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The authors would like to acknowledge Joseph A. Witkowski for his contributions to this chapter.
Evidence Levels: A Double-blind study B Clinical trial ≥ 20 subjects C Clinical trial < 20 subjects D Series ≥ 5 subjects E Anecdotal case reports
Pressure ulcers (decubitus ulcers, bed sores, pressure sores, to torsion stress) represent damage within the skin and soft tissue that can extend through the subcutaneous tissue and muscle layer onto the underlying bone. They generally occur over bony prominences, the most common being the sacrum, ischial tuberosities, greater trochanters, calcaneus, and lateral malleoli.
Repositioning is a significant part of prevention. A patient in an ordinary bed who is at risk for developing a pressure ulcer should be repositioned at frequent intervals; however, the correct timing for turning has never been established. The National Pressure Ulcer Advisory Panel (NPUAP) has admitted that evidence on repositioning every 2 hours is arbitrary and varies from country to country, even from facility to facility, and that repositioning at 2–4-hour intervals may be more appropriate.
Pillows and foam wedges are used to maintain an appropriate position and to keep bony prominences apart. Completely immobile patients should have their heels raised from the bed by a pillow or boot and not be placed on their trochanters, unless a specialized bed is used. To avoid the latter, use a 30-degree position from the horizontal lying on the side. The head of the bed should not be raised more than 30 degrees from the horizontal for an extended period. Knees should be flexed at 5–10 degrees to minimize the risk of deep-vein thrombosis.
Where possible, use lifting devices or draw sheets to reposition or to transfer patients. Minimize pressure from medical devices, such as catheters, oxygen tubing, and restraints. Finally, when appropriate, the patient should be placed on a pressure-reducing device such as alternating air, gel, or water mattress . Foam rings, foam cut-outs, or donut-style devices should not be used, as these devices distribute pressure inappropriately.
A patient sitting in a wheelchair should be repositioned frequently, perhaps every hour, and be taught to shift weight every 15 minutes. A pressure-reducing device made of foam, gel, air, or a combination of each is indicated. Unfortunately, even in paraplegics, the exact time interval for repositioning has never been accurately determined.
Barrier creams are useful for conserving the intact skin of incontinent patients and of those at risk for skin breakdown.
Theoretically, pressure ulcers should be preventable, but despite these measures, many simply are not. If they are associated with immobility, sustained pressure, and the loss of pain sensibility, these problems can and should be addressed. In practice, successful prevention is often foiled by our limited understanding of the pathogenesis, as well as by complicating comorbidities. There is also some evidence that many deep ulcers are initiated by multiple microthromboses of deep tissues. This indicates that dehydration, along with any factor that might increase blood coagulability, should be addressed.
The management of skin lesions caused by pressure is based on these principles:
Elimination of relative/sustained pressure
Reposition of the patient regularly and frequently
Removal of necrotic debris
Maintenance of a moist wound environment
Correction of the underlying contributing factors
Nutritional supplements and screening for nutritional deficiencies
Wound care with topical products and/or dressing
The patient should not lie on the ulcer. A patient who is at risk for developing additional ulcers and can assume a variety of positions without lying on the ulcer should be placed on a static support surface (i.e., air, foam, or water) . If the patient cannot assume various positions without lying on the ulcer or bottoms out while on a static surface, or if the ulcer does not heal after 2–4 weeks of optimal care, place the patient on a dynamic support surface when possible. These supporting surfaces can be categorized as constant low-pressure (CLP) devices conforming to body shaper or replacing pressure devices that alter pressure mechanically. CLP devices, such as high-specification foam mattresses with overlays, and bead-filled and water-filled mattresses, may lessen the development of pressure ulcers and tend to be more successful than standard foam hospital mattresses. Alternating-pressure (AP) mattresses and overlays include a variety of compartments filled with air inflating and deflating in a coordinated way to alter pressure continually across the body. Unfortunately, there is no proof to show exactly which type is better for protection and treatment; however, both CLP and AP devices are more successful than standard hospital mattresses for prevention and treatment.
Debridement is required to expose granulation tissue, decrease infection risk, and improve healing, especially when there is an extensive eschar or necrotic tissue. Debridement can be conducted through surgical (sharp) and nonsurgical (enzymatic, autolytic, mechanical, and biologic). The debridement method is dependent on several factors, including the characteristics of the patient, the wound, the risk of infection risk, and even the cost.
Surgical debridement is indicated for infected ulcers with necrotic debris, if the patient has advancing cellulitis and systemic infection, devitalized tissue, and eschars other than those on the heel; however, the extent of tissue needing to be removed is highly variable. An eschar on the heel should be excised only if it is fluctuant, draining, or surrounded by cellulitis, and if the patient is septic. If there is a high index of suspicion that a biofilm is present (i.e., wound failing to heal despite proper wound care and antimicrobial therapy), then surgical debridement is required.
Major debridement is performed in the operating room, but serial sharp debridement can be performed at the bedside. The use of systemic antimicrobials should be considered to prevent bacteremia during significant debridement. A bone biopsy is recommended while debriding ulcers, when bone is exposed, and for non-healing deep ulcers (stage 3 or 4) after 2–4 weeks of optimal therapy.
Mechanical debridement methods, such as hydrotherapy, whirlpool baths, and wound irrigation are among other measures that have benefits, such as improving local circulation, reducing pain and fever, relieving debris and bacteria, helping with wound removal, and accelerating wound healing. Saline wet-to-dry gauze is an additional alternative.
Autolytic debridement provides a moist wound area that allows the body enzymes to digest necrotic tissue. Similarly, enzymatic debridement uses enzymes for the liquefaction of dead tissue in the wound and clears them with dressings like collagenase to remove necrotic tissue, and moist wounds are the best place for them to work. Autolytic and enzymatic debridement is indicated for non-infected ulcers that are unlikely to get infected.
Biologic debridement utilizes non-infectious larvae and maggots, which has been observed to have increased complete debridement over conventional therapy (80% versus 48%, respectively).
The choice of a synthetic dressing depends on the presence of infection, amount of exudate, status of the periulcer skin, and amount of pain experienced by the patient. Saline dressings and alginates are indicated for infected ulcers. Synthetic dressings (i.e., films) are used on ulcers with minimal exudate, hydrocolloid wafers for moderate exudate, and foam wafers and alginates for ulcers with a large amount of exudate. Ulcers with fragile or dermatitic periulcer skin should be covered with hydrogel wafers or non-adherent foam wafers . All occlusive dressings relieve pain, when present, but the hydrogel wafers are best for this purpose.
Attention to the medical status is important; diabetes mellitus, nutritional conditions (malnutrition, hypoproteinemia, anemia), peripheral vascular disease, deep venous thrombosis, congestive heart failure, lower extremity edema, cardiac disease, malignancy, mental health problems, and even Alzheimer disease may prevent any ulcer healing. Unfortunately, even the best medical care may not permit healing.
Treatment of the pressure ulcer can be simplified and made more effective if the following recommendations are considered:
It is essential that the heels are inspected at least daily and any changes are recorded
Saline should be used to clean most pressure lesions; soap and disinfectants are too irritating for more than occasional use. Scrubbing may prove too irritating, so gentle washing is indicated
When ulcers are not infected, synthetic dressings should be changed only if they become dislodged or wound fluid escapes from under the dressing
Periulcer skin must be kept dry not only to avoid maceration but also to permit the dressing to adhere to the skin
To obliterate dead space, fill deep ulcers loosely with a hydrocolloid, a hydrogel wound filler, or an alginate rope before applying a synthetic dressing. This same material should be placed under the edge of the ulcer when undermining is present. Bleeding after serial surgical debridement can often be controlled with an alginate dressing. Moistening with saline can loosen an alginate dressing that adheres to granulation tissue
A clean ulcer failing to show signs of healing and revealing inflammatory signs of erythema, edema, and warmth, purulent discharge and persistent excessive exudate, discoloring or darkening of granulation tissue, giving off a foul odor, and presenting with heightened local pain should be treated with antibacterial agents, such as 1% silver sulfadiazine, cadexomer iodine, triple antibiotic, or retapamulin , for 2 weeks to reduce the bacterial burden; however, topical antimicrobials may create the risk of resistant bacterial strains emerging. Metronidazole gel would be the exception, as the odor of an infected ulcer can often be eliminated by applying it to the ulcer bed. Increased bacterial burden may impede healing before clinical signs of infection become apparent. Cytotoxic agents, such as hydrogen peroxide and povidone-iodine, should be avoided
Clinical observation is the key to making the diagnosis. Cutaneous biopsies will not be helpful, although biopsies for aerobic and anaerobic bacteriology cultures could be useful if infection is suspected
Systemic antibiotics are recommended only in the presence of bacteremia, sepsis, advancing cellulitis, or osteomyelitis. Bacterial testing and analysis with comprehensive swabbing cannot provide all the information required. Infection that is described as a variety of bacteria bigger than 10 5 CFU/g of tissue is partially relevant. It is recommended the wound is controlled for signs of infections: pain, warmth, erythema, drainage, bad odor, and/or systemic manifestations. Osteomyelitis usually accompanies stage 4 pressure ulcers and deep ulcers. X-rays, MRI, and bone biopsy should be used to check for osteomyelitis
Although most synthetic dressings relieve pain, treatment for moderate-to-severe pain can include topical anesthetics (lidocaine), non-steroidal antiinflammatory drugs, opiates, antidepressants, and sedatives
Observe for:
Blanchable erythema
Non-blanchable erythema
Superficial ulcer
Deep ulcer
Eschar
Necrosis
Gangrene
Decubitus dermatitis
Blanchable and non-blanchable erythema represent the initial development of the pressure ulcer. The early lesions of non-blanchable erythema are bright red; later, they become dark red to purple. Both can be treated with adherent synthetic dressings to protect the lesion from friction and shear, topical corticosteroids, or zinc oxide paste . The bright red lesion can also be treated with 2% nitroglycerin ointment ; 0.5–1 cm of the ointment is applied over the lesion and covered with an impermeable plastic wrap (such as Saran Wrap) for 12 hours daily.
Superficial and deep ulcers without necrotic debris are treated with saline wet-to-dry gauze or an adherent synthetic dressing. Deep ulcers should be loosely filled with a synthetic wound filler before applying a synthetic dressing.
The deep ulcer with necrotic debris requires debridement and is then treated as a clean ulcer. Covering the lesion with an adhesive occlusive dressing for several days after scarification will often soften the eschar before excision is undertaken. The firmly adherent dry eschar that is not attached to underlying bone can often be separated from the surrounding skin with 5% 5-fluorouracil cream . After scarification and application of zinc oxide paste to protect the surrounding skin, 5-fluorouracil is applied to the eschar, including its margin, and then covered with an impermeable plastic wrap. Application is repeated every 8 hours. When separation occurs, it can be excised.
Decubitus dermatitis is treated with topical corticosteroids, vaseline gauze, or a hydrogel wafer. Large bullae may be debrided before applying the dressing.
Patients at risk need to be considered in terms of the underlying disease process:
Spinal cord injury in an otherwise healthy person
Neurologic disease with no medical disease but a devastating condition, such as multiple sclerosis or a cerebral vascular accident compromising the body integrity
Debilitation with a multitude of medical diseases affecting the patient (e.g., arteriosclerosis, diabetes mellitus, Parkinson disease, Alzheimer disease, malignancy, malnutrition, and peripheral vascular disease)
Surgical procedures requiring lengthy positioning on the operating table for cardiovascular or orthopedic procedures
Grading or evaluation can be accomplished by dermatologic observation and staging. Bear in mind that ulcer staging is arbitrary and does not reflect the dynamics of ulcer formation.
Stages are as follows:
Stage 1: Non-blanchable erythema of intact skin
Stage 2: Partial-thickness skin loss with exposed dermis. Adipose or deeper tissues are not exposed
Stage 3: Full-thickness skin loss. Adipose tissue is visible in the ulcer bed, which may have undermining and tunneling (see figure)
Stage 4: Full-thickness skin and tissue loss. Fascia, muscle, tendon, ligament, cartilage, or bone is exposed; undermining, tunneling, and epibole may be present
Unstageable: Obscured full-thickness skin and tissue loss. Extent of tissue damage within the ulcer is obscured by slough or eschar and cannot be determined; removal of slough or eschar reveals a stage 3 or 4 pressure injury
Deep tissue pressure injury: Persistent non-blanchable deep red, maroon, or purple discoloration (may be seen with intact or non-intact skin)
NPUAP recently have added two further pressure injury types to their definitions, both of which are caused by medical devices. Medical devices can lead to pressure injury and injury to mucosal membranes; staging is not possible for these types of pressure injury.
Most superficial ulcers do not progress to stage 2 or even 3 or 4 ulcers. The concept of staging need not be thought of as a progression.
Accumulating evidence suggests that a number of ulcers (most stages 3 and 4) may initially originate in the deep tissue compartment and progress outward to the dermis and epidermis (inside-out theory).
Blackburn J, Ousey K, Taylor L, et al. J Wound Care 2020; 29: 4–12.
The most important risk factors in pressure ulcer etiology are ischemia, recovery of blood flow, and the pathologic effect of pressure and shear. Among other risk factors are force and pressure (shear force, type of force, the relative position of external forces compared to bony prominences), agedness, spinal cord injury, and type 1 diabetes with cardiac autonomic neuropathy.
Parish LC, Lowthian PT. Exp Rev Dermatol 2008; 3: 287–91.
Pressure ulcers continue to have an uncertain etiology.
Park SH, Lee YS, Kwon YM. West J Nurs Res 2016; 38: 459–83.
Typical screening tools (Braden, Norton, and Waterloo scales) utilized for pressure ulcer risk are limited as to their validity and accuracy among older adults due to heterogeneity throughout studies.
Moore ZE, Patton D. Cochrane Database Syst Rev 2019; 1: CD006471.
No proof suggesting the reduction of the incidence or the severity of pressure ulcers is available on the use of structured and systematic pressure ulcer risk assessment tools.
Wei M, Wu L, Chen Y, et al. Nurs Crit Care. 2020; 25: 165-70.
Braden scale provided a moderately predictive validity and had a fair sensitivity and low specificity in critically ill adult patients.
Chun X, Lin Y, Ma J, et al. Pediatr Res 2019; 86: 436–43.
The Braden Q scale anticipated the risk in the pediatric intensive care unit moderately accurate.
Parish LC, Sibbald RG. Adv Skin Wound Care 2012; 25: 57–8.
Role of staging may provide more confusion than merit.
Edsberg LE, Black JM, Goldberg M, et al. Revised National Pressure Ulcer Advisory Panel. J Wound Ostomy Continence Nurs 2016; 43: 585–97.
The European Pressure Ulcer Advisory Panel developed a staging system in 1998 that is composed of four stages: Grade 1 to Grade 4. The classification system most popularly adopted and used is the one presented in 1989 by the NPUAP. This classification system has been updated and revised. A new stage, suspected deep tissue injury, was incorporated in 2016. The extent of the tissue loss present and the presence and absence of anatomical features in the stage of the injury is described in each definition. The revised description of a stage 2 pressure injury aims to demonstrate the difference between moisture-associated skin damage and injury led by pressure and/or shear. The suspected definition has been eliminated from the Deep Tissue Pressure Injury diagnostic label.
Hariri A, Chen F, Moore C, et al. Wound Repair Regen 2019; 27: 488–96.
Q-switched Nd:YAG laser and light-emitting diode (LED)-based photoacoustic imaging systems analyze photoacoustic intensity and photoacoustic depth. The average and standard deviation of ulcer depths from 10 different A-lines are measured with this new technology.
Salomé GM, Ferreira LM. Adv Skin Wound Care 2018; 31: 1–6.
The current study defines the planning and development of a mobile application to prevent and treat pressure injuries for use by providers. The application outlines the risk factors for pressure injury development, supplies an assessment of the wound, suggests wound clearing procedures, maintains pressure injury staging, and suggests treatment interventions.
Lima Serrano M, González Méndez MI, Carrasco Cebollero FM, et al. Med Intensiva 2017; 41: 339–46.
The occurrence of pressure ulcers cannot be explained by a single factor. Risk factors predictive of pressure ulcer development are usually age, length of ICU stay, diabetes, time of MAP <60–70 mmHg, length of mechanical ventilation, intermittent hemodialysis or continuous veno-venous hemofiltration therapy, vasopressor support, sedation, and turning.
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