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  • What does a Dermal Clinician or therapist get paid? A snippet of the ASDC guidance document.

    With a national award rate existing for Beauty Therapists, but not for Dermal Clinicians, this is a question asked constantly throughout the Beauty and Aesthetics industry. The Australian Society of Dermal Clinicians often receive queries from Dermal Clinicians, Dermal Therapists, employer groups and those thinking of entering into the profession particularly around the questions "What will I/should I get paid?" After extensive research and legal counsel, ASDC can now provide some much-needed clarity on this topic. To do so, we have put together an extensive guidance article, which includes information regarding the issues or considerations that may be involved in the determination of what 'a fair wage' is to inform workplace negotiations and discussions. There is a lot to consider when it comes to establishing a Dermal Therapist or Clinician’s salary, and the full guidance article covers a lengthy discussion of award/s members may be covered by as well as the implications that employment setting, and job description or duties can have when determining whether you will be paid under a particular award. Also provided in the piece is information about the industry average according to ASDC commissioned industry research and how this compares to other allied and health professions. As the peak professional body representing Dermal Clinicians and Therapists, the ASDC aim to provide general guidance and information regarding industry pay rates based on previous data collected - in addition to expertly-curated content that will benefit our members. Therefore, this pay guidance in its entirety will be reserved for our ASDC financial members (including student members). If you aren’t already a member, we highly encourage you to join us in order to receive this type of tailored information in addition to other amazing benefits such as career opportunities, exclusive connections with peers, and discounted education and industry events. If you’d like a sneak peak of the pay guidance piece, here is a snapshot of the average pay rates we’ve uncovered: Industry Average Pay Rates for the Dermal Therapy Sector In 2017, the average pay rate for those working in the dermal therapy sector was $33-35 per hour. There was variance based on the clinical setting with those in medical settings being paid a higher rate than those working in beauty settings. The study had 82 respondents, 61.33% with a bachelor degree and 13.33% with an advanced diploma in Dermal Therapy. The remaining percentage either had no formal qualification, had trained overseas or identified as having a qualification other than dermal therapy-specific qualifications such as nurses working in the dermal therapy sector. Other findings reported in this survey of industry pay rates included: · Increased years of experience resulted in higher rates of pay. It was reported that those with several years of experience were able to earn up to $45 per hour in some work settings. · Postgraduate study also related to a higher average pay rate. · At the time this research was carried out, respondents reported that pay increases were expected in the next 12 months but didn't necessarily occur on an annual basis. The ASDC aim to update this information with another survey over the next twelve months and will provide this information when available on the member portal via the ASDC website. This is of course only one tiny piece of the puzzle. Other considerations include how your Dermal Clinicians affect your insurance costs (they could lower your rates), can you use their knowledge in order to facilitate educational programs and events in your business, the overall quality of patient care they provide, and how they may be operating within the scopes of practice of multiple professions to bring you added value as an employee. If you are an ASDC member, you can access the full guidance article through your member portal. You can find out more about becoming a member at www.dermalclinicians.com.au

  • Unraveling the mysteries of the lymphatic system.

    For many decades the lymphatic system was the forgotten circulatory system. Currently the study of Lymphology is experiencing its Renaissance. More has been learned about the lymphatic system in the last 5-15 years than in the 100 years before. With advances in lymphatic imaging, DNA assays, inflammatory and molecular markers we begin to unravel and understand this complex and amazing system. Emerging evidence demonstrates the vital role the lymphatic system has to play in our health and the onset of disease including obesity, arteriosclerosis, autoimmune diseases, problems with wound healing and cancer. Following is a snap shot from our full scientific review... head over to our blog for the full article. Starling's & Fick's Law: Theories Revisited Starling's Law and Fick's Law modelled the movement of fluid and solutes between cardiovascular capillaries and the interstitium based on hydrostatic and oncotic pressure gradients. Past Understanding: 8 litres of fluid filtration occurred at the capillary bed over a 24 hour period approximately 90% reabsorbed into the venous network (Tortora, 2014). 10% picked up by initial lymphatic vessels. Present Understanding Recent research indicates all interstitial fluid (100%) under normal conditions that leaves the cardiovascular system at the capillary bed is returned through the lymphatic system (Adamczyk et al, 2016). Approximately 40% of the fluid within lymphatic vessels (Lymphatic load) is returned to the venous circulation through veins connected to lymph nodes (Cooper et al, 2016; Huxley & Scallan, 2011; Keast et al, 2014). New understanding into forces effecting contractile function. Lymphangions are the intrinisic (active) pump inside lymphatic vessels. These are small muscular units found within larger collecting lymphatic vessels The lymphatic system also relies on pressure gradients within the blind ended initial lymphatic vessels, which draw fluid into them like straws. The negative pressure within these vessels aids in movement of fluid deeper into the network of larger vessels. Once reaching the collecting vessels positive pressure is created by lymphangions with their synchronised peristaltic contractions. The pulse rate of the lymphatic system is about 5-8 beats per minute with a systolic pressure of 3-5 mmHg and diastolic pressure of 0-1mmHg (Chikly, 2017). This makes the pumping of the lymphatics undetectable to feel or observe without imaging techniques. As seen in the video below using tracer dyes and near infrared light provide real time insight into how this system performs in health and disease. This video below demonstrates the bolus of lymphatic fluid as it moves from one lymphangion unit to the next within deeper collecting vessels. Emerging Evidence Animal studies have established that lymphangion muscular structure is unique as it has properties of both smooth and striated muscle. This unique combination allows for lymphangions to have similar alterations in contractile activity and tone as vascular smooth muscle with stimulus such as pressure changes, vasoactive substances, mechanical and neuro-modulatory factors. However the striated muscle allow for rapid changes in contractile force and pace in response to pressure on the walls of lymphatic vessels created by changes in fluid load (Chakraborty et al, 2015). Lymphangions can alter the frequency or strength of contractions. Lymphangions alter their function in response to how quickly their muscular segments are filling with fluid as well as how much fluid there is inside the vessel or in the interstitium. This is detected by pressure or stretch exerted on the muscular walls (Chakraborty et al, 2015; Huxley & Scallan, 2011; Gashev et al, 2010). Acute Inflammation, Chronic Inflammation and Oedema: What's the connection? The Lymphatic system exhibits great plasticity to remodel itself. Evidence reports on the important role the lymphatic system has in resolving acute inflammation through activation of lymphatic vessels. This process is mediated by the interplay between many chemical mediators as well as mechanical stresses. These forces influence lymphatic vessel hyper permeability, hyperplasia, lymphangiogenesis, involution and remodelling. Nitric Oxide (NO), VEGF-A along with VEGFR-3, VEGF-C and VEGF-D are some of the cytokines that mediate this process. Along with mechanical stresses on the tissue caused by the fluid itself. (Goldman, et al, 2007; Huggenberger et al, 2011; Adamczyk et al, 2016). Emerging Evidence Immediately after injury there is a temporary lymphatic insufficiency caused by lymphangion reflux (inefficient filling and emptying) which appears to be mediated by NO. Interestingly for the first 4 hours these effects are systemic. This is hypothesised to facilitate immune functions ensuring that pathogens do not move beyond the regional lymphatics and lymph nodes. Decreased contractile activity local to the injury is observed for up to 3 days with normal function returning by 7 days post injury. These studies did note that there are anatomical variations in these responses and that these observations should be investigated in more depth. Increased density of lymphatic vascular networks through lympangiogenesis and hyperplasia are not observed during the first 7 days, however the vessels in the area are dilated, and hyper permeable. This points to theories that acute inflammation that resolves after 7-10 days is mostly facilitated by vascular repair and remodelling of existing lymphatic architecture as well as return of normal contractile function (Lachance et al, 2013; Aldrich & Sevick-Muraca, 2013). Chronic inflammation and oedema is a self perpetuating cycle that can occur if acute inflammation and oedema fail to resolve. The effects of a lymphatic system under stress can also have systemic effects impacting on other organs and tissues. This has been observed in links between lymphatic dysfunction and chronic inflammatory skin conditions as well as inflammatory bowel disease, rheumatoid arthritis, obesity, and asthma (Huggenberger & Detmar, 2011; Varricchi et al, 2015). Fluid with high protein content and pro-inflammatory cell and chemical content will result in continued oncotic pull of fluid to the area. Over time the development of fibrosis (scarring) can also trap fluid within the area. Lymphatic vessel contractile function is further affected by the presence of pro-inflammatory cells and mediators resulting in decreased effectiveness or cessation of lymphangion pumping altogether (Chakraborty et al, 2015) TGF-B which is known to cause tissue fibrosis during chronic inflammation also exhibits inhibitory effects on Lymphatic endothelial cells and inhibits lymphangiogenesis. Lymphatic vasculature that is produced is hyper permeable, disorganised and incompetent (Clavin et al, 2008; Varricci, et al, 2015). Dysfunctional and incompetent lymphatic system also has negative effects on immunity. including increased risk of infections, development of chronic diseases including arteriosclerosis, inflammatory bowel diseases and cancer (Adamczyk et al, 2016; Yuan et al, 2019; Lund et al, 2016) Lymphatic Dysfunction: Plumbing problem or inflammatory condition? Up until recently conditions that result in oedema have been managed as primarily problems of poor plumbing. Clinically this has translated to using techniques such as MLD and compression to move fluid out of the affected area. Whilst these will remain to be two of the four pillars of managing chronic oedema along with skin management and physical activity, new targets for therapy are emerging. The main focus is now on the interplay in inflammatory cells and mediators in lymphatic dysfunction. Investigation continues into their effects on lymphatic vascular regeneration, remodelling, contractile function as well as tissue fibrosis and how all of these contribute to chronic oedema formation. Potential targets for therapy include Lymphatic endothelial cell specific markers including VEGFR-3, VEGF-C and D, Lieukotriene B4 as well as genes that may predispose individuals to lymphatic dysfunction. Multiple trials have been conducted using NSAIDS including Ketoprofen as well as T-cell immunosuppressive drugs (Tacrolimus). These studies reported positive effects in the management of lymphatic dysfunction. However continued research is undergoing in this field in order to understand the possible clinical applications of these findings (Liao & von der Weid, 2014; Dietrich et al, 2014; Jiang et al, 2018; Lund et al, 2016; Tian et al, 2017; Rockson et al, 2018; Gardenier et al, 2017). Implications: Research to Clinical Practice Most of the research reported in this review is obtained from animal studies. It is therefore important to follow findings that emerge in the following years and translation to human models. Current understanding in how lymphatics pump, the effects of chronic inflammation within skin, as well as conditions that may affect the ability to resolve inflammation and oedema are important to the Dermal Clinician/Therapist. This is to optimise managing inflammation, wound repair and oedema to prevent complications in the future. Translation of science to practice will be important through developing more clinical and case studies. As Dermal Clinicians we will need to evaluate questions such as: When is the best time to implement manual lymphatic drainage (MLD) after an injury? In what situations is it better practice to use compression? Are their topical formulations or modalities that can aid in lymphatic regeneration and function? In the next blog the ASDC Education team will provide insight into how oedema can be assessed and managed, informed by current best practice and the latest evidence. Want to keep up with the latest research? Access the Medline (Ebscohost) Database (free) as a benefit of your ASDC membership. The ASDC access puts 1300 Journals at your finger tips with FULL TEXT available! Not a member yet? What's stopping you? We now have both annual and monthly subscription options. JOIN NOW! References Adamczyk. L., Gordon. K., Kholova. I., Meijer-Jorna. L., Telinius. N., Gallagher. P., van der Wal. A. & Baandrup. U. (2016). Lymph vessels: The forgotten second circulation in health and disease. Virchows Archiv, 469, 3-17 Aldrich. M., & Sevick-Muraca. (2013). Cytokines are systemic effectors of lymphatic function in acute inflammation. Cytokine. 64. 362-369 Clavin. N., Avraham. T., Fernandez. J., Dahuvoy. S., Soares. A., Chundhry. A. & Mehara. B. (2008). TGF-B is a negative regulator of lymphatic regeneration during wound repair. American Journal of Physiology-Heart Circulation Physiology. 295, H2113-H2127 Chakraborty. S., Davis. M. & Muthuchamy. M. (2015). Emerging trends in the pathophysiology of lymphatic contractile function. Seminars in Cell Development and Biology. 38, 55-66 Chikly. B. (2017). Silent Waves: Theory and Practice of Lymph Drainage Therapy 3rd Edition. The Chikly Health Institute Cooper. L., Heppell. J., Clough. G., Ganapathisubramani. B. & Roose. T. (2016). An image-based model of fluid flow through lymph nodes. Bulletin of Mathemadical Biology. 78, 52-71 Doi 10.1007/s11538-015-0128-y Dietrich. L., Seidel. C & Detmar. M. (2014). Lymphatic vessels: new targets for the treatment of inflammatory diseases. Angiogenesis. 17(2), 359-371 Gardenier. J., Kataru. R., Hespe. G., Savetsky. I., Torrisi. J., Nores. G., Jowhar. D., Nitti. M., Schofield. R., Carlow. D. & Mehara. B. (2017). Topical tacrolimus for the treatment of secondary lymphedema. Nature Communications. 8:14345 Doi: 10.1038/ncomms14345 Gashev. A., Nagai. T. & Bridenbaugh. E. (2010). Indocyanine green and lymphatic imaging: current problems. Lymphatic Research and Biology. 8(2). 127-130 Heart Foundation. (2017). Where our funds go. Retrieved from https://www.heartfoundation.org.au/about-us/what-we-do/where-our-funds-go Goldman. J., Conley. K., Raehl. A., Bodny. D., Pytowski. B., Swartz. M., Ruthkowski. J., Jaroch. D., & Ongstad. E. (2007). Regulation of lymphatic capillary regeneration by interstitial flow in skin. American Journal of Physiology-Heart Circulation Physiology. 292- H2176-H2183 Huggenberger. R., & Detmar. M. (2011). The cutaneous vascular system in chronic skin inflammation. Journal of Investigative Dermatology Symposium Proceedings. 15, 24-32 Huggenberger. R., Siddiqui. S., Brander. D., Ullmann. S., Zimmermann. K., Antsiferova. M., Werner. S., Akitalo. K., & Detmar. M. (2011). An important role of lymphatic vessel activation in limiting acute inflammation. Blood. 117(17), 4667-4678 Huxley. V. & Scallan. J. (2011). Lymphatic fluid: Exchange mechanisms and regulation. Journal of Physiology. 589, 2935-2943 Jian. X., Nicolls. M., Tian. W., Rockson. S (2018). Lymphatic dysfunction, leukotrienes and lymphoedema. Annual Review of Physiology. 80(4), 4.1-4.21 Keast. D., Despartis. M., Allen. J. & Brassard. A. (2014). Chronic Oedema/Lymphoedema: under-recognised and under-treated. International Wound Journal. Doi:10.1111/wj.12224 Lachance. P., Hazen. A. & Sevick-Muraca. E. (2013). Lymphatic vascular response to acute inflammation. PLoS ONE 8(9), e76078 Doi 10.1371/journal.pone.0076078 Liao. S. & von der Weid. P. (2014). Inflammation-induced lymphangiogenesis and lymphatic dysfunction. Angiogenesis. 17(2). 325-334 Lund. A., Medler. T., Leachman. S. & Coussens. L. (2016). Lymphatic vessels, inflammation and immunity in skin cancer. Cancer Discovery. 6(1), 22-35 Lymphoedema Action Alliance (2018). EQUITABLE ACCESS TO QUALITY LYMPHOEDEMA SERVICES IN NSW. retrieved from https://www.actionalliance.org.au/about-us National Institute of Health. (2018). Estimates of Funding for Various Research, Condition, and Disease Categories (RCDC). retrieved from https://report.nih.gov/categorical_spending.aspx Negrini. D. & Moriondo. A. (2011). Lymphatic anatomy and biomechanics. Journal of Physiology. 589, 2927-2934 Rockson. S., Tian. W., Jiang. X., Kuznetsova. T., Haddad. F., Zampell. J., Mehara. B., Sampson. J., Roche. L., Kim. J., Nicolls. M. (2018). Pilot studies demonstrate the potential benefits of antiinflammatory therapy in human lymphoedema. Journal of Clinical Investigation Insight. 3(20). e123775 Doi: 10.1172/jci.insight.123775 Tian. W., Rockslon. S., Jiang. X., Kim. J., Begaye. A., Shuffle. E., Tu. A., Cribb. M., Nepiyushchikh. Z., Feroze. A., Zamanian. R., Dhillon. G., Voelkel. N., Peters-Golden. M., Kitajewski. J., Dixon. B., Nicolls. M. (2017). Leukotriene B4 antagonism ameliorates experimental lymphoedema. Science Translational Medicine. 9, eaal3920 Doi: 10.1126/scitranslmed.aal3920 Tortora. G. & Derickson. B. (2014). Principles of Anatomy and Physiology 14th Ed Wiley. Varricchi. G., Loffredo. S., Genovese. A., & Marone. G. (2015). Angiogenesis and lymphangiogenesis in inflammatory skin disorders. Journal of the American Academy of Dermatology. 73(1), 144-153 Villeco. J. (2012). Edema: A silent but important factor. Journal of Hand Therapy. 25, 153-162 Yuan. Y., Arucci. V., Levy. S. & Archen. M. (2019). Modulation of immunity by lymphatic dysfunction and lymphoedema. Frontiers in Immunology. 10(76), Doi 10.3389/fimmu.2019.00076

  • What's a little swelling?

    The importance of skin health and integrity for those that suffer from acute, problematic and chronic swelling shouldn't be underestimated. In Part 1 of the Oedema Series we revise what causes swelling, when it becomes a problem and what your role is in identifying problematic swelling. In following posts we will focus on some of the emerging evidence in relation to understanding more about how swelling occurs and resolves, therapies for management and what this may mean for the Dermal Clinician and Therapist. What causes swelling? Swelling or its medical term Oedema is caused by an accumulation of fluid in the interstitial spaces between cells. This can happen within the body, for example pulmonary oedema (fluid in the lungs) and cerebral oedema (swelling of the brain). However in Dermal Science and Therapy we are concerned with the more common occurrence of oedema within the skin (peripheral oedema). The regulation, balance and movement of water and solutes within different compartments in the body relies on many different systems to maintain homeostatic function. These include neurological (nervous stimuli), renal (kidney), cardiovascular (heart and blood vessels), integumentary (skin) and the lymphatic system. For most of us, swelling is something that we live with at some point or another. This may be due to an injury, medication we have been taking, pregnancy or perhaps even a surgery. Dermal Clinicians and Therapists know that swelling is an expected side effect of any treatment that causes inflammation in the skin. We even use that as a positive endpoint, as regeneration of the skin requires inflammation and associated swelling to allow much needed cells and co-factors for healing to get to the site. However any swelling that is disproportionate, persists for an extended period of time, causes considerable discomfort or affects daily activities is cause for concern and further investigation. Swelling that occurs in the elderly, with medical conditions such as diabetes, cardiovascular disease and cancer should not be ignored. When is swelling a problem? Swelling is a normal and expected function of human healing. In response to tissue damage or injury, the body will have an inflammatory response. This results in vascular hyper permeability allowing for movement of cells and fluid to the area. This process facilitates immunological functions and repair or removal of damaged cells and tissues. Normal acute inflammation and swelling will usually peak at 3-7 days after the injury and then will slowly dissipate. How long this takes varies depending on how extensive the injury was, but usually within 4-12 weeks swelling will be markedly improved or gone altogether. Problematic oedema can be defined as acute oedema that is disproportionate and causing issues such as pain or discomfort, problems with movement and activities of daily living and causing risk to skin integrity. Whilst oedema is a normal part of healing, due to many factors it can negatively impact on optimal healing. Early management and support will improve wound repair, reduce risk of or degree of scarring, improve range of movement and prevent further complication in the future. Chronic oedema is under recognised as a problem and under managed. Chronic oedema can be diagnosed medically when swelling has been present for more than three months. It is a multi-factorial condition, meaning that the condition is not often caused by one thing. It is the contribution of many factors over time. However, it is known that the lymphatic system is responsible for returning fluid from the interstitial spaces to the cardiovascular network. Therefore degeneration of this system and its ability to do this task is seen as being the resulting problem. Patients with chronic oedema will often say that there was a defining event where the problem made itself known. What they didn't realise is that they probably actually had sub-clinical oedema for many years before this. Chronic oedema may or may not be reversible depending on what is exacerbating the issue and how long it has been present. Risk factors that can result in chronic oedema at some point in a persons life include obesity, pregnancy, venous insufficiency, heart or kidney problems, medications that cause fluid retention, significant or ongoing injury and increasing age. Genetic predisposition may also play a role. Early identification of problematic and chronic oedema is important to ensure that the condition is managed to prevent further problems and degeneration. Lymphoedema is a form of chronic oedema. However lymphoedema is caused by dysfunction or failure of the lymphatic system itself. Chronic oedema if present and unmanaged can develop into lymphoedema. However lymphoedema can also occur due to malformation or genetic predisposition to lymphatic dysfunction. As the lymphatic system is responsible for returning fluid to the cardiovascular network, when it is not working the fluid will not resolve on its own and the condition is not reversible. Early identification and management can prevent the condition from worsening or causing significant health problems. It is reported that 1 in 30 people globally suffer from lymphoedema, however this may not be accurate as most people only seek diagnosis when there is already significant swelling. Therefore mild forms may not be picked up in this data. In Australia, lymphoedema is mostly associated with cancer and its treatment, though it can be the result of many factors that can damage the lymphatic system. 1 in 5 woman with breast cancer and treatment will have to manage lymphoedema afterwards. In most cases this presents within the first 12 months of treatment. However it can occur at any stage afterward. Any cancer that results in removal of lymph nodes, radiation or chemotherapy increases the risk of developing lymphoedema. This includes melanoma which reports an incidence of 6-58% cases of lymphoedema, 18% incidence rate in gynaecological cancers and 25-66% for prostrate cancer. The not so missing link: Skin, lymphatics and oedema The skin (integumentary system) and Lymphatic system are inextricably linked. Together they work to provide immune functions and protect against the outside world. When the skin is intact, it reduces the load on the lymphatic system to provide this defence. When the skin barrier is compromised this will result in inflammation and the lymphatic system having to work harder. This increase in load is due to the lymphatic system both attempting to resolve inflammation by removing the fluid but also due to working to neutralise any pathogens and other substances that could damage the body. On the other hand, when there is significant oedema in the short term, this can result in stretching or even breaking of the skin barrier and damage to the skin including wounds. When oedema has been present for a long period of time, the inflammation in the skin can result in tissue changes including fibrosis, thickening and other dermatoses such as fungal infections, xerosis (dry skin), fissures and dermatitis. Therefore we need to know that any skin that is not intact particularly for long periods of time, will result in chronic inflammation, oedema and ultimately is a risk for overloading the lymphatic system in time. Conversely providing simple management strategies to manage oedema and skin barrier can assist in improving the outcomes for those with swelling. The role of the Dermal Clinician. Skin and lymphatic wellbeing is definitely within the scope of Dermal Clinicians. They study as part of their Bachelor degree programs, anatomy and physiology of both the lymphatic and integumentary systems as well as its management in health and disease. The Dermal Clinician and Therapist also play a really important role in education of those that may be at risk of lymphatic dysfunction as well as early detection. In our clinical settings we often have clients presenting with early signs of vascular insufficiency (leg veins and capillaries), obesity, increasing age, planning surgical procedures and dermatological conditions that are associated with increasing lymphatic load. Therefore implementing assessment of lymphatic and skin health, as well as simple education and management strategies to assist with optimal lymphatic function, could play an important role in reducing the incidence and severity of lymphatic dysfunction. In following posts we will explore the tools and techniques available to assess and manage skin health and lymphatic function. The ASDC at the Australasian Lymphology Association (ALA) Symposium 2019 This May in Sydney, Marnina Diprose and Jennifer Byrne as representatives of the ASDC will be conducting a workshop for ALA delegates on the role of Dermal Clinicians in the interdisciplinary management of lymphoedema. This conference is a great opportunity for Dermal Clinicians with a special interest in skin and lymphatic health to undertake some professional development and networking. Click Here for more information. 2019 ASDC SkinCon This year at the annual ASDC education conference, rebranded as SkinCon we will have a variety of speakers all discussing inter professional client management. One of our speakers will be presenting on the importance of lymphatic health.... stay tuned. Click Here to stay in touch with what's happening at our conference. #asdcassociation #dermalclinician #SkinCon References Al-Kofahi. M., Yun. J., Minagar. A & Alexander. J. (2017). Anatomy and roles of lymphatics in inflammatory disease. Clinical and experimental Neuroimmunology. 8(3), 199-214 Alitalo. K. (2011). The lymphatic vasculature in disease. Nature Medicine. 17, 1371–1380 Chatham. N., Thomas. L. & Molyneaux. M. (2013). Dermatologic Difficulities: Skin problems in patient with chronic insufficiency and phlebolymphoedma. Wound Care Advisor. 2(6), 30-36 Flour. M. (2013). Dermatological issues in lymphoedema and chronic odedma. Journal of Community Nursing. 27(2), 27-32 Haesler. E. (2016). Evidence Summary: Lymphoedema: Skin Care. Journal of Australian Wound Management Association. 24(4), 236-238 Huggenberger. R. & Detamar. M. (2011). The cutaneous vascular system in chronic skin inflammation. Journal of Investigative Dermatology Symposium Proceedings. 15, 24-32 Huggenberger. R., Siddiqui. S., Brander. D., Ullmann. S., Zimmermann. K., Antsiferova. M., Werner. S., Akitalo. K., & Detmar. M. (2011). An important role of lymphatic vessel activation in limiting actute inflammation. Blood. 117(17), 4667-4678 Huxley. V. & Scallan. J. (2011). Lymphatic fluid: Exchange mechanisms and regulation. Journal of Physiology. 589(12), 2935-2943 Keast. D., Despatis. M. Allen. J., Brassard. A. (2015). Chronic oedema/lymphoedema: under-recognised and under-treated. International Wound Journal. 12, 328–333 Lymphoedema Action Alliance. (2015). Submission to The Standing Committee on Health: Inquiry into Chronic Disease Prevention and Management in Primary Health Care. Submission 33 Negrini. D. & Moriondo A. (2011). Lymphatic anatomy and biomechanics. Journal of Physiology. 589(12), 2927-2934 Noowicki. J. & Siviour. A. (2013). Best practice skin care management in lymphoedema. Wound Practice and Research. 21(2), 61-65 Savetsky I. et al. (2015). Lymphatic Function Regulates Contact Hypersensitivity Dermatitis in Obesity. Journal of Investigative Dermatology, 135(11), 2742-2752 Tian. W et al. (2017).Leukotriene B4 antagonism ameliorates experimental lymphedema. Science Translational Medicine, 9(389). DOI: 10.1126/scitranslmed.aal3920 Todd. M. (2013). Chronic oedema impact and management. British Journal of Nursing. 22(11). 16-20 Varricchi. G., Loffredo. S., Genovese. A. & Marone. G. (2015). Angiogenesis and lymphangiogenesis in inflammatory skin disorders. Journal of American Academy of Dermatology. 73(1), 144-153

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  • Find a Dermal Clinician | The ASDC

    USE THE MAP BELOW TO FIND A DERMAL CLINICIAN NEAR YOU We have members located in most states of Australia and New Zealand

  • Skin Health Education and Management | Australian Society of Dermal Clinicians

    The Australian Society of Dermal Clinicians Who we are The Australian Society of Dermal Clinicians (ASDC) are a not-for-profit professional association for Dermal Clinicians, Dermal Therapists and industry associates. The ASDC is a collaborative professional community of practitioners, educators, researchers and industry representatives. As a professional body the ASDC advocate on behalf of our members, industry representatives, and consumers in maintaining standards of safety and ethical practice. Our members have expertise in skin health, integrity as well as a special interest in the support and clinical management of those that experience skin conditions, disorders and disease. The ASDC encourages research and evidence based, best practice that is patient centred in order to empower those with skin concerns and improve their overall health and well-being. Learn More Our Purpose The board, advisory committees and members of the Australian Society of Dermal Clinicians are leading practitioners, educators, industry members as well as students and consumers. They wok together with a common focus to support and guide the profession with an aim to ensure standards and safety in the provision of skin health services. Support Increasing recognition and awareness of the profession within government, health, allied health and aesthetic forums. Advocacy Advocating on behalf of our members, industry representatives and consumers to ensure standards of safety and ethical practice. Education Providing ongoing professional education and guidance regarding formal and informal pathways for education. Connection A collaborative community connecting clinicians, educators, researchers and our industry partners. JOIN US What the benefits of Membership? Join a rapidly growing and dynamic professional community made up of clinicians, educators, researchers and industry affiliates. Read More FIND A CLINICIAN What is a Dermal Clinician? Dermal Clinicians are allied health professionals with an AQF 7 Bachelor of Health Science. They have expertise in assessing and managing the skin in health and disease Read More MEET THE BOARD Governance of the ASDC The Australian Society of Dermal Clinicians Board members are all dedicated Dermal Clinicians with expertise in clinical practice, education and research. Read More

  • Scope of Practice | The ASDC

    Scope of Practice Dermal Clinicians are independent allied health practitioners; however, they often work in practices collaboratively with General Practitioners, Skin Cancer Medical Practitioners, Dermatologists, Cosmetic Physicians, Plastic Surgeons, Vascular Surgeons, and Oncology specialities among others. ​ Dermal Clinicians can independently (within their scope of practice) provide therapeutic management of the skin using a variety of non-surgical, minimally invasive techniques. ​ You can find Dermal Clinicians in independent private practice, or working in community health settings, in medical speciality health services such as plastic surgery, skin cancer and vascular clinics or other outpatient hospital services. Dermal Clinicians are patient centred and evidence based allied health professionals. In providing skin management strategies they can employ a variety of techniques to suit client needs and preferences and take into account individual personal circumstances. ​ Dermal Clinicians work on what is called an intervention ladder based on clinical need. We provide a management plan that is most likely to address your needs that is supported by evidence, is cost and time effective and is the lowest risk possible to achieve the desired outcome. This means that your Dermal Clinicians won't recommend therapies you don't need or are not right for your individual situation. ​ Dermal Clinicians work around the pillars of skin management, at the centre of all skin health management is client education and support. Your Dermal Clinician may also use a variety of therapeutic interventions including skin care (topically applied), manual techniques or energy devices. ​ If you would like to know more about the pillars of skin management you can view the infographic below and contact info@dermalclinciians.com.au for more detail Pillars of Skin Management Scope of Practice & Education The scope of practice of Dermal Clinicians is defined by their education and training. The ASDC recognises that there are many professionals, with varying levels of education, knowledge and skill particularly within the non-surgical cosmetic industry providing treatments. There is also interchangeable use of titles “Dermal Therapist”, “Skin Therapist” or “Dermal Clinician” which can be misleading or confusing for consumers and colleagues in the industry. ​ For more information about the education of dermal clinicians, use of titles and what questions to ask you skin health professional before receiving skin health services see the links below. Education Thinking of studying to become a Dermal Clinician? Learn more Read More Professional Titles What are the ASDC endorsed titles? Learn More Read More What does a Dermal Clinician Do? Want to know more about the role of Dermal Clinicians in skin health? Learn More Read More Questions to ask your Dermal Clinician Before receiving any skin therapy advice ask these quesitons Button Read More Back

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