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Wound Series Part 3: Pressure Ulcers and Injuries-Risk Factors, Diagnosis, Staging, Management

2.00 Contact Hours
This course is applicable for the following professions:
Advanced Registered Nurse Practitioner (ARNP), Certified Nursing Assistant (CNA), Clinical Nurse Specialist (CNS), Home Health Aid (HHA), Licensed Practical Nurse (LPN), Licensed Vocational Nurses (LVN), Medical Assistant (MA), Occupational Therapist (OT), Occupational Therapist Assistant (OTA), Physical Therapist (PT), Physical Therapist Assistant (PTA), Registered Nurse (RN)
This course will be updated or discontinued on or before Thursday, March 11, 2021

AOTA Classification Code: CAT 2: Client Factors
Education Level: Intermediate
AOTA does not endorse specific course content, products, or clinical procedures. AOTA provider number 9575.

FPTA Approval:CE19-649249. Accreditation of this course does not necessarily imply the FPTA supports the views of the presenter or the sponsors.
Course Description
The goal of this continuing education course is to enable the participants to identify strong risk factors for pressure ulcer development, describe pressure ulcer staging and documentation, and discuss evidence-informed pressure ulcer prevention and management strategies. Through this course, the Occupational therapist and physical therapist will be able to identify strong risk factors for pressure ulcer development, describe pressure ulcer staging and documentation, and discuss evidence-informed pressure ulcer prevention and management strategies. The OT and PT will understand the interprofessional relationship and be able to incorporate strategies throughout the continuum of care. Through this course, the Occupational Therapy Assistant and Physical Therapy Assistant will understand and identify risk factors for pressure ulcer development, staging, documentation and evidence-based prevention and management strategies. The OT and PT Assistants will understand the interprofessional relationship, development of the p.o.c. and be able to understand strategies used for prevention of pressure ulcers.
CEUFast Inc. did not endorse any product, or receive any commercial support or sponsorship for this course. The Planning Committee and Authors do not have any conflict of interest.

Last Updated:
To earn of certificate of completion you have one of two options:
  1. Take test and pass with a score of at least 80%
  2. Reflect on practice impact by completing self-reflection, self-assessment and course evaluation.
    (NOTE: Some approval agencies and organizations require you to take a test and self reflection is NOT an option.)
Author:    Linda J. Cowan (PHD, ARNP, FNP-BC, CWS)

Outcomes

The purpose of this continuing education course is to enable the participants to identify strong risk factors for pressure ulcer development, describe pressure ulcer staging and documentation, and discuss evidence-informed pressure ulcer prevention and management strategies.

Objectives

After completing this continuing education course, the participant will be able to meet the following objectives:

  1. Describe at least three etiological factors of pressure ulcers/injuries
  2. Identify at least four common risk factors of pressure ulcers/injuries
  3. Describe at least two common pressure ulcer/injury risk assessment tools
  4. Identify at least five pressure ulcer/injury stages
  5. Describe at least one recent change in terminology published in NPUAP in 2016
  6. Identify at least two evidence-based interventions to consider in the management of pressure ulcers/injuries.

Pressure Ulcer Background and Significance

Pressure ulcers have been known as “bedsores” for hundreds of years. Historically, the term decubitus ulcer or decubiti has also been used to describe these wounds related to pressure and/or immobility. The term “pressure ulcer” was replaced by “pressure injury” in the updated National Pressure Ulcer Advisory Panel Pressure Injury Staging System by the National Pressure Ulcer Advisory Panel (NPUAP) and Pan Pacific Pressure Injury Alliance in April, 2016.1 The NPUAP now defines a pressure injury as, “localized damage to the skin and/or underlying soft tissue usually over a bony prominence or related to a medical or other device. The injury can present as intact skin or an open ulcer and may be painful. The injury occurs as a result of intense and/or prolonged pressure or pressure in combination with shear. The tolerance of soft tissue for pressure and shear may also be affected by microclimate, nutrition, perfusion, co-morbidities and condition of the soft tissue.”1 Many, but not all healthcare organizations have adopted the new terminology. However, coding systems such as the International Statistical Classification of Diseases and Related Health Problems – version 10 (ICD-10) continue to use the term pressure ulcers (L89 codes). For the purpose of this educational course, we will be using the term pressure ulcer (PU) with no disrespect intended to the NPUAP. The presence of avoidable facility acquired PUs are recognized internationally as a quality of care indicator for healthcare organizations.2 Despite this, CMS reports PUs were present in 3.7 to 7.3 % of residents in the majority of long term care facilities (nursing homes) in the United States (US) in 2014, with no change in the rate between 2013 and 2014. This represents an annual cost of over 3.3 billion US dollars for PUs in long term care settings alone.3 In a National Inpatient Sample of over 6 million persons discharged from acute care facilities (hospitals) in the US, 94,758 individuals had a discharge diagnosis of pressure ulcer.4 However, this number only accounts for patients who had a pressure ulcer diagnosis code documented at discharge. The real numbers of incident PUs (those that start in the facility) are difficult to estimate since studies report widely varied rates of PUs across healthcare settings and most of these rates are prevalence rates (any PU present over a given time span).5,6 Furthermore, individuals with spinal cord injuries (SCI) are particularly vulnerable to PUs. The National Spinal Cord Injury Statistical Center 2017 Annual Statistical Report7 indicates about 25% of all persons with SCI in their surveillance program have developed a PU within the first 12 months of the SCI, and 35% have developed at least one PU past the 1st 12 months post-SCI. Others estimate approximately 30 to 60% of all persons with spinal cord injuries (SCI) will experience a PU in their lifetime,8,9 and 7 to 8% of deaths in persons with SCI are attributed to PUs.10 The Agency for Healthcare Research and Quality (AHRQ)11 report about 60,000 persons in the US die each year as a direct result of pressure ulcers, but it is unclear where this statistic comes from, or how it was calculated, though it has been cited in many manuscripts.

It is evident from the scientific literature PUs are painful, prone to infection, reduce quality of life, and create a world-wide economic dilemma.4,5,12 Health care costs related to the management and treatment of chronic wounds (including PUs) in the U.S. exceeds $20 billion annually.11 While the quality of health care and medical technology has improved in the United States during the past 20 years, facility-acquired pressure ulcers have not been eliminated.3,13 Concurrent with this advancing technology, modern-day patients live longer and are typically hospitalized with higher acuity levels than patients hospitalized years ago. Healthcare organizations must continuously improve in order to adequately impact this important quality of care indicator.6,14,15

Etiology of Pressure Ulcers

Historically, pressure ulcers have been described in medical literature since at least the 1500s when Fabricius Hildanus first documented his hypotheses of the causes and characteristics of bedsores. He highlighted the role of “internal supernatural” and “external natural” factors that interrupt the supply of blood and nutrients to tissue as causes of bedsores. Mechanical pressure and incontinence were first identified and key factors in the development of PUs by French surgeon de la Motte in 1722.16 Major risk factors identified for PU development in the scientific literature since 1987 include increased age, impaired mobility, decreased physical activity, poor nutrition, urinary and/or fecal incontinence, and sensory impairment.5,17,18,19 Other studies have identified additional risk factors including smoking status, diabetes mellitus (DM), coronary artery disease (CAD), intensive care unit (ICU) stay greater than 3 days, ventilator dependency, pneumonia, sepsis, obesity, surgery, female gender, and peripheral vascular disease (PVD).20,21,22 Most PUs are considered to be avoidable, therefore, preventable.1,2,23,24 An “avoidable” PU means that the patient developed a PU and the facility or health caregivers did not perform (or document) one or more of the following: evaluate the patient’s / resident’s clinical condition and PU risk factors; define and implement interventions that are consistent with resident needs, resident goals, and recognized standards of practice; monitor and evaluate the impact of the interventions; or revise the interventions as appropriate. Thomas (2001)25 suggests there may be a few instances where PUs are unavoidable. “Unavoidable” means the patient/resident developed a PU despite the fact that the facility and health care providers had evaluated (and documented) the resident’s clinical condition and PU risk factors; defined and implemented interventions that are consistent with resident needs, goals, and recognized standards of practice; monitored and evaluated the impact of the interventions; and revised the approaches as appropriate – all within a timely manner.26 Kennedy ulcers (a specific type of PU often seen at the end of life due to organ/system failure) are one example of “unavoidable” PUs.

Exploring Risk Factors for Pressure Ulcers

Fogerty et al.4 conducted a very large retrospective case-control study reviewing admission and discharge data from over six million subjects in the Nationwide Inpatient Sample (NIS) to identify risk factors and demographic differences between those who developed PUs and those that did not. Some may describe their study as a nested case-control27 because they identified a cohort (inpatients in the NIS dataset), followed their records retrospectively from their hospital admission until hospital discharge (during 2003), and separated them into 2 groups: those who developed PUs (cases) and those that did not (controls). There were 94,758 incident PUs documented among a final discharge sample of 6,610,787 persons. Utilizing multivariate logistic regression analysis on 45 common diagnoses identified in persons with PUs, they reported odds ratios (estimate of relative risk) for the most significant risk factors associated with developing PUs. Analysis was also conducted stratifying the sample by age, race and gender. Age over 75 years was the strongest PU risk factor identified with an Odds Ratio (OR) of 12.63 (meaning people over 75 years are almost 13 times more likely to develop PUs than younger age groups). Other strong risk factors identified (listed in descending order) include: diagnosis of gangrene (OR 10.94, 95% CI 10.43-11.48), septicemia (OR 9.78, 95% CI 9.33- 10.26), osteomyelitis (OR 9.38, 95% CI 8.81-9.99), nutritional deficiencies (OR9.18, 95% CI 8.81-9.99), pneumonitis (OR 8.70, 95% CI 8.33-9.09), urinary tract infection (OR 7.17, 95% CI 6.96-7.38), paralysis (OR 10.30, 95% CI 9.69-10.96), age 59 to 75 years (OR 5.99, no CI reported), and African American race (OR 5.71, 95% CI 5.35-6.10). Fogerty et al. also reported a statistically significant interaction between race and age, such that as African Americans age, their risk of developing PUs increases faster than the risk Caucasians experience as they age, indicating noteworthy racial disparities. Other significant findings identified in their study highlight some of the strongest risk factors are non-modifiable (age, paralysis, race) while others are potentially modifiable (infection, nutritional deficiencies). Therefore, exploration is needed to determine when interventions are most effective in those persons with non-modifiable risk factors (such as age > 75, darker skin, or paralysis) or if interventions should be initiated in all persons over 75 years old, with darker skin, or with paralysis. Investigations should also examine the most effective interventions to reduce or eliminate the identified modifiable risk factors (infection and nutritional deficiencies) and ways to accurately identify them in patients.

The purpose of identifying a risk factor is to intervene and lower the associated risk. Identifying the strongest PU risk factors is important to be able to provide evidence-based interventions and thereby lower the likelihood of someone developing a PU or halting the progression of the PU. PU risk assessment tools provide a tangible way to quantify potential risk so that interventions may be reserved for those at highest risk and avoid unnecessary interventions and higher financial expenditures on those who may not need them.28

Interpreting Research Pearl: When reading results of research studies reporting Odds Ratios (OR), here are some tips to interpreting the data:

If the OR number is a number more than 1.0 (2, 3, 4, 13, etc.), this can be interpreted to say the associated risk is higher with the test group or exposure group than with the control group or comparison group. Example: An Odds Ratio (of developing lung cancer) of 7.0 associated with smokers versus non-smokers could indicate that those who smoke are 7.0 times more likely to develop lung cancer than those who do not smoke.

If the OR number is a number less than 1.0 (0.9, 0.7, 0.2, etc.) then you can subtract (in your head) this number from 1 and turn it into a percentage to say the associated risk is less in the test group than the control or comparison group. Example: An Odds Ratio of 0.25 of developing a Deep Vein Thrombosis (DVT) when you fly long distances by plane if you wear compression stockings versus if you do not wear compression stockings could indicate a 75% risk reduction in the compression stocking group. We got to this number by taking the OR of 0.25 and subtracting it from 1 = 0.75, then turned it into a percentage = 75%.

These OR interpretations are only worth something meaningful if the study was large enough (had enough subjects), was carried out with scientific rigor (done the best way to answer the question), and the 95% Confidence Interval (CI) does not contain numbers on both sides of 1.0. For instance, an OR of 7.0 with a 95% CI of 3.0 – 9.0 means that the estimated risk associated with whatever they are looking at is 7 times higher in the exposure or test group AND you can be 95% confident that the real risk is somewhere between 3 times higher risk and 9 times higher risk. If the OR was 7.0 with 95% CI of 0.5 to 8.0, then it is essentially worthless – you don’t get meaningful results if the risk might be 50% less or up to 8 times greater. It should be either less risk or more risk but if the real measure of risk could be either, don’t use these results as evidence to change practice! Therefore, anytime OR is reported, the authors should also report a 95% Confidence Interval (95% CI).

Cowan et al. (2012)22 conducted a retrospective analysis in a Veteran population to identify the strongest PU predictive model which demonstrated four medical factors (malnutrition, surgery, pneumonia, candidiasis) were more predictive of PU than total Braden Scale for Predicting Pressure Ulcer scores. The finding of a diagnosis of candidiasis as a risk factor for PUs may be related to medical conditions where candidiasis is most common (could it be a proxy variable for impaired immune function?). More research is needed to explore these relationships. Nevertheless, this research provides valuable information that may enhance current risk factor assessments. Identification of factors affecting the development of PUs is imperative in the present day population in order to select patients for effective prevention interventions. Furthermore, evaluation of the efficacy of existing preventive interventions must be ongoing, and new innovative interventions must be explored in order to impact PU incidence and prevalence significantly.4,29

One criticism of existing PU risk assessment tools is that “neither risk factors nor the weights attributed to them have been identified using adequate statistical techniques.”30 Risk factors are those factors or conditions that are noted to be most strongly associated with the outcome of interest. In order to provide evidence-based measures in the prevention of PUs, an effective means of identifying those at highest risk is imperative. Other criticism of PU risk assessment tools includes the lack of clear evidence that risk assessment tools have significant impact on clinical outcomes such as PU incidence rates,31-33 the subjective nature of some of the assessments,32,33 the lack of tools for specific settings such as the perioperative environment,34,35 and the fact that no one assessment tool could account for every risk factor.33 Current risk assessment tools may require further development, improved statistical evaluation, and possible modification in order to remain applicable to present-day populations.

Thomas25 posits an explanation for an unchanging incidence of PUs as “a failure of known effective prevention treatment to be applied, or the failure of prevention strategies to be effective despite being applied” (p.298). Effective preventive measures may not be applied if individuals are not appropriately identified as being at risk. Risk-screening tools are useless if they are not applicable to the population being screened, if they are used inconsistently, or scored incorrectly.25,32,36

Risk Assessment Tools

Norton Scale

The PU risk assessment tools most frequently utilized around the world are the Norton Scale (published in 1962) and the Braden Scale (published in 1987) or modified versions of these. Doreen Norton (along with Rhoda McLaren and Dr. Norman Exton-Smith) developed the Norton Scale in Great Britain during the 1950s.37-39 It is the first of all of the PU risk assessment scales; indeed it is one of the earliest risk assessment scales of any kind. At first, Norton et al. devised a data collection tool with columns to describe all factors noted in every patient that “might be relevant to PU development”38 (p.39) such as patient’s weight, build, appetite, medications, preventive measures (14 different skin care products), treatment measures, site and condition of skin, and skin changes. They developed a rating ‘scale’ (at a time when rating scales were uncommon) with 5 elements that had weighted descending values for each element from 4 to 1. The “elements” or factors in their tool were listed as column headings for general physical condition (including overall nutritional state), mental condition, mobility, activity, and incontinence. Norton reports the tool was scored ‘4’ for a normal or good function in each factor and ‘1’ for very poor or bad function, with a total possible high score of 20 (patient in good overall condition) and low score of 5 (patient in poor overall condition). Norton explains, “A descending scale was selected because it correlated with a decline in the patient’s condition”38 (p.39). The Norton conceptual model is a simple model based on their observed factors of general physical condition, mental condition, mobility, activity, and incontinence with a Likert-type scale for each of these factors totaled as one independent variable and “pressure ulcer RISK” as the dependent or outcome variable. This model posits that higher total scores have a strong positive association with higher pressure ulcer risk.37-39 Norton states her scale was frequently misinterpreted as “over-predicting pressure ulcer lesions”38 (p.41) when used incorrectly as a predictive tool. In addition, it was criticized for leaving out nutritional assessment. However, according to Norton, nutritional assessment was included in their data collecting form and was intended as an integral part of overall “general condition” assessment. In retrospect, Norton (p.42)38 regretted not having an explicit user’s guide to go along with her original tool and suggests that all future risk assessment tools remain simple and easy to use and have a Rater’s Guide explaining specifically how to utilize the tool.

Braden Scale

The Braden Scale was first published in 198739,40-42 and is probably the most widely used PU risk assessment tool available today.39 The theoretical framework is based on a physiological model depicting factors that contribute to the development of PUs. It includes factors affecting intensity and duration of pressure (decreased mobility, decreased activity, and decreased sensory perception), which combine with intrinsic factors (age, nutrition, vascular perfusion) and extrinsic factors (increased moisture, increased friction, and increased shear forces) that affect tissue tolerance.40-43 The Braden Scale is publicized as the most extensively tested and studied of the assessment tools. The Braden Scale has a potential score ranging from 6 to 23 derived from the total scores of its six subscales (sensory perception, mobility, activity level, moisture/incontinence, nutrition, and friction/shear). Lower scores on the Braden Scale indicate greater risk for PU development. For example: Very high risk = 9 or below; High risk = 10-12; Moderate risk= 13-14; and Mild risk = 15-18. There is literature by Braden to suggest that if a person has other major risk factors present (age, fever, poor nutrition, hemodynamic instability), their score should be advanced to the next highest level of risk (i.e., next lower score), yet observational studies suggest this is not routinely done by nurses.39-45

Clinical Pearl:

Nurses who are being tasked with conducting daily pressure ulcer risk assessments should take them very seriously and make sure to score them accurately, taking into account any change in the patient’s condition and risk not assessed by the specific tool being used. It is always better to overestimate risk than to underestimate risk! And sometimes this means assigning a lower score, if lower scores indicate higher risk on the risk screening tool you are using (such as the Braden Tool). If the person’s sub-score falls between numbers, always select the lower number to try and capture any possible risk. For instance, if the patient’s nutritional sub-score falls between a “2” and “3” on the Braden Tool, always mark it a “2”.

Reports of sensitivity and specificity of the Braden and Norton Scales may be misleading. Jalali and Rezaie23 report sensitivity to be “the percent of individuals who developed a pressure ulcer who were assessed at being at risk” for a PU by the tool (Norton, Braden, Waterlow, or Gosnell scales), and specificity to be “the percent of individuals who do not develop a pressure ulcer who were assessed to not be at risk” (p.94). They report sensitivity and specificity (respectively) for the Norton scale to be 49% and 100%, the Braden scale was 53% and 100%, the Gosnell scale was 85% and 83%, and Waterlow was 63% and 82.5%. As Norton posits, in using the tool at all, you may be providing an intervention; therefore, the “predictive validity” scores may accurately depict a lower percent sensitivity for the more effective tools because they are effectively lowering the incident number of PUs in those identified as higher risk. The specificity of 100% (Braden and Norton scales) depicts the tool’s ability to correctly identify those not at risk for developing a PU and suggests the Gosnell and Waterlow scales were not as successful in this regard. Therefore, a word of caution should accompany research studies seeking to ‘validate’ risk assessment scales in this manner rather than investigating the impact of their use on the incidence of PUs.23

Defloor16 criticized Braden & Bergstrom’s inclusion of “tissue tolerance” in a causal pathway toward PU development in their conceptual model stating, “Tissue tolerance cannot cause pressure sores. The existence of pressure and/or shearing force is needed. Tissue tolerance is looked upon as an intermediate variable and not a causal factor"16 (p.207). Defloor went on to say that the Braden & Bergstrom conceptual model did not include factors identified in other studies as strongly associated with PU development such as “specific diseases, dehydration, protein deficiency, body build, position, etc.” He described his own conceptual scheme of pressure sore formation, utilizing known risk factors and pathophysiology and expanding on the factors listed in the Braden & Bergstrom model. Defloor’s 1999 model depicts Compressive Force and Shearing Force as independent variables that interact and Tissue Tolerance for Pressure as well as Tissue Tolerance for Oxygen as intermediate (moderating) variables toward the dependent variable of Pressure Sores. Defloor also noted that more research is needed especially in regards to factors such as smoking and low protein, as well as the influence of preventive measures. Defloor concluded (p.214) that many authors on the subject of PU development limit themselves to identifying risk factors, stating, “it is important to gain insight into how these risk factors interact, not only for a better understanding of the pathophysiology of pressure sores and of preventive measures, but also for the development of valid risk scales.”16

Jalali & Rezaie23 tested the “predictive power” of the 4 most common PU risk assessment scales (RAS) side by side in a prospective study evaluating incident PUs in 3 educational hospitals in Iran between 2000 and 2002. They examined a total of 230 patients (100 men + 130 women) over 21 years old who were admitted to the hospital without a PU. They used 4 common PU risk scales (Norton, Braden, Waterlow, and Gosnell) and a uniform skin assessment tool requiring the researcher to document the skin condition of all bony prominences for every patient within 48 hours of admission and every 24 hours afterward for 14 days. All incident PUs were staged and recorded according to the AHCPR (now AHRQ) PU treatment guidelines staging that contained Stage I – Stage IV (no unstageable or deep tissue injury stages). Four separate researchers each evaluated the patient using one of the 4 RAS, but there were some limitations associated with the study. Deep tissue injury discoloration could be misclassified as Stage I. Researchers report the patients were assessed for a minimum of 14 days under their methods section and a maximum of 14 days under the procedure section. The average number of days the sample was followed was not clear; however, it seems apparent that patients were followed only 2 weeks. This is a limitation to the study especially as far as negative predictive value (NPV) and positive predictive value (PPV) they report regarding the scales. Norton and Braden demonstrated 100% PPV in this study, but Gosnell and Waterlow demonstrated only 59 and 61% PPV, while Gosnell and Waterlow demonstrated 95% and 84% NPV and Norton and Braden only had 52% and 58% NPV. Assuming these values to be true for the sake of argument, perhaps patients developed PUs at day 15 or 20. If more patients developed ulcers later, it would alter some of these results. If the study followed the patients longer, it would be more supportive of the author’s premise regarding the scales. Furthermore, the Youden’s Index (developed in 1950 to evaluate the accuracy of diagnostic tools/tests) was used to report predictive validity or “predictive power” for the four scales, but the index data was not reported uniformly. Jalali & Rezaie reported that Youden’s Index “assumes that sensitivity and specificity have equal importance” (p.94),23 however it is unclear if sensitivity and specificity of PU risk scales do or should have equal importance. Is it more important that PU risk assessment scales predict who will get a PU or who will not?

Cultural and Social Issues

In the Jalali & Rezaie study,23 the Iran subjects ranged from 21 to 89 years with a mean age of 60 years. Jalali and Rezaie designed their study observation period based on findings from Pang & Wong,46 who reported most PUs developed in the first 2 weeks (in a Hong Kong rehabilitation hospital with an older sample of mostly Chinese individuals). The average life expectancy in Iran is lower than both Asian and Western developed countries. The authors did not mention the cultural, economic or social differences between these study populations, yet they mention they do not use pressure-reducing equipment and their study demonstrated a 32.2% higher acute care PU prevalence rate than other acute care studies. In addition, Jalali and Rezaie collected their data in acute care settings (intensive care, neurology, orthopedic, and medical units). They also report that nursing care for the Iran sample was “similar in all patients,” but go on to describe subjects in their study as having “neurological problems such as cerebrovascular accident and intracranial hemorrhage, decreased mobility, and decreased level of consciousness, inadequate nutrition, and incontinence” (p.96).23 How can nursing care be similar across 3 different educational hospitals and in different acuity levels? It is also unclear why limb massage was reported by the authors as an intervention that could help prevent PUs, when studies from the 1980s demonstrated that limb massage is not evidence-based or recommended.47 Are there any cultural or social reasons barriers to utilizing effective evidence-based interventions? Health care providers in American and the western world may not be able to fathom the difficulties in providing even basic nursing care that faces our colleagues in other countries.

Age as Social Factor

Multiple studies demonstrate the elderly are particularly vulnerable to PUs.4,48-51 The US aging population is growing. The US Census Bureau for 2000 reported 35 million people (12.4% of population) in the US were over 65 years old in the year 2000. That number is projected to rise to 54 million (16.3% of population) by the year 2020, and 86.7 million (20.7% of population) by the year 2050. Pressure ulcers are a critical problem that is growing in the United States. Many changes in aging skin, as well as progressive immobility, may contribute to higher risks of PU in aging populations (thinning of epidermal and dermal layers and loss of rete ridges), sensory changes, changes in the composition of body fat and muscle mass, etc.).24

Doreen Norton38 conducted her research involving 600 patients (average age 79) in the geriatric firm of a London hospital (over a 2-year period of time) in the 1950s. Her scale is based on observed factors in that population. Braden built on what Norton had done and modified her scale to fit observed factors of the 1980s. In addition, a recent study suggests that even after specific in-depth training on how to use the Braden Scale, nurses produced reliable Braden Scores only 65% of the time after training.52 Indeed, there have been documented problems with nurse’s knowledge and inconsistent use of PU risk assessment tools. Not to mention the lack of adequate implementation of effective PU prevention protocols and interventions once risk has been identified.44,52,53

Nutrition as a Risk Factor

The research published by Fogerty et al. in 20084 and Cowan et al. in 201222 along with many others have demonstrated just how important adequate nutrition and hydration are to maintaining intact skin, as well as facilitate wound healing. Individuals who are nutritionally compromised are at greater risk of PU. Unfortunately, the Braden Scale may not do a great job of adequately capturing nutritional risk. Further analysis of the Cowan et al. retrospective PU risk study54 explored the relationship between the Braden subscore of Nutrition (documented by nurses) and the nutritional assessment conducted and documented by licensed/registered dieticians. The results of this analysis will be published soon and suggest there is poor agreement between these two assessments on the same patients. There also appears to be poor agreement with the Braden subscore and nutritional lab indices (better agreement between LD/RD nutritional assessments and lab indices). This may indicate the Braden Scale itself is too vague in the subscore of Nutrition, or nurses may need more specific education on how to assess nutritional risk and capture that risk with the Braden instrument. Regardless, assessing every patient for nutritional risk and then acting quickly (perhaps with a LD/RD nutrition consult) to address nutritional deficits is a critical consideration in preventing and managing PUs.

Diagnosis

Pressure ulcers or “bed sores” have been documented for thousands of years. Diagnosing pressure ulcers largely depends on assessing possible pressure, shear and moisture- related etiological factors as well as location of the tissue damage. The first question in your mental wound assessment “checklist” should be: “Is it over a boney prominence?” While pressure ulcers may develop over any boney prominence on the body, the sacrum, coccyx, buttocks, and heels of the feet are the most prevalent sites for pressure ulcers.55-57 Other common locations may include greater trochanters, ischial tuberosities, ankles, knees, elbows, scapulas, shoulders, and occiput. In addition, pressure-related injury may also be related to devices such as oxygen tubing, cervical collars, endotracheal tubes, oxygen saturation monitor probes, drain tubes, foley catheters, etc.. Device-related PUs may be observed over the ears, around the urethral opening of the genitals or other soft tissue location not associated with a bony prominence.58 Furthermore, this type of device-related injury may cause full thickness tissue damage which is difficult to stage because, as in the case of the ears, there is no subcutaneous tissue evident - a very shallow wound may result in the exposure of cartilage (full thickness wound) without the involvement of muscle, tendon or bone. Again, it is important to note that while the onset of pressure ulcers is associated with unrelieved pressure, of course, it can also be caused by a combination of pressure, friction and shearing forces. Evaluating these potential forces (head of bed raised for long periods, patient sliding down in the bed, chair transfers, improper overhead sling positioning, etc.) is imperative when assessing your patient’s skin integrity risks.

Pressure Ulcer Stages

Pressure ulcer staging provides a way to communicate the degree of tissue damage in pressure ulcers. The staging system was defined by Shea in 1975 and provides a name to the amount of anatomical tissue loss. The original definitions were confusing to many clinicians and lead to inaccurate staging of ulcers associated or due to perineal dermatitis and those due to deep tissue injury.59 The original stages ranged from Stage I (less obvious and potentially reversible damage) to Stage IV (damage extending to muscle, tendon and/or bone). “Unstageable” and “suspected Deep Tissue Injury” (sDTI) were added as additional ‘stages’ or descriptors in 2007.59 In April, 2016, the NPUAP again revised their PU staging system to include new “pressure injury” terminology to replace “pressure ulcer” terms, deleting “suspected” from Deep Tissue Injury classification, clarification about moisture-related skin damage, specifics on assessment of darkly pigmented skin, adding medical device-related pressure injury and mucosal pressure injury definitions, and using Arabic numbers to replace Roman numerals.1,60,61 Please see the new NPUAP Staging system in the clinical pearls box below.

Updated NPUAP Pressure Injury Stages and Terminology:
Stage 1 Pressure Injury: Non-blanchable erythema of intact skin

Intact skin with a localized area of non-blanchable erythema, which may appear differently in darkly pigmented skin. Presence of blanchable erythema or changes in sensation, temperature, or firmness may precede visual changes. Color changes do not include purple or maroon discoloration; these may indicate deep tissue pressure injury.

Stage 2 Pressure Injury: Partial-thickness skin loss with exposed dermis

Partial-thickness loss of skin with exposed dermis. The wound bed is viable, pink or red, moist, and may also present as an intact or ruptured serum-filled blister. Adipose (fat) is not visible and deeper tissues are not visible. Granulation tissue, slough and eschar are not present. These injuries commonly result from adverse microclimate and shear in the skin over the pelvis and shear in the heel. This stage should not be used to describe moisture associated skin damage (MASD) including incontinence associated dermatitis (IAD), intertriginous dermatitis (ITD), medical adhesive related skin injury (MARSI), or traumatic wounds (skin tears, burns, abrasions).

Stage 3 Pressure Injury: Full-thickness skin loss

Full-thickness loss of skin, in which adipose (fat) is visible in the ulcer and granulation tissue and epibole (rolled wound edges) are often present. Slough and/or eschar may be visible. The depth of tissue damage varies by anatomical location; areas of significant adiposity can develop deep wounds. Undermining and tunneling may occur. Fascia, muscle, tendon, ligament, cartilage and/or bone are not exposed. If slough or eschar obscures the extent of tissue loss this is an Unstageable Pressure Injury.

Stage 4 Pressure Injury: Full-thickness skin and tissue loss

Full-thickness skin and tissue loss with exposed or directly palpable fascia, muscle, tendon, ligament, cartilage or bone in the ulcer. Slough and/or eschar may be visible. Epibole (rolled edges), undermining and/or tunneling often occur. Depth varies by anatomical location. If slough or eschar obscures the extent of tissue loss this is an Unstageable Pressure Injury.

Unstageable Pressure Injury: Obscured full-thickness skin and tissue loss<

Full-thickness skin and tissue loss in which the extent of tissue damage within the ulcer cannot be confirmed because it is obscured by slough or eschar. If slough or eschar is removed, a Stage 3 or Stage 4 pressure injury will be revealed. Stable eschar (i.e. dry, adherent, intact without erythema or fluctuance) on the heel or ischemic limb should not be softened or removed.

Deep Tissue Pressure Injury: Persistent non-blanchable deep red, maroon or purple discoloration
Intact or non-intact skin with localized area of persistent non-blanchable deep red, maroon, purple discoloration or epidermal separation revealing a dark wound bed or blood filled blister. Pain and temperature change often precede skin color changes. Discoloration may appear differently in darkly pigmented skin. This injury results from intense and/or prolonged pressure and shear forces at the bone-muscle interface. The wound may evolve rapidly to reveal the actual extent of tissue injury, or may resolve without tissue loss. If necrotic tissue, subcutaneous tissue, granulation tissue, fascia, muscle or other underlying structures are visible, this indicates a full thickness pressure injury (Unstageable, Stage 3 or Stage 4). Do not use DTPI to describe vascular, traumatic, neuropathic, or dermatologic conditions.

Additional pressure injury definitions.

Medical Device Related Pressure Injury:
This describes an etiology. Medical device related pressure injuries result from the use of devices designed and applied for diagnostic or therapeutic purposes. The resultant pressure injury generally conforms to the pattern or shape of the device. The injury should be staged using the staging system.

Mucosal Membrane Pressure Injury: Mucosal membrane pressure injury is found on mucous membranes with a history of a medical device in use at the location of the injury. Due to the anatomy of the tissue these ulcers cannot be staged.

Courtesy of the National Pressure Ulcer Advisory Panel

It is important to note PUs (pressure injuries) should never be “back-staged,” meaning once a wound is identified as a Stage 3 pressure ulcer/injury, it is never referred to as a Stage 1 or 2. Rather, the Stage 3 pressure ulcer/injury which is healing would be referred to as a “healing Stage 3 pressure ulcer/injury.” In addition, only pressure ulcers/injuries are “staged.” Diabetic foot ulcers may be “graded” (such as Wagner Grades) but no other wounds are “staged.”

Cost of Pressure Ulcers

Whittington & Briones49 estimated annual medical costs in the United States (US) associated with treating pressure ulcers exceed $5 billion dollars annually. Fogerty et al.4 estimated this cost to be higher at $10,845 per patient, exceeding a total $18.5 billion dollars annually. Furthermore, studies suggest it costs less to prevent a pressure ulcer than to treat a pressure ulcer.23, 62 Individuals with pressure ulcers have higher mortality rates63, 64 and up to five-fold increased hospital length of stay.65,66 Updated in 2014, the AHRQ document “Preventing Pressure Ulcers in Hospitals: 1. Are we ready for this change?” reports Medicare estimated each pressure ulcer added $43,180 in costs to a hospital stay in 2007.11 Additionally, AHRQ indicates the cost of pressure ulcers is $9.1-$11.6 billion dollars annually in the US with costs of individual patient care related to PUs go from $20,900 to 151,700 per pressure ulcer.11 Interestingly, Barbara Braden gave a NPUAP lecture, “Costs of Pressure Ulcer Prevention: Is it really cheaper than treatment?” Given May 9, 2013, she discussed the fact that when pressure ulcer prevention interventions are put in place, patient falls are also noted to decrease.67

Political, Economic, and Other Implications of Pressure Ulcers

Political issues affecting pressure ulcer prevention and treatment may include scenarios like the one in Iran, where pressure reducing equipment is scarce or other situations where lack of healthcare resources prevent global implementation of even basic preventative measures. Government sponsored or subsidized medical care, private insurance, homelessness, drug addiction, war, economic crisis, limited transportation and/or food sources are but a few huge issues affecting healthcare today. In America, Medicare and Medicaid services come to mind when considering economic, social, and political implications on research findings regarding pressure ulcer risk. To highlight this point, a roundtable discussion of the International Expert Wound Care Advisory Panel entitled, “Opportunities to Improve Pressure Ulcer Prevention and Treatment: Implications of the CMS Acute Care Present on Admission (POA) Indicators/Hospital-Acquired Conditions (HAC) Ruling”29 highlights one pressure ulcer specific ramification of Deficit Reduction Act of 2005. The expert panel detailed subsequent changes in the Centers for Medicare and Medicaid Services (CMS) financial reimbursement amounts for long-term and acute care settings such as nursing homes and hospitals. Beginning in October 2008, CMS no longer reimburse higher rates for patients that develop stage III or IV pressure ulcers (full-thickness tissue loss) after admission.29 This represents a potentially very large economic loss to health care facilities. This is thought to provide additional motivation to acute and long-term care facilities to evaluate and improve their documentation and pressure ulcer prevention programs. This discussion is significant, as it stresses the urgency of a consensus among health care providers and particularly the wound care community in providing quality research and evidence-based (and innovative) interventions that are effective.

Limitations of Research Evidence and Data

Comment on Limited Use of Randomized Control Trails for Pressure Ulcer Research

There are few (if any) current randomized controlled trials (RCTs) where random vulnerable patients are assigned to receive an intervention suspected of “causing” full thickness pressure ulcers because that would be unethical. Three important documents impact biomedical research around the world by helping to determine what is ethically right or wrong. These documents are: The Nuremberg Code (1947), the World Medical Association’s Declaration of Helsinki (originally adopted in 1964), and the Belmont Report of the National Commission for the Protection of Human Subjects in the United States.68 In a nutshell, these documents came about after tragic medical research practices were disclosed to the world. The Nuremberg Code was written in 1946-1947 after the horrific, criminal medical research on Jews and other prisoners in Nazi concentration camps came to light. The Code’s purpose is described as providing ten directives for human experimentation, including informed consent and assurance within research protocols that “all unnecessary physical and mental suffering and injury” as a result of the experimentation process is avoided. The Declaration of Helsinki built on these directives in a document that has been revised by the World Medical Association at least six times.69-71 These documents and a report describing other unethical medical research practices discovered in the United States (The Belmont Report) led to the development of the US National Research Act in 1974 to ensure the protection of all human research subjects is a standard practice.69-70 The ethical dilemma for pressure ulcer research arises when you want to do a RCT where the dependent variable of interest is a poor medical outcome like a stage III pressure ulcer. It would not be ethical to divide two elderly groups of people into experimental and control groups and apply some type of intervention to one group and not to others while you observed both groups to see who developed a stage III pressure ulcer. Ethically, researchers should desire to prevent harm (pressure ulcers) in all of the subjects, and if something were to cause skin or tissue injury, you would want to intervene immediately. To merely record how bad things got in one group or the other would go against biomedical ethical principles of “not causing harm.” However, RCTs can be conducted that investigate potentially positive outcomes. Several RCTs have been reported involving patients deemed at risk for pressure ulcers that introduce a theoretically preventative intervention (such as a new support surface) versus standard care (existing mattress) to see which is more effective at preventing pressure ulcer development.

Problems with Using Data from Studies Conducted Twenty Years Ago

In particular, with regard to pressure ulcer risk prediction, using data collected from research studies on populations twenty years ago poses a problem for application to the current population. Many of the pressure ulcer prevention guidelines available today are based on those risk factors identified over twenty years ago, and these may not carry the same relevance today.72-74

Clinical Pearl: Access to Guidelines.

Unfortunately, in the US, AHRQ made the decision to stop hosting the National Guideline Clearinghouse website in 2018.

However, there continues to be national and international guidelines available to healthcare providers on other websites such as those listed below:

Health Information Technology (HIT) and Patient Safety approaches have changed dramatically over the past 2 decades.74-78 These advances are likely to meet the increased needs of patients who are admitted to acute care facilities. Vincent et al.78 describe medical technology and clinical procedure advances, as well as, process of care (organizational/policy) changes within the emergency medicine and intensive care unit (ICU) arenas over the past 25 years. In addition, more patients are having procedures done on an outpatient basis, so fewer patients with “minor” conditions are being admitted to the hospital.79-80 These changes are likely to alter acuity levels,74 numbers of patient transfers within facilities, and length of stays for patients being admitted to hospitals. Essentially, these factors are apt to change the “face” of the inpatient population and impact characteristics of those at risk of a pressure ulcer.

Evidence-Based Management of Pressure Ulcers

Please see the AHRQ toolkit for preventing PU in hospitals (content last reviewed in October, 2014)11 online here. The approach to managing pressure ulcers should always focus on PREVENTION. Prevent the ulcer in the first place! If the patient develops pressure related injury (despite preventive measures), then evidence-based practice related to wound healing should be administered but always with PREVENTION in the treatment plan. Prevent further breakdown. Prevent the pressure ulcer from deteriorating or worsening to a deeper stage. Evidence suggests that offloading and pressure reduction/redistribution should be a primary goal of treatment of pressure ulcers, along with eliminating shearing and friction forces. Addressing other key contributing or risk factors is also critical. Knowing what intrinsic and extrinsic factors contribute to skin breakdown is important. Intrinsic factors such as age, immune function, nutrition and disease states (co-morbid conditions) should be considered. Extrinsic factors such as dry skin, friction, transfer equipment, medications, and moisture should also be addressed.

Maintaining adequate nutrition and hydration should be an essential component of PU management plans. Nutritional assessments should include: current and usual weight, history of involuntary weight loss, nutrition intake (protein, calories, fluid), appetite, dental health, chewing, swallowing or feeding problems, medical or surgical history affecting intake or absorption, drug / nutrient interactions, psychosocial factors (mood, finances, cooking ability, culture, preferences) and appropriate laboratory values. Common laboratory analysis includes serum albumin (20 days half-life indicates chronic disease state, values below 3.5g/dl indicates increased risk); serum pre-albumin has a 2 to 3 day half-life, which some providers feel may provide a more current reflection of protein stores (values below 15 mg/dl indicates increased risk); a total lymphocyte count is an indicator of protein-calorie malnutrition (values below 1,800 mm3 indicates risk); serum transferring is also a malnutrition indicator (values below 200 mg/dl indicates risk).

Managing excessive moisture (incontinence, sweat, spilled liquids) on the skin surface of patients at risk for PU is another critical preventive and management goal. Managing incontinence includes establishing a bowel and bladder program, cleansing the skin after soiling with pH balanced cleansers, and using incontinence skin barriers (creams, ointments, etc.) to protect and maintain intact skin. Consider a pouching system or collection device to protect from effluence if fecal incontinence is an issue. Indwelling catheters may be indicated for short term use with severe incontinence-related dermatitis and difficult to manage urinary incontinence. In addition, limit the use of diapers, but if briefs, diapers or underpads are used, make sure they are the type that wick moisture from the skin.

Addressing impaired mobility includes patient and caregiver education and establishing a turning/repositioning schedule for patients confined to the bed or a chair. This should include repositioning the patient every 2-4 hours with the support of bony prominences. Keep the head of the bed at 30 degrees or less except for tube fed patients (but allow elevation for 1 hour after meals). Avoid “donuts” (rings meant for under coccyx areas), and pulling of the patient across the bed or a chair surface. Place pressure-redistribution surfaces on bed and chair surfaces.

Pressure Reduction and Redistribution

There are many ways to help reduce or redistribute pressure under bony prominences. The most common are repositioning and the use of support surfaces. Examples of support surfaces include mattresses and mattress overlays, integrated bed systems, seat cushions, seat overlays, and heel floatation devices. Mattresses and mattress overlays include 3 groups. Group 1 support surfaces do not require electricity, are relatively inexpensive and are for patients at low or moderate risk of pressure ulcers; Group 2 support surfaces may or may not be dynamic-powered devices and are appropriate for patients at moderate or high risk; Group 3 support surfaces include air-fluidized beds and are for patients at very high risk. The goal of these surfaces is to assist in creating an environment that enhances tissue viability and will assist in promoting healing. The surface should prevent “bottoming out” when the patient is positioned on it. The surface should also assist in the prevention of shearing of tissue.24

Wound Healing

Open pressure ulcers are wounds. Many become chronic wounds and stage 3-4 pressure ulcers have been associated with a higher complication rate (especially infection and sepsis) and higher mortality rate than some other chronic wounds. Wound healing principles have been discussed in previous educational papers, but as a brief summary, we will review some helpful mnemonics to guide wound bed preparation and wound management of full-thickness open wounds. The first mnemonic is T-I-M-E. Schultz et al.,81 (updated by Leaper et al.)82 have written pivotal articles describing T-I-M-E as a way to guide clinicians in the management of full-thickness wounds.

  • T stands for tissue: address non-viable tissue in the wound bed. Removing dead and necrotic tissue from the wound bed promotes wound healing, inflammation and reduces bacterial breeding grounds.

  • I stands for infection and inflammation: address potential sources of bacterial contamination. Use excellent technique when changing the dressings and providing wound care. Identify early signs of infection and address them. Culture the wound bed if warranted using appropriate methods (quantitative tissue cultures). Chronic wounds tend to be stuck in an inflammatory phase of wound healing. High levels of wound enzymes (MMPs or Matrix metalloproteinases) and inflammatory chemical messengers (cytokines) dominate the wound fluid of these wounds, making a very inhospitable environment for healing processes and cells. Consider wound dressings and topical therapies which address this and help minimize it.

  • M stands for moisture. Maintaining adequate moisture in the wound is necessary for healing cells to migrate and microcellular processes to continue optimally. A dry wound bed may take almost 50% longer to heal than a moist wound environment. Too much moisture, on the other hand, perpetuates high levels of MMPs and cytokines and may contribute to the chronic inflammatory state of a chronic wound.

  • E stands for the edges of the wound (and surrounding tissue). Healthy wound edges have a “beachfront” look to them, as if the edges of the wound were the sand on the water’s edge of the beach gently flowing down into the water. If the edge of the wound is rolled under, like a cliff instead of a beach, or if it is undermined as if a cave were hiding under the wound edge, then skin cells (keratinocytes/epithelial cells) cannot migrate easily, and the wound will not contract (get smaller) normally. These problematic wound edges need to be addressed and smoothed out in order to facilitate or stimulate wound healing. In some cases rolled edges may be addressed by chemical cauterization with silver nitrate on a stick by a professional who is trained to do this within their scope of practice.
Clinical Pearl:

Undermining (a underground cave, “lip” or shelf under the edge of a wound is often caused by shearing forces (such as when a person slides down in bed or someone slides harshly on a transfer board). Eliminating these forces is the only way to prevent/reduce this undermining in pressure ulcers, particularly sacral, coccyx and ischial PU.

Dorothy Doughty83 gave the following mnemonic to illustrate similar principles for topical wound therapy:

  • D – Debride any non-viable tissue (necrotic tissue is an impediment to wound healing)
  • I – Identify and treat infection – infection is a powerful impediment to wound healing (get a biopsy versus a swab culture)
  • P – Pack dead space LIGHTLY – the wound environment should be friendly to fibroblasts (the white cells that manufacture new granulation tissue in full-thickness wounds). Packing a wound too tightly, reduces the fibroblast activity, impairs cellular migration and may actually cause some tissue ischemia in the wound bed if excessive pressure results from the packing.
  • A – Absorb EXCESS exudate
  • M – Maintain MOIST wound surface
  • O – Open or excise closed wound edges
  • P – Protect healing wound from trauma/infection
  • I – Insulate (maintain body temp. at normal to reduce vasoconstriction and enhance cellular activity).

Stillman84 suggested this DIDN’T HEAL mnemonic device to help remember factors that adversely affect wound healing:

  • D = Diabetes: The long-term effects of diabetes impair wound healing by diminishing sensation and arterial inflow. In addition, even acute loss of diabetic control can affect wound healing by causing diminished cardiac output, poor peripheral perfusion, and impaired polymorphonuclear leukocyte phagocytosis.
  • I = Infection: Infection potentiates collagen lysis. Bacterial contamination is a necessary condition but is not sufficient for wound infection. A susceptible host and wound environment are also required. Foreign bodies (including sutures) potentiate wound infection.
  • D = Drugs: Steroids and antimetabolites impede proliferation of fibroblasts and collagen synthesis.
  • N = Nutritional problems: Protein-calorie malnutrition and deficiencies of vitamins A, C, and zinc impair normal wound-healing mechanisms.
  • T = Tissue necrosis, resulting from local or systemic ischemia or radiation injury, impairs wound healing. Wounds in characteristically well-perfused areas, such as the face and neck, may heal surprisingly well despite unfavorable circumstances. Conversely, even a minor wound involving the foot, which has a borderline blood supply, may mark the onset of a long-term nonhealing ulcer. Hypoxia and excessive tension on the wound edges also interfere with wound healing because of local oxygen deficits.
  • H = Hypoxia: Inadequate tissue oxygenation due to local vasoconstriction resulting from sympathetic overactivity may occur because of blood volume deficit, unrelieved pain, or hypothermia, especially involving the distal extent of the extremities.
  • E = Excessive tension on wound edges: This leads to local tissue ischemia and necrosis.
  • A = Another wound: Competition between several healing areas for the substrates required for wound healing impairs wound healing at all sites.
  • L = Low temperature: The relatively low tissue temperature in the distal aspects of the upper and lower extremities (a reduction of 1-1.5°C [2-3°F] from normal core body temperature) is responsible for slower healing of wounds at these sites.

Keys to PU Wound Management and Summary

Prevention is paramount! Off load!

Address healing impediments, especially nutrition, moisture, friction and shear.

Use appropriate mnemonics to help guide wound bed preparation and wound healing approaches.

Any topical wound therapy that you select should show expected improvement in 2 to 4 weeks. If not, then re-evaluate the wound and evaluate for possible infection (quantitative tissue analysis). Consider measures to address etiologic and systemic factors (nutrition, shear, and diabetes or comorbid disease control). Change to another product. If the wound continues to worsen or does not improve after doing these things, consider malignancy (biopsy for histopathology) or autoimmune disease(s) as potential contributing factors such as Pyoderma Gangrenosum.

Summary. As stated before, many changes have occurred in health care over the past 20 years. Nursing care delivery, hospital organizational frameworks, quality improvement, financial coverages, not to mention technology (including electronic records), and perhaps the overall face of our present-day patient population.74-80 Yet, even with multiple pressure ulcer prevention programs implemented nationwide, pressure ulcer incidence and prevalence (and number of deaths attributed to pressure ulcers annually by the CDC) have not changed significantly in many facilities. Researchers need to determine why and develop innovative approaches to solve this dilemma. The effectiveness of pressure ulcer prevention and treatment interventions must be determined. Guidelines must be based on current, high-quality scientific evidence, and impediments to guideline implementation must be addressed. There are significant gaps in the scientific literature regarding pressure ulcer risk assessment, particularly in regard to present-day populations, and how pressure ulcer risk assessment may impact patient outcomes.33 New conceptual models of pressure ulcer development, risk assessment, and effective pressure ulcer prevention interventions may need to be developed.5,11,29

Case Study Scenario

Patient

A 76-year-old African American Male presented to ER at 4pm for fractured right hip after falling at home. No other complaints. History includes type II diabetes (well-controlled with oral medication and diet), hypertension (no current medication, ran out 3 months ago); height 5’10” weight 150 lbs. (recent weight loss of 25 lbs. over past 3 months after wife recently died). Lives alone with a son living 2 hours away who visits every 2 weeks. Uses walker to ambulate for past 2 years since he is “not too steady” on his feet sometimes. Reports he sometimes dribbles urine after urinating, but otherwise no incontinence of urine or stool. Current pain level is 8 out of 10. BP is 170/98. Current labs HgbA1C = 7.2; serum glucose is 125.

PU Risk Assessment

Braden Tool used by admission RN: Sensory Perception: 4 “no impairment”; Moisture: 4 “rarely moist”; Activity: 3 “walks occasionally”; Mobility: 3 “slightly limited”; Nutrition: 3 “Adequate”; Friction & Shear: 3 “No apparent problem” – Total score: 20 (not at risk); Visual skin assessment head-to-toe reveals no redness over any boney prominence. Skin tear noted on left forearm from fall at home.

Prevention Intervention Strategies

Foam mattress (standard for the medical-surgical unit the patient was admitted to) while awaiting hip surgery in the AM; patient is NPO after midnight and no nutrition consult is placed yet. Patient is on bedrest and opioid ordered for pain relief before surgery scheduled. Using urinal for voiding during night. Patient does not want to be turned to side during night due to pain.

Initial Clinical Outcomes

Patient goes to surgery without additional skin assessment and no-one documents any skin warmth at sacral area or right heel, perianal moisture is present but not documented by transfer personnel. Patient is prepped for surgery and perioperative skin assessment notes intact but slightly darker skin and skin is warm to touch over sacral area, some right hip bruising (diffuse bruising over most of right lateral hip and thigh – not particularly over trochanter boney prominence), right heel bogginess and warmth, and the left forearm skin tear.

PU Staging

Perioperative nurse documents right hip bruising likely due to fracture injury, sacral stage 1 PU and right heel stage 1 PU; left forearm skin tear is not staged because it is not a pressure ulcer; right hip is not staged due to nature of bruising consistent with fall injury and fracture.

PU Management Strategies

Perioperative staff implement specialty gel operating table padding and careful foam padding to non-operative extremities, head, etc., and take care to float heels. In post-op recovery, alternating pressure redistribution surface is used, small adjustments to patient’s position are made hourly to relieve pressure to sacral area, and heels continue to be floated. Vital signs - high blood pressure after surgery (200/110) and elevated heart rate (110/min), labs are unremarkable. Patient is transferred to SICU for observation. SICU beds have alternating pressure mattresses and beds with “turn assist” capability. When patient awakes, he reports pain is 4 out of 10. Post-operative opioids are ordered for pain. Patient remains NPO. The perioperative staff points out all skin findings to ICU staff. When patient was admitted to ICU Braden risk score was Sensory Perception: 2 “very limited”; Moisture: 2 “often moist”; Activity: 1 “bedfast”; Mobility: 2 “very limited”; Nutrition: 1 “very poor”; Friction & Shear: 1 “problem” – Total score: 9 (severe risk); Nutrition consult is ordered and wound consult by wound specialist.

Outcomes

Patient stabilizes within 1 day and is transferred to regular medical-surgical floor (on an alternating pressure specialty mattress). Sacral PU is now documented by med-surg staff as Stage 2 -superficial open blister but no purple discoloration, and right heel is now deep purple color, intact, and still boggy (documented but staff as stage 1). Interdisciplinary team discusses PU management plan and steps to initiate on care plan to prevent progression of existing PU and prevent any new PU. Physical therapy initiates a mobility and strengthening plan of care, and patient starts to ambulate with assistance. A regular turning schedule is implemented at least every 2 hours, and sips of fluid are offered with turning schedule. A moisture barrier cream is ordered for perineum, and the head of bed is kept at 30 degrees or below (when in bed) except for meals and 30 minutes after meals. Pain that may be present with turning is addressed, and nutrition interventions have been initiated. Social worker and team discuss best location to discharge patient to, and potential need for home assistance, and safety assessment of home environment. Patient is discharged 12 days later after resolution of stage 2 sacral PU and no further evolution of heel pressure ulcer. Right hip bruising is resolved, left forearm skin tear is closed. BP, pulse and labs are unremarkable at discharge.

Strengths of the Case

Perioperative skin assessment is thorough and accurately notes Stage 1 sacral PU and right heel PU. They correctly note right hip bruising due to injury and not PU (diffuse bruising over most of right lateral hip and thigh – not particularly over trochanter boney prominence) and the left forearm skin tear (not a PU). Perioperative staff also implement PU prevention strategies during surgery (specialty gel operating table padding and careful foam padding to non-operative extremities, head, etc., and take care to float heels). In post-op recovery, ICU and regular floor, alternating pressure redistribution surface is appropriately used, with addition of small adjustments to patients position regularly made to relieve pressure to sacral area, and heels continue to be floated. ICU staff correctly score Braden Risk Assessment as “9”: Sensory Perception: 2 “very limited” – because patient is over 65 years old, and some sensory decline is normal in ages over 65 as well as diabetics (peripheral neuropathy present in feet), and patient is on pain medication (decreases sensory perception, and pain may also distract patient from feeling more minor discomforts); Moisture: 2 “often moist” (patient using urinal was noted to frequently spill a little, and perineal moisture was noted even pre-operatively, which could be sweat as well) ; Activity: 1 “bedfast” (patient was bedfast for several days); Mobility: 2 “very limited” (mobility was impaired severely for more than 3 days); Nutrition: 1 “very poor” (NPO for > 24 hours, 25 lb. weight loss prior to admission, and potential appetite changes due to grieving since wife recently died); Friction & Shear: 1 “problem” (the nurse really felt the score was between a 1 or 2 because the patient was slipping down in bed frequently needing staff to lift him back up – he was also most in the perineal area increasing friction, but selected 1 to capture the most risk possible, in order to intervene if possible)– Total score: 9 (severe risk) was accurate at the time of admission to ICU. Appropriate interventions based on the level of risk45 indicates appropriate interventions to be considered for a Braden Total Score of 9 include: Frequent turning; maximal remobilization (early mobility, PT/OT involvement if feasible and patient’s condition allows); protect heels (float heels but take care to not cause increased focused pressure to Achilles tendon – if using pillows, use one lengthwise behind each leg at calf and with enough height that heels do not touch bed surface); manage moisture (may include moisture barrier creams, avoid drying the skin, bed pads that wick moisture away from body, address cause of moisture if possible, etc.), manage nutrition and hydration (nutrition consult, increase protein intake, supplement if needed, offer liquids with turn schedules if patient is able to take oral liquids), and friction and shear (maintain head of bed below 30 degrees when not eating if condition is stable, use trapeze when indicated, use lift sheet to move patient, protect elbows and heels during movement if exposed to friction); pressure relieving support surface; turning schedule (low air loss beds or mattress overlays do not substitute for turning schedules); use of foam wedges for 30 degree lateral positioning (if medical condition allows for this); and supplementing turn schedules with small shifts in position more frequently. The actions of the staff in the case scenario addressed some of these with: Physical therapy initiated a mobility and strengthening plan of care; a regular turning schedule was implemented at least every 2 hours, and sips of fluid were offered with turning schedule. A moisture barrier cream was ordered for perineum, and the head of bed was kept at 30 degrees or below (when in bed) except for meals and 30 minutes after meals. Pain that may be present with turning was addressed, and nutrition interventions have been initiated. Nutrition and Wound consults were placed. Interdisciplinary team and social worker were involved with discharge planning, and home safety assessment was ordered (to prevent further falls). Self-care needs at home were also evaluated/addressed.

Weakness of the Case/Room for Improvement

The initial Braden score obtained on admission to the hospital facility did not account for the real measure of PU risk, and did not account for the patient’s age (not accounted for by the Braden tool).40-43 The admission assessment documented: Sensory Perception: 4 “no impairment”; Moisture: 4 “rarely moist”; Activity: 3 “walks occasionally”; Mobility: 3 “slightly limited”; Nutrition: 3 “Adequate”; Friction & Shear: 3 “No apparent problem” – Total score: 20 (not at risk). However, this would have been scored more accurately if these sub-scores were marked in this way: Sensory Perception: 2 (between 2 “Very limited” and 3 “slightly limited” so select the lower score) due to the patient’s age, diabetes diagnosis, peripheral neuropathy, extreme pain, and he was on opioids; Moisture: 3 “occasionally moist” (especially at perineum); Activity: 1 “Bedfast” (the patient had a newly fractured hip and would not be up walking until at least after surgery, and he was in severe pain, which impaired his mobility even in bed - so at the time of the assessment he should have been considered bedfast); Mobility: 2 “very limited” (for same reasons as activity); Nutrition: 1 (between 1 “very poor” and 2 “probably inadequate” for NPO status that would start after midnight, and recent significant weight loss); Friction & Shear: 1 (between 1 “ problem” and 2 “potential problem” due to patient’s severe immobility at the start of hospitalization due to hip fracture and severe pain – Total admission should have been between 10 and 12 (both are high-risk scores). Appropriate pressure ulcer prevention interventions may have been initiated earlier if this level of risk had been communicated.

Room for improvement for the medical-surgical staff pressure ulcer staging relate to the right heel which was incorrectly staged as Stage 1 by med-surg staff but was deep purple color, intact, and still boggy (should have been staged as a deep tissue injury). Quicker implementation of a powered pressure redistribution support surfaces and better attention to offloading heels pre-operatively may have helped prevent the 2 PUs that developed.1

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References

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