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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 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.
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