The Basics of Pressure Ulcers

Essentials of Wound and Burn Care

By John Roark

B

urns, punctures, cuts, surgical incisions, pressure sores and diabetic ulcers are all wounds that can easily become infected. Preventative measures must be taken to avoid this danger.

Simply put, an infected wound contains a greater number of microorganisms than a contaminated wound. Proper wound cleansing and debridement can prevent bacterial colonization from reaching the point of clinical infection. Acute wounds are more susceptible to infection than chronic wounds. Wounds that have not been debrided of necrotic tissue can predispose the patient to systemic infection; therefore, measures to prevent wound infection must include debridement of eschar or necrotic tissue and meticulous wound cleansing, along with measures to prevent wound dehydration.1

Factors that predispose wounds to infection are well documented and influence the way colonized wounds respond. Patient-specific factors include advancing age, diabetes, steroid therapy and other immuno-suppressants, extreme obesity, severe malnutrition, compromised circulation, and infection in remote sites.2

“More than 90 percent of all wounds have bioburden, and greater than 50 percent of chronic wounds will progress from having organisms present to an overt infection,” says Cynthia Fleck, RN, ET/WOCN, a certified wound care specialist, secretary of the American Academy of Wound Management and Medline’s vice president of clinical education. “Systemic antibiotics rarely reach adequate levels in the granulation tissue of chronic wounds to effectively control superficial proliferating bacteria. In addition, the bacterial resistance issue is alive and well in the chronic wound care arena.”

Chronic wounds by nature tend to get “stuck” in the inflammatory stage of healing, and don’t follow the normal complex therapeutic cascade. “Key cells ‘fall asleep’ or become senescent and unlock the wound’s susceptibility to infection,” says Fleck. “Infection occurs when homeostasis among the host, the microorganism and the environment is out of sync. The first line of defense is the skin. If the skin is open, as with a wound, defense is diminished and an infection can occur. The larger, deeper and older the wound is, the greater the chance for infection. If the host is compromised, such as with various co-morbid states, diseases like diabetes, immune challenges and the like, infection is more prevalent. Also, wounds in typically ‘dirty’ areas such as perineal and perianal areas are more prone to infection due to an increase in microorganisms.”

Bacteria present within a wound can be divided into four distinct categories:

Contamination

— The presence of bacteria on the wound surface that are not actively multiplying. All wounds are contaminated. This condition does not elicit a host reaction and does not impair healing.

Colonization

— Defined as the presence of replicating microorganisms, which do not cause injury to the host. Pathogens attach themselves to the surface of the open wound, but do not invade healthy tissue surrounding the wound.

Critical Colonization

— The presence of replicating microorganisms, which are beginning to cause local tissue damage. These are wounds with an increased bacterial burden, moving between the category of colonization and local infection. Bacteria also excrete metabolic byproducts that can be toxic to cells, and may also promote the cellular production of high levels of protein-degrading enzymes in the wound.

Infection

— Defined as 105 microorganisms/gram of tissue, a critical load. This occurs when organisms are present in the wound and surrounding soft tissue that result in a host response and leads to non-healing or decline in the wound.2

Aseptic technique must be exercised in order to aid in wound recovery and avoid infection. “It is imperative that a wound/burn site and the hands of the healthcare professional be free of any bio-burden or contaminants,” says Sherry L. Brereton, MSM, MBA, executive vice president of Care-Tech® Laboratories, Inc. “This means cleansing with proper surfactant chemistry, which will emulsify and rapidly remove debris without harming the cellular structure of the dermis or tissue. In addition, a non-toxic antimicrobial/antiseptic agent will eliminate harmful pathogens. Both of these functions should be accomplished with proper formulations, which do not cause additional irritation, dryness or cell damage.”

Effective cleansing at each and every dressing change as well as prudent debridement of any and all devitalized material is key, says Fleck.

Evaluating the Wound

“Good assessment skills can capture a critically colonized wound before it progresses to full infection and consequent tissue damage,” says Fleck. “Education is of prime importance. Clinicians who perform wound care must be alert to the overt signs and symptoms of infection or impending cellulites and be able to identify a wound ‘in trouble,’ putting the right wound management in action to prevent further problems. Activating a protocol and/or getting the correct wound care experts involved is critical and should be taught at all levels in the care continuum.”

The first step in wound care is evaluating the clinical condition of the wound and the ability of the wound to heal. Physical characteristics of the wound (size and depth), the presence of undermining (tissue destruction underlying intact skin along the wound margins), tunneling (a pathway that can extend in any direction from the wound, resulting in dead space; also called sinus tract), foreign bodies (such as sutures, staples, drain tubes or environmental debris) and exposed bones factor into the healing timeline.

Tissue surrounding the wound can indicate the presence of or potential for infection. Conditions to be aware of include:

Erythema

— redness which may be from infection, irritation from drainage, urine/feces or dermatitis/trauma from tape or dressing. Redness from infection may be seen as diffuse and indistinct, or as intense with demarcated borders, or red streaking. Dark skin may appear purple or have a gray hue, or deepening of the ethnic skin color.

Edema and induration

— observed as slight swelling and firmness at the wound edge. If accompanied by warmth, may indicate infection; induration is a hardened mass or formation with defined edges.

Crepitus

— an accumulation of air or gas in tissues. “Rice Krispies” feeling in the skin surrounding the wound. The gas bubbles come from the bacteria fermenting carbohydrates into carbon dioxide and hydrogen. Gas bubbles under the skin cause the crepitus.

Temperature

— normal temperature ranges from cool to warm and is dependent upon vasoconstriction or vasodilatation. Warmth may reflect infection or a new wound.

Color changes

— reddish skin tone may reflect infection.3

Dr. Andres Alfonso Gutierrez, head of the cell therapy unit, National Institute of Rehabilitation (CNR) in Mexico City, and an advisory board member for Oculus Innovative Sciences stresses that the infection site must be properly controlled in order to avoid edema and microthrombi in capillaries. “Both factors severely stop blood flow in the infected area and impair healing,” he says. “If you do not control the local infection properly, it would be necessary to keep the patient on systemic antibiotics for longer periods of time at the hospital, increasing morbidity and costs of attention.”

It is also essential to avoid the spread of the infection to the blood stream (e.g. bacteremia) and the possible development of a septic shock, says Gutierrez. The latter is a serious systemic disorder with multiple organ failure and high mortality rates. “Its severity depends on numerous factors in the host (e.g. nutrition, perfomance status, immunocompromised status, etc.) as well as the severity and type of infection. For example, septicemia due to hospital infections with Pseudomonas or antibiotic-resistant bacteria like Methicillin-resistant Staphylococcus aureus (MRSA) and vancomycin-resistant Enterococcus (VRE), could be lethal to the patients.”

“In the last few years, the term ‘wound bed preparation’ has been coined and is now in increasing use,” says Robert J. Goldman, MD, associate professor of rehabilitation medicine at the University of Pennsylvania Health System (UPHS), Philadelphia, and director of the rehabilitation wound clinic at Presbyterian University of Pennsylvania Medical Center. What it implies is you are coaxing the wound bed out of the critically colonized state. “The wound bed has multiple states. When wounds are critically colonized they don’t heal, but they don’t have signs and symptoms of classic infection like fever, chills, sweats, high blood pressure, erythema far from the wound. The wounds just won’t heal.”

Goldman frequently uses antibiotics to prepare the wound bed. “A lot of times you use local agents like the antimicrobial dressings. In many cases, a wound that has been open for a long time will get to a point and then stop — it won’t close. I’ve seen that if you use an antimicrobial dressing, it makes a big difference. It will coax the wound and it will start to granulate very quickly.”

Burn Care

According to the Wound Care Information Network, 2 million people in the United States are treated for burn injuries each year; 100,000 of those patients require hospitalization. Burns are susceptible to infection because of the local alteration in the skin’s immune system. The epidermis is almost invariably lost with even a slight burn and the epidermis is what prevents bacteria from penetrating the skin into the bloodstream.

Burns create unique challenges. With deep burns, decreased blood flow from the burn-injured vessels further impairs local immune function because of the inability of the wound to get antibodies and nutrifils.

Secondly, the systemic effects of a large burn impair systemic immune function. “It’s very similar to a transplant patient on immunosuppressant drugs,” says Robert H. Demling MD, director of the burn center at Brigham & Women’s Hospital, Boston, Mass. “Their immune function is severely impaired. So you have the local problem, and the inability systemically to manage the local infection.”

The third component relates to management. “If hospitalized, you’re putting this patient — whose local and systemic immune function is impaired — into an environment where there’s a high risk for nosocomial infection,” says Demling. “It’s kind of the worst of all worlds, exposing someone who is immunocompromised in an environment that is loaded with resistant organisms.”

Generally, a large wound is managed with cross-contamination-preventive measures — mainly gloves, gowns and masks. With a burn you tend to go one step further, says Demling. “Say you have a wound patient. You walk in the room and do your physician or nursing care, but you don’t really put gowns, gloves or masks on unless you’re taking the wound down and dressing it. Any time you are around a burn patient, you always wear caps, gowns, gloves and booties, and change them every time you go into and out of the room. It’s very similar to what you do with a bone marrow transplant patient, because you’re not simply worried about the wound, you’re worried about bacteria to the patient. Bacteria on not-burned skin can make its way to burned skin. The contamination precautions are total, all the time.”

Another challenge unique to burns is the difficulty of diagnosing infection. “An infection is very difficult to assess clinically, because allburns are going to grow some bacteria,” says Demling. “All burns have fevers and they look like they have an infection as a result of the inflammation response to the burn. It’s often difficult to detect that there’s a superimposed infection. The best clinical way of assessing it is if the wound appears to be getting deeper.”

Once diagnosis is made — either through quantitative swab cultures or quantitative biopsies of the eschar — the patient automatically begins systemic antibiotics. “They’ll already be treated with topical antibiotics,” says Demling, “a deep burn always has topical antibiotics on it, and a superficial burn tends not to get infected.”

Deep burn management has changed dramatically over the past 20 years. “Given the fact that a deep burn is at risk of getting infected and getting deeper, we now turn to surgical debridement and skin grafting very early — in the first week or several days,” says Demling.

“The point when you can no longer be concerned is when the wound is totally closed. A deep burn typically won’t close until you remove the deep burn and put a skin graft on it. In the past, or still today in some countries, you just wait it out until it heals. But we no longer do that here in the states. It’s actually rapid removal of the source of infection, and then closing the wound. At that point we can say the patient is home free.”

The critical care management of a burn patient has advanced along with critical care in general. According to Demling, the leading cause of death with a major burn is respiratory failure, not the wound itself.

Another advance has been aggressive nutritional management. “The burn consumes so many nutrients that it’s extremely important that an aggressive high-calorie, high-protein, nutrient-rich diet be initiated from the very beginning,” says Demling.

An increased use of anabolic agents, which actually stimulate healing, is another area of care that has evolved. Anabolic agents will promote and accelerate the healing process and minimize the effect of the burn on the patient, which is usually weight loss. “Keeping the patient strong and stimulating the healing process accelerates the time it takes to get better,” says Demling.

Bacterial Biofilms

One of the roadblocks to wound and burn recovery is the formation of bacterial biofilm. “Biofilm is a matrix of assorted types of bacteria that forms a polysaccharide coating on top,” says Fleck. “It is slimy to the touch. Most bacteria in moist environments are found in biofilm, which doesn’t attach to viable tissue. The problem with biofilm is that it is impermeable to topical and systemic antimicrobial/antibiotic therapy. The bacteria are under the protection of the polysaccharide coating, much like we are protected from the rain while under an umbrella. It then exchanges genetic antibiotic resistance information, making it nearly impossible to obliterate without physical manipulation and surfactants. It is therefore recommended to abandon the use of simple normal saline as a wound cleanser and adopt the use of a safe, non-cytotoxic wound cleanser that utilizes surfactants as well as enough pressure to remove non-viable tissue and debris while minimizing tissue damage. Another big issue is that macrophages, phagocytes and white blood cells do not recognize biofilm as bacteria.

“Biofilms are a three-dimensional connection of numerous species of bacteria that live in a ‘stuck together’ extracellular matrix made of polysaccarides, unlike free-floating planktonic bacteria,” Fleck elaborates. “Imagine the JELL-O molds that your grandma made with pieces of fruit, such as peaches. The gelatin is analogous to the polysaccharide matrix and the peach pieces are analogous to the bacteria. Much like it is difficult to isolate the peaches in the gelatin mold, bacteria in a biofilm are less susceptible to antimicrobial therapies due to the polysaccharide matrix that protects them. Additionally, channels within the polysaccharide matrix allow the flow of nutrients and communication chemicals, making these tenacious films difficult to overcome.

“Since most antimicrobials bind to protein, biofilms are surrounded by a carbohydrate-rich sugar matrix devoid of protein, which offers them a level of protection against antimicrobials,” Fleck continues. “So, the basics of wound bed preparation such as cleansing and debriding are paramount.”

Bacterial biofilms can occur on any wound, but they present more of a predicament with burns, because the burn wound is open longer, explains Demling. “The biofilm is kind of like a wall built around the bacteria, shielding them from antibiotics. The bacteria get together and basically secrete a film that allows them to continue to replicate, but doesn’t allow topical or systemic antibiotics to approach it.”

Currently, the only successful way of dealing with bacterial biofilms is excising the wound surface, and trying to close the wound to actually remove the bacterial biofilm. “It’s much easier to remove it and close the wound than it is to treat it with today’s technology, because different bacteria produce a different kind of biofilm,” says Demling.

“There’s no anti-biofilm out there that’s universal. There are a number of agents that are being developed for that very purpose, but just like flu vaccine, they may have to be species-specific.”

The Silver Lining

Silver is the most common topical antimicrobial used in burns, and has become the most prominent topical antimicrobial used in wounds as well.

The use of silver in wound care has been around since about 1965, says Demling. “The silver was originally cream-based, and applied as an ointment. The problem with that is that the silver is short-lived; it’s usually silver salt, and once the silver is released from the salt, it disappears relatively quickly. This entails fairly frequent reapplications of the silver ointments or creams. In the last few years has come the advent of silver-releasing dressings, which, when laid on the wound, will release silver and bacterial-killing concentrations for five to seven days. The wound doesn’t need to be changed very frequently, which is good, because you don’t want to disrupt the wound biology. Secondly, you’re constantly barraging the bacteria with very potent microbialsaddled silver. Up until now, there are very few organisms that have shown resistance to silver.”

But, that could change, says Demling. “Silver is the universal management, the antimicrobial of choice for burns and wounds. It’s not easy to get mutations in silver, because if you use it in high enough concentration, it just kills everything on contact. But if you were to use lower concentrations — similar to lower concentrations of antibiotic — then you breed the potential for mutations and bacterial resistance. The silver has to be provided in high enough concentrations to be totally bacterialcidal, and the problem here is you’ve got to be vigilant to change and reapply new silver dressings at frequent enough intervals to avoid bacterial overgrowth.”

“The technology is here, you’ve just got to use it correctly,” he continues. “You have the tendency to want to stick on a piece of silver dressing and leave it there, send the patient home and have them come back in two weeks. That’s when you’re going to breed bacteria, because as the silver concentration begins to drop, then some bacteria survive, and they become more resistant. It took a long time for staph to get resistant to penicillin. It may take awhile, but it’s kind of inevitable.”

Wound/Burn Care Products

There have been a great number of advances in wound care in recent years,” says David G. Armstrong, professor of surgery, chair of research and assistant dean, Dr. William M. Scholl College of Podiatric Medicine at Rosalind Franklin University of Medicine and Science in North Chicago, Ill. “Many modalities, such as negative pressure wound therapy (aka VAC therapy) have reduced the need for extensive plastic surgical flaps and grafts. Bioengineered tissues and topical cytokines have also enjoyed a good deal of success in specific areas of wound healing. Other advances in antibiotics are allowing us, in concert with our colleagues in infectious disease, to treat many mild to moderate infections on an outpatient basis. One such antibiotic is Linezolid, which is effective (in its oral formulation) against resistant Gram positive organisms. While very expensive, it has shown to be cost- effective in allowing us to deliver short-term oral outpatient therapy to many patients who would otherwise require intravenous inpatient or outpatient therapy.”

With the gamut of wound care products on the market and the evolution of healing mediums, what separates the gimmicks from the legitimate technological advancements?

An effective wound care product will address the most important aspects of infection control, says Glenn Carter of 3M. “It should provide protection to the wound site barrier to outside contamination, viruses and bacteria. It should control microbial load reduction in the wound and should manage and contain wound fluid — preventing wound exudate leakage to healthcare works or other patients.”

“Does the product stand up to its claims?” asks Kip Kilpatrick, national accounts manager for Aqua Guard, who also poses the following queries: What are the benefits to the patient? Is it easy to apply and to remove? Does it protect against pathogens? Does it help patients resume their normal daily activities, such as showering? Is it readily available?

Carter adds to the list. “Is it a brand that is known, trusted and supported by comprehensive educational services, professional and technical support, reimbursement and health economic consultants, as well as ongoing research and development?

It is not only efficacy that matters, but safety as well, stresses Gutierrez. “The efficacy depends on the range of microorganisms that can be killed with that particular product. For example, some agents kill bacteria but not mycobacteria or spores. EPA grants a disinfectant claim to any solution which will destroy Staph aureus, Pseudomonas aeruginosa, and Salmonella choleraesius using an official AOAC procedure. Label claims do not include efficacy against bacterial spores or Mycobacterium tuberculosis. It does not imply efficacy against viruses either.”

Gutierrez enumerates the efficacy levels of available disinfectants: “Only high-level disinfectants are capable of killing all microorganisms. This level is equivalent to sterilization when contact is long enough and efficacy of solution is maintained. Intermediate-level disinfectants kill all vegetative bacteria, fungi, tuberculosis bacilli and most viruses. Low-level disinfectants destroy vegetative bacteria and fungus and most enveloped viruses.”

The major problem is that high level disinfectants — such as glutaraldehyde — are toxic for humans and not intended for wound/ burn care. Others, like povidone iodine or alcohol, kill most bacteria but might not destroy antiobiotic-resistant strains, e.g. Methicillin-resistant Staph aureus (MRSA) or Vancomycin-resistant Enterococcus (VRE), Mycobacteria or spores. “A 3 percent hydrogen peroxide solution could exert a better antimicrobial control than the previous agents, but all these agents interfere with wound healing,” says Gutierrez. “In fact, none of them is recommended for the treatment of burns.”

Gutierrez considers the most important element in selecting a wound/burn-care product to be the cost-benefit ratio. There are various factors to be considered in this respect, he says. “If one product can control the infection efficiently without side effects and decreasing the use of systemic antibiotics (or avoiding its use), minimizing adjuvant therapies (e.g. skin grafts, expensive special dressings) and reducing hospital stay, then you have a good cost-benefit ratio. If in addition, the same product possesses a direct or indirect healing effect on the wound/burn, then your product could be a golden standard therapy.”

What does the future hold for wound and burn treatment? There are several modalities increasing in use for wounds that are prepared, says Goldman. “They include synthetic skin grafts — living skin cells which promote all the events surrounding wound healing. In a prepared wound bed without infection, it probably increases healing rate. Growth factors have been on the market for a long time. Most of them turned out not to be successful. There are clinical trials on gene therapy using growth factors. They’re not yet approved, and the process will take a long time. You actually inject growth factor DNA transcripts into certain viruses, and the viruses then transfect wound cells. Then the wound cells churn out growth factor for a period of a week or two, and then the whole thing is self-limited and it resolves. It’s purpose is for wounds which otherwise won’t heal.”

“I believe science is on its way to researching and developing products to safely prevent infection in all wounds,” says Fleck. “This would completely eliminate the need for treatment, focusing 100 percent on prevention, without resistance or sensitivity. Ionic silver is one of these cutting-edge products that allows clinicians to nip infection in the bud. Much more in the way of in vivo testing is needed to attain this goal.”


References:

1. McGuckin M. et al. The clinical relevance of microbiology in acute and chronic wounds. Advances In Skin & Wound Care: The Journal for Prevention and Healing. Jan/Feb 2003, vol. 16 No. 1.

2. Wound Care Education Institute, Inc. Comprehensive wound assessment.

3. Ibid.

Deb Lauren, RN, BC, WCC, COS-C was a contributing source for this article.


The Basics of Pressure Ulcers

According to information from the Wound Care Information Network, pressure ulcers arise due to a combination of situations and factors. On a cellular level, ischemia occurs to tissue when too much pressure is applied to one area for a prolonged period of time. This pressure is usually from a bony prominence on one side and a hard surface on the other side. The soft tissue between these two surfaces is subjected to abnormal pressure. The ischemia produced leads to tissue necrosis. The tissue closest to the bone is typically the first tissue to undergo necrosis; therefore, visible skin discoloration or redness may actually be an indicator of underlying adipose or muscular necrosis. It has been demonstrated that the capillary pressure on the arterial side is around 30-32 mmhg and around 12 mmhg on the venous side.

Sustained pressures at values higher than these may result in circulatory compromise and tissue necrosis. Frictional and shearing forces also play roles in tissue necrosis and must be reduced or eliminated. General health, skin texture and turgor, patient’s mobility, nutritional status and body weight must all be evaluated and corrected in order to reduce the risk of a pressure sore.

The AHCPR Guideline Agency for Health Care Policy and Research (AHCPR) Clinical Practice Guideline for the Treatment of Pressure Ulcers makes the following points about managing bacterial colonization and infection:

  • All stage 2, 3, and 4 ulcers are invariably colonized by bacteria. Topical antibiotics are appropriate; watch for response and sensitivity.
  • Swab cultures should not be used; they will only show surface contaminants.
  • Use needle aspiration to obtain fluid or soft tissue biopsy for determining infecting organism.
  • Bone biopsy is the gold standard for assessing osteomyelitis. WBC, ESR and plain x-ray have a positive predictive value 69 percent when all three tests are positive.
  • Use appropriate systemic antibiotic therapy for patients with bacteremia, sepsis, advancing cellulitis or osteomyelitis.
  • Use sterile instruments and clean dressings during wound care. Treat the most contaminated ulcer last in patients with multiple wounds. Change gloves and wash hands between patients.

According to the Wound Care Information Network, the difference between infection and contamination/colonization lies in the concentration of organisms in the wound. An infected wound contains a larger number of microorganisms than a contaminated wound. According to the AHCPR, stage 2, 3 and 4 pressure ulcers should all be considered as colonized with bacteria. Proper wound cleansing and debridement should prevent bacterial colonization from proceeding to the point of clinical infection. A contaminated wound will heal, an infected wound will not.

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