Category Archives: Level 2

Level 0, Level 1, Level 2, Level 3, Level 4

The Harm Scale

Comment

Caroline Fife suggested I should publish a simple scale for tissue damage and call it the “Harm Scale”.

Here it is.

Analysing wounds requires to have a look at it at five levels, from the molecule up to the social environment of the patient. To understand events in wounded cells and tissue, it is important to realise that cells and tissues have a range of states related to damage. The linguistic problem is that damage is considered as, well, damage but in reality, cell and tissue damage ranges from no damage to death. Therefore, perhaps, we may refer to the scale as loss of homeostasis. Here the normal state means there is no loss of homeostasis, and the dead state means there is a maximum loss of homeostasis. This also makes sense because the body considers homeostasis the optimum and any loss of homeostasis will evoke a reaction. But the easiest option is, as Caroline pointed out, to use the word harm, which can be seen as a measure of loss of homeostasis.

What is harm?

Harm stands for how much problems a cell or a tissue has in its normal function.

Logically a cell or tissue can be in six states of harm:

  1. Normal,
  2. Adapted,
  3. Stressed,
  4. Injured,
  5. Damaged,
  6. Dead.

 

Normal is the normal state, where the cell or a tissue is well adapted to the circumstances and it is able to fulfil its required role. Here, the cell and tissue are in a state homoeostasis.

Adapted, if there are changes in the environment, cells or tissue adapt by changing its anatomy, physiology or behaviour. Adaptation causes cells and tissues to communicate their changed state with their environment, and the body detects those signals (Pakos‐Zebrucka et al. 2016; Erguler, Pieri, and Deltas 2013)

Stressed, when the changes lead to problems in the cells or tissue’s anatomy, physiology or behaviour becomes stressed. Here it is no longer able to fulfil all its activities normally. Stressed cells and tissues start sending out distress signals like reactive oxygen species, HIF-1a and other signals (Andreeva et al. 2015; Bohovych and Khalimonchuk 2016). These signals are not only detected by the body but some signals can also be detected in laboratory analysis (Görlach et al. 2015; Pichu et al. 2018).

Injured, if the changes have led to small-scale damage, like a leaking cell membrane or tissue damage, problems can begin to arise. Leaking for instance ATP and calcium through membranes and other forms of damage (DAMPS) are interpreted as unwelcome events (Horn and Jaiswal 2018; Tang and Marshall 2017). This implies that the signals resulting from cell and/or tissue injury may already elicit an inflammatory response (Jagannathan and Tucker-Kellogg 2016; Rathinam and Chan 2018). Often injury may be repaired, allowing for full regeneration.

Damaged, if the resultant harm has led to irreversible, yet non-lethal, damage, there are inevitable consequences. For example, loss of a limb, may not kill you, but it will reduce your functionality. The body will detect damage and respond. It might do so by apoptosis, the controlled killing of damaged cells (Karch and Molkentin 2015). IApart from liver or skin tissue, full regeneration of damage is not an option. Here the negative consequence of fibrotic repair can take place (Whyte, Smith, and Helms 2012; Greaves et al. 2013; Nyström and Bruckner-Tuderman 2018).

Dead, a dead cell is, well … dead. If a dead cell or tissue is not cleaned up properly, but is destructed instead, it’s organelles and DNA function as a danger signal, the so-called DAMP’s (danger associated molecular patterns) invoking inflammation and other tissue repair or regeneration processes (Pandolfi et al. 2016; Maslanik et al. 2013).

The Harm Scale has dimensions of level, size and time. A single cell moving up the Harm Scale, does not imply that the tissue containing that cell is also adapted, injured or damaged. The tissue it is in,  might very well be in perfect homeostasis. However, if more cells in the tissue start to get damaged or die, in time the tissue itself may start moving on the Harm Scale. And similarly, if a tissue is moving up the Harm Scale does not mean your body or parts of it are damaged.

Nevertheless, an inflammatory response is always imminent, inflammation is good but at the price of remaining scars, even at the molecular level (Fulop et al. 2018). Chronic inflammation is a source for age-related disease. (Franceschi et al. 2018)

So, even if harm doesn’t necessarily lead to direct damage, even little harm may cause problems over time in the li=ong run (Ashcroft, Mills, and Ashworth 2002).

 

Why is this important?

The body detects and responds to any deviation from homeostasis and will react to regain homeostasis. If the reaction is insufficient, the tissue damage will increase in size and magnitude and cause serious problems for the patient.

If you consider most non-traumatic wounds result from an underlying condition, the Harm Scale begins to make sense. It draws attention to the pre-clinical events which impact the clinical events to follow. If the harm is not handled properly, you are setting up your topical treatment for failure.

Flatly, if you fail to recognise the obstructed vessel, your dressing is not going to do much.

Even stressed cells may already have an impaired ability to handle harm, this condition may worsen if the harm moves up the scale. If the surrounding cells or tissues are in a grave state, the situation can spiral out of control, like in the case of skin failure at the end of life (Levine 2016).

Recognising the existence of harmed tissue highlights how a patient, who does not yet have a wound, might still suffer enough from harm to develop a wound in the near future. Or even worse, a closed wound does not mean there is no tissue damage, setting the stage for recurrence.

Neglecting the level of harm in tissue, can cause to you take action which may result in an avoidable lesion. (Black et al. 2011)

The Harm Scale also points out that, not only the tissue in the wound but also the cells and tissue surrounding the wound may be harmed, impairing the ability to repair or regenerate tissue. In general, it will be safe to say that processes, like proliferation, will take place outside the wound, even perhaps outside of the inflamed zone (Park et al. 2017). This means that the quality of the surrounding tissue plays an important role in the wound healing process.

Figure 1 Schematic representation of harm in and outside the wound.

In this paper we treat the Harm Scale at level 2 of the Five Level Model for Wound Analysis and Treatment. The five level model is a system to describe factors influencing the cause and resolution of wounds at a normal (0), general (1), local (2), systemic (3) and cellular-molecular (4) level. The levels represent a connection between where problems occur and common clinical and scientific practice. (Smit 2018)

Level 2 is local, the level of the wound. However, the Harm Scale also exists at other levels, examples are:

  • Level 1; inflammaging (Chen et al. 2014),
  • Level 3; organ-system damage (San Miguel-Ruiz and García-Arrarás 2007) and
  • Level 4; (epigenetic) DNA damage (Nanduri, Semenza, and Prabhakar 2017; Jasiulionis 2018).

Using the Harm Scale at all 5 levels opens up the possibility of making use of preventive and curative toolkits used in other types of tissue damage like renal, brain or heart damage. It also allows us to make use of the insights from inflammation research, like inflammaging (Castellani et al. 2016).

 

How the Harm Scale can help.

In today’s wound care we only casually touch on the subject of tissue damage, because the most used solution for a wound is a dressing. The Harm Scale may help us in evaluating tissue in, under and around wounds.

Having some kind of definition of harm will improve communication on the complexities of the state tissues and cells are in. Acquiring a better understanding of the level of harm in tissue allows us for assessment and modalities to maintain homeostasis.

It may be helpful to notice that, though adapted, stressed, injured and damaged cells signal their harm state to their environment, the body can under- or over-react. If the patient is compromised these early signals may be missed, masking what is really happening. On the other hand, if injured, damaged and dead cells invoke a dramatic response, this in itself, may spiral out of control in a compromised patient.

The Harm Scale is also helpful in determining where to inject growth factors, miRNA’s and other interventions. Zones in which cells are barely surviving maybe not the best place for your intervention. You have to locate the proper location in, around and under the wound for a (maximal) effect (Berlanga et al. 2013).

Perhaps, if we start diagnosing and treating issues which reduce the body’s ability to repair or regenerate tissue, we might find better ways to predict and/or prevent wounds. A Harm Scale type assessment can be a useful addition to the toolbox.

And in the process, we will learn how to achieve much better results from our current treatment modalities.

© Harm Smit (2018)

Ps. It is really weird, writing a text like this when your name is … Harm.

 

References

Andreeva, Elena R., Margarita V. Lobanova, Olga O. Udartseva, and Ludmila B. Buravkova. 2015. “Response of Adipose Tissue-Derived Stromal Cells in Tissue-Related O2 Microenvironment to Short-Term Hypoxic Stress.” Cells Tissues Organs 200 (5): 307–15. https://doi.org/10.1159/000438921.

Ashcroft, Gillian S, Stuart J Mills, and Jason J Ashworth. 2002. “Ageing and Wound Healing.” Biogerontology 3 (6): 337–45. https://doi.org/5100237 [pii].

Berlanga, Jorge, D V M Ms, José I Fernández, Ernesto López Ms, Pedro a López, Amaurys Río, Carmen Valenzuela Ms, et al. 2013. “Heberprot-P: A Novel Product for Treating Advanced Diabetic Foot Ulcer.” Medic Review 15: 11–15. https://www.ncbi.nlm.nih.gov/pubmed/23396236

Black, Joyce M, Laura E Edsberg, Mona M Baharestani, Diane Langemo, Margaret Goldberg, Laurie McNichol, Janet Cuddigan, and National Pressure Ulcer Advisory Panel. 2011. “Pressure Ulcers: Avoidable or Unavoidable? Results of the National Pressure Ulcer Advisory Panel Consensus Conference.” Ostomy/Wound Management 57 (2): 24–37. http://www.ncbi.nlm.nih.gov/pubmed/21350270.

Bohovych, Iryna, and Oleh Khalimonchuk. 2016. “Sending Out an SOS: Mitochondria as a Signaling Hub.” Frontiers in Cell and Developmental Biology 4 (October): 109. https://doi.org/10.3389/fcell.2016.00109.

Castellani, Gastone C., Giulia Menichetti, Paolo Garagnani, Maria Giulia Bacalini, Chiara Pirazzini, Claudio Franceschi, Sebastiano Collino, et al. 2016. “Systems Medicine of Inflammaging.” Briefings in Bioinformatics 17 (3): 527–40. https://doi.org/10.1093/bib/bbv062.

Chen, Pei-Yu, Lingfeng Qin, Zhen W Zhuang, George Tellides, Irit Lax, Joseph Schlessinger, and Michael Simons. 2014. “The Docking Protein FRS2α Is a Critical Regulator of VEGF Receptors Signaling.” Proceedings of the National Academy of Sciences of the United States of America 111 (15): 5514–19. https://doi.org/10.1073/pnas.1404545111.

Erguler, Kamil, Myrtani Pieri, and Constantinos Deltas. 2013. “A Mathematical Model of the Unfolded Protein Stress Response Reveals the Decision Mechanism for Recovery, Adaptation and Apoptosis.” BMC Systems Biology 7: 16. https://doi.org/10.1186/1752-0509-7-16.

Franceschi, Claudio, Paolo Garagnani, Paolo Parini, Cristina Giuliani, and Aurelia Santoro. 2018. “Inflammaging: A New Immune–metabolic Viewpoint for Age-Related Diseases.” Nature Reviews Endocrinology. https://doi.org/10.1038/s41574-018-0059-4.

Fulop, Tamas, Anis Larbi, Gilles Dupuis, Aurélie Le Page, Eric H. Frost, Alan A. Cohen, Jacek M. Witkowski, and Claudio Franceschi. 2018. “Immunosenescence and Inflamm-Aging As Two Sides of the Same Coin: Friends or Foes?” Frontiers in Immunology 8 (January). https://doi.org/10.3389/fimmu.2017.01960.

Görlach, Agnes, Katharina Bertram, Sona Hudecova, and Olga Krizanova. 2015. “Calcium and ROS: A Mutual Interplay.” Redox Biology 6: 260–71. https://doi.org/10.1016/j.redox.2015.08.010.

Greaves, Nicholas S., Kevin J. Ashcroft, Mohamed Baguneid, and Ardeshir Bayat. 2013. “Current Understanding of Molecular and Cellular Mechanisms in Fibroplasia and Angiogenesis during Acute Wound Healing.” Journal of Dermatological Science 72 (3): 206–17. https://doi.org/10.1016/j.jdermsci.2013.07.008.

Horn, Adam, and Jyoti K. Jaiswal. 2018. “Cellular Mechanisms and Signals That Coordinate Plasma Membrane Repair.” Cellular and Molecular Life Sciences, no. 0123456789. https://doi.org/10.1007/s00018-018-2888-7.

Jagannathan, N. Suhas, and Lisa Tucker-Kellogg. 2016. “Membrane Permeability during Pressure Ulcer Formation: A Computational Model of Dynamic Competition between Cytoskeletal Damage and Repair.” Journal of Biomechanics 49 (8): 1311–20. https://doi.org/10.1016/j.jbiomech.2015.12.022.

Jasiulionis, Miriam G. 2018. “Abnormal Epigenetic Regulation of Immune System during Aging.” Frontiers in Immunology 9 (FEB): 1–14. https://doi.org/10.3389/fimmu.2018.00197.

Karch, Jason, and Jeffery D. Molkentin. 2015. “Regulated Necrotic Cell Death: The Passive Aggressive Side of Bax and Bak.” Circulation Research 116 (11): 1800–1809. https://doi.org/10.1161/CIRCRESAHA.116.305421.

Levine, Jeffrey M. 2016. “Skin Failure: An Emerging Concept.” Journal of the American Medical Directors Association 17 (7): 666–69. https://doi.org/10.1016/j.jamda.2016.03.014.

Maslanik, Thomas, Lucas Mahaffey, Kate Tannura, Lida Beninson, Benjamin N. Greenwood, and Monika Fleshner. 2013. “The Inflammasome and Danger Associated Molecular Patterns (DAMPs) Are Implicated in Cytokine and Chemokine Responses Following Stressor Exposure.” Brain, Behavior, and Immunity 28: 54–62. https://doi.org/10.1016/j.bbi.2012.10.014.

Nanduri, Jayasri, Gregg L. Semenza, and Nanduri R. Prabhakar. 2017. “Epigenetic Changes by DNA Methylation in Chronic and Intermittent Hypoxia.” American Journal of Physiology-Lung Cellular and Molecular Physiology 313 (6): L1096–1100. https://doi.org/10.1152/ajplung.00325.2017.

Nyström, Alexander, and Leena Bruckner-Tuderman. 2018. “Injury- and Inflammation-Driven Skin Fibrosis: The Paradigm of Epidermolysis Bullosa.” Matrix Biology, no. 2017: 1–14. https://doi.org/10.1016/j.matbio.2018.01.016.

Pakos‐Zebrucka, Karolina, Izabela Koryga, Katarzyna Mnich, Mila Ljujic, Afshin Samali, and Adrienne M Gorman. 2016. “The Integrated Stress Response.” EMBO Reports 17 (10): 1374–95. https://doi.org/10.15252/embr.201642195.

Pandolfi, Franco, Simona Altamura, Simona Frosali, and Pio Conti. 2016. “Key Role of DAMP in Inflammation, Cancer, and Tissue Repair.” Clinical Therapeutics 38 (5): 1017–28. https://doi.org/10.1016/j.clinthera.2016.02.028.

Park, Sangbum, David G. Gonzalez, Boris Guirao, Jonathan D. Boucher, Katie Cockburn, Edward D. Marsh, Kailin R. Mesa, et al. 2017. “Tissue-Scale Coordination of Cellular Behaviour Promotes Epidermal Wound Repair in Live Mice.” Nature Cell Biology 19 (2): 155–63. https://doi.org/10.1038/ncb3472.

Pichu, Sivakamasundari, Selvaraj Vimalraj, Jayalalitha Sathiyamoorthy, and Vijay Viswanathan. 2018. “Association of Hypoxia Inducible Factor-1 Alpha Exon 12 Mutation in Diabetic Patients with and without Diabetic Foot Ulcer.” International Journal of Biological Macromolecules 119: 833–37. https://doi.org/10.1016/j.ijbiomac.2018.08.011.

Rathinam, Vijay A.K., and Francis Ka Ming Chan. 2018. “Inflammasome, Inflammation, and Tissue Homeostasis.” Trends in Molecular Medicine xx (3): 1–15. https://doi.org/10.1016/j.molmed.2018.01.004.

San Miguel-Ruiz, José E., and José E. García-Arrarás. 2007. “Common Cellular Events Occur during Wound Healing and Organ Regeneration in the Sea Cucumber Holothuria Glaberrima.” BMC Developmental Biology 7: 1–19. https://doi.org/10.1186/1471-213X-7-115.

Smit, Harm Jaap. 2018. “A Five-Level Model for Wound Analysis and Treatment.” Wounds UK 14 (4): 24–29. https://www.wounds-uk.com/journals/issue/548/article-details/five-level-model-wound-analysis-and-treatment.

Tang, Sindy K Y, and Wallace F Marshall. 2017. “Self-Repairing Cells: How Single Cells Heal Membrane Ruptures and Restore Lost Structures.” Science (New York, N.Y.) 356 (6342): 1022–25. https://doi.org/10.1126/science.aam6496.

Whyte, J. L., a. a. Smith, and J. a. Helms. 2012. “Wnt Signaling and Injury Repair.” Cold Spring Harbor Perspectives in Biology 4 (8): a008078–a008078. https://doi.org/10.1101/cshperspect.a008078.

Ps. It is really weird, writing a text like this when your name is … Harm.

 

Level 0, Level 1, Level 2, Level 3, Level 4

Five levels, how to do it.

Comment

The original 5-level article was published in WoundsUK, you can find it here.

The five levels model provide you with a holistic checklist and allow you to map what is driving the events in any given wound.

Even though it is tempting to immediately jump in, that would lead to an almost incomprehensible list of factors to check. Perhaps it is easier to do it in an iterative way, where you have a very simple first pass and then, if you do not find a proper explanation for what is happening in the wound, you do further iterative passes. Depending on the findings of the previous pass(es), you zoom in and cast a finer net.

 

The basic idea behind a five-level wound analysis contains three ideas:

  1. You divide your problem into two new problems and keep doing that.
  2. Use the 5 levels as a checklist to see if you have missed something.
  3. If you do not find a solution,  redo 1 and 2 asking more questions and a larger checklist.

 

As any professional will know; wound healing is a complex field requiring knowledge, skills and tools on a variety of issues at all levels. The amount of knowledge, skills and tools needed increases at each round of questioning or pass.  Applying the 5-level system requires experience and a profound knowledge of tissue repair and regeneration. It requires understanding and ability to execute diagnostic tests. Finally, it requires knowledge of many comorbidities, lab values and medication.

The five levels are a result of 4 questions mapping your problem.

  1. Will this wound heal normal or not?
  2. If not will it heal by itself or will it not heal?
  3. If it will heal by itself, does it require advanced wound care or can it do without?
  4. If it will not heal by itself, is it because of organ system failure (usually vascular problems or repetitive damage) or because of cellular, molecular or genetic disorders?

By definition, any complex wound will have phenomena acting simultaneously on all levels. Having a full picture will provide a better understanding of the problems and possible remedies.

First pass, analysis

  • First question: will this wound heal normally, yes or no?
    • If yes, you have a level 0 wound. Take good care of the wound. It can be as simple as putting a bandage on; any bandage.
    • Chances it is a no, is when the wound exists for a longer period, your patient is over 65 years of age and/or has diabetic, dyslipidaemic, social, mobility, cardiovascular, neurological, immunologic or renal issues.
    • If no, the wound will heal not normally, leading to the
  • Second question: will this wound heal by itself or will this wound not heal by itself?
    • If yes, it is a level 1 or 2 wound. Consider minimal intervention, intervention means disruption of the normal life which can cause issues by itself.
    • A level 1 wound does not need special care.
    • Al level 2 wound requires wound care.
    • If no, the wound will not heal by itself, it is a level 3 or 4 wound, leading to.the
  • Third question: what is preventing the wound from healing?
    • Chances it is a wound resulting from arterial problems, venous problems or tissue damage due to repetitive forces. Figure out how grave the problem is and how to handle it.
    • Level 3 wounds require specialist care to solve the cause.
    • Level 4 wounds require specialist care. Currently, most level 4 diagnostic tools and interventions are in a research stage.
    • If needed appropriate, consider referring to a specialist able to solve or reduce the problem. It can be a specialised nurse, dermatologist, vascular surgeon, internal doctor or a podiatrist. Optimally all of them combined in a specialised wound care construction (not necessarily at one location).

 

First pass, checklist.

  • Check all 5 levels for issues which cause the wound or which may be not a direct cause for the wound but influence its trajectory. They are listed in the article.

 

First pass; act.

Select and apply your interventions.  Less is more.

 

First pass; review.

  • If the wound improves, redo the first pass for any changes or signals the wound might not improve on the next visit.
  • If the wound does not improve it is time for the second pass.
  • The goal of the second pass is to redo the first pass:
    • double check your assumptions.
    • have a closer look at the factors influencing the wound trajectory.

Having a closer look at the factors influencing the wound is important because, for instance, an infection can have a dramatic effect on the wound healing. But there are many more factors worth investigating. Causal and correlating factors have to be considered simultaneously. Most correlating factors are found on level 1. On the other levels, both causing and correlating factors can be found.

 

 

 

Second pass; analysis.

  • Is the cause well defined?
    • If yes, focus in the second pass on factors related to the cause. You can use the concise checklist for generating ideas.
  • Check level 1 for any causal or correlating factors which may point to problems on level 2, 3 and 4.
    • Consider other or more precise tests.
    • Identify possible tests and issues
  • Check level 2 for any causal or correlating factors which may point to problems on level 3 and 4.
    • Consider other or more precise tests.
    • Identify possible tests and issues, debride the wound thoroughly.
  • Check level 3 for any causal or correlating factors which may point to problems on level 3 and 4.
    • Consider other or more precise tests.
    • Identify possible tests and issues
  • Check level 4 for any causal or correlating factors which may point to problems on level 1, 2, 3 and 4.
    • Consider other or more precise tests. This includes a closer look at lab values.
    • Identify possible tests and issues.

 

  • Consider all issues and tests, look for connections which help explain what is going on.
    • Decide which test may improve your understanding or underpin possible interventions
    • Decide which intervention(s) will have the most impact on the wound trajectory.

 

Second pass; act.

  • Select and apply your tests and interventions, consider referring the patient.

 

Second pass, review

  • See if the wound has improved as a result of your interventions
  • If the wound improves, redo the first pass for any changes or signals the wound might not improve on the next visit.
  • If the wound does not improve, do a third pass by redoing the second pass.

 

Third pass

  • Is the cause well defined?
  • If yes, focus in the third pass on factors related to the cause.
  • But also consider marginal interventions, not aimed at resolving the cause but at improving the body’s ability to maintain, repair or regenerate tissue.
  • Check for patterns in issues, factors can be related or even appear in an interrelated fashion.
  • Try to learn from the previous pass(es).
  • Try to improve your knowledge, skills and tools by seeking options for discussion and learning.

 

Conclusion

It will be clear that even answering question one seems simple enough, it is not, this judgement requires quite some experience. But progress in the wound after one or two weeks will tell you if the judgement was justified. After running the analysis you will have a better idea of what is happening in your patient and the wound. This will help you in finding better ways to intervene. You will also learn what the limitations are in terms of available knowledge, experience and tools. Some are unavailable to you, others do not exist.

Even though this simple way is focussing on existing wounds, the insights resulting from it can also be used to predict and prevent wounds. Especially because harm may well exist prior to the formation of a wound or lesion, it is detectable and treatable.

Harm Smit

 

If you have any questions, do not hesitate to ask.

 

 

 

 

 

 

Level 0, Level 1, Level 2, Level 3, Level 4

An open letter to the Presidents of NPUAP and EPUAP

Comment

Open letter to the Presidents of NPUAP and EPUAP

(https://www.linkedin.com/pulse/open-letter-presidents-npuap-epuap-phil-strong )

Dear Madam Presidents,

We have been engaged and working within the ‘inbed’ * patient care sector for over 20 years; as health and social care practitioners, researchers and product developers. Today, we are deeply concerned that the NPUAP changes in ‘pressure injury’ terminology and ‘pressure ulcer’ classifications do not reflect the underlying causes of skin and tissue damage and that there has been selective use of the research from which the review was initiated.

We call on EPUAP during its review of the terminology and classifications to consider the views below and we suggest both NPUAP and its Staging Task Force to consider – in the light of the points below – whether their process really did produce the best outcome.

The pressure ulcer staging consensus is a further development of the original guidelines published in 1975. The updating processes in is described in the your first reference [1].  The procedure was divided in two parts, statements from which are backed by research and are a result of the consensus processes. However, it is not clear on what ground decisions were referred to either research or consensus. For example:

  • “Do not use DTPI to describe vascular, traumatic, neuropathic, or dermatologic conditions”

This is in conflict with the research findings where vascular disease is a causing factor of deep tissue injury[2–6].

  • The statement from the first reference in the document: “The staging system for pressure injury of the skin cannot be used to stage mucosal membrane pressure injury”.

In what way are mucosal membranes so different anatomically that not one of the proposed seven stages is applicable?

  • The literature selection process: “The CINAHL and MEDLINE electronic databases were searched individually; this search yielded 3652 articles. Task Force members completed title and abstract reviews, along with full text review. Two hundred forty-two articles were deemed relevant to the task at hand. In addition, references submitted by stakeholders and the public during the comment period were retrieved and reviewed for relevance to the goals of the Task Force.”

This statement Is biased due to the addition of stakeholder references for two reasons. Firstly, adding extra articles by stakeholders implies the original algorithm is sub optimal. Secondly, hand picking articles is biased by definition; especially since they added to the original 242 articles.

  • It appears the consulted professional and government or regulatory organisations are primarily nursing-based organisations rather than a balanced sample of stakeholders.

Position Statement 1: The diagnosis of a “pressure injury” does not mean that the health care provider(s) “caused” the injury.

Tissue damage associated with patients being cared for ‘inbed’ have been historically called pressure ulcers, pressure sores, bed sores/ulcers, decubitus ulcers and other names. The latest term being used is pressure injury. Since the word pressure is used to describe pressure, shear and tension depending on the direction of the forces involved, a more accurate description is ‘force-related tissue damage’ and so we will be using this term throughout this response.

The fact that an entire paragraph is dedicated to the word “injury”, indicates that the NPUAP foresees legal problems in the words used.

For example, anticipatory design of both products and practices must be used to enable tissue damage prevention when moving and stabilising a patient being cared for ‘inbed’ by:

  • creating the correct resting-surface/patient synergetic support layers
  • requiring the products/practices to work with gravity, rather than against it.
  • preventing tissue strain in static and moving situations

Position Statement 2: Some pressure injuries are unavoidable despite provision of evidence based care by the health care team.

The second position statement is on the avoid-ability of force-related tissue damage. However, NPUAP fails to provide qualitative or quantitative data on the number of an unavoidable force related injuries.

  • Whilst the references speak of unavoidable “pressure sores”, they do so in relation to the availability of high-quality care. This qualitative approach indicates a larger chance of developing an “unavoidable “ulcer yet no quantitative evidence is provided to substantiate this.
  • However well-intentioned the currently accepted and evidence-based ‘inbed’ care practices and products are, patients are still suffering. Some patients are more prone and of a higher risk to tissue damage (for example due to spinal cord injury or are of older age). However, there are those patients who don’t fit into these categories that are also prone and are at risk to tissue damage when the body’s threshold of resistance and/or ability to recover from damage, is exceeded.
  • The real issue of this statement is a cost-benefit analysis and indicates that the number of so-called unavoidable ulcers can be reduced even further with the use of advanced medical and nursing techniques. A casual glance at related medical fields like cardiology, nephrology and brain research shows there are many readily available diagnostic techniques and interventions to prevent and/or resolve forced-induced injuries. However, this raises the question whether society is able or willing to carry the cost involved with avoiding “the last ulcer”.

The second part of paragraph 2 points the eventual plaintiff towards asking if the best available care has been applied. Available care would include current available standard medical procedures which are applicable for wound care. It would be fair to say that the non-availability of these tools would and should not be accepted as a reasonable argument by a judge in 2017. This raises the question why non-availability of basic medical procedures is acceptable for a health care provider or any other medical professional.

The best available care would indicate that all the ways external forces can compromise a patient’s ‘inbed’ tissue integrity have been avoided. These would include:

  • Avoiding any unnecessary external forces that can be generated by how the patient is rested, how they are moved and how they are re-stabilised, both during and after their body mass has been re-orientated.
  • Avoiding harmful forces generated as a result of both inconsistent manual handling practices and the use of mechanical means that are working against gravity and trying to overcome the gravitational pull forces that are keeping the patient stable.
  • That these external forces are controlled in a way that any patient movement and stabilisation works with rather than against gravity. Allowing the body to move and be re-orientated safely, further compliments and supports the body’s innate homeostasis to keep the patients skin and tissues within its natural threshold of resistance and repair. Thereby, maintaining its optimum tissue integrity.

NPUAP and EPUAP needs to recognise that new research is available to show that the best available care would also include managing the one major external factor in the patient’s environment in all ‘inbed’ tissue damage occurrences: the patient interfaces with a resting/support surface.

Position Statement 3: The numerical staging system does NOT imply linear progression of pressure injuries from Stage 1 through Stage 4, nor does it imply healing from Stage 4 through Stage 1.

The fact that the third position statement actually states that there is no logical connection between the stages in the consensus document is interesting because the four-stage wound healing process is exactly describing healing from stage 4 to stage 1 (Wikipedia).

By stating this, NPUAP appears to be concluding that each stage has its own specific aetiology and that underlying pathology may be a connection between the stages. We agree and challenge NPUAP and EPUAP that force related tissue injuries should therefore be staged/classified based on the underlying pathology.

Position Statement 4: The NPUAP Staging System classifies pressure injuries based on the type of tissue loss that can be visualized or directly palpated.

The fourth position statement is identifying the exact problem. The classification is based on type of tissue loss that can be visualised or directly palpated. Not only is the classification superficial, it also denies underlying pathology, for example, why is a mucosal force related injury unstageable?

Imagine what the clinical relevance a classification based on type of tissue that can be visualised directly palpated for any type of wound would be? It is immediately clear that this classification is descriptive but bears no relation to the aetiology or possible interventions and is therefore not clinically relevant. Categorising a wound as unstageable can, under circumstances, be considered evidence of neglect due to lack of debridement.

Classical diagnostic tools such medication (STOPP/START) screening [7,8], lab values[9,10], biomarkers[11,12], tissue sampling[13,14] and imaging[15,16] are not mentioned in the guidelines. Advanced diagnostic tools such as (epi) genetic[13,17–19], proteomic[20] and metabolomic[21,22] screening are also not mentioned.

Position Statement 5: The pressure injury may be more extensive than initially apparent. The wound base and surrounding tissue should be assessed for variations in sensation, temperature, firmness, color and any expression of drainage from surrounding tissues when palpated.

Position statement five is claiming that there is more than meets the eye. However, these findings are to be noted but are neither qualified, quantified or part of the staging process. This is a very true statement. There are at least 22 internal factors that can contribute to the loss of optimum tissue integrity i.e. that can cause/contribute to both a reduction in the tissue resistance threshold and/or a reduction in tissue recovery. These include generic factors (such as stress), systematic factors, structural factors and local factors.

It would be better therefore, if statement 5 would be reframed to diagnosis of pre-clinical events leading to stress, injury and damage at a molecular, cellular, tissue organ and organism level. That would be a nice starting point for bringing wound care to this century.

Position Statement 6: Deep Tissue Pressure Injury (DTPI) may evolve into a full thickness wound despite optimal care.

Position statement six is actually the same as position statement five. In court, however, this would make a difference. Interesting statements such as NPUAP’s “Off-loading the area still offers the best chance for tissue that is ischemic or injured, but not infarcted” is in conflict with medical ethics where chance should be avoided at all times. You may consider: “diagnostic tools for assessing and grading DTI, endothelial status and reperfusion injury are being investigated”.

Position Statement 7: Any pressure injury should be treated in accordance with current evidence-based practices and monitored closely for changes that require re-evaluation of treatment strategies.

Position statement seven is correct. However, guidelines do not allow proper execution of the statement. Close monitoring for changes that require re-evaluation of treatment strategies based on the six stages is dangerous and ethically questionable. NPUAP appears to realise this because they provide examples of deep tissue injury developing into a stage IV injury. However, having to explain this implies that the current guidelines are not sufficient for prescribing and handling the events related to force related injuries.

However, we challenge NPUAP and EPUAP to promote that force-related tissue damage prediction and  prevention rather than treatment is always the preferred approach to maintaining optimum tissue integrity. Evidence-based care should be demonstrating that

  • The patient’s ‘inbed’ environment provides the optimal synergetic resting support surface layers including the bed frame, bed mattress, bed mattress cover, sheets, any incontinence slide, the patient’s clothing, the patient’s skin and tissue
  • That external forces are controlled in a way that any patient movement and stabilisation works with rather than against gravity to maintain optimum tissue integrity. i.e. allows the body to move and be re-orientated safely, by allowing the body’s innate homeostasis to keep the patients skin and tissues within its natural threshold of resistance and repair.
  • The care provided allows the body to protects and repairs its internal environment by using both physiological and biomechanical mechanisms (tensegrity) and homoeostasis to maintain optimum tissue integrity.

Conclusion

The NPUAP document on current staging of pressure related injuries is superficial and does not make use of current available knowledge and techniques. It does not measure up to modern standards of care.  The fact that the methodology used is entirely ignoring underlying pathology in a way that it would be criminal to use pressure injury staging methodology on, for instance, a leg ulcer.

The claim that,” The NPUAP has provided the gold standard for diagnosis and classification of pressure injuries for nearly three decades, and counting.” Is therefore not entirely correct.

The document focuses solely on treatment rather than prevention:

  • It does not address the gap of what should be and what is available for both the caregiver and the care receiver.
  • It does not promote the best-practice for designing out unsafe practice (higher-level hierarchy risk control),
  • It does not eliminate the use of unsuitable products
  • It continues to rely on monitoring compliance
  • It overlooks the designing-in prevention and a safer care trajectory

By taking this safer, combined ergonomic and biomechanical approach, NPUAP and EPUAP can make a real difference to the occurrence of force-related tissue damage and remove the risks to both carers and patients associated with ‘inbed’ care and positioning.

NPUAP and EPUAP need to promote the evaluation and use of technology to fill in the gaps for inconsistencies in patient care and should give the patient and carer what they need:

  • Patients need a safe environment (social or hospital) to enhance their care.
  • Whilst being cared for ‘inbed’, they need to avoid tissue damage.
  • They require effective infection control that prevents them contracting other infections whilst receiving their care.
  • They need to be at an optimum temperature.
  • Nurses and carers need products that are intuitive and easy to use, and are compliant with safe patient care expectations and regulation.

Signed:

Phil Strong SRN RNMS Cert. Ed CT NT, Managing Director & Product Designer, Ergo-Ike Ltd, Associate Member of the CIEHF

Harm J Smit MSc, Wound Care Biologist, BioMedServ

*    By “inbed” we mean: any resting /support surface facility which enables the patient to receive care, support and movement. This can include for example: beds (domestic/clinical), theatre tables, theatre trolleys, gurneys and X-ray tables, chairs and wheelchairs. Although this list is not exhaustive.

References

http://www.npuap.org/wp-content/uploads/2012/01/NPUAP-Position-Statement-on-Staging-Jan-2017.pdf

1           Edsberg LE, Black JM, Goldberg M, et al. Revised National Pressure Ulcer Advisory Panel Pressure Injury Staging System: Revised Pressure Injury Staging System. J wound, ostomy, Cont Nurs Off Publ Wound, Ostomy Cont Nurses Soc2016;43:585–97. doi:10.1097/WON.0000000000000281

2           Farid KJ. Applying observations from forensic science to understanding the development of pressure ulcers. Ostomy Wound Manage 2007;53:26–8, 30, 32 passim.http://www.ncbi.nlm.nih.gov/pubmed/17449915

3           Mekkes JR, Pasch MC, Meijs M, et al. Acquired arteriovenous malformation induced by pressure: a case report. Vasc Med 2003;8:201–2. doi:10.1191/1358863x03vm497cr

4           Nagel T, Loerakker S, Oomens CWJ. A theoretical model to study the effects of cellular stiffening on the damage evolution in deep tissue injury. Comput Methods Biomech Biomed Engin 2009;12:585–97. doi:10.1080/10255840902788603

5           Loerakker S, Solis LR, Bader DL, et al. How does muscle stiffness affect the internal deformations within the soft tissue layers of the buttocks under constant loading? Comput Methods Biomech Biomed Engin 2013;16:520–9. doi:10.1080/10255842.2011.627682

6           Solis LR, Liggins AB, Seres P, et al. Distribution of internal strains around bony prominences in pigs. Ann Biomed Eng 2012;40:1721–39. doi:10.1007/s10439-012-0539-y

7           Hill-Taylor B, Walsh KA, Stewart S, et al. Effectiveness of the STOPP/START (Screening Tool of Older Persons’ potentially inappropriate Prescriptions/Screening Tool to Alert doctors to the Right Treatment) criteria: Systematic review and meta-analysis of randomized controlled studies. J Clin Pharm Ther 2016;41:158–69. doi:10.1111/jcpt.12372

8           Levine JM. The Effect of Oral Medication on Wound Healing. Adv Skin Wound Care 2017;30:137–42. doi:10.1097/01.ASW.0000512112.60254.28

9           Gould LJ, Olney CM, Nichols JS, et al. Spinal Cord Injury survey to determine pressure ulcer vulnerability in the outpatient population. Med Hypotheses2014;83:552–8. doi:10.1016/j.mehy.2014.08.027

10         Callahan D, Keeley J, Alipour H, et al. Predictors of Severity in Diabetic Foot Infections. Ann Vasc Surg Published Online First: 2015. doi:10.1016/j.avsg.2016.01.003

11         Lindley LE, Stojadinovic O, Pastar I, et al. Biology and Biomarkers for Wound Healing. Plast Reconstr Surg 2016;138:18S–28S. doi:10.1097/PRS.0000000000002682

12         Tegl G, Schiffer D, Sigl E, et al. Biomarkers for infection: enzymes, microbes, and metabolites. Appl Microbiol Biotechnol 2015;99:4595–614. doi:10.1007/s00253-015-6637-7

13         Januszyk M, Gurtner GC. High-Throughput Single-Cell Analysis for Wound Healing Applications. Adv wound care 2013;2:457–69. doi:10.1089/wound.2012.0395

14         Voegeli D, Lwaleed B. Back to basics: histological, microbiological and biochemical sampling in wound care. J Wound Care 2013;22:650–2, 654. doi:10.12968/jowc.2013.22.11.650

15         Stekelenburg A, Strijkers GJ, Parusel H, et al. Role of ischemia and deformation in the onset of compression-induced deep tissue injury: MRI-based studies in a rat model. J Appl Physiol 2007;102:2002–11. doi:10.1152/japplphysiol.01115.2006

16         Linder-Ganz E, Gefen A. Stress analyses coupled with damage laws to determine biomechanical risk factors for deep tissue injury during sitting. J Biomech Eng 2009;131:11003. doi:10.1115/1.3005195

17         Anderson AE, Galko MJ. Rapid clearance of epigenetic protein reporters from wound edge cells in Drosophila larvae does not depend on the JNK or PDGFR/VEGFR signaling pathways. Regeneration 2014;1:11–25. doi:10.1002/reg2.12

18         Zhang S, Duan E. Epigenetic regulations on skin wound healing: implications from current researches. Ann Transl Med 2015;3:227. doi:10.3978/j.issn.2305-5839.2015.07.12

19         Cutroneo KR, Chiu JF. Comparison and evaluation of gene therapy and epigenetic approaches for wound healing. Wound Repair Regen 2000;8:494–502. doi:10.1046/j.1524-475X.2000.00494.x

20         Förster Y, Schmidt JR, Wissenbach DK, et al. Microdialysis sampling from wound fluids enables quantitative assessment of cytokines, proteins, and metabolites reveals bone defect-specific molecular profiles. PLoS One 2016;11:1–24. doi:10.1371/journal.pone.0159580

21         Zang T, Broszczak DA, Broadbent JA, et al. The biochemistry of blister fluid from pediatric burn injuries: proteomics and metabolomics aspects. Expert Rev Proteomics 2016;13:35–53. doi:10.1586/14789450.2016.1122528

22         Kalkhof S, Förster Y, Schmidt J, et al. Proteomics and Metabolomics for In Situ Monitoring of Wound Healing. Biomed Res Int 2014;2014:1–12. doi:10.1155/2014/934848

 

 

 

https://www.linkedin.com/pulse/open-letter-presidents-npuap-epuap-phil-strong

 

Level 1, Level 2

3 reasons, marine sponges are interesting for wound healing.

Comment

Looking at a simpler model of something as complex as wound healing usually provides interesting insights. Sponges are animals with a very simple structure and are known for their regenerating capacity. The reason they are interesting are:

  1. obvious similarities between sponge and human response to injury.
  2. not so obvious similarities between sponge and human response to injury.
  3. clues what to look for in human response to injury.

This tells us something about the basic events in wound healing. Translating these findings to human wound healing is tempting, but should be considered with caution.

Sponges are animals with a very simple structure and are known for their regenerating capacity.

The sponge consists of layers of pinacocytes and choanocytes which resemble the epithelium of more complex animals. This layer covers a gel type body wherein the cells move freely. They do not have a nervous system but are nevertheless able to respond to be environment by means of neurotransmitters which guides movement. (https://en.wikipedia.org/wiki/Sponge) A sponge actually has two types of cells which play a role in regeneration. Cells which provide matrix (collencytes) and cells which proliferate into other cells (archeocytes).

sponge2

Structurally a sponge has a primitive version of an epidermis, a dermis and a skeleton and its regeneration system runs roughly on two types of cells. The similarities are striking1,2,3,4.

The obvious similarity between sponge and human response to injury.

  • Age matters, tissue age limits regeneration. Young tissue regenerates faster.
  • Genotype matters, regeneration varies among genetically distinct sponges.
  • Wound size matters, larger wounds heal slower than small wounds.
  • Wound depth matters, as more deep tissue and skeletal elements are involved wounds heal slower.
  • Wound location matters, distal wounds heal faster than wounds on the base of a sponge. In general, if the transport of material for regeneration is easy, wounds heal faster.
  • Water temperature matters, in warmer water the metabolism runs faster, and thus regeneration is faster.
  • Food availability, if more nutrients are available, there are also more nutrients available for regeneration.
  • Sedimentation matters, if more sedimentation falls into the wound, more energy is needed to remove it and this energy is not available for regeneration.
  • Disturbance history, previously injured sponges are more likely to be damaged.

 

The not so obvious similarity between sponge and human response to injury.

  • Post regeneration strategies are aimed at closing the “skin” as fast as possible to prevent fouling, the marine version of a biofilm.
  • Wound perimeter matters, a circular wound heals faster than a linear wound of the same surface area.
  • Energy balance is important, regeneration draws energy from the organism. Actually, there is a competition for resources between regeneration and other functions of life.
  • Size matters, larger sponges generate better, simply because they have a larger metabolic capacity.

 

Clues what to look for in human response to injury.

  • The G1 checkpoint; reduced growth of cells adjacent to the wound be due to cells being halted in their progression through the cell cycle as a result of insufficient energy to progress past the G1 checkpoint in eukaryotic cell division.
  • Distance; cell proliferation is lower at 1 cm from the wound compared to cell proliferation 3 cm from the wound.

 

And the sponge is only one of several model organisms for wound care.

Have fun.

#proudtobeabiologist

 

 

Refs: these articles are cited “loosely”.

 

  1. Henry, L. A. & Hart, M. Regeneration from injury and resource allocation in sponges and corals – A review. Int. Rev. Hydrobiol. 90, 125–158 (2005).
  2. Alexander, B. E. et al. Cell kinetics during regeneration in the sponge Halisarca caerulea : how local is the response to tissue damage? PeerJ 3, e820 (2015).
  3. Wulff, J. Regeneration of sponges in ecological context: Is regeneration an integral part of life history and morphological strategies? Integr. Comp. Biol. 50, 494–505 (2010).
  4. Hoppe, W. F. Reproductive patterns in three species of large coral reef sponges. Coral Reefs 7, 45–50 (1988).
Level 2

Everything you always wanted to know about biofilms but …

Comment

The question: “Is there a biofilm in the wound?” reveals it is still hard to understand biofilms for wound care professionals.

To ask this simple question is uncovering a knowledge gap.

There is no such thing as A biofilm. Her are two thoughts which may enlighten you.

  1. most microbes are able to produce biofilms.
  2. If a biofilm will increase their chance of survival they will produce one, if it does not they will not.

This immediately implies that every imaginable combination of species and numbers of each species will have an influence on the biofilm.

This also implies no two biofilms are the same, stay the same or that there is only one biofilm in the wound. There will be deep tissue biofilms and superficial biofilms. The whole combination of microbes and biofilms may be more comparable to a city than a glass house. Its appearance will depend on the size of the city and the number of different inhabitants and their needs.

Luckily even biofilms will have to follow some natural or mathematical rules and therefore the number of clinical relevant biofilms may be not infinite.

Not all biofilms are bad either. As we know, every nine out of ten cells in your body are not really you. There are biofilms in the intestine which are essential for a proper functioning body. They are so important the appendix functions as a special reservoir for spare biofilms in the case something goes wrong.

In the wound it is very well imaginable that a biofilm has a ECM like function. So presumably not all biofilms are bad.

So in the end, the question is not if there is a biofilm in the wound, the question is if there is a (good or bad) clinical relevant microbiome in the wound.

For more information: Elisabeth Bik has a nice blog on biofilms and the microbiome. Here you may find this nice example of biofilm dynamics.

https://npjbiofilmscommunity.nature.com/users/6679-elisabeth-m-bik/posts/3967-the-biofilm-hunger-games

 

Level 2

Basic steps in wound care: debridement

Comment

Debridement is considered a cornerstone in wound care. Common sense dictates only a clean wound heals. Observing animals lick their wounds adds to this.
It remains the question if and how debridement translates to the clinical practice.

IF: Wilcox checked this in 2013. In  a study of 154 644 patients with 312 744 wounds of all causes debridement were checked as a parameter.  He found the following. The more frequent the debridements, the better the healing outcome. Although limited by retrospective data, this study’s strength was the analysis of the largest wound data set to date.

m_doi130027f5

The bias is in the quality of the data where you do not know if debridement was the only parameter which differs between the groups, however this is offset by “n”, the sheer number of subjects. They explain further in the article.

The best way to debride is to surgical debridement were all dead material is removed using scalpels, forceps, scissors etcetera. If sharp debridement is not possible alternative methods may be used.

It is important to also keep biofilms in mind, they may be not visible. In a non-healing wound it should be removed, in a healing wound it may be wise to leave it in situ. Common sense dictates removing is more damaging than leaving it in situ.

Frequency of Debridements and Time to Heal: A Retrospective Cohort Study of 312 744 Wounds.  James R. Wilcox, RN ; Marissa J. Carter, PhD, MA; Scott Covington, MD
http://archderm.jamanetwork.com/article.aspx?articleid=1720508

HOW: debridement works seems simple but leads to other questions. It works because you remove debris and other causes of infection in the wound.You also help the body removing unwanted material.  But if you rephrase the answer to it works because you remove barriers to healing you may have to take a second look. Not only debris itself but also tissue directly adjacent to the wound may be a barrier to healing. This leads to the question: which living tissue is a barrier to healing. ..the road to debridement 2.0

Debridement 2.0
Sometimes it may make sense to debride the wound to the point where you remove some living tissue as well. For instance in burns. Presumably in the near future we discover other instances where removing living tissue. Al in all the affected area is usually larger than the wound itself. This is often overlooked in research. Subjects: burn wounds, but also scar tissue and, but we do not know that, metabolically impaired tissue. This is one of the almost uncharted areas in wound care.

nihms235813f4In some cases a closer observation will reveal which “visible” healthy tissue is compromised. This allows to identify and remove more damaged tissue. In the future, this may speed up healing.

Using Gene Transcription Patterns (Bar Coding Scans) to Guide Wound Debridement and Healing
Marjana Tomic-Canic, PhD, RN, Director, Elizabeth A. Ayello, PhD, RN, ACNS-BC, ETN, FAPWCA, FAAN, President, Olivera Stojadinovic, MD, Instructor, Michael S. Golinko, MD, MA, General Surgery Resident, and Harold Brem, MD, Chief   http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2948232/
and
Surgical wound debridement sequentially characterized in a porcine burn model with multispectral imaging.
King DR, Li W, Squiers JJ, Mohan R, Sellke E, Mo W, Zhang X, Fan W, DiMaio JM, Thatcher JE. http://www.ncbi.nlm.nih.gov/pubmed/26073358

 

 

 

Take away:

  1. Proper debriding makes sense.
  2. Proper means clean but also by using the right knowledge and skills.
  3. And thinking on something as simple a removing stuff from a wound may bring progress.
  4. Agree to disagree…discussion improves wound care

Here is a lecture on debridement.

Level 2

Diagnosis of wound infections

Comment

 

Brilliant lecture by Benjamin Lipsky on diagnosis of wound infections. It appears we have no tools (yet) to really analyse what is going on in the wound. This means we also do not understand exactly what the role of each bacterium is in wound healing.
This lecture rightfully  increases your uncertainty towards wound infections.

My concluson is that anyone who appears confident while making a comment on wound infection should be treated with care 🙂

Level 2, Level 4

Microbiome; the shepherd and the flock

Comment

Many bacteria in the wound are unknown to us. This is why they call it dark matter in the article below. We know it is there but cannot see it. The entire system in a wound bed is called the microbiome, it may be compared to a city in its diversity and complexity. We are now beginning to understand what this means to wound healing. In a healthy subject, the microbiome may well be part of the normal wound healing process whereas in a compromised wound it may have a very different role.

One reason for looking into this is pure curiosity. Another may be to discover new bacteria and new ways bacteria and human cells live together in the wound. The last and more intriguing reason is S aureus and P. aeruginosa may be just the flock while we still have to find the shepherd. Like P. gingivalis is a shepherd in gingivitis. In the article of Hajishengallis it is described that a les abundant microbe is actually controlling the mouth microbiome like a shepherd controls a flock. Metagenomic research may bring us something, if only if S.aureus and P.aeruginosa are flock or shepherd. Hopefully, it will unravel the systems in the wound which may be more important that the individual cells. (meaning the system describes roles to be fulfilled and which organism actually fulfills it is less important.) Anyway, let us hope we are abele to discern between detrimental microbes and microbes which have a more positive role in wound healing.

In the end, this type of research will allow us to decide when and how to remove the microbiome or when it makes sense to take a more probiotic approach.

  1. http://www.nature.com/news/mining-the-microbial-dark-matter-1.17774
  2. Hajishengallis, G. Lamont, R. J. Breaking bad: Manipulation of the host response by Porphyromonas gingivalis.  Eur. J. Immunol. 44.2.1521-4141  http://dx.doi.org/10.1002/eji.201344202
  3. http://www.nature.com/nrmicro/posters/metagenomics/posters.pdf
  4. https://microbewiki.kenyon.edu/index.php/Pseudomonas_aeruginosa_infection
  5. http://www.nature.com/nrmicro/posters/pseudomonas/posters.pdf
Level 1, Level 2

Diabetic Foot Complications

Comment

As we read through the literature we get a view on the severity of diabetic foot ulcerations. Copy/pasting from the articles below we get the following picture.

Chronic nonhealing neuropathic foot ulcers occur in approximately 15% of patients with diabetes. In 2011, there were an estimated 366,000,000 adults with diabetes. Worldwide global projections indicate that this figure will increase to 552,000,000 by 2030. It is estimated (2003) that 24.4% of the total health care expenditure among diabetic population is related to foot complications and the total cost of treating diabetic foot complications is approaching 11 billion USD in USA and 456 million USD in UK. Wound care in general costs 2-5% of your national health expenditure. (billions) Hospital-based studies have shown that mortality rates in individuals with diabetic foot ulcers are about twice those observed in individuals with diabetes without foot ulcers.

To sum it up, diabetic foot lesions involve a lot of people, a lot of suffering, a lot of money and time and they “have legs for breakfast” and may “kill you overnight”.

So what do we do about it… not much!

Despite the effort of many dedicated clinicians who, we cannot thank them enough, take up the Sisyphean task of point out the importance of prevention, monitoring and treatment we still are stuck with an ever increasing number of diabetics suffering from ulcers. Some policy makers even cut cost on this issue with dramatic effects.  The number of diabetic foot ulcers can be reduced significantly. Therefore it is today still shocking to see how many “chronic” ulcers heal within 7 weeks in the right hands.

Just to make sure; anyone dealing with diabetic ulcers is supposed to know and apply the national and international guidelines;  http://iwgdf.org/

Make no mistake, diabetic ulcers can be very hard to treat for many reasons and some will never heal. The problems “behind the ulcers” are daunting and need to be solved. Nevertheless, as often, the first steps to treat a foot ulcus are straightforward.

First and best is to make sure someone who has a diabetic foot wound gets basic wound care. It is not rocket science but for some reason the average medical professional is having a tough time to set up prevention and often is not able to deliver level 1 and 2 wound care.

What is level 1 and 2 wound care?

Level 1 and 2 wound care are on both sides of the wound healing equilibrium.

A healthy person can handle most wounds without much ado (Vigor), level 1 is aimed at increasing Vigor. If the wound is large or complicated the body will need help (Severity). Level 2 is aimed at reducing severity.

Ergo, the equilibrium:        Balans-EN

Level 1 is to make sure the patient has the best possible health under the circumstances: 1. take care of diabetes regulation 2. remove stress (and get some sleep) 3. eat properly and 4 mobilize as much as you can.

Level 2 is debride the wound at least twice a week (debriding = remove anything which is not living cells (debriding is not mopping a wound with a gauze)) and secondly apply enough pressure to the wound to handle oedema. That is it.

If you do not know how to debride a wound properly or are not able to; transfer the patient to someone who is better able to treat the ulcer.

If the wound does not start healing in 2 weeks, step up your effort or even better, transfer the patient to someone who is better able to treat the ulcer.

Once healed, step up prevention and monitoring to the max.

 

http://www.jci.org/articles/view/32169/pdf

http://poi.sagepub.com/content/39/1/29.abstract  (Thank you Lian)

http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0124446

http://care.diabetesjournals.org/content/37/9/e196.extract

(Debriding is a medical intervention which only skilled medical professionals are allowed to do. A non-healing wound has to be seen by a specialised doctor or nurse.)