By 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…)
A court case answers the question as to whether a pressure ulcer was preventable
By Nancy J. Brent, MS, RN, JD
Pressure ulcers are a major health risk for every adult patient. Risk factors include sepsis, hypotension, and age 70 or older. These risk factors became all too real when Mr. M developed pressure ulcers after being admitted to a Texas hospital.
Background
Mr. M, age 81, presented at a medical center’s emergency department on January 2 complaining of abdominal pain. After undergoing an assessment, he was diagnosed with gallstones and admitted to the hospital. The next day, he had gallbladder surgery. He subsequently developed a bowel obstruction and had to undergo two more surgeries for this condition over the next 10 days.
On January 13, he was transferred to the intensive care unit (ICU) because of multiple serious medical conditions, including respiratory distress syndrome (necessitating ventilatory support), septic shock, a “blood infection” that caused his blood pressure to drop, and multiorgan failure. His primary physician discontinued tube feedings out of concern they might exacerbate his renal failure; he wrote a do-not-resuscitate order and ordered sedation.
Mr. M was unable to turn or position himself in any way. While in the ICU, he developed a “skin tear” on the tailbone (coccyx) that progressed to a serious pressure ulcer. On February 6, his condition improved enough to allow his transfer to a rehabilitation hospital, where he developed pressure ulcers on his heels. He was transferred to another hospital; the ulcer on his coccyx healed by August. He remained in that hospital for 1 year before being discharged home.
Despite healing of the pressure ulcer on his coccyx, the wound area remained hard and painful, and Mr. M experienced “daily discomfort” there. Also, he was unable to do many of the things he’d been able to do before his hospitalization.
Mr. M files a medical malpractice suit
Mr. M sued the medical center, alleging the hospital was negligent by failing to prevent the pressure ulcer from forming through the use of known “pressure relief” methods, and that the hospital failed to provide proper care and treatment of the wound once it was discovered.
At trial, the medical center lawyers argued that Mr. M’s grave condition caused the pressure ulcer to develop. The jury returned a verdict for Mr. M, finding that the medical center’s negligence proximately caused the injuries he sustained. It awarded him $35,000 for medical expenses; $135,000 for past physical pain and mental anguish; $25,000 for future physical pain and mental anguish; $25,000 for past physical impairment; and $25,000 for future physical impairment. The medical center appealed the decision.
Medical center appeals the verdict
Several issues were raised by the medical center on appeal. Of particular interest to nurses and wound care practitioners was the “cause in fact” or the “proximate cause” of Mr. M’s pressure ulcer on the coccyx. Because an expert witness must establish proximate cause based on a reasonable degree of medical certainty, Mr. M’s case became a battle of the experts regarding the care he received, or lack of care, relative to development of the pressure ulcer.
Expert witness testimony for Mr. M
The first nurse expert to testify was Mr. M’s highly qualified expert. She testified about the various acceptable ways to provide pressure relief, including turning the patient or, if the patient can’t be turned, repositioning. The latter requires use of foam wedges or pillows to elevate a particular body part. The nurse expert testified that if a patient can’t be turned or repositioned, that fact must be documented along with the reason for inability to carry out this nursing care.
Proper assessment of the pressure ulcer is required so that other team members can “see” the wound; the clinician who assesses the wound should draw a picture of exactly what he or she saw when documenting the note in the patient’s chart. The nurse expert testified that the assessment should include the color, duration, and depth of the pressure ulcer; presence or absence of infection; and whether the tissue was dead or perfused.
After reviewing the medical center’s policies and protocols on pressure relief, which required nurses to provide pressure relief every 2 hours, and the depositions of the nurses who’d cared for Mr. M, the nurse expert testified there was no documentation showing Mr. M received any pressure relief from January 13 to January 16. She said she could only conclude that the nurses failed to turn or reposition him during those days. The only notation made about his skin condition was when nurses discovered the “skin tear” on January 14. After this discovery, the physician wasn’t notified of it until January 19. On that date, the physician ordered a wound care consult, but the actual consultation didn’t occur until 3 days later. Even with the wound consultant’s specific, written orders to care for the wound, only one notation existed showing that the orders were followed. Also, the wound care orders weren’t entered into Mr. M’s care plan until January 28. Additionally, in their depositions, the nurses caring for Mr. M couldn’t recall changing the dressing as ordered.
Therefore, in the nurse expert’s opinion, the pressure ulcer on Mr. M’s coccyx was caused directly by failure of the ICU nurses to provide pressure relief from January 14 to January 16 and that providing the wound care that was ordered would have prevented the ulcer from getting worse and would have healed the ulcer.
Although a physician serving as a second expert for Mr. M also testified that pressure relief should have been provided, he couldn’t say that development of the pressure ulcer was unpreventable.
Expert witness testimony for the medical center
Not surprisingly, the medical center’s expert witnesses, two of whom were physicians, testified that because of Mr. M’s general medical condition, he would have developed the pressure ulcer even if hospital policies and protocols had been followed. The hospital’s nurse expert witness stated that Mr. M’s pressure ulcer was not preventable because of his medical condition, regardless of whether or not he was turned. In her opinion, the active range of motion his nurses put him through was enough to reperfuse the area.
Appellate court’s decision
The appellate court upheld the trial court jury’s verdict, stating that evidence presented at the trial was legally and factually sufficient to support that verdict.
Take-away points
Mr. M’s case undoubtedly was complicated by his age and general medical condition, as well as disagreement among expert witnesses as to the cause of the pressure ulcer on his coccyx. Even so, the appellate court held that the evidence at trial (specifically that presented by Mr. M’s nurse expert witness) was sufficient legally and factually to support the verdict in favor of Mr. M. This case illustrates many areas of importance for nurses in terms of formation and care of pressure ulcers. They include the following: • Risk factors supporting potential formation of pressure ulcers can’t be overlooked or underestimated by nursing staff. • A plan to prevent pressure ulcers should be initiated on admission for every patient who is immobile or has other risk factors for pressure ulcers. • Documentation of every aspect of nursing care that’s initiated and continued to prevent pressure ulcers from forming must be carried out as ordered and pursuant to hospital policy and protocol. • Care plans, communications with other health team members, and carrying out of orders must be done as soon as possible. • Assessment and documentation of pressure ulcers should include enough detail so other health team members can visualize what the nurse entering the documentation has seen. • The nurse should assess and stage the pressure ulcer at each dressing change. • One’s expert witness must be credentialed, educated, and experienced in would care prevention and treatment, because his or her testimony can win or lose a case.
Nursing remains at the forefront of protecting and safeguarding patients from pressure ulcers. Although not every ulcer can be prevented, the goal is to prevent as many ulcers as possible. If a pressure ulcer does occur, caregivers’ essential focus must be on healing or preventing further deterioration and infection.
Selected references Columbia Medical Center Subsidiary, L.P., d/b/a/ North Central Medical Center, Appellant, v. John Meier, Appellee. 198 S.W. 3d 408 (Ct. Appeals 2006).
Lyder CH, Ayello EA. Pressure ulcers: A Patient Safety Issue. In: Hughes RG, ed. Patient Safety and Quality: An Evidence-Based Handbook For Nurses. Rockville, MD: Agency For Healthcare Research and Quality. April 2008. www.ncbi.nlm.nih.gov/books/
NBK2650/. Accessed November 1, 2012.
Nancy J. Brent is an attorney in Wilmette, Illinois. The information in this article is for educational purposes only and doesn’t constitute legal advice.
There’s an app for that! Here are a variety of medical apps that you might want to try. You can download them in the iTunes store, and the basic service is free.
Medscape
More than 1.4 million healthcare professionals use this app from WebMD, which includes:
• medical news
• clinical reference information, such as drugs and diseases
• medical calculators (not available for iPad).
The app is available for Android, iPad, and iPhone/iPod touch devices.
Use this app to take a photo of a wound. The app segments the image into red, yellow, and black to help with ulcer classification. You can also use the app to track changes in the wound over time. The app is available for iPad and iPhone/iPod touch devices. Note: This is free for a limited time.
The ePSS (Electronic Preventive Services Selector) app allows you to search and browse the U.S. Preventive Services Task Force recommendations on the Web or a mobile device. The app is from the U.S. Department of Health & Human Services and is available for Android, iPad, and iPhone/iPod touch devices.
This app from the University of Michigan Health System allows users to complete and store photographs of the skin. Features include:
• guidance on performing a skin cancer self-exam and full-body photographic survey
• tracking of detected skin lesions and moles for changes over time
• notifications/reminders to perform self-exams on a routine basis
• storage of photos for baseline comparisons during routine follow-up self-
exams
• informational videos and literature on skin cancer prevention and healthy skin as well as a skin cancer risk calculator function.
The app is available for iPad and iPhone/iPod touch devices.
This data storage utility app is perfect for your patients with diabetes who want all their information in one place. Users can manually enter their glucose results, carbohydrate consumption, insulin dosages, and activities, and then view the data in a free glucosebuddy.com online account. Another option is the ability to set reminders for when it’s time to check blood glucose.
The app is available for Android, iPad, and iPhone/iPod touch devices.
Use this app to learn more about pressure ulcer staging. It includes information about 3M pressure ulcer products.
The app is available for iPad and iPhone/iPod touch devices.
This evidence-based tool is helpful for assessing and classifying peristomal skin lesions. Click here for more information about the SACS Instrument.
The app is available for iPad and iPhone/iPod touch devices.
Do you experience chronic stress? Is your body stiff and inflexible? Does your mind seem dull and sluggish, your spirit exhausted?
Restorative yoga may help “open” your joints, ease your mind, and revive your spirit. It’s based on the concept that we’re overstimulated and don’t get enough rest. Constant stimulation activates the sympathetic nervous system, overtaxing the fight-or-flight response. The body responds by increasing cortisol and glucose production, which (along with additional unhealthy responses) raises the risk of metabolic syndrome.
Restorative yoga promotes active relaxation, helping to halt the overstimulation cycle. It promotes balance by alternately stimulating and relaxing the body, which is supported in yoga poses with such props as blankets, pillows, yoga mat, and eye covers. Research suggests restorative yoga may ease hot flashes in postmenopausal women and may promote a calm, positive mood in women with ovarian or breast cancer.
Five facets of restorative yoga
Restorative yoga takes a five-faceted approach to relieve the effects of stress. Over time, you’re likely to notice a new awareness of and appreciation for your body, mind, and spirit.
Simply put, networking is an information exchange, a forum for communicating your needs or agenda and, in return, listening and responding to others’ needs or agendas. Good networking requires emotional reciprocity, which means caring about the needs and agendas of the people you network with. Caring about others’ needs is what nurses do, so networking really shouldn’t be that difficult for a nurse.
1. Using props, restorative yoga supports the body in yoga poses, helping muscles and joints release tension and achieve muscular balance.
2. The restorative poses move the spine in all directions—flexion, extension, rotation, and lateral flexion. This enhances spinal flex-ibility, lubricates vertebrae, and strengthens the deep muscles that stabilize the spine.
3. Inverted poses, in which the feet and legs are elevated, counter the effects of gravity and promote lymph and fluid drainage to the heart.
4. The poses compress and release internal organs, cleansing them while aiding removal of cellular waste and renewing oxygen and nutrients.
5. Finally, the poses balance the body’s male (prana) and female (apana) energies.
Learning the poses
To learn the poses, consider taking a restorative yoga class. (See Finding an instructor.) Beforehand, make sure to tell the instructor about any special health concerns you have, so the instructor can modify the poses for you. Expect to bring your own blankets, pillows, eye covers, and yoga mat. The class will last from 60 to 90 minutes.
Restorative yoga typically doesn’t involve active (hatha) yoga poses, although it may include stretching poses to warm muscles and joints before the restorative poses begin. The instructor will help you use your props to make the poses right for you, and will direct you into a pose using them. Expect to stay in the pose for 5 to 10 minutes. The instructor will guide you by helping you focus on your breath and turn your attention inward. If your mind wanders and your body stays active, accept this reaction and don’t judge yourself. Over time, you’ll learn to use your breath to release tension and to focus and calm your mind.
After you hold the pose for the required duration, the instructor will help you into the next one. Generally, the class is near-silent, with minimal talking; the lights are low and music may play.
When the class ends, you may feel more relaxed and in touch with yourself. If you feel restless and jittery instead, accept your reaction. Don’t judge yourself. Try again. Give yourself the opportunity to experience something different.
Restorative yoga is just one method to renew and reconnect with your inner being. Only you can know if it’s right for you. n
Selected references
Cohen B, Kanaya A, Macer J, Shen H, Chang A, Grady D. Feasibility and acceptability of restorative yoga for treatment of hot flushes: a pilot trial. Maturitas. 2007;56(2):198-204.
Danhauer SC, Tooze JA, Farmer DF, Campbell CR, McQuellon RP, Barrett R, Miller BE. Restorative yoga for women with ovarian or breast cancer: findings from a pilot study. J Soc Integr Oncol. 2008;6(2):47-58.
Lisa Marie Bernardo is the managing member of The PIlates Centre, LLC, in Hampton Township, Pennsylvania, and adjunct faculty at Carlow University School of Nursing in Pittsburgh, Pennsylvania.
To find a certified yoga instructor in your area, check the Yoga Alliance website at www.yogaalliance.com. Restorative Yoga Teachers (www.restorativeyogateachers.com) focuses exclusively on restorative yoga. This site is operated by Judith Hansen Lasater, PhD, the leader in restorative yoga practice.
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.
Traditional treatment approaches
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.
Elevation
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
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.
Pneumatic compression pump
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.
Surgery
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.
Diuretics
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
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.
Complete decongestive therapy: The current treatment approach
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.)
Manual lymph drainage
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
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
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.
Skin and nail hygiene
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.
Self-care education
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.
An underrecognized and mistreated problem
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.
Staphylococcus aureus is one of the most feared human pathogens, causing a wide range of infections. Most wound care professionals can expect to frequently encounter patients with S. aureus infections. Soft-tissue infections caused by S. aureus include impetigo, cellulitis, and cutaneous abscesses, as well as such life-threatening processes as necrotizing fasciitis and pyomyositis (a hematogenous intramuscular abscess). Serious non-soft-tissue infections include septic arthritis, osteomyelitis, pneumonia, endocarditis, and sepsis.
Why is S. aureus such a nasty bug?
S. aureus produces various cellular and extracellular factors involved in the pathogenesis of infection. S. aureus protein A, an important surface protein, helps the organism resist phagocytosis. Also, S. aureus produces several cytotoxins and enzymes that contribute to infection spread and severity. In addition, some strains produce toxins (including toxic shock syndrome toxin-1) that function as superantigens—molecules that nonspecifically trigger release of large amounts of cytokines, leading to a sepsislike condition. Taken together, such factors combine to make S. aureus a dangerous pathogen.
MRSA emergence
When penicillin was introduced in the 1940s, virtually all S. aureus isolates were sensitive to that drug. But soon thereafter, S. aureus strains that produced a β-lactamase enzyme capable of inactivating penicillin became widespread. During the 1950s, outbreaks of penicillin-resistant S. aureus occurred in many U.S. hospitals. Introduction of penicillinase-resistant antibiotics, such as methicillin and oxacillin, temporarily restored the ability to treat all strains of this pathogen using penicillin antibiotics. The first strain of methicillin-resistant S. aureus (MRSA) was described in 1961 shortly after introduction of penicillinase-resistant antibiotics.
The mechanism of methicillin resistance involves a mutation in one of the bacterial cell-wall proteins to which penicillins must bind to kill the bacterium. This mutation renders the organism resistant to all penicillins and penems and almost all cephalosporins.
MRSA incidence has increased steadily to the point where it currently constitutes up to 60% of S. aureus isolates in many U.S. hospitals. These organisms commonly carry genetic material that makes them resistant to various non-β lactam antibiotics as well, leading some to suggest that the term MRSA should stand for multiply resistant S. aureus. S. aureus has continued to mutate in the face of persistent antibiotic pressure. Vancomycin-intermediate S. aureus (VISA) was described in 1997; vancomycin-resistant S. aureus (VRSA), in 2003. Fortunately, these two strains remain rare and haven’t become established pathogens. (See Strains of antibiotic-resistantS. aureus by clicking the PDF icon above.)
Healthcare- versus community-acquired MRSA
Although MRSA initially arose and spread within healthcare settings (chiefly acute-care hospitals), a community-based variant was described in 1998. Called community-
acquired MRSA (CA-MRSA), this variant differs from healthcare-associated MRSA (HCA-MRSA) in more ways than the acquisition site. CA-MRSA occurs predominately in otherwise healthy children and young adults.
It most commonly presents as recurrent cutaneous abscesses, although life-threatening infections (such as necrotizing fasciitis and pneumonia) also have occurred. The propensity to cause cutaneous abscesses isn’t fully understood but may relate partly to production of the Panton-Valentine toxin by many CA-MRSA isolates.
In contrast, HCA-MRSA afflicts mainly older patients, particularly those with chronic illnesses, including chronic wounds. It typically causes wound infections, urinary tract infections, pneumonia, and bacteremia.
Besides these epidemiologic and clinical differences, many CA-MRSA isolates derive from a single clone, known as clone USA 300, whereas HCA-MRSA is composed of multiple non-USA 300 clones. Finally, many CA-MRSA isolates are sensitive to non-β
lactam antibiotics, whereas most HCA-MRSA isolates resist multiple antibiotics. More recently, the distinction between CA-MRSA and HCA-MRSA has been blurred as evidence emerges that CA-MRSA now is being transmitted in healthcare settings as well as in the community.
S. aureus carrier state
Staphylococci are frequent colonizers of humans. Common colonization sites include the skin, anterior nares, axillae, and inguinal regions. Individuals can be colonized continuously or transiently, with nasal carriage rates varying from 20% to 40%. Most S. aureus infections result from the strain carried by the infected patient.
Three patterns of S. aureus carriage exist in humans:
• 20% of individuals are continuously colonized.
• 30% of individuals are intermittently colonized.
• 50% of individuals are never colonized.
The highest carriage rates occur in patients receiving frequent injections (such as insulin-dependent diabetics, hemodialysis patients, and I.V. drug users) and those with chronic skin conditions (for instance, psoriasis or eczema). In the general population, MRSA carriage rates have increased to 1% or 2%, with clinical consequences hinging on the colonizing strain (CA-MRSA versus HCA-MRSA) and host characteristics. The most consistent carriage site is the anterior nares, but many other sites may carry this pathogen, including the axillae, inguinal regions, and perirectal area.
MRSA treatment
Therapy for MRSA infection depends on the infection location and antibiotic sensitivity of the infecting strain.
• Cutaneous abscesses are treated by incision and drainage; antibiotics play a secondary role to adequate drainage.
• Therapy for necrotizing fasciitis caused by MRSA involves aggressive debridement with removal of all necrotic tissue, plus adequate antibiotic therapy. Typically, patients require serial debridement followed by subsequent careful wound care, often with eventual skin grafting.
• Pyomyositis treatment entails drainage of the muscle abscess (which sometimes can be done with percutaneous tube placement instead of open drainage), plus appropriate antibiotic therapy.
Vancomycin has been the mainstay of I.V. therapy for MRSA for decades, but some clinicians are concerned that its effectiveness may be declining due to slowly increasing minimum inhibitory concentrations (the minimum concentration of an
antibiotic needed to inhibit pathogen growth). Other parenteral options have emerged in the last few years. (See I.V. drugs used to treat MRSA by clicking the PDF icon above.) Several oral antibiotics also are available for MRSA treatment. (See Oral agents used to treat MRSA by clicking the PDF icon above.)
Knowing the antibiotic sensitivity pattern of the infecting MRSA strain is crucial to ensuring that the patient receives an appropriate antibiotic. Treatment duration for soft-
tissue infections usually ranges from 7 to 14 days, but bacteremia and bone or joint infections call for more prolonged therapy.
Efforts to eradicate MRSA carriage
Because the carrier state increases the risk of subsequent S. aureus infection, efforts have been made to eradicate carriage. Unfortunately, this has proven to be difficult. A commonly used regimen involves 5 days of twice-daily mupirocin nasal ointment with either chlorhexidine gluconate showers or immersion up to the neck in a dilute bleach solution. However, success in eliminating carriage is limited, although the bleach bath seems to improve eradication rates better than other modalities.
Controlling MRSA in hospitals
How best to control MRSA spread within hospitals is controversial. Some experts advocate an aggressive, “search and destroy” approach involving screening all patients for nasal carriage on admission and initiating contact precautions with subsequent decolonization efforts. Others focus on improving the overall level of hand hygiene and other general infection-control measures, arguing that nasal screening misses at least 20% of MRSA-colonized patients and thus gives an unwarranted sense of security.
Many hospitals use a mixed approach, screening patients suspected to be at high risk for MRSA carriage (such as those admitted from extended-care facilities or to the intensive care unit), while simultaneously trying to improve hand hygiene and general infection-control measures. Recent data suggest MRSA colonization and infection rates have stopped increasing and are beginning to decline.
MRSA is one of the most problematic pathogens encountered on a regular basis, and among the most dangerous pathogens we face. While some MRSA infections are relatively mild, many are serious or life-threatening. Severe soft-tissue infections, such as necrotizing fasciitis and pyomyositis, require surgical debridement or drainage, appropriate antibiotic therapy, and assistance from a wound-care professional to achieve optimal outcomes. n
Selected references
Calfee DP. The epidemiology, treatment and prevention of transmission of methicillin-resistant Staphylococcus aureus. J Infus Nurs. 2011 Nov-Dec;34(6):359-64.
DeLeo FR, Otto M, Kreiswirth BN, Chambers HF. Community-associated meticillin-resistant Staphylococcus aureus. Lancet. 2010 May 1;375(9725): 1557-68.
Ippolito G, Leone S, Lauria FN, et al. Methicillin-resistant Staphylococcus aureus: the superbug. Int J Infect Dis. 2010 Oct;14 Suppl 4:S7-11.
Landrum ML, Neumann C, Cook C, et al. Epidemiology of Staphylococcus aureus blood and skin and soft tissue infections in the US military health system, 2005-2010. JAMA. July 4;308:50-9.
Lee AS, Huttner B, Harbarth S. Control of methicillin-resistant Staphylococcus aureus. Infect Dis Clin North Am. 2011 Mar;25(1):155-79.
Moellering RC Jr. MRSA: the first half century. J Antimicrob Chemother. 2012 Jan;67(1):4-11.
Otter JA, French GL. Community-associated meticillin-resistant Staphylococcus aureus strains as a cause of healthcare-associated infection. J Hosp Infect. 2011 Nov:79(3):189-93.
Rivera AM, Boucher HW. Current concepts in antimicrobial therapy against select gram-positive organisms: methicillin-resistant Staphylococcus aureus, penicillin-resistant pneumococci, and vancomycin-resistant enterococci. Mayo Clin Proc. 2011 Dec;86(12):1230-43.
Simor AE. Staphylococcal decolonization: an effective strategy for prevention of infection? Lancet Infect Dis. 2011 Dec;11(12):952-62.
Joseph G. Garner is director of the infectious disease division and hospital epidemiologist at the Hospital of Central Connecticut and a professor of medicine at the University of Connecticut.
In health care, we frequently use the terms formulary and protocol interchangeably even though they have different meanings. A formulary is an official list of available dressings, products, and medications. A protocol is a roadmap or guideline on how to use the formulary.
Formularies became popular several years ago when reimbursement changed to bundling and wound-product costs were included in the routine cost of care rather than separately billable. In an effort to control costs, hospitals, home health agencies, and long-term care facilities began exclusive partner agreements with supply and buying groups. (“You use our products exclusively and we’ll give you a huge discount on cost.”)
A good formulary not only can help save money. It can also assist in streamlining care delivery, reducing waste, and directing treatment decisions. But on the flip side, using formularies can have disastrous results. I realized this last week while speaking on the phone with a wound clinician who’d called to ask for wound treatment ideas for a hospice patient. As she described the situation, it became apparent that the patient’s symptoms definitely pointed to high levels of bacteria in the wound. As I began sharing recommendations for treatment ideas, she kept responding: “Nope. Can’t use that, not on our formulary.” “Nope, not on formulary.” The only options available on her hospice formulary were hydrocolloid, hydrogel, or foam dressings, none of which had antibacterial properties.
Providing an appropriate standard of care shouldn’t be dictated by a formulary, and choosing substandard care just because the patient is in hospice isn’t acceptable or appropriate. Evidence-based guidelines, wound characteristics, underlying complications, and patient care goals should dictate management and treatment.
To ensure your formulary is adequate, determine if it includes a variety of product categories, and negotiate the ability to go off formulary if needed. Although cost control is essential, clinicians need access to products and therapies that yield positive outcomes. One size doesn’t fit all in wound care.
Donna Sardina, RN, MHA, WCC, CWCMS, DWC, OMS
Editor-in-Chief Wound Care Advisor
Cofounder, Wound Care Education Institute
Plainfield, Illinois
Before discharge, a new ostomy patient and caregiver have a lot to learn, including how to empty the pouch, establish a schedule for pouch changes, measure the stoma to ensure protection from effluent, and use accessory supplies appropriately.
Lymphedema is characterized by regional immune dysfunction, distorted limb contours, and such skin changes as papillomas, hyperkeratosis, and increased girth. The condition may involve the limbs, face, neck, trunk, and external genitals; its effects may include psychological distress. For optimal patient management, clinicians must understand what causes lymphedema and how it’s diagnosed and treated.
This two-part series provides an overview of lymphedema. Part 1 covers etiology, pathology, and diagnosis. Part 2, which will appear in the November-
December issue, will focus on treatment.
Causes of lymphedema
Lymphedema occurs when protein-rich fluid accumulates in the interstitium due to impaired lymphatic function. Proteins, other macromolecular wastes, and water constitute lymphatic loads. These wastes rely on specially structured absorptive and transport structures in peripheral regions for their return to central circulation.
When lymph stasis prevails, inflammatory processes and lymphostatic fibrosis trigger tissue-density changes, further entrapping superficial vessels and accelerating mechanical insufficiency. (See Physiologic changes caused by lymphatic disruption by clicking the PDF icon above.)
Classifying lymphedema
Lymphedema can be primary or secondary. Primary lymphedema either is congenital (present at birth) or arises around puberty. In the vast majority of cases, it is associated with structural changes in the lymphatic system and isn’t associated with another disease or condition. Most structural changes (87%) manifest before age 35 and cause hypoplasia of vessels and nodes. Syndromes involving hyperplasia, node fibrosis, or aplasia also may occur, although they’re much less common. Dysplasia (either hypoplasia, hyperplasia, or aplasia) predisposes drainage regions to inadequate lymph collection, resulting in edema and secondary tissue changes, such as chronic inflammation and reactive fibrosis. Genetic variability in lymphatic constitution may explain why seemingly similar patients receiving the same surgical protocol have different lymphedema risks over time. Secondary lymphedema stems from a significant insult to lymphatic tissues, as from lymphadenectomy, radiation therapy, trauma, infection, or cancer. It commonly results from direct trauma to regional nodes or vessel structures. Slow degradation of lymphatic function also occurs when adjacent tissues (such as superficial and deep veins) become diseased, when cellulitis occurs, or when accumulations
of adipose or radiation fibrosis mechanical-ly disrupt drainage of skin lymphatics.
Lymphedema stages
Lymphedema progresses in stages, which involve secondary connective-tissue disease combined with disturbed fluid update and transport. These conditions cause a universal and classic clinical picture.
• Stage 0 (latency stage) is marked by reduced transport capacity and functional reserve. The patient has no visible or palpable edema, but has such subjective complaints as heaviness, tightness, and waterlogged sensations.
• In Stage 1 edema (reversible lymphedema), edema decreases with elevation. Pitting edema is present, but fibrosis is absent.
• During Stage 2 (spontaneously irreversible lymphedema), lymphedema doesn’t resolve entirely, although it may fluctuate. Pitting is more pronounced and fibrosis is present.
• Stage 3 (lymphostatic elephantiasis) is marked by dermal hardening, nonpitting edema, papillomas, hyperkeratosis, and in some cases, extreme girth.
Assessment and diagnosis
Diagnosing lymphedema can be challenging because edema may be associated with other diseases and disorders. For a summary of signs and symptoms, see Clinical findings in lymphedema by clicking the PDF icon above.
Discomfort and skin appearance
Lymphedema rarely causes pain because the skin accommodates gradual, insidious fluid accumulation. However, secondary orthopedic discomfort may result from increased weight of the affected limb due to deconditioning or decreased range of motion.
Because lymphedema usually progresses slowly, gravity and centrifugal forces pull fluids toward distal limb areas, causing an entrenched, stubborn pitting edema. Later, further valvular incompetence contributes to worsening distal edema in the fingers, toes, and dorsal regions of the hand and foot. Prominent lower-extremity structures, such as the malleolus, patella, tibia, anterior tibialis tendon, and Achilles tendon, become progressively less distinct. This creates a columnar limb appearance; the swollen limb has the same girth from distal to proximal aspects, unlike the natural cone shape of a normal limb.
Lymphatic failure doesn’t tax the venous system, so skin color remains normal. Blood supply remains patent, helping to prevent secondary ulcers.
Severity
Lymphedema severity correlates directly with such factors as onset of the condition and extent of cancer therapy, if given (number of nodes resected, number of positive nodes, and use of radiotherapy). Lymphedema may worsen with a greater number of infection episodes, weight gain, injury, diuretics, limb disuse, pneumatic compression therapy (when used for pure lymphedema), and ill-fitting compression garments. The single most important contributor to increasing lymphedema severity is lack of patient education, which can result in improper treatment or none at all.
Opportunistic infections
Lymphedema causes regional immune suppression and leads to an increase in opportunistic infections such as cellulitis. As skin integrity suffers, scaling and dryness allow resident skin pathogens (such as streptococci and staphylococci) to gain access through the defective skin barrier into protein-rich interstitial fluid, creating a medium favorable to bacterial colonization. Lymphocyte migration decreases, and dissected or irradiated nodal sites are slow to detect invaders. Furthermore, stagnant lymph promotes further delays in the immune response. Patients with opportunistic infections may exhibit high fever, local erythema, regional hypersensitivity or acute pain, flulike symptoms, and rapidly advancing “map-like” borders in the skin.
Differential diagnosis
Several methods can aid differential diagnosis. Clinical findings. Lymphedema can be diagnosed from patient history, physical examination, palpation, and inspection. Trauma to lymph nodes (each of which governs a distinct body region) decreases the transport capacity of lymph formed in that region, in turn causing local swelling (lymphedema). Trauma to the axillary or inguinal lymph nodes, which exist on both the left and right of the body and in both the upper and lower regions, predisposes these quadrants to swelling. Therefore, if lymph nodes on only one side are damaged, lymphedema occurs only on that side of the body. Using the universal characteristics cited above as a guide, while ruling out cancer recurrence, acute deep vein thrombosis, or plasma protein abnormalities, yields sufficient data to form a diagnosis. Imaging. Lymphography involves subcutaneous injection of a lymph vessel–
specific dye (Patent Blue V), followed by X-ray. Although it provides high-resolution images of lymphatic structures, this technique is invasive, painful, damaging to lymphatics, and potentially lethal—and therefore is no longer recommended.
Lymphangioscintigraphy (LAS) uses interdigital subcutaneous injection of protein-labeled radioisotopes, followed by
imaging at specific intervals to gather information about uptake and transport time. Images are hazy and false-negatives are common, so well-trained radiotherapists familiar with lymphology and lymphedema should administer and interpret the test. Also, experts don’t agree on standard criteria for LAS administration, so measures may not be similarly conclusive. Limb-measuring instruments and methods. Serial measurement of affected limb circumference using a standard garment tape measure is the most widely accessible approach. Intra-rater reliability is comparable to that of currently used tools; however, these methods can’t be used for early detection, for screening, or when various raters are used to assess the same patient. Circumferences are measured at four points and are considered positive if a distance of 2 cm or more separates the involved from uninvolved extremity in comparison. Water displacement techniques for limb-volume calculation, although accurate, are impractical in most clinical settings and rarely used.
Various devices have been used to obtain measurements. For instance, the Perometer® uses optoelectronic volumetry. By scanning the limb with infrared beams circumferentially, the device accurately records girth at 4-mm intervals along the limb length and transmits these measurements to a computer. The Perometer is used mainly in the research setting. Preoperative and postoperative measurements at intervals can detect lymphedema early.
Impedimed XCA® uses bioelectrical
impedance to calculate ratios of intracellular to extracellular fluid. A weak electrical current is passed through affected and unaffected limbs, allowing comparison of results. Impedance is lower in edematous tissue, supporting an accurate diagnosis.
Next step: Treatment
Once a diagnosis is made, the next step is treatment. Part 2 of this series covers lymphedema treatment.
Selected references
Foeldi M. Foeldi’s Textbook of Lymphology: For Physicians and Lymphedema Therapists. 3rd ed. St. Louis, MO: Mosby; 2012.
Kubik S, Manestar M. Anatomy of the lymph capillaries and precollectors of the skin. In: Bollinger A, Partsch H, Wolfe JHN, eds. The Initial Lymphatics. Stuttgart: Thieme-Verlag; 1985:66-74.
Lee B, Andrade M, Bergan J, et al. Diagnosis and treatment of primary lymphedema. Consensus document of the International Union of Phlebology (IUP)—2009. Int Angiol. 2010 Oct;29(5):454-70.
Lerner R. Chronic lymphedema. In: Prasad H, Olsen ER, Sumpio BE, Chang JB, eds. Textbook of Angiology. Springer; 2000.
Mayrovitz HN. Assessing lymphedema by tissue indentation force and local tissue water. Lymphology. 2009 June;42(2):88-98
Pecking AP, Alberini JL, Wartski M, et al. Relationship between lymphoscintigraphy and clinical findings in lower limb lymphedema (LO): toward a comprehensive staging. Lymphology. 2008 Mar;41(1):1-10.
Stanton AW, Northfield JW, Holroyd, B, et al. Validation of an optoelectronic volumeter (Perometer). Lymphology. 1997 June;30(2):77-97
Weissleder H, Schuchhardt C. Lymphedema: Diagnosis and Therapy. 4th ed. Viavital Verlag GmbH; 2007.
Steve Norton is cofounder of Lymphedema & Wound Care Education and executive director of the Norton School of Lymphatic Therapy in Matawan, New Jersey.
Every year, thousands of people of all ages have ostomy surgery in the United States. That means no matter where you work, you’re likely to care for patients with new ostomies and teach them to care for themselves. (See Why patients need ostomy surgery by clicking the PDF icon above.)
These patients present two challenges: staying up-to-date on ostomy equipment and procedures and having only 3 to 5 days after surgery to teach basic ostomy care to patients who are unlikely to be physically or emotionally ready to learn. This review and update of ostomy care should help you meet both challenges. Let’s start with the common types of stomas and ostomies.
Reviewing stoma types
The three common types of stomas are the end stoma, loop stoma, and double-barrel stoma. The patient’s surgeon decides on the most appropriate type based on the disease or injury, the amount of intestine available, and the patient’s health status.
To create an end stoma, the most common type, a surgeon creates a small opening in the abdominal wall, then resects the intestine and pulls it through the opening. Next, the surgeon turns the end of the intestine onto itself—somewhat like cuffing a sock—and sutures the stoma to the skin. Next to the stoma, the surgeon may create a mucous fistula, which secretes mucus from the nonfunctioning portion of the intestine.
A loop stoma is usually created for a temporary ostomy. The surgeon creates a small opening in the abdominal wall and pulls a loop of intestine through it. With an external rod or bridge placed under the loop to keep it from slipping back into the peritoneal cavity, the surgeon cuts the top of the loop to form the apex of the stoma. Next, the surgeon everts the intestine around the opening and sutures the stoma edges to the skin. After a few days, the rod is removed, and the stoma stays above skin level on its own. Double-barrel stomas aren’t common in adults, but they are used frequently in neonates. For this type, a surgeon cuts through the bowel to create two separate end stomas, one to evacuate stool and the other to evacuate mucus. The two stomas can be placed next to each other, so one pouching system can be used for both. If the stomas are further apart, the patient may need two pouches. If mucus secretions are slight, you may be able to apply a nonadherent dressing after gently cleaning the stoma and peristomal skin, instead of using a pouch.
An ideal stoma protrudes above the skin surface and has a flat peristomal skin surface that allows the ostomy barrier to adhere to it. (See Characteristics of an ideal stoma by clicking the PDF icon above.) A healthy stoma is red and moist and looks like gum tissue. In fact, the entire alimentary canal from mouth to anus has the same type of tissue. Keep in mind that while cleaning a stoma, you’ll commonly see a small amount of bleeding, just as your gums may bleed when you brush your teeth too vigorously. If you note excessive bleeding, report it immediately.
Reviewing types of ostomies
The three most common types of ostomies you’ll see are a colostomy, an ileostomy, and a urostomy.
A surgeon creates a colostomy by making an opening in the large intestine and connecting it to the stoma. The location of the surgical opening will affect the consistency of the stool exiting the body through the stoma: The lower the opening, the firmer the consistency. A colostomy produces flatus because of the high bacterial content in the large intestine. A colostomy can be temporary or permanent, depending on the diagnosis and the patient’s ability to heal.
To create an ileostomy, a surgeon makes an opening in the small intestine and forms a stoma. Patients with ileostomies are prone to dehydration because a large amount of enzymatic fluid is discharged through the ileostomy instead of being absorbed in the disconnected large intestine. Teach your patient to be alert for the signs and symptoms
of dehydration—thirst; decreased urination; darker, concentrated urine; warm, flushed skin; fever; and malaise. Also, warn the patient to keep enzymatic effluent off the skin because it can quickly cause skin breakdown. As with a colostomy, an ileostomy may be temporary or permanent.
To create a urostomy, a surgeon removes the diseased bladder and uses a portion of resected small intestine to create a conduit. The ureters, which were connected to the bladder, are sutured into the resected small intestine so urine can exit the body through the stoma. Urostomies are permanent.
Choosing the right pouching system
An ostomy pouching system has two parts: an adhesive barrier that attaches to the skin around the stoma and a pouch connected to the barrier that collects effluent. Determining the right ostomy pouching system for your patients will depend on their needs and preferences. Let’s look at some of the important choices.
A pouching system may come in one or two pieces. With one-piece systems, the barrier (also called the wafer, flange, or baseplate) and pouch come as a single unit. (See One- and two-piece ostomy pouching systems by clicking the PDF icon above.) One-piece systems are easier to apply and more flexible. Plus, they’re flatter and thus more discreet.
With two-piece systems, the barrier and pouch are separate components that must be attached. Depending on the product, the patient may need to press the pouch onto the barrier or use a locking ring mechanism or an adhesive coupling system. Two-piece systems allow the patient to remove the pouch without removing the barrier. Also, a patient can apply a smaller pouch, such as a stoma cap or close-ended pouch, before exercise or intimate relations.
Today, ostomy pouching systems offer many options that weren’t available just a few years ago—options such as built-in, varying levels of convexity and integrated closures. Skin-friendly barriers now eliminate the need for accessory products, such as skin prep, ostomy powder, and stoma paste. By knowing the new options, you can help simplify the pouch application process for your patient and increase patient satisfaction.
Selecting barriers
Barriers may be cut-to-fit or precut. Cut-to-fit barriers are used during the postoperative period while the stoma size is changing and for oval or irregularly shaped stomas. Precut sizes are convenient for round stomas after they stabilize.
The choice of a barrier also depends on abdominal contours and the effluent consistency. A standard-wear barrier is appropriate for thicker output. An extended-wear barrier is better for loose or watery output and for problematic ostomies.
Convex barriers can be used to push down the peristomal skin and help the stoma project into the pouch. These barriers help ensure that the effluent goes into the pouch and not between the skin and the barrier, causing leakage.
For ostomies that are difficult to manage and frequently leak, you may select an ostomy belt. This device helps secure a convex pouching system by increasing its pressure. The plastic hooks at the end of the belt attach to the belt loops of the pouching system. Depending on the manufacturer, the belt loops may be on the barrier or the pouch.
Selecting pouches
Pouches can be transparent or opaque. Transparent pouches allow you to see the stoma postoperatively and allow patients to watch as they place the pouch over the stoma. Opaque pouches, of course, have the advantage of concealing the effluent.
Some pouches have filters. Colostomy patients usually prefer filtered pouches because they eliminate the need to burp the pouch to remove gas. Ileostomy output is usually watery, so the charcoal filters may get wet and quit working.
The appropriate type of pouch closure also varies, depending on the type of output and the patient’s needs and preferences. A patient with a colostomy or ileostomy needs a drainable pouch. Newer clamps and integrated closures can make closing the pouch easier for the patient.
Close-ended pouches are available for patients who empty their pouch once or twice a day. Reimbursement guidelines for Medicare, which most insurance companies follow, allow 60 close-ended pouches a month. Thus, someone who empties once or twice a day will have enough pouches.
Patients with urostomies use pouches with spigots on the end to allow for urine drainage.
Urostomy pouches can be connected to a continuous urinary drainage bag at bedtime or to a leg bag during the day for those in a wheelchair.
Dealing with complications
Report the following postoperative complications to the surgeon and the ostomy clinician caring for the patient:
• allergic reaction
• candidiasis
• contact dermatitis
• folliculitis
• ischemic or necrotic stoma
• mechanical irritation
• mucocutaneous separation
• parastomal hernia
• prolapse.
Many complications result from surgical technique or the patient’s disease status, but complications also result from an incorrect fit or an ostomy that frequently leaks. To determine why and where leakage occurred, examine the back of the barrier. If leakage results from a flush or recessed stoma or an irregular surface around the stoma, the patient may need a convex barrier. Or the patient may need a convex barrier and an ostomy belt.
Remember that a firm abdomen requires a soft, flexible barrier that conforms to the abdominal contours. A soft belly, on the other hand, may need the rigidity of a convex barrier to help the stoma empty into the pouch.
For weepy, extremely denuded skin, apply ostomy powder, brush off the excess, and dab an alcohol-free skin sealant, such as No-Sting by 3M, on the area. Allow the area to air-dry before applying the barrier.
Discharge planning and patient teaching
Because the postoperative length of stay is short, start preparing for discharge and teaching the pouch-change procedure at your first hospital encounter with the patient. Teaching the patient at each encounter creates a continuum of care throughout hospitalization and recovery. If possible, include the caregiver. (See Teaching your patient to change an ostomy pouch by clicking the PDF icon above.) Before discharge, give the patient two or three ostomy pouches to take home, step-by-step printed instructions on applying pouches, a list of supplies the patient will need, and a list of ostomy product suppliers in the area.
Also, teach the patient about complications, activity, diet, and drug therapy and provide the names of local support groups. (See Finding support by clicking the PDF icon above.)
Complications at home
Tell the patient to call the physician if any of the following occurs: fever, increased pain or discomfort, diarrhea, dehydration, or signs and symptoms of infection at the surgical site. The patient should also call the physician if there’s no output from the stoma for more than 24 hours.
Patients with urostomies who develop the following signs and symptoms may have a urinary tract infection: fever, chills, abdominal or retroperitoneal pain, and bloody, cloudy, or foul-smelling urine. Clear urine with mucus shreds is normal.
Increasing activity
Explain that after surgery the patient should feel a little bit stronger every day. Teach the patient to alternate rest and activity periods and to increase the activity period a little each day while building endurance. Refer the patient to the physician for clearance to resume exercise and sexual relations.
Dietary considerations
After ostomy surgery, your patient will start on a clear liquid diet and progress to a normal, preoperative diet. The patient should reintroduce one food at a time to help determine if it’s well tolerated. High-fiber foods should be introduced slowly.
Tell your patient to expect his or her body to tolerate the food as it did before surgery: if onions caused gas before surgery, they will do so after surgery, too, but the stoma will expel the gas. Make the patient aware of other gas-forming foods, such as hard-boiled eggs, spicy foods, fish, dried beans, carbonated beverages, and beer.
Tell the patient to chew food well and to drink plenty of liquids, which will prevent blockage. Explain the importance of hydration to avoid constipation, dehydration, and urinary tract infection. To prevent dehydration, ileostomy patients who are not on fluid restriction should drink 64 ounces of fluid a day. Teach these patients to replace fluids by drinking a glass of water every time they empty their pouches.
Drug therapy
Tell the patient to adhere to the prescribed regimen and to call the physician before using any new drugs. Instruct patients with ileostomies not to take laxatives because they may become dehydrated. These patients should tell their pharmacist that they have an ileostomy, so the proper form of prescription drugs can be ordered. Extended-release tablets will not break down in time and may be found in the pouch.
Rewarding work
Keeping up with the changes in ostomy equipment and care and teaching new ostomy patients the skills they need can be challenging. But helping these patients regain the confidence and learn the skills they need to improve their quality of life makes the rewards much greater than the challenges.
Selected references
Colwell J. Principles in stoma management. In: Colwell JC, Goldberg MT, Carmel JE, eds. Fecal and Urinary Diversions Management Principles. St. Louis, MO: Mosby; 2004:240-262.
Discharge Planning for a Patient with a New Ostomy: Best Practice for Clinicians. Glenview, IL: Wound, Ostomy and Continence Nurses Society; 2004.
Hampton BG, Bryant RA. Ostomies and Continent Diversions: Nursing Management. St. Louis, MO: Mosby; 1992.
McCann E. Common ostomy problems. In: Milne C, Corbett L, Dubuc D. Wound, Ostomy, and Continence Nursing Secrets: Questions and Answers Reveal the Secrets to Successful WOC Care. Philadelphia, PA: Hanley & Belfus, Inc; 2004.
The Sarah Cole Hirsh Institute for Best Nursing Practices Based on Evidence. State of the evidence review hospital to home: Planning the transitions. 2000; Cleveland, OH.
Goranka Paula Bak is an Ostomy Sales Territory Manager for Coloplast Corporation.
In the current healthcare environment, wound care practitioners need to capitalize on all available reimbursement avenues for care delivery and wound care supplies and dressings. And when it comes to reimbursement, there’s one constant: The rules change constantly. Whether these changes always benefit the patient is questionable. Nowhere is this more evident than in acute-care settings. Clinicians constantly are challenged to make sure their patient-care decisions comply with current Medicare reimbursement guidelines. (And if you’re not sure about today’s guidelines, be prepared for the guidelines to change tomorrow.) (more…)
Necrotizing fasciitis (NF) results from an infection that attacks the fascia and subcutaneous tissues. The primary bacterial etiology is group A streptococcus, a facultative anaerobic bacterium. However, other bacteria may contribute. Sometimes called the “flesh-eating” disease because of the potentially devastating effect on the afflicted patient, NF can be monomicrobial or polymicrobial.
The four typical settings for NF are:
surgical bowel or abdominal trauma surgery
pressure ulcer and perianal abscess
injection sites (especially in drug users)
Bartholin abscess or minor vulvovaginal infection.
Because of the rapid course and ravaging nature of acute NF, clinicians must maintain a high index of suspicion if the patient has suggestive signs and symptoms. In 1990, puppeteer Jim Henson (best known for creating the Muppets) died from NF. At that time, little was known about the progression of group A streptococcal infection.
The disease can quickly cause death, so starting immediate treatment is even more crucial than confirming the diagnosis. Once the disease is suspected, antibiotics must be given immediately and the patient must be prepared for surgery at once. NF spreads rapidly, capable of progressing from a small lesion to death in days to weeks. Thus, delayed diagnosis increases the risk of death. Lack of knowledge about the disease and inability to recognize it promptly are the main reasons many victims die. This article can improve your knowledge base.
Overview
NF was discovered in 1871 by Joseph Jones, a Confederate Army surgeon. At that time, it was called hemolytic streptococcal gangrene, nonclostridial gas gangrene, nonclostridial crepitant cellulitis, necrotizing or gangrenous erysipelas, necrotizing cellulitis, bacterial synergistic gangrene, or synergistic necrotizing cellulitis.
NF involves the fascia, muscle compartments, or both. It can affect not only the muscle fascia but the superficial fascia. NF and cellulitis differ in the amount of tissue involved and extent of tissue involvement.
The most common areas of infection are the abdominal wall, perineum, and extremities. When NF affects the perineum and scrotum, it’s called Fournier gangrene, after the French dermatologist and virologist Alfred Jean Fournier.
The most common causes are trauma, surgery, and insect bites. The disease can affect persons of any age. Such comorbidities as diabetes, chronic renal failure, immunosuppressive therapy, hypertension, obesity, and malnutrition increase susceptibility.
Pathophysiology
NF falls into four classifications based on wound microbiology. Type 1, the most common, involves polymicrobial bacteria. Type 2 results from trauma and is associated with comorbidities. Type 3, rare in this country, stems from gram-negative marine bacteria. Type 4 is a fungal infection occurring mostly in immunocompromised persons. (See Comparing types of necrotizing fasciitis by clicking the PDF icon above.)
Disease progression
The four types of NF progress in a similar way. Bacteria secrete pyrogenic exotoxin A, which stimulates cytokines. These cytokines damage the endothelial lining; fluid then leaks into the extravascular space.
M proteins in streptococci and β-hemolytic streptococci exacerbate the immune reaction by inhibiting phagocytosis of polymorphonuclear leukocytes and normal neutrophil chemotaxis. As the immune reaction increases, blood vessels dilate, allowing toxins to leak through vessel walls, which in turn decreases blood flow. As the cascade continues, hypoxic conditions cause facultative aerobic organisms to grow and become anaerobic. These bacteria exacerbate destruction of surrounding cells and lead to release of carbon dioxide, water, hydrogen, nitrogen, hydrogen sulfide, and methane. As the infection continues to progress, toxins spread throughout the bloodstream and the patient becomes septic.
Assessment
Obtain the patient’s medical history and description of the wound. Determine when the changes first appeared and whether the affected area seemed to get worse recently.
In all NF types, patients commonly present with a small, painful area (possibly with entry marks) but no other signs or symptoms. The wound may appear as a bulla, cellulitis, or dermatitis, representing an infection developing in underlying tissues. The skin may have a wooden-hard feel as the infection progresses to the subcutaneous space and causes necrosis. The wound becomes discolored and necrotic; drainage is rare until surgical debridement begins. The patient quickly develops fever, chills, nausea, and vomiting. As NF progresses, bullae become dark purple with darkened edges; the patient grows disoriented and lethargic, and organ failure and respiratory failure
ensue. Without treatment, the patient dies.
Diagnosis
Diagnostic tests usually include magnetic resonance imaging, complete blood count with differential, comprehensive metabolic panel, and cultures. (See Diagnostic findings in necrotizing fasciitis by clicking the PDF icon above.)
Treatment
Immediate surgical debridement and broad-spectrum antibiotics are needed to stop the immune response to infection. Clindamycin, gentamicin, penicillin, or metronidazole may be given alone or in combination until culture results are available. Supportive care includes total parenteral nutrition for nutritional support, I.V. fluids, and oxygen. Limb amputation should be done only as a last resort.
Surgical debridement involves penetrating deep into the fascia and removing all necrotic tissue. After the first debridement, release of “dishwater fluid” may occur.
Administering hyperbaric oxygen therapy (HBOT) after the first debridement increases tissue oxygenation, thus reducing tissue destruction by anaerobic bacteria. During HBOT (usually given as a 90-minute treatment), the patient breathes 100% oxygen in an environment of increasing atmospheric pressure.
HBOT should be given in conjunction with surgical debridement (usually after each debridement) and should continue until necrotic tissue ceases and cell destruction stops. HBOT also promotes collagen synthesis and neoangiogenesis (new blood vessel growth), which boosts blood supply and oxygen to tissues.
Adverse effects of HBOT include ear pain, oxygen toxicity, and seizures. Ear pain can be minimized by swallowing or yawning. If the patient continues to have ear pain, ear tubes may be inserted by an otolaryngologist. During HBOT, air breaks (intervals of breathing room air) are important in controlling oxygen toxicity (the main cause of seizures).
Throughout the HBOT treatment period, wound dressings must be simple. Well-moistened gauze dressings and an abdominal pad provide good support. Once necrotic destruction occurs, dressings depend on wound size and the need to fill cavities. The patient may require a diverting colostomy, depending on wound
location and the amount of uncontrolled diarrhea. Blood glucose levels must be monitored before and after HBOT, as this treatment affects blood glucose.
Supportive care and follow-up treatment
During initial treatment, patients need supportive care and monitoring. Once they’re out of danger, begin teaching them how to prevent NF recurrences. Advise them to control blood glucose levels, keeping the glycated hemoglobin (HbA1c) level to 7% or less. Caution patients to keep needles capped until use and not to reuse needles. Instruct them to clean the skin thoroughly before blood glucose testing or insulin injection, and to use alcohol pads to clean the area afterward.
Before discharge, help arrange the patient’s aftercare, including home health care for wound management and teaching, social services to promote adjustment to lifestyle changes and financial concerns, and physical therapy to help rebuild strength and promote the return to optimal physical health. One helpful patient resource is the National Necrotizing Fasciitis Foundation. The Centers for Disease Control and Prevention section on necrotizing fasciitis includes “Common sense and great wound care are the best ways to prevent a bacterial skin infection.”
The life-threatening nature of NF, scarring caused by the disease, and in some cases the need for limb amputation can alter the patient’s attitude and viewpoint, so be sure to take a holistic approach when dealing with the patient and family. Today, NF has a much better survival rate than 2 decades ago when Jim Henson died. In my practice, I’ve seen four NF cases. Thanks to early identification, good wound care, and HBOT, these patients suffered only minimal damage.
Selected references
Boyer A, Vargas F, Coste F, et al. Influence of surgical treatment timing on mortality from necrotizing soft tissue infections requiring intensive care management. Intensive Care Med. 2009;35(5):847-853. doi:10.1007/s00134-008-1373-4.
Cain S. Necrotizing fasciitis: recognition and care. Practice Nurs. 2010;21(6):297-302.
Centers for Disease Control and Prevention. Notes from the field: fatal fungal soft-tissue infections after a tornado—Joplin, Missouri, 2011. MMWR. 2011;60(29):992.
Chamber AC, Leaper DJ. Role of oxygen in wound healing: a review of evidence. J Wound Care. 2011; 20(4):160-164.
Christophoros K, Achilleas K, Vasilia D, et al. Postraumatic zygomycotic necrotizing abdominal wall fasciitis with intraabdominal invasion in a non immunosuppressed patient. Internet J Surg. 2007;11(1). doi:10.5580/17a8.
Ecker K-W, Baars A, Topfer J, Frank J. Necrotizing fasciitis of the perineum and the abdominal wall-surgical approach. Europ J Trauma Emerg Surg. 2008;
34(3):219-228. doi:10.1007/s00068-008-8072-2.
Hunter J, Quarterman C, Waseem M, Wills A. Diagnosis and management of necrotizing fasciitis. Br J Hosp Med. 2011;72(7):391-395.
Magel DC. The nurse’s role in managing necrotizing fasciitis. AORN J. 2008;88(6):977-982.
Phanzu MD, Bafende AE, Imposo BB, Meyers WM, Portaels F. Under treated necrotizing fasciitis masquerading as ulcerated edematous Mycobacterium ulcerans infection (Buruli ulcer). Am J Trop Med Hyg. 2012;82(3):478-481.
Ruth-Sahd LA, Gonzales M. Multiple dimensions of caring for a patient with acute necrotizing fasciitis. Dimens Crit Care Nurs. 2006;25(1):15-21.
Stevens DL, Bisno AL, Chambers HF, et al; Infectious Diseases Society of America. Practice guidelines for the diagnosis and management of skin and soft-tissue infections. Clin Infect Dis. 2005;41(10):1373-1406.
Su YC, Chen HW, Hong YC, Chen CT, et al. Laboratory risk indicator for necrotizing fasciitis score and the outcomes. ANZ J Surg. 2008;78(11):968-972.
Taviloglu K, Yanar H. Necrotizing fasciitis: strategies for diagnosis and management. World J Emerg Surg. 2007;2:19.
Lydia Meyers is a medical reviewer for National Government Services in Castleton, Indiana, and a clinical liaison at CTI Nutrition in Indianapolis. She has 11 years of wound care experience in nursing homes, wound clinics, and home health.
