Dermatologic difficulties: Skin problems in patients with chronic venous insufficiency and phlebolymphedema By Nancy Chatham, RN, MSN, ANP-BC, CWOCN, CWS; Lori Thomas, MS, OTR/L, CLT-LANA; and Michael Molyneaux, MD
Skin problems associated with chronic venous insufficiency (CVI) and phlebolymphedema are common and often difficult to treat. The CVI cycle of skin and soft tissue injury from chronic disease processes can be unrelenting. If not properly identified and treated, these skin problems can impede the prompt treatment of lymphedema and reduce a patient’s quality of life.
This article reviews skin problems that occur in patients with CVI and phlebolymphedema and discusses the importance of using a multidisciplinary team approach to manage these patients. (more…)
By Nancy Chatham, RN, MSN, ANP-BC, CCNS, CWOCN, CWS, and Lori Thomas, MS, OTR/L, CLT-LANA
An estimated 7 million people in the United States have venous disease, which can cause leg edema and ulcers. Approximately 2 to 3 million Americans suffer from secondary lymphedema. Marked by abnormal accumulation of protein-rich fluid in the interstitium, secondary lymphedema eventually can cause fibrosis and other tissue and skin changes. (more…)
One of the worst fears of a wound care clinician is inadvertently compressing a leg with critical limb ischemia—a condition marked by barely enough blood flow to sustain tissue life. Compression (as well as infection or injury) could lead to necrosis, the need for amputation, or even death. The gold standard of practice is to obtain an ankle-brachial index (ABI) before applying compression. However, recent research and expert opinion indicate an elevated or normal ABI is deceptive in patients with advanced diabetes. What’s worse, in the diabetic foot, skin may die from chronic capillary ischemia even when total blood perfusion is normal. For information on how to perform an ABI and interpret results, click on this link. (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.
By Nancy Chatham, MSN, RN, ANP-BC, CWOCN, CWS, and Carrie Carls, BSN, RN, CWOCN, CHRN
Moisture-related skin breakdown has been called many things-perineal dermatitis, irritant dermatitis, contact dermatitis, heat rash, and anything else caregivers could think of to describe the damage occurring when moisture from urine or stool is left on the skin. At a 2005 consensus conference, attendees chose the term incontinence-associated dermatitis (IAD).
IAD can be painful, hard to properly identify, complicated to treat, and costly. It’s part of a larger group of moisture-associated skin damage that also includes intertrigo and periwound maceration. IAD prevalence and incidence vary widely with the care setting and study design. Appropriate diagnosis, prompt treatment, and management of the irritant source are crucial to long-term treatment.
Causes
IAD stems from the effects of urine, stool, and containment devices on the skin. The skin’s pH contributes to its barrier functions and defenses against bacteria and fungus; ideal pH is 5.0 to 5.9. Urine pH ranges from 4.5 to 8.0; the higher range is alkaline and contributes to skin damage.
Skin moisture isn’t necessarily damaging. But when moisture that contains irritating substances, such as alkaline urine, contacts the skin for a prolonged period, damage can occur. Urine on the skin alters the normal skin flora and increases permeability of the stratum corneum, weakening the skin and making it more susceptible to friction and erosion. Fecal incontinence leads to active fecal enzymes on the skin, which contribute to skin damage. Fecal bacteria can penetrate the skin, increasing the risk of secondary infection. Wet skin has a lower temperature than dry skin; wet skin under a pressure load has less blood flow than dry skin.
Containment devices, otherwise known as adult diapers or briefs, are multilayer disposable garments containing a superabsorbent polymer. The polymer is designed to wick and trap moisture in the containment device. This ultimately affects the skin by trapping heat and moisture, which may cause redness and inflammation that can progress to skin erosion. This trapping can lead to increased pressure against the skin, especially if the device has absorbed liquid and remains in contact with the skin.
Categorizing IAD
IAD is categorized as mild, moderate, or severe. (See Picturing IAD by clicking the PDF icon above.)
Screening for IAD
Screen the patient’s skin for persistent redness, inflammation, rash, pain, and itching at least daily. To differentiate IAD from pressure ulcers, keep in mind that:
IAD can occur wherever urine or stool contacts the skin. In contrast, pressure ulcers arise over bony prominences in the absence of moisture.
With IAD, affected skin is red or bright red. With a pressure ulcer, skin may take on a bluish purple, red, yellow, or black discoloration.
The skin-damage pattern in IAD usually is diffuse. With a pressure ulcer, edges are well defined.
The depth of IAD-related skin damage usually is partial-thickness without necrotic tissue. With a pressure ulcer, skin damage depth may vary.
Preventing IAD
The three essentials of IAD prevention are to cleanse, moisturize, and protect.
Cleanse the skin with a mild soap that’s balanced to skin pH and contains surfactants that lift stool and urine from the skin. Clean the skin routinely and at the time of soiling. Use warm (not hot) water, and avoid excess force and friction to avoid further skin damage.
Moisturize the skin daily and as needed. Moisturizers may be applied alone or
incorporated into a cleanser. Typically, they contain an emollient such as lanolin to replace lost lipids in the stratum corneum.
To protect the skin, apply a moisture-barrier cream or spray if the patent has significant urinary or fecal incontinence (or both). The barrier may be zinc-based, petrolatum-based, dimethicone-based, an acrylic polymer, or another type. Consider using an algorithm developed by wound and skin care specialists that’s customized for skin care products your facility uses. (See Skin care algorithm by clicking the PDF icon above.)
If the treatment protocol fails, the patient should be referred to an appropriate skin care specialist promptly.
To help prevent urine or stool from contacting the patient’s skin, consider using a male external catheter, a female urinary pouch, a fecal pouch, or a bowel management system. Avoid containment devices. If the patient has a containment pad, make sure it’s highly absorbent and not layered, to decrease pressure under the patient.
Managing IAD
A comprehensive multidisciplinary approach to IAD is essential to the success of any skin care protocol. Identify skin care champions within your facility and educate them on IAD. Incorporating administrators, physicians, nursing staff, therapists, and care assistants makes implementation of protocols and algorithms within an institution seamless.
Administrators support the skin care program in the facility, including authorizing a budget so product purchases can be made. The certified wound clinician is the team expert regarding skin care, incontinence, prevention, and product recommendation. The physician oversees protocol development and evaluates and prescribes additional treatment when a patients fails to respond to treatment algorithms. Nursing staff identify patients at risk, incorporate the algorithm into the patient’s plan of care, and direct care
assistants. Therapists address function, strength, and endurance issues to improve the patient’s self-care abilities in activities of daily living to manage or prevent episodes of incontinence.
In severe inflammation, topical dressings, such as alginates and foam dressings, may be used along with topical corticosteroids. In complex IAD, antifungals or antibiotics may be required if a secondary fungal or bacterial infection is suspected.
Additional diagnostic tests may be done to identify and treat secondary infections. These tests may include skin scraping, potassium hydroxide test or Gram’s stain for fungal components, or a swab culture and sensitivity for bacterial infections. If your patient has a suspected secondary fungal or bacterial infection, use appropriate treatments for the full course of recommended therapy. In severe secondary fungal infection, an oral agent may be added to topical therapy. If cost is a concern, consider using a pharmacy knowledgeable about compounding for topical combination therapies.
Referrals and education
For assessment and treatment of under-lying incontinence, refer the patient to a continence specialist if appropriate. Teach the patient strategies for managing incontinence through dietary measures, toileting programs, pelvic-floor muscle training, clothing modification, and mobility aids.
Selected references
Beguin A, Malaquin-Pavan E, Guihaire C, et al., Improving diaper design to address incontinence associated dermatitis. BMC Geriatrics. 2010;10:86. http://www.biomedcentral.com/1471-2318/10/86. Accessed March 15, 2012.
Black JM, Gray M, Bliss DZ, et al. MASD part 2: incontinence-associated dermatitis and intertriginous dermatitis. J Wound Ostomy Continence Nurs. 2011; 38(4):359-370.
Bliss DZ, Zehrer C, Savik K, et al. An economic evaluation of four skin damage prevention regimens in nursing home residents with incontinence: economics of skin damage prevention. J Wound Ostomy Continence Nurs. 2007;34(2):143-152.
Denat Y, Khorshid L. The effect of 2 different care products on incontinence-associated dermatitis in patients with fecal incontinence. J Wound Ostomy Continence Nurs. 2011;38(2):171-176.
Doughty DB. Urinary and Fecal Incontinence: Current Management Concepts. 3rd ed. St. Louis, MO: Mosby Elsevier; 2006.
Gray, M. Optimal management of incontinence-associated dermatitis in the elderly. Am J Clin Dermatol. 2010;11(3):201-210.
Gray M, Beeckman D, Bliss DZ, et al. Incontinence-associated dermatitis: a comprehensive review and update. J Wound Ostomy Continence Nurs. 2012;39(1):61-74
Gray M, Bliss DZ, Doughty DB, et al. Incontinence-associated dermatitis: a consensus. J Wound Ostomy Continence Nurs. 2007;34(1):45-54.
Gray M, Bohacek L, Weir D, et al. Moisture vs pressure: making sense out of perineal wounds. J Wound Ostomy Continence Nurs. 2007;34(2):134-42.
Junkin J, Lerner-Selekof JL. Prevalence of incontinence and associated skin injury in the acute care inpatient. J Wound Ostomy Continence Nurs. 2007;34(3):260-269.
Landefeld CS, Bowers BJ, Feld AD, et al. National Institutes of Health state-of-the-science conference statement: prevention of fecal and urinary incontinence in adults. Ann Intern Med. 2008;148(6):449-458.
Langemo D, Hanson D, Hunter S, et al. Incontinence and incontinence-associated dermatitis. Adv Skin Wound Care. 2011;24(3):126-142.
Nancy Chatham is an advanced practice nurse at Passavant Physician Associates in Jacksonville, Illinois. Carrie Carls is the nursing director of advanced wound healing and hyperbaric medicine at Passavant Area Hospital in Jacksonville, Illinois.
