1. Description of the problem

Pressure ulcers can develop within 2-6 hours. Preventive measures should be instituted for all patients upon arrival in the intensive care unit, but it is important to identify patients at risk. Although conclusive evidence is lacking relating to risk factors for development of pressure ulcers in critically ill patients, the following are most commonly implicated:

  • Number and duration of surgery

  • Fecal and urinary incontinence

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  • Decreased preoperative protein and albumin concentration

  • Immobility and impaired sensory perception

  • Skin moisture

  • Compromised circulation

  • Vasoactive drugs

  • Diabetes mellitus

  • Inability to turn due to instability

  • High APACHE II score

  • Hemodynamic instability

  • Septic shock

  • Peripheral vascular disease

  • Cerebrovascular disease

Because of the myriad risk factors cited in the literature, pressure ulcer prediction tools are widely used. The two most commonly used tools in the United States are the Norton Scale and the Braden Scale. The Norton Scale has 5 clinical categories (physical condition, mental state, activity, mobility, and incontinence), with a score of 16 or less indicating increased risk for pressure ulcer development. The Braden Scale has 6 clinical categories (sensory perception, moisture, activity, mobility, nutrition, and friction and shear), with a score of 18 or less indicating increased risk for pressure ulcer development. Both of these tools have been well validated, but they tend to overpredict the number of patients at risk.

A scale used more commonly in Europe is the Waterlow Scale, which consists of 10 categories: build/weight for height, continence, skin type/visual risk area, mobility, sex/age, appetite, tissue malnutrition, neurological deficit, major surgery/trauma and medication. Each category contains several subscales. Each subscale has a risk score ranging from 0 (most favorable) to 6/8 (the least favorable). To sum the total risk score, the category scores are first obtained and then the subcategory scores are totaled. A score between 10 and 14 places a patient at risk, a score between 15 and 19 is high risk, and greater than 20 constitutes very high risk. Unfortunately the sensitivity of the Waterlow Scale is much too high and the specificity is much too low.

Pressure ulcers are considered a good indicator of quality of care (part of pay-for-performance measures); failure to prevent or heal them can lead to litigation. It is important, then, that the primary focus centers around prevention. Although many preventive measures have not been rigorously evaluated, it is widely accepted that excessive pressure for a prolonged period of time may result in pressure ulcer occurrence. The first major intervention consists of redistributing pressure around sensitive areas of the body. A 2-hour repositioning schedule is now considered the minimal interval for patients at risk.

The use of support surfaces is the next important consideration in pressure redistribution. Support surfaces are divided into three categories:

Group 1: These surfaces are static and do not require electricity (air, foam, gel and water). Ideal for patients at low risk for pressure ulcer development.

Group 2: These devices are considered dynamic in nature and are powered by electricity (alternating and low-air-loss mattresses). These mattresses are useful for patients who are at moderate to high risk for pressure ulcers or have full-thickness pressure ulcers. When reactive hyperemia is noted on bony prominences using group 1 surfaces, these devices should be considered.

Group 3: These devices are also considered dynamic. An example is electric beds that contain silicone-coated beads (air is pumped through the beds and the beads become liquified). These are most useful for patients with non-healing full-thickness pressure ulcers.

Maintaining adequate nutritional status is absolutely essential to prevent skin breakdown and promote healing and maintain immune function. For patients in the prone position, prone head support systems are recommended. Also, in patients requiring non-invasive positive pressure ventilation, masks with larger cushioned surfaces should be used.

Clinical features of the condition

Pressure ulcers usually present as persistent non-blanching erythematous hyperemic areas of the skin. However, blistering, discoloration, localized warmth, edema and induration may also be present. In patients with darkly pigmented skin, discoloration will be the most prominent feature. Pressure ulcers occur most commonly on the back of the head, shoulder blades, lower back, pelvic bone and heels. In addition, patients with nasogastric and nasal feeding tubes are at risk to develop pressure ulcers on their nares. Other common sites include the ear, shoulder, elbow, hip, and between the knees and ankles. However, with the use of prone positioning and non-invasive positive-pressure ventilation, pressure ulcers are occurring with greater frequency on anterior weight-bearing sites, such as the face, thorax, iliac crest, breast and knee.

Key management points

Dressings represent one of the most important interventions in the management of pressure ulcers. The primary objective in using a dressing is maintaining a moist wound environment. Nongauze dressings are more expensive than gauze dressings but may represent cost savings over time because of faster healing rates and lower infection rates. Newer dressings impregnated with hyaluronic acid have proven benefit in healing recurring pressure ulcers.

Adjunctive therapies are used when pressure ulcers have failed to heal over a 12-week period. These interventions are expensive and may not be reimbursed by insurance companies.

Electrical stimulation increases collagen synthesis and produces an increase in growth factor receptor sites and fibroblast production. Radiant heat increases blood flow and promotes fibroblast production. Other investigations involving cytokine growth factors and fibroblast growth factors are ongoing.

Pressure ulcers with large amounts of drainage benefit from the use of vacuum-assisted devices. These devices use sub-atmospheric negative pressure that when applied to the surface and margins of the ulcer removes excess fluid from the wound. This increases localized blood flow and promotes the formation of granulation tissue. These devices are contraindicated for ulcers with osteomyelitis, eschar and exposed blood vessels or organs.

Surgery is an option for full-thickness pressure ulcers. However, surgically closed pressure ulcers have a high rate of recurrence. Free flaps and musculocutaneous flaps in addition to skin grafting and skin flaps are also used as surgical options. Prophylactic ischiectomy is no longer employed because of the high rate of perineal ulcer and urethral fistula. Procedures for fecal diversion (diverting colostomy, diverting ileostomy) are sometimes undertaken to prevent fecal soiling of the ulcer site.

Nutrition is critical for optimal wound healing and immune response. Many critically ill patients are malnourished; therefore, maintaining adequate protein stores is vital to the recovery process. It is important to maintain an adequate caloric intake either parenterally or enterally in all critically ill patients. Surprisingly, there is little evidence at this stage to show that these interventions significantly increase pressure ulcer healing. In addition, there is scant empirical evidence to show that the use of vitamin or mineral supplements in the absence of a deficiency actually aids in pressure-ulcer healing or prevention. However, most critical care clinicians will agree that optimizing every patient’s nutrition status is essential in preventing and treating pressure ulcers.

2. Emergency Management

In general there are few emergencies relating to decubitus ulcers. However, if after inspection of the ulcer it appears that a blood vessel is exposed with active bleeding, steps should be taken to remedy this as soon as possible. This may require immediate surgical intervention, especially if the patient is hemodynamically unstable.

In addition, if a patient presents in septic shock with an infected decubitus ulcer as the source, steps should be taken immediately to incise and debride the infected area, and appropriate antibiotic coverage should be instituted immediately.

Management points not to be missed

Surgical Intervention – for an exposed blood vessel with active bleeding, immediate steps must be undertaken if the patient is hemodynamically unstable.

Source Control – if an infected decubitus ulcer is the source of severe sepsis or septic shock, steps should be taken to emergently incise and debride the infected area, and appropriate antibiotic coverage should be instituted immediately. To distinguish bacterial infection from simple contamination, a tissue biopsy is recommended. This will allow for quantitative wound cultures and assist in antibiotic selection. If bone is visible within the ulcer, osteomyelitis should be presumed, and thus the patient should be treated accordingly for a systemic infection.

3. Diagnosis

Pressure ulcers usually present as persistent non-blanching erythematous hyperemic areas of the skin. However, blistering, discoloration, localized warmth, edema and induration may also be present. In patients with darkly pigmented skin, discoloration will be the most prominent feature. Pressure ulcers occur most commonly on the back of the head, shoulder blades, lower back, pelvic bone and heels. Other common sites include the ear, shoulder, elbow, hip, and between the knees and ankles. However, with the use of prone positioning and non-invasive positive-pressure ventilation, pressure ulcers are occurring with greater frequency on anterior weight-bearing sites, such as the face, thorax, iliac crest, breast and knee. As stated above, patients with nasogastric tubes or nasal feeding tubes are at risk for developing nares ulcers.

The European Pressure Ulcer Advisory Panel and the National Pressure Ulcer Advisory Panel have developed staging systems for pressure ulcers:

Stage 1: An observable pressure-related alteration of intact skin whose indicators, as compared with the adjacent or opposite area on the body, may include changes in 1 or more of the following: skin temperature (warmth or coolness), tissue consistency (firm or boggy feel), and/or sensations (pain, itching). The ulcer appears as a defined area of persistent redness in lightly pigmented skin, whereas in darker skin tones, the ulcer may appear with persistent red, blue, or purple hues.

Stage 2: Partial-thickness skin loss involving epidermis or dermis, or both. The ulcer is superficial and presents clinically as an abrasion, blister, or shallow crater.

Stage 3: Full-thickness skin loss involving damage or necrosis of subcutaneous tissue, which may extend down to but not through underlying fascia. The ulcer presents clinically as a deep crater, with or without undermining adjacent tissue.

Stage 4: Full-thickness skin loss with extensive destruction, tissue necrosis, or damage to muscle, bone, or supporting structures (such as tendon, joint capsule).

Confirmatory tests

In a study evaluating the incidence of pressure ulcers in patients at risk in three different intensive care units at a university hospital in Turkey, Sayar and colleagues found that C-reactive protein was significantly associated with the development of pressure ulcers in this institution. However, multiple stepwise logistic regression analysis determined that length of stay and activity level were the most influential factors for pressure ulcer development. It is not recommended that C-reactive protein levels be measured on a routine basis to assess a patient’s risk for pressure ulcer development.

Pathophysiology

Prolonged immobilization, paralysis, general anesthesia, or physical restraint applies external pressure on prominent body surfaces that exceeds capillary pressure (approximately 32 mm Hg) within tissue beds. This interrupts circulation and results in hypoxic tissue damage and eventually necrosis. The amount of ischemic time necessary to result in a pressure injury varies widely among individuals: it is believed to be somewhere between 30 and 240 minutes. Other factors contribute to variable tissue tolerance to ischemia.

For example, patients with peripheral arterial occlusive disease are at risk for not only pressure ulcer development, but also poor wound healing. This is believed to be due to a delayed reperfusion time after removal of the external pressure. These processes are most influential on bony or cartilaginous prominences with only a thin covering of soft tissue. In addition, ischemia-reperfusion injury may play a role in damage that ensues after circulation is restored. Other forces that can result in skin damage include friction at the skin surface, shearing forces (lateral displacement of the skin whose layers are of differing firmness), and moisture.

Epidemiology

Pressure ulcers have been found in the remains of Egyptian mummies, and were described in the scientific literature in the early 19th century. The prevalence rate of pressure sores in nursing home residents is approximately 17-28%. Sixty-six percent of pressure sores occur in patients older than 70 years. The annual incidence rate of pressure sores in those who are neurologically impaired is believed to be 5-8%, with a lifetime risk estimated to be 25-85%. In addition, they are believed to be the direct cause of death in 7-8% of all paraplegics.

Acutely ill patients who have undergone hospitalization have a pressure sore incidence rate of 3-11%. A recent study of hip fracture patients who underwent surgery revealed that 36.1% developed a pressure sore within 32 days of hospital admission. This 32-day period included time spent by patients in nursing homes and rehabilitation facilities; however, the highest incidence of pressure sores occurred during the hospital stay.

At present, the cost of treatment of pressure sores in the United States exceeds $1 billion annually. Of concern, patients who achieve wound healing through either medical or surgical therapy experience recurrence rates as high as 90%. Of note, a recent study involving nursing home residents found the incidence of pressure sores to be higher in black residents than white residents. These data included 113,869 nursing home residents, all of whom were without pressure sores at admission.

Post-admission pressure sores were discovered in 4.7% of black residents and 3.4% of white residents. The difference in pressure sore incidence displayed a gender preference as well as a racial one. The differences between black and white men occurred in residents who were dependant in mobility. In females the differences between black and white residents were manifest in those who were bed-fast and residing in facilities with fewer than 200 beds.

Special considerations for nursing and allied health professionals.

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What's the evidence?

Description:

De Laat, EH, Schoonhoven, L, Pickkers, P. “Epedemiology, risk and prevention of pressure ulcers in critically ill patients: a literature review”. Journal of Wound Care. vol. 15. 2004. pp. 269-275. (A well-written comprehensive overview with 41 references).

Sayar, S, Turgut, S, Dogan, H. “Incidence of pressure ulcers in intensive care unit patients at risk according to the Waterlow scale and factors influencing the development of pressure ulcers”. Journal of Clinical Nursing. vol. 18. 2008. pp. 765-774. (A well-written study done in Turkish ICUs that explains the Waterlow scale and its limitations; multiple stepwise logistic regression analysis found the most influential factors for pressure ulcer development to be length of stay and activity level).

Kottner, J. “(2009) Incidence of pressure ulcers in intensive care unit patients at risk according to the Waterlow scale and factors influencing the development of pressure ulcers”. Journal of Clinical Nursing. vol. 18. 2008. pp. 775-779. (A commentary on reference #2).

Lyder, CH. “Pressure Ulcer Prevention and Management”. JAMA. vol. 289. 2003. pp. 223-226. (A comprehensive overview of interventions for prevention and managment is presented here. The section on dressings is concise yet thorough.)

Shahin, ESM, Dassen, T, Halfens, RJG. “Incidence, prevention and treatment of pressure ulcers in intensive care patients: A longitudinal study”. International Journal of Nursing Studies. vol. 46. 2009. pp. 413-421. (A longitudinal study where pressure ulcer incidence was low in comparison to other studies, preventive measure such as foam and alternating air pressure mattresses were instituted and hydrocolloid dressing was found to increase the healing rate)

Xakellis, GC, Chriscilles, EA. “Hydrocolloids versus saline gauze dressings in treating pressure ulcers: a cost-effective analysis”. Arch Phys Med Rehabil.. vol. 73. 1992. pp. 463-469. (This study demonstrated that nongauze dressings, although more expensive than gauze dressings, are more cost-effective over time due to less frequent dressing changes, faster healing rates, and decreased rates of infection).

Kloth, LC, McCulloch, JM. “Promotion of wound healing with electrical stimulation”. Adv Wound Care.. vol. 9. 1996. pp. 42-45. (This paper descibes how this treatment modality increases numbers of fibroblasts, macrophages and neutrophils, stimulates collagen and DNA synthesis, and increases the number of growth factor receptor sites specific for wound healing).

Baker, L, Rubayi, S, Villar, F. “Effects of electrical stimulation wave form on healing of ulcers in human beings with spinal cord injury”. Wound Repair Regen.. vol. 4. 1996. pp. 21-28. (As above in reference #7 except included only patients with spinal cord injury.)

Xia, Z, Sato, A, Hughes, MA. “Stimulation of fibroblast growth in vitro by intermittent radiant warming”. Wound Repair Regen.. vol. 8. 2000. pp. 138-144. (In vitro study demonstrating the effect radiant heat has on increasing blood flow and increasing other factors that serve to promote pressure ulcer healing.)

Kloth, LC, Berman, JE, Dumit Minkel, S. “Effects of a normothermic dressing on pressure ulcer healing”. Adv Skin Wound Care.. vol. 13. 2000. pp. 69-74. (As above in reference #9)

Bello, YM, Phillips, TJ. “Recent advances in wound healing”. JAMA.. vol. 283. 2000. pp. 716-718. (Nice treatment and overview of recent advances, particularly as it relates to the experimental use of cytokine growth factors, fibroblast growth factors and skin equivalents.)

Philbeck, TE, Whittington, KT, Millsap, MH. “The clinical and cost-effectiveness of externally applied negative pressure wound therapy in the treatment of wounds in home healthcare Medicare patients”. Ostomy Wound Manage.. vol. 45. 1999. pp. 41-50. (Excellent treatement of externally applied negative pressure wound therapy and its cost-effectiveness. Great read about a treatment that is becoming more and more prevalent.)

El-Toraei, I, Chung, B. “The management of pressure sores”. J Dermatol Surg Oncol.. vol. 3. 1977. pp. 507-511. (Good overview, but one must keep in mind that many of the current therapies were not available in 1977).

Relander, M, Palmer, B. “Recurrence of surgically treated pressure sores”. Scand J Plast Reconstr Surg Hand Surg.. vol. 22. 1988. pp. 89-92. (This paper describes the factors underlying the high rate of recurrence of surgically treated pressure sores)

Hengstermann, S, Fischer, A, Steinhagen-Thiessen, E. “Nutrition status and pressure ulcer: what we need for nutrition screening”. Journal of Parenteral and Enteral Nutrition.. vol. 31. 2007. pp. 288-294. (Excellent treatment of the nutritional considerations in patients with pressure ulcers. Many current and relevant references provide additional reading on this absolutely essential component of pressure ulcer healing.)

Emergency Management:

Anders, J, Heinemann Axel, Leffman, C. “Decubitus Ulcers: Pathophysiology and Primary Prevention”. Dtsch Arztebl Int .. vol. 107. 2010. pp. 371-382. (Perhaps the most current and best review available on this topic)

Diagnosis:

“European Pressure Ulcer Advisory Panel and National Pressure Ulcer Advisory Panel: Prevention and treatment of pressure ulcers: clinical practice guideline”. National Pressure Ulcer Advisory Panel. 2009. (Gold standard for classifying pressure ulcers)

Black, J, Baharestani, M, Cuddigan, J. “National Pressure Ulcer Advisory Panel's updated pressure ulcer staging system”. Dermatol Nurs.. vol. 19. 2007. pp. 343-349. (Update of reference #17)

Pathophysiology:

Gefen, A. “Reswick and Rogers pressure-time curve for pressure ulcer risk. Part 1”. Nurs Stand. vol. 23. Jul 15-21 2009. pp. 64-66,68. (A good description of the time course for pressure ulcer risk and development)

Gefen, A. “Reswick and Rogers pressure-time curve for pressure ulcer risk. Part 2”. Nurs Stand. vol. 23. Jul 22-28 2009. pp. 40-44. (As above in reference #19)

Schweinberger, MH, Roukis, TS. “Effectiveness of instituting a specific bed protocol in reducing complications associated with bed rest”. J Foot Ankle Surg.. vol. 49. 2010. pp. 340-347. (Single-center observational cohort study evaluating interventions that included specific positioning, continuous heel off loading, frequent position changes and upper and lower body bed exercises. Findings suggested that institituting specific protocols can reduce complications like pressure ulcers in patients in whom strict bed rest is indicated.)

Zhao, G, Hilttabidel, E, Liu, Y. “A cross-sectional descriptive study of pressure ulcer prevalence in a teaching hospital in China”. Ostomy Wound Manage. vol. 56. 2010. pp. 38-42. (A cross-sectional study conducted at one teaching hospital in China; results are fairly consistent and supportive of current literature.)

Epidemiology:

Thompson, RJ. “Pathological changes in mummies”. Proc R Soc Med.. vol. 54. 1961. pp. 409(Interesting read from a half-century ago, before we could probe more deeply into the anatomy of mummies with modern imaging devices like CT and MRI scanners)

Stausberg, J, Kiefer, E. “Classification of pressure ulcers a systematic literature review”. Stud Health Technol Inform.. vol. 146. 2009. pp. 511-515. (A well-written systematic review)

Conway, H, Griffin, BH. “Plastic surgery for closure of decubitus ulcers in patients with paraplegia; based on experience with 1000 cases”. Am J Surg.. vol. 91. 1956. pp. 946-975. (Old reference with a large number of cases but good treatment of requirements in paraplegic patients)

Fogerty, M, Guy, J, Barbul, A. “African Americans show increased risk for pressure ulcers: A retrospective analysis of acute care hospitals in America”. Wound Repair Regen.. vol. 17. Sept-Oct 2009. pp. 678-684. (The authors looked at discharge diagnoses and found that African Americans exhibited a higher prevalence of pressure ulcers as compared to Caucasians. African Americans demonstrated a tendency to develop pressure ulcers at a younger age. Socioeconomic factors failed to provide an explanation for these findings.)

Baumgarten, M, Margolis, DJ, Orwig, DL. “Pressure ulcers in elderly patients with hip fracture across the continuum of care”. J Am Geriatr Soc.. vol. 57. 2009. pp. 863-870. (Excellent study examining the prevalence in the elderly patient population)

Howard, DL, Taylor, YJ. “Racial and gender differences in pressure ulcer development among nursing home residents in the Southeastern United States”. J Women Aging.. vol. 21. 2009. pp. 266-278. (This study also found that the incidence of pressure ulcers was higher in black residents than white residents. There were also gender differences as well. The differences between black and white males occurred in individuals who were dependant in mobility. The differences in females involved those who were bed-fast and in facilities with fewer than 200 beds.)

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