Essential Treatment Tips For Decubitus Ulcers
Given the prevalence and problematic nature of decubitus ulcers in at-risk patients, these authors review proper staging, keys to debridement and other principles for facilitating successful wound closure.
Over the last decade, the prevalence of pressure sores in hospitalized patients has reportedly ranged between 14 to 21 percent.1 With the costs to heal a single full-thickness pressure sore soaring as high as $70,000 and overall annual costs estimated between $5 billion and $8.5 billion, it is not only an unnecessary and preventable complication but also a costly epidemic.1,2
Furthermore, the costs of treating National Pressure Ulcer Advisory Panel (NPUAP) stage IV ulcers are reported to be about 10 times more than the cost of treating stage II ulcerations.3 The most effective method to reducing these costs is early recognition and treatment to prevent progression. Understanding the mechanism of insult is key not only for early recognition but, more importantly, prevention.
Decubitus ulcers develop when there is prolonged pressure on the skin, soft tissue, muscle and bone above capillary filling pressure (approximately 32 mmHg). Pressure, shear forces and friction cause microcirculatory occlusion, resulting in ischemia, inflammation and tissue anoxia, which can eventually lead to cell death, necrosis and ulceration. Irreversible damage may occur in as little as two hours of uninterrupted pressure. The skin itself can withstand ischemia from direct pressure for up to 12 hours but the underlying muscle, which has higher metabolic requirements for oxygen, may have already had significant damage by the time the skin shows any signs of injury.4
While we know prolonged, uninterrupted pressure causes the ulcers, impaired mobility and sensation are what predispose patients to developing the ulcers. Accordingly, the first step is acknowledging that every patient with limited mobility is at risk for developing pressure ulcerations. At-risk patients also include those with decreased neurological sensations or those on certain medications that decrease or eliminate stimuli for repositioning and pressure relief.5 Skin integrity can also be compromised by malnutrition and systemic diseases that affect skin turgor and make skin more susceptible to breakdown.
A Guide To Assessing The Patient
In developing a treatment plan, the clinician should not only assess the wound but the patient as well. This includes obtaining a complete history and physical, identifying comorbidities and the potential for complications, nutritional assessment and assessing the risk for additional pressure ulcers. Pay special attention to identifying and facilitating the management of illnesses that might impede healing. Such illnesses include peripheral vascular disease, diabetes, collagen vascular diseases, malignancies and depression. Physicians may control contractures or spasticity pharmacologically with benzodiazepines or other muscle relaxants.
Nutritional status assessment and management are essential to the successful treatment of pressure ulcers. One must ensure that patients have an adequate intake of protein and calories. Not only have researchers demonstrated that malnutrition increases the risk of development of new pressure ulcers, a recent meta-analysis showed positive effects of oral nutritional supplementation on pressure ulcer healing as well as risk reduction.6,7
When treating decubitus ulcerations, offloading and wound care are key. First, identify the cause of pressure. Frequent repositioning of the patient (every two hours), specialized bedding (air mattress) and protective foam padding/boots are all current mainstays in care. Individuals with existing pressure ulcers are at a higher risk for developing additional ulcers on either the contralateral side or in a new area of pressure on the ipsilateral side. It is important to make sure that the current offloading techniques are not magnifying pressure in a new location. A doughnut-type device, while offloading the actual ulceration site, unfortunately increases the pressure on the surrounding uninvolved sites. The goal of tissue load management is to create an environment that enhances soft tissue viability and promotes healing of the pressure ulcer.8
What You Should Know About Evaluating And Staging The Wound
When one first identifies a wound, the podiatrist should initiate an immediate treatment protocol, which involves not only the patients and their caregivers but the primary care physician, physical therapists and nursing staff as well. One should assess the wound for location, stage, base appearance and size as well as the presence of exudate, undermining, tunneling or fluctuance. Monitor the wound regularly and clearly document detailed findings, measurements, staging of the wound and the treatment plan. An accurate initial assessment of the wound is crucial in order to ensure comprehensive treatment.
Pressure ulcers are generally classified by the degree of tissue damage involved. The stages, as outlined by the NPUAP, are as follows.9
Stage 0. This is a suspected deep tissue injury, consisting of a purple or maroon localized area of discolored, intact skin or a blood-filled blister due to damage to the underlying soft tissue from pressure and/or shear forces.
Stage I. This stage includes intact skin with signs of impending ulceration including blanchable erythema/reactive hyperemia.
Stage II. In this stage, there is a partial thickness loss of skin involving the epidermis and dermis, which appears as an open shallow ulcer with a pink wound bed.
Stage III. The patient has a full thickness loss of skin with extension into subcutaneous tissue but not through the underlying fascia.
Stage IV. This stage comprises a full thickness loss of skin with extension into the muscle, bone, tendon or joint capsule. Slough or eschar may be present in the wound along with a possibility of osteomyelitis.
Unstageable. Wounds that cannot be staged include a full thickness loss of tissue in which the base of the ulceration is covered by slough or eschar to the point where one cannot appreciate the full depth of the wound. Until one removes the eschar, the ulcer remains unstageable.
Key Strategies For Treating The Wound
One can address wound care in accordance with the corresponding stage of the wound and its clinical appearance. An ideal dressing should protect the wound, be biocompatible and provide ideal hydration. The challenge, however, is to keep the wound moist but the surrounding intact skin dry. For draining wounds, the dressing should control the exudate but not desiccate the base.
If the wound has signs of contamination, a silver-based dressing would be most suitable due to its bactericidal properties. For example, Silvadene is effective against gram-positive organisms, gram-negative organisms and yeast. There are many other dressings with silver that sufficiently contain contamination such as Acticoat (Smith and Nephew), Actisorb Silver (Systagenix), Silvercel (Systagenix) and Aquacel Ag (Convatec).
Stable, granular wounds with minimal drainage would benefit from hydrocolloid dressings such as DuoDerm (Convatec) or a hydrogel as they maintain the moist environment while preventing bacterial contamination. On the other hand, stable granular wounds with heavy drainage would benefit from an alginate dressing. When it comes to ulcerations with necrotic tissue or fibrinous exudate, one may pursue mechanical debridement with wet-to-dry dressings or chemical debridement with an enzymatic debrider such as collagenase (Santyl, Healthpoint Biotherapeutics).
Although eschar makes it hard to stage the wound, it is a natural protective cover for the wound. One should only debride eschar in the presence of erythema, edema, fluctuance and/or drainage. Otherwise, one should place a dry dressing on the eschar and allow it to self-avulse. When the eschar starts to avulse, the use of a chemical debridement agent can help accelerate the process.
A Closer Look At Methods Of Debridement
An important adjunct to wound care is debridement. Moist, devitalized tissue supports the growth of pathological organisms. Therefore, the removal of such tissue favorably alters the healing environment of the wound. When it comes to pressure ulcers, one may employ three types of debridement: sharp, chemical and/or mechanical debridement.
Sharp debridement is the fastest and most effective way to remove devitalized tissue. One should only perform this on patients with adequate vascular supply. Debridement can occur in the operating room under sterile conditions if the wound needs extensive debridement. However, most sharp wound debridement is minor and can be performed at the patient’s bedside. Regardless of where care occurs, one should always use sterile instruments and apply a moist dressing afterward. In wounds with signs of infection, sharp debridement is urgently indicated.
Mechanical debridement includes the use of wet-to-dry dressings at prescribed intervals (twice daily or every eight hours), wound irrigation and hydrotherapy. When one removes wet-to-dry dressings, they adhere to the devitalized tissue so take caution when removing the dressing as it may be painful for the patient. Hydrotherapy and wound irrigation are useful for softening and mechanically removing eschar and debris.
Chemical or enzymatic debriders or topical debriding agents, such as collagenase, are useful for those who cannot tolerate surgery, those who are in long-term facilities or those receiving care at home. However, this should not be a substitute for when the wound is in need of a surgical debridement.
When Surgery Is Warranted
In the case of infection or intractable ulcerations secondary to positional problems, surgery may be warranted. Patients with osteomyelitis will need thorough debridement including resection of underlying infected bone and bone biopsy with culture-driven antibiotic therapy. Although contracture releases or joint fusions are not commonly done in patients with positional contractures, they may benefit from this when it comes to keeping the foot in a plantigrade and/or rectus position to relieve pressure areas.
When it comes to surgical planning with wound closure techniques, the surgeon needs to determine the simplest technique that will restore the missing tissue and blood supply without sacrificing function. Physicians rarely use primary closure for decubitus wounds due to inadequate soft tissue, which can lead to wound dehiscence and/or skin tension. Skin grafts are good for repair of shallow ulceration although they only provide a skin barrier.
A more practical method of closure that would not only release the skin tension but also provide padding at the site of the bony prominence would either be a musculocutaneous or fasciocutaneous flap. These flaps are ideal in a paraplegic patient but in ambulatory patients, one must weigh the risks of sacrificing functional muscle against the benefits.
Musculocutaneous flaps are effective in managing osteomyelitis because they provide a physiologic barrier to infection, eliminate dead space in the wound and improve vascularity. Increased vascularity increases local oxygen tension and thereby enhances the delivery of systemic antibiotics.10 Flaps are preferred in treatment of Stage III and Stage IV ulcers because they provide more durable tissue than scar tissue.
The ultimate guide in treating decubitus wounds is the progress of healing. A stagnant or increasing wound is indicative of the need for a change in the current regimen of care. Once a wound is healed, however, the goal then shifts to preventing recurrence or a formation of a new ulceration. Unfortunately, recurrence rates for decubitus ulcers are as high as 90 percent in the literature.11
Case Study: When A Patient Presents With An Infected Decubitus Ulcer Complicated By Several Comorbidities
A 63-year-old male presented to the clinic with an infected decubitus ulceration with surrounding cellulitis and exposed tendon. His medical history was significant for scleroderma, peripheral vascular disease, skin cancer (following multiple resections on the face), meningioma, Raynaud’s disease, pulmonary fibrosis, hypothyroidism and second toe amputation secondary to osteomyelitis. In addition, the patient had CREST syndrome, which consists of calcinosis, Raynaud’s phenomenon, esophageal dysmotility, sclerodactyly and telangiectasia.
After admitting the patient to the hospital from the clinic, we started IV antibiotics and performed serial debridements in the operating room to the level of fascia. The underlying tendon was viable and no bone was exposed. Further debridement optimized the wound in the operating room and due to the exposed tendon, we utilized Integra (Integra Life Sciences) and subsequent placement of Vacuum Assisted Closure therapy (VAC therapy, KCI) over the wound.
This case was complicated by the patient’s comorbidities and poor nutritional status. While the patient was in the hospital, an internist, rheumatologist, infectious disease specialist, nutritionist and vascular surgeon were involved in care of the patient.
Over the next two months, the patient underwent further debridements. After granulation occurred over the tendon, surgeons placed Apligraf (Organogenesis) on the wound. Unfortunately, despite the forward progression of healing, two months later, the patient presented to the emergency room with an abscess and necrosis of the Achilles tendon. He underwent subsequent debridements and a partial calcanectomy because he had osteomyelitis in his posterior heel.
Once the infection cleared, we utilized a free gracilis muscle flap to cover the exposed bone and fill the soft tissue deficit. We then placed a split thickness skin graft over the flap and subsequently employed an external fixator. We then discharged the patient to a rehabilitation center for continuing care.
Two months later, part of the gracilis flap was deemed non-viable and the patient went to the operating room again for further debridement and placement of Integra and VAC therapy. He had osteomyelitis of the calcaneus and had to have further debridement of the calcaneus. One month later, the external fixator was removed and the wound closed with a combination of a plantar heel flap and a split thickness skin graft. The patient has subsequently been able to maintain a healed wound.
Despite the challenges with the patient’s collagen vascular disease and other comorbidities, the patient healed seven months after the initial presentation. Extra precautions were necessary due to the fragility of integument. However, success ultimately occurred via a multidisciplinary approach.
Good pressure ulcer care consists of: a thorough evaluation of the patient; nutritional assessment; examination and documentation of the wound appearance, and tracking of healing rates; serial debridements as needed; and offloading. One should implement all of these principles not only to heal the wound but to help prevent recurrence. It is particularly important to emphasize the concept of prevention and one must stress prevention to patients and their caregivers.
Dr. Siddiqui is a Diabetic Limb Salvage Fellow in the Department of Plastic Surgery at Georgetown University Hospital in Washington, D.C.
Dr. Steinberg is an Associate Professor in the Department of Plastic Surgery at the Georgetown University School of Medicine in Washington, D.C. He is a Fellow of the American College of Foot and Ankle Surgeons.
1. Gallagher SM. Outcomes in clinical practice: pressure ulcer prevalence and incidence studies. Ostomy Wound Manag. 1997;43(1):28-32, 34-5, 38.
2. Fogerty MD, Abumrad NN, Nanney L, Arbogast PG, Poulose B, Barbul A. Risk factors for pressure ulcers in acute care hospitals. Wound Repair Regen. 2008;16(1):11-8.
3. Brem H, Maggi J, Nierman D, et al. High cost of stage IV pressure ulcers. Am J Surg. 2010; 200(4):473-7.
4. Reuler JB, Cooney TG. The pressure sore: pathophysiology and principles of management. Ann Intern Med. 1981;94(5):661-6.
5. Kenkel JM. Pressure sores (overview). Selected Read Plast Surg. 1998; 8(39):1-29.
6. Schols JM, Heyman H, Meijer EP. Nutritional support in the treatment and prevention of pressure ulcers: An overview of studies with an arginine enriched oral nutritional supplement. J Tissue Viability. 2009;18(3):72-9.
7. Cereda E, Gini A, Pedrolli C, Vanotti A. Disease-specific, versus standard, nutritional support for the treatment of pressure ulcers in institutionalized older adults: a randomized controlled trial. J Am Geriatr Soc. 2009;57(8):1395-402.
8. Black J, Baharestani M, Cuddigan J, Dorner B, Edsberg L, Langemo D, et al. National Pressure Ulcer Advisory Panel's updated pressure ulcer staging system. Dermatol Nurs. 2007;19(4):343-9.
9. Bergstrom N, Allman RM, Bennett MA. Treatment of pressure ulcers: Clinical Practice Guideline. Rockville, Maryland, U.S. Department of Health and Human Services. Agency for Healthcare Policy and Research; 2007. AHCPR Publication: 21-88.
10. Anthony JP, Hunstmans WT and Mathes SJ. Changing trends in the management of pelvic pressure ulcers: a 12-year review. Decubitus 1992; 5(3):44-7, 50-1.
11. Relander M, Palmer B. Recurrence of surgically treated pressure sores. Scand J Plast Reconstr Surg Hand Surg. 1988; 22(1):89-92.