Baromedical Nurses Association (BNA) - Letter from the President

  • Annette M. Gwilliam, BSN, RN, CWON, ACHRN - President, BNA & Laura Josefsen, RN, ACHRN
  • Volume 10 - Issue 2

Baromedical Nurses Association (BNA)
Letter from the President

Hello Hyperbaric Nurses,

Thanks to all who planned, presented, and listened to our 2nd Annual HBO Nurses’ Day in-service on April 2, 2019. (Next year the 1st Tuesday in April is the 7th, so mark your calendars). The in-service is now available on line as a Category A CEU for those of you who missed it. Our theme this year was “HBO Nurses: The Key to Quality.” Our in-service covered assessment in both the mono- and multiplace programs. As we all know, assessment is a very important part of the HBO nurse’s responsibility.

We have a few news items to share this month.

  1. 1. The BNA research committee has been diligently working on a project. You should all be receiving a survey and we would like to get as many responses back as we can. Let’s work together to forward the recognition and research of HBO nursing!
  2. 2. Check out the website for a new page! Hover over the “Research” tab to access the drop downs. You will see two posters that were presented by BNA board members. WE’D LOVE TO ADD YOUR POSTER! Send to Robin at This email address is being protected from spambots. You need JavaScript enabled to view it. and we will publish you! Please share all the good work you do.
  3. 3. Congratulations to the dual winners of the new “Rising Star” BNA award! Mindi Skjordal (Iowa Methodist, Des Moines, Iowa) and Samantha Wooldridge (Cox Health, Springfield, Missouri) are co-winners and will each receive a trophy and a $250 honorarium. This award honors a nurse who is a member of the BNA, has worked in hyperbarics less than 5 years, and has demonstrated a commitment for growth and leadership in hyperbaric nursing.
  4. 4. The UHMS ASM is coming soon in Puerto Rico (June 27-29). The BNA and UHMS associates will be having valuable presentations on safety and other pertinent information.
  5. 5. The Annual BNA membership meeting will be held this year at the Gulf Coast Chapter UHMS meeting in Dallas (September 6, 2019). It will also be available as a live broadcast if you are unable to attend in person. The BNA will have a huge presence at the conference, including several speakers and presentation of our annual BNA awards! Come join us.

Do you have any ideas for research? Quality improvement in HBO? Ways the BNA can improve your practice? Contact any board member! Our addresses are on the BNA website.

Thanks again for supporting hyperbaric nursing by being a member of the Baromedical Nurses Association!

Annette M. Gwilliam, BSN, RN, CWON, ACHRN
Baromedical Nurses Association, President
This email address is being protected from spambots. You need JavaScript enabled to view it.

Read more: Baromedical Nurses Association (BNA) - Letter from the President

Challenges of Wound Healing

  • Michael B. Strauss, MD, FACS, AAOS, Stuart S. Miller, MD, & Igor V. Aksenov, MD, PhD
  • Volume 10 - Issue 2

Challenges of Wound Healing

This article was originally published in WCHM during its second year of publication in 2010. Dr. Strauss has reviewed this content to ensure its current applicability.


The healing of problem wounds is a matter of concern. Even with “advanced therapies,” 20% of diabetic foot wounds proceed to a major lower limb amputation.1 Why are the statistics so grim, and can such dismal results be mitigated? First, not all wounds that present healing challenges are the same; Second, not all patients have the same healing abilities and potential for useful function; Third, the patient’s goals and aspirations may not be conducive to wound healing; Fourth, not all wounds heal at the same rate (relativity!); Fifth, healing of wounds evolve through defined stages (evolution!); Sixth, specific treatment interventions predictably guarantee healing in almost all problem wounds; and Seventh, defined prevention measures avert problem wounds from recurring and ensure durable results. This paper addresses these considerations, provides an explanation why problem wounds fail to heal, describes interventions that promote healing, and discusses measures to prevent wound recurrences. The inspiration for these objectives comes from Masterminding Wounds by Michael B. Strauss, Stuart S. Miller, and Igor V.Aksenov where full chapters of information can be found on subjects that are only given one or two paragraphs of coverage this article.2

Wound healing is a complicated process that involves substrates, growth factors, oxygen availability, temporal relationships, and an appropriate environment. During wound healing, most of these factors are assumed to be present and contributing to wound healing in a normal fashion. Some factors can be assessed objectively, such as oxygen availability with juxta-wound transcutaneous measurements. Others can be inferred, such as using biochemical nutrition parameters (albumin and prealbumin) to make assumptions about the adequacy of substrates. Much attention is now being given to appropriate environment through debridements and agents to cover the wound base. For the latter, over 2,000 choices exist and more than 5 billion dollars a year are spent on these products in the United States.3,4 A new buzz phrase, “Advanced Therapies,” is permeating the literature and purports to be the answer for problem wound healing. There are over a dozen different “Advanced Therapies” (Table 1). Some have good supporting evidence, such as negative pressure wound therapy, while others are based on observations and theoretical explanations for their effectiveness.

TABLE 1. Examples of Advanced Therapies*

There are lessons to be learned from Einstein’s Theory of Relativity and Darwin’s Theory of Evolution that can be applied to healing of problem wounds. From Einstein, the time factor, the fourth dimension, has relevance to evaluation and management of problem wounds. Wound healing has a timeline and is relative not only to the patient (i.e., the observer), but also to the character of the wound. Postulates can be made about predictability of wound healing based on size reduction at finite time intervals. For example, 50% reduction of surface area in 4 weeks predicts eventual satisfactory healing.5 However, this observation is relative to the wound characteristics, location and the management interventions as well as the patient’s healing potential. A better choice to predict healing is the observation of objective improvement in one or more wound characteristics over a relative period of time. This improvement may not be confirmed by a reduction in wound size, but rather by a decrease in bioburden, the formation of healthy granulation tissue in the wound base, an improvement in the appearance of the skin surrounding the wound, achievement of glycemic control, the patient’s subjective impression that he/she is feeling better, or combinations of these.

Evolution also has analogies to wound healing. Wounds evolve through distinct stages and their outcomes are a function of the environment in which the wound is placed. Environment management of the wound has five cardinal strategies that include: 1) Preparation of the wound’s base, 2) Protection and stabilization of the wound, 3) Optimal medical management of comorbidities, 4) Selection of the optimal wound dressing agent(s) and 5) Adequate oxygenation of the wound.6 Without the proper environment, a wound will not evolve from one stage to the next. In reality, the wound actually improves in a continuum fashion. With relativity and evolution analogies introduced when appropriate, each of the 7 considerations will now be addressed.

First, not all wounds that present healing challenges are the same. Classification systems have been generated to grade the severity of wounds. Most are generic descriptions of one or more wound characteristics and miserably fail as a tool for scoring the seriousness of the wound, guiding management, or predicting outcomes. This further adds to the challenges of evaluating the effectiveness of “advanced therapies” because of not comparing “like with like” wound types when using these agents. In order to meet these challenges we have developed an easy to use, rapidly generated Wound Score based on 5 assessments which are the most important for the evaluation and management of a wound.7 Each assessment is graded with objective criteria from 2 (best) to 0 (worst) to generate a 0 to 10 score (Table 2). High wound scores predict healing. Conversely, very low wound scores predict failure and the need to proceed to an amputation (Table 3). The real challenge to the wound care provider is the middle score (4-7) group which we label the “problem” wound. With appropriate interventions as will be described later, almost 90% of this group will heal without the need for a major lower limb amputation.7,8



Second, not all patients have the same healing abilities and potential for useful function. The HOST-FUNCTION SCORE provides a quick and easy assessment of the patient’s potential for healing and for return of function after wound healing (Table 4). It is a second 0 to 10 score, and like the WOUND SCORE summates 5 assessments. The 5 host-function assessments (also, each graded from 2 to 0) help answer the healing and potential for return of function questions. The HOST-FUNCTION SCORE quantifies the host status as “healthy,” “impaired” or “decompensated” (Table 4).


However, other factors, most of which are remedial, cannot be ignored. These include the three fundamental problems that present challenges to wound healing: 1) Inadequately managed deformities, as is so often the cause of the malperforans ulcer, 2) Unresolved infections, usually due to underlying osteomyelitis, infected scar/bursa tissue and/or biofilms, and 3) Ischemia/ hypoxia of sufficient severity to thwart healing responses. These three fundamental problems, which account for the majority of the reasons wounds fail to heal, will be further amplified in section 6. Our observations indicate that when these problems are addressed and resolved, healing of “problem” wounds approach 95%. That leaves only a small percentage of “problem” wounds for which “Advanced Therapies” need to be considered.

Malnutrition is another reason wounds fail to improve. This problem can be quantified utilizing biochemical markers such as albumin and prealbumin (coupled with the C-reactive protein) and managed with a continuum of interventions ranging from oral food supplements, nasogastric tube feedings, gastrostomy/enterostomy food delivery, and finally to hyperalimentation. The significance of other reasons postulated to interfere with wound healing, such as lack of growth factors, accumulation of matrix metalloproteinase inhibitors, wound desiccation, use of the wrong wound dressing agent, unresolved edema, inability to up-regulate growth factors, diabetes mellitus, collagen vascular diseases, and the use of steroids/antimetabolites and microangiography is largely guess work somewhat based on empirical observations. Our sophistication in objectively assessing the rolls these factors contribute to non-healing of wounds is still in the infancy stage. In most clinical situations, the use of “Advanced Therapies” has not reached a point to objectively justify their use to mitigate wound healing problems.

Third, the patient’s goals and aspirations may not be conducive to wound healing. The GOAL-ASPIRATION SCORE quantifies the patient’s (and family’s) desires to avoid a lower limb amputation (Table 5). A GOAL-ASPIRATION SCORE greater than 4 points provides quantification for doing everything possible to heal the wound and prevent a lower limb amputation. Without factoring in the patient’s aspirations with regard to healing of the wound, the wound caregiver, will be working as if blindsided. The usefulness of the GOAL-ASPIRATION SCORE becomes fully appreciated after the patient leaves the hospital and/or a step-down facility when the majority of the patient’s care is left to the patient and the family. The patient’s care not only includes dressing changes for the wound, but also adherence to protection and off-loading the wound site, following medical management (especially with regard to diabetes), diet and utilization of medications, maintaining wound and adjacent skin hygiene, utilizing edema reduction measures, and participation in physical therapy and rehabilitation.


Because of home health providers’ budgetary limitations and visitation restrictions, which are becoming increasingly more stringent, it becomes impossible for the professional caregiver to adequately provide for all of these needs. This is where the patient (and the family) must assume responsibility for the 98.5% of the time (assuming 1-hour visits by the visiting home health nurse 3 times a week) professional caregivers are not attending to the patient’s wound and other care needs. Our most resounding successes in healing the most complicated lower limb threatening wounds are observed when the patient and the family become the caregivers. Naturally, this only occurs after the wound has transitioned from the acute, sepsis management phase to the repair, epithelialization phase. The GOAL-ASPIRATION SCORE provides the factual information to make the determination that the patient’s and family’s aspirations are sufficient to assume the responsibility for wound healing once the patient leaves the acute and/or sub acute hospital settings.

Fourth, not all wounds heal at the same rate (relativity!). WOUND healing is time-related and relative (aka Einstein) not only to the patient, but also to the care providers. What this means is that multiple factors determine the time course of healing. The most important factors, of course, are the 5 assessments used to compute the WOUND SCORE (Table 2). To label a wound as not making satisfactory progress if it fails to decrease in size by 50% in a month’s time does not reflect the relativity of the most challenging wounds, that is, those that are truly limb-threatening. A wound in a patient admitted with a septic foot, ascending tenosynovitis and necrotizing soft tissue infection may take weeks to establish a healthy, free of infection wound base even after optimal debridement surgery, wound care and antibiotic therapy. Other wounds with healthy wound bases may seemingly stop progressing only to subsequently rebound with a “growth spurt” of improvement after weeks of time.

From a patient’s perspective, progress becomes relative to “feeling better” and returning to home or a lower level of care, even though dressing changes are required and the wound is only improving slowly. From a caregiver’s perspective, wound healing is relative to observing objective improvement regardless of time intervals. The improvement may be manifested by control of sepsis, the development of granulation in the wound base, the reduction in edema and/ or observation of wound contraction. Many cavitary wounds, especially in the presacral region, often managed with negative pressure wound therapy, take months to heal and progress is only measured by formation of granulation tissue in the wound base and not reduction in the surface area of the wound. Conversely, wound size reduction is relative time-wise to surgical interventions. A couple of appropriately placed sutures to partially approximate a wound can reduce the wound volume by 50 percent while coverage/closure techniques eliminate the wound and in reality reduce the wound size by 100 percent. Thus, time is not a good factor to judge healing of complicated wounds because of its relativity. Rather, progress should be the determining factor. If progress is not observed, then other interventions including “Advanced Therapies” need to be considered.

Fifth, healing of wounds evolve through defined stages (evolution!). Although it is not exactly accurate to say that the fittest wounds are the ones that survive (and heal), several analogies with respect to evolution can be made: First the healthier (i.e., the “fittest”) the wound, the more likely healing will occur. Second, the environment, both internal and external, of the wound dictates the direction wound healing takes. Finally, wounds “evolve” through clearly defined stages directed by the environment in which the wound is placed. The concept behind the first analogy stating that healthy wounds heal was already discussed in the first section of our paper. The WOUND SCORE (Tables 2 and 3) provides a means to quantify the healthiness of a wound and predict its healing ability.

The environment of a wound is crucial for healing to occur. Environmental factors can be classified as internal or external. Even a “healthy” wound (i.e. WOUND SCORE of 8 to 10 points) will fail to heal if the blood supply to the wound base becomes disrupted or caustic agents are introduced for dressing materials. Other internal environmental factors include growth factors, signaling mechanisms to induce growth factor functions, substrates, oxygen availability, edema control, underlying deformities and deep infection. Some internal environmental factors need to be present, such as growth factors and oxygen; others need to be eliminated, such as deformities, deep infection, and matrix metalloproteinase inhibitors. External environmental factors include selection of the “ideal” dressing material for the particular stage of wound healing (Figure 1). Subsidiary considerations include maintenance of a moist environment, secretion management, bioburden control, protection of the wound from trauma, and stabilization. Just as the environment influences how the evolution of species advance, the environment determines how wound healing progresses.

Figure 1

Wounds evolve through 4 defined stages of healing (Table 6). The healthier the wound is, the smoother the transition from one stage to the next. Conversely, the more challenging the wound is, the more problematic the transitions are through the stages. The stages, in reality, represent a continuum of responses that we have artificially classified into four components based on the predominant characteristics of the wounds. They include a deterioration phase, which is determined by the etiology of the wound; a resting stage, where neither improvement nor deterioration are observed; an angiogenesis stage, where the wound base becomes healthy enough to consider coverage/closure options; and the coverage stage itself, which may be epithelialization/ keratinization of the margins or surgical coverage techniques in an operating room, such as skin grafting (Figure 2). Each stage varies in time from being transient, such as the deterioration phase of a traumatic wound, to weeks in duration, as needed for a large wound to epithelialize.

Table 6

Figure 2

Goals of the deterioration phase are removal of necrotic and infected material to provide an entry point for the wound to evolve through the other stages. During the resting phase, neither improvement nor worsening occurs. The environment must be made as conducive to wound healing as possible during this stage with attention to bioburden and biofilm control, maintenance of a moist environment, debridement of obviously non-viable tissues and optimal medical management with glucose control and nutrition support. In the healthiest of wounds, the latency phase may be sidestepped with transition from the deterioration phase, such as in a venous stasis disease ulcer or traumatic wound, directly (after debridement of non- viable tissue) to the angiogenesis stage. The angiogenesis stage occurs when healthy granulation tissue appears in the wound base. At this point, the wound dressing agents should be as physiological as possible with the goal of maintaining a moist, bioburden-controlled environment (Figure 1). Of the four stages through which a wound evolves, the coverage/closure stage has the most therapeutic options and is the one which “Advanced Therapies” receive the most attention. Before considering “Advanced Therapies,” more fundamental approaches, such as healing by secondary intention, skin grafting and/or flap coverage should not be discounted.

Sixth, specific treatment interventions predictably guarantee healing in almost all problem wounds. In our experiences, as stated in section 2, 3 reasons explain why nearly 95% of problem wounds fail to evolve through the four healing stages. These reasons include 1) Inadequately managed deformity; 2) Unresolved infection; and 3) Insufficient perfusion/oxygenation (Figure 3). Specific interventions for each reason almost always resolve the problem and allow healing to go on to a successful outcome.

Figure 3

Inadequately managed deformity is almost always the reason a wound fails to heal in the absence of ischemia and deep infection. Deformity wounds can vary from mild, as seen with a wound at the apex of a proximal interphalangeal joint of a clawed toe, to a malperforans ulcer under a depressed metatarsal head, to a seemingly impossible to manage ulcer associated with a Charcot arthropathy deformity. Although deformity is usually attributed to bone, underlying bursa and cicatrix are often contributing factors and develop as a “frustrated” effort by the body to generate protective padding over the bone deformity problem.

Off-loading with protective footwear is the initial intervention for dealing with deformities. If ulcers develop in the forefoot, total contact casting (TCC) is recommended by many authorities for this problem. We have been disappointed in our experiences with TCC. Healing may take months, requiring biweekly cast changes. There is a high incidence of recurrence of ulceration once casting is stopped after healing occurs since the deformity was not corrected and wound complications, such as progressive necrotizing soft tissue infection, have been reported to develop in the wound between cast changes.10 Because of these observations, we recommend surgical interventions for deformities that are not adequately managed with protective footwear. These can be as simple as correcting a claw toe deformity with tenotomies or elevating a depressed metatarsal head by percutaneous drilling of the metatarsal neck and manual osteoclasis. Ostectomies (bumpectomies), debridement of overlying bursa and cicatrix and partial or complete wound closure is the next level of surgical complexity in managing deformities. The most complicated management for deformity correction is done for Charcot arthropathy and may require debridements, osteotomies, ostectomies and bone realignment/stabilization with a ring (Ilizarov) external fixator. Convalescence from this typically requires a year’s time and in about half the cases, additional surgeries such as bumpectomies, skin grafting and/or intramedullary ankle rodding are needed.

Unresolved infection is typically attributed to osteomyelitis in the bone at the wound base. When the bone is avascular, antibiotics are ineffective for management of the infected bone. Swelling associated with the infection/ inflammatory response can cause a tamponading effect (ala a compartment syndrome) on the blood vessels and be the cause of avascularity of the bone, especially in the patient with co-existent peripheral artery disease and microangiopathy.

Infected bursa and cicatrix, both relatively avascular tissues, can also be a cause of unresolved infection. When these findings are present, surgical debridement in conjunction with organism specific antibiotics is invariably necessary for resolving the infection. Other causes of unresolved infection included retained infected hardware, biofilms and avascular fibrous membranes in the wound base. Debridement with probably hardware removal, if present, is the essential intervention for these problems.

Insufficient perfusion/oxygenation is the third of the triad of reasons the majority of wounds fail to heal. Wound oxygen tensions of 30 to 40 mmHg are required for wound healing.11 Obviously if the oxygen tensions are very low, tissues will die and debridement or more proximal amputation is required. If intermediate between this and the lowest oxygen tensions needed for healing, the wound will remain in a refractory state. In essence, the wound is hibernating- oxygen availability is sufficient to keep the tissues alive, but insufficient to meet the estimated 20-fold increase in metabolic activity required for wound healing to occur.12 Five interventions can improve perfusion/oxygenation to wounds and include: 1) Improved flow through revascularization, angioplasty, thrombectomy, clot lysis and/or stenting; 2) Hyperbaric oxygen; 3) Edema reduction; 4) Optimizing cardiac function to improve blood circulation; and 5) Use of pharmacological agents such as anticoagulants, platelet adhesion inhibitors, vasodilators and red blood cell deforming agents. Unfortunately, the revascularization techniques to improve flow are not effective, are insufficient, or have already been done in about 1/3 of our patients who have a limb-threatening combination of peripheral artery disease and a non-healing wound.

Hyperbaric oxygen is the one intervention than can improve tissue oxygenation even with inadequate perfusion. Its mechanism is to increase plasma oxygen tensions.13,14 In essence, each “drop” of blood at two atmospheres absolute hyperbaric oxygen pressure that is delivered through the capillary has 10 times the amount of oxygen in its plasma as normoxic, normobaric blood. This improvement in oxygen tension is often sufficient to transform the wound from its hibernating state to a healing situation. We reported 88% healing rates of problem wounds when juxta-wound oxygen tensions exceeded 200 mmHg during a hyperbaric oxygen exposure regardless of what the juxta-wound oxygen tension was in room air.15 Angiogenesis and fibroblast function, so essential for wound healing, are secondary effects of hyperoxygenation from hyperbaric oxygen.

It requires a “leap of faith” to believe that a WOUND SCORE of 3 quantifies a “futile” wound with no chance of healing and a score one point higher (i.e. “problem wound” with 4 points) almost always “guarantees” healing of the patient’s wound. To resolve this matter, we use the term “end-stage” wound for wounds that have a WOUND SCORE in the 2 1/2 to 4 1/2 range. In order to sensibly manage these wounds (i.e., make a decision between attempt at limb salvage or lower limb amputation), we utilize the HOST-FUNCTION AND GOAL-ASPIRATION SCORES (Tables 4 and 5).

Scores greater than 4 support the decision to attempt to salvage the limb while scores of 4 or less help to justify a lower limb amputation. With these tools, sensible interventions (including the measures just discussed in this section) and predictable outcomes occur for the “end-stage” wounds transitional in the continuum between “problem” wounds and “futile” wounds.

Seventh, defined prevention measures avert problem wounds from recurring and ensure durable results. Wound healing outcomes need to be measured by the durability of their results, not just healing. This is frequently observed with healed forefoot malperforans ulcers that recur after total contact casting has stopped.10 With appropriate prevention measures, wounds that are ischemic will usually remain healed since the metabolic demands of healed wounds are a fraction of that required for healing. Unfortunately, for unresolved infection and underlying deformities, there is high likelihood of recurrences after antibiotics are discontinued and/ or ambulation is resumed. Four generic prevention measures are effective in preventing wound recurrences or new problem wounds from developing. These include: 1) Patient education; 2) Foot, ankle skin, and toenail care; 3) Appropriate protective footwear selection; and 4) Proactive surgeries. Important components of patient education include education in awareness of the risk factors such as deformity, ischemia, neuropathy, etc., that lead to wounds, knowledge of the “dos and don’ts” to prevent wounds, and selection and adherence to appropriate levels of activity.

Proper skin and toenail care serve two purposes. First, they maintain these tissues in the best possible condition in order to avoid wounds developing from skin shear and pressure stresses. Second, they can be used to measure patient compliance and help determine how often rechecks with the primary and/or wound care specialist are needed. The GOAL-ASPIRATION SCORE can quantify how often return visits are needed (Table 7). There is a hierarchy of protective footwear choices ranging from quality walking-type shoes, to off-the-shelf diabetic footwear, to prescription shoe alterations (lifts, wedges, braces, etc.), to custom-molded shoes, and finally, to the Charcot Restraint Orthotic Walker (CROW) boot. The more complex the healed foot and ankle problem, the higher up the protective footwear selection needs to be. Finally, proactive, minimally invasive surgeries should be done to correct muscle imbalances and deformities before wounds develop in this at risk group of patients.

Table 7


Much information has been presented in this paper in as concise a fashion as possible. Almost every paragraph is deserving of a full book chapter of information. The following are some “take home” points. First, challenging wounds have a variety of presentations. The Wound Score provides objectivity to evaluation, management, and judging effectiveness of interventions, especially for similarly scored wounds. Second, the Host-Function Score and Goal-Aspiration Score help in decision making, especially as to whether to do everything possible to heal the wound or recommend immediate lower limb amputation. Third, challenging wounds heal at different rates (i.e., relativity) that have ramifications for both the patient as well as the caregiver. Fourth, wounds evolve through defined stages with the times and durations a function of the environment in which the wound is placed (i.e., evolution). While Einstein and Darwin might not be totally comfortable with applying their theories to wound healing, the analogies fit well into our evaluation, management, and prevention of wounds approach. Fifth, unresolved deformities, infection and/or ischemia/hypoxia are the reasons the majority (95% in our experiences) of challenging wounds fail to heal, and when these 3 reasons are appropriately addressed, uniformly good healing outcomes can be anticipated. Finally, preventive measures avoid recurrences of healed wounds and the onset of new wounds to ensure durable results.


1. Moulik PK, Mtonga R, Gill GV. Amputation and mortality in new-onset diabetic foot ulcers stratified by etiology. Diabetes Care. 2003 Feb;26(2):491-4

2. Strauss MB, Aksenov IV, Miller SS. MasterMinding Wounds. Best Publishing Company; Flagstaff AZ; 2010

3. Hess CT. Clinical Guide: Wound Care. 5th ed: Lippincott Williams & Wilkins, Philadelphia, PA; 2005, pg 101

4. Zaleski T. “Active” Products Drive Wound-Care Market: BioMarket Trends: May 1 2008 (Vol. 28, No. 9)

5. Coerper S, Beckert S, Küper MA, et al. Fifty percent area reduction after 4 weeks of treatment is a reliable indicator for healing--analysis of a single-center cohort of 704 diabetic patients. J Diabetes Complications. 2009 Jan-Feb;23(1):49-53. Epub 2008 Apr 3

7. Strauss MB, Aksenov IV, Miller S. MasterMinding Wounds Part III, The Strategic Management of Problem Wounds. Best Publishing Company, Flagstaff AZ 2010; p129-285

8. Strauss MB, Aksenov IV. Evaluation of diabetic wound classifications and a new wound score. Clin Orthop Relat Res. 2005 Oct;439:79-86

9. BorerKM, Borer RC Jr., Strauss MB. Prospective Evaluation of a Clinical Wound Score to Identify Lower Extremity Wounds for Comprehensive Wound Management. Undersea Hyperbaric Med, 2000. 27(suppl) #81 p.34

10. Myerson M, Papa J, Eaton K, Wilson K. The total-contact cast for management of neuropathic plantar ulceration of the foot. J Bone Joint Surg Am. 1992 Feb;74(2):261-9

11. Frigg A, Pagenstert G, Schäfer D, Valderrabano V, Hintermann B. Recurrence and prevention of diabetic foot ulcers after total contact casting. Foot Ankle Int. 2007 Jan;28(1):64-9

12. Hunt TK, Zederfeldt B, Goldstick TK Oxygen and Healing. Am J Surg. 1969 Oct;118(4):521-5

13. Strauss MB. Diabetic foot and leg wounds: principles, management and prevention. Primary Care Reports. 2001;7:187-198

14. Strauss MB, Aksenov IV, Miller S. MasterMinding Wounds, Best Publishing Company; Flagstaff AZ; 2010 Chapter 10 p253-285

15. Boerma I, Meyne NG, Brummelkamp WH, et al. Life without blood: A study of the influence of high atmospheric pressure and hypothermia on dilution of blood. J Cardiovascular Surgery 1960; 1:133-146

17. Strauss MB, Bryant BJ, Hart GB. Transcutaneous oxygen measurements under hyperbaric oxygen conditions as a predictor for healing of problem wounds. Foot Ankle Int. 2002;23:933-937

About the Author

Michael Strauss, M.D., an orthopaedic surgeon, is the retired medical director of the Hyperbaric Medicine Program at Long Beach Memorial Medical Center in Long Beach, California. He continues to be clinically active in the program and focuses his orthopaedic surgical practice on evaluation, management and prevention of challenging wounds. Dr. Strauss is a clinical professor of orthopaedic surgery at the University of California, Irvine, and the orthopaedic consultant for the Prevention-Amputation Veterans Everywhere (PAVE) Problem Wound Clinic at the VA Medical Center in Long Beach. He is well known to readers of WCHM from his multiple articles related to wounds and diving medicine published in previous editions of the journal. In addition, he has authored two highly acclaimed texts, Diving Science and MasterMinding Wounds. Dr. Strauss is actively studying the reliability and validity of the innovative, user-friendly Long Beach Wound Score, for which he already has authored a number of publications.

Read more: Challenges of Wound Healing

Press Release from Smith & Nephew

  • Smith & Nephew
  • Volume 10 - Issue 2

Press Release from Smith & Nephew

New NICE guidance recognizes that Smith & Nephew’s PICO™ sNPWT provides better outcomes than standard dressings in patients at high risk of surgical site infections, at similar overall cost

Smith & Nephew (NYSE:SNN; LSE:SN), the global medical technology business, welcomes the launch of new medical technologies guidance from the UK National Institute for Health and Care Excellence (NICE). In the guidance, NICE recommends that PICO Single Use Negative Pressure Wound Therapy System (sNPWT) should be considered as an option for closed surgical incisions in patients who are at high risk of surgical site infections (SSIs).1 Key patient risk factors include a high BMI, diabetes, renal insufficiency and smoking.2

NICE concluded that PICO sNPWT is associated with fewer SSIs and seromas compared with standard wound dressings across several types of surgery. Cost modeling suggests that compared with standard wound dressings, PICO sNPWT provides extra clinical benefits at similar overall cost to the NHS.1 For some types of surgery, PICO sNPWT is cost saving.1

When making its recommendations, NICE considered a review of 31 studies, 15 of which were randomized controlled trials.1 A supporting meta-analysis showed that PICO reduced the risk of SSIs by 63%, the risk of seroma by 77% and the risk of dehiscence by 30%.3 Significantly, it also showed there was an almost two-day reduction in length of hospital stay, providing substantial cost savings and efficiency gains across the healthcare system.3

“Surgical site complications are an increasing concern for healthcare providers and patients,” said Simon Fraser, President, Advanced Wound Management, Smith & Nephew. “NICE’s recognition of the proven impact PICO can make on both clinical outcomes and cost efficiencies will hopefully challenge existing standards of care around the world.”

The PICO sNPWT dressing includes a proprietary AIRLOCK™ Technology layer that uniformly and consistently delivers sufficient NPWT across a surgical incision and the surrounding zone of injury.4,5 This unique feature is designed to help reduce the risk of wound complications by reducing post-operative fluid6,7 and tension*8 around a closed surgical incision, when compared with standard dressings. The combination of these actions helps reduce the risk of surgical wound dehiscence3 and SSIs3, the two most common surgical site complications.

To learn more about the NICE recommendations and PICO sNPWT please visit


  1. NICE Medical Technology Guidance MTG43. PICO Negative Pressure Wound Dressings for closed surgical incisions. May 9 2019
  2. World Union of Wound Healing Societies (WUWHS) Consensus Document. Closed surgical incision management: understanding the role of NPWT. Wounds International, 2016
  3. Smith & Nephew. April 2019. Outcomes following PICO compared to conventional dressings when used prophylactically on closed surgical incisions: systematic literature review and meta-analysis. Report reference EO/AWM/PICO/004/v3
  4. Smith & Nephew October 2017. Project Opal PICO 7 System Stability Testing, Initial Time Point. Internal Report. DS/17/253/R.
  5. Malmsjö M, Huddleston, E., and Martin, R., .Biological Effects of a Disposable, Canisterless Negative Pressure Wound Therapy System. ePlasty. 2014;14.
  6. Karlakki SL, Hamad AK, Whittall C, et al.Incisional negative pressure wound therapy dressings (iNPWTd) in routine primary hip and knee arthroplasties: A randomised controlled trial. Bone Joint Res. 2016;5(8):328-337.
  7. Payne C, Edwards D.Application of the Single Use Negative Pressure Wound Therapy Device ( PICO ) on a Heterogeneous Group of Surgical and Traumatic Wounds. ePlasty. 2014:152-166.
  8. Loveluck J, Copeland, T., Hill, J., Hunt, A., and Martin, R., .Biomechanical Modeling of the Forces Applied to Closed Incisions During Single-Use Negative Pressure Wound Therapy. ePlasty. 2016.

NICE has checked the use of its content in this product.
NICE is independent of any company or product advertised.

* as demonstrated in biomechanical modelling

About Smith & Nephew

Smith & Nephew is a portfolio medical technology business with leadership positions in Orthopaedics, Advanced Wound Management and Sports Medicine. Smith & Nephew has more than 16,000 employees and a presence in more than 100 countries. Annual sales in 2018 were $4.9 billion. Smith & Nephew is a member of the FTSE100 (LSE:SN, NYSE:SNN). For more information about Smith & Nephew, please visit our corporate website and follow us on Twitter, LinkedIn or Facebook.

To learn more about how we can help you get CLOSER TO ZERO™ surgical site complications, please visit

Forward-looking Statements

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Over 10 Years of Practice-Relevant Content At Your Fingertips

  • Note from the Editor
  • Volume 10 - Issue 2

Over 10 Years of Practice-Relevant Content At Your Fingertips

The staff at WCHM continues to recognize the advancements and accomplishments over the past 10 years in wound care and hyperbaric medicine. The magazine has launched its own website so past articles can be readily found/accessed by all practitioners via keywords and google searches. The articles can also be used for continuing education and reference sources. In a few short months, the website has received over 550 visitors. Check it out.

In this issue, WCHM continues to spotlight an archived article that had an impact in wound care, hyperbaric medicine, facility safety, quality control, billing and coding, legal issues, and/or continuing medical education (CME). Generous sponsors and prolific and knowledgeable contributing authors are recognized.

This issue’s archived article is from Michael Strauss, MD, who has been a WCHM contributor since its inception over 10 years ago. Dr. Strauss has been the largest contributor to WCHM with over 30 articles submitted in wound care, diving medicine, and hyperbaric medicine. His archived article can be found in the wound care section and discusses the challenges of wound healing. Go to the magazine website to find all of his past articles.

WCHM is the only free online magazine covering all topics under pressure: wound care, hyperbaric medicine, and diving medicine with a circulation of over 13,000 wound care and hyperbaric medicine practitioners and interested parties.

The magazine’s past and present role continues to be a fair, objective, nonpartisan, international publication dedicated to reporting and commenting on the knowledge and advances in science and technology encompassing wound care and hyperbaric oxygen therapy. It reports on currently accepted and emerging clinical applications as well as the associated economic, social, and political issues and events that influence the administration, growth, and development of the field.

Please contact us at This email address is being protected from spambots. You need JavaScript enabled to view it. to contribute an article in 2019.

Read more: Over 10 Years of Practice-Relevant Content At Your Fingertips

Pressure Ulcers

  • Aimee D. Garcia, MD, CWS, FACCWS
  • Volume 10 - Issue 2

Pressure Ulcers

Excerpt from Textbook of Chronic Wound Care

The following is an excerpt from Textbook of Chronic Wound Care, editors Jayesh B. Shah, MD, Paul J. Sheffield, PhD, and Caroline E. Fife, MD.

Introduction and epidemiology

Pressure ulcers continue to be a significant health-care issue in the United States and around the world. The two most common groups that develop pressure ulcers are the elderly and individuals with spinal cord injuries. The main risk factor in both of these populations is immobility. An estimated 2.5 million patients are treated for pressure ulcers in the acute-care setting yearly.(1-2) The cost of pressure ulcers to the health-care system in the United States ranges from $9.1–11.6 billion per year. As per Medicare data from 2007, treatment of a pressure ulcer added an additional $43,180 in cost to a hospital stay.(3) The additional cost includes additional hospital days, dressings, nursing time, and therapeutic modalities, such as negative pressure therapy or electrical stimulation therapy. If the patient experiences complications from pressure ulcers, additional costs might include IV antibiotic therapy, surgical debridement, and more complex treatments such as diverting colostomy or rotational flaps to promote wound healing. In addition, patients who develop pressure ulcers during hospitalizations are more likely to require long-term care placement as opposed to going home, adding additional cost to the health-care system. The development of a single pressure ulcer can increase the length of stay in the hospital fivefold.(4)

Despite the advances in technologies, dressings, and support surfaces, the prevalence and incidence of pressure ulcers has not significantly decreased in the last 20 years. Although the average life expectancy has increased, we have not significantly impacted functional status or chronic medical conditions; therefore these conditions continue to plague individuals into their older years.(5) As of 2012, 11.5% of the world’s population was over the age of 60.(6) Given the global aging population, it is estimated that 20% of the population will be over the age of 65 by the year 2030, with the fastest-growing segment of the population being individuals over the age of 80.(7) Seventy percent of pressure ulcers occur in individuals over the age of 70, which is by far the largest group in which pressure ulcer occurs.(4) In the spinal cord injury population, it is expected that 25%–40% of individuals will develop a pressure ulcer in their lifetime.(8)

I. Pathophysiology

The National Pressure Ulcer Advisory Panel has changed the terminology for pressure ulcer staging by removing the word “ulcer” and replacing it with “injury.” The NPUAP definition of a pressure injury as revised in April 2016 now reads:

“A pressure injury is localized damage to the skin and/or underlying soft tissue usually over a bony prominence or related to a medical or other device. The injury can present as intact skin or an open ulcer and may be painful. The injury occurs as a result of intense and/or prolonged pressure or pressure in combination with shear. The tolerance of soft tissue for pressure and shear may also be affected by microclimate, nutrition, perfusion, comorbidities and condition of the soft tissue.”(9)

Since the term “injury” is now used by the NPUAP to denote both changes in skin color which are not yet open ulcers as well as open ulcers requiring some sort of dressing, in this chapter we will use the term “ulcer” to designate open skin lesions. The amount of time and the amount of pressure can vary among individuals, but it is well documented that pressures above 32 mmHg will cause capillary collapse. The amount of time is dependent on the amount of pressure. The more pressure is placed on a specific area of tissue, the less time necessary to lead to tissue necrosis.(10-11)

Contributing factors to the development of pressure ulcers include both intrinsic and extrinsic factors. Intrinsic factors are those inherent to the patient, including medical conditions, age, functional status and nutrition.(12) In addition, a history of previous pressure ulcers would also be a consideration. These factors cause changes to the skin that may predispose the patient to skin breakdown. The more comorbidities a patient has, the more significance it may have on skin integrity. For example, if a patient has a history of congestive heart failure, end stage renal disease on dialysis, incontinence secondary to diuretics, hypotension due to dialysis, limited mobility from being short of breath, and that patient also requires dialysis three times a week which will impact mobility, fluid status and potentially blood pressure, the cumulative effect of these various factors will increase that individual’s risk for the development of a pressure ulcer. It is therefore important to take a holistic view of the patient when assessing risk factors.

Extrinsic factors include pressure, friction, shear, and moisture. Pressure is the major risk factor for pressure ulcers. The main cause is immobility, although there can be pressure from external sources such as medical devices as well. Poor mobility may be secondary to underlying comorbidities such as cerebrovascular accident, spinal cord injury or progressive neurologic disorders, or advanced age leading to functional decline. When assessing the patient’s risk from mobility, it is important to look not only at the patient’s ability to transfer and ambulate, but at bed mobility as well. Patients with limited bed mobility in the home environment still need to be repositioned frequently by caregivers if they cannot make shifts in body positioning. Friction is defined as the force when two objects rub against each other. In patients at risk for pressure ulcers, friction can cause additional damage to the skin. Some examples commonly noted are patients using their heels to push themselves up in the bed or patients who are dragged across the sheets instead of being lifted. In both these scenarios, friction can lead to superficial damage to the epidermis or blisters when fluid enters the space between the epidermis and dermis. Preventive strategies would be the use of trapezes to allow the patient to use his or her upper body for mobility, use of offloading boots to prevent use of heels for pushing up in the bed, and appropriate turning strategies to prevent dragging patients instead of lifting them with draw sheets. Shear force occurs when the head of the bed is elevated above 30 degrees, and the patient begins to slide down the mattress. The blood vessels in the sacral area are sheared by the opposing forces and can lead to skin breakdown in the sacral/coccyx area. In some clinical situations, the clinician has no choice but to elevate the head of the bed due to underlying medical issues. In these scenarios, prevention strategies such as sacral dressings to minimize tension on the tissue might be utilized. Moisture is another extrinsic factor in the development of pressure ulcers. Moisture can occur from numerous sources including urinary and bowel incontinence, wound drainage, obesity, and excessive sweating. When the skin is exposed to excess moisture, it leads to maceration of the tissue. This makes the skin friable and more susceptible to damage from friction and shear forces.

II. Pathway

© Best Publishing Company, Wound Care Certification Study Guide 2nd edition Adapted with permission by Jayesh B. Shah, MD

Case study: evaluation of the pressure ulcer patient

See Pressure Ulcer Management Pathway. Mrs. S is an 88-year-old female who lives in an assisted-living facility. The patient has multiple medical problems including a history of cerebrovascular accident, hypertension, diabetes mellitus, and early dementia. The staff at the assisted-living facility noted Mrs. S had not been seen in the dining room in the past 24 hours. Upon entering her room, they found Mrs. S sitting in her recliner. She was noted to be very confused and lethargic and had incontinence episodes. 911 was called, and the patient was sent to the emergency room. Upon evaluation, she was noted to have a urinary tract infection and be dehydrated. On evaluation of the patient’s skin, she was noted to have an area of skin breakdown on the sacrum measuring 3.5 x 2.5 cm, partial thickness with no noted necrotic tissue. There is minimal serous drainage, no odor, and no surrounding erythema.

When the clinical team evaluates a patient, a wound-care history needs to be performed. In the same way that a comprehensive history is obtained to find out the background of any clinical problem, a wound-care history incorporates many elements to gain insight into the wound.(13) Some questions that might be asked specifically in the case of a pressure ulcer include the following items:

  • How long has the pressure ulcer been present?
  • What treatments have been implemented for wound healing?
  • What comorbidities are present that might impact wound healing?
  • Has the patient had previous pressure ulcers, and if so, where? What stage?
  • Has there been a change in functional status?
  • Is the patient able to offload?
  • Are there any preventive devices currently being used, such as a wheelchair cushion or specialty support surface?
  • Does the patient have any social support?

After a comprehensive history has been completed, there needs to be a comprehensive wound assessment done of the wound. Please refer to Chapter 5: Wound Assessment. The patient also needs to have a risk assessment done. A risk-assessment tool does not replace clinical judgment, but it does give the wound-care team a basis on which to implement protocols for prevention. Risk assessment should be done at the time of initial evaluation of the patient and at scheduled intervals, depending on the facility’s protocol. A new assessment should also be completed when there is a change in clinical condition. The most-validated pressure ulcer risk assessment tool is the Braden Scale. Other validated risk-assessment tools include the Norton and the Waterloo scales. The Braden Scale contains six domains to determine risk: sensory perception, activity, mobility, moisture, nutrition, and friction/shear. The highest number that can be achieved is 23.(14) A patient is considered at risk when the score is 18 or below. The lower the score on the scale, the higher the clinical risk for pressure ulcer development. The Norton Scale has five domains: physical condition, mental condition, activity, mobility, and incontinence. A score of 14 or less denotes clinical risk.(15) The Waterloo Scale was developed in 1987 and is used mostly in Europe. It looks at the BMI, continence, skin type, mobility, age, and nutrition. In addition, it takes into account special conditions such as tissue malnutrition, surgery or trauma, medications, and neurologic deficit.(16) Whatever risk-assessment tool is used at the clinical site, the health-care providers need to understand the elements and levels of risk associated with the different tiers. There are elements, such as underlying clinical diagnoses, that are not included in these scales, so the clinician needs to make a comprehensive assessment of the patient’s risk in addition to the risk-assessment tool.

Staging of the wound is the next step in management. Many health-care settings have developed protocols based on the staging of pressure ulcers. There are six stages of pressure ulcers as defined by the National Pressure Ulcer Advisory Panel, and as per the 2016 NPUAP consensus conference they are defined as the following:(9)

STAGE I. Pressure injury: non-blanchable erythema of intact skin
The skin is intact with a localized area of nonblanchable erythema, which may appear differently in darkly pigmented skin. Presence of blanchable erythema or changes in sensation, temperature, or firmness may precede visual changes. Color changes do not include purple or maroon discoloration; these may indicate deep tissue pressure injury. Since the ICD-10 coding system continues to use the term “ulcer”, we will use that term for this chapter.

STAGE II. Pressure Injury: partial-thickness skin loss with exposed dermis
The wound bed is viable, pink or red, moist, and may also present as an intact or ruptured serum-filled blister. Adipose (fat) is not visible and deeper tissues are not visible. Granulation tissue, slough, and eschar are not present. These injuries commonly result from adverse microclimate and shear in the skin over the pelvis and shear in the heel. This stage should not be used to describe moisture associated skin damage (MASD) including incontinence associated dermatitis (IAD), intertriginous dermatitis (ITD), medical adhesive related skin injury, or traumatic wounds (skin tears, burns, abrasions).

STAGE III. Pressure injury: full-thickness skin loss
Full-thickness loss of skin, in which adipose (fat) is visible in the ulcer and granulation tissue and epibole (rolled wound edges) are often present. Slough and/or eschar may be visible. The depth of tissue damage varies by anatomical location; areas of significant adiposity can develop deep wounds. Undermining and tunneling may occur. Fascia, muscle, tendon, ligament, cartilage, and/or bone are not exposed. If slough or eschar obscures the extent of tissue loss this is an unstageable pressure injury.

STAGE IV. Pressure Injury: full-thickness skin and tissue loss
Full-thickness skin and tissue loss with exposed or directly palpable fascia, muscle, tendon, ligament, cartilage, or bone in the ulcer can occur. Slough and/or eschar may be visible. Epibole (rolled edges), undermining and/or tunneling often occur. Depth varies by anatomical location. If slough or eschar obscures the extent of tissue loss this is an unstageable pressure injury.

Unstageable pressure injury: obscured full-thickness skin and tissue loss
Full-thickness skin and tissue loss occurs, in which the extent of tissue damage within the ulcer cannot be confirmed because it is obscured by slough or eschar. If slough or eschar is removed, a Stage 3 or Stage 4 pressure injury will be revealed. Stable eschar (i.e. dry, adherent, intact without erythema or fluctuance) on the heel or ischemic limb should not be softened or removed.

Deep tissue pressure injury (DTPI): persistent nonblanchable deep red, maroon or purple discoloration
Intact or nonintact skin occurs with localized area of persistent nonblanchable deep red, maroon, purple discoloration or epidermal separation revealing a dark wound bed or blood filled blister. Pain and temperature change often precede skin color changes. Discoloration may appear differently in darkly pigmented skin. This injury results from intense and/or prolonged pressure and shear forces at the bone-muscle interface. The injury may evolve rapidly to reveal the actual extent of tissue damage and subsequent ulceration, or may resolve without tissue loss. If necrotic tissue, subcutaneous tissue, granulation tissue, fascia, muscle or other underlying structures are visible, this indicates a full thickness pressure injury (unstageable, Stage 3 or Stage 4). Do not use DTPI to describe vascular, traumatic, neuropathic, or dermatologic conditions.

Two additional definitions related to pressure ulcer include the following:

Medical device related pressure injury
This describes an etiology. Medical device related pressure injuries result from the use of devices designed and applied for diagnostic or therapeutic purposes. The resultant pressure injury generally conforms to the pattern or shape of the device. The injury should be staged using the staging system.

Mucosal membrane pressure injury
Mucosal membrane pressure injury is found on mucous membranes with a history of a medical device in use at the location of the injury. Due to the anatomy of the tissue, these injuries cannot be staged.

If the provider is unsure how to stage the pressure ulcer or is unsure that the wound is a pressure ulcer, it is better to describe the wound clinically than to assign a diagnosis or stage. Many regulatory bodies such as Centers for Medicare & Medicaid Services (CMS) will withhold payment or penalize health-care systems for development or worsening of pressure ulcers. If a wound that is not a pressure ulcer is described as such, or if a wound is incorrectly staged, the facility can face fines that are not justified. If there is any doubt, it behooves the provider to obtain a wound history and describe the wound per the assessment as outlined in Chapter 5: Wound Assessment and to obtain a wound-care consult for assessment of the site.

FIGURE 1. Redness on right buttock; checking for blanching.

Courtesy of Caroline E. Fife, MD

FIGURE 2. Nonblanchable redness on right buttocks; NPUAP Stage 1 Pressure Injury

Courtesy of Caroline E. Fife, MD

FIGURE 3. NPUAP: Stage I Pressure Injury Left buttock - intact skin with nonblanchable redness on buttock.

Courtesy of Caroline E. Fife, MD

FIGURE 4. NPUAP -Stage II Pressure Ulcer Both buttocks - partial thickness loss of dermis presenting as a shallow open ulcer

Courtesy of Caroline E. Fife, MD

FIGURE 5. Stage II on sacrum

Courtesy of Caroline E. Fife, MD

FIGURE 6. Stage II on heel

Courtesy of Caroline E. Fife, MD

FIGURE 7. Stage III on sacrum

Courtesy of Caroline E. Fife, MD

FIGURE 8. Stage III on ischium

Courtesy of Caroline E. Fife, MD

FIGURE 9. NPUAP - Stage III Pressure Ulcer - full thickness tissue loss; sacrum - subcutaneous fat may be visible but bone, tendon, or muscle is not exposed.

Courtesy of Jayesh B. Shah, MD

FIGURE 10. Stage IV on ischium

Courtesy of Caroline E. Fife, MD

FIGURE 11. Stage IV on sacrum and coccyx.

Courtesy of Caroline E. Fife, MD

FIGURE 12. Unstageable Pressure Ulcer Full - thickness tissue; left buttock - loss with exposed bone, tendon, or muscle.

Courtesy of Jayesh B. Shah, MD

FIGURE 13. Deep tissue injury of heel.

Courtesy of Caroline E. Fife, MD

FIGURE 14. Deep tissue injury of bilateral buttocks

Courtesy of Caroline E. Fife, MD

FIGURE 15. Deep tissue injury of both gluteal regions

Courtesy of Caroline E. Fife, MD

After risk assessment and staging have been performed, the clinician needs to determine how best to offload the patient. A turning regimen needs to be developed as part of routine, overall care. The current standard of turning every two hours was based entirely on animal data. Until recently, this “standard of care” had never been subjected to a prospective, randomized, controlled study in humans.

A recent study by Bergstrom et al. demonstrated in a prospective trial that even among patients at high risk for pressure ulcers, according to the Braden Scale, the patients did not have an increased incidence of ulcer formation if they were turned every four hours rather than every two hours.(17) This study has profound implications for clinical care and supports the findings of Defloor et al. that pressure ulcer formation is lowest among patients turned every four hours.(18) However, there are patients for whom turning every two hours is insufficient to prevent pressure ulcer formation; therefore, clinical judgement is required when turning schedules are recommended on a given patient.

Given that incontinence is a major factor in the moisture-associated risk for pressure ulcer development, it should be part of the clinical evaluation of the patient to assess their level of incontinence. For urinary incontinence, scheduled voiding methods can be used to help the patient remain dry. Use of a Foley catheter may be indicated if risk of wound contamination is high, but there needs to be a clear understanding that an indwelling Foley catheter will increase the patient’s risk of urinary tract infection. With fecal incontinence, management may be easier. The patient can be put on a bowel regimen to regulate the bowel movements, which makes perineal care easier to control. In patients with loose stools or diarrhea, use of a fecal containment system may be appropriate. When there is high risk of fecal contamination to the wound bed, the clinical team may consider a diverting colostomy to bypass the rectum until the pressure ulcer is healed.

The evaluation of nutrition is another clinical component that requires clinical assessment. In the geriatric population, nutritional compromise is common. Appetite decreases as individuals age, but in addition, factors such as dentition, poor health conditions, medications, or lack of access to food can put patients at nutritional risk. Patients with underlying malignancy or significant weight loss, regardless of age, are also at risk for nutritional compromise that can impact the skin and increase the risk for pressure-ulcer development or poor wound healing. Health-care providers used the prealbumin or albumin levels as markers of underlying nutrition. These markers may be helpful to assess overall clinical prognosis, but they do not necessarily correlate well with clinical assessment of nutritional status. The NPUAP white paper on nutrition indicates that these markers are not good markers of nutrition as they are affected by many underlying clinical conditions.(19) A study by Langkamp- Henken and colleagues concluded that use of a mini-nutritional screening tool was superior to use of visceral protein screening in determining atrisk patients.(20) Obtaining a nutritional consult early in the evaluation of an at-risk patient is a good clinical practice to address underlying nutritional risk at the beginning of the clinical course and potentially impact nutrition to decrease risk or increase wound healing.

Managing infection in a pressure ulcer patient

Infection can be an issue when dealing with pressure ulcers, especially when the area of breakdown is in the buttocks/ perineal area. In this region, there is a high risk of contamination of the wound bed if the patient is incontinent of bowel and bladder. It is important to understand that every pressure ulcer is colonized with bacteria, since our skin and the environment are colonized with bacteria. This does not mean a wound is infected. The gold standard of assessment of a potentially infected wound is tissue biopsy for quantitative culture. With this technique, a sample of tissue is obtained and cultured for growth of bacteria so that the number of bacterial colonies can be reported in relation to grams of tissue. Quantitative cultures allow a clinician to determine whether the bacteria present in a wound are merely colonizing agents or are likely to represent an infection requiring treatment.

A superficial swab of the wound will only grow the organisms that are on the surface of the wound, and not necessarily the organism that is actually causing clinical infection, if present. If a superficial swab is the only method available for quantitative analysis, the Levine method should be utilized. Areas of necrotic tissue or slough should be avoided and the deepest part of the wound selected. Before culture by the Levine technique, it is recommended to clean the wound with normal saline. Once the wound is cleaned, the swab is applied to a clean area (1 cm2 area) in the deepest section for 30 seconds. That sample is then sent for analysis.(21)

The levels of infection of a wound are defined as colonization, critical colonization, and cellulitis. Colonization is bacteria in the wound bed, but not to a level where the bacteria are negatively affecting wound healing. Every wound is colonized, but not every wound is infected. Critical colonization is when bacteria have reached a level where they are now affecting the wound bed and inhibiting healing. This is defined as 1 x 105 bacteria. Depending on the time frame the wound has been open, different types of bacteria are more likely to be present. For wounds present less than one month, gram-positive organisms will be more prevalent. For wounds present greater than one month, or if the patient has medical conditions that make him or her immunocompromised, the clinician should also consider gram-negative and anaerobic organisms. At this point, there are no systemic signs of infection, although local signs such as change in the quality of the tissue in the wound, increased drainage, pain, friable granulation tissue, and odor may be present. Critical colonization may also be noted when a clean wound is not showing signs of healing within a 14-day period despite appropriate wound care.(22) It is important to note that when critical colonization is present, systemic antibiotic therapy is not indicated. Treatment of the critical colonization should be done at the level of the wound with a topical antimicrobial or antiseptic agent. Antimicrobial agents for wounds include topical antibiotics, manuka honey, cadexomer iodine, and silver dressings. Antiseptic agents include povidone iodine, chlorhexidine, acetic acid, and sodium hypochlorite. The provider should become familiar with the products available in his or her health-care setting. These agents should only be used for a limited time to decrease bacterial load and achieve bacterial balance in the wound, at which time treatment should be changed to moist wound healing. Topical antibiotic use is becoming increasingly common for wounds that have moderate or high bacterial loads. A more aggressive stage of infection is cellulitis. It is defined as a soft-tissue infection where bacteria has now invaded the deeper tissue and is causing tissue necrosis and clinical signs and symptoms of infection, which include edema, erythema, pain, and odor. At this level, systemic antibiotic therapy with oral or intravenous agents is indicated. A deeper infection should also be considered any time a wound probes to bone. If bone is visible or palpable, a work-up for osteomyelitis may be appropriate depending on the plans for surgical debridement and/or closure. In some cases, the infected bone can be removed at the time of surgery and/or debridement, or a bone biopsy may be obtained for definitive treatment. Thus, an extensive work up for osteomyelitis prior to a planned surgical procedure may not be appropriate.

Plastic surgery approach in management of a pressure ulcer

If a pressure ulcer is full thickness or affecting quality of life, surgical intervention might be indicated for management. Prior to pursuit of surgical intervention, the clinician needs to manage the underlying factors that may affect healing. Factors such as nutritional maximization, management of underlying infection, and pressure redistribution must be managed, or the likelihood of postoperative complications will increase. If there is significant fecal soiling occurring in the wound bed, a diverting colostomy may be indicated. Referral to a general or plastic surgeon will depend on what type of surgical intervention is required. If excisional debridement of a pressure ulcer is needed, general surgery is appropriate, but if a surgical flap procedure is warranted, a plastic surgery consult is required. The decision to pursue a specific surgical intervention is going to be dependent on the surgeon’s level of expertise and his or her preference.(23) Surgical procedures may include debridement, deep cultures, or flap procedures. When a surgical debridement is performed, the surgeon will remove all devitalized and nonhealing tissue from the wound bed. This may include subcutaneous tissue, fat, muscle, or bone. Removal of necrotic tissue will decrease bacterial load in the wound bed and facilitate wound healing. At this point, the surgeon can choose to heal the wound via secondary intention, or he or she will consider primary closure with a flap. Factors the surgeon will consider prior to determination of what procedure he or she will pursue will be location of the pressure ulcer and the size and the depth of the wound. The most commonly used flaps in the treatment of pressure ulcers are musculocutaneous and fasciocutaneous flaps, as these surgical interventions provide vascularized tissue for coverage of the defect. A posterior lateral thigh V-Y procedure is also indicated for pressure ulcer management. There has been no study that has compared the effectiveness of myocutaneous flaps versus fasciocutaneous flaps.

The decision to pursue surgical intervention is not without inherent risk. A review of the literature of all of the previously mentioned flaps performed for ischial pressure sores found an overall complication rate ranging from 0% to 80% and a recurrence rate from 0% to 33.3%.(24) The most-common complication after a flap surgery is suture line dehiscence.(25) If the patient has surgical resection of bone prior to flap surgery, the incidence of dehiscence increases. Hospitalized patients who develop pressure ulcers tend to have multiple underlying comorbidities including osteomyelitis and are at increased risk for death.(26)

Support surfaces for patients with pressure ulcers See Pathway 11. Management of a pressure ulcer begins with pressure redistribution, as this is the primary factor that caused development of the wound. A Cochrane analysis of 52 randomized trials reported that patients at high risk for pressure ulcers should have a specialized support surface as opposed to a standard hospital mattress.(27) The first step is evaluation of the patient’s functional status. Is the patient bedbound, or does he or she spend the majority of time in a chair? Pressure redistribution should be considered for both settings. For the wheelchair, the patient should be referred to occupational or physical therapy for evaluation. Wheelchair cushions should be ordered for all patients who spend significant time in a wheelchair, since the seat upholstery is not designed to offer support.(28) The therapist will assess seating balance and will determine what type of seating surface is most appropriate. The four basic categories of cushions include foam, air, viscous fluid, and elastomeric cushions. The therapist will choose the correct type of cushion depending on patient’s functional status, ability to transfer, continence status, and seating balance.

The choice of mattress support surface is going to depend on whether the patient has a pressure ulcer or not. If the patient has no open wounds, most payers will not cover the cost for a preventive support surface unless the patient is completely immobile in the bed or has partial mobility and skin breakdown. Many facilities have purchased their own pressure redistribution surfaces for prevention, and if the facility has these support surfaces, a static air, gel, or foam mattress can be used for prevention. As per CMS, the categories for ordering of a pressure redistribution surface are as follows:(29)

  • Group 1 - Support surfaces are generally designed to either replace a standard hospital or home mattress or as an overlay placed on top of a standard hospital or home mattress. Products in this category include mattresses, pressure pads, and mattress overlays (foam, air, water, or gel).
  • Group 2 - Support surfaces are generally designed to either replace a standard hospital or home mattress or as an overlay placed on top of a standard hospital or home mattress. Products in this category include powered air flotation beds, powered pressure reducing air mattresses, and non-powered advanced pressure reducing mattresses.
  • Group 3 - Support surfaces are complete bed systems, known as air-fluidized beds, which use the circulation of filtered air through silicone beads.

CMS and most payers will only cover the cost of a support surface with appropriate documentation of clinical need. The patient has to meet certain criteria for each type of mattress. CMS requirements are outlined below:(29)

  • Group 1 - A Group 1 support surface is covered if the patient is completely immobile. Otherwise, he or she must be partially immobile, or have any stage pressure ulcer and demonstrate one of the following conditions: impaired nutritional status, incontinence, altered sensory perception, or compromised circulatory status. A physician order must be obtained prior to delivery of the equipment and should be kept on file by the supplier.
  • Group 2 - A Group 2 support surface is covered if the patient has a Stage II pressure sore located on the trunk or pelvis, has been on a comprehensive pressure sore treatment program (which has included the use of an appropriate Group 1 support surface for at least one month), and has sores which have worsened or remained the same over the past month. A Group 2 support surface is also covered if the patient has large or multiple Stage III or IV pressure sores on the trunk or pelvis, or if he or she has had a recent myocutaneous flap or skin graft for a pressure sore on the trunk or pelvis and has been on a Group 2 or 3 support surface.
  • Group 3 – A Group 3 support surface is covered if the patient has a Stage III or Stage IV pressure ulcer, is bedridden or chair-bound, would be institutionalized without the use of the Group 3 support surface, the patient is under the close supervision of the patient’s treating physician, at least one month of conservative treatment has been administered (including the use of a Group 2 support surface), a caregiver is available and willing to assist with patient care, and all other alternative equipment has been considered and ruled out. The other situation in which a Group 3 surface would be utilized would be in a patient who had a post-flap procedure or a patient in which multiple turning surfaces are affected by pressure ulcers, therefore limiting the ability of the patient to be turned and repositioned.

In 2015, McNichol et al. created an evidence-based and consensus-based algorithm to help clarify the selection of specialty support surfaces.(30)

A group of clinical experts convened to look at systematic reviews and publications related to support surfaces. When evaluating a patient for a support surface, a multitude of factors should be considered. Some of the factors include the patient’s weight, rehab potential, level of pain, and whether the patient has any contraindications to being on a support surface. The type of support surface used in the past for prevention and treatment of pressure ulcers is also a consideration. Once a support surface is selected, the clinician must implement a turning and repositioning schedule, as a specialty support surface will not decrease pressures below capillary closing pressure and pressure necrosis can still occur. The only category of specialty support surface on which a patient does not have to be turned and repositioned is a high-air-loss mattress. The other aspect noted by the consensus panel is that for the support surface to effectively offload the patient, it must be in good working order and must be used appropriately by the clinical staff to achieve maximum benefit.

Preventing recurrence of pressure ulcers

The majority of publications on recurrence of pressure ulcers are focused on the spinal cord injury population. Studies have shown a recurrence rate of 31% to 79%. Some of the characteristics associated with a higher recurrence rate in this population include male, younger patients, African American ethnicity, residence in a nursing home, and a history of previous pressure ulcer surgery.(31) In the elderly population, clinical evidence supports the fact that a patient who has developed a pressure ulcer in the past is usually at high risk for further development of pressure ulcers unless the factors leading to development are modified.

Full-thickness pressures heal with scar tissue. A Stage 1 pressure ulcer heals with offloading. There is never a break in the skin, therefore no re-epithelialization or scar tissue formation occurs. A Stage 2 pressure ulcer is partial thickness and therefore heals with re-epithelialization. In Stage 3 or Stage 4 pressure ulcers, healing of the pressure ulcer occurs with laying down of scar tissue as these injuries are full thickness and involve the subcutaneous tissue. Based on the wound-healing cascade, the time frame for remodeling can be up to 1.5 years. The tensile strength of the scar tissue is at maximum 70%–80% of the surrounding tissue; therefore the patient is always going to be more susceptible to having recurrence of a pressure ulcer at that site.(32) Once a patient is identified as having a history of a healed, full-thickness pressure ulcer in an area, it is important to be especially vigilant. This includes monitoring of the patient’s skin closely, maintaining moisture balance, and attenuating underlying internal and external risk factors. Maintenance of moisture balance may include use of moisture-barrier creams to protect the skin from excessive moisture, such as bowel or bladder incontinence. If the skin is excessively dry, use of emollients to keep the skin hydrated are utilized to prevent cracks and fissures in the skin.

Prevention requires the use of proper equipment to minimize the risk of recurrence. As discussed previously, a correct pressure redistribution cushion for a wheelchair is necessary if the patient spends many hours a day up in a chair. Other types of seating surfaces also need to be considered, such as Gerichairs. If a patient is spending multiple hours a day on this type of seating surface, the patient needs to be turned and repositioned, and pressure needs to be offloaded if the patient is at risk for pressure ulcers. In terms of a prevention surface for the bed, there is no current CMS payment source for prevention unless the patient is completely immobile. Use of Group 1 support surfaces are usually adequate for prevention of pressure ulcers. For heel pressure ulcers, prevention includes floating the heels with pillows and use of offloading boots. If the patient is in a wheelchair, use of appropriate footwear to prevent excessive pressure from the footrests is required. The patient’s skin should be assessed on a daily basis and during routine clinical care.

Given that immobility is one of the main risk factors for pressure-ulcer development, improvement of activity and mobility will decrease risk of pressure-ulcer recurrence. Referral of a patient to physical and occupational therapy, if appropriate, can improve strength, balance, and mobility. The individual will then need to maintain that level of activity to prevent losing any forward progress. Nutritional assessment and maximization should be achieved. The use of prophylactic dressings might also be considered. As per the NPUAP clinical practice guidelines, there were four studies that demonstrated a reduction in the occurrence of pressure ulcers with polyurethane foam dressing applied to at-risk anatomical locations. These clinical trials included patients that were critically ill and immobile patients in critical care setting.(33)


Pressure ulcers continue to be a significant and costly clinical condition. As a health-care system, we need to utilize consistent protocols to identify and minimize the risk of pressure ulcer development. Although there is no way to eliminate the risk of pressure ulcers completely, we can continue to develop clinical strategies to attenuate the impact to patient care and quality of life.


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Additional Resources

  1. Allman R, Good PD, Burst N, Bartolucci AA, Thomas DR. Pressure ulcer, hospital complications, and disease severity: implications of hospital costs and length of stay. Adv Wound Care. 1999;12(1):22-30.
  2. National Pressure Ulcer Advisory Panel [Internet]. Washington DC: National Pressure Ulcer Advisory Panel. Available from:
  3. Levine SM, Sinno S, Levine JP, Saadeh PB. An evidence-based approach to the surgical management of pressure ulcers. Ann Plast Surg. 2012 Oct;69:482-4.
  4. Becker H. The distally based gluteus maximus muscle flap. Plast Reconstr Surg. 1979;63:653-656.
  5. Kroll SS, Rosenfield L. Perforator-based flaps for low posterior midline defects. Plast Reconstr Surg. 1988;81:561-566.
  6. Park C, Park BY. Fasciocutaneous V-Y advancement flap for repair of sacral defects. Ann Plast Surg. 1988;21:23-26.
  7. Brown G. Long-term outcomes of full-thickness pressure ulcers: healing and mortality. Ostomy Wound Manage. 2003;49:42–50.

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