Pressure Injury Risk Factors in Adult Critical Care Patients: A Review of the Literature

Critically ill patients require complex care in a technologically sophisticated environment where they are highly vulnerable to pressure-related injuries. However, pressure injury (PI) development remains a multifactorial phenomenon in critically ill persons; true risk is both pervasive and elusive. The purpose of this comprehensive review of the empirical literature was to examine the risk factors associated with PIs among adult patients admitted to contemporary intensive care units (ICUs).Inclusion criteria stipulated publications were to be peer-reviewed, quantitative studies with a focus on pressure ulcer (PU) risk factors in adult critical care patients published between 2010 and 2016 in which statistical analysis involved multivariate analysis using PU development as the outcome variable. Studies not available in English, those in which the primary focus was on PU prevention or treatment, and those that focused solely on the use of PU risk assessment scales were excluded. A comprehensive review of the OVID and PubMed computerized databases using the search terms pressure ulcer, critical care, intensive care, and risk factors yielded 540 reports; 358 remained after duplicates were eliminated and 28 after the inclusion/exclusion criteria were applied. Following examination, 16 studies were suitable for inclusion. A total of 43 risk factors emerged. Of those, 7 were identified in 3 or more studies in multivariate regression analysis; these included age, prolonged ICU admission, diabetes mellitus, cardiovascular disease, hypotension, prolonged mechanical ventilation, and vasopressor administration. To facilitate results interpretation, risk factors from multivariate analyses were grouped in 6 broad categories: demographic/patient characteristics, comorbidities, intrinsic factors, iatrogenic/care factors, PI risk assessment scales, and severity of illness/mortality risk. The shared attribute of the 7 risk factors identified was they are all potentially nonmodifiable. Advancing the science regarding the pathogenesis of PI development is imperative when trying to better understand unavoidable pressure-related injuries. The need for large multisite studies and studies using large datasets capable of validating risk factors unique to this population persists. Additionally, the need for enhanced PI risk quantification for adult ICU patients remains.

Almost 6 million people are admitted into intensive care units (ICUs) across the United States annually,¹ where they face life-threatening illnesses that require care in a technologically sophisticated environment. Of the top 5 patient conditions requiring admission to an ICU, respiratory failure requiring ventilator support is the most common, followed by acute myocardial infarction, intracranial hemorrhage, sepsis/septicemia requiring ventilator support, and percutaneous cardiovascular procedures.² To manage these and a myriad of other critical illnesses, modern day critical care units are equipped with many life-saving technologies of which a single patient may require concomitant use for treatment. As a result, critically ill patients are surviving illnesses today that just a decade ago may have proved fatal.  

Critically ill patients, the most medically fragile and vulnerable population in the hospital setting, require care by highly trained professionals to minimize complications and improve outcomes. As a consequence of the complexity of their care and the high burden of illness, it is logical to deduce ICU patients would be highly vulnerable to pressure-related injuries. In fact, pressure ulcer (PU) prevalence in the ICU population is cited as the highest among hospitalized patients, ranging from 13% to 45.5%.³

However, determining PU or pressure injury (PI) risk becomes challenging in this population. Although standard PU risk assessment using a validated tool such as the Braden Scale⁴ addresses some of the risk factors that confront ICU patients, many patients are exposed to a multitude of risk factors not accounted for in PU risk assessment scales. In fact, a 2014 consensus meeting convened by the National Pressure Ulcer Advisory Panel (NPUAP)⁵ determined that potentially nonmodifiable extrinsic and intrinsic risk factors could influence PU development and may render the development of a pressure-related injury unavoidable — that is, injuries that occur despite the implementation and monitoring of evidenced-based PU prevention strategies aimed at an individual’s risk.⁵ Examples such as respiratory instability, an unstable spine, compromised tissue tolerance due to arterial insufficiency, neurologic deficits, medically necessary treatments such as fluid resuscitation and vasopressor administration, nutritional depletion, malnutrition/cachexia, septic shock, and impaired cardiopulmonary status all are purported to be related to unavoidable PUs and are all conditions likely to affect the critically ill population.⁵ 

Technology is omnipresent in the ICU setting. Consequently, PI risk factors may change as sequelae of technological advances coupled with the subsequent heightened burden of illness experienced by patients who require intensive care. Thus, the aim of this review was to examine the PI risk factors identified in the recent empirical literature that are associated with PIs in critically ill patients admitted to contemporary ICUs.

The author performed a comprehensive search of the OVID and PubMed computerized databases using the terms pressure ulcer, critical care, intensive care, and risk factors. Inclusion criteria established for this review stipulated publications needed to be English-language, peer-reviewed, published quantitative studies with a focus on PU risk factors in adult critical care patients published between 2010 and 2016 in peer-reviewed journals and subject to multivariate (eg, regression) analysis with PU development as the outcome variable of interest. Studies published before 2010 were excluded from review because the focus of this literature review was on critical care patients receiving care in present day ICU settings; also excluded were studies in which the primary focus was on PU prevention or treatment and studies focused solely on the use of PU risk assessment scales. In addition, ancestry searching (defined as using citations from relevant studies to track down additional potential research on the same topic) was employed as a secondary search technique. For this descriptive review, level of evidence was not a consideration. 

The initial search of the indices yielded 540 published reports; 358 publications remained after deleting duplications. When inclusion/exclusion criteria were applied, 28 were examined for possible inclusion; 12 studies were eliminated because they did not meet the predetermined inclusion criteria: no multivariate analysis (2); single risk factor (1); focus only on risk assessment scale (4); focus on nursing documentation (1); focus on PU healing (1); trauma population (1); conceptual model development (1); and comparison study (1). This exclusion yielded the 16 studies ultimately identified and included in this review.^6-21 Across these 16 studies, 43 potential risk factors were identified in multivariate analyses. For ease of interpretation, these risk factors were grouped under 6 broad headings: demographic/patient characteristics, comorbidities, intrinsic factors, iatrogenic/care factors, PI risk assessment scales, and severity of illness/mortality risk. After examination of these risk factors, 7 emerged in 3 or more studies and included age, ICU length of admission, diabetes mellitus, cardiovascular disease, hypotension, prolonged mechanical ventilation, and vasopressor agents.

Of the 16 studies, 7 were conducted in the United States^{7,8,13,14,16,18,20} and 9 were conducted internationally, representing Brazil,^9,17 Greece,¹⁰ Iran,¹¹ Italy,¹⁵ Japan,²¹ Saudi Arabia,⁶ Spain,¹⁹ and Turkey.¹² ICU settings represented included medical surgical ICUs (5),^7,8,10,11,18 cardiovascular ICUs (3),^7-9 and surgical ICUs (2)^16,20; 2 studies included multiple types of ICUs^7,8 and in 8 studies, the type of ICU was not specified.^{6,12-15,17,19,21} With regard to study design, 7 were retrospective^7,8,13-16,18, and 9 were prospective^{6,9-12,17,19-21} (see Table 1A, 1B, 1C).

Study sample characteristics. Across the studies, the mean age of critical care patients ranged from 52 years⁶ to 71 years.⁸ The most common ICU admitting diagnoses were respiratory-^10,12,17,18 and cardiac-related.^8,9,15 Mean ICU length of admission was reported^{6-9,11,12,16-19,21} and ranged from 5 days¹⁸ to 17 days.¹²  A measure of patient severity of illness/mortality risk was reported in 10 of the studies^{6,8-10,12,14,17-19,21} using a variety of instruments including the Acute Physiologic and Chronic Health Evaluation (APACHE) II, APACHE III, Sequential Organ Failure Assessment (SOFA),  Simplified Acute Physiologic Score (SAPS II),²² and All Patients Refined Diagnosis Related Group (APR-DRG). The APACHE II was the most common tool used to measure illness severity (6 studies^{8-10,12,18,21}), with mean scores across these studies ranging from 9.5²¹ (indicating an 8% mortality risk) to 22⁹ (indicating a 40% mortality risk).²³ The American Society of Anesthesiologist’s risk classification was used in 1 study to determine surgical risk, but no mean score for the study sample was reported¹³ (see Table 2A, 2B). 

PI characteristics in studies. PU occurrence rates across the study populations varied from 9.4%¹⁶ to 39.3%.⁶ When stratified by stage, 5 studies identified Stage 2 PI,^{9,10,13,18,21} 4 identified Stage 1,^6,9,11,12 1 identified Stage 3,¹⁵ and 1⁸ identified deep tissue injury (DTI) as most common. In 6 studies,^{7,14,16,17,19,20}, the most common stage of PU was not recorded. With regard to PU location, 7 of the 9 studies that used this descriptor identified the sacrococcygeal region as the most common anatomical site.^{7-10,12,18,19} In 1 study,²¹ the ear, scapula, and heels were documented as the most common sites for PU development; in another,⁶ the heel was the most common location. With regard to the application of PU prevention strategies, 7 studies^{6,8,11,12,18,19,21} reported the presence of or consideration for PU prevention strategies as part of the design and implementation of the study (see Table 2A, 2B).

Risk factors. Numerous potential PU risk factors were examined in the studies in this review. Table 3 (3A, 3B, 3C, 3D) highlights the significant predictors found in each study according to its multivariate analysis in addition to risk factors found to be significant in univariate analysis, those found to be nonsignificant, and other risk factors considered in the study design. 

Overall, 43 risk factors were found to be significant predictors across the studies in this review and were grouped into 6 broad categories as previously described; 7 were found significant in multivariate analysis in 3 or more studies (see Table 4). These risk factors included age, ICU length of admission, diabetes mellitus, cardiovascular disease, hypotension, prolonged mechanical ventilation, and vasopressor agents. 

Demographic/patient characteristics. Age was the most frequently reported predictor and found to be significant in 6 studies.^6,9,11,18-20 However, the mean age of patients in these 6 studies ranged from 55 to 69 years, representing middle-aged to younger elder adults. When the mean age of patients who developed a PU across these 6 studies was examined, ages ranged between 60 years and 73 years. In multivariate analysis, 1 prospective cohort study⁹ of 370 cardiopulmonary ICU patients found age >42.5 years to be a significant predictor of PU development. In a prospective 2-phase study of 369 surgical ICU patients, Slowikowski and Funk²⁰ found age ≥70 years to be a significant predictor. Advancing age has long been considered a risk factor for PU development, as earlier studies^24,25 in the ICU population noted. 

Length of stay. Length of stay was the second most common predictor across these 16 studies and was found to be significant in 5 studies.^6,9,11,17,18 In a prospective cohort study of 84 ICU patients in Saudi Arabia, Tayyib et al⁶ reported the average length of stay for patients who developed a PU was 13.3 ± 8.3 days as compared to the PU-free group with 9.1 ± 6.6 days. In multivariate analysis, length of stay was found to be a significant predictor for patients with any stage of PI (odds ratio [OR] 1.8, 95% confidence interval [CI] 1.01-3.30; P = .045) as well as for patients with Stage 2 through Stage 4 PI (OR 1.2, 95% CI 1.08-1.39).⁶ Campanili et al⁹ found an ICU admission of >9.5 days was a significant predictor of PU development. Patients with a PU were found to have a mean length of stay of 14 days as compared to patients who remained PU-free at 4.5 days (P <.001). A prospective study of 160 ICU patients in Brazil by Cremasco et al¹⁷ also found length of stay to be predictive for patients who developed PU (OR 1.12, 95% CI 1.04-1.20; P = .002), with a mean number of ICU days of 23.9 days as compared to those that remained PU-free at 9.4 days (P <.001). Similarly, a retrospective study of 347 medical/surgical ICU patients by Cox¹⁸ found length of stay to be significant in multivariate analysis for all stages of PI (OR 1.033, 95% CI 1.003-1.064; P = .03) and for Stage 2 or greater PIs (OR 1.008, 95% CI 1.004.-1.012; P <.001) and reported a mean length of stay of 281 hours (12 days) in patients that developed a PU compared to 81 hours (3 days) for patients who remained PU-free (P <.01). In their prospective study of 352 medical/surgical ICU patients, Nassaji et al¹¹ also reported ICU length of stay as a significant predictor (OR 1.19, 95% CI 1.13-1.25; P <.001).

Comorbidities. Significant comorbidities found across these studies included diabetes mellitus, cardiovascular disease, renal disease/failure, pulmonary disease, trauma, and anemia. Of these, diabetes mellitus^11,15,20 and cardiovascular disease^13,15,18 were each found to be significant in multiple studies. These 2 comorbidities are known to be strongly associated with PU development across patient populations.³ 

Diabetes mellitus was identified as a significant predictor in 3 studies.^11,15,20 Slowikowski and Funk²⁰ found a history of diabetes was a significant predictor of PU development (OR 1.93, 95% CI 1.11-1.35; P = .019), as did Nassaji et al.¹¹ The latter study found PU development was more than 5 times more likely in patients with a history of diabetes (OR 5.58, 95% CI 1.83-18.7; P = .003). In a retrospective study of 610 critical care patients, Serra et al¹⁵ found both diabetes and congestive heart failure to be significant predictors, (OR 2.25, 95% CI not reported. P = .047; OR 2.25, 95% CI: not reported; P = .0047, respectively [in women]). Results of a retrospective, observational study by O’Brien et al¹³ showed a preoperative history of congestive heart failure to be predictive of ICU PU development (OR 1.78, 95% CI 1.27-2.49; P = .001), and a history of cardiovascular disease was found to be predictive of PU development in a retrospective, correlational study¹⁸ among medical-surgical ICU patients (OR 2.9, 95% CI 1.3-6.4; P = .007). One (1) retrospective study⁸ of 306 cardiovascular and medical surgical ICU patients found cardiovascular disease protective of PU development (OR 0.035, 95% CI 0.002-0.764; P = .03), which may have been a reflection of the sampling methodology. 

Intrinsic factors. Hypotension is defined by the Society for Critical Care Medicine Sepsis 3 guidelines²⁶ as a systolic blood pressure <90 mm Hg, mean arterial pressure (MAP) <60 mm Hg or 70 mm Hg, or a drop in systolic blood pressure >40 mm Hg. Hypotension denotes that perfusion is impaired.²⁷ Blood is shunted from the periphery in an ongoing effort to preserve vital organ function, affecting tissue tolerance as capillaries close at lower tissue interface pressures.²⁸ Hypotension was found to be a significant predictor of PUs in 3 studies.^7,8,16  In their retrospective, 345 ICU-patient study, Bly et al⁷ reported a systolic blood pressure <90 mm Hg was predictive of PU development (OR 3.5, 95% CI 1.24-9.91: P <.05), and results of the retrospective cohort study by Wilczewski et al¹⁶ reported prolonged periods of MAP <70 mm Hg as the only predictor associated with PU development in a sample of 95 spinal cord injured patients in a surgical ICU. Cox and Roche⁸ found longer mean hours of MAP <60 mm Hg while on vasopressor agents to be predictive of PU development (OR 1.096, 95% CI 1.020-1.178; P = .01). Cox¹⁸ found MAP <60 mm Hg was significant in univariate analysis but not in multivariate analysis. 

Iatrogenic/care factors. Prolonged mechanical ventilation was found to be a significant predictor in 3 studies.^8,10,19 Cox and Roche⁸ found patients who required mechanical ventilation for >72 hours were 23 times more likely to develop a PU (OR 23.604, 95% CI 6.4-86.6; P <.001), and in a prospective study of 216 ventilated patients in 2 medical/surgical ICUs, Apostolopulou et al¹⁰ reported mechanical ventilation for >20 days was a significant predictor of PU development (OR 7.225, 95% CI 2.46-21.201; P <.001). In their prospective cohort study of 299 ventilated medical/surgical ICU patients, Manzano et al¹⁹ found the time on mechanical ventilation before PU development was an independent risk factor (OR 1.042, 95% CI 1.005-1.080; P =.024), with PU risk increasing by 4.2% for each day on mechanical ventilation. O’Brien et al¹³ identified the presence of an endotracheal or tracheostomy airway in an ICU patient before the surgical procedure was a significant predictor of postoperative PU development (OR 1.663, 95% CI 3.63-7.67; P <.001). 

Vasopressor agents. Vasopressors are potent vasoconstricting agents used to raise MAP in patients with profound hypotension unresponsive to fluid resuscitation²⁹; administration commonly is confined to critically ill patients in the ICU setting. Common agents include norepinephrine, epinephrine, phenylephrine, vasopressin, and dopamine. In this review, 4 studies^7,8,14,18 found vasopressor agents to be significant predictors of PU development. Bly et al⁷ found patients receiving more than 1 vasopressor (type not specified) were 3.3 times more likely to develop a PI (OR 3.71; 95% CI 1.65-6.62; P <.05). Cox and Roche⁸ found vasopressin administration to be independently associated with PU development (OR 4.816, 95% CI 1.66-13.92; P = .004). Vasopressin is usually a second-line agent used to manage shock states refractory to a single vasopressor agent. Cox and Roche⁸ postulate the addition of a second vasopressor agent (usually vasopressin) was considered the tipping point for PU risk. The retrospective cohort study by Tschannen et al¹⁴ reported patients who received vasopressor agents (type not specified) were 33 times more likely to develop a PU (OR 1.33, 95% CI 1.03-1.73; P = .03). Cox¹⁸ found norepinephrine to be an independent predictor of Stage 2 or greater PUs (Stage 3, Stage 4, DTI, unstageable). Apostolopoulou et al¹⁰ found vasopressor agents to be significant in univariate analysis only; however, in this study the variable inotropic agents (medications primarily indicated to improve cardiac contractility) was used. Although 4 studies^9,13,16,21 did not find significant associations between these agents and PU development, in most of these studies the vasopressor agents under investigation were not stated and as such the ability to draw meaningful conclusions was impaired. Additionally, changes in treatment protocols such as the SEPSIS 3 guidelines²⁶ have recently modified the hierarchy of vasopressor agent selection, potentially compromising knowledge of their effect on PU development.

Pressure ulcer risk assessment scales. The Braden Scale is the most well-known PU risk assessment scale and is used across the care continuum, including ICUs. The Braden Scale measures PU risk on 6 subscales (sensory perception, activity, mobility, moisture, friction/shear, and nutrition). Cumulative scores range from 6 to 23, with lower scores indicating greater PU risk. Used mostly abroad, the Jackson-Cubbin Scale³⁰ is a tool designed for use in ICUs and measures risk based on 12 risk factors (age, weight, past medical history, general skin condition, mental condition, mobility, hemodynamics, respirations, oxygen requirements, nutrition, incontinent, hygiene). Cumulative scores range from 9 to 48, with lower scores indicating greater risk. 

The total Braden Scale score was found to be a significant predictor in 2 studies.^14,20 Tschannen et al¹⁴ found that a lower Braden score on admission was a significant risk factor in multivariate analysis (OR 0.89, 95% CI 0.86-0.93; P <.001); Slowikowski and Funk²⁰ also cited the total Braden Scale score (time of measurement not specified) as an independent risk factor (OR 1.30, 95% CI 1.15-1.47; P <.001). In the study by Cox¹⁸ that measured the total Braden score and the individual subscale scores on admission to the ICU, the total Braden score was found to be significant in univariate analysis only (r = -0.276, P ≤.01), and the subscales friction/shear and mobility were independent predictors of PU development (OR 5.715, 95% CI 1.423-22.95; P = .01; and  OR 0.439, 95% CI 0.21-0.95; P = .04, respectively). In other studies that included the Braden Scale score in data analysis, 1 found it to be significant in univariate analysis only,⁸ while another found no relationship between the Braden Scale score and PU development.⁹

In the 1 study that employed the Jackson-Cubbin Scale to measure PU risk, Apostolopoulou et al¹⁰ found a Jackson-Cubbin score ≤29 to be a significant predictor of PU development (OR 0.015, 95% CI 0.005-0.050; P <.001). A comparative review³¹ of PU risk assessment scales found the Jackson-Cubbin superior to the Braden Scale in the ICU population. A systematic review and meta-analysis³² of the predictive validity of PU risk assessment scales used in the critical care population concluded the Braden scale was the best PU risk assessment scale for this population due to a lack of large studies using alternative PU risk assessment scales including the Jackson-Cubbin Scale. To date, no critical care-specific PU risk assessment scale has been validated in multiple empirical investigations using larger sample sizes in the critical care population. As such, a need for a PU risk assessment tool in this population persists.

Severity of illness. Severity of illness/mortality risk measures were reported in 10 of the studies in this review.^{6,8-10,12,14,17-19,21} Scales used to measure severity of illness included the APACHE II,^{8-10,12,18,21} APACHE III,¹⁹ SOFA,¹⁹ and SAPS II.¹⁷ In addition, APR-DRG¹⁴ and ASA Risk Classification^13,33 were used as indicators of severity of illness; these are not tools specific to the ICU population. Of these scales, 4 were found in individual studies to be significant predictors of PU development.^13,14,17,19 Cremasco et al¹⁷ found the SAPS II to be a significant predictor of PU (OR 1.058, 95% CI 1.004-1.114; P =.035); using the SOFA scale. Manzano et al¹⁹ found the fourth day cardiovascular SOFA score and the first day respiratory SOFA scores to be predictive (OR 1.33 95% CI 1.066-1.664; P = .12; and OR 1.56, 95% CI 1.026-2.360; P = .37, respectively). The APACHE III score also was measured in this study and found to be nonsignificant in univariate analysis. The ASA risk classification was used in a study of intraoperative risk factors in 2695 critical care patients; higher anesthesia risk classes of 4 or 5 as compared to lower risk classes of 1, 2, or 3 were found to be predictive of PU development (OR1.63, 95% CI 1.19-2.23; P = .003).¹³ Tschannen et al¹⁴ measured risk for mortality using the APR-DRG and found patients in the highest mortality risk categories were 11 times more likely to develop a PU (OR 11.15, 95% CI 7.1-17.5; P <.001). Higher APACHE II scores were found to be significantly associated to PU development in univariate analysis in 4 studies,^8,12,18,21 while in 2 studies^9,10 no relationship between PUs and the APACHE II score emerged. The use of multiple severity of illness/mortality indices across these studies makes it difficult to determine if any of these tools offers some insight into the relationship between severity of illness measures and PI risk. Although validated tools to measure severity of illness and mortality risk may help describe the burden of illness experienced in the ICU population, these may not translate to valid indicators of PI risk.

PU characteristics. In 6 studies, PU stage was not reported^{7,16,17,19-21} and in 7 studies PU location was not reported.^11,13-17,20 Of the studies that reported PU stage, Stage 2  was the most common,^{9,10,13,18,21} with the sacrococcygeal region cited as the most common location in 6 studies,^7-9,11,18,19 which is consistent with the literature.³⁴

Interestingly, only 1 study⁸ (conducted in the United States) reported DTI as the most common stage. This finding may reflect the difference in staging classification utilized in the United States and abroad. In the 2009 NPUAP/European Pressure Ulcer Advisory Panel (EPUAP) International Pressure Ulcer guidelines,³⁵ the categories termed DTI (now termed DTPI) and unstageable PU were only recognized in the United States. DTPI begins at the muscle-bone interface and occurs as a result of tissue deformation due to a short period of intense pressure and/or as a result of tissue ischemia due to prolonged periods of immobility.^36,37 Critical illness coupled with prolonged immobility may render a patient vulnerable to the effects of pressure; thus, it would be logical this population would be at higher risk for more severe PIs. In fact, in a large United States prevalence study,³⁴ critical care patients had a higher prevalence of severe PUs (Stage 3, Stage 4, DTPI, or unstageable) as compared to the general hospital population. 

The 7 PU risk factors found to be significant across multiple studies included age, length of ICU admission, diabetes mellitus, cardiovascular disease, hypotension, mechanical ventilation, and vasopressor agents. An attribute shared by these risk factors is that they could be considered nonmodifiable. Patient-related factors such as age, comorbidities (diabetes, cardiovascular disease), and hypotension are intrinsically driven, and iatrogenic factors such as mechanical ventilation and vasopressors are lifesaving measures that cannot be terminated in an effort to avert PI risk, potentially diminishing the ability to prevent PI. 

Age. According to the NPUAP,³ age may be a confounding variable that has the potential to influence mobility level, perfusion/oxygenation status, nutritional intake, and skin moisture level. In the pathogenesis of PI, these factors may mediate tissue tolerance and can affect the overall architecture of the skin. In the critically ill population, the overall burden of illness and complex care requirements may need to be considered an equally tenable confounding factor influencing tissue tolerance, subsequently escalating PI risk. Thus, in this population, all adults and not just older or elderly adults should be considered vulnerable to the potential for PI.

Length of stay. In the United States, mean ICU length of stay is estimated to be 3.8 days but may vary based on both the patient and ICU attributes.¹ It is logical to infer that the longer a patient remains in the ICU, the greater the probability that PI can occur. Prolonged ICU admission may act as a proxy for overall illness burden. Longer ICU length of stay connotes that a patient’s condition requires a higher level of care to manage the critical nature of his/her illness and prolonged recovery. Additionally, because longer length of stay is also a factor of time, the odds of developing a PI may increase with the passage of time. 

When evaluating length of ICU admission as a risk factor, it is equally important to evaluate the time to PI development in determining PI risk. In the studies that reported this finding,^{6,7,9,12,15,17-19} the mean times ranged from 3 days⁹ to 14 days¹⁹; the majority of the studies noted the first week of ICU admission was the most vulnerable timeframe. This finding is consistent with previous studies in the ICU population.^38-40 The first week of a critical illness may be the time period in which the patient may be hemodynamically labile and physiologically unstable, so care priorities are focused on life preservation. This is the time that heightened PI prevention should be implemented within the context of the patient’s critical illness. Conversely, this time period may be ripe for the development of the unavoidable PIs due to the overall condition of the patient. 

Diabetes and cardiovascular disease. Pathophysiologically, diabetes mellitus is associated with microvascular complications leading to capillary damage resulting from oxidative stress and poor perfusion. Macrovascular changes associated with diabetes are known to lead to peripheral arterial disease, coronary artery disease, and stroke.⁴¹ The prevalence of coronary artery disease increases with the longevity of a diabetes diagnosis, and the incidence of congestive heart failure is also higher in persons with diabetes.⁴¹ For persons with cardiovascular disease without concomitant diabetes, obstruction of vessels with atherosclerotic plaques impairs tissue perfusion and can lead to major ischemic events.⁴¹ In the setting of a critical illness, the sequelae of either comorbidity can complicate recovery and impair tissue perfusion and oxygenation; these comorbidities are worthy of consideration when establishing PI risk.

Hypotension. Hemodynamic instability is 1 of the primary clinical presentations of patients admitted to the ICU setting. In 3^7,8,16 of the 4 studies that measured hypotension, it was found to be a significant predictor and in 1 study it was found to be significant in univariate analysis.¹⁸ In previous ICU research^39,42 hypotension was not found to be related to PU development in this population or was found to be related  in univariate analysis only.^43,44 However, the multivariate results from this review of more recent studies suggest prolonged hypotension should be strongly considered as an intrinsic PI risk factor in the ICU population. 

Mechanical ventilation. According to the Society of Critical Care Medicine,¹ respiratory failure requiring ventilator support is the most common reason that requires admission to the ICU in the United States. Mechanical ventilation is indicated when the patient’s spontaneous ventilation is inadequate to sustain life; physiologic indications include respiratory or mechanical insufficiency and ineffective gas exchange, which can impair tissue perfusion and tissue oxygenation.⁴⁵ Prolonged mechanical ventilation as a PI risk factor also may reflect a patient’s overall severity of illness as well as be considered a proxy for immobility. Although progressive mobility in ventilated patients advocated by the American Association of Critical Care Nurses⁴⁶ is implemented in the ICU setting, this intervention could be either contraindicated or cautioned in many mechanically ventilated ICU patients. Additionally, mechanically ventilated patients require continuous head elevation when receiving this modality, predisposing the patient to greater shear forces, a major contributor to PI development, especially deeper injuries that originate at the fascial level overlying a bony prominence. When exposed to shear, blood vessels angulate and stretch and when combined with friction caused by head elevation, shear can cause thrombosis and compromise blood flow to the sacrococcygeal area.²⁸ 

Vasopressor agents. As potent vasoconstrictors, vasopressor agents are used to increase MAP in critically ill patients with impaired tissue and organ perfusion.²⁹ The pharmacodynamics of these agents suggest these medications can contribute to altered tissue tolerance, thus contributing to PI development.  In this review, 4 studies^7,8,14,18 found vasopressor agents to be significant in multivariate analysis, with 2 specific agents (norepinephrine, vasopressin) identified in 2 studies.^8,18 Vasopressin is commonly administered as a second line agent; Cox and Roche⁸ suggest the addition of a second vasopressor agent may be the time period during which PI risk escalates in critically ill patients. Although evidence supporting vasopressor agents as a PI risk factor in critical care is strengthening, further empirical investigation is warranted into the role of specific agents in addition to the duration and dose administered of these agents. 

Clinical implications: unavoidable PI. Although evidenced-based PU prevention programs have been successfully implemented and have been shown through ICU quality improvement initiatives to impact PU rates,^47-50 there are patients — specifically, critically ill patients — for whom PI occurrence may at times be unavoidable. However, the determination that a PI was unavoidable cannot be made without consideration for PI prevention strategies. In this review, 7 studies^{6,8,11,12,18,19,21} reported PU prevention strategies were in place when the study was conducted and in 2 studies, infrequent repositioning was found to be a significant predictor of PU development.^6,21 In order to validate that PI was beyond the control of care providers, it is important for future investigations to consider PI prevention interventions in the study design. 

The ability to label a PI “unavoidable” creates a clinical paradox for caregivers as unavoidable pressure injury currently is not recognized in the hospitalized patient; regulatory and quality indicators at this time give credence to the notion that all PIs are preventable. For example, in 2007 the Centers for Medicare and Medicaid Services⁵¹ deemed the occurrence of Stage 3 and Stage 4 hospital-acquired PUs as “never events,” restricting reimbursement to facilities for care necessary to treat these conditions. Moreover, the National Database of Nursing Quality Indicators⁵² includes hospital-acquired PUs as nurse-sensitive quality indicators, linking PU occurrence to the quality of care delivered by nurses. Litigation exposure is an ever-present threat to caregivers; more than 17 000 lawsuits related to PUs are filed annually, second only to wrongful death and more common than patient falls.⁵³ Based on the current health care climate, it is a research imperative to develop the clinical criterion to validate the unavoidable PI in the hospitalized patient, especially in the critically ill population, in an effort to assist bedside caregivers in more accurate distinction of this clinical phenomenon.

The future of the Braden Scale in critical care. Formalized PI risk assessment of the ICU patient continues to be a facet of prevention that needs to be modified in the critical care population. Although the Braden Scale remains the most common tool used in critical care and most settings across the United States, questions remain regarding its clinical utility in the critical care population and its ability to discriminate true risk. In the studies in this review that considered formalized PI risk assessment as either a descriptive variable or as part of the data analysis, all patients were found to be at moderate to high risk for PI. Although the total Braden scale score was found predictive in 2 studies^14,20 and in 2 of the subscales (mobility and friction/shear) in 1 study,¹⁸  it is noteworthy that none of these elements was found to be predictive in multiple studies in this review. The need for the development and testing of a critical care PI risk tool to accurately detect PI risk persists to provide caregivers a potential edge in the application of evidence-based prevention strategies.

The author recognizes this review has limitations. First, differences in methodologic approaches and risk factors chosen for inclusion and analysis create a degree of difficulty in interpreting and synthesizing these results. Secondly, differences in prevention strategies across the study sites cannot be controlled; thus, for some of these studies it was unclear whether PU prevention strategies were in place at the time of the study. 

PI development in critically ill patients remains a multifactorial phenomenon for which true risk is both pervasive and elusive. This review identified 7 risk factors (age, prolonged ICU admission, diabetes mellitus, cardiac disease, hypotension, vasopressor use, and prolonged mechanical ventilation) as significant predictors in 3 or more studies, with the majority of these factors nonmodifiable and potential contributors to unavoidable PIs. Advancing the science regarding the pathogenesis and physiologic mechanisms that accelerate PI development is imperative in any effort to better understand unavoidable PI. The need for large multisite studies and studies using large datasets capable of validating risk factors unique to the critical care population remains. Enhanced PI risk quantification for this population will aid caregivers in earlier and more targeted risk detection, which has the potential to impact the care delivered to this complex and vulnerable patient population. 

Dr. Cox is an Associate Clinical Professor, Rutgers School of Nursing, Newark, NJ; and an advanced practice nurse/CWOCN, Englewood Hospital and Medical Center, Englewood, NJ.

Please address correspondence to: Jill Cox, PhD, RN, APN-C, CWOCN, 350 Engle Street, Englewood, NJ 07631; email: jillcox@sn.rutgers.edu; jill.cox@ehmchealth.org