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Practical Issues in Wound, Skin and Ostomy Management
The resources below will help you address issues in your practice.
Use of the hand check to determine “bottoming out” of support systems should be limited to static air overlay mattresses, according to a position statement from the National Pressure Ulcer Advisory Panel (NPUAP). (more…)
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One in three patients enters a hospital malnourished. Fight malnutrition by viewing six short videos from the Alliance to Advance Patient Nutrition, including “Rapidly Implement Nutrition Interventions” and “Recognize and Diagnose All Patients at Risk of Malnutrition.” The videos show how to collaborate with the care team to become champions of nutrition and help improve patient outcomes. Watch the videos online or download them for later viewing. (more…)
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By Todd Zortman, RN, WCC, and James Malec, PhD
Pressure ulcers are a chronic healthcare burden for both patients and providers. Over 2.5 million patients in the United States are affected annually by pressure ulcers, with nearly 60,000 of those cases directly resulting in death. From a provider’s perspective, the cost of individual care ranges anywhere from $500 to $70,000 per pressure ulcer, which translates to annual costs in the U.S. approaching $11 billion. (more…)
Read MoreBy Carrie Carls, BSN, RN, CWOCN, CHRN; Michael Molyneaux, MD; and William Ryan, CHT
Every year, 1.9% of patients with diabetes develop foot ulcers. Of those, 15% to 20% undergo an amputation within 5 years of ulcer onset. During their lifetimes, an estimated 25% of diabetic patients develop a foot ulcer. This article discusses use of hyperbaric oxygen therapy (HBOT) in treating diabetic foot ulcers, presenting several case studies.
HBOT involves intermittent administration of 100% oxygen inhaled at a pressure greater than sea level. It may be given in a:
• multi-place chamber (used to treat multiple patients at the same time), compressed to depth by air as the patient breathes 100% oxygen through a face mask or hood (more…)
Editor’s note: Part 1 of this series, published in the September-October issue, discussed lymphedema pathology and diagnosis. This article, Part 2, covers treatment.
Traditionally, lymphedema treatment has been approached without a clear understanding of the underlying structure and function of lymphatic tissues. Ineffective traditional treatments include elevation, elastic garments, pneumatic pumps, surgery, diuretics, and benzopyrones (such as warfarin). Because many traditional treatments are still overused and some may be appropriate for limited use, it’s important for clinicians to understand these approaches.
As a sole therapy for lymphedema, elevation of the affected part provides only short-lived results. Ever-increasing macromolecular wastes retain water against the effects of gravity. Increased interstitial colloid osmotic pressure must be addressed by interventions targeted at improving lymphatic function—not just a position change. Otherwise, lymphedema will progress. Furthermore, elevation alone is impractical, promotes deconditioning, and alters lifestyle for prolonged periods.
Elastic garments prove inadequate because they attempt to treat lymphedema with compression alone. Medically correct garments are engineered with thoughtful attention to high-quality textiles and offer gradient support, which promotes proximal flow. However, without precise tissue stimulation leading to improved lymphangioactivity (lymph-vessel pulsation), macromolecular wastes can’t be removed.
Interstitial pressure increases caused by compression garments impede further fluid accumulation. When these garments are removed, the spontaneous girth increase causes an imprecise fit, and the garment rapidly leads to a countertherapeutic effect. Furthermore, compression garments don’t combat the osmotic forces generated by ever-increasing interstitial wastes. Except in patients diagnosed with stage 0 or stage 1 lymphedema, disease progression involving metaplasia ensues. Although elastic compression garments are a cornerstone of long-term management, they shouldn’t be used as a stand-alone treatment.
Formerly, the pneumatic compression pump (PCP) was considered the standard of care for lymphedema. However, when inflated, the pump doesn’t increase the frequency of lymph-vessel contraction or enhance lymph capillary absorption. What’s more, accelerated fibrosis development and rapid tissue refilling occur when a PCP is removed. Also, PCP use disregards the ipsilateral territory of the excised regional nodes, effectively dumping fluid from the leg into the trunk. A PCP is appropriate only when nothing else is available, as it may worsen the patient’s condition.
Surgical approaches to treating lymphedema involve either excisional (debulking) or microsurgical techniques. The most extensive surgical technique, the radical Charles procedure, completely debulks all involved tissue down to the muscle fascia. Split-thickness grafts are then harvested from excised skin and donor sites, and applied to the fascia to achieve so-called limb reduction.
Most debulking procedures have been applied to lower-extremity lymphedema and offer poor cosmetic results. Less radical surgeries favor long incisions, preserving the skin but excising subcutaneous edematous portions to reduce girth. Although less cosmetically alarming, these procedures effectively amputate the subcutaneous space where lymph vessels reside. Other surgical approaches are beyond the scope of this article.
Generally, surgery isn’t a good approach for any patient, as it’s linked to significant morbidity, such as skin necrosis, infection, and sensory changes. In the future, less invasive procedures may be available that yield significant improvement without these adverse effects.
Although diuretics are prescribed appropriately to address water-rich edemas of venous origin, they disregard the fact that lymphedema is a protein-rich edema. Long-term, high-dose diuretic therapy leads to treatment-resistant limbs, similar to those that have received intensive pneumatic compression.
Benzopyrones such as warfarin decrease swelling by combating protein accumulation in fluid. Such drugs have undergone clinical trials abroad. Their mechanism is to promote macrophage migration into interstitial fluid, as well as subsequent proteolysis. Due to significant risk of liver damage or failure, benzopyrones haven’t been approved for treating lymphedema.
Currently, the gold standard for lymphedema treatment is complete decongestive therapy (CDT). Michael Foeldi and Etelka Foeldi, who originated this method, discovered a unique symbiotic relationship among five distinct modalities that addresses the challenges of lymphedema treatment. In 1989, CDT was brought to the United States by Robert Lerner and has become the mainstay of lymphedema treatment here.
CDT is a two-phase approach involving an intensive clinical effort followed by a semi-intensive home-care program geared toward autonomous management, stabilization, and continual improvement. It involves manual lymph drainage (MLD), compression bandaging, exercise, skin and nail hygiene, and self-care education. (See Phases of complete decongestive therapy by clicking the PDF icon above.)
A type of soft-tissue mobilization, MLD provides skin traction, stimulating superficial lymph vessels and nodes. Lymph capillaries contain large inter-endothelial inlets called swinging tips, akin to overlapping shingles. Each overlapping cell is tethered to the interstitial matrix by anchoring filaments, so that fluid increases cause immediate distention and lymph inflow. Manual skin traction using MLD promotes greater lymph fluid uptake by stretching these filamentous structures, opening the swinging tips.
MLD also provides extrinsic stimulation of the lymphangion (the segment of a lymph vessel between a distal and proximal valve), drawing fluid into the system at the capillary level and promoting flow at the vessel level toward regional lymph nodes. Usually, these segments contract and relax in a rhythmic fashion six times per minute. MLD triples this output to 18 or 20 times per minute, greatly enhancing systemic transport.
MLD requires intensive daily treatment sessions to strengthen collateral flow as a pathway to circumventing surgical or developmental lymphatic disruption. Treatment strategies further recruit more deeply situated lymphatics such as the thoracic duct, as well as lumbar trunks that empty at the juncture of the internal jugular and subclavian veins to improve global uptake. MLD thus stimulates deeper vessel angioactivity to help drain the superficial vessels that drain toward them.
Compression bandaging provides tissue support after MLD to prevent reflux, slow new fluid formation, and mechanically soften fibrotic areas. Bandaging techniques provide a high working pressure to harness the muscle and joint pumps as a propellant for lymph while resisting retrograde flow created by gravity and centrifugal forces during movement. Pure cotton materials coupled with specialized padding create a soft, castlike environment, which confines swollen tissues without constriction. By relying on high working pressure and low resting pressures to decrease limb swelling, this strategy achieves greater control over intensity (level of compression/pressure exerted), with little to no soft-tissue injury or discomfort.
The patient wears this bulky inelastic complex after each MLD treatment until the next day’s session to ensure limb-volume reduction in a stable, linear fashion. Once a plateau is reached, tissue stabilization and self-care education are the goals of additional sessions.
Exercise always must be done with adequate support to counteract fluid formation. During the intensive CDT phase, limbs are bandaged to provide complete around-the-clock containment. Gentle exercises encourage blood flow into the muscle; during muscle contraction, this creates a favorable internal pressure that effectively squeezes the subcutaneous space between the bandage wall and muscle. Because every bandage strives to provide a gradient of support, fluid tends to drain proximally to the bandage—in most cases, to the trunk.
Without intact, well-hydrated skin, cellulitic infections occur in many lymphedema patients whose immune response has been diminished by regional lymphadenectomy or inherited deficiencies. To prevent infection caused by avoidable external events, patients receive clear guidelines to reinforce appropriate behavior. As most cellulitis results from resident skin pathogens (streptococci and staphylococci), maintaining a low skin pH helps control colonization. Ways to avoid recurrent infections include maintaining an acid mantle on the skin using low-pH-formulated lotions and avoiding injury from daily tasks that may scratch, puncture, burn, or abrade the skin. Patients should receive lists of self-care precautions at the time of treatment.
Because lymphedema is a chronic condition, patients must receive self-care education for daily management to avoid lymphedema destabilization, which can lead to tissue saturation and subsequent skin changes. Therapists must provide patients with appropriate self-care tools and knowledge to maintain adequate treatment results. Teaching topics include how to apply and remove compression garments and bandages and how to exercise safely, preserve skin integrity, monitor for infection, and respond appropriately to infection and significant changes in limb mobility.
Lymphedema remains an underrecognized and mistreated condition, even though CDT yields safe, reliable results. Early detection, accurate staging, proper diagnosis, and appropriate treatment can slow the inevitable progression of lymphedema. Wound care specialists should adapt wound therapy to address not just the wound but the edematous environment responsible for delayed wound resolution.
Selected references
Al-Niaimi F, Cox N. Cellulitis and lymphedema: a vicious cycle. J Lymphoedema. 2009;4:38-42.
Browse N, Burnand KG, Mortimer PS. Diseases of the Lymphatics. London: Hodder Arnold; 2003.
Casley-Smith JR, Casley-Smith JR. Modern Treatment for Lymphoedema. 5th ed. The Lymphoedema Association of Australia; 1997.
Cooper R, White R. Cutaneous infections in lymphoedema. J Lymphoedema. 2009:4:44-8.
Foeldi M. Foeldi’s Textbook of Lymphology: For Physicians and Lymphedema Therapists. 3rd ed. St. Louis, MO: Mosby; 2012.
International Society of Lymphology. The diagnosis and treatment of peripheral lymphedema. Consensus Document of the International Society of Lymphology. Lymphology. 2009 Jun;42(2):51-60.
Leduc A, Bastin R, Bourgeois P. Lymphatic reabsorption of proteins and pressotherapies. Progress in Lymphology XI. 1988:591-2.
National Lymphedema Network Medical Advisory Committee. Position Statement: Lymphedema Risk Reduction Practices. Revised May 2012. http://www.lymphnet.org/pdfDocs/nlnriskreduction.pdf. Accessed September 5, 2012.
Pappas CJ, O’Donnell TF Jr. Long-term results of compression treatment for lymphedema. J Vasc Surg. 1992 Oct;16(4):555-62.
Whittlinger H. Textbook of Dr. Vodder’s Manual Lymphatic Drainage. Vol 1. 7th ed. New York, NY: Thieme; 2003.
Steve Norton is cofounder of Lymphedema & Wound Care Education and executive director of the Norton School of Lymphatic Therapy in Matawan, New Jersey.
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By Matthew Steinhauser, University of Pittsburgh
I recently visited an 83-year-old patient in the hospital after EMTs rushed her to the ER with an infected leg wound. Her ordeal started inconspicuously when she bumped into the sharp edge of a table and developed a small cut. The patient’s wound didn’t close, but she ignored it until she woke up in pain one morning two weeks after first injuring her leg. Her daughter called 911 after noticing angry, red skin discoloration and pus – both signs of an infection. Our medical team treated her with IV antibiotics and cleared up the infection, but the wound did not fully close until at least a month later, well after she was discharged from the hospital.
How different the story is when children get a cut. They may scream initially, but within days, the scab falls off, revealing new skin. Why was healing so delayed in my 83-year-old patient compared to a healthy child?
The answer is age. Decades of life slow down healing for most tissues, and wounds in skin can offer a window into why this slowdown occurs.
I am physician who studies how aging predisposes patients to diseases like diabetes and whether behavioral changes such as intermittent fasting may slow down aging. In order to understand why the skin wound in my older patient healed so slowly, it is important to first understand how wounds heal under the ideal conditions of youth.
The wound healing process is classically categorized into three stages.
Right after a wound occurs, the inflammatory response begins.
Jpbarrass via Wikimedia Commons
The first stage is inflammation, essentially the body’s attempt to clean the wound. During the inflammatory phase, immune cells called phagocytes move into the wound, kill any contaminating bacteria, and ingest and dispose of dead cells and debris.
Inflammation sets the stage for the regenerative phase, where several processes work in concert to regrow damaged skin. Replacement skin cells are born when cells at the edge of the wound divide, while fibroblast cells lay down a supportive scaffolding called the extracellular matrix. This holds the new cells together. Any damaged supporting structures of the skin, such as the blood vessels that supply critical oxygen and nutrients, also need to regrow. The second stage effectively closes the wound and restores a protective barrier against bacteria.
The regenerative phase is a relatively quick, but tenuous fix – new skin is fragile. The final remodeling phase plays out over a couple of years as the new skin is progressively strengthened by several parallel processes. The extracellular matrix, which was initially laid down in a haphazard fashion, is broken down and replaced in a more durable way. Any residual cells from prior phases that are no longer needed – such as immune cells or fibroblasts – become inactive or die. In addition to strengthening the new skin, these collective actions also account for the tendency of scars to visibly fade with time.
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One major way aging can derail the orderly and efficient progression through the stages of healing is through the health problems that stem from diseases of old age.
Diabetes is one example of a disease that is strongly associated with older age. One of the many ways that diabetes negatively affects healing is by causing blood vessels to narrow. As a consequence of inadequate circulation, crucial nutrients and oxygen do not reach the wound in sufficient quantities to fuel the second regenerative phase.
Diabetes is just one of many age-related diseases that disrupts normal processes in the body such as wound healing.
Aside from the negative impacts of age-associated diseases, cells themselves age. In an extreme sign of aging called cellular senescence, cells permanently lose the ability to divide. Senescent cells accumulate in skin and many other organs as people age and cause a host of problems.
When cells divide more slowly – or when they stop dividing altogether due to senescence – skin becomes thinner. The replacement of fat cells, which form a cushioning layer under the skin, also declines with age. The skin of older patients is therefore more prone to injury in the first place.
Once an older person’s skin is injured, the skin has a harder time healing properly as well. Aging and senescent immune cells cannot defend against bacteria, and the risk of serious skin infection rises. Then in the regenerative stage, slow rates of cell division translate into slow skin regrowth. My patient exhibited all of these negative effects of age – her thin, almost translucent skin ruptured from a minor bump, became infected and took nearly two months to fully regrow.
But senescent cells are more than just dysfunctional bystanders. For reasons that are not yet fully understood, senescent cells release toxic byproducts that damage surrounding tissue and drive inflammation – even when there’s no bacterial threat present. Some of these byproducts can even accelerate senescence in neighboring cells. This suggests that intrinsic aging of cells is in essence contagious and senescent cells actively fuel an uncontrolled cycle of inflammation and tissue damage that further impedes successful regeneration and healing.
As the most outwardly visible tissue of the body, the skin provides a window into why people heal more slowly with age, but all tissues can be injured and are susceptible to the effects of aging. Injuries may be small, repetitive and build up over time – like the effect of smoking on the lungs. Or they may be discrete and dramatic – such as the death of heart cells with a heart attack. Different tissues may heal in different ways. Yet all tissues share a sensitivity to the repercussions of an aging immune system and a decline in the ability to regrow dead or damaged cells.
Understanding why healing slows down with age is important, but my patient asked a very practical question that physicians often face in one form or another: “Doctor, what can you do for me?”
Unfortunately, current treatment of wounds is fairly old-fashioned and often ineffective. Some of the options available include wound dressing changes, antibiotics when the wound is infected or treatment in a high oxygen chamber when circulation is bad due to diabetes.
There is hope, though, that medicine can do better and that progress in understanding the aging process will lead to new therapies. Neutralizing senescent cells in mice, for example, improves a variety of age-associated diseases. While it is way too early to say that researchers have discovered the fountain of youth, I am optimistic for a future when physicians will bend the aging curve and make skin and other organs heal faster and better.
Matthew Steinhauser, Associate Professor of Medicine, University of Pittsburgh
This article is republished from The Conversation under a Creative Commons license. Read the original article.
By Robert A. Schwartz, Rutgers University
The word “leprosy” conjures images of biblical plagues, but the disease is still with us today. Caused by infectious bacteria, some 200,000 new cases are reported each year, according to the World Health Organization. In the United States, leprosy has been entrenched for more than a century in parts of the South where people came into contact with armadillos, the principle proven linkage from animal to humans. However, the more recent outbreaks in the Southeast, especially Florida, have not been associated with animal exposure.
The Conversation talked with Robert A. Schwartz, professor and head of dermatology at Rutgers New Jersey Medical School, to explain what researchers know about the disease.
Leprosy is caused by two different but similar bacteria — Mycobacterium leprae and Mycobacterium lepromatosis — the latter having just been identified in 2008. Leprosy, also known as Hansen’s disease, is avoidable. Transmission among the most vulnerable in society, including migrant and impoverished populations, remains a pressing issue.
This age-old neglected tropical disease, which is still present in more than 120 countries, is now a growing challenge in parts of North America.
Leprosy is beginning to occur regularly within parts of the southeastern United States. Most recently, Florida has seen a heightened incidence of leprosy, accounting for many of the newly diagnosed cases in the U.S.
The surge in new cases in central Florida highlights the urgent need for health care providers to report them immediately. Contact tracing is critical to identifying sources and reducing transmission.
Traditional risk factors include zoonotic exposure and having recently lived in leprosy-endemic countries. Brazil, India and Indonesia have each noted more than 10,000 new cases since 2019, according to the World Health Organization data, and more than a dozen countries have reported between 1,000 to 10,000 new cases over the same time period.
Evidence suggests that leprosy has plagued civilization since at least the second millennium B.C.
From that time until the mid-20th century, limited treatments were available, so the bacteria could infiltrate the body and cause prominent physical deformities such as disfigured hands and feet. Advanced cases of leprosy cause facial features resembling that of a lion in humans.
Many mutilating and distressing skin disorders such as skin cancers and deep fungal infections were also confused with leprosy by the general public.
Fear of contagion has led to tremendous stigmatization and social exclusion. It was such a serious concern that the Kingdom of Jerusalem had a specialized hospital to care for those suffering from leprosy.
Research shows that prolonged in-person contact via respiratory droplets is the primary mode of transmission, rather than through normal, everyday contact such as embracing, shaking hands or sitting near a person with leprosy. People with leprosy generally do not transmit the disease once they begin treatment.
Armadillos represent the only known zoonotic reservoir of leprosy-causing bacteria that threaten humans. These small mammals are common in Central and South America and in parts of Texas, Louisiana, Missouri and other states, where they are sometimes kept as pets or farmed as meat. Eating armadillo meat is not a clear cause of leprosy, but capturing and raising armadillos, along with preparing its meat, are risk factors.
The transmission mechanism between zoonotic reservoirs and susceptible individuals is unknown, but it is strongly suspected that direct contact with an infected armadillo poses a significant risk of developing leprosy. However, many cases reported in the U.S. have demonstrated an absence of either zoonotic exposure or person-to-person transmission outside of North America, suggesting that transmission may be happening where the infected person lives. But in many cases, the source remains an enigma.
Some people’s genetics might make them more susceptible to leprosy infections, or their immune systems are less capable of resisting the disease.
Stigma and discrimination have prevented people from seeking treatment, and as a result, “concealed” cases contribute to transmission.
Leprosy primarily affects the skin and peripheral nervous system, causing physical deformity and desensitizing one’s ability to feel pain on affected skin.
It may begin with loss of sensation on whitish patches of skin or reddened skin. As the bacteria spread in the skin, they can cause the skin to thicken with or without nodules. If this occurs on a person’s face, it may rarely produce a smooth, attractive-appearing facial contour known as lepra bonita, or “pretty leprosy.” The disease can progress to causing eyebrow loss, enlarged nerves in the neck, nasal deformities and nerve damage.
The onset of symptoms can sometimes take as long as 20 years because the infectious bacteria have a lengthy incubation period and proliferate slowly in the human body. So presumably many people are infected long before they know that they are.
Fortunately, worldwide efforts to screen for leprosy are being enhanced thanks to organizations like the Order of Saint Lazarus, which was originally founded in the 11th century to combat leprosy, and the Armauer Hansen Research Institute, which conducts immunologic, epidemiological and translational research in Ethiopia. The nongovernmental organization Bombay Leprosy Project in India does the same.
Leprosy is not only preventable but treatable. Defying stigma and advancing early diagnosis via proactive measures are critical to the mission of controlling and eradicating it worldwide.
Notably, the World Health Organization and other agencies provide multi-drug therapy at no cost to patients.
In addition, vaccine technology to combat leprosy is in the clinical trials stage and could become available in coming years. In studies involving nine-banded armadillos, this protein-based vaccine delayed or diminished leprous nerve damage and kept bacteria at bay. Researchers believe that the vaccine can be produced in a low-cost, highly efficient manner, with the long-term prospect of eradicating leprosy.
If health care professionals, biomedical researchers and lawmakers do not markedly enhance their efforts to eliminate leprosy worldwide, the disease will continue to spread and could become a far more serious problem in areas that have been largely free of leprosy for decades.
The World Health Organization launched a plan in 2021 for achieving zero leprosy.
Robert A. Schwartz, Professor and Head of Dermatology, Rutgers New Jersey Medical School, Rutgers University
This article is republished from The Conversation under a Creative Commons license. Read the original article.
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American Nurse Today, Woundcare Advisor and Angelini present: Innovations in Wound Care: Case Studies Basic Wound Cleansing and use of Collagen in Diabetic Foot Ulcer
This 30-minute presentation featurea learning opportunities that will provide in-depth instruction and demonstration in wound care treatments. After this webinar, the learner will be able to:
Martha Kelso, RN, HBOT, CEO, WCP Wound Care Plus, LLC, is the founder and Chief Executive Officer of Wound Care Plus, LLC (WCP). As a visionary and entrepreneur in the field of mobile medicine, she has operated mobile wound care practices nationwide for many years. She enjoys educating on the art and science of wound healing and how practical solutions apply to healthcare professionals today. Martha enjoys being a positive change in healthcare impacting clients suffering from wounds and skin issues of all etiologies. Martha started her career as a Certified Nurse Aide at the age of 15 in Kansas before moving to Kansas City, MO to attend nursing school. Long Term Care nursing was her first love and her biggest challenge.