Baromedical Nurses Association (BNA)

  • Laura Josefsen, RN, ACHRN - Chairman, BNA Publications Committee
  • Volume 10 - Issue 4

Baromedical Nurses Association (BNA)

The very active BNA board has had a busy year and is looking forward to the new decade! Do you know that 2020 will be the 35th anniversary of the Baromedical Nurses Association?

The BNA board is busy planning the 3rd annual Hyperbaric Nurses Day on Saturday, April 4, 2020. Be sure to check the BNA website for this exciting day at for updates, time, presentations, and events.

You are invited to check the new and improved BNA website for the latest news and information. The tabs include, but are not limited to, the following:

  • About Us: Gives you information about the board members and committee chairs. You are encouraged to nominate yourself or another nurse for any of these positions or committees. A description of the positions and committee responsibilities are in this area. You will make a great difference in the growth and success of the BNA.
  • Membership: RN and LVN/LPN
  • Education: Offers Category A credits free to BNA members and at a nominal charge for nonmembers and provides education and resources for your nursing practice.
  • Certification: Includes requirements, updates, and discounted fees to take the exam for BNA members
  • Safety: Includes safety drills and hot topics
  • Members-Only Forum
  • Chamber Spotlight: Includes international facilities
  • Newsletters: Up-to-date info on hyperbaric nursing
  • Research: This very active committee is developing the first BNA research project
  • Awards: There are now four awards to recognize outstanding contributions

Are you familiar with the “BNA Guidelines of Nursing Care for the Patient Receiving Hyperbaric Oxygen Therapy (HBO2) Position Statement?” It states: “These hyperbaric nursing guidelines reflect and promote actual knowledge and judgment to practice hyperbaric nursing safely. It is recommended that each facility develop guidelines based on, but not limited to, the hyperbaric nursing guidelines, the Policy and Procedure Guidelines for Hyperbaric Facilities, the National Fire Protection Association (NFPA 99) and their own facility guidelines.” There are 17 problem guidelines, each with detailed goals and interventions to assist the hyperbaric nurse with assessment, documentation, and safety. These guidelines are reviewed and updated on a regular basis.

You are invited to be active in the BNA. The total membership of experienced and new members this past decade has resulted in tremendous growth of hyperbaric nursing. The next decade holds promise of an exciting future. The BNA has an active presence in the UHMS annual meetings as well as the chapter meetings. You are invited to visit the BNA table at each of the meetings to see familiar as well as nurses new to the hyperbaric field. We look forward to seeing you!

About the Author

LAURA JOSEFSENLAURA JOSEFSEN, RN, ACHRN, has been involved in hyperbaric nursing since 1982. A founding member of the Baromedical Nurses Association (BNA) in 1985, she served as BNA president from 1996 to 1998 and as a board member in several positions throughout the years. She served on the Undersea and Hyperbaric Medical Society (UHMS) Associates Council for six years, with two of those years as Nurse Representative on the UHMS Board of Directors. She is a member of the UHMS Accreditation Team as a nurse surveyor, served for many years as an executive board member of the National Board of Diving and Hyperbaric Medical Technology and is a previous chairman of the BNA Certification Board. She is a member of the UHMS Associates, former member of Divers Alert Network, and former member of the Hyperbaric Technologists and Nurses Association (HTNA) of Australia. She has numerous publications and is an internationally recognized speaker in the field of hyperbaric medicine. Her passions are quality improvement and education to promote hyperbaric nursing, safety, and optimal standards of care and practice for patients and the community.

Hyperbaric Medicine

Read more: Baromedical Nurses Association (BNA)

Clinic In Focus: St. Vincent Wound Care Clinic and Hyperbaric Oxygen Therapy

  • WCHM Staff
  • Volume 10 - Issue 4

Clinic In Focus: St. Vincent Wound Care Clinic and Hyperbaric Oxygen Therapy

  • Clinic In Focus:

    Vincent Wound Care Clinic and Hyperbaric Oxygen Therapy

  • Location:

    3801 Bellemeade Ave. Suite 110
    Evansville, IN 47714

  • Website/Phone:

    (812) 485-7330

  • How long in business:

    Wound Care: 6 years
    Hyperbarics: 3 years

  • How many chambers:


  • Chamber type(s):

    Perry Baromedical Sigma 36 and Sigma 40

  • How many physicians/nurses/CHTs:

    2 physicians
    1 chamber technician
    1 safety director/program director
    6 RNs

  • Medical director:

    Maureen P. Kuhrt, MD

  • Podiatrist:

    Sarah Voelkel, DPM

  • Date of UHMS accreditation:

    September 18, 2018

If an accredited facility, how has seeking UHMS accreditation affected your clinic? Seeking and obtaining accreditation has helped us keep the utmost important safety and policies at the forefront of our care. We have always treated with a mindset of “safety first,” however, this gives us the extra check and balance system in order to excel. It keeps our attention on smaller things that have the potential to be overlooked. Our patients can feel confident in the fact they are receiving the very best care, knowing that no detail is overlooked and no step is missed. Accreditation has also given our amazing clinicians the recognition they deserve.

What are the most common indications treated at your clinic? At this time, we aren’t set up to treat emergent indications for hyperbaric oxygen therapy, but, this is an eventual goal of ours for the future. Most commonly treated indications at our clinic include the following:

Hyperbaric Oxygen Therapy:

  1. Wagner Grade 3 diabetic foot ulcers
  2. Osteoradionecrosis
  3. Soft tissue radiation injury
  4. Chronic refractory osteomyelitis
  5. Flap failure
  6. Idiopathic sudden sensorineural hearing loss

Wound Clinic:

  1. Diabetic foot ulcers
  2. Ulcers related to venous insufficiency
  3. Ulcers related to arterial insufficiency
  4. Burns and traumatic wounds
  5. Pressure related injuries/ulcers

What is the most memorable treatment success story that has come out of your clinic? In March of this year, we had a 48-year-old female with a new diagnosis of Type 2 Diabetes. She presented to us with a very large diabetic foot ulcer (8.6 cm x 7.1 cm x .1 cm) with underlying osteomyelitis and at risk for a life-altering amputation. Thankfully we were able to treat her with hyperbaric oxygen therapy. After 42 dives, in conjunction with advanced wound care, she was completely healed and able to return back to her normal daily activities.

Do you work with a management company? If so, which one? Yes! We proudly work with Outpatient Integrated Strategies.

If you had to pick one thing to attribute your clinic’s success to, what would it be? Dedication and teamwork! Without a doubt, our clinicians are the most loyal/dedicated group of individuals. We have a very low (staff) turnover rate and each one of them shows up daily, dedicated to providing the utmost quality care to our patients. They work together, no matter how large or small the task, to get things done safely and correctly. They truly are the backbone of our clinic.

What is one marketing recommendation that you can make to help clinics increase their patient load? Do your research. We all know what indications are typically approved, but that doesn’t mean they are prevalent to your specific demographical area. The key is keeping it simple and directly related to the individual practices and/or groups to which you’re marketing. Make traveling marketing materials indication-specific to keep the attention of the potential referring provider. They are all very busy, so being clear and concise will go a long way.

Hyperbaric Medicine

Read more: Clinic In Focus: St. Vincent Wound Care Clinic and Hyperbaric Oxygen Therapy

Influence of Oxygen Tensions in Viral Infections

  • Rodney E. Willoughby Jr., Charles C. Falzon, Aliyah Keval, and Harry T. Whelan
  • Volume 10 - Issue 4

Influence of Oxygen Tensions in Viral Infections

Excerpt from Chapter 16: Effects of Hyperbaric Oxygen in Infectious Diseases: Basic Mechanisms in Hyperbaric Medicine Practice 4th edition, Harry T. Whelan and Eric P. Kindwall, editors

With flu season among us, you may find the following information helpful from Hyperbaric Medicine Practice 4th Edition.

Presently there is no evidence of direct beneficial effects of HBO2 in viral infections. However, it appears that oxygen tensions affect the growth and virulence of certain viruses. Hypoxia (3% O2) causes marked alterations in growth characteristics of some viruses. Plaque diameter and plating efficiency of adenoviruses cultured under hypoxic conditions are markedly reduced. In contrast, polioviruses are not adversely affected by hypoxic conditions. Replication of rubella virus in hamster kidney cells was not altered during exposure to oxygen tensions ranging from 1 to 330 mmHg.

Reactive oxygen species cause single-strand breaks in DNA. Viral DNA may be particularly susceptible to oxidative damage because viruses lack antioxidants and DNA repair mechanisms. Exogenous SOD and catalase combine to confer protection against inactivation of viruses. Therefore, it is possible that antioxidants in the host cells may protect viruses against free radicals. Thus, exogenous antioxidants may account, at least in part, for the viral resistance to hyperoxia.

Effects of various oxygen tensions in murine models of viral infections have been examined. In a model of encephalomyocarditis caused by the MM virus, hypobaric hypoxia (21% O2 at 0.5 ATA) significantly increased mortality as compared to normoxia. Exposure to hypobaric normoxia (100% O2 at 0.2 ATA) also increased mortality in mice infected with influenza A virus. However, neither normobaric hypoxia (11% O2 at 1 ATA) nor hyperoxia (77% O2 at 1 ATA) altered mortality. Thus, it appears that decreased atmospheric pressure, rather than oxygen tension, influenced mortality due to influenza A virus in that study. In contrast, Ayers et al. found that exposure to hyperoxia (99% O2 at 1 ATA) resulted in influenza-infected mice dying 3 to 4 days earlier than normoxic controls. One possible explanation is the finding by Naldini et al. that the antiviral activity of interferon-alpha (and interferon-gamma) is decreased in vitro under “normoxic” conditions (140 mmHg O2) compared to “hypoxic” conditions (14 mmHg O2). Exposure to hypoxia (11% O2) increased mortality and viral titers in tissue of mice infected with Coxsackie B-1 virus. Interestingly, hypobaric hypoxia (21% O2 at 0.5 ATA) increased viral titers, but not mortality. In addition, HBO2 (100% O2 at 3 ATA) enhanced mortality in mice infected with Coxsackie B-1 virus. Pretreatment of mice with HBO2 significantly increased viral titers in heart muscle and brown fat by three days after inoculation of the virus. The effects of HBO2 may have been mediated through free radicals since, in another model of Coxsackie B3 myocarditis, polyethylene-conjugated SOD reduced cellular infiltration, myocardial necrosis, and calcification scores, compared to the control group at day 14, after intraperitoneal challenge in C3H/He mice. There were no differences in viral titers among the three groups at day 7 and viral titers were no longer detected by day 14 in any of the treatment groups.

Another recent study investigated the basis of treating chronic hepatitis with HBO2 and to compare the changes in hepatic function, immunity, pathologic morphology, ultrastructure and HBV in hepatic tissues before and after treatment. The experimental group was treated with six courses of HBO2 while the control group was treated for 60 days with standard therapy. There were significant differences between the experimental and control groups after treatment; for the experimental group, all markers of hepatic function and hepatocyte degeneration or necrosis were decreased, but the fibrosis and fat-storing cells in the liver were not reduced.

In summary, oxygen tensions appear to influence the outcome of viral infections in animal models. Hyperoxia appears to increase mortality in mice infected with influenza A virus or Cocksackie B-1 virus. Hypoxic conditions also increase mortality in Coxsackie B-1 infected mice. Treatment of chronic HBV with HBO2 appears to be effective, and should be considered as an adjunct to standard pharmacologic therapy. HBO2 has not been shown to be effective at reversing liver fibrosis.

Hyperbaric Medicine

Read more: Influence of Oxygen Tensions in Viral Infections

Emerging Paradigms Integrating the Lymphatic and Integumentary Systems: Clinical Implications

  • by Robyn Bjork MPT, CLWT, CWS, CLT-LANA and Heather Hettrick PT, PhD, CWS, CLT-LANA, CLWT
  • Volume 10 - Issue 4

Emerging Paradigms Integrating the Lymphatic and Integumentary Systems: Clinical Implications

This is an archived article reprinted with permission from Volume 9 Issue 2 of WCHM. Robyn Bjork and Heather Hettrick are leading experts in the field of wound care and lymphedema management.


Ernest Starling, in the late 1880s, introduced a model of capillary fluid exchange, based on hydrostatic and oncotic pressures (Starling, 1894). It was thought that increased hydrostatic pressure on the arterial side of the blood capillaries forced fluid into the interstitium, while lower hydrostatic pressure, coupled with higher oncotic pressure on the venous side of the blood capillaries, resulted in reabsorption of fluid. Until more recently, this was the prevailing understanding of fluid homeostasis, and formed the basis of wound, edema, and lymphedema education.

More recently, it has been established that the endothelial glycocalyx layer (EGL) controls the movement of proteins and fluid across the blood capillary wall. Despite prevailing principles regarding Starling’s Law, it is now understood that there is no reabsorption of fluid back into the venous side of blood capillaries. Rather, there is only diminishing net filtration across the capillary bed, and fluid and blood proteins are removed from tissues via reabsorption through lymphatic capillaries alone. Consequently, a new paradigm that all edemas are on a lymphedema continuum has emerged (Bjork, Hettrick, 2018).

Evidence suggests that areas of lymphatic failure produce regions of integumentary vulnerability subject to inflammation, infection and carcinogenesis, essentially, skin barrier failure (Carlson, 2014). This may be the basis behind most integumentary dysfunction and contribute to the development of various wound pathologies (complicated by underlying disease processes and comorbidities). These combined findings highlight the interconnectedness of the lymphatic and integumentary systems and the need for a more unified clinical approach for the management of patients with chronic wounds and lymphedema.

Structure & Function of the Endothelial Glycocalyx Layer

In 1940, Danielli first introduced the concept of a protein-based lining of all blood vessels that plays a vital role in fluid filtration. And, in 1966, Luft visualized this layer for the first time through electron microscopy. By 2007, the EGL gained recognition as controlling the movement of proteins and fluid across the blood capillary wall. Subsequently, Levick and Michel (2010) mathematically demonstrated that there is no net reabsorption of fluid back into the venous side of the blood capillaries, rather only diminishing net filtration into the interstitium. Then, in 2014, Mortimer and Rockson integrated this new understanding of “no net reabsorption” into their review “New developments in clinical aspects of lymphatic disease”, bringing it to the forefront of edema management.

A healthy EGL is approximately 0.5 um thick in the blood capillaries; it is progressively thicker in larger vessels, up to 4.5 um in carotid arteries (Reitsma et al., and Weinbaum, Tarbell, and Damiano, 2007). The EGL is made up of two continuous layers. The base is a slimy layer that coats the endothelial cells of the vessel wall. This slime or gel matrix is made up of chains of glycoproteins and proteoglycans that attach directly into the membranes of the endothelial cells, creating “backbones” (Reitsma et al., and Weinbaum, Tarbell, and Damiano, 2007). These backbones are linked together by a web of glycosaminoglycans that can absorb 10,000 times their weight in water (Biddle, 2013), thus creating a slimy gel layer. This sophisticated layer lines the endothelial cells of blood vessels and is integral in keeping fluid in or out, based on physiologic requirements. Within this base layer are wavy clefts, or channels, with tight junctions that control movement of fluid and protein through the EGL into the interstitium (Weinbaum, Tarbell, and Damiano, 2007). The EGL’s essential role is maintaining vascular homeostasis.

The second layer of the EGL is made up of soluble plasma components linked to each other in a direct way or via soluble proteoglycans and/or glycosaminoglycans (Reitsma et al., 2007). This layer is visualized as hair-like projections, extending into the lumen of the blood vessel, organized into a hexagonal matrix with roots that attach to the “backbone” proteins of the gel base layer (Weinbaum, Tarbell, and Damiano, 2007) (Figure 1). Since the “backbone” proteins are tethered into the endothelial cell membranes of the capillary wall, and crosslinked in the gel matrix, blood flow shear forces acting on the hairlike projections mechanically transmit this information into the endothelial cells themselves. The endothelial cells respond to the mechanical signals, such as producing and releasing nitric oxide, which dilates the vessel (Biddle, 2013).

The composite EGL, including soluble proteins and other components that bind to it, has a negative charge that repels red blood cells (RBCs) and platelets so they do not touch the vessel wall. This space between the RBCs and the EGL is called the “exclusion zone” (Reitsma et al., 2007). The EGL is dynamic and can “shed” in response to stimuli, such as during inflammation or disease states. During inflammation, this shedding of the hair-like projections allows more fluid to escape through the EGL. Shedding also exposes adhesion molecules (Reitsma et al., 2007) to which platelets or white blood cells (WBCs) attach. WBCs are squeezed tightest in the blood capillary where they enter the venule and are known to crush the EGL temporarily by 20% (Weinbaum, Tarbell, and Damiano, 2007). It is here that WBCs tether to exposed adhesion molecules and then remain tethered as they roll across the venule wall to exit into the tissues, known as diapedesis.

The EGL is particularly sensitive to ischemia, which can result in rapid shedding as a protective mechanism. A high fat, high cholesterol diet, oxidative low-density lipoproteins, and hyperglycemia also cause shedding of the EGL, and the EGL has been found to be thinner in areas prone to atherosclerosis (Reitsma et al., 2007). The EGL plays an important role in diabetes mellitus, peripheral arterial disease, reperfusion injury, intravenous fluid mismanagement, renal disease, and dialysis (Biddle, 2013). It also has an antithrombotic effect due to “enzyme docking” and plays an important role in reducing oxidative stress (Biddle, 2013). With this, it is important to appreciate the role and implications the EGL has with respect to integumentary dysfunction—inclusive of lymphatic and cutaneous disease.

To summarize, the functional importance of the vascular endothelial glycocalyx layer cannot be overemphasized. (See Figure 1.) Biddle, 2013, eloquently details the EGL’s functions as: regulation of vascular permeability, mechanotransducer regulating vascular tone, moderator for leukocyte and platelet adhesion, provides antithrombotic effect in vasculature, repulses red blood cells from the vascular endothelium, and reduces oxidative stress.

FIGURE 1. Vascular endothelial glycocalyx (Biddle, 2013). This figure is used with permission from the author.

No Net Reabsorption Exception

Once the interstitial fluid enters the lymphatic capillary, the lymph is funneled through pre-collectors and into collectors that propel the lymph toward lymph nodes via sequenced contraction of lymphangions coupled with one-way valves. Under normal conditions, ~4L of lymph re-enters the venous system at the venous angles in the neck. However, a sum of ~8L/day of fluid moves out of the blood capillaries and into the tissues (Levick, 2010; Renkin, 1986). The structure and function of the lymph nodes is essential to reconciling this apparent discrepancy.

In 1983, Knox et al. found that ~50% of the fluid portion of lymph is reabsorbed into the venous circulation via the blood capillaries within canine lymph nodes. The same year, Adair and Guyton demonstrated that increasing the venous pressure in canine lymph nodes resulted in movement of fluid back into the node, thereby reducing the concentration of proteins in the efferent lymph vessels. This highlights the role of the lymph nodes and lymphatics in fluid homeostasis, as well as the impact of chronic venous hypertension. Elevated venous pressure not only results in ultrafiltration from the blood capillaries but also slows reabsorption of fluid from the lymph nodes back into the venous circulation. The dense, capsular design of the lymph nodes, their placement in joint areas that are mechanically compressed by movement, and the presumed absence of EGL, all work synergistically to facilitate fluid reabsorption back into the venous system. Conversely, immobility and decreased joint movement through the full range of motion, lymph node removal, or venous hypertension can have a significant impact on fluid retention in the dermis and subcutaneous tissues. Ultimately, this stagnant fluid may lead to fibrosclerosis and deleterious alterations within these tissues.

New Paradigm: All Edemas Are on a Lymphedema Continuum

All edemas are on a lymphedema continuum. Since we now know that all swelling is managed by reabsorption by the lymphatic capillaries alone, the patency of dermal lymphatics and the efficiency of lymphatic drainage are paramount to edema management and wound healing. Interventions to help prevent damage to lymphatic capillaries, and techniques to facilitate lymphatic drainage and lymphangiogenesis need to be considered as part of wound management. As early as 1994 (Scelsi, et al.), damage to dermal lymphatics was observed in skin biopsies from patients affected by chronic venous insufficiency (CVI). In more recent studies using near-infrared fluorescence lymphatic imaging (NIRFLI) technology, baseline imaging showed impaired lymphatic function and bilateral dermal backflow in all subjects with chronic venous insufficiency, even those without ulcer formation (Rasmussen et al., 2016). As edema progresses to chronic edema, pathophysiological changes occur as a result of localized lymphatic insufficiency or failure. For example, swelling post-orthopedic surgery or traumatic injury or chronic edema surrounding a venous leg ulcer can lead to localized protein accumulation and degradation, resulting in localized inflammation and connective tissue proliferation. According to Foldi, “. . . stagnating high protein edema develops a pathohistological state of chronic inflammation, with infiltration of the tissue by mononuclear cells, angiogenesis, proliferation of connective tissue, fibrosis and fibrosclerosis . . .” He further goes on to describe how oxidation and degradation of interstitial proteins attracts monocytes (macrophages) that, in turn, ingest proteins and activate fibroblasts and adipocytes. This activation results in connective tissue and adipose proliferation. As such, wounds and impaired cutaneous function are highly associated with inflammation and fibrosis associated with lymphatic dysfunction.

Clinical Diagnosis

In 1976, Robert Stemmer defined a test used for differential diagnosis of lymphedema, which later was corroborated sonographically, macroscopically and microscopically by Brenner, Putz, and Moriggl in 2007. In its original description by Stemmer, “a thickened longitudinal skinfold when pinching the toes is a clinical sign for the early diagnosis of a lymphoedema, and delimits it from a pure venous oedema” (Stemmer, 1976). In the Best Practice for the Management of Lymphoedema (Framework, 2006), the Stemmer test is described as being performed on the second toe or middle finger, attempting to pinch and lift the skin. The test is considered positive for lymphedema when a skin fold cannot be raised, but a negative sign does not exclude lymphedema. In 2007, Brenner, Putz, and Moriggl showed that in individuals with lymphedema and a positive Stemmer sign, both the dermis and subcutaneous tissue of the second toe were thickened and the structure of the dermal layers destroyed, as well as an accumulation of edematous fluid in free spaces within the subcutaneous tissue.

In light of the new paradigm that all edemas are on a lymphedema continuum, co-author Robyn Bjork proposes an expanded version of the Stemmer test. This new test, named the “Bjork Bow Tie Test,” can be performed anywhere on the body to assess for inflammation and thickening of the integument that can occur with lymphatic dysfunction, such as around chronic wounds. To perform the test, in one maneuver gently pinch, lift and rotate the skin between the thumb and pointer finger, noting quality of tissue texture and thickness. Healthy skin can be lifted and pinched, should feel slippery between the layers, and produce a “bow tie” of wrinkles when rotated. (See Figures 2 and 3.) Skin that is positive for lymphedema will be thickened, less pliable, less able to be pinched and lifted, more difficult to rotate, and produce limited or no “bow tie” of wrinkles.

FIGURES 2 and 3. Pictured are Bjork Bow Tie Tests performed on different areas of skin with varying thicknesses. Both tests are negative for lymphedema, exemplified by the distinguishing “bow tie” of wrinkles.

For skin that may be distended from edema and cannot be lifted because of it, still observe for the “bow tie” of wrinkles when performing the technique. Areas of skin should be demarcated on a body map to indicate where the test is positive (+) or negative (-). Even a slightly positive test should be marked as positive (+). The subcutaneous tissue should also be assessed in a similar fashion. A negative test does not exclude lymphedema but means that the dermis and subcutaneous tissues have not yet developed the pathohistological changes described previously.

Relationship Between Lymphatic and Integumentary Systems

It is well established that there is a paucity and lack of standardization with respect to wound and lymphedema education in traditional medical and health professions education. If such education is provided, it is likely segmented and taught in separation rather than in parallel or unison. In 2008, a study by Patel et al. compared wound education in medical school curricula between the United States, Germany and the United Kingdom. The results of this retrospective indicated that the “total hours of required wound education received in the United States was 9.2 hours in the 4 years of medical school. In the United Kingdom, the total time devoted to wound-related issues equaled 4.9 hours over 5 years. In Germany, a total of 9 hours of wound education was provided over 6 years.” This study concluded that there is a deficiency with respect to wound education in preparing future physicians to manage wounds.

With respect to lymphedema, the education is even more sparse. A survey study published in 2011 by Vuong, Nguyen and Piller regarding the level of lymphatic education provided in medical schools around the United States, indicated that most programs devoted 30 minutes or less to teaching lymphatic function in the first two years of medical school. Further, nearly 40% of respondents indicated that 1-3 hours of time was devoted to the lymphatic system, while 25% indicated that 15 minutes or less was spent on the topic. The apparent lack of dedicated time in traditional medical education is further compounded by the fact that these two systems are highly interdependent, meaning impairment in one system directly impacts the other.

Carlson describes in his 2014 review article how lymphatic failure produces a cutaneous region susceptible to infection, inflammation and carcinogenesis, which he describes as a locus minoris resistentiae or path of least resistance. He explains in his article how lymphatic failure causes a disruption of adaptive immunity by “decreasing or obstructing immune trafficking by antigen, lymphocytes, macrophages and dendritic/antigen presenting cells (Langerhans cells) to the lymph node crating a cutaneous region of immunosuppression. All these abnormalities create a region of immunosuppression . . . or a condition called lymphatic dermopathy, which is failure of the skin as an immune organ.” In essence, lymphatic impairment can lead to integumentary dysfunction and integumentary dysfunction can exacerbate lymphatic dysfunction. For clinicians, it is important to recognize the interdependence these systems have on one another so proper diagnosis and interventions can be delivered.


To summarize, the EGL is the gatekeeper for blood capillary fluid exchange. There is only diminishing net fluid filtration, and no reabsorption across the blood capillaries of the dermis and subcutaneous tissues. All fluid and blood proteins moving into the interstitium must be removed via reabsorption through the lymphatic capillaries alone. Thus, all edemas are on a lymphedema continuum and are at risk of developing chronic inflammation, dermal thickening and connective tissue proliferation. The new, “Bjork Bow Tie Test” can be used to test for these integumentary changes anywhere on the body, including around wounds. Skin that is positive for lymphedema will be thickened, less pliable and produce limited or no “bow tie” of wrinkles.

Assessment of the lymphatics is important in chronic wound management, as impairment in one system indicates impairment in the other with varying levels of complexity and clinical presentation. Improved collaboration is needed between physicians, vascular/vein specialists, wound specialists, lymphedema therapists and other health care professionals, to establish cohesiveness of paradigms and common language. By working more closely together, progress toward effective, multi-disciplinary care, particularly for individuals with lower extremity lymphedemas and chronic wounds, is achievable.


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About the Authors

Emerging Paradigms Author 01ROBYN BJORK, PT, CLWT, CWS, CLT-LANA is the founder and CEO of the International Lymphedema & Wound Training Institute (ILWTI). She is a physical therapist who is an expert in the field of wound care and lymphedema management and has over 20 years experience, spanning outpatient, inpatient, transitional, long-term, home-care and private practice settings.

Bjork is a featured speaker at national and international conferences, such as the Symposium on Advanced Wound Care, European Wound Management Association, Canadian Association of Wound Care, Wild on Wounds, National Lymphedema Network International Conferences, the Lymphatic Education & Research Network’s Symposium Series, and numerous regional lymphedema and wound conferences. Bjork has written, produced, and implemented over 155 hours of advanced, accredited curriculum for certifying wound and lymphedema specialists in the United States and abroad ( She is co-author on the chapter on lymphedema in Textbook of Chronic Wound Care: An Evidence-Based Approach to Diagnosis and Treatment and has authored articles in Wounds International, Pathways and Wound Care Advisor.

Bjork is a Certified Lymphedema and Wound Therapist through the International Lymphedema & Wound Training Institute, a Certified Wound Specialist through the American Board of Wound Management, and a Certified Lymphedema Therapist through the Lymphology Association of North America. She is a proud member of the American Physical Therapy Association, the Lymphology Association of North America, the Association for the Advancement of Wound Care, the World Alliance of Wound and Lymphedema Care, and the American College of Phlebology.

Bjork is a board member and past secretariat of the World Alliance of Wound and Lymphedema Care. She is an international expert in the morbidity management of podoconiosis and lymphatic filariasis and a chapter author on podoconiosis for a soon-to-be-published global wound and lymphedema management handbook for WAWLC and the World Health Organization. In recognition of her international work, in 2011 Bjork received the Central Florida Humanitarian Award and was featured in the commemorative edition of Space Coast Medicine magazine. She also received a Certificate of Special Congressional Recognition in appreciation of excellence in medicine.

Emerging Paradigms Author 02HEATHER HETTRICK PT, PHD, CWS, CLT-LANA, CLWT is an associate professor in the Physical Therapy Program at Nova Southeastern University in Ft. Lauderdale, Florida. As a physical therapist, her expertise resides in integumentary dysfunction where she holds three board certifications.

Heather has diverse work experience in academia and the private sector. She is a key opinion leader and is actively involved in numerous professional organizations, conducts research, and publishes, presents and teaches nationally and internationally on integumentary related issues.

Dr. Hettrick is a past president of the American Board of Wound Management and is an active board member of the Association for the Advancement of Wound Care and World Alliance of Wound and Lymphedema Care.

Wound Care

Read more: Emerging Paradigms Integrating the Lymphatic and Integumentary Systems: Clinical Implications

Letter from the Editor

  • Lorraine Fico-White
  • Volume 10 - Issue 4

WCHM closes out its 10-year anniversary in 2019 with an important announcement. This will be the last issue of WCHM as a digital magazine. In the future, the staff of WCHM will be restructuring content into practical applications and provide information on wound care and hyperbaric medicine through various media channels. We’d love your input/feedback as to how we can bring this content to you in a usable and effective format. We invite you to visit and mark it as a “favorite.”

Sadly, our last issue recognizes the loss of three beloved icons in the field of hyperbaric medicine and diving: Dr. Alfred Bove, Dr. Carl Edmonds, and Dr. Fiona Sharp. They will be missed.

In hyperbaric medicine news, the American Board of Preventive Medicine announces expanded eligibility requirements for its three subspecialties. The Baromedical Nurses Association (BNA) shares their quarterly news. An excerpt from Hyperbaric Medicine Practice 4th edition section provides helpful information on the influence of oxygen tensions in viral infections . . . appropriate as flu season descends upon us. This issue’s clinic in focus spotlights St. Vincent Wound Care and Hyperbaric Oxygen Therapy.

In wound care news, our last archived article spotlighting the magazine’s prolific authors is from Robyn Bjork and Heather Hettrick, experts in the field of wound care and lymphedema. The Whats and Hows of Wound Care Certification Exams by Jayesh B. Shah, Paul J. Sheffield, and Caroline E. Fife provides expert advice on preparing and taking the wound care certification exams.

Thank you to all of our fabulous sponsors and expert authors the staff of WCHM have worked with over the past 10 years! We have appreciated your valuable insights in the fields of hyperbaric medicine, wound care, and diving medicine!

Wishing everyone a healthy 2020!

Lorraine Fico-White
Managing Editor, WCHM Magazine

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