitosis and regeneration), which is how some chemotherapy agents function to prevent cancer cell growth. While that may be a desirable trait for cancer treatment, it may not be as desirable for a wound cleanser!
Ohio State University Medical Center (OSUMC) Department of Inpatient Nursing (2002) published a nice patient education pamphlet, “How to Make Dakin’s Solution” (available at: (View document) . This pamphlet describes diluting 3 ounces of common (unscented) household bleach (5.25% sodium hypochlorite solution) with 32 ounces of clean, boiled water (buffered with ½ teaspoon baking soda/sodium bicarbonate) to make a full strength Dakin’s solution (0.5% sodium Hypochlorite solution).
To make ½ strength Dakin’s solution (0.25% sodium hypochlorite), use only 3 tablespoons (48ml) bleach mixed with the same amount of water (32 ounces) and baking soda (1/2 tsp). OSUMC reports tightly sealed jars of these solutions may be stored at room temperature up to one month (in a dark jar), but once opened, any unused solution should be discarded within 48 hours. University of Virginia Health System also created a similar document accessible at: (View document)
Many clinicians are badly informed concerning Dakin’s solution, when to use and not to use, storage, documentations and strengths.
Here are some things every clinician should know about Dakin’s:
In most cases, wound experts recommend using water or saline to cleanse the wound (Fernandez, Griffiths, & Ussia, 2007). Some articles suggest tap water may be appropriate to cleanse a chronic wound. However, a Cochrane systematic review of research exploring this tap water question concluded, “The decision to use tap water to cleanse wounds should take into account the quality of water, nature of wounds and the patient’s general condition, including the presence of co-morbid conditions” (Fernandez et al., 2007). They also point out that for tap water to be considered for wound cleansing, it must be potable. Caution may be warranted for several reasons when considering tap water. Most of the studies in the systematic review were small and did not have adequate sample sizes to determine significant differences between groups. It is not known if the water used for wound cleansing vs. normal saline was tested for bacteria, cysts, fungi or presence of any other contaminants. Tap water if obtained from a well may contain contaminants such as bacteria or other contaminants, undetectable to the human eye. Alternatively, “city water” is typically chlorinated at around 3 parts per million or 0.3mg/L and also typically contains fluoride (0.5mg/L to 1.0mg/L) - it is unknown what effect this may have on cellular activity in the wound bed, and this was not reported on by the studies included in the Cochrane systematic review. Therefore, the author recommends using primarily saline or a proven non-cytotoxic wound cleanser.
Cleansers or killers? Wilson et al. (2005) reported on the cellular toxicity of common skin and wound cleansers such as dilute Acetic acid (0.25% vinegar), Cara-Klens, Dermal Wound Cleanser, Dial Liquid Antimicrobial Soap, Hibiclens, Hydrogen peroxide (3%), diluted Dakin’s solution (0.025% sodium hypochlorite/bleach), Povidone Iodine (10%), Puriclens, Restore Wound Cleanser, SAF-Clens, Saline (0.9% sodium chloride), Shur-Clens, Biolox, Techni-Care, etc. Their study revealed that only Shur-Clens, SAF-Clens and Saline were non-cytotoxic to fibroblasts (Toxicity index 0) without being diluted. Only Biolex, Shur-Clens and Techni-Care were non-cytotoxic to epidermal keratinocytes (Toxicity index 0) without being diluted. Some cleansers had higher toxicity indices such as 10 (need to dilute 10 times to reach a non-cytotoxic strength), 100, 1000, 10,000 or 100,000 (need to dilute 100,000 times to reach a non-cytotoxic strength). The higher the index, the more cytotoxic the cleanser. The cleansers which had the highest toxicity index against fibroblasts included Hibiclens (10,000), Dial Antibacterial Soap (100,000) and Ivory Liqui-Gel (100,000). The cleansers which had the highest toxicity index (100,000) against epidermal keratinocytes included Hydrogen peroxide, Povidone Iodine, and Dakin’s Solution.
An exception to using cytotoxic wound cleansers is when the benefits outweigh the risks. For instance, in the case of localized bacterial invasion in which the host is unable to overcome the bioburden of the infecting organism(s) with its own immune defenses (such as pseudomona aeruginosa infection resulting in further wound deterioration), the fibroblasts and epidermal keratinocytes are not likely to survive this hostile wound environment anyway. Therefore, it may justify using a short-term application of cytotoxic wound cleanser such as a dilute Dakin’s solution (sodium hypochlorite) just long enough to eradicate the infecting organisms. Yes,
this is likely to impair cellular function temporarily but the infecting organisms would do far worse if you did not address/control them. Once you have “cleaned up” the wound (perhaps a few weeks), you should return to non-cytotoxic moist wound healing principles for wound care.
“Cleansing” the wound should not only address washing or rinsing a wound but also includes debridement or addressing removal of non-viable (necrotic) tissue from the wound bed. Necrotic tissue is a breeding ground for bacteria and impairs wound healing (Schultz et al., 2003; Doughty & McNichol, 2016). Removing this unhealthy tissue (debridement) may be achieved by a variety of means: Sharp debridement, either selective or non-selective (with scalpel, scissors, curette); enzymatic (collagenase ointment or similar); autolytic (promoting the body’s own enzymatic activities); mechanical (rough friction or wet-to-dry) and larval debridement (maggots) (Schultz & Dowsett, 2012; Doughty & McNichol, 2016)
Necrotic tissue in the wound bed provides a breeding ground for bacteria, impairs optimal cellular communication and proliferation, and acts as a physiological barrier to new tissue deposition and wound contraction (Schultz & Dowsett, 2012; Schultz et al., 2003; Sussman & Bates-Jensen, 2012). In almost all cases, necrotic tissue should be removed when safely possible. This includes slough (white, yellow, grey “chicken fat” appearing tissue), fibrin (adherent, white yellow or grey fibrous non-viable tissue), and eschar (typically thick, brown to black, “leathery” dead tissue). There are a few exceptions to this rule. One very important exception is in the case of intact, hard, black eschar on the heel of the foot. There is no way to determine the depth of tissue damage underneath this eschar, so removing it may expose bone and predispose the patient to infection and osteomyelitis. “Intact” is the key word here. If this eschar is dry, and NOT soft or boggy or fluctuant, and does not have any lifting at any of the wound edges or drainage, then it may actually be beneficial to leave this eschar alone. Of course, pressure should be off-loaded from the area, and the eschar should be kept clean and dry. Cover the eschar with dry gauze for protection and “paint” it daily with a small amount of Betadine solution – (letting it air dry thoroughly before applying dry gauze for protection and padding). With this tissue in place, it may act as a protective “body bandage” – keeping bacteria and contaminants out of the wound. The wound healing process under this eschar may continue if other wound healing impediments are addressed (offloading pressure, adequate nutrition & blood flow, adequate immune function and tissue perfusion). If the wound under the eschar follows a healing trajectory, the eschar may lift itself after several weeks and display newly epithelialized skin underneath. In some cases, it may lift prematurely at an edge or start feeling boggy or fluctuant underneath the eschar and may start draining. In this case, it may be best to remove the eschar (Sussman & Bates-Jensen, 2012; Bryant & Nix, 2016; Doughty & McNichol, 2016).
Typical methods of debridement include sharp debridement, mechanical, autolytic, enzymatic and larval debridement. Sharp debridement is usually performed with a scalpel, curette, and/or scissors. This may occur in a surgical suite by a surgeon or at the bedside by a physician, PA, ARNP, or certified wound specialist if allowed by state board scope of practice limitations. Enzymatic debridement is typically achieved by applying ointment (collagenase) to the wound bed. Mechanical debridement may be accomplished by wet-to-dry dressings, by rubbing/friction while cleansing the wound, or by pulsed water jets & hydrotherapy (pulsed lavage, whirlpool). Autolytic debridement occurs by promoting natural enzymes in wound fluid to degrade non-viable tissues – usually by placing an occlusive or semi-occlusive dressing over the non-viable tissue. In addition, autolytic debridement may be accomplished by osmotic wound products such as medical grade honey or gauze saturated with a hypertonic sodium chloride since these products “draw” fluid from wound bed tissues into the wound product and loosen necrotic tissue. Larval debridement is performed by allowing sterile maggots to remove non-viable tissue (Bradley, et al., 1999; Sussman & Bates-Jensen, 2012; Schultz & Dowsett, 2012; Baranoski & Ayello, 2014; Bryant & Nix, 2016; Doughty & McNichol, 2016).
Maggots are the unsung heroes of wound healing. Maggot(s) or larval debridement therapy (MDT or LDT) has been utilized for medical purposes for hundreds or thousands of years. Mayan Native Americans and other ancient cultures have documented reports of maggots being used in certain medical treatments, especially for wound care. Larvae of certain fly species, such as Lucilia sericata (green bottle fly), remove only dead tissue while promoting healthy tissue in the wound bed, helping wounds heal faster.
Dr. John Forney Zacharias (1837-1901), a Confederate American Civil War surgeon, is recognized as the first healthcare provider in the US who intentionally applied maggots for wound care/debridement purposes. He noted that "maggots could clean a wound better in one day" than any other agent they had at their disposal. He also accredited maggots with saving many soldier's lives. In WWI, an orthopedic surgeon named Dr. William S. Baer recognized the efficacy of maggots to “clean up” compound fractures and large open flesh wounds when he discovered them in several untended war wounds from the battlefield. He credited the blow fly larvae with preventing sepsis in these battlefield cases. He was very impressed with the usefulness of maggots as a medical treatment, and after his battlefield experiences, he determined to conduct research using blow fly larvae at Johns Hopkins. In 1929 he started using maggots he found in the neighborhood or those he grew on a windowsill. Two patients contracted tetanus from contaminated maggots (one died), so he developed sterile maggot growing procedures. He used maggot therapy in 21 patients with chronic osteomyelitis which did not respond to other treatment. He demonstrated rapid wound debridement of necrotic tissue, a return of the wound bed to an alkaline ph environment, the reduction of bacteria, reduced odor levels, and complete healing of the osteomyelitis infections within six weeks (Sherman, 2009; Baer, 2011; Schultz & Dowsett, 2012; Sherman, 2014).
Regrettably, with the development of antibiotics in the 1940's and various skin and wound antiseptics, the use of LDT declined. It became a standard of care to use antibiotics in and on the body and antiseptics on the skin and in the wound. Maggot therapy was essentially abandoned in favor of more modern or “easier” methods. Arguably, one of the biggest reasons LDT may have lost favor in clinician's eyes was not ineffectiveness (for they remain a most effective form of debridement) but rather was the "yuck factor" - patients, their caregivers and clinicians found it distasteful to apply small squirming worms that could crawl out of a wound.
Fortunately, with the advent of antibiotic-resistant organisms and increasing drug sensitivities, there was a renewed interest in the “natural” aspect of Maggot therapy in the 1980's. The Food and Drug Administration (FDA) cleared medicinal maggots (Phaenicia or Luciliasericata) for debriding non-healing necrotic skin and soft tissue wounds including diabetic foot ulcers, pressure ulcers, non-healing surgical or traumatic wounds and venous stasis ulcers. In the US, larval therapy with maggots is classified as a medical device. However, in Europe, Canada and Japan maggots are classified as medicinal drugs. Maggots used in the US for larval debridement therapy are all processed under controlled laboratory conditions and are sterile (both free of disease as well as unable to reproduce). Larval debridement of non-viable tissue within chronic wounds results partly from the proteolytic digestive enzymes liquefying the necrotic tissue, which the larvae then suck up (along with bacteria and biofilm) and remove from the wound bed. As such, they are a most efficient way to debride a wound without the typical pain or bleeding associated with other forms of debridement such as sharp debridement. Research suggests they are very effective at eliminating drug-resistant organisms such as MRSA (methicillin-resistant staphylococcus aureus), and they do not excrete any bacteria into the wound (Sherman, 2009; Cowan et al., 2013; Sherman, 2014).
In many cases, wound inflammation is often mistaken for wound infection, since the signs of inflammation are warmth, edema, pain, and localized redness. Patients with these symptoms are often placed on antimicrobial treatment regimens without the benefit of microbiological studies to guide them (no quantitative tissue cultures from the wound). This may be one contributing factor in the development of drug resistant organisms. There has been much written about wound infection and other authors can address this better than this brief wound care review (Schultz, Davidson, Kirsner, Bornstein, & Herman, 2011; Schultz & Dowsett, 2012; Sussman & Bates-Jensen, 2012; Wolcott et al., 2010; Krasner, 2014; Bryant & Nix, 2016; Doughty & McNichol, 2016). Nevertheless, it is one of the most requested topics of basic wound care courses (to know when to treat and when not to treat “infection”). Therefore, we will quickly summarize some important facts and helpful tips regarding wound infection:
As a general rule of thumb, the wound care provider who is ordering the wound care should re-evaluate the wound for progress at least 2 weeks after the initial wound orders are placed. If the wound is stable, the topical wound treatment is performing as anticipated, and the wound is progressing as expected, the wound treatment may be continued and the follow-up could be extended to once every 2 to 4 weeks. If the wound has not improved after the initial 2 weeks, but the wound has not worsened, the clinician should make a decision if a change of wound treatment is in order or if there are other factors which need to be addressed which may be impairing wound healing (nutrition, medications, glycemic control, infection, etc.). After addressing these factors, have the patient return to the clinic in another week or two to re-evaluate progress with the current treatment. If no progress is noted, or the wound worsens at all, a change in treatment may be warranted (Sussman & Bates-Jensen, 2012; Baranoski & Ayello, 2016; Bryant & Nix, 2016; Doughty & McNichol, 2016).
Many forms now exist to document and monitor wounds. The Sussman Wound Healing Tool (SWHT), the Bates-Jensen Wound Assessment Tool (BWAT), and the Pressure Ulcer Scale for Healing (PUSH) are just a few (Sussmant & Bates-Jensen, 2012). Wound documentation (especially at the initial visit) should at least consist of these following components: Chief Complaint; History of Present Illness; Medical, Family and Social History; Review of Systems; Physical Assessment; Risk Assessment; Manual Assessment; Skin and Wound Assessment (including T-I-M-E, wound measurements, exudate amount and color, wound bed description, odor, edema, pain, etc.); Procedures Performed; Supplies and Tests Ordered; Patient/Caregiver Education Provided (and response); Care Plan; and Discharge/Follow-up Plan (Hess, 2013).
Measuring the wound is an essential component of wound monitoring and documentation. Wounds may be measured using a variety of techniques but the two most common techniques are the clock method and the longest axis method. The measurement method used should be performed consistently by all care providers. Only one method should be used for all wound measurement documentation for the entire facility to minimize confusion and inconsistency in the patient’s charts. The clock method consists of imagining the top of the patient’s head to be at the 12 o’clock position of a clock and the soles of the feet to be at the 6 o’clock position of an imaginary clock. All wounds are measured with length being the measure of the wound along the 6 to 12 o’clock axis and the width being the measure of the wound opening along the 3 to 9 o’clock axis. This works well to get the same measures no matter what position the patient is lying or sitting in. The longest axis method consists of taking the wound opening measurements along the longest axis of the wound as the length and the width measurement as the measurement of the wound opening along the perpendicular axis. Wound depth is measured the same way for both of these methods. Using the blunt end of a cotton tipped applicator, hold the stick lightly resting upon the deepest portion of the wound and using a gloved hand, grasp the stick at the wound edge and measure the straight depth of the wound at the deepest portion of the wound and record this as straight depth. Tunnels or tracking in the wound or undermining (lip under the inner aspect of the wound edge) should be measured at most shallow and deepest points. It should also be noted if tunneling or tracking connects two wounds or connects with any joint space or underlying structures (Baranoski & Ayello, 2016; Bryant & Nix, 2016; Sussman & Bates-Jensen, 2012).
Photographing the wound (if desired) as an additional component of wound monitoring includes establishing a routine frequency of photographic documentation, a consistent camera and distance from the wound for all photographs, and a measuring ruler in the frame next to the wound for size reference. It is imperative that you consider who is taking the photos. If another person is taking the pictures, make sure they follow infection control practices and do not touch the patient with the camera or anything in the patient’s room, especially if they will be taking the camera back to a central work area or other patient’s room. If it is the same clinician performing the dressing change, care should be taken to follow strict infection control protocols concerning handling the camera and where it is stored during wound care. For example, it should not be laid on the patient’s bed or bedside table without a clean barrier under it. It should not be handled after touching the patient, the wound dressing or wound care supplies without first washing your hands. Hands should be washed again after handling the camera. The camera should not be in close proximity to the wound during dressing changes if at all possible. During dressing changes, bacteria may be aerosolized and could contaminate the camera. The camera should not be taken from one patient’s room to another for other photos without first using some kind of disinfecting wipe or changing camera covers if disposable covers are used.
If photographs are to be used in the electronic health record, the author recommends that a photo of the patient’s ID bracelet be taken, followed by a photo of the wound, then the ID bracelet again, so that this sequence of photos may be uploaded into the appropriate electronic health record, and minimize the chance of the picture being uploaded to the wrong patient’s chart. In most cases, identifiers such as patient name, initials, date, etc. should not be included in any photo that may be used for educational purposes. However, follow your facility’s protocols for taking and uploading wound photographs.
One of the main functions of a wound dressing or wound therapy is moisture management. Specifically, to maintain a moist wound bed while also eliminating excessive wound drainage. Since George Winter’s seminal work in 1962, demonstrating open wounds treated with dressings which maintained a moist environment healed almost 50% faster than wounds allowed to dry out, no published studies have been able to refute the effectiveness of moist wound healing. In fact, current scientific investigations not only support what has been known about moist wound healing, but serve to further explain the role of a moist wound bed in relation to the local cellular activity associated with wound healing (cytokine signaling, fibroblast cell proliferation, collagen and matrix synthesis, epithelial cell migration, etc.) (Sussman & Bates-Jensen, 2012; Krasner, 2014; Bryant & Nix, 2016; Doughty & McNichol, 2016).
There are hundreds of commercially available wound care products in the United States. Numerous dressings or topical wound care applications have reported successful wound healing results in clinical trials, yet wet-to-dry dressings are still one of the most frequently ordered wound care modalities in nearly all healthcare settings (Cowan & Stechmiller, 2009; Fleck, 2009). Wet-to-dry dressings are no longer evidenced-based practice for wound care. As the name implies, a wet-to-dry dressing ultimately results in a dry wound bed (even if for limited amounts of time). Research demonstrates these dressings disrupt granulating tissue, impair epithelial cell migration, leaves behind foreign bodies in the wound bed, increase the risk of infection, aerosolize bacteria, and cause severe pain upon removal (Cowan & Stechmiller, 2009; Fleck, 2009). Nevertheless, wet-to-dry dressings have been a standard, traditional or ‘default’ dressing for decades (Mulder, 1995; Cowan & Stechmiller, 2009; Sussman & Bates-Jensen, 2012; Bryant & Nix, 2016). Modern wet-to-dry dressings are accomplished by moistening sterile cotton gauze with a solution (usually 0.9% normal saline) and placing it in the wound, allowing it to dry, then removing it dry from the wound bed (along with tissue that adheres to it), thus performing mechanical debridement. There are several reasons why this form of debridement may be detrimental to the wound bed, and unnecessary with so many other forms of wound debridement available today. Cost, compliance, pain, increased risk of infection and re-injury to healthy granulating tissue are several of these reasons (Mulder, 1995; Cowan & Stechmiller, 2009; Doughty & McNichol, 2016).
It is the author’s belief that most healthcare providers have continued with wet-to-dry dressings more out of misunderstood tradition rather than evidence-based wound care practices. Furthermore, the use of wet-to-dry dressings as a wound care modality may be outdated and used with inappropriate frequency in today’s health care arena (Cowan & Stechmiller, 2009).
If not wet-to-dry, then what? How do you select a moist wound dressing? There are so many to choose from. What dressing has the most evidence supporting it? How often should you change the dressing? Unfortunately, several systematic reviews have failed to produce strong evidence in favor of one specific dressing type for all wounds. Most clinicians who are not very familiar with modern wound products just want to know, “if not wet-to-dry, then what one product can safely be used in its place?” The answer to this question should be, “it depends.”
Wound experts now realize the “one size fits all” approach is not ideal for wound care or dressing product selection. Multiple EBP wound treatment algorithms exist to assist the clinician in selecting wound treatment approaches. Krasner, Sibbald & Woo (2012) developed a Conceptual Framework for Wound Dressing Product Selection©. This model reminds healthcare providers that wound care should be delivered using a “Holistic, Interprofessional, and Patient-Centered Approach©.” This approach should also be in agreement with the principles of evidence-based practice (EBP). The principles of EBP affirm that health care should be delivered based on the strongest and most current research evidence + the clinician’s experience & expertise + the patient’s (and family’s) preferences and values (Sackett, 1999; Sackett et al., 2000; Titler, 2008).
Before you can determine anything about the wound, you must assess the wound. However, the wound is only one small part of a person. In assessing the wound, don’t forget to assess and talk to the person attached to the wound. Assess the person (physically as well as psychosocially). What are the preferences, personal needs, likes, dislikes of the patient (as well as their caregiver)? What are their feelings about the wound/wound care? For a caregiver who gets sick and faints at the sight of blood, asking them to empty bloody drainage from a drainage tube may not be a good choice. As you assess the wound itself, identify the etiology of the wound and co-morbid conditions which may affect wound healing. In Krasner, Sibbald & Woo’s model (2012), they suggest approaching wound care with one of 3 options or “goals” in mind.
Probably the most effective and economical substitute for saline moistened gauze (wet-to-dry) dressings are wound gel moistened or impregnated gauze dressings. However, there are now a myriad of evidence-supported wound dressings to address specific needs of various types of wounds. This section is an introduction to some common dressings which have at least moderately strong evidence supporting their use. Please see Table 1 for list of common wound dressings and suggestions for frequency of dressing changes. Resources for all of this information were obtained from 5 main sources: (Baranoski & Ayello, 2004; Bryant & Nix, 2007; Hess, 2005; Krasner et al., 2012; Sussman & Bates-Jensen, 2007). In addition, the Agency for Healthcare Research & Quality (AHRQ) has several evidence synthesis summaries and technical assessments published or currently in progress (such as a review of skin substitutes for chronic wounds) which may be pertinent to wound care.
The ideal dressing should promote the best environment in the wound bed to promote wound healing. In other words, it should maintain a moist wound bed, be thermally insulating, protective to the wound, free of particles that could remain in the wound and become foreign bodies in the wound, be vapor permeable, hypoallergenic, non-toxic, comfortable, and cost effective (Carville, 2006; Hess, 2005; Jones, Grey, & Harding, 2006; Mulder, 1995). Health care providers should consider patient and/or caregiver cognitive and physical limitations/abilities when ordering a wound dressing, if the patient or caregiver will be expected to do the wound care. In addition, if at all possible, the wound dressing should also be aesthetically acceptable to the patient/caregiver (taking their preferences into account) and promote the patient continuing as many activities of daily living as possible (within the limits of his co-morbid conditions) (Krasner et al., 2012). The average health care provider or medical clinic should have at least a familiarity with the following products, and probably have at least one of each type of dressing on hand/in stock:
Gauze comes in a plethora of forms, sizes, shapes, and layered products. The most common gauze products are sterile or aseptic (packaged individually, in packages of 2 or in bulk packages of 50 or 200 cotton, woven, 8 or 12 layered, 4” x 4” or 2” x 2” sizes. Telfa is gauze which is coated with a plastic film to help render it “non-adhesive.” Gauze also comes in larger bulk dressings such as “abdominal dressings.” These dressings are commonly made today with bulky absorptive layers of cotton batting and woven gauze in larger sizes such as 5”x 9” or 8” x 10.” Gauze dressings are also manufactured in woven gauze of one rolled length (roll gauze) in a variety of widths (such as 2” of 4” or 6” widths). Gauze may be impregnated with other substances such as calamine, petrolatum, wound gels, silver, etc. In addition, combination products may have layers of gauze combined with layers of other wound products such as charcoal, alginates, adhesive backings or borders.
Whereas, wet to dry dressings are moistened with saline and allowed to dry out, wound gels are a good alternative that effectively maintains a moist wound bed. The clinician may moisten gauze with a wound gel, or use a pre-packaged gel impregnated gauze. Typically, this only needs to be changed once a day instead of 2-3 times per day. Wound gel dressing changes would be less painful than wet-to-dry. Wound gels come in amorphous gels (in tubes) or in sheets of flexible semisolid gel. Wound gels are commonly made of organic polymers that maintain moisture in the wound bed but also swell with water or wound drainage. In addition, wound gel may contain silicone, water, glycerin, polyethylene oxide, alginate or collagen. Common brand names of these wound gels include (this is not meant to be all-inclusive): Saf-Gel, Vigilon, Elastogel, Curasol, Solugel, Intrasite Gel, Purulon Gel, DuoDERM gel, Nu-gel, Stimulen collagen gel, etc. Some gel sheets such as “Vigilon” come with polyethylene film covers on each side that should be removed before placing gel sheet on wound (this will allow more vapor permeability). Gel products may absorb up to 5 or more times their body weight in wound drainage yet will not dry out or dissolve. Typically, the gel product is placed in the wound bed and covered with a secondary dressing to secure in place (such as gauze or foam). These products are normally changed daily, though gel sheets on certain wounds such as superficial wounds and skin tears may be left on for 1 week if the skin tear is clean (non-infected) with a well approximated flap and is not heavily exudating. Wound gel sheets that come with adhesive borders may be changed 3 times per week. Wound gels are appropriate for full thickness, shallow or deep wounds with scant to small amounts of drainage or varying amounts of drainage where the wound bed may dry out at times. Silicone gel sheets may also be useful in preventing or treating wound scarring (keloid/hypertrophic tissue) for up to one year after wound closure.
Care should be taken to manage moisture so that excessive moisture is not allowed to seep out over the surrounding wound edges causing maceration. Skin Barrier wipes or creams may be useful to protect periwound skin from adhesives (barrier wipes) or excessive moisture (barrier creams such as zinc oxide, or dimethicone). These are applied at each dressing change.
Another simple dressing to use is impregnated gauze. Pre-packaged impregnated gauze products are typically impregnated with petrolatum, hydrogel, Bismuth Tribromophenate, hypertonic sodium chloride, zinc, or crystalline iodine compound (iodoform). Common brand names of these dressings include (this is not meant to be all-inclusive): Vaseline Gauze, Adaptic, Xeroform, Curasalt, Mesalt, etc. The most basic and inexpensive of the petrolatum impregnated gauze may average $40 or less per box of 50. These dressings are conforming and may be good choice when filling tunnels or tracking as long as one piece and not multiple pieces are packed loosely into the tunnel. These dressings provide non-drying and moisture retaining wound interface, they conform to the wound bed, and petrolatum impregnated products may help protect periwound skin if they are shallow abrasions, so may be placed on the wound overlapping the edges. Normally these dressings are changed daily, and covered with a secondary dressing such as gauze pads or roll gauze, foam, bandage / wraps.
Hydrocolloid dressings are typically opaque, self-adherent “patch” type dressings made of sodium carboxymethylcellulose, pectin and gelatin mixed with polymers and adhesives. They also have a semipermeable film or foam sheet covering which makes them generally waterproof. However, waterproof does not mean it can be submersed such as in a bathtub or pool. These dressings are flexible wafers of differing sizes, thicknesses and shapes (some may be cut to desired size and shape). They can conform to many areas of the body. Common brand names of these dressings include (this is not meant to be all-inclusive): Restore, DuoDERM, DuoDERM CGF, Tegasorb, Comfeel, Granuflex, and 3M Tegaderm hydrocolloid thin. When exposed to exudate (wound drainage), the polysaccharides & other polymers absorb water and swell but remain contained in the adhesive matrix. Some have marks to tell you when the wound drainage is exceeding the dressing's limit and it is time to change. Most if cut to size, should be cut larger than wound. These dressings are typically changed every 2-5 days and it is best to use a skin barrier wipe applied to the periwound skin before application of the hydrocolloid.
Alginates are super absorbent fibers typically composed of calcium alginate manufactured from brown seaweed that becomes gel-like when exposed to sodium-rich wound exudates. It resembles angle hair and is manufactured from brown seaweed. They may absorb up to 20 times their weight in wound exudates. This makes them a good choice for highly exudating wounds. However, they are not recommended for dry or only slightly moist wound beds, as they will not remain a gel without the presence of moisture from the wound bed. Thus, they may dehydrate the wound bed, or allow the wound bed to dry out. Alginates may be available as sheets or pads and ropes and also are known for some hemostatic properties, making them a good choice for a wound bed that may be oozing a small amount of blood after sharp debridement. In addition, some alginates may have silver incorporated into the fibers as an antimicrobial agent. Alginates typically require a secondary cover dressing such as gauze or ABD pad and are changed daily or as necessary to manage wound exudates.
Hydrofiber dressings are non-wicking, absorptive primary dressings made of sodium carboxymethyl-cellulose fibers that absorb wound drainage and turn into a gel sheet. They may also keep the wound bed moist if the wound is sometimes dry (you would moisten them with saline or water). Hydrofibers act somewhat like an alginate but will not promote hemostasis like alginates. Some hydrofiber dressings include 1.2% silver as an antimicrobial component (usually delineated by the silver element symbol “AG” in the hydrofiber name). They are appropriate for full thickness wounds with minimal to moderate amounts of drainage. They are typically changed once every 1 to 3 days and require a secondary cover dressing.
Foam dressings are typically both absorptive and protective. They may be selected to provide conforming padding and may be used in combination with other products (such as alginates or hydrofibers) if needed; Foams may be used as a packing material in large wounds to fill dead space. Not all foam dressings are appropriate for infected wounds. Check manufacturer guidelines if infection is an issue. Some foam dressings are impregnated with silver or other antimicrobial material (such as Methylene Blue and Gentian Violet or polyhexamethylene biguanide/PHMB) or coated with a silicone interface.
Silver ions may be incorporated in wound gels, woven fabric dressings, foam, rope, alginates or hydrofiber dressings. Most silver fabric dressings are not very absorbent, they are used primarily to deliver silver ions to wound bed for the silver’s antimicrobial effects. However, silver alginates, hydrofibers, foams, or composite dressings are absorbent. Silver ions are activated by wound exudates or water; some silver products (Acticoat 3 days or 7 days) should not be moistened with sodium chloride (saline). Most silver products should not be mixed with hydrogen peroxide or sodium hypochlorite (Dakin’s or DiDaksol) solutions because the ions will inactivate each other. Silver products should not be combined with iodine products for the same reason. Silver dressings may need secondary dressings and may be changed daily up to every 7 days, depending on the product.
In general, povidone iodine should not be used in chronic wound care due to its cytotoxic properties. However, a cadexomer iodine is available which is antimicrobial while remaining non-cytotoxic to the wound bed. Cadexomer iodine is available in a wound gel (thick paste) or a flexible pad which is typically applied to the wound bed with a secondary dressing on top and left in the wound bed for 3 days, or until the color changes from an orange-brown to a grey-brown. They are used for antimicrobial effects on infected wounds and are effective against most bacteria including pseudomonas, staphylococcus aureus and streptococcus as well as fungus.
Compression dressings or bandage wraps are primarily used for lower extremity venous insufficiency. Compression garments are also appropriate for extremities effected by lymphedema (such as after mastectomies with axillary lymph node removal) or burns. Short-stretch compression is typically used for lymphedema (these are NOT ace bandages). Long-stretch compression (multilayer wraps and ace-type bandage) is also the typical treatment venous leg wounds. It is important to verify arterial perfusion to affected limb before applying compression. Compression may be applied in 2 to 4 layers, with a therapeutic layer such as zinc-oxide or calamine impregnated strips applied first, an absorptive layer next, possibly a bandage layer and/or Coban layer on top. These dressings may be applied every few days to weekly, depending upon amount of wound exudates. Once edema is under control and wounds healed, lifelong compression stockings should be worn by the patient (apply daily first thing in the morning before ambulating and remove at night just before retiring to bed).
Composite dressings are combination dressings of various sizes that are made up of two or more separate materials to address unique needs of certain wounds. These dressings tend to be layered with a contact layer (may be non-adhesive), an absorptive layer, and possibly an antimicrobial layer or odor absorbing layer (such as charcoal). They also may have an adhesive border to secure them to the wound site.
Tissue engineered skin substitutes, matrix dressings, collagen products and negative pressure wound therapy are some of the advanced wound therapies to be discussed in a future article.
|Type of product||Examples *Brands/Names||Types of wounds||Action|
|Petrolatum or Hydrogel Impregnated gauze ($)||Vaseline Gauze, Adaptic, Xeroform; Skintegrity, Elta, Restore, Dermagauze, Curafil||Shallow and dry wounds; abrasions, skin tears, etc.||Provides non-drying and moisture retaining wound interface, conforms to the wound bed, petrolatum impregnated products may help protect periwound skin if shallow abrasions. Typically changed daily, though may be left in place over well-approximated, non-infected skin tears up to 1 week.|
|Wound Gels/Hydrogels ($-$$)?||Saf-Gel, Vigilon, Elastogel, Curasol, Solugel, Intrasite Gel, Purulon Gel, DuoDERM gel, Nu-gel, Stimulen collagen gel||Dry to minimally draining wounds; partial and full thickness depth, 2nd degree burns, exposed tendons||Organic polymers that maintain moisture in the wound bed but also swell with water/drainage (some can absorb up to 5x their own weight in exudate). These gels typically will not dry out or dissolve. May be changed daily, though some gel sheets such as on skin tears may be left on for 1 week if a well approximated flap. Some gel sheets may also be used over scars to reduce hyperkeratosis (keyloid formation).|
|Hydrocolloids ($-$$)||Restore, DuoDERM, DuoDERM CGF, Tegasorb, Comfeel, Granuflex, 3M Tegaderm hydrocolloid thin||Partial and full thickness wounds; minimal to moderate drainage||Typically a flexible wafer of differing sizes, thicknesses and shapes (some may be cut to desired size and shape); forms an Impermeable barrier (most are waterproof); self-adhesive; may contain gelatin, pectin and carboxy-methylcellulose together with other polymers and adhesives. When exposed to exudate (wound drainage), the polysaccharides & other polymers absorb water and swell but remain contained in the adhesive matrix. May be changed every 3-5 days.|
|Transparent films ($-$$)||Op-Site, 3M Tegaderm, PolySkin, Suresite, Blisterfilm, Argomed and Argomed plus TPU films, Mefilm, Uniflex, AcuDerm||Partial thickness or shallow wounds with minimal to small drainage||Most are polyurethane films; provide moisture retention and may provide skin protection. May also assist with autolytic debridement. Most are oxygen or vapor permeable (not 100% occlusive). Sometimes used to "waterproof" a wound|
|Hydrofiber ($$-$$$)||Aquacel, Aquacel AG||mostly shallow; partial to full thickness; minimal to moderate drainage||Non-wicking, absorptive dressing made of sodium carboxymethyl-cellulose fibers that absorb wound drainage and turn into a gel sheet. They may also keep wound bed moist if wound is sometimes dry (moisten with saline or water). Act somewhat like an alginate but will not promote hemostasis like alginates. Typically changed 1-3 days.|
|Non-adherent polyurethane foam or Silicone interfaced foam; ($$)||Optifoam, Mepilex, Mepilex Border, Mepilex Transfer, Allevyn, PolyMem, Lyofoam, Hydrasorb||shallow wounds to those with some depth; partial to full tickness; minimal to heavy drainage||Absorptive & protective - provides conforming padding and may be used in combination with other products (such as alginates or hydrofibers) if needed; Some have self-adhesive borders. Foams that have a silicone contact layer may be useful in reducing hypertrophic (keyloid) scarring. Some have multiple layers (such as polyurethane foam+ polyacrylate fibers + waterproof film in Mepilex). Typically changed 1-3 days.|
|Calcium Alginate ($$)||CalciCare, AlgiSite M, Maxsorb||Moderate to heavily draining wounds with no necrotic tissue||Highly absorptive fiber (rope or pad) product made from brown seaweed. Turns to gel when moistened with wound drainage. Change daily.|
|Foams ($$)||Optifoam, Mepilex, Hydrasorb||Deeper, full tickness; moderate to heavy drainage||Absorptive and protective - provides conforming padding and may be used in combination with other products (such as alginates or hydrofibers) if needed; Foams may be used as a packing material in large wounds to fill dead space.|
|Silicone ($$)||Mepitel, Elastogel, etc.||Dry to exudating wounds or delicate wound beds (exposed tendons, etc.); or over newly closed wounds with high risk of scarring||Some are fenestrated (have holes in them such as Mepitel) and may be applied directly to wound bed under negative pressure wound therapy or other dressing as a non-stick primary dressing. Some are thicker and used over shallow wounds or newly closed wounds to prevent hypertrophic (keyloid) scarring. May be changed every 2-7 days.|
|Roll Gauze ($)||Deeper, full tickness; moderate to heavy drainage||Absorptive and may be used to fill dead space; may also be used in combination with other products (such as alginates or hydrofibers) if needed; Kerlix not recommended due to loose fibers|
|Antimicrobial silver impregnated woven fabric||Acticoat Burn (3day), 7day, flex, surgical site dressings||Not for very dry wounds||Not very absorbant - used primarily to deliver silver ions to wound bed for antimicrobial effects. Silver ions are activated by wound exudates or water; some silver products should not be moistened with sodium chloride (saline) or sodium hypochlorite (Dakins or DiDaksol) solutions because the ions will inactivate each other. Silver products should not be combined with iodine products.|
|Other silver products||silver wound gels; Silver gel sheets (Silvasorb), silver alginate; silver hydrofiber, silver foam||Application varies by type of base product||Use silver gels as you would other wound gels, use silver alginates you would other alginates, silver foams as you would other foam dressings, etc.|
|Compression||Profore, Profore lite, Unna Boots (with zinc oxide or calamine impregnated contact layer) or multilayer (2-4 layer) wraps, ace wraps,||for lower extremity venous wounds||Long-stretch compression (multilayer wraps and ace bandage) is typical treatment of choice for venous insufficiency and venous leg wounds. Verify arterial perfusion to affected limb first!|
|Silver Nitrate sticks||same||see notes||Applied directly to rolled wound edges, hypergranulating tissue in wound bed; chemically cauterizes acute bleeding|
|Collagenase ointment||Santyl||wounds with necrotic tissue in wound bed||only FDA approved active enzymatic ointment to help remove necrotic tissue from wound bed|
|Antifungal skin products||2% miconazole nitrate in powder, spray, cream, lotion, or ointment. Aloe Vesta Antifungal; Monistat 1, Neosporin AF, Baza Antifungal; Carrington Antifungal; Fungoid; Lotrimin AF, etc.||Skin with fungal rash||Generally for fungal rash affecting skin around wound. Typically apply small amount, gently rubbing into skin so it is no longer visible. Powder may be applied with a light dusting, then gently rub onto affected skin (and may blot with skin barrier liquid to seal in, if excessive moisture is present or under ostomy appliance).|
The Joint Commission for Accreditation of Health Care Organizations (JCAHO) lists pain management a quality indicator for acute care settings (Sussman & Bates-Jensen, 2012). Basic pain management includes an accurate assessment and documentation of wound pain. While pain management may be addressed most in burn wound settings, it is being increasingly addressed in other chronic wounds (and rightly so!). The gold standard for an accurate assessment of the patient’s pain is the patient’s self-reported pain level. Whether a pain scale of 0 (no pain) to 10 (excruciating pain) is used, or smiling faces/grimacing faces, the level of pain should be documented exactly as the patient reports it (Hess, 2013). The quality of pain (stabbing, shooting, throbbing, sharp, dull, constant or intermittent) along with what factors relieve the pain or make the pain worse (walking, standing, elevating the leg, etc.) should be ascertained and documented. Worsening wound pain is one hallmark of a deteriorating wound and may be more indicative of infection than other observable signs such as edema, warmth and erythema surrounding chronic wounds (Sussman & Bates-Jensen, 2012; Hess, 2013; Baranoski & Ayello, 2016; Doughty & McNichol, 2016). Woo and Sibbald (2007) developed a Chronic Wound Associated Pain (WAP) model to address the patient, the cause, and the wound (Krasner, 2014). This algorithm may be helpful in determining an evidence-based approach to wound pain management. Persistent chronic pain is highly individualized and requires highly specialized medical care (Sussman & Bates-Jensen, 2012). If wound-related pain is not well managed, patients should be referred to a specialist who can address their wound pain.
Pain with dressing changes may be managed by topical anesthetic products such as 2% or 4% topical Lidocaine Jelly, or EMLA cream, or systemic medications such as NSAIDS or opioids. Topical anesthetics (Lidocaine, Prilocaine, etc.) should be applied with enough time prior to dressing change or debridement for the medication to take effect (approximately 10 min). Similarly, systemic pain medication should also be administered with enough time for pain relief (at least 30 minutes) (Sussman & Bates-Jensen, 2012; Bryant & Nix, 2016; Doughty & McNichol, 2016). Addressing the pain when infection is suspected would include addressing the infection. Certain wound products may assist with pain management in specific types of wounds. Matrix applications using small intestine submucosa (SIS) technology (typically porcine) have been successful in relieving some wound pain, particularly over donor sites from split thickness skin grafts. Glycerin or silicone based gel sheets as well as hydrogel sheets (cross-linked polyethylene oxide and water) such as Vigilon may be cool and soothing to partial thickness wounds such as second degree burns and silicone is helpful in reducing scarring after wound closure (Sussman & Bates-Jensen, 2012; Hess, 2013; Doughty & McNichol, 2016). Be on the alert for new, different (especially worsening), or persistent pain associated with chronic wounds. Persistent pain in a neuropathic extremity with a chronic wound, as well as may be associated with osteomyelitis (Schultz & Dowsett, 2012; Sussman & Bates-Jensen, 2012; Krasner et al., 2014; Doughty & McNichol, 2016).
Baer, W. S. (2011). The classic: The treatment of chronic osteomyelitis with the maggot (larva of the blow fly). 1931. Clinical orthopaedics and related research, 469(4), 920–944. doi:10.1007/s11999-010-1416-3
Baranoski, S., and Ayello, E. (2016). Wound Care Essentials: Practice Principles. Fourth Edition. Philadelphia, PA: Wolters Kluwer, Lippincott Williams & Wilkins.
Bradley, M., Cullum, N., & Sheldon, T. (1999). The debridement of chronic wounds: a systematic review. Core Research.
Bryant, R., & Nix, D. (2016). Acute and Chronic Wounds: Current Management Concepts (5rd ed.). St. Louis, MO: Mosby.
Carville, K. (2006). Which dressing should I use? It all depends on the “TIMEING”. Australian family physician, 35(7), 486–489.
CDC - 2011 National Estimates - 2011 National Diabetes Fact Sheet - Publications - Diabetes DDT. (n.d.). Retrieved January 1, 2013 (Visit Source).
CDC, C.-C. for D. C. and. (2012). CDC - Hygiene and Handwashing - Water-related Emergencies and Outbreaks - Healthy Water. Prevention. Retrieved January 1, 2013 (Visit Source).
Cowan, L. J., & Stechmiller, J. (2009). Prevalence of wet-to-dry dressings in wound care. Advances in skin & wound care, 22(12), 567–573. doi:10.1097/01.ASW.0000363469.25740.74
Cowan, L., Phillips, P., Stechmiller, J., Yang, Q., Wolcott, R., Schultz, G. (2013) Chapter 4: Antibiofilm strategies and antiseptics. In: Willy, C, ed. Antiseptics in Surgery - update 2013. Ulm, Germany: Lindqvist Book Publishing.
Cowan, L., Stechmiller, J., Phillips, P., Schultz, G. (2012). Science of Wound Healing: Translation of Bench Science into Advances for Chronic Wound Care. In: Krasner, D, Sibbald, G, Rodeheaver, G, (eds.) Chronic Wound Care: A Clinical Source Book for Healthcare Professionals 5th Edition. King of Prussia, PA: Health Management Publications.
Doughty, D.B. & McNichol, L.L. (2016) (Eds) Wound Management: Core Curriculum of the Wounds, Ostomy and Continence Nurses Society; Philadelphia, PA: Wolters Kluwer.
Fernandez, R. S., Griffiths, R., & Ussia, C. (2007). Water for wound cleansing. International journal of evidence-based healthcare, 5(3), 305–323. doi:10.1111/j.1479-6988.2007.00068.x
Fleck, C. A. (2009). Why “Wet to Dry”? The Journal of the American College of Certified Wound Specialists, 1(4), 109–113. doi:10.1016/j.jcws.2009.09.003
Hess, C. T. (2013). Clinical Guide to Skin and Wound Care. Seventh Edition. Amber, PA: Lippincott Williams & Wilkins.
Gillespie, B., Chaboyer, W., Allen, P., Morely, N., Nieuwenhoven, P. (2014). Wound care practices: a survey of acute care nurses. J Clin Nurs. 2014 Sep;23(17-18):2618-26. doi: 10.1111/jocn.12479.
Jones, V., Grey, J. E., & Harding, K. G. (2006). Wound dressings. BMJ (Clinical research ed.), 332(7544), 777–780. doi:10.1136/bmj.332.7544.777
Jones, V., Harding, K., Stechmiller, J., Schultz, G. (2012). Acute and Chronic Wound Healing. In: Baranoski S, Ayello E (eds.) Wound Care Essentials: Practice principles. Third Edition. Baltimore, MD: Wolters Kluwer, Lippincott Williams & Wilkins.
Krasner, D. L. (Ed.) (2014). Chronic Wound Care: The Essentials - A Clinical Source Book for Healthcare Professionals. Malvern, PA: HMP Communications, LLC.
Krasner, D. L., Ed, Rodeheaver, G. T., Sibbald, R. G., & Woo, K. Y. (Eds.). (2012). Chronic Wound Care: A Clinical Soure Book for Healthcare Professionals (5th ed., Vol. I). Malvern, PA: HMP Communications, LLC.
Leaper, D.J., Schultz, G., Carville, K., Fletcher, J., Swanson, T., and Drake, R. (2012). Extending the TIME concept: what have we learned in the past 10 years? Int Wound J. Suppl 2:1-19. doi: 10.1111/j.1742-481X.2012.01097.x.
Mulder, G. D. (1995). Cost-effective managed care: gel versus wet-to-dry for debridement. Ostomy/wound management, 41(2), 68–70, 72, 74 passim.
Rabenberg, V. S., Ingersoll, C. D., Sandrey, M. A., & Johnson, M. T. (2002). The Bactericidal And Cytotoxic Effects Of Antimicrobial Wound Cleansers. Journal of Athletic Training, 37(1), 51–54.
Scales, B.S., and Huffnagle, G.B. (2013). The microbiome in wound repair and tissue fibrosis. The Journal of Pathology, 229(2): 323-331.
Schultz, G. S., Barillo, D. J., Mozingo, D. W., & Chin, G. A. (2004). Wound bed preparation and a brief history of TIME. International wound journal, 1(1), 19–32. doi:10.1111/j.1742-481x.2004.00008.x
Schultz, G. S., Barillo, D. J., Mozingo, D. W., & Chin, G. A. (2004). Wound bed preparation and a brief history of TIME. International Wound Journal, 1(1), 19–32. doi:10.1111/j.1742-481x.2004.00008.x
Schultz, G. S., Davidson, J. M., Kirsner, R. S., Bornstein, P., & Herman, I. M. (2011). Dynamic reciprocity in the wound microenvironment. Wound repair and regeneration: official publication of the Wound Healing Society [and] the European Tissue Repair Society, 19(2), 134–148. doi:10.1111/j.1524-475X.2011.00673.x
Schultz, G. S., & Dowsett, C. (2012). Wound bed preparation revisited. Wounds International, 3(1), 25–29.
Schultz, G. S., Sibbald, R. G., Falanga, V., Ayello, E. A., Dowsett, C., Harding, K., … Vanscheidt, W. (2003). Wound bed preparation: a systematic approach to wound management. Wound repair and regeneration: official publication of the Wound Healing Society [and] the European Tissue Repair Society, 11 Suppl 1, S1–28.
Sherman, R. A. (2009). Maggot therapy takes us back to the future of wound care: new and improved maggot therapy for the 21st century. Journal of diabetes science and technology, 3(2), 336–344.
Sherman, R. A. (2014). Mechanisms of Maggot-Induced Wound Healing: What Do We Know, and Where Do We Go from Here? Evidence-Based Complementary and Alternative Medicine?: eCAM, 2014, 592419. http://doi.org/10.1155/2014/592419
Sibbald, R.G., Ovington, L.G., Ayello, E.A., Goodman, L., and Elliott, J.A. (2014). Wound bed preparation 2014 update: management of critical colonization with a gentian violet and methylene blue absorbent antibacterial dressing and elevated levels of matrix metalloproteases with an ovine collagen extracellular matrix dressing. Adv Skin Wound Care, 27(3 Suppl 1):1-6. doi: 10.1097/01.ASW.0000443269.63406.f9.
Sussman, C., & Bates-Jensen, B. M. (2012). Wound Care: A Collaborative Practice Manual. Lippincott Williams & Wilkins.
Wilson, J., Mills, J., Prather, I., & Dimitrijevich, S. D. (2005). A toxicity index of skin and wound cleansers used on in vitro fibroblasts and keratinocytes. Advances in Skin and Wound Care, 18(7), 373–378.
Winter, G. D. (1962). Formation of the Scab and the Rate of Epithelization of Superficial Wounds in the Skin of the Young Domestic Pig. , Published online: 20 January 1962; | doi:10.1038/193293a0, 193(4812), 293–294. doi:10.1038/193293a0
Wolcott, R. D., Rumbaugh, K. P., James, G., Schultz, G., Phillips, P., Yang, Q., … Dowd, S. E. (2010). Biofilm maturity studies indicate sharp debridement opens a time- dependent therapeutic window. Journal of wound care, 19(8), 320–328.
Wound prevalence and wound management, 2012-2020. MedMarket Diligence, LLC; Report #S190 and Report #S249. http://sumo.ly/lpQI via @medmarket
Zhao, G., Usui, M. L., Lippman, S. I., James, G. A., Stewart, P. S., Fleckman, P., & Olerud, J. E. (2013). Biofilms and Inflammation in Chronic Wounds. Advances in Wound Care, 2(7), 389–399 (Visit Source).