Management of pressure ulcer
Pressure ulcers are areas of local tissue trauma, usually developing where soft tissues are compressed between bony prominences and any external surface for prolonged time periods. Thus, they are most commonly found over bony prominences subject to external pressure. A pressure ulcer is a sign of local tissue necrosis: The skin may be involved or there may be major muscle and subcutaneous fat tissue destruction underneath intact skin.
Incidence of Pressure Ulcers
The exact incidence and prevalence of pressure ulcers remain unclear. Data from the National Pressure Ulcer Advisory Panel (NPUAP) in the United States indicate that the incidence varies widely, from 0.4 to 38 % in acute care, 2.2–23.9 % in long-term care, and 0–17 % in home care. Prevalence rates show the same variability: 10–18 % in acute care, 2.3–28 % in long-term care, and 0–29 % in home care. Therefore, the incidence of pressure ulcers is high, especially among certain high-risk groups of patients. These groups include elderly patients admitted to a hospital for femoral fractures (66 %) and critical care patients (33 %); in a study of quadriplegic patients, the prevalence was 60 % . In spinal cord injury (SCI) patients, the pressure ulcer prevalence rate ranged from 8 % in the ﬁrst year following the onset of spinal cord injury to 33 % for community resident individuals with SCI.
Cost of Pressure Ulcer Management
The cost of managing pressure ulcers has increased dramatically in hospitals and in the community due to the overall increase in health-care costs worldwide. The impact of pressure ulcers is signiﬁcant in terms of both ﬁnancial and nonmonetary costs. Its reported that the cost to heal complex pressure ulcers was $100,000; less serious pressure ulcers cost $20,000 to $30,000 to heal (National Pressure Ulcer Advisory Panel 1989, U.S. Department of Health and Human Services 1990).
The medico-legal implications of pressure ulcer development are an urgent issue all worldwide. Pressure ulcers are viewed as a quality indicator of care. Hence, the development of pressure ulcers can constitute a failure in the healthcare system. In the United States, federal health agencies regard pressure ulcers as a surrogate for how well the healthcare team is functioning in monitoring the quality of care for the patient. The increasing recognition of pressure ulcer development as a marker for quality of care has led to a greater number of pressure ulcer litigations against clinicians and their employers. The public has been made aware through the media like television and Internet that pressure ulcers can be prevented and treated effectively. The development of pressure ulcers is considered to be the result of negligence by the healthcare provider. Pressure ulcers can cause sepsis and even death in certain groups of patients, in addition to causing changes in patients’ quality of life. A number of lawsuits have been brought against hospitals, nursing homes, physicians, and even plastic surgeons. If greater attention were paid to preventing development of pressure ulcers and to enforcing some basic rules of prevention, there would be fewer of these litigations
Advances in Prevention
In the twenty-ﬁrst century, pressure ulcers are seen as a preventable disease, and thus, prevention is a priority and a necessity in their management. This can be accomplished through continuing education for all healthcare staff on detecting the early signs of pressure ulcers and assessing patients for the risk of pressure ulcer development. In hospitals, nursing homes, convalescent homes, and patients’ homes, measures for prevention include: the patient’s repositioning and turning schedule; preventing and treating excessive body moisture and fecal and urinary incontinence; using advanced equipment, such as special beds, mattresses, and wheelchair cushions; attention towards the patient’s nutritional intake; and patient and family education. All of these measures are today’s standard of care and have become the foundation for pressure ulcer prevention.
Complications and Life- Threatening Risks of Pressure Ulcers
Fifty years ago, pressure ulcers were among the major diseases predisposing in shortening the life expectancy in the spinal cord injury patient. In the twenty-ﬁrst century, advances in antibiotics, local wound care, and early surgical interventions have tremendously reduced the morbidity and mortality rates and prolonged life expectancy in spinal cord injury patients. However, the medical literature documents many complications that can occur in patients with chronic pressure ulcers, including acute sepsis, amyloidosis, heterotopic ossiﬁcation, septic joint, perineal and urethral ﬁstula , squamous cell carcinoma changes in pressure ulcers, and the most common complication, acute or chronic osteomyelitis of the bone underlying the ulcer. To avoid and prevent these complications, prevention and early detection of pressure ulcers in spinal cord patients are important for the patients’ healthcare and to provide quality of life and longer life expectancy. This responsibility falls on all healthcare providers.
PRESSURE ULCER PATHOPHYSIOLOGY
It has been observed that the application of constant pressure of 70 mmHg for more than 2 h produced irreversible tissue damage. Minimal tissue damage was observed when the pressure exceeded 240 mmHg, providing there was intermittent pressure relief.
Pressure ulcers are the result of mechanical injury to the skin and underlying tissues. Traditionally, pressure (stress), shear, and friction were considered the primary external factors involved in pressure ulcer development. More recently, deformation (strain), heat, reperfusion injury, and impaired lymphatic function have been considered as additional primary forces involved in pressure damage.
Four hypotheses for the pathophysiology behind pressure ulcer development include
- Ischemia caused by capillary occlusion
- Impairment in lymphatic ﬂow with increase in metabolic waste products.
- Reperfusion injury (damage that occurs because of the inﬂammatory response that occurs when blood ﬂow resumes to the ischemic tissues).
- Deformation of tissue cells.
Shear forces are an etiologic factor in development of pressure, and ulcers are caused by movement of boney prominence against the subcutaneous tissues. This occurs when the position of the patient, for example, in bed, is shifted in a way that the skin remains stationary in relation to the support of the body and, as a result of the movement, the subepidermal vessels are bent at a right angle. Shear alone does not cause tissue necrosis; however, it is a predisposing factor in causing pressure ulcers. Shear forces are seen more frequently in clinical practice when a patient loses weight and tissue sliding can occur over the boney prominences. Friction forces relate to rubbing of the skin against linen or clothing, or even when lifting a patient on a sling. Most abrasion injuries are caused by friction, although friction does not lead to all pressure ulcers; it can damage the epidermis and make the skin susceptible to pressure ulcers.
Signiﬁcant Factors in Development of Pressure Ulcers
The most important factor in the development of pressure ulcers is skin moisture. The skin is the largest organ of the body and one of its important functions is to protect the body. There are many factors that can alter and decrease the resistance of the skin. Moisture is a contributing factor in the etiology of pressure ulcers because it macerates the epidermis. The epidermis becomes easily eroded and tissue necrosis can occur. Moisture is a condition that can be seen clinically with incontinence of urine and stool, excessive sweating, excessive vaginal discharge, wound discharge, and sometimes wound dressings that can cause. skin irritation. Uncontrolled skin moisture by itself is considered a risk factor in developing pressure ulcers in certain patients. Because the skin is an organ, poor nutrition has shown to be a factor in its breakdown. In addition, loss of fat and muscle increases the pressure of the boney prominences. In aging skin, changes take place in collagen synthesis that result in the tissue of the body having lower mechanical strength and increased stiffness . There are also changes in the barrier properties in aging skin, reduced immunity, slower wound healing, and diminished pain reception. The patient’s physique also plays a role; if pressure is distributed evenly, the patient is less likely to develop pressure ulcers. A thin patient with little subcutaneous fat and poor muscle bulk will be inclined to develop pressure ulcers over the boney prominences. An extremely obese individual has much greater weight but better padding to distribute the weight; however, these patients have poor circulation and are more liable to be affected by shear and friction.
Site of Pressure Ulcer Development
A study by the model system of spinal cord injury patient care in the United States found that during early treatment in the acute phase of the spinal cord injury at trauma centers, for stabilization of the spinal shock and the spine, patients were kept in the supine position in bed for numerous medical reasons. The ﬁndings for the common ulcer site areas were occipital = 2.6 %, scapular = 4.3 %, spinous process = 1.3 %, iliac crest = 1.8 %, sacrum = 37.4 %, trochanteric = 3.8 %, ischium = 9.2 %, elbow = 2.0 %, knee = 1.5 %, and malleolar = 3 %. The anatomical distribution of the ulcer sites somewhat changed when patients were followed in the ﬁrst year post injury, when the common sites were the sacrum = 20 %, ischium = 18.3 %, trochanteric = 12.4 %, heel = 16.6 %, elbow = 2.6 %, and malleolar 8.7 %. The reasons for the ulcer distribution at this phase of a patient’s life were sitting in a wheelchair and resuming normal life without practicing pressure relief as instructed in rehabilitation post injury. Laying down in bed in the supine position or lateral position without a pressure relief mattress can predispose to ulcer development in the sacrococcygeal area and trochanteric area.
Early Pressure-Induced Tissue Damage
The immediate response of the tissues to a sustained period of pressure are related to the inﬂammatory response and are manifest as elevated temperature, subepidermal edema, and erythema. Skin temperature and subepidermal edema are reﬂections of the nonvisible spectrum of pressure-induced tissue damage. Elevated skin surface temperature, as compared with that of healthy tissues can be evaluated by palpation, skin thermistors, or thermography. Subepidermal edema can be assessed using ultrasound and surface electrical capacitance methods. If pressure is not relieved, pressure-induced tissue damage progresses to the visible spectrum. The ﬁrst visible indicator of pressure damage is blanchable erythema. Erythema presents as redness of a ﬂat, nonraised area of the skin larger than 1 cm. The discoloration varies in intensity from pink to bright red in persons with light skin tones. In persons with dark skin tones, the discoloration appears as a deeper than normal pigmentation or a purple or blue-gray hue to the skin.
Stage I Pressure Ulcers
If pressure is not relieved, the damage progresses to stage I category, with additional temperature, coloration, and texture changes seen. As the tissues become more disturbed, the temperature may decrease, signaling underlying tissue damage. Nonblanchable erythema develops, in which the color of the skin becomes more intense, varying from dark red to purple or cyanotic in both light- and dark-skinned patient In addition, skin texture changes. The skin may feel hard and indurated, and observation may reveal heightened skin features or an orange-peel appearance. This stage of tissue destruction is also reversible, although tissues may take 1 to 3 weeks to return to normal. Additionally, the patient may report pain at the site.
Stage II Pressure Ulcers
Stage II category pressure ulcers are superﬁcial ulcers most often the result of the mechanical force of friction on the epidermis. Stage II pressure ulcers involve damage to the epidermis and part of the dermis, they are partial-thickness lesions. The ulcer is superﬁcial, with indistinct margins and a red pink, shiny base . It is usually surrounded by blanchable or nonblanchable erythema. If not dealt with aggressively, stage II ulcers can progress to involve deeper tissues. Still, if properly treated, the situation may resolve in 2 to 4 weeks.
Stage III and IV Pressure Ulcers
Whereas superﬁcial or partial-thickness ulcers such as stage II ulcers begin at the skin surface and progress to deeper layers, deep, full-thickness ulcers do not originate at the skin surface; they begin at the bony prominence–soft tissue interface at the muscle tissue layer and spread to involve the skin structures.The chronic deep ulcer usually has a dusky red wound base and does not bleed easily.It is surrounded by blanchable or nonblanchable erythema or deepening of normal skin tone, induration, possible edema, change in temperature compared to healthy tissues, and possible mottling with or without hemosiderin staining. Undermining and tunneling may be present with a large necrotic cavity.
Unstageable Pressure Ulcers
Pressure ulcers that present covered with devitalized necrotic tissue are classiﬁ ed as unstageable because the depth of tissue destruction is not visible. The necrotic tissue may be slough or eschar. Eschar is the formation of an acellular dehydrated compressed area of necrosis, usually surrounded by an outer rind of blanchable or nonblanchable erythema Eschar formation indicates a full-thickness loss of skin and may be the result of both pressure and shear forces. Slough is devitalized tissue with a higher water content than eschar. Slough appears as yellow or tan material that is thickly adherent to wound bed tissues . Slough also indicates full-thickness tissue damage.
Suspected Deep Tissue Injury
Pressure-induced skin damage that manifests as purple, blue, or black areas of intact skin may be suspected DTI areas. These lesions commonly occur on the sacrum and heels and signal more severe tissue damage below the skin surface . DTI lesions reflect tissue damage at the bony tissue interface and may progress rapidly to large tissue defects.
Comprehensive Clinical Wound Evaluation
With pressure ulcers, like any other wounds or illnesses, a complete medical history prior to examination of the wound is important to understanding the nature of the wound. The pressure ulcer is always secondary to the primary illness or trauma, and consequently a management plan is developed according to the information obtained from the patient or the caregiver. Therefore, examining a wound without a comprehensive medical history is considered incomplete diagnosis or management. History of spinal cord injury, level of injury, and whether it’s a complete or incomplete injury should be ascertained to determine the level of sensation in the patient, the level of muscle function, and whether the patient is ambulatory, walks with aids, or is wheelchair conﬁned. Other primary diagnosis, for example, spina biﬁda, stroke, or neurological disease, will help determine how to treat the wound, either by conservative or surgical treatment. The medical history should include a complete history of illnesses and the medications the patient is taking. Illnesses such as heart disease, lung disease, diabetes, and vascular disease affect healing and the ability of the patient to tolerate general anesthesia if surgery is indicated. History of bowel and urinary control is important knowledge for the postoperative management of the patient. History of the existing of muscle spasms should be investigated and controlled to avoid postoperative morbidities. Psychosocial evaluation is important for the success of the surgery, as the compliance of patient is important in the postoperative period.
Assessment of the Individual with a Pressure Ulcer
- Complete an initial assessment of the individual with a pressure ulcer, to include: The individual’s and family’s goals of care. If the individual is unable to participate, consult with family and/or significant others.
- A complete health/medical and social history.
- A focused physical examination that includes:
- Factors that may affect healing (e.g., impaired perfusion,impaired sensation, systemic infection)
- Vascular assessment in the case of extremity ulcers (e.g.,physical examination, history of claudication, and ankle brachial index or toe pressure)
- Laboratory tests and x-rays as needed
- Nutritional assessment
- Pain related to pressure ulcers
- Risk for developing additional pressure ulcers
- Psychological health, behavior and cognition.
- Social and financial support systems.
- Functional capacity, particularly in regard to positioning, posture,and the need for assistive equipment and personnel.
- The employment of pressure-relieving maneuvers.
- Adherence to pressure-relieving maneuvers.
- Integrity of seating and bed surfaces (wear and tear).
- The individual’s/family member’s knowledge and belief about developing and healing pressure ulcers.
- Reassess the individual if the ulcer does not show signs of healing as expected despite adequate local wound care, pressure redistribution, and nutrition.
- Expect some signs of healing in most individuals within 2 weeks.
- Adjust expectations in the presence of multiple factors (particularly unmodifiable factors) that impair wound healing (e.g., persistent undernutrition, poor perfusion, and co-morbidities known to impair wound healing).
- Teach the individual and his/her family about the normal healing process and keep them informed about progress (or lack of progress) toward healing, including signs and symptoms that should be brought to the professional’s attention.
Pressure Ulcer Assessment
- Assess the pressure ulcer initially and re-assess it at least weekly, documenting findings.
- With each dressing change, observe the pressure ulcer for developments that may indicate the need for a change in treatment (e.g., wound improvement, wound deterioration, more or less exudate, signs of infection, or other complications).
- Assess and accurately document physical characteristics such as location, Category/Stage, size, tissue type(s), wound bed and periwound condition, wound edges, sinus tracts, undermining, tunneling, exudate, necrotic tissue, odor, presence/absence of granulation tissue, and epithelialization.
- Use a validated tool such as the Pressure Ulcer Scale for Healing (PUSH©) Tool or the Bates-Jensen Wound Assessment Tool (BWAT), formerly known as the Pressure Sore Status Tool (PSST).
Role of Nutrition in Pressure Ulcer Healing
- Screen and assess nutritional status for each individual with a pressure ulcer at admission and with each condition change — and/or when progress toward pressure ulcer closure is not observed.
- Provide 30-35 kcalories/kg body weight for individuals under stress with a pressure ulcer. Adjust formula based on weight loss, weight gain, or level of obesity. Individuals who are underweight or who have had significant unintentional weight loss may need additional kcalories to cease weight loss and/or regain lost weight.
- Offer 1.25 to 1.5 grams protein/kg body weight daily for an individual with a pressure ulcer when compatible with goals of care, and reassess as condition changes
- Provide additional fluid for individuals with dehydration, elevated temperature, vomiting, profuse sweating, diarrhea, or heavily draining wounds.
- Offer vitamin and mineral supplements when dietary intake is poor or deficiencies are confirmed or suspected
Manage General Pain
- Organize care delivery to ensure that it is coordinated with pain medication administration and that minimal interruptions follow. Set priorities for treatment.
- Encourage individuals to request a ―time out‖ during any procedure that causes pain.
- Reduce pressure ulcer pain by keeping the wound bed covered and moist, and using a non-adherent dressing.
- Use dressings less likely to cause pain and/or those likely to require less frequent dressing changes (e.g., hydrocolloids, hydrogels, alginates, polymeric membrane foams, foam, soft silicone dressingsNote: Gauze dressings are more likely to cause pain.
- For an individual with pain from a pressure ulcer, music, meditation, distraction, conversations, and guided imagery are sometimes beneficial.
- Administer pain medication regularly, in the appropriate dose, to control chronic pain following the World Health Organization Dosing Ladder.
- Use adequate pain-control measures, including additional dosing at times of wound manipulation, wound cleansing, dressing change, debridement, etc.
- Manage persistent pressure ulcer pain (neuropathic) with a local anesthetic or an adjuvant (antidepressant or antiepileptic), as well as with transcutaneous nerve stimulation, warm applications, or tricyclic antidepressants.
Support Surfaces for Treatment of Pressure Ulcers
Support surfaces alone neither prevent nor heal pressure ulcers. They are to be used as part of a total program of prevention and treatment. When pressure ulcers deteriorate or fail to heal, the professional should consider replacing the existing support surface with one that will improve pressure redistribution and microclimate (heat and moisture control) for the individual. Changing the support surface is only one of several strategies to consider. The individual and his/her pressure ulcer should be re-evaluated. Preventive interventions and local wound care should also be intensified as needed. A significant increase in risk status may also prompt such re-evaluation of the individual and the support surface.
- Replace the existing mattress with a support surface that provides better pressure redistribution, shear reduction, and microclimate control for the individual if she or he:
- Cannot be positioned off of the ulcer
- Has pressure ulcers on two or more turning surfaces (e.g., the sacrum and trochanter), limiting turning options
- Fails to heal or demonstrates ulcer deterioration despite appropriate comprehensive care
- Is at high risk for additional ulcers
- Bottoms out‖ on the existing support surface
- Inspect the skin for additional damage each time the individual is turned or repositioned while in bed. Do not turn the individual onto a body surface that is damaged or still reddened from a previous episode of pressure loading, especially if the area of redness does not blanch
- Limit head-of-bed elevation to 30 degrees for an individual on bedrest, unless contraindicated by medical Encourage individuals to sleep in a 30- to 40-degree side-lying position or flat in bed if not contraindicated.
- Use transfer aids to reduce friction and Lift — don’t drag — the individual while repositioning.
- Do not use ring- or donut-shaped devices.
- Consider higher-specification foam or similar nonpowered pressure redistribution support surfaces for Category/Stage I and II pressure ulcers. Use hydrocolloid or silicone foam dressing for sensitive skins.
- Relieve pressure under the heel(s) with Category/Stage I or II pressure ulcers by placing legs on a pillow to ―float the heels‖ off the bed or by using pressure-reducing devices with heel suspension. Use foam or silicone heal guards to prevent pressure sores.
- Debride devitalized tissue within the wound bed or edge of pressure ulcers when appropriate to the individual’s condition and consistent with overall goals of care.
- Select the debridement method(s) most appropriate to: the individual’s condition; goals of care; ulcer/periulcer status; type, quantity, and location of necrotic
- Use mechanical, autolytic, enzymatic, and/or biosurgical methods of debridement when there is no urgent clinical need for drainage or removal of necrotic tissue.
- Perform surgical debridement in the presence of advancing cellulitis, crepitus, fluctuance, and/or sepsis secondary to ulcer-related
- Use sharp debridement with caution in the presence of: immune incompetence, compromised vascular supply to the limb, or lack of antibacterial coverage in systemic Relative contraindications include anticoagulant therapy and bleeding disorders.
- Perform a thorough vascular assessment prior to debridement of lower extremity pressure ulcers
- Do not debride stable, hard, dry eschar in ischemic
Wound dressings are a central component of pressure ulcer care. The selection of the dressing should be based on the tissue in the ulcer bed, the condition of the skin around the ulcer bed, and the goals of the person with the ulcer. Generally maintaining a moist ulcer bed is the ideal when the ulcer bed is clean and granulating to promote healing or closure. Several moisture-retentive dressings are available. However, the type of dressing may change over time as the ulcer heals or deteriorates.
- Use hydrocolloid dressings for clean Category/Stage II pressure ulcers in body areas where they will not roll or melt.
- Consider using hydrocolloid dressing on noninfected, shallow Stage III pressure ulcers.
- Change the hydrocolloid dressing if feces seep beneath the dressing.
- Consider using filler dressings beneath hydrocolloid dressings in deep ulcers to fill in dead space.
- Consider using hydrocolloid dressings to protect body areas at risk for friction injury or risk of injury from tape.
Transparent Film Dressings
- Consider using film dressings to protect body areas at risk for friction injury or risk of injury from tape.
- Consider using film dressings for autolytic debridement when the individual is not immunocompromised.
- Consider using film dressings as a secondary dressing for ulcers treated with alginates or other wound filler that will likely remain in the ulcer bed for an extended period of time (e.g., 3-5 days).
- Do not use film dressings as the cover dressing over enzymatic debriding agents, gels, or ointments.
- Consider alginate dressings for the treatment of moderately and heavily exudating ulcers.
- Consider alginate dressings in infected pressure ulcers when there is proper concurrent treatment of infection.
- Consider lengthening the dressing-change interval or changing the type of dressing if the alginate dressing is still dry at the scheduled time for dressing change.
- Consider using foam dressings on exudative Category/Stage II and shallow Category/Stage III pressure ulcers.
- Avoid using single small pieces of foam in exudating cavity ulcers.
- Consider using foam dressings on painful pressure ulcers.
- Consider placing foam dressings on body areas and pressure ulcers at risk for shear injury.
- Consider use of silver dressings for pressure ulcers that are infected or heavily colonized.
- Consider use of silver dressings for ulcers at high risk of infection.
- Avoid prolonged use of silver dressings; discontinue when the infection is controlled.
- Consider use of silver sulfadiazine in heavily contaminated or infected pressure ulcers until definitive debridement is accomplished.
- Consider using silicone dressings as a wound contact layer to promote atraumatic dressing changes.
- Consider using silicone dressings to prevent tissue injury when the ulcer or periwound tissue is fragile or friable.
Assessment and Treatment of Infection
Bacteria are present on all skin surfaces. When the primary defense provided by intact skin is lost, bacteria reside on the wound surface also. When the bacteria (by numbers or virulence) cause damage to the body, infection is present. An impaired host has a reduced ability to combat bacteria. The number of bacteria and their effect on the host can be categorized as contamination, colonization, critical colonization, or infection. Infection is not common in Category/Stage I or II ulcers, and assessment of infection should focus on Category/Stage III and IV ulcers. Infection may spread beyond the pressure ulcer, resulting in serious systemic infections such as cellulitis, fasciitis, osteomyelitis, systemic inflammatory response syndrome (SIRS), or sepsis.
- Have a high index of suspicion for local wound infection in individuals with diabetes mellitus, protein-calorie undernutrition, hypoxia or poor tissue perfusion, autoimmune disease, or
- Have a high index of suspicion for local infection in pressure ulcers when there are no signs of healing for 2 weeks, or when friable granulation tissue, foul odor, increased pain in the ulcer, increased heat in the tissue around the ulcer, increased drainage from the wound, an ominous change in the nature of the wound
- Consider a diagnosis of spreading acute infection if the pressure ulcer has signs of acute infection, such as erythema extending from the ulcer edge, induration, new or increasing pain, warmth, or purulent The acutely infected ulcer may also be increasing in size or have crepitus, fluctuance, or discoloration in the surrounding skin. The individual may also have systemic signs of infection such as fever, malaise, and lymph node enlargement. Elderly individuals may develop confusion/delirium and anorexia.
- Determine the bacterial bioburden of the pressure ulcer by tissue biopsy or quantitative swab technique.
The gold standard method for examining microbial load is quantitative culture of viable wound tissue. Surface swabs will only reveal the colonizing organism, and may not reflect deeper tissue infection. An acceptable alternative to quantitative tissue culture is the Levine quantitative swab technique:
- Cleanse wound with normal saline. Blot dry with sterile gauze.
- Culture the healthiest-looking tissue in the wound bed.
- Do not culture exudate, pus, eschar, or heavily fibrous tissue.
- Rotate the end of a sterile alginate-tipped applicator over a 1 cm x 1 cm area for 5 seconds.
- Apply sufficient pressure to swab to cause tissue fluid to be expressed.
- Use sterile technique to break tip of swab into a collection device designed for quantitative cultures.
Consider a diagnosis of pressure ulcer infection if the culture results indicate bacterial bioburden of > 105 CFU/g of tissue and/or the presence of beta hemolytic streptococci.
- In general, topical antibiotics are not recommended for pressure ulcers. Reasons for this include inadequate penetration for deep skin infections, development of antibiotic resistance, hypersensitivity reactions, systemic absorption when applied to large wounds, and local irritant effects, all of which can lead to further delay in wound However, short courses of silver sulfadiazine, topical antibiotic solutions, or topical metronidazole can be useful in certain circumstances — for example, on wounds that have been debrided and cleansed, yet still have a bacterial bioburden of > 105 CFU/g of tissue and/or the presence of beta hemolytic streptococci. Topical metronidazole might be used for the treatment of malodor in fungating wounds or wounds with anaerobic infection.
- Use systemic antibiotics for individuals with clinical evidence of systemic infection, such as positive blood cultures, cellulitis, fasciitis, osteomyelitis, systemic inflammatory response syndrome (SIRS), or sepsis.
Biophysical Agents in Pressure Ulcer Management
- Consider the use of direct contact (capacitative) electrical stimulation (ES) in the management of recalcitrant Category/Stage II, as well as Category/Stage III and IV pressure ulcers to facilitate wound healing.
- Consider a course of ultraviolet light as an adjunctive therapy to reduce bacterial burden in clean, but critically colonized Category/Stage III and IV pressure ulcers.
- Negative Pressure Wound Therapy Consider NPWT as an early adjuvant for the treatment of deep, Category/Stage III and IV pressure ulcers. Debride the pressure ulcer of necrotic tissue prior to the use of
- There is insufficient evidence to support the use of biological dressings in the treatment of pressure
- The combined clinical evidence on platelet-derived growth factor (PDGF) suggests that PDGF-BB may improve healing of pressure ulcers.
- There is insufficient evidence to recommend hyperbaric oxygen therapy for the treatment of pressure ulcers.
- There is insufficient evidence to recommend topical oxygen for the treatment of pressure ulcers.
- Consider use of high-frequency (MHz) ultrasound as an adjunct for the treatment of infected pressure ulcers
Surgery for Pressure Ulcers
- Evaluate the need for surgical consultation for operative repair in individuals with Category/Stage III or IV pressure ulcers that are not closing with conservative treatment, or for individuals who desire more rapid closure of the ulcer.
- Wound which shows no signs of healing at 2 wks must be evaluated for usage of alternative therapy if no signs of healing present despite complete patient optimization and patient mobilizing consider surgical closure.